1
Q
A 53-year-old woman has brief episodes of vertigo lasting seconds, triggered by head movement. No tinnitus, hearing loss, gait issues, or neuro deficits. T1–T3 viscerosomatic reflex noted.
Which mechanism best explains her condition?
A. Accumulation of endolymph
B. Embolic-induced ischemia
C. CN VIII compression
D. Inflammation of the labyrinth
E. Otolith displacement
A
E — Otolith displacement
Diagnosis: Benign paroxysmal positional vertigo (BPPV)
Caused by dislodged otoliths (canaliths) in semicircular canal
Brief vertigo induced by head position changes (<20 sec)
No auditory symptoms
Positive Dix-Hallpike
2
Q
Which vertigo disorder is caused by endolymph accumulation and presents with vertigo + tinnitus + ear fullness?
A. Vestibular neuritis
B. BPPV
C. Ménière disease
D. Acoustic neuroma
E. Brainstem stroke
A
C — Ménière disease
Vertigo + tinnitus, hearing loss, ear fullness
Endolymphatic hydrops (↑ endolymph)
3
Q
A 28-year-old woman presents with episodic vertigo, nausea, vomiting, right ear fullness, tinnitus, and fluctuating hearing loss. Exam: tympanic membranes intact. Rinne: AC > BC. Weber: lateralizes to left ear. MRI normal. What is the most likely cause of her condition?
A. Acute suppurative inflammation
B. Excess cerumen
C. Hydropic dilation of the cochlea
D. Keratin-filled cyst of the middle ear
E. New bone formation around the stapes
A
Hydropic dilation of the cochlea
Diagnosis: Ménière disease
Episodic vertigo + sensorineural hearing loss + aural fullness + tinnitus
Pathophysiology: Excess endolymph (endolymphatic hydrops)
Rinne: AC > BC; Weber: lateralizes opposite affected ear
Imaging normal; ENT referral recommended
Management: low-sodium diet, diuretics, vestibular rehab
4
Q
A 24-year-old postpartum woman develops gradual bilateral hearing loss over 6 months. Exam: intact tympanic membranes, clear auditory canals. Family history: mother also had hearing loss. Rinne test: hears tuning fork longer on mastoid than in front of ear canal. What is the most likely diagnosis?
A. Benign paroxysmal positional vertigo
B. Cerumen impaction
C. Otosclerosis
D. Presbycusis
E. Vestibular schwannoma
A
C — Otosclerosis
Type of hearing loss: Bilateral conductive hearing loss
Inheritance: Autosomal dominant with incomplete penetrance
Typical onset: Late teens to 40s; often worsens during pregnancy
Pathophysiology: Stapes fixation at the oval window interferes with sound conduction
Rinne test: Bone conduction > air conduction (positive for conductive loss)
Otoscopic exam: Normal
Other notes: Presbycusis → sensorineural, age-related; BPPV → vertigo without hearing loss; vestibular schwannoma → usually unilateral sensorineural loss
5
Q
A patient experiences brief episodes of spinning vertigo lasting seconds to minutes, provoked by turning in bed or tilting the head backward. Symptoms include nausea and vomiting, but no hearing loss, tinnitus, or ear pain. What is the most likely diagnosis and underlying mechanism?
A
Benign paroxysmal positional vertigo (BPPV)
Mechanism: Dislodged calcium otoliths in the semicircular canal
Key features:
Recurrent vertiginous episodes triggered by head movements
Short duration (seconds to minutes)
Associated nausea/vomiting
No auditory symptoms (hearing loss, tinnitus, ear pain)
Treatment: Epley maneuver (canalith repositioning)
6
Q
A 24-year-old male presents with 36 hours of nausea, vomiting, dizziness, and a sensation of swaying after a recent upper respiratory infection. Exam shows left horizontal nystagmus suppressible with visual fixation, intact hearing, and no neurological deficits. Symptoms are slightly improving. What is the most appropriate next step in management?
Options:
A. CT scan of the brain
B. Electromyogram
C. MRI of the brain
D. Reassurance with symptomatic treatment
E. Video EEG
A
D. Reassurance with symptomatic treatment
Key Points:
Most likely diagnosis: Vestibular neuritis (postviral peripheral vestibular dysfunction)
Classic features:
Acute onset vertigo, nausea, vomiting
Preserved hearing (differentiates from labyrinthitis)
Horizontal, unidirectional nystagmus
Patient can still ambulate
Symptoms improve within 48 hours
Diagnosis: Clinical; no imaging needed if no red flags (neurological deficits, atypical nystagmus, cardiovascular risk factors)
Treatment: Supportive care, antiemetics, vestibular rehabilitation if needed
7
Q
A patient presents with sudden onset vertigo, nausea, vomiting 1–2 days after a viral upper respiratory infection. Hearing is intact, and neurological exam is otherwise normal. What is the most likely diagnosis?
A
Vestibular neuritis
Key Points:
Pathophysiology: Acute inflammation of the vestibular nerve (CN VIII), usually post-viral
Clinical features:
Severe vertigo lasting hours to days
Nausea and vomiting
No hearing loss (distinguishes from labyrinthitis)
Nystagmus: horizontal, unidirectional, suppressed by visual fixation
Ambulation: patient can usually walk, though unsteady
Diagnosis: Clinical; imaging not required unless atypical features
Treatment:
Supportive care (hydration, antiemetics, antihistamines)
Vestibular rehabilitation if symptoms persist
Symptoms usually improve within a few days
8
Q
A 200-participant sleep study monitors patients with EEG, EOG, and EMG. Two hours after falling asleep, one patient shows irregular, jerky, rapid conjugate eye movements on EOG. Which neurotransmitter change is responsible for this stage of sleep?
Options:
A. High dopamine levels
B. High melatonin levels
C. Increase in muscle tone
D. Rise in acetylcholine
E. Slow, high-amplitude EEG waves
A
D – Rise in acetylcholine
Key Points:
Stage: REM sleep
Biochemical changes:
↑ Acetylcholine → triggers REM sleep onset
↓ Norepinephrine
Polysomnography findings:
EEG: Low-voltage, mixed pattern, sawtooth waves (2–6 Hz)
EOG: Rapid, irregular, conjugate eye movements
EMG: Atonia of muscles (except diaphragm & extraocular)
Other notes:
REM sleep is associated with dreaming, memory consolidation, and cortical activation.
REM sleep behavior disorder is rare and occurs when muscle atonia fails.
Mnemonic: “Ach = Active Eyes in REM” → rise in acetylcholine triggers eye movements and cortical activity during REM.
9
Q
A 22-year-old male presents after a suicide attempt. He has intense, unstable relationships, frequent mood swings triggered by perceived slights, and angry outbursts. History includes childhood trauma. No psychosis or mania. Which long-term treatment is most appropriate?
Options:
A. Aripiprazole
B. Dialectical behavior therapy
C. Escitalopram
D. Exposure-based therapy
E. Lithium
A
B – Dialectical Behavior Therapy
Notes:
First-line psychotherapy for borderline personality disorder
Focuses on:
Emotion regulation
Distress tolerance
Interpersonal effectiveness
Mindfulness
Reduces self-harm, suicidal behavior, and hospitalizations
Medications are adjunctive, not primary treatment
10
Q
Which personality disorder is characterized by unstable relationships, impulsivity, mood swings, fear of abandonment, and recurrent self-harm?
Options:
A. Narcissistic PD
B. Borderline PD
C. Histrionic PD
D. Antisocial PD
E. Avoidant PD
A
B – Borderline Personality Disorder
Notes:
Key features: interpersonal instability, affective dysregulation, impulsivity, self-harm/suicidality, chronic emptiness
Often triggered by perceived abandonment
11
Q
During which sleep stage is a patient alert with beta waves on EEG?
Options:
A. Awake (eyes open)
B. Awake (eyes closed)
C. NREM 1
D. NREM 2
E. REM
A
A – Awake (eyes open)
Notes:
Clinical: alert and active
Disorders: insomnia, hypersomnolence
12
Q
A patient experiences light sleep with hypnic jerks. Theta waves are seen on EEG. Which sleep stage is this?
Options:
A. NREM 1
B. NREM 2
C. NREM 3
D. REM
E. Awake
A
Back:
✔ Answer: A – NREM 1
Notes:
Clinical: light sleep, hypnic jerks
Disorder association: OSA ↑ NREM 1 sleep length
13
Q
During which stage does 45–55% of total sleep occur with sleep spindles and K-complexes on EEG?
Options:
A. NREM 1
B. NREM 2
C. NREM 3
D. REM
E. Awake
A
B – NREM 2
Notes:
Disorders: bruxism (teeth grinding)
14
Q
Which sleep stage is deepest non-REM sleep with delta waves and is associated with sleepwalking, night terrors, and nocturnal enuresis?
Options:
A. NREM 1
B. NREM 2
C. NREM 3
D. REM
E. Awake
A
C – NREM 3
Notes:
Slow-wave sleep
NREM 3 ↓ with age
15
Q
Which EEG waveform is characteristic of deep slow-wave sleep (NREM 3)?
