Endocrinology — MCQs

A 47-year-old woman presents with increasing headaches and visual changes. On examination, her pupils are normal and reactive to light, the extraocular movements are normal, and there are visual field defects of the outer half in both eyes (bitemporal hemianopsia). Which of the following is the most likely diagnosis?

Q25Medium

Lisch nodules and a pancreatic somatostatinoma are seen in which condition?

Q26Medium

What is the earliest presentation of hypopituitarism in adults?

Q27Medium

Which of the following findings does not occur in a patient with gastrinoma?

Q28Medium

An 80-year-old woman, previously in sinus rhythm, developed atrial fibrillation with rapid ventricular response during an ICU stay for sepsis. She was treated with amiodarone, converted to sinus rhythm, and was discharged on maintenance amiodarone. In the following weeks, she presented with increasing fatigue, dry skin, and constipation. Laboratory tests revealed a TSH of 25 mIU/L. What is the best management approach in this situation?

Q29Easy

Which gene is NOT associated with Diabetes Mellitus?

Q30Medium

Which of the following statements about MODY is false?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 21: SIADH secretion is seen in all of the following conditions except?

A. Meningitis
B. Interstitial Nephritis (Correct Answer)
C. Hypothyroidism
D. Lung cancer

Explanation: The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by the excessive release of ADH from the posterior pituitary [1] or an ectopic source, leading to water retention and dilutional hyponatremia [2]. **Why Interstitial Nephritis is the correct answer:** Interstitial nephritis is a primary renal parenchymal disease. It often leads to **Nephrogenic Diabetes Insipidus (NDI)** rather than SIADH. In NDI, the renal tubules become resistant to ADH [3], leading to the inability to concentrate urine and resulting in polyuria and hypernatremia. Therefore, it is physiologically opposite to SIADH. **Analysis of Incorrect Options:** * **Meningitis:** Central Nervous System (CNS) disorders (meningitis, encephalitis, trauma, or tumors) are classic causes of SIADH. Any irritation or pressure on the hypothalamus/pituitary axis can trigger unregulated ADH release [4]. * **Hypothyroidism:** Severe hypothyroidism (Myxedema) is a well-known cause of SIADH. The mechanism involves decreased cardiac output and glomerular filtration rate (GFR), which triggers non-osmotic release of ADH. * **Lung Cancer:** Specifically, **Small Cell Carcinoma of the Lung** is the most common ectopic source of ADH. It is a classic paraneoplastic syndrome frequently tested in NEET-PG. **High-Yield Clinical Pearls for NEET-PG:** 1. **Diagnosis:** SIADH is a diagnosis of exclusion. Criteria include: Euvolemic hyponatremia, low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg). 2. **Drug Causes:** Common triggers include Carbamazepine, Cyclophosphamide, and SSRIs. 3. **Treatment:** Fluid restriction is the first-line treatment. For chronic management, Vaptans (Vasopressin antagonists) or Demeclocycline may be used. 4. **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis).

Question 22: Which of the following statements regarding thyroid hormones is correct?

A. Majority of the circulating T3 remains in bound form (Correct Answer)
B. Only 50% of the circulating T3 is secreted by the thyroid
C. TSH estimation is not a sensitive test for the diagnosis of primary hypothyroidism
D. Fetal pituitary-thyroid axis is dependent to a large extent on the maternal pituitary-thyroid axis

Explanation: ### Explanation **Correct Option: A. Majority of the circulating T3 remains in bound form** Thyroid hormones (T3 and T4) are highly hydrophobic and require carrier proteins for transport in the blood [1]. Approximately **99.7% of T3** and **99.97% of T4** circulate in bound form. The primary binding proteins are **Thyroxine-Binding Globulin (TBG)**, transthyretin, and albumin [1]. Only the unbound (free) fraction is biologically active and capable of entering target cells [1]. **Why the other options are incorrect:** * **Option B:** In reality, only about **20%** of circulating T3 is directly secreted by the thyroid gland. The remaining **80%** is produced via the peripheral deiodination of T4 (pro-hormone) by Type 1 and Type 2 deiodinase enzymes in tissues like the liver and kidney. * **Option C:** TSH is the **most sensitive** screening and diagnostic test for primary hypothyroidism. Due to the negative feedback loop, even a slight decrease in T4 levels leads to a logarithmic increase in TSH, often making it elevated even before T4 falls below the normal range (Subclinical Hypothyroidism). * **Option D:** The fetal pituitary-thyroid axis is **independent** of the maternal axis. The placenta is largely impermeable to TSH. While small amounts of maternal T4 cross the placenta to support early brain development, the fetus begins synthesizing its own thyroid hormones by the end of the first trimester (approx. 12 weeks). **High-Yield Clinical Pearls for NEET-PG:** * **Potency:** T3 is 3–4 times more potent than T4 and has a much shorter half-life (1 day vs. 7 days for T4) [2]. * **Wolff-Chaikoff Effect:** Transient inhibition of thyroid hormone synthesis due to high iodine intake. * **Amiodarone:** A high-yield drug that can cause both hypo- and hyperthyroidism due to its high iodine content and structural similarity to T4.

