Endocrine Pharmacology Practice Questions

Q: Finasteride acts by blocking which of the following?

5–α reductase enzyme. **Explanation:** **Mechanism of Action:** Finasteride is a competitive and specific inhibitor of the **Type II 5-α reductase enzyme**. This enzyme is responsible for the intracellular conversion of Testosterone into **Dihydrotestosterone (DHT)**, primarily in the prostate gland and hair follicles. DHT is a more potent androgen than testosterone; by blocking its production, Finasteride reduces the size of the prostate and prevents hair follicle miniaturization. **Analysis of Options:** * **Option A (α-receptors):** Drugs like Tamsulosin and Prazosin block α1-receptors. While used for BPH, they act by relaxing smooth muscles in the bladder neck rather than altering hormone levels. * **Option C (Androgen receptors):** Drugs that block androgen receptors are called anti-androgens (e.g., **Flutamide, Bicalutamide, Spironolactone**). Finasteride does not block the receptor; it reduces the concentration of the ligand (DHT). * **Option D (β-receptors):** β-blockers (e.g., Propranolol) are used in cardiovascular conditions and have no role in androgen metabolism. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Uses:** Finasteride is FDA-approved for **Benign Prostatic Hyperplasia (BPH)** and **Male Pattern Baldness (Androgenetic Alopecia)**. * **Dosing:** 5 mg/day for BPH; 1 mg/day for Alopecia. * **Dutasteride:** A related drug that inhibits both Type I and Type II 5-α reductase. * **Teratogenicity:** Finasteride is highly teratogenic (Category X). Pregnant women should not even handle crushed tablets, as it can cause hypospadias in a male fetus. * **Side Effects:** Decreased libido, erectile dysfunction, and gynecomastia.

Q: All of the following agents are useful in acromegaly EXCEPT:

Nafarelin. **Explanation:** Acromegaly is caused by the excessive secretion of **Growth Hormone (GH)**, usually due to a pituitary adenoma. Management focuses on inhibiting GH release or blocking its action. **Why Nafarelin is the correct answer:** Nafarelin is a **GnRH (Gonadotropin-Releasing Hormone) agonist**. While continuous administration of GnRH agonists suppresses the pituitary-gonadal axis (useful in precocious puberty, endometriosis, and prostate cancer), it has **no therapeutic role** in suppressing Growth Hormone. Therefore, it is ineffective in treating acromegaly. **Analysis of Incorrect Options:** * **Bromocriptine:** This is a **Dopamine (D2) agonist**. While dopamine normally stimulates GH in healthy individuals, it paradoxically inhibits GH release from the pituitary tumor in patients with acromegaly [2]. * **Somatostatin:** This is the endogenous **Growth Hormone Inhibiting Hormone (GHIH)**. It directly inhibits the secretion of GH from the anterior pituitary [1]. * **Octreotide:** This is a potent, long-acting **synthetic analog of Somatostatin** [1]. It is the preferred medical treatment for acromegaly because it has a longer half-life and is more effective than natural somatostatin [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Medical):** Somatostatin analogs like **Octreotide** or **Lanreotide** [1]. * **GH Receptor Antagonist:** **Pegvisomant** is used for resistant cases; it blocks the peripheral action of GH rather than its secretion [2]. * **Dopamine Agonists:** **Cabergoline** is generally preferred over Bromocriptine due to better efficacy and fewer side effects [2]. * **Side Effects of Octreotide:** Steatorrhea and **cholelithiasis** (gallstones) due to inhibition of cholecystokinin (CCK) and gallbladder contractility [3].

Q: Which oral hypoglycemic agent is known to cause cholestatic jaundice?