Options:
A. Alpha
B. Beta
C. Theta
D. Delta
E. Gamma
A
: D – Delta
16
Q
Which neurologic finding is classically associated with subfalcine herniation?
A. Downward gaze palsy
B. Ipsilateral pupil dilation
C. Mental status changes & return of primitive reflexes
D. Ataxia and dysmetria
A
C. Mental status changes & return of primitive reflexes
17
Q
Subfalcine herniation most commonly compresses which artery, risking ischemia?
A. Middle cerebral artery
B. Anterior cerebral artery
C. Posterior cerebral artery
D. Basilar artery
A
B. Anterior cerebral artery
18
Q
Which herniation type is most associated with uncal herniation, not subfalcine?
A. Compression of ACA
B. CN III palsy
C. Midline shift under falx cerebri
D. Leg weakness
A
B. CN III palsy
19
Q
Subfalcine herniation occurs when which brain structure herniates across the midline under the falx cerebri?
A. Uncus of temporal lobe
B. Cingulate gyrus
C. Cerebellar tonsil
D. Hippocampus
A
B. Cingulate gyrus
20
Q
Transcalvarial herniation most commonly occurs in which of the following situations?
A. Increased intracranial pressure leading to cerebellar tonsil displacement through the foramen magnum
B. Displacement of brain tissue through a skull defect following trauma or craniectomy
C. Herniation of the cingulate gyrus under the falx cerebri
D. Herniation of the medial temporal lobe past the tentorium causing CN III palsy
E. Elevated CSF volume due to brain atrophy without increased ICP
A
B. Displacement of brain tissue through a skull defect following trauma or craniectomy
Extra Info (Back of Card):
Transcalvarial herniations occur when portions of brain matter herniate through disruptions in the skull. They can present as sequelae of skull fractures as well as after craniectomies (removal of a portion of the skull to relieve intracranial pressure). Although a patient may have head trauma, transcalvarial herniation requires a skull defect.
21
Q
A 19-year-old man has 6 weeks of disorganized thoughts, auditory hallucinations when not intoxicated, social withdrawal, and decline in functioning. He skips classes to smoke marijuana but symptoms persist when sober. Which diagnosis is most likely?
A. Brief psychotic disorder
B. Marijuana addiction
C. Schizoaffective disorder
D. Schizophrenia
E. Schizophreniform disorder
A
E. Schizophreniform disorder
Extra Info (Back of Card):
Schizophreniform disorder presents with schizophrenia-like symptoms lasting ≥1 month but <6 months.
Brief psychotic disorder: <1 month
Schizophrenia: ≥6 months
Schizoaffective disorder: mood symptoms present for majority of illness + psychosis ≥2 weeks without mood symptoms
22
Q
A 35-year-old woman is started on doxepin for depression with insomnia. What is the mechanism of action of this medication?
A. Blocking dopamine receptors
B. Blocking serotonin and norepinephrine reuptake
C. Blocking the metabolic breakdown of dopamine
D. Blocking the metabolic breakdown of norepinephrine
E. Increasing serotonin reuptake
A
B. Blocking serotonin and norepinephrine reuptake
Extra Info (Back of Card):
TCAs (e.g., doxepin, amitriptyline, imipramine) inhibit NE & 5-HT reuptake
Side effects: anticholinergic, orthostatic hypotension, sedation, weight gain, cardiac arrhythmias (QT prolongation)
Useful for MDD with insomnia
23
Q
Q: A 40-year-old man presents with fatigue and trouble concentrating. He lives alone, avoids eye contact, has monotonous speech, shows little emotional expression, and is indifferent to criticism from his sister about his messy apartment. He prefers solitary work and social isolation and is only superficially engaged in conversation. Which feature is most consistent with the likely diagnosis?
A. Enjoyment of a small number of activities
B. Envious of others or believes others are envious of him
C. Excessive conscientiousness and scrupulousness about morals and ethics
D. Excessive involvement in pleasurable activities that are high risk
E. Excessive social anxiety
A
A. Enjoyment of a small number of activities
24
Q
A 42-year-old woman reports difficulty with intimate relationships but is actively seeking companionship. She wishes to volunteer at her church but feels out of place and has low self-esteem. She desires social interaction but avoids it due to fears of inadequacy. Which of the following is another characteristic seen with this disorder?
A. Distrust of others
B. Unstable self-image
C. Fear of rejection
D. Fear of social situations
E. Wants to be taken care of
A
C. Fear of rejection
Key Facts (Back of Card)
Diagnosis: Avoidant Personality Disorder
Core traits:
Social inhibition
Feelings of inadequacy
Fear of rejection & criticism
Strong desire for relationships (vs schizoid = no desire)
Differentiation:
A (Distrust): Paranoid PD
B (Unstable self-image): Borderline PD
D (Fear of social situations): Social anxiety, but avoidant PD also fears rejection — chronic & personality-based
E (Wants to be taken care of): Dependent PD
25
: A 20-year-old female presents with altered mental status and seizures after suspected overdose. Vitals show fever, hypotension, and tachycardia. Exam reveals dilated pupils, poor gag reflex, and withdrawal to pain. ECG shows widened QRS. Which medication is most likely responsible?
A. Alprazolam
B. Amitriptyline
C. Amlodipine
D. Fluoxetine
E. Sertraline
B. Amitriptyline
26
A 44-year-old woman reports heat intolerance, hair thinning, and unintentional 12-lb weight loss over 2 months. She thinks she is entering menopause. Which lab finding is most likely?
A. Antinuclear antibodies
B. Autoantibodies to thyroid peroxidase
C. Autoantibodies to TSH receptor
D. Elevated TSH level
E. Elevated TRH level
C. Autoantibodies to TSH receptor
Key Points (Back of Card)
Diagnosis: Graves disease (most common cause of hyperthyroidism)
Key lab: TSH receptor-stimulating antibodies
Symptoms: heat intolerance, weight loss, hair thinning, tremor, palpitations, diarrhea
Mechanism: antibodies stimulate TSH receptor → ↑T3/T4, ↓TSH
Treatment: beta-blockers + antithyroid meds / radioactive iodine / surgery
27
A 74-year-old woman presents with chronic crusting and ulceration of the left nipple and a palpable subareolar mass. Symptoms have been present for months and did not respond to lotion. What is the most likely diagnosis?
A. Inflammatory carcinoma
B. Intraductal papilloma
C. Invasive ductal carcinoma
D. Invasive lobular carcinoma
E. Squamous cell skin cancer
C. Invasive ductal carcinoma
Key Points (Back of Card)
Paget disease of the breast = chronic eczematous nipple changes + underlying malignancy
Strongly associated with invasive ductal carcinoma or DCIS (~90%)
Presentation: nipple crusting, scaling, itching, ulceration; may have palpable mass
Histology: Paget cells (malignant intraepithelial adenocarcinoma cells in epidermis)
Workup: mammography ± ultrasound
28
An 8-year-old girl with sickle cell disease presents with fever and worsening leg pain despite cefazolin. X-ray shows periosteal reaction and cortical irregularity consistent with osteomyelitis. Which organism is most likely responsible?
A. Neisseria gonorrhoeae
B. Pasteurella multocida
C. Pseudomonas aeruginosa
D. Salmonella enteritidis
E. Streptococcus pyogenes
D. Salmonella enteritidis
Back of Card – Key Facts
Sickle cell disease → functional asplenia → ↑ risk osteomyelitis
Most common organisms:
Salmonella spp. (classically)
Staph aureus (still common!)
Failure to improve on cefazolin → think Salmonella (Gram-negative)
X-ray: periosteal elevation, cortical irregularity, demineralization
Treatment: Fluoroquinolone (e.g., ciprofloxacin) + anti-Staph coverage
29
A 20-year-old woman presents with right-sided weakness for 1 week. She had prior transient gait difficulty. History of migraines. Family history of SLE. Exam shows 3/5 strength in right upper extremity and 4/5 in right lower. Which CSF finding is most likely?
A. Acetylcholine receptor antibodies in plasma
B. Elevated 14-3-3 protein in CSF
C. Increased immunoglobulins in CSF
D. Increased white blood cells in CSF
E. Xanthochromia in CSF
C. Increased immunoglobulins in CSF
Back of Card – Key Facts
Presentation suggests multiple sclerosis
Young woman
Neurologic symptoms separated in time and space
Prior episode (gait issues), now focal weakness
CSF in MS
↑ Ig (oligoclonal bands)
Other options:
A → Myasthenia gravis
B → Creutzfeldt-Jakob disease
D → Infection/meningitis
E → Subarachnoid hemorrhage
30
A 25-year-old man presents with recurrent, severe headaches occurring daily for 6 weeks. Pain lasts 30 minutes, described as stabbing in the left eye. During attacks he paces and cannot rest. Simple analgesics ineffective. Similar episode years ago lasting 3 months. Exam normal.
Which additional history finding is most consistent with the diagnosis?