Question 23: What is the most likely complication of insulin therapy in ketoacidosis?

A. Dilutional hyponatremia
B. Hypoglycemia (Correct Answer)
C. Increased bleeding tendency
D. Pancreatitis

Explanation: **Explanation:** The management of Diabetic Ketoacidosis (DKA) involves aggressive fluid resuscitation and continuous intravenous insulin infusion. **Hypoglycemia** is the most common complication of insulin therapy in this setting [1]. This occurs because insulin promotes glucose uptake into cells and inhibits hepatic gluconeogenesis. If the insulin infusion rate is not adjusted or if dextrose is not added to the intravenous fluids once blood glucose levels drop below **200–250 mg/dL**, the patient’s blood sugar can plummet rapidly. **Analysis of Options:** * **A. Dilutional Hyponatremia:** This is incorrect. In DKA, patients often have "pseudohyponatremia" due to the osmotic effect of hyperglycemia [2]. As insulin therapy lowers blood glucose, water shifts back into cells, and the serum sodium concentration typically **rises**. * **C. Increased Bleeding Tendency:** There is no direct physiological link between insulin therapy and coagulopathy or platelet dysfunction. * **D. Pancreatitis:** While acute pancreatitis can be a *trigger* for DKA (due to metabolic stress), it is not a complication caused by insulin therapy itself. **NEET-PG High-Yield Pearls:** 1. **The "Big Three" Complications:** The most common complications of DKA management are **Hypoglycemia** [1], **Hypokalemia** (due to insulin shifting K+ into cells), and **Cerebral Edema** (most common in children due to rapid fluid shifts) [3]. 2. **Protocol Tip:** To prevent hypoglycemia, switch from Normal Saline to **5% Dextrose (D5NS)** when plasma glucose reaches **200 mg/dL**, while continuing the insulin infusion to resolve the underlying ketosis. 3. **Potassium Rule:** Never start insulin if the serum potassium is **<3.3 mEq/L**, as insulin will further worsen the hypokalemia, potentially leading to fatal arrhythmias.

Question 24: A 47-year-old woman presents with increasing headaches and visual changes. On examination, her pupils are normal and reactive to light, the extraocular movements are normal, and there are visual field defects of the outer half in both eyes (bitemporal hemianopsia). Which of the following is the most likely diagnosis?

A. pituitary adenoma (Correct Answer)
B. falx meningioma
C. craniopharyngioma
D. aneurysm of the internal carotid artery

Explanation: ### Explanation **Correct Answer: A. Pituitary Adenoma** The clinical presentation of **bitemporal hemianopsia** (loss of the outer half of the visual field in both eyes) is the hallmark sign of a lesion compressing the **optic chiasm**. The optic chiasm is located directly above the sella turcica. In adults, the most common cause of a mass in this region leading to chiasmal compression is a **pituitary adenoma** (specifically a macroadenoma, >10 mm) [1]. As the tumor expands superiorly out of the sella, it compresses the decussating nasal retinal fibers, which are responsible for temporal vision. **Analysis of Incorrect Options:** * **B. Falx Meningioma:** These tumors arise from the dural fold between the cerebral hemispheres. They typically cause lower limb weakness (paraparesis) or focal seizures, not bitemporal hemianopsia. * **C. Craniopharyngioma:** While these also cause bitemporal hemianopsia, they follow a **bimodal age distribution** (primarily seen in children aged 5–14 or older adults >65). In a 47-year-old, a pituitary adenoma is statistically much more likely. * **D. Aneurysm of the Internal Carotid Artery:** An aneurysm in the cavernous sinus or supraclinoid portion usually causes **ipsilateral nasal hemianopsia** (by compressing the non-decussating lateral fibers) or cranial nerve palsies (III, IV, VI), which are absent here. **High-Yield Clinical Pearls for NEET-PG:** * **Visual Field Defect:** Pituitary tumors compress the chiasm from *below*, often affecting the **upper temporal quadrants** first ("pie in the sky") [1]. Urgent treatment is required if there is evidence of pressure on visual pathways [1]. * **Craniopharyngioma:** Often compresses the chiasm from *above*, affecting the **lower temporal quadrants** first. Look for "eggshell calcification" on imaging. * **Prolactinoma:** The most common functional pituitary adenoma; presents with galactorrhea/amenorrhea in females and decreased libido in males [1]. In a sellar mass lesion, it is crucial that serum prolactin is measured [1]. * **Management:** Transsphenoidal surgery is the treatment of choice for most symptomatic macroadenomas, except for prolactinomas (treated first with Dopamine agonists like Cabergoline).

