Endocrine Pharmacology Practice Questions

Q: All of the following are adverse effects of long-term corticosteroid use EXCEPT?

Hypoglycaemia. **Explanation:** **Corticosteroids** are potent metabolic and anti-inflammatory agents. The correct answer is **Hypoglycaemia** because corticosteroids actually cause **Hyperglycaemia**. 1. **Why Hypoglycaemia is the correct answer:** Glucocorticoids (like Prednisolone or Dexamethasone) are "counter-regulatory" hormones. They increase blood glucose levels by stimulating **gluconeogenesis** in the liver and decreasing peripheral glucose uptake in muscles and adipose tissue (anti-insulin effect). Long-term use can lead to "Steroid-induced Diabetes." Therefore, hypoglycaemia is not an adverse effect. 2. **Analysis of Incorrect Options:** * **Psychosis (Option B):** Corticosteroids affect the CNS, leading to "Steroid Psychosis," mood swings, euphoria, or depression. * **Peptic Ulcers (Option C):** They increase gastric acid secretion and decrease protective mucus production, especially when used concurrently with NSAIDs. * **Osteoporosis (Option D):** This is a hallmark side effect. Steroids inhibit osteoblast activity, stimulate osteoclasts, and decrease intestinal calcium absorption, leading to bone loss and pathological fractures. **High-Yield Clinical Pearls for NEET-PG:** * **Cushingoid Features:** Long-term use leads to moon facies, buffalo hump, and truncal obesity. * **Ocular Effects:** Steroids are notorious for causing **Posterior Subcapsular Cataracts** and **Glaucoma** (due to increased intraocular pressure). * **Wound Healing:** They delay healing by inhibiting fibroblast proliferation and collagen synthesis. * **Withdrawal:** Abrupt cessation after long-term use can cause **Acute Adrenal Insufficiency** (Addisonian crisis) due to HPA axis suppression. Always taper the dose.

Q: Which of the following is NOT a therapeutic use of progesterone?

Treatment of breast tumors. **Explanation:** The correct answer is **C. Treatment of breast tumors**. Progesterone and its derivatives (progestins) are generally contraindicated or not used in the treatment of breast tumors because many breast cancers are **progesterone-receptor positive**. Progestins can potentially stimulate the proliferation of these malignant cells. In fact, antiprogestins (like Mifepristone) or hormonal antagonists (like Tamoxifen) are more relevant in breast cancer management. **Analysis of other options:** * **A. Postponement of menstruation:** Administering progestins during the luteal phase maintains the endometrial lining, preventing the withdrawal bleed. Menstruation occurs only after the drug is discontinued. * **B. Post-coital pill:** High-dose progestins (e.g., Levonorgestrel 1.5mg) act as emergency contraception by delaying ovulation and altering cervical mucus to prevent fertilization. * **C. Treatment of abnormal uterine bleeding (AUB):** Progestins are the mainstay for treating AUB caused by "unopposed estrogen" (e.g., PCOS or anovulatory cycles). They stabilize the endometrium and ensure a controlled, synchronized shedding. **High-Yield Clinical Pearls for NEET-PG:** * **Luteal Phase Support:** Progesterone is essential in IVF cycles to support embryo implantation. * **Endometrial Protection:** In Hormone Replacement Therapy (HRT), progestins are added to estrogen to prevent endometrial hyperplasia and carcinoma. * **Diagnostic Use:** The "Progestin Withdrawal Test" is used to evaluate secondary amenorrhea; a positive bleed indicates adequate endogenous estrogen and a functional outflow tract. * **Endometrial Cancer:** While not used for breast cancer, high-dose progestins (Medroxyprogesterone acetate) are used in the palliative treatment of endometrial carcinoma.

Q: Both decreased bone resorption and increased bone formation are caused by which of the following agents?