A. Early morning vomiting
B. Heavy caffeine consumption
C. Nasal congestion on side of pain
D. Snoring with nonrestorative sleep
E. Visual aura before onset of pain
C. Nasal congestion on side of painCluster headache
Recurrent, severe, unilateral periorbital pain
Short duration (15–180 minutes)
Daily for weeks → cluster period
Pacing/agitation during attacks (vs lying still in migraine)
Associated autonomic symptoms on pain side:
Nasal congestion
Lacrimation
Rhinorrhea
Ptosis
Conjunctival injection
Other choices:
31
An 8-year-old girl has frequent daily episodes of “spacing out” with no recollection. Prior trial of ethosuximide was ineffective and poorly tolerated.
What is the most appropriate next treatment?
A. Carbamazepine
B. Diazepam
C. Levetiracetam
D. Topiramate
E. Valproic acid
E. Valproic acid
Back (Explanation)
Absence seizures
Frequent brief staring spells (3–20 sec)
No postictal confusion
Occur many times daily
First-line treatment: ethosuximide
If ethosuximide is ineffective or not tolerated → valproic acid
Why others are wrong
Carbamazepine → can worsen absence seizures
Diazepam → for acute seizures, not chronic absence
Levetiracetam → broad-spectrum but not first- or second-line for absence
Topiramate → not for absence seizures
Mnemonic:
Absence = E.T. first (Ethosuximide → if fails, Valproic Acid)
32
A 35-year-old woman presents with headaches, diarrhea, mental fogginess, and a rash. She has a history of alcohol use disorder, rheumatoid arthritis, and is significantly underweight.
Which nutritional deficiency is most likely?
A. Folate
B. Iron
C. Niacin
D. Riboflavin
E. Zinc
C. Niacin
Back (Explanation)
Pellagra (niacin deficiency) is characterized by the 3 D's + 1:
Dermatitis: photosensitive, often on hands, neck, face
Diarrhea: gastrointestinal symptoms
Dementia: mental confusion, irritability
Death: if untreated
Risk factors:
Alcoholism → poor dietary intake and impaired absorption
Malnutrition / underweight
Chronic diseases increasing nutritional needs
Why others are less likely:
Folate → megaloblastic anemia, fatigue, glossitis, not classically dermatitis + diarrhea + dementia
Iron → microcytic anemia, pallor, fatigue
Riboflavin → cheilitis, glossitis, eye symptoms
Zinc → dermatitis, alopecia, diarrhea, impaired wound healing (can overlap but mental changes are less prominent)
Mnemonic:
“Diarrhea, Dermatitis, Dementia – remember Niacin!”
33
A 53-year-old female presents with recurrent, sudden, sharp pain on the left side of her face, under the eye and along the side of the nose. Episodes last 10–15 seconds, occur multiple times per day, and can be triggered by light touch or a breeze. She has no visible lesions. She had a similar problem in the past that responded to medication, but she cannot recall the name.
What is the first-line medication for her condition?
A. Acetaminophen
B. Carbamazepine
C. Gabapentin
D. Meloxicam
E. Oxycodone
B. Carbamazepine
Back (Explanation)
Diagnosis: Trigeminal neuralgia (TN)
Presentation: Sudden, unilateral, brief, stabbing pain along one or more branches of the trigeminal nerve (V1–V3)
Triggers: Light touch, chewing, talking, breeze
Physical exam: Usually normal between episodes, no lesions
First-line treatment:
Carbamazepine or oxcarbazepine
Mechanism: Sodium channel blocker, reduces hyperexcitability of trigeminal nerve fibers
Other options:
Gabapentin: Second-line or adjunct therapy
Acetaminophen, NSAIDs (meloxicam), opioids: Not effective for trigeminal neuralgia
Takeaway:
Carbamazepine is highly effective for TN and is the first-line therapy for acute and chronic management.
34
A 55-year-old female with hyperlipidemia is on simvastatin and amlodipine. She is prescribed a new medication to lower cholesterol. Shortly afterward, she experiences facial flushing and a pruritic rash on her torso and upper extremities.
Which mechanism of action most likely explains the lipid-lowering effects of this medication?
A. Blocking reabsorption of bile acids by the intestines
B. Blocking reabsorption of cholesterol by the intestines
C. Decreasing hepatic synthesis of very-low-density lipoprotein (VLDL)
D. Increasing lipoprotein lipase
E. Inhibiting HMG-CoA reductase
C. Decreasing hepatic synthesis of VLDL
Back (Explanation)
Diagnosis: Niacin (Vitamin B3) toxicity
Mechanism of action:
Decreases hepatic synthesis of VLDL → reduces secretion of VLDL into circulation
Inhibits lipolysis in adipose tissue → less free fatty acids for VLDL production
Result: ↓ LDL, ↓ triglycerides, ↑ HDL (most potent HDL-raising agent)
Adverse effects:
Cutaneous flushing and pruritus (face, neck, torso, arms) – mediated by prostaglandins
Hyperglycemia
Hyperuricemia
Flushing can be reduced with aspirin or NSAIDs prior to dosing
Other lipid-lowering mechanisms (for comparison):
A: Bile acid sequestrants (eg, cholestyramine) → bind bile acids in gut
B: Ezetimibe → inhibits intestinal cholesterol absorption
D: Fibrates → activate lipoprotein lipase
E: Statins → inhibit HMG-CoA reductase
Takeaway: Niacin is rarely used clinically today but is important for exam recognition, especially due to flushing.
35
Which of the following is a primary effect of parathyroid hormone (PTH) on the kidney?
A. Increases phosphate reabsorption in the proximal tubule
B. Decreases calcium reabsorption in the distal convoluted tubule
C. Inhibits phosphate reabsorption in the proximal tubule and promotes calcium reabsorption in the distal convoluted tubule
D. Increases calcium excretion in the urine
E. Inhibits calcitriol production
C. Inhibits phosphate reabsorption in the proximal tubule and promotes calcium reabsorption in the distal convoluted tubuleKey points about PTH:
Produced by chief cells of the parathyroid glands
Released in response to low serum calcium
Kidney effects:
Proximal tubule: inhibits phosphate reabsorption → phosphaturia
Distal convoluted tubule: promotes calcium reabsorption → reduces calcium excretion
Other actions:
Stimulates osteoclast activity indirectly → bone resorption → ↑ serum calcium
Increases 1,25-dihydroxyvitamin D production in kidney → ↑ intestinal calcium absorption
Takeaway: PTH primarily raises blood calcium while lowering phosphate reabsorption in the kidney.
36
A 51-year-old man with a history of mild myopia notices gradual improvement in his distance vision over the past year and rarely needs glasses. Visual acuity at 20 feet is 20/30 in both eyes without corrective lenses. Eye exam is otherwise normal.
What is the most likely underlying cause of this improvement?
A. Age-related demyelination
B. Blood vessel proliferation
C. Loss of lens elasticity
D. Microvascular ischemia
E. Trabecular meshwork obstruction
C. Loss of lens elasticity
Explanation:
This patient’s improved distance vision is due to age-related loss of lens elasticity (presbyopia).
Mechanism:
With age, denaturation of lens proteins and altered curvature reduces lens flexibility.
Normally, the ciliary muscles relax and contract the zonules to allow the lens to accommodate for near vision.
In presbyopia, the lens cannot properly change shape, making near vision difficult.
Patients with mild myopia may notice improved distance vision as the fixed lens curvature shifts the focal point closer to the retina for far objects.
Other options:
Age-related demyelination → affects neural conduction, not refraction.
Blood vessel proliferation → retinal disease (e.g., diabetic retinopathy).
Microvascular ischemia → retinal ischemia; causes vision loss.
Trabecular meshwork obstruction → glaucoma; causes vision loss.
Key Point: Presbyopia can paradoxically improve distance vision in mild myopia.
37
A 70-year-old woman presents with sudden onset dyspnea and right-sided pleuritic chest pain 5 days after right total knee arthroplasty. She missed 2 doses of rivaroxaban postoperatively. Vital signs show tachycardia and hypoxemia. Pulmonary exam reveals decreased breath sounds at the right lung base. D-dimer is elevated, and CT pulmonary angiogram shows a filling defect in the right lower lobe pulmonary artery.
This patient’s clinical picture is most likely due to an increase in:
A. Alveolar fluid accumulation
B. Airway resistance
C. Physiologic dead space
D. Pulmonary vascular resistance
E. Right-to-left shunting
C. Physiologic dead space
Explanation:
The patient has an acute pulmonary embolism (PE), evidenced by:
Recent orthopedic surgery (major risk factor)
Acute pleuritic chest pain and dyspnea
Hypoxemia and tachycardia
CT pulmonary angiogram showing filling defect
Pathophysiology:
Pulmonary artery occlusion by an embolus reduces perfusion to ventilated alveoli.
Ventilation continues but perfusion is absent → high V/Q ratio → physiologic dead space.
Other options:
Alveolar fluid accumulation → seen in pulmonary edema, ARDS.
Airway resistance → asthma or COPD.
Pulmonary vascular resistance → can increase in chronic pulmonary hypertension; acute PE mainly causes dead space.
Right-to-left shunting → causes hypoxemia refractory to oxygen, not typical in PE.
Key Point: In PE, ventilation is preserved but perfusion is blocked, leading to wasted ventilation (increased physiologic dead space).
38
A 14-year-old boy presents with acute onset diffuse abdominal pain that migrated to the right lower quadrant, intractable vomiting, and fever. Examination shows rebound tenderness, rigidity, and guarding. Labs reveal mild leukocytosis.
