Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 621: Manifestations of endemic cretinism include:

A. Deafness and facial nerve involvement
B. Blindness and hypothyroidism
C. Strabismus and spastic diplegias (Correct Answer)
D. Multinodular goitre and mental retardation

Explanation: Endemic cretinism occurs in populations living in iodine-deficient areas and is primarily classified into two distinct clinical syndromes: **Neurological** and **Myxedematous**. [2] 1. **Why Option C is Correct:** The **Neurological type** is the most common form of endemic cretinism. It results from severe maternal iodine deficiency during the first and second trimesters, leading to impaired fetal brain development. [1] Characteristic features include **spastic diplegia** (or tetraplegia) due to pyramidal tract involvement, **strabismus** (squint), deaf-mutism, and profound intellectual disability. The spasticity typically affects the lower limbs more than the upper limbs. 2. **Why Other Options are Incorrect:** * **Option A:** While sensorineural **deafness** is a hallmark of neurological cretinism, **facial nerve involvement** is not a standard feature of the syndrome. * **Option B:** While hypothyroidism is the underlying cause, **blindness** is not a feature of cretinism. Optic atrophy or primary visual loss is not associated with iodine deficiency. * **Option D:** While mental retardation is present, **Multinodular goitre (MNG)** is a compensatory mechanism seen in adults with chronic iodine deficiency; cretinous children may have a goiter, but "Multinodular Goitre" specifically is not a defining manifestation of the cretinism syndrome itself compared to the neurological deficits. **High-Yield Clinical Pearls for NEET-PG:** * **Neurological Cretinism:** Predominant features are deaf-mutism, spasticity, and strabismus. Patients are usually euthyroid at birth. [1] * **Myxedematous Cretinism:** Predominant features are severe growth retardation (dwarfism), dry skin, and coarse features. These patients are clinically hypothyroid. * **Key Difference:** Neurological cretinism is due to iodine deficiency during early gestation, whereas Myxedematous cretinism involves iodine deficiency and potentially thiocyanate toxicity (from cassava) in late gestation or early neonatal life. * **Prevention:** Iodized salt is the most cost-effective intervention to prevent endemic cretinism. [2]

Question 622: What substance is deposited in Bronze diabetes?

A. Bronze
B. Copper
C. Iron (Correct Answer)
D. Carbon

Explanation: **Explanation:** **Bronze Diabetes** is the clinical triad of skin hyperpigmentation, diabetes mellitus, and cirrhosis [1]. It is the classic presentation of **Hereditary Hemochromatosis**, an autosomal recessive disorder (most commonly involving the *HFE* gene mutation) [1], [4]. **Why Iron is the correct answer:** In Hemochromatosis, there is an inappropriate increase in intestinal iron absorption. This excess **Iron** is deposited in various organs as **hemosiderin** [1]. * **Skin:** Iron deposition stimulates melanin production, leading to a "bronze" or metallic-gray skin discoloration [1]. * **Pancreas:** Iron deposits cause selective destruction of beta cells in the Islets of Langerhans, resulting in insulin deficiency and secondary diabetes mellitus [1], [3]. * **Liver:** Deposition leads to micronodular cirrhosis and increases the risk of Hepatocellular Carcinoma (HCC) [1], [2]. **Why other options are incorrect:** * **Bronze:** This is a metal alloy (copper and tin) and not a physiological substance found in the body. The name "Bronze diabetes" refers only to the skin color, not the deposit. * **Copper:** Excess copper deposition is the hallmark of **Wilson’s Disease**, which typically presents with Kayser-Fleischer (KF) rings and basal ganglia involvement, not diabetes. * **Carbon:** Carbon deposition (Anthracosis) is commonly seen in the lungs of smokers or coal miners and does not cause diabetes. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Serum Transferrin Saturation (Best initial test; >45% is suggestive). * **Confirmatory Test:** Genetic testing for *HFE* gene (C282Y mutation) [2], [4]. * **Gold Standard:** Liver biopsy (Perls' Prussian Blue stain shows iron) [2]. * **Treatment of Choice:** Therapeutic Phlebotomy [2]. * **Other manifestations:** Restrictive cardiomyopathy, "Square-off" bone spurs in the 2nd/3rd MCP joints, and hypogonadotropic hypogonadism [1].

