Answer: C. Anterior Cruciate Ligament Injury. Based on this patient’s history, presentation of injury mechanism, examination findings, and MRI results, the diagnosis is likely Anterior Cruciate Ligament Tear. ACL tears are one of the most common knee injuries among athletes. They are most common in late adolescence, affecting females 2-8 times more than males2. Athletes who are at greatest risk for tearing their ACL include skiers, soccer players, snow boarders, basketball players, and football players2,3. There are reported average of 90,000 ACL repairs performed in the United States annually, with 1/3,000 reported ACL ruptures2. These numbers vary depending on the gender, sport, and level of competition. There are many risk factors for injuring an ACL. Some intrinsic factors include decreased flexibility or strength, abnormal foot morphology, genetic predisposition, and ligament/leg dominance2. Extrinsic factors to consider include shoe-surface interaction, wet/muddy/uneven playing surface, higher/more aggressive competition, and extreme temperature changes2. Females are reported to have a greater risk of injury due to their anatomy; larger pelvic width, smaller ACL size, increased q angle, valgus deformity, narrow intercondylar notch, generalized joint laxity, and quad dominance2.
The anterior cruciate ligament runs through the knee joint, connecting the posterior lateral femoral condyle to the anterior tibia3. The ACL is the primary source of stabilization for the knee. It helps with rotational stability of the tibia on the femur as well as, more importantly, controlling anterior translation of the tibia on the femur3. ACL injuries can occur due to both contact and noncontact forces. Noncontact injuries make up about 70% of ACL injuries2. Typically, the mechanism is either caused by forceful quadriceps contraction during deceleration of lower extremity, along with a change in direction such as internal rotation with hyperextension (noncontact), or is due to a planted foot with a torque (valgus blow) applied to the lower extremity causing the tissue to tear (contact)2.
Patient’s usually present with a chief complaint of knee pain following an injury where they most often report hearing a “pop” or feeling a “pop” at the time. Often they will mention their pain developed immediately following, with swelling within the next few hours. When asking questions, depending on time since injury, patients will often report decreased range of motion of the knee, stiffness, and feeling of instability3. Upon physical exam, a Lachman test is the most sensitive and useful for testing anterior laxity of the knee4. The anterior drawer test is often positive as well, although not as sensitive. It may show excessive anterior translation of the tibia in comparison to the other knee. Also on exam, decreased ROM and effusion are commonly noted.
As with most orthopedic injuries, x-rays are often the first imaging study to be done. In a case of ligament injury, an x-ray is more important to rule out fracture or other underlying problem but will not help in diagnosing a ligament injury. More detailed than an x-ray, an MRI can diagnose an ACL tear with 95% or better accuracy4. Along with visualizing the tear, 80% of the time bone bruises are seen along both the lateral tibial plateau and lateral femoral condyle4.
Unlike most other ligaments in the knee, the ends of a torn ACL do not reconnect. Therefore, if the patient is young or hoping to return to physical activity, ACL tears require reconstruction via surgery. Prior to surgery, if the injury is strictly ACL related, physical therapy is recommended to help regain range of motion of the knee as well as to strengthen the muscles surrounding the knee. If the patient chooses a nonsurgical approach, they may attempt to return to physical activity slowly following PT clearance. If the patient hopes to return to activity and regain stability, surgical reconstruction is needed. The most commonly used and most successful include autograft bone-patellar tendon-bone, semitendinosus/gracilis hamstring autograft, and bone-patellar tendon-bone allograft reconstructions4. A more recent option, currently still being studied at Boston Children’s Hospital, is the Bridge-Enhanced ACL Repair Clinical Trial (BEAR Trial). This study, currently on stage 3, uses stitches and a scaffold sponge injected with the patient’s blood to act as a bridge to help stimulate healing of the torn ACL1. The benefit is no graft is needed and the patient’s own ACL tissue will be preserved. The goal is to help improve long term health benefits and decrease risk of arthritis in the future.
Overall, studies have shown at least 90% of patients are able to return to play following an ACL tear with physical therapy rehab protocols4. They are typically out of sports for 6 months, then slowly able to return as their quad and hamstrings strengthen. Most patients return to sports following a successful surgery, but there is always the possibility of re-tearing their ACL. The rate can be up to 20% risk of re-tear in teenagers1. Another complication is the increased risk of arthritis 15-20 years post-op, roughly 80% risk1. With the surgical advances today, more and more ACL’s are being reconstructed allowing athletes to return back to what they love to do.

There are many other differential diagnoses to consider when someone presents with a knee injury. Often if it’s an acute injury the patients pain will be diffuse and hard to pinpoint. They also may present with swelling that makes the knee hard to evaluate on physical exam. Another difficulty is the patient guarding on exam or not relaxing the knee due to the pain. All these factors can affect your diagnosis. In this patient’s case, it was less likely a meniscus injury because we would have expected a positive McMurry’s test with more significant joint line tenderness. A tear of the posterior collateral ligament was also less likely based on the mechanism of injury, negative posterior drawer test, and low occurrence of PCL tears in teenage female athletes. Medial/Lateral collateral ligament injuries are less likely based on the patient’s physical exam, with no laxity/significant pain with valgus or Varus stress on the knee. Patellar instability is also a common problem in this population. The patient denied feeling her patella dislocate. Also, if this is what happened, the patient would likely have less pain with minimal effusion still present. Overall, the only way to ensure diagnosis is an MRI and x-ray. In this case, although our history and exam pointed in the direction of an ACL tear, the MRI was able to confirm that therefore ruling out the other possible diagnoses.

References:

1. Bridge-Enhanced ACL Repair Clinical Trial | Boston Children’s Hospital. Boston Children’s Hospital. http://www.childrenshospital.org/aclbeartrial. Accessed December 2, 2018.

2. DynaMed Plus. Anterior Cruciate Ligament (ACL) Injury. https://www.dynamed.com/ topics/dmp~AN~T114675/Anterior-cruciate-ligament-ACL-injury. Published 1995. Updated June 26, 2017. Accessed December 1, 2018.

3. McPhee Sj, Papadakis MA, Rabow MW. Current medical diagnosis & treatment 2017. New York: McGraw Hill Education; 2017.

4. Skinner HB, McMahon PJ. Current Diagnosis & Treatment Orthopedics . 5th ed. McGraw-Hill Education; 2014.

Explanation:
The answer is not seborrheic keratosis. Seborrheic keratoses do not typically bleed and are not erythematous by nature. They do not have rolled borders with central ulcerations, but instead a greasy, stuck-on appearance. The answer is not squamous cell carcinoma. Although skin cancers do bleed sometimes, squamous cell carcinoma has a different appearance. Squamous cell carcinoma appears as a red, elevated thickened nodule with white scaly, or crusted margins. This description is different from basal cell carcinoma. Benign nevus is incorrect because they are usually flesh colored, not pearly or crusty, and do not bleed. Basal cell carcinoma is the correct answer. This diagnosis fits the description in the case vignette.

Bibliography

1. Samarasinghe V, Madan V, Lear JT. Focus on Basal Cell Carcinoma. Journal of Skin Cancer. 2011;2011:328615. doi:10.1155/2011/328615.

2. Long-term recurrence rates in previously untreated (primary) basal cell carcinoma: implications for patient follow-up. Rowe DE, Carroll RJ, Day CL Jr J Dermatology Surgery Oncology. 1989 Mar; 15(3):315-28.

3. Tallon, B. (2016, December). Basal cell carcinoma pathology. Retrieved from https://www.dermnetnz.org/topics/basal-cell-carcinoma-pathology/

4. Wong CSM, Strange RC, Lear JT. Basal cell carcinoma. BMJ: British Medical Journal. 2003;327(7418):794-798.

5. Baheti, A. D. (2015). Basal Cell Carcinoma: A Comprehensive Review for the Radiologist. American Journal of Roentgenology. Retrieved from https://www.ajronline.org/doi/pdf/10.2214/AJR.14.13160

Correct answer is B. The patient is presenting with common symptoms of carpal tunnel syndrome therefore, EMG Nerve Conduction studies are the most appropriate modality. This modality has an over 95% specificity and is able to determine the severity and location of the nerve compression. MRI is incorrect because it is only recommended when the clinical picture is not straightforward or if nerve conduction studies are inconclusive.
Carpal tunnel syndrome is a collection of symptoms caused by compression of the median nerve as it travels through the carpal tunnel in the wrist. Symptoms include pain, paresthesia of the fingers, and less commonly weakness, in the distribution of the median nerve which includes the thumb, index, middle finger and radial half of the ring finger. The classic examination includes performing the Phalen and Tinel test. The Phalen maneuver involves fully flexing the palm at the wrist with the elbow in full extension. Alternatively, the backs of the hands are placed against each other to provide hyperflexion of the wrist with the elbows remaining flexed. Pain and/or paresthesia in the median nerve distribution with one minute of wrist flexion is a positive test. Sensitivity is 68%, specificity is 73%. The Tinel test involves percussion over the proximal or directly on top of the carpal tunnel region. Again, pain and/or paresthesia is a positive test with a 50% sensitivity anda 77% specificity. Treatment options involve splinting, clucocorticoid injection, or surgical decompression.

Sources:
1) Middleton WD, e. (2018). MR imaging of the carpal tunnel: normal anatomy and preliminary findings in the carpal tunnel syndrome. – PubMed – NCBI. [online] Ncbi.nlm.nih.gov. Available at: https://www.ncbi.nlm.nih.gov/pubmed/3492109 [Accessed 8 Jul. 2018].

2) W,B.(2018). Radiologic imaging of the caroal tunnel. –PubMed- NCBI. [online] Ncbi.nlm.nih.gov available at: http://www.ncbi.nlm.nih.gov/pubmed/9283839 [accessed8 Jul. 2018].

3) UpToDate

The answer is B. The patient presents with the signs and symptoms of emphysema. The patient has an FEV1/FVC ration of <70% which indicates an obstructive condition as well as diminished lung sounds which are consistent with emphysema.Chronic bronchitis patients will typically be overweight and cyanotic while those with emphysema will present with a barrel chest, accessory muscle use, and will appear underweight utilizing a puff-like inhalation technique.
Pulmonary function tests (PFTs) are used to confirm the diagnosis and help to determine the type of COPD that a patient has as well as the effectiveness of treatment regimens. The most widely accepted criteria in determining the appropriate treatment according to the disease stage is the GOLD criteria which is composed of 4 stages. Stage 1 = FEV1  80% and the patient should receive a short acting bronchodilator as well as vaccines for pneumonia and influenza. Stage 2 = FEV1 of 50-79% and the patient should add a long acting bronchodilator. Stage 3 = FEV1 of 30-50% and the patient should undergo pulmonary rehabilitation as well as receive an inhaled corticosteroid for acute flare-ups. Stage 4 = cor pulmonale, heart or respiratory failure or an FEV1  30%. These patients should add oxygen therapy to their regimen. Additionally, if the SPO2% drops below 88% or the PaO2 drops below 55mmHg then the patient should also begin oxygen therapy.

References:
1. COPD. dynamed.com. http://www.dynamed.com/topics/dmp~AN~T115557#Epidemiology. Published January 19, 2018. Accessed February 7, 2018.
2. Ferguson G, Make B. Management of Stable Chronic Obstructive Pulmonary Disease. UpToDate.
3. Papadakis MA, McPhee SJ, Rabow MW. 2017 Current medical diagnosis and treatment. New York.,
NY: McGraw Hill Education; 2017.
4. Williams DA. PANCE prep pearls: a medical study and review guide for the PANCE, PANRE & medical
examinations. North Charleston, SC: CreateSpace Independent Publishing Platform; 2017.

Answer: B, Endometrial biopsy
Endometrial cancer is the most common gynecologic malignancy and is most common in women who are perimenopausal or postmenopausal 3. It is a malignancy of the lining of the uterus. Ninety six percent of all uterine cancers occur in women who are older than 40 1. Endometrial cancer most commonly presents with abnormal uterine bleeding, in this case, postmenopausal bleeding. However, patient’s may also present with pelvic pain, abdominal pain, or changes in urination or bowel function 3. Risk factors include unopposed estrogen, nulliparity, history of infertility, irregular menses, obesity, high blood pressure, and a first degree relative with endometrial cancer 2. The patient may have a history of obesity, hypertension, or diabetes mellitus as these are common comorbid conditions 2. Transvaginal ultrasound with or without saline infused sonohysterography may be performed to measure the thickness of the endometrial lining. An endometrial lining greater than 4mm is an indication for biopsy of the endometrium 1. Diagnosis is confirmed via biopsy with histology. In patient’s whose biopsy comes back and is non-diagnostic, dilation and curettage may be performed 1. Dilation and curettage is more invasive than an endometrial biopsy and is therefore not a first line diagnostic tool for endometrial cancer unless there are complicating factors such as cervical stenosis or significant discomfort with biopsy 1. Pap smears are not a diagnostic tool for endometrial cancer. Pap smears that come back normal do not rule out endometrial cancer 1. If a pap smear comes back with abnormal cells in a patient that has endometrial cancer, it may be evidence of advanced disease 1. Pap smears should be performed on all women without history of cervical cancer or HPV every 3-5 years between the ages of 21 and 65 to screen for cervical dysplasia. Laparoscopy is the diagnostic tool of choice for patients with endometriosis where endometrial tissue may be found outside of the uterus for example on the ovaries or in the pelvis 2. Laparoscopy will typically not show any abnormalities with endometrial cancer unless there is metastasis into the abdominal cavity or the primary tumor involves the bladder and bowel 1. Staging is based on the primary tumor, the regional lymph nodes, and whether or not there is distant metastasis 1. The primary treatment for endometrial cancer is to perform a total abdominal hysterectomy with bilateral salpingo-oopgorectomy. Lymphadenectomy should be done based on the stage of cancer 3. Chemotherapy and radiation may be used as an added treatment modality 1. Radiation therapy alone may be used in patients who are not candidates for surgery such as those who are morbidly obese, have unresectable disease, or have other medical contraindications 3. Patients who have recurrence may be managed with high dose progestins or antiestrogens 2. Regular follow ups for pelvic and rectal exams should be done for patients with endometrial cancer every 3-6 months for 2 years and then every 6 months for 3 years 1.

References:
1. Endometrial Cancer. In DynaMed Plus [database online]. EBSCO Information Services. http://www.dynamed.com/topics/dmp~AN~T113952/Endometrial-cancer. Updated May 24, 2017. Accessed February 1, 2018.
2. O’Connell C. A Comprehensive Review For The Certification And Recertification Examinations For Physician Assistants. 5th ed. Lippincott Raven; 2015:151-153.
3. Endometrial Carcinoma. In UpToDate [database online]. Wolters Kluwer. https://www.uptodate.com/contents/overview-of-endometrial-carcinoma. Updated August 22, 2017. Accessed February 2, 2018.

Correct answer is A. Campylobacter jejuni, a gram-negative bacterium, is the most common cause of bacterial enteritis in the US and the second most common cause of foodborne disease behind Salmonella. It typically comes from the intestinal tracts of animals, the most common being poultry, but can also come from contaminated water and unpasteurized milk. Typical incubation period is no more than 3 days. Shigella sonnei is usually associated with more severe diarrhea described as explosive with mucous or blood. Vibrio Cholera usually causes high volume diarrhea that is odorless and described as “rice water.” Giardia lamblia is associated with swimming or drinking from a fresh water source commonly associated with camping or outdoor activities. The diarrhea from Giardia is more described as “frothy, greasy or foul.” E. coli is usually associated with more significant bloody diarrhea and is most commonly found in beef.

Other symptoms associated with Campylobacter include fever, body aches, headache, dizziness and sometimes vomiting that may occur before the onset of diarrhea. Neurological symptoms such as progressive muscle weakness may indicate Guillain-Barre syndrome as Campylobacter is the most commonly identified causing agent of this disorder. The diagnosis is most commonly made with a stool culture. Campylobacter induced enteritis is usually self-limited. Most cases do not require antibiotics and education on supportive care with hydration and correcting electrolyte imbalances is sufficient. Antibiotics may shorten the duration if infection. Azithromycin 1 gram single dose or 500mg twice a day for 3 days can be used. Fluoroquinolones are also effective but have increased incidence of resistance and should not be first line.

References:
1. Williams DA. PANCE Prep Pearls: A Medical Study and Review Guide for the PANCE, PANRE & Medical Examinations. 2nd ed. North Charleston, SC: CreateSpace Independent Publishing Platform; 2017.
2. Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment 2017. (Rabow MW, ed.). McGraw Hill Education and Lange Medical Publications; 2017.
3. Russell SM. Salmonella and Campylobacter: A Methods Update. Food Safety Magazine. https://www.foodsafetymagazine.com/magazine-archive1/december-2004january-2005/salmonella-and-campylobacter-a-methods-update/. Published 2005.
4. Allos BM. Uptodate: Clinical manifestations, diagnosis, and treatment of Campylobacter infection. UpToDate, Inc. https://www.uptodate.com/contents/clinical-manifestations-diagnosis-and-treatment-of-campylobacter-infection?search=infectious colitis&source=search_result&selectedTitle=5~150&usage_type=default&display_rank=5. Published November 3, 2017.

Correct answer is C. The risk factors associated with Peptic Ulcer Disease (PUD) include: Helicobacter Pylori, NSAID use, smoking, cytomegalovirus, Crohn’s disease, genetic factors, and associated conditions (hiatal hernia, Meckel diverticulum). H. pylori has a high urease activity that protects it from gastric acid secretions and stimulates increased acid secretion which can result in ulcers in the stomach or duodenum. Patients typically described a “gnawing” pain in the epigastric region which usually starts 2-5 hours after eating a meal and is relieved with eating and with antacids.
Testing options include breath, stool and serology samples. Treatment typically involves one of two options: triple therapy (PPI, clarithromycin, and amoxicillin or metronidazole) or quadruple therapy (bismuth subsalicylate, metronidazole, tetracycline and a PPI), either is given X 14 days.
References:
1. Peptic Ulcer Disease. Dynamed. http://www.dynamed.com/topics/dmp~AN~T116374/Peptic-ulcer-disease#General-Information. Accessed February 7, 2018.
2. National Institute for Health and Clinical Excellence (NICE). Dyspepsia and gastro-esophageal reflux disease: Investigation and management of dyspepsia, symptoms suggestive of gastro-esophageal reflux disease, or both. NICE 2014 Sep:CG184 PDF
3. Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. Lancet. 2009 Oct 24;374(9699):1449-61, commentary can be found in Lancet 2010 Feb 13;375(9714):553

Correct answer is D. The ascending weakness/paralysis described is characteristic of Guillain-Barre syndrome (GBS) and can affect not only the muscles of the extremities but also the respiratory muscles and less commonly, the bulbar muscles. Because of this many patients with GBS develop respiratory failure as the syndrome progresses. Fasciculations are commonly found in patients with ALS who will likely also have hyperreflexia. Optic Neuritis is a common symptom of Multiple Sclerosis and there is usually hyperreflexia and a positive Babinski. Ptosis is a common symptom of patients with Myasthenia Gravis and can be fatigable. Reflexes and sensation are usually normal throughout.

GBS is defined as an immune-mediated acute polyneuropathy that is most often preceded by an infection and usually presents as ascending weakness and absent or decreased deep tendon reflexes with mild sensory deficits. Symptoms progresses over two weeks’ time reaching the end at four weeks. Diagnostic criteria include: 1) progressive weakness of legs and arms, which can range from mild to paralyzing and 2) decreased reflexes or areflexia in the effected extremities. Diagnosis is typically supported by CSF which characteristically demonstrates elevated protein with normal white cell count.

Supportive care is the key to treatment of all patients with GBS. It is common for patients to be monitored in the ICU due to cardiac and respiratory complications of the disease, as upwards of 30% of patients develop respiratory failure during their course of the disease requiring mechanical ventilation. Plasma exchange or Immune Globulin (IVIG) is the standard of care. Deciding between the two treatments options is based on availability and patient/provider preference. Patients and their families must be aware that it can take upwards two to three months before some patients are able to walk without assistive devices.

References:
1. Dimachkie MM, Barohn RJ. Guillain-Barré Syndrome and Variants. Neurologic clinics. 2013;31(2):491-510. doi:10.1016/j.ncl.2013.01.005.
2. Hahn AF. Guillain-Barre syndrome. Lancet. 1998 Aug 22;352(9128):635-41.
3. Seneviratne U. Guillain-Barre syndrome. Postgrad Med J. 2000 Dec;76(902):774-82.
4. Vriesendorp, F., MD. Guillain-Barré syndrome in adults: Clinical features and diagnosis. 2017, August 21.

The answer is C. A Lisfranc injury is a disruption of the tarsometatarsal joint (TMT) causing a displacement between the 1st and 2nd metatarsals either with or without fracture. A Jones fracture is a fracture through the diaphysis of the fifth metatarsal. A Maisonneuve fracture is a spiral fracture of the proximal fibula. It is caused by the rupture of the distal talofibular syndesmosis and the interosseous membrane due to a distal medial malleolar fracture and/or a deltoid ligament rupture. A Charcot’s joint occurs when the joint of the midfoot is damaged and destroyed secondary to peripheral neuropathy from diabetes mellitus or peripheral vascular disease. Radiographs of a Charcot foot will show obliteration of the joint space.

The diagnosis of a Lisfranc injury requires a high degree of clinical suspicion. Injuries to the tarsometatarsal joint can be very subtle and are not always seen on radiographs. Approximately, 20% of the Lisfranc injuries initially go undiagnosed and nearly 40% do not receive treatment within the first week. AP, lateral and obliques radiographs are recommended to help diagnose a Lisfranc injury. Comparing views in weight bearing x-rays are sometimes helpful if non-weightbearing films are inconclusive.

Treatment of Lisfranc injuries can be both operative and nonoperative depending on the severity of the joint damage. Nonoperative injuries include sprains and nondisplaced ligamentous injuries. These patients are placed in a non-weight bearing cast for six weeks followed by a weight bearing cast for an additional four to six weeks. The most common surgical approach to a Lisfranc injury is open reduction internal fixation (ORIF). Approximately 25% of patients who undergo ORIF for a Lisfranc injury will experience complications including broken hardware and arthritis. Posttraumatic arthritis, compartment syndrome, infection, complex regional pain syndrome, neurovascular injury, and nonunion are potential complications.

References
1. Physiopedia contributors. Foot and Ankle Structure and Function. Physiopedia. https://www.physio-pedia.com/Foot_and_Ankle_Structure_and_Function. Published February 8, 2018.

2. Taylor T. Gliding Joint – Pivot Joints. InnerBody. http://www.innerbody.com/image_skel07/skel32.html#continued.

3. Egol KA, Koval KJ, Zuckerman JD. Handbook of Fractures. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.

4. Jain M. Lisfranc’s amputation. LinkedIn Corporation. https://www.slideshare.net/mahaksayz/lisfranc-injury-72776736. Published March 3, 2017.

5. Blomberg J. Lisfranc Injury (Tarsometatarsal fracture-dislocation). Orthobullets. https://www.orthobullets.com/foot-and-ankle/7030/lisfranc-injury-tarsometatarsal-fracture-dislocation.

6. Fischer SJ. Lisfranc (Midfoot) Injury – OrthoInfo – AAOS. Lisfranc (Midfoot) Injury. https://orthoinfo.aaos.org/en/diseases–conditions/lisfranc-midfoot-injury/.

7. Wheeless CR. Wheeless’ Textbook of Orthopaedics. Wheeless Online. http://www.wheelessonline.com/ortho/orif_of_lisfrancs_fracture. Published September 4, 2012.

8. Williams DA. PANCE PREP PEARLS. 2nd ed. North Charleston, SC: CreateSpace Independent Publishing Platform; 2017.

Correct answer is C. The patient’s symptoms are most consistent with intermittent claudication secondary to peripheral artery disease (PAD). Deep Vein thrombosis (DVT) occurs when a blood clot develops in the deep venous system. On presentation, there will be unilateral leg pain, pitting edema, increase calf circumference and possible tenderness at the site of the clot. Chronic venous insufficiency is a condition in which the valves in the leg veins are not working effectively. This causes blood to collect in these veins resulting in progressive pitting edema of the leg. For superficial venous thrombosis, the pain is localized to the site of the superficial thrombus. The skin is generally indurated, warm, and tender with a possible palpable cord extending along the superficial vein and is most common along the saphenous vein.

The most common cause of PAD in adults older than 40 years old is atherosclerosis. The other causes of PAD are thrombosis, embolism, trauma, vasculitis (Giant cell and Takayasu’s arteritis), fibromuscular dysplasia, and entrapment (thoracic outlet syndrome). Risk factors believed to contribute to the plaque formation are cigarette smoking, diabetes mellitus, hypercholesterolemia, and hypertension. Symptoms include pain, aching, cramping, numbness or muscle fatigue or atrophy. An ankle brachial index (ABI) of  0.9 is diagnostic of PAD. All pt’s with PAD should be counseled on smoking cessation and aggressive management of risk factors (BP, cholesterol, and glucose control). The primary medication with evidence for improved claudiacation is cilostazol, a phosphodiesterase inhibitor that suppresses platelet aggregation and is a direct arterial vasodilator. Antiplatelet agents may provide some improvement. Surgical options include angioplasty/stenting and bypass graft.

Reference
1. Peripheral Artery Disease. National Heart Lung and Blood Institute. https://www.nhlbi.nih.gov/health-topics/peripheral-artery-disease.

2. Deep vein thrombosis (DVT). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557. Published July 12, 2017.

3. Superficial Thrombophlebitis. Background, Pathophysiology, Etiology. https://emedicine.medscape.com/article/463256-overview. Published August 17, 2017.

4. Venous Insufficiency. Background, Anatomy, Pathophysiology. https://emedicine.medscape.com/article/1085412-overview. Published September 29, 2017.

5. Clinical features and diagnosis of lower extremity peripheral artery disease. Uptodate.
https://www.uptodate.com/index.html#!/contents/clinical-features-and-diagnosis-of-lower-extremity-peripheralarterydisease?search=Peripheral%20artery%20disease&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 .

Correct answer: C (Primary hyperparathyroidism).

Rationale:
Normally, elevated plasma calcium suppresses PTH secretion. However, in primary hyperparathyroidism (PHPT), PTH secretion from autonomously functioning parathyroid adenomas or parathyroid hyperplasia is not suppressed. This patient has hypercalcemia with an elevated PTH level, suggesting PHPT. PHPT leads to increased bone turnover, low bone mineral density, and increased fracture risk. These effects are, however, preferentially seen in the distal forearm, which is rich in cortical bone. Bone density is lowest at the forearm in patients with PHPT, and the worst T-score is commonly found in the distal forearm in patients with PHPT9.

Choice A: Incorrect. Milk-alkali syndrome is characterized by hypercalcemia caused by ingestion of large amounts of calcium and absorbable alkali (e.g., calcium-containing antacids). Calcium would be elevated, but PTH would be suppressed. Dietary supplements taken to prevent osteoporosis are common sources of calcium and alkali.10

Choice B: Incorrect. Hyperthyroidism, if left untreated, can cause rapid bone loss, leading to osteoporosis and increased risk of fracture. All patients with primary hyperthyroidism have a low TSH. However, the TSH in this patient is normal, suggesting that she does not have hyperthyroidism.11

Choice D: Incorrect. Hypoparathyroidism is characterized by low serum calcium, increased serum phosphate, and low serum parathyroid hormone levels. This patient has hypercalcemia with an elevated PTH level.12

References:

1. Riggs BL, Melton LJ 3rd. The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone. 1995;17(5 Suppl):505S.

2. National Osteoporosis Foundation, http://www.nof.org 2011.

3. Hudec SM, Camacho PM. Secondary causes of osteoporosis. Endocr Pract. 2013;19(1):120-128.

4. Griebeler ML, Kearns AE, Ryu E, Hathcock MA, Melton LJ, Wermers RA. Secular Trends in the Incidence of Primary Hyperparathyroidism Over Five Decades (1965-2010). Bone. 2015;73:1-7.

5. Bilezikian JP, Silverberg SJ. Clinical practice. Asymptomatic primary hyperparathyroidism. N Engl J Med. 2004;350(17):1746.

6. Cosman F, de Beur SJ, LeBoff MS, et al. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-81.

7. Silverberg SJ, Shane E, Jacobs TP, et al. A 10-year prospective study of primary hyperparathyroidism with or without parathyroid surgery. N Engl J Med. 1999; 341(17):1249-1255.

8. Hofbauer LC, Hamann C, Ebeling PR. Approach to the patient with secondary osteoporosis. Eur J Endocrinol. 2010;62(6):1009-1020.

9. Wood K, Dhital S, Chen H, Sippel RS. What is the utility of distal forearm DXA in primary hyperparathyroidism? Oncologist. 2012; 17(3):322-325.

10. Patel AM, Adeseun GA, Goldfarb S. Calcium-Alkali Syndrome in the Modern Era. Nutrients. 2013;5(12):4880-4893.

11. De Leo S, Lee SY, Braverman LE. Hyperthyroidism. Lancet (London, England). 2016;388(10047):906-918.

12. Abate EG, Clarke BL. Review of Hypoparathyroidism. Frontiers in Endocrinology. 2016;7:172.

Correct answer is E. Schizophrenia is a mental disorder in which the mind of the patient and reality do not agree. Drug addiction could fit the scenario, but her pupils are reactive and her affect is flattened. Bipolar disorder is characterized by episodes of mania, hypomania, and major depression with delusions and hallucinations possible but usually without frank paranoia. Brief psychotic disorder would only have symptoms lasting less than six months. B-12 deficiency can cause some psychological symptoms, very closely resembling schizophrenia but the psychotic symptoms occur along with anxious symptoms. This patient did not have the hyper-anxious symptoms and exhibited more flattened symptoms.
Schizophrenia commonly occurs in late adolescence or early adulthood, between ages of 16-45. Males will have a slightly younger onset age than females. Symptoms should be present for 6 months to confirm the diagnosis. Risk factors include genetics, environmental and socioeconomic factors. The period of onset is referred to as the prodromal phase which is characterized by the negative symptoms of the disease. Negative symptoms of schizophrenia include lack of motivation, lack of attention and social isolation, decline in self-care, and flattened affect. Positive symptoms which are more difficult to notice in the patient are hallucinations, delusions, debilitating thoughts. Patients with paranoid schizophrenia can be so overwhelmed by the positive symptoms that they are unable to lead a normal life.
Antipsychotics are the treatment of choice to ease the positive symptoms. First generation medications for schizophrenia include Chlorpromazine, Fluphenazine, Haloperidol, Perphenazine, and Thiothixene. Second generation medications include Aripiprazole, Asenapine, Olanzapine, Quetiapine, and Risperidone. These medications can be used alone or in a cocktail to provide the greatest relief to the patients for symptom relief. These medications have a lot of side effects that can be a deterrent to the patient including weight gain, sexual problems, drowsiness, dizziness, restlessness, dry mouth, constipation, blurred vision, hypotension, and seizures.

References
1. Childhood trauma linked to schizophrenia. ScienceDaily. https://www.sciencedaily.com/releases/2012/04/120419102440.htm. Published April 19, 2012. Accessed July 8, 2018.
2. Misdiagnosis of Schizophrenia, Paranoid Schizophrenia. The History of Schizophrenia. http://schizophrenia.com/family/misdiag.html. Accessed July 8, 2018.
3. Paranoid Schizophrenia: Overview of Causes, Symptoms, & Treatments. PsyCom.net – Mental Health Treatment Resource Since 1986. https://www.psycom.net/paranoid-schizophrenia. Accessed July 8, 2018.
4. schizophrenia P. What Is Paranoid Schizophrenia? WebMD. https://www.webmd.com/schizophrenia/guide/schizophrenia-paranoia#1. Accessed July 8, 2018.
5. Tufan AE, Bilici R, Usta G, Erdoğan A. Advances in pediatrics. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3404901/. Published 2012. Accessed July 8, 2018.

A. Agranulocytosis is a blood dyscrasia. It is characterized by symptoms such as sore throat, fever, malaise, and mouth sores, as well as possibly other flu like symptoms. Agranulocytosis is diagnosed using a CBC w/Differential to determine the presence of leukopenia, or agranulocytosis. Patients at risk for developing agranulocytosis are either conventional or atypical antipsychotics. If not properly diagnosed and treated, agranulocytosis can result in death. Treatment generally includes removing the offending agent and monitoring for any signs/symptoms of infection and treating those accordingly.

B. Serotonin Syndrome is associated with the use of SNRIs/SNRIS/MAOIs and is characterized by abdominal pain, diarrhea, diaphoresis, fever, tachycardia, elevated blood pressure, delirium, muscle spasms, increased motor activity, irritability/mood swings, hostility, irrational thought process, and seizures. In severe cases, fever can become dangerously high and there is risk of cardiovascular shock and even death. Serotonin Syndrome is rare but life-threatening and is the possible result of too high a dose of an antidepressant medication or interactions with other medications. Risk for Serotonin Syndrome is highest when an SSRI/SNRI is combined with an MAOI or when an MAOI is given to someone who was taking an SSRI/SNRI without at least a 14 day (but up to 5 week) washout period of the SSRI/SNRI.

C. Neuroleptic Malignant Syndrome (NMS) is associated with the use of antipsychotic medications and is characterized by reduced consciousness, muscular rigidity, tachycardia, diaphoresis, hyperpyrexia, drooling, tachypnea, and labile hypertension. NMS is a life threatening medical emergency and thought to be connected to a change in brain dopamine activity. While it usually occurs early in therapy, it can occur at any point during medication therapy. Approximately 10% of cases result in death.

D. Tardive Dyskinesia (TD) is associated with the use of antipsychotic medications and is characterized by involuntary tonic muscular contractions of the face, limbs, or trunk. While TD is serious, it is not life threatening. Women and older adults are more at risk for developing TD. It affects up to 50% of those receiving long term antipsychotic medications. Symptoms involving the face include protruding/rolling tongue, smacking or licking of the lips, blowing type movement of the lips. Symptoms involving the limbs include pill rolling (fingers), choreic movements (rapid, purposeless, irregular) and/or athetoid movements (slow, complex, serpentine-like). Symptoms involving the trunk include neck and shoulder movements, hip movements (jerks and rocking motions).

References:
Herzog, E. A. & Varcarolis, E. M. (2010). Schizophrenia. In Varcarolis, E. M. & Halter,
M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 306-343). St. Louis, MO: W.B. Saunders.

Kozy, M. &Varcarolis, E. M. (2010). Depressive Disorders. In Varcarolis, E. M. &
Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 246-279). St. Louis, MO: W.B. Saunders.

Generalized Anxiety Disorder (GAD), which lasts 6 months or more, is characterized by excessive anxiety or worry about numerous things, usually in excess of the event or situation about which the person is worried. Worries are usually related to daily life stressors, such as finances, relationships, job related concerns, etc. Symptoms include restlessness, fatigue, an inability to concentrate/focus, irritability, tension, and poor sleep.

Acute Stress Disorder shares symptoms similar to Post-Traumatic Stress Disorder (PTSD), such as poor sleep, irritability, flashbacks, avoidant behaviors, etc. However, there are 3 hallmark differences between the two disorders: length of time to onset of symptoms (within one month following the traumatic event for Acute Stress Disorder), length of time to resolution of symptoms (no more than 4 weeks for Acute Stress Disorder) and presence of at least 3 dissociative symptoms either during or after the traumatic event (Acute Stress Disorder). Dissociative symptoms include emotional numbing/detachment, reduced awareness of surroundings, depersonalization (sense of unreality related to self), derealization (sense of unreality related to the environment), and loss of memory of an important aspect of the trauma.

Obsessive Compulsive Disorder (OCD) is characterized by obsessions and/or compulsions. Obsessions, (thoughts, impulses, or images) are pervasive and unable to be dismissed. Typically, individuals experiencing obsessive thoughts don’t want to have the thoughts and being unable to stop them causes severe anxiety. Compulsions (the behaviors) are ritualistic in nature and individuals feel driven to perform them in an attempt to temporarily reduce or relieve the anxiety. Because the relief is only temporary, the compulsive act must be repeated again and again. Obsessions and compulsions are considered problematic when they begin to interfere with daily functions and lead to an inability to focus on anything but the obsession or compulsion.

Post-Traumatic Stress Disorder (PTSD) refers to a set of symptoms experienced after witnessing or being a part of a traumatic event, such as a car accident, fire, natural disaster, etc. Symptoms can occur any time after the traumatic event-as early as a few months after, or as long as several years after the event. Symptoms include: re-experiencing the event, including flashbacks, nightmares, and intrusive thoughts, and can be triggered by internal or external factors. Diagnostic criteria also includes avoidant type behaviors, such as staying away from people, places, or things that trigger thoughts of the event, feeling numb and disinterested, including anhedonia, feelings of guilt or depression, and an inability to recall the traumatic event. People with PTSD tend to be hypervigilant, have an easy startle response, difficulty sleeping, and are described as irritable or edgy. PTSD also includes symptoms such as inability to focus/concentrate, poor memory regarding the traumatic event, and a negative outlook. To make the diagnosis, symptoms have to be present for at least one month duration and a person must experience at least one re-experiencing and one avoidance symptom, and two each of the arousal/reactivity and mood/cognition criteria.

References

National Institute of Mental Health. (2016). Post-Traumatic Stress Disorder. Retrieved
March 20, 2016, from http://www.nimh.nih.gov/health/topics/post-traumatic-stress-disorder-ptsd/index.shtml.

Halter, M. J., Varcarolis, E. M. & Shoemaker, N. C. (2010). Anxiety and Anxiety Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 212-245). St. Louis, MO: W.B. Saunders.

Pancreatitis is a medical condition, specifically an inflammatory disorder of the pancreas. While it can be associated with chronic alcohol use, this is not always the cause of pancreatitis. Symptoms are typically physical in nature, and do not include psychiatric symptoms, as mentioned in the above patient. Symptoms of pancreatitis include, but are not limited to, nausea and vomiting, abdominal pain and distention.

Delirium tremens (DTs), also referred to as alcohol withdrawal delirium, generally occurs 2 to 3 days (though onset can occur later than that) after alcohol cessation or reduction in alcohol intake, and can last for 2 to 3 days. Delirium tremens/alcohol withdrawal delirium is characterized by agitation, insomnia, anxiety, change in cognition (confusion, disorientation, etc.), hallucinations (visual, tactile, etc.), and mood disturbance. Physical symptoms include elevated blood pressure, tachycardia, and diaphoresis. Delirium tremens/alcohol withdrawal delirium is considered a medical emergency and can result in death even if treated.

Post-acute withdrawal syndrome (also known as protracted withdrawal) can occur any time after the acute withdrawal phase has passed, usually at least 7 days after last use of alcohol. It can last anywhere from a few days or weeks up to two or three years. Symptoms can include, but are not limited to, sleep disturbance, anxiety, mood lability, including irritability and depression, short-term memory difficulties, and fatigue.

Sleep deprivation occurs when one doesn’t get enough sleep, sleeps at the wrong time of the day, or does not get good quality sleep. Signs and symptoms can include feeling tired and unrested upon awakening, poor focus and concentration, difficulty remembering things, difficulty learning things, low frustration tolerance, difficulty making decisions, slowed reaction time (i.e. such as when driving a car), slower to finish tasks and likely to make more mistakes, irritability, and worried thinking.

References

Councill III, J., Halter, M.J. & Smith-Dijulio, K. (2010). Addictive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 402-432). St. Louis, MO: W.B. Saunders.

Huether, S.E. (1998). Alterations of Digestive Function. In McCance, K.L. & Huether, S.E. (Eds), Pathophysiology: The Biologic Basis for Disease in Adults and Children (pp. 1322-1379). St. Louis, MO: Mosby-Year Book, Inc.

U.S. Department of Health & Human Services, National Institutes of Health, National Heart, Lung and Blood Institute. (2012). What are Sleep Deprivation and Deficiency? Retrieved March 20, 2016 from http://www.nhlbi.nih.gov/health/health-topics/topics/sdd. U.S. Department of Health & Human Services, Substance Abuse and Mental Health Services Administration, Center for Substance Abuse Treatment. (2010).

Venlafaxine is not a recommended choice due to the patient’s history of non-compliance with medications. Abrupt discontinuation of venlafaxine without a taper over the course of several weeks, is known to cause an intolerable discontinuation syndrome. Symptoms of discontinuation syndrome include anxiety, dysphoria, various flu like symptoms (i.e. sweats, chills, body aches, nausea), dizziness, excessive sweating, and insomnia.

Sertraline is the best choice at this time. While all SSRIs have the potential to cause a discontinuation syndrome when abruptly stopped, sertraline is among the safer SSRIs due to its longer half-life. Fluoxetine is the safest. However, the patient could not remember the past benefits, if any, and therefore a retrial is not necessarily indicated. The results of abrupt discontinuation are an important consideration in patients with a history of non-compliance. Sertraline is also effective for binge eating behaviors.

Bupropion is contraindicated when there is a history of anorexia/bulimia, or when there has been an abrupt discontinuation of alcohol use. Bupropion is associated with an increased risk for seizures and is contraindicated for use in patients who purge. Bupropion is known to lower the seizure threshold. Purging also lowers the seizure threshold due to causing imbalance in electrolytes.

Although it is possible that fluoxetine helped this patient in high school, her condition ultimately worsened, suggesting that the medication failed and that a different one is warranted.

References

Hirsch, M. & Birnbaum, Robert J. Selective serotonin reuptake inhibitors:pharmacology, administration, and side effects. In: UpToDate, Post TW (Ed.), UpToDate, Waltham, MA. (Accessed on February 7, 2016.)

Hirsch, M. & Birnbaum, Robert J. Atypical antidepressants: Pharmacology,administration, and side effects. In: UpToDate, Post TW (Ed.), UpToDate, Waltham, MA. (Accessed on February 7, 2016.)

Harvey, Richard A. & Champe, Pamela C. (Eds.). (2009). Pharmacology. Baltimore:Lipincott Williams & Wilkins.

Although indicated for other anticholinergic syndromes, the use of physostigmine is contraindicated in the setting of TCA toxicity due to association with cardiac arrest.

Procainamide is also contraindicated, as it is an inhibitor of rapid sodium channels, which will only heighten the TCAs effect.
The use of magnesium sulfate is known to help control cardiac arrhythmias, but is reserved only for cases of TCA toxicity which are refractory to initial sodium bicarbonate treatment.

Sodium bicarbonate is the correct answer. The patient is experiencing symptoms of a toxic exposure to tricyclic antidepressants (TCAs), as revealed in her history of taking more than the prescribed dose of amitriptyline. TCA overdose commonly presents as cardiac toxicity, usually in the form of tachycardic arrhythmias. QRS prolongation and other ECG findings, such as exaggerated S and R waves, are usually found in the setting of cardiac toxicity. Other symptoms include anticholinergic effects such as flushing, dry mouth, blurred vision, urinary incontinence, sedation, confusion, etc. The anticholinergic effects of TCAs are further precipitated by alcohol consumption. Rapid intravenous (IV) sodium bicarbonate is the initial management for TCA toxicity with cardiac manifestations. This will work to decrease the QRS interval and prevent the potential evolution of fatal tachyarrhythmia, such as ventricular tachycardia (VT) or ventricular fibrillation (VF).

References

Kerr, G. W., McGruffie, A. C., & Wilkie, S. (n.d.). Tricyclic antidepressant overdose: A review. In Emerg Med J 2001;18:236–241. Retrieved June 11, 2016, from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1725608/pdf/v018p00236.pdf

Schneider, G. (May 2003). Never Use Physostigmine in a TCA Overdose. In Emergency Medicine News, 25(5); 44. Retrieved June 11, 2016, from http://journals.lww.com/em-news/Fulltext/2003/05000/Never_Use_Physostigmineiin_a_TCA_Overdose.30.aspx

Stevens-Johnson Syndrome is characterized by symptoms such as tongue/facial swelling, hives, skin pain, red or purple rash that spreads within a few hours up to several days, and blistering and shedding of the skin. These symptoms can be precipitated by more generalize flu-like symptoms such as fever, cough, fatigue, and sore throat. Stevens-Johnson Syndrome is often associated with medications, such as lamictal. It is a medical emergency and requires medical intervention, including hospitalization. Treatment includes removing the offending agent (if it’s medication induced), fluid and nutrition management, medications to treat pain, itching, or infection, wound care, and eye care if the symptoms involve the eyes.

Cellulitis is a skin infection caused by staphylococcus and affects the dermis and subcutaneous layers of the skin. Cellulitis is generally secondary to a skin wound, ulcer, infected hair follicles, or boils. Presentation of the affected area includes swelling, pain, and erythema. Treatment includes antibiotics.

