The correct answer is D. A is incorrect as this is the typical murmur associated with mitral stenosis. B is incorrect as this is the typical murmur associated with coarctation. C is incorrect as this is the murmur associated with patent ductus arteriosus. E is incorrect as this is the murmur associated with aortic regurgitation.

The above case and question represent a specific valvular heart condition known as aortic stenosis (AS). Aortic stenosis is a disease process affecting the leaflets of the aortic valve. The valves become stenotic and the opening becomes narrow, causing a left ventricular outflow obstruction of blood flow across the valve. (1) Gradually over time the outflow obstruction and pressure load on the heart muscle increases causing left ventricular dysfunction. (1) According to Lester and Abbas (2016) aortic stenosis is the most common indication for valve replacement in North America and Europe. (2)

Two of the most common causes of AS is calcification and degeneration of a trileaflet or congenitally abnormal unicuspid or bicuspid valve, rather than tricuspid. Calcific and degenerative aortic stenosis, is thought to be related to calcium deposition due to processes similar to what occurs in atherosclerotic vascular disease. Approximately 25% of patients over age 65 years and 35% of those over age 70 years have echocardiographic evidence of aortic valve thickening (sclerosis). (4) About 10–20% of these will progress to hemodynamically significant aortic stenosis over a period of 10–15 years. (4)

Patients with congenitally abnormal valves may develop symptoms during childhood or adolescence if the stenosis is severe enough (1). However, patients do not typically become symptomatic until their 50’s or 60’s when calcification and degeneration of the valve develops(8).
A less common cause of AS is rheumatic valve disease. Since the development of antibiotics it has become a rare cause of valve disease in industrialized countries. However, it still remains a prevalent cause in developing countries(4). Other rare causes of AS are connective tissue diseases such as systemic lupus erythematosus and orchronosis. Some common risk factors associated with AS include hypertension, hypercholesterolemia, and smoking (8).

Patients with AS develop symptoms gradually overtime. Initially they start out asymptomatic until the stenosis becomes more severe. The most common symptoms patients usually present with is exertional dyspnea. Two other common symptoms patients often develop is chest pain and syncope associated with exertion as well. Together these three symptoms make up, what is known as the classic triad of AS.

The most classic physical exam finding associated with AS is the crescendo-decrescendo systolic ejection murmur heard short after S1 and just before S2(8). The murmur is a low pitched, harsh murmur heard best at the 2nd intercostal space in the right upper sternal boarder and radiates to the carotids(8). The murmur decreases with squatting and increases with valsalva maneuver (8). In mild or moderate cases where the valve is still pliable, an ejection click may be heard before the murmur. Some other symptoms that tend to be associated with more severe AS are; a palpable LV heave or thrill, a weak to absent aortic second sound, or reversed splitting of the second sound, weak and delayed carotid upstroke (pulsus parvus et tardus) and pulses alternans (8).

The diagnostic test of choice for determining valvular heart disease and measuring the severity of the valve disease is an echocardiograph/Doppler(1,5,8). Catheterization can also be used a test to measure the severity of the valve disease and is usually reserved for cases where there is a discrepancy between symptoms and the echocardiography/doppler information(1). An electrocardiogram (EKG) may show non-specific findings of left ventricular hypertrophy or secondary repolarization changes, or it can be normal (3).

The only definitive treatment for AS is an aortic valve replacement (AVR)(8). Due to the invasiveness of the valve replacement and the high risk involved, patients do not undergo replacement until the patients with severe AS becomes symptomatic (2). In the meantime noninvasive medical therapy is used to treat symptomatic patients that do not yet qualify for valve replacement. In these patients medical treatment is aimed at treating the patients symptoms associated with their AS.

