Endocrine Pharmacology Practice Questions

Q: What is the primary route of administration for GnRH analogues?

Subcutaneous. **Explanation:** **1. Why Subcutaneous is Correct:** GnRH (Gonadotropin-Releasing Hormone) analogues, such as **Leuprolide, Goserelin, and Nafarelin**, are synthetic decapeptides. Because they are peptides, they are susceptible to rapid degradation by proteolytic enzymes in the gastrointestinal tract if taken orally. The **subcutaneous (SC)** route is preferred because it allows for the formulation of **depot preparations**. These depots provide a sustained, slow release of the drug over weeks or months, which is essential for achieving the therapeutic goal of "medical castration" (downregulation of GnRH receptors to suppress FSH and LH). **2. Why Other Options are Incorrect:** * **Oral:** As mentioned, GnRH analogues are peptides. They have poor bioavailability due to gastric acid degradation and first-pass metabolism. * **Intravenous (IV):** While possible, the IV route results in a very short half-life (minutes) and lacks the sustained-release profile required for chronic conditions like prostate cancer or endometriosis. * **Transdermal:** The large molecular size and hydrophilic nature of these peptides make them unsuitable for passive diffusion through the skin barrier. **3. Clinical Pearls for NEET-PG:** * **Biphasic Action:** Initial administration causes a "flare-up" (transient increase in LH/FSH), followed by downregulation and desensitization of pituitary GnRH receptors. * **Alternative Route:** **Intranasal** administration (e.g., Nafarelin) is used for shorter-term indications like endometriosis or precocious puberty, though SC remains the primary route for long-term therapy. * **Therapeutic Uses:** Prostate cancer, endometriosis, uterine fibroids, and central precocious puberty. * **Antagonists vs. Agonists:** Unlike analogues (agonists), GnRH **antagonists** (e.g., Degarelix, Cetrorelix) produce immediate suppression without the initial flare-up.

Q: All of the following are side effects of steroids except?

Osteomalacia. **Explanation:** The correct answer is **Osteomalacia** because glucocorticoids (steroids) cause **Osteoporosis**, not osteomalacia. 1. **Why Osteomalacia is incorrect:** Osteomalacia is a defect in bone *mineralization* (soft bones), usually due to Vitamin D deficiency. Steroids, however, cause a decrease in bone *density* (brittle bones) by inhibiting osteoblast activity, stimulating osteoclasts, and decreasing intestinal calcium absorption. This leads to **Osteoporosis** and an increased risk of avascular necrosis of the femoral head. 2. **Analysis of other options:** * **Hyperglycemia:** Steroids are "diabetogenic." They increase gluconeogenesis in the liver and decrease peripheral glucose uptake (insulin resistance), often leading to steroid-induced diabetes. * **Infection:** Steroids are potent immunosuppressants. They inhibit NF-κB, decrease cytokine production (IL-1, IL-2), and cause lymphopenia, masking signs of inflammation and increasing susceptibility to opportunistic infections (e.g., Tuberculosis reactivation). * **Peptic Ulcer:** Steroids inhibit phospholipase A2, reducing protective prostaglandins in the gastric mucosa. When used with NSAIDs, the risk of peptic ulceration and perforation increases significantly. **Clinical Pearls for NEET-PG:** * **Mnemonic for Steroid Side Effects:** "CUSHINGOID" (Cataracts, Ulcers, Striae/Skin thinning, Hypertension, Immunosuppression, Necrosis of femoral head, Glucose elevation, Osteoporosis, Impaired wound healing, Depression/Psychosis). * **Ocular effects:** Steroids cause **posterior subcapsular cataracts** and can increase intraocular pressure (glaucoma). * **Growth:** In children, they cause growth retardation due to premature closure of epiphyseal plates.

Q: Which of the following is true about Metformin?

Reduces lipogenesis in adipose tissue.. **Explanation:** Metformin, a Biguanide, is the first-line oral hypoglycemic agent for Type 2 Diabetes Mellitus. Its primary mechanism involves the activation of **AMP-activated protein kinase (AMPK)**. **Why Option C is Correct:** Activation of AMPK leads to the inhibition of **Acetyl-CoA carboxylase (ACC)**. This results in decreased fatty acid synthesis (**reduced lipogenesis**) and increased fatty acid oxidation. In adipose tissue, this metabolic shift helps improve insulin sensitivity and contributes to the weight-neutral or weight-loss profile of the drug. **Analysis of Incorrect Options:** * **Option A:** Metformin is an **"euglycemic"** agent, not a hypoglycemic one. It does not stimulate insulin release; therefore, the risk of hypoglycemia is negligible when used as monotherapy. * **Option B:** Metformin **decreases** hepatic gluconeogenesis (the primary mechanism for lowering fasting blood glucose) by inhibiting mitochondrial glycerophosphate dehydrogenase (mGPD). * **Option D:** Metformin does not affect the pancreatic beta cells; it **increases peripheral glucose uptake** (sensitizes tissues to existing insulin) rather than increasing insulin secretion. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** First-line for T2DM and Polycystic Ovarian Syndrome (PCOS). * **Side Effects:** Most common are GI-related (diarrhea, abdominal pain). The most dreaded is **Lactic Acidosis** (avoid in renal failure, CrCl <30 ml/min). * **Vitamin Deficiency:** Long-term use can lead to **Vitamin B12 deficiency** due to interference with its absorption in the terminal ileum. * **Pleiotropic Effect:** It is associated with a reduced risk of certain cancers and cardiovascular mortality.

