Explanation: The initial presentation of squamous cell carcinoma is typically a nonhealing ulcer or growth on a sun exposed area. The patient in this case question presents with this common presentation specifically.
Choice A: Melanoma is typically diagnosed by a pigmented lesion that varies in color and/or diameter, height, or asymmetry of borders.
Choice C: Basal Cell Carcinoma is typically diagnosed by a slowly enlarging lesion that does not heal and may bleed when traumatized. These lesions often have a central dimple as well.
Choice D: Seborrheic Keratosis is a benign growth that often appears as a waxy stuck –on-the-skin look. They often start small and slowly develop a warty appearance. They can range in color from white to black.
Squamous Cell Carcinoma

Squamous Cell Carcinoma is the second most common type of skin cancer following behind basal cell carcinoma. Approximately 700,00 new cases are diagnosed in the U.S. each year (3). Unfortunately, up to 8,000 people die of this disease each year and the incidence has increased two hundred percent in the last three decades (2). This type of cancer typically appears on sun-exposed areas of the body such as the dorsal aspect of the hand, face, neck, lips, and ears. Women may commonly get them on the lower legs as well (1). Unlike Basal Cell Carcinoma, this type of skin cancer is more likely to spread to other parts of the body although it is still unlikely (1). Squamous Cell Carcinoma often appears as red scaly patches, open sores, appear to have a central ulceration, or may even take on a warty appearance (2). Although they are most common on sun exposed areas Squamous Cell Carcinoma may also appear on mucous membranes and genitals (2).

Risk factors for Squamous Cell Carcinoma include pale or light colored skin, light eyes, blonde hair, inability to tan, significant sun exposure, use of tanning beds, exposure to cancer-causing chemicals, and smoking. Previously, diagnosed actinic keratosis also known as solar keratosis may evolve into SSC, although there is only about a 5-7% chance (3). SSC occurs in men twice as much as woman and typically in individuals over the age of 50. Incidence of women in their 30-40s being diagnosed with SCC has increased due to increased use of indoor tanning bed (2). Skin inflammation, chronic infections, and a weakened immune system from HIV, chemotherapy, or anti-rejection drugs all increase the risk of developing squamous cell carcinoma (2). A tumor suppressor gene called TP53 is the gene most often altered in SCC. When TP53 is altered it allows abnormal cells to go on to live longer and potentially become cancerous (1).

Symptoms of Squamous Cell Carcinoma include a small, pink, dry, scaly patch on the skin. This spot may feel rough or irritated to the touch. The lesion may also cause the patient a burning or itching sensation on the spot. When SCC affects the lips it may present as consistently feeling dry and may have a whitish color and feel scaly (3). SCC often appears as sores on the skin that over time refuse to heal and may even slowly progress to a larger lesion (1). Unfortunately, the appearance of SCC can vary greatly from patient to patient so it is most important to pay close attention to new or changing skin growths, spots that don’t heal, or areas that itch, bleed, or burn (1). From time to time SSC may arise unprovoked on otherwise normal or healthy looking skin and researchers tend to believe these lesions are inherited and that there is a familial factor involved (1).

In the office, a dermatologist along with obtaining a history and physical exam, including the palpitation of lymph nodes, may also use a dermoscopy. This is also called a epiluminescence microscopy which allows the provider to see the skin more closely and clearly (1). The only way to obtain a definitive diagnosis of Squamous Cell Carcinoma or any type of skin cancer is with a skin biopsy. Typically, this is done by a simple shave biopsy, but a punch biopsy may also be done (3). Another option is an incisional versus excisional biopsy. An incisional biopsy involves just removing only a portion of the tumor while an excisional biopsy removed the entire tumor (1). Although it is rare sometimes both Squamous Cell Carcinoma and Basal Cell Carcinoma may spread beyond the skin. When it does spread the first place it typically travels to is nearby lymph nodes. If a patient presents with lymphadenopathy and a positive biopsy a fine needle aspiration biopsy may be performed to analyze for any cancer cells. At times fine needle aspiration biopsies come back negative but a provider may still have a strong clinical suspicion that the cancer has spread to the lymph system. In this case a surgical excisional lymph node biopsy may be performed (1).

For Squamous Cell Carcinoma it is often important to use a staging system in order determine a patient’s prognosis and chose the best treatment options. For Basal Cell Carcinoma and Squamous Cell Carcinoma often the American Joint Commission on Cancer TNM system. T represents the main tumor and its site, location, and how far it has extended within the skin. N represents the spread to nearby lymph nodes. M represents metastasis to other parts of the body (1).

Squamous Cell Carcinoma when diagnosed and treated in the early stages is usually always curable. If not treated over time they will invade underlying tissue and become disfiguring. A very small percentage can even spread to the lymph system, other tissues, and even organs becoming fatal (2). One treatment option included MOHs surgery which offers the highest cure rate for difficult Squamous Cell Cancers. In this procedure the provider cuts out the lesion in addition to a very small amount of normal looking skin. The provider then uses a microscope to analyze the frozen cross section of the specimen to see if any cancer cells can be identified. If the margins are not clear the provider will continue to go back and remove more tissue and repeat the process until clear margins are obtained. MOHs is often used in difficult areas or areas where tissue conservation is important such as the face, scalp, neck, hands, and shins. Excision is also a method of treatment use for SCC in which the lesion is excised along with 4-8mm of surrounding healthy tissue. The tissue is then sent out to a pathologist to be checked to make sure there are clear margins. Radiation is a treatment option that is only used for lesions that can’t be cut out. For early SCCs curettage and electrodessication or laser treatments may be used. Chemotherapy cream such as 5-fluorouracil (5-FU) can also be used to treat SCC in its early stages (3).