Chlorpropamide. **Explanation:** **Chlorpropamide**, a first-generation sulfonylurea, is the correct answer. While all sulfonylureas can potentially cause hepatic dysfunction, Chlorpropamide is classically associated with **cholestatic jaundice** as an idiosyncratic reaction. This occurs due to hypersensitivity leading to bile stasis within the canaliculi. **Why Chlorpropamide is the correct choice:** Chlorpropamide has a long half-life (approx. 32 hours) and is notorious for specific side effects not commonly seen with newer generations. Beyond cholestatic jaundice, it is famous for causing a **Disulfiram-like reaction** with alcohol and **SIADH** (Syndrome of Inappropriate Antidiuretic Hormone), leading to dilutional hyponatremia. **Analysis of Incorrect Options:** * **A. Tolbutamide:** A first-generation sulfonylurea with a very short half-life. While it can cause skin rashes or GI upset, it is significantly less associated with cholestatic jaundice compared to Chlorpropamide. * **B & C. Glibenclamide and Glipizide:** These are second-generation sulfonylureas. They are more potent and generally have a better safety profile regarding idiosyncratic hepatic reactions. Their primary side effect is hypoglycemia (especially Glibenclamide due to active metabolites). **NEET-PG High-Yield Pearls:** 1. **Chlorpropamide Mnemonic (The 3 Cs):** **C**holestatic jaundice, **C**hlorpropamide-alcohol flush (Disulfiram-like), and **C**oncentrated urine (SIADH). 2. **Safety in Elderly:** Chlorpropamide is generally avoided in the elderly due to the prolonged risk of hypoglycemia and hyponatremia. 3. **Renal Failure:** Most sulfonylureas are avoided in renal impairment; however, **Gliquidone** is primarily excreted in bile and is safer, while **Glipizide** is also preferred over Glibenclamide.

Q: All of the following are rare but life-threatening adverse effects of thioamide group of anti-thyroid drugs except?

Lung fibrosis. **Explanation:** Thioamides (Propylthiouracil and Methimazole/Carbimazole) are the mainstay of medical management for hyperthyroidism. While generally well-tolerated, they are associated with specific rare but severe idiosyncratic reactions. **Why Lung Fibrosis is the Correct Answer:** **Lung fibrosis** is not an adverse effect associated with thioamides. It is a classic high-yield side effect of other drugs like **Amiodarone** (an anti-arrhythmic that can cause thyroid dysfunction), **Bleomycin**, and **Busulfan**. **Analysis of Incorrect Options:** * **Agranulocytosis (A):** This is the most feared life-threatening complication (incidence 0.1–0.5%). It usually occurs within the first 3 months of therapy. Patients are strictly advised to report immediately if they develop a sore throat or fever. * **Aplastic Anemia (B):** Though extremely rare, thioamides can cause bone marrow suppression leading to pancytopenia/aplastic anemia. * **Liver Toxicity (C):** Both drugs are hepatotoxic but manifest differently. **Propylthiouracil (PTU)** is associated with severe **fulminant hepatic failure** (Black Box Warning), whereas **Methimazole** more commonly causes **cholestatic jaundice**. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Methimazole is preferred due to its longer half-life and lower risk of liver failure, except in specific scenarios. * **Pregnancy:** **PTU** is the drug of choice in the **1st trimester** (less teratogenic; Methimazole causes *Aplasia Cutis*). **Methimazole** is preferred in the **2nd and 3rd trimesters** to avoid PTU-induced maternal hepatotoxicity. * **Thyroid Storm:** PTU is preferred because it also inhibits the peripheral conversion of T4 to T3. * **ANCA-associated vasculitis** is another rare, life-threatening side effect specifically linked to PTU.

Q: Which of the following drugs does NOT cause thyroid dysfunction?

Paracetamol. **Explanation:** **Paracetamol (Acetaminophen)** is the correct answer because it is a centrally acting analgesic and antipyretic that has no significant interaction with the hypothalamic-pituitary-thyroid axis or thyroid hormone metabolism. It does not interfere with iodine uptake, hormone synthesis, or peripheral conversion. **Why the other options are incorrect:** * **Amiodarone:** This iodine-rich antiarrhythmic frequently causes thyroid dysfunction. It can lead to **hypothyroidism** (Wolff-Chaikoff effect) or **hyperthyroidism** (Jod-Basedow phenomenon or destructive thyroiditis). It also inhibits the peripheral conversion of T4 to T3. * **Lithium:** Used in bipolar disorder, lithium inhibits the release of thyroid hormones from the gland. It is a well-known cause of **drug-induced hypothyroidism** and goiter. * **Cholestyramine:** This bile acid sequestrant binds to thyroid hormones in the gastrointestinal tract, interfering with their enterohepatic circulation and significantly **reducing the absorption** of oral levothyroxine. **High-Yield Clinical Pearls for NEET-PG:** * **Wolff-Chaikoff Effect:** Autoregulation where high iodine levels (e.g., from Amiodarone) inhibit thyroid hormone synthesis. * **Drugs inhibiting T4 to T3 conversion:** Propranolol, Glucocorticoids, Amiodarone, and Propylthiouracil (PTU). * **Phenytoin/Carbamazepine:** These induce hepatic enzymes (CYP450), increasing the metabolism of T4 and potentially necessitating higher doses of levothyroxine. * **Amiodarone Content:** Each 200mg tablet contains approximately 75mg of organic iodine.