Patients with heart failure are typically treated cautiously with low doses of diuresis and angiotensin-converting enzyme (ACE) inhibitors(1,5,6,8). Digoxin is used for patients with left dysfunction and or atrial fibrillation (1,5,6,8). Once patients reach the point that surgical intervention is warranted patients can undergo surgical replacement or a transcatheter approach. Typically patients that have multiple comorbidities and are high risk surgical candidates undergo the transcatheter aortic valve repair TAVR). (2)

References

1. Bojar R. Manual Of Perioperative Care In Adult Cardiac Surgery. Chichester, UK: Wiley-Blackwell; 2011:18-26.
2. Brecker S, Gaasch W, Aldea G. Transcatheter aortic valve replacement: Indications and outcomes. Transcatheter aortic valve replacement: Indications and outcomes. https://www.uptodate.com/contents/transcatheter-aortic-valve-replacement-indications-and-outcomes. Published October 25, 2016. Accessed October 20, 2016.
3. Gaasch, MD W. Indications for valve replacement in aortic stenosis in adults. Up to date. 2016. Available at: https://www.uptodate.com/contents/indications-for-valve-replacement-in-aortic-stenosis-in-adults?source=search_result&search=aortic%20stenosis&selectedTitle=2~150#H1. Accessed October 20, 2016.
4. Gaasch, MD W. Natural history, epidemiology, and prognosis of aortic stenosis. Up to date. 2016. Available at: https://www.uptodate.com/contents/natural-history-epidemiology-and-prognosis-of-aortic-stenosis?source=search_result&search=aortic%20stenosis&selectedTitle=5~150. Accessed October 20, 2016.
5. Otto, MD C. Clinical manifestations and diagnosis of aortic stenosis in adults. Uptodate. 2016. Available at: https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-aortic-stenosis-in-adults?source=search_result&search=aortic%20stenosis&selectedTitle=1~150. Accessed October 20, 2016.
6. Otto, MD Cooper, MD S. Medical management of symptomatic aortic stenosis. Up to date. 2016. Available at: https://www.uptodate.com/contents/medical-management-of-symptomatic-aortic-stenosis?source=search_result&search=aortic%20stenosis&selectedTitle=3~150#H1. Accessed October 20, 2016.
7. Ren, MD X. Aortic Stenosis: Practice Essentials, Background, Pathophysiology. Emedicinemedscapecom. 2016. Available at: http://emedicine.medscape.com/article/150638-overview?src=refgatesrc1. Accessed October 20, 2016.
8. McPhee SJ, Papadakis MA. Current Medical Diagnosis &Amp; Treatment 2011. New York: McGraw-Hill Medical; 2011.

Osgood-Schlatter’s Disease (OSD) or traction apophysitis is an inflammation of the growth plate at the tibial tubercle where the patella tendon attaches. OSD occurs in adolescents during peak growth age, which is when skeletal growth outpaces the stretch of surrounding tendons. In OSD, the tight patella tendon pulls on the tibial apophysis causing inflammation and in some cases, partial or complete avulsion of the tibial tubercle. A partial avulsion will cause a noticeable bump on the anterior tibia which is a common finding in patients with long standing OSD.  Pain, tenderness, and swelling will be present over the tibial tubercle during palpation and pain is made worse with resisted active knee extension. The lateral radiograph of the knee is the most telling in patients with OSD, often showing irregularity and fragmentation of the tibial tubercle. 1,2

Symptoms generally resolve with a period rest, activity modification, ice, and NSAIDs. Physical therapy can help patients stretch their quadriceps muscle to relieve tension on the tibial apophysis. OSD may cause pain for several months so a lengthy period of conservative treatment may be necessary. Athletes may play through mild pain if tolerable. An infrapatella strap may be used during sport participation to help with the pain. Severe pain may signal an impending avulsion fracture and the athlete should rest accordingly.  The pain generally subsides with rest or when skeletal growth completes, which is generally around age 14 for girls and 16 for boys. Patients should be advised however that a bump on the anterior tibia, if present, will persist through adulthood. 1

References

1. Pihlajamaki HK, Mattila VM, Parviainen M, Kiuru MJ, Visuri TI. Long-Term Outcome After Surgical Treatment of Unresolved Osgood-Schlatter Disease in Young Men. JBJS 2009; 91: 2350-8.
2. Osgood-Schlatter’s disease. http://www.orthobullets.com. Accessed on 2/18/2017.

A. Concomitant infection can slow healing of corneal abrasions so prophylactic antibiotics are often prescribed, although there is a lack of evidence to support this.  Polymyxin B/trimethroprim eye drops are a good choice for antibiotic coverage in this patient.