References:
Basal and Squamous Cell Skin Cancer. American Cancer Society. https://www.cancer.org/cancer/basal-and-squamous-cell-skin-cancer.html. Accessed October 21, 2017.
Skin Cancer Foundation. Squamous Cell Carcinoma (SCC) – SkinCancer.org.
http://www.skincancer.org/skin-cancer-infortmation/squamous-cell-carcinoma. Accessed October 21, 2017.
Squamous cell carcinoma. Squamous cell carcinoma American Academy of Dermatology. https://www.aad.org/public/diseases/skin-cancer/squamous-cell-carcinoma. Accessed October 21, 2017.

Ureteral stenting is the correct answer. In this scenario the patient is noted to have a dilated right renal pelvis proximal to the visualized stone. This means the patient is obstructed. This requires an urgent referral to urology and the immediate insertion of a ureteral stent past the obstruction with a cystoscope. If the pressure on the kidney is not relieved expediently kidney damage can result.
SWL is not the correct answer because it is not guaranteed to work to relieve the obstruction and cannot be coordinated quickly enough to be of use. SWL can however be used once the stent has been placed to fragment the stone.
PCNL does not have an application here because it is only useful in large renal stones. Also it cannot be coordinated in time to be of use.
Medical expulsive therapy is inappropriate because there is a currently great risk to the kidney. It may be true that expulsive therapy with alpha blockers and CCB will relax the ureter enough for the stone to pass but this is not a given and cannot be relied upon. Stenting is the quickest and most effective treatment.

Etiology:
Renal calculi develop when normally soluble components of urine such as calcium, uric acid, oxalate, and sodium become supersaturated and fall out of suspension 1. When this happens they precipitate within the urinary tract and over time collect more solute. If they grow large enough they can irritate tissues and even block the flow of urine.
Epidemiology: Renal stones are more prevalent in men than women 3:1. More prevalent in whites than others. More prevalent in hot and dry geographic locations. Most common in the 4th to 6th decades of life but rates are rising in younger populations. There is a positive correlation between renal calculi and BMI 1.
Pathophysiology: It appears that the pathophysiology of renal calculi is still not well understood. Certainly the precipitation of supersaturated solutes in the urine plays a role but it is not undisputed which part of the kidney this takes place in. Some studies have shown that plaques can form within the loop of Henle 3. These plaques may provide a collecting point for solutes to form on before they travel distally and collect in the calyces, renal pelvis, ureters, and bladder.

History & physical exam: The common presentation of acute renal colic is one of a patient waking from sleep with excruciating flank pain. Depending on the location of the stone the pain has different radiculopathy patterns. If the stone is in the kidney, most of the time it is asymptomatic unless the flow of urine has been obstructed. If obstruction is present the pain will be in the deep flank without radiation to the groin. There may be some associated nausea and vomiting because the kidney shares nerve innervation with the stomach and intestines. If the stone is in the upper ureter it will cause severe colicky flank pain that often radiates anterior and caudally 2. This pain may be accompanied by nausea. If the stone is impacted at the UO a patient may experience radiation to the groin or testicle/labia majora. This may be accompanied by urinary frequency and dysuria. Once the stone has passed into the bladder it is most times passed without incident.
On physical exam a patient will be in severe pain and writhing in contrast to a patient with peritonitis who will stay very still. Most often there will be the presence of microhematuria on UA. They may have migrating flank pain with radiation to groin. Hypoactive bowel sounds may be present. Fever is absent unless they have developed an infection secondary to obstruction.
Diagnostics:Non contrast CT is most widely used and sensitive diagnostic imaging test. Some will order a KUB if the patient is a known stone factory and their stones can be seen on KUB. Ultrasound can be used for children or pregnant women when radiation exposure is of greater concern. IVP is declining in use but is a useful exam that demonstrates the urinary tract anatomy and function. It requires IV contrast which carries a risk of allergy. A urinalysis will show microhematuria 85% of the time 2. It can show the offending crystals which is a big clue. Leukocytes, nitrites, and pH can show infection. CMP will show renal function and electrolyte abnormalities which may explain the propensity to form stones. A 24 hour urine collection will show if there are elevated crystals or other abnormalities in the urine. CBC may show elevated WBC count if infection present.