Which organism is most commonly associated with this condition?
A. Bacteroides fragilis
B. Campylobacter jejuni
C. Clostridioides difficile
D. Helicobacter pylori
E. Staphylococcus aureus
A. Bacteroides fragilis
Explanation:
The patient has acute appendicitis, suggested by:
Periumbilical pain migrating to the right lower quadrant (McBurney point)
Nausea, vomiting, and fever
Signs of peritonitis (guarding, rigidity, rebound)
Pathophysiology:
Usually caused by luminal obstruction (fecalith, lymphoid hyperplasia, seeds, parasites, neoplasm)
Obstruction → stasis → bacterial overgrowth → inflammation → possible perforation
Microbiology:
Appendiceal infections are polymicrobial
Most common bacteria: Bacteroides fragilis (anaerobe) and Escherichia coli (facultative anaerobe)
Management:
Appendectomy (surgical removal)
Broad-spectrum antibiotics covering Gram-negative and anaerobic organisms
Key Point: In acute appendicitis, Bacteroides fragilis is a primary pathogen in perforated or complicated cases.
39
A 34-year-old woman presents with a 6-month history of worsening shortness of breath. Vital signs: BP 130/85 mmHg, HR 90/min. Exam reveals wheezing on forced exhalation. FEV1 is reduced by 20%. Allergy testing is negative.
Which mechanism of action corresponds to the most appropriate initial treatment?
A. Blockade of beta1-adrenergic receptors
B. Blockade of histamine H1 receptors
C. Stimulation of alpha1-adrenergic receptors
D. Stimulation of beta2-adrenergic receptors
E. Stimulation of muscarinic M3 receptors
D. Stimulation of beta2-adrenergic receptors
Explanation:
The patient likely has asthma, suggested by:
Wheezing on exhalation
Reduced FEV1 (airflow obstruction)
Chronic shortness of breath
Pathophysiology:
Asthma → airway inflammation, mucus accumulation, and bronchial smooth muscle constriction
Mechanism of initial treatment:
Beta2-adrenergic receptor agonists (e.g., albuterol) stimulate receptors on bronchial smooth muscle → bronchodilation
Other options:
A (beta1 blockade): Affects heart rate, not bronchodilation
B (H1 blockade): Not effective in non-allergic asthma
C (alpha1 stimulation): Causes nasal vasoconstriction, not bronchodilation
E (M3 stimulation): Causes bronchoconstriction; M3 antagonists relieve symptoms instead
Key Point: Short-acting beta2 agonists are the first-line treatment for acute bronchoconstriction in asthma.
40
A 70-year-old woman with colorectal cancer receives her first cycle of paclitaxel. Two weeks later, she complains of hair loss, noting clumps of hair falling out when brushing or washing. Scalp examination shows diffuse thinning across the vertex and crown.
What is the most likely mechanism of her hair loss?
A. Cell-mediated autoimmune destruction
B. Disruption of follicular keratinocyte proliferation
C. Impaired formation of the mitotic spindle
D. Impaired transition to the catagen phase of hair growth
E. Widespread transition to the telogen phase of hair growth
B. Disruption of follicular keratinocyte proliferation
Anagen: Active growth; most follicles are in this phase → targeted by chemotherapy
Catagen: Transition; hair growth stops
Telogen: Resting; hair sheds naturally
Clinical course: Hair loss is usually diffuse, occurs 1–3 weeks after chemotherapy, and is typically reversible after treatment ends.
Key Point: Chemotherapy-induced hair loss is primarily due to direct cytotoxic effects on proliferating follicular keratinocytes.
41
Front (Question)
A 3-year-old boy presents with:
Constant involuntary contraction of skeletal muscles
Cleft palate
Oral Candida albicans overgrowth
Hypocalcemia
Absent thymus on chest radiograph
Which congenital cardiac abnormality is most likely in this patient?
A. Persistent truncus arteriosus
B. Pulmonary atresia
C. Total anomalous pulmonary venous return
D. Transposition of the great vessels
E. Tricuspid atresia
A. Persistent truncus arteriosus
Explanation:
This patient has DiGeorge syndrome (22q11.2 deletion), caused by defective development of the third and fourth pharyngeal pouches.
Classic features include:
C: Cleft palate
H: Hypocalcemia (parathyroid hypoplasia)
A: Abnormal facies
T: Thymic hypoplasia → immunodeficiency (recurrent viral/fungal infections)
C: Conotruncal cardiac defects
Most common cardiac defect in DiGeorge syndrome:
Persistent truncus arteriosus
Others include interrupted aortic arch, tetralogy of Fallot, vascular rings, atrial/ventricular septal defects.
Pathophysiology: Absence of thymus → T-cell deficiency → immunocompromised → Candida infections. Hypocalcemia due to absent parathyroids.
Key point: In a child with hypocalcemia, absent thymus, and conotruncal heart defect, think DiGeorge syndrome; the most frequent associated heart defect is persistent truncus arteriosus.
42
How does TSST-1 activate the immune system?
A. ADP-ribosylation of G proteins
B. Binding to MHC-II and T-cell receptors simultaneously, activating T cells to release IFN-γ and IL-2
C. Inhibition of acetylcholine release
D. Direct activation of B cells to release antibodies
E. Stimulation of neutrophil chemotaxis only
B. Binding to MHC-II and T-cell receptors simultaneously, activating T cells to release IFN-γ and IL-2
43
A 65-year-old woman presents with morning stiffness lasting over 1 hour, fatigue, and occasional fevers. She reports pain when trying to grasp objects and has a deformity of her left little finger that has been present for the past year. Osteopathic manipulative treatment is considered, but the physician avoids cervical HVLA techniques due to concern for joint instability.
Which of the following is the most likely cause of her finger deformity?
A. a mixed inflammatory infiltrate within a hyperplastic synovium
B. a reduction of bone mass without joint involvement
C. eroded cartilage with little inflammation, plus osteophyte formation
D. failure of normal bone resorption
E. uric acid deposition within the joints
A
Explanation:
This patient has classic features of rheumatoid arthritis (RA):
Morning stiffness >1 hour
Symmetric small joint involvement (hands, MCPs, PIPs)
Systemic symptoms (fatigue, low-grade fevers)
Joint deformities (e.g., ulnar deviation, swan-neck, boutonnière)
Pathophysiology of Deformity in RA:
Chronic autoimmune inflammation of the synovium leads to pannus formation, a hyperplastic synovial tissue infiltrated by T cells, B cells, plasma cells, and macrophages.
Pannus erodes cartilage and bone, causing joint deformities and instability.
Cervical spine involvement (especially atlantoaxial subluxation) can make HVLA techniques dangerous.
Other Options:
B. Osteoporosis: Reduction in bone mass, but no joint inflammation or deformity.
C. Osteoarthritis: Degenerative; features include osteophytes, joint space narrowing, and minimal inflammation. Morning stiffness is usually <30 minutes, and deformities are Heberden’s (DIP) and Bouchard’s (PIP) nodes.
D. Osteopetrosis: Failure of bone resorption; bones are dense and brittle, not inflamed.
E. Gout: Deposition of monosodium urate crystals, causing acute, intermittent attacks, often at the MTP of the big toe, not symmetric hand involvement.
High-Yield USMLE Points:
RA → MCP, PIP, not DIP (OA affects DIP)
Systemic symptoms + positive inflammatory markers (ESR, CRP)
Morning stiffness >1 hour is typical
Anti-CCP antibodies are highly specific
44
A 10-year-old boy presents with nocturnal cough and exercise-induced wheezing, especially in cold air. He has a history of atopic dermatitis and seasonal allergies. Vital signs are normal. Examination reveals diffuse expiratory wheezing, T4–T5 paraspinal hypertonicity, scalene hypertonicity, and a restricted right diaphragm.
In addition to a short-acting drug, which of the following is appropriate for chronic management of asthma and allergic symptoms?
A. albuterol
B. diphenhydramine
C. ipratropium
D. montelukast
E. theophylline
D – Montelukast
Explanation:
This patient likely has mild persistent asthma characterized by:
Nocturnal symptoms
Exercise-induced symptoms
History of atopy (eczema, seasonal allergies)
Chronic Management:
Montelukast (leukotriene receptor antagonist):
Reduces airway inflammation and bronchoconstriction
Particularly effective in allergic asthma and exercise-induced bronchospasm
Other Medications:
A. Albuterol: Short-acting β2 agonist (SABA); rescue therapy only
B. Diphenhydramine: Antihistamine; treats allergic symptoms, not first-line for asthma control
C. Ipratropium: Short-acting muscarinic antagonist; mainly for acute exacerbations, often in ER
E. Theophylline: Oral methylxanthine; rarely used in children due to narrow therapeutic window and side effects
High-Yield USMLE Points:
Persistent asthma in children is treated with daily controller medications: inhaled corticosteroids are first-line, but leukotriene antagonists like montelukast are appropriate for mild cases.
SABAs are for rescue only.
Atopic history increases likelihood of allergic asthma.
