COMSAE Form 110 – Complete Exam
with Answer Key & Step-by-Step
Explanations | Ideal for COMLEX Level 1
Review
Question 1
A 58-year-old man with hypertension and type 2 diabetes presents with progressive exertional
dyspnea and orthopnea for 2 weeks. On exam: BP 150/90 mmHg, HR 96 bpm, JVD to the angle
of the mandible when sitting at 45°, bibasilar crackles, and 2+ bilateral pitting edema. Cardiac
exam: S3 gallop. Echocardiogram shows LVEF 30% with global hypokinesis. He is euvolemic
after diuresis but still has orthopnea. Which of the following medications is recommended to
reduce mortality in this patient and should be started (assuming no contraindication)?
A. Metoprolol succinate (β1 selective blocker)
B. Verapamil (non-dihydropyridine calcium channel blocker)
C. Hydrochlorothiazide
D. Diltiazem
E. Digoxin
Correct answer: A. Metoprolol succinate (β1 selective blocker)
Rationale — step-by-step
1. Clinical interpretation (cardiology): Presentation consistent with chronic systolic heart
failure (reduced EF) with signs of congestion and S3; guideline-directed medical therapy
(GDMT) for HFrEF includes ACE inhibitors (or ARNI/ARB), β-blockers (evidence-
based agents), mineralocorticoid receptor antagonists, SGLT2 inhibitors, etc. β-blockers
reduce mortality and improve remodeling in HFrEF when used with ACEi/ARB.
2. Why metoprolol succinate? Metoprolol succinate (extended release) is an evidence-
based β1-selective blocker proven to reduce mortality in HFrEF. Start low and titrate.
3. Why not verapamil/diltiazem (B/D)? Non-dihydropyridine CCBs can worsen systolic
dysfunction and are contraindicated in HFrEF with reduced EF.
4. Why not hydrochlorothiazide (C)? Thiazides are useful for hypertension and mild fluid
retention but do not reduce mortality in HFrEF the way β-blockers do; also thiazides less
effective with reduced renal perfusion.
, 5. Why not digoxin (E)? Digoxin can improve symptoms and reduce hospitalizations but
does not reduce mortality; it's not first-line for mortality benefit.
6. Osteopathic note: In HFrEF, consider somatic dysfunctions (e.g., thoracic lymphatic
pump restrictions, rib dysfunctions) — OMT (lymphatic techniques, thoracic inlet
release) may help with pulmonary congestion and symptom relief but do not replace
GDMT; coordinate OMT timing when patient is stable and euvolemic.
Question 2
A 32-year-old woman presents with fever, severe dysuria, urinary urgency, and pelvic pain.
Urine dipstick: positive nitrites and leukocyte esterase. Urine culture grows >100,000 CFU/mL
Escherichia coli that produces extended-spectrum β-lactamases (ESBL). She has no drug
allergies. Which is the best single-agent oral option for outpatient therapy?
A. Trimethoprim-sulfamethoxazole (TMP-SMX)
B. Nitrofurantoin
C. Ciprofloxacin
D. Amoxicillin-clavulanate
E. Ceftriaxone (single IM dose)
Correct answer: B. Nitrofurantoin
Rationale — step-by-step
1. Microbiology: ESBL-producing E. coli are resistant to many penicillins and
cephalosporins (including amoxicillin-clavulanate) and often resistant to TMP-SMX and
fluoroquinolones depending on local patterns — but ESBL enzymes do not confer
resistance to nitrofurantoin, which has a different mechanism and is effective for lower
urinary tract infections when kidney function is adequate.
2. Clinical choice: Nitrofurantoin is indicated for uncomplicated cystitis (lower UTI) due
to E. coli including many ESBL producers and is oral. It achieves high urinary
concentrations but is not appropriate for pyelonephritis or systemic infection.
3. Why not TMP-SMX (A)? Resistance is common with ESBL strains; local susceptibility
should guide use — not the best empiric for ESBL.
4. Why not ciprofloxacin (C)? Fluoroquinolones can be active but rising resistance and
collateral effects (C. difficile, tendinopathy); many ESBL isolates co-carry quinolone
resistance. Reserve for when indicated and susceptible.
5. Why not amoxicillin-clavulanate (D) or ceftriaxone (E)? ESBLs hydrolyze many β-
lactams; ceftriaxone is often ineffective for ESBL; carbapenems are preferred for
systemic ESBL infections. Ceftriaxone IM single dose is sometimes used for gonococcal
infection, not ESBL UTI.
