Endocrinology — MCQs
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Which of the following is associated with A-V block?
A 40-year-old woman presents with weakness and amenorrhea. She has a history of hypertension and diabetes mellitus. Which of the following conditions can explain these clinical findings?
An 82-year-old female presents with a year-long history of worsening symptoms, including abdominal pain, inability to eat, weakness, and dependence on others for basic activities. She denies symptoms of depression. Her vital signs are notable for supine blood pressure of 90/54 mmHg, which drops to 76/40 mmHg upon standing. Physical examination reveals a bronze skin discoloration on the elbows and palmar creases. What laboratory abnormality would you expect to find in this patient?
Jod-Basedow phenomenon refers to which of the following?
A patient with tuberculosis presents with low levels of sodium, chloride, and bicarbonate. The patient also has hyperpigmentation of palmar creases. What is the most probable diagnosis?
Which of the following is NOT a feature of hypercalcemia?
Lamina dura is lost or partially lost in which of the following conditions?
What is true about thyroid storm?
Angiofibromas are seen in which of the following conditions?
MEN-2A is associated with which of the following findings?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1071: Which of the following is associated with A-V block?
- A. Hypothyroidism (Correct Answer)
- B. Hyperthyroidism
- C. Cushing disease
- D. Pheochromocytoma
Explanation: **Explanation:** **Hypothyroidism (Correct Answer):** Hypothyroidism is characterized by a generalized slowing of metabolic processes, which significantly impacts the cardiovascular system. Thyroid hormones normally increase the expression of calcium-handling proteins and beta-adrenergic receptors in the myocardium. In hypothyroidism, a deficiency of these hormones leads to **decreased conduction velocity** and an increased refractory period within the specialized conduction system (SA node, AV node, and His-Purkinje system). This results in characteristic ECG findings such as sinus bradycardia, prolonged PR interval, and varying degrees of **Atrioventricular (A-V) block** [2]. Additionally, the accumulation of mucopolysaccharides in the interstitium (myxedema) can further impair electrical conduction. **Incorrect Options:** * **Hyperthyroidism:** Typically causes a hyperdynamic state. It is associated with sinus tachycardia, atrial fibrillation (most common arrhythmia), and shortened PR intervals, rather than conduction blocks. * **Cushing Disease:** Excess cortisol leads to hypertension and hypokalemia. While it can cause left ventricular hypertrophy, it is not classically associated with A-V blocks. * **Pheochromocytoma:** Excess catecholamines lead to tachyarrhythmias (sinus tachycardia, PVCs) and potentially catecholamine-induced cardiomyopathy, but not primary A-V conduction delay. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Triad of Hypothyroidism:** Bradycardia, Low voltage complexes (due to myxedema or pericardial effusion), and T-wave flattening/inversion. * **Reversibility:** A-V blocks in hypothyroidism are often reversible with Levothyroxine replacement. * **Wolff-Parkinson-White (WPW) Syndrome** is sometimes associated with hyperthyroidism, whereas **A-V blocks** [1] are a hallmark of the "slowed" state of hypothyroidism.
Question 1072: A 40-year-old woman presents with weakness and amenorrhea. She has a history of hypertension and diabetes mellitus. Which of the following conditions can explain these clinical findings?