Folliculitis is a bacterial infection of the hair follicle, typically caused by staphylococcus aureus that has spread in to the opening of the hair follicle. Folliculitis presents as pustules surrounded by erythema, generally without systemic symptoms. Contributing factors to folliculitis include poor hygiene, prolonged moisture on the skin, and/or skin trauma. Treatment may include topical antibiotics as well as cleaning the area with warm water and soap.

Eczema is a general term that refers to various types of skin swelling. Eczema is also referred to as dermatitis. Eczema generally refers to an inflammatory skin disorder that causes dry, itchy skin, as well as rashes on the face, hands, and feet as well as inside the elbow and behind the knees. There is not a known cause, though it can be related to environmental factors, such as skin irritants or various allergies. Treatment depends upon the cause of the eczema but may include use of moisturizers, antihistamines or topical steroids to help reduce the itching, and avoiding anything that is known to worsen the condition.

References

Huether, S.E. (1998). Structure, Function, and Disorders of the Integument. In McCance, K.L. & Huether,S.E. (Eds), Pathophysiology: The Biologic Basis for Disease in Adults and Children (pp. 1517-1554). St. Louis, MO: Mosby-Year Book, Inc.

Stevens-Johnson syndrome. (n.d.). Retrieved May 14, 2016, from http://www.mayoclinic.org/diseases-conditions/stevens-johnson-syndrome/basics/treatment/con-20029623

Pancreatitis is a medical condition, specifically an inflammatory disorder of the pancreas. While it can be associated with chronic alcohol use, this is not always the cause of pancreatitis. Symptoms are typically physical in nature, and do not include psychiatric symptoms, as mentioned in the above patient. Symptoms of pancreatitis include, but are not limited to, nausea and vomiting, abdominal pain and distention.

Cirrhosis is an inflammatory disease of the liver and is irreversible. Cirrhosis typically develops slowly over a number of years, though severity and rate of progression are dependent upon the cause. Contributing factors can include alcoholism and hepatitis. Signs and symptoms of cirrhosis can include, but are not limited to, jaundice, nausea, weight loss, fatigue, swelling, accumulation of fluid in the abdomen.

Hypothyroidism refers to an underactive thyroid, meaning it does not produce enough thyroid stimulating hormone (TSH). While hypothyroidism is physiological in nature, it can often times present like a depressive disorder. Signs and symptoms of hypothyroidism can include, but are not limited to, weight loss, fatigue, depression, poor memory, body aches, and muscle weakness. Hypothyroidism can be the result of things such as autoimmune disorders, treatment of hyperthyroidism, and medications. Hypothyroidism is usually diagnosed by obtaining a TSH level, and at times, other thyroid tests such as Free T3 and T4. Treatment is usually with a thyroid hormone replacement medication, such as levothyroxine.

Serotonin Syndrome is associated with the use of SNRIs/SNRIS/MAOIs and is characterized by abdominal pain, diarrhea, diaphoresis, fever, tachycardia, elevated blood pressure, delirium, muscle spasms, increased motor activity, irritability/mood swings, hostility, irrational thought process, and seizures. In severe cases, fever can become dangerously high and there is risk of cardiovascular shock and even death. Serotonin Syndrome is rare but life-threatening and is the possible result of too high a dose of an antidepressant medication or interactions with other medications. Risk for Serotonin Syndrome is highest when an SSRI/SNRI is combined with an MAOI or when an MAOI is given to someone who was taking an SSRI/SNRI without at least a 14 day (but up to 5 week) washout period of the SSRI/SNRI.

References

Cirrhosis. (2016). Retrieved May 14, 2016, from http://www.mayoclinic.org/diseases-conditions/cirrhosis/home/ovc-20187218

Huether, S.E. (1998). Alterations of Digestive Function. In McCance, K.L. & Huether, S.E. (Eds), Pathophysiology: The Biologic Basis for Disease in Adults and Children (pp. 1322-1379). St. Louis, MO: Mosby-Year Book, Inc.

Kozy, M. &Varcarolis, E. M. (2010). Depressive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 246-279). St. Louis, MO: W.B. Saunders.

Bipolar Disorder, also known as manic-depression, is a chronic and recurrent illness. Bipolar disorder is characterized by extreme mood swings. Highs (mania or hypomania) are a period of persistently elevated or irritable mood, with symptoms such a grandiosity, inflated self-esteem, decreased need for sleep, hyperverbal and/or pressured speech, perception that thoughts are racing, flight of ideas, distractibility, impulsivity (i.e. excessive spending or sexual indiscretions), and increase in goal directed activity with trouble completing tasks. Elevated moods often alternate with periods of severe depression and both typically require hospitalization for safety and stabilization. However, there can be periods of normal functioning. To make a diagnosis of bipolar disorder, symptoms of mania must be present for at least one week OR symptoms of hypomania must be present for at least 4 days.
Schizophrenia is a thought disorder that can affect one’s ability to think logically, perceive reality accurately, socialize and communicate with others, and control emotions. Schizophrenia is typically characterized by the presence of delusions, hallucinations, disorganized speech, thoughts, or behavior, as well as flat affect, avolition, and poverty of speech.

Post-Traumatic Stress Disorder (PTSD) refers to a set of symptoms experienced after witnessing or being a part of a traumatic event, such as a car accident, fire, natural disaster, etc. Symptoms include: re-experiencing the event, including flashbacks, nightmares, and intrusive thoughts, and can be triggered by internal or external factors. Other symptoms include avoidant type behaviors, such as staying away from people, places, or things that trigger thoughts of the event, feeling numb and disinterested, including anhedonia, feelings of guilt or depression, and an inability to recall the traumatic event. People with PTSD tend to be hypervigilant, have an easy startle response, difficulty sleeping, and are described as irritable or edgy. PTSD also includes symptoms such as inability to focus/concentrate, poor memory regarding the traumatic event, and a negative outlook.

Borderline Personality Disorder is probably the most well-known of the personality disorders. It can be easily confused with bipolar disorder, due to the mood instability and impulsivity. While there is typically marked emotional dysregulation associated with borderline personality disorder, these symptoms are intermittent and typically only last from a few hours to no more than a few days. Other symptoms associated with borderline personality disorder include intense and/or unstable interpersonal relationships (tend to see either the positive (idealization) or negative (devaluation) in others, but not both), ineffective coping and self-soothing skills such as cutting or engaging in reckless behaviors (i.e. promiscuity, substance use, etc), negative self-image, feelings of emptiness and abandonment (real or perceived), paranoid ideation that is transient in nature and stress/anxiety induced, and recurrent suicidal/parasuicidal thoughts, behaviors, and gestures. While there are no medications indicated for the treatment of borderline personality disorder per se, medication therapy is typically aimed at targeting symptoms, such as anxiety, depression, anger, etc. Effective therapy modalities include individual therapy, cognitive behavioral therapy, dialectical behavior therapy, and group therapy.

References

Cihlar, C.A. & Shoemaker, N.C. (2010). Personality Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 433-460). St. Louis, MO: W.B. Saunders.

Halter, M. J., Varcarolis, E. M. & Shoemaker, N. C. (2010). Anxiety and Anxiety Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 212-245). St. Louis, MO: W.B. Saunders.

Halter, M. J. & Varcarcolis, E.M. (2010). Bipolar Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 280-305). St. Louis, MO: W.B. Saunders.

Herzog, E. A. & Varcarolis, E. M. (2010). Schizophrenia. In Varcarolis, E. M. & Halter,
M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 306-343). St. Louis, MO: W.B. Saunders.

Renal failure refers to the gradual loss of kidney function, and is typically a chronic process. Early stages of renal failure may be asymptomatic, with symptoms not presenting until late stage failure. Usual signs and symptoms of renal failure are generalized and non-specific and can look like numerous other illness processes. The signs and symptoms of renal failure include nausea, vomiting, poor appetite, fatigue, poor sleep, weakness, muscle cramping/twitching, swelling, changes in urine output, cognitive changes, and possibly chest pain, shortness of breath, and HTN if fluids build up in/around the heart and lungs. Causes of renal failure include, but are not limited to, diabetes, HTN, and recurrent infections.

Lithium toxicity is associated with lithium levels greater than 1.2 mEq/L. Therapeutic levels are considered to be between 0.6-1.2 mEq/L. Toxicity symptoms range from mild to severe and/or life threatening. Common side effects of lithium can include fine tremors, mild thirst, frequent urination, and mild GI discomfort. While these symptoms can be present for the duration of lithium therapy, they are often self-limited and subside during treatment. Early symptoms of toxicity (levels < 1.5 mEq/L) include nausea, vomiting, diarrhea, excessive thirst, frequent urination, fine hand tremors, muscle weakness, lethargy, and slurred speech. As toxicity progresses (1.5-2.0 mEq/L), tremors become more exaggerated, mental status becomes altered with changes in EEG noted, gait becomes uncoordinated, and there is increased sedation. Severe toxicity symptoms (2.0 to > 2.5 mEq/L) include, but are not limited to, significant changes in EEG, ataxia, confusion, blurred vision, seizures, stupor, coma, and in extreme cases, death. Treatment includes holding the lithium and checking levels, re-evaluating dosage based on blood level. In moderate to severe cases, hospitalization may be required and in extreme cases, hemodialysis may be required to expedite the removal of lithium from the blood.

Tardive Dyskinesia (TD) is associated with the use of antipsychotic medications and is characterized by involuntary tonic muscular contractions of the face, limbs, or trunk. While TD is serious, it is not life threatening. Women and older adults are more at risk for developing TD. It affects up to 50% of those receiving long term antipsychotic medications. Symptoms involving the face include protruding/rolling tongue, smacking or licking of the lips, blowing type movement of the lips. Symptoms involving the limbs include pill rolling (fingers), choreic movements (rapid, purposeless, irregular) and/or athetoid movements (slow, complex, serpentine-like). Symptoms involving the trunk include neck and shoulder movements, hip movements (jerks and rocking motions).

Agranulocytosis is a blood dyscrasia. It is characterized by symptoms such as sore throat, fever, malaise, and mouth sores, as well as possibly other flu like symptoms. Agranulocytosis is diagnosed using a CBC w/Differential to determine the presence of leukopenia, or agranulocytosis. Patients at risk for developing agranulocytosis are either conventional or atypical antipsychotics. If not properly diagnosed and treated, agranulocytosis can result in death. Treatment generally includes removing the offending agent and monitoring for any signs/symptoms of infection and treating those accordingly.

References

Chronic kidney disease. (n.d.). Retrieved May 15, 2016, from http://www.mayoclinic.org/diseases-conditions/kidney-disease/basics/definition/con-20026778

Halter, M. J. & Varcarcolis, E.M. (2010). Bipolar Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 280-305). St. Louis, MO: W.B. Saunders.

Herzog, E. A. & Varcarolis, E. M. (2010). Schizophrenia. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 306-343). St. Louis, MO: W.B. Saunders.

Catatonia is typically associated with schizophrenia, though it can also be part of a severe and/or treatment resistive depression. Catatonia is often characterized by either a complete lack of movement or grossly delayed movements (psychomotor retardation) fast, strange, or unpredictable movements (psychomotor agitation), and mutism. While a stuporous presentation (no movement at all) is the most common, catatonia can also present with intermittent increases in movement, often times referred to as stereotyped behaviors/movements, as they are repetitive and serve no logical purpose. A person experiencing catatonia may be able to follow simple commands in a robot-like fashion, may do the opposite of what is asked, or they may not be able to follow commands at all. A patient with catatonia may also demonstrate statue-like behavior, referred to as waxy flexibility (i.e. the provider raises the patient’s arm and the patient holds it there even once the provider has let go).

Delusions refer to an altered thought process whereby one experiences false fixed beliefs that do not respond to reality testing. The person with delusions believes his/her thoughts to be reality. Types of delusions include persecutory or paranoid, grandiose, religious, or somatic. Delusional thinking can also refer to one’s belief that he/she can thought broadcast or insert/withdraw thoughts from other’s minds. Delusions are considered to be a positive symptom (presence of something that is not normally present) of a thought disorder, such as schizophrenia.

Hallucinations, another positive symptom of an illness such as schizophrenia, is an alteration in sensory perception. A patient with hallucinations has a sensory experience despite lack of stimulus to create such an experience (i.e. feels a bug crawling on his/her body even though there is nothing there). Hallucinations can be experienced across all five senses. They can be tactile (feeling bodily sensations), auditory (hearing voices, noises, sounds, music), olfactory (smelling odors), visual (seeing objects or people), and gustatory (experiencing tastes).

Tardive Dyskinesia (TD) is associated with the use of antipsychotic medications and is characterized by involuntary tonic muscular contractions of the face, limbs, or trunk. While TD is serious, it is not life threatening. Women and older adults are more at risk for developing TD. It affects up to 50% of those receiving long term antipsychotic medications. Symptoms involving the face include protruding/rolling tongue, smacking or licking of the lips, blowing type movement of the lips. Symptoms involving the limbs include pill rolling (fingers), choreic movements (rapid, purposeless, irregular) and/or athetoid movements (slow, complex, serpentine-like). Symptoms involving the trunk include neck and shoulder movements, hip movements (jerks and rocking motions).

References

Electroconvulsive therapy (ECT). (n.d.). Retrieved May 23, 2016, from http://www.mayoclinic.org/tests-procedures/electroconvulsive-therapy/basics/why-its-done/prc-20014161

Herzog, E. A. & Varcarolis, E. M. (2010). Schizophrenia. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 306-343). St. Louis, MO: W.B. Saunders.

Dopamine is a monoamine neurotransmitter that is naturally occurring in the brain. It is involved in fine muscle movement, including walking and talking, the integration of emotions and thoughts, decision making ability, and it stimulates the hypothalamus to release various hormones. A decrease in dopamine levels can result in conditions such as Parkinson’s disease or psychiatric conditions such as depression. An increase in dopamine levels can result in psychiatric conditions such as schizophrenia and mania.

Gamma-aminobutyric acid (GABA), an amino acid, is another naturally occurring neurotransmitter in the brain. Its effects are known to calm nervous activity through inhibiting nerve transmission. GABA also has a possible role in pain perception, possesses anticonvulsant and muscle-relaxing properties, and may, in some instances, impair cognition as well as motor functioning. A decrease in GABA is associated with anxiety disorders, schizophrenia, mania, and Huntington’s disease. An increase in GABA is known to reduce anxiety. Benzodiazepines, including medications such as Ativan (lorazepam) and Valium (diazepam), bind to GABA receptors and enhance the effect of GABA, leading to a reduction in anxiety.

Serotonin is yet another naturally occurring monoamine neurotransmitter in the brain. Serotonin’s effects are known to effect sleep regulation, mood regulation, hunger, pain perception, sexual behavior, aggression, and hormonal activity. A decrease in serotonin levels is associated with depression and an increase in serotonin levels is associated with anxiety. The SSRI and SNRI classes of medication are typically used to target mood and anxiety symptoms believed to be related to changes in serotonin levels.

Glutamate, like GABA, is classified as an amino acid, and is another neurotransmitter in the brain. It is broken down in to two receptors-AMPA and NMDA. Glutamate is an excitatory neurotransmitter. The glutamate receptor AMPA is known to have an effect on learning and memory. A decrease in NMDA levels is associated with psychosis. Increased levels of NMDA can be neurotoxic if the elevated levels persist for a long period of time. Increases in NMDA are also associated with the neurodegeneration seen in Alzheimer’s. Increases in AMPA are known to improve cognitive performance.

References

Gutierrez, M.A. & Raynor, R. (2010). Biological Basis for Understanding Psychotropic Drugs. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 45-75). St. Louis, MO: W.B. Saunders.

THE BRAIN FROM TOP TO BOTTOM. (n.d.). Retrieved May 23, 2016, from http://thebrain.mcgill.ca/flash/d/d_04/d_04_m/d_04_m_peu/d_04_m_peu.html

Generalized Anxiety Disorder (GAD), which lasts 6 months or more, is characterized by excessive anxiety or worry about numerous things, usually in excess of the event or situation about which the person is worried. Worries are usually related to daily life stressors, such as finances, relationships, job related concerns, etc. Symptoms include restlessness, fatigue, an inability to concentrate/focus, irritability, tension, and poor sleep.

Anorexia Nervosa is an eating disorder that is characterized by abnormally low body weight (i.e. less than 85% of that expected for height), failure to thrive (i.e. unable to make expected weight gain during a period of growth that leads to a body weight less than 85% of that expected for height), an intense fear of gaining weight despite being grossly underweight, the denial of the seriousness of low body weight, and disturbance in perceived body weight or shape. Anorexia nervosa typically involves severely restricting the amount of food eaten to prevent weight gain or induce further weight loss. However, periods of restriction can also be interspersed with recurrent episodes of binging and purging behaviors. A person with anorexia nervosa might also exercise excessively and/or misuse diet aids and laxatives. The weight loss associated with anorexia nervosa can lead to metabolic changes as well as problems with muscle atrophy, nutritional deficiencies, and onset of amenorrhea (for at least 3 consecutive menstrual cycles) in girls/women.

Obsessive Compulsive Disorder (OCD) is characterized by obsessions and/or compulsions. Obsessions, (thoughts, impulses, or images) are pervasive and unable to be dismissed. Typically, individuals experiencing obsessive thoughts don’t want to have the thoughts and being unable to stop them causes severe anxiety. Compulsions (the behaviors) are ritualistic in nature and individuals feel driven to perform them in an attempt to temporarily reduce or relieve the anxiety. Because the relief is only temporary, the compulsive act must be repeated again and again. Obsessions and compulsions are considered problematic when they begin to interfere with daily functions and lead to an inability to focus on anything but the obsession or compulsion.

Bulimia Nervosa is a potentially life threatening eating disorder that is characterized by recurrent episodes of binge eating followed by recurrent inappropriate compensatory behaviors to prevent weight gain. Compensatory behaviors include things such as purging; abusing/misusing laxatives, diuretics, diet aids, or other medications; excessive exercise; or fasting. Binge eating is characterized by consuming a larger amount of food, in a particular period of time, than most people would consume in the same time period and under similar circumstances. People with bulimia nervosa often binge eat in discrete places. There is a sense of lack of control over eating and feeling that one cannot stop eating or control what they are eating.

References

Anorexia nervosa. (2016). Retrieved June 03, 2016, from http://www.mayoclinic.org/diseases-conditions/anorexia/home/ovc-20179508

Bulimia nervosa. (2016). Retrieved June 03, 2016, from http://www.mayoclinic.org/diseases-conditions/bulimia/home/ovc-20179821

Enright, C. R. & Ibrahim, K. (2010). Eating Disorders. In Varcarolis, E. M. & Halter, M.
J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 344-368). St. Louis, MO: W.B. Saunders.

Halter, M. J., Varcarolis, E. M. & Shoemaker, N. C. (2010). Anxiety and Anxiety Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 212-245). St. Louis, MO: W.B. Saunders.

Benadryl is an antihistamine medication that is also known to have anticholinergic properties. It is typically used to treat or prevent symptoms associated with allergies, such as sneezing, runny nose, and itchy, watery eyes. Benadryl can also be used to treat insomnias through its effect on the histamine receptors. When histamine levels are decreased, sedation can result. Benadryl, because of its anticholinergic properties, can also be used to treat stiffness and tremors associated with Parkinson’s disease as well as some of the extrapyramidal side effects (EPS) associated with the use of antipsychotics. Benadryl is not indicated for the management of alcohol withdrawal.

Librium is a long acting benzodiazepine often times used to manage symptoms of alcohol withdrawal. It is one of the most widely used medications for the management of alcohol withdrawal, with a well-documented efficacy profile. Librium doses can be scheduled, to try and minimize withdrawal symptoms, or given as needed if symptoms are identified through the use of a detox protocol, such as the CIWA. The dosage of Librium given depends upon the severity of the withdrawal symptoms. Librium can help decrease withdrawal symptoms, stabilize vital signs (i.e. BP and pulse) and help to prevent complications such as seizures or delirium tremens (DTs). Because of its long half-life, Librium is a self-tapering medication, which helps to minimize the risk of withdrawal associated with benzodiazepines.

Prozac is an antidepressant, and is classified as a selective serotonin reuptake inhibitor (SSRI). SSRIs are considered the first line of treatment for major depression. Prozac is indicated for the treatment of symptoms associated with depressive disorders as well as anxiety disorders. Prozac increases the activity of serotonin in the brain by blocking the reuptake of serotonin. Prozac is not indicated for the management of alcohol withdrawal.
Seroquel is a second generation atypical antipsychotic. It is used in the treatment of both schizophrenia and bipolar disorder. The newer Seroquel XR has an additional indication as an adjunct for the treatment of depressive disorders. Seroquel is effective in treating both the positive and negative symptoms of schizophrenia. When used to treat bipolar disorder, Seroquel targets both the depressive and manic episodes, and is an effective maintenance medication as well. Seroquel is not indicated for the management of alcohol withdrawal.

References

Antihistamine (Oral Route, Parenteral Route, Rectal Route). (n.d.). Retrieved June 03, 2016, from http://www.mayoclinic.org/drugs-supplements/antihistamine-oral-route-parenteral-route-rectal-route/description/drg-20070373

Councill III, J., Halter, M.J., & Smith-Dijulio, K. (2010). Addictive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 402-432). St. Louis, MO: W.B. Saunders.

Halter, M. J. & Varcarcolis, E.M. (2010). Bipolar Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 280-305). St. Louis, MO: W.B. Saunders.

Herzog, E. A. & Varcarolis, E. M. (2010). Schizophrenia. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 306-343). St. Louis, MO: W.B. Saunders.

Kozy, M. &Varcarolis, E. M. (2010). Depressive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 246-279). St. Louis, MO: W.B. Saunders.

Prater, C.D., Miller, K.E., & Zylstra, R. G. (1999). Outpatient Detoxification of the addicted or Alcoholic Patient. American Family Physician, 60(4):1175-1182. http://www.aafp.org/afp/1999/0915/p1175.html

Selective Serotonin Reuptake Inhibitors (SSRIs) are a class of antidepressant medications, and include medications such as Prozac, Zoloft, and Lexapro. These medications act by blocking the reuptake of serotonin, which allows for serotonin to act at its receptor sites in the brain for extended periods of time. This in turn can lead to improvement in both mood and anxiety symptoms. SSRIs are considered the first line of treatment for depressive disorders.

Dopamine antagonists generally refer to the atypical antipsychotics used to treat schizophrenia and bipolar disorder. These include medications such as Seroquel, Clozaril, Risperdal, and more. These medications work by blocking dopamine which in turn leads to a decrease in psychotic symptoms. However, a decrease in dopamine can lead to some untoward effects, including extrapyramidal side effects (EPS), cognitive changes, and possibly drug-induced parkinsonism, which can include symptoms such as hypersalivation and drooling. Therefore, a dopamine antagonist would not be a treatment choice to alleviate drooling as in the above scenario.

Anticholinergic medications act to block or inhibit the action of the neurotransmitter acetylcholine, which helps to send messages from nerves to muscles. Examples of anticholinergic medications are Cogentin (benztropine mesylate) and Glycopyrrolate. Both of these medications are known to be effective in the treatment of drooling due to their effects on the parasympathetic innervation of the salivary gland. Anticholinergic agents tend to be drying, thereby improving hypersalivation and drooling. In addition to dry mouth, other side effects of anticholinergic medications include, but are not limited to, blurry vision, drowsiness, urinary retention, and memory impairment.

Antihypertensive medications are comprised of several classes of medications, and are used to treat high blood pressure as well as other heart related conditions. Classes of antihypertensive medications include adrenergic blockers, diuretics, calcium channel blocker, and angiotensin-converting enzyme (ACE) inhibitors. All of the medications within these classes reduce blood pressure through their effect(s) on various mechanisms of action within the body. Antihypertensive medications are used in an effort to prevent the complications of high blood pressure, such as stroke and myocardial infarction.

References

Bavikatte, G., Sit, P.L., & Hassoon, A. (2012). Management of Drooling of saliva. British Journal of Medical Practitioners, 5(1);a507. http://www.bjmp.org/content/management-drooling-saliva

Brashers, V.L., Haak, S.W., & Richardson, S. J. (2010). Alterations of Cardiovascular Function. In McCance, K.L. & Huether, S.E. (Eds), Pathopyhsiology: The Biologic Basis for Disease in Adults and Chidren (pp. 1024-1092). St. Louis, MO: Mosby-Year Book, Inc.

Gutierrez, M.A. & Raynor, R. (2010). Biological Basis for Understanding Psychotropic Drugs. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 45-75). St. Louis, MO: W.B. Saunders.

Saltz, B.L., Robinson, D.G., & Woerner, M.G. (2004). Recognizing and Managing Antipsychotic Drug Treatment Side Effects in the Elderly. Prim Care Companion J Clin Psychiatry, 6(suppl 2): 14–19. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487007/

Conduct Disorder is a disorder of childhood and adolescence, and one of the most frequently diagnosed disorders amongst these age groups. Characteristics of conduct disorder include persistent disregard for age-appropriate societal norm and rules as well as a range of antisocial types of behavior where the rights of others are violated. Conduct disorder involves ongoing emotional and behavioral problems that may lead to complications such as impulsivity, substance misuse, academic failure, school suspensions, and legal involvement. Childhood onset occurs prior to 10 years of age and is more common in males. Conduct disorder can be characterized as aggression towards people or animals, property destruction, theft/deceit, and serious violations of rules.

Evidence of conduct disorder with onset prior to 15 years of age is one of the criteria for diagnosis of antisocial personality disorder. Conduct disorder can be characterized as aggression towards people or animals, property destruction, theft/deceit, and serious violations of rules.
Oppositional Defiant Disorder (ODD) is another disorder of childhood and adolescence. There are some similarities to conduct disorder in that there is a recurrent pattern of negative behaviors, including angry/irritable moods, defiance, and hostility aimed at authority figures. Unlike conduct disorder, ODD does not involve aggression towards people or animals, there is no property destruction, no pattern of deceit, and no serious violations of the basic rights of others. Children with ODD tend to be stubborn, argumentative, unwilling to compromise, unable to accept responsibility/blame for poor behaviors/choices, and will repeatedly test limits that are set. Evidence of ODD is usually present before 8 years of age, and more common in males until puberty, after which the rate is equal.

Attention Deficit Hyperactivity Disorder (ADHD) is a childhood disorder characterized by an inability to maintain an age-appropriate degree of attention, an inability to control impulses, and hyperactivity. Symptoms must be present and cause dysfunction and/or impairment in at least 2 separate settings. Additionally, onset of symptoms must occur prior to 12 years of age to make a diagnosis. Symptoms of inattention include difficulty with focus and concentration, difficulty paying attention, difficulty listening and following directions, and forgetfulness. Symptoms of impulsivity and hyperactivity include difficulty sitting still, fidgeting, unable to play quietly, difficulty with being patient and tends to be impulsive as a result (i.e. blurts out answers, trouble waiting for own turn, interrupts others, etc). While ADHD can often look similar to conduct disorder and ODD, it’s important to note that children with the latter two disorders tend to display consistent patterns of negative behavior and look for arguments regardless of the situation. Children with ADHD tend to display negative behaviors consistent with thei inability to tolerate situational and environmental stressors.

Reactive Attachment Disorder is considered to be rare but serious in nature. A child is at risk for developing a reactive attachment disorder when as an infant or younger child, they are unable to form healthy bonds and relationships with their primary caregivers. When basic needs for comfort, stability, affection, and nurturing are not met, children are at risk for an inability to establish stable attachments to others. Reactive attachment symptoms can start as early as infancy and it is still unclear as to whether the disorder occurs in children 5 years of age and older. Symptoms include an inability to respond when comfort is given, an inability to seek comfort when it is offered, isolation and withdrawal, lack of social interaction with others, appearance of being sad, fearful, or irritable, and failure to ask for help/support when needed. Children with reactive attachment disorder tend to withdraw inside themselves and are not known to display any negative behaviors towards others.

References

Cihlar, C.A. & Shoemaker, N.C. (2010). Personality Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 433-460). St. Louis, MO: W.B. Saunders.

Conduct disorder: MedlinePlus Medical Encyclopedia. (n.d.). Retrieved June 12, 2016,from https://www.nlm.nih.gov/medlineplus/ency/article/000919.htm

Erwin, E.H. & Colson, C. W. (2010). Disorders of Children and Adolescents. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 626-652). St. Louis, MO: W.B. Saunders. Reactive attachment disorder. (n.d.). Retrieved June 11, 2016, from http://www.mayoclinic.org/diseases-conditions/reactive-attachment-disorder/basics/definition/con-20032126

Acute Stress Disorder shares symptoms similar to Post-Traumatic Stress Disorder (PTSD), such as poor sleep, irritability, flashbacks, avoidant behaviors, etc. However, there are 3 hallmark differences between the two disorders: length of time to onset of symptoms (within one month following the traumatic event for Acute Stress Disorder), length of time to resolution of symptoms (no more than 4 weeks for Acute Stress Disorder) and presence of at least 3 dissociative symptoms either during or after the traumatic event (Acute Stress Disorder). Dissociative symptoms include emotional numbing/detachment, reduced awareness of surroundings, depersonalization (sense of unreality related to self), derealization (sense of unreality related to the environment), and loss of memory of an important aspect of the trauma.

Malingering is a condition considered to be related to the factitious disorders. It is characterized by a conscious motivation to act for the purpose of deceiving, in order to achieve material gain. There is a conscious act to feign or exaggerate an illness or symptoms for the purpose of trying to become eligible for disability benefits, obtain prescription medications (likely narcotics), and/or avoid legal issues. Symptoms are consciously fabricated and not supported by any medical findings, and are generally vague and hard for providers to prove or disprove (i.e. stomach pain, back pain, head pain, dental pain). Malingering is thought to be more common in men than women, and is often associated with antisocial personality disorder.

Generalized Anxiety Disorder (GAD), which lasts 6 months or more, is characterized by excessive anxiety or worry about numerous things, usually in excess of the event or situation about which the person is worried. Worries are usually related to daily life stressors, such as finances, relationships, job related concerns, etc. Symptoms include restlessness, fatigue, an inability to concentrate/focus, irritability, tension, and poor sleep.

Hypochondriasis is known as an illness anxiety disorder, and is characterized by fears of having a serious illness or disease, or the idea that one is going to become seriously ill. These fears and/or ideas persist despite appropriate medical testing that does not support these fears or ideas. Reassurance that there are no obvious medical issues also does nothing to alleviate the fears or ideas of having a serious illness. People with hypochondriasis typically have no, or very mild, symptoms to support their belief of having a major illness. These patients seek frequent medical attention, frequently check their bodies for signs of illness, avoid doing things or being with people due to fear it will impact their health, constantly talking about their health and possible illnesses, and scour the internet for information on their perceived symptoms and possible illness/causes for such symptoms. Preoccupation with these fears or ideas typically causes significant impairment in social and/or occupational functioning and/or causes significant distress in general. In order to diagnose hypochondriasis, other delusional disorders and types of somatoform disorders must first be ruled out.

References

Grund, F.J. & Shoemaker, N.C. (2010). Somatoform, Factitious, and Dissociative Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 502-526). St. Louis, MO: W.B. Saunders.

Illness anxiety disorder. (n.d.). Retrieved June 12, 2016, from
http://www.mayoclinic.org/diseases-conditions/illness-anxiety-disorder/basics/symptoms/con-20124064

Narcan, or naloxone, is an opiate antagonist used in the treatment of opiate (i.e. heroin, narcotic pain medication) overdose. Narcan blocks the effects of opiates and reverses the respiratory and central nervous system depression caused by the overdose. The mechanism of action is to push the opiate out of the opiate receptors in the brain, thus allowing the Narcan to occupy the opiate receptors. Length of time to onset of efficacy is generally 5 minutes with most of the Narcan being metabolized within 90 minutes. In some cases, duration of action of the Narcan may be less than that of the opiate ingested and additional doses of Narcan may be required. Narcan does not promote physical or psychological dependence and cannot be used to get high due to its mechanism of action. It is not known to have any effect, positive or negative, when given to someone who has not ingested opiates.

Librium is a long acting benzodiazepine often times used to manage symptoms of alcohol withdrawal. It is one of the most widely used medications for the management of alcohol withdrawal, with a well-documented efficacy profile. Librium doses can be scheduled, to try and minimize withdrawal symptoms, or given as needed if symptoms are identified through the use of a detox protocol, such as the CIWA. The dosage of Librium given depends upon the severity of the withdrawal symptoms. Librium can help decrease withdrawal symptoms, stabilize vital signs (i.e. BP and pulse) and help to prevent complications such as seizures or delirium tremens (DTs). Because of its long half-life, Librium is a self-tapering medication, which helps to minimize the risk of withdrawal associated with benzodiazepines.

Benadryl is an antihistamine medication that is also known to have anticholinergic properties. It is typically used to treat or prevent symptoms associated with allergies, such as sneezing, runny nose, and itchy, watery eyes. Benadryl can also be used to treat insomnias through its effect on the histamine receptors. When histamine levels are decreased, sedation can result. Benadryl, because of its anticholinergic properties, can also be used to treat stiffness and tremors associated with Parkinson’s disease as well as some of the extrapyramidal side effects (EPS) associated with the use of antipsychotics.

Seroquel is a second generation atypical antipsychotic. It is used in the treatment of btoh schizophrenia and bipolar disorder. The newer Seroquel XR has an additional indication as an adjunct for the treatment of depressive disorders. Seroquel is effective in treating both the positive and negative symptoms of schizophrenia. When used to treat bipolar disorder, Seroquel targets both the depressive and manic episodes, and is an effective maintenance medication as well. Seroquel is not indicated for the management of alcohol withdrawal.

References:
Antihistamine (Oral Route, Parenteral Route, Rectal Route). (n.d.). Retrieved June 03,2016, from http://www.mayoclinic.org/drugs supplements/antihistamine-oral-route-parenteral-route-rectal-route/description/drg-20070373

Councill III, J., Halter, M.J., & Smith-Dijulio, K. (2010). Addictive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 402-432). St. Louis, MO: W.B. Saunders.

Halter, M. J. & Varcarcolis, E.M. (2010). Bipolar Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 280-305). St. Louis, MO: W.B. Saunders.

Naloxone – Medical Countermeasures Database. (n.d.). Retrieved June 10, 2016, from https://chemm.nlm.nih.gov/countermeasure_naloxone.htm

Prater, C.D., Miller, K.E., & Zylstra, R. G. (1999). Outpatient Detoxification of the addicted or Alcoholic Patient. American Family Physician, 60(4):1175-1182. http://www.aafp.org/afp/1999/0915/p1175.html

Anorexia Nervosa is an eating disorder that is characterized by abnormally low body weight (i.e. less than 85% of that expected for height), failure to thrive (i.e. unable to make expected weight gain during a period of growth that leads to a body weight less than 85% of that expected for height), an intense fear of gaining weight despite being grossly underweight, the denial of the seriousness of low body weight, and disturbance in perceived body weight or shape. Anorexia nervosa typically involves severely restricting the amount of food eaten to prevent weight gain or induce further weight loss. However, periods of restriction can also be interspersed with recurrent episodes of binging and purging behaviors. A person with anorexia nervosa might also exercise excessively and/or misuse diet aids and laxatives. The weight loss associated with anorexia nervosa can lead to metabolic changes as well as problems with muscle atrophy, nutritional deficiencies, and onset of amenorrhea (for at least 3 consecutive menstrual cycles) in girls/women.

Bulimia Nervosa is a potentially life threatening eating disorder that is characterized by recurrent episodes of binge eating followed by recurrent inappropriate compensatory behaviors to prevent weight gain. Compensatory behaviors include things such as purging; abusing/misusing laxatives, diuretics, diet aids, or other medications; excessive exercise; or fasting. Binge eating is characterized by consuming a larger amount of food, in a particular period of time, than most people would consume in the same time period and under similar circumstances. People with bulimia nervosa often binge eat in discrete places. There is a sense of lack of control over eating and feeling that one cannot stop eating or control what they are eating.
Borderline Personality Disorder is probably the most well-known of the personality disorders. It can be easily confused with bipolar disorder, due to the mood instability and impulsivity. While there is typically marked emotional dysregulation associated with borderline personality disorder, these symptoms are intermittent and typically only last from a few hours to no more than a few days. Other symptoms associated with borderline personality disorder include intense and/or unstable interpersonal relationships (tend to see either the positive (idealization) or negative (devaluation) in others, but not both), ineffective coping and self-soothing skills such as cutting or engaging in reckless behaviors (i.e. promiscuity, substance use, etc), negative self-image, feelings of emptiness and abandonment (real or perceived), paranoid ideation that is transient in nature and stress/anxiety induced, and recurrent suicidal/parasuicidal thoughts, behaviors, and gestures. While there are no medications indicated for the treatment of borderline personality disorder per se, medication therapy is typically aimed at targeting symptoms, such as anxiety, depression, anger, etc. Effective therapy modalities include individual therapy, cognitive behavioral therapy, dialectical behavior therapy, and group therapy.

Dysthymic Disorder is a depressive disorder in which a depressed mood occurs for most of the day, more days than not, over a 2 year period. Dysthymia is chronic in nature and therefore difficult to distinguish the depressed mood from usual pattern of mood and functioning. Symptoms include changes in appetite, changes in sleep patterns, decreased energy and/or chronic fatigue, trouble with focus and concentration, difficulty with making decisions, feelings of hopelessness, and a decrease in self-esteem. People with dysthymia typically demonstrate significant distress in various aspects of functioning, including social and occupational. However, symptoms are not usually severe enough that hospitalization is warranted, such as in a major depressive disorder.

References

Cihlar, C.A. & Shoemaker, N.C. (2010). Personality Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 433-460). St. Louis, MO: W.B. Saunders.

Enright, C. R. & Ibrahim, K. (2010). Eating Disorders. In Varcarolis, E. M. & Halter, M.J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 344-368). St. Louis, MO: W.B. Saunders.

Kozy, M. &Varcarolis, E. M. (2010). Depressive Disorders. In Varcarolis, E. M. & Halter, M. J. (Eds.), Foundations of Psychiatric Mental Health Nursing: A Clinical Approach (pp. 246-279). St. Louis, MO: W.B. Saunders.

The correct answer is B. The chest x-ray shows a pneumonic process in the right middle lobe. Because the patient has dementia, one should suspect aspiration to be the cause. Dementia patients will often have a progressively worsening dysphagia, and are unable to adequately protect their airways. Aspiration often occurs on the right side. The right mainstem bronchus is large and oriented in a vertical position, allowing gravity to aid in the passage of foreign materials (food, secretions) into this region. Clindamycin is the best answer because it is in IV form and covers anaerobic bacteria. It is the least expensive drug and has a low rate of post-treatment infection with MRSA. Although Streptococcus Pneumoniae and Staphylococcus Aureus remain the most common causes of bacterial pneumonia, potential anaerobes implicated here include Fusobacterium and Peptostreptococcus. Flagyl is an inappropriate answer when used as a single agent, because it has a high failure rate against aerobic streptococci and microaerophilic isolates. Augmentin is incorrect because the patient is septic and requires hospitalization. In this instance an IV medication, as opposed to something by mouth, is far more appropriate. Zithromax is an outpatient regimen that covers atypical pneumonia and is incorrect. Thoracentesis would not be a first line treatment for aspiration pneumonia and is also incorrect.

References

1. Sanders CV, Hanna BJ, Lewis AC. Metronidazole in the treatment of anaerobic infections. Am Rev Respir Dis 1979; 120:337.

2. Kadowaki M, Demura Y, Mizuno S, et al. Reappraisal of Clindamycin IV monotherapy for treatment of mild-to-moderate aspiration pneumonia in elderly patients. Chest 2005; 127:1276.

The correct answer is D. The American Diabetes Association recommends initial treatment of systolic blood pressure readings in the 120-139mmHg range with diet and exercise. This is also true of diastolic readings in the 80-89mmHg range. In the case described above, the patient has already been counseled on diet and exercise, yet his blood pressure remains high. Although it is unlikely good blood pressure control will be achieved with a singular agent, an angiotensin converting enzyme inhibitor (ACE) is an excellent medication to start first. They are generally well tolerated. A dry cough is a common side effect, for which an angiotensin receptor blocker (ARB) can be substituted. ACE inhibitors protect against diabetic nephropathy. There is also some evidence to suggest that these drugs lower plasma glucose by increasing responsiveness to insulin. Norvasc is incorrect. Although used in the treatment of hypertension and diabetes, it is not a first line agent. It is often used in combination with an ACE inhibitor though. Lasix is incorrect. It is a diuretic and would be considered in a patient without diabetes as first line management. It can dehydrate patients and worsen renal failure if already present. Metoprolol is often used in diabetics, but it also is not a first line agent. This medication has been known to mask symptoms of hypoglycemia and may worsen peripheral arterial disease. Imdur is a drug often used to medically manage angina and coronary artery disease. It is typically initiated in diabetics but after patients have already developed complications of their disease.

References

1. Messerli FH, Bangalore S, Julius S. Risk/benefit assessment of beta-blockers and diuretics precludes their use for first-line therapy in hypertension. Circulation 2008; 117:2706.

2. Alkharouf J, Nalinikumari K, Corry D, Tuck M. Long-term effects of the angiotensin converting enzyme inhibitor captopril on metabolic control in non-insulin-dependent diabetes mellitus. Am J Hypertens 1993; 6:337.

The correct answer is D. Atrial fibrillation is a supraventricular tachyarrhythmia. It is characterized by uncoordinated atrial electrical activity resulting in an irregularly irregular heart rate. Atrial fibrillation is a relatively common cardiac condition and its incidence increases with age. Men are more often affected than women. An EKG with atrial fibrillation is without P waves as described above. The three cornerstones of treating atrial fibrillation are rate control, rhythm control, and anticoagulation to prevent thromboembolism. Patients with atrial fibrillation should be placed on long-term anticoagulation therapy to maintain an INR of 2 to 3, according to their CHADS2 VASc score. Patients with a CHADS2 score of greater than or equal to 2 should receive anticoagulation unless contraindicated. Those with a score of 1 should be treated with anticoagulation or aspirin. Those patients with a score of 0 can receive aspirin or no treatment at all. Other agents such as Pradaxa (Direct Thrombin Inhibitor), Eliquis and Xarelto (Factor Xa Inhibitors) can also be used for anticoagulation in place of Warfarin.

All of the above are viable treatment options for atrial fibrillation, but the only appropriate answer in this vignette is answer D. The question implies that the patient has most likely been in atrial fibrillation for 3-4 days. For those patients who are hemodynamically stable and in atrial fibrillation for greater than 48 hours, the treatment protocol is to anticoagulate for a period of approximately 4 weeks before proceeding with electrical cardioversion. Blood can sometimes pool in the chambers of the heart as it fibrillates. This can cause clot formation. The clots can become dislodged and cause an embolic stroke. Answer A puts the patient at significant risk for an embolic stroke because anticoagulation has not been initiated. Answer B is not the best choice either. Although it is an option for rhythm control, it is not as safe and efficacious as option D. Rate control with a calcium channel blocker, followed by beta blocker therapy, is widely accepted. Initiation of an anti-arrhythmic such as Amiodarone is done if the rate is refractory to those initial measures. Amiodarone requires hospital monitoring for loading doses to be administered. It is also known for its pulmonary and hepatic toxicity, and is not the best choice. Answer C is a good option for refractory atrial fibrillation but is not a first line treatment. Answer E is incorrect because the patient requires inpatient monitoring of her heart rate and hemodynamic stability.

References

1. Domino FJ, Baldor RA, Golding J, Stephens MB, Maloney ME, Ceci L. The 5-Minute Clinical Consult Premium 2016. 24th edition. Philadelphia, PA: Wolters Kluwer; 2015 Papadakis MA, McPhee SJ, Rabow MW. Current Medical Diagnosis & Treatment 2015. New York, NY: McGraw Hill Education; 2014

2. Kasper D, Fauci A, Hauser S, Longo D, Jameson JL. Harrison’s Principles of Internal Medicine. 19th Edition. New York: McGraw-Hill Education; 2015.

3. What Is Atrial Fibrillation? – NHLBI, NIH 2014. Available at: http://www.nhlbi.nih.gov/health/health-topics/topics/af. Accessed February 9, 2016.