, Question 3
A 24-year-old man with newly diagnosed phenylketonuria (PKU) is seen for counseling. Which
of the following dietary strategies most effectively prevents intellectual disability in PKU?
A. High-protein diet with vitamin B6 supplementation
B. Low-phenylalanine diet with tyrosine supplementation
C. Low-tyrosine diet with phenylalanine supplementation
D. High-phenylalanine diet with tetrahydrobiopterin (BH4)
E. Normal diet but start levodopa
Correct answer: B. Low-phenylalanine diet with tyrosine supplementation
Rationale — step-by-step
1. Biochemistry of PKU: PKU results from deficiency of phenylalanine hydroxylase
(PAH) or BH4 cofactor problems, leading to accumulation of phenylalanine and
decreased tyrosine (tyrosine becomes conditionally essential). High phenylalanine causes
neurotoxicity and cognitive impairment.
2. Effective therapy: Dietary restriction of phenylalanine from infancy prevents
accumulation and subsequent intellectual disability. Tyrosine supplementation is
necessary because conversion from phenylalanine is impaired.
3. Why not other choices:
o (A) High-protein would worsen phenylalanine load. Vitamin B6 is a cofactor for
some enzymes but not a primary fix for PAH deficiency.
o (C) Low-tyrosine would be harmful; tyrosine is needed.
o (D) BH4 supplementation helps a subset with BH4-responsive PKU but not by
giving high phenylalanine.
o (E) Levodopa addresses dopamine deficiency but not the primary metabolic
derangement; not appropriate.
Question 4
A 45-year-old man presents with a 3-week history of cough productive of rusty sputum, pleuritic
chest pain on the right, and fever. Chest x-ray shows lobar consolidation in the right lower lobe.
He has diabetes but is otherwise healthy. Sputum Gram stain shows gram-positive lancet-shaped
diplococci. He is allergic to penicillin (anaphylaxis). Which is the best antibiotic choice?
A. Azithromycin
B. Levofloxacin
C. Doxycycline
D. Ceftriaxone
E. Vancomycin
with Answer Key & Step-by-Step
Explanations | Ideal for COMLEX Level 1
Review
Question 1
A 58-year-old man with hypertension and type 2 diabetes presents with progressive exertional
dyspnea and orthopnea for 2 weeks. On exam: BP 150/90 mmHg, HR 96 bpm, JVD to the angle
of the mandible when sitting at 45°, bibasilar crackles, and 2+ bilateral pitting edema. Cardiac
exam: S3 gallop. Echocardiogram shows LVEF 30% with global hypokinesis. He is euvolemic
after diuresis but still has orthopnea. Which of the following medications is recommended to
reduce mortality in this patient and should be started (assuming no contraindication)?
A. Metoprolol succinate (β1 selective blocker)
B. Verapamil (non-dihydropyridine calcium channel blocker)
C. Hydrochlorothiazide
D. Diltiazem
E. Digoxin
Correct answer: A. Metoprolol succinate (β1 selective blocker)
Rationale — step-by-step
1. Clinical interpretation (cardiology): Presentation consistent with chronic systolic heart
failure (reduced EF) with signs of congestion and S3; guideline-directed medical therapy
(GDMT) for HFrEF includes ACE inhibitors (or ARNI/ARB), β-blockers (evidence-
based agents), mineralocorticoid receptor antagonists, SGLT2 inhibitors, etc. β-blockers
reduce mortality and improve remodeling in HFrEF when used with ACEi/ARB.
2. Why metoprolol succinate? Metoprolol succinate (extended release) is an evidence-
based β1-selective blocker proven to reduce mortality in HFrEF. Start low and titrate.
3. Why not verapamil/diltiazem (B/D)? Non-dihydropyridine CCBs can worsen systolic
dysfunction and are contraindicated in HFrEF with reduced EF.
4. Why not hydrochlorothiazide (C)? Thiazides are useful for hypertension and mild fluid
retention but do not reduce mortality in HFrEF the way β-blockers do; also thiazides less
effective with reduced renal perfusion.
, 5. Why not digoxin (E)? Digoxin can improve symptoms and reduce hospitalizations but
does not reduce mortality; it's not first-line for mortality benefit.