B. Corneal abrasions often require frequent follow up to reevaluate and reassess, especially if healing is delayed or the epithelial defect is enlarging. This would most definitely be a part of treatment, as you want to see the patient back in your clinic to ensure his symptoms are resolving.

C. Since this patient notes mild pain an NSAID eye drop is a good idea to alleviate some of the patient’s discomfort. This type of drop is not indicated in all types of corneal abrasion, but is however useful if the patient is in pain.

D. Correct answer: Eye patching is not indicated for the treatment of corneal abrasion. Since this patient is presenting in mild distress and with a small corneal abrasion, it would not be indicated to include patching in this patient. Eye patching is often contraindicated in patients who are contact lens wearers, or if the mechanism of injury of the corneal abrasion involves fingernails, or vegetable matter.

Reference
1. Ehlers J, Shah CP. The Wills Eye Manual; Office and Emergency Room Diagnosis and Treatment of Eye Disease. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins; 2008.

This patient’s x-ray findings of the left hip include flattening of the femoral head and advanced degenerative changes consistent with the diagnosis of avascular necrosis (AVN) of the femoral head. Hip AVN is a relatively common condition that is caused by a disruption of the blood supply to the femoral head. The condition is so common in fact that 10% of all total hip replacements performed in the United States are for AVN. Taking oral steroids has been linked to the disease and could potentially be the cause in this patient. AVN can occur bilaterally in up to 80% of patients so bilateral hip x-rays should always be ordered if the diagnosis has been made or is suspected. If the diagnosis of AVN is made on x-ray than no further imaging is necessary.

Symptoms of hip and lumbar spine pathology can often overlap causing a delayed diagnosis. Knowing key physical exam findings and symptoms that differentiate the two can help prevent a delay in diagnosis and treatment. The most common symptoms that occur when the hip is the source of pathology includes groin, thigh, and buttock pain. Pain from hip pathology is usually made worse with hip flexion and internal rotation. Lumbar spine pathology usually causes back and buttock pain, and with lumbar nerve impingement, radiating pain that travels distally past the knee. Pain to palpation over the lumbar spine and a positive straight leg raise are common symptoms associated with lumbar spine pathology. This case is a great example of how a careful history and physical exam must be performed in order to make an accurate initial diagnosis. 2

References
1. Avascular necrosis of the Hip. http://www.orthobullets.com . Accessed on 2/14/2017.
2. Buckland AJ, Miyamoto R, Patel RD, Slover J, Razi AE. Differentiating hip pathology from lumbar spine pathology: key points of evaluation and management. JAAOS 2017; 25: 23-24.

Group A Streptococci is correct. The patient presents with exudate on her tonsils, tender anterior cervical lymph nodes, fever, and an absent cough. All of these symptoms are suggestive of streptococcal pharyngitis.

Incorrect: A. Mononucleosis. It is common with patients who are infected with Mono to have a prodromal period of malaise, myalgia, fatigue and low grade fever for 1-2 weeks before it becomes infectious pharyngitis. This patient has an onset of sore throat, fever, and fatigue for the past 3 days. The time course of mononucleosis is usually longer onset whereas Group A Strep is more of a “sudden onset”. B. Rhinovirus. Patients infected with rhinovirus usually present with nasal congestion, nasal discharge, sneezing, and/or cough. This patient did not have any of these symptoms. D. Gonorrhea infection of the pharynx is more commonly asymptomatic or mild symptoms. Patient is not sexually active or had any orogential contact.

Reference
1. Pharyngitis. http://www.medbullets.com. Accessed on 2/24/17.

The answer is D: High-potency topical steroids. The patient presents with vitiligo that is localized (<10% TBSA) and located on the back. Clinical trials and current recommendations from the AAD advise that medium to high potency steroids be used as first line treatment for vitiligo that is involving <10% TBSA and not involving the face.

(A) Topical antifungal is incorrect as the diagnosis is not due to a superficial fungal infection.
(B) Low-potency steroids would not be effective; topical steroids MOA in vitiligo is via modulation of the immune response and this would not be achieved with low-potency steroids.
(C) Topical calcineurin inhibitors are an effective treatment for vitiligo. Their indication is normally reserved for cases that involve sensitive areas such as the face, or as combination therapy with topical steroids. Head to head trials of high-potency topical steroids vs. topical calcineurin inhibitors in patients with non-facial vitiligo demonstrate a lower success rate in those who used topical calcineurin inhibitors alone.