Question 623: Albright's syndrome includes all except?

A. Polyostotic fibrous dysplasia
B. Precocious puberty in girls
C. Patchy pigmentation (Correct Answer)
D. Pseudohypoparathyroidism

Explanation: This question highlights a common point of confusion in medical entrance exams: the distinction between **McCune-Albright Syndrome** and **Albright’s Hereditary Osteodystrophy (AHO)**. ### Why "Patchy Pigmentation" is the Correct Answer The question asks for what is **NOT** part of Albright’s syndrome (referring here to Albright’s Hereditary Osteodystrophy/Pseudohypoparathyroidism). While "patchy pigmentation" (Café-au-lait spots) is a hallmark of **McCune-Albright Syndrome**, it is not a feature of **Pseudohypoparathyroidism**. Therefore, in the context of this specific question, it is the "except" option. ### Analysis of Options * **A. Polyostotic fibrous dysplasia:** This is a classic feature of **McCune-Albright Syndrome**. * **B. Precocious puberty in girls:** This is the most common endocrine manifestation of **McCune-Albright Syndrome**, caused by autonomous ovarian activation. * **D. Pseudohypoparathyroidism (PHP):** This is also known as **Albright’s Hereditary Osteodystrophy (AHO)**. It is characterized by PTH resistance, short stature, round facies, and short 4th/5th metacarpals [1]. ### Clinical Pearls for NEET-PG To avoid confusion, remember these two distinct "Albright" entities: 1. **McCune-Albright Syndrome:** * **Triad:** Polyostotic fibrous dysplasia, Café-au-lait spots (Coast of Maine borders), and Precocious puberty. * **Pathophysiology:** Somatic mutation in the **GNAS1 gene**, leading to constitutive activation of adenylate cyclase [1]. 2. **Albright’s Hereditary Osteodystrophy (Pseudohypoparathyroidism Type 1a):** * **Features:** Short stature, obesity, round face, **brachydactyly** (short 4th/5th metacarpals), and subcutaneous calcification [1]. * **Biochemistry:** High PTH, Low Calcium, High Phosphate (due to end-organ resistance to PTH) [1]. * **Genetics:** Also involves the **GNAS1 gene** but via imprinting/inheritance patterns [1]. **High-Yield Tip:** If you see "Coast of Maine" spots, think McCune-Albright. If you see "Short 4th metacarpal (Archibald’s sign)," think Albright’s Hereditary Osteodystrophy.

Question 624: What is the most common cause of hyperparathyroidism?

A. Carcinoma
B. Hyperplasia
C. Adenoma (Correct Answer)
D. Familial isolated hyperparathyroidism

Explanation: ### Explanation Primary Hyperparathyroidism (PHPT) is characterized by the autonomous overproduction of parathyroid hormone (PTH), leading to hypercalcemia [1]. **1. Why Adenoma is Correct:** A **solitary parathyroid adenoma** is the most common cause of primary hyperparathyroidism, accounting for approximately **85–90%** of cases [4]. It typically involves a single gland, while the remaining three glands remain suppressed due to high serum calcium levels. **2. Analysis of Incorrect Options:** * **Hyperplasia (Option B):** Diffuse enlargement of all four parathyroid glands accounts for about **10–15%** of cases. It is frequently associated with hereditary syndromes like MEN 1 and MEN 2A [3]. * **Carcinoma (Option A):** Parathyroid carcinoma is a very rare cause, occurring in **<1%** of patients. It is usually suspected when calcium levels are extremely high (>14 mg/dL) and a palpable neck mass is present. * **Familial Isolated Hyperparathyroidism (Option D):** This is a rare genetic condition and does not represent the majority of cases in the general population [3]. **3. Clinical Pearls for NEET-PG:** * **Most common presentation:** Today, most patients are **asymptomatic**, discovered via routine biochemical screening (incidental hypercalcemia) [4]. * **Classic Symptom Triad:** "Stones (renal calculi), bones (osteitis fibrosa cystica), abdominal groans (peptic ulcers/pancreatitis), and psychic overtones (depression)" [2][3]. * **Radiological Hallmark:** Subperiosteal bone resorption, most classically seen on the radial side of the middle phalanges. * **Biochemical Profile:** High Serum Calcium, Low Serum Phosphate, and inappropriately High/Normal PTH [4]. * **Localization:** Sestamibi scan (Technetium-99m) is the investigation of choice to localize an adenoma before surgery [2].