6. Osteopathic note: In HFrEF, consider somatic dysfunctions (e.g., thoracic lymphatic
pump restrictions, rib dysfunctions) — OMT (lymphatic techniques, thoracic inlet
release) may help with pulmonary congestion and symptom relief but do not replace
GDMT; coordinate OMT timing when patient is stable and euvolemic.
Question 2
A 32-year-old woman presents with fever, severe dysuria, urinary urgency, and pelvic pain.
Urine dipstick: positive nitrites and leukocyte esterase. Urine culture grows >100,000 CFU/mL
Escherichia coli that produces extended-spectrum β-lactamases (ESBL). She has no drug
allergies. Which is the best single-agent oral option for outpatient therapy?
A. Trimethoprim-sulfamethoxazole (TMP-SMX)
B. Nitrofurantoin
C. Ciprofloxacin
D. Amoxicillin-clavulanate
E. Ceftriaxone (single IM dose)
Correct answer: B. Nitrofurantoin
Rationale — step-by-step
1. Microbiology: ESBL-producing E. coli are resistant to many penicillins and
cephalosporins (including amoxicillin-clavulanate) and often resistant to TMP-SMX and
fluoroquinolones depending on local patterns — but ESBL enzymes do not confer
resistance to nitrofurantoin, which has a different mechanism and is effective for lower
urinary tract infections when kidney function is adequate.
2. Clinical choice: Nitrofurantoin is indicated for uncomplicated cystitis (lower UTI) due
to E. coli including many ESBL producers and is oral. It achieves high urinary
concentrations but is not appropriate for pyelonephritis or systemic infection.
3. Why not TMP-SMX (A)? Resistance is common with ESBL strains; local susceptibility
should guide use — not the best empiric for ESBL.
4. Why not ciprofloxacin (C)? Fluoroquinolones can be active but rising resistance and
collateral effects (C. difficile, tendinopathy); many ESBL isolates co-carry quinolone
resistance. Reserve for when indicated and susceptible.
5. Why not amoxicillin-clavulanate (D) or ceftriaxone (E)? ESBLs hydrolyze many β-
lactams; ceftriaxone is often ineffective for ESBL; carbapenems are preferred for
systemic ESBL infections. Ceftriaxone IM single dose is sometimes used for gonococcal
infection, not ESBL UTI.
, Question 3
A 24-year-old man with newly diagnosed phenylketonuria (PKU) is seen for counseling. Which
of the following dietary strategies most effectively prevents intellectual disability in PKU?
A. High-protein diet with vitamin B6 supplementation
B. Low-phenylalanine diet with tyrosine supplementation
C. Low-tyrosine diet with phenylalanine supplementation
D. High-phenylalanine diet with tetrahydrobiopterin (BH4)
E. Normal diet but start levodopa
Correct answer: B. Low-phenylalanine diet with tyrosine supplementation
Rationale — step-by-step
1. Biochemistry of PKU: PKU results from deficiency of phenylalanine hydroxylase
(PAH) or BH4 cofactor problems, leading to accumulation of phenylalanine and
decreased tyrosine (tyrosine becomes conditionally essential). High phenylalanine causes
neurotoxicity and cognitive impairment.
2. Effective therapy: Dietary restriction of phenylalanine from infancy prevents
accumulation and subsequent intellectual disability. Tyrosine supplementation is
necessary because conversion from phenylalanine is impaired.
3. Why not other choices:
o (A) High-protein would worsen phenylalanine load. Vitamin B6 is a cofactor for
some enzymes but not a primary fix for PAH deficiency.
o (C) Low-tyrosine would be harmful; tyrosine is needed.
o (D) BH4 supplementation helps a subset with BH4-responsive PKU but not by
giving high phenylalanine.
o (E) Levodopa addresses dopamine deficiency but not the primary metabolic
derangement; not appropriate.
Question 4
A 45-year-old man presents with a 3-week history of cough productive of rusty sputum, pleuritic
chest pain on the right, and fever. Chest x-ray shows lobar consolidation in the right lower lobe.
He has diabetes but is otherwise healthy. Sputum Gram stain shows gram-positive lancet-shaped
diplococci. He is allergic to penicillin (anaphylaxis). Which is the best antibiotic choice?
A. Azithromycin
B. Levofloxacin
C. Doxycycline
D. Ceftriaxone
E. Vancomycin