Q: Which among the following is not an androgen receptor blocker?

Finasteride. **Explanation:** The correct answer is **Finasteride** because it is not an androgen receptor blocker; rather, it is a **5-alpha reductase inhibitor**. **1. Why Finasteride is the correct answer:** Finasteride works by inhibiting the enzyme 5-alpha reductase (specifically Type II), which converts Testosterone into its more potent metabolite, **Dihydrotestosterone (DHT)**. It does not bind to or block the androgen receptor itself. It is primarily used in the treatment of Benign Prostatic Hyperplasia (BPH) and Male Pattern Baldness (Androgenetic Alopecia). **2. Why the other options are incorrect:** * **Cyproterone:** This is a steroidal anti-androgen that acts as a competitive antagonist at the androgen receptor. It also has progestational activity, which suppresses LH secretion, further reducing testosterone levels. * **Flutamide:** This is a non-steroidal (pure) anti-androgen that competitively blocks androgen receptors. It is frequently used in the management of metastatic prostatic carcinoma. **High-Yield NEET-PG Pearls:** * **Dutasteride:** Unlike Finasteride, Dutasteride inhibits both Type I and Type II 5-alpha reductase. * **Bicalutamide & Enzalutamide:** Newer non-steroidal anti-androgens preferred over Flutamide due to better safety profiles (lower hepatotoxicity). * **Spironolactone:** Primarily a potassium-sparing diuretic, but also acts as a weak androgen receptor blocker, often used clinically for hirsutism in females. * **Side Effects:** Finasteride can cause erectile dysfunction and decreased libido due to reduced DHT levels. Cyproterone can cause hepatotoxicity and gynecomastia.

Q: Which insulin has a late onset of action, longer duration of action, and no pronounced peak?

Glargine. ### Explanation **Correct Option: C. Glargine** Insulin Glargine is a **long-acting basal insulin analog**. Its unique pharmacokinetic profile is due to its chemical structure: the addition of two arginine residues and the substitution of glycine. * **Mechanism:** It is soluble at an acidic pH (4.0) but **precipitates** into micro-crystals upon subcutaneous injection (neutral pH). These crystals dissolve slowly, resulting in a steady, slow release into the bloodstream. * **Profile:** This provides a "peakless" (flat) concentration curve, a late onset (1–2 hours), and a long duration of action (up to 24 hours), mimicking the natural basal secretion of the pancreas. **Incorrect Options:** * **A. NPH (Neutral Protamine Hagedorn):** An intermediate-acting insulin. Unlike Glargine, it has a **distinct peak** (4–10 hours) and a shorter duration (12–18 hours), which increases the risk of nocturnal hypoglycemia. * **B. Glulisine & D. Aspart:** These are **rapid-acting insulin analogs**. They have a very fast onset (5–15 mins), a sharp peak (1 hour), and a short duration (3–5 hours). They are used specifically for postprandial (mealtime) glucose control. **NEET-PG High-Yield Pearls:** 1. **Basal Insulins:** Glargine, Detemir, and Degludec. **Degludec** has the longest half-life (>40 hours). 2. **Mixing:** Glargine should **not** be mixed in the same syringe with other insulins because its acidic pH can cause the other insulin to precipitate. 3. **Safety:** Because Glargine is peakless, it carries a significantly **lower risk of nocturnal hypoglycemia** compared to NPH. 4. **Rapid-acting Mnemonic:** "No **LAG**" (**L**ispro, **A**spart, **G**lulisine).

Q: Antithyroid drugs are indicated in which of the following conditions, except?

Prophylaxis of endemic goiter. **Explanation:** The primary goal of **Antithyroid Drugs (ATDs)** like Methimazole, Carbimazole, and Propylthiouracil (PTU) is to inhibit the synthesis of thyroid hormones by blocking the enzyme thyroid peroxidase. **Why Option D is the Correct Answer:** **Endemic goiter** is primarily caused by **iodine deficiency**, leading to low T3/T4 levels and a compensatory rise in TSH, which causes thyroid enlargement. Treating or preventing this condition with antithyroid drugs is contraindicated because ATDs further decrease hormone synthesis, which would worsen the hypothyroidism and exacerbate the goiter. The correct management for endemic goiter is **Iodine supplementation** (e.g., iodized salt). **Analysis of Incorrect Options:** * **A. Graves' Disease:** This is an autoimmune condition causing hyperthyroidism. ATDs are the first-line medical management to achieve remission. * **B. Toxic Nodular Goiter:** Characterized by hyperfunctioning nodules. While surgery or radioiodine is often definitive, ATDs are used to control thyrotoxic symptoms and render the patient euthyroid before surgery. * **C. Along with Radioactive Iodine (RAI):** ATDs are used **before** RAI to deplete thyroid hormone stores (preventing a thyroid storm post-radiation) and **after** RAI to maintain euthyroidism until the radiation effect fully manifests (which can take 3–6 months). **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Methimazole is generally preferred over PTU due to its longer half-life and lower hepatotoxicity. * **Pregnancy:** **PTU** is preferred in the **1st trimester** (less teratogenic; Methimazole causes *Aplasia Cutis*). **Methimazole** is preferred in the **2nd and 3rd trimesters** (to avoid PTU-induced hepatotoxicity). * **Most Serious Side Effect:** **Agranulocytosis** (presents as fever and sore throat); requires immediate discontinuation of the drug.

