USMLE Step 1 USMLE Step 1 Practice Test 2025

The correct answer is (c) Radial nerve. The radial nerve runs in the spiral groove of the humerus at the midshaft level, making it vulnerable to injury in midshaft humeral fractures. Injury at this level causes wrist drop (inability to extend the wrist and fingers) and sensory loss over the posterior forearm and dorsum of the hand. The triceps reflex is intact because the branch to the triceps arises proximal to the spiral groove.

(a) Axillary nerve -- This nerve innervates the deltoid and teres minor and provides sensation to the lateral shoulder (regimental badge area). It is injured in surgical neck fractures of the humerus or anterior shoulder dislocations, not midshaft fractures.

(b) Musculocutaneous nerve -- This nerve innervates the anterior compartment of the arm (biceps brachii, brachialis, coracobrachialis) and provides sensation to the lateral forearm. Its injury would cause weakness in elbow flexion, not wrist drop.

(d) Median nerve -- This nerve innervates most forearm flexors and thenar muscles. Its injury causes loss of thumb opposition and sensory loss in the lateral palm, not wrist drop.

(e) Ulnar nerve -- This nerve innervates intrinsic hand muscles and provides sensation to the medial hand. It is most commonly injured at the medial epicondyle, not the midshaft of the humerus.

The correct answer is (b) Glucose-6-phosphatase. This presentation is classic for Von Gierke disease (glycogen storage disease type I), caused by deficiency of glucose-6-phosphatase. This enzyme catalyzes the final step of both glycogenolysis and gluconeogenesis -- the conversion of glucose-6-phosphate to free glucose. Its absence causes fasting hypoglycemia, hepatomegaly, lactic acidosis, and hyperuricemia. The glycogen structure is normal because it is synthesized correctly.

(a) Glycogen phosphorylase -- Deficiency causes McArdle disease (type V, muscle) or Hers disease (type VI, liver). Type VI presents with milder hepatomegaly and hypoglycemia but without the severe lactic acidosis and hyperuricemia.

(c) Branching enzyme -- Deficiency causes Andersen disease (type IV), presenting with hepatosplenomegaly, cirrhosis, and abnormal glycogen structure (long unbranched chains), not normal glycogen structure.

(d) Acid maltase (acid alpha-glucosidase) -- Deficiency causes Pompe disease (type II), presenting with cardiomegaly, hypotonia, and muscle weakness, not fasting hypoglycemia with lactic acidosis.

(e) Debranching enzyme -- Deficiency causes Cori disease (type III), which can mimic type I but typically shows milder lactic acidosis and has glycogen with abnormally short outer branches.

The correct answer is (d) Operating on the flat portion of a depressed Frank-Starling curve. This patient has heart failure with elevated filling pressures but a reduced cardiac output. In heart failure, the entire curve is shifted downward and flattened, so despite high preload (evidenced by elevated filling pressures), the cardiac output remains low. The patient is on the flat portion of this depressed curve.

(a) Operating on the ascending portion of a normal Frank-Starling curve -- This would describe a healthy heart with increasing preload leading to increasing cardiac output. The low cardiac output despite high filling pressures excludes this.

(b) Operating on the ascending portion of a depressed Frank-Starling curve -- If on the ascending portion, increasing preload would still produce meaningful increases in cardiac output. The very high filling pressures with persistently low output suggest the plateau has been reached.

(c) Operating on the flat portion of a normal Frank-Starling curve -- A normal heart achieves adequate cardiac output before reaching its plateau. This patient has both low output and high filling pressures, indicating a depressed curve.

(e) Operating on a curve shifted upward and to the left -- This indicates enhanced contractility, which would produce higher cardiac output at any given preload. This is the opposite of what is observed.

The correct answer is (c) Inhibition of angiotensin-converting enzyme (ACE). ACE inhibitors (e.g., lisinopril, enalapril) are first-line agents for hypertension in diabetic patients because they provide renoprotective effects. However, they can cause hyperkalemia (by reducing aldosterone secretion, which decreases potassium excretion) and can increase serum creatinine (by dilating the efferent arteriole of the glomerulus, reducing glomerular filtration pressure). These two side effects together are characteristic of ACE inhibitors or ARBs.