Epidemiology
Worldwide occurrence of vitiligo is approximately 1-2%; with a rate of 1% in the United States alone. Vitiligo affects males and females equally, with no specific affinity to racial, ethnic, or socio-economic factors. Vitiligo may appear at any time from birth to late adulthood; peak onset occurring at 10-30 years (mean average of 20 years old). Approximately one-third of patients with vitiligo are children, and 70-80 percent of adult patients develop vitiligo prior to age 30 years.1,2

Etiology
The etiology of vitiligo is unknown. Patients commonly attribute the onset of their disease to specific triggering events such as physical injury or illness, sunburn, emotional stress, or pregnancy, but there are no data supporting a causative role for these factors. The frequency of comorbid autoimmune diseases is significantly elevated in patients with vitiligo and in their first-degree relatives, suggesting an autoimmune etiology for this disorder. Finally, family clustering of vitiligo suggests a genetic basis for the disease.2

Pathophysiology
Vitiligo is a multifactorial disorder related to various factors. It is generally agreed that there is an absence of functional melanocytes in vitiligo skin. Genetic studies indicate a multifactorial, polygenic inheritance pattern; with 25-50 percent of patients with affected relatives. Genetic studies have identified approximately 36 susceptibility loci; with the majority of the susceptibility genes encode either immunoregulatory proteins or melanocyte proteins. Specifically, AIS1 is a major susceptibility locus in Caucasians, while chromosome 4q13-q21 appears to be the main locus in Chinese families.2

Historically, vitiligo has been associated with several autoimmune diseases, including Hashimoto’s thyroiditis, Graves’ disease, type 1 diabetes mellitus, alopecia areata, pernicious anemia, rheumatoid arthritis, and psoriasis. Multiple cytokines have also been implicated in the destruction of melanocytes in vitiligo. Several studies have documented increased expression of tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-10, and IL-17. Many hypotheses exist regarding the true pathophysiology behind vitiligo; including, but not limited to: the melanocyte self-destruction hypothesis, oxidative stress, neural hypothesis, and convergence theory.2,4

Pertinent historical & Physical findings
Vitiligo most commonly presents as totally amelanotic macules or patches surrounded by normal skin. The lesions characteristically have discrete margins, and can be round, oval, irregular or linear in shape. The borders are usually convex, as if the depigmenting process were “invading” the surrounding normal skin. Progressive lesions enlarge over time, at a slow or rapid rate, with macules and patches range from millimeters to centimeters in diameter and often vary in size within areas of involvement.4

The current accepted classification system for vitiligo divides the disease into three types: localized, generalized, and universal. Localized vitiligo is described as focal, segmental, or mucosal. Focal is defined as one or more macules in a single area but not in a segmental distribution. Segmental is one or more macule involving a unilateral segment of the body, but stops at midline. Mucosal involves mucous membranes alone. Generalized category can be vulgaris, acrofacial, or mixed. Vulgaris are scattered patches that are widely distributed, while acrofacial affects only distal extremities and the face. Mixed is described as a various combination of segmental, acrofacial and/or vulgaris. Finally, universal vitiligo is complete or nearly complete depigmentation of the skin surface.4

Other dermatological findings have been strongly correlated with vitiligo. Poliosis, a decrease or absence of color in head hair, eyebrows, and/or eyelashes, is frequently found prior to or simultaneously with the classic amelanotic macules/patches of vitiligo. Halo nevi have been identified as a precursor for vitiligo in up to 25% of patients. Lastly, friction and other types of physical trauma such as scratching, chronic pressure, or cuts along with allergic or irritant contact reactions may trigger vitiligo on areas such as the neck, elbows, and ankles. This is known as the Koebner phenomenon and has been reported in 20-60 percent of vitiligo patients.2,4