Question 625: A 45-year-old patient has a Fasting Blood Sugar (FBS) of 111 mg/dL, Postprandial Blood Sugar (PPBS) of 181 mg/dL, and HbA1c of 6.1%. What is the diagnosis?

A. Pre-diabetes (Correct Answer)
B. Type 2 Diabetes Mellitus
C. Type 1 Diabetes Mellitus
D. Stress hyperglycemia

Explanation: ### Explanation The diagnosis of **Pre-diabetes** (also known as Intermediate Hyperglycemia) is based on blood glucose levels that are higher than normal but do not yet meet the threshold for a diagnosis of Diabetes Mellitus [1]. According to the American Diabetes Association (ADA) criteria, a patient is diagnosed with pre-diabetes if they meet **any** of the following: 1. **Impaired Fasting Glucose (IFG):** FBS between 100–125 mg/dL. (Patient: 111 mg/dL) [1] 2. **Impaired Glucose Tolerance (IGT):** 2-hour post-load glucose (OGTT) or PPBS between 140–199 mg/dL. (Patient: 181 mg/dL) [1] 3. **HbA1c:** Between 5.7% and 6.4%. (Patient: 6.1%) Since all three parameters in this patient fall within these specific ranges, the diagnosis is Pre-diabetes. [1] **Why other options are incorrect:** * **Type 2 & Type 1 Diabetes Mellitus:** Diagnosis requires FBS ≥126 mg/dL, PPBS/Random ≥200 mg/dL, or HbA1c ≥6.5% [1]. This patient’s values are below these cut-offs. * **Stress Hyperglycemia:** This refers to transiently elevated glucose levels (usually >140 mg/dL) during acute illness or physiological stress in patients without prior diabetes. While the sugars are elevated here, the HbA1c of 6.1% indicates a chronic state of dysglycemia rather than an acute spike. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Values:** FBS <100 mg/dL, 2hr-PPBS <140 mg/dL, HbA1c <5.7%. * **Screening:** In asymptomatic adults, screening for pre-diabetes/diabetes should begin at age 35 (recently lowered from 45). * **Management:** Lifestyle modification (weight loss and exercise) is the first-line treatment. Metformin is considered for high-risk pre-diabetics (BMI ≥35, age <60, or women with prior GDM).

Question 626: What is the characteristic feature of primary aldosteronism?

A. Low serum sodium
B. High plasma renin
C. Low serum potassium (Correct Answer)
D. High serum creatinine

Explanation: **Explanation:** Primary aldosteronism (Conn’s syndrome) is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, independent of the renin-angiotensin system. **Why Low Serum Potassium is Correct:** Aldosterone acts on the principal cells of the distal convoluted tubule and collecting duct [1]. It promotes the reabsorption of sodium and the **secretion of potassium and hydrogen ions** into the urine [1]. This excessive potassium wasting leads to **hypokalemia**, which clinically manifests as muscle weakness, fatigue, or cardiac arrhythmias [1]. **Analysis of Incorrect Options:** * **A. Low serum sodium:** Aldosterone increases sodium reabsorption. While patients are hypervolemic, they rarely show significant hypernatremia due to "aldosterone escape" (atrial natriuretic peptide release causing pressure natriuresis) [2], but they definitely do **not** have hyponatremia. * **B. High plasma renin:** This is the hallmark of *secondary* aldosteronism. In primary aldosteronism, high aldosterone levels suppress renin production via negative feedback, leading to a **low plasma renin activity (PRA)**. * **C. High serum creatinine:** Primary aldosteronism does not typically cause renal failure unless there is long-standing, untreated hypertensive nephrosclerosis. **NEET-PG High-Yield Pearls:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio >20-30** is highly suggestive. * **Confirmatory Test:** Oral or IV Saline Suppression Test (failure to suppress aldosterone). * **Classic Triad:** Hypertension, Hypokalemia, and Metabolic Alkalosis. * **Most Common Cause:** Adrenal Adenoma (Conn’s Syndrome), followed by Bilateral Adrenal Hyperplasia.

