Block 1

1. B- The formula for a 95% confidence interval for data that follow a normal distribution is x̅ +/- (1.96 x Standard Error), where x̅ is the mean. The lower end of the confidence interval is thus 130 – (1.96 x 5), which equals 120.2, and the higher end of the confidence interval is 130 + (1.96 x 5) which equals 139.8. This best matches the range of 120-140.
2. E- Six weeks ago, this patient developed acute renal failure and ischemia-induced acute tubular necrosis (ATN) in the setting of cardiac arrest due to underlying coronary artery disease. This was most likely due to severe renal ischemia due to impaired cardiac output. The diagnosis of ATN is supported by his oliguria, azotemia, and urinary granular casts. Two weeks after his initial cardiac arrest, the oliguria and azotemia resolved, representing the recovery of acute tubular necrosis. Most patients with ATN will experience tubular re-epithelialization and spontaneous full recovery. This is not uncommon after several weeks. Severe acute kidney injury can be lethal if not properly managed, although the question states that this patient’s death was secondary to a cardiac arrhythmia, likely due to damage sustained from ischemia during cardiac arrest.
3. D- For a normal distribution of data, mean (average) is the most reliable measure of central tendency. In this example, the mean leukocyte count is 7500 cells/mm3. Based on this, 50% of individuals will have leukocyte counts greater than 7500 and 50% will have leukocyte counts less than 7500.
4. A- This patient has vaginal pain, pruritus, and dyspareunia. Physical exam reveals edematous, erythematous vaginal mucosa with white discharge, suggestive of a candidal infection. A vaginal smear reveals the presence of normal vaginal epithelium and pseudohyphae, confirming the diagnosis of vaginal candidiasis. This patient is at risk for the development of this condition based on her history of type 2 diabetes mellitus.
5. E- Emphysema is a component of chronic obstructive pulmonary disease characterized by loss/damage of alveolar elastin and lung parenchyma due to a protease/antiprotease imbalance. This causes increased alveolar collapse on expiration, air trapping and hyperinflation, impaired ventilation, and increased dead space, leading to hypoxemia and hypercapnia. Patients may experience shortness of breath and dyspnea on exertion/at rest. Over time patients may develop severe hyperinflation and a barrel chest. Breathing through pursed lips is performed in order to prevent expiratory alveolar collapse (auto-PEEP). Pulmonary function testing classically reveals decreased FEV1:FVC ratio (<70%), increased residual volume (obstruction), and impaired diffusion (decreased DLCO).  For additional information check out MedSchool Bootcamp’s video on COPD.
6. A- Bipolar I disorder is characterized by at least one episode of mania. This is defined as seven or more days of abnormal and persistently elevated, irritable, or expansive mood along with increased goal-directed activity, behavior, or energy that are not attributed to another medical condition, psychotic disorder, or substance abuse. This patient has evidence of psychotic features, including delusions (married to the president's brother, receiving specific instructions from higher being) that further support this diagnosis. For additional information check out MedSchool Bootcamp's video on Bipolar Disorders.
7. B- Peak A represents the initial antibody production by B cells that are exposed to this live attenuated bacteria’s antigens for the first time (clonal selection). Between Peaks A and B, some of these cells become memory B cells, awaiting future infections/exposures. Peak B is characterized by amplification of the antibody production response due to previous exposure (clonal expansion). This “second exposure” achieves a more robust response than the “first exposure” in a shorter amount of time. Following this second peak, a lack of continued stimulation leads to cellular apoptosis in the majority of the antibody producing cells. A small population remains as memory cells. For additional information check out MedSchool Bootcamp's video on Antibody Properties.
8. B- This patient has evidence of exocrine pancreatic insufficiency, including fatty stools (large volume, floating) and significant weight loss. In the setting of insufficient pancreatic enzyme secretion and activation (e.g., lipase), fat-soluble vitamins (A,D,E,K) are likely to become deficient. This patient has symptoms of vitamin A deficiency (e.g., xerosis cutis). For additional information check out MedSchool Bootcamp's video on Pancreatic Insufficiency.
9. G- Serum prostate-specific antigen (PSA) is a high value test, where a high value indicates a positive result. At the original threshold, values > 4.1 ng/mL were considered a positive result. If the threshold is lowered to 2.0 ng/mL, some patients who were previously considered negative will be considered positive. This population of newly positive patients with PSA levels between 2.0 and 4.1 ng/mL will have a higher proportion of false positive results compared to the population of patients with a PSA > 4.1 ng/mL. Overall this will lead to more false positives, which decreases the reliability of a positive test result. Thus, the PPV will decrease. Meanwhile, the NPV will increase, because the patients with a PSA between 2.0 and 4.1 had a higher chance of being a false negative with the original threshold, so changing the threshold such that these patients become positive decreases the amount of false negatives and increases the reliability of a negative result. For additional information check out MedSchool Bootcamp's video on Diagnostic Test Thresholds.
10. D– Absorbing and understanding complex information is extremely difficult shortly after receiving unexpected and emotional news. By providing only a small amount of the most need-to-know information, the physician gives the family time to process and understand that information before giving additional details that may otherwise be forgotten.
11. H- Physiologic changes of exercise include increases in venous return (preload), contractility, and heart rate. Point X on the diagram represents the steady state condition regarding right atrial pressure and cardiac output in this patient prior to exercise. The slope of the cardiac function curve (solid line) is increased by increases in contractility and heart rate as demonstrated with exercise (left-upward shift of the curve). Point G represents baseline venous return (as we have not left the initial vascular/venous return curve). Point F represents pathologic decreases in venous return, while point H correctly corresponds to physiologic increases in venous return in the setting of exercise.
12. B- This patient is experiencing lower urinary tract symptoms, including impaired bladder emptying, urinary hesitancy, and postvoid dribbling, indicating lower urinary tract obstruction. Physical exam revealed a diffusely enlarged, firm, and nontender prostate—consistent with benign prostatic hyperplasia (BPH). BPH is a very common condition of advancing age. It is due to prostate stimulation by dihydrotestosterone (DHT) which is converted from testosterone by 5 alpha-reductase. This stimulation leads to hyperplasia of the periurethral lobes (lateral and middle) of the prostate and subsequent symptomatology.
13. E- This patient with sickle cell disease (SCD) is presenting with symptoms of biliary colic (e.g., postprandial RUQ pain, nausea, lack of fever) in the presence of gallstones confirmed by ultrasound. This is most likely secondary to underlying hemolysis linked to the patient’s sickle cell disease. Typical lab findings in hemolysis include a decreased haptoglobin, increased LDH, and increased unconjugated bilirubin. The elevation in unconjugated bilirubin results from heme catabolization and can increase the risk of pigmented calcium bilirubinate gallstone formation. For additional information check out MedSchool Bootcamp's video on Hemolysis.
14. D- This patient has evidence of autosomal dominant familial hypercholesterolemia, supported by tendinous xanthomas (hands and Achilles), familial history of early onset atherosclerosis (coronary artery disease) affecting males and females, and hypercholesterolemia on serum lipid studies. Patients with Apo C-II or lipoprotein lipase deficiency commonly develop familial hyperchylomicronemia with hypertriglyceridemia and its possible sequelae (pancreatitis, eruptive xanthomas) with no increased risk of atherosclerosis.
15. A- Controlled cellular destruction (shrinkage, cytoplasmic budding, noninflammatory, plasma membranes intact) is indicative of apoptosis. Apoptosis is a highly programmed self-contained process of cell destruction. This can occur via two general pathways: extrinsic and intrinsic. The intrinsic pathway is initiated by a stimulus (p53, loss of regulating factor) that leads to a change in the intracellular balance of pro-apoptotic (Bax, Bak, Bad) and anti-apoptotic (Bcl-2, Bcl-xL) proteins. These pro-apoptotic proteins enhance mitochondrial membrane permeability, leading to cytochrome c release (increases in cytochrome c) into the cytosol, and eventual activation of caspase 9 that then activates additional caspases. For additional information check out MedSchool Bootcamp's video on Apoptotic Pathways.
16. D- Increasing the sample size from 500 to 1500 will increase the power of the study, which is the ability of a study to correctly reject the null hypothesis when the null hypothesis is false. If the chances of the study correctly rejecting the null hypothesis increase, the chances of the study failing to reject the null hypothesis when the null hypothesis is false will decrease. This means the chances of making a type II error will decrease. Mathematically, the power = 1 -  probability of making a type II error, so if the power increases, the probability of making a type II error must decrease.
17. A- Reactive gliosis is the process involved in repairing CNS tissue after injury. This is mediated by the proliferation of astrocytes within the CNS. These cells facilitate nervous tissue repair and scar formation. Astrocytes are the most abundant form of glial cell, functioning as structural support for neurons, supporting and forming the blood brain barrier, removing and metabolizing neurotransmitters (glymphatic system), extracellular potassium buffering, and acting as a glycogen reserve. For additional information check out MedSchool Bootcamp's video on Histologic Timeline of Stroke.
18. C- Cardiac function during a myocardial infarction is severely compromised. This patient’s ECG reveals ST-segment elevations and new Q waves in leads V4-V6, representing occlusion of the distal LAD/LCX. This infarcted tissue comprises a large portion of the left ventricle. During the acute setting, ventricular contractility will decrease in an effort to balance oxygen supply and demand. This is seen as a large drop in cardiac output. This decreased output leads to increased retention of blood within the left ventricle, as an increased end-diastolic volume (EDV). This is represented by a change from W to Z on the graph. For additional information check out MedSchool Bootcamp's video on Cardiac Function and Venous Return Curves.
19. A- This patient has signs and symptoms of hypercalcemia, including increased urinary frequency, constipation, and fatigue in the presence of elevated calcium and decreased parathyroid hormone on serum lab studies. This suggests an extra-endocrine cause of hypercalcemia that is leading to parathyroid suppression (non-PTH-mediated hypercalcemia). A chest x-ray reveals bilateral hilar adenopathy and interstitial infiltrates, pathognomonic for sarcoidosis, a granulomatous disorder. Sarcoidosis is classically associated with calcium homeostasis dysregulation due to overactivation of macrophages and increased extra-renal production of 1-alpha hydroxylase. This increased enzymatic expression leads to increased conversion of 25-vitD to 1,25-vit D, causing increased gastrointestinal calcium and phosphate absorption, increased renal calcium reabsorption, and increased bone resorption. This is seen as hyperphosphatemia, hypercalcemia, hypervitaminosis D, and suppression of PTH levels.
20. C- Patients with Parkinson disease are commonly prescribed levodopa in order to increase central nervous system dopamine levels. They are also co-prescribed carbidopa to decreased peripheral conversion of levodopa (able to cross blood brain barrier) to dopamine (unable to cross blood brain barrier) by DOPA decarboxylase. This combination is the classic treatment of choice for Parkinson disease but is commonly affected by periods of on-off phenomenon. This effect can be mitigated by using a monoamine oxidase type B inhibitor, such as selegiline or rasagiline. This prevents the central conversion of dopamine into DOPAC (3,4-dihydroxyphenylacetic acid), prolonging the effect of the neurotransmitter. For additional information check out MedSchool Bootcamp's video on Parkinson Disease.
21. F- Infusion of high-dose epinephrine in isolation produces a net “pressor effect” due to increased systolic blood pressure (alpha 1 effect) and a mild decrease in diastolic blood pressure (beta 2 effect). In other words, the alpha effect predominates at higher doses. This alpha 1 effect is mediated through Gq receptor activation, leading to phospholipase C production and increased conversion of PIP2 to IP3 and DAG. IP3 leads to increased intracellular calcium concentrations and subsequent protein kinase C activation, while DAG activates protein kinase C. These combined effects lead to smooth muscle contraction and increased peripheral resistance. With the addition of doxazosin (alpha antagonist), the beta-2 effect predominates. Beta 2 activation leads to Gs receptor activation and subsequent adenylate cyclase upregulation. This leads to increased conversion of ATP to cAMP, protein kinase A activation, and inhibition of myosin light chain kinase, culminating in inhibition of smooth muscle contraction and decreased peripheral resistance.