Diagnostic Correlation
The standard for diagnosis of vitiligo is through the use of a Wood’s lamp. The lamp is a handheld device emitting UVA light at 365 nm wavelength. Under the Wood’s light, the depigmented areas emit a bright blue-white fluorescence and appear sharply demarcated, confirming amelanosis. Although not necessary, a skin biopsy can also be used to distinguish between hypopigmentation and depigmentation. On histology, vitiligo would present as complete loss of melanin pigment in the epidermis and absence of melanocytes, with occasional lymphocytes at the advancing border of the lesions.2

Management & Treatment
The primary goals of vitiligo treatment are stabilization of the depigmentation and subsequent re-pigmentation. The choice of therapy depends on the extent, location, and activity of disease. In general, a period of at least 2–3 months is required to determine whether a particular treatment is effective. The areas of the body that typically have the best response to medical therapy are the face, neck, mid extremities and trunk, while the distal extremities and lips are the most resistant to treatment. 4

For patients who have progressive vitiligo, stabilization is the primary goal and can be achieved with oral prednisone 5-10 mg per day in children and 10-20 mg per day in adults for a maximum of two weeks. If needed, treatment can be repeated in four to six weeks. Those who have stabilized and are seeking re-pigmentation have various treatment options depending on the extent of the disease. 3

In patients who have less than 10% TBSA (total body surface area), mid or high potency topical steroids are considered first line therapy. Topical calcineurin inhibitors are considered first line alternatives if the depigmentation occurs on areas that are at risk for skin atrophy, such as the face or genitals. Targeted UVB phototherapy (bi-weekly) can be used as adjunct therapy for those who do not respond to topical treatment or would like to be treated more aggressively. For patients with greater than 10% TBSA affected, UVB therapy 2-3x/week is considered first line treatment, with supplemental topical steroid and/or topical calcineurin inhibitors. Assessment of response to therapy should be done after 15-20 NB-UVB treatments. 3,4

Surgical therapies involving the autologous transplantation of healthy melanocytes in depigmented areas are an option for patients with localized or segmental vitiligo that has been stable for a minimum of 6 months. These procedures primarily are made up of different types of grafts, melanocyte cultures, and epidermal suspensions that transfer a reservoir of healthy melanocytes to affected skin for proliferation and migration into areas of depigmentation.3

References

1) Emedicine.medscape.com. Vitiligo: An overview. 2016. Available at: http://emedicine.medscape.com/article/1068962-overview. Accessed September 18, 2016

2) UpToDate.com. Vitiligo: pathogenesis, clinical features, and diagnosis. 2016. Available at: https://www.uptodate.com/contents/vitiligo-pathogenesis-clinical-features-and-diagnosis?source=search_result&search=Vitiligo&selectedTitle=3~115#H14676582. Accessed September 18, 2016

3) UpToDate.com. Vitiligo: Management and Prognosis. 2016. Available at: https://www.uptodate.com/contents/vitiligo-management-and-prognosis?source=search_result&search=Vitiligo&selectedTitle=1~115#H4083146597. Accessed September 18, 2016

4) Bolognia JL, Jorizzo JL, Schaffer JV. Vitiligo. In: Dermatology. 3rd ed. New York, NY: Elsevier Saunders; 2012: 1023-1030.

Answer is C. This patient presents with moderate-persistent asthma in which the preferred treatment is with a low-dose inhaled glucocorticoid and a long-acting beta-2 agonist (LABA) in addition to the Albuterol inhaler PRN. The treatment plan in Choice A is for a patient with intermittent asthma. Choice B represents the treatment for a patient with mild-persistent asthma and choice D is for a patient with severe-persistent asthma. Classification of severity is based on the frequency of symptoms, nighttime awakenings, use of a short-acting beta-2 agonist (SABA), interference with normal activity, and lung function tests.

Asthma Case Discussion:

Epidemiology:
Asthma affects millions of patients worldwide. In the U.S. it has been found that asthma is more prevalent in African Americans than Caucasians. Recently, there has been an increase in the prevalence and morbidity of asthma which is likely due to air pollution, smoking, and exposure to environmental allergens. Asthma is also more common in boys during childhood years and is greater in females after puberty. The majority of cases are diagnosed before adulthood and about half of all children with asthma have less severe symptoms by early adulthood although symptoms may develop at any age.