Management and treatment: The first line managements for renal or ureteral colic are supportive measures. These may include fluids, pain relief with morphine or ketorilac, and anti emetics. Medical expulsive therapy which consists of alpha blockers and CCBs is used for non obstructing stones smaller than 1cm 1. Most stones pass within 4-6 weeks and if they don’t will need to be operated on if symptomatic. Obstruction is an indication for cystoscopy and stent insertion. Infection will need to be managed with IV antibiotics and relief of obstruction. If the stone is larger than 1cm it is unlikely that it will pass on its own. In such scenarios extracorporeal shockwave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy can be performed. The benefits of ESWL are that general anesthesia is not requited, it is the least invasive option, and complication rates are low (but not unheard of). Unfortunately ESWL success rates are lower than other interventions. Ureteroscopy requires general anesthesia and entering the urinary system. It’s success rates are higher for most locations of stones except for proximal ureter and renal stones larger than 2cm. For large renal stones PCNL is most effective. It involves general anesthesia and entering the kidney percutaneously through the flank. Risks of complication are higher with this procedure but is the last resort for many large renal stones.
Depending on the chemistry of the patient’s urine there are certain alkalization agents and binders that can be prescribed to keep the offending salt from forming stones. Uric acid stones can be dissolved by potassium citrate and sodium bicarbonate which lowers the urine pH. Goal pH is 6.5-7 1. Allopurinol can be used for recurrent calcium oxalate stones in patients with a normal urine calcium. Recurrent calcium stones with hypercalciuria can be treated with HCTZ or potassium supplement. Intractable struvite stones can be treated with a urease inhibitor. In addition to these medications 2L of urine output should be maintained along with a low sodium, low protein, low oxalate diet.

Sources
1. Antonelli J. Nephrolithiasis. Point of Care Medical Applications | Epocrates. http://www.epocrates.com/. Published April 6, 2017. Accessed October 30, 2017.
2. Chirag D. Nephrolithiasis. Medscape. http://www.medscape.com. Published December 3, 2016. Accessed October 30, 2017.
3. McCance KL, Huether SE. Pathophysiology: the biologic basis for disease in adults and children. St. Louis, MO: Elsevier; 2014.

Alopecia areata is usually diagnosed clinically, with a biopsy rarely being needed. Exclamation hairs, which are short broken off hairs that are narrower closer to the scalp, are pathognomonic for Alopecia areata, but are not always seen in the disease (2,4). While Tinea capitis is a cause of alopecia, it has a slightly different presentation then that of alopecia areata. Tinea capitis tends to begin as small erythematous papules that become scaly and typically become ring-like in form. This presentation would warrant an KOH prep examination (2). Telogen effluvium presents with increased shedding and the patients hair will appear thinner, however, there will be no areas of total alopecia in patients with this condition. Telogen effluvium may have a metabolic cause so it is important to check common causes such as hypothyroidism or iron deficiency anemia, which are both common and easily corrected (2). Systemic Lupus Erythematosus is another cause of alopecia, as it is an autoimmune disorder that can affect any organ system. It is most common to have hair loss on the scalp that thins gradually, however, some people may lose hair in clumps. If lupus is suspected, it is important to get labs checking the presence of Antinuclear antibodies (1).

Case Discussion
Epidemiology
The prevalence of Alopecia areata in the general population is .1-.2% with a lifetime risk of developing the condition of 2.1% (1,3). It effects approximately 6.8 million people in the U.S. alone (1). There is noted to be a slight female predominance of the condition, but all races seem to be effected equally. This condition can occur at any age, however, peak incidence is between 15-29 years of life (1,2).
Etiology and Pathophysiology
The cause of Alopecia areata is unknown, however there are several hypotheses on what may contribute to this condition, the most supported being that it is an autoimmune mediated process. Studies have found that this is likely a T cell mediated disease, with biopsies showing lymphocytic infiltrate around the hair follicles of effected patients (2). It is unclear what triggers the autoimmune reaction to the hair follicle.
It is also apparent that genetics play a role in the development in this condition as well. It has been shown that in patients with alopecia areata, around 10-20% of the patients have family members with the same condition (2). Studies have focused primarily on Human leukocyte antigen DQ3 , which has been found to be in more than 80% of patients with alopecia areata (2,3). However, this disease is said to be a “polygenic disease,” meaning multiple genes contribute to the expression of the condition (1).
Research has been completed targeting nerve and blood supply to the area of scalp affected by this condition , as it is believed to be correlated to symptoms of itching and pain in these patients, however it is unclear whether the findings are significant (2,3). Other studies have been conducted to determine if there is an infectious cause of this condition, however, most studies have been negative.
History and Physical exam
Patients with alopecia areata can often present with a precipitating factor in their history, such as a major life event, febrile illness, drugs, pregnancy, or trauma (2). These patients are often asymptomatic other than the discreet patches of hair loss, which are smooth and without scarring (4). A majority of patients have a single patch. On occasion, some patients complain of burning or pruritis in the area. This condition is primarily found on the scalp but can affect any hair bearing areas, including beard, eyebrows and eyelashes (4,2). There are several patterns used to classify alopecia areata, which include reticular, ophiasis, sisaipho, and alopecia universalis. Extensive alopecia areata is less common but involves >50% of hair, which can often lead to total hair loss (alopecia totalis). Patients with alopecia areata also have the presence of small hairs 2-3mm in length called “exclamation hairs” which are pathognomonic but not always found (4). They often border new patches of alopecia areata and indicate that the patch is expanding. Telogen hairs, or hairs in the resting phase, can be easily dislodged with the “Pull test” in this condition.
Diagnostics
In most cases alopecia areata is diagnosed clinically. On occasion, a scalp biopsy can be taken when the diagnosis in unclear, however, this is rarely needed (2). On biopsy, peribulbar lymphocytic infiltrate is seen, often resembling a “swarm of bees.” An increase in vellus hairs versus terminal hairs is often seen as well (2).
Management
Patients with alopecia areata have several options available to them. However, treatment is not necessary as the condition is benign and spontaneous remissions are also common. The goal of treatment is to stimulate hair growth in the affected areas. The type of treatment varies based on presentation and extent of hair involved.
Intralesional steroid injections, usually with Kenalog, are often used in the treatment of alopecia areata and are first line in patients with localized lesions (3,4). Regrowth is often seen within 4-6 weeks in patients that respond to this treatment. Topical steroids are often useful in patients who cannot tolerate injections, especially in children (4). Topical immunotherapy is another treatment option that involves stimulating the area with an antigen that can initiate an allergic response which may hopefully trigger regrowth (2,3). Minoxidil is effective in patients with extensive hair loss. It is well tolerated and regrowth can be seen within 12 weeks.
Systemic treatments are also an option for patients with extensive disease. This includes UV therapy, systemic steroids, cyclosporine, and methotrexate. Additionally, interleukin 2, which targets T regulatory cells, and ruxolitinib, which inhibits JAK are new treatments that may help with immune modulation (4). Unfortunately, alopecia areata is a highly unpredictable disease and these treatments are no guarantee for a cure, thus it is important to counsel these patients on support groups and camouflage techniques that are used as coping mechanisms for living with the disease (2,1).
 