The correct answer is E. The patient has severe aortic stenosis and is symptomatic. He describes having intermittent chest pain and exertional dyspnea. Additionally, he describes symptoms consistent with congestive heart failure (i.e. swollen ankles and wet cough). Worse yet, he syncopized with exertion. In the context of aortic stenosis, syncope is thought to occur because there is systemic vasodilation and a fixed cardiac output that ultimately drops the patient’s systolic blood pressure. Sublingual nitroglycerin is contraindicated because the patient is not having active chest pain and nitrates would worsen the systemic vasodilation already present. Lasix is a good treatment option for the management of congestive heart failure, but the patient’s lungs are clear, and he is not having an active exacerbation at this time. A cardiac catheterization is more diagnostic than therapeutic in this instance. Although the patient could have concomitant coronary disease, the aortic valve is the problem here. Patients with severe aortic stenosis have a high risk of sudden death. The mortality rate is as high as 50% in a 3-year period if the valve is not replaced. It is imperative that these patients receive prompt referral to cardiothoracic surgery to determine if they are good surgical candidates. For sicker patients and in instances where surgery might be prohibited, TAVR (transcutaneous aortic valve replacement) can be pursued instead.

References

Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 63:e57.

Tintinalli JE, Kelen GD, Stapczynski JS, eds. Valvular emergencies. 6th ed. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill; 2004. 54.

Vahanian A, Alfieri O, Andreotti F, Antunes MJ, Barón-Esquivias G, Baumgartner H, et al. Guidelines on the management of valvular heart disease (version 2012): The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2012 Oct. 33(19):2451-96. [Medline].

Blase A. Carabello. (2002). “Evaluation and management of patients with aortic stenosis.” Circulation.

The correct answer is A. Sumatriptan is widely accepted as a first line agent for cluster headaches. Cluster headaches commonly affect males and their onset occurs in the late third and early fourth decade of life. They tend to occur at the same time each day and last anywhere from 15-20 minutes on average. Longer headaches can go on for an hour and a half or more. Patients will describe the headache as a severe stabbing pain behind the eye, sometimes accompanied by tearing, nasal congestion, and/or visible swelling in the region. Neurologists will often obtain MRI with/without contrast and/or a head CT to evaluate the pituitary gland, rule out tumor, and to assess for possible AVM. Octreotide is used in the treatment of cluster headaches but is felt to be inferior to Sumatriptan in terms of its overall response time. Lidocaine is a topical treatment that is inexpensive and somewhat effective, but not as helpful as Sumatriptan. The patient is depressed because of his headaches. It should be noted that many patients with cluster headaches voice wanting to pursue suicide due to the severity of their symptoms. They should be screened for suicidal ideation and treated aggressively. Prozac is indicated for the treatment of depression, but will not abort the headaches. Augmentin is incorrect because it treats acute sinusitis. Although the tearing, swelling, and nasal congestion can occur with cluster headaches, the pain from acute sinusitis is likely to be more constant and associated with fever or general malaise.

References

PubMed. Triptans for acute cluster headache. AU. Law S, Derry S, Moore RA, Cochrane Database Syst Rev. 2010.

Treatment of acute cluster headache with sumatriptan. The Sumatriptan Cluster Headache Study Group. N Engl J Med. 1991;325(5):322.

Cluster headache: pathogenesis, diagnosis, and management. May A. Lancet. 2005;366(9488):843.

The correct answer is B. This patient has Obsessive Compulsive Disorder or OCD. This condition is characterized by recurrent intrusive thoughts that compel one to repeat or ritualize unrelated behaviors. For instance, in the vignette described above the patient deals with his social anxiety by showering for “hours” each day. He is focused on a sense of cleanliness and is afraid of contamination associated with public restrooms. Zoloft is a selective serotonin re-uptake inhibitor (SSRI). These drugs are generally well tolerated and are the first line treatment for OCD. Side effects include impotency and occasional gastrointestinal distress. Clonipramine is an effective drug but has more adverse side effects than its counterpart, Zoloft. These include somnolence, dry mouth, constipation, and even cardiac conduction delay. Xanax is incorrect because it is short acting and can become habit forming. Lithium is used in the treatment of bipolar disorder and Geodon is used primarily for schizophrenia.

References

Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). Soomro GM, Altman D, Rajagopal S, Oakley-Browne, Cochrane Database Syst Rev. 2008;

Practice guideline for the treatment of patients with obsessive-compulsive disorder. Koran LM, Hanna GL, Hollander E, Nestadt G, Simpson HB, American Psychiatric Association. Am J Psychiatry. 2007;164(7 Suppl):5.

The correct answer is E. The patient has developed Red Man Syndrome or a hypersensitivity reaction to vancomycin. Interestingly, this reaction is traditionally only seen with intravenous administration of the medication. Neck and facial flushing can occur, and as the reaction worsens, it can spread to the face and torso. The redness can be accompanied by erythema of the affected areas along with pruritis. The reaction occurs more frequently at higher infusion rates. It is therefore prudent to stop the medication and give Benadryl. An H2 blocker such as Zantac also offers additional antihistamine coverage. Epinephrine is incorrect because it is typically reserved for more severe reactions. It would be appropriate when hypotension is observed or the patient is experiencing anaphylactic shock. Decreasing the rate of vancomycin administration is incorrect because it doesn’t mitigate the patient’s ongoing symptoms and prevent progression to a more severe reaction. Normal Saline, although used to flush and dilute the medication in the patient’s system, is not treating the patient’s symptoms. Doing absolutely nothing is negligent. It is advised that a period of at least 4 hours pass before attempting to restart this medication and providers should cut the initial rate of administration in half. Most patients can be expected to make a full recovery.

References

PubMed. Mechanisms of vancomycin-induced histamine release from rat peritoneal mast cells.
Horinouchi Y, Abe K, Kubo K, Oka M. Agents Actions. 1993;40(1-2):28.

PubMed. Vancomycin-induced histamine release and “red man syndrome”: comparison of 1- and 2-hour infusions. Healy DP, Sahai JV, Fuller SH, Polk. Antimicrob Agents Chemother. 1990;34(4):550.

The correct answer is C. Acute pancreatitis is a condition marked by severe epigastric discomfort. The pain is described as being constant and is almost always accompanied by nausea and vomiting. Serum lipase has a high sensitivity and specificity for acute pancreatitis. Amylase is also a marker of this condition but is not as helpful as lipase in making the diagnosis. Lipase rises within 4-8 hours and peaks at 24 hours. Amylase rises in 6-12 hours after the initial onset of pancreatic inflammation, but has a short half life. Thus lipase elevations occur earlier and last longer, making it the better test, particularly if the patient presents greater than 24 hours after the onset of initial symptoms. A blood alcohol level will confirm whether or not the patient has alcohol in his system, but does not aid in making a diagnosis of acute pancreatitis. H. pylori is implicated in reflux disease and is an inappropriate marker to order. Total bilirubin is utilized to screen for the presence of liver disease and/or to follow chronic liver conditions.

References

PubMed. Comparative evaluation of the diagnosis of acute pancreatitis based on serum and urine enzyme assays. Gwozdz GP, Steinberg WM, Werner M, Henry JP, Pauley C, Clin Chim Acta. 1990;187(3):243.

Amylase normal, lipase elevated: is it pancreatitis? A case series and review of the literature.
Frank B, Gottlieb K, Am J Gastroenterol. 1999 Feb;94(2):463-9.

The correct answer is C. Statins, like Lipitor, have been found to not only prevent initial strokes but recurrent ones too. This is an interesting point, because in and of itself, hyperlipidemia is not a significant risk factor for stroke. It is hypothesized that perhaps the statins have a plaque stabilizing effect by reducing inflammation. Metoprolol is not the best choice. Many patients with an acute stroke have elevated blood pressures that are compensatory and intended to increase cerebral perfusion. This elevation in blood pressure should not be treated unless it is excessively high. Although stroke patients may often suffer from dizziness, Meclizine is intended for symptomatic treatment. It is not the best answer because it does not alter the disease course, as a statin does. The same is true of Fioricet. This medication is used for headache relief, commonly for migraines. Prilosec may be utilized to prevent gastrointestinal upset associated with the use of aspirin, but does not prevent a stroke from reoccurring.

References

PubMed. High-dose atorvastatin after stroke or transient ischemic attack. Amarenco P, Bogousslavsky J, Callahan A 3rd, Goldstein LB, Hennerici M, Rudolph AE, Sillesen H, Simunovic L, Szarek M, Welch KM, Zivin JA, Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Investigators.

PubMed. Antiatherothrombotic properties of statins: implications for cardiovascular event reduction. Rosenson RS, Tangney CC.

The correct answer is B. Early Lyme disease is characterized by a bull’s eye rash (erythema migrans), myalgias, lymphadenopathy, and fever. Interestingly, the rash is not always present. Unfortunately this patient is allergic to doxycycline, the preferred treatment for Lyme. It is preferred because it is a once daily regimen and can also treat a coexisting infection transmitted by ticks, Anaplasma phagocytophilum. If doxycycline cannot be used, however, Amoxicillin is the correct choice. It has equal efficacy to doxycycline and is well tolerated. Zithromax has been shown to be ineffective in the treatment of Lyme disease. Resistance to macrolides has been demonstrated amongst some strains of Some strains of B. burgdorferi. Longer courses of these antibiotics have not been studied and so their true efficacy is not known. Additionally first generation cephalosporins such as Keflex also have a high failure rate. Penicillin G is incorrect because it is used in later disease stages when neurological symptoms have developed. The patient described is presumed to have early disease, given that the tick bite was 3 days prior to her presentation. Levaquin is not appropriate. An erythema migrans rash may sometimes give the appearance of a cellulitis for which levaquin would be a reasonable choice, however, it is not utilized in the treatment of Lyme disease.

References

PubMed. Azithromycin compared with amoxicillin in the treatment of erythema migrans. A double-blind, randomized, controlled trial. Luft BJ, Dattwyler RJ, Johnson RC, Luger SW, Bosler EM, Rahn DW, Masters EJ, Grunwaldt E, Gadgil SD. Ann Intern Med. 1996;124(9):785.

PubMed. Failure of treatment with cephalexin for Lyme disease. Nowakowski J, McKenna D, Nadelman RB, Cooper D, Bittker S, Holmgren D, Pavia C, Johnson RC, Wormser GP. Arch Fam Med. 2000;9(6):563.

The correct answer is E. Systemic steroids such as IV solumedrol have been shown to improve lung function, diminish symptoms of shortness of breath, and decrease the length of hospital stay for patients experiencing an acute exacerbation of COPD. Giving this medication is a means to rapidly address the patient’s compromised respiratory status. Zithromax is often used in conjunction with steroids for COPD exacerbations, mainly to protect the patient from an ongoing bacterial infection that may actually caused the flare. It is not going to help this patient in a more immediate sense, however. Advair is a maintenance medication for COPD and is not indicated acutely. Mucinex helps to clear bronchial secretions and can be used in these patients, but it is not the best answer. Some mucoactive agents may actually make patients’ symptoms worse. Finally, magnesium is sometimes utilized in the treatment of respiratory emergencies, specifically asthma exacerbations. With asthma it has been shown to have a bronchodilating effect. It is important to note however, this is not true of COPD.

References

PubMed. Controlled clinical trial of methylprednisolone in patients with chronic bronchitis and acute respiratory insufficiency. Albert RK, Martin TR, Lewis SW. Ann Intern Med. 1980;92(6):753.

PubMed. Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. Niewoehner DE, Erbland ML, Deupree RH, Collins D, Gross NJ, Light RW, Anderson P, Morgan NA. N Engl J Med. 1999;340(25):1941.

PubMed. Effect of intravenous magnesium sulfate on chronic obstructive pulmonary disease exacerbations requiring hospitalization: a randomized placebo-controlled trial. Abreu González J1, Hernández García C, Abreu González P, Martín García C, Jiménez A.
Arch Bronconeumol. 2006 Oct;42(10):491.

The correct answer is B. Beta blockers are contraindicated for cocaine-induced MI. Cocaine causes vasoconstriction of the coronary arteries. It does this by stimulating alpha-adrenergic receptors and increasing the levels of endothelin-1. It also limits the chances of vasodilation by decreasing the body’s production of nitric oxide, a natural vasodilator. It also increases heart rate, contractility, and blood pressure, which all result in increased cardiac demand. Beta-blockers can cause unopposed alpha-constriction, increased blood pressure, and coronary vasospasm, leading to further ischemia. Nitroglycerin, aspirin, and benzodiazepines are all acceptable treatment modalities in the setting of a cocaine-induced MI. Nitroglycerin is a vasodilator that will help decrease cardiac demand by decreasing the preload and increase myocardial blood supply. Aspirin helps prevent platelet aggregation and activation. It will not break up an existing clot, but will help prevent new ones from forming. “Benzodiazepines decrease the central stimulatory effects of cocaine, which indirectly reduce cardiovascular toxicity. It also decreases neuropsychiatric symptoms associated with cocaine, which are closely related to cardiovascular complications.”2 Ace inhibitors are utilized with myocarditis or cardiomyopathy which are often seen secondary to the use of cocaine.

References

Williams, D. PANCE Prep Pearls. CreateSpace; 2014.

McCord J, Hani J, Hollander J, el al. Management of Cocaine-Associated Chest Pain and Myocardial Infarction. American Heart Association. 2008; 117: 1897-1907.

The correct answer is A. The two most common causes of pancreatitis are alcohol abuse and gallstones. In this case, this man has acute pancreatitis due to his alcohol abuse. Key things that would lead you to the possible diagnosis of acute pancreatitis would be epigastric pain, history of alcohol abuse as well as elevated liver enzymes, lipase, and WBC. The diagnostic test of choice to make the official diagnosis of acute pancreatitis is an abdominal CT scan.

Abdominal X-ray can also be used to diagnose pancreatitis, but it is not considered the test of choice. On x-ray you may see dilated small bowel in the LUQ, which is known as a sentinel loop. You also may see abrupt collapse of the colon near the pancreas. Sometimes pleural effusions can be seen at the lung bases and often an elevated hemidiaphragm will be present. HIDA scan is the gold standard for diagnosing cholecystitis. Cholecystitis is inflammation/infection of the gallbladder. Common signs of acute cholecystitis are episodic RUQ/epigastric pain usually precipitated by a fatty meal. Liver enzymes would be elevated with cholecystitis, but you would expect the patient to have a positive murphy’s sign on exam. Liver biopsy is used to diagnose cirrhosis. Although this man has a history of alcohol abuse, you would expect to find more signs on physical exam such as jaundice, ascites, and hepatosplenomegaly. Yes, his liver enzymes would be elevated, but you would also expect his bilirubin to be to elevated as well. Also, cirrhosis is due to chronic liver disease which this man has no history of. This is not a disease process that would occur within the mentioned time frame. An echocardiogram could be performed to ensure this patient does not have alcohol induced cardiomyopathy or acute pericarditis. An echo would also tell you if there is any valvular disease or ischemia that has resulted in wall motion abnormalities of the heart. This test is not really indicated in cases of acute pancreatitis though and would not help you to make the diagnosis.

References

Williams, D. PANCE Prep Pearls. CreateSpace; 2014.

Respiratory complications in acute pancreatitis. Ranson JH, Turner JW, Roses DF, Rifkind KM, Spencer FC. Ann Surg. 1974;179(5):557.

The correct answer is E. Infective endocarditis is a very serious condition in which bacteremia can result in damage to the heart valves and/or colonization of an intracardiac device. The Modified Duke Criteria are used to determine the pretest probability of IE. Per the Duke Criteria, infective endocarditis is definitively present if a vegetation can be confirmed with echocardiogram testing or if blood cultures are positive. These represent the major criteria. Minor criteria include: recreational IV drug abuse, fever, Janeway lesions, and/or evidence of emboli. The patient in the above vignette has Janeway lesions on her palms and soles. She admits to injecting IV heroin, which puts her at significant risk for IE. The other associated symptoms are consistent with her bacteremia. Although a transthoracic echocardiogram can be obtained in this circumstance, and is often the first test performed, transesophageal echocardiogram testing is more sensitive. It is better at detecting aneurysm, abscess, and other potential cardiac complications. A chest CT would be helpful in determining distant sites of metastatic infection but does not aid in making the initial diagnosis.

References

Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications: A Scientific Statement for Healthcare Professionals From the American Heart Association. Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Tleyjeh IM, Rybak MJ, Barsic B, Lockhart PB, Gewitz MH, Levison ME, Bolger AF, Steckelberg JM, Baltimore RS, Fink AM, O’Gara P, Taubert KA, American Heart Association Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young, Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and Stroke Council. Circulation. 2015;132(15):1435.

Diagnostic value of echocardiography in suspected endocarditis. An evaluation based on the pretest probability of disease. Lindner JR, Case RA, Dent JM, Abbott RD, Scheld WM, Kaul S
Circulation. 1996;93(4):730.

014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD. J Am Coll Cardiol. 2014;63(22):e57.

The correct answer is D. Epiglottitis is an inflammation of the epiglottis. It can be caused by bacteria or trauma. In this case, the NG tube placement may have been responsible for causing trauma to the affected area. Adults can experience fever, hoarseness, sore throat, drooling, and even respiratory compromise. Airway compromise is less common in adults than children though, because of the larger anatomic structures they possess. Radiographs will often show a “thumb sign” or an enlarged epiglottis protruding out from the hypopharynx. Adult patients with epiglottitis frequently require ICU monitoring and empiric antibiotic therapy. A third generation cephalosporin with staph coverage is generally recommended. The course of treatment may vary but is routinely prescribed for 7-10 days. Pneumonia is not the correct answer. It is in the differential diagnosis, but is generally not responsible for causing a sore throat or drooling. Pharyngitis is typically accompanied by fever and sore throat, but symptoms of headache, malaise, anorexia, and swollen glands are also present. Infectious mononucleosis has some overlapping symptoms with epiglottitis, but is also known for causing profound and prolonged fatigue. White or even green colored exudates can be seen on the tonsils in this condition. A foreign body is the incorrect answer. The patient would likely have noticed something obstructing his airway upon removal of the NG tube, instead of experiencing a more gradual onset of his symptoms.

References

Radiographic parameters in adult epiglottitis. Schumaker HM, Doris PE, Birnbaum G
Ann Emerg Med. 1984;13(8):588.

Diagnosis and management of supraglottitis (epiglottitis). Glynn F, Fenton JE
Curr Infect Dis Rep. 2008;10(3):200.

The correct answer is E. This patient is presenting with the typical symptoms of streptococcal pharyngitis. Although the most common cause of strep is viral, this patient has a bacterial infection. This is most commonly caused by Group A Beta Hemolytic Streptococcus. The Centor Criteria for strep throat consists of: Fever (>100.4 degrees fahrenheit), tender anterior cervical lymphadenopathy, absence of a cough, and pharyngotonsillar exudate. Each symptom is worth 1 point. Any patient with 2-3 points should get a throat culture. This patient presents with 3 of the 4 symptoms (fever, anterior cervical lymphadenopathy, and no cough), giving her a score of 3 points and therefore needing a throat culture. Choice A, a rapid influenza test via nasopharyngeal swab is incorrect. The common symptoms for influenza do include fever, myalgias, and chills but also a cough, nasal congestion, coryza, and headaches. This patient is not experiencing a majority of these symptoms, so therefore a rapid influenza test would not be the best choice. Choice B, MonoSpot test followed by Epstein Barr titers is incorrect. Mononucleosis is a good option to keep in the differential, but a key symptom that would be a negative indication of mononucleosis is “anterior” cervical lymphadenopathy. Most patients with mononucleosis will have posterior cervical lymphadenopathy. Although patients with mononucleosis will have a sore throat and fever, they will also complain of severe fatigue as well as abdominal discomfort. This patient denied these symptoms. The abdominal pain is due to the inflammation of the spleen and liver that occurs during the disease. Patients who have an enlarged spleen or liver should avoid contact sports and trauma for at least 1 month in order to avoid possible rupture. On physical exam, bilateral lid edema known as Hoagland sign and conjunctival hemorrhaging may be present as well. Answer C is done if epiglottitis is suspected. A thumb print sign is a positive finding. The patient’s airway should be protected and intubation should be considered. Choice D, do nothing because it’s viral, is not the correct answer. This patient has been experiencing high fevers for multiple days which would indicate more of a bacterial infection rather than viral. Most viral infections have lower grade fevers as opposed to bacterial infections where fevers tend to be higher. Also, in bacterial infections the fever will get worse a few days into the illness rather than getting better.

References

Williams D.A. PANCE Prep Pearls. CreateSpace. 2014.
Papadakis M, McPhee S, Rabow M. Current Medical Diagnosis & Treatment 2015. 2015

Duke University Health System. Is it a Bacterial Infection or Virus?. DukeMedicine. https://www.dukemedicine.org/blog/it-bacterial-infection-or-virus. Published Oct. 1, 2013. Accessed Jan. 25, 2016.

The answer is B. Transverse myelitis is a rare inflammation of the spinal cord which makes it an upper neuron lesion. About 1400 people per year develop transverse myelitis effecting males and females equally. However, in female there is an association with Multiple Sclerosis. This could happen at any age (3) . Transverse myelitis is caused by a number of conditions such as infection, secondary to Multiple Sclerosis, Neuromyelitis Optica, connective tissues, sarcoidosis and other autoimmune disorders (4) . A postinfectious patient could presents with a combination of bilateral pain, numbness, weakness, ataxia, spasticity, hyperreflexia, bladder and bowel dysfunction. There is no one diagnostic test for Transverse Myelitis. MRI, Lumbar puncture, chest CT, infectious and other immunological tests should be order. Enhanced MRI should show inflammation at the suspected region. CSF should show inflammation such as pleocytosis, elevated IgG and protein, and normal glucose (3,5) . For the treatment of TM , IV glucocorticoid is the first line for acute idiopathic cause. Plasma exchange may also be consider. The underlying cause should be thoroughly investigated and treated (3). Parkinson and TIA are incorrect because they are unlikely in a 38 year old. Parkinson is a chronic progressive disease, it is unlikely to start with a 2 day history of an acute neurological episode (6) . TIA by definition does not last longer than 24 hr, therefore among other reasons, this is not the case (7) . Guillain Barre syndrome is an immune mediated lower neuron neuropathy which starts at the distal portion of the nerve and move centrally. GBS presents with weakness and hyporeflexia or areflexia, while Transverse Myelitis is an upper neuron lesion which is hyperreflexia and spastic (8).

References

1. Bennetto. L, N Scolding. Inflammatory/postinfectious encephalomyelitis. Journal of Neurology, Neurosurgery & Psychiatry. 2004;75:i22i28 doi:10.1136/jnnp.2003.034256. Accessed date 5/31/2016

2. Brenton. J, nicholas. Acute disseminated encephalomyelitis clinical presentation. Medscape.
http://emedicine.medscape.com/article/1147044clinical#b4 . Last update dec 30, 2015. Accessed date
5/31/2016

3. Krishnan, Chitra. Transverse myelitis. Uptodate. http://www.uptodate.com/contents/transversemyelitis?source=search_result&search=transverse+myelitis&selectedTitle=1%7E101 . Last update Mar 07 2016. accessdate:5/25/2016

4. Greenberg BM, Frohman EM, Immunemediated Myelopathies. Continuum. 2015; 21(1) 121131.

5. Eisen, andrew, disorders affecting the spinal cord. Uptodate. http://www.uptodate.com/contents/disordersaffectingthespinalcord?source=search_result&search=transverse+myelitis&selectedTitle=4%7E101 . Last update May 5 2015. Accessed date 5/26/2016

6. Chou. Kelvin. Diagnosis and differential diagnosis of parkinson disease. Uptodate.
. http://www.uptodate.com/contents/diagnosisanddifferentialdiagnosisofparkinsondisease?
source=search_result&search=parkinson&selectedTitle=3%7E150 . Last update Feb 29 2016. Accessed date 5/26/2016

7. Furie, Karen. Etiology and clinical manifestation of transient ischemic attack. Uptodate.http://www.uptodate.com/contents/etiologyandclinicalmanifestationsoftransientischemicattack?
source=machineLearning&search=TIA&selectedTitle=2%7E150&sectionRank=1&anchor=H7#H7 . Last update. Jan 10, 2014. Access date 5/26/2016

8. Vriesendorp, Francine. Clinical features and diagnosis of Guillainbarre syndrome in adults. Uptodate. http://www.uptodate.com/contents/clinicalfeaturesanddiagnosisofguillainbarresyndromeinadults?source=search_result&search=guillain+barre&selectedTitle=1%7E150 . Last update Mar 16 2016. Accessed date 5/26/2016.

Answer D, refer to a cardiac surgeon for placement of an LVAD. This man is clearly showing signs and symptoms of heart failure, which is refractory to medical management, stage D heart failure. Increasing Lisinopril would be inappropriate in this patient as his serum creatinine is elevated. Though adding an inotrope would increase his ejection fraction, it would further increase his blood pressure and/ or heart rate and put this man at risk for an arrhythmia. Increasing his Lasix dose may improve the patients’ shortness of breath; it has no effect on mortality. Due to this patients advancing age, he most likely would not be a candidate for a heart transplant. Also, if this man was candidate, the likelihood that he would receive a donor heart in time is slim.

“Heart failure (HF) is a major public health issue, with a prevalence of over 5.8 million in the USA. The lifetime risk of developing HF is one in five… [and it] carries substantial morbidity and mortality, with 5-year mortality that rival those of many cancers.”1 In simple terms, heart failure can be defined as a “condition in which the heart can’t pump enough blood to meet the body’s needs.”1 The increase in life expectancy coupled with the steady rise in obesity rates has lead to an increased prevalence in heart failure patients. Heart failure is a clinical syndrome that can be broken down into systolic and/or diastolic failure and can affect the left and/or right side of the heart. The most prevalent type is systolic heart failure of the left ventricle. The key risk factors that have been isolated in the development of heart failure include hypertension, coronary artery disease, diabetes, valvular heart diseases, cardiomyopathy and being greater than 65 years old. 2

The pathophysiology of chronic systolic heart failure is complex but fundamentally results from long periods of increased stress. As the heart begins to become an inefficient pump and the body senses that it’s not getting enough blood supply, a physiological response will occur. This response is an increase in blood pressure and heart contractility by neurohormones, such as epinephrine and norepinephrine, and activation of the RAAS. The Frank-Starling law of the heart states that an increase in end diastolic volume will create a proportional increase in stroke volume. In order to keep up with these demands, the myocardium hypertrophies. In prolonged periods of stress, myocyte apoptosis occurs which subsequently leads to a slow remodeling of the heart. Ultimately, the end result of this process is a weakened myocardium with dilated ventricles.3

With diastolic heart failure, the ventricles become thickened and stiff. The total volume of the ventricle is reduced which concomitantly decreases the end diastolic volume.4 The end point of systolic and diastolic dysfunction is comparable. In both instances, there is a decreased stroke volume, cardiac output and cardiac index.

Patients in heart failure may present with non-specific and constitutional symptoms. A majority of the symptoms are the result of fluid overload or inadequate perfusion. Cough and shortness of breath are common and typically due to excess fluid in the lungs as the left side of the heart is not able to efficiently eject the blood. Fluid retention is evident by swelling in the legs, feet abdomen and is the result of blood getting backed up on the venous side from the right side of the heart. Other common symptoms include fatigue, weakness, and chest pain. On physical exam, the findings depend on the type and severity of heart failure. Pitting edema, rales, murmurs, and increased JVD may be observed.

A full workup should be started in a patient who presents with possible heart failure as it is a serious condition and there is not one gold standard test or lab to rule the disease in or out. Basic chemistries, a CBC, LFT’s, TSH and urinalysis should be drawn to assess possible other diagnosis’ or complications of the heart failure. A BNP should be drawn and is a valuable lab to assess the presence and severity of an individuals’ heart failure. A chest x-ray should be obtained to assess for pulmonary edema, pleural effusions and cardiomegaly, all signs of heart failure. An echocardiogram can also be a valuable tool to evaluate the filling, contractility, valve function and ejection fraction of the heart. Individuals in systolic heart function will have a decreased ejection fraction while diastolic heart failure will have either a normal or increased ejection fraction. CT scan, MRI and EKG can be used as well to rule out other diseases with similar presentations.

As indicated above, a diagnosis of heart failure is not a benign issue and is often fatal. Lifestyle modifications such as maintaining a balanced diet low in sodium and regular exercise should be implemented early. There are numerous medications on the market indicated for heart failure, however there is no magic pill that can reverse heart failure. Beta-blockers such as, Metoprolol Tartrate, Bisoprolol, and Carvedilol, as well as ACE-I and ARBs have been proven to reduce mortality and slow the disease process down. Diuretics, Digoxin, and various other medicines have shown to decrease symptoms but have no effect on survival rates.

Unfortunately, the only true treatment of end-stage heart failure is a heart transplant. In the United States, there is a large discrepancy between those with end stage hear failure that is refractory to medication and the number of available hearts that are available for transplants. Fortunately, a device called a Ventricular Assist Device (VAD) has become a favorable option. These can be implanted in patients who are ineligible for a heart transplant or who need support in the interim of a new heart. As left systolic heart failure is the most prevalent type of health failure, an LVAD device is the most common inserted VAD. Essentially, a VAD works in a similar fashion a healthy ventricle should. In the instance of an LVAD, a cannula is inserted into the left ventricle, which connects to a small pump that is located outside of the heart but within the chest cavity. On the opposite end of the LVAD is a graft that is stitched in to the ascending aorta. The VAD is continuously creating a negative pressure to suction the blood from the left ventricle and eject it into the systemic arterial system.

Heart failure is and has been an epidemic due to obesity and technological advances that are leading to increased longevity. The mismatch in individuals with this disease and the number of hearts that become available for transplants is tragic. VAD’s have proven to decrease the number of lives that would have been taken prematurely due to heart failure. Though the outlook of many diseases is grim, technology has once again paved the way to the future of medicine.

References

1. Bui AL, Horwich TB, Fonarow GC. Epidemiology and risk profile of heart failure. Nature reviews Cardiology. 2011;8(1):30-41. doi:10.1038/nrcardio.2010.165.

2. What Is Heart Failure? National Heart, Lung, and Blood Institute . https://www.nhlbi.nih.gov/health/health-topics/topics/hf. Accessed June 8, 2016.

3. Dumitri I. Heart Failure. Medscape. http://emedicine.medscape.com/article/163062-overview#a4. Published January 11, 2016.

4. Zile MR, Gaasch WH. Pathophysiology of diastolic heart failure. UpToDate. http://www.uptodate.com/contents/pathophysiology-of-diastolic-heart-failure. Published September 15, 2014.

Correct A. This patient presents with an acute exacerbation of congestive heart failure with a decrease in exertional capacity, dyspnea, significant weight gain, JVD, and signs of fluid overload. The most appropriate treatment would be a loop diuretic like Furosemide, which is the most effective treatment for symptom relief of mod-severe CHF with fluid overload. It works by inhibiting water transportation across the loop of Henle resulting in an increased excretion of water, chloride, sodium and potassium.5,7,8 Since this patient is having an acute onset, intravenous treatment is necessary for rapid relief of symptoms.

Incorrect B This patient has negative troponins and a normal EKG and is not currently having angina or AMI. Isosorbide mononitrate does decrease the preload via venous relaxation but it is not the most effective treatment for immediate symptom relief.

Incorrect C ACE inhibitors along with diuretics are first line treatment for CHF patients, but the Lisinopril takes 7-10 days for its pharmacological effect. ACE inhibitors are initiated as first line if the patient is not in fluid overload. Therefore, a diuretic would be the most appropriate rather than lisinopril.5,7

Incorrect D Metoprolol Succinate takes about 7-10 days for its pharmacological effects to take place. It works by decreasing the patients HR and BP, improving the left ventricular function and dilation, improving symptoms within 7-10 days. It does not help with fluid excretion or the immediate relief of symptoms after the first dose, like Furosemide.5,7

Reference: Mann D, Chakinala M. Heart Failure and Cor Pulmonale. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012: 1901-1913

Correct answer: Malaria. Fever, malaise, anemia and thrombocytopenia are common findings in a patient infected with malaria. In this case, ring forms were identified on the smear for parasites. Dengue Fever will typically present with fever and usually severe myalgia (termed “break-bone”) and a maculopapular rash starting on the trunk and progressing to the extremities. Anemia in Dengue Fever usually only occurs if the condition becomes hemorrhagic. Ebola presents with fever and myalgia as well but is almost always accompanied by chest pain with cough, vomiting, diarrhea, and altered mental status and possibly progress to bleeding and hemorrhage. Leukopenia, in addition to thrombocytopenia, is usually present. Influenza is generally an abrupt onset of fever, chills, myalgia and is usually associated with a cough. Influenza is generally not associated with a bandemia or thrombocytopenia. Typhoid usually results in fever and abdominal pain. A rash, described as “rose spots”, occurs in up to 30% of cases. Thrombocytopenia is less commonly found with Typhoid.

Malaria is a protozoan disease found mostly in Central and South America, Africa and Asia. There are five species of the protozoa Plasmodium which can be transmitted to humans via mosquito bites with the species P. falciparum being responsible for the vast majority of deaths related to malaria. Incubation times between the bite and clinical symptoms varies based on the specific species that the host is infected with and can be between 9-40 days. During this time the protozoa are replicating with the host’s liver. Symptoms typically include headache, fatigue, irregular fevers and sweats leading to myalgias, arthralgias, abdominal pain, vomiting and diarrhea. Rash and lymphadenopathy are very uncommon. Giemsa stain with thick and thin smears are used to assess for parasitemia. Thrombocytopenia is a more common finding than anemia. Treatment options include quinine plus doxycycline or tetracycline, amodiaquine, or a combination drug of atovaquone-proguanil. Chloroquine is still used however resistance has been occurring. There is no currently approved vaccine so travelers to these parts of the world are generally advised to use prophylactic medications. With proper treatment, outcome is very good and fevers usually resolve within 1-2 days.

Dengue Fever is the transmission of the flavivirus to a human host also by a mosquito bite and is prevalent in similar geographic as malaria. Incubation time from bite is 3-14 days and classic symptoms include abrupt onset of fevers, headache, retroorbital pain, and severe myalgias. Adults are more often symptomatic than children. Macular rash, lymphadenopathy and vesicles on the palate are also possible as well as hemorrhagic symptoms. Leukopenia, thrombocytopenia, and elevated transaminases are seen in lab testing and the diagnosis is confirmed with IgM and IgG ELISA’s. Treatment is supportive care until the virus runs it’s course.
Influenza A and B are prevalent in temperate countries throughout the world and are spread via respiratory droplets with a 1-4 day incubation time. Symptoms onset is generally abrupt and includes fevers and chills, fatigue, myalgias and cough as well as occasional vomiting and diarrhea. Physical exam is usually unremarkable except for the appearance of fatigue and discomfort. The diagnosis is made either clinically or via influenza testing using a nasal swab. CBC is generally normal or may reveal leukopenia. Treatment is supportive or an anti-influenza medication may be prescribed for more severe symptoms or for those with other underlying health conditions if the patient presents within 48 hours of symptom onset.

Typhoid (enteric fever) is an infection with Salmonella typhi and usually occurs in areas with poor sanitary conditions within India, China, Africa and Southeast Asia. Incubation time is typically 10-14 days and classic symptoms are fever and abdominal pain. Headache as well as a rash are also relatively prevalent. The rash is usually maculopapular on the trunk and chest consisting of faint, pink, blanchable areas which have been described as “rose spots”. Definitive diagnosis on positive cultures of blood, bone marrow or stool. The Widal test for “febrile agglutinins” may be helpful but is not definitive. Treatment is usually with ciprofloxacin but ceftriaxone, azithromycin, amoxicillin or trimethoprim-sulfamethoxazole and others are also used with good success rates.

References:

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2015 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2015. Print.

Influenza. In DynaMed Plus® – the next-generation clinical information resource designed to decrease time to answer. DynaMed Plus. Available at: http://www.dynamed.com/home/. Accessed March 10, 2016.

Correct answer is A. Activated protein C resistance (Factor V Leiden) is the most common cause of pulmonary embolus in white patients. Other hypercoagulabe states include malignancy, deficiencies of protein C, protein S, and antithrombin III, extensive burns, recent long distance travel, and oral contraceptives. Von Willebrands, Factor 7 deficiency, and idiopathic thrombocytopenia purpura are bleeding disorders that reduce the body’s ability to clot.

The most common cause of sudden death is cardiac related while the second most common cause is pulmonary emboli (PE). 1 “PE & deep vein thrombosis (DVT) are immediate & intermediate causes of death, respectively.”2 A PE is defined as the blockage of one or more pulmonary arteries. A blockage at the bifurcation of the pulmonary trunk is defined as a saddle embolus. PE is not a disease, but rather a complication of a venous thromboembolism; the most common is DVT.1

A PE is considered acute if its location is central within the lumen or completely occludes the vessel. A PE is considered chronic if it is “eccentric & contiguous with the vessel wall, it reduces arterial diameter by more than 50%, evidence of recanalization within thrombus is present, & an arterial web is present.” 1 A central PE is located in the “main pulmonary artery, left and right main pulmonary artery, anterior trunk, right and left interlobar arteries, left upper lobe trunk, right middle lobe artery and right and left lower lobe arteries” whereas a peripheral PE is located in the ”segmental and subsegmental arteries of the right upper lobe, right middle lobe, right lower lobe, left upper lobe, lingual, and left lower lobe”. 1 A massive PE includes bilateral pulmonary arteries or results in hemodynamic compromise. 1

The etiology of a PE can be attributed to Virchow’s Triad: stasis, hypercoagulability, and intimal damage.3 The most common etiology is a DVT but others include air, amniotic fluid, fat, foreign body, parasite eggs, septic emboli, and tumor cells. 4 Factor V Leiden, resistance to activated protein C, is the most common inherited etiology in the white population.1

Of the percentage of patients that die in hospitals, around 60% have a PE and were misdiagnosed around 70% of times. For every 1,000 people, there is one case of PE per year. Between 60-80% of patients with DVTs end up with PEs, but, over 50% present asymptomatically. 1 The 3rd most common cause of deaths in hospitalized patients is PE. 1, 4

A PE caused by right ventricle or pulmonary artery obstruction leads to the venous blood being damned which causes distention of venous vessels and flow through the pulmonary circuit to the left side of the heart to slow. This slowing of blood to the left heart and aorta cause the mechanical collapse of the entire cardiovascular system.5 The thrombus that causes the PE begins as a “platelet nidus”1, usually on a lower extremity venous valve. It continues to grow by accumulation of fibrin and platelets then progresses to a red fibrin thrombus. This can embolize or cause complete occlusion of the vessel.1

The ‘classic’ presentation of PE, “abrupt onset pleuritc chest pain, shortness of breath, and hypoxia”1, is actually less common than the other signs and symptoms. Symptoms can include: dyspnea, chest pain, cough, leg pain, palpitations, wheezing, and aginal pain. Signs may include: tachypnea, rales, accentuated second heart sound, tachycardia, fever, diaphoresis, S3 and S4 gallop, hemoptysis, pleural friction rub, and cyanosis.1 The most common symptom is dyspnea while the most common sign is tachypnea.3 A PE may present with a normal pulmonary exam and (+) Homan’s sign.3
A PE can be worked up with many diagnostic imaging studies. A plain chest radiograph (CXR) is most often normal but if the patient has hypoxia in the setting of a normal CXR, there should be a high suspicion for PE. There may or may not be a pleural effusion or atelectasis. There are classic findings on CXR indicating a PE, but these are not common. 3 The classic findings include Westermark’s Sign, Hampton’s Hump, and Fleischner Sign 3,6. On electrocardiograph, there may be changes in Lead I showing a deep, wide S and in Lead III Q waves and inverted T waves can be seen as well. This is written in medical abbreviation as S1Q3T3.3,6 Respiratory alkalosis on initial ABG will, with time, convert to respiratory acidosis. A D dimer has low specificity but high sensitivity. This can be helpful if it is negative to rule a PE out of the differential diagnosis. Other studies include CT and V/Q scans. A pulmonary angiography is the gold standard but is only performed if the following criteria are met: either CT or V/Q are negative and the clinician has a high suspicion. On ultrasound, the most common finding is DVT.3

Treatment for a PE can be medical or mechanical. Medical treatment consists of anticoagulation, via heparin or low molecular weight heparin in combination with warfarin, or thrombolytic, via t-PA (Alteplase). “Heparin binds to and accelerates the ability of antithrombin to inactivate thrombin, factor Xa and factor IXa. It thus retards additional thrombus formation, allowing endogenous fibrinolytic mechanisms to lyse existing clot.”4 “Streptokinase, urokinase, and recombinant tissue plasminogen activator (rt-PA; Alteplase) increase plasmin levels and thereby directly lyse intravascular thrombi.”4 Mechanical treatment is rare but includes: inferior vena cava filter, pulmonary embolectomy, and pulmonary thromboendarterectomy.4

References

1. Ouellette D. Pulmonary Embolism: Practice Essentials, Background, Anatomy. Emedicinemedscape.com. 2016. Available at: http://emedicine.medscape.com/article/300901-overview#showarll. Accessed February 1, 2016.

2. Dolinak D, Matshes E, Lew E. Forensic Pathology. Boston: Elesevier Academic Press; 2005:104.

3. Williams D. PANCE Prep Pearls. Lexington, KY: CreateSpace; 2014:98-100.

4. Papadakis M, McPhee S, Rabow M. Current Medical Diagnosis & Treatment 2015. 54th ed. New York, NY: McGrawHill; 2015:293-299.

5. Spitz W, Spitz D. Fischer R. Spitz And Fischer’s Medicolegal Investigation of Death. 4th ed. Springfield, Ill.: Charles C. Thomas; 2006:331-332.

6. Hrciz C. Pulmonary (Venous Thrombo)embolism (PE). [PowerPoint] Manchester, NH: MCPHS Physician Assistant Program; 2015

Answer: Sinus rhythm. This EKG demonstrates a moderate amount of baseline artifact however the QRS complexes are at regular intervals and leads V1 and V2 demonstrate p waves followed by QRS complexes. These 2 findings exclude atrial fibrillation and flutter. A Mobitz II block consists of a fixed, prolonged PR interval with an occasional non-conducted P wave resulting in a dropped beat. There are no dropped beats on this EKG. The rate is approximately 80bpm which eliminates supraventricular tachycardia (>100bpm).

Artifacts on an EKG tracing can be due to one or more of several reasons including an expired electrode, poor skin contact, breakdown of the conduction gel in the center of the electrode, tautness of the skin underlying an electrode, and finally, patient movements including breathing, tremors or any other muscle use. These artifacts can mimic a wide variety of arrhythmias and the importance of a thorough assessment of all EKG leads as well as a complete assessment of the patient including any obvious signs of instability and a manual palpation of the pulse should be conducted when attempting to make a determination between artifact and an actual abnormal finding. If the patient is stable, any possible arrhythmia on a rhythm strip should be confirmed with a 12-lead EKG.

When evaluating a 12-lead EKG, if sinus rhythm is not completely apparent, assess all leads for P followed by QRS. Many times P waves can be more easily appreciated in lead V1. Also, each column of leads (for example: leads I, II, III on a standard format) represents the same period of time, therefore, any irregularity noted in one lead should also be present in the other two that correspond to the same point in time. In the case of the attached EKG, P waves are most visible in V1 and V2 and there is no significant artifact which would correspond to the same timeframe as the lead II rhythm strip immediately below those leads.

References

Ortega R, Mazzini M, Xue K, Espaillat D. Electrocardiographic Monitoring in Adults. New England Journal of Medicine N Engl J Med 2015;372(8).

El-Sherif N, Turitto G. Ambulatory Electrocardiographic Monitoring between Artifacts and Misinterpretation, Management Errors of Commission and Errors of Omission. Ann Noninvasive Electrocardiol Annals of Noninvasive Electrocardiology 2014;20(3):282–289.

Dubin D. Rapid Interpretation of EKG’s: an Interactive Course. Tampa, FL: Cover Pub. Co.; 2000.

Answer:  Hyperkalemia.  The bradycardia, flattened P waves, widened QRS complex, biphasic QRS-T complexes and conduction delay are all findings consistent with hyperkalemia.  Hypercalcemia can cause bradycardia and widened T waves however, it usually causes a shortened QT interval.  Hypermagnesemia EKG changes are usually a result of simultaneous hyperkalemia and not from the elevated magnesium itself.  Hypernatremia is not generally associated with specific EKG changes.

Hyperkalemia is commonly associated with the phrase “peaked T waves”, however, the condition has been known to cause a multitude of other changes as well.  In addition to the findings mentioned above, hyperkalemia can also cause a first-degree block, bundle branch or atrioventricular blocks, deep S waves, ST elevations, and a merging of the S and T waves which can eventually develop into a since-wave and asystole.