- A. Pituitary tumor
- B. Adrenal tumor
- C. Ectopic ACTH production
- D. Any of the above (Correct Answer)
Explanation: ### Explanation The clinical presentation of **weakness, amenorrhea, hypertension, and diabetes mellitus** is a classic constellation of symptoms for **Cushing’s Syndrome** (hypercortisolism). **1. Why the correct answer is "Any of the above":** All three options are established causes of endogenous Cushing’s Syndrome, leading to excessive cortisol production: * **Pituitary tumor (Cushing’s Disease):** An ACTH-secreting pituitary adenoma stimulates the adrenal glands to produce excess cortisol. This is the most common endogenous cause (approx. 70%). * **Adrenal tumor:** A primary adrenal adenoma or carcinoma autonomously secretes cortisol, independent of ACTH. * **Ectopic ACTH production:** Non-pituitary tumors (most commonly **Small Cell Carcinoma of the Lung** or bronchial carcinoids) secrete ACTH, leading to bilateral adrenal hyperplasia and hypercortisolism. **2. Pathophysiology of symptoms:** * **Weakness:** Cortisol causes muscle catabolism (proximal myopathy). * **Amenorrhea:** High cortisol levels inhibit the GnRH pulse generator, disrupting the HPO axis. * **Hypertension:** Cortisol has mineralocorticoid-like effects and increases vascular sensitivity to catecholamines. * **Diabetes:** Cortisol is a "stress hormone" that promotes gluconeogenesis and causes insulin resistance. **3. High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Overnight Dexamethasone Suppression Test (ONDST) or 24-hour urinary free cortisol. * **Gold Standard for localization:** Inferior Petrosal Sinus Sampling (IPSS) helps differentiate between a Pituitary source and an Ectopic source of ACTH. * **Ectopic ACTH Clue:** Often presents with rapid onset, severe hypokalemia, and significant hyperpigmentation (due to very high ACTH/POMC levels). * **Most common cause overall:** Iatrogenic (exogenous steroid use).
Question 1073: An 82-year-old female presents with a year-long history of worsening symptoms, including abdominal pain, inability to eat, weakness, and dependence on others for basic activities. She denies symptoms of depression. Her vital signs are notable for supine blood pressure of 90/54 mmHg, which drops to 76/40 mmHg upon standing. Physical examination reveals a bronze skin discoloration on the elbows and palmar creases. What laboratory abnormality would you expect to find in this patient?
- A. Low serum calcium
- B. Low serum potassium
- C. Low serum sodium (Correct Answer)
- D. Normal serum potassium
Explanation: This patient presents with classic signs of **Primary Adrenal Insufficiency (Addison’s Disease)**. The key clinical markers are chronic abdominal pain, profound weakness, orthostatic hypotension (90/54 to 76/40 mmHg), and characteristic **hyperpigmentation** (bronze skin) in sun-exposed areas and pressure points like elbows and palmar creases [1]. ### Why Low Serum Sodium is Correct In Primary Adrenal Insufficiency, there is a deficiency of both cortisol and **aldosterone** due to destruction of the adrenal cortex [1]. * **Aldosterone deficiency** leads to "salt wasting": the kidneys fail to reabsorb sodium and fail to excrete potassium and hydrogen ions. This results in **hyponatremia**, hyperkalemia, and metabolic acidosis. * Additionally, cortisol deficiency leads to increased ADH secretion (loss of negative feedback), further worsening hyponatremia through water retention. ### Why Other Options are Incorrect * **A. Low serum calcium:** Addison’s disease is actually associated with **hypercalcemia** (seen in ~10-20% of cases), likely due to decreased renal calcium excretion and increased bone resorption. * **B. Low serum potassium:** This is incorrect. Aldosterone deficiency causes **hyperkalemia** (high potassium), not hypokalemia [2]. * **D. Normal serum potassium:** While it can occur in secondary adrenal insufficiency (where aldosterone is intact), in this patient, the hyperpigmentation confirms a **primary** pathology (high ACTH), making hyperkalemia the expected finding [2]. ### NEET-PG High-Yield Pearls 1. **Hyperpigmentation** occurs only in **Primary** Adrenal Insufficiency because high ACTH levels (derived from POMC) cross-react with Melanocyte Stimulating Hormone (MSH) receptors. 2. **Cosyntropin Stimulation Test:** The gold standard for diagnosis [2]. 3. **Electrolyte Triad:** Hyponatremia + Hyperkalemia + Azotemia. 4. **Treatment:** Requires both Glucocorticoid (Hydrocortisone) and Mineralocorticoid (Fludrocortisone) replacement [3].
Question 1074: Jod-Basedow phenomenon refers to which of the following?