Strontium ranelate. **Explanation:** The correct answer is **Strontium ranelate**. This agent is unique in the management of osteoporosis because it possesses a **dual mechanism of action**. It acts as a "Dual Acting Bone Agent" (DABA) by: 1. **Increasing bone formation:** It stimulates the proliferation of osteoblasts and increases collagen synthesis. 2. **Decreasing bone resorption:** It inhibits osteoclast differentiation and activity while promoting osteoclast apoptosis. This "uncoupling" of bone remodeling—where formation is stimulated while resorption is suppressed—distinguishes it from other drugs that typically only affect one side of the process. **Analysis of Incorrect Options:** * **B. Ibandronate:** This is a **Bisphosphonate**. Bisphosphonates are purely **anti-resorptive** agents; they inhibit osteoclasts but do not stimulate new bone formation. * **C. Teriparatide:** This is a recombinant human PTH analogue. It is a purely **anabolic** agent (at intermittent low doses) that stimulates bone formation. It does not decrease resorption; in fact, long-term use can eventually increase resorption. * **D. Calcitonin:** This is an **anti-resorptive** hormone that directly inhibits osteoclast activity. It has no bone-forming (anabolic) properties. **NEET-PG High-Yield Pearls:** * **Strontium Ranelate Side Effects:** It is associated with an increased risk of **cardiovascular events** (myocardial infarction) and **DRESS syndrome** (Drug Reaction with Eosinophilia and Systemic Symptoms). Due to cardiac risks, its use is now strictly restricted. * **Teriparatide Limit:** Due to the theoretical risk of **osteosarcoma** (seen in rat studies), clinical use is generally limited to a maximum of 24 months. * **Bisphosphonates:** The drug of choice for most osteoporosis cases; watch for **osteonecrosis of the jaw (ONJ)** and atypical subtrochanteric fractures.

Q: What is the action of oxytocin in small doses when used as an intravenous infusion in a full-term uterus?

Induces uterine contractions. **Explanation:** **Correct Answer: B. Induces uterine contractions** Oxytocin is a peptide hormone synthesized in the hypothalamus and released by the posterior pituitary. Its primary pharmacological action on the full-term uterus is the stimulation of rhythmic contractions. * **Mechanism:** Oxytocin acts via G-protein coupled receptors (Gq) to increase intracellular calcium in the myometrium. At **small doses (low-dose IV infusion)**, it increases the frequency and force of uterine contractions, mimicking natural labor. These contractions are followed by complete relaxation, ensuring fetal oxygenation is maintained. **Why other options are incorrect:** * **A. Relaxes uterus:** This is physiologically incorrect. Oxytocin is an oxytocic (stimulant); it never relaxes the myometrium. Drugs that relax the uterus are called tocolytics (e.g., Ritodrine, Nifedipine). * **C. Causes cervical dilatation:** Oxytocin does not have a direct biochemical effect on the cervix. Cervical dilatation is a **secondary result** of the mechanical pressure exerted by the fetal head during oxytocin-induced uterine contractions. For direct cervical ripening, Prostaglandins (PGE2 - Dinoprostone) are used. **High-Yield NEET-PG Pearls:** 1. **Sensitivity:** The uterus is most sensitive to oxytocin at full term due to a massive increase in oxytocin receptor expression. 2. **High Dose Risks:** At high doses, oxytocin can cause **tetanic contractions** (sustained contraction without relaxation), leading to fetal distress or uterine rupture. 3. **ADH-like effect:** Because it is structurally similar to Vasopressin, high-dose oxytocin can cause **water intoxication** and hyponatremia. 4. **Drug of Choice:** Oxytocin is the drug of choice for both **Induction of Labor** and the prevention/treatment of **Postpartum Hemorrhage (PPH)**.

Q: Corticosteroids cause all of the following except:

Muscular hypertrophy. **Explanation:** Corticosteroids, specifically glucocorticoids, are primarily **catabolic** in nature regarding peripheral tissues. The correct answer is **Muscular hypertrophy** because steroids actually cause **muscular atrophy (myopathy)**. 1. **Why Muscular Hypertrophy is incorrect:** Glucocorticoids promote the breakdown of muscle proteins into amino acids (proteolysis) to provide substrates for gluconeogenesis in the liver. This leads to muscle wasting and proximal myopathy, characterized by weakness in the shoulder and hip girdles. 2. **Peptic Ulceration:** Steroids increase gastric acid and pepsin secretion while reducing the protective mucosal barrier (by inhibiting prostaglandin synthesis). This increases the risk of peptic ulcers, especially when co-administered with NSAIDs. 3. **Psychosis:** Steroids have significant CNS effects. They can cause a range of psychiatric symptoms, from mild euphoria and insomnia to severe "steroid psychosis," mania, or depression. 4. **Suppression of Pituitary-Adrenal Axis:** Exogenous steroids exert negative feedback on the hypothalamus (CRH) and anterior pituitary (ACTH). Prolonged use leads to atrophy of the adrenal cortex, which can result in acute adrenal insufficiency if the drug is stopped abruptly. **High-Yield Clinical Pearls for NEET-PG:** * **Redistribution of Fat:** Steroids cause "Centripetal Obesity" (Buffalo hump, Moon facies, and potbelly) despite peripheral muscle wasting. * **Bone Health:** They cause osteoporosis by inhibiting osteoblast activity and decreasing calcium absorption. * **Ocular Effects:** Long-term use is a known risk factor for **Glaucoma** and **Posterior Subcapsular Cataracts**. * **Metabolic:** They cause hyperglycemia (Steroid-induced Diabetes) by increasing gluconeogenesis and decreasing peripheral glucose uptake.

Q: Carboprost, used for 2nd-trimester abortion, is an analogue of which prostaglandin?

PGF2α. Explanation: **Carboprost (15-methyl PGF2α)** is a synthetic analogue of naturally occurring **Prostaglandin F2α** [1]. The addition of a methyl group at the C-15 position increases its metabolic stability and duration of action by resisting rapid degradation by the enzyme 15-OH prostaglandin dehydrogenase [1]. **Why PGF2α is correct:** Prostaglandins of the F series are potent stimulators of uterine smooth muscle (myometrium) throughout pregnancy. Carboprost induces forceful uterine contractions and cervical ripening, making it highly effective for: 1. **Second-trimester abortions** (13–20 weeks) [1]. 2. **Postpartum Hemorrhage (PPH):** It is a second-line agent used when oxytocin fails, as it causes powerful uterine contraction to control bleeding [1]. **Analysis of Incorrect Options:** * **PGE2 (Dinoprostone):** While also used for cervical ripening and abortion, Carboprost specifically belongs to the F2α class [1]. PGE2 is primarily used for induction of labor at term [1]. * **PGI2 (Prostacyclin):** Analogues like Epoprostenol or Iloprost are used as vasodilators and inhibitors of platelet aggregation, primarily in pulmonary hypertension. * **PGD2:** This prostaglandin is involved in allergic responses and sleep regulation; it has no clinical application in obstetrics. **High-Yield NEET-PG Pearls:** * **Side Effects:** Carboprost frequently causes diarrhea and vomiting (due to GI smooth muscle stimulation) and can cause **bronchoconstriction** [1]. * **Contraindication:** It is strictly contraindicated in patients with **Asthma** [1]. * **Other PG Analogues:** * **Misoprostol:** PGE1 analogue (used for medical abortion with Mifepristone) [1]. * **Alprostadil:** PGE1 analogue (used to keep ductus arteriosus patent). * **Latanoprost:** PGF2α analogue (used in Glaucoma).

Q: What is the most common side effect of mifepristone?

Diarrhea. **Explanation:** Mifepristone is a selective progesterone receptor modulator (SPRM) used primarily for medical termination of pregnancy (MTP). While it is generally well-tolerated, it has a distinct side effect profile. **1. Why Diarrhea is Correct:** The most common side effect associated with mifepristone administration is **gastrointestinal upset**, specifically **diarrhea**. This occurs due to the drug’s secondary effects on the gastrointestinal tract and its interaction with prostaglandin pathways. While abdominal pain and cramping are also frequent, they are often attributed to the subsequent administration of Misoprostol; however, even when used alone, mifepristone frequently induces nausea and diarrhea. **2. Analysis of Incorrect Options:** * **A. Fever:** Fever and chills are very common side effects of **Misoprostol** (a PGE1 analogue), not Mifepristone. In NEET-PG, it is crucial to differentiate between the two drugs in the MTP regimen. * **C. Headache:** While reported by some patients, it is a non-specific symptom and occurs much less frequently than GI disturbances. * **D. Rash:** Skin rashes or allergic reactions are rare adverse effects and are not considered characteristic of the drug. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Mifepristone acts as an anti-progestogen by blocking receptors, leading to decidual breakdown and sensitization of the myometrium to prostaglandins. * **MTP Dosage:** The standard WHO/RCOG regimen is **200 mg Mifepristone orally**, followed 24–48 hours later by **800 mcg Misoprostol** (vaginal/sublingual/buccal). * **Contraindication:** Chronic adrenal failure (due to its anti-glucocorticoid activity) and uncontrolled asthma. * **Key Distinction:** If the question asks for the most common side effect of the *combined* MTP regimen, the answer is usually **pain/cramping** or **bleeding**. If asking specifically for Mifepristone, think **GI upset (Diarrhea/Nausea)**.

