Endocrine Pharmacology — MCQs

Endocrine Pharmacology Indian Medical PG Practice Questions and MCQs

Question 521: Which one of the following is true of adrenal suppression due to steroid therapy?

A. It is not associated with atrophy of the adrenal glands
B. It does not occur in patients receiving inhaled steroids
C. It should be expected in anyone receiving greater than 5 mg of prednisolone daily (Correct Answer)
D. Following cessation, the stress response normalizes after 8 weeks

Explanation: ### Explanation **1. Why Option C is Correct:** Adrenal suppression occurs via the **negative feedback loop** of the Hypothalamic-Pituitary-Adrenal (HPA) axis. Exogenous glucocorticoids inhibit the release of CRH and ACTH. Chronic suppression leads to the inability of the adrenal cortex to produce endogenous cortisol. The threshold for suppression is generally considered to be **>5 mg of Prednisolone daily** (or equivalent) for more than 3 weeks. At this dose, the exogenous steroid exceeds the physiological daily cortisol production, signaling the HPA axis to shut down. **2. Why the Other Options are Incorrect:** * **Option A:** Chronic lack of ACTH stimulation leads to **disuse atrophy** of the adrenal cortex (specifically the *zona fasciculata* and *reticularis*). * **Option B:** While systemic effects are less common with inhaled steroids, **high-dose inhaled corticosteroids** (especially fluticasone) can be absorbed systemically and cause HPA axis suppression, particularly in children. * **Option D:** Recovery of the HPA axis is a slow, multi-stage process. While basal cortisol levels might return sooner, the full **stress response** (the ability to increase cortisol during surgery or infection) can take **up to 6–12 months** to normalize after long-term therapy. **3. High-Yield Clinical Pearls for NEET-PG:** * **Steroid Cover:** Patients with HPA suppression require "stress doses" of hydrocortisone during surgery or trauma to prevent an **Addisonian Crisis**. * **Tapering Rule:** Never stop steroids abruptly if used for >3 weeks; tapering allows the HPA axis to "wake up." * **Equivalent Doses:** 5 mg Prednisolone ≈ 0.75 mg Dexamethasone ≈ 4 mg Methylprednisolone ≈ 20 mg Hydrocortisone. * **Mineralocorticoid Sparing:** Dexamethasone and Betamethasone have zero mineralocorticoid activity, making them preferred for cerebral edema but not for primary adrenal insufficiency.

Question 522: Cinacalcet acts by which of the following mechanisms?

A. Inhibiting RANK-ligand
B. Activating osteoblasts
C. Decreasing parathyroid hormone secretion (Correct Answer)
D. Increasing vitamin D levels

Explanation: **Mechanism of Action** Cinacalcet is a **calcimimetic** agent. It works by increasing the sensitivity of **calcium-sensing receptors (CaSR)** located on the chief cells of the parathyroid gland to extracellular calcium. By mimicking the action of calcium, it "tricks" the gland into sensing that calcium levels are high, thereby suppressing the synthesis and release of **Parathyroid Hormone (PTH)**. **Analysis of Options** * **Option A (Inhibiting RANK-ligand):** This is the mechanism of **Denosumab**, a monoclonal antibody used in osteoporosis to prevent osteoclast maturation. * **Option B (Activating osteoblasts):** Teriparatide (recombinant PTH 1-34) acts as an anabolic agent by stimulating osteoblasts when given in intermittent doses. * **Option D (Increasing Vitamin D levels):** Vitamin D analogs (like Calcitriol or Paricalcitol) are used to suppress PTH, but Cinacalcet does not increase Vitamin D; in fact, it is often used alongside Vitamin D sterols. **Clinical Pearls for NEET-PG** * **Indications:** Secondary hyperparathyroidism in Chronic Kidney Disease (CKD) on dialysis and Parathyroid Carcinoma. * **Side Effects:** The most common side effect is **hypocalcemia** (since it lowers PTH) and GI upset (nausea/vomiting). * **Etelcalcetide:** A newer intravenous calcimimetic that also targets the CaSR. * **Key Distinction:** Unlike Vitamin D analogs, Cinacalcet lowers PTH without increasing intestinal absorption of calcium and phosphorus, making it ideal for patients with high calcium-phosphorus products.