Question 627: Which of the following is NOT a steroid?

A. Estrogen
B. Progesterone
C. Relaxin (Correct Answer)
D. Testosterone

Explanation: **Explanation:** The classification of hormones based on their chemical structure is a high-yield topic for NEET-PG. Hormones are generally divided into three categories: **Steroids**, **Peptides/Proteins**, and **Amino acid derivatives**. **Why Relaxin is the correct answer:** Relaxin is a **peptide hormone** (specifically a protein belonging to the insulin superfamily). It is produced primarily by the corpus luteum in females and the prostate in males. Its primary physiological role is to relax the pelvic ligaments and soften the cervix during childbirth. Because it is a protein, it acts via cell-surface receptors (G-protein coupled receptors) [1], unlike steroids which typically act on intracellular receptors [1]. **Why the other options are incorrect:** * **Estrogen, Progesterone, and Testosterone** are all **steroid hormones** [2], [3]. * Steroid hormones are derived from **cholesterol** and are lipid-soluble [2]. * They are secreted by the adrenal cortex (cortisol, aldosterone), ovaries (estrogen, progesterone), and testes (testosterone) [2]. **Clinical Pearls for NEET-PG:** 1. **Steroid Hormones mnemonic:** Remember "The **Adrenal Cortex** and the **Gonads**." (Cortisol, Aldosterone, Estrogen, Progesterone, Testosterone) [2]. Vitamin D is also a steroid hormone [1]. 2. **Mechanism of Action:** Steroids are lipophilic; they cross the cell membrane and bind to **intracellular/nuclear receptors** to alter gene transcription [1]. 3. **Relaxin’s Clinical Role:** In pregnancy, it increases glomerular filtration rate (GFR) and renal blood flow, contributing to the physiological changes of gestation. 4. **Quick Check:** If a hormone name ends in **"-one"** or **"-ol"** (e.g., Aldosterone, Cortisol, Estradiol), it is almost always a steroid [2]. Relaxin is a notable exception to the "sound-alike" rule.

Question 628: Which of the following is not involved in MEN II syndrome?

A. Pituitary tumor (Correct Answer)
B. Medullary carcinoma of thyroid
C. Pheochromocytoma
D. Parathyroid adenoma

Explanation: Multiple Endocrine Neoplasia (MEN) syndromes are autosomal dominant conditions characterized by tumors involving two or more endocrine glands. The distinction between MEN I and MEN II is a high-yield topic for NEET-PG. **1. Why Pituitary Tumor is the correct answer:** Pituitary tumors are a hallmark of **MEN I (Wermer Syndrome)**, not MEN II. MEN I is classically defined by the "3 Ps": **P**ituitary adenoma (most commonly prolactinoma), **P**arathyroid hyperplasia/adenoma, and **P**ancreatic islet cell tumors (e.g., Gastrinoma, Insulinoma). **2. Why the other options are incorrect (Components of MEN II):** MEN II (Sipple Syndrome) is caused by a mutation in the **RET proto-oncogene** and is characterized by: * **Medullary Thyroid Carcinoma (MTC):** Occurs in 100% of cases; it is the most common and earliest manifestation. * **Pheochromocytoma:** Occurs in approximately 50% of patients, often bilateral. * **Parathyroid Adenoma/Hyperplasia:** Seen specifically in **MEN IIA** (not IIB). **High-Yield Clinical Pearls for NEET-PG:** * **MEN IIA (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid hyperplasia. * **MEN IIB (Gorlin Syndrome):** MTC + Pheochromocytoma + Mucosal neuromas + Marfanoid habitus (Note: Parathyroid involvement is **absent** in MEN IIB). * **Screening:** For MEN II, the first step in a suspected patient is to screen for Pheochromocytoma (via urinary/plasma metanephrines) before performing thyroid surgery to prevent a hypertensive crisis during anesthesia. * **Prophylactic Thyroidectomy:** Often recommended in RET mutation carriers due to the high penetrance of MTC.