- A. Iodine excess causing suppression of TSH
- B. Iodine excess causing hyperthyroidism (Correct Answer)
- C. Iodine excess causing transient decrease in thyroid hormone production
- D. Iodine excess causing regression of Multinodular Goiter (MNG)
Explanation: **Explanation:** The **Jod-Basedow phenomenon** refers to **iodine-induced hyperthyroidism**. It occurs when an excess load of iodine (from dietary sources, contrast media, or drugs like Amiodarone) is administered to a patient with an underlying thyroid pathology, such as a multinodular goiter (MNG) or Graves' disease. In these patients, the thyroid loses its ability to autoregulate iodine uptake, leading to autonomous and excessive synthesis of thyroid hormones [1]. **Analysis of Options:** * **Option B (Correct):** This is the definition of Jod-Basedow. It typically occurs in iodine-deficient areas when people are suddenly exposed to iodine supplementation. * **Option A (Incorrect):** While hyperthyroidism eventually leads to TSH suppression via negative feedback, the phenomenon itself describes the *induction of hyperthyroidism*, not the mechanism of TSH suppression. * **Option C (Incorrect):** This describes the **Wolff-Chaikoff effect**, which is the transient *inhibition* of thyroid hormone synthesis following an iodine bolus (the physiological opposite of Jod-Basedow). * **Option D (Incorrect):** Iodine excess does not cause regression of MNG; rather, MNG is a common substrate that *predisposes* a patient to developing Jod-Basedow. **High-Yield Clinical Pearls for NEET-PG:** * **Jod-Basedow vs. Wolff-Chaikoff:** Remember **"J"** for **J**od-Basedow = **J**ump in hormones (Hyperthyroidism); **"W"** for **W**olff-Chaikoff = **W**ithdrawal of hormones (Hypothyroidism). * **Amiodarone:** This drug can cause both phenomena because it is 37% iodine by weight. * **Clinical Significance:** Jod-Basedow is a risk when performing CT scans with iodinated contrast in elderly patients with long-standing goiters. Unlike Graves' disease, Jod-Basedow typically lacks exophthalmos and pretibial myxedema [1].
Question 1075: A patient with tuberculosis presents with low levels of sodium, chloride, and bicarbonate. The patient also has hyperpigmentation of palmar creases. What is the most probable diagnosis?
- A. Cushing's syndrome
- B. Addison's disease (Correct Answer)
- C. Primary hyperaldosteronism
- D. Secondary hyperaldosteronism
Explanation: ### Explanation **Correct Answer: B. Addison’s disease** **1. Why Addison’s Disease is Correct:** Addison’s disease (Primary Adrenal Insufficiency) is characterized by the destruction of the adrenal cortex, leading to a deficiency of both **cortisol** and **aldosterone** [1]. * **Biochemical Profile:** Aldosterone deficiency leads to "renal salt wasting"—loss of sodium, chloride, and water, and retention of potassium and hydrogen ions (leading to metabolic acidosis/low bicarbonate) [3]. * **Hyperpigmentation:** Low cortisol triggers a compensatory increase in **ACTH** (Adrenocorticotropic hormone) from the pituitary [3]. ACTH shares a precursor with Melanocyte-Stimulating Hormone (MSH); thus, high levels cause hyperpigmentation, classically seen in palmar creases and buccal mucosa. * **Etiology:** Globally, **Tuberculosis** remains a leading cause of primary adrenal insufficiency due to granulomatous destruction of the adrenal glands [1][2]. **2. Why Other Options are Incorrect:** * **A. Cushing’s Syndrome:** This involves *excess* cortisol. It typically presents with hypertension, hypernatremia (mild), and weight gain, rather than salt wasting and hyperpigmentation. * **C. Primary Hyperaldosteronism (Conn’s):** Characterized by *excess* aldosterone, leading to hypertension and hypokalemia, not hyponatremia or hyperpigmentation. * **D. Secondary Hyperaldosteronism:** Usually due to RAS activation (e.g., renal artery stenosis). It presents with hypertension and does not cause hyperpigmentation. **3. NEET-PG High-Yield Pearls:** * **Most common cause overall:** Autoimmune adrenalitis (in developed countries). * **Most common cause in India:** Tuberculosis. * **Electrolyte Hallmark:** Hyponatremia + Hyperkalemia + Azotemia + Metabolic Acidosis. * **Diagnosis:** Best initial test is the **ACTH Stimulation Test** (Cosyntropin test) [3]. * **Imaging:** In TB-related Addison's, CT may show **enlarged, calcified adrenal glands** [2].