Question 523: Steroids are indicated in all of the following conditions except?

A. Edema following extractions
B. Oral ulcers in AIDS patients (Correct Answer)
C. TMJ arthritis
D. Angioneurotic edema

Explanation: **Explanation:** The correct answer is **B. Oral ulcers in AIDS patients.** **1. Why "Oral ulcers in AIDS patients" is the correct choice:** Corticosteroids are potent immunosuppressants. In patients with AIDS, the immune system is already severely compromised (low CD4 counts). Administering steroids can further suppress local and systemic immunity, leading to the worsening of the underlying infection (viral, fungal, or bacterial) causing the ulcer [2]. Furthermore, steroids can mask signs of secondary infections and delay wound healing [3]. In AIDS patients, oral ulcers are often opportunistic (e.g., CMV, Herpes, or Fungal), where steroids are generally contraindicated unless specifically combined with potent anti-infectives for major aphthous ulcers [2]. **2. Analysis of incorrect options:** * **A. Edema following extractions:** Steroids (like Dexamethasone) are frequently used in oral surgery to reduce post-operative inflammation and edema by inhibiting the phospholipase A2 pathway and reducing capillary permeability. * **C. TMJ arthritis:** Intra-articular steroid injections are a standard treatment for non-infectious inflammatory conditions of the Temporomandibular Joint (TMJ) to reduce pain and improve mobility. * **D. Angioneurotic edema:** Steroids are a mainstay in managing acute allergic reactions and angioedema [1]. They help prevent the "late-phase" response and reduce vascular permeability, although Adrenaline remains the first-line drug for life-threatening laryngeal edema. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Steroids induce **Lipocortin (Annexin A1)**, which inhibits Phospholipase A2, blocking both Prostaglandin and Leukotriene synthesis. * **Contraindications:** "S-I-C-K-P-U-B" (Psychosis, Ulcer (Peptic), Chronic Infections (TB/Fungal), Keratitis (Herpes), Pancreatitis, Uremia, Bones (Osteoporosis)) [3]. * **Drug of Choice:** Steroids are the DOC for **Replacement therapy in Addison’s disease** and **Nephrotic syndrome**.

Question 524: All of the following are true regarding adverse effects of chlorpropamide except?

A. Releases ADH
B. Less incidence of hypoglycemia (Correct Answer)
C. More incidence of weight gain
D. Disulfiram like reaction may occur

Explanation: **Explanation:** Chlorpropamide is a **first-generation sulfonylurea** used in the management of Type 2 Diabetes Mellitus. Understanding its unique pharmacokinetic profile is key to identifying its adverse effects. **Why Option B is the Correct Answer:** Chlorpropamide has an exceptionally **long half-life (approx. 32–36 hours)** and is excreted slowly by the kidneys. Because of its prolonged duration of action, it actually carries a **higher incidence of severe and prolonged hypoglycemia** compared to other sulfonylureas, especially in elderly patients or those with renal impairment. Therefore, the statement "Less incidence of hypoglycemia" is false. **Analysis of Other Options:** * **A. Releases ADH:** Chlorpropamide is unique among sulfonylureas because it increases the secretion of Antidiuretic Hormone (ADH) and enhances the sensitivity of renal tubules to ADH. This can lead to **SIADH** and **dilutional hyponatremia**. * **C. More incidence of weight gain:** Like all sulfonylureas, chlorpropamide stimulates insulin release. Insulin is an anabolic hormone that promotes lipogenesis, leading to weight gain as a common side effect. * **D. Disulfiram-like reaction:** Chlorpropamide can inhibit aldehyde dehydrogenase. If a patient consumes alcohol while on this medication, they may experience flushing, nausea, and tachycardia (the **Disulfiram-like reaction**). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice for DI?** Chlorpropamide was historically used in **Partial Central Diabetes Insipidus** due to its ADH-potentiating effect. * **The "C" Rule:** Remember **C**hlorpropamide causes **C**onfusion (due to hyponatremia), **C**holestatic jaundice, and **C**hlorpropamide-alcohol flush. * **Avoid in Elderly:** Due to the high risk of prolonged hypoglycemia and hyponatremia, it is generally avoided in geriatric populations (Beers Criteria).

