A patient with primary hyperaldosteronism is started on spironolactone. Which
laboratory trend best confirms therapeutic efficacy while minimizing
hyperkalemia risk?
A. Rising serum potassium with normalization of the aldosterone-to-renin
ratio
B. Falling serum potassium with rising plasma renin activity
C. Rising serum sodium with suppressed plasma renin activity
D. Falling serum bicarbonate with normalization of serum potassium
Correct Answer: B - Falling serum potassium with rising plasma
renin activity
RATIONALE
Spironolactone blocks aldosterone receptors, which should lower
blood pressure, normalize potassium, and-because the
renin-angiotensin system is no longer suppressed-increase plasma
renin activity. Option A is incorrect because the aldosterone-to-renin
ratio typically remains elevated in primary hyperaldosteronism.
Option C reflects continued aldosterone effect, and option D suggests
metabolic acidosis, which is not the therapeutic goal.
Question 2
Which molecular mechanism best explains why combined oral contraceptives
remain effective despite variable absorption of ethinyl estradiol?
A. Progestin-mediated suppression of gonadotropin-releasing hormone
pulsatility is the primary contraceptive mechanism.
B. Ethinyl estradiol's 17-ethinyl group resists first-pass metabolism,
ensuring consistent hepatic delivery.
C. Enterohepatic recirculation of estradiol metabolites provides a
sustained estrogen reservoir.
D. Progesterone receptor antagonism at the endometrium prevents
implantation independent of ovulation.
Page 2
,Correct Answer: A - Progestin-mediated suppression of
gonadotropin-releasing hormone pulsatility is the primary
contraceptive mechanism.
RATIONALE
The dominant contraceptive effect of combined oral contraceptives is
progestin-induced suppression of GnRH pulsatility, which inhibits the
LH surge and ovulation. While the 17-ethinyl group does slow hepatic
metabolism (making option B partially true), it is not the primary
reason for contraceptive efficacy. Options C and D describe
mechanisms that are not the principal basis for contraceptive
effectiveness.
Question 3
A patient with type 1 diabetes and gastroparesis is prescribed pramlintide.
Which concurrent medication adjustment is most critical to prevent severe
hypoglycemia?
A. Reduce prandial insulin dose by 50%
B. Increase basal insulin by 20%
C. Add a DPP-4 inhibitor
D. Switch from insulin glargine to NPH
Correct Answer: A - Reduce prandial insulin dose by 50%
RATIONALE
Pramlintide slows gastric emptying and suppresses glucagon, which
reduces postprandial glucose excursions; prandial insulin must be
reduced by approximately 50% to avoid hypoglycemia. Increasing
basal insulin (B) would worsen hypoglycemia risk. Adding a DPP-4
inhibitor (C) does not address the immediate insulin adjustment, and
switching to NPH (D) does not mitigate the pramlintide effect.
Page 3
, Question 4
Which finding best distinguishes secondary syphilis from primary syphilis on
physical examination?
A. A single, painless, indurated genital ulcer
B. A diffuse maculopapular rash involving palms and soles
C. Painless inguinal lymphadenopathy
D. A painless, non-tender chancre at the site of inoculation
Correct Answer: B - A diffuse maculopapular rash involving
palms and soles
RATIONALE
Secondary syphilis is characterized by a diffuse maculopapular rash
that classically involves the palms and soles, often with mucous
membrane lesions. Options A and D describe the primary chancre, and
option C (lymphadenopathy) can occur in both stages but is not
specific to secondary syphilis. The palmoplantar rash is the hallmark
distinguishing feature.
Question 5
In a patient with suspected thyroid storm, which pathophysiologic mechanism
best explains the exaggerated catecholamine response despite normal serum
catecholamine levels?
A. Increased density of beta-adrenergic receptors on target tissues
B. Direct catecholamine release from thyroid follicular cells
C. Autoantibody stimulation of the TSH receptor
D. Decreased hepatic clearance of catecholamines
Correct Answer: A - Increased density of beta-adrenergic
receptors on target tissues
Page 4