References

1. Alopecia Areata | National Alopecia Areata Foundation. Naaforg. 2017. Available at: https://www.naaf.org/alopecia-areata. Accessed October 23, 2017.
2. Bolduc, MD C. Alopecia Areata: Practice Essentials, Background, Pathophysiology. Emedicinemedscapecom. 2017. Available at: https://emedicine.medscape.com/article/1069931-overview. Accessed October 23, 2017.
3. Dainichi T, Kabashima K. Alopecia areata: What’s new in epidemiology, pathogenesis, diagnosis, and therapeutic options?. Journal of Dermatological Science. 2017;86(1):3-12. doi:10.1016/j.jdermsci.2016.10.004.
4. McPhee S, Papadakis M. Current Medical Diagnosis & Treatment 2016. 1st ed. New York: McGraw-Hill Medical; 2016.

A) Ciprofloxacin would be a good choice for broad spectrum coverage of acute bacterial conjunctivitis. Although this patient does exhibit unilateral injection, her recent contact with “pink eye” is more indicative of a viral, highly contageous, conjunctivitis. She also has clear discharge instead of the purulent discharge, which would be expected with bacterial etiology. 1

C) Emergent ophthalmologist referral is essential in the setting of acute angle closure glaucoma. However, for this diagnosis we would expect sudden decrease in vision, in addition to a red and painful eye. Discharge would not be as likely and physical exam would find a mid-dialated and non reactive pupil. More concerning finding such as sudden nausea and vomiting would also be expected.1

D) Artificial tears and lubricating ointment are the treatent of choice for Keratoconjunctivits sica. However, a more insidious onset would be expected with only mild scleral injection. Foreign body sensation is consistent with this diagnosis, however discharge is not.1

B) Cold compress and good hygeine are the best choice in the setting of viral conjunctivitis. This patient’s presentation of injected, painful eyes with clear discharge is most consistent with viral etiology. Recent infectious contact and lack of purulent discharge make the diagnosis of bacterial conjunctivitis less likely. The sudden onset and severe injection are not consistent with Keratoconjunctivits sicca. Finally, because this patient’s vision is intact, and physical exam finds PERRLA, the diagnosis of acute angle closure Glaucoma is presumptively ruled out. 1

Conjunctivits refers to a broad category of disorders which involve inflammation of the conjunctiva. These may be infectious or non infectious, acute or chronic. Infectious etiologies may be viral or bacterial. Non-infectious subtypes include allergic, mechanical (irritative or toxic), immune mediated or even neoplastic causes. Acute conjunctivitis is present for 3 to 4 weeks, whereas chronic disease must be present for greater than 4 weeks. 2
Much like the common cold, viral conjunctivitis is so common that statistics pertaining to epidemiology are often under reported and inaccurate. Outbreaks are particularly common in schools, families, and the military. Acute bacterial conjunctivitis accounts for 1% of all primary care visits in the US with 135 cases per 10,000 people. 3
The most common etiology for viral conjunctivitis is Adenovirus, although other causes such as Herpes Simplex, Herpes Zoster and Molluscum Contagiosum are possible. Bacterial etiologies include non gonococcal (Staphylococci and Streptococci) and gonococcal, as well as Chlamydia infection. 2
The epithelial layer of conjunctiva is a crucial barrier against infection. If this defence is disrupted, dangerous alterations in flora or viral contact may occur. Swimming, contact lense use, or self inoculation are all possible mechanisms of contamination. Infection may spread from the adjacent eye, especially in the case of viral disease, or remain isolated on one side. 3
In the setting of acute viral conjunctivitis, the patient commonly complains of sudden onset of eye irritation, redness, and photophobia. These symptoms may be unilateral or bilateral. Recent contact with conjunctivitis or URI may be noted. On physical exam, the provider is likely to find conjunctival injection, eyelid edema, erythema and watery discharge. Lymphadenopathy and subconjunctival hemorrhage are rare findings. In contrast, bacterial conjunctivitis is associated with purulent drainage and is usually unilateral. 2
Diagnosis is based heavily on clinical findings. Although secondary bacterial infection is rare in the setting of viral conjunctivitis, culture may be indicated. Culture is also helpful to confirm the diagnosis and guide treatment in simple bacterial infection. 2
Treatment for viral conjunctivitis consists largely of supportive care. This includes cold compress, artificial tears, and in some cases Anti-histamines. Hand and eye hygiene are also very important elements of patient education. Contact lenses and cosmetics should be temporarily discontinued. Individuals who work with food, young children, or in the health care setting should refrain from work until symptoms resolve. 2
Topical antibiotic may be considered if bacterial etiology is suspected. These include Ciprofloxacin, Azithromycin, Gentamicin and other broad spectrum choices. Close follow-up is recommended, in four days to one week, but this is typically a self-limiting disease. Ophthalmology referral should be obtained if symptoms do not begin to improve in one week, or more severe disease is suspected.