Q: A teenage girl complains of increased facial hair growth. Her menstrual cycle is regular and she has normal body weight. Which of the following may be used in the treatment of hirsutism, EXCEPT?

Mifepristone. **Explanation:** The clinical presentation describes **hirsutism** (excessive terminal hair growth in a male-pattern distribution). Treatment for hirsutism focuses on reducing androgen production or blocking androgen receptors. **Why Mifepristone is the Correct Answer:** **Mifepristone (RU-486)** is a potent **progesterone and glucocorticoid receptor antagonist**. It is primarily used for medical termination of pregnancy (up to 7 weeks) and in the management of Cushing’s syndrome (to control hyperglycemia). It has **no significant anti-androgenic activity**; therefore, it is ineffective in treating hirsutism. **Analysis of Incorrect Options:** * **Spironolactone (A):** An aldosterone antagonist that also possesses significant anti-androgenic properties. It works by blocking androgen receptors and inhibiting 5-alpha reductase. It is a first-line pharmacological treatment for hirsutism. * **Flutamide (B):** A pure non-steroidal anti-androgen that competes with testosterone and dihydrotestosterone (DHT) for binding to androgen receptors. While effective for hirsutism, its use is often limited by potential hepatotoxicity. * **Cyproterone Acetate (C):** A synthetic progestin with potent anti-androgenic activity. It blocks androgen receptors and suppresses LH/FSH, reducing ovarian androgen production. It is frequently used in combination with ethinylestradiol (as a COCP) for hirsutism. **NEET-PG High-Yield Pearls:** * **Finasteride:** Another option for hirsutism; it acts by inhibiting **Type II 5-alpha reductase**, preventing the conversion of testosterone to the more potent DHT. * **Eflornithine:** A topical cream used for hirsutism that inhibits the enzyme **ornithine decarboxylase** in hair follicles. * **First-line treatment:** Combined Oral Contraceptive Pills (COCPs) are generally the initial choice for hirsutism in women not seeking pregnancy.

Q: Prostaglandin derivatives are used in the following conditions, except:

Abortion. **Explanation:** Prostaglandin (PG) derivatives are widely used in obstetrics and gynecology due to their ability to cause cervical softening and uterine contractions. However, the question as presented contains a typographical error in the options. In the context of NEET-PG, this question typically tests the **contraindications** or **limitations** of PG use. **Understanding the Correct Answer:** Prostaglandins (like **Misoprostol/PGE1** and **Dinoprostone/PGE2**) are standard treatments for **Cervical Ripening** and **Abortion** (both medical and missed). If the "Except" option is meant to be a condition where they are avoided, it usually refers to **Previous Cesarean Section** (due to risk of uterine rupture) or **Glaucoma** (specifically for PGF2α, though Latanoprost is used topically). *Note: Given the repetitive options provided, the intended "Except" answer in standard exams is often "To maintain patency of Ductus Arteriosus" (which uses PGE1) vs "To close it" (which uses NSAIDs).* **Analysis of Options:** * **Cervical Ripening:** PGE2 (Dinoprostone) gel or inserts are the gold standard for ripening the cervix before induction of labor. * **Abortion:** Misoprostol (PGE1) is used in combination with Mifepristone for medical termination of pregnancy (MTP) up to 9-11 weeks and for second-trimester abortions. * **Postpartum Hemorrhage (PPH):** Carboprost (PGF2α) and Misoprostol are used to control bleeding by causing uterine contraction. **High-Yield NEET-PG Pearls:** 1. **Alprostadil (PGE1):** Used to keep the Ductus Arteriosus open in cyanotic heart disease. 2. **Latanoprost (PGF2α):** First-line for Open-Angle Glaucoma (increases uveoscleral outflow). 3. **Epoprostenol (PGI2):** Used in Pulmonary Hypertension. 4. **Misoprostol Side Effect:** Most common side effect is diarrhea. It is also used for NSAID-induced peptic ulcers.