Question 25: Lisch nodules and a pancreatic somatostatinoma are seen in which condition?

A. Neurofibromatosis (Correct Answer)
B. Multiple endocrine neoplasia 2A
C. Turcot syndrome
D. Familial adenomatous polyposis

Explanation: **Explanation:** The correct answer is **Neurofibromatosis Type 1 (NF1)**. **1. Why Neurofibromatosis is correct:** Neurofibromatosis Type 1 (von Recklinghausen disease) is an autosomal dominant neurocutaneous syndrome caused by a mutation in the *NF1* gene on chromosome 17. * **Lisch Nodules:** These are melanocytic hamartomas of the iris, appearing as well-defined, dome-shaped brown papules. They are a hallmark diagnostic feature of NF1. * **Somatostatinoma:** While rare, there is a specific and high-yield association between NF1 and **duodenal/pancreatic somatostatinomas**. These tumors often contain psammoma bodies and are part of the spectrum of neuroendocrine tumors associated with the NF1 mutation [1]. **2. Why other options are incorrect:** * **MEN 2A:** Characterized by Medullary Thyroid Carcinoma, Pheochromocytoma, and Parathyroid Hyperplasia. It is not associated with Lisch nodules or somatostatinomas. * **Turcot Syndrome:** A variant of FAP or HNPCC involving colonic polyposis associated with CNS tumors (Medulloblastoma or Glioblastoma). * **Familial Adenomatous Polyposis (FAP):** Characterized by thousands of colonic adenomas and extracolonic manifestations like osteomas and desmoid tumors (Gardner syndrome), but not Lisch nodules. **3. Clinical Pearls for NEET-PG:** * **NF1 Diagnostic Criteria (NIH):** Remember the mnemonic **CAFE SPOT** (Café-au-lait spots, Axillary/inguinal freckling, Fibromas [Neurofibromas], Eye [Lisch nodules], Skeletal [Sphenoid dysplasia], Positive family history, Optic Tumor [Glioma]). * **Somatostatinoma Triad:** Diabetes mellitus, Steatorrhea, and Cholelithiasis (due to inhibition of insulin, pancreatic enzymes, and CCK) [1]. * **NF1 + Hypertension:** Always rule out **Pheochromocytoma** or **Renal Artery Stenosis** (due to fibromuscular dysplasia).

Question 26: What is the earliest presentation of hypopituitarism in adults?

A. Growth failure
B. Anosmia
C. Visual field defects
D. Hypogonadism (Correct Answer)

Explanation: **Explanation:** In adults with progressive pituitary destruction (such as from a non-functioning pituitary adenoma), there is a characteristic sequence of hormonal loss [1]. The correct answer is **Hypogonadism** because gonadotropins (LH and FSH) are typically the first hormones to be affected when the anterior pituitary is compressed or damaged [4]. **Why Hypogonadism is correct:** The gonadotroph cells are highly sensitive to pressure. In males, this manifests early as decreased libido and erectile dysfunction. In females, it presents as amenorrhea or infertility [4]. Growth Hormone (GH) deficiency actually occurs concurrently or even slightly earlier at a biochemical level, but because adults have already completed linear growth, GH deficiency is often clinically silent or vague (presenting as fatigue or increased adiposity), making **symptomatic hypogonadism** the earliest recognizable clinical presentation [1]. **Analysis of Incorrect Options:** * **A. Growth failure:** This is the earliest sign in **children**, not adults [3]. In adults, epiphyses are fused, so GH deficiency does not cause growth failure. * **B. Anosmia:** This is associated with **Kallmann Syndrome** (hypogonadotropic hypogonadism with failure of olfactory bulb development), but it is a congenital feature, not a presentation of acquired hypopituitarism [1]. * **C. Visual field defects:** These are "mass effects" caused by large tumors (typically bitemporal hemianopia). While common, they are mechanical complications rather than the earliest hormonal manifestation [2]. **High-Yield NEET-PG Pearls:** * **Sequence of Hormone Loss:** "Go Look For Adenoma" → **G**H > **L**H/**F**SH > **T**SH > **A**CTH. * **Life-threatening deficiency:** While LH/FSH are lost first, the loss of **ACTH** (secondary adrenal insufficiency) is the most acutely dangerous. * **Postpartum Pituitary Necrosis:** Known as **Sheehan Syndrome** [1]; the earliest sign is typically the failure to lactate (prolactin deficiency).