The “peaked” or “tented” T waves are generally the earliest changes (5.5-6.5 mEq/L) related to hyperkalemia and are a result of an acceleration to the terminal repolarization.  P wave flattening (6.5-7.5 mEq/L) as well as PR and QRS prolongation occurs are next to occur (7-8 mEq/L) as potassium continues to rise and are caused by a depression in conduction between adjacent myocytes.  As potassium continues to rise, the SA and AV node conduction is suppressed which can lead to escape beats, heart block, QRS widening leading to a sine-wave (>8 mEq/L) and eventually ventricular fibrillation or asystole.  These changes vary from individual to individual and are not necessarily present in all cases or at similar potassium levels from one person to another.

Hypokalemia can also cause EKG changes, including:  low amplitude T wave, ST depression, broad-based U wave formation.  As hypokalemia becomes more profound, ventricular tachycardia, PVC’s, and ventricular fibrillation are possible.

References:

2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.  Part 10.1: Life-Threatening Electrolyte Abnormalities. Circulation 2005;112(24_suppl).

Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: a Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division; 2004.

Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2015 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2015. Print.

Webster A. Recognizing signs of danger: ECG changes resulting from an abnormal serum potassium concentration. Emergency Medicine Journal 2002;19(1):74–77.

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Answer:  Calcium gluconate.  All of the answers are appropriate treatments for hyperkalemia, however, calcium gluconate is the only one which is directly responsible for stabilizing the myocytes while initiating treatment to lower the extracellular potassium levels.

Hyperkalemia is most commonly caused by renal failure or insufficient dialysis once the patient has been  started on chronic dialysis.  Other somewhat common causes include use of potassium-sparing diuretics, aldosterone deficiency, and rhabdomyolysis.  Pseudohyperkalemia is seen with hemolysis during the venipuncture process and can occur during a diabetic ketoacidosis (DKA) event.  During DKA, potassium is shifted into the extracellular space in exchange of hydrogen causing serum levels to be elevated.  However, in patients with good renal function, much of the potassium is excreted in the urine due to the hyperglycemic state causing osmotic diuresis.  This diuresis results in a depleted total body potassium state.

A patient with hyperkalemia can present with palpitations, nausea/vomiting, myalgias or paresthesias, however, some patients may be asymptomatic if only mild elevations of potassium are present or if levels have gradually increased over a period of time.  Hyperkalemia is classified according to the serum potassium level and not necessarily the degree of symptoms.  Mild hyperkalemia is between 5.5-6.5 mEq/L, moderate is 6.5-7.5 mEq/L, and severe is a potassium greater than 7.5 mEq/L.  As levels increase, various EKG changes can occur.  “Peaked” or “tented” T waves are generally the earliest changes followed by P wave flattening, PR and QRS prolongation occurs are next to occur which can eventually lead to heart block, QRS widening, sine-wave formation and eventually ventricular fibrillation or asystole.

Treatment of hyperkalemia in the non-DKA patient involves several medications which work on a variety of physiologic levels.  Mild hyperkalemia which is asymptomatic and without accompanying EKG changes may resolve spontaneously if the underlying cause is reversible and addressed.  Moderate to severe hyperkalemia requires both shifting the potassium back into the cells as well as removal of potassium from the body.  This is accomplished with insulin, glucose, albuterol (nebulized or intravenous), furosemide (Lasix), and sodium polystyrene (Kayexalate).  Insulin and glucose should both be provided and the typical doses are 10 units of regular insulin with 50 grams of glucose IV.  Albuterol 2.5mg nebulized can also be provided.  These three treatments will assist in shifting potassium back to the intracellular space.  Sodium bicarbonate 50-100 mEq IV will also promote some intracellular shift but is usually reserved for severe cases with acidosis and it’s efficacy is less predictable.  Furosemide (Lasix) 40mg IV will promote renal excretion of the potassium unless the patient has end-stage renal disease, in which case, dialysis would be needed.  Sodium polystyrene (Kayexalate) 25-50 grams oral or rectal will bind to enteral potassium and prevent it from being resorbed into the system, allowing for it to be excreted from the GI tract.

Calcium chloride (10%) or calcium gluconate (10%) 10ml IV is necessary to initially stabilize the myocyte membrane potential while other agents are being given time to work.  Calcium gluconate is preferred due to the lack of potential tissue necrosis if the medication infiltrates at the injection site.  The onset of action is 1-3 minutes and the duration of effect can last up to 50 minutes.  Some sources cite using calcium in any patient with EKG changes, others recommend a more conservative use and reserve it for the following conditions:  widened QRS or sine wave, cardiac arrest due to hyperkalemia, or rapid changes in the EKG due to an ongoing process.  Calcium will narrow the QRS and improve bradycardia.  Calcium should be given with extreme caution to a patient taking digitalis (Digoxin) due to the possibility that the hypercalcemia could lead to cardiac tetany (“stone heart”) or ventricular arrhythmias.  Some studies have disproven this association.

References:

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Lehnhardt A, Kemper MJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol Pediatric Nephrology 2010;26(3):377–384.

Pfennig C, Whitmore S, Slovis C. ACEP. Focus On… Critical Decisions: Hyperkalemia //. Available at: http://www.acep.org/education/continuing-medical-education-(cme)/focus-on/focus-on—-critical-decisions–hyperkalemia/. Accessed March 16, 2016.

Levine M, Nikkanen H, Pallin DJ. The Effects of Intravenous Calcium in Patients with Digoxin Toxicity. The Journal of Emergency Medicine 2011;40(1):41–46.

Answer:  Pericarditis.  The pt. has a history consistent with a recent viral illness and the report of increasing pains with lying supine, thus improved with sitting up, leaning forward are classic findings in a patient with pericarditis.  While subtle, the EKG does show diffuse ST elevations consistent with pericarditis.  Costochondritis is usually much more reproducible with palpation of the chest wall and is less likely to improve with leaning forward.  Pleuritis would be diagnosed with the presence of pleural rubs on auscultation.  Neither costochondritis nor pleuritis should be associated with EKG changes.  Pulmonary embolus is less likely to be positional, is generally associated with tachycardia and if present, would have different EKG changes.  ST elevation MI by definition is 1mm or more of ST segment elevation in 2 contiguous leads.  This EKG does not meet that criteria.

The pericardium is a 3-layered fibrous and elastic structure surrounding the heart.  Between the innermost (visceral) layer and the middle (parietal) pericardium is the pericardial cavity, or sack, which usually contains 5-15ml of fluid.  The purpose of the pericardium is to contain the myocardium, restrict chamber dilation, and to minimize friction and transference of infection between the heart, lungs, and vessels.  Inflammation of this structure, referred to as pericarditis, is most often due to viral etiologies.  Other causes include:  bacterial, fungal, tuberculous, recent myocardial infarction (Dressler’s syndrome), uremia, systemic inflammatory conditions, cancer, radiation, cardiac procedures and trauma.  The majority of cases are found in males less than 50 years of age and cases can be both acute and chronic.

The classic history of pericarditis is a sharp, stabbing, substernal pain which is usually pleuritic and made significantly worse by lying supine, relieved with sitting forward.  Some patients will report shortness of breath as well.  Pertinent history questioning should inquire about recent illness, trauma, MI, or insect bites (including ticks).  In addition, a past medical history of cancer or renal failure, as well as, autoimmune and inflammatory disorders should be sought out.

The most common physical exam findings is a pericardial friction rub, occurring in approximately 85% of these patients.  Pericardial effusions develop in approximately 75% of these patients which can cause diminished heart sounds and tachycardia.  Tenderness along the sternal boarder or with epigastric palpation can also occur.

A complaint of “substernal chest pain” dictates obtaining an EKG.  With pericarditis, the EKG can go through 4 phases over the course of several weeks.  Phase 1 is diffuse ST elevations and PR depressions.  Phase 2 is a return to normal, followed by T wave inversions (phase 3) and finally another return to normal however it may take several weeks to months for the T inversions to resolve.  In patients with an associated pericardial effusion, low voltage will be present.  Laboratory tests may reveal elevations of CK-MB and troponin which is then diagnosed as myopericarditis.  In the patient above, the initial troponin was 2.98 with a peak of 16.7.  Additional labs that can be helpful in the workup if there is not a clear-cut viral or traumatic etiology are: CBC, chemistry, sed rate, C reactive protein, anti-nuclear antibody, rheumatoid factor and PPD.  A chest x-ray may reveal cardiomegaly if a moderate effusion is present.

Treatment for viral etiologies includes rest and NSAIDS, including indomethacin.  Prednisone can also be beneficial for refractory cases or those secondary to connective tissue disorders.  Other potential etiologies should be addressed appropriately if the history is inconsistent with a viral cause.  Complications can include a chronic pericardial effusion, constrictive pericarditis or pericardial tamponade.

References:

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: a Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division; 2004.

Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2015 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2015. Print.

Andreeff, Renee A. MS, MPAS, PA-C. Quick Recertification Series:  Acute Pericarditis. Journal of the American Academy of Physician Assistants 2014;27(3):49-50.

Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial Disease: Diagnosis and Management. Mayo Clinic Proceedings 2010;85(6):572–593.

Answer:  Pleural effusion.  There is opacification from the base to the mid-lung fields well delineated with a horizontal cutoff and darker (normal) lung above.

Pleural effusions are accumulation of fluid within the pleural space secondary to either an abnormality of absorption by the pleural lymphatics or by excess production via the pleural capillaries.  Cirrhosis leads to an increase in fluid production either by causing a decrease in oncotic pressure or by migration of fluid from ascites through the lymphatic system.  Other etiologies of pleural effusions are:  congestive heart failure, pneumonia, uremia, pancreatitis, ARDS, TB, malignancy and trauma to the thoracic duct (Chylothorax) or a blood vessel (hemothorax).

The patient’s symptoms are generally related to the length of time that the effusion takes to develop.  A slow developing effusion allows for compensation whereas a rapid accumulation results in acute shortness of breath.  Effusions can also be associated with pleuritic pain, dry cough and even fever depending on the underlying etiology.  Physical exam will reveal diminished breath sounds over the affected lung base, depending on the size of the effusion.  Dullness to percussion and decreased tactile fremitus are also present depending on the size of the effusion.  Tachypnea and hypoxia will be present with large or rapidly accumulating effusions.

A chest x-ray is the most commonly used modality to diagnose a pleural effusion.  As little as 50ml of fluid can be visualized on the lateral x-ray compared to a minimum of 175-200ml being needed to be visible on a frontal view.  The first indication of an effusion is blunting of the normally sharp costophrenic angle(s).  Poor demarcation of the hemi-diaphragm and atelectasis may also be present.  A lateral decubitus film may be useful to distinguish between loculated and free flowing effusions.  Ultrasound can detect as little as 3-5ml of pleural fluid but is usually reserved for the treatment phase.

Treatment may involve observation if small and asymptomatic however for symptom relief or to assist in diagnosis a thoracentesis is generally performed and the fluid obtained can be sent for analysis.  Lights criteria can aid in the determination between exudative and transudative fluids.  Exudative fluids must meet at least one of the following characteristics:  pleural fluid protein to serum protein ration > 0.5, or pleural fluid LDH to serum LDH ration of > 0.6, or pleural fluid LDH > 2/3rds of the upper limit of normal serum LDH.  Other treatment options include thoracostomy or pleurodesis for frequent reoccurrences.

The patient in this case has required bi-weekly thoracentesis for some time and frequently has approximately 2L removed.  Despite this rather large amount of fluid, her PO2 was 100% RA.

References:

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Papadakis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2015 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2015. Print.

Pleural Effusion. In DynaMed Plus, EBSCO Information Services (Accessed April 1, 2016)

Answer:  Staphylococci aureus.  Given the patient’s history of IV drug use and lack of an apparent site of infection, endocarditis should be at the top of the differential diagnosis.  While all of these pathogens can be responsible for endocarditis, Staph aureus is by far the most common cause in an IV drug abuser, accounting for approximately 68% of cases.  Listeria risk factors include pregnancy, elderly or immunocompromised, and those patients with a history of an underlying valvular or structural abnormality.  Enterococci endocarditis has been associated with patients recently undergoing colonoscopies or dental procedures, especially in the presence of an underlying prosthetic valve.  Candida generally presents with a slow progression of symptoms and risk factors include:  indwelling catheters, artificial valves, pacemakers, IV drug abusers and immunosuppressive states.

Endocarditis is refers to an infectious lesion which develops most commonly on a heart valve but can also occur on ventricular septal defect or on intracardiac devices.  These lesions consist of an infectious component, platelets, fibrin and inflammatory cells.  The elderly and those with prosthetic valves are at the highest risk due to some degree of damaged endothelium.  The risk of prosthetic valve infection is greatest during the first 6-12 months after replacement and then gradually declines to a relatively low rate.  Whether mechanical or bioprosthetic, the rate of infection is roughly the same.

Symptoms of endocarditis can be vague and progress over several days to weeks.  Fever occurs in 80-90% of patients and a new murmur is found in nearly as many.  Other common symptoms include myalgias, arthralgias, fatigue, and malaise.  Less common findings include Osler’s nodes, Janeway lesions, Roth’s spots and splinter hemorrhages.  Roth’s spots are retinal hemorrhages and splinter hemorrhages are found under the nails.  Osler’s nodes are painful, erythematous nodules of the pads of fingers or toes whereas Janeway lesions are non-painful, erythematous nodules of the palms or soles.

The definitive diagnosis of endocarditis is made when vegetative endocardial lesions are located and examined.  In the absence of vegetative lesion examination, Duke criteria is commonly used when endocarditis is high on the differential.  It consists of two major criteria and five minor.  Major criteria include positive blood cultures in a patient with no other source and either a positive echocardiogram or a new valvular regurgitation.  Minor criteria include the following:  underlying risk factors, fever > 100.4°F, vascular findings consistent with endocarditis, immunologic findings consistent with endocarditis, and positive blood cultures which fall outside of the more specific major criteria blood culture specifics which are not mentioned here.  A patient is considered to have endocarditis if both major criteria have been met, one major and three minor, or all five minor criteria are positive.

Treatment consists of appropriate intravenous antimicrobial therapy either started empirically or based on culture sensitivities.  Penicillin G, ceftriaxone, vancomycin, and nafcillin or oxacillin are the most commonly used antibiotics.  Surgical removal of lesions may be required for more complicated patients.  The patient mentioned above was started on vancomycin and cefepime at the advice of the infectious disease physician and the following day an echocardiogram revealed a 2cm X 1cm tricuspid valve lesion, the most common site of endocarditis in an IV drug abuser.

References:

Summa C, Walker SAN. Endocarditis Due to Listeria monocytogenes in an Academic Teaching Hospital: Case Report. CJHP The Canadian Journal of Hospital Pharmacy 2010;63(4). doi:10.4212/cjhp.v63i4.935.

Sexton, D, Chu, V. Infective endocarditis in injection drug users. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on April 11, 2016.)

Prasad, P.  Infective endocarditis.  In:  DynaMed Plus, EBSCO Information Services (Accessed April 13, 2016)

Marle MGD. Infective endocarditis from Enterococcus faecalis complicating colonoscopy in Heyde’s syndrome. Postgraduate Medical Journal 2004;80(948):619–620. doi:10.1136/pgmj.2004.019711.

Urbano, F.  Peripheral Signs of Endocarditis.  Hospital Physician 2000:41-46

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Correct answer is B; V-paced pacer should be installed. Answer A is incorrect because AV pacing would be indicated if the patient’s underlying rhythm was sinus, not AF. 2Answer B is correct because of the patient’s underlying rhythm of AF. The AV conduction is not intact which would indicate V-pacing. 2 Answer C is incorrect because ICD’s are used for tachydysrhythmias such as ventricular tachycardia or ventricular fibrillation which this patient does not have. A pace-maker is indicated which differs from an ICD. 2 Answer D is incorrect because AV conduction is not intact during AF with pause, which is indicated for A-pacing. 2

Discussion:

Atrial fibrillation (AF) is defined as disorganized, irregular and rapid atrial activation resulting in loss of effective atrial contractility and an irregularly irregular ventricular response.2 AF is the most common sustained arrhythmia, see Figure 14. When looking at an EKG you will see a lack of discrete P waves and an irregularly irregular ventricular response (QRS complex). Etiology includes heart failure, hypertension, coronary artery disease, valvular disease, acute hyperthyroidism, acute alcohol intoxication, atrial enlargement, post-operative after a major surgery. AF is seen more in the age group over 65, men verse women, and Whites more than Blacks, Hispanics, or Asians. There are different types of AF, paroxysmal (returning to normal baseline within 7 days), persistent (lasting longer than 7 days and will require treatment), permanent (condition lasting indefinitely, and no further attempts to restore normal rhythm have been discussed). 1

Symptoms vary in AF and include, fatigue, dizziness, SOB, weakness, rapid and irregular heartbeat, thumping in chest, and chest pain/pressure.2,3 Taking a full cardiac history of any patient suspected with AF is very important. Knowing all medications, heart disease, valvular disease, alcohol use are all important questions to ask. Upon examination, watching the vital signs, especially heart rate is extremely important. Patients will have an irregularly irregular pulse and commonly be tachycardiac. There may be a displaced PMI or S3 which would suggest ventricular enlargement and elevated LV pressure. Head and neck exam may show elevated JVP, cyanosis, carotid bruits, thyromegaly, or exophthalmos. Heart failure may be presents with rales and pleural effusions.2

To diagnosis AF, an EKG is the golden standard. An EKG will reveal an irregularly irregular rhythm, no discrete P waves and narrow QRS complexes. An echocardiogram may be ordered to show any structural problems. CBC, BMP, TSH are also usually ordered to see if there is an underlying cause. Heart monitors can also be worn by the patient if they go in and out of AF to try and see is there is a cause correlated. 1,2,3

Treatment and management for AF has three goals: control the rate, restore sinus rhythm (if possible), and decrease risk of clot formation which could lead to CVA.2 Pharmacological treatments include calcium channel blockers, beta blockers, and amiodarone for rate control. Amiodarone is used in refractory cases and better for those in heart failure. Chemical cardioversion using IV Ibutilide has seen to be about 50% successful.2,3 Direct current cardioversion is used in patient with an onset of >48 hours to restore a normal sinus rhythm.1,3 Cardiac ablation is also an option. During this nonsurgical procedure, lesions are destroyed, usually around the pulmonary veins, which trigger the abnormal heart rhythm thus creating an entrance and exit block from triggering foci. To help reduce the risk of a CVA warfarin or newer anticoagulants (in non-valvular AF) are used. The CHADS2 and CHA2DS2-VASc are tools to help determine a patient’s risk of developing a clot who have AF, by simply answering yes or no to certain risk factors. 3

References:

1 Brady WJ, Laughrey TS, Ghaemmaghami CA. Cardiac Rhythm Disturbances. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com.ezproxymcp.flo.org/content.aspx?bookid=1658&Sectionid=109426644. Accessed April 11, 2016.

2 Prystowsky EN, Padanilam BJ, Waldo AL. Chapter 40. Atrial Fibrillation, Atrial Flutter, and Atrial Tachycardia. In: Fuster V, Walsh RA, Harrington RA. eds. Hurst’s The Heart, 13e. New York, NY: McGraw-Hill; 2011. http://accessmedicine.mhmedical.com.ezproxymcp.flo.org/content.aspx?bookid=376&Sectionid=40279769. Accessed April 11, 2016.

3 Scheinman MM. Chapter 12. Atrial Fibrillation. In: Crawford MH. eds. Current Diagnosis & Treatment: Cardiology, 4e. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com.ezproxymcp.flo.org/content.aspx?bookid=715&Sectionid=48214544. Accessed April 11, 2016.

 Answer: D. The PERC Criteria, developed in 2008, should be the first choice to guide your medical decision-making regarding a possible PE. It involves eight questions: Age >50?, HR >100?, SaO2 <95%?, hemoptysis?, estrogen use?, surgery/trauma w/hospitalization in last 4wks?, prior VTE?, and unilateral leg swelling?

The PERC Criteria does not give specific guidance about when to order further testing but instead gives a general impression about the likelihood of a diagnosis of PE. If you can answer no to all the above questions and your impression is low based on your gestalt, the PE miss rate is found be only 1.8%. This has been deemed an acceptable level of error based on the risk/benefit of additional testing. If any question is answered yes and suspicion is increased, proceed to the Well’s Criteria as the next step in evaluation.

 Beck’s Triad are the three clinical signs associated with acute cardiac tamponade: low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.

 Charcot’s Triad are the three clinical signs associated with acute cholangitis: jaundice, fever and right upper quadrant abdominal pain.

 Well’s Criteria would be the second step in evaluation if PERC Criteria had raised suspicion of PE. The Well’s Criteria provides a numeric grading scale based on four clinical questions similar to the PERC questions. The tally of the score is used to determine the usefulness of ordering a D-dimer test on the patient. The D-dimer test is sensitive (95-98%) but not specific (40-55%) for PE. A high Well’s score significantly increases the positive predictive value of a (+) D-dimer test, bringing the probability of PE to 79.6%.   This information will justify ordering the next level of testing, a CTA which is ~95% specific for PE.

Reference

Kosowsky, J., Zane, R., Pocket Emergency Medicine 3rd Edition, Wolters Kluwer, 2015, p. 1-16-18

Answer C. This patient has infectious flexor tenosynovitis, which is considered an orthopedic emergency.  The most appropriate next step would be to consult an orthopedic surgeon now for possible surgical intervention. The incidence of infectious tenosynovitis has been difficult to determine1; however, there is an increased risk of a concomitant infection when a penetrating injury potentially inoculates the tendon sheath.1

As it is with our patient, the majority of cases of infectious tenosynovitis are the result of some kind of penetrating trauma.1,3 In all likelihood, our patient’s current medical condition is a direct result of the cut to her finger more than a week prior to her presenting to the ED. Other causes, though, may also be from surgery or dissemination from the blood.2

The most common pathogens involved are Staphylococcus aureus and streptococci, with S. aureus being the more common. It is not unusual, however, for a combination of the two to cause infection.1,2,3 Other potential agents are pseudomonas and mycobacterium.1,3

Infection is most often the result of direct inoculation or colonized S. aureus around damaged skin gaining access into tissue through a wound,1,2,3  a likely scenario for our patient given her history of a cut to her finger.  The bacteria then attach to and further colonize the exposed damaged tissue.2 Specialized molecules on the cell wall of S. aureus enable the bacteria to adhere to different tissue surfaces, and with the aid of elaborating enzymes like proteases and lipases, the bacteria are then able to spread locally.2 It is likely that over time the infection worked its way to the patient’s tendon sheath, where its supply of synovial fluid provides a rich medium for bacterial growth.

Our patient has recently sustained a penetrating injury to her left middle finger, and now the finger demonstrates Kenaval’s four cardinal signs of flexor tenosynovitis:  fusiform swelling, tenderness along the flexor tendon sheath, finger held in slightly flexed position, and exquisite pain upon passive extension.  These findings are pathognomonic for infectious flexor tenosynovitis.3

An x-ray of the finger obtained the day before ruled out the presence of a foreign body or any bony involvement.  The results of the complete blood count (CBC) and the erythrocyte sedimentation rate (ESR) confirmed the presence of an inflammatory response, which helps support the suspicion of an infectious cause.

Infectious tenosynovitis is considered an orthopedic emergency,1,3 so surgical consult with subsequent admission to the OR is the appropriate next immediate step in this patient’s care. The non-operative approaches also listed might be appropriate if the case had presented and been diagnosed earlier in the process, but the fact that antibiotic treatment for this patient has already failed is an indication for surgical drainage.1

References

Foster, MR. Tenosynovitis. http://emedicine.medscape.com/article/2189339. Updated 10/2015. Accessed 03/10/2016.

Lowy, FD. Staphylococcal infections. In Longo, DL [et al], eds. Harrison’s principles of internal medicine-eighteenth edition. McGraw Hill: New York. 2012: 1160-70.

Tsai, E; Failla, JM. Hand infections in the trauma patient. Hand clinics.  1999, May; 15(2): 373-86.

Correct Answer C. CT scan without contrast is the most appropriate initial step in confirming the presence of a subdural hematoma. In patients presenting with acute head trauma, subdural hematomas have been reported to occur in 5-25% of individuals. Subdural hematomas consists of an intracranial mass of blood or calcified emulsions below the inner layer of the dura but external to the brain and arachnoid membrane.  It is the most common type of traumatic intracranial mass lesion.1 and are, also more common in the elderly population for multiple reasons including comorbidities and trauma. Subdural hematomas are typically seen as concave toward the brain and unlimited by suture lines.  Midline shifting is usually present.  Generally, acute subdural hematomas are less than 72 hours old and are hyperdense compared to the brain.

This patient’s demographic and recent history of a fall (pertinent historical feature) with neurological deficits should elicit concern for a subdural hemorrhage (SDH).  He also presented with an therapeutic INR of 2.5, a level within normal limits for a patient on Warfarin.  This also raises the risk of developing a subdural hemorrhage (SDH).

Choices A and B are incorrect because magnetic resonance imaging of any sort would take too much time to indicate a possibly life-threatening SDH.  Patients suspected of having a SDH should have intervention as soon as possible by means of surgery if applicable.  Choice B may be utilized if the initial choice of scan showed an isodense matter representing a subacute SDH (or if the initial image was difficult to interpret.)

Choice D is incorrect because contrast is not necessary to visualize a SDH on a CT scan. It also carries a risk of causing a hypersensitivity reaction, and it may be contraindicated due to renal impairment – a common comorbidity of elderly patients.

References:

1. Meagher RJ, Young WF. Subdural Hematoma. Medscape. 2015. http://emedicine.medscape.com/article/1137207-overview. Accessed February 9, 2016.
2. Centers for Disease Control and Prevention. Home and recreational safety: important facts about falls. http://www.cdc.gov/homeandrecreationalsafety/falls/adultfalls.html. Accessed February 09, 2016.
3. Stevens JA, Corso PS, Finkelstein EA, Miller TR. The costs of fatal and nonfatal falls among older adults. Injury Prevention 2006;12:290–5.
4. Atkinson JL, Lane JI, Aksamit AJ. MRI depiction of chronic intradural (subdural) hematoma in evolution. J Magn Reson Imaging. 2003 April 17(4):484-6.
5. VirtualMedStudent. Subdural hematomas: diagnosis. http://www.virtualmedstudent.com/links/neurological/subdural_hematoma.html. Accessed February 9, 2016.
6. Brain Trauma Foundation, AANS, Joint Section of Neurotrauma and Critical Care. Guidelines for the management of severe head injury. Neurotrauma. 1996 November. 13(11):641-734.

Correct Answer: C 24-hour urine catecholamine. The patient is suffering from a symptomatic tumor of the adrenal medula and sympathetic ganglion known as a pheochromocytoma.  This tumor produces norepinephrine and epinephrine (catecholamines). This can be identified in 1/500 hypertensive individuals. It is most commonly found in 40-60 year olds. Associated risk factors include MEN-II, von Hippel-Lindau disease, and family history. The classic triad includes: palpitations, headache, episodic diaphoresis.  Fifty percent of patients will present with hypertension.  Other symptoms include pallor, flushing, anxiety, weight loss, tachycardia, and hyperglycemia.

The Mayo Clinic found that a 24 hour urine fractionated metanephrines and catecholamine collection is the most reliable case-detection method with a sensitivity of 98% and a specificity of 98%. To ensure adequate sample include a urinary creatinine.  There is an unfortunate high false positive rate due to the normal range being derived from a normotensive group of individuals. A urine screen should look for Vanillyl Mandelic Acid (VMA), metanephrines, and normetanephrine.  A serum epinephrine/norepinephrine level should also be gathered.

The patient could also be hyperglycemic as epinephrine increases glucose while norepinephrine decreases insulin.  They could also show signs of polycythemia from volume depletion.

Plasma fractionated metanephrines are regarded as first line if the patient falls into a high risk for pheochromocytoma.  These include family history, MEN II, previous pheo resection, and an incidental adrenal mass found on imaging showing characteristic features.  Definitive tumor localization should be found by imaging including CT, MRI, I-MIBG, PET scan, or OctreoSCan.

A troponin is indicated during evaluation of patients suspected of having acute coronary syndrome.  The patient is not experiencing angina, nausea, or vomiting, and denies history of cardiac problems therefore making cardiac etiology less likely.   In the setting of palpitations and shortness of breath a troponin may still be indicated.

Thyroid Stimulating Hormone (TSH) is released by the anterior pituitary gland and causes release of thyroid hormone from the thyroid.  A TSH is indicated when there is concern for hyper/hypothyroidism.  Although the patient does report “anxiety” and palpitations the the patient does not endorse other historical findings consistent with hyperthyroidism including: neck fullness, heat intolerance, diarrhea, restlessness, double vision, lethargy, or changes in hair or skin.

A D-dimer is indicated when evaluating a patient for suspected venous thromboembolic disease.  A patient has a low pretest probability for PE/DVT and is therefore more unlikely to have a significant thromboembolic event.

References

Clinical presentation and diagnosis of pheochromocytoma. Clinical presentation and diagnosis of pheochromocytoma. Available at: http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of-pheochromocytoma?source=search_result. Accessed February 16, 2016.

Mahadevan SV, Garmel GM. An Introduction To Clinical Emergency Medicine Guide for Practitioners in the Emergency Department. Cambridge: Cambridge University Press; 2005.

Blackbourne LH. Surgical Recall. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2009.

Correct answer is B. The most likely diagnosis of this patient is acute diverticulitis. This is an obese patient presenting with a fever and crampy LLQ pain, all suggestive of the diagnosis. The patient’s pain is in the LLQ (unlikely appendicitis), denies dysuria (unlikely a UTI), denies a burning sensation (unlikely GERD) and she moved her bowels (unlikely a bowel obstruction). The most appropriate next step would be to obtain an abdominal CT to confirm the diagnosis. Option A is not the correct antibiotic for diverticulitis. Option C is not indicated for diverticulitis unless there are complications and the patient fails medical management. Option D is inappropriate as the patient needs antibiotics (and mostly likely morphine for pain management).

Diverticulosis is the existence of diverticula, which are bulges in the colon wall, and they may or may not have symptoms. Diverticular disease is when they bleed, become inflamed or ischemic. Diverticulitis is when there is inflammation of a diverticulum and it can become complicated by abscesses, fistulas or bowel obstructions.
Diverticulosis prevalence varies based on age. It occurs in under 20 percent of individuals under 40 years old but increases to 60 percent of people by 60 years old. Diverticulitis is present in about 4-15% of individuals who have diverticulosis. In western countries, the disease occurs most often in the left side of the colon and in Asian countries, it occurs more often on the the right side. It is more common in men before the age of 50. Between the ages of 50 and 70, women slightly predominate and over 70, women have a much higher incidence.

The etiology of diverticular disease is unclear but there are numerous risk factors. Some studies indicate that a diet low in fiber increases the rate of the disease. However, increasing the intake of fiber does not decrease symptoms in patients already suffering from the disease. It may, though, decrease the rate of the disease progression by lowering inflammation in the intestines and changing the microflora of the gut. Another risk factor is obesity. The rate of diverticulitis was much greater in those with a higher waist circumference. Individuals who smoke are at a greater risk for the disease. Lastly, medications such as NSAIDs, steroids and opiates are correlated with an increased risk.

Diverticula occur when there is herniation of small mucosal layers that protrude through the intestine and smooth muscle. They herniate through natural openings that have been produced by the vasa recta or vessels in the colon wall. “True” diverticulae include all layers of the GI wall while “false” diverticulae only contain submucosa or mucosa layers. These herniations can happen anywhere within the GI tract but most often occur in the colon, particularly the sigmoid colon, which has the greatest intraluminal pressure. Diverticulosis, which is when the diverticula are not inflamed, increases with age and the cause is not fully understood. Diverticulitis occurs when single or multiple diverticula become inflamed and its cause is uncertain as well. It is thought that fecal matter or food pieces that were undigested can accumulate in the pouches. An obstruction then occurs, leading to distention due to buildup of mucous and increased growth of bacteria. Vessels can become compromised and small or large perforations can follow. Another theory is that there is increased pressure in the lumen which leads to break-down of the diverticular wall. This leads to inflammation, perforation and tissue death. The disease can be mild with small perforations but when they are large, abscesses can form and in rare instances, they may lead to rupture of the intestines or peritonitis.

The most common symptom of patients presenting with diverticulitis is left lower quadrant pain and it is present in up to 70 percent of patients. However, the symptoms will vary depending on the site of the inflamed diverticulum. Patients often note the pain is crampy and their bowel movements may be affected. Associated symptoms may include feeling nauseas, vomiting, having constipation or diarrhea, and experiencing flatulence and bloating. A very small perforation may present without any symptoms or signs of infection. However, it may lead to a more contained outgrowth and signs of systemic disease can arise. Severe forms of the disease is often seen with decreased appetite, nausea and vomiting. Patients usually note that they have been experiencing pain for several days and it is very intense and is only in one area of their abdomen. They are often constipated and a small minority note symptoms of the urinary system, including urgency and dysuria.

There are numerous physical findings that can be present due to diverticulitis and they will correlate with the degree of inflammation and existence of any complications. In uncomplicated diverticulitis, the patient will present with fever and the abdomen is tender over a specific area. Most commonly, the left lower quadrant is tender as most diverticula are present in the sigmoid colon. If the diverticulitis is complicated with an abscess, often a palpable mass that is tender can be appreciated. If there is peritonitis, there may be generalized tenderness along with rebound tenderness or guarding. There may be distention of the abdomen and bowel sounds are often decreased or absent.

Acute diverticulitis is often diagnosed based on the history and physical exam. However, lab tests are often helpful. These include a complete blood count which often show leukocytosis and a left shift which would demonstrate the presence of an infection. However, 20-40% of patients have a normal WBC count, especially those who are immunocompromised, elderly or in those in whom the disease is not severe. A hemoglobin level should be noted when the patient mentions blood in his or her stool. A basic metabolic panel should be obtained if the patient has been vomiting or had diarrhea in order to evaluate electrolyte disturbances. Liver function tests will help to rule out other etiologies. It is also important to get blood cultures before giving antibiotics, especially those who are very sick. Lastly, a pregnancy test should also be done on a woman of childbearing age.
The imaging modality most often used in diagnosis is an abdominal CT. It may show pericolic fat stranding (linear areas of soft tissue around the colon), diverticula, bowel wall thickening and abscesses. If there is an abscess, the CT can help in localizing the site for drainage. Plain x-rays are not informative in diagnosing diverticulitis but it may show a bowel obstruction if one is present.
Diverticulitis treatment can be divided into uncomplicated or complicated disease. If the disease is acute and uncomplicated, conservative treatment is successful in 70-100% or patients. Patients are normally put on a clear liquid diet along with 7-10 days of broad-spectrum antibacterial therapy, covering both anaerobic and aerobic microorganisms. Typically, ciprofloxacin and metronidazole are administered. The clear liquid diet is then slowly adjusted as the patient improves. Patients are hospitalized if they demonstrate an infection with systemic symptoms or are unsuccessful with outpatient treatment. In addition, patients are usually administered morphine for pain. It usually takes 2-3 days in the hospital before patients’ symptoms improve. In complicated diverticulitis, patients may need surgery due to uncontrolled sepsis or an intestinal obstruction.
Once a patient has recovered, he or she is advised to have a colonoscopy in order to determine if there is a malignancy. They should also consume a high-fiber diet for the rest of their lives. The disease’s recurrence is extremely variable and is based on the illness’ severity, any complications or comorbidities.

References

Cunha, John P. A Picture Guide to Diverticulitis. MedicineNet.com. http://www.medicinenet.com/diverticulitis_diverticulosis_pictures_slideshow/article.htm. Reviewed December 24, 2014. Accessed March 14, 2016.

Elmasry, Mohamed. Diverticulitis of the Sigmoid Colon with Fat Stranding on CT Scan. Radiology Spirit. Published July 28, 2010. Accessed March 14,2015.

Pemberton, John. UpToDate. Clinical manifestations and diagnosis of acute diverticulitis in adults. Published December 15, 2015. Accessed March 14, 2016.

Shahedi, Kamyar. Diverticulitis. Medscape. http://emedicine.medscape.com/article/173388-overview#a6. Updated January 14, 2015. Accessed March 14, 2016.18.

The correct answer is D, acute pancreatitis, likely drug induced, as she is taking HCTZ, a drug with high potential for inducing acute pancreatitis .  She also has epigastric pain radiating to the back with nausea, and tenderness to the epigastric and LUQ regions; this is a typical picture of acute pancreatitis, as will be discussed below.  Options A, B, and C are distracters.  Acute cholecystitis is a possible diagnosis, as this is an overweight female in her forties with epigastric pain.  However, she does not have a fever, and PE is benign with no indication of Murphy’s sign; these are two main factors to consider when making the diagnosis.   Acute MI is a distracter as this is a woman with epigastric pain, but it is incorrect as the patient would not have reproducible pain on PE.   GERD is a distracter as it is a common diagnosis with epigastric pain in overweight adults and can radiate to the back; however, nausea is not usual in GERD, and the patient does not have typical GERD symptoms of burning, dysphagia, and regurgitation.

Acute pancreatitis is an inflammatory condition of the pancreas that lasts for several hours and heals over the course of several days.  The incidence of the disease has been increasing in recent years, with approximately 40 cases per year per 100,000 adults.  Incidence is greater in men than woman; however, this does depend on etiology, as alcohol related disease occurs more commonly in men, and women tend to present more as biliary disease.  Idiopathic pancreatitis has no sex-related patterns.  Etiology and pathophysiology of acute pancreatitis are vast.  Thirty to forty percent of cases occur due to cholelithiasis; if a stone from the gallbladder obstructs the ampulla, bile can flow backwards into the pancreatic duct, causing an inflammation.1  Thirty percent of cases in the US is due to alcohol; therefore, this must be one of the pertinent questions asked during the patient interview.  The exact pathophysiology of alcoholic pancreatitis is unclear, but proposed mechanisms include ethanol increasing the protein content of pancreatic juice, thereby eventually leading to protein plugs in the ducts that block outflow.  This blockage leads to inflammation.  Acute pancreatitis can also develop after ERCP to treat choledocholithiasis.5  Other etiology include triglyceride levels above 1000, abdominal trauma, infections such as Hepatitis B and Varicella, and genetic mutations.  There is an extensive list of medications that are known to trigger episodes of acute pancreatitis, including diuretics, atorvastatin, metformin, and Lisinopril.  Pancreas divisum is an anatomic abnormality where two pancreatic ducts are formed, causing an overflow obstruction, as the minor papilla are not able to manage the volume of pancreatic juice flowing into it; this can lead to an inflamed state.  If none of these etiologies are present in a patient, idiopathic acute pancreatitis becomes the answer, as in the case presented above.1

Historical findings in a patient with acute pancreatitis correlate to the array of etiologies mentioned above.  In addition, these patients will usually present with severe, constant epigastric pain with or without radiation to the left upper quadrant.  Pain also radiates to the back and is relieved when sitting leaning forward, as in the case above.  Nausea, vomiting, and dyspnea are associated symptoms.  On physical examination, tenderness to the epigastric region is present.  Hepatomegaly is commonly present in alcoholic pancreatitis.  In gallstone pancreatitis, jaundice and scleral icterus is present if the stone has dislodged and caused an obstruction in the common bile duct.  In severe cases, abdominal distention and hypoactive bowel sounds should raise red flags for ileus.
There are certain laboratory markers to indicate acute pancreatitis.  To make the diagnosis, serum amylase or lipase levels must be elevated three times or greater than the upper limit of normal (or, a combination of epigastric pain radiating to the back and evidence on imaging must be present to make the diagnosis).  An elevated AST, ALT, ALP, and total bilirubin are suggestive of gallstone pancreatitis.  Elevated cholesterol and triglycerides would suggest hyperlipidemia pancreatitis.  Additionally, IgG 4 levels can be checked to determine if an autoimmune pancreatitis is occurring; this marker will be elevated.  Abdominal ultrasound is the first imaging test of choice, as it can detect gallstones.  A CT scan would be necessary if the pain has been present for several days, and a walled-off necrosis or pseudocyst is suspected.6  An MRCP can also be performed if choledocholithiasis is a concern.5

Treatment of acute pancreatitis includes keeping the patient NPO, administering IV fluids, and providing adequate pain relief.  If gallstones or biliary sludge is noted on imaging, a cholecystectomy is performed during the same admission, as future episodes of pancreatitis are now more likely to be triggered.  As the patient’s pain begins to lessen, clear liquids to full liquids to eventual regular diet is followed; once caloric intake is adequate and serum lipase/amylase have trended down to near normal, the patient can be discharged.  Any complications noted on imaging require intensive care admission.  The patient should be followed as an outpatient within 7-10 days to be certain his/her symptoms have resolved.5

References

1. Vege, Santhi Swaroop. Etiology of acute pancreatitis. UpToDate website. http://www.uptodate.com/contents/etiology-of-acute-pancreatitis?source=preview&search=acute+pancreatitis&language=en-US&anchor=H13#H13. Updated May 7, 2015. Accessed June 5, 2016.

2. Afdhal, Nezam, Zakko, Salam. Acute cholecystitis: Pathogenesis, clinical features, and diagnosis. UpToDate website. http://www.uptodate.com/contents/acute-cholecystitis-pathogenesis-clinical-features-and-diagnosis?source=machineLearning&search=acute+cholecystitis&selectedTitle=1~77&sectionRank=1&anchor=H15#H15. Updated August 26, 2015. Accessed June 5, 2016.

3. Cayley, William. Diagnosing the Cause of Chest pain. American Family Physician website. http://www.aafp.org/afp/2005/1115/p2012.html. Updated November 15, 2005. Accessed June 5, 2016

4. Kahrilas, Peter. Clinical manifestations and diagnosis of gastroesophageal reflux in adults. UpToDate website. http://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-gastroesophageal-reflux-in-adults?source=machineLearning&search=gerd&selectedTitle=4~150&sectionRank=2&anchor=H13575781#H13575781. Updated March 11, 2015. Accessed June 5, 2016.

5. Gardner, Timothy B. Acute Pancreatitis. Medscape website. http://emedicine.medscape.com/article/181364-overview#a1. Updated April 1, 2015. Accessed June 5, 2016.

6. Vege, Santhi Swaroop. Clinical manifestations and diagnosis of acute pancreatitis. UpToDate website. http://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-acute-pancreatitis?source=search_result&search=acute+pancreatitis&selectedTitle=2~150. Updated December 14, 2015. Accessed June 7, 2016.

7. Kirkman-Oh, Myriam. Biliary tract obstruction caused by a gallstone in the distal common bile duct. American Family Physician Website. http://www.aafp.org/afp/2000/0701/p164.html. Updated July 1, 2000. Accessed June 7, 2016

Correct Answer A. Activated Protein C resistance (Factor V Leiden) is the most prevalent inherited hypercoagulable disorder & is found in about 30% of all individuals presenting with deep vein thrombosis (DVT). It is primarily observed in individuals of European ancestry & approximately 5% of the European & U. S. white population are heterozygous for this mutation whereas it is essentially absent in the African-American, Native Americans & Asian populations. In this disorder the gene for Factor V has a single point mutation that makes Factor Va resistant to inhibition by activated Protein C & thus leads to an overabundant conversion of prothrombin to thrombin & more fibrin is created leading to excessive thrombus. Hypercoagulability is differentiated into whether it results from primary (inherited) or secondary (acquired) acquired causes. Primary causes include defects in proteins involved in hemostasis.

Protein C & S deficiency are inherited in an autosomal dominant pattern but not all patients with heterozygous defects develop inappropriate thrombosis. Von Willebrands is the most common congenital bleeding disorder present in 1% of the population.

References

Longo, DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012

McCance KL, Huether SE, Brashers VL, Rote NS, Pathophysiology The Biological  Basis for Disease in Adults and Children. Missouri: Mosby Elsevier; 2010

Papadikis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2011 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2011. Print

Tintinalli JE, Stapczynski,JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Pub. Division; 2011

Correct answer: B, endoscopy. Due to the profuse amount of blood loss & that the patient is severely hypotensive with limited improvement in blood pressure after IV fluid resuscitation, it is imperative that the source of his bleed be found.  Upper GI endoscopy is the gold standard as it allows for direct visualization & therapeutic intervention to treat the active bleeding site & its ability to predict the likelihood of recurrent bleeding. In cases like this of severe active bleeding endoscopy should be performed as soon as the patient has been appropriately fluid resuscitated & is hemodynamically stable.