Question 629: Pituitary adenomas are regarded as macroadenomas when their size is:

A. > 1 cm (Correct Answer)
B. > 1.5 cm
C. > 2 cm
D. > 2.5 cm

Explanation: Pituitary adenomas are benign tumors of the anterior pituitary gland and are classified primarily based on their size, which dictates both clinical presentation and surgical approach. **1. Why the correct answer is right:** The standard radiological classification (based on MRI findings) divides pituitary adenomas into two categories [3]: * **Microadenomas:** < 1 cm (10 mm) in diameter [3]. These usually present with symptoms of hormonal excess (e.g., prolactinoma or Cushing’s disease) before they are large enough to cause mass effects [1]. * **Macroadenomas:** **> 1 cm (10 mm)** in diameter [3]. These are significant because they are large enough to compress adjacent structures, such as the optic chiasm (causing bitemporal hemianopia) or the normal pituitary tissue (causing hypopituitarism) [2], [4]. **2. Why the incorrect options are wrong:** * **Options B, C, and D (> 1.5 cm, > 2 cm, > 2.5 cm):** While these sizes technically qualify as macroadenomas, they do not represent the established diagnostic threshold. A tumor is labeled a macroadenoma the moment it exceeds the 1 cm mark [3]. Tumors exceeding 4 cm are specifically termed **Giant Pituitary Adenomas**. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common type:** Prolactinoma is the most common secretory pituitary adenoma. * **Mass Effect:** Macroadenomas typically present with the "classic triad": Headache, bitemporal hemianopia (due to optic chiasm compression), and hypopituitarism [2]. * **Imaging Gold Standard:** Contrast-enhanced MRI of the Sella Turcica [3]. * **Treatment:** For most macroadenomas, **Transsphenoidal surgery** is the first-line treatment [1], *except* for Prolactinomas, where medical management (Dopamine agonists like Cabergoline) is preferred regardless of size [2], [4].

Question 630: A 45-year-old female presents with symptoms of thyrotoxicosis. The RAIU scan shows increased uptake. Which of the following is the most likely diagnosis?

A. Hashimoto's thyroiditis
B. Struma ovarii
C. Thyrotoxicosis factitia
D. Choriocarcinoma (Correct Answer)

Explanation: The clinical presentation of thyrotoxicosis with **increased Radioactive Iodine Uptake (RAIU)** indicates that the thyroid gland is actively synthesizing new thyroid hormone (hyperthyroidism). [1] **Why Choriocarcinoma is correct:** Choriocarcinoma is a germ cell tumor that secretes extremely high levels of **human chorionic gonadotropin (hCG)**. The alpha-subunit of hCG is identical to that of **TSH**. At very high concentrations, hCG cross-reacts with TSH receptors in the thyroid gland, stimulating thyroid hormone production and increasing iodine trapping. This results in a high RAIU scan, similar to Graves' disease but without the ophthalmopathy. [2] **Why the other options are incorrect:** * **Hashimoto’s Thyroiditis:** Typically presents with hypothyroidism. During the initial "Hashitoxicosis" phase, thyrotoxicosis occurs due to the release of pre-formed hormones from gland destruction, resulting in **low/decreased RAIU**. [1] * **Struma Ovarii:** This is ectopic thyroid tissue within an ovarian teratoma. While it causes thyrotoxicosis, the iodine uptake occurs in the pelvis. The **neck RAIU scan will be low** because the endogenous TSH is suppressed. * **Thyrotoxicosis Factitia:** Caused by the exogenous ingestion of thyroid hormones. Since the thyroid gland is suppressed by the external hormone, the **RAIU scan will be low/absent**. [1] **High-Yield Clinical Pearls for NEET-PG:** * **High RAIU (>30%):** Graves’ Disease, Toxic Multinodular Goiter, Toxic Adenoma, TSH-secreting pituitary adenoma, and hCG-mediated thyrotoxicosis (Choriocarcinoma/Hydatidiform mole). [3] * **Low RAIU (<5%):** Thyroiditis (Subacute, Silent, Hashimoto's), Iodine overload (Jod-Basedow), Factitious thyrotoxicosis, and Ectopic thyroid (Struma ovarii). [1] * **Key Concept:** If thyrotoxicosis is present but the neck scan is "cold," always consider thyroiditis or an extrathyroidal source.

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