(a) Blockade of L-type calcium channels -- Calcium channel blockers (e.g., amlodipine) cause peripheral vasodilation but do not typically cause hyperkalemia or significant rises in creatinine.

(b) Blockade of beta-1 adrenergic receptors -- Beta-blockers (e.g., metoprolol) reduce heart rate and contractility. While they can mildly increase potassium, they do not cause the acute creatinine rise described.

(d) Inhibition of the Na-Cl symporter in the distal convoluted tubule -- Thiazide diuretics (e.g., hydrochlorothiazide) inhibit this transporter. They typically cause hypokalemia (not hyperkalemia).

(e) Antagonism of alpha-1 adrenergic receptors -- Alpha-1 blockers (e.g., prazosin) cause vasodilation and may cause orthostatic hypotension. They do not cause hyperkalemia or creatinine elevation.

The correct answer is (b) Squamous cell carcinoma. The histological findings of intercellular bridges (desmosomes visible between squamous cells) and keratin pearls (concentric laminations of keratin) are pathognomonic for squamous cell carcinoma. This type of lung cancer is strongly associated with smoking and typically arises centrally (hilar location), as described in this case.

(a) Adenocarcinoma -- The most common type of lung cancer overall, more common in non-smokers and women. Histologically shows glandular differentiation with mucin production, not keratin pearls. Typically presents as a peripheral lung mass.

(c) Small cell carcinoma -- A highly aggressive neuroendocrine tumor presenting as a central mass in smokers. Histologically shows small round blue cells with scant cytoplasm, nuclear molding, and a high mitotic rate.

(d) Large cell carcinoma -- A diagnosis of exclusion characterized by large, undifferentiated cells lacking the specific features of squamous, adenocarcinoma, or small cell carcinoma.

(e) Carcinoid tumor -- A low-grade neuroendocrine tumor presenting as a central endobronchial mass, often in younger patients. Shows uniform cells with a salt-and-pepper chromatin pattern.

The correct answer is (d) Escherichia coli O157:H7. This enterohemorrhagic E. coli (EHEC) strain is classically associated with consumption of undercooked ground beef. It produces Shiga-like toxins that damage intestinal epithelium (causing bloody diarrhea) and endothelial cells of small blood vessels (causing hemolytic-uremic syndrome, or HUS). Key features: non-sorbitol-fermenting colonies on MacConkey-sorbitol agar and the triad of HUS (microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure).

(a) Salmonella enteritidis -- Causes gastroenteritis from contaminated poultry or eggs. Does not typically cause HUS.

(b) Shigella dysenteriae -- While Shigella produces Shiga toxin and can rarely cause HUS, it does not grow as non-sorbitol-fermenting colonies. Transmission is typically person-to-person.

(c) Campylobacter jejuni -- Most common cause of bacterial diarrhea in the US, often from undercooked poultry. Grows on special media at 42 degrees C. Can trigger Guillain-Barre syndrome but not typically HUS.

(e) Clostridium difficile -- A gram-positive, spore-forming anaerobe causing pseudomembranous colitis typically following antibiotic use. Not associated with undercooked meat consumption or HUS.

The correct answer is (c) Type III (immune complex-mediated) hypersensitivity. This patient has hypersensitivity pneumonitis (farmer lung), caused by repeated inhalation of thermophilic actinomycetes spores from moldy hay. The 4-8 hour delay after exposure is characteristic of a type III reaction, in which preformed IgG antibodies bind inhaled antigens to form immune complexes that deposit in the alveolar walls, activate complement, recruit neutrophils, and cause inflammation.

(a) Type I (immediate) hypersensitivity -- Mediated by IgE antibodies bound to mast cells, causing immediate (within minutes) responses such as anaphylaxis or allergic asthma. The 6-hour delay and IgG precipitins exclude this.