Question 27: Which of the following findings does not occur in a patient with gastrinoma?

A. Epigastric pain
B. Diarrhea
C. Basal acid output (BAO) less than 15 mEq/litre (Correct Answer)
D. Serum gastrin levels > 200 pg/ml

Explanation: Explanation: Gastrinoma (Zollinger-Ellison Syndrome) is a neuroendocrine tumor that secretes excessive amounts of gastrin, leading to hyperchlorhydria and severe peptic ulcer disease [2]. **Why Option C is correct:** In gastrinoma, the hallmark is **marked gastric acid hypersecretion** [2]. The diagnostic criteria for BAO in a patient with an intact stomach is **>15 mEq/hour** (not less than 15). If the patient has had previous gastric surgery, the threshold is >5 mEq/hour. A BAO <15 mEq/hour would actually point away from a diagnosis of gastrinoma. **Why the other options are incorrect:** * **A. Epigastric pain:** This is the most common presenting symptom (seen in >90% of patients) due to multiple, refractory, or atypically located peptic ulcers caused by hyperacidity [1]. * **B. Diarrhea:** This occurs in about 30–50% of patients. It is caused by the high acid volume overwhelming the small intestine, inactivating pancreatic enzymes (steatorrhea), and damaging the intestinal mucosa. * **D. Serum gastrin levels > 200 pg/ml:** Normal fasting gastrin is typically <100 pg/ml. In gastrinoma, levels are almost always elevated (>200 pg/ml), and values >1000 pg/ml are highly suggestive of the diagnosis [2]. **NEET-PG High-Yield Pearls:** * **Most common location:** The "Gastrinoma Triangle" (Passaro’s Triangle)—bounded by the cystic duct/CBD junction, the junction of the 2nd and 3rd parts of the duodenum, and the neck of the pancreas. * **Association:** Approximately 25% of cases are associated with **MEN1 syndrome** (3Ps: Parathyroid, Pancreas, Pituitary). * **Confirmatory Test:** The **Secretin Stimulation Test** is the most sensitive and specific provocative test; a rise in serum gastrin >200 pg/ml after secretin injection is diagnostic. * **Drug of Choice:** High-dose Proton Pump Inhibitors (PPIs).

Question 28: An 80-year-old woman, previously in sinus rhythm, developed atrial fibrillation with rapid ventricular response during an ICU stay for sepsis. She was treated with amiodarone, converted to sinus rhythm, and was discharged on maintenance amiodarone. In the following weeks, she presented with increasing fatigue, dry skin, and constipation. Laboratory tests revealed a TSH of 25 mIU/L. What is the best management approach in this situation?

A. Discontinue amiodarone and monitor TSH and clinical symptoms.
B. Initiate low-dose levothyroxine and repeat TSH in 6 weeks. (Correct Answer)
C. Start a beta-blocker and gradually withdraw amiodarone.
D. Measure anti-thyroid peroxidase (TPO) antibodies to guide treatment.

Explanation: ### Explanation **1. Understanding the Correct Answer (Option B)** The patient has developed **Amiodarone-Induced Hypothyroidism (AIH)**. Amiodarone is iodine-rich (37% by weight); a standard 200 mg dose releases massive amounts of free iodine. In most individuals, the thyroid acutely inhibits hormone synthesis in response to iodine excess (**Wolff-Chaikoff effect**) but "escapes" this effect within days. AIH occurs when the thyroid fails to escape this inhibition, often in patients with underlying autoimmune thyroiditis. [2] In this scenario, **levothyroxine** is the treatment of choice. [1] Unlike amiodarone-induced thyrotoxicosis, amiodarone **does not need to be discontinued** if it is required for arrhythmia control. [2] In an 80-year-old with a history of rapid AF, maintaining rhythm stability is a priority. Treatment should start with a **low dose** (e.g., 25–50 mcg) due to her age and cardiac history to avoid precipitating ischemia or tachyarrhythmias. [1][3] **2. Why Other Options are Incorrect** * **Option A:** Discontinuing amiodarone is often unnecessary and risky. Amiodarone has a very long half-life (up to 100 days), so stopping it will not resolve the hypothyroidism quickly. [2] Furthermore, the drug may be essential for her cardiac stability. * **Option C:** Beta-blockers are used for hyperthyroidism, not hypothyroidism. Withdrawing amiodarone without a clear cardiac alternative could trigger a recurrence of AF with RVR. * **Option D:** While TPO antibodies are often positive in AIH, their presence does not change the immediate management (which is hormone replacement). [1] **3. Clinical Pearls for NEET-PG** * **Wolff-Chaikoff Effect:** Transient inhibition of T4/T3 synthesis due to high iodine levels. * **Jod-Basedow Phenomenon:** Iodine-induced *hyperthyroidism* (opposite of AIH). * **Amiodarone & Thyroid:** It inhibits 5’-deiodinase, decreasing the conversion of T4 to T3, which can cause a transient rise in TSH even in euthyroid patients. * **Monitoring:** Patients on chronic amiodarone should have TSH monitored every 6 months.

