Endocrine pharmacology: growth hormone mechanisms MCQs With Answer

Endocrine pharmacology: growth hormone mechanisms MCQs With Answer

This question set is designed for M.Pharm students to deepen understanding of growth hormone (GH) pharmacology and its molecular mechanisms. It emphasizes receptor biology, intracellular signaling cascades (JAK-STAT, MAPK, PI3K-Akt), regulation by hypothalamic peptides and IGF‑1, clinical drugs (somatropin, pegvisomant, somatostatin analogs, GHRH/GHRP analogs), and pharmacokinetic/pharmacodynamic considerations. Each MCQ targets core concepts useful for therapeutics, drug development, and interpretation of endocrine assays. These questions will help you connect basic receptor mechanisms to clinical management of GH deficiency and excess, identify drug actions and adverse effects, and prepare for advanced pharmacy examinations and research discussions.

Q1. Which intracellular pathway is the primary mediator of growth hormone-induced transcriptional activation of IGF-1 in hepatocytes?

• cAMP-dependent PKA pathway
• JAK2-STAT5 signaling pathway
• PKC-ERK pathway initiated by GPCRs
• Wnt/β-catenin pathway

Correct Answer: JAK2-STAT5 signaling pathway

Q2. Pegvisomant is an effective drug for acromegaly because it primarily:

• Inhibits somatostatin release from the hypothalamus
• Acts as a GH receptor antagonist by preventing receptor dimerization
• Stimulates IGF-1 degradation in the liver
• Enhances proteasomal degradation of circulating GH

Correct Answer: Acts as a GH receptor antagonist by preventing receptor dimerization

Q3. Somatostatin analogs (e.g., octreotide) reduce GH secretion mainly by:

• Directly blocking pituitary GH receptor signaling
• Activating somatostatin receptors on pituitary somatotrophs to inhibit adenylate cyclase
• Increasing hypothalamic GHRH release to produce negative feedback
• Enhancing peripheral IGF-1 action to suppress GH synthesis

Correct Answer: Activating somatostatin receptors on pituitary somatotrophs to inhibit adenylate cyclase

Q4. Which physiologic regulator acts as a potent GH secretagogue by binding to a specific GPCR in the hypothalamus and pituitary?

• Somatostatin
• Ghrelin (via GHS-R)
• Insulin-like growth factor-1 (IGF-1)
• Leptin

Correct Answer: Ghrelin (via GHS-R)

Q5. Laron syndrome (primary GH insensitivity) is most commonly caused by mutations in the:

• IGF-1 gene leading to loss of IGF-1 secretion
• GH1 gene causing absence of GH synthesis
• GH receptor gene leading to defective GH signaling
• Somatostatin receptor gene increasing inhibition of GH

Correct Answer: GH receptor gene leading to defective GH signaling

Q6. Which effect of GH is mediated predominantly via hepatic IGF‑1 rather than direct GH action on peripheral tissues?

• Acute lipolysis in adipose tissue
• Stimulating linear bone growth through chondrocytes
• Rapid glucose uptake into skeletal muscle
• Immediate catabolism of muscle proteins

Correct Answer: Stimulating linear bone growth through chondrocytes

Q7. A somatropin preparation used for GH replacement therapy differs from endogenous GH mainly by:

• Being a GH analog with modified receptor-binding domain causing antagonism
• Being recombinant human GH identical in amino acid sequence to pituitary GH
• Containing additional somatostatin to reduce side effects
• Having truncated peptides that preferentially activate IGF-1

Correct Answer: Being recombinant human GH identical in amino acid sequence to pituitary GH

Q8. Which laboratory change is most consistent with effective pegvisomant therapy in acromegaly?

• Decreased serum GH concentration with increased IGF‑1
• Unchanged GH but decreased serum IGF‑1 concentration
• Marked reduction in GH-binding protein levels
• Increased hepatic expression of GH receptor mRNA

Correct Answer: Unchanged GH but decreased serum IGF‑1 concentration

Q9. Which statement correctly describes GH receptor activation on target cells?

• GH binding induces cytosolic proteases to liberate transcription factors
• GH binds to preformed receptor dimers causing conformational change and JAK2 activation
• GH binding to GPCRs increases cAMP to activate PKA and STATs
• GH directly enters the cell to interact with nuclear DNA

Correct Answer: GH binds to preformed receptor dimers causing conformational change and JAK2 activation

Q10. Which intracellular negative regulator attenuates GH signaling by targeting JAK-STAT components?