45
A 25-year-old woman presents with diplopia that began several weeks ago. She reports intermittent bladder incontinence, fatigue, and a history of optic neuritis 5 years ago. Diplopia occurs with extraocular movements but she denies ptosis or vision loss. Symptoms worsen with heat.
On examination, pupils are equal and reactive; no afferent pupillary defect is noted.
What is the most likely abnormal finding on examination?
A. Fasciculations
B. Hyporeflexia
C. Hypotonia
D. Right eye appears inferior and laterally deviated
E. Right eye does not move past midline when attempting left gaze
E – Right eye does not move past midline when attempting left gaze
Explanation:
This patient has multiple sclerosis (MS) presenting with internuclear ophthalmoplegia (INO). Key features:
Age 20–40, female
History of optic neuritis
Diplopia with extraocular movements
Uhthoff phenomenon: symptoms worsened with heat
CNS demyelinating lesions in different locations over time
Internuclear Ophthalmoplegia (INO):
Caused by a lesion in the medial longitudinal fasciculus (MLF)
Characterized by:
Impaired adduction of the ipsilateral eye
Nystagmus of the abducting contralateral eye
Example: Right MLF lesion → Right eye cannot adduct when looking left; left eye abducts with nystagmus
Other options:
A. Fasciculations: Seen in LMN lesions like ALS
B. Hyporeflexia: LMN; MS is UMN
C. Hypotonia: LMN; MS usually has spasticity
D. Right eye inferior/lateral deviation: Suggestive of oculomotor nerve palsy, not INO
High-Yield Points:
Diplopia + history of optic neuritis + Uhthoff phenomenon → think MS
INO is a classic localizing sign to the MLF in the brainstem
46
A 35-year-old woman presents preoperatively for a cholecystectomy with nausea, lethargy, and multiple joint and muscle pains for several weeks. Physical exam reveals hyperpigmentation of axillae and buccal mucosa. Labs show low aldosterone.
Which of the following medications could worsen her underlying condition?
A. Cranial osteopathic manipulative treatment (OMT)
B. Etomidate
C. Hydrocortisone
D. Ketamine
E. Thiopental
B – Etomidate
Explanation:
Patient has Addison disease (primary adrenal insufficiency):
Features: fatigue, nausea, hypotension, myalgias/arthralgias, hyperpigmentation
Labs: low aldosterone, low cortisol
Etomidate:
Induction agent for anesthesia
Inhibits 11β-hydroxylase, blocking conversion of 11-deoxycortisol → cortisol
Even a single dose can worsen adrenal insufficiency and precipitate an Addisonian crisis, especially under surgical stress
Other options:
A. Cranial OMT: Safe; may relieve musculoskeletal pain
C. Hydrocortisone: Treatment, not harmful
D. Ketamine: Sympathomimetic; does not impair cortisol
E. Thiopental: GABAergic; no direct effect on adrenal function
High-Yield:
Avoid etomidate in patients with primary adrenal insufficiency.
Hyperpigmentation differentiates primary from secondary adrenal insufficiency (secondary → ACTH low → no hyperpigmentation).
47
A 35-year-old woman with Addison disease presents with diffuse joint pain and hyperpigmentation. What lab finding supports primary adrenal insufficiency?
A. High cortisol, low ACTH
B. Low cortisol, high ACTH
C. Low cortisol, low ACTH
D. High aldosterone, low renin
B – Low cortisol, high ACTH
Explanation:
Primary adrenal insufficiency (Addison disease):
Adrenal glands fail → low cortisol & aldosterone
Pituitary responds → high ACTH, which also causes hyperpigmentation
Secondary/tertiary adrenal insufficiency:
ACTH low → no hyperpigmentation
High aldosterone: Seen in secondary/tertiary adrenal insufficiency only
48
A 63-year-old female is brought to the emergency department after a minor motor vehicle accident. She reports 2 prior near collisions under similar circumstances. She has a history of asthma, chronic back pain, headaches, and cervical fusion surgery 2 years ago.
Vital signs: T 36.8°C, BP 112/74 mmHg, HR 94, RR 18.
Neurologic examination: pupils 4 mm and reactive, intact extraocular movements, markedly decreased peripheral vision bilaterally, motor strength 5/5, deep tendon reflexes normal. Osteopathic exam: lumbar paraspinal tenderness.
Question: Hyperplasia of which pituitary cell type is most likely in this patient?
A. Corticotroph
B. Gonadotroph
C. Lactotroph
D. Somatotroph
E. Thyrotroph
C – Lactotroph
Explanation:
The patient presents with bitemporal hemianopsia (loss of lateral visual fields bilaterally), a classic sign of optic chiasm compression.
In postmenopausal women, the most common functioning pituitary adenoma is a prolactinoma, caused by lactotroph hyperplasia.
Clinical presentation:
Premenopausal women: amenorrhea, galactorrhea, infertility
Postmenopausal women: headache, visual field deficits (bitemporal hemianopsia), due to mass effect
Other pituitary adenomas:
Corticotroph: ACTH → Cushing disease; presents with weight gain, striae, hyperpigmentation
Gonadotroph: FSH/LH; usually nonfunctioning; may cause mass effect but rarely hypersecretory symptoms
Somatotroph: GH → acromegaly; enlarged hands, jaw, coarsened facial features
Thyrotroph: TSH → hyperthyroidism; rare
Key Point:
Pituitary macroadenomas (>1 cm) in postmenopausal women often present with mass effect (headache, visual field deficits) rather than hormonal hyperfunction.
Bitemporal hemianopsia is the hallmark finding for optic chiasm compression from a pituitary mass.
Osteopathic pearl:
Spinal somatic dysfunction (lumbar paraspinal hypertonicity) may be found in patients with chronic pain but is not directly related to pituitary pathology.
49
A 28-year-old female with a history of bulimia nervosa and chronic smoking presents for follow-up. She has previously failed nicotine gum and patches. She wants to quit smoking and is a good candidate for pharmacotherapy.
Which of the following best describes the mechanism of action of the drug most likely to be prescribed to her?
A. Acetylcholine receptor antagonist
B. Inhibits reuptake of norepinephrine and dopamine
C. Muscarinic receptor agonist
D. Partial agonist at opiate receptors
E. Partial agonist of nicotinic acetylcholine receptors
E – Partial agonist of nicotinic acetylcholine receptors
Explanation:
This patient has failed first-line nicotine replacement therapy and is a candidate for varenicline, a pharmacologic agent for smoking cessation.
Mechanism of action:
Varenicline is a partial agonist at α4β2 nicotinic acetylcholine receptors in the CNS.
It stimulates moderate dopamine release, reducing withdrawal symptoms.
It blocks nicotine from binding, reducing the rewarding effects of smoking.
Other options:
A. Acetylcholine receptor antagonist: e.g., mecamylamine (rarely used for smoking cessation)
B. Inhibits reuptake of norepinephrine and dopamine: e.g., bupropion, another first-line therapy for smoking cessation (good alternative if varenicline not tolerated)
C. Muscarinic receptor agonist: unrelated to smoking cessation
D. Partial agonist at opiate receptors: e.g., buprenorphine (used in opioid use disorder)
Key Points:
First-line pharmacotherapy for smoking cessation: nicotine replacement, varenicline, or bupropion.
Varenicline is particularly effective in patients who have failed nicotine replacement previously.
Side effects: nausea, vivid dreams, sleep disturbances, and rare neuropsychiatric symptoms.
50
A 28-year-old female wants to quit smoking. She has previously tried nicotine gum and patches without success. Which of the following drugs acts as a partial agonist at nicotinic acetylcholine receptors, reducing nicotine cravings while blocking the rewarding effects of smoking?
A. Bupropion
B. Varenicline
C. Mecamylamine
D. Nicotine patch
E. Clonidine
B – Varenicline
Explanation:
Varenicline is a partial agonist at α4β2 nicotinic acetylcholine receptors.
Mechanism:
Stimulates moderate dopamine release → reduces withdrawal
Blocks nicotine binding → reduces pleasure from smoking
First-line therapy, especially for patients who fail nicotine replacement.
Side effects: nausea, vivid dreams, rare neuropsychiatric symptoms.
51
A 35-year-old male is trying to quit smoking. He chooses a medication that inhibits the reuptake of norepinephrine and dopamine, which helps reduce nicotine cravings and withdrawal symptoms. Which drug does this describe?
A. Varenicline
B. Nicotine gum
C. Bupropion
D. Mecamylamine
E. Clonidine
C – Bupropion
Explanation:
Bupropion is an atypical antidepressant used for smoking cessation.
Mechanism: inhibits norepinephrine and dopamine reuptake, reducing cravings and withdrawal symptoms.
Also beneficial in patients with depression.
Side effects: insomnia, dry mouth, rare risk of seizures.
Can be combined with NRT or varenicline if needed.
52
A 60-year-old woman with type II diabetes mellitus on metformin presents for a routine check-up. Her blood pressure is 150/90 mmHg, consistent with previous readings. Urinalysis reveals 2+ proteinuria. Which of the following is the most appropriate medication to initiate at this time?