References:
1) Agabi SS. Step up to medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2004
2) Dynamed.com.
http://www.dynamed.com/topics/dmp~AN~T116741/Infectious-conjunctivitis. Accessed October 20, 2017.
3) Silverman M, Bessman E. Acute Conjunctivitis (Pink Eye). Overview, Clinical Evaluation, Bacterial Conjunctivitis. https://emedicine.medscape.com/article/797874-overview. Published August 17, 2017. Accessed October 20, 2017.

A. This medication would be used to induce remission in a patient with Ulcerative Colitis. Ulcerative colitis is a chronic inflammatory disease of the colon or rectal mucosa that usually begins in adolescence or young adulthood. Abdominal pain and left lower quadrant tenderness are present in this patient, but she denies hematochezia and tenesmus, two common symptoms of UC. Therefore, UC is unlikely the cause of symptoms in this patient’s case.1

B. This treatment plan would be appropriate for a patient experiencing paralytic ileus, which is decreased or absent peristalsis. Common causes of paralytic ileus include medications such as narcotics and anticholinergics. Other common causes include hospitalization, immobilization, shock, and spinal cord injury. This patient is an otherwise healthy female who denies any medication use, significant past medical history, or past surgeries so paralytic ileus is highly unlikely.1

C. This patient admits to 2-3 bowel movements a week with small hard stools and episodes of diffuse cramping abdominal pain. These symptoms are consistent with constipation. Modification of lifestyle factors is the first line approach to symptomatic constipation. Patients should increase fiber in their diet, and reduce consumption of red meat, fried and fatty foods, and dairy. It is also recommended that patients increase their water intake to 1.5-2 liters a day. Patient should also work to increase their daily physical activity.3

D. This medication would be used to treat a patient with Ogilvie’s Syndrome, specifically with a cecal diameter > 12 cm. Ogilvie’s Syndrome is a colonic pseudo-obstruction, meaning dilation of the colon in the absence of mechanical obstruction. Symptoms include constipation and abdominal pain. However, the hallmark of Ogilvie’s Syndrome is abdominal distention. This patient was found to have a non-distended abdomen upon physical exam so Ogilvie’s Syndrome is a doubtful diagnosis.4

Constipation is defined as unsatisfactory defecation with infrequent or difficult to pass stools, or both.3 It is a symptom, rather than a disease. It is the most common digestive complaint in the US, affecting 2-27% of the North American population.2,3 Risk factors for constipation include female sex, age older than 65 years, a low fiber diet, lack of physical activity, or having an endocrine or neuromuscular disorder.
Constipation can be divided into two main groups, primary and secondary constipation. There are three types of primary constipation: functional constipation, slow transit constipation, and outlet dysfunction constipation. Functional constipation is either idiopathic or caused by irritable bowel syndrome. Slow transit constipation is caused by idiopathic colonic inertia or delayed movements. Outlet dysfunction constipation is most commonly due to the inability of pelvic floor and anal muscles to relax during straining. Other causes of outlet dysfunction constipation include Hirschsprung disease or impaired rectal sensation.3 Secondary constipation can be due to dietary issues and reduced levels of exercise.2 Many medications can contribute to constipation such as narcotic analgesics, antacids, calcium channel blockers, and anticholinergics. Structural causes of secondary constipation include anal fissures, thrombosed hemorrhoids, and obstructing tumors. Systemic diseases such as scleroderma, hypothyroidism, hypercalcemia, and diabetic autonomic neuropathy can also cause secondary constipation.1
The Rome criteria were initially introduced in 1988 to become the research-standard definition of constipation. It has been modified twice since then, and is now the Rome III criteria. In order to meet the Rome III criteria for constipation, a patient must have experienced at least two of the follow symptoms over the preceding three months: fewer than 3 bowel movements per week, straining during bowel movements, lumpy or hard stools, sensation of anorectal obstruction or incomplete defecation, or manually facilitating defecations. Additionally, the patient should not meet criteria for irritable bowel syndrome and loose stools are rarely present without laxatives. 2
Review the patient’s current medication list, ask about past abdominal and pelvic surgeries, and medical conditions with increased risk for constipation. Always review potentially modifiable risk factors for constipation such as daily fiber, fluid intake, and level of physical activity. It is important to ask the patient about “red flag” signs and symptoms that may be suggestive of a colorectal malignancy. These signs and symptoms include rectal bleeding, change in the caliber of stool, bloody stools, weight loss, anemia, or family history of colorectal cancer.3
Physical exam findings may include a distended abdomen with tenderness upon palpation. Palpation of the abdomen may also reveal a palpable colon with hard stool, nonfecal masses, and scars from previous abdominal or pelvis surgeries. External anorectal exam may reveal fistulas, fissures, hemorrhoids, or rectal mucosal prolapse. Other physical exams may include assessment of the anal wink, perineal descent, and digital rectal exam. Evaluate the patient’s anal wink by stroking the surrounding anal skin and looking for a reflexive external sphincter contraction. Assess patient’s perineal descent by observing the patient’s perineum both at rest and while bearing down. Normal perineal descent is 1.0-3.5 cm. A descent < 1 cm may indicate the inability to relax the pelvic floor muscles. A descent >3.5 cm may indicate laxity of perineum. A digital rectal exam may reveal the presence of a mass of stool impaction. Also feel for possible strictures, assess sphincter tone, and note any tenderness. Ask women to perform a Valsalva maneuver to evaluate for pelvic organ prolapse, specifically a rectocele.3
Constipation is usually diagnosed clinically using problem specific history and physical exam and the Rome III criteria. Routine use of blood tests, x-rays, or endoscopy is not recommended in patients without alarm symptoms or other significant comorbidities.3 An extensive workup would be performed after 3-6 months of failed medical management. Additional studies for refractory constipation or those without an unknown underlying cause include lower GI endoscopy, colonic transit study, defecography, anorectal manometry, surface anal electromyography, and balloon expulsion.2
The first line approach to symptomatic chronic constipation is lifestyle modifications. Recommend patients intake 1.5 L-2.0 L of water a day and 20-35 grams of fiber a day. Types of dietary fiber include oat or wheat bran. Patients can also try eating prunes for mild to moderate constipation. Educate patients on reducing fried and fatty foods, red meat, and large amounts of dairy products. First line medications can include bulk-forming agents such as methylcellulose powder, polycarbophil, or psyllium powder. Osmotic laxatives such as polyethylene glycol and lactulose are also appropriate for treating chronic constipation. Second line therapy can include stimulant laxatives such as bisacodyl (Dulcolax), but only for short-term use. Consider prosecretory agents, lubiprostone and linaclotide, for constipation refractory to dietary modifications, osmotic laxatives, and stimulant laxatives. There is insufficient evidence to support the use of enemas and probiotics in chronic constipation, but suppositories may be effective for short-term use.3