There is already enough information to formulate a list of suspected diagnoses, which is why continuing the history and physical exam (C) in more detail is unnecessary and may actually be detrimental to the patient’s condition. In a patient this young there are very few possible diagnoses to suspect.  While his risk factors are minimal (tobacco use, male gender, medications), his presentation is strongly suggestive of a profuse upper GI bleed, of which PUD is the most common cause.  While a urea breath test (A) could be used to detect H. pylori, this would be an inappropriate test in this setting as it would not help determine the source of the patient’s GI bleed.  Likewise, an abdominal U/S (D) may assist in differentiating a source of right upper quadrant pain, however his combined history and physical exam give no indication that this would be helpful or necessary.

References

1. Swartz, M. Chapter 14 the abdomen. In: Textbook of Physical Diagnosis: History and Exam. 7th ed. Philadelphia, PA: Elsevier; 2014: 429-467.
2. Williams, DA. Chapter 3: Gastrointestinal/nutrition. In: PANCE Prep Pearls: A practical comprehensive study and review guide for the PANCE and PANRE. 1st ed. Lexington, KY: CreateSpace; 2015: 154-161.
3. Collins, RD. Hematemesis and melena, Rectal bleeding. In; Differential Diagnosis in Primary Care. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012: 208-213,367-371.
4. National Institute of Health. Norflex – Orphenadrine citrate tablet, extended release, Orphenadrine citrate injection. April 2007. Available from: http://dailymed.nlm.nih.gov/dailymed/search.cfm?labeltype=all&query=orphenadrine (Accessed February 2016).
5. Papadikis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2011 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2011. Print
6. Tintinalli JE, Stapczynski,JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Pub. Division; 2011

Correct answer: Rapid Strep Test followed by a Strep Culture if negative – This patient is presenting with the typical symptoms of streptococcal pharyngitis. Although the most common cause of pharyngitis is viral, this patient is presenting with signs and symptoms of a bacterial infection. This is most commonly caused by Group A Beta Hemolytic Streptococcus.1  The Centor Criteria for strep throat consists of: Fever (>100.4 degrees Fahrenheit), tender anterior cervical lymphadenopathy, absence of a cough, and pharyngotonsillar exudate.1 Each symptom is worth 1 point. Any patient with 2-3 points should get a throat culture.1 This patient presents with 3 of the 4 symptoms (fever, anterior cervical lymphadenopathy, and no cough), giving her a score of 3 points and therefore needing a throat culture.

A rapid influenza test via nasopharyngeal swab is incorrect. The common symptoms for influenza do include fever, myalgias, and chills but also a cough, nasal congestion, coryza, and headaches.2  This patient is not experiencing a majority of these symptoms, so therefore a rapid influenza test would not be the best choice.

MonoSpot test followed by Epstein Barr titers is incorrect. Mononucleosis is a good option to keep in the differential, but a key symptom that would be a negative indication of mononucleosis is “anterior” cervical lymphadenopathy. Most patients with mononucleosis will have posterior cervical lymphadenopathy.1  Although patients with mononucleosis will have a sore throat and fever, they will also complain of severe fatigue as well as possible abdominal discomfort.

Do nothing because it’s viral, is not the correct answer. This patient has been experiencing high fevers for multiple days which would indicate more of a bacterial infection rather than viral. Most viral infections have lower grade fevers as opposed to bacterial infections where fevers tend to be higher.3 Also, in bacterial infections the fever will get worse a few days into the illness rather than getting better.3

Resources:

1. Williams D.A. PANCE Prep Pearls. CreateSpace. 2014.
2. Papadakis M, McPhee S, Rabow M. Current Medical Diagnosis & Treatment 2015. 2015
3. Duke University Health System. Is it a Bacterial Infection or Virus?. DukeMedicine. https://www.dukemedicine.org/blog/it-bacterial-infection-or-virus. Published Oct. 1, 2013. Accessed Jan. 25, 2016.
4. Wald, E. R. Approach to diagnosis of acute infectious pharyngitis in children and adolescents. UpToDate. http://www.uptodate.com/contents/approach-to-diagnosis-of-acute-infectious-pharyngitis-in-children-and-adolescents?source=search_result. Published Aug. 11, 2015. Accessed Jan. 28, 2016.
5. Marquez-Carrillo M.A. Bacterial Pharyngitis. Medscape. http://emedicine.medscape.com/article/225243-overview. Published Jul. 28, 2015. Accessed Feb. 1, 2016.

The correct answer is Nephrolithiasis (kidney stone) – The classic symptom complex is an acute onset of a colic like pain (crampy intermittent pain) that originates in the flank & radiates to the groin. The pain originates from the hollow viscus ureter & is visceral in nature without any associated peritoneal irritation & is due to the subsequent hydronephrosis creating pressure against Gerota fascia causing flank pain. Stones contained within the kidneys themselves are usually painless, it is once they are released into the ureter that the pain begins. In contrast to the patient with an acute abdomen the patients with renal colic are constantly moving & the pain is wave like & episodic. The pain is commonly accompanied by nausea & vomiting & the adrenergic response to the pain can result in tachycardia. Microscopic hematuria is present in approximately 85% of patients with renal colic, whereas only 30% have gross hematuria. The location of the pain correlates somewhat with the location of the stone. Patients who have a stone in the upper ureter are more likely to have flank pain, whereas those with a mid-ureter stone the pain radiates to the lower anterior quadrant of the abdomen. 75% of stones diagnosed are in the distal ureter & refer the pain to the groin. Stones positioned at the urethral vesicular junction (UVJ) can mimic a urinary tract infection (UTI) with frequency, urgency & dysuria. Confirmation, position & measurement of the size of the stone is achieved with non-contrast abdominal & pelvic CT. Treatment for symptomatic nephrolithiasis includes IV hydration & pain control. NSAID’s are the primary choice (Ketorolac 15-30 mg IV) as they have a direct action on the ureter by inhibiting prostaglandin synthesis. IV or po narcotics may also be indicated but do not affect the cause of the pain. IV antiemetics are indicated for nausea & vomiting. In most cases stones measuring < 5 mm will pass & the patient can be discharged home, if there is no associated infection, with a prescription for an oral opiate & NSAID & instructions to strain their urine & follow up with their PCP and/or urology. Those patients with a stone > 5 mm should be directly referred to urology for intervention as the stone most likely will not pass. In patients who have an associated infection with obstruction, fever & systemic illness admission is indicated & they should be started on IV antibiotics gentamycin or tobramycin 3 mg/kg/day every 8 hours in divided doses plus one of the following ampicillin 1-2 grams IV every 4 hours, piperacillin-tazobactam 3.375 g IV every 6 hours, cefepime 2 grams IV every 8 hours, ticaricillin-clavulinic acid 3.1 grams IV every 6 hours or ciprofloxacin 400 mg IV every 12 hours based on culture & sensitivities.

Pyelonephritis is an infection of the upper urinary tract that can present in a similar fashion to nephrolithiasis but almost always presents with fever which may be absent in an uncomplicated nephrolithiasis. If CT is performed emphysematous pyelonephritis may be detected instead of the urethral stone.

Abdominal Aortic Aneurysm (AAA) must be considered in all patients with risk factors as many times rupturing or expanding AAA is misdiagnosed as nephrolithiasis & CT will help to evaluate.

Cholecystitis can also present similar to nephrolithiasis especially if biliary colic is present, however on exam there is usually right upper quadrant tenderness to palpation that is not normally found with nephrolithiasis.

Pancreatitis can also present similar to nephrolithiasis but will usually have diffuse tenderness to palpation of the abdomen & will have an elevated lipase.

References:

Longo, DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012

Mahadevan SV, Garmel GM. An Introduction to Clinical Emergency Medicine. Cambridge: Cambridge University Press; 2012

McCance KL, Huether SE, Brashers VL, Rote NS, Pathophysiology The Biological  Basis for Disease in Adults and Children. Missouri: Mosby Elsevier; 2010

Papadikis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2011 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2011. Print

Tintinalli JE, Stapczynski,JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Pub. Division; 2011

Correct Answer: D. Pulmonary embolism: PE is very difficult to diagnose & you must be vigilant to ensure that you do not miss it, as the clinical presentation is variable. The clinical findings depend on both the size of the embolus & the patient’s pre-existing cardiovascular status. The utilization of the PERC criteria & Wells criteria have been very helpful in determining whether to pursue PE as a diagnosis. The PERC rule can be applied to patients where the diagnosis of PE is being considered, but the patient is deemed low-risk. A patient deemed low-risk by provider’s gestalt who is also The hallmark of PE is dyspnea unexplained by auscultory findings, ECG changes, or obvious diagnosis on chest x-ray. Dyspnea occurs in 75-85% & pain on inspiration occurs in 65-75% of patients with PE. Routine cardiopulmonary testing in the ED generally demonstrates non-specific findings. The most common findings for PE on EKG are sinus tachycardia seen in about 44% of all cases & non-specific ST-T wave changes. When the PE causes the right ventricular systolic pressure to exceed 40 mm Hg the EKG begins to manifest more specific changes including T wave inversion in V1-V4 & leads II, III, & aVF, incomplete or complete right bundle branch block.. However an S1-Q3-T3 indicative of cor pulmonale is the classic finding on EKG for PE. On chest x-ray the most common finding is clear lungs & absence of pulmonary edema. However the Westermark sign from complete lobar artery obstruction & Hampton’s Hump indicative of pulmonary infarction are relatively specific findings seen in <5% of patient’s. The definitive diagnostic test is chest CT angiography which identifies a clot as a filling defect in contrast enhanced pulmonary arteries.

The time to treatment with therapeutic anticoagulation has an inverse relationship with outcome & anticoagulation should be initiated in any patient with high suspicion for PE while waiting for the diagnostic confirmation. The use of low molecular weight heparin (1 mg/kg BID or 1.5 mg/kg daily) as a bridge to therapeutic anticoagulation with Warfarin sodium (dosing based on the INR) has become the standard of treatment.

References

Slovis B. MDCalc. http://www.mdcalc.com/wells-criteria-for-pulmonary-embolism-pe/. Accessed June 16, 2016

Slovis B. MDCalc. http://www.mdcalc.com/perc-rule-for-pulmonary-embolism/. Accessed June 16, 2016

Longo, DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012

Mahadevan SV, Garmel GM. An Introduction to Clinical Emergency Medicine. Cambridge: Cambridge University Press; 2012

Papadikis, Maxine A., Stephen J. McPhee, and Michael W. Rabow. 2011 Current Medical Diagnosis & Treatment. New York: McGraw-Hill Education/Medical, 2011. Print

Tintinalli JE, Stapczynski,JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD. Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill Pub. Division; 2011

The correct answer is (C) idiopathic intracranial hypertension. This is the correct choice based on the symptoms of headache, blurry vision, papilledema, no MRI brain findings and elevated cerebrospinal fluid pressures. The patient was also recently treated with a tetracycline, is overweight and suffers from polycystic ovarian syndrome. The answer cannot be (B) tension headache because there is papilledema and no history of pulsatile headache. (D) Subarachnoid hemorrhage and (E) glioblastoma multiforme are ruled out based on the negative MRI findings. (A) Migraine headache is more difficult to rule out but typically, patients don’t have papilledema, and concerning vision symptoms, photophobia is more common than blurry vision.

Idiopathic intracranial hypertension affects 1-2 per 100,000 yearly, it is vastly more common in the obese, especially women between the ages of 15 and 44 years old, although it can occur at any age and any habitus. 1

Risk factors include women of childbearing age, recent weight gain of over 4 pounds in recent months. 1 Some drugs appear to have an increased risk of IIH including growth hormone, tetracycline antibiotics, hypervitaminosis A and retinoids including retinoic acid, retinol and isotretinoin. 1  Associated conditions include Addison’s disease, hypoparathyroidism, anemia, sleep apnea, Lupus, Behcet’s Syndrome, PCOS, coagulation disorders, uremia and hypovitaminosis A. 1

The etiology is unknown, it must have an explanation as to why there is increased intracranial pressure. Some people believe there is a cerebral venous outflow abnormality in these patients with IIH. The most prominent and significant finding is the venous sinus thrombosis. Less supported theories include central obesity functioning in increasing intracranial pressure and cerebral edema, which is not supported by MRI. An inconsistent theory is based off of vitamin A intoxication, but not all patients have this feature. 1

The most common symptom of IIH is headache, followed by visual effects that are usually transient and photopsia. Patients can also present with complaints of pain in the back and retrobulbar areas. Additionally, pulsatile tinnitus and more visual effects including diplopia or sustained visual loss. 2

As the most common presenting symptom, headaches are usually described as more severe than normal and they may have a throbbing, pulsatile nature to the pain. Headaches can be daily or less frequent and sometimes are associated with nausea and vomiting.2 In patients who present with papilledema, many will complain of visual symptoms, including bouts of transient obstruction in their visual fields along with photopsia. These vision changes are more common when a patient changes position, with valsalva maneuvers, light and with movement of the eyeball. 2

Tinnitus with pulsations is common in IIH in combination with a headache, the two together strongly suggest an IIH diagnosis. The sound of running water or wind can also be considered tinnitus in this case.2 Lastly, patients complain of diplopia, this is most commonly horizontal and it is associated with a sixth nerve palsy that develops from increased intracranial pressure. 2

On physical exam papilledema, visual field loss and sixth nerve palsy are the most common presenting signs.2 Papilledema, found on fundoscopic exam, is one of the hallmark signs of IIH and it can be bilateral or unilateral. Also on fundoscopic exam one will find flame hemorrhages and macular exudates.2 In the event subretinal hemorrhages are present with papilledema a poor prognosis of visual return is likely. 2

While testing the extraoccular eye movements, one may find a sixth never palsy when asking the patient to follow their eyes horizontally from right to left. The positive finding involves the effected eye not fully moving outward. This is commonly associated with the symptom, diplopia.2 Visual loss is a poor prognostic indicator, some patients will lack return of their vision permanently. Visual acuity is less commonly affected than visual field loss. 2

The patient needs to have blood testing to check a complete blood count, erythrocyte sedimentation rate, serum iron and iron-binding capacity, antinuclear antigen profile and a coagulation profile.2 The ANA testing is to specifically rule out lupus erythematous. Lyme screening is also common in those with a history due to the association between the two illnesses. 2

It is also required to run a MRI of the brain with contrast to first look for any masses that could be causing headache or diplopia and papilledema.2 In a patient with IIH, the MRI studies should be normal. You can also use ultrasound to measure the diameter of the optic nerve. 2

Finally, the best diagnostic study is the lumbar puncture, this is indicated after a mass is ruled out using the MRI. With the lumbar puncture, the opening pressure should be increased well above the normal range of 12-20cm H2O. The cerebrospinal fluid is collected and sent for cell count, cytology, culture, glucose, protein and electrolyte counts.2 In the diagnostic radiology department, lumbar punctures are performed prone with only local lidocaine, the x-ray’s guide the needle into the spinal canal where CSF is easily drawn off.

It is important for patients to try to make lifestyle changes that promote weight loss. If they can’t loose weight or continue to have symptoms they can try medical therapy.3 The first line pharmacologic therapy is Diamox, this therapy is best at removing the headache from IIH symptoms. Dosing can be 500 mg twice daily with room to increase until you reach 3-4 grams per day. At high doses patients experience more adverse effects from the Diamox, including paresthesias, fatigue, decreased libido and metallic tastes. If a patient can’t tolerate Diamox, the second line treatment is furosemide, but it doesn’t have the same efficacy. 3Patients can also consider bariatric surgery for their treatment in effort to lose weight. 3

When patients lack papilledema, but present with chronic headaches, standard migraine headache prophylaxis can also help, examples are amitriptyline, Topamax and propranolol. In a patient with severe papilledema, steroids can help to reduce inflammation in the optic disc and optic nerve, this will assist with vision restoration. Patients can not go on chronic steroids for IIH, the side effects are not worth the benefit. 3

A lumbar puncture with removal of some CSF fluid should provide immediate relief for patients with IIH. If there is a need for frequent lumbar puncture, there is an option to create a CSF shunt. Surgeons prefer to create a ventricular shunt either ventirculoperitoneal or ventriculoatrial shunts. 3 They like these positions because the valve of the shunt can be manipulated from the skin surface. The shunt creates a path from the intracranial space into the abdomen. When the pressure is to high, the shunt is told to release CSF into the abdomen for the body to absorb and destroy. 3

Optic nerve sheath fenestration is a treatment option for patients who struggle with continued vision loss due to papilledema, the fenestration is a creation of slits in the dura around the optic nerve. The slits allow CSF to leak into the orbit where the body absorbs it. There are contraindications to fenestration including: diplopia, optic nerve injury, vessel occlusion or hemorrhage, tonic pupils and infection. 3

Most patients tolerate treatment in the outpatient setting, in the rare case of admission a common reason why is due to visual loss that is chronic with acute worsening. These patients will receive high dose intravenous steroids. If there is no response to steroids and surgery is not an option, the second line pharmacologic treatment is intravenous mannitol, the goal here is to decrease the CSF pressure which should also create relief for the optic nerve. 3

References:

1. Lee, Andrew G, Wall, Michael. Idiopathic Intracranial Hypertension (pseudotumor cerebri): Epidemiology and Pathogenesis. https://www.uptodate.com/contents/idiopathic-intracranial-hypertension-pseudotumor-cerebri-epidemiology-and-pathogenesis?source=search_result&search=Idiopathic+intracranial+hypertension&selectedTitle=3%7E72. Accessed May 23, 2016.
2. Lee, Andrew G, Wall, Michael. Idiopathic Intracranial Hypertension (pseudotumor cerebri): Clinical Features and Diagnosis. UpToDate. https://www.uptodate.com/contents/idiopathic-intracranial-hypertension-pseudotumor-cerebri-clinical-features-and-diagnosis?source=search_result&search=pseudotumor+cerebri&selectedTitle=1%7E72. Accessed May 23, 2016.
3. Gans, Mark S. Idiopathic Intracranial Hypertension Treatment & Management. Medscape. http://emedicine.medscape.com/article/1214410-treatment#showall. Accessed May 23, 2016.

Correct Answer: (C): An ectopic pregnancy is one in which the fertilized egg implants outside of the endometrial cavity, most commonly the ampulla of the fallopian tube.1,2 The classic triad of ectopic pregnancy is abdominal pain, amenorrhea, and vaginal bleeding.1 The B-hCG is utilized to differentiate between normal and abnormal pregnancies.1,2 This patient’s B-hCG was below the discriminatory zone of 2000 mIU/mL, which is the level in which a gestational sac can be recognized on transvaginal ultrasound imaging studies.1 In a normal pregnancy the B-hCG should double every 48-72 hours for the first 40 days of pregnancy.1,2 Since this was not the case, an ectopic pregnancy is the most likely diagnosis.  This patient should undergo a Dilation and Curettage or Methotrexate therapy as to avoid rupture of the ectopic pregnancy.1,2 If this were to be a (D) spontaneous abortion, the B-hCG should have decreased in 48 hours, and would have continued to decrease in each serum test thereafter. (B) Ovarian cyst is in the differential diagnoses because a mass measuring 2cm in early pregnancy with lower abdominal pain lateralized to one side has potential to be a corpus luteal cyst, which is formed at the site of ovulation. An ovarian cyst would likely present with adnexal tenderness rather than fullness.3 The corpus luteum cyst will start to regress around 10 weeks in pregnancy.3 (A) Pelvic Inflammatory Disease (PID) often presents with cervical motion tenderness, chronic lower abdominal pain and abnormal uterine bleeding or dysmenorrhea.4 Often times, the patient has a fever and an increased WBC count.5 The most common organisms responsible for PID are Neisseria gonorrhoeae and Chlamydia trachomitis.4,5 The patient presenting with PID would not have a positive B-hCG.

References

Sepilian VP. Ectopic Pregnancy. Medscape. http://emedicine.medscape.com/article/256448-clinical#b3. Updated November 15, 2015. Accessed June 28, 2016.

Tulandi T. Clinical manifestations, diagnosis, and management of ectopic pregnancy. UpToDate. http://www.uptodate.com. 2016. Accessed June 28, 2016.

Sharp HT. Evaluation and management of ruptured ovarian cyst. UpToDate. http://www.uptodate.com. 2016. Updated November 25, 2015. Accessed June 28, 2016.

Shepherd SM. Pelvic Inflammatory Disease. Medscape. http://emedicine.medscape.com/article/256448-clinical#b3. Updated September 28, 2015. Accessed June 28, 2016.

O’Connell CB. Gynecology. In: A comprehensive review for the certification and recertification examinations for physician assistants. 5th ed. Baltimore, MD: Wolters Kluwer Health; 2015:161-162.

The correct answer is D, acute bacterial sinusitis. Chronic sinusitis is a distracter because chronic sinusitis is defined as symptoms lasting for 12 weeks or more. Here, the patient has symptoms for only three weeks. Initial management of acute sinusitis is to observe for 7 days and treat with antibiotics only if there is no clinical improvement and the patient is febrile. Option B, Acute viral sinusitis should have been resolved within 7-10 days if it was viral in etiology. In this case, patient symptoms are going on from past 3 weeks. Option C, allergic rhinitis would cause symptoms including rhinorrhea, nasal congestion, but would not consist of purulent nasal discharge, sinus pressure or tenderness, low grade fever, or productive cough.

In the United States, 1 out of every 7 adults have an episode of acute rhinosinusitis (ARS) each year and approximately 30 million individuals are diagnosed each year. It is more common in women than men. Highest incidence among adults is seen between ages 45y.o to 64yo. Risk factors include older age, smoking, allergies and asthma, dental disease, and immunodeficiency. Acute bacterial rhinosinusitis (ABRS) comprise of 0.5 – 2.0% of ARS episodes. The pathophysiology of acute rhinosinusitis is associated with three factors including obstruction of the ostia or sinus drainage pathways, ciliary impairment, and altered mucus quantity and quality. Allergic, non-allergic or viral insults can predispose the sinuses to obstruction and reduced ciliary function leading to inflammation and edema of the sinus and nasal mucosa. The inflammation and edema results in decreased ciliary clearance of sinus secretions and/ or obstruction of the ostium leading to retention of secretions, negative sinus pressure, and decrease in partial pressure of oxygen, thereby, allowing infection by bacteria.

Acute bacterial rhinosinusitis (ABRS) is most commonly associated with viral URI. Additionally, it can result as a complication of trauma, granulomatous diseases, dental infection, mechanical obstruction, allergy or non-allergic rhinitis, immunodeficiency, ciliary dysfunction, cystic fibrosis, and other factors that disrupt sinus drainage. Approximately 75% cases of ABRS comprise of Streptococcus pneumoniae, and Haemophilus influenza as the pathogens. Other pathogens include Moraxella catarrhalis, Pseudomonas aeruginosa, Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae. Acute sinusitis pathogens can also be very commonly viral and rarely fungal agents. Patient can have a history of recent URI that lasts more than 7 days or worsens after 7 days, in this case, consider acute sinusitis. ABRS has three common clinical presentations including onset with persistent, severe, or worsening symptoms (nasal drainage, cough). Symptoms of ABRS include sinus pressure, tenderness over the sinus areas, hyposmia, nasal congestion, thick and purulent nasal drainage, postnasal drip, cough, sore throat, fever, fatigue, maxillary dental pain, ear fullness. On physical exam, common findings include tenderness on palpation and percussion of the maxillary and/or frontal sinuses, purulent nasal secretions, mucosal and facial erythema, periorbital edema. Transillumination may show opacification of the maxillary or frontal sinuses.
ABRS is a clinical diagnosis and does not require any imaging or tests unless complications, alternate diagnosis or treatment failure is suspected. One of the following is required to diagnose a patient with ABRS: (1) symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of upper respiratory symptoms, 1 or (2) symptoms or signs of acute rhinosinusitis worsen within 10 days after an initial improvement. X-ray or CT-scan may be used to determine etiology or for confirmation of sinusitis. Sinus aspiration can be performed to determine etiology as well. For treatment or management, Antibiotics are the mainstay for treatment of ABRS, but watchful waiting can be considered for up to 7 days if follow-up is assured. Antibiotic after 7 days should be started if patient’s condition fails to improve. If a decision is made to treat ABRS with an antibiotic agent, prescribe amoxicillin with or without clavulanic acid as first-line therapy for 5 to 10 days for most adults according to current guidelines. Doxycycline or levofloxacin or moxifloxacin is recommended as alternative first line agents for patients with penicillin allergy. Other commonly used antibiotics for second line treatment include third-generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie, clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and clindamycin.3Additionally, recommendations include drinking plenty of fluids, rest, analgesics, topical intranasal steroids, and/or nasal saline irrigation for symptomatic relief of ABRS.

References

Rosenfeld RM, Piccirillo JF, Chandrasekhar SS, et al. Clinical practice guideline (update): Adult sinusitis. Official Journal of American Academy of Otolaryngology—Head and Neck Surgery Foundation. 2015; 152(2S): S1–S39. doi: 10.1177/0194599815572097

JAMA. 2009; 301(17):1844. doi:10.1001/jama.301.17.1844.

Brook I. Acute sinusitis. Medscape website. http://emedicine.medscape.com/article/232670-overview. Updated July 29, 2015. Accessed February 4, 2016.

Hwang PH, Patel ZM. Acute sinusitis and rhinosinusitis in adults: Clinical manifestation and diagnosis. UpToDate website. http://www.uptodate.com/contents/acute-sinusitis-and-rhinosinusitis-in-adults-clinical-manifestations-and-diagnosis?source=search_result&search=acute+sinustis&selectedTitle=2~150. Updated January 22, 2016. Accessed February 2, 2016.

The correct answer is B. Based on the history, this patient has classic symptoms of carpal tunnel syndrome. The Phalen’s maneuver is the only exam listed that is considered a diagnostic test for carpal tunnel syndrome. During this maneuver, the patient is asked to maximally flex their wrists together for one minute. If the patient feels tingling or numbness along the median nerve pathway (the first three fingers and the radial side of the forth finger on the palm side) the test is considered a pertinent positive for the diagnosis of CTS. The test is designed to reproduce the patient’s symptoms during an office visit.

Answer A is the diagnostic test for DeQuervain’s tenosynovitis. This test would be performed if the patient was having pain more focused around the thumb and along the radial aspect of the wrist. This condition is not associated with any nerve entrapment, which is the contrasting feature from CTS. Finkelstein’s test involved the patient placing their thumb inside their hand to make a fist and ulnar deviating the wrist. This would elicit pain over the anatomical snuff box. Answer C is used to determine arterial circulation of the hand. The radial and ulnar arteries are held simultaneously and after the hand is blanched, one of the arteries is released to determine the patency of the vessels. This answer is incorrect in the case of this patient since the test would not reproduce her symptoms and is not related to the median nerve. Answer D is most commonly used to diagnose thoracic outlet syndrome. This answer is incorrect as the patient only has focused pain in the hands, not in the neck or proximal upper extremity.

References

1. Filius A, Thoreson AR, Yang T, Vanhees M, An K, Zhao C and Amadio PC. The Effect of Low- and High-Velocity Tendon Excursion on the Mechanical Properties of Human Cadaver Subsynovial Connective Tissue. 32: 1: 123-128, 2014.
2. Bezuhly Michael, O’Brien J, Lalonde D. Nerve Entrapment Syndromes. In: Neligan P, 3rd edition. Plastic Surgery. Seattle, WA: Elsevier Inc; 2013
3. Carpal Tunnel Syndrome. University of Maryland Medical Center. Published 2016. Accessed April 23, 2016. http://umm.edu/health/medical/reports/articles/carpal-tunnel-syndrome
4. Gejyo F and Narita I. Current clinical and Pathogenetic Understanding of Beta2-m Amyloidosis in Long-Term Haemodialysis Patients. Nephrology (Carlton) 8 Suppl: S45-S49; 2003.
5. Tosti R and Ilyas AM. Acute Carpal Tunnel Syndrome. Orthop.Clin.North Am. 43: 4: 459-465; 2012.

Answer C.  About 80-90% of UTIs are caused by E. coli. It has been suggested that E. coli originate in the gastrointestinal flora and take a fecal-vaginal-urethral route to infection in women. The infection ascends from the urethra into the bladder. Invasion appears to be related to the adhesion process where the bacteria adhere and penetrate into bladder epithelial cells. The bacteria replicate and form a stable reservoir for bladder colonization. The other 5-10% of UTI are caused by Staph. Saprophyticus, particularly in sexually active young women. Rarely, acute cystitis can be caused by a virus or fungus. There is a wider range of causative pathogens in nosocomial infections, including E. coli (27%), Klebisella (11%), Pseudomonas (11%) and Candida albicans (9%). These are typically caused by urinary catherization where the bacteria invade through a contaminated catheter.

Uncomplicated cystitis in women can be treated with short-term antimicrobial therapy. The suggested regime is a fluoroquinolone such as Ciprofloxacin or nitrofurantoin (Macrobid) for 3 to 5 days4. Bactrim DS can be used as an alternative to a quinolone in resistant E.Coli, however resistance to Bactrim is also becoming increasingly emergent. Since UTI is rare in men, the duration of antibiotic therapy depends on the underlying etiology. Complicated cases are treated with IV or PO fluoroquinolones or aminoglycosides.  Pregnant patient’s best respond to 7-14 days of amoxicillin or Macrobid. Bactrim and Cipro should not be taken during pregnancy.

Increasing fluids, avoiding intercourse and hot sitz baths are helpful. There is not enough evidence to conclude that drinking cranberry juice is beneficial, although a theory exists that pure cranberry juice acidifies the urine and prevents bacteria from adhering to the bladder wall. Phenazopyridine is a urinary analgesic that cannot be used for more than 48 hours because of the side effects of methemoglobinemia and hemolytic anemia, but it is useful for symptom relief. The patient should be warned that the urine will turn dark orange. Infections typically respond quickly to therapy and failure to respond suggests further investigation.

Future infections can be prevented with proper hygiene, such as avoiding washing with soap or using baby wipes and urinating after intercourse. Women who have more than three episodes of UTI a year are candidates for prophylatic antibiotic therapy. Hospitals should strive to only use indwelling catheters when necessary, implement prompt removal of catheters when they are no longer necessary and maintain proper insertion techniques.

References

1. Meng MV, Walsh TJ, Chi TD. Urologic Disorders. In: Papadakis MA, McPhee SJ, CURRENT Medical Diagnosis & Treatment. 54th ed. United States of America: McGraw-Hill Education; 2015: 931-933.
2. Foxman, B. Epidemiology of Urinary Tract Infections: Incidence, Morbidity, and Economic Costs. Am J Med. 2002; 113(1A): 5S-13S. doi: 10.1067/mda.2003.7
3. Salvatore S, Salvatore S, Cattoni E, et al. Urinary tract infections in women. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2011;156(2):131-136. doi: http://dx.doi.org.ezproxymcp.flo.org/10.1016/j.ejogrb.2011.01.028.
4. O’Connell CB. Urinary Tract Infection. In: Certification and Recertification Examinations for Physician Assistants. 5th ed. Baltimore, Maryland: Wolters Kluwer Health; 2015: 136.

5 Williams, DA. Genitourinary System. In: PANCE Prep Pearls. 1st edition. United States of America: Dwayne A. Williams; 2014: 335.

6. Cranberry xyloglucan structure and inhibition of escherichia coli adhesion to epithelial cells. – J Agric Food Chem. (- 23):- 5622. doi: – 10.1021/acs.jafc.5b00730.

The answer is B. Self-monitoring glucose finger sticks are not appropriate to make a diagnosis of type 2 diabetes.  Glucometers are sometimes inaccurate in glucose readings and many times readings may fluctuate between fingers and hands. Finger stick readings are the main way for patients to log their blood sugars at home and give a clinician a good idea if a patient’s current diet and pharmacotherapy regimen is adequate.  However, in the clinical setting for an official diagnosis a finger stick is not sufficient.  Lab work is mandatory for a diagnosis.

A: Fasting plasma glucose (FPG) is the most common and least expensive test used to assess impaired glucose metabolism. A fasting plasma glucose ≥ 126 mg/dL is considered the threshold for diabetes.  The range between 100-125 mg/dL is in the pre diabetic zone, while 70-99 mg/dL is considered normal blood glucose levels. This test needs to have the patient fasting for a minimum of eight hours prior to venipuncture to receive an accurate result. If this test shows ≥ 126 mg/dL on two separate occasions, it is diagnostic of type 2 diabetes mellitus. Another option using the FPG is a random plasma glucose. If the results are ≥ 200 mg/dL and the patient is experiencing symptoms (i.e. polydipsia, polyuria, fatigue, etc.) this also acceptable diagnostic criteria.

C:  The OGTT, although more sensitive than the FPG test, it is less convenient to administer. In non-pregnant adults, 75 grams of a glucose beverage is consumed in over 5 minutes.  Blood is drawn 2 hours later to determine the insulin response. If the 2 hour plasma glucose reports ≥ 200mg/dL, it is diagnostic of diabetes mellitus. If the result is between 140-199 mg/dL, it is indicative of impaired glucose tolerance (IGT) or prediabetes.  Before this glucose challenge, a patient needs to be fasting a minimum of 8 hours.

D:  Hemoglobin A1C ≥6.5% is indicative of diabetes mellitus and chronic hyperglycemia. This test measures the glycated hemoglobin levels for the past 90 days in a patient and gives the clinician an average blood sugar range for that period of time. The “pre-diabetes” range of A1C is 5.7-6.4%. A normal A1C level should be below 5.6%. Once a patient receives a diagnosis of diabetes, an A1C should be checked twice yearly at minimum. If a patient requires closer monitoring, than more frequent testing is acceptable.

References

Alter DN, Laposata M. Pancreatic Disorders. In: Laposata M. eds. Laboratory Medicine: The Diagnosis of Disease in the Clinical Laboratory. New York, NY: McGraw-Hill; 2014.

Molina PE. Chapter 7. Endocrine Pancreas. In: Molina PE. eds. Endocrine Physiology, 4e. New York, NY: McGraw-Hill; 2013.

Pagana KD, Pagana TJ. Mosby’s Manual of Diagnostic and Laboratory Tests. St. Louis, MO: Mosby/Elsevier; 2010.

Answer is B. Polymyalgia Rheumatica (PMR) is an inflammatory disease that causes muscle pain and stiffness particularly in areas of the shoulder girdle, upper arms, neck, lower back and thighs (1). A patient’s symptoms develop very quickly and tend to be worse in the mornings (1). This condition typically affects individuals greater than 65 years old and rarely occurs in those under 50 years old (1). While this is an inflammatory condition, PMR does not cause swelling of the joints, which is one aspect that has made it increasingly hard to recognize (1). However, one way providers have been able to distinguish PMR from other similarly presenting conditions is by the quick response time patients with PMR have to a low dose course of daily corticosteroids (1).

There are three main risk factors associated with occurrence of polymyalgia rheumatic: age, sex, and race/region (2). Most often, PMR affects older individuals above the age of 50 and is not typically seen in those any younger. The average age of PMR onset is 73 years old (2). Polymyalgia rheumatica is two times more likely to occur in females than males, even more so in Caucasian females in northern European populations (2). Due to the association found between PMR and giant cell arteritis, Caucasian women over the age of 50 are at the highest risk for developing both of these conditions (3). While women are at an increased risk for the two disorders, research has shown that men with giant cell arteritis are more likely to experience potentially worse eye involvement, often progressing to blindness (3). Both PMR and giant cell arteritis are quite prevalent conditions (4). It was determined that there are an estimated 711,000 American individuals with PMR and an estimated 228,000 with giant cell arteritis in the United States (4).

In contrast with many other rheumatic disease states, the target of inflammation in PMR is still unknown (5). It is believed that the synovial membrane is the most likely target, as synovitis around the joints of the shoulders, hips, knees, wrists, and metacarpalphalanges have been revealed via sonographic and immunohistochemical methods (5,7). Additionally, there is an increased frequency of peripheral arthritis in patients with PMR, which further supports this theory (5). Both polymyalgia rheumatica and giant cell arteritis have a similar course of pathophysiology, with underlying “abnormalities of cellular immunity leading to vessel and systemic inflammation” (6). One major difference being, however, that in patients with PMR, it has been studied that inflammation is mainly confined to the articular and perarticular tissues (6). In those with giant cell arteritis, there is evidence of severe inflammation confined to the vessels due to the presence of large-vessel vasculitis (6). Regardless of location, cytokines, specifically IL-6, and tumor necrosis factor-alpha play a major role in the progression of inflammation in those with either condition (6). Individuals with PMR or giant cell arteritis typically have an elevated level of IL-6, which is the most likely cause of the systemic inflammatory response that occurs (7). The majority of studies done on patients with PMR have revealed that a decrease in circulating IL-6 levels is directly associated with resolution of clinical manifestations in patients (7). There is also thought to be an autoimmune correlation to PMR. There may be an “imbalance between the immunosuppressive T-regulatory lymphocytes (T-reg) and proinflammatory T-helper 17 (Th-17) cells in both PMR and giant cell arteritis (8). There has shown to be a decreased incidence of circulating T-reg cells compared to an increased number of Th-17 cells in patients with PMR (8). Unfortunately, not enough data has been gathered to support any conclusions regarding the association of other circulating cytokines (interleukins, tumor necrosis factor-alpha) to PMR (7). However, recent studies have revealed that interferon-gamma (IFN-gamma) is present in about 70% of temporal artery biopsy samples taken from individuals with giant cell arteritis (7). This interferon-gamma has not been found in individuals with pure PMR, which can lead researchers to believe that IFN-gamma may be pertinent to the development of the vasculitis so characteristically associated with giant cell arteritis (7). Findings such as these are crucial for providers to know and understand as they can assist greatly in the differentiation between two similar conditions.

PMR is a condition of generalized aching pain and stiffness throughout an individual’s body (1,2). Typically, the first symptom that a patient experiences is an ache or pain in their shoulders (2). Aches or pains in the neck, upper arms, wrist, elbows, buttocks, hips, thighs or knees can then follow (2). In addition to the pain, a severe stiffness will present in the affected areas (2). Majority of times the signs and symptoms of PMR occur bilaterally (1), The symptoms of PMR have been found to develop as quickly as overnight, or more commonly, over the course of a couple of days to weeks (1). Most often, this stiffness will be most noticeable in the morning, lasting a minimum of 30 minutes, and/or after long periods of inactivity (1,2). Patients also experience a decreased range of motion in the affected areas (2). Aside from the musculoskeletal symptoms, there may also be some general, flu-like symptoms, which include fever, fatigue, malaise, loss of appetite, and unexpected weight loss (2). PMR can have significant effects on an individual’s ADLs (2). The characteristic pain and stiffness associated with PMR can result in a struggle to carry everyday activities such as bathing, trouble lifting one’s arms over their head, brushing or doing one’s hair, getting out of bed, getting dressed, standing up from a chair, getting in or out of a car, and even trouble sleeping (2).  Polymyalgia rhuematica is clinically diagnosed on the basis of 3 main factors – patient’s medical history, symptoms and physical exam (6). Majority of the time, physical exam findings will include pain with movement that inhibits active range of motion in the shoulder and hips (6). The patient’s passive range of motion, in addition to their muscle strength, should be normal (6). It is important to note that fundamentally muscle weakness is not a symptom of PMR (7). However, true muscle weakness can be difficult to evaluate in a patient with PMR due to the significant pain and discomfort they experience (7).

Unfortunately, there is no single gold standard test or method of imaging that can conclusively diagnose PMR (3). However, there are a variety of lab tests now utilized by health care professionals to aid in verifying a diagnosis or ruling out a different diagnosis or cause of the patient’s symptoms (3). In patients with PMR, one of the most common lab findings is an elevated erythrocyte sedimentation rate (ESR) or sed rate (3). This is a measurement test of inflammation based on how long it takes for red blood cells to fall to the bottom of a test tube filled with unclotted blood (3). Red blood cells that fall quickly signify the presence of inflammation in the body. While this lab test is sensitive for PMR, the ESR is not specific (3). An elevated ESR level strictly indicates active inflammation in the body. The problem is that this is a finding of a number of other arthritic and rheumatic conditions (3).  Therefore, an abnormal ESR measurement cannot solely confirm a PMR diagnosis (3). For this reason, there are other specific tests used to help definitively rule out other disease presentations that can mimic that of PMR. One is the C-reactive protein (CRP), which is another measurement of inflammation (3). Like the ESR, the CRP level will be elevated in the majority of PMR patients (3).

Polymyalgia rheumatica is a chronic, limiting condition; therefore, the primary goals of therapy for patients with PMR include managing painful myalgia, improving muscle stiffness and ultimately resolving disease progression (7). The first line treatment of choice for PMR is corticosteroid therapy, typically that of Prednisone or prednisolone (6,7). This has been the foundation of successful PMR management since 1951 (6,7). Corticosteroids have been found to not only result in total or near-total symptom resolution, but also play a role in normalizing the elevated ESR level (7). Once initiated, patients can expect to experience symptom relief within 2-3 days (7). If, however, the symptoms are not relieved or controlled within 1 week, the corticosteroid dose may be increased (7). At this point, it is imperative for a patient’s provider to consider the possibility of a giant cell arteritis diagnosis, especially if the patient is still not experiencing symptom control with 20mg of Prednisone (7). Once the patient demonstrates a sufficient response to the corticosteroids, the starting dose should be sustained for 1 months duration before gradually starting to taper downward to the lowest effective dose (6). The tapering of Prednisone in these patients plays a huge role in remission on their PMR. If started at 15mg Prednisone, it was found that a slow tapering, of less than 1mg/month, correlated with fewer occurrences of relapse (7). Once tapered down to 10mg per day, a gradual taper of Prednisone by 1 mg every 2 months until therapy cessation was found to correlate with optimal regulation of disease activity (7).

It is important to note that it is very common for disease flare-ups to occur throughout ones corticosteroid taper and typically these require temporary increases in treatment (6). Tapering in general should be directed based on a patient’s clinical response to treatment. This includes monitoring levels of “decreased pain and stiffness, decreased morning stiffness, and decreased shoulder pain or limitation on exam” (7). In addition to patient’s responses to corticosteroid therapy, overall physical function, mental function, and normalization of patient’s inflammatory markers are other important factors to consider as measures of disease activity and treatment response (7). However, they are not factors which on their own should act as indicators for alterations to or cessation of treatment (7). Patients should expect to continue their specific corticosteroid therapy for a minimum of 1-2 years (6). In addition to possible flare-ups, the majority of patients also have a minimum of 1 relapse during their corticosteroid taper (6). “The factors associated with an increased risk of relapse include persistently high levels of IL-6 and CRP despite treatment, in addition to a rapid rate of prednisone withdrawal (6).” Relapses are most likely to happen within the first 18 months of corticosteroid treatment and then within 1 year of withdrawal (7). Therefore, it is important for all patients to be closely monitored for any signs of symptoms reappearance during their corticosteroid tapering, in addition to 12 months after therapy is discontinued (7). The next step in potential PMR treatment and management is non-steroidal anti-inflammatory drugs, or NSAIDs, such as Ibuprofen or Naproxen (6,7). If there are no contraindications for a patient’s use of NSAIDs, they may be helpful in offering additional pain relief. However, in a study of 232 patients with PMR, an association between NSAIDs and drug-related morbidity was found (7). Therefore, it is suggesting that proceeding with NSAID and corticosteroid treatment should be cautious and perhaps only considered if patients have unbearable adverse effects from corticosteroids (7). Overall, once treated polymyalgia rheumatic usually resolves as quickly as 2-3 days. With the help of a timely diagnosis and sufficient treatment, patients with PMR have a tremendous prognosis (7). Even without treatment, it will resolve on its own but may take as long as several years.

References

1. Docken W P. Polymyalgia Rheumatica. American College of Rheumatology. http://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Polymyalgia-Rheumatica. June 2015. Accessed March 4, 2016.

2. Polymyalgia Rhuematica. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/polymyalgia-rheumatica/basics/symptoms/con-20023162. September 17, 2015. Accessed March 4, 2016.

3. Polymyalgia Rheumatica and Giant Cell Arteritis. National Institute of Arthritis and Musculoskeletal and Skin Disease. http://www.niams.nih.gov/Health_Info/Polymyalgia/. April 2015. Accessed March 4, 2016.

4. Helmick CG, Felson DT, Lawrence RC, Gabriel S, Hirsch R, Kwoh CK, et al.; National Arthritis Data Workgroup. Estimates of the Prevalence of Arthritis and Other Rheumatic Conditions in the United States, Part II. Arthritis Rheum. 2008 January ; 58(1): 26?35. doi:10.1002/art.23176

5. Cimmino M A. Genetic and Environmental Factors In Polymyalgia Rheumatica. Annals of the Rheumatic Diseases – The Eular Journal. 1997: 56;576-577 doi: 10.1136/ard.56.10.576

6. Clifford A, Hoffman G S. Polymyalgia Rheumatica and Giant Cell Arteritis. Cleveland Clinic – Center for Continuing Education. June 2014. Accessed March 4, 2016.