A. Beta-adrenergic receptor antagonist
B. Alpha1-adrenergic receptor antagonist
C. Captopril
D. Furosemide
E. Hydrochlorothiazide
C – Captopril
Explanation:
This patient has hypertension with proteinuria in the setting of type II diabetes, suggesting diabetic nephropathy.
ACE inhibitors (like captopril) are first-line therapy because they:
Reduce intraglomerular pressure → decrease proteinuria
Slow progression of diabetic kidney disease
Lower blood pressure
Mechanism: Inhibit conversion of angiotensin I → angiotensin II, causing efferent arteriole dilation and reduced glomerular filtration pressure.
Other antihypertensives (beta-blockers, diuretics) can lower blood pressure but do not provide renal protection in proteinuric diabetic patients.
Monitor: serum creatinine and potassium after initiation.
High-Yield Point:
Any diabetic patient with proteinuria should have an ACE inhibitor or ARB, regardless of baseline blood pressure, for renal protection.
53
A 56-year-old woman with heart failure and a sulfonamide allergy needs a loop diuretic. Which is the safest choice?
Options:
A. Furosemide
B. Chlorthalidone
C. Ethacrynic acid
D. Indapamide
E. Acetazolamide
C. Ethacrynic acid
Explanation:
Ethacrynic acid is the only loop diuretic without a sulfonamide group, making it safe for patients with sulfa allergies. Furosemide contains a sulfonamide group and is contraindicated in these patients. Thiazides (chlorthalidone, indapamide) are also sulfonamides and less potent for fluid overload. Acetazolamide is a carbonic anhydrase inhibitor, not a loop diuretic.
54
What is the mechanism of action of ethacrynic acid?
Options:
A. Inhibits Na+/Cl- transporter in distal tubule
B. Inhibits Na+/K+/2Cl- cotransporter in thick ascending loop of Henle
C. Carbonic anhydrase inhibitor in proximal tubule
D. Aldosterone receptor antagonist in collecting duct
E. Osmotic diuretic in proximal tubule and loop of Henle
B. Inhibits Na+/K+/2Cl- cotransporter in thick ascending loop of Henle
Explanation:
Loop diuretics block the Na+/K+/2Cl- cotransporter → decrease reabsorption of sodium, chloride, potassium, water, magnesium, and calcium → potent diuresis.
55
Which loop diuretic is safe for a patient with a sulfonamide allergy?
Options:
A. Furosemide
B. Bumetanide
C. Torsemide
D. Ethacrynic acid
E. Chlorthalidone
D. Ethacrynic acid
Explanation:
All other listed diuretics are sulfonamide derivatives and could trigger an allergic reaction.
56
Which of the following is a main indication for loop diuretics?
Options:
A. Hypertension only
B. Edema from heart failure, cirrhosis, nephrotic syndrome
C. Glaucoma
D. Diabetes insipidus
E. Osteoporosis
B. Edema from heart failure, cirrhosis, nephrotic syndrome
Explanation:
Loop diuretics are used for fluid overload states, not for mild hypertension, glaucoma, or osteoporosis.
57
A 50-year-old man with newly diagnosed diabetes has proteinuria and a renal biopsy showing nodular glomerulosclerosis (Kimmelstiel-Wilson nodules). What is the underlying pathophysiologic mechanism?
Options:
A. Decreased angiotensin II levels
B. Dilation of the efferent glomerular arteriole
C. Hypofiltration of the glomerulus
D. Isolated afferent hyaline arteriolosclerosis
E. Mesangial expansion
E. Mesangial expansion
Explanation:
Diabetic nephropathy is caused by chronic hyperglycemia → nonenzymatic glycosylation of proteins → increased mesangial matrix deposition and hypertrophy. This leads to mesangial expansion, nodular glomerulosclerosis (Kimmelstiel-Wilson nodules), glomerular basement membrane thickening, and eventual proteinuria.
58
Which histologic lesion is diagnostic for diabetic nephropathy?
Options:
A. Fibrinoid necrosis
B. Kimmelstiel-Wilson nodules
C. Crescent formation
D. Tubulointerstitial fibrosis
E. Hyaline arteriolosclerosis
B. Kimmelstiel-Wilson nodules
Explanation:
Kimmelstiel-Wilson nodules are pink, hyaline nodules in glomerular mesangium caused by mesangial matrix expansion. They are pathognomonic for diabetic nephropathy.
59
What is the earliest morphologic change in diabetic nephropathy?
Options:
A. Podocyte injury
B. Mesangial expansion
C. Glomerulosclerosis
D. Basement membrane thickening
E. Efferent arteriole dilation
B. Mesangial expansion
Explanation:
Mesangial expansion occurs first due to hyperglycemia-induced matrix deposition. Over time, it progresses to GBM thickening, podocyte injury, and eventually Kimmelstiel-Wilson nodules.
60
Which medication can slow progression of diabetic nephropathy?
Options:
A. Loop diuretics
B. ACE inhibitors
C. Beta-blockers
D. Calcium channel blockers
E. NSAIDs
B. ACE inhibitors
Explanation:
ACE inhibitors (and ARBs) dilate the efferent arteriole, lowering intraglomerular pressure and reducing proteinuria, which slows nephropathy progression.
61
Which of the following fundoscopic findings is most consistent with diabetic retinopathy?
Options:
A. Cotton-wool spots, retinal neovascularization, macular edema
B. Cherry-red spot
C. Retinal pallor
D. Drusen
E. Optic disc cupping
A. Cotton-wool spots, retinal neovascularization, macular edema
Explanation:
Chronic hyperglycemia → retinal microvascular damage → diabetic retinopathy, which can include microaneurysms, hemorrhages, cotton-wool spots, neovascularization, and macular edema.
62
A 64-year-old man presents with progressive tightening of his hand, thickened palmar skin with nodular cord-like bands, and difficulty extending fingers. Family history is positive. Which digit(s) are most likely permanently contracted?
Options:
A. All phalanges will be maintained in a claw-like pattern
B. First and second digits
C. Fourth and fifth digits
D. Third, fourth, and fifth digits
E. Second and third digits
C. Fourth and fifth digits
Explanation:
This is Dupuytren contracture, a fibroproliferative disorder of the palmar fascia.
Digits most commonly affected: fourth (ring) and fifth (little) fingers. Third finger can be affected less often; radial digits rarely.
Clinical features: painless nodules in the palm → thickened, cord-like bands → progressive flexion contractures.
Risk factors: male sex, age >50, diabetes mellitus, family history (strong hereditary component), Northern European ancestry.
Treatment: mild cases monitored; severe cases may require fasciectomy or collagenase injection.
63
What is the underlying pathophysiology of Dupuytren contracture?
Options:
A. Neuropathy of the median and ulnar nerves
B. Fibroblastic proliferation with disordered collagen deposition
C. Inflammatory arthritis causing joint destruction
D. Tendon sheath inflammation and thickening
E. Autoimmune destruction of synovium
B. Fibroblastic proliferation with disordered collagen deposition
Explanation:
Dupuytren contracture is a benign fibroblastic proliferation of the palmar fascia.
Leads to type III collagen deposition, cord formation, and eventual flexion contracture.
Not primarily inflammatory or autoimmune; the neurologic exam is usually normal.
64
Which of the following is most commonly associated with Dupuytren contracture?
Options:
A. Rheumatoid arthritis
B. Type 2 diabetes mellitus
C. Chronic gout
D. Psoriasis
E. Carpal tunnel syndrome
B. Type 2 diabetes mellitus
Explanation:
Dupuytren contracture is strongly associated with diabetes, age >50, male sex, and family history.
It is also more common in Northern European ancestry.
65
A 41-year-old man develops intense polyuria and polydipsia immediately after transsphenoidal pituitary surgery. What is the most likely cause?
A. Adenohypophysis injury
B. Adverse drug effect
C. Ectopic pulmonary lesion
D. Neurohypophysis injury
E. Pancreatic beta-cell destruction
D. Neurohypophysis injury
Damage to the posterior pituitary (neurohypophysis) → loss of ADH secretion → central diabetes insipidus
High serum osmolality
Low urine osmolality
Hypernatremia
Treatment: Desmopressin (ADH analog)
66
Which hormone is deficient in central diabetes insipidus?
A. Aldosterone
B. Vasopressin
C. Oxytocin
D. Cortisol
B. Vasopressin (ADH)
Posterior pituitary releases ADH + oxytocin.
Loss of ADH → kidneys cannot reabsorb water → polyuria + polydipsia
67
What is the treatment for central diabetes insipidus?
A. Thiazide diuretic
B. Mannitol
C. Desmopressin
D. ACE inhibitor
C. Desmopressin
Synthetic ADH analog restores kidney water reabsorption.
68
Where is ADH produced?
A. Posterior pituitary
B. Anterior pituitary
C. Hypothalamus
D. Adrenal cortex
C. Hypothalamus
Made in hypothalamic nuclei
Stored/released by posterior pituitary
69
Which postoperative condition is most associated with damage to the posterior pituitary?
A. SIADH
B. Central diabetes insipidus
C. Hyperthyroidism
D. Hypocortisolism
B. Central diabetes insipidus
Loss of ADH release → inability to concentrate urine.