References
1. Agabegi ED, Agabegi SS, undefined undefined undefined. Diseases of the Gastrointestinal System. In: Step-up to medicine. Philadelphia: Wolters Kluwer; 2016:114-120.
2. Basson M. Constipation. Medscape. https://emedicine.medscape.com/article/184704-overview. Published March 28, 2017. Accessed October 21, 2017.
3. Ostrovsky DA. Constipation in Adults. dynamed.com. http://www.dynamed.com/topics/dmp~AN~T116186/Constipation-in-adults. Accessed October 21, 2017.
4. Williams DA. PANCE prep pearls: a practical study guide to preparing for physician assistant national certifying exam (PANCE), recertification (PANRE) & clinical rotations. Lexington, KY: CreateSpace; 2014.

A. Is incorrect because COPD is a obstructive breathing issue and the PFT test shows results for a restrictive breathing issue.
B. Asthma is incorrect because most asthma is diagnosed as a child and not in 60 year olds. Also, asthma is an obstructive breathing issue and the PFT test shows results for a restrictive breathing issue.
C. Pneumonia is not the answer because symptoms have been going on for a few months with no signs of infection, fever, fatigue, or myalgias.
D. Pleural effusion is not the answer because on physical exam you would find decreased or absent breath sounds at the bases from the fluid collection.
E. Interstitial pulmonary fibrosis is the correct answer because of the worsening symptoms, the work place environment that could be causing her to breath in pollutants and chemicals for the past 40 years. Also, IPF is a restrictive lung disease which is consistent with the PFT findings.

Interstitial lung disease (ILD) is a large umbrella term for many different lung issues. The most common type of ILD is idiopathic pulmonary fibrosis (IPF) which accounts for 40% of all ILDs. IPF is a common cause of restrictive lung disease that causes scar tissue formation in the parenchymal of the lungs (Meltzer and Noble, 2008). It can be caused by inhalation of harmful substances, drugs, infections, radiation or autoimmune conditions (Martino 2016). One of these come in contact with the lungs causing a hypersensitivity reaction which causes inflammation. Our bodies are in charge of wound healing and if something goes wrong in the process our lungs can develop fibrosis or scarring to the tissue. The lung fibrosis then has an issue with expanding causing decreased ventilation, hypoxemia and a restrictive lung disease.

The prevalence of IPF is 20 cases per 100,000 persons for males and 13 cases per 100,000 persons for female. 66% of patients who are diagnosed with IPF are 60 years of age or older and have a poor prognosis estimating 2-5 years to live from diagnosis (Martino 2016). When these patients arrive to their primary providers most of the symptoms are nonspecific. The most common symptoms are dyspnea on exertion and or a nonproductive cough. The most important part of diagnosis IPF is getting a complete history. The patient could have a social history of smoking, travel history, occupational history of exposure to pollutants, exposure history of asbestos in a house or medications that cause lung fibrosis years after use like Amiodarone, Bleomycin and Nitrofurantoin. Other history needs to be ruled out also such as tuberculosis and human immunodeficiency virus. The physical exam on IPF patients could be positive for fine bibasilar inspiratory crackles which is called Velcro crackles in IPF. The patient should be evaluated for digital clubbing which could occur slowly overtime and found in 50% of IPF patients (Meltzer and Noble, 2008).