Etiology & Pathophysiology:
Asthma is a chronic inflammatory disorder that involves airway hyper-responsiveness as well as increased mucus production which ultimately leads to decreased respiratory airflow. However, the exact cause of asthma is not completely understood as it is a very complex disorder. Environmental exposures, genetic factors, allergens, foods, as well as infectious processes are among the strongest risk factors. There are several prenatal risk factors which include maternal smoking, diet, stress, and even the use of antibiotics. Childhood risk factors include allergic sensitization, environmental tobacco smoke, animal dander, gender, and even socioeconomic status. Allergens plays one of the largest role in asthmatics, particularly in those with a history of atopy (allergies, atopic dermatitis, and allergic rhinitis). In fact, total serum IgE levels, markers for allergen sensitivity, are often associated with a higher incidence of asthma as IgE is closely linked with airway hyperresponsiveness. There is increasing evidence that indoor allergens play a large role in the development of asthma and recurrent wheezing in children. Such allergens include house dust mites, animal proteins, cockroaches, and fungi. In adult onset asthma, the most common etiologies include occupational exposures such as chemicals used by hairdressers, paint used by mechanics, as well as commercial cleaning solutions. Smoking may also contribute to asthma-like symptoms in the adult population.

History and Physical Exam Findings:
Patients usually present with a typical history of respiratory symptoms that occurred following exposure to certain triggers that usually revolve after avoiding the stimuli or with asthma medication. The most common triggers include exercise, allergen exposure, or recent viral infection. Patients often report the most common symptoms of asthma which include wheeze, cough (worse at night), and shortness of breath. Typically, patients also have a personal history of atopy which includes atopic dermatitis, seasonal allergic rhinitis as well as asthma.
On physical exam, patients often have diffuse high-pitched expiratory wheezes on auscultation. In patients with severe airflow obstruction, physical exam findings may include tachypnea, tachycardia, prolonged expiration, use of accessory muscles, and the patient may be in the “tripod” position. Other findings in asthmatic patients include pale or swollen nasal mucus membranes, nasal polyps, or atopic dermatitis.

Diagnostic Labs/Imaging:
Laboratory testing and chest imaging are not routinely used in the diagnosis of asthma, but often used to rule out other differential diagnoses. Pulse oximetry may be useful for assessing the severity and response to treatment. Pulmonary function testing (PFT) is the diagnostic test of choice in asthma. PFTs test airflow limitation and are useful in identifying airway hyper-responsiveness. Spirometry testing, in particular, measures the amount your lungs can inhale, exhale, and how quickly you do so. This testing measures forced expiratory volume in one second (FEV1) and forced vital capacity (FVC). When there is a suspected diagnosis of asthma, it is important that providers obtain baseline results to have a comparison for when there is a possible asthma exacerbation or uncontrolled symptoms. Compared to baseline, a reduced FEV1/FVC ratio represents the presence of airway obstruction. Spirometry can be used to determine the amount of obstruction present, assess the response to bronchodilators, characterize the severity of airflow limitation, and identify any restrictive patterns.

Other testing includes the methacholine/histamine challenge or bronchoprovocation testing. It is most commonly used to assess airway hyper-responsiveness in patients with atypical presentations or normal spirometry results. During the test, methacholine or histamine (provocative substances) are used to cause constriction of the bronchioles. Asthmatics will be more sensitive to these stimuli than patients without asthma. Peak expiratory flow is a simple and inexpensive test that is measured during forceful expiration. It is more useful in monitoring patients with asthma rather than diagnosing asthma. A reduced peak flow value at the time a patient is experiencing respiratory symptoms is suggestive of asthma or an exacerbation. Also, a 20% or greater improvement in peak flow after administration of a SABA is also indicative of asthma.