• SOCS (suppressor of cytokine signaling) proteins
• CREB-binding protein (CBP)
• Heat-shock protein 90 (Hsp90)
• Protein kinase A regulatory subunit

Correct Answer: SOCS (suppressor of cytokine signaling) proteins

Q11. Which pharmacologic agent would most likely increase GH secretion when administered acutely?

• Octreotide
• Clonidine (α2-adrenergic agonist)
• Insulin infusion causing hypoglycemia
• Exogenous IGF-1

Correct Answer: Insulin infusion causing hypoglycemia

Q12. Growth hormone causes insulin resistance primarily through which mechanism?

• Direct inhibition of pancreatic insulin secretion
• Activation of hepatic glucokinase to lower hepatic glucose uptake
• Induction of lipolysis leading to increased free fatty acids that impair insulin signaling
• Upregulation of GLUT4 translocation in adipocytes

Correct Answer: Induction of lipolysis leading to increased free fatty acids that impair insulin signaling

Q13. Which drug class is used to suppress GH hypersecretion and is most effective for patients with pituitary adenomas unresponsive to surgery?

• GH receptor antagonists only
• Somatostatin analogs (octreotide, lanreotide)
• Thyroid hormone replacement agents
• Estrogen receptor modulators

Correct Answer: Somatostatin analogs (octreotide, lanreotide)

Q14. Which property of pegylated GH preparations improves their clinical utility compared to native GH?

• Increased affinity for the GH receptor leading to stronger signaling
• Reduced immunogenicity and prolonged plasma half-life
• Complete resistance to proteolytic degradation in the gut allowing oral dosing
• Ability to cross the blood-brain barrier and modulate hypothalamic release

Correct Answer: Reduced immunogenicity and prolonged plasma half-life

Q15. IGF-binding proteins (IGFBPs) modulate IGF-1 action primarily by:

• Accelerating IGF-1 degradation to terminate signaling
• Sequestering IGF-1 in circulation and regulating its bioavailability
• Transporting IGF-1 into mitochondria for metabolic effects
• Directly binding IGF-1 receptors to activate downstream kinases

Correct Answer: Sequestering IGF-1 in circulation and regulating its bioavailability

Q16. Which laboratory pattern is characteristic of GH deficiency in adults?

• Elevated IGF-1 with suppressed GH on stimulation testing
• Low IGF-1 and blunted GH response to stimulation tests
• Normal IGF-1 with excessive nocturnal GH pulses
• High GH-binding protein with low IGF-1

Correct Answer: Low IGF-1 and blunted GH response to stimulation tests

Q17. Which statement correctly explains why GH therapy may worsen glucose tolerance?

• GH directly stimulates pancreatic β-cell apoptosis leading to insulin deficiency
• GH increases hepatic glucose uptake and storage, lowering blood sugar
• GH antagonizes insulin action in peripheral tissues, reducing glucose uptake
• GH binds to insulin receptors competitively, blocking insulin signaling

Correct Answer: GH antagonizes insulin action in peripheral tissues, reducing glucose uptake

Q18. Tesamorelin, a synthetic GHRH analog used clinically, exerts its effect by:

• Direct antagonism of the GH receptor in peripheral tissues
• Stimulating pituitary somatotrophs via GHRH receptor to increase GH release
• Mimicking somatostatin to inhibit GH pulses
• Binding to IGF-1 receptors to increase negative feedback

Correct Answer: Stimulating pituitary somatotrophs via GHRH receptor to increase GH release

Q19. In the JAK-STAT pathway activated by GH, STAT5 phosphorylation primarily leads to:

• Immediate cytoskeletal rearrangements without transcriptional change
• Nuclear translocation of STAT5 and transcriptional activation of IGF-1 and other genes
• Direct inhibition of ribosomal RNA synthesis
• Targeted degradation of GH receptor by lysosomes

Correct Answer: Nuclear translocation of STAT5 and transcriptional activation of IGF-1 and other genes

Q20. Which adverse effect is most commonly associated with long-term supraphysiologic GH therapy?

• Hypoglycemia due to increased insulin sensitivity
• Carpal tunnel syndrome and edema due to soft tissue overgrowth
• Progressive hypotension from decreased vascular tone
• Marked hyperpigmentation from melanocyte stimulation

Correct Answer: Carpal tunnel syndrome and edema due to soft tissue overgrowth

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