Q: Sulfonylurea drugs produce hypoglycemia due to all the following mechanisms except?

Increases biosynthesis of insulin in islet tissues. **Explanation:** Sulfonylureas (SUs) are oral hypoglycemic agents that primarily act as **insulin secretagogues**. Their mechanism of action is centered on the release of pre-formed insulin rather than the production of new insulin. **1. Why Option B is the correct answer:** Sulfonylureas do **not** increase the biosynthesis (synthesis) of insulin. They act by binding to the **SUR1 subunit** of the ATP-sensitive $K^+$ channels on the pancreatic $\beta$-cell membrane. This leads to channel closure, membrane depolarization, $Ca^{2+}$ influx, and the subsequent exocytosis of **pre-stored insulin granules**. Since they trigger the release of what is already made, they do not stimulate the genetic or ribosomal machinery to synthesize more insulin. **2. Analysis of incorrect options:** * **Option A:** This is the primary mechanism. By closing $K_{ATP}$ channels, SUs directly trigger the release of insulin. * **Option C:** Chronic administration of SUs is known to have "extrapancreatic effects," which include increasing the number of insulin receptors on target tissues (like muscle and fat) and improving insulin sensitivity. * **Option D:** SUs "prime" the $\beta$-cells, making them more responsive to the natural glycemic stimulus (glucose), thereby enhancing glucose-mediated insulin secretion. **Clinical Pearls for NEET-PG:** * **First Generation SUs:** Tolbutamide, Chlorpropamide (associated with Disulfiram-like reactions and SIADH). * **Second Generation SUs:** Glibenclamide, Glipizide, Glimepiride (more potent). * **Side Effects:** Hypoglycemia (most common) and weight gain. * **Safety:** Glipizide is preferred in patients with mild renal impairment as it is primarily metabolized in the liver.

Question 1

All of the following are adverse effects of long-term corticosteroid use EXCEPT?

Accepted Answer

Hypoglycaemia

Answer

Psychosis

Answer

Peptic ulcers

Answer

Osteoporosis

Question 2

Which of the following is NOT a therapeutic use of progesterone?

Accepted Answer

Treatment of breast tumors

Answer

Postponement of menstruation

Answer

Post-coital pill

Answer

Treatment of abnormal uterine bleeding

Question 3

Both decreased bone resorption and increased bone formation are caused by which of the following agents?

Accepted Answer

Strontium ranelate

Answer

Ibandronate

Answer

Teriparatide

Answer

Calcitonin

Question 4

What is the action of oxytocin in small doses when used as an intravenous infusion in a full-term uterus?

Accepted Answer

Induces uterine contractions

Answer

Relaxes uterus

Answer

Causes cervical dilatation

Answer

All of the above

Question 5

Corticosteroids cause all of the following except:

Accepted Answer

Muscular hypertrophy

Answer

Peptic ulceration

Answer

Psychosis

Answer

Suppression of pituitary-adrenal axis

Question 6

Carboprost, used for 2nd-trimester abortion, is an analogue of which prostaglandin?

Accepted Answer

PGF2α

Answer

PGE2

Answer

PGI2

Answer

PGD2

Question 7

What is the most common side effect of mifepristone?

Accepted Answer

Diarrhea

Answer

Fever

Answer

Headache

Answer

Rash

Question 8

A teenage girl complains of increased facial hair growth. Her menstrual cycle is regular and she has normal body weight. Which of the following may be used in the treatment of hirsutism, EXCEPT?

Accepted Answer

Mifepristone

Answer

Spironolactone

Answer

Flutamide

Answer

Cyproterone

Question 9

Prostaglandin derivatives are used in the following conditions, except:

Accepted Answer

Abortion

Answer

Cervical ripening

Question 10

Sulfonylurea drugs produce hypoglycemia due to all the following mechanisms except?

Accepted Answer

Increases biosynthesis of insulin in islet tissues

Answer

Increases release of insulin from islet tissue

Answer

Increases number of insulin receptors

Answer

Sensitization of cells of islets to glucose

Endocrine Pharmacology — MCQs

Endocrine Pharmacology — MCQs

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