The most important work up for IPF is a pulmonary function test which will show restrictive lung disease. The Total Lung Capacity (TLC) will be reduced, Forced Expiratory Volume in 1 second (FEV1) will be increased, Forced Vital Capacity (FVC) will be reduced and FEV1/FVC will be increased (Martino 2016). Chest x-rays are also useful which will show small irregular opacities less than 1.5mm in diameter, ground-glass opacities, and honey combing which is small translucency in the lungs. The more superior option to diagnosing IPF is by using a High-Resolution Computed Tomography (HRCT). This will imaging tool will diagnosis, assesses disease severity and can find ILD in patients with a negative chest x-ray. The next step in IPF is getting a lung biopsy. Depending on the location of the IPF biopsies can be taken by bronchoscopy, bronchoalveolar lavage or thoracoscopic wedge biopsy.

The definitive treatment for IPF is lung transplant. There are some new medications that can help with the disease if the patient is not a lung transplant candidate which is Tyrosine Kinase Inhibitors and Antifibrotic Agents. Tyrosine Kinase Inhibitor called Nintedanib was FDA approved for the treatment of IPF in 2014 after it found improvement of FVC in patients and less acute exacerbations (Godfrey, 2017). The common side effect of the medication is diarrhea which caused less than 5% of patients to stop treatment. Nintedanib targets platelet derived growth factor receptors, vascular endothelial growth factor receptors and fibroblast growth factor. The FDA also approved an Antifibrotic Agent called Pirfenidone for IPF in 2014 after it was found to improve FVC over a 52 week time span and less progression of the disease and longer survival (Raghu, 2017). Complications of IPF are increased pulmonary pressures causing pulmonary hypertension or cor pulmonale, repeat acute exacerbations of pulmonary fibrosis or pneumonia (Martino 2016). All IPF patients need to be evaluated for obstructive sleep apnea and lung cancer. If the patient is a current smoker they should be given smoking cessation. These patients need to receive the influenza and pneumococcal vaccine due to their high risk of development with an underlying lung condition. These patients need to stay active, exercise regularly, loss weight if needed, eat a healthy diet. Their provider should start by prescribing pulmonary rehab to help them.

References

Godfrey, Amanda M K. Emedicine.medscape.com. (2017). Idiopathic Pulmonary Fibrosis Medication: Tyrosine Kinase Inhibitors, Antifibrotic Agents, Corticosteroid, Systemic, Immunosuppressant Agent. [online] Available at: https://emedicine.medscape.com/article/301226-medication [Accessed 25 Oct. 2017].
Martino, Linda. Idiopathic pulmonary fibrosis. MCPHS PowerPoint Lecture on April 4, 2016.
Meltzer, E. and Noble, P. (2008). Idiopathic pulmonary fibrosis. Orphanet Journal of Rare Diseases, [online] 3(1), p.8. Available at: https://ojrd.biomedcentral.com/articles/10.1186/1750-1172-3-8 [Accessed 25 Oct. 2017].
Raghu, G. Selman, M. Atsjournals.org. (2017). Nintedanib and Pirfenidone. New Antifibrotic Treatments Indicated for Idiopathic Pulmonary Fibrosis Offer Hopes and Raises Questions | American Journal of Respiratory and Critical Care Medicine. [online] Available at: http://www.atsjournals.org/doi/full/10.1164/rccm.201411-2044ED [Accessed 25 Oct. 2017].

Choice (B) is correct. Since this patient is possibly having an Inferior wall NSTEMI, you should avoid Nitroglycerin and Morphine because it decreases preload. The right side of the heart is more dependent on preload to maintain cardiac output. Therefore, if this patient is actually having an NSTEMI and preload is decreased, it could be fatally harmful for this patient.
(A) is not harmful because per ACLS guidelines, a patient with suspected MI should receive full dose ASA and Oxygen and present to the cath lab with a time window of 90 minutes.
(C) is not harmful because if this patient presented within an hour of onset, initial cardiac enzymes would not be elevated. They begin to elevate in 4-6 hours and peak in 12-24 hours.
(D) is not harmful because if this patient had ischemia/infarct to their myocardium, abnormal wall motions would show on ECHO. ECHO is useful because it is a noninvasive way to assess the function of the heart.