Q: Which type of insulin is used to manage a case of diabetic ketoacidosis?

Regular. **Explanation:** In the management of **Diabetic Ketoacidosis (DKA)**, the primary goal is to suppress ketogenesis and normalize blood glucose levels. **Regular (Soluble) Insulin** is the gold standard and the only insulin formulation recommended for **intravenous (IV) administration** in DKA. **Why Regular Insulin is Correct:** Regular insulin is a short-acting insulin that, when given intravenously, has an immediate onset of action and a very short half-life (approx. 5–10 minutes). This allows for precise, minute-to-minute titration via a continuous infusion pump, which is essential to prevent rapid shifts in osmolarity and to manage the dynamic metabolic state of a DKA patient. **Why Other Options are Incorrect:** * **Lispro and Aspart (Options B & D):** These are ultra-short-acting insulin analogs. While they can be used subcutaneously in mild DKA, they are not the standard for IV management in acute, severe cases. They are more expensive than Regular insulin without providing additional benefits in an IV setting. * **Glargine (Option C):** This is a long-acting, peakless insulin analog used for basal coverage. It has a slow onset and is never used for the acute management of DKA because its effects cannot be quickly reversed if hypoglycemia occurs. **High-Yield Clinical Pearls for NEET-PG:** * **Route of Choice:** IV bolus followed by continuous IV infusion (0.1 units/kg/hr) is the preferred protocol. * **The "Switch":** Transition from IV Regular insulin to subcutaneous insulin only when the **anion gap has closed**, the patient is conscious, and is able to tolerate oral intake. * **Potassium Warning:** Always check potassium levels before starting insulin; insulin shifts $K^+$ into cells, potentially worsening hypokalemia. * **Bicarbonate:** Not routinely used unless pH is < 6.9.

Q: All of the following drugs are useful in nephrogenic diabetes insipidus, except?

Chlorpropamide. **Explanation:** **Nephrogenic Diabetes Insipidus (NDI)** occurs when the kidneys are unresponsive to Antidiuretic Hormone (ADH). Therefore, drugs that work by enhancing ADH action or mimicking it are ineffective. **Why Chlorpropamide is the Correct Answer:** Chlorpropamide is a first-generation sulfonylurea used in **Central Diabetes Insipidus**. It works by sensitizing the renal tubules to the action of ADH and increasing ADH release from the posterior pituitary. Since the fundamental defect in NDI is renal resistance to ADH, chlorpropamide has no therapeutic effect in this condition. **Analysis of Incorrect Options:** * **Thiazide Diuretics (e.g., Hydrochlorothiazide):** Paradoxically used in NDI. They cause mild hypovolemia, leading to increased proximal tubule reabsorption of salt and water, which reduces the volume of filtrate delivered to the distal nephron, thereby decreasing urine output. * **Amiloride:** This is the **drug of choice for Lithium-induced NDI**. It blocks the Epithelial Sodium Channels (ENaC) in the collecting duct, preventing lithium from entering the cells and exerting its toxic effects. * **Indomethacin:** NSAIDs inhibit prostaglandin synthesis. Since prostaglandins (PGE2) normally antagonize ADH action, inhibiting them enhances water reabsorption and reduces renal blood flow, decreasing urine volume. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for Central DI:** Desmopressin (dDAVP). * **Drug of Choice for NDI (General):** Thiazides. * **Drug of Choice for Lithium-induced NDI:** Amiloride. * **Most common cause of NDI in adults:** Lithium therapy. * **Most common cause of NDI in children:** X-linked recessive mutation in the V2 receptor.