7. Saad E R. Polymyalgia Rheumatica. Medscape. http://emedicine.medscape.com/article/330815-overview. September 23, 2015. Accessed March 4, 2016.

8. Kermani T A, Warrington K J. Advances and Challenges In The Diagnosis and Treatment of Polymyalgia Rheumatica. Therapeutic Advances in Musculoskeletal Disease. February 2014; 6(1):8-19.

9. Lyme Disease Tests. Lab Tests Online – AACC. https://labtestsonline.org/understanding/analytes/lyme/tab/test/.  October 16, 2015. Accessed March 4, 2016.

The answer is C. This patient has a history of MGUS which can progress to multiple myeloma, which could present as a renal injury. A urine dipstick only detects albumin in the urine and no other proteins such as Bence Jones proteins as seen with multiple myeloma. The 24 hour urine will also give a more accurate creatinine clearance. Renal biopsy is performed after other less invasive exams have been exhausted and not rendered a diagnosis for increasing renal injury. Although Aleve should be discontinued as it decreases blood flow to the kidneys and can cause renal injury, a 24-hour urine collection needs to be ordered. Tylenol would be a better option for pain management. This patient has a weak urinary stream and it is important to make sure this patient does not have an obstruction causing hydro nephrosis and kidney damage. CT has a high dose of radiation and is expensive. An ultrasound is a better option for first imaging studies and should be ordered to rule out an obstruction.

MGUS is the most common plasma cell proliferative disorder and occurs in approximately 2-3% of the white population of greater than 50 years of age. Men are more commonly affected and it is 2-3 times more common among the black population. There is no discrimination between the white and black population when it comes to progression of MGUS to multiple myeloma (MM). There is a genetic component. Patients who have a first degree relative with MGUS or MM are at a two-to-threefold higher risk of developing MGUS. Obesity and immunosuppression also increase your risk of developing MGUS. 1

The cause of progression from MGUS to MM are not well understood. There are, however, different types of MGUS that progress to different malignancies. The IgA and IgG variant have shown progression to MM, primary amyloidosis, plasma-cell leukemia or light-chain deposition disease. The IgM variant has an increased risk of progression to Waldenstrom macroglobulinemia, CLL, or other types of non-Hodgkin lymphoma and very rarely progresses to MM.2
MGUS is most often asymptomatic and an incidental finding when working up an older patient with several common symptoms and laboratory abnormalities in which a serum-protein electrophoresis or immunofixation is ordered. A monoclonal (M) protein is often found in the serum or urine. Patient that are symptomatic usually have the IgM variant and present with peripheral neuropathies. This can easily be overlooked in patients already suffering from diabetic neuropathy. This finding does require a multiple myeloma work up. MGUS differs from MM in that it does not have any of the CRAB criteria for multiple myeloma. For the diagnosis of MGUS the patient cannot have hypercalcemia, renal failure, anemia and lytic bone lesions attributed to plasma-cell proliferative disorders.2

The diagnostic tests are serum protein electrophoresis with immunofixation and measurement of serum immunoglobulins. In MGUS the patient is positive for monoclonal (M) protein of There is no treatment for MGUS and it often does not cause any complications. It often goes undetected for many years since it is asymptomatic. The practitioner should be aware of alarming symptoms that could mean the MGUS has progressed to MM or other malignant disorders and know what exams to order. In our case above, the patient came to the nephrology clinic due to an increase in his creatinine levels, indicating worsening of renal function. This patient was fairly asymptomatic except for neuropathy in his lower extremities, most likely from his diabetic neuropathy. He was taking Lasix but was taken off of it 3 days prior to the appointment with us. He was still taking Aleve. The Lasix could have made him volume depleted. The Aleve is decreasing blood flow to the kidneys. Both of these cause a pre-renal injury and cause a spike in serum creatinine levels. His urinary frequency and weak stream could be a sign of an obstruction and an ultrasound should be ordered to check for hydronephrosis. We did a urinalysis in the office and it was pretty benign with trace protein. Since he has a history of MGUS and one of the signs of progression to MM is worsening kidney functions, the urine should be evaluated for Bence Jones proteins also known as light chain proteins. We ordered a 24-hour urine collection since it gives a more accurate creatinine clearance than serum calculated levels and gives us the total protein excreted. Dip stick urinalysis are good at detecting albumin in the urine but does not do a good job at detecting smaller proteins such as light chains. We followed up with our patient after two weeks and his 24-hour urine collection showed a creatinine of 1.7 (decreased but still elevated) and an abnormally high amount of kappa light chains. This could mean that he has light chain MGUS which is benign but can progress to MM or that he has light chain deposition disease in his kidneys which has a poor prognosis. The only way to get a better understanding of what is happening in his kidneys and to determine if it is something that should be treated is to do a renal biopsy. We performed a renal biopsy on this patient but results are pending. In this case the renal biopsy will tell us if the patient has something that can be treated and prevent further renal injury or if treatment is not indicated.4

References

1. Greer, John P., and Maxwell Myer Wintrobe. Wintrobe’s Clinical Hematology. Philadelphia, PA: Lippincott Williams & Wilkins, 2014.

2. Epocrates. MGUS https://online.epocrates.com/u/29611173/Monoclonal+gammopathy+of+undetermined+significance. Accessed February 10, 2016.

3. Damon LE, Andreadis C. Blood Disorders. In: Papadakis MA, McPhee SJ, Rabow MW. eds. Current Medical Diagnosis & Treatment 2015. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com.ezproxymcp.flo.org/content.aspx?bookid=1019&Sectionid=57668605. Accessed February 10, 2016.

4. Watnick S, Dirkx T. Kidney Disease. In: Papadakis MA, McPhee SJ, Rabow MW. eds. Current Medical Diagnosis & Treatment 2015. New York, NY: McGraw-Hill; 2014. http://accessmedicine.mhmedical.com.ezproxymcp.flo.org/content.aspx?bookid=1019&Sectionid=57668614. Accessed February 10, 2016.

Answer C. Right knee will show evidence of increased in narrowing in the lateral space joint compared to the medial space joint. Subchondral sclerotic bone development on the lateral aspect and osteophytes.  c) is the correct answer because patients with valgus alignment will have the most stress on the lateral aspects of their knees due to the load bearing axis being shifted to the outer compartments of their knees.3 The image to the right best represents a valgus deformity of an osteoarthritic knee on X-ray.5 There is evidence of joint space narrowing more on the lateral aspect of the knee compared to the medial aspect. This confirms that the misalignment effects the joint region and the mechanical stresses that occurs. 2

Osteoarthritis (OA) or also known as primary OA, is a degenerative joint disease involving multiple factors which determine the progression of the disease. Compared to secondary osteoarthritis, this type involves underlying conditions that can enhance the risk of developing osteoarthritis such as congenital or bone disorders. 1 Both types of osteoarthritis are commonly diagnosed clinically. Diagnosis is based on patient’s overall age, history and physical, and radiographic findings. Idiopathic OA can be localized or general, and usually occurs in the hands, hips, knees and feet.1 Common risk factors include increasing age, female, obesity, muscle weakness, repetitive use, previous injury and genetics. 1 The patient that is mentioned in the question above has several of these risk factors: her advanced age, female and she is obese. Another risk factor for osteoarthritis is misalignment of the knees. Having a valgus or varus deformity causes a shift in neutral alignment of the hip, knee and ankle. This affects the load bearing axis causing an uneven distribution of mechanical forces. 2

Pathophysiology: Since osteoarthritis is a chronic disease, it involves the progression of joint degeneration, articular cartilage and synovial fluid damage. It was once thought to be a non-inflammatory process but recent studies have revealed that an inflammatory process does play a role in the disease progression. 1 The degradation process includes the pro-inflammatory factors that produce enzymes that are accountable for the overall joint destruction. Other factors that are found to expedite this process include the risk factors that have been mentioned earlier. Mechanical factors such as repetitive use will result in stimulation of these pro-inflammatory factors. Also, weight bearing status has proven to be a major risk factor to increasing the progression of the disease. Patients who are obese increase their weight bearing load along their hips, knees and ankles, thus causing irritation to the joints.

History and physical exam findings: Completing a history and physical is essential to the diagnosis. Older adult patients usually complain of localized or general joint pain that is exacerbated with activity and relieved by rest. Joint stiffness is noted to increase throughout the day and even correlated with weather changes.1 On the physical exam, these patients will have limited range of motion and tenderness to palpation on the medial and/or lateral joint line. Pertaining to the patient mentioned in the above question, this patient may have crepitus, where there is arthritic changes in the patellofemoral area.1 Also, patients with varus or valgus alignment are associated with an increase in progression of osteoarthritis and will have pain on varus or valgus stress of the joint. 2

Diagnostics: Diagnosing osteoarthritis is primarily based on clinical findings. Imaging is pertinent to confirming and assessing the progression of the disease. Radiographic imaging is used to assess the severity and presence of the disease. Findings may include: narrowing of the joint space, subchondral sclerotic bone, osteophytes and/or subchondral cysts. 1 Magnetic resonance imaging (MRI) can be used to confirm the diagnosis by evaluating the presence of cartilage abnormalities, edema, and other pathology. However, it is not necessary to order an MRI for the diagnosis of osteoarthritis. 1 Lab values that can used for part of the patient assessment include, aspiration and evaluation of the synovial fluid, rheumatoid factor (RF) titers, and erythrocyte sedimentation rate (ESR). 1

Management and Treatment: Treatment of this disease includes conservative management and surgical options. Initial treatment of osteoarthritis tends to favor conservative options such as acetaminophen and other non-inflammatory medications. Patients are also encouraged to participate in exercise programs and weight loss counseling to further symptom relief. 5 Another option for patients that have persistent symptoms are intra-articular injections, which can be cortisone or hyaluronic acid. When patients fail conservative treatment and continue to be symptomatic, surgical consultation is indicated. Total joint replacement is the definitive treatment option for osteoarthritis. It relieves patients’ symptoms and improves joint functionality.1

References

1. Kalunian, K.C., Tugwell, P, et al. Clinical manifestations of osteoarthritis. UpToDate. http://www.uptodate.com/contents/clinical-manifestations-of-osteoarthritis?source=machineLearning&search=valgus+osteoarthritis++knee&selectedTitle=4~130&sectionRank=1&anchor=H5#H5. Updated December 30, 2013. Accessed April 23, 2016.
2. Sharma, L. The role of varus and valgus alignment in knee osteoarthritis. Arthritis and Rheumatism. http://onlinelibrary.wiley.com/doi/10.1002/art.22514/pdf. Published November 4th 2007. Accessed April 23, 2016.
3. Eustice, C. What is Varus or valgus knee deformity? Verywell. https://www.verywell.com/what-is-varus-or-valgus-knee-deformity-2552048. Updated March 3rd, 2016. Accessed April 23, 2016.
4. Venables, P.J.W., Maini, R.N., et al. Clinical manifestations of rheumatoid arthritis. UpToDate. http://www.uptodate.com/contents/clinical-manifestations-of-rheumatoid-arthritis?source=machineLearning&search=rheumatoid+arthritis+knee&selectedTitle=1~150&sectionRank=1&anchor=H12#H1598951. Updated November 28th, 2015. Accessed April 23, 2016.

The correct answer is B) Esophagogastroduodenoscopy (EGD). The patient’s hemoptysis, in addition to tremor, hepatomegaly, abdominal distention, headaches, and elevated BP, are all common presenting symptoms of advanced alcoholic liver disease. He is likely experiencing an irritated, or perhaps torn/ruptured, esophageal varix resulting in blood appearing in his mucus secretions. The increased alcohol consumption is a likely trigger for the progression of an already existing problem. Upon investigating his past medical history, it would be found that this patient is an alcoholic. His lorazepam is taken as needed for withdrawal symptoms. He is on a multivitamin due to the number of nutritional deficits that may develop in alcoholics.

If the patient also presented with fever and produced a positive lung examination, one would consider a pneumonia or other respiratory infection as the cause of his hemoptysis. If this were the case, then plain radiography and peripheral blood cultures would both be diagnostic of a lung consolidation or the potential systemic manifestations of infection, respectively. A pneumonia, other lung infection, or malignancy would also be high on the differential diagnosis if the patient were a chronic tobacco smoker or had other concomitant comorbidities that would decrease his immunity. The patient does not need an emergent abdominal CT scan as he is not presenting with acute abdominal symptoms. However, he may require further imaging of his liver in the future to screen for hepatic pathology such as hepatocellular carcinoma, a deadly complication of advanced stage liver disease.

References

Kazushige Beppu, MD,   Kiyoshi Inokuchi, MD, PhD, FACS,   Nobuhiro Koyanagi, MD,   Shinichi Nakayama, MD,   Hisanobu Sakata, MD,   Seigo Kitano, MD,   Michio Kobayashi, MD. Prediction of variceal hemorrhage by esophageal endoscopy. Gastrointestinal Endoscopy. Volume 27, Issue 4, November 1981, Pages 213-218.

Dagradi, Angelo E.The Natural History of Esophageal Varices in Patients with Alcoholic Liver Cirrhosis. American Journal of Gastroenterology . Jun1972, Vol. 57 Issue 6, p520-540

The Correct answer is D. A hordeolum, also known as a stye,  is a common staphylococcal abscess characterized by an acute erythematous, swollen, and painful upper or lower eyelid margin. Warm compresses and topical antibiotic ointment are recommended initially. Incision and drainage may be recommended if swelling and pain fails to improve after 48 hours of conservative treatment.

Entropion is characterized by an inward turning of the eyelid without swelling. The eyelid and skin may rub against the eye causing irritation and discomfort.  Entropion usually occurs in older adults as a result of degeneration of the lid fascia. Lubricating eye drops may help relieve symptoms but surgery is often necessary to prevent corneal injury.

Blepharitis is characterized by inflammation of the eyelid causing symptoms of irritation, burning, and tearing.  The eye lids are usually thickened with crust and debris around the lashes. Inflammation may be caused by infection, surrounding seborrheic dermatitis, acne rosacea, or blocked meibomian glands. Initial treatment involves warm compresses and gentle eye washing to remove irritants.

Dacryocystitis is an infection of the lacrimal sac characterized by pain, swelling, tenderness, and redness in the tear sac area.  Purulent discharge may be expressed from the blocked lacrimal sac. Treatment of acute dacryocystitis usually includes systemic antibiotics.

References

McPhee SJ, Papadakis MA. 2010 Current Medical Diagnosis & Treatment.  McGraw-Hill Companies. 2010.

American Family Physicians. http://www.aafp.org/afp/1998/0601/p2695.html. Retrieved on 10/6/14.

Answer is D. Varicose veins are present as dilated, tortuous superficial veins in the lower extremities. Risk factors for developing varicose veins includes female gender, pregnancy, a family history, prolonged standing requirements, and a history of phlebitis.  Symptoms may include dull aching and heaviness of the lower extremities.  Compression stockings and prolonged elevation is recommended initially. Surgery may be indicated if persistent or disabling pain exists.  Common procedures include vein ligation and stripping.

Superficial thrombophlebitis is characterized by induration, redness, and tenderness along a superficial vein.  Superficial thrombophlebitis may occur with varicose veins and commonly occur with a history of trauma such as an intravenous line insertion.

Chronic venous insufficiency can be caused by DVT, phlebitis, varicose, veins, and other conditions causing poor venous circulation.  The leg and ankles become progressively swollen and the skin is usually shiny, thin, and cyanotic.

The cause of deep vein thrombosis (DVT) is often described by Virchow’s triad (stasis, vascular injury, and hypercoagulability).  A history of major surgery, such as total knee and hip arthroplasty, or prolonged immobilization is common.  DVT’s can present with dull aching, cramping, or pain in the back of the knee and calf. Homan’s sign, or pain on passive dorsiflexion of the ankle, is positive in 50% of cases.

An acute arterial occlusion is a sudden severe pain in the leg caused by an obstruction to the arterial system. The skin distal to the occlusion may become pale, cold to the touch, and pulses may be weak or absent.

References

McPhee SJ, Papadakis MA. 2010 Current Medical Diagnosis & Treatment.  McGraw-Hill Companies. 2010.

Samina S, Collins L. Diagnosis and Treatment of Venous Ulcers.  Am Fam Physician. 2010 Apr 15;81(8):989-996

Answer is A. Immunoglobulins (Ig), also known as antibodies in the blood, are proteins made by the plasma cells of the immune system to fight antigens such as bacteria, virus, and toxins.  The five classes of immunoglobulins include IgG, IgM, IgA, IgD, and IgE.  IgG is the smallest of all immunoglobulins and by far the most abundant of all found throughout the body.  IgG is the only class of Ig that crosses the placenta and provides passive immunity from the mother to the newborn.  The mother has a history of chickenpox exposure and the infant is exhibiting passive immunity acquired from the mother in utero.  IgG constitutes 90% of all antibodies in the fetus due to the maternal passive immunity.  Maternal IgG provides the infant with maternal antibodies during the first 4 months of life.   Around 2-3 months after birth, the infant’s immune system begins to produce other immunoglobulins. IgM is the first Ig that appears in the infant’s circulation after immunization and is the most abundant antibody produced in neonatal period.  IgM antibodies are the first antibodies to respond to an infection.  IgA predominately protects against enteric organisms and is not produced until several weeks after birth. IgD is not well understood but seems to be involved in the allergic response and hypersensitivity reactions.  IgE antibodies are found in high levels in the lungs, skin, and mucous membranes.  IgE antibodies induce an allergic response to foreign antigens and are found in high levels in people with allergies. Breast milk also contains all five types of maternal antibodies which can also help the infant against diseases and infection.

Reference

Hay WW, Levin MJ, Detarding RR, Abzug MJ. Current Diagnosis and Treatment Pediatrics. 22nd Edition. McGraw-Hill Companies. 2012.

Answer is D. Prolonged elevated blood sugars in diabetic patients often results in damage to the kidneys over time.  Hypertension can also damage the filtering ability of the kidneys, and if left untreated in diabetic patients, can result in kidney failure.  Diabetes is the leading cause of chronic kidney disease and renal failure in the United States. An early sign of kidney damage includes the presence protein in the urine (proteinuria) and a decreased glomerular filtration rate. Treatment of HTN in diabetics has been shown to reduce the incidence of proteinuria and improve kidney function.  ACE inhibitors, such as enalapril, are the first line medications for hypertensive diabetics. ACE inhibitors are renoprotective by reducing systemic vascular resistance and renal perfusion pressure.  ACE inhibitors also cause intrarenal vasodilation further reducing perfusion pressure which protects the filtering glomeruli.  Enalapril, an ACE inhibitor, would be the best option for this patient.

References

Management of Diabetic Hypertension. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230084/. Accessed on 11/9/14.

Kidney Disease in Diabetes. http://kidney.niddk.nih.gov/kudiseases/pubs/kdd/.  Accessed on 11/9/14.

The answer is C. In the diagnosis of Group A streptococcal pharyngitis, Centor’s criteria is an important clinical tool that physicians use for the management and treatment of GABHS. Centor’s criteria consists of: anterior cervical lymphadenopathy, pharyngotonsillar exudate, a temperature of 100.9°F, and the absence of cough. Streptococcal pharyngitis is diagnosed in over 11 million patients each year1, with the highest incidence occurring among children 5 to 15 years of age.  This infection is present most commonly in the winter and the early spring.  Risk factors for developing streptococcal pharyngitis include chronic medical illnesses such as diabetes, immunodeficiency, being within crowded environments such as schools, and exposure through infected persons.

Although viruses are the most common causes of acute pharyngitis, Group A beta-hemolytic Streptococcus (GABHS) is the most common bacterial cause of pharyngitis.  Some of the respiratory viruses that cause acute pharyngitis include adenovirus, inflenza virus, RSV, and rhinovirus, among many others.  However, GABHS accounts for about 15-30% of cases of acute pharyngitis in children and 5-20% of cases in adults.  This infection is transmitted through respiratory droplets, which means that the bacteria is spread through the droplets after an infected person coughs or sneezes.  It is important in preventing the spread of infection by practicing good hand washing techniques, refraining from drinking from the same glass as an infected person, or eating food that an infected person had eaten.

The microorganism Group A beta-hemolytic streptococci (Streptococcus pyogenes), is a gram positive extracellular bacterial pathogen that colonizes the throat or skin.  There are few individuals that have chronic GABHS colonization, but they do not have clinical symptoms of the disease, and these individuals are at low risk of transmitting the disease to others.  In the majority of individuals, the proliferation of GABHS in the pharynx causes the clinical signs and symptoms of the infection.  This is due to the fact that GABHS has many surface proteins and it produces extracellular products that cause evasion of the immune system.  Specifically, the M protein is responsible for the virulence and clinical symptoms that are seen in infected individuals.

In the clinical diagnosis of GABHS in patients, it is important to first differentiate the clinical differences between the viral and bacterial etiologies of acute pharyngitis.  Patients with bacterial etiology (GABHS) present with sudden onset of a sore throat, odynophagia, and fever.  In children, headache, nausea, vomiting, and abdominal pain may be present.  On examination, there is inflammation of the pharynx and tonsils with or without exudates and enlarged anterior cervical lymph nodes.  Clinicians often use the “Centor Criteria” for the diagnosis which includes temperature >100.4°F, anterior cervical lymphadenopathy, absence of a cough, and pharyngotonsillar exudate. Conversely, patients with acute pharyngitis of viral origin present with conjunctivitis, cough, hoarseness, coryza, viral exanthems, diarrhea, and the absence of a fever.  It is also important to ask the patient if they have a history of exposure to an infected person with GABHS, as this is significant information to aid in the diagnosis.

The diagnostic tests that are useful in detecting GABHS include the rapid antigen detection test (RADT) and throat culture.  The culture of a throat swab for detecting the presence of GABHS has a sensitivity of 90-95%6, whereas the RADT for strep is slightly less sensitive.  Using the Centor criteria, clinicians identify which patients need a rapid antigen test or throat culture.  When the patients have met >2 out of the 4 criteria, these patients require further testing.  When >3 out of the 4 criteria are present, then the rapid antigen testing sensitivity is over 90%.  With less than 2 out of the 4 criteria present, GABHS is not likely.  This being said, if the patient has more than 2 out of the 4 criteria, the clinician will perform the RADT or throat culture.  If the RADT is positive, then it is not necessary to perform a throat culture.  However, if a RADT is negative in high prevalence settings and clinical suspicion is high for the infection, a throat culture should be performed.  For children and adolescents, all negative RADT results should be followed with a throat culture.  Due to the lower incidence of streptococcal infection in adults and low risk of rheumatic fever, it is not necessary to confirm the diagnosis of the infection with a throat culture following a negative RADT.

Group A streptococcal pharyngitis is a often a self-limited disease, which means that the fever and constitutional symptoms reside in 3-4 days without the use of antibiotic therapy.  However, the use of antibiotics is indicated for those patients experiencing symptoms of the infection with a positive throat culture or rapid antigen detection test.  In addition, if there is a high index of suspicion for the infection, and the clinician is waiting for laboratory results, the patient should also be placed on antibiotics. The Centor criteria is also used in the management of the disease, thus when patients have 4 criteria met, antibiotics should be started. The antibiotics that are effective in treating GABHS include penicillin, ampicillin, amoxicillin, clindamycin, certain cephalosporin and macrolides.  The course of treatment for the antibiotics is usually 10 days.  The treatment of choice for GABHS pharyngitis remains penicillin due to its efficacy and safety, low cost, and narrow spectrum6.  However, amoxicillin can be used instead with equal effectiveness and more tolerable taste.  For non-compliant patients who are not able to finish a full 10 day course of antibiotics, it is recommended that they be treated with a single IM dose of penicillin G benzathine.  Also, treatment guidelines state that those with a penicillin allergy should be treated with erythromycin or second generation macrolides azithromycin or clarithromycin.  Rarely, there are patients with erythromycin-resistant strain of GABHS and when they are unable to tolerate beta lactam antibiotics, clindamycin is the appropriate choice.  In addition, symptomatic treatment includes acetaminophen for reducing fever, cough drops as needed for throat discomfort, rest, and plenty of fluids.

References

Choby, B. Diagnosis and Treatment of Streptococcal Pharyngitis. American Family Physician . 2009;79(5):383–390.

Gerber, M, Baltimore, R, Eaton, C, et al. Prevention of Rheumatic Fever and Diagnosis and Treatment of Acute Streptococcal Pharyngitis. American Heart Association. 2009;119:1541–1551.

Chahine, E, Chamoun, J, Sucher, A. Update on the Management of Streptococcal Pharyngitis. US Pharmacist. 2013;38(7):51–56.

Strep Throat. National Center for Biotechnology Information. Available at: http://www.ncbi.nlm.nih.gov/pubmedhealth/pmht0024690/. Accessed March 10, 2016.

Cunningham, M. Pathogenesis of Group A Streptococcal Infections. Clinical Microbiology Reviews. 2000;13(3):470–511.

Alan, B., Gerber, M., Gwaltney, J., Kaplan, E., Schwartz, RH. Practice Guidelines For The Diagnosis And Management Of Group A Streptococcal Pharyngitis. Infectious Diseases in Clinical Practice. 2002;35:113–123.

Papadakis MA, McPhee SJ, Rabow MW. 2015 Current Medical Diagnosis and Treatment. New York: McGraw-Hill Education/Medical 2015.

Answer is C. Cervical cancer is the third most common gynecological cancer, after endometrial and ovarian cancer. There are two types of cervical carcinoma. Squamous cell accounts for 90% of the cervical carcinomas, while adenocarcinomas account for the other 10%. The average age of diagnosis is 45 years old. HPV infection is associated with 99.7% of cervical carcinomas. The most common HPV types associated are 16, 18, 31, and 33. Risk factors include early onset of sexual activity, an increased number of sexual partners, smoking, CIN, DES exposure, immunosuppression, and a history of sexually transmitted infections.

The current guidelines to screen for cervical cancer, are to start testing with Paps alone at age 21 regardless of sexual activity or risk factors. Paps should then be performed every 3 years until age 30. For women 30 years old and older with 10 previous, consecutive, negative Paps, the recommendation is to have a Pap with HPV co-testing and repeat in 5 years if both are negative. If the Pap is done alone the recommendation is to repeat in 3 years if negative. Women greater than 65 years old can discontinue Pap and HPV screening if they have had 3 previous negative Paps or 2 previous negative co-tests within the past 10 years with the last test being within the past 5 years. Also, they cannot have a history of CIN2 or higher in the past 20 years.

The results typically reported after a Pap test are normal, atypical squamous cells of undetermined significance (ASC-US), low grade squamous intraepithelial lesion (LSIL), high grade squamous intraepithelial lesion (HSIL).  Any level of dysplasia found on a Pap smear more significant than ASC-US should be evaluated with a colposcopy regardless of HPV testing or prior Pap test results.  ASC-US with positive HPV would also warrant a colposcopy, while ASC-US with negative HPV would require a repeat Pap in one year.  A repeat ASC-US at that time would result in colposcopy.

References

Cervical Cancer. Centers for Disease Control and Prevention 2014. Available at: http://www.cdc.gov/cancer/cervical. Accessed March 9, 2016.

Williams DA. PANCE Prep Pearls: a Practical Study Guide to Preparing for Physician Assistant National Certifying Exam (PANCE), Recertification (PANRE) &Amp; Clinical Rotations. 1st ed. Lexington, KY: CreateSpace; 2014.

The salmon colored or hyperpigmented lesions of pityriasis rosea are somewhat inflammatory, and are characterized as macular to slightly raised plaques that are oval or annular in shape. Lesions are located on the trunk and proximal regions of the extremities.  Itching is a common symptom and few experience sore throat, headache and fatigue as a prodrome. The exanthem is common in the spring and fall months, and begins with a “herald” patch measuring 2-5 cm in diameter that develops a scale. Central clearing occurs leaving behind the classic “collarette” of a scale. In a matter of days or weeks, smaller lesions cluster in the typical distribution along cleavage lines forming the characteristic “Christmas tree” pattern on the back. A v shaped pattern may arise on the chest. The lesions resolve within 4-6 weeks, however they can persist for a period of months. Atypical presentations may occur in children. For example the nature of the lesions may be more papular, vesicular, or purpuric and the distribution may include the face, scalp, groin, axillary areas and distal extremities. The absence of a herald patch due to partial resolution of the exanthem may make diagnosis more difficult. Management is expectant with the aim to control pruritus.  Effective options include the use of antihistamines, topical steroids and possibly UVB treatment.

If a patient presents acutely with a herald patch, one may mistake this lesion for tinea corporis due to its similar annular shape, central clearing and peripheral scale. Patients manifesting multiple lesions of pityriasis rosea can be differentiated from those with tinea corporis as tinea corporis is generally more localized with fewer annular lesions that may have multiple concentric circles rather than one. Branching hyphae are seen on the KOH scraping in patients with tinea corporis. Hypopigmented or hyperpigmented macules characteristic of tinea versicolor  present on the neck and trunk may also be confused with pityriasis rosea. These lesions lack erythema and have a fine scale rather than the classic “collarette” of a scale. There is no “herald” patch present. KOH scrapings show Pityrosporum described as a “spaghetti and meatball” pattern.

Cutaneous manifestations of secondary syphilis should be considered in sexually active patients. Pityriasis rosea spares the palms and soles while the red to brown macules of secondary syphilis do not.  Patients with syphilis do not report the appearance of a “herald” patch but may have noticed signs of a chancre.

Guttate psoriasis is common amongst children regardless of previous psoriasis history. Patients do not recall the presence of a “herald” patch, but may report recent strep infection prior to the eruption. The lesions of guttate psoriasis also occur on the trunk as oval or round erythematous plaques which have a thick, adherent scale.

References

Goldstein, AO and Goldstein, BG. Pityriasis Rosea. In: UpToDate, Orfori, AO (Ed), Waltham,         MA. (Accessed on May, 11, 2016).

Lawley LP, McCall CO, Lawley TJ. Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J,        Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 19e. New York, NY:         McGraw-Hill; 2015.

Usatine RP, Smith MA, Chumley HS, Mayeaux EJ, Jr.. Chapter 153. Pityriasis Rosea. In:    Usatine RP, Smith MA, Chumley HS, Mayeaux EJ, Jr.. eds. The Color Atlas of Family         Medicine, 2e. New York, NY: McGraw-Hill; 2013.

The answer is D: inverse psoriasis. Inverse psoriasis is a variant of psoriasis that refers to a presentation involving the intertriginous areas, including the inguinal, perineal, genital, intergluteal, axillary, or inframammary regions. This presentation is called “inverse” since it is the reverse of the typical presentation on extensor surfaces. The risk factors of age, smoking, and drinking history, as well as the chronic nature of the rash, are all common in the history of patients with psoriasis.

Seborrheic Dermatitis (A) is characterized by erythematous plaques with greasy-looking, yellowish scales. Although Seborrheic dermatitis can appear in intertriginous areas, it normally presents on areas that are abundant in sebaceous glands: such as the scalp, face and ears. Furthermore, the patient above presents without any scale.

Tinea (B) is due to superficial fungal infections (dermatophyte) that can cause well demarcated erythematous plaques in all parts of the body – including the axillae and groin. However, the lack of response to the anti-fungal treatment the patient has been using, as well as the negative KOH prep makes this choice unlikely

Erythrasma (C) is a superficial infection of the skin caused by Corynebacterium minutissimum. The infection typically presents as erythematous to brown patches or thin plaques in intertriginous areas. A Wood’s lamp examination depicting coral-red fluorescence confirms the diagnosis of erythrasma; therefore, a negative wood’s lamp test would rule out the diagnosis.

According to the National Institutes of Health (NIH), psoriasis affects approximately 2.2% of the population in the United States. Worldwide prevalence of psoriasis in adults varies significantly, with rates occurring from 0.91 to 8.5 percent in adults, and 0 to 2.1 percent in children. Geographic location has a direct influence of the likelihood of having psoriasis, with prevalence having a positive correlation with increasing distance from the equator. The incidence of psoriasis is slightly more common in women then men, as well as a higher incidence in whites (2.5%) compared to African Americans is (1.3%). Although psoriasis can begin at any age, the disease is less common in children than adults. The age of onset occurs in two peaks: one between the ages of 30 and 39 years and another between the ages of 50 and 69 years. 1,2

Etiology

One of the primary mechanism of action is hyperproliferation of the keratinocytes in the epidermis, which in turn, increases the epidermal cell turnover rate. The cause of hyperproliferation of the keratinocytes is unknown but is highly attributed to genetic, immunologic, and external factors. In regards to genetic factors, several studies have identified multiple susceptibility loci for psoriasis, including those that involve immune system regulation. Approximately 40% of patients with psoriasis and/or psoriatic arthritis have a family history of these disorders. The major locus identified is PSORS1 on chromosome 6p21. HLA-Cw6 and HLA-B17 are the most important alleles identified within psoriasis, with HLA-Cw6 associated with early-onset disease and HLA-B17 linked to more severe phenotype. HLA associations explain only a portion of genetic susceptibility to psoriasis. Factors that are associated with psoriasis include smoking, obesity, medications, alcohol, psychogenic stress, infections, and the koebner phenomenon. Both former and current smokers are at higher risk for development of psoriasis, specifically palmoplantar pustulosis subtype. Patients with larger BMI may develop more severe psoriasis due to increased levels of cytokines. The most common medication “offenders” include beta-blockers, lithium, and antimalarial drugs. Alcohol has been linked to psoriasis due to numerous reports of alcohol consumption involved in both the development of psoriasis, as well as worsening of psoriasis. Stress is a well-established triggering factor in psoriasis; it has been associated with initial presentations of the disease as well as flares of pre-existing psoriasis. Infections, specifically streptococcal and HIV, are highly associated with the development of psoriasis. Finally, the Koebner phenomenon (the elicitation of psoriatic lesions by injury to the skin) is observed in approximately 25% of patients with psoriasis. 2,4

Pathophysiology

Psoriasis is a complex immune-mediated disorder that presents as inflammatory plaques in the skin. Dysregulation of components of the immune systems, keratinocyte function, and vascular structure contribute to the manifestations of this disease Plasmacytoid and myeloid dendritic cells are key contributors to development of inflammation in psoriasis. Specifically, Plasmacytoid dendritic cells stimulates the activation of myeloid dendritic cells via IFN-alpha. Consequently, Myeloid dendritic cells produce an array of inflammatory cytokines that influence T cell activity, as well cytokines IL-23 and IL-12. IL-23 and IL-12 promote the development of Th17 and Th1 cells, respectively. Th17 appears to play a major role in the pathogenesis of psoriasis via production of an array of other inflammatory cytokines (IL22, IL17, and TNF-alpha). These particular cytokines have been the target for the various biologics developed to treat psoriasis.

Epidermal hyperplasia is another major component of psoriasis that is driven by cytokines (IL-20 and IL-22). The typical clinical findings of erythema and scaling are the result of hyperproliferation. The hyperproliferative state is characterized by an increased number of epidermal stem cells, increased number of cells undergoing DNA synthesis, shortened cell cycle time of keratinocytes (36 hours instead of the normal 311 hours of normal skin), and decreased turnover time of the epidermis.2,5

Pertinent historical & Physical findings

There are multiple clinical subtypes of psoriasis. The various variants of psoriasis include chronic plaque, guttate, inverse, pustular, and erythrodermic. Patients with chronic plaque type psoriasis usually present with symmetrically distributed cutaneous plaques. The scalp, extensor elbows, knees, and back are common sites for involvement. The plaques are erythematous with sharply defined margins and a thick silvery scale. In patients with dark skin, postinflammatory hyperpigmentation may be a characteristic feature. Positive koebner phenomenon and Auspitz’s sign may be present. Guttate psoriasis is characterized by the abrupt appearance of multiple small psoriatic papules and plaques, particularly on the trunk and proximal extremities. It typically occurs as an acute eruption in a child or young adult with no previous history of psoriasis. There is a strong association with a recent streptococcal infection.

Erythrodermic psoriasis is an uncommon manifestation that may be acute or chronic. It is characterized by generalized erythema and scaling from head to toe, with increased risk of complications such as dehydration, infection, and sepsis. Pustular psoriasis presents with the acute onset of widespread erythema, scaling, and several superficial pustules. Presentation is commonly associated with pregnancy, infection, and the withdrawal of oral glucocorticoids. These variant is high risk for complications as well, such as malaise, fever, diarrhea, leukocytosis, and hypocalcemia. Inverse psoriasis refers to a presentation involving the intertriginous areas, including the inguinal, perineal, genital, intergluteal, axillary, or inframammary regions. Other manifestations of psoriasis include nail psoriasis and psoriatic arthritis, both of which will not be discussed within this review.1,2

Diagnostic Correlation

Psoriasis is a clinical diagnosis that is derived from a thorough physical examination and history. If necessary, other diagnostic procedures can be completed to help diagnose psoriasis. If a guttate variant is present, a throat culture may yield previous or current streptococcal pharyngitis. Other tests include KOH prep to rule out dermatophyte infection or a Wood’s Lamp evaluation to determine presence of corynebacteria bacteria. For definitive diagnosis, a punch biopsy of an active lesion or plaque would produce histological results that are consistent with psoriasis, which would include findings such as: hyperplasia of the epidermis, elongation of the dermal papillae, dilated blood vessels, hypogranulosis, and parakeratosis.4

Management & Treatment

For most patients, treatment entails identifying their psoriasis as either mild to moderate or moderate to severe. Most patients will be exposed to either topical and/or systemic therapy. Mild to moderate cases may start with topical treatment only, while those with moderate to severe cases may require systemic treatment with supplementation of topical treatment as well. For many, topical therapy may provide symptomatic relief and minimize required doses of systemic medications.

In regards to treatment options for the psoriatic patient, the range of options includes topicals, light therapy, and systemic treatment (oral vs. injectable biologics). For topical therapy, all psoriatic patients should implement an emollient into their treatment to maintain proper skin hydration, prevent irritation, and help with itching. The most effective ointments are petroleum jelly or thick creams, especially when applied immediately after bathing. Tar has been a longstanding treatment that is commonly recommended due to its low side effect profile and anti-inflammatory effects. Topical steroids remain the mainstay of topical psoriasis treatment due to its antiinflammatory, antiproliferative, and immunosuppressive actions. Steroids range from low to high potency and are chosen dependent on site, plaque thickness, and patient compliance. The “typical” topical regimen includes using emollients 1-2x/day and corticosteroids 2x/day when psoriasis is active. Other topical alternatives include Vitamin D analogs, such as calcipotriene, and Calcineurin inhibitors such as Tacrolimus. The advantage of using these alternatives are to give patients who have chronic psoriasis a “vacation” from corticosteroid, or a topical option for those who do not opt to use corticosteroids in general.

Light therapy has long been recognized as beneficial for psoriasis. UV radiation may act via antiproliferative effects (slowing keratinization) and anti-inflammatory effects (inducing apoptosis of pathogenic T-cells in psoriatic plaques). Consequently, many patients with a new psoriasis flare or those with widespread psoriasis frequently combine UVB light therapy with topical steroid use to clear their condition. For those with localized areas, Excimer laser offers a focused treatment.

Oral and injectable biologic therapies are normally indicated for moderate to severe psoriasis. For oral treatment, options include methotrexate, apremilast, and acitretin. Methotrexate has the most years of clinical usage and is commonly considered one of the primary treatments for moderate to severe psoriasis. The medication is taken once weekly and is titrated up until the lowest effective dose is found. Monitoring includes CBC/LFTs to monitor hepatic and immune function. Folic acid is prescribed concomitantly to mitigate common side effects of MTX. Acitretin is normally given for patients of the pustular or erythrodermic variants; monitoring for hypertriglyceridemia and hepatotoxicity are required. Aprimelast, a PDE-4 inhibitor, is the newest oral medication for the treatment of psoriasis. The dose is commonly titrated due to side effects and is relatively expensive at this time. GI side effects are common, and there is no monitoring needed.

For patients with severe or refractory psoriasis, biologics are normally indicated. The four most common injectable treatments are etanercept, adalimumab, ustekinumab and secukinumab. Etanercept and adalimumab are more widely studied and are considered the initial choice for patients starting treatment. Entanercept and adalimumab mechanism of action is focused on inhibiting TNF-alpha, while ustekinumas and secukinumab function through the inhibition of IL-22 and IL-17, respectively. Clinicians must check for TB via quantiferon gold or T-spot prior to initiating treatment, as well as monitoring for any infection and signs of lymphoma during treatment. Injection schedule includes the following: once weekly for etanercept, once every two weeks for adalimumab, once monthly for secukinumab and once every three months for ustekinumab.3,4

References

1) Emedicine.medscape.com. Psoriasis: epidemiology. 2016. Available at: http://emedicine.medscape.com/article/1943419-overview. Accessed April 18, 2016

2) UpToDate.com. Epidemiology, clinical manifestations, and diagnosis of Psoriasis. 2016. Available at: http://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-psoriasis?source=search_result&search=inverse+psoriasis&selectedTitle=1~11. Accessed April 18, 2016

3) UpToDate.com. Treatment of Psoriasis. 2016. Available at: http://www.uptodate.com/contents/treatment-of-psoriasis?source=search_result&search=inverse+psoriasis&selectedTitle=2~11. Accessed April 18, 2016

4) Bolognia JL, Jorizzo JL, Schaffer JV. Psoriasis. In: Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012: 137-155.

5) UpToDate.com. Pathophysiology of Psoriasis. 2016. Available at: http://www.uptodate.com/contents/pathophysiology-of-psoriasis?source=see_link#H481234. Accessed April 18, 2016

The correct answer is (A) Chelation therapy. This patients Ferritin 775 (normal 11-307) and Serum Iron 211 (normal 40-155) so she needs chelation therapy to avoid build-up of iron in her liver, heart and endocrine glands. Iron becomes toxic to organs in large amounts so it is best to start chelation therapy as soon as the serum levels of ferritin and iron are out of range. Answer (D) No treatment is incorrect because of the high levels of serum ferritin and serum iron as well as the Liver Iron Index. This patient is clearly has anemia and is iron overloaded. Answer (B) PRBC transfusion is incorrect because this patient denies all other symptoms of anemia except for DOE. In addition, adding more RBCs to the system will cause an increase in system iron content, which this patient clearly doesn’t need. Answer (C) Iron supplementation is not correct because the patient’s system is already far too high in iron content. Any additional iron added to the system will cause more build up in the organs and cause further toxicity.

Alpha thalassemias are commonly inherited and autosomal recessive in nature. There is no predilection for men or women, they are affected equally. Alpha thalassemias are most frequently seen in persons of Chinese or southeast Asian descent. In the U.S., these conditions have been considered somewhat uncommon. However, with the immigration of populations into the U.S. it is becoming more common and seen more often.

There are 4 alpha globin genes in total, they are housed in pairs on each copy of chromosome 16. Each type of alpha thalassemia is determined by how many alpha globin genes are either deleted or contain a defect that causes them to make less alpha globin chain than they should. Gene deletion is the most common source of the alpha thalassemias. There are four types of alpha thalassemias that can be present: (1) Alpha Thalassemia Silent Carrier, (2) Alpha Thalassemia Trait, (3) Alpha Thalassemia Intermedia/Hemoglobin H Disease and (4) Thalassemia Major with Hemoglobin Bart’s, which causes the fatal condition called Fatal Hydrops Fetalis.

The deletion of one alpha globin gene causes Alpha Thalassemia Silent Carrier (2). The silent carrier is asymptomatic and has no hematologic abnormalities (1) . Since there are no hematologic abnormalities there is no need for treatment or long-term monitoring. There is no change to the life expectancy for individuals that have this form of thalassemia.

The deletion of two alpha globin genes, either homozygous or heterozygous, causes Alpha Thalassemia Trait (2). This condition does not exhibit anemia but they do exhibit microcytosis. The blood smear in this case will show hypochromia and microcytes as well as a few target cells and acanthocytes (1). Since people with thalassemia trait do not usually have iron deficiency anemia there is no need for treatment or long-term monitoring. Again, there is no change in life expectancy for this form of thalassemia.  Should someone will alpha thalassemia trait decide to have children genetic counseling should be considered since two partners that both carry some form of alpha thalassemia have a higher probability of having a child a more severe form of the condition.