Question 525: A 54-year-old obese patient with type 2 diabetes mellitus and a history of alcoholism should probably not receive metformin because it can increase the risk of:

A. Disulfiram-like reaction
B. Hypoglycemia
C. Lactic acidosis (Correct Answer)
D. Severe hepatic toxicity

Explanation: **Explanation:** **Correct Option: C. Lactic Acidosis** Metformin, a biguanide, works primarily by inhibiting hepatic gluconeogenesis and increasing peripheral glucose uptake. However, it also inhibits the enzyme **pyruvate carboxylase** and mitochondrial respiration (Complex I). This leads to an accumulation of lactate because pyruvate cannot be converted back into glucose. In a patient with **alcoholism**, the metabolism of ethanol increases the **NADH/NAD+ ratio**, which further shifts the equilibrium from pyruvate toward lactate. The combination of metformin and chronic alcohol consumption significantly impairs lactate clearance, creating a synergistic risk for **Metformin-Associated Lactic Acidosis (MALA)**, a rare but potentially fatal metabolic emergency. **Why Incorrect Options are Wrong:** * **A. Disulfiram-like reaction:** This is classically associated with drugs like Sulfonylureas (1st generation like Chlorpropamide), Metronidazole, and certain Cephalosporins. Metformin does not interfere with aldehyde dehydrogenase. * **B. Hypoglycemia:** Metformin is an "euglycemic" agent. Unlike sulfonylureas or insulin, it does not stimulate insulin secretion; therefore, it carries a negligible risk of hypoglycemia when used as monotherapy. * **D. Severe hepatic toxicity:** While metformin is contraindicated in severe hepatic impairment (due to decreased lactate clearance), it is not inherently hepatotoxic. In fact, it is often studied for its potential benefits in Non-Alcoholic Fatty Liver Disease (NAFLD). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Metformin Contraindications:** **"CHAIR"** – **C**HF (unstable), **H**epatic failure, **A**lcoholism, **I**nfection/Ischemia, **R**enal failure (eGFR <30 mL/min). * **Renal Threshold:** Metformin must be discontinued if eGFR is <30 mL/min and should not be initiated if eGFR is <45 mL/min. * **Radiology Alert:** Metformin should be withheld for 48 hours after procedures involving **IV iodinated contrast** to prevent acute kidney injury-induced lactic acidosis. * **Vitamin Deficiency:** Long-term metformin use is associated with **Vitamin B12 deficiency** due to interference with calcium-dependent absorption in the terminal ileum.

Question 526: Which selective V2 receptor agonist is useful for the treatment of central diabetes insipidus?

A. Arginine vasopressin
B. Desmopressin (Correct Answer)
C. Lypressin
D. Terlipressin

Explanation: **Explanation:** **Desmopressin (dDAVP)** is the drug of choice for **Central Diabetes Insipidus (CDI)**. It is a synthetic analogue of Vasopressin (ADH) with two specific modifications: deamination of cysteine and substitution of L-arginine with D-arginine. These changes result in a **selective V2 receptor agonist** profile with minimal V1 (vasoconstrictor) activity. By acting on V2 receptors in the renal collecting ducts, it increases water reabsorption via aquaporin-2 channels. It also has a longer duration of action (6–24 hours) compared to natural ADH. **Analysis of Incorrect Options:** * **A. Arginine Vasopressin (AVP):** This is the naturally occurring ADH. It acts on both V1 (causing vasoconstriction) and V2 receptors. It has a very short half-life (10–20 minutes), making it impractical for the long-term management of CDI. * **C. Lypressin:** A synthetic analogue (8-lysine vasopressin) formerly used for CDI. However, it is less potent and has a shorter duration of action than Desmopressin, making it obsolete. * **D. Terlipressin:** A prodrug of lysine vasopressin with high **V1 selectivity**. It is primarily used for managing esophageal variceal bleeding and Hepatorenal Syndrome, not for its antidiuretic effects. **High-Yield Clinical Pearls for NEET-PG:** * **Routes of Desmopressin:** Available as nasal spray (most common), oral tablets, and parenteral injections. * **Other Uses of Desmopressin:** Nocturnal enuresis, Hemophilia A, and von Willebrand Disease (Type 1) because it releases Factor VIII and vWF from endothelial storage (Weibel-Palade bodies). * **Side Effect:** The most serious adverse effect is **water intoxication** leading to hyponatremia. * **Diagnostic Tip:** Desmopressin is used in the **Water Deprivation Test** to differentiate Central DI (responds to dDAVP) from Nephrogenic DI (no response).