Q: Tamoxifen is known to predispose patients to which of the following conditions?

Endometrial cancer. **Explanation:** Tamoxifen is a **Selective Estrogen Receptor Modulator (SERM)**. Its mechanism of action is tissue-specific: it acts as an **antagonist** in the breast (used for treating ER-positive breast cancer) but acts as a **partial agonist** in the uterus. 1. **Why Endometrial Cancer is Correct:** In the postmenopausal uterus, Tamoxifen’s estrogenic effect leads to endometrial proliferation. Chronic stimulation can result in endometrial hyperplasia, polyps, and a 2- to 3-fold increased risk of **Endometrial Adenocarcinoma** (specifically Type I). 2. **Why Other Options are Incorrect:** * **Ovarian Cancer:** Tamoxifen does not have a significant stimulatory effect on the ovarian epithelium; in fact, some studies suggest it may have a protective or neutral effect. * **Cervical and Vaginal Cancer:** These are primarily associated with High-risk HPV infection (Cervical) or DES exposure in utero (Clear cell adenocarcinoma of the vagina), rather than SERM therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Raloxifene:** Unlike Tamoxifen, Raloxifene is an estrogen antagonist in both the breast and the uterus, meaning it **does not** increase the risk of endometrial cancer. * **Monitoring:** Routine endometrial biopsy or ultrasound is not recommended for asymptomatic women on Tamoxifen. However, any **postmenopausal bleeding** in these patients must be investigated immediately with Transvaginal Ultrasound (TVS) and biopsy. * **Other Side Effects:** Tamoxifen increases the risk of **Thromboembolism** (DVT/PE) and causes vasomotor symptoms (hot flashes). * **Benefit vs. Risk:** Despite the risk of endometrial cancer, the benefit of Tamoxifen in preventing breast cancer recurrence far outweighs the risk in most patients.

Question 1

What is the primary route of administration for GnRH analogues?

Accepted Answer

Subcutaneous

Answer

Oral

Answer

Intravenous

Answer

Transdermal

Question 2

All of the following are side effects of steroids except?

Accepted Answer

Osteomalacia

Answer

Hyperglycemia

Answer

Infection

Answer

Peptic ulcer

Question 3

Which of the following is true about Metformin?

Accepted Answer

Reduces lipogenesis in adipose tissue.

Answer

Hypoglycemia is very common.

Answer

Increases hepatic gluconeogenesis.

Answer

Increases the secretion of insulin.

Question 4

Which of the following is an irreversible aromatase inhibitor?

Accepted Answer

Exemestane

Answer

Anastrozole

Answer

Letrozole

Answer

Vorozole

Question 5

Which among the following is not an androgen receptor blocker?

Accepted Answer

Finasteride

Answer

Cyproterone

Answer

Flutamide

Answer

None of the above

Question 6

Which insulin has a late onset of action, longer duration of action, and no pronounced peak?

Accepted Answer

Glargine

Answer

NPH

Answer

Glulisine

Answer

Aspart

Question 7

Antithyroid drugs are indicated in which of the following conditions, except?

Accepted Answer

Prophylaxis of endemic goiter

Answer

Graves' disease

Answer

Toxic nodular goiter

Answer

Along with radioactive iodine

Question 8

Beta blockers are used in hyperthyroidism:

Accepted Answer

As short-term symptomatic therapy until the effect of carbimazole develops

Answer

As long-term therapy after subtotal thyroidectomy

Answer

In patients not responding to carbimazole

Answer

To potentiate the effect of radioactive iodine

Question 9

Tamoxifen is known to predispose patients to which of the following conditions?

Accepted Answer

Endometrial cancer

Answer

Ovarian cancer

Answer

Cervical cancer

Answer

Vaginal cancer

Question 10

A 62-year-old female presents to the emergency with acute severe low back pain after sitting down quickly. She has a history of rheumatoid arthritis and bronchial asthma and reports being on multiple medications for several years. X-ray shows a fracture of the fifth lumbar vertebra. Which of the following drugs is likely responsible for the patient's condition?

Accepted Answer

Prednisolone

Answer

Methotrexate

Answer

Indomethacin

Answer

Salbutamol

Endocrine Pharmacology — MCQs

Endocrine Pharmacology — MCQs

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