70
A 61-year-old woman with long-standing type II diabetes has micro-hemorrhages on fundoscopy and decreased lower-extremity monofilament sensation. If renal biopsy were done, what would be seen?
A. Tram-track basement membrane
B. Immune deposits along GBM
C. Podocyte foot process effacement only
D. Spike and dome pattern
E. Uniform GBM thickening
E. Uniform GBM thickening
Diabetic nephropathy results from chronic hyperglycemia → non-enzymatic glycosylation →
Uniform glomerular basement membrane (GBM) thickening
Mesangial expansion
Kimmelstiel-Wilson nodules (nodular glomerulosclerosis)
Leads to albuminuria → nephrotic-range proteinuria
Key clinical clues:
Diabetic retinopathy (micro-hemorrhages)
Peripheral neuropathy (loss of monofilament sensation)
Treatment: ACE inhibitors/ARBs to reduce intraglomerular pressure & proteinuria
71
Mechanism of diabetic nephropathy?
A. Immune complexes
B. Non-enzymatic glycosylation of basement membrane proteins
C. Podocyte fusion due to viral infection
D. Complement activation
B. Non-enzymatic glycosylation
Chronic hyperglycemia → glycosylation →
Thickened, leaky GBM
Mesangial expansion
Glomerulosclerosis
72
A 57-year-old man with type 2 diabetes has a rising A1c >7% despite no lifestyle or medication changes. An additional medication is started to inhibit dipeptidyl-peptidase-4 (DPP-4) and prevent incretin breakdown. Which drug was added?
A. Acarbose
B. Exenatide
C. Glipizide
D. Pramlintide
E. Sitagliptin
E. Sitagliptin
🧠 Explanation
DPP-4 inhibitors (e.g., sitagliptin, saxagliptin) block breakdown of incretins (GLP-1, GIP), leading to:
↑ glucose-dependent insulin release
↓ glucagon release
↓ gastric emptying
Mild weight loss or weight-neutral effect
Used to improve glycemic control when metformin alone isn’t enough.
73
A 65-year-old obese woman has "shock-like" sensations in her legs, decreased vibration in feet, decreased ankle reflexes, and hyperglycemia. What is the most likely mechanism?
A. Accumulation of excess sorbitol in nervous tissue
B. Compression of the posterior tibial nerve
C. Compression of the sciatic nerve
D. Herniation of the lumbar nucleus pulposus
E. Immune reaction against axonal membrane
A. Accumulation of excess sorbitol in nervous tissue
Explanation:
Chronic hyperglycemia → excess glucose shunted to polyol pathway → converted to sorbitol by aldose reductase → sorbitol accumulation damages nerves → diabetic peripheral neuropathy.
74
What enzyme converts glucose → sorbitol, contributing to diabetic neuropathy?
A. Hexokinase
B. Aldose reductase
C. Sorbitol dehydrogenase
D. Glucokinase
E. Pyruvate kinase
B. Aldose reductase
Extra Note:
Sorbitol accumulation causes osmotic + oxidative nerve damage.
75
Which peripheral nerve finding is most characteristic of diabetic neuropathy?
A. Pure motor loss
B. Loss of vibration first
C. Increased ankle reflexes
D. Spasticity
E. Early bowel/bladder incontinence
B. Loss of vibration first
Extra Note:
Large-fiber sensory loss (vibration, proprioception) → then small-fiber pain symptoms.
76
A 21-year-old thin woman has mild hyperglycemia (fasting glucose 120), HbA1c 7.4%, normal C-peptide, no autoantibodies, normal lipids, no neonatal issues, family-pattern diabetes suspected.
Dx: MODY.
Which mutation is most likely?
A. Glucokinase
B. Hepatocyte nuclear factor 4α
C. Hepatocyte nuclear factor 1β
D. Human leukocyte antigen
E. Paired box gene 4
Answer: A. Glucokinase (MODY-2)
Why?
Young, lean, mild diabetes
Normal C-peptide
No autoantibodies → NOT Type 1
Not insulin-resistant → NOT Type 2
Mild, stable hyperglycemia = MODY2 (GCK mutation)
Key features of MODY-2
Glucokinase mutation → higher glucose threshold for insulin release
Mild hyperglycemia, often stable
Often needs no treatment
77
Which MODY subtype has mild stable fasting hyperglycemia and often requires no treatment?
A. MODY-1
B. MODY-2
C. MODY-3
D. MODY-5
B. MODY-2
Due to glucokinase mutation
Mild hyperglycemia, stable
Usually diet only
78
Which MODY subtype responds dramatically to sulfonylureas?
A. MODY-1 (HNF4A)
B. MODY-2 (GCK)
C. MODY-3 (HNF1A)
D. MODY-5 (HNF1B)
Back:
C. MODY-3 (HNF1A)
Progressive diabetes
Sulfonylureas work extremely well
79
A 52-year-old man presents with bilateral, nontender gynecomastia. He takes medications for HTN, HLD, type 2 diabetes, and CHF. Which medication is the most likely cause?
A. Digoxin
B. Glyburide
C. Lisinopril
D. Metformin
E. Metoprolol
A. Digoxin
Digoxin
Isoniazid
Spironolactone
Cimetidine, ketoconazole
Oestrogen/anti-testosterone (finasteride)
80
A 62-year-old female with hypertension and low DEXA z-score (-1.7) is started on an antihypertensive that can also help with bone density. Which class of drug is likely prescribed?
A. Spironolactone / Eplerenone (Mineralocorticoid receptor antagonist)
B. Thiazide diuretics
C. ACE inhibitors
D. Beta-blockers
E. Calcium channel blockers
B. Thiazide diuretics
Explanation:
Thiazides (eg, hydrochlorothiazide, chlorthalidone) reduce calcium excretion in the urine → mild protective effect on bone density.
Indicated for hypertension and can improve DEXA scores.
Mechanism: inhibit Na+/Cl- cotransporter in distal convoluted tubule, causing mild diuresis and calcium retention.
81
A 65-year-old male with a history of smoking and lung mass presents with altered mental status, seizures, hyponatremia, high urine sodium, and high urine osmolality. What is the most likely diagnosis?
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Explanation:
Common paraneoplastic syndrome associated with small cell lung cancer.
Labs: hyponatremia, low serum osmolality, high urine osmolality (>100 mOsm/kg), urine sodium >40 mmol/L.
Clinical: confusion, seizures, weakness.
82
What is the pathophysiologic mechanism of SIADH in small cell lung cancer?
✅ Excess ADH (vasopressin) secretion by tumor cells → V2 receptor activation in collecting ducts → water retention → hyponatremia
Key Point:
V2 receptor activation increases aquaporin-2 insertion → water reabsorption → dilutional hyponatremia.
83
A patient with SIADH develops seizures from severe hyponatremia. Which is the most appropriate pharmacologic therapy?
A. Carbamazepine
B. Conivaptan
C. Desmopressin
D. Lithium
E. Spironolactone
B. Conivaptan
Explanation:
Conivaptan / Tolvaptan: V2 receptor antagonists → block ADH effect → excrete free water.
Used when fluid restriction is insufficient or hyponatremia is severe/symptomatic.
Other options:
Carbamazepine → can treat mild SIADH (enhances ADH)
Desmopressin → treats central diabetes insipidus, contraindicated here
Lithium → nephrogenic DI, rarely used
Spironolactone → mild benefit in chronic SIADH, not acute/severe
84
A 15-year-old male with DKA is started on insulin and fluids. Two hours later, he develops muscle weakness and palpitations. ECG shows flattened T waves and U waves. What is the most likely cause?
Answer Choices:
A. Anaphylactoid reaction to insulin
B. Decreased liver glycogenolysis
C. Hypokalemia
D. Increased muscle proteolysis
E. Untreated infection
C. Hypokalemia
Explanation: Insulin shifts potassium into cells via the Na⁺/K⁺ ATPase. Even if baseline K⁺ is normal, DKA treatment can precipitate hypokalemia, causing muscle weakness and arrhythmias.
85
A 35-year-old woman at 25 weeks gestation presents with polyuria and polydipsia. Oral glucose tolerance test shows:
Fasting: 110 mg/dL (normal <95)
1 hour: 195 mg/dL (normal <180)
2 hour: 160 mg/dL (normal <155)
Which mechanism is most likely causing her hyperglycemia?A. Decreased insulin production
B. Enlargement of the pituitary gland
C. Increased production of thyroid-binding globulin
D. Production of human placental lactogen
E. Release of tissue factor into maternal circulation
D. Production of human placental lactogen (HPL)
Explanation:
HPL is produced by the placenta and acts as an insulin antagonist, decreasing maternal insulin sensitivity and increasing lipolysis. This leads to gestational diabetes, which is typically screened for between 24–28 weeks gestation.
86
What is the first-line management of gestational diabetes mellitus?
Answer Choices:
A. Insulin therapy immediately
B. Lifestyle modification (diet and exercise)
C. Metformin as first-line
D. Sulfonylureas
B. Lifestyle modification (diet and exercise)
Explanation:
Lifestyle modification is the initial management. If hyperglycemia persists, pharmacologic therapy with insulin or metformin may be used.