The deletion of three alpha globin genes causes Alpha Thalassemia Intermedia, which is also called Hemoglobin H Disease (2). In this case there is a shortage of alpha globin chains that allows for an over-abundance of beta globin chains. These beta globin chains form beta4 tetramers, or Hemoglobin H. These patients are not necessarily transfusion dependent. Often they only require sporadic transfusions for symptomatic anemia. Hemolysis due to viral infection or exposure to oxidative drugs can trigger an acute episode where transfusion may be needed. The decision to transfuse is generally based on the severity of their clinical condition, not just lab numbers. These patients will often have a baseline hemoglobin lower than the expected normal values. Patients with this condition will exhibit hematologic abnormalities such as microcytic anemia, splenomegaly and hemolysis. The blood smear will show microcytosis, hypochromia, target cells and poikilocytosis (1). As discussed with alpha thalassemia trait above, genetic counseling should be considered should child bearing be desired.

The deletion of all four alpha globin genes results in Thalassemia Alpha with Hemoglobin Bart’s which will lead to fatal Hydrops Fetalis (2). It can be determined if a fetus has this type of thalassemia by use of chorionic villus sampling. Should the fetus have thalassemia alpha with hemoglobin Bart’s the risk of toxemia and post-partum bleeding is increased (2). Hemoglobin Bart’s has no available effective treatment (3).

Iron overload is more often associated with beta thalassemia patients because they are more dependent on blood transfusions. However, it can occur with alpha thalassemias as well. In iron overload, excess iron in the body is deposited in visceral organs including the liver and heart. The patients will often have labs that show increased ferritin levels, low TIBC levels and high iron saturation levels as well as microcytic anemias. In the alpha thalassemias the iron overload is more commonly seen in the liver and can be triggered by events such as increased absorption of dietary iron due to anemia or hemolysis. In order to prevent toxicity to the visceral organs, patients with iron overload are usually treated with chelation therapy. There are two therapies that are currently available – Deferoxamine IV or subcutaneously or Exjade/Deferasirox, which has oral dosing (2). Chelation therapy is recommended if Liver Iron Concentration (LIC) > 5 mg/g or if ferritin levels are > 800 ng/L (4). In addition to chelation therapy, iron levels are checked every 6 months and monthly checks are done for CBC, CMP, Phos and Ferritin.

References

1. Papadakis, M., McPhee S. CURRENT Medical Diagnosis & Treatment 2015. New York: McGraw-Hill Education Medical; 2015.
2. Munchie, M.D. H.L., Campbell, M.D. J.S. Alpha and Beta Thalassemias. American Family Physician. 2009; 80(4):339-344.
3. Galanello, M.D. R., Cao M.D. A. Alpha-thalassemia. Genetics in Medicine. 2011; 13(2): 83-87.
4. Ricchi P., Marsella M. Profile of Deferasirox for the Treatment of Patients with Non-Transfusion Dependent Thalassemia Syndromes. Drug Des Devel Ther. 2015; 16(9):6475-82.

Answer, D. Wide, fixed-split S2, is pathognomonic for ASD.  The test of choice to confirm this diagnosis is an echocardiogram.Atrial Septal Defects are the second most common congenital structural heart condition in the US. ASD occurs in roughly 1 in 1000 live births and appears more frequently in female versus male gender. Primary etiology is congenital, and can arise as one of four variants: Ostium primum, Ostium Secundum (most common), sinus venosus and coronary sinus. After birth, the majority of the population will undergo a fusion of the septum primum and secundum giving rise to the septal wall between the left and right atria. Persisting communication between these two chambers resulting from maladhesion of the septae, is the pathophysiologic catalyst of atrial septal defects. Clinical presentation is dependent on the size and location of the defect in addition to presence of other comorbidities. Typically, symptoms of ASD present during the patients 20’s-30’s.

The most pertinent finding with respect to history and physical, is the exclusive murmur (fixed, split S2). Symptoms that support this finding are right heart related in nature, most commonly dyspnea on exertion. Test of choice for ASD is echo. Typically, a transthoracic echo is suffice, and it is less invasive. While TEE are considered superior by some clinicians, it is typically reserved for cases in which diagnosis via TTE are uncertain. Echocardiography determines location, size, and additional defects of the heart if present.

Treatment is based on patient symptoms (which suggest RV volume overload), overall heart function, and severity of the defect +/- complications. The main indications for surgical repair (closure) of an ASD are patients with clinically severe complications such as a paradoxical emboli, arrhythmias, significant shunting of blood between the atrial chambers, and RV dysfunction. It may be noted however, that if patients have progressed to shunt reversal, ASD closure is an absolute contraindication.

Practice Question Recap: Pertinent findings from the history include: dyspnea on exertion, increased fatigue, and family history (mild familial patterns exist). Thus, choice a, can be eliminated as it represents patent ductus arteriosus. Most PDA patients are asymptomatic, and if symptoms to present they are typically associated with Left Heart pathology. All of the choices aside from letter D, can be eliminated with physical exam findings, specifically, auscultatory findings. Paradoxical split S2 represents severe Aortic Stenosis. The holosystolic murmur represents a Ventricular Septal Defect, which has a few similar presenting symptoms, however the primary symptoms are left heart related in nature with VSD, and in addition, these patients are at an elevated risk of presenting with Eisenmenger’s Syndrome.

References

Toy, E; Faulx, M. Case Files: Cardiology .  NewYork, New York. Mcgraw Hill, 2015

Williams, D. PANCE PREP PEARLS  Lexington,KY; CreateSpace an Amazon company, 2016

Connolly, H. MD; Indications for Closure and Medical Management of Atrial Septal Defects in Adults. Up to Date, Jan. 2015. Accessed June 3, 2016.

Correct answer: D. 1-2 sessions of in-office Canalith repositioning. Canalith repositioning (CRP) is the treatment of choice for confirmed BPPV by positive Dix-Hallpike. The most common CRP is the Epley maneuver which general principle is to return the particles in the semi-circular canal back to its original place so that the vestibular system is no longer out of balance.

Incorrect answers:

1. Decrease dosage of HCTZ. The patient has not had a change in dosage in this medication for the past 2 years. Any cardiogenic vertigo would have presented earlier and closer to the time of a dosage change.
2. Increase dosage of Meclizine. It is possible that a higher dose may treat her vertigo however her normal dose provided no relief when it has in the past. There is a better treatment option that provides immediate relief without an increased risk of side effects.
3. Immediate ENT surgical consult. The surgical route is reserved for patients whose vertigo is unresolved with CRP. Surgery is not recommended until all other options are exhausted because it is invasive and poses a risk of nerve damage.

Epidemiology: BPPV is prevalent among every 64 per 100,000 people. Gender distribution is slightly higher towards females (64%). BBPV occurs in an older population with an average age of 51-57 years of age. It is a rare incident in patients younger than 35 years without a history of prior head trauma. There is insignificant data correlating racial affinity. Some predisposing factors for BPPV include inactivity, acute alcoholism, major surgery, and central nervous system disease. Many patients may have concurrent ear pathology including: idiopathic, trauma, ear diseases, otitis media, vestibular neuritis, Meniere disease, otosclerosis, sudden sensorineural hearing loss, vestibular basilar insuffiency, acoustic neuroma, and cervical vertigo.

Etiology: BPPV is an abnormal sensation that is evoked by provocative positions that usually trigger certain eye movements like nystagmus. The cause of BPPV is categorized into 2 groups: canalithiasis and cupulolithiasis. Canalithiasis or canal rocks occur when particles are present in the canal of the semi-circular canals. These rock particles are free floating and mobile leading to vertigo by exertion of force. Cupulolithiasis, or cupula rocks, are affixed to the cupula of the crista ampullaris. In contrast, these densities are non-mobile present in the ampulla of the semi-circular canals.

Pathophysiology: In the cupulolithiasis explanation, basophilic particles are attached to the cupula rendering the posterior semicircular canal (PSC) overly sensitive to gravity. The abnormally attached structures can impinge on the cupula. The additional weight of the cupula rocks makes the pole unstable and more difficult to maintain a neutral position. The unstable cupula is prone to stay in one direction depending on the tilt of the head. Once a position is made, the weight of the cupula rocks keeps the cupula from recoiling back to a neutral position. This results in persistent nystagmus and dizziness, especially when a patient is in a specific position, ie tilted backwards.

In the canalithiasis explanation, symptoms of BPPV are related to the mobile canaliths in the posterior semi-circular canal. When the head is upright, the densities are at the most gravity-dependent position. When the head is tilted back supine, the particles circumduct approximately 90 degrees up along the arc of the PSC. After a transient lag, the particles move back down the arc by gravitational force. The downward movement of the particles causes the endolymph to flow away from the ampulla and the cupula to be deflected. The bending of the cupula results in nystagmus. When the head returns to an upright position, the rotation and cupular deflection is reversed, thus dizziness with nystagmus flickering in the opposite direction occurs. The canalithiasis explanation is analogous to pebbles inside a tire. As the tire rotates, the pebbles are picked up temporarily then fall back down with gravity. The tumbling results in dizziness. Reversal of the tire rotation makes the flow and dizziness go in opposite direction. Canalithiasis explains the delay (latency), transient nystagmus and reversal on return to upright.

Pertinent historical and physical findings: The onset of BPPV is sudden. Most patients will awake with these symptoms, often noticing vertigo while trying to sit up suddenly. Positional vertigo is variable from days and weeks to even months or years. Symptoms may resolve then recur. Severity is also variable. In extreme instances, the faintest head movement will elicit nausea and vomiting. There can be strong nystagmus, while others will be unfazed. Sensation of dizziness is not constant. Head movement triggers severe dizziness. In between episodes, patients will have few or no symptoms. Some patients may complain of a foggy or cloudy sensation.

Classic BPPV symptoms are triggered by suddenly moving from an erect position to supine position while the head is angled 45 degrees towards the side of the affected ear. After reaching the provocative position, a delay of a few seconds occurs before the dizzy spell strikes. The patient feels like they are suddenly thrown into a rolling spin toward the side of the affected ear. Symptoms begin very violently and usually resolve within 20 to 30 seconds. The sensation is triggered once again when returning to sitting erect, but the nystagmus is in the opposite direction. Generally physical findings are unremarkable. Neurological exam findings are normal except those from the Dix-Hallpike maneuver. However, abnormal neurological exam findings do not rule out a BPPV diagnosis.

Diagnostic correlations (labs/imaging): The standard clinical test for BPPV is the Dix-Hallpike maneuver. A patient with classic rotatory nystagmus with latency and limited duration is also considered diagnostic for BPPV. In the Dix-Hallpike maneuver, the patient is moved rapidly from a sitting position to a supine position with the head 45 degrees to one side. In approximately 20 to 30 seconds, the patient is then returned to the sitting position. If there is an absence of nystagmus, the maneuver is performed with the head turned to the opposite side.

Management/treatment: Medical care includes watchful waiting, vestibulosuppressant medication, vestibular rehabilitation, canalith repositioning, and surgery. BPPV can resolve with watchful watching, however it may take weeks to months for symptoms-leaving the patient in discomfort and vertigo until resolution. In addition, patients may be at risk for a fall or other events from a vertigo episode. Vestibulosuppressant medication does not control vertigo but it may provide minimal relief of symptoms. Patients may feel groggy or sleepy with this medication. Vestibular rehabilitation is noninvasive therapy that can be successful only after a considerable period of time. While the therapeutic maneuvers are performed, vertigo is repeatedly stimulated.

Canalith repositioning procedure (CRP) is a first choice treatment option due to its high benefit-to-risk ratio and its simple noninvasive treatment to cure BPPV in 1-2 sessions. There are 2 methods in canalith repositioning therapy: Epley maneuver and Semont maneuver. Both options involve head repositioning to rearrange the displaced particles, however the Epley is gentler.

In the Epley maneuver the patient begins in a sitting position with the head turned 45 degrees towards the affected side. In position 1, the patient slowly reclines to the supine position. The rate of recline is so that no nystagmus is elicited- usually about 30 seconds. In position 2, the patient continues to recline supine until 15 degrees Trendelenburg is reached and head turned 45 degrees toward affected side. It takes about 10 seconds to recline with another 20 seconds in Trendelenburg position. In position 3, the body is still in supine 15 degrees Trendelenburg with the head turned 45 degrees towards the contralateral side. In position 4, the body is turned from position 3 so that the shoulders are perpendicular to the floor with the affected ear facing upwards. The head is turned farther so that the nose extends 45 degrees below the horizon. This takes 40 seconds. In position 5, the patient is raised back to sitting with the head still turned away from affected side (at least 90-135 degrees toward contralateral side). In position 6, the head is returned to midline.

After the completion of the Epley maneuver, a Dix-Hallpike test is performed immediately. If nystagmus is observed, the Epley maneuver is repeated. After CRP treatment, patients should avoid lying down completely flat for 24-48 hours. They should sleep with the head elevated. They are also advised to avoid aggravating activities such as jumping or flipping. Patients may also want to adjust their sleeping position to prevent recurrence.

If CRP fails, surgical options are considered. They are invasive and hold risks of complications (hearing loss and facial nerve damage). Surgical options for vertigo control include: labyrinthectomy, posterior canal occlusion, singular neurectomy, vestibular nerve resection, and transtympanic aminoglycoside application. Labyrinthectomy and vestibular nerve resection are only considered in extreme cases. Singular neurectomy is difficult and has been mastered by only a select number of surgeons. The most practical surgical option is posterior canal occlusion. The posterior canal is collapsed and therefore the particles are immobilized in the canal. This procedure takes the mastoidectomy approach- the hard bone is drilled through with diamond burrs to expose the labyrinth without spilled excessive perilymphatic fluid. The labyrinth is compressed so that the flow of endolymphatic fluid and movement of particles are disrupted.

References

Anagnostou E, Kouzi I, Spengos K. Diagnosis and Treatment of Anterior-Canal Benign Paroxysmal Positional Vertigo: A Systematic Review. J Clin Neurol. 2015;11(3):262-7. http://reference.medscape.com/medline/abstract/26022461. Accessed             May 26th, 2016.

Huppert D, Strupp M, Mückter H, Brandt T. Which medication do I need to manage dizzy patients?. Acta Oto-laryngologica. 2011;131(3):228-41.  https://www.ncbi.nlm.nih.gov/pubmed/21142898. Accessed May 26th, 2016.

Correct Answer: B. The patient has actinic keratosis which is often considered to be an early form of squamous cell carcinoma. The chief complaint of a “rough, red spot” on a fair-skinned male of an advanced age who works outside and rarely uses sunscreen protection are all classic for a patient presenting with AKs.2 With option A, it is unlikely JM already has invasive skin cancer based on the presentation (non-tender) and squamous cell carcinoma has a low mortality rate. However, a biopsy should be performed. Option C is inappropriate has all AKs should be treated due to their ability to evolve into SCC. With option D, rosacea can appear erythematous and scaly on the cheeks but should be disregarded as it is not normally one solitary lesion and patient’s history does not support the diagnosis.

Actinic keratosis (AK) (sometimes referred to as solar keratosis) is a lesion of the skin that presents due to excess growth of atypical epidermal keratinocytes and can sometimes develop into squamous cell carcinoma. AKs are one of the most common reasons why a patient would present to a dermatologist. Fourteen percent of dermatology office visit in the United States between 1990 and 1999 were due to AKs. People with lighter skin are more likely to develop the lesions.1 The prevalence in Australia is believed to be between 40-60% of individuals older than 40.2 Other risk factors include ultraviolet radiation (causes mutations in the p53 tumor suppressor gene), extensive sun exposure (particularly individuals who work outdoors), a history of more than six painful sunburns in a lifetime, male sex and an increase in age. The immunosuppressed are at in increased risk and HPV may also play a role but further studies are still needed.1

Histologically, AKs share many similarities with squamous cell carcinoma. AKs are lesions of the skin characterized by collections of atypical keratinocytes (keratin-producing cells) at the skin’s basal layer which ascends to include the granular and cornified layers of the skin. The epidermis will begin to show abnormal structures, such as acanthosis (thickening of the skin), parakeratosis (nuclei remain in the stratum corneum and causes thinning of the granular layer) and dyskeratosis (abnormal keratinization). The cells appear atypical and keratinocytes will be various sizes and shape. Often, an inflammatory component is present. It is argued that AKs are early signs of squamous cell carcinoma but others believe calling them “pre-cancerous” unnecessarily alarms patients.2

Patients who present with AKs are almost always white and sun-sensitive. The incident of the lesions increases with age and men have a slight increased risk. Individuals often have had extensive UV exposure, particular those with occupations that require them to work outdoors. The lesions will often be located on the patient’s body where there has been long-term sun exposure such as the face, ears, scalp (in bald men), forearms and hands. They will often start as small spots that feel rough (sandpaper texture) and are often more easily felt than visualized. Over time, the lesions will increase in size and develop into a red and scaly lesion (usually 3-10mm but they can be larger).2

In order to confirm that the lesion is an AK, a skin biopsy is advised in order to rule out squamous cell carcinoma or another advanced skin lesion. A biopsy should also be performed if the lesion is recurring or it does not respond to treatment. Under the microscope, AKs will show dysplasia (proliferation of abnormal cells) and the cell architecture will appear disordered. The keratinocytes will be abnormal in both size and shape. These abnormalities will often ascend into a thinning granular layer. A Wood lamp may also be used as the lesions will emit a pink fluorescence.2

AKs that are untreated may stay the same, they may spontaneously resolve or they can progressive to squamous cell carcinoma. There is no way to determine their course. The chance of progression to SCC is relatively low (about 10%) but if the patient has multiple lesions, the chance increases. In addition, AKs are often difficult to differentiate from other skin malignancies and thus all lesions should be treated. Treatment is determined based on the how many lesions are present and the effectiveness of the treatment. Both medical and surgical treatments are available. With medical treatment, the patient should be educated to limit sun exposure and use sunscreen and protective clothing at all times. With medical therapy, large areas are able to be treated. However, the treatment course is long and involves irritating and uncomfortable medications. The most common topical therapy is 5-FU which acts by inhibiting the enzyme thymidylate synthetase and leads to cell destruction of actively proliferating cells. During treatment, the lesions will become red and uncomfortable. If the treatment is successfully completed, though, the patient’s complexion will become smooth and there will be substantial improvement of the AKs.2 Another medical option is photodynamic therapy (PDT). A light-sensitizing compound builds up in AK cells and is then activated by a specific wavelength of light. It is then converted by enzymes and oxygen free radicals are produced which leads to cell death. The therapy a good cosmetic outcome, however, a major drawback is that the technique is very painful.2,4

Surgical therapy involves total destruction of the AK but limiting damage to the healthy skin surrounding the lesion. If the diagnosis is uncertain, a biopsy should be performed, though it will usually leave a scar. Cryosurgery is used which utilizes cryogen to decrease the temperature of the skin and cause cell death. Liquid nitrogen is most commonly used.  The low temperature destroys keratinocytes but other structures surrounding it are spared as they are more resistant to the cold. Other surgical options include cosmetic resurfacing, which includes deep chemical peels and dermabrasion. However, insurances do not normally cover the cost of these procedures.2

All patients should be educated to use sunscreen with an SPF of at least 30 and to avoid sun exposure as much as possible. They should follow-up regularly with their dermatologist, especially if any new lesions appear. If the lesion does not resolve, a biopsy may need to be performed at a later date if not already done prior to treatment.2

References:

1. Padilla, Steven. Epidemiology, natural history, and diagnosis of actinic keratosis. UpToDate. 2015. https://www.uptodate.com/contents/epidemiology-natural-history-and-diagnosis-of-actinic-keratosis?source=search_result&search=actinic+keratosis&selectedTitle=2%7E79. Accessed May 21, 2016.
2. Spencer, J. Actinic Keratosis. Medscape. 2016. http://emedicine.medscape.com/article/1099775-overview. Accessed May 21 2016.
3. American Academy of Dermatology. Actinic Keratosis. https://www.aad.org/public/diseases/scaly-skin/actinic-keratosis. Accessed May 21 2016.
4. Kessels, JP. Laser-mediated Photodynamic Therapy: An Alternative Treatment for Actinic Keratosis? Acts Derm Venereol. 2016. https://www.ncbi.nlm.nih.gov/pubmed/26551377. Accessed May 21 2016.

Answer is C. Lichen sclerosis is most common in postmenopausal women causing signs and symptoms of pruritus and vulvar pain. Skin is typically erythematous with white wrinkled lesions along the vulva and can include perianal region. Often times maceration and lichenification will result. Lichen sclerosis is diagnosed by biopsy that shows thin hyperkeratotic and epithelial layers, flattened papillae with deep lymphocytic infiltrations. Stopping the itch-scratch cycle is the best way to manage the chronic condition of lichen sclerosus. If the patient stops scratching, the tissue can heal and prevent excoriation and maceration. It is important to educate patient on loose wearing undergarments, cleaning daily with gentle soap, and drying the vulvar area with blow dryer. Oral antihistamine can also be used to help with itching. Patients with lichen sclerosis have a higher rate of squamous cell cancer. Although it is important to biopsy all new lesions it does not manage the symptoms of lichen sclerosis. Cancer actually develops mainly in those who continue to suffer from vulvar itching. Intralesional injections of steroids are used as a last option for those who do not find relief from topical steroids such as clobestasole. Although use of water based lubricants during sexual intercourse may help some with the dyspareunia, it does not help to manage the lichen sclerosis condition itself.

(A) Vitiligo is common along the vulva but may also include other areas of the skin. It does not cause pruritus or pain. (B) Lichen simplex chronicus causes similar symptoms but on biopsy, tissue is thickened and papillae are elongated. This is typically a result of chronic irritation. (D) Psoriasis is considered a red lesion when it involves the vulva because it often times lacks the white scales and usually shows as erythematous lesions and can look like candidal infections. Patient lacks other lesions on her extensor surfaces or scalp which also helps to rule psoriasis.

References

Decherney A, Nathan L, Laufer N, Roman A. Current Diagnosis & Treatment Obstetrics & Gynecology. 11th ed. United States: McGraw-Hill Companies; 2013.

Cooper S, Arnold S. Vulvar lichen sclerosus. UpToDate.com Web site. http://www.uptodate.com/contents/vulvar-lichen-sclerosus. Accessed May 15, 2016

We Are Macmillan. Cancer Support Web site. http://www.macmillan.org.uk Accessed May 15, 2016.

Answer: A. Echocardiogram with Doppler is test of choice for evaluating severity and progression of AS by assessing LVEF (heart’s ability to pump blood past stenotic valve). It can also assess LV wall mass as consequence of patient’s long standing HTN and pressure gradient across leaflets. Echo also looks at valves for motion abnormalities and can measure pressure needed to open leaflets enough to pass blood. (B) Exercise stress testing is contraindicated for symptomatic AS patients because of possible exacerbation of hemodynamic instability. It is appropriate modality for asymptomatic patients as a low-risk procedure and can show abnormal BP changes. (C)BNP does not assess severity of AS. It is used a prognostic evaluation to predict symptom onset for someone with severe AS by increasing BNP levels. However, they are already symptomatic so it is apparent that treatment is needed. (D)EKG is not reliable to assess AS. In this case it might show LV hypertrophy but critical AS cannot be ruled out if there is no LVH. Also, because of patient’s history of MI, voltage may be abnormal already. This modality could be used to r/o ischemia or arrhythmias, but he is not complaining of it so it is not specific enough.
Aortic stenosis (AS) is a valvar heart disease characterized by obstruction of blood flow across the aortic valve during systole when blood is pumped from the left ventricle into the ascending aorta and out into the peripheral vascular system. The problem with a stenotic aortic valve is that it becomes resistant to smooth blood flow and causes some back up of blood leading to increased pressures in the heart. The increased pressure within the left ventricle because vastly different from the aorta leading to a pressure gradient. The left ventricle is designed to be resistant to this increased pressure and compensates by thickening thus becoming hypertrophied.
Initially, as with most patients, the left ventricle is still able to contract and pump blood appropriately for many years. Eventually, patients may notice DOE and other symptoms with exercise due to a fall in cardiac output. With this, what is left in the left ventricle after contraction, the end-diastolic pressure, will be more causing a backup in the heart and into the pulmonary capillary beds, also known as systolic dysfunction. This may ultimately lead to HF and heart failure symptoms.

The pathophysiology behind aortic stenosis will likely involve diastolic dysfunction as it progresses as noted above. The hypertrophic walls of the left ventricle have a more difficult time relaxing and thus the atria will need to work harder to fill. This extra struggle that the atria has may eventually wear out the atria, causing atrial dilation, and other potential valvular disease, such as insufficiencies, as the entire system begins to get congested little by little.
Unfortunately, as the heart is now having to work harder as the AS progresses, oxygen requirements of the heart increase leading to reduced coronary flow reserve. Once myocardial perfusion is compromised, angina is now possible1. With that, myocardial ischemia and infarction could be likely.

AS occurs from two different pathways, either acquired or congenital. Unicuspid, bicuspid, tricuspid, and quadricuspid valves are possible, bicuspid being the most common in adults and unicuspid valves being the most common cause of symptomatic AS in adolescents and infants. It is not the bicuspid valves themselves that cause the obstruction to blood flow but rather the constant turbulent flow of blood across the valve that start to damage the leaflets over time and lead to fibrosis, calcification, and stenosis. Surprisingly, most adults with congenital bicuspid valves, are not aware nor are symptomatic until after 40-years-old.

Acquired degenerative calcific AS, on the other hand, is the most common cause for aortic valve replacement (AVR). Risk factors for developing degenerative calcific AS is hypertension, hyperlipidemia, DM, and smoking. These increase the risk of AS because they put constant hemodynamic stress on the leaflets leading to limited normal motion during systole.
There are also many other causes of AS but among them are rheumatic heart disease, often causing symptoms after 50 yo. RHD leads to commissural fusion and fibrosis causing both stenosis and regurgitation of aortic valve. It is not uncommon to have coexisting mitral valve insufficiency.
The incidence of AS increases with age second to long standing histories of above risk factors. These environments cause sclerosing that initially is non-obstructing but degenerates to stenosis. Percentages range as high as 29% over 65-year-old to 37% over 75-years-old. Prevalence of AS is 2-9%, most commonly in 75-year-old males and older.

Symptoms of AS gradually progress so a patient might be followed closely for as much as 10-20 years before they start to experience symptoms. Screening questions range greatly when interviewing a patient that you might suspect symptomatic AS. It is important to ask about DOE as this is often the initial complaint followed by exertional chest pain, and progressive inability to exercise. The chest pain felt with AS is often relieved with rest which could be hard to differentiate from angina pectoris of CAD.

Symptoms for these patients are typically exacerbated by activity and they might start to notice lightheadedness and syncope with activity. It is possible to correlate to syncopal events to different etiologies. When it occurs with activity, it is likely due to systemic vasodilation or tachyarrhythmias.
The classic triad of AS is not complete without heart failure symptoms. These heart failure symptoms can occur from either systolic or diastolic dysfunction as discussed above. To remind you, PND, orthopnea, DOE, and SOB should point to CHF.

Most clues you might find when physically examining an AS patient will be found with either your stethoscope or finger tips. On palpation of different pulses, you might find delayed upstroke and decreased amplitude of the carotid arteries known as pulsus tardus. When examining the Jugular venous pulse, pulsus alternans may be identified. Remember, this is due to poor ability of the right ventricle to welcome more blood due to left sided and septal hypertrophy.

When placing the stethoscope to the precordium, you may notice abnormalities in A2, which is often diminished or unheard because of its immobility. Paradoxical splitting might also be heard of S2 as A2 will close late due to calcification. Although, if pulmonary hypertension is presents as well, P2 might also be delayed. You may even hear an ejection click in children with congenital AS, heard best along LLSB after S1. Another extra heart sound you might hear is S4. If you recall, it is caused by atrial forcefully contracting to fill hypertrophied LV second to long standing hemodynamic pressures.

Unfortunately with Aortic stenosis, you have to decode the dreaded and confusing murmurs. The classic murmur of AS is crescendo-decrescendo murmur best heard in the 2nd ICS of the right upper sternal border during midsystole. It often sounds rough or harsh in nature and can radiate to both carotid arteries. It is key to remember that it is not the loudness or intensity of the murmur that should clue to into the severity but rather the duration. Longer duration equals more severe AS. Fun fact, valsalva will decrease the intensity of the AS murmur. Why is that? Well think about it, valsalva causes less blood to enter LV so less blood is trying to push through stenotic aortic valve.
Some patients may even have consequences of aortic regurgitation also. This murmur would be a diastolic high-pitch and blowing sound heard in the area of the apex.

Diagnostic studies to confirm aortic stenosis always include a two-dimensional and doppler echocardiography, the modality of choice. Not only is it used to diagnose AS but it is also used to assess LV size, function, and hemodynamics, reevaluate patients with known AS with changing symptoms or even asymptomatic, and to assess severity (must use doppler echo). The structure and function of all valves can be assessed with this modality although three findings are indicative of severe AS. These include echo-dense aortic valve without cusp movement, decreased separation between cusps (< 8 mm), and unexplained left ventricular hypertrophy.

Severity is measured using transvalvular gradient across the valve with mild being < 25 mmHg and sever being > 40 mmHg. Sometimes however, the echocardiogram may show minimal severity when in fact the AS appears clinically severe. In this case, evaluation with a cardiac catheterization may be necessary. The cardiac cath can measure the EF and the heart’s ability to pump past the stenotic valve, assess the need for AVR, among other things. A coronary arteriography is also indicated in those over 35-year-old before AVR to rule out symptomatology second to CAD3. It is known that 50% of patients over 50-years-old with AS have coexisting CAD.

Other tests might be suggested to better assess the patient. Exercise stress testing can be used only in asymptomatic AS patients with severe aortic stenosis to assess exercise capacity, hemodynamics, and to establish if low-gradient AS is present. Chest radiography can be used to support diagnosis, though it is nonspecific to AS. Electrocardiography may be used to assess for LV hypertrophy, although if absent, severe AS cannot be ruled out. Lastly, B-type Natruietic peptide (BNP) can be used to assess prognosis. A rise in BNP could predict upcoming symptoms in an asymptomatic patient and may suggest the need for AVR.

A big takeaway from this discussion is that the only definitive treatment for AS is aortic valve replacement (AVR). Once, symptoms of AS develop, it is pertinent that the patient be evaluated for AVR. Research shows that if your patient is asymptomatic, they can be followed closely until symptoms arise while optimizing other cardiac factors such as blood pressure, hydration, physical activity, blood sugar management, and smoking cessation. But, AVR is recommended for asymptomatic patients that have severe AS and left ventricle dysfunction.

Fortunately, EF and LV mass improve within months of AVR. AVR 5-year survival rate for adults is 80-94%. AVR is completed with either bioprosthetic or mechanical valve placement. After surgery, endocarditis prophylaxis is no longer necessary or recommended.

When a patient is not a good candidate for AVR or refuses, palliative treatment could be initiated. Percutaneous balloon valvuloplasty can be considered for patient with short life expectancy second to comorbidity, to bridge those critically ill until they can undergo AVR, and pregnant patients.
Medical treatment is not possible with AS. However, managing AS can be done but it is limited. Caution should be taken with diuretics, ACE-I, beta blockers, and other vasodilators because they may cause exacerbation.

References

1. Xiushui (Mike) Ren, MD. Aortic Stenosis Pathophysiology. Medscape.com Web site. http://emedicine.medscape.com/article/150638-overview#a3. Accessed April 8, 2016.

2. Papadakis M, McPhee S. Current Medical Diagnosis & Treatment. 54th ed. United States: McGraw-Hill Education; 2015.

3. William H Gaasch, MD. Understanding history, epidemiology, and prognosis of Aortic Stenosis. Uptodate.com Web site. http://www.uptodate.com/contents/search?search=aortic+stenosis+ pathophysiology&sp=0&searchType=PLAIN_TEXT&source=USER_INPUT&searchControl=TOP_PULLDOWN&searchOffset=. Accessed April 7, 2016.

The correct answer is C. This patient is presenting with the typical symptoms of streptococcal pharyngitis. Although the most common cause of strep is viral, this patient has a bacterial infection. This is most commonly caused by Group A Beta Hemolytic Streptococcus.1  The Centor Criteria for strep throat consists of: Fever (>100.4 degrees Fahrenheit), tender anterior cervical lymphadenopathy, absence of a cough, and pharyngotonsillar exudate.1 Each symptom is worth 1 point. Any patient with 2-3 points should get a throat culture.1 This patient presents with 3 of the 4 symptoms (fever, anterior cervical lymphadenopathy, and no cough), giving her a score of 3 points and therefore needing a throat culture.

Choice A, a rapid influenza test via nasopharyngeal swab is incorrect. The common symptoms for influenza do include fever, myalgias, and chills but also a cough, nasal congestion, coryza, and headaches.2  This patient is not experiencing a majority of these symptoms, so therefore a rapid influenza test would not be the best choice.

Choice B, MonoSpot test followed by Epstein Barr titers is incorrect. Mononucleosis is a good option to keep in the differential, but a key symptom that would be a negative indication of mononucleosis is “anterior” cervical lymphadenopathy. Most patients with mononucleosis will have posterior cervical lymphadenopathy.1  Although patients with mononucleosis will have a sore throat and fever, they will also complain of severe fatigue as well as abdominal discomfort. This patient denied these symptoms. The abdominal pain is due to the inflammation of the spleen and liver that occurs during the disease. Patients who have an enlarged spleen or liver should avoid contact sports and trauma for at least 1 month in order to avoid possible rupture.1 On physical exam, bilateral lid edema known as Hoagland sign and conjunctival hemorrhaging may be present as well.2

Choice D, do nothing because it’s viral, is not the correct answer. This patient has been experiencing high fevers for multiple days which would indicate more of a bacterial infection rather than viral. Most viral infections have lower grade fevers as opposed to bacterial infections where fevers tend to be higher.3 Also, in bacterial infections the fever will get worse a few days into the illness rather than getting better.3

Resources

1. Williams D.A. PANCE Prep Pearls. CreateSpace. 2014.
2. Papadakis M, McPhee S, Rabow M. Current Medical Diagnosis & Treatment 2015. 2015
3. Duke University Health System. Is it a Bacterial Infection or Virus?. DukeMedicine. https://www.dukemedicine.org/blog/it-bacterial-infection-or-virus. Published Oct. 1, 2013. Accessed Jan. 25, 2016.
4. Wald, E. R. Approach to diagnosis of acute infectious pharyngitis in children and adolescents. UpToDate. http://www.uptodate.com/contents/approach-to-diagnosis-of-acute-infectious-pharyngitis-in-children-and-adolescents?source=search_result. Published Aug. 11, 2015. Accessed Jan. 28, 2016.
5. Marquez-Carrillo M.A. Bacterial Pharyngitis. Medscape. http://emedicine.medscape.com/article/225243-overview. Published Jul. 28, 2015. Accessed Feb. 1, 2016.

The Answer is C. Gout is an inflammatory arthritis condition caused by the interaction between phagocytes and monosodium urate (MSU). Gout can be acute or chronic and involve one or multiple joints. MSU crystals are deposited in the joints and periarticular tissues. A gout flare can be triggered by a release of uncoated crystals or precipitation of crystals in a supersaturated microenvironment. The MSU crystals interact with intracellular and surface receptors of local immune system cells. This interaction in turn incites signals to activate parts of the pro-inflammatory innate immune system. This condition is predominantly a disease of adult men. Gout is rarely seen in pre-menopausal women since estrogen is uricosuric. The incidence of gout is increasing and the prevalence of gout is approximately 9-14 per 1000 (Mikuls T et all 2005).

Hyperuricemia can occur as a result of overproduction, under-excretion, or both of uric acid. Overproduction of uric acid can be caused by rapid cell turnover, excessive dietary purine intake, or inherited disorders of purine nucleotide biosynthesis. Under-excretion of uric acid by the kidney is the most common cause of hyperuricemia. Mixed overproduction and under-excretion of uric acid, most commonly results from excessive alcohol consumption. Acute flares are often precipitated by trauma, initiation of diuretics, dehydration, dietary, systemic illness/surgery resulting in bed rest, and progressive renal insufficiency. It should be noted that not all patients with hyperuricemia have gout.

An acute gout flare typically occurs as a rapid onset with a peak at about 12-24 hours after onset. The patient may present with a very painful, swollen, red, mono-articular joint. Common sites of acute flares are olecranon bursa, elbow, wrist, fingers, knee, ankle, subtalar, and midfoot. Patients with chronic gout may experience about 1-2 gout attacks per year. Whereas for others, gout can be a relapsing problem with multiple attacks without complete resolution.  Advanced gout is characterized by tophi, chronic pain, and deformities.

Diagnosis of gout can be made from uric acid crystals in synovial fluid, elevated serum uric acid level, or the presence of tophi. During an acute gout attack, the presence of uric acid crystals in aspirated synovial joint fluid or tophi is definitive diagnostic finding.  For analysis, the fluid is examined under a polarized light microscope. Serum uric acid concentration is a supportive diagnostic feature. MSU crystallization occurs when the serum level of urate is greater than 6.8 mg/dL, which is the physiologic limit of solubility.  However, serum uric acid levels can be normal during a gout flare. Radiographic findings comprise of soft tissue swelling early in the disease process compared to overhanging edges and asymmetric erosions in the mid to late stage of the disease process.

The goal of treating acute gout flares is rapid relief of pain and inflammation. Response to treatment typically occurs within the first 24-36 hours of the attack. Medical treatment of acute gout flares comprise of oral NSAIDs, Colchicine, or Corticosteroids. Management of chronic gout involves the use of uric acid lowering medications. These medications are indicated in those with several attacks per year, tophi, urate kidney stones, and x-ray changes of gout. Uric acid lowering medications can reduce the frequency of gout attacks over time, tophi formation, and the risk of joint destruction. Medication options for uric acid lowering include: Probenecid, Allopurinol, Febuxostat, and Pegloticase.  Patients with chronic gout should also be advised to avoid foods high in purines such as shellfish, red meat, anchovies, kidneys, yeast, and trout.

References

Aromdee E, Michet C, Crowson C, O’Fallon M, Gabriel S. Epidemiology of gout: is the incidence rising? J Rheumatology 2002; 29:2403–6.

Fravel MA, Ernst ME. Management of gout in the older adult. American Journal of Geriatric Pharmacotherapy. 2011 Oct. 9(5):271-85

Martinon F, Glimcher LH. Gout: new insights into an old disease. The Journal of Clinical Investigation. 2006;116(8):2073-2075. doi:10.1172/JCI29404.

Mikuls T, Farrar J, Bilker W, Fernandes S, Schumacher Jr. H, Saag K. Gout epidemiology: results from the UK General Practice Research Database 1990-1999. Ann Rheum Dis. 2005; 64:2 267-272. doi:10.1136/ard.2004.024091.

Singh JA, Reddy SG, Kundukulam J. Risk factors for gout and prevention: a systematic review of the literature. Current Opinion in Rheumatology. 2011 Mar. 23(2):192-202.

The correct answer is C. Pelvic ultrasound (transvaginal and abdominal) is the first test you would order when trying to rule out ovarian pathology. Other reasonable answers would have included a serum marker CA125, or a pelvic x-ray, both of which were not answer options provided but are often included in the workup in conjunction with orders for a pelvic ultrasound.

Abdominal CT scan is more often indicated in the evaluation of abdominal pain, of which this patient does not present with. Abdominal CT can be used in the evaluation of ovarian pathology, although it is not the standard first-line test, partly for the reason that CT scans subject the patient to radiation and ultrasound testing does not. Occasionally, abdominal or pelvic CT is needed to help clarify ultrasound findings.

Abdominal ultrasound is partially correct, as it is often used in conjunction with a transvaginal ultrasound to evaluate for ovarian pathology. Abdominal ultrasound alone would not be the best choice given above, as the transvaginal combined with the abdominal ultrasound provides more information about the uterus and ovaries.

DXA scan is used in the evaluation of bone mineral density and the screening and diagnosis of osteoporosis. The patient presentation in this case is note related to symptoms and findings related to bone density.

Most women with epithelial ovarian cancer have pelvic or abdominal symptoms prior to their diagnosis. Women with ovarian pathology most typically present with symptoms related to the abdomen (77% of cases), gastrointestinal (70%), pain (58%), constitutional (50%), urinary (34%), and pelvic (26%).   The most common symptoms are bloating, urinary urgency or frequency, difficulty eating or feeling full, and/or abdominal or pelvic pain. Women who complain of these symptoms should be evaluated for a thorough history that includes frequency and severity of each symptom. Persistent abdominal distention, rather than fluctuating, can be more specific for ovarian pathology.

A symptom index has been developed to aid clinicians in evaluating women for early symptoms of epithelial ovarian cancer (although it is not recommended at this time for clinical use). The symptom index is considered to be positive if a woman reports any of the following symptoms that are: new to her within the past year and occur more than 12 times per month: pelvic or abdominal pain, increased abdominal size or abdominal bloating, or difficulty eating or feeling full quickly. Physical exam findings suggestive of epithelial ovarian cancer include adnexal mass, abdominal ascites, “omental cake” or mass in the mid to left upper abdomen, pleural effusion, and groin or supraclavicular lymphadenopathy.

Cancer of the ovary most often requires surgery for diagnosis, staging, and initial management. Most of the time, this involves a surgical total hysterectomy with salpingo-oophorectomy, where the doctor removes the ovaries, the fallopian tubes, and the uterus. Staging and initial surgical management should be performed by a gynecologic oncologist whenever possible to ensure better outcomes. Further treatment will depend a lot on the stage of the cancer, a woman’s age, and her other medical problems. Some women might not need any further treatment after surgery. Other women might need chemotherapy.

Risk assessment for ovarian cancer depends upon age and family history. Ovarian cancer occurs most often in women ages 50 to 65. Ovarian cancer is the second most common gynecologic malignancy and the most common cause of death among women with gynecologic cancer. Most women are diagnosed at an advanced stage, while early stages of the disease are potentially curable. Screening programs for epithelial ovarian cancer using pelvic imaging or tumor markers have not yet been successful. The identification of epithelial ovarian cancer symptoms to aid early detection has become a focus of clinical research. Epithelial carcinoma of the ovaries, fallopian tubes, and peritoneum are clinically similar. Evidence suggests that these diseases have a common pathogenesis and may be initiated in the fallopian tubes. Almost 80 percent of women have lymph node or distant metastases at the time of diagnosis. Five-year survival rates for advanced disease are 19 to 32 percent.

References

http://www.uptodate.com/contents/screening-for-ovarian-cancer?source=machineLearning&search=ovarian+cancer&selectedTitle=2~150&sectionRank=1&anchor=H9#H9

http://www.uptodate.com/contents/epithelial-carcinoma-of-the-ovary-fallopian-tube-and-peritoneum-clinical-features-and-diagnosis source=search_result&search=ovarian+cancer&selectedTitle=1~150

http://www.uptodate.com/contents/overview-of-dual-energy-x-ray-absorptiometry?source=machineLearning&search=dexa+scan&selectedTitle=1~123&sectionRank=1&anchor=H5#H6

http://www.uptodate.com/contents/search?search=clinical+presentation+ovarian+cancer&sp=0&searchType=PLAIN_TEXT&source=USER_INPUT&searchControl=TOP_PULLDOWN&searchOffset=

http://www.uptodate.com/contents/evaluation-of-the-adult-with-abdominal-pain?source=search_result&search=abdominal+ct+scan&selectedTitle=1~150

The correct answer is B. The most common cause of mitral stenosis is rheumatic heart disease, which this patient has a history of. Also, mitral stenosis is a diastolic murmur. The mitral valve should close during diastole, but since the valve is insufficient the patient gets back flow into the left atria causing the murmur. An opening snap is also characteristic for mitral stenosis. Aortic regurgitation is also a diastolic murmur and can be a result of rheumatic fever, but it will not have an opening snap. The murmur will also be best heard at the left upper sternal border rather than the apex, and it will have a decrescendo or blowing sound. Mitral valve prolapse (MVP) is most common in patients with connective tissue disorders, such as Marfan’s or Ehlers Danlos. The characteristic murmur for MVP is a mid systolic ejection click heard best at the apex. Aortic stenosis is a systolic murmur heard best at the right upper sternal border and will have a crescendo-decrescendo sound. Some other exam findings you may find with aortic stenosis are radiation to the carotids, narrow pulse pressure, and a weak/delayed pulse. Patent ductus arteriosus or PDA is a machine-like murmur found in neonates and/or pediatric patients and is incorrect. It occurs when the ductus arteriosis does not close after birth. Symptoms include poor weight gain and shortness of breath.

References

Williams D.A. PANCE Prep Pearls. CreateSpace. 2014.

Mitral stenosis. Chandrashekhar Y, Westaby S, Narula J. Lancet. 2009 Oct;374(9697):1271-83. Epub 2009 Sep 9.