22. D- This patient has developed a urinary tract infection (UTI), evidenced by dysuria, increased urinary frequency, microscopic hematuria, pyuria, nitrite/leukocyte esterase/bacteria positivity. This is likely due to a gram negative bacterium, such as Escherichia coli. Risk factors for the development of UTIs include female sex, sexual intercourse, abnormalities of the urinary tract (e.g., BPH, nephrolithiasis, congenital malformations), pregnancy, prior conditions (e.g., diabetes mellitus, immunosuppression), and prolonged indwelling urinary catheter usage (CAUTI). This patient has no signs of current pregnancy and is most likely experiencing irregular periods due to perimenopause. UTIs are more common in females due to the shorter length of the urethra and close proximity of the anal-genital regions. This combination allows easier bacterial spread from the anal region, vaginal colonization, and subsequent ascension of the urinary tract.
23. E- This patient is experiencing occupational-related allergic contact dermatitis due to latex exposure. This is characterized by a type IV hypersensitivity reaction, presenting with delayed symptoms following exposure to latex (e.g, gloves). Contact dermatitis is mostly a clinical diagnosis, evidenced by a limited erythematous rash that is confined to the area of exposure. Other causes include exposure to poison ivy/oak/sumac, nickel, neomycin, perfumes, soaps, and many others. Latex is a very common cause of allergic contact dermatitis. For additional information check out MedSchool Bootcamp's video on Type IV Hypersensitivity Reactions.
24. B- This patient has developed signs of meningismus (e.g., fever, headache, nuchal rigidity, photophobia) in the context of similar illness experienced by those around him. Lumbar puncture findings are consistent with a viral cause (e.g., increased opening pressure, lymphocytosis, increased protein, normal glucose). Enteroviruses (e.g., echoviruses, coxsackieviruses) are the most common cause of viral meningitis in all age groups.
25. A- The baroreceptor reflex functions to maintain blood flow during changes in position (standing, supine, seated). This patient transitioned from standing to supine. During this process, blood goes from relatively pooled in the lower extremities (due to gravity) to equalized (head and feet are the same height). This increases venous return to the heart (increased atrial stretch) and distends the carotid sinus (increasing their firing frequency). Through a vasomotor center brainstem reflex arc, this leads to increased parasympathetic efferent activity and decreased sympathetic efferent activity. The net effect is vasodilation, decreased heart rate, stroke volume, and blood pressure. For additional information check out MedSchool Bootcamp's video on Sensory Receptors of the Vasculature.
26. B– This statement shows the patient that the physician is honest and committed to understanding the patient’s perspective. It would not be appropriate to respond in a way the patient might perceive as being told she is “making up” her experience (A, C, E). It would also not be appropriate to ignore her past medical records and history (D). For additional information check out MedSchool Bootcamp's video on Disorders of Somatization and Hypochondriasis.
27. A- This 3-week-old female presents with one week of jaundice, scleral icterus, acholic stools, and dark urine. Additional remarkable findings include hepatomegaly, direct hyperbilirubinemia, and mild elevations in AST/ALT. In a newborn, this clinical picture is consistent with biliary atresia. The infant is capable of conjugated bilirubin but is unable to secrete it into the small intestine. This leads to increased total and direct bilirubin and subsequent hepatomegaly, varying levels of transaminitis, and symptoms of hyperbilirubinemia (e.g., jaundice, scleral icterus). (B) Crigler-Najar syndrome type I is characterized by increased indirect bilirubin due to inability to conjugate. (C) Gilbert syndrome is a benign condition characterized by decreased ability to conjugate bilirubin (less severe than Crigler-Najar) that typically presents in adolescence as benign jaundice in periods of physiologic stress (e.g., surgery, infection, fasting, alcohol use). (D) Hemolytic disease of the newborn presents with significant intravascular hemolysis that can potentially lead to severely increased indirect hyperbilirubinemia and possible kernicterus. (E) Physiologic jaundice is an indirect hyperbilirubinemia that presents after the first day of life. It is due to a decreased life of fetal erythrocytes and immature hepatic conjugation of bilirubin. This condition is benign. For additional information check out MedSchool Bootcamp's video on Jaundice.
28. A- This patient presents with medically uncontrolled hypertension. Lab studies reveal increased renin in the absence of other significant findings. Angiography reveals a high-grade stenotic lesion of the proximal right renal artery, pathognomonic for atherosclerotic renal artery stenosis. This stenosis leads to relative hypoperfusion of the right kidney. This causes increased activation of the renin-angiotensin-aldosterone system in the right kidney, leading to difficult-to-control hypertension. The unaffected (left) kidney typically maintains adequate electrolyte balance, explaining the normal electrolytes in this patient. On the other hand, fibromuscular dysplasia is a common cause of distal renal artery stenosis that classically affects young women. For additional information check out MedSchool Bootcamp's video on Secondary Hypertension.
29. A- The correlation coefficient is a value between -1 and 1 that describes how well two variables display a linear relationship. Correlation coefficients less than 0 mean that the slope of the linear relationship between the two variables is negative. Correlation coefficients that are greater than 0 mean that the slope of the linear relationship between two variables is positive. A correlation coefficient of 0 means there is no linear relationship. A correlation of 0.6 means that the two variables, serum LDL and serum hs-CRP, have a positive linear relationship, meaning that high values of serum LDL will be associated with high values of hs-CRP. Importantly, two variables being associated does not imply that one causes the other.  
30. A- Potency is defined as the concentration of a drug required to achieve a desired clinical response. Potency is represented by distribution along the X axis while efficacy is represented by distribution along the Y axis. Drug X achieves a ~50% clinical response at a much lower level than drugs Y or Z, indicating greater potency. Drugs Y and Z have similar efficacy (same height) and are both more efficacious than drug X.
31. B- This patient presents with key findings of plethora and splenomegaly in the setting of a normal oxygen saturation, increased hemoglobin, hematocrit, leukocyte count, and leukocyte alkaline phosphatase level with occasional giant platelets observed on peripheral blood smear. These findings are consistent with a diagnosis of polycythemia vera (PV), a malignant hematopoietic neoplasm caused by abnormally high activity of transduction of growth signals in the kinase domain. JAK2 is integral to the regulation of erythropoiesis, thrombopoiesis, and granulopoiesis. The primary hematologic defect in PV (usually a JAK2 gain of function mutation) is at the level of the hematopoietic stem cells (can affect multiple cell lines). Of note an abnormally low oxygen saturation would be more suggestive of a secondary polycythemia as observed in COPD. For additional information check out MedSchool Bootcamp's video on Polycythemia Vera.
32. C- This patient has a 10 year history of heartburn that occurs after known triggers. His condition has been uncomplicated (e.g., no weight loss, dysphagia, stricture). His physical exam is unremarkable but endoscopy reveals erythema and ulceration of the distal esophagus above the Z line. This represents gastroesophageal reflux disease (GERD). GERD is most commonly due to transient loss of lower esophageal tone and reflux of gastric contents into the distal esophagus. This patient has no indication of decreased saliva production (not a smoker), esophageal dysmotility (no dysphagia), or gastrinoma (no duodenal ulcer noted). For adidtional information check out MedSchool Bootcamp's video on Esophagitis.
33. D- This patient presents with classic signs of carbon monoxide poisoning (e.g., headache, nausea, dizziness for a specified period of time). He currently lives in the basement of a large home during the winter months and smokes 1.5 PPD. The physician should inquire further about the method of heating for this patient’s living quarters. Common sources of carbon monoxide include wood-burning stoves, furnaces, gas heaters, house fires, and vehicle exhaust in an enclosed, poorly ventilated space. Of note, those who smoke tobacco generally have higher baseline levels of carboxyhemoglobin. For additional information check out MedSchool Bootcamp's video on Carbon Monoxide Poisoning.
34. D- This patient has developed left sided hydronephrosis in the setting of recurrent urinary tract infections. The T2-weighted MRI shows a proximal obstruction at the level of the ureteropelvic junction—site where the ureter leaves the renal collecting pelvis. This is a more common site of ureteric obstruction than the uterovesical junction (site where the ureter enters the bladder). The hydronephrosis develops as a result of increased back pressure on the proximal renal system. Obstructed areas are viewed as dark areas of T2-weighted MRI followed by relatively diminished intensity due to impaired contrast movement around the obstruction (some leaks through).
35. C- This patient is experiencing dysmenorrhea without other significant medical issues. The first-line treatment in an otherwise healthy young female is non-steroidal anti-inflammatory agents (NSAIDs), such as ibuprofen. Primary dysmenorrhea is due to endometrial PGF2-alpha production that leads to localized vasoconstriction and ischemia as well as increased uterine contractions in order to prevent blood loss. This is experienced by patients as intense lower abdominal cramping and discomfort that typically radiates to the back. The use of NSAIDs prevents prostaglandin synthesis, improving these symptoms. Other methods of relief include local heat application (e.g, heating pad) and implementation of oral contraception (OCPs). For additional information check out MedSchool Bootcamp's video on Menstrual Cycle Disorders.
36. A- This patient presents with a mild injury. He is subsequently found to have a megaloblastic macrocytic anemia, evidenced by a hypersegmented neutrophil (> 5 lobes) and erythrocytes with central pallor. In the context of significant daily alcohol intake (4-6 beers/day and double on weekends) and rudimentary dietary intake (“tea and toast” diet), the most likely cause of this is folic acid (folate) deficiency. Affected patients are unable to maintain the 1 carbon pool due to inability to regenerate folate equivalents (tetrahydrofolate). This impairs conversion of homocysteine to methionine, leading to hyperhomocysteinemia and potential cardiovascular sequelae. Lack of folate cycling also prevents the conversion of dUMP to dTMP for DNA synthesis. For additional information check out MedSchool Bootcamp's video on Folate Deficiency.
37. C- This otherwise healthy newborn is found to have a penile-appearing structure with hypospadias located above the vaginal introitus. If this infant is found to have a 46, XX karyotype, this is most likely caused by maternal exposure to androgens while pregnant causing virilization. (A) 17alpha-hydroxyprogesterone is converted to 11-deoxycortisol and then cortisol. Deficiency would lead to adrenal insufficiency, hypertension, and impaired stress response. This would not likely lead to virilization as less 17 alpha-hydroxyprogesterone would be converted to androstenedione for testosterone production.  Normal female external genitalia would be expected at birth, although 21-beta hydroxylase deficiency and 11-beta hydroxylase deficiency can present with virilization. (B & D) Increased concentration of mullerian-inhibiting substance and/or the presence of sex-determing region Y would lead to expression of Wolffian duct structures and a lack of the uterus, fallopian tubes, and upper vagina. Ambiguous external genitalia would be unlikely in this case as the XX fetus would produce estrogen, causing the formation of female external genitalia. (E) 5alpha-reductase deficiency is a disorder of 46, XY males in which testosterone cannot be converted to dihydrotestosterone (DHT). This prevents the adequate maturation of the external male genitalia during development resulting in internal male genitalia and external female-appearing genitalia. This classically resolves at puberty as the substantial increase in testosterone leads to the maturation of male external genitalia. For additional information check out MedSchool Bootcamp's video on Disorders of Sexual Development.
38. E- Ischemic reperfusion injury occurs when oxygen is reintroduced into an environment of prior ischemia. This is frequently observed in peripheral vascular disease and acute coronary syndrome. This may also be secondary to interventions, including percutaneous coronary intervention when reperfusion is attempted. The mechanism of reperfusion injury involves the production of free radicals and tissue damage. This may progress to necrosis (nonphysiologic cell death), in this case of the myocardial tissue. Necrosis results in mitochondrial edema and swelling of other organelles secondary to lack of ATP production that eventually leads to nuclear changes, including karyolysis (disintegration of the nucleus) and plasma membrane damage secondary to acute rises in intracellular calcium. Of these options, only lysis of the plasma membrane is directly responsible for troponin (an intracellular enzyme) leaking into the systemic circulation. For additional information check out MedSchool Bootcamp's video on Necrosis.
39. A- The formula for absolute risk reduction (ARR) is the risk in the riskier procedure minus the risk in the less risky procedure. The question stem states that the risk for wound infection for Procedure A is 12/1000, and the risk for Procedure B is 18/1000. ARR = Procedure B – Procedure A = (18/1000) – (12/1000). For additional information check out MedSchool Bootcamp's video on Additional Calculations of Relative Risk.
40. B- This patient presents with a concern for traumatic spinal cord injury from cervical subluxation in proximity to the C6 vertebrae. Elbow flexion is supplied by the C5 nerve roots and would be most cephalad to the lesion from the options presented. Wrist flexion is primarily supplied by C6-C7, elbow extension C7, thumb abduction C8, and finger abduction T1. Of additional note, cervical spinal nerve roots exit the canal above the vertebrae that correspond to the segment of the root.

Block 2

1. D- This patient experienced symptoms of hypoglycemia (e.g., restlessness, sweating, and confusion) due to over-supplementation of exogenous insulin. Mistakes in calculating the necessary insulin dosage after a high-carbohydrate meal are common. When adjusting insulin doses for a specific meal, typically the shorter-acting insulin formulation is adjusted while the basal insulin formulation is left the same. This patient’s father increased the doses of both of her insulin formulations around a high-carbohydrate meal with good intent to prevent hyperglycemia. This adjustment most likely led to overcompensation of this child’s carbohydrate intake, causing a brief period of symptomatic hypoglycemia. These symptoms are multifactorial, including autonomic (e.g., sweating, restlessness) and neuroglycopenic (e.g., confusion) in nature.
2. B- This patient is experiencing symptoms of cardiac obstruction (e.g., fainting). She is subsequently found to have S3 and S4 heart sounds and a pedunculated intracardiac mass, pathognomonic for a cardiac myxoma. Biopsy findings of scattered mesenchymal cells surrounded by gelatinous material (composed of glycosaminoglycans) further support this diagnosis. Cardiac myxomas are most commonly found in the left atrium. These tumors act as a ball-valve obstruction, causing intermittent symptoms, including dizziness, palpitations, and syncope. Weight loss, fever, pallor, chills, fatigue, and other constitutional symptoms are also possible as these tumors frequently secrete IL-6.
3. A- This infant has polycystic kidney disease leading to Potter’s sequence. Since genetic testing reveals two copies of a genetic mutation, that suggests this is an autosomal recessive condition. The Hardy-Weinberg principle states that in a population at equilibrium, the genotypic proportions will follow the formula p²+2pq+q²=1, where p² is the frequency of homozygous dominants, 2pq is the frequency of heterozygotes, and q² is the frequency of homozygous recessives. The frequency of each allele occurring in the population will follow p+q=1, where p is the frequency of the dominant allele, and q is the frequency of the recessive allele. Since this is an autosomal recessive condition, only homozygous recessive individuals will have the disease, so the disease frequency and the q² is 1/10,000. The mutation rate, which is the same as the frequency of recessive alleles in the population, can be calculated by taking the square root of 1/10,000, which comes out to q = 1/100. For additional information check out MedSchool Bootcamp's video on Hardy-Weinberg Genetics.
4. B- This elderly female has evidence of worsening osteoarthritis involving her wrists and hands that causes her significant pain and loss of function, especially when buttoning her coat. The image of her hand reveals Heberden and Bouchard nodes (especially of the 3rd PIP). Osteoarthritis occurs due to chronic mechanical forces translated across joints and age-related decreases in proteoglycan synthesis. This process leads to the loss of cartilage elasticity and subsequent degeneration and inflammation of the cartilage. This can be seen as subchondral sclerosis and joint space narrowing, especially on imaging.
5. D- This previously health patient has developed severe left-sided flank pain, tachycardia, and hypertension (likely from pain). Further evaluation reveals microscopic hematuria and a small ureteric calculus (kidney stone) composed of uric acid. Uric acid stones are a relatively uncommon finding of nephrolithiasis, as most are calcium based. Patients with underlying impairments in uric acid metabolism (underexcretion or overproduction) are more likely to develop nephroliths composed of uric acid. Conditions associated with these stones include gout, high cell turnover (e.g., tumor lysis syndrome, myelodysplastic syndromes), hyperuricemia, and hyperuricosuria. Out of the listed choices, an impairment in purine metabolism (adenine, guanine) is the most likely cause of his presenting illness. (E) Urea cycle abnormalities include ornithine transcarbamylase deficiency, arginase deficiency, carbamoyl phosphate synthetase 1 deficiency, and N-acetylglutamate synthase deficiency. These disorders involve dysfunction of ammonia conversion into urea for excretion. They are not involved in purine metabolism and/or uric acid production. For additional information check out MedSchool Bootcamp's video on Purine Metabolism.
6. A- This patient has developed worsening symptoms of hypothyroidism (e.g., cold intolerance, constipation, and severe fatigue) after beginning calcium carbonate supplementation for lumbar spine osteopenia. Lab studies reveal elevated TSH and decreased free T4 concentrations, confirming worsening hypothyroidism. This is most likely due to nonspecific complex formation between calcium and levothyroxine within the intestinal lumen. It is known that taking these two medications within a four hour window can significantly decrease the absorption and bioavailability of levothyroxine.
7. A- This elderly patient presenting with a 5-day history of a painful rash that does not cross the midline likely is suffering from herpes zoster (shingles). Herpes zoster classically presents in a dermatomal distribution that does not generally cross the midline. Lesions are often vesicular and painful in nature. Reactivation of varicella-zoster virus is thought to contribute to the development of shingles in immunocompromised individuals secondary to deficiencies in cellular immunity. Cellular immunity is essential in the identification and destruction of intracellular pathogens, such as viruses, through the use of MHC class I proteins on host tissue. For additional information check out MedSchool Bootcamp's video on Herpes Simplex and Varicella Skin Infections.
8. E- This patient is found to have accessory spleens after suffering crush injuries in a motor vehicle collision. The most likely origin of this congenital anomaly is a thickening of the dorsal mesogastrium. This occurs due to an incomplete fusion of mesenchymal buds during development. During the fifth week of development, a primitive spleen forms in the midline from the mesoderm of the dorsal mesogastrium (in the midline). This rotates to the left side as the foregut develops. The unfused mesenchymal buds can form accessory spleens in any position between the original primitive spleen formation and the final site of the spleen (LUQ). Of note, accessory spleens can also be formed by the descent of the gonads during development—the spleen initially forms near the urogenital ridge. Due to this physical proximity, it is possible for the primitive gonadal tissue to become fused to some of the mesenchymal buds. As the gonads develop and descend, they can drag accessory splenic tissue with them; this leads to the placement of accessory spleens in the pelvis or groin.
9. C- Benzodiazepines are the first-line agents in the management of alcohol withdrawal. Longer acting agents (e.g., chlordiazepoxide, diazepam) are classically preferred in most patients, but shorter acting agents (e.g., lorazepam, temazepam) are preferred in patients with altered drug metabolism (e.g., liver disease, elderly). These agents are indirect GABA-A receptor agonists that increase the action of GABA binding by increasing the frequency of chloride channel opening. This leads to postsynaptic membrane hyperpolarization and decreased symptoms associated with neuronal excitability (e.g., anxiety, insomnia, tremor, palpitations, sweating, seizures). For additional information check out MedSchool Bootcamp's video on Alcohol Withdrawal.
10. B- This patient has poorly controlled type II diabetes mellitus. This is most likely due to her travel and work situation, leading her to eat excessive amounts of “fast” food (e.g., overly processed, high-carbohydrate density foods) and forget to measure her blood glucose concentration. The best action by the physician would be to further explore and inquire about the barriers this patient is experiencing when it comes to diet adherence (e.g., financial ability, time requirement, food macronutrient knowledge). (C, D, G) Increasing this patient’s medications may be necessary but is likely to be less effective if the patient’s dietary adherence is the primary issue. Referral to a nutritionist could be helpful if a lack of macronutrient knowledge and healthy food choices is a source of this patient’s problem. (E) Measuring the blood glucose concentration is unlikely to be helpful as it is more than likely elevated. This patient displays no signs of HHS or DKA so this is unwarranted. (F) Though monitoring of renal function is essential in patients with diabetes mellitus, this is unlikely to help improve her level of disease control. (A) Creating an exercise regimen for a patient who already feels time constraints and cannot handle the current level of intervention is unlikely to be helpful.
11. D- This young male presents with bilateral parotid gland swelling, fever, malaise, and decreased appetite. This presentation is classic for an infection with Mumps virus—a highly contagious viral infection transmitted via airborne droplets, contaminated saliva and/or respiratory secretions. Mumps classically effects the salivary glands (especially the parotid gland) before disseminating to lacrimal, thyroid, mammary glands, ovaries, testes, pancreas and/or central nervous system. This can be differentiated by other causes of parotid gland swelling due to its bilateral nature, painful presentation, and fever. Sialadenitis is typically unilateral and painful, sialolithiasis is unilateral and partial with prandial pain, and salivary gland tumors are typically unilateral, painless +/- signs of invasion (e.g., facial nerve compression and palsy), systemic signs (e.g., weight loss, fatigue.
12. A- This patient has developed multiple episodes of angioedema (e.g., throat tightness and swelling of the face, lips, and tongue) six weeks after beginning an ACE inhibitor. She has no signs of urticaria (hives). This is most likely due to increased levels of bradykinin caused by impaired catabolism in the presence of an ACE inhibitor. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II in the treatment of hypertension; they also prevent the inactivation of bradykinin into physiologically inactive peptides. A buildup of bradykinin leads to overactivation of B2 receptors, causing the release of prostacyclin, NO, and other endothelium-derived relaxing and hyperpolarizing factors. This leads to vasodilation and possible hypotension, seen clinically as angioedema. For additional information check out MedSchool Bootcamp's video on Antihypertensives.
13. B- This patient has a left-sided varicocele, due to an abnormal enlargement, tortuosity, and distention of the scrotal pampiniform plexus—network of small veins that runs in the spermatic cord, providing testicular venous drainage. This is most commonly due to proximal obstruction of the testicular vein. The left side is more commonly affected as the left testicular vein enters the left renal vein at a ~90° angle. The right testicular vein enters the IVC directly. The left renal vein passes between the superior mesenteric artery and the aorta, leaving it susceptible to period compression (nutcracker syndrome). The increased pressure within the left renal vein transmits to the left testicular vein, leading to scrotal pampiniform plexus distension—over time this leads to enlargement and tortuosity. This can be exacerbated by increased intraabdominal pressure (e.g., Valsalva) and observed with doppler ultrasound of the affected testicle. For additional information check out MedSchool Bootcamp's video on Male Reproductive Anatomy.
14. B- This patient has developed chronic myelogenous leukemia with the presence of the Philadelphia chromosome. This is due to a translocation between chromosomes 9 and 22, t(9;22). Fusion of the ABL1 gene from chromosome 9 with the BCR gene from chromosome 22 leads to the formation of a BCR-ABL gene. This encodes for a non-receptor tyrosine kinase that has enhanced enzymatic activity. The results of the translocation include inhibition of apoptosis and increased baseline mitotic activity. Translocations represent the recombination of chromosomal regions between nonhomologous chromosomes. For additional information check out MedSchool Bootcamp's video on Chronic Myeloid Leukemia.
15. A- This patient presents with signs and symptoms of cystic fibrosis, an autosomal recessive disease due to a defect in the CFTR gene on chromosome 7. This gene encodes the cystic fibrosis transmembrane conductance regulator—a chloride and bicarbonate channel responsible for fluid secretions nd extracellular alkalinization. Patients with cystic fibrosis are unable to secrete bicarbonate adequately, leading to organ specific manifestations (e.g., pancreatic insufficiency, dental caries, impaired gastrointestinal mucous secretion, cervical mucous thickening, impaired fertility). Kunzelmann K, Schreiber R, Hadorn HB. Bicarbonate in cystic fibrosis. J Cyst Fibros. 2017;16(6):653-662. doi:10.1016/j.jcf.2017.06.005. For additional information check out MedSchool Bootcamp's video on Cystic Fibrosis.
16. C- This patient has suffered damage to the upper trunk due to right clavicular fracture. His current deficits include decreased DTRs in the biceps (C5-6) and brachioradialis (C5-6) and decreased sensation over the right shoulder (Axillary nerve- C5-6). Out of the listed options, impaired shoulder abduction (due to impaired axillary nerve transduction) is the most likely. (A) Elbow extension is maintained by the extensor compartment innervated by an intact radial nerve (C5-T1). (B) Finger abduction is maintained by the dorsal interossei innervated by an intact ulnar nerve (C8-T1). (D) Thumb flexion is maintained by flexor pollicis longus (median nerve and brevis (superficial: median, deep: ulnar) innervated by intact median nerve (C6-T1) and ulnar nerves (C8-T1). Wrist flexion is also maintained by intact ulnar and median nerves via multiple muscles of the anterior compartment.
17. C- This patient presents with signs of platelet dysfunction (e.g., nosebleeds, easy bruisability, gingival bleeding) in the presence of a family history, normal platelet count, normal ristocetin cofactor response assay, and impaired thrombin-mediated platelet aggregation. This is most likely due to Glanzmann thrombasthenia—an aggregation disorder due to an autosomal recessive deficiency in platelet receptor GpIIb-IIIa. Most affected patients are asymptomatic or develop minor bleeding (e.g., petechiae, menorrhagia, epistaxis, purpura, gingival bleeding). Lab findings include increased bleeding time, normal platelets, and impaired platelet aggregation studies (impaired thrombin-mediated platelet aggregation). PT/INR, aPTT, D-dimer, and fibrin degradation products will all be within normal limits. For additional information check out MedSchool Bootcamp's video on Platelet Disorders.
18. E- This patient has developed new-onset shortness of breath after living at high-altitude for a period of 2 years. Findings include jugular venous distention and lower extremity pitting edema. This is most likely due to group 3 pulmonary hypertension—high altitude. High altitude exposure is associated with decreased PiO2 (atmospheric oxygen). Along with tachypnea, and renal bicarbonate excretion that occurs acutely, pulmonary vascular resistance increases (D) in response to hypoxic pulmonary vasoconstriction. Over time, this leads to pulmonary hypertension and eventual concentric right ventricular hypertrophy (F). As the wall of the right ventricle thickens, diastolic compliance decreases. As a result, the height of the P waves in lead I increase (P pulmonale, right atrial enlargement) (A), height of R waves in lead V1 increase (increased right ventricular mass) (B). Compensation to chronic hypoxia also includes erythroid expansion (erythropoiesis), increased erythrocyte mass, and increased hematocrit (C). For additional information check out MedSchool Bootcamp's video on Pulmonary Hypertension.
19. E- This patient has primary pulmonary tuberculosis. The typical treatment regimen consists of two months of rifampin, isoniazid, pyrazinamide, and ethambutol followed by four months of rifampin and isoniazid. Rifampin inhibits bacterial DNA-dependent RNA polymerase, preventing transcription and mRNA synthesis. This leads to impaired bacterial protein synthesis and cell death.
20. D- This patient is found to have a large hepatic laceration involving the right and left lobes. Hepatic bleeding is often controlled via the Pringle maneuver—temporary occlusion of the hepatoduodenal ligament via vascular clamp or surgeon’s hand in order to decrease blood flow to the liver through the hepatic artery and portal vein. For additional information check out MedSchool Bootcamp's video on GI Gross Anatomy.
21. C- This 1-month-old male has developed signs and symptoms of bronchiolitis (e.g., fever, cough, intercostal retractions, diffuse wheezing). He is subsequently found to have blood cultures growing coagulase-negative, catalase-positive, gram-positive cocci in clusters. This is representative of Staphylococcus epidermidis. Bronchiolitis is most commonly caused by respiratory syncytial virus (RSV) and occasionally with parainfluenza virus. This blood culture result is most likely due to contamination of blood culture vials with normal skin flora.
22. C- Increases in trans-fatty acid intake are known to adversely affect serum lipid studies, owing to a greater risk of atherogenesis and coronary artery disease. Trans-fatty acid intake is linked with reduced HDL, increased total cholesterol and increased LDL.                
23. D- Clearance of a drug is defined as the volume of plasma cleared of a drug in a unit of time (typically hours). It can be calculated by dividing the rate of elimination of a drug by the plasma drug concentration. The rate of elimination of this drug is unknown, necessitating another equation to be used. Infusion rate = Clearance x Steady state concentration. In this case, 100mg/hr = Clearance x 50 mg/L. Solving for clearance = 100mg/hr divided by 50 mg/L = 2 L/hr. 
24. D- This patient has developed acute tubular necrosis (e.g., muddy brown casts, acute kidney injury, elevated creatinine) in the setting of E. coli sepsis. This is most likely due to decreased renal blood flow caused by hypotension and renal ischemia. The most likely areas of the kidney to be affected by ischemia include the proximal convoluted tubular and the thick ascending limb due to greater levels of metabolic activity and oxygen consumption.
25. E- This patient with a past medical history of myasthenia gravis has developed increasing weakness, shortness of breath, and abdominal cramping. Further evaluation reveals bradycardia, tachypnea, weak cough, impaired inspiratory force, hyperactive bowel sounds, myogenic fasciculations, and decreased deep tendon reflexes. In the context of this patient’s medical history of medication use (prednisone and pyridostigmine), this is most likely due to an overdose of pyridostigmine. This agent is an acetylcholinesterase inhibitor used in patients with myasthenia gravis to improve synaptic ACh levels and decrease neuromuscular symptoms. In excess, this can lead to multiple cholinergic side effects, including bradycardia, hypotension, nausea, abdominal pain, diarrhea, hypoventilation, lethargy, weakness, paralysis, bronchospasm, etc. For additional information check out MedSchool Bootcamp's video on Myasthenia Gravis.
26. B- Paracentric chromosomal inversions involve two breaks in one chromosome to create an intervening segment. This segment does not contain the centromere. The segment is then inverted (180 degrees) and re-inserted. These inversions can survive for long periods of time, through multiple generations. Normally, during prophase I, each pair of chromosomes come together and exchange genetic material (crossing over). A single chromosome containing a paracentric inversion may present structural challenges to crossover events, requiring the chromosomes to form a loop, allowing the inverted segment of one chromosome to align its genes accordingly with the normal segment of the other corresponding chromosome. If a crossover event occurs within the loop formed, two disproportionate chromosomal segments are produced. One chromosome may contain 2 centromeres, whereas the other may contain none. If a fetus is conceived with either of these two formed chromosomes, the pregnancy would be at risk for early spontaneous abortions. A liveborn child, would likely be the result of a crossover event occurring outside of the loop, in which case, two structurally similar chromosomal segments would be produced, and thus not be associated with aneuploidy. 
27. D- This young boy has a family history significant for Huntington disease in a maternal grandfather, colon cancer in paternal grandfather, numbers colonic polys in father necessitating colectomy, and a confirmed heterozygous APC frameshift gene mutation in his father. Based on this patient’s current risk for genetic disease, investigating his risk of familial adenomatous polyposis (APC gene-adenomatous polyposis coli) is most appropriate. Since this patient’s father has a frameshift mutation it is appropriate to look for this directly. Though he may be at risk of Huntington disease, this is less important to test for as there is no preventative or curative treatment available. For additional information check out MedSchool Bootcamp's video on Single Stranded DNA Repair.
28. A- This 53-year-old female presents with six years of stiffness and pain in her hands that causes her difficulty buttoning her clothes. She is subsequently found to have multiple Swan Neck deformities (PIP hyperextension, DIP flexion). This is most likely representative of rheumatoid arthritis (RA). RA is associated with anti-citrullinated peptide antibodies ( > 90% specificity), rheumatoid factor (less specific, elevated in infectious disease, other autoimmune diseases, some healthy individuals), and antinuclear antibodies. RA is also associated with a genetic disposition with HLA-DR4 an HLA-DR1 proteins. 
29. F- This patient is a known amphetamine drug abuser presenting with irritability, restlessness, tremor, palpitations, tachycardia, tachypnea, and hypertension. This is most likely due to recent amphetamine use. Amphetamines cause these symptoms via the increased synaptic release and inhibited reuptake of biogenic amines (epinephrine, norepinephrine, serotonin, and dopamine). This leads to sympathetic overstimulation and hallucinogenic effects. For additional information check out MedSchool Bootcamp's video on Amphetamines.
30. B- This young female has developed dysentery (blood diarrhea), acute kidney injury (oliguria, elevated creatinine), anemia, and thrombocytopenia, representing hemolytic uremic syndrome. This is most likely due to infection with the O157:H7 serotype of enterohemorrhagic Echerischia coli. Gastrointestinal inflammation facilitates the systemic circulation of bacterial toxins (Shiga-like toxin, verotoxin). This toxin preferentially causes endothelial damage, especially in the glomerulus (due to Gb3 receptor expression). Once damage, endothelial cells release cytokines that promote further damage, vasoconstriction, microthrombi formation and microangiopathic hemolytic anemia (MAHA). This leads to end-organ ischemia and damage, most commonly in the kidneys (large percentage of total blood flow), leading to acute kidney injury (e.g., decreased GFR, azotemia). 
31. D- In healthcare settings, a professional interpreter must be used whenever a patient is not fluent in English. It would not be appropriate to delay care or communications with the patient and their family to wait for the hospital interpreter, so using a telephone interpreter service is the most appropriate option in this scenario.
32. E- This patient has developed neutropenic fever, a common oncologic emergency in patients receiving chemotherapy. This is caused by a severe decrease in absolute neutrophil count (ANC < 500 or expected to decrease to that level based on trends) that can lead to life-threatening infections. Though these infections can be severe (gram-negative rod bacteremia), patients often present with mild symptoms (e.g., low grade fever, tachycardia, lack of erythema) due to lack of neutrophil-mediated inflammation. Patients should receive early empiric antibiotic therapy and investigation for source should be rapid and thorough (e.g., central line associated blood stream infection workup, blood cultures, imaging). For additional information check out MedSchool Bootcamp's video on Cell Cycle Dependent Drug Targets.
33. B- This patient with distant right colon resection and chemotherapy presents with fatigue on follow-up examination. CT imaging reveals multiple new hepatic and pulmonary masses, consistent with cancer recurrence and metastasis. This patient’s primary gastrointestinal malignancy most likely traveled through the right-sided mesenteric venules into the superior mesenteric vein and into the portal vein, through the liver (depositing hepatic metastases), and into the inferior vena cava before reaching the lungs. For additional information check out MedSchool Bootcamp's video on Veins, Anastomoses, and Hemorrhoids.
34. A- This patient with a past medical history of acute lymphoblastic leukemia is seen for follow-up. The physician adds an agent to decrease the toxicity of high-dose methotrexate on his normal cells. This agent is most likely folinic acid, also known as leucovorin or active folic acid. This bypasses the requirement for normal healthy cells to activate folic acid via dihydrofolate reductase—the enzymatic target of methotrexate. This “rescues” the normal cells from methotrexate’s adverse effects. This is known as salvage therapy or leucovorin rescue therapy. For additional information check out MedSchool Bootcamp's video on Clinical Applications of Pyrimidine Pathway.
35. C- This newborn male is found to have a small blind pit at the midline of the tongue at the intersection of the anterior two-thirds and posterior-one third and a mass adhered to the hyoid bone. This small blind pit represents the foramen cecum of the tongue—this serves as the embryonic origin of the thyroglossal duct. During embryogenesis, the thyroid normally descends through the thyroglossal duct into its adult anatomical position in the neck. In some cases, the thyroid fails to descend completely, leading to a lingual thyroid, as seen in this patient. The cells within the thyroid produce tetraiodothyronine (T4) and triiodothyronine (T3) that have many physiologic effects, including CNS development, metabolism regulation, catecholaminergic receptor expression, respiratory center stimulation, musculoskeletal system maturation, bone growth, and many others. Thyroid hormones (mainly T3) enter target cells, binds to nuclear thyroid hormone receptors (TR) that are heterodimerized with RXR. This leads to disruption of nuclear corepressor binding and promotion of coactivator binding, which causes recruitment of polymerases and initiation of gene transcription. For additional information check out MedSchool Bootcamp's video on the Pharyngeal Apparatus.
36. C- This receptor has found that are deficient in a specific eosinophil protein are more susceptible to filarial parasitic infections. This is most likely representative of a major basic protein deficiency. Major basic protein is an eosinophilic protein that is involved in host defense against parasites. It is produced in response to IgE antibody-dependent cell-mediated cytotoxicity. Release leads to destruction of pathogens via cytotoxic mechanisms as well as the release of histamine from mast cells and basophils, and the recruitment of neutrophils and macrophages. For additional information check out MedSchool Bootcamp's video on Eosinophils.
37. D- Keratosis pilaris (KP) is a common dermatologic condition characterized by keratinized hair follicles that are most commonly found on the extensor surfaces of the arms and thighs. KP is a benign condition that is sometimes associated with atopic dermatitis. It typically consists of nonpruritic and nonpainful erythematous bumps but, as in this patient, is sometimes a source of social embarrassment. There is typically no need to treat KP but keratolytic medications are sometimes prescribed if patient’s develop worry or social impairment. For additional information check out MedSchool Bootcamp's video on Dermatologic Histopathology.
38. B- This patient with a known history of obstructive sleep apnea (OSA) on continuous positive airway pressure device has developed increasing daytime somnolence and signs of cyanosis (e.g., blue lips, earlobes, and nail beds). Arterial blood gas reveals a hypercarbic, hypoxic respiratory acidosis. OSA is a common cause of increased hemoglobin concentration, termed appropriate absolute polycythemia. This is due to appropriate increase in erythryocyte mass due to increased erythropoietin stimulation from chronic oxygen desaturation. (A) Serum bicarbonate is most likely to be increased as a renal compensation for chronic respiratory acidosis. (C) Total lung capacity is most likely decreased in the morbidly obese patient due to musculoskeletal restriction. (D) OSA is a likely cause of group 3 pulmonary hypertension (chronic-lung disease etiology) that can lead to right ventricular hypertrophy (cor pulmonale). For additional information check out MedSchool Bootcamp's video on Sleep Apnea.
39. F- This patient with chronic kidney disease is found to have elevated creatinine and hyperphosphatemia. This is most likely due to impaired renal function. Patients with severely impairred renal dysfunction are unable to secrete phosphate. This retained phosphate deposits within the vasculature and organs as calcium-phosphate products, depleting the serum calcium level. This is sensed by the parathyroid glands, stimulating the release of parathyroid hormone in attempt to raise serum calcium. The damage kidneys are unable to upregulate 1-alpha-hydroxylase to form active 1,25 vit D. This leads to an inability to increase renal calcium reabsorption and phosphate secretion as well as impaired gastrointestinal calcium and phosphate absorption. Over time, the continued PTH secretion can lead to bone pain and increased risk of fractures (renal osteodystrophy)
40. E- This patient has congestive heart failure insufficiently treated with an ACE inhibitor. Because of continued symptomatology, her physician adds a potassium sparing diuretic (e.g., spironolactone, eplerenone, triamterene, amiloride). These agents work within the late distal convoluted tubule and collecting tubule, leading to decreased sodium reabsorption and potassium excretion. This patient was most likely prescribed spironolactone as it has been shown to reduce mortality in heart failure with reduced ejection fraction. Amiloride and triamterene are more commonly co-prescribed with thiazide diuretics to maintain a normal potassium level. Eplerenone is rarely used as an initial agent.

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Block 3

1. D- This patient is performing a high-intensity long-distance activity (half marathon) and avoiding liquid intake due to a pre-existing medical condition. She is likely to develop hypernatremia during exercise due to lack of liquid intake and increased water loss compared to salt. She is also likely to become significantly dehydrated. Both of these result in the release of antidiuretic hormone (ADH). ADH regulates plasma osmolality via the V2 receptors, inserting aquaporin channels in the principal cells of the collecting duct and distal convoluted tubule in order to enhance water reabsorption. It also increases the rate of urea absorption within the collecting duct in order to drive the corticomedullary gradient in favor of free water reabsorption and urine concentration. ADH release also leads to vasoconstriction via V1 receptors in states of hypovolemia and hypotension. For additional information check out MedSchool Bootcamp's video on Sodium.

2. D- Development of the aorticopulmonary septum requires proper neural crest cell migration. In a state of genetic modification leading to lack of cardiac neural crest cell development, this can not take place. This animal model is most likely to develop persistent truncus arteriosus due to a lack of neural crest cells and subsequent lack of septum formation. A commonly mistaken cardiac defect is transposition of the great vessels which results from improper spiraling of the aorticopulmonary septum, leaving the right ventricle empting into the aorta and the left ventricle into the pulmonary artery. This occurs after proper neural crest cell migration and septum formation have occurred. It is associated with infants born to diabetic mothers and DiGeorge syndrome. For additional information check out MedSchool Bootcamp's video on the Truncus Arteriosus.

3. E- This patient is undergoing an outpatient laparoscopic cholecystectomy. This procedures requires the visualization of the cystic artery within the hepatocystic triangle (triangle of Calot) created by the cystic duct laterally, the common hepatic duct medially, and the liver edge superiorly. This is of great importance as the triangle is the most common location for the course of the cystic artery. The cystic artery is a terminal branch of the right hepatic artery, branching off at the proximal end immediately after division of the proper hepatic artery into its right and left branches (C). (D) The right gastric artery is the first branch of the common hepatic artery, supplying the inferior portion of the lesser curvature of the stomach. (A) The gastroduodenal artery is a terminal branch of the common hepatic artery that supplies the gastric pyloris, proximal duodenum, and head of the pancreas. (B) The left gastric artery is one of the three branches of the celiac trunk. It supplies the superior portion of the lesser curvature of the stomach. For additional information check out MedSchool Bootcamp's video on GI Blood Supply.

4. C- This patient presents with 2 weeks of a generalized prodromal symptom complex, including fever, exudative pharyngitis, tachycardia, hypotension, diffuse lymphadenopathy, anemia, leukopenia, and thrombocytopenia in the absence of definitive lab testing. This symptom complex is consistent with a diagnosis of primary HIV infection, which commonly presents with a mononucleosis-like syndrome (e.g., fever, fatigue, myalgia, headache, generalized lymphadenopathy, oropharyngeal symptoms). (A) This is unlikely to be EBV as a heterophile antibody test was negative. (B) Patients with gonococcal pharyngitis are likely to present with sore throat, pharyngeal exudates, and cervical lymphadenitis consistent with localized infection. Diffuse lymphadenopathy is less likely. (D) Lymphogranuloma venereum (LGV) is caused by serotypes L1-L3 of Chlamydia trachomatis. It is most common in tropical countries, with increasing incidence in men who have sexual contact with men. Primary infection results in the formation of small, painless genital ulcerations that heal spontaneously. This is following by painful inguinal adenopathy with abscess formation and systemic toxicity. (E) Streptococcal pharyngitis is unlikely to cause cytopenias to this degree and is likely to resolve spontaneously in 2-5 days even if untreated.

5. D- This patient has developed focal neurologic deficits in the context of rheumatic mitral valve disease and likely related atrial fibrillation. Her deficitis include right-sided weakness, Broca’s aphasia (inability to speak), right lower facial weakness, and dysphagia. This is most likely due to thromboembolic stroke involving the left middle cerebral artery from atrial fibrillation, affecting the motor and sensory cortices as well as Broca’s area within the inferior frontal gyrus. For additional information check out MedSchool Bootcamp's video on Types of Strokes.

6. A- This patient presents to his primary care physician with difficulty with his omeprazole working for his gastroesophageal reflux around the holiday season. This level of specificity in lack of drug efficacy is unusual. After further assessment the patient brags about his increased food and alcohol intake during the holidays. The most appropriate response would be to inquire about the severity and quantity of this increase. This type of bingeing behavior is likely worsening his reflux to the point to where his medication cannot work. He is also at risk of medication:alcohol interactions. Alcohol can lead to lower esophageal sphincter (LES) relaxation and worsening of reflux. Increased gastric distention from overeating can also increase intragastric pressure, forcing the LES open and causing reflux. (B, C, D, E) While these may be needed, it most appropriate for the physician to explore the degree of this patient’s increased intake prior to changing medical management.

7. C- This patient’s presentation is consistent with pernicious anemia (e.g., weakness, paresthesias, altered mental status, spasticity, loss of vibratory sensation). This is further supported by findings of antiparietal cell antibodies, methylmalonic acidemia, homocysteinemia, and megaloblastic anemia. A type II hypersensitivity reaction, leading to antibody formation against gastric parietal cells, leads to decreased gastric acid and intrinsic factor production. This ultimately results in impaired vitamin B12 absorption in the terminal ileum. Anti-intrinsic factor antibodies may also be seen. B12 is required for the conversion of homocysteine to methionine via impaired methionine synthase function (requires B12 cofactor). Deficiency leads to homocysteine elevation and methionine deficiency. This conversion also normally recycles tetrahydrofolate. Without this, DNA synthesis is impaired, leading to the formation of megaloblastic hematopoeitic cells. B12 is also responsible for the conversion of methymalonyl CoA to succinyl CoA via methylmalonyl CoA mutase, with deficiency leading to elevations in methymalonyl CoA (methylmalonic acid).

8. D- This newborn is exhibiting respiratory distress, as evidenced by cyanosis, grunting, and retractions. Further evaluation reveals bowel loops in the left chest. This is most likely due to a congenital diaphragmatic hernia, specifically a Bochdalek hernia (posterolateral left-sided diaphragmatic hernia). This results form impaired development of the pleuroperitoneal membrane, leading to a persistent diaphragmatic defect. Within the pleuroperitoneal membrane, the septum transversum cannot fuse posteriolaterally, creating this defect. These defects present most commonly on the left side due to impaired herniation on the right as a result of the liver being in the way. For additional information check out MedSchool Bootcamp's video on Diaphragmatic Hernias.

9. E- This patient with alcohol use disorder presents with hematuria without pain. He has known exposure to naphthylamine and chronic tobacco exposure. Imaging reveals a mass within the renal pelvis. Based on his exposure history, this is most likely due to urothelial (transitional cell) carcinoma. This is the most common malignancy of the bladder, ureter, and renal pelvis. When the renal pelvis is involved, the classic presentation consists of painless hematuria throughout micturition and flank pain.

10. A- This adolescent female presents with chest pain, preceding fever, and shortness of breath. She is found to be afebrile with a friction rub. Out of the choices, Coxackievirus is the most likely causal agent. Coxsackievirus B infection can cause pleurodynia (Bornholm’s disease, Devil’s grip) characterized by fever, flu-like symptoms and painful spasms of the chest and upper abdominal quadrants due to pleural and muscular irritation. Diagnosis is clinical but may be supported by viral culture or PCR and serological testing. In severe cases, pericarditis may occur, with the development of a pleural friction rub.