87
A 40-year-old man presents with polyuria, polydipsia, fatigue, nausea, vomiting, and abdominal pain. Labs show:
Glucose: 612 mg/dL
Bicarbonate: 10 mEq/L
Anion gap: 23 mEq/L
Potassium: 6.5 mEq/L
Sodium: 155 mEq/L
Which physiological property is decreased in this patient?
Answer Choices:
A. Ferrous state of hemoglobin
B. Hemoglobin affinity for oxygen
C. Oxygen release in peripheral tissues
D. Partial pressure of carbon dioxide
E. Partial pressure of oxygen
B. Hemoglobin affinity for oxygen
Explanation:
This patient has diabetic ketoacidosis (DKA), a high-anion-gap metabolic acidosis. In acidosis, hemoglobin's affinity for oxygen decreases (Bohr effect), facilitating oxygen release to tissues.
88
A 65-year-old male presents with 6 weeks of bilateral joint pain and stiffness in his hands, affecting the metacarpophalangeal and proximal interphalangeal joints, with morning stiffness lasting over an hour. Labs are significant for high titers of autoantibodies. Which target is most likely recognized by these antibodies?
Answer Choices:
A. Centromere A
B. Double-stranded DNA
C. Fragment crystallizable (Fc) portion of immunoglobulin G
D. Myeloperoxidase
E. Serine proteinase 3
C. Fragment crystallizable (Fc) portion of immunoglobulin G
Explanation:
This presentation is classic rheumatoid arthritis (RA): symmetrical small joint involvement, prolonged morning stiffness, extraarticular features (e.g., pleurisy).
Rheumatoid factor (RF) is an autoantibody directed against the Fc portion of IgG.
RF is present in up to 80% of RA patients and high titers predict severe disease with extraarticular involvement.
Other serologic markers include anti-citrullinated peptide antibodies (anti-CCP), which have high specificity for RA.
Treatments: methotrexate ± biologics (e.g., TNF-α inhibitors) and steroids for flares.
Mnemonic to remember RF target:
“RF = Really Fc” → Rheumatoid Factor targets Fc portion of IgG.
89
A 22-year-old male with type 1 diabetes presents to the emergency department with episodic sweating, tremors, and palpitations, especially after skipping meals. He becomes unconscious in the ED. He is immediately given IV fluids and a medication to raise blood sugar.
Which of the following is the primary effect of this medication?
A. decreased insulin secretion
B. decreased proteolysis
C. increased glycogenolysis
D. increased glycogenesis
E. increased lipogenesis
C. increased glycogenolysis ✅
Explanation:
The patient is experiencing severe hypoglycemia, likely due to missed meals while on insulin therapy.
In unconscious hypoglycemia, the emergency treatment is IV dextrose or IM/SC glucagon.
Glucagon acts via Gs-coupled receptors → ↑ cAMP.
Primary hepatic effects of glucagon:
Glycogenolysis (breakdown of glycogen → glucose)
Gluconeogenesis (glucose from amino acids and lactate)
Lipolysis and ketogenesis
Amino acid breakdown
Other effects:
Raises blood glucose
Increases heart rate and contractility
Helps restore homeostasis
Key point: Glucagon mobilizes glucose rapidly in hypoglycemia, making glycogenolysis the main mechanism.
90
A 12-year-old boy is brought to the office with a 3-week history of polyuria, polydipsia, and a 4.5-kg (10-pound) weight loss. He has become increasingly fatigued and has difficulty concentrating. Physical examination reveals a thin-appearing child with mild dehydration. Laboratory studies show:
Glucose: 485 mg/dL
Hemoglobin A1c: 12.8%
C-peptide: 0.2 ng/mL
Anti–glutamic acid decarboxylase antibodies: positive
The development of this patient’s condition is most strongly associated with:
A. HLA-A29 and HLA-B27 alleles
B. HLA-DR3 and HLA-DR4 alleles
C. HLA-DR7 and HLA-DR15 alleles
D. mitochondrial DNA mutations
E. TCF7L2 gene polymorphisms
B. HLA-DR3 and HLA-DR4 alleles ✅
Explanation:
This patient has type 1 diabetes mellitus (T1DM): childhood onset, polyuria/polydipsia/weight loss, low C-peptide, and positive anti-GAD antibodies.
T1DM is an autoimmune destruction of pancreatic β-cells, and the strongest genetic risk is conferred by HLA-DR3 and HLA-DR4 alleles.
91
A 6-year-old male presents with gradual onset of fatigue for the last 2 months. He has not been playing at recess, stating he is too tired. He has increased appetite and increased frequency of urination. There is no history of night sweats, cough, or diarrhea, and none of his classmates have similar symptoms. Physical examination is notable only for slightly increased pulse and dry skin. There is no pallor, lymphadenopathy, heart murmur, wheezing, or hepatosplenomegaly. Laboratory results including CBC, glucose, BUN, creatinine, and urinalysis are pending.
Among the following, which is most likely present?
A. amyloid deposition in the islets of Langerhans
B. disease or injury involving the posterior pituitary gland
C. fibrosis and cystic changes in the pancreas and mutated CFTR
D. lymphocytic infiltration of the islets of Langerhans
E. primitive white blood cells in the bone marrow and peripheral blood
D. lymphocytic infiltration of the islets of Langerhans ✅
Explanation:
The patient presents with classic type 1 diabetes mellitus (T1DM) symptoms: fatigue, polyphagia, and polyuria due to insulin deficiency.
Pathophysiology: autoimmune destruction of pancreatic beta cells. Lymphocytes infiltrate the islets of Langerhans, leading to absolute insulin deficiency.
Other options:
A: Amyloid deposition → type 2 diabetes
B: Posterior pituitary disease → diabetes insipidus (polyuria without hyperglycemia)
C: CFTR mutations → cystic fibrosis, pancreatic exocrine insufficiency
E: Primitive WBCs → leukemia
T1DM often has autoantibodies against GAD or insulin and is associated with HLA-DR3/DR4 alleles.
92
A 70-year-old woman with type 2 diabetes presents with sweating, tremors, palpitations, and dizziness 30 minutes after taking her medication. Blood glucose during these episodes is 55–60 mg/dL. She reports increased appetite and weight gain over the past month.
Which of the following drugs is the most likely cause?
A. glucagon
B. glyburide
C. metformin
D. propranolol
E. rosiglitazone
B. glyburide ✅
Explanation:
Sulfonylurea (glyburide)–induced hypoglycemia: triggers excess insulin secretion, leading to symptomatic hypoglycemia.
Key clues: timing after medication, blood glucose 55–60 mg/dL, elderly patient, weight gain due to increased caloric intake after hypoglycemia.
Other drugs:
Glucagon → raises glucose
Metformin → rarely causes hypoglycemia
Propranolol → masks hypoglycemia symptoms
Rosiglitazone → weight gain but not hypoglycemia
93
A 32-year-old African American woman with obesity (BMI 34) presents with hyperpigmented, thickened, velvety plaques on the back of her neck and axillae. She takes an oral contraceptive daily.
This skin condition is most likely caused by:
A. autoimmune destruction of thyroid follicles
B. increased production of proopiomelanocortin
C. overproduction of glucagon by pancreatic islet cells
D. transactivation of insulin on IGF-1 receptors
E. water-soluble vitamin deficiency
D. transactivation of insulin on IGF-1 receptors ✅
Explanation:
This is acanthosis nigricans, characterized by velvety hyperpigmented plaques, commonly on the neck and axillae.
Most often associated with insulin resistance (obesity, type 2 diabetes, PCOS).
Mechanism: hyperinsulinemia → insulin transactivates IGF-1 receptors → increased keratinocyte and melanocyte proliferation → thickened, hyperpigmented skin.
Other options:
A: Autoimmune thyroid disease → no acanthosis
B: POMC overproduction → Cushing disease
C: Glucagonoma → necrolytic migratory erythema
E: Vitamin deficiency → unrelated skin findings
94
A 57-year-old man with type 2 diabetes has an HbA1c of 8.2% despite lifestyle modifications. The physician decides to start metformin.
Metformin improves glycemic control primarily through which mechanism?
A. decreased glucagon release via inhibition of the DPP-4 enzyme
B. decreased hepatic gluconeogenesis via inhibition of mitochondrial glycerophosphate dehydrogenase
C. delayed carbohydrate hydrolysis and glucose absorption
D. increased endogenous production of insulin via closure of K+ channels in the β-cell membrane
E. increased insulin sensitivity via activation of a nuclear receptor
B. decreased hepatic gluconeogenesis via inhibition of mitochondrial glycerophosphate dehydrogenase ✅
Explanation:
Metformin is a first-line agent for type 2 diabetes.
Primary mechanism: inhibits mitochondrial glycerophosphate dehydrogenase, leading to reduced hepatic gluconeogenesis → lowers fasting glucose.
Other effects: increases glycolysis and peripheral insulin sensitivity.
Other options:
A: DPP-4 inhibition → gliptins (sitagliptin, etc.)
C: Delayed carbohydrate absorption → α-glucosidase inhibitors
D: Stimulate insulin release → sulfonylureas
E: Activate nuclear receptor → thiazolidinediones (TZDs)
95
Comlex 1
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