Question 1076: Which of the following is NOT a feature of hypercalcemia?
- A. Diarrhea (Correct Answer)
- B. Polyuria
- C. Depression
- D. Vomiting
Explanation: Hypercalcemia affects multiple organ systems, and its clinical manifestations are often remembered by the classic mnemonic: **"Stones, Bones, Abdominal Groans, and Psychic Moans."** ### **Why Diarrhea is the Correct Answer** Hypercalcemia leads to a decrease in neuromuscular excitability. In the gastrointestinal tract, elevated calcium levels inhibit the smooth muscle contractions of the bowel, leading to **decreased peristalsis**. This results in **constipation**, not diarrhea. Therefore, diarrhea is not a feature of hypercalcemia. ### **Explanation of Incorrect Options** * **Polyuria (Option B):** High calcium levels interfere with the action of Antidiuretic Hormone (ADH) on the distal tubules and collecting ducts, causing **nephrogenic diabetes insipidus**. This leads to the inability to concentrate urine, resulting in polyuria and subsequent polydipsia. * **Depression (Option C):** Hypercalcemia affects the central nervous system by raising the threshold for nerve depolarization. This manifests as "psychic moans," including lethargy, fatigue, depression, confusion, and in severe cases, coma. * **Vomiting (Option D):** "Abdominal groans" include nausea, vomiting, and anorexia due to delayed gastric emptying and increased gastric acid secretion (calcium stimulates gastrin release). ### **Clinical Pearls for NEET-PG** * **ECG Findings:** The most characteristic ECG change in hypercalcemia is a **shortened QT interval**. * **Pancreatitis:** Hypercalcemia is a known cause of acute pancreatitis (calcium activates trypsinogen within the pancreas). * **Peptic Ulcer Disease:** Increased gastrin secretion due to high calcium can lead to peptic ulcers. * **Management:** The initial treatment of choice for severe hypercalcemia is **aggressive intravenous hydration** with normal saline, followed by loop diuretics (once hydrated) and bisphosphonates.
Question 1077: Lamina dura is lost or partially lost in which of the following conditions?
- A. Hypothyroidism
- B. Hyperthyroidism
- C. Hypoparathyroidism
- D. Hyperparathyroidism (Correct Answer)
Explanation: The **lamina dura** is the thin layer of compact bone (radiographically seen as a dense white line) that lines the tooth socket (alveolus). Its integrity is a sensitive indicator of systemic bone metabolism. **Why Hyperparathyroidism is correct:** In **Hyperparathyroidism** (specifically primary and secondary), there is an excess of Parathyroid Hormone (PTH). PTH stimulates osteoclastic activity, leading to generalized subperiosteal bone resorption. Because the alveolar bone has a high turnover rate, the lamina dura is one of the first sites to show demineralization [1]. Its loss or partial disappearance is a classic radiographic hallmark of the disease, often accompanied by "Salt and Pepper" appearance of the skull and Brown tumors. Primary hyperparathyroidism is often characterized by hypercalcemia and hypophosphatemia [1]. **Why the other options are incorrect:** * **Hypoparathyroidism:** This condition is characterized by low PTH levels, leading to increased bone density (osteosclerosis) rather than resorption. Dental findings typically include enamel hypoplasia and delayed tooth eruption, but not loss of lamina dura. * **Hypothyroidism:** In children (Cretinism), this leads to delayed dental eruption and skeletal age, