Block 1 June 2022

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. For additional information check out
MedSchool Bootcamp's video on Physiologic Changes 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 (Bad, 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 doxazon (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. Fibromuscular dysplasia
is a common cause of renal artery stenosis, classically affected young women with distal renal
 arterial stenosis. 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.

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 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 these 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 hookworm
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, chilld with rigors,
and myaglias 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
filtrum, 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 relief 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 endemic-type Burkitt lymphoma due to
underlying EBV infection. The description of a rapidly enlarging neck mass with neoplastic
histopathologic results is a classic association for this form of lymphoma. For additional
information check out MedSchool Bootcamp's video on Burkitt Lymphoma.

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.