Management & Treatment:
The most important components in the management of asthma are routine monitoring of lung function, education, trigger avoidance, control of comorbid conditions, as well as pharmacologic therapy. Aside from avoiding triggers, the pharmacologic treatment of asthma is multi-faceted and depends on severity of symptoms. The mainstay of pharmacologic management includes the use of short-acting beta-2 agonists, long-acting beta-2 agonists, inhaled corticosteroids, leukotriene receptor antagonists, and omalizumab. Of course, effective management requires prevention of symptoms and exacerbations and when the asthma is not well-controlled, therapy should be “stepped-up” or “stepped-down” when symptoms are well-controlled. Almost all asthmatics should have a prescription for an Albuterol inhaler (SABA) to use as needed for symptoms. However, the use of Albuterol inhalers more than two days per week for symptom relief typically represents inadequate symptom control and the need to step up treatment. Severe asthma exacerbations are often treated with nebulized albuterol, intravenous/oral steroids, and occasionally helium-oxygen.

Work Cited:

1. Zhang Y, McConnell R, Gilliland F, Berhane K. Ethnic differences in the effect of asthma on pulmonary function in children. Am J Respir Crit Care Med. 2011 Mar 1. 183(5):596-603. [Medline]
2.Subbarao P, Mandhane PJ, Sears MR. Asthma: epidemiology, etiology and risk factors. CMAJ. 2009;181(9):E181-90.
3.Litonjua A et al. Risk Factors For Asthma. UpToDate. 2016. Available at: https://www.uptodate.com/contents/risk-factors-for-asthma?source=search_result&search=asthma+epidemiology&selectedTitle=4%7E150.
Accessed September 12, 2016.
4.Fanta M.D. C. Diagnosis of Asthma in Adolescents and Adults. UpToDate. 2016. Available at: https://www.uptodate.com/contents/diagnosis-of-asthma-in-adolescents-and-adults?source=search_result&search=asthma+history+and+physical&selectedTitle=3%7E150. Accessed September 15, 2016.
5.Fanta C. An Overview of Asthma Management. UpToDate. 2016. Available at: https://www.uptodate.com/contents/an-overview-of-asthma-management?source=search_result&search=asthma+treatment&selectedTitle=1%7E150. Accessed September 15, 2016.

Answer is D. Mitral valve prolapse is a disease where the leaflets of the mitral valve project back into the left atrium with systolic pressure. Patients with connective tissue disorders such as Marfan Syndrome are at increased risk for the disease.1 Most patients are asymptomatic, but those with symptoms can have left sided chest pain, sweats, dyspnea, orthopnea, fatigue, and edema.3 The classic murmur for mitral valve prolapse is a midsystolic click over the mitral valve area (fifth intercostal space left midclavicular line).6 Echocardiogram is the definitive diagnostic tool for this condition.1 The remaining choices can be ruled out because tricuspid regurgitation presents with a blowing holosystolic murmur over the left sternal border, mitral stenosis presents with a diastolic low, rumbling decrescendo murmur heard at the apex, pulmonary stenosis presents with a diastolic, crescendo-decrescendo murmur at the left second intercostal space, and aortic regurgitation presents with a decrescendo, high-pitched diastolic murmur over the right parasternal third intercostal space.6

References
1. Problem: Mitral Valve Prolapse. http://www.heart.org/HEARTORG/Conditions/More/Heart
ValveProblemsandDisease/Problem-Mitral-Valve-prolapse_UCM_450441_
Article.jsp#.WIodtYWcHIU. Published October 16, 2016. Accessed January 26, 2017.
2.How is Mitral Valve Prolapse Treated? National Institutes of Health.
https://www.nhlbi.nih.gov/health/health-topics/topics/mvp/treatment. Published June 22,
2016. Accessed January 26, 2017.
3. Mitral valve prolapse. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/mitral-valve-
prolapse/basics/definition/con-20024748. Published April 5, 2014. Accessed January 26, 2017.
4. The Evolution of Mitral Valve Prolapse: Insights from the Framingham Heart Study. Circulation American Heart Association. 2016;37(1):327-335. doi:10.1353/crb.0.0100.Epidemiology and
5. Pathophysiology of Mitral Valve Prolapse. Contemporary Reviews in Cardiovascular Medicine. 2014;37(1):327-335. doi:10.1353/crb.0.0100
6.Types of Heart Murmurs. The Society for Cardiovascular Angiography and Interventions. http://www.secondscount.org/pediatric-center/pediatric-detail-2/types-of-heart-murmurs#.WI0P5YWcHIU. Published January 12, 2015. Accessed January 28, 2017.