Question 29: Which gene is NOT associated with Diabetes Mellitus?

A. PPARγ
B. KCNJ11
C. CTLA4
D. PDGF-R (Correct Answer)

Explanation: The correct answer is **D. PDGF-R** (Platelet-Derived Growth Factor Receptor). This receptor is primarily involved in cell growth, proliferation, and angiogenesis. While it plays a role in wound healing and atherosclerosis (complications of diabetes), it is not a genetic locus associated with the pathogenesis or susceptibility of Diabetes Mellitus itself. **Analysis of Options:** * **PPARγ (Peroxisome Proliferator-Activated Receptor Gamma):** This is a nuclear receptor essential for adipocyte differentiation and glucose metabolism. Mutations in the *PPARG* gene are strongly associated with **Type 2 Diabetes (T2DM)** and insulin resistance. It is the molecular target for Thiazolidinediones (e.g., Pioglitazone). * **KCNJ11:** This gene encodes the Kir6.2 subunit of the ATP-sensitive potassium (K-ATP) channel in pancreatic beta cells. Mutations in this gene are a well-known cause of **Neonatal Diabetes Mellitus** and are associated with an increased risk of T2DM. * **CTLA4 (Cytotoxic T-Lymphocyte Associated Protein 4):** This is an immune checkpoint molecule. Polymorphisms in the *CTLA4* gene are associated with autoimmune susceptibility, specifically **Type 1 Diabetes Mellitus (T1DM)**, as well as Graves' disease and Addison’s disease [1]. **High-Yield Clinical Pearls for NEET-PG:** * **MODY Type 3:** The most common form of Maturity-Onset Diabetes of the Young, caused by mutations in the **HNF1A** gene. * **MODY Type 2:** Caused by **Glucokinase (GCK)** mutations; usually presents with mild, stable fasting hyperglycemia. * **HLA Association:** T1DM is most strongly linked to **HLA-DR3 and HLA-DR4** [2]. * **TCF7L2:** Currently considered the strongest common genetic risk factor for Type 2 Diabetes in various ethnic groups.

Question 30: Which of the following statements about MODY is false?

A. Onset typically before 25 years of age
B. Characterized by impaired insulin secretion
C. Often responsive to sulfonylureas
D. Requires insulin therapy (Correct Answer)

Explanation: Maturity-Onset Diabetes of the Young (MODY) is a group of monogenic disorders characterized by non-insulin-dependent diabetes caused by mutations in genes affecting beta-cell function, rather than insulin resistance or autoimmune destruction [1]. Why Option D is the Correct Answer (False Statement): Unlike Type 1 Diabetes, MODY is primarily a defect in insulin secretion "sensing" or production, not a total absence of insulin. Most patients (especially those with MODY 1 and 3) have significant residual beta-cell function and do not require insulin therapy, at least in the early stages [1]. Many can be managed effectively with oral hypoglycemic agents or diet alone. Analysis of Incorrect Options: * Option A: MODY typically presents in adolescence or early adulthood, usually before age 25, distinguishing it from Type 2 Diabetes [1]. * Option B: The pathophysiology involves impaired insulin secretion due to genetic mutations (e.g., HNF1A, GCK), while insulin sensitivity remains normal. * Option C: Patients with MODY 3 (the most common type) and MODY 1 are exquisitely sensitive to Sulfonylureas, which is often the first-line treatment. High-Yield Clinical Pearls for NEET-PG: 1. Inheritance: Autosomal Dominant (look for a strong family history across 3 generations) [1]. 2. MODY 3 (HNF1A): Most common form; highly sensitive to low-dose sulfonylureas. 3. MODY 2 (GCK): Characterized by mild, stable fasting hyperglycemia; usually requires no treatment (diet only). 4. Diagnostic Clue: Absence of pancreatic autoantibodies (GAD, IA-2) and low/normal BMI.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

Want unlimited practice?

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

Start For Free