NSTEMI
Epidemiology: Approximately one-third of deaths in individuals over the age of 35 is attributed to coronary heart disease (CHD). A total of 16.5 million people in the United States live with CHD. Males are more common than women and risk increases with age proportionately. (2)
Etiology: CHD is due to accumulation of plaques as each individual ages. Unstable plaques have properties within them that can cause platelets to activate and aggregate together and cause adhesions. This leads to a coagulation cascade which can cause a thrombus to form and dislodge and cause a transient or near-complete occlusion. (1)
Pathophysiology: NSTEMI occurs when myocardial oxygen demand exceeds oxygen supply, most likely due to a decrease perfusion due to a partially obstructed vessel. In addition, decreased perfusion to the myocardium leads to ischemia. Ischemia over a period of time can cause elevations in troponins. Severity of STEMI depends on duration of ischemia, extent of occlusion, degree of underlying atherosclerosis and presence of other comorbidities. (1)
Pertinent historical findings: Generally, most symptoms include chest pain with exertion or at rest. The pain can radiate to their jaw, shoulder or down their arm. They may experience nausea, diaphoresis, dizziness and lightheadedness. Symptoms vary from person to person, especially in women and diabetics, who are likely to have atypical variations of symptoms. Many patients will admit to progressively worsening and more intermittent chest pain with exertion. (3)
Pertinent physical findings: Physical findings can also vary from person to person depending on degree of severity. Typically, these patients are in acute chest pain, clenching their chest with their first. They can use accessory muscles to breath and be short of breath. They can also be diaphoretic. However, other patients can present asymptomatically and have stable vital signs and be in no acute distress. The presentation really varies from person to person. (3)
Diagnostic Correlation (Labs/Imaging): Findings depend on the time of onset of symptoms to presentation to the hospital setting. Initiate labs can be negative therefore it is important to continue to trend cardiac enzymes and monitor for an elevation indicating ischemia or infarct. Cardiac enzymes include CK-MB and troponins. EKG can also vary but typically, NSTEMI presents with depressed ST segments. EKG can also show T wave flattening or inversion and new Q waves not previously present on prior EKGs. ECHOs are also a noninvasive imaging technique that is useful to show wall abnormalities due to wall infarct or ischemia. Stress tests are useful in stable patients who present with a concerning history of chest pain worsening with exertion. Different stress tests include exercise stress test but those who cannot tolerate exercise stress tests will be given a pharmacological stress test and an ECHO can be used to show whether ischemia is reversible or not. The gold standard of imaging is a cardiac catherization which can outline and show occlusions to the vessel. A cardiac catherization is considered diagnostic and interventional management as well. (2)
Management/Treatment: Once it is determined that a patient is having ACS, specifically a NSTEMI, the patient should be given ASA 324mg, Oxygen if O2 sat <94% and Nitrates. If nitrates do not relieve the pain, IV Morphine is added onto the regimen. Aside from relieving the pain, Morphine is also a vasodilator that increases the perfusion of blood. The patient should also be started on antithrombotics such as Heparin or Enoxaparin. Ideally, the protocol to the cath lab from entering the emergency room should be less than 90minutes. Within the cath lab, the coronary blockages are identified and if one of two vessels are involved that does not involve the main LCA, a drug eluting stent or bare metal stent is placed. If more than three vessels are involved or the left main coronary artery is involved, the ideal situation is to go to for CABG where the occluded coronary arteries are bypassed. Patients should go home with ASA 81mg, Clopidagrel 75mg, Nitroglycerin SL prn for chest pain, Beta blockers and a high intensity statin such as Atorvastatin or Rosuvastatin. If the EF <40%, an ACE-I/ARB/ARNI should be initiated to decrease progression of heart failure and provide neurohormonal blockade. The patient should follow up with his cardiologist when discharged. (2)

References
1. Non-ST Elevation Myocardial Infartion. https://online.epocrates.com/diseases/15124/Non-ST-elevation-myocardial-infarction/Etiology. Accessed 23 October 2017.
2. Overview of the acute management of Non-ST elevation acute coronary syndromes. https://www.uptodate.com/contents/overview-of-the-acute-management-of-non-st-elevation-acute-coronary-syndromes?source=search_result&search=nstemi&selectedTitle=1~150#H2. Accessed 23 October 2017.
3. Papadakis MA, McPhee SJ, Rabow MW. 2015 current medical diagnosis & treatment. New York: McGraw-Hill Education/Medical; 2015.

An understanding of anatomy is crucial for early recognition of injuries to tendons, muscles, and nerves. An accurate assessment of the injury and physical exam findings is also necessary to determine if the patient can be washed out and sent home from the ED or if urgent nerve, artery, and/or tendon repair is necessary.
On the flexor or palmar aspect of the forearm the most superficial layer is made of 4 muscles that arise from the medial epicondyle and fan out across the forearm. From a radial to ulna direction these muscles include the pronator teres, flexor carpi radialis, palmaris longus, and flexor carpi ulnaris. The “mobile wad” of muscle that arises from the lateral epicondyle on the lateral and palmar aspect of the forearm is made of the brachioradialis and the extensor carpi radialis longus and brevis. 1,2
The location of the nerves and vessels of the anterior forearm is relatively simple to remember. The radial nerve runs down the radial or lateral side of the forearm with the radial artery running along the medial side of the nerve at the distal half of the forearm. The ulnar nerve runs down the unlar side of the forearm with the ulnar artery running along the lateral boarder of the nerve at the distal half of the forearm. The median nerve courses down the middle of the forearm. The anterior interosseous nerve, a branch of the median nerve, courses deep to the median nerve in the mid forearm. 1,2
The depth and location of this patient’s laceration suggest that the superficial muscles of the mid forearm may have been injured including the brachioradialis, flexor carpi radialis, palmaris longus, and the flexor carpi ulnaris muscles. The wound is deepest in the middle of the forearm which suggest the median nerve is at the highest risk of being injured.
References
1. Flexor Tendon Injuries. http://www.orthobullets.com. Accessed 7/23/17.
2. Thompson JC. Netter’s Concise Atlas of Orhtopedic Anatomy. Elsevier, Inc. Philadelphia, PA. 2002. Pages 108-114.