11. A- This patient presents with hemoptysis, shortness of breath, lower extremity edema, and dark urine (hematuria). He is hypertensive and hypoxemic with diffuse inspiratory crackles on auscultation. His labs support a diagnosis of acute kidney injury and hematuria with dysmorphic urinary RBCs and rare casts. Biopsy reveals crescentic (rapidly progressive) glomerulonephritis and linear IgG deposition along the glomerular capillaries. This presentation is pathognomonic for Goodpasture syndrome—a cause of nephritic syndrome and proliferative glomerulonephritis due to the formation of anti-base membrane antibodies directed at type IV collagen int he renal and pulmonary capillary basement membranes. For additional information check out MedSchool Bootcamp's video on Rapidly Progressive Glomerulonephritis.

12. A- This statement encourages the patient to explore their motivations for changing behavior without resorting to fear (B, D) or shaming (C, E) tactics. For additional information check out MedSchool Bootcamp's video on the Transtheoretical Model of Change.

13. F- This patient presents with increased urinary frequency and excessive thirst. His urine osmolality is 50 mOsmol/kg. After administration of ADH, his urine osmolality is in the reference range (50-1200 mOsmol/kg). This patient was likely experiencing central diabetes insipidus due to impaired ADH secretion by the supraoptic nucleus of the hypothalamus. This is differentiated from nephrogenic diabetes insipidus by adequate response to exogenous ADH, as seen in this patient. For additional information check out MedSchool Bootcamp's video on Sodium.

14. B- This patient presents with a knife wound through his right chest, tachycardia, normotension, tachypnea, and leftward tracheal shift. This is most likely due to a traumatic pneumothorax. Significant hemothorax is essentially ruled out due to his hemodynamic stability. Patients with a pneumothorax have various physical exam findings, including:

- Opposite tracheal shift due to air filling the pleural space and forcing the contents to the other side of the chest.

- Hyperresonance on percussion due to the presence of intrathoracic air.

- Decreased breath sounds on the ipsilateral side due to lung collapse.

- Decreased fremitus on the ipsilateral side. Air is a poor conductor of low sound frequencies whereas solid or dense tissue increases the transmission of these frequencies. Therefore, a hemithorax full of air will conduct sound less readily than normal heterogeneous lung (air and parenchyma). Increase fremitus can be noted in conditions such as pneumonia (increased pulmonary density and fluid).

For additional information check out MedSchool Bootcamp's video on Pneumothorax.

15. C- This patient has started lisinopril due to proteinuria in the context of type 2 diabetes mellitus and persistent hypertension. Lisinopril is an angiotensin converting enzyme (ACE) inhibitor that prevents the conversion of angiotensin I to angiotension II (ATII). This prevents the effects of angiotensin II as well as aldosterone (release mediated by angiotensin II). The results of ACE inhibitor administration include:

- Increased renal blood and decreased blood pressure due to decreased vasoconstrictive effects of ATII

- Decreased aldosterone secretion and decreased sodium/water reabsorption leading to decreased blood pressure

- Decreased ultrafiltration pressure due to decreased efferent arteriolar constriction (normally mediated by ATII), leading to decreased hydrostatic glomerular capillary pressure and increased ease of flow from afferent arterioles through glomerular capillaries and into the efferent arterioles. Glomerular filtration rate decreases for the same reason.

16. B- This newborn female is found to have ambiguous genitalia, increased 17-hydroxyprogesterone, and a 46, XX karyotype (confirming female sex). This is most likely representative of female virilization due to underlying androgen excess in the context of 21-hydroxylase deficiencym the most common cause of congenital adrenal hyperplasia (~95% of cases). This deficiency leads to an inability to convert:

- Progesterone to 11-deoxycorticosterone in the synthesis of aldosterone

- 17-hydroxy-pregnenolone to 17-hydroxy-progesterone in the synthesis of cortisol

This leads to increased shunting of mineralocorticoid and glucocorticoid precursors into the androgenic steroid synthesis pathway (testosterone, estradiol). This classically presents with female virilization, due to testosterone excess. Patients may also development symptomatic adrenal insufficiency (e.g., salt-wasting, hypotension, shock). For additional information check out MedSchool Bootcamp's video on Disorders of Sexual Development.

17. B- This patient with a past medical history of hypertension presents with shortness of breath after a cross-country flight, tachycardia, tachypnea, and hypertension. Physical exam reveals evidence of a right lower extremity deep venous thrombosis with extension to the popliteal vein (pain behind right knee). This is concerning for a pulmonary embolism. Out of the listed options, Factor V Leiden mutation is a cause of inherited thrombophilia. This mutation results in the inability for activated protein C to inactivate clotting factor V, leading to enhanced thrombin activation and increased risk of thromboembolic events (e.g., deep venous thrombosis, cerebral venous thrombosis, recurrent pregnancy loss). (A) Antithrombin III deficiency is most commonly asymptomatic, discovered when patients receive heparin that has diminished activity. (C) Glanzmann thrombasthenia is a functional platelet disorder that results in microbleeding (e.g., petechiae, purpura). (D) Protein C deficiency is rarer than Factor V Leiden. This deficiency puts patient at a higher risk of developing warfarin-induced skin necrosis. (E) von Willebrand disease is the most common inherited bleeding disorder characterized by microbleeding (e.g., petechiae, purpura) and, in some cases, factor VIII deficiency (inc. PTT). For additional information check out MedSchool Bootcamp's video on Thrombophilias.

18. D- This patient has classic symptoms of hypokalemic period paralysis, an autosomal dominant disorder characterized by recurrent episodes of muscle weakness that typically develop after certain triggers, including strenuous exercise (e.g., football), alcohol ingestion, dietary changes, medication use, stress, etc. This is due to mutations in sodium and calcium channel genes causing intracellular shifting of serum potassium and resulting muscular paralysis/weakness. Laboratory analysis during an attack is most likely to show hypokalemia.

19. D- This patient has developed symptomatic syringomyelia. The most important thing to evaluate in this case would be an incidence of trauma, as a small percentage of patients develop this as a complication. This is thought to be due to traumatic inflammatory obstruction of the central canal of the spinal cord, leading to cavitary dilatation and subsequent compression of cord structures, including:

- Lateral spinothalamic tract fibers at the anterior white commissure (loss of pain and temperature)

- Lower motor neuron compression at anterior horns (bilateral weakness, paresis, and muscle atrophy at level of syrinx)

- Upper motor neuron compression in medial portion of lateral corticospinal tract (spastic paresis below syrinx)

- Posterior column (loss of proprioception and vibratory sensation)

For additional information check out MedSchool Bootcamp's video on Central Cord Syndromes.

20. A- This patient presents with signs of herpes labialis (e.g., painful ulcerations/blisters, neuralgia, and fever). This is most likely caused by HSV-1 infection—enveloped dsDNA virus. Treatment includes antiviral treatment wit acyclovir or valacyclovir—antiviral agents that inhibit viral DNA polymerase and subsequent DNA replication via chain termination. These drugs are guanosine analogs that are activated by HSV/VZV encoded thymidine kinase. These active intermediates are then phosphorylated by cellular kinases into their triphosphate forms.

21. D- This patient sustained an injury to the ulnar nerve, leading to severe weakness, muscle atrophy, and decreased sensation in the nerve’s distribution. As this is a peripheral nerve, Schwann cells are essential in the recover of neurologic function within this patient. Schwann cells are responsible for the myelination of axons of the peripheral nervous system (PNS), including the radial n. (and CN III-XII). Each single Schwann cell is capable of myelinating an internodal segment of one neuron. This is essential after neuronal damage if repair is to occur. (B) This is contrast to oligodendrocytes, which are responsible for myelination within the CNS. Each oligodendrocyte myelinates multiple neurons. (A) Astrocytes are the most abundant cell within the CNS, providing structural support, acting as an extracellular buffer, and playing a role in the glymphatic system. (C) Satellite cells are skeletal muscle cell precursors, responsible for myoregeneration. (E) Tanycytes are specialized ependymal cells found within the third and fourth ventricles that are in direct contact with blood vessels. Their function is to transport a multitude of substances between the blood and the ventricles. For additional information check out MedSchool Bootcamp's video on Neuronal Cell Types.

22. D- This young male presenting with painful left eye bulging without a history of trauma or medication use. Imaging reveals a small mass involving the ocular muscles and subsequent biopsy reveals malignant cells with striations. This is most likely representative of a rhabdomyosarcoma—tumor of primitive skeletal muscle cells, known as rhabdomyoblasts. This tumor type is the most common malignant orbital tumor in children.

23. B- This 11-year-old female has developed scant pubic hair, the initial formation of a breat bud (areolar tissue enlargement), and an increase in areolar diameter. This is indicative of Breast and Pubic Hair Tanner stage 2 development. These characteristics are the initial findings of puberty. Of note, thelarche (breast development) classically precedes a growth spurt and pubarche (pubic hair growth) in females. For additional information check out MedSchool Bootcamp's video on Childhood Development.

24. A- This young male has developed bloody stool consisting of hard “pebbles” and blood on toilet paper when wiping himself. His most recent bowel movement was 5 days prior that caused him pain. Further examination reveals abdominal distension, hypoactive bowel sounds, and a rectal mucosal prolapse. This constellation of findings is most likely due to constipation. Constipation can lead to abdominal pain and the need to increase intraabdominal pressure during defection, leading to anal fissures, hemorrhoids, and/or rectal prolapse. (D) While whipworm infestation (Trichuris trichiura) is a potential cause of rectal prolapse, this is a very rare cause in developed countries. For additional information check out MedSchool Bootcamp's video on Veins, Anastomoses, and Hemorrhoids.