Q: Which thyroid inhibitor produces the fastest response?

Lugol's iodine. **Explanation:** The speed of response in treating hyperthyroidism depends on whether the drug inhibits the **synthesis** of new hormones or the **release** of pre-formed hormones. **1. Why Lugol’s Iodine is Correct:** Lugol’s iodine (potassium iodide) acts by inhibiting the **release** of thyroid hormones from the colloid into the circulation. This occurs via the **Wolff-Chaikoff effect**, where high concentrations of iodine acutely suppress thyroid peroxidase and endocytosis of thyroglobulin. Because it acts on pre-formed hormones already stored in the gland, the clinical response is seen within **1–2 days**, making it the fastest-acting agent. **2. Why the Other Options are Incorrect:** * **Propylthiouracil (PTU):** This is an antithyroid drug (thioamide) that inhibits the **synthesis** of new hormones by blocking thyroid peroxidase. It does not affect stored hormones; therefore, it takes **1–3 weeks** to show clinical effects as the existing stores must first be depleted. * **Radioactive Iodine (I-131):** This works by emitting beta particles that destroy thyroid tissue. The process of follicular destruction is slow, usually taking **2–3 months** for full effect. * **Lithium Carbonate:** While lithium can inhibit hormone release (similar to iodine), it is significantly less potent and slower than Lugol's iodine. It is rarely used clinically for this purpose due to its narrow therapeutic index. **NEET-PG High-Yield Pearls:** * **Pre-operative use:** Lugol’s iodine is given 10 days before thyroidectomy to decrease the **vascularity and size** of the gland, making it firm and easier to operate on. * **Escape Phenomenon:** The effect of iodine lasts only for 10–14 days, after which the thyroid "escapes" the inhibition and thyrotoxicosis may worsen. * **Drug of Choice in Pregnancy:** PTU is preferred in the **1st trimester** (due to less teratogenicity), while Methimazole is preferred in the 2nd and 3rd trimesters.

Question 1

Finasteride acts by blocking which of the following?

Accepted Answer

5–α reductase enzyme

Answer

α-receptors

Answer

Androgen receptors

Answer

β–receptors

Question 2

Which of the following is NOT a mechanism of action of an oral contraceptive containing a combination of oestrogen-progestin?

Accepted Answer

A change in the cervical mucus

Answer

Inhibition of ovulation

Answer

Inhibition of motility of the uterine tubes

Answer

Inhibition of motility of sperm

Question 3

All of the following agents are useful in acromegaly EXCEPT:

Accepted Answer

Nafarelin

Answer

Bromocriptine

Answer

Somatostatin

Answer

Octreotide

Question 4

Which oral hypoglycemic agent is known to cause cholestatic jaundice?

Accepted Answer

Chlorpropamide

Answer

Tolbutamide

Answer

Glibenclamide

Answer

Glipizide

Question 5

All of the following are rare but life-threatening adverse effects of thioamide group of anti-thyroid drugs except?

Accepted Answer

Lung fibrosis

Answer

Agranulocytosis

Answer

Aplastic anemia

Answer

Liver toxicity

Question 6

Which of the following drugs does NOT cause thyroid dysfunction?

Accepted Answer

Paracetamol

Answer

Amiodarone

Answer

Lithium

Answer

Cholestyramine

Question 7

Which type of insulin is used to manage a case of diabetic ketoacidosis?

Accepted Answer

Regular

Answer

Lispro

Answer

Glargine

Answer

Aspart

Question 8

All of the following drugs are useful in nephrogenic diabetes insipidus, except?

Accepted Answer

Chlorpropamide

Answer

Amiloride

Answer

Indomethacin

Answer

Thiazide diuretics

Question 9

Use of Ergotamine is contraindicated in which of the following conditions?

Accepted Answer

Ischaemic heart disease

Answer

Diabetes mellitus

Answer

Anemia

Answer

Postpartum hemorrhage

Question 10

Which thyroid inhibitor produces the fastest response?

Accepted Answer

Lugol's iodine

Answer

Propylthiouracil

Answer

Radioactive iodine

Answer

Lithium carbonate

Endocrine Pharmacology — MCQs

Endocrine Pharmacology — MCQs

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