(b) Type II (antibody-mediated cytotoxic) hypersensitivity -- Involves IgG or IgM antibodies directed against cell-surface antigens, leading to cell destruction (e.g., autoimmune hemolytic anemia). Does not explain pulmonary infiltrates from inhaled antigen.

(d) Type IV (delayed-type) hypersensitivity -- T-cell-mediated, typically manifesting 24-72 hours after antigen exposure. While chronic hypersensitivity pneumonitis may have a type IV component, the acute 4-8 hour presentation with IgG precipitins is primarily type III.

(e) Type V (stimulatory) hypersensitivity -- A subtype of type II in which antibodies stimulate rather than destroy target cells (e.g., Graves disease). Not relevant to this pulmonary presentation.

The correct answer is (b) 75%. Sensitivity is the ability of a test to correctly identify patients who have the disease (true positive rate). Sensitivity = True Positives / (True Positives + False Negatives) = 120 / (120 + 40) = 120 / 160 = 0.75 = 75%.

(a) 80% -- This is the positive predictive value (PPV), not sensitivity. PPV = TP / (TP + FP) = 120 / (120 + 30) = 120 / 150 = 80%.

(c) 86% -- This does not correspond to any standard test characteristic calculation from the given data.

(d) 96% -- This approximates the specificity. Specificity = TN / (TN + FP) = 810 / (810 + 30) = 810 / 840 = 96.4%.

(e) 67% -- This does not correspond to sensitivity, specificity, PPV, or NPV from the given data. The NPV = TN / (TN + FN) = 810 / (810 + 40) = 810 / 850 = 95.3%.

The correct answer is (a) Honor the patient wishes and provide comfort measures only. The principle of autonomy is the cornerstone of medical ethics. A competent adult patient has the right to refuse any medical treatment, including life-sustaining treatment. The psychiatric evaluation confirmed intact decision-making capacity. The durable power of attorney is only activated when the patient lacks decision-making capacity; since this patient is alert, oriented, and confirmed competent, his own wishes take precedence over those of his healthcare proxy.

(b) Follow the daughter wishes since she holds power of attorney -- The durable power of attorney is activated only when the patient cannot make decisions for himself. Since the patient retains capacity, his proxy authority is not yet in effect.

(c) Convene an ethics committee before making any changes -- This situation does not present an ethical dilemma. A competent patient refusal of treatment is well-established in medical ethics and law. Delaying action would violate the patient autonomy.

(d) Continue current treatment while arranging a second psychiatric opinion -- The patient has already been evaluated by a psychiatrist who found no impairment. Ordering additional evaluations to override a competent patient decision is paternalistic.

(e) Discharge the patient against medical advice -- The patient is requesting a change in goals of care to comfort care, not requesting discharge. Palliative care should be provided in the current setting.

The correct answer is (c) Autosomal recessive. Key features: (1) Both parents are unaffected carriers (confirmed by carrier testing), each carrying one copy of the recessive allele. (2) The disorder skips generations -- the maternal grandfather was affected, his daughter is an obligate carrier, and one grandchild is affected. (3) Both males and females are equally affected, excluding X-linked inheritance. (4) Unaffected parents producing an affected child is the hallmark of recessive inheritance (25% chance per offspring).

(a) Autosomal dominant -- In autosomal dominant inheritance, at least one parent of an affected individual must also be affected (assuming complete penetrance). Both parents are unaffected here.

(b) Autosomal dominant with incomplete penetrance -- While incomplete penetrance can cause apparently unaffected carriers, the confirmation that both parents carry a single allele without being affected is more consistent with recessive inheritance.

(d) X-linked recessive -- In X-linked recessive inheritance, the disorder predominantly affects males. This pedigree shows equal sex distribution of the disease.

(e) Mitochondrial inheritance -- Mitochondrial (maternal) inheritance would require all children of an affected mother to be affected. The mother is unaffected, and the pattern is not consistent with mitochondrial inheritance.