25. C- This patient has a 2-week history of intermittent bloody stools. Further evaluation reveals mild anemia and occult blood in his stool with follow-up colonscopy findings. This presentation and set of findings is most representative of a hamartomatous polyp. Hamartomatous polyps are characterized by normal findings for location on histopathologic analysis. This patient’s biopsy reveal smooth muscle hyperplasia (bands of light pink cells) and glandular hypertrophy without distorted architecture, representative of this polyp type. Hamartomatous polyps can be associated with juvenile polyposis syndrome, Peutz-Jeghers syndrome, Cowden syndrome, and others. For additional information check out MedSchool Bootcamp's video on Hereditary Polyposis.

26. C- This patient has a complex medical history and many risk factors for falls, including bilateral below-the-knee amputations with wheelchair dependence, elderly age, Alzheimer dementia, medications (e.g., amlodipine, insulin), and alcohol intake. She lives with family members who endorse that they do the best they can. She is found to have scattered bruising over her abdomen (likely due to insulin administration) and all extremities (maybe due to falls x 2). Though this patient has a potential mechanism and medical explanation for her physical condition, it is important to assess her relationship with her family to ensure she is receiving adequate care and help while also ruling out forms of elderly abuse. Medical care providers are mandated reporters of elderly abuse and must be aware of potential warning signs.

27. C- This researcher notices that neutrophils are unable to adhere to the vascular endothelium after the administration of glucocorticoids. It is known that glucocorticorids mediate this effect by causing neutrophil demargination. The process of leukocyte margination and rolling requires the expression of various molecules, including P-selectin, E-selectin, GlyCAM-1, and CD34 on endothelial cells as well as Sialyl-Lewisx, and L-selectin on leukocytes. (B, D, E) These are involved in leukocyte tight binding (adhesion)—the step that follows margination and rolling. (A) Cadherin is a calcium-dependent transmembrane protein that is responsible for intercellular adhesion. Impaired cadherin function is associated with neoplastic metastatic transformation. For additional information check out MedSchool Bootcamp's video on Neutrophil Migration.

28. E- This patient presents with worry about memory loss. Though he has some signs of forgetfulness, he is able to live alone and manage his ADLs (e.g., feeding, toileting, dressing) and IADLs (e.g., finances, cooking, shopping) while also continuing to work part-time. His exam is unremarkable and he is found to have a full range of affect, euthymic mood, intact concentration, math skills, proper object recognition and recall, and commands recognition and enaction. The most appropriate response is to counsel the patient that some forgetfulness is normal with aging. There is no evidence of pathological memory loss in this patient’s history and exam (A, C), and it would be inappropriate to continue workup without indications to do so (B, D).    

29. E- This patient has developed myalgia, fatigue, cough, sore throat, rhinorrhea, fever, tachycardia, tachypnea, hypertension, and a severe, painful, rapidly spreading bullous rash over her body and mouth that began 10 days after treatment with a sulfonamide antibiotic (TMP-SMX). Exam reveals a positive Nikolsky sign. Biopsy reveals diffuse epidermal keratinocyte necrosis with minimal lymphocytic infiltration in the dermis. This is a classic description of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Of the choices, TEN is the most likely. TEN involves > 30% of the body surface area, while SJS involves < 10%. This is likely caused by a delayed (type IV) hypersensitivity reaction of drug-specific cytotoxic T lymphocytes, leading to release of cytolytic proteins (e.g., granulysin) and subsequent keratinocyte damage. The most common cause of SJS and TEN is drug exposure (e.g., sulfonamides, aminopenicillins, antiepileptics, NSAIDs, allopurinol). Other causes include infection (e.g., CMV, HSV, mycoplasma), vaccinations, graft-versus-host disease (GVHD), and various unknown mechanisms. For additional information check out MedSchool Bootcamp's video on Reactive Disease.

30. D- This patient has developed a spontaneous vertebral fracture with no history of trauma. She has signs of hypercortisolism (e.g., weight gain, thin extremities, central adiposity, purple striae), likely due to Cushing syndrome (e.g. high normal ACTH, elevated urinary free cortisol). The most likely cause of her fracture is an increase in osteoclast lifespan and activation due to corticosteroid mediated upregulation of RANKL expression.

31. D- This patient has developed fever, headache, light-headedness, dizziness, chills with rigors, and myalgias after beginning therapy for Lyme disease caused by Borrelia burgdorferi. This is a classic description of a Jarisch-Herxheimer reaction. This is an acute, systemic reaction that occurs in response to release of bacterial endotoxin-like substance release that occurs after initiation of antibiotic therapy, most commonly with spirochete infections (e.g., Borrelia, Treponema, Leptospira).

32. D- This newborn is at risk for fetal alcohol syndrome (FAS) due to his mothers alcohol intake (e.g., vodka). Findings of FAS include developmental delay, microcephaly, smooth hypoplastic philthrum, down-slanting short palpebral fissures, epicanthal folds, heart defects (e.g., VSD), and many others. (A) Hypospadias is a common congenital malformation due to incorrect positioning of the external urethral meatus as a result of impaired urethral folds and foreskin fusion. (B) Limb hypoplasia is seen in various syndromes and can be due to drug use (e.g., thalidomide) and sequence limb development (e.g. Potter sequence). (C) Neck webbing is classically associated with Turner syndrome. (E) Spasticity is commonly associated with disorders of the central nervous system (e.g., cerebral palsy). For additional information check out MedSchool Bootcamp's video on Teratogenic Medications.

33. B- This cirrhotic patient (irregular liver surface, jaundice, caput medusae) has developed esophageal variceal bleeding and is about to undergo a TIPS procedure. TIPS is a transjugular intrahepatic portosystemic shunt that is used to decrease portal venous pressure and relieve pressure within anatomically relevant portocaval anastomoses (e.g., left gastric:esophageal, paraumbilical:small gastric, superior rectal:middle/inferior rectal). During this procedure, a needle catheter is inserted into the internal jugular vein and passed to the hepatic vein. Once inside, the needle is used to pierce through the liver parenchyma, creating a new shunt between the portal vein and the inferior vena cava (via the hepatic vein). (A, C, D, E) are all veins within the portal venous system. Thus, creating a shunt between one of them and another portal venous structure would not relieve intraportal pressure. For additional information check out MedSchool Bootcamp's video on Veins, Anastomoses, and Hemorrhoids.

34. B- This patient has a history of chronic back pain with evidence of bone loss on MRI. This is seen as loss of lumbar vertebral body height, bulging intervertebral discs, and spinal stenosis with evidence of impingement. A major risk factor for bone loss and the development of osteoporosis is cigarette smoking. Others include malabsorption, malnutrition, anorexia, medications (e.g., anticonvulsants, corticosteroids, PPIs, anticoagulants). (A) Excessive alcohol consumption is a risk factor but this patient had not drank in 5 years and only drank two beers per day when he did.

35. B- This patient has developed a rapidly enlarging neck mass in the posterior triangle. Biopsy results reveal squamous epithelium (overlying skin), enlarged atypical nuclei (neoplastic lymphocytes), and absent keratin formation (not epidermal material). Although this vignette does not mention immigration or place of birth, this is most likely nasopharyngeal carcinoma due to underlying EBV infection. The description of a rapidly enlarging neck mass with neoplastic histopathologic results is a classic association for this type of neoplasm.

36. A- This patient has developed slipped capital femoral epiphysis (SCFE). This is evidenced by knee pain (referred), reduced hip range of motion on internal rotation, abduction, and flexion, and anterior hip tenderness. SCFE is most common in adolescent males (ages 10-16). It is commonly associated with obesity. This patient has exam findings of obesity and insulin resistance (BMI > 30), including acanthosis nigricans. (A) Although a family history of SCFE is a risk factor, this patient does not endorse such a history. (C) Medication use, especially corticosteroids, is associated with avascular necrosis. This is a potential complication of SCFE but not a risk factor. (D) Previous fractures do not increase the risk of SCFE, although current trauma does. (E) Physical activity is associated with potential overuse myalgia and arthralgia but is unlikely to cause SCFE.

37. B- The most appropriate response in this situation is to explore what the patient understands about her treatment options and their pros and cons. This information will help the physician better understand what the patient might value in making this decision. It would be inappropriate to push this decision back onto the patient when she is clearly asking for the physician’s advice (A, E, F). It would also be inappropriate for the physician to make assumptions about the patient's values (C, D, G).

38. C- This patient is unknowingly pregnant while taking an ACE inhibitor (lisinopril). This is a teratogenic agent known to cause various manifestations. During the first trimester, cardiovascular and CNS malformations are common. During the second and third trimesters, fetal renal damage with resulting oligohydramnios, impaired cranial ossification, and potential fetal demise are possible. ACE inhibitors are thought to produce these effect via inhibition of fetal urine production due to impaired renal blood and filtration flow dynamics. For additional information check out MedSchool Bootcamp's video on Teratogenic Medications.

39. D- This patient developed palpitations and heat intolerance after delivering a child. Exam findings are pertinent for tachycardia, palmar sweating, lid lag, enlarged, nontender thyroid, and increased DTRs. Labs reveal TSH suppression and elevated T4/T3. This is most likely due to postpartum thyroiditis, a subtype of subacute lymphocytic thyroiditis. This is due to follicular cell damage with lymphocytic infiltration, leading to the release of preformed thyroid hormone. The condition is typically self-limited, arising within a year of delivery.

40. F- This elderly male had developed dyspnea on exertion. Physical examination is unremarkable and no significant murmurs are heard on auscultation. This is most likely due to calcific aortic sclerosis (calcification and fibrosis if aortic valve leaflets) due to age-related valvular damage. This is the most common cause of aortic stenosis, affecting 1 out of 3 of those between the ages of 75 and 85. Symptoms (e.g. dyspnea on exertion, lightheadedness, dizziness) are caused by a relative inability to increase blood flow across the stenotic valve during periods of exertion. For additional information check out MedSchool Bootcamp's video on Aortic Stenosis.

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