Question 527: Which of the following contains emergency contraception?

A. Cyproterone
B. Desogestrel
C. Levonorgestrel (Correct Answer)
D. Medroxyprogesterone

Explanation: **Levonorgestrel (LNG)** is the gold standard for hormonal emergency contraception [1]. It is a second-generation synthetic progestin. When used as emergency contraception (the "morning-after pill"), it is typically administered as a single **1.5 mg dose** within 72 hours of unprotected intercourse [1]. Its primary mechanism of action is the **delay or inhibition of ovulation** by suppressing the LH surge. It is not an abortifacient and is ineffective once implantation has occurred. **Analysis of Incorrect Options:** * **Cyproterone:** An anti-androgenic progestin used primarily in the treatment of severe acne, hirsutism (PCOS), and as part of combined oral contraceptives (e.g., Diane-35) [2]. * **Desogestrel:** A third-generation progestin commonly used in "mini-pills" (Progestogen-only pills) for daily contraception [2]. It is not used in the high doses required for emergency intervention. * **Medroxyprogesterone (MPA):** Primarily used as an injectable contraceptive (**DMPA/Antara**) given every 3 months (150 mg IM). It provides long-term depot contraception rather than emergency post-coital prevention. **High-Yield Clinical Pearls for NEET-PG:** * **Yuzpe Regimen:** An older method using high doses of combined OCPs (Ethinylestradiol + Levonorgestrel); it is less effective and causes more nausea than LNG alone. * **Ulipristal Acetate:** A selective progesterone receptor modulator (SPRM) that is now considered more effective than LNG, especially between 72–120 hours [1]. * **Copper T (IUCD):** The **most effective** method of emergency contraception if inserted within 5 days of unprotected intercourse. * **Mifepristone:** Can also be used as emergency contraception at low doses (10–25 mg).

Question 528: Which of the following is NOT an established use of estrogen?

A. Treatment of senile vaginitis
B. Treatment of carcinoma of the prostate
C. Treatment of breast cancer (Correct Answer)
D. Management of delayed puberty

Explanation: **Explanation:** The correct answer is **C (Treatment of breast cancer)**. Estrogens are generally contraindicated in breast cancer because most breast tumors are **estrogen-receptor (ER) positive** [3]. Estrogen acts as a growth factor for these malignant cells, promoting tumor progression [2]. Instead, the management of breast cancer typically involves **anti-estrogens** (like Tamoxifen) or **Aromatase Inhibitors** (like Letrozole) to block estrogenic effects [3]. **Analysis of other options:** * **A. Senile Vaginitis:** Post-menopausal estrogen deficiency leads to thinning of the vaginal epithelium (atrophic vaginitis). Topical or systemic estrogen restores the mucosal integrity and is a standard treatment. * **B. Carcinoma of the Prostate:** While not the first-line treatment today (due to the availability of GnRH analogs), high-dose estrogen (e.g., Diethylstilbestrol) was historically used to suppress LH secretion via negative feedback, thereby reducing testosterone levels which drive prostate cancer. * **D. Delayed Puberty:** In girls with primary hypogonadism (e.g., Turner Syndrome), estrogen is used to induce the development of secondary sexual characteristics and ensure proper bone maturation. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Estrogen is the most effective treatment for **postmenopausal vasomotor symptoms** (hot flashes) [4]. * **Risk Factor:** Unopposed estrogen therapy increases the risk of **endometrial carcinoma**; therefore, progestins are always added in women with an intact uterus [1]. * **Side Effect:** Estrogens increase the risk of **thromboembolism** by increasing the synthesis of clotting factors (II, VII, IX, X) and decreasing Antithrombin III. * **Exception:** While estrogen generally promotes breast cancer, very high-dose estrogen was paradoxically used in the past for postmenopausal breast cancer, but it is **not** an established or standard use in modern practice.

