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MCQ Answers (Questions 8-15)

Q8. PCOS - Physiological Change Responsible for Symptoms

Answer: C. Increased LH levels

In PCOS, the key hormonal derangement is an increased LH:FSH ratio. Elevated LH drives excess androgen production from theca cells in the ovaries (not decreased - ruling out B). Insulin resistance leads to hyperinsulinemia, which further stimulates ovarian androgen production. The excess androgens cause hirsutism (excess hair growth) and the irregular cycles result from anovulation. Option A is wrong (insulin resistance - not increased sensitivity). Option D is wrong (estrogen is not low; it may actually be elevated from peripheral aromatization of androgens).

Why C over D: Increased LH is the direct driver of the pathophysiology. The LH surplus stimulates thecal androgen excess - the hallmark hormonal finding in PCOS.

Berek & Novak's Gynecology: "Insulin resistance results in a compensatory hyperinsulinemia, which stimulates ovarian androgen production in an ovary genetically predisposed to PCOS"

Q9. Pallidotomy - Most Likely Outcome

Answer: A. Improvement in motor symptoms of Parkinson's disease

Pallidotomy destroys the internal segment of the globus pallidus (GPi). In Parkinson's disease, the dopamine deficit leads to overactivity of the indirect pathway, which causes excessive GPi inhibitory output to the thalamus, suppressing voluntary movement. Destroying the GPi relieves this excessive inhibition, improving motor symptoms (rigidity, bradykinesia, tremor).

It does NOT worsen motor symptoms (B), cause dystonia (C), or improve cognition (D) - Parkinson's cognitive symptoms are tied to cortical and cholinergic changes, not the globus pallidus.
Neuroanatomy through Clinical Cases, 3rd Ed.: "Lesions in this location [GPi] are thought to be beneficial for Parkinson's disease because of..."

Q10. Snellen's Chart - Visual Acuity 6/24

Answer: A. The subject can see at 6 meters what a normal person can see at 24 meters

Snellen notation is: Distance tested / Distance at which a normal person reads the same line

6/24 means the patient stands at 6 meters and reads letters that a normal person can read at 24 meters
This means the patient's vision is worse than normal (4x worse)
Option B reverses the numerator/denominator - incorrect
Option C is wrong (normal acuity would be 6/6)
Option D is wrong (6/6 = normal acuity)

Q11. Multiple System Atrophy - Dizziness on Standing

Answer: D. Autonomic dysfunction

Multiple System Atrophy (MSA) is a synucleinopathy that prominently affects the autonomic nervous system, causing orthostatic (postural) hypotension - dizziness and lightheadedness when standing. This is one of the hallmark features of MSA (formerly called Shy-Drager syndrome when autonomic failure predominated).

Option A (decreased sympathetic tone) is a component but is too narrow - the root cause is global autonomic failure
Option C (impaired baroreflex) is also a mechanism within autonomic dysfunction, but "autonomic dysfunction" is the most complete and accurate answer
Option B (increased parasympathetic tone) is incorrect
Goldman-Cecil Medicine: "The prominent involvement of brainstem areas critical for cardiovascular control...explains the early and severe orthostatic hypotension...that characterize multiple system atrophy"

Q12. Positive Babinski Sign

Answer: A. Upper motor neuron lesion

The Babinski sign (dorsiflexion of the great toe + fanning of other toes on plantar stimulation) is a pathological reflex indicating upper motor neuron (UMN) lesion - i.e., damage to the corticospinal tract above the level of the anterior horn cell.

Lower motor neuron lesions (B) cause flaccid paralysis, hyporeflexia, fasciculations, and atrophy - NOT a Babinski sign
Peripheral neuropathy (C) affects LMN and peripheral nerves - no Babinski
Myopathy (D) affects the muscle directly - no Babinski
Neuroanatomy through Clinical Cases: "Increased tone, spastic gait, and hyperreflexia including Babinski's sign, Hoffmann's sign, and jaw jerk reflex are upper motor neuron signs"

Q13. Chorea + Psychiatric Disturbances + Caudate Atrophy

Answer: B. Huntington's disease

This is the classic triad of Huntington's disease:

Chorea (involuntary movements)
Psychiatric disturbances (depression, psychosis, personality changes)
Cognitive decline (dementia)
Caudate nucleus atrophy on imaging - the pathological hallmark
Parkinson's (A): tremor at rest, bradykinesia, rigidity - no caudate atrophy
Wilson's disease (C): liver disease + neuropsychiatric symptoms, due to copper accumulation
Sydenham's chorea (D): post-streptococcal, in children, self-limiting, no cognitive decline or caudate atrophy
Harrison's Principles of Internal Medicine 22E: "Progressive atrophy of the head of the caudate nucleus...The disease predominantly affects the striatum but progresses to involve the cerebral cortex"

Q14. 46,XY with Ambiguous Genitalia, Normal Testosterone, Low DHT

Answer: A. 5-alpha reductase deficiency

The clinical scenario is textbook 5-alpha reductase type 2 deficiency:

46,XY karyotype (genetically male)
Normal testosterone (testes function normally and produce testosterone)
Low DHT (dihydrotestosterone) - which requires 5-alpha reductase to convert testosterone to DHT
Ambiguous genitalia: DHT is required for external male genital virilization (scrotum, penis formation); without it, external genitalia appear ambiguous or female
17-beta hydroxysteroid dehydrogenase deficiency (B): affects testosterone synthesis itself, so testosterone would also be low
Aromatase deficiency (C): would cause virilization of a female (46,XX), not ambiguous genitalia in a 46,XY
21-hydroxylase deficiency (D): causes CAH, virilizes females (46,XX), does NOT produce this pattern

Q15. Fatigue + Cold Intolerance + Weight Gain + Low Free T4 + Inappropriately Low TSH

Answer: B. Anterior pituitary

The key is "inappropriately low TSH" in the setting of low free T4:

Pathology	Free T4	TSH
Primary hypothyroidism (thyroid gland)	Low	High (TSH rises to stimulate thyroid)
Secondary hypothyroidism (anterior pituitary)	Low	Low or normal (pituitary can't produce TSH)
Tertiary hypothyroidism (hypothalamus)	Low	Low or normal (TRH deficit)

The thyroid gland (A) failing causes high TSH - not what we see here
Hypothalamus (C) failure is tertiary hypothyroidism - possible, but the TSH would also be low. However, the key distinguishing clue is that pituitary failure is more common in secondary hypothyroidism, and the question says "inappropriately low TSH," pointing to the source of TSH = anterior pituitary
Posterior pituitary (D) does not produce TSH (it releases ADH and oxytocin)
Costanzo Physiology 7th Ed.: "If the defect is in the hypothalamus or pituitary, then TSH levels will be decreased"
Henry's Clinical Diagnosis: "In the setting of secondary (pituitary) and tertiary (hypothalamic) hypothyroidism the TSH is inappropriately normal [or low] for the low levels of T4"

Summary Table

Q	Answer	Key Concept
8	C	Increased LH → androgen excess in PCOS
9	A	Pallidotomy (GPi) improves Parkinson's motor symptoms
10	A	6/24 = patient sees at 6m what normals see at 24m
11	D	MSA causes autonomic dysfunction → orthostatic hypotension
12	A	Babinski = UMN lesion sign
13	B	Huntington's = chorea + psych + caudate atrophy
14	A	5-alpha reductase deficiency = normal T, low DHT, ambiguous genitalia
15	B	Low T4 + low TSH = anterior pituitary (secondary hypothyroidism)

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