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Portage Learning - 240 Questions
This exam assesses mastery of the endocrine system, including hormone synthesis, receptor signaling, feedback
loops, and pathophysiological disruptions. Questions require integration of molecular mechanisms, clinical
correlations, and experimental data interpretation. It contains 240 multiple-choice questions, each with four
distractors and a fully worked rationale that explains why the keyed answer is correct. Content is organized into 9
focused sections: Endocrine System, Cardiovascular System: Heart and Blood Vessels, Lymphatic System and
Immunity, Respiratory System, Digestive System, Urinary System, Fluid, Electrolyte, and Acid-Base Balance,
Reproductive System, Development and Heredity. Targeted learning outcomes include: Analyze hormone synthesis
pathways and their regulation by feedback mechanisms.; Predict physiological outcomes of receptor-level
disruptions and endocrine pathologies.; Interpret laboratory and diagnostic data to differentiate endocrine
disorders.; Evaluate the interplay between endocrine glands and target tissues in homeostasis.. Every item has
been reviewed for clinical accuracy, current guidelines, and clarity so that students can study with confidence and
self-correct as they work through the bank. Use it as a high-yield review immediately before the exam, or as a
structured practice tool during the unit - the rationales double as concise teaching notes. The recommended
writing time is 3 hours, with a passing score of 70%. Aligned with Designed to meet US university standards for
upper-division biology courses, aligned with HAPS guidelines. standards and reflects the question style commonly
Section 1: Endocrine System (Questions 1-28)
1 A researcher treats cultured thyroid follicular cells with a TSH receptor
antagonist. Which of the following changes in gene expression would be
most directly reduced?
A) Sodium-iodide symporter (NIS) mRNA
B) Thyroglobulin (Tg) mRNA
C) Thyroid peroxidase (TPO) mRNA
D) Calcitonin mRNA
Answer: C
Rationale: TSH stimulates TPO expression via cAMP-PKA pathway; NIS and
Tg are also upregulated but TPO is the rate-limiting enzyme for thyroid
hormone synthesis. Calcitonin is produced by parafollicular C cells, not
regulated by TSH.
2 Which of the following best explains why cortisol administration suppresses
CRH and ACTH secretion, but not vasopressin secretion from the supraoptic
nucleus?
A) Cortisol receptors are absent on vasopressin neurons
B) Vasopressin secretion is primarily regulated by osmolality
,C) CRH neurons express glucocorticoid receptors, but vasopressin neurons do
not
D) Vasopressin is co-secreted with CRH and is not independently regulated
Answer: B
Rationale: Vasopressin (AVP) from the supraoptic nucleus is mainly regulated
by plasma osmolality and baroreceptors, not by glucocorticoid negative
feedback. CRH neurons in the paraventricular nucleus express glucocorticoid
receptors and are suppressed. Option C is incorrect because some vasopressin
neurons do express glucocorticoid receptors, but their secretion is less
sensitive.
3 A patient has a mutation in the 11-hydroxysteroid dehydrogenase type 2
(11-HSD2) enzyme. Which of the following laboratory findings would most
likely be observed?
A) Elevated serum cortisol with low aldosterone
B) Elevated serum aldosterone with low renin
C) Elevated serum cortisol with low ACTH
D) Elevated serum deoxycortisol with low cortisol
Answer: A
Rationale: 11²-HSD2 converts cortisol to cortisone in renal collecting ducts,
protecting the mineralocorticoid receptor from cortisol activation. Deficiency
allows cortisol to bind MR, causing apparent mineralocorticoid excess
(hypertension, hypokalemia) but with low aldosterone. Aldosterone is
suppressed due to volume expansion; renin is low. ACTH may be normal or
slightly suppressed.
4 Which of the following statements correctly describes the effect of a
noncompetitive antagonist of the insulin receptor on glucose metabolism?