The correct answer is D. Serum bilirubin, sodium, and INR all are necessary to calculate the MELD score. Other information needed would be serum creatinine and whether or not the patient received dialysis in the past week. MELD scores are intended to help providers predict 3 month survival rates of patients who have end stage liver disease. The United Network of Organ Sharing adopted the MELD score as a way to prioritize patients awaiting liver transplantation. Historically, before the 1990s, priority was given to patients who had been on the transplant list the longest, rather than to those who were the most critical. A more equitable system was sought out though, and MELD scores allowed for organs to be allocated the sickest patients first. The scoring range is from 6-40, with 6 being less ill and 40 being severely ill. Labs should be checked every 7 days for a score greater or equal to 25, every 30 days for a score 24-19, every 90 days for a score 18-11, and every year for a score equal or less than 10. By adopting the MELD score as a way of distributing available organs for transplantation, some unintended consequences occurred. The number of patients who not only received a liver but also a renal transplant increased because of the emphasis on Creatinine in the equation. Women somehow became disadvantaged in the MELD system, and have a greater likelihood of dying or becoming too ill for transplantation. It is suggested that this may have to do with their lower Creatinine levels when compared with men. Additionally, MELD scoring removed race from impacting who receives a liver transplant and who is more likely to die while awaiting surgery.

MELD and the Waiting List for Liver Transplant.Sutter Health CPMC. http://www.cpmc.org/advanced/liver/patients/topics/MELD.html#What%20is%20MELD?%20How%20will%20it%20be%20used?. Accessed May 11, 2016.

https://optn.transplant.hrsa.gov/search-results?q=MELD (Accessed on January 24, 2014).

The new liver allocation system: moving toward evidence-based transplantation policy.
Freeman RB Jr, Wiesner RH, Harper A, McDiarmid SV, Lake J, Edwards E, Merion R, Wolfe R, Turcotte J, Teperman L, UNOS/OPTN Liver Disease Severity Score, UNOS/OPTN Liver and Intestine, and UNOS/OPTN Pediatric Transplantation Committees. Liver Transpl. 2002;8(9):851.

The correct answer is C. This patient likely has a right lower extremity deep vein thrombosis, DVT. A palpable cord is indicative of a thrombosed vein. Homan’s sign is when the patient experiences pain in the calf or behind the knee with forced dorsiflexion of the foot. It should be noted that a positive Homan’s sign isn’t necessarily indicative of DVT and a negative sign does not completely rule it out either. Compression ultrasonography is highly sensitive and specific for DVT and is noninvasive. An abdominal CT might be indicated for bilateral lower extremity swelling in order to rule out something such as a mass. Bilateral lower extremity edema might occur if something were obstructing venous return from the legs. In this case however, the patient’s symptoms are unilateral. Plain films such as an x-ray of the lower leg would better inform you of an injury or deformity and would not be indicated here. Peripheral vascular resistance testing is done if there is suspected arterial or venous insufficiency. As a provider, you would see ulcerations, or dusky skin discoloration on your patient. The limb might be cool to the touch and pulseless. Some lower extremity DVTs have been confused with cellulitis due to the similar skin changes that can occur for both conditions. Certainly antibiotics are appropriate if cellulitis is present, but there is signifiant morbidity and mortality associated if a DVT is missed.

References

ABC of arterial and venous disease. Non-invasive methods of arterial and venous assessment.
Donnelly R, Hinwood D, London NJ. BMJ. 2000;320(7236):698.

Real-time ultrasound for diagnosis of symptomatic venous thrombosis and for screening of patients at risk: correlation with ascending conventional venography. Monreal M, Montserrat E, Salvador R, Bechini J, Donoso L, MaCallejas J, Foz M. Angiology. 1989;40(6):527.

The correct answer is B. Spontaneous bacterial peritonitis is an infection of the ascitic fluid present in the abdomen without any other identifiable surgical source. It almost always occurs in patients who have a history of cirrhosis. Typical symptoms include abdominal distention and pain, fever, general malaise, and often altered mentation due to metabolic encephalopathy. Gut pathogens are usually implicated including E.coli. Other causative agents include Klebsiella, Staph and Strep. Trimethoprim-sulfamethoxazole is an appropriate treatment for SBP prophylaxis but is not indicated in the case of active infection. The patient in this vignette requires hospitalization and close monitoring to evaluate for the possibility of decompensation. Cefotaxime is the best choice because it achieves high blood and ascitic fluid levels with IV dosing. Treatment should commence as quickly as possible once paracentesis has been performed to secure a fluid sample. The antibiotics can then be appropriately tailored to whatever culture results are obtained. Cipro does cover intestinal pathogens, but because it is an oral medication, it is not appropriate in this instance. SBP can be life threatening and is only indicated for patients who are asymptomatic. This particular patient is symptomatic given his weakness, fever, and abdominal pain. Levaquin can be used for SBP but is not the best choice because it can be nephrotoxic. The kidneys are already underperfused in the context of liver cirrhosis and there are better alternatives to Levaquin. Additionally, it does not have good penetration of ascitic fluid. Answer E is incorrect because once SBP has developed, patients have a greater mortality risk, when maintained on a nonselective beta-blocker. Nadolol should be discontinued to prevent complications including a prolonged hospital stay and precipitation and/or worsening of hepatorenal syndrome.

References

Cabrera J, Arroyo V, Ballesta AM, Rimola A, Gual J, Elena M, Rodes J. Aminoglycoside nephrotoxicity in cirrhosis. Value of urinary beta 2-microglobulin to discriminate functional renal failure from acute tubular damage. Gastroenterology. 1982;82(1):97.

Terg R, Cobas S, Fassio E, Landeira G, Ríos B, Vasen W, Abecasis R, Ríos H, Guevara M. J Hepatol. Oral ciprofloxacin after a short course of intravenous ciprofloxacin in the treatment of pontaneous bacterial peritonitis: results of a multicenter, randomized study.
2000;33(4):564.

Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M, Hagmann M, Blacky A, Ferlitsch A, Sieghart W, Trauner M, Peck-Radosavljevic M, Reiberger T. Nonselectiveβblockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology. 2014;146(7):1680.

Answer is D. The above clinical vignette displays the classic scenario of Acute Respiratory Distress Syndrome (ARDS). The Berlin Definition defines ARDS as an acute (less than one week) onset of symptoms, bilateral opacities not explained by effusions classically described as a “white out pattern” sparing the costophrenic angels, respiratory failure refractory to 100% oxygen, which is not secondary to cardiac failure or fluid overload as proven by clinical examination or a PCWP > 18cm H2O, and a PaO2/FiO2 ratio Although acute respiratory distress syndrome is an inflammatory process defined as diffuse alveolar damage, IV steroids are not indicated as first line treatment and have not been found to be beneficial as standard of care in ARDs patients. 6

While Furosemide is beneficial in the treatment of CHF exacerbation, the given CXR showed a “white out pattern” which spared the costophrenic angles. This description is not typical of a patient in congestive heart failure, steering the reader away from this pathology. The radiograph of a patient with cardiogenic CHF may show cardiomegaly, pulmonary hypertension and pleural effusions, unlike in non-cardiac cases of CHF, where those are absent. The edema is also diffuse and does NOT spare the periphery of the mid or upper lungs. 5

Prone positioning IS a standard therapy in the treatment of ARDS due to recent evidence of improving oxygenation in patients with clinically diagnosed ARDS, however, a 12 to 24 hour stabilization period prior to the initiation of proning is recommended, along with maintaining prone ventilation for greater than 12 to 18 hours. 4, 6

Discussion:
Acute respiratory distress syndrome (ARDS) is a form of pulmonary edema, non-cardiac in origin which is characterized by diffuse alveolar injury and carries an average mortality rate of 30%. According to Sweeny and McAuley, “7% of patients in the intensive care unit and 16% of those receiving mechanical ventilation, have acute respiratory distress syndrome”. The cause ARDS can be classified into two broad categories: pulmonary or systemic (non-pulmonary in origin). Underneath the pulmonary category lies the two biggest risk factors for ARDS which also carry the highest mortality rate, pneumonia and aspiration. Other common causes include sepsis, trauma, multiple blood transfusions, pancreatitis, inhalation injury and certain types of drug toxicity. 1, 2, 6

ARDS occurs in response to a primary illness, either a direct pulmonary or indirect extrapulmonary insult, which causes severe alveolar inflammation and injury to the epithelial of lung capillaries. Due to increased epithelial and endothelial permeability, cytokines, plasma proteins and macrophages flood the damaged alveolar epithelium, causing an inflammatory response which results in loss of surfactant production, epithelial ion channels, disrupted gas diffusion and increased permeability which all lead to alterations in vasomotor tone, the formation of microthrombi and subsequent pulmonary hypertension. As a result of pulmonary hypertension, there is an increase in right ventricular afterload which can be worsened by fluid overload and mechanical ventilation. 6

In 2012, The Berlin Definition for acute respiratory distress syndrome was established. This states that in order for the diagnosis of ARDS to be met, ALL of the following criteria must be present: Within one week of a known clinical insult, or new/worsening respiratory symptoms, bilateral opacities not explained by effusions, lobar/lung collapse or nodules on chest radiography/CT, respiratory failure is not secondary to cardiac failure or fluid overload as proven by objective measures (ECHO, lung ultrasonography), and lastly, hypoxemia with severity determined by the PaO2/FiO2 ratio: Mild (200-300 mmHg), Moderate (100-200 mmHg), and Severe ( The management of ARDS is focused on assessing the underlying condition as well as specific targeted therapy. The current recommendations include protective mechanical ventilation with a low tidal volume of 6ml/kg IBW, Pplat

References

1. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2000.

2. Kallet R, Campbell A, Dicker R, Mackersie R. TIDAL VOLUME (VT) AND WORK OF BREATHING (WOB) DURING LUNG-PROTECTIVE VENTILATION (LPV) IN ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS). Critical Care Medicine. 2004.

3. Williams D. PANCE Prep Pearls. Lexington, KY: CreateSpace; 2014.

4. Marino PSutin K. The ICU Book. Philadelphia: Lippincott Williams & Wilkins; 2007.

5. Singh V. Congestive Heart Failure Imaging: Overview, Radiography, Computed Tomography. Emedicinemedscapecom. 2016. Available at: http://emedicine.medscape.com/article/354666-overview. Accessed May 24, 2016.

6. Mac Sweeny R. Acute respiratory distress syndrome. The Lancet. 2016.

A Comprehensive Metabolic Panel (CMP) refers to a group of blood tests that look at overall chemical balance and metabolism of the body. The blood tests look at organ function, such as that of the liver and kidneys. It also measures serum electrolyte levels, such as sodium, potassium, and chloride. Serum glucose levels and protein levels are also measured through a CMP. Abnormal results typically indicate the presence of conditions such as liver or kidney disease or diabetic complications.

Blood Count with Differential (CBC w/diff) is used to look at overall health status and the presence of conditions such as anemia, leukemia, and infections. It can also be used to detect the presence of other life threatening conditions such as agranulocytosis, which is often associated with atypical antipsychotics, most commonly Clozaril. A CBC w/diff looks at various components of the blood including red and white blood cells, hematocrit and hemoglobin, and platelet count. Increases or decreases in cell counts may be indicative of an underlying disease process.

Arterial Blood Gases (ABGs) are a means to measure the amount of oxygen and carbon dioxide in the blood, as well as the pH level to determine acidosis or alkalosis. The blood used for ABGs is taken directly from an artery. Red blood cells (RBCs) transport oxygen and carbon dioxide throughout the body. The blood passes through the lungs were oxygen and carbon dioxide are exchanged-the oxygen enters the blood through the lungs while the carbon dioxide flows out of the blood and into the lungs to be exhaled. Low levels of oxygen in the blood are indicative of hypoxemia. High pH levels are indicative of a process called alkalosis, while low pH levels are associated with acidosis. Abnormal levels of oxygen and carbon dioxide, as well as pH imbalance, can help detect the presents of liver and kidney disease as well as various respiratory diseases, such as asthma and COPD. You may also see alterations in any of the above as a result of drug overdose, chemical poisoning, hemorrhage, organ failure, or shock.

A Lipid Profile is used to measure the level of cholesterol and triglycerides in the blood. Monitoring cholesterol levels can help determine the presence of plaque build-up in the arteries, which leads to narrowing and or occlusion of vessels. Elevated cholesterol and triglyceride levels do not cause any symptoms, which is why blood tests are so important, and are a known risk factor for development of heart disease. A lipid profile measures total cholesterol level and then further breaks it down to level of High Density Lipoprotein (HDL, “good” cholesterol), Low Density Lipoprotein (LDL, “bad” cholesterol), and triglycerides (fat in the blood).

References

Blood Gas Test. (n.d.). Retrieved May 23, 2016, from http://www.healthline.com/health/blood-gases#Overview1. Cholesterol test. (2016). Retrieved May 23, 2016, from http://www.mayoclinic.org/tests-procedures/cholesterol-test/home/ovc20169526?_ga=1.242328459.866837476.1462205784

Complete blood count (CBC). (n.d.). Retrieved May 23, 2016, from http://www.mayoclinic.org/tests-procedures/complete-blood-count/basics/definition/prc-20014088. National Institute of Health, U.S. National Library of Medicine (2015).

Comprehensive Metabolic Panel. Retrieved May 23, 2016, from https://www.nlm.nih.gov/medlineplus/ency/article/003468.htm

Answer:  Hypothermia.  Leads V4 and V5 demonstrate classic Osborne (J) waves, defined as an additional upward deflection to the terminal portion of the QRS complex.  Other findings on this EKG consistent with hypothermia are baseline artifact related to shivering, inverted T waves and prolonged QT interval.  Atrial flutter is characterized by the classic “saw tooth pattern” and should have a faster rate than this EKG with atrial rates of 240-400 bpm.  Hyperkalemia EKG findings are usually:  bradycardia, flattened P waves, widened QRS complex, biphasic QRS-T complexes, upright peaked T waves and ST elevations.  Ischemia would be represented by ST depressions and pulmonary embolus EKG findings are usually tachycardia and/or the “S1Q3T3” pattern.

Hypothermia is generally defined as a core temperature of less than 35 degrees C or 95.8 degrees F with severe hypothermia at a temp of less than 82.4 degrees F.  Rectal or esophageal temperatures are most accurate.  In addition to a prolonged exposure to a cold environment (primary hypothermia), secondary causes of hypothermia include endocrine disorders, spinal cord transection leading to neurogenic shock, hypothalamic dysfunction, toxins, diabetic or alcoholic ketoacidosis, and sepsis.  This particular patient had underlying diabetic ketoacidosis with a pH of 7.10 and an anion gap of 28.

History and physical exam may reveal irritability, lethargy to confusion to coma, reduced respiratory rate, bradycardia, and/or signs of frostbite (hyperemia, edema, vesicles, hemorrhagic blisters, or necrosis).  EKG findings include Osborne waves (present in approximately 80% of cases), baseline artifacts, QT prolongation, bradycardia, atrial fibrillation with slow ventricular response, premature ventricular beats, ventricular tachycardia or fibrillation, and asystole.  The Osborne, or “J”, wave size usually corresponds to the severity of the hypothermia and will diminish in size as the patient’s core temperature is warmed.  Ventricular tachycardia and fibrillation are most commonly found during the rewarming process.

Treatment of hypothermia is targeted at rewarming as well as addressing any potential secondary causes that may be responsible.  Rewarming should occur somewhat slowly to avoid inducing potential arrhythmias unless the patient is profoundly hypothermic, in which case a more aggressive rewarming strategy has been suggested to get the patient to 30-32 degrees C (86-89.6 degrees F).  Rewarming techniques once the patient has been removed from a cold environment include warm blankets or more commonly a forced warm air blanket found in most hospitals.  With more profound hypothermia, more invasive techniques are required.  These include:  warm IV fluids, humidified oxygen, GI, peritoneal, pleural or bladder lavage, and even cardiac bypass. Frostbite should be rapidly rewarmed in warm water baths once the chance of re-freezing has passed.

References:

Slovis C. ABC of clinical electrocardiography: Conditions not primarily affecting the heart. Bmj 2002;324(7349):1320–1323.

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: a Comprehensive Study Guide. New York: McGraw-Hill, Medical Pub. Division; 2004.

Accidental hypothermia. In DynaMed Plus® – the next-generation clinical information resource designed to decrease time to answer. DynaMed Plus. Available at: http://www.dynamed.com/home/. Accessed March 16, 2016.

Answer:  Second-degree AV block – Mobitz Type II.  This EKG shows a fixed prolongation of the PR interval with a non-conducted P wave resulting in an absence of a QRS complex.  A first-degree block could appear similar but all P waves should result in a corresponding QRS.  Mobitz I blocks have a PR interval which becomes more prolonged with each successive beat, eventually resulting in a missed QRS complex.  Third-degree, or complete, heart block shows a constant interval between P waves but no association to the QRS complexes.

These various blocks are disorders of the electrical conduction through the atrioventricular node caused by numerous potential etiologies including:  congenital anomalies, ischemia, infectious/inflammatory diseases, metabolic abnormalities, medications, cardiac procedures, and post-radiation, to name a few.

The patient may present with complaints of dizziness, syncope, fatigue, chest pain, dyspnea or be completely asymptomatic.  History should include inquiry about current medications, tick or other possible infectious disease exposures, angina-like symptoms, or symptoms consistent with previously undiagnosed conditions such as:  sarcoidosis, amyloidosis, lupus, rheumatoid arthritis, scleroderma, and even sleep apnea.

The diagnosis is usually made with a 12 lead EKG, however, an intermittent block might be more likely diagnosed using a Holter or event monitor, exercise testing, or with an electrophysiological (EP) study.  A first-degree block has a PR interval of > 200 milliseconds and every P is followed by a QRS.  Second-degree type I blocks have either a progressive lengthening of the PR interval eventually resulting in a missed QRS complex (Wenckebach) or a fixed PR interval with 2 P waves before a QRS is conducted.  Second-degree type II blocks usually have a fixed prolongation of the PR interval with an intermittent non-conducted QRS complex, however, they can also have a 2:1 or greater pattern similar to the second-degree type I mention but usually found in conjunction with an intraventricular conduction delay.  Third-degree blocks are characterized by a complete absence of AV node or His-Purkinje system conduction of the P wave impulse.  This requires an area from within the AV node or the ventricle itself to initiate the QRS complex resulting in a complete disassociation between the P and QRS waves.  Mixed second-degree type II and third-degree can also occur.

Treatment involves addressing underlying systemic causes if any are present.  Temporary or permanent pacing is indicated for almost all patients with a second-degree type II or higher with biventricular pacing for those also associated with heart failure.  Atropine may be of short-term benefit.

References:

Zipes DP. Second-degree atrioventricular block. Circulation 1979;60(3):465–472.

Longo DL, Kasper D, Jameson J, Fauci A, Hauser S, Loscalzo J. Harrison’s Principles of Internal Medicine. New York: McGraw-Hill; 2012.

Atrioventricular conduction disorders. In DynaMed Plus® – the next-generation clinical information resource designed to decrease time to answer. DynaMed Plus. Available at: http://www.dynamed.com/home/. Accessed March 10, 2016.

Inflammatory bowel disease (IBD), specifically Crohn’s disease, is a complex, chronic autoimmune disease of unknown etiology characterized by relapsing and remitting inflammation anywhere in the GI tract from mouth to anus. The disease has a bimodal age peak: 15-30 and 60-80 years. Symptoms of Crohn’s generally include anorexia, malnutrition, diarrhea (from epithelial damage), abdominal pains and cramps, possibly obstructive symptoms and sometimes perianal manifestations (eg, skin tags, abscess, fistula, anal ulcers, anal stenosis). Ulcerative colitis (UC) is the other manifestation of IBD, but there is generally no perianal involvement.

Irritable bowel syndrome (IBS) is a functional disorder, marked by nonspecific abdominal symptoms (eg, pain, flatulence, cramps) in association with altered bowel habits (eg, constipation, diarrhea or both). Unlike IBD, IBS has no morphologic or biochemical abnormalities. Instead, it is thought to result from disturbance of the brain/gut interaction, resulting in abnormal processing of physiologic stimuli, which triggers altered motility, increased contractility/spasticity, and visceral hypersensitivity, and is associated with a reduced intestinal volume tolerance. There is no perianal disease component to this disorder.

Celiac disease is an immunologic disorder of the small bowel, resulting in enhanced immunogenic response to gliadin (alcohol-soluble portion of gluten). This results in intense local inflammation of the villi of the small intestine, followed by villous atrophy and significantly decreased absorptive surface area. While many cases are asymptomatic, symptoms can include diarrhea, fatigue, weight loss, abdominal distention, excessive flatus, or large, bulky, foul smelling stools. Like IBS, there is no associated perianal manifestation of this disease, as there is in Crohn’s. Symptoms are related to dietary gluten intake. Management involves eliminating gluten from the diet.

Lactose intolerance is the inability to digest milk and some dairy products, leading to abdominal bloating, cramping and diarrhea. The enzyme lactase is generally present in the small intestine at birth, but levels start to decline by the age of 5 years, and 95% of birth lactase levels are lost by early childhood. Lactase continues to decrease with aging, and as a result patients can become increasingly symptomatic. Treatment is aimed at limiting consumption of milk and other lactose-containing foods. There is no perianal manifestation of lactose intolerance.

References

1. Lichtenstein GR, et al. Practice Parameters Committee of American College of Gastroenterology. Management of Crohn’s disease in adults. Am J Gastroenterol 2009; 104:465.
2. Kamp EJ, et al. Irritable Bowel Syndrome and Microscopic Colitis: A Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol 2016; 14:659.
3. Mattar, et al. Lactose intolerance: diagnosis, genetic, and clinical factors. Clin Exp Gastroenterol. 2012; 5: 113–121.

C. diff., or pseudomembranous colitis, presents a wide clinical spectrum from mild diarrhea to fulminant and potentially fatal colitis. The infection is most often associated with antibiotic use and resulting overgrowth of the commensal anaerobe C. difficile. It can occur from a few days to up to 10 weeks after antibiotic use. For mild symptoms, treatment consists of, first, discontinuing the offending agent; then, initiation of a 10-14 day course of oral antibiotics. Metronidazole 250mg-500mg po TID or vancomycin 125mg-250mg QID are first line agents. For severe cases or patients with significant comorbidities, IV metronidazole may be used.

Antidiarrheal agents are contraindicated as long as the infection is uncontrolled.

The indications for operative treatment of C. diff. are fulminant disease, toxic megacolon, colonic perforation or failure to improve with medical therapy.

References

1. Bagdasarian N, et al. Diagnosis and treatment of Clostridium difficile in adults: a systematic review. JAMA 2015; 313:398.

2. Cohen SH, et al. Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the society for healthcare epidemiology of America (SHEA) and the infectious diseases society of America (IDSA). Infect Control Hosp Epidemiol 2010; 31:431.

This patient has most likely developed an anal fissure. A fissure is a longitudinal tear/wound in the anus, typically located in the posterior midline, and is associated with high anal sphincter tone. The main risk factors for fissure are constipation and chronic diarrhea, but fissure can also occur with normal bowel movements. Acute fissure will heal in 40-60% of patients with appropriate improved stool management and decreasing anal sphincter tone. A daily fiber supplement will help keep stool soft, bulky and easy to pass. Sitz baths will provide comfort and relaxation of the sphincter muscles. Topical nitroglycerine (0.2%) is a vasodilator that acts to increase bloodflow to the wound to aid in healing, but also has a relaxing effect on the sphincter muscles.

Rubber band ligation is used to treat Grade I – II hemorrhoids, and has no role in the treatment of fissures.

References

1.  Zaghiyan KN, Fleshner P. Anal fissure. Clin Colon Rectal Surg 2011; 24:22.Perry WB, et al. Practice parameters for the management of anal fissures (3rd revision). Dis Colon Rectum 2010; 53:1110.

2. Perry WB, et al. Practice parameters for the management of anal fissures (3rd revision). Dis Colon Rectum 2010; 53:1110.

Carcinoembryonic antigen (CEA) is used to monitor people who have been diagnosed with colorectal cancer. An initial CEA test is typically ordered prior to treatment as a “baseline” value. If the level is elevated, then the test can be used to monitor a patient’s response to therapy and to determine whether the cancer has progressed or recurred. The test in not diagnostic, but can be used as an adjunct in colorectal cancer diagnosis, staging and post-treatment surveillance.

A complete blood count (CBC) will provide useful information regarding white and red blood cell counts, but is not routinely used to monitor recurrence of colorectal cancer; it can provide information on anemia, infection, inflammation or a bleeding disorder. Cancer antigen 125 (CA-125) is used as a marker for cancers such as ovarian, breast or cervical. Alpha-fetoprotein (AFP) is used to monitor for hepatocellular carcinoma, testicular cancer, pancreatic cancer or gastric cancer.

 References

1.https://www.fascrs.org/sites/default/files/downloads/publication/practice_guideline_for_the_surveillance_of

Esophageal varices are dilations of the veins of the esophagus, generally at the distal end. The most common cause in adults is cirrhosis, either from alcohol abuse or chronic viral hepatitis. Varices are generally asymptomatic until they bleed, at which point they can become life-threatening. In a stable patient with no recent bleeding, upper endoscopic exam is the preferred method to screen for esophageal varices, looking for dilated veins, red streaks and red spots, all of which may indicate a significant risk of bleeding.

In this patient, evidence of recent bleeding is unlikely given her history of no symptoms for the past 4 or 5 months. Treatment can be undertaken to prevent further bleeding. Use of NSAIDS can exacerbate bleeding, so should be avoided. Beta blockers can be used to reduce pressure in the portal vein, thereby decreasing the risk of bleeding.

Octreotide is a pharmacologic vasoconstrictor, and would be a treatment option if the patient were actively bleeding. It is commonly used with endoscopic therapy to slow the flow of blood from internal organs to the portal vein. Octreotide is typically continued for 5 days following a bleeding episode.

References

1. Garcia-Tsao G, et al. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology 2007; 46:922.

2. Sanyal AJ, Shiffman ML. The pharmacologic treatment of portal hypertension. Annu Rev Gastrointest Pharmacol 1996; :242.

3. Bañares R, et al. Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a meta-analysis. Hepatology 2002; 35:609.

Early mobilization of patients as soon as possible after surgery is thought to reduce the chances of venous thrombosis because it stimulates calf muscles and puts pressure on the calf and leg veins, thus discouraging stasis and venous pooling of blood in the lower extremities. Likewise, sequential compression with pneumatic leg compression enhances blood flow in the deep veins of the legs. Lovenox is a low molecular weight heparin. It is an excellent therapeutic choice in high-risk VTE patients (i.e., patients over 40 years of age, patients undergoing major surgery, patients with concurrent risk factors for VTE). Prophylactic low-molecular-weight heparin should be given subcutaneously once or twice daily until the patient is ambulating well.

An IVC filter can be considered when anticoagulation is contraindicated (eg, due to heightened bleeding risk), but is generally not first line therapy.

 References

1. Hemmila MR, et al. Prophylactic Inferior Vena Cava Filter Placement Does Not Result in a Survival Benefit for Trauma Patients. Ann Surg 2015; 262:577.

2. Snow V, et al. Management of venous thromboembolism: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Fam Med 2007; 5:74.

3. Blann AD, Lip GY. Venous thromboembolism. BMJ 2006; 332:215.

4. Morris RJ, Woodcock JP. Intermittent pneumatic compression or graduated compression stockings for deep vein thrombosis prophylaxis? A systematic review of direct clinical comparisons. Ann Surg 2010; 251:393.

This patient most likely has Zollinger-Ellinson syndrome (ZES). In ZES, a gastrin-secreting tumor (gastrinoma) causes hypergastrinemia, which results in refractory peptic ulcer disease (PUD). The excess gastric acid leads to peptic ulcers, acid reflux, abdominal pain, diarrhea and other symptoms. The clinical presentation is indistinguishable from PUD, except that ZES is typically more advanced or refractory to PUD treatment (eg, PPIs and H2 blockers), as with this patient.

In this case, the patient should be advised that symptoms may be due to a tumor, and that further work-up is advised. A fasting gastrin lab should be obtained—a level >150pg/mL indicates hypergastrinemia. Follow with a secretin test to confirm the diagnosis.

Dietary modifications and weight loss will not change the course of the gastrinoma, so will not likely ameliorate symptoms.

Endoscopy, CT or MRI may be helpful to localize the tumor.

References

1. Ellison EC, Johnson JA. The Zollinger-Ellison syndrome: a comprehensive review of historical, scientific, and clinical considerations. Curr Probl Surg 2009; 46:13.

2. Metz DC. Diagnosis of the Zollinger–Ellison syndrome. Clin Gastroenterol Hepatol 2012; 10:126.

In the United States, the recommended primary therapies for H. pylori infection include: a PPI twice daily, clarithromycin 500mg BID, and amoxicillin1,000mg BID. For patients allergic to penicillin, metronidazole can be substituted for amoxicillin. Treatment duration of 14 days has typically been employed. When given at the recommended doses, most recent studies report eradication rates in the range of 70–80%.

H. pylori is naturally resistant to several commonly used antibiotics, including vancomycin, trimethoprim and sulfonamides.

Antibiotics are required to eradicate H. pylori infection; fiber powder and probiotics will not cure the infection.

 References

1. http://gi.org/guideline/management-of-helicobacter-pylori-infection/

2. Almeida et al. Triple Therapy with High-Dose Proton-Pump Inhibitor, Amoxicillin, and Doxycycline Is Useless for Helicobacter pylori

Eradication: A Proof-of-Concept Study. Helicobacter 19: 90–97 (2014).

The presence of gallstones (cholelithiasis) is common, particularly in Western populations. In the United States, gallstones are seen in approximately 6 percent of men and 9 percent of women. Most individuals with gallstones are asymptomatic throughout their life and are referred to as having “incidental” gallstones. Prophylactic cholecystectomy is not indicated for most patients with asymptomatic gallstones. Adult patients with silent or incidental gallstones should be observed and managed expectantly, with few exceptions.

Decision analysis models have shown no benefit with prophylactic cholecystectomy, whether laparoscopic or open. Waiting until a patient becomes symptomatic before performing cholecystectomy prevents unnecessary surgery since the majority of patients with incidental gallstones will never develop biliary colic. However, prophylactic cholecystectomy should be performed in patients at high risk of gallbladder carcinoma. The specific groups at high risk of gallbladder cancer include patients with asymptomatic gallstones who are Pima Indians or who have a calcified gall-bladder, gallbladder polyps greater than 10 mm, gallstones greater than 2.5 cm or anomalous pancreaticobiliary ductal junction, and carriers of Salmonella typhosa.

ERCP to evaluate the biliary tree is not indicated for asymptomatic gallstones.

References 

1. Ahmed A, et al. Management of Gallstones and Their Complications. Am Fam Physician. 2000 Mar 15;61(6):1673-1680.

2. Ransohoff DF, et al. Prophylactic cholecystectomy or expectant management for silent gallstones. A decision analysis to assess survival. Ann Intern Med. 1983;99(2):199.

3. Gracie WA, Ransohoff DF. The natural history of silent gallstones: the innocent gallstone is not a myth. N Engl J Med. 1982;307:798–800.

Crohn’s disease is characterized by transmural inflammation that can affect any part of the gastrointestinal tract, from the mouth to the anus. It is associated with segmental involvement with skip lesions. Strictures and perianal disease (eg, abscess, fistula) are also seen with Crohn’s disease but are exceedingly rare in ulcerative colitis. In patients who have undergone removal of the colon and rectum to treat presumed ulcerative colitis but who later develop symptoms elsewhere in the GI tract, including the perianal area, Crohn’s disease must be considered. The patient in this scenario is experiencing recurrent perianal abscess with likely fistula in ano, which is not a characteristic of ulcerative colitis.

Ulcerative colitis is characterized by inflammation that is confined to the mucosal and submucosal layers of the colon. It generally starts in the rectum and progresses proximally. Surgical excision of the colon and rectum cures ulcerative colitis, though not the extra-intestinal manifestations of the disease.

Perianal abscess is not a feature of irritable bowel syndrome.

Anal cancer typically presents with signs of bleeding from the anus, a lump near the anus or pain, pressure, itching or discharge near the anus. Symptoms are generally not cyclic in nature.

References

1. Zoeten E, et al. Diagnosis and Treatment of Perianal Crohn Disease: NASPGHAN Clinical Report and Consensus Statement. JPGN Volume 57, Number 3, September 2013.

2. Thornton M, Solomon MJ. Long-term indwelling seton for complex anal fistulas in Crohn’s disease. Dis Colon Rectum 2005; 48:459.

Primary sclerosing cholangitis (PSC) is a chronic thickening of the bile duct walls of unknown etiology, although 80% of cases are associated with inflammatory bowel disease, generally ulcerative colitis. Endoscopic retrograde cholangiopancreatography (ERCP) is the mainstay for accurate assessment of the hepatobiliary tree to establish a diagnosis of PSC. Management is multidisciplinary. Antihistamines can be used for pruritus. Bile that backs up in narrowed or blocked ducts causes frequent bacterial infections. To prevent and treat these infections, people with PSC may take repeated courses of antibiotics. Liver transplant is the only known cure for PSC.

Resecting the pancreas (pancreatectomy) in PSC is not indicated unless signs and symptoms of pancreatitis are present.

 References

1. Lindor, K. et al. High Dose Ursodeoxycholic Acid for the Treatment of Primary Sclerosing Cholangitis. Hepatology. 2009 Sep; 50(3): 808–814.

2. Tharian B, et al. What is the current role of endoscopy in primary sclerosing cholangitis? World J Gastrointest Endosc. 2015 Aug 10; 7(10): 920–927.

3. Koro N, Alkaade S. Role of Endoscopy in Primary Sclerosing Cholangitis. Curr Gastroenterol Rep (2013) 15:361.

Recommendations for colorectal cancer (CRC) screening when there is a single first-degree with CRC or advanced adenoma diagnosed at age <60 years is colonoscopy every 5 years beginning at age 40 years or 10 years younger than age at diagnosis of the youngest affected relative.

References

1. http://gi.org/guideline/colorectal-cancer-screening/

Wound dehiscence can range from splitting open of the skin layers to complete breakdown of the muscle and fascia, exposing internal organs. Occasionally, the skin layers remain intact, but deeper layers break down resulting in an incisional hernia.

Many factors are associated with surgical dehiscence. Age, malnutrition, male sex and long-term steroid use are thought to influence the incidence of abdominal dehiscence. Smoking, diabetes and rheumatoid arthritis can impair healing by affecting the microcirculation. Obesity can influence wound breakdown due to reduced tissue oxygenation, increased subcutaneous dead space rendering the patient more susceptible to hematoma and seroma formation and increased incidence of infection.

Once wound infection has been ruled out, treatment of the dehisced wound will depend on the depth of tissue interruption. In this case, the only breakdown is at the level of the skin and subcutaneous tissue. For such superficial dehiscence, remove any staples that have been in place for the required amount of time (depending on location), usually 12-14 days for abdominal incisions. There is no added benefit to leaving the staples when the wound has clearly dehisced. Explore the wound to see how deep it goes, assessing if the fascia is intact. Do not restaple or suture the dehisced wound; instead, allow it to heal by secondary intention using wet to dry packing of the wound.

There is no indication in this scenario for returning to the operating room for abdominal washout in the absence of intra-abdominal contamination or infection.

References

1. Orsted H, et al. Best Practice Recommendations for the Prevention and Management of Open Surgical Wounds. Wound Care Canada, Volume 8, Number 1, 2010, p.6-34.

Internal hemorrhoids are classified by their degree of prolapse, which helps determine management:

Grade One:     No prolapse

Grade Two:     Prolapse that goes back in on its own

Grade Three: Prolapse that must be pushed back in by the patient

Grade Four:   Prolapse that cannot be pushed back in by the patient (often very painful).

Bleeding attributed to internal hemorrhoids is usually bright red and can be quite brisk. It may be found when wiping, dripping into the toilet bowl, or streaked on the bowel movement (BM) itself. Not all patients with symptomatic internal hemorrhoids will have significant bleeding. Instead, prolapse may be the main or only symptom. Prolapsing tissue may result in significant irritation and itching around the anus. Patients may also complain of mucus discharge, difficulty with cleaning themselves after a BM, or a sense that their stool is “stuck” at the anus with BMs. Patients without significant symptoms from internal hemorrhoids do not require treatment based on their appearance alone.

References

1. Hemorrhoids: Expanded Version. American Society of Colon and Rectal Surgeons, https://www.fascrs.org/patients/disease-condition/hemorrhoids-expanded-version.

Squamous cell carcinoma of the anus is an uncommon tumor, representing only 1.5% of gastrointestinal tract tumors. Concurrent chemoradiotherapy is the current standard of treatment for anal cancer. Until the mid-1970s, anal cancer was most commonly treated with radical surgery consisting of abdominoperineal resection (APR), which involved removal of the anal sphincters and placement of a permanent colostomy. The use of chemoradiotherapy was introduced in 1974, initially as neoadjuvant therapy preceding APR. However, with the finding that many patients were rendered free of cancer by this pre-operative regimen, CRT became the widely accepted definitive therapeutic option, sparing the patient the need for permanent colostomy, and replacing radical surgery as the primary treatment of choice for anal cancer.

Topical immunomodulators (eg, Aldara, Condylox) and cryotherapy are treatment for anal warts, not anal cancer.

References

1. Spithoff K, et al. Chemoradiotherapy for Squamous Cell Carcinoma of the Anal Canal: A Systematic Review. Clinical Oncology 26 (2014) 473-487.

2. http://www.cdc.gov/std/treatment/2010/genital-warts.htm

In the U.S., the most common reason for needing a liver transplant is cirrhosis caused by chronic viral hepatitis C infection, followed by cirrhosis caused by long-term alcohol abuse. Primary biliary cirrhosis and autoimmune hepatitis are also possible causes, though not as common.

 References

1. https://www.niddk.nih.gov/health-information/liver-disease/liver-transplant

2. Burra P, et al. Hepatitis C virus and liver transplantation: where do we stand? Transpl Int. 2016 Feb;29(2):135-52.

Hepatitis is inflammation of the liver, a vital organ that processes nutrients, filters the blood, and fights infections. When the liver is inflamed or damaged, its function can be affected. Heavy alcohol use, toxins, some medications, and certain medical conditions (eg, Wilson’s disease, autoimmune hepatitis) can cause hepatitis. However, hepatitis is most often caused by a virus. In the United States, the most common types of viral hepatitis are Hepatitis A, Hepatitis B, and Hepatitis C.

References 

1. http://www.cdc.gov/hepatitis/abc/

Toxic megacolon is a rare but potentially fatal complication of colitis, most commonly associated with inflammatory bowel disease. It is defined as a segmental or total colonic dilatation of >6cm in the presence of acute colitis and signs of systemic toxicity. Early detection and intervention have a profound impact on survival. Toxic megacolon can occur in any patient with colitis, regardless of age, gender or race. Toxic megacolon is a diagnosis based on clinical signs of systemic toxicity in combination with radiographic evidence of colonic dilatation. The radiologic diagnosis is made using plain films of the abdomen, assessing for dilatation > 6cm.

Toxic megacolon features found by plain film may indicate the need for subsequent CT to determine the cause of the megacolon, and is an important tool in the diagnosis of abdominal complications such as colonic perforation.

Stool studies and culture should be sent for patients with a history of antibiotic use or chemotherapy, assessing for C. diff as the etiology of the megacolon.

Colonoscopy to assess the inside of the colon should not be performed in suspected toxic megacolon due to the increased risk of colonic perforation.

References

1. Woodhouse, E. Toxic Megacolon: A Reviewfor Emergency Department Clinicians. Journal of Emergency Nursing, Volume 42, Issue 6 (2016), p. 481-486.

2. Autenrieth D, Baumgart D. Toxic Megacolon. Inflamm Bowel Dis 2012;18: 584-591 (2012).

Irritable bowel syndrome (IBS), one of the most common gastrointestinal (GI) disorders in the world, is characterized by abdominal pain, discomfort, bloating, and disturbed defecation. It has four types: IBS with diarrhea (IBS-D), IBS with constipation (IBS-C), mixed IBS (IBS-M), and unsubtyped IBS (IBS-U).

Because IBS lacks characteristic imaging features and has no diagnostic biomarkers, symptom-based criteria (Rome III) are recommended for its diagnosis, defined as: Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated with two or more of the following:

• Improvement with defecation.
• Onset associated with a change in frequency of stool.

o   Onset associated with a change in form (appearance) of stool.

Lactose intolerance and celiac disease are both related to dietary intake, which is not indicated in this scenario.

Inflammatory bowel disease is characterized by inflammation of all or part of the GI tract, and usually presents with severe diarrhea, pain, fatigue and weight loss, which is not indicated in this scenario.

References

1. Ohgo H, et al. Irritable bowel syndrome evaluation using computed tomography colonography. World J Gastroenterol 2016 November 14; 22(42): 9394-9399.

VTE is a common cause of preventable death in hospitalized patients. Approximately one-third of the 150,000 to 200,000 VTE-related deaths per year in the United States occur following surgery. In patients undergoing general and abdominal-pelvic surgery, the risk of VTE varies depending on both patient-specific and procedure-specific factors. Examples of relatively low-risk procedures include laparoscopic cholecystectomy, appendectomy, transurethral prostatectomy, inguinal herniorrhaphy, and unilateral or bilateral mastectomy. Open abdominal and open-pelvic procedures are associated with a higher risk of VTE. VTE risk appears to be highest for patients undergoing abdominal or pelvic surgery for cancer. Patient-specific factors also determine the risk of VTE, including age >60, prior VTE, anesthesia > 2 hours, bedrest > 4 days and sepsis.

 References 

1. Gould MK, et al. Prevention of VTE in nonorthopedic surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e227S-77S.

Answer is B. Given this patients vitals, physical exam, values showing blood loss and leukocytosis and CT scan with free air and fluid this patient has a perforation somewhere in his abdomen, mostly likely due to a peptic ulcer The patients age, sex, history of tobacco use, and daily ASA use put him at increased risk of developing peptic ulcers (1,2,3,4,5). GI bleeds and gastrointestinal perforations are common complications of peptic ulcers (1, 2, 3, 4, 5). Due to the fact that he is hemodynamically unstable, and he has free air and fluid on the CT scan, just giving a unit of pRBC and IVF and monitoring him would not be adequate care. The best treatment option for this patient would be emergent exploratory surgery to locate the perforation and repair it (4). Given the above, admitting him for observation and repeating the CT in the morning is not the right answer.

Case Discussion:

The above case and question represent a common complication associated with peptic ulcer disease. Peptic ulcers are the result of a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa.^1,2 Peptic ulcers occur when the protective mucosal factors decrease and damaging factors such as acid and pepsin increase.¹ Duodenal ulcers are 5 times more common than gastric ulcers and tend to occur in patients between the ages of 30-55,^1,5 whereas gastric ulcers occur in patients between the ages of 55-70.¹ However, ulcers can occur at any age.¹ Ulcers in general are slightly more common in men than women with a ratio of 1.3:1.¹ Some common risk factors associated with people who have ulcers are smoking and long term use of NSAIDs.

Two major etiologies associated with peptic ulcer disease is Helicobacter pylori (H. pylori) infection and the long term use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, indomethacin, ketorolac, Motrin, Aleve.^1,2 Less common causes are acid hypersecretory states like Zollinger Ellison syndrome.¹

Mucosal injury occurs when the balance between the protective factors like mucous, bicarbonate, prostaglandins, and blood flow and the destructive factors like pepsin and acid are disrupted.^1,3 The imbalance leads to increased acid exposure to the mucosal lining of the stomach or the duodenum causing gastric metaplasia.¹

NSAID-induced ulcers occur due to suppression of gastric prostaglandin synthesis.⁴ Prostaglandins are important for mucosal integrity. Once inhibited, it makes the mucosal lining more susceptible to destruction in the setting of increased pepsin and acid. The most common presenting symptom in patients with peptic ulcer disease is dyspepsia.² However, most patients may not have any symptoms until they develop complications of the ulcers like obstruction or perforation. According to Vakil, “80 percent of patients with endoscopically diagnosed ulcers have epigastric pain.”²

Those that complain of gastrointestinal symptoms describe the pain as dull, gnawing, aching, localized to the epigastrium area.¹ The pain is typically related to eating.^1,2,3,4,5 Duodenal ulcers usually occurs a couple hours after meals and in the middle of the night.^1,2 While patients with peptic ulcers have pain with eating.^1,2,3,4,5 Other gastrointestinal symptoms include: belching, epigastric fullness, early satiety, nausea and occasional vomiting.¹ Patients with uncomplicated peptic ulcer decease usually have nonspecific findings on physical exam.¹ They may or may not have mild epigastric tenderness on palpation and guaiac-positive stools.¹