Question 529: All of the following are anti-androgens except:

A. Finasteride
B. Flutamide
C. Cyproterone acetate
D. Dihydrotestosterone (Correct Answer)

Explanation: **Explanation:** The correct answer is **Dihydrotestosterone (DHT)**. To answer this question, one must distinguish between an androgen (agonist) and an anti-androgen (antagonist or synthesis inhibitor). **Why Dihydrotestosterone is the correct answer:** Dihydrotestosterone is a potent, naturally occurring **androgen** (agonist). It is the active metabolite of testosterone, converted by the enzyme 5-alpha reductase. DHT has a higher affinity for androgen receptors than testosterone and is responsible for the development of male external genitalia, prostate growth, and male-pattern baldness. Since it promotes androgenic effects, it is not an anti-androgen. **Why the other options are incorrect:** * **Finasteride:** It is a **5-alpha reductase inhibitor**. By preventing the conversion of testosterone to DHT, it acts as an anti-androgen. It is primarily used for Benign Prostatic Hyperplasia (BPH) and androgenic alopecia. * **Flutamide:** It is a **pure androgen receptor antagonist**. It competes with DHT for binding sites on the target cell. It is frequently used in the management of metastatic prostatic carcinoma. * **Cyproterone acetate:** It is a **steroidal androgen receptor antagonist** that also possesses progestational activity. It inhibits the feedback loop by suppressing LH secretion and is used for treating hirsutism in females and precocious puberty. **High-Yield Clinical Pearls for NEET-PG:** * **Spironolactone:** A potassium-sparing diuretic that also acts as an androgen receptor antagonist (used in PCOS). * **Abiraterone:** A CYP17 inhibitor used in castration-resistant prostate cancer to block all androgen synthesis. * **Bicalutamide:** Preferred over Flutamide for prostate cancer due to less hepatotoxicity and once-daily dosing. * **Teratogenicity:** 5-alpha reductase inhibitors (Finasteride/Dutasteride) are contraindicated in pregnancy as they can cause feminization of a male fetus.

Question 530: What is a common cause of gynecomastia and infertility in men?

A. Digitalis
B. Omeprazole
C. Erythromycin
D. Cimetidine (Correct Answer)

Explanation: **Explanation:** **Cimetidine**, a first-generation H2-receptor antagonist, is a classic cause of gynecomastia and infertility in men due to its unique endocrine side-effect profile. It acts through two primary mechanisms: 1. **Anti-androgenic effects:** It binds to androgen receptors and inhibits the action of dihydrotestosterone (DHT). 2. **Hyperprolactinemia:** It inhibits the metabolism of estradiol and can increase prolactin levels, especially when administered intravenously. These effects lead to an altered estrogen-to-androgen ratio, resulting in breast tissue enlargement (gynecomastia) and reduced sperm count (oligospermia/infertility). **Analysis of Incorrect Options:** * **A. Digitalis:** While chronic Digoxin use is associated with gynecomastia (due to its steroid-like structure which can mimic estrogen), it is not a primary or common cause of infertility compared to the potent anti-androgenic action of Cimetidine. * **B. Omeprazole:** As a Proton Pump Inhibitor (PPI), it is generally devoid of significant anti-androgenic or pro-estrogenic effects. * **C. Erythromycin:** This is a macrolide antibiotic. Its primary side effects are GI upset and QT prolongation; it does not affect the endocrine system or fertility. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Gynecomastia (DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone, **C**imetidine, **O**estrogens. * **Cimetidine & P450:** It is a potent **enzyme inhibitor**, leading to increased levels of drugs like Warfarin, Theophylline, and Phenytoin. * **Modern H2 Blockers:** Newer agents like Ranitidine, Famotidine, and Nizatidine do **not** cause these endocrine side effects.

Practice by Chapter

Hypothalamic and Pituitary Hormones

Practice Questions

Thyroid Drugs and Antithyroid Agents

Practice Questions

Insulin and Oral Hypoglycemic Agents

Practice Questions

Adrenocorticosteroids

Practice Questions

Sex Hormones: Estrogens and Progestins

Practice Questions

Androgens and Anabolic Steroids

Practice Questions

Hormonal Contraceptives

Practice Questions

Drugs Affecting Calcium Metabolism

Practice Questions

Drugs for Osteoporosis

Practice Questions

Pharmacological Management of Obesity

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free