A) It reduces insulin binding but does not alter maximal response
B) It reduces the maximal response to insulin without affecting its affinity
C) It shifts the insulin dose-response curve to the right without reducing
maximum
D) It increases insulin degradation and reduces half-life
Answer: B
Rationale: A noncompetitive antagonist binds to the receptor at a site distinct
from the orthosteric site, reducing the number of functional receptors and thus
,the maximal response (efficacy). It does not affect insulin binding affinity (Kd)
but reduces the maximum effect. Option A describes a competitive antagonist;
C is also competitive; D is not a direct receptor effect.
5 A researcher measures intracellular cAMP levels in ovarian granulosa cells
after FSH stimulation. Which of the following additional treatments would
most effectively blunt the cAMP increase?
A) Addition of a phosphodiesterase inhibitor
B) Addition of a Gs inhibitor
C) Addition of a Gi activator
D) Addition of a protein kinase A inhibitor
Answer: C
Rationale: FSH receptor is coupled to G±s, which activates adenylyl cyclase to
produce cAMP. Activating Gi (e.g., via pertussis toxin-sensitive pathways)
would inhibit adenylyl cyclase, reducing cAMP. A phosphodiesterase inhibitor
would increase cAMP. A Gs inhibitor would also reduce cAMP, but Gi
activation is more direct and potent. PKA inhibitor acts downstream of cAMP.
6 A 45-year-old individual presents with hypertension, hypokalemia, and
metabolic alkalosis. Laboratory results show low renin and high aldosterone.
A CT scan reveals a unilateral adrenal adenoma. Which of the following
hormonal profiles would most likely be found in the contralateral adrenal
gland?
A) Atrophy of zona glomerulosa with suppressed aldosterone synthase
expression
B) Hypertrophy of zona fasciculata with increased cortisol secretion
C) Normal zona glomerulosa with increased renin receptor expression
D) Hyperplasia of zona reticularis with elevated DHEA-S
Answer: A
Rationale: In primary aldosteronism due to an aldosterone-producing adenoma,
the high aldosterone suppresses renin, leading to low angiotensin II. The
contralateral adrenal's zona glomerulosa, which depends on angiotensin II for
trophic support, undergoes atrophy and downregulates aldosterone synthase
(CYP11B2). Zona fasciculata and reticularis are not primarily affected.
, 7 A patient with a pituitary tumor secreting excess growth hormone (GH) has
elevated serum IGF-1 but normal GH levels. Which of the following best
explains this discrepancy?
A) GH is secreted in a pulsatile manner and a single measurement may miss
peaks
B) IGF-1 has a longer half-life and integrates GH secretion over time
C) The tumor secretes a GH variant that is not detected by standard
immunoassay
D) Peripheral resistance to GH leads to compensatory IGF-1 production
Answer: B
Rationale: GH is secreted episodically with peaks and troughs, so a random GH
level may be normal. IGF-1, produced in response to GH, has a longer half-life
(12-15 hours) and reflects integrated GH secretion over 24 hours, making it a
better screening test for acromegaly. Option A is true but does not explain why
IGF-1 is elevated; B directly addresses the integration.
8 Which of the following experimental observations would most strongly
support the hypothesis that leptin acts primarily through the arcuate nucleus
to regulate appetite?
A) Leptin injection into the third ventricle reduces food intake more
effectively than peripheral injection
B) Leptin receptor knockout mice are hyperphagic and obese
C) Leptin stimulates POMC neurons and inhibits AgRP neurons in the
arcuate nucleus
D) Leptin crosses the blood-brain barrier via a saturable transport system
Answer: C
Rationale: Direct demonstration that leptin alters the activity of specific
neuronal populations (POMC and AgRP) in the arcuate nucleus provides
mechanistic evidence for its site of action. Option A supports central action but
not specifically arcuate. B shows necessity but not sufficiency for arcuate. D is
a prerequisite but not evidence of action.
9 A researcher discovers a novel hormone that activates a receptor coupled to
Gq. Which of the following second messenger changes would be expected
upon receptor activation?
A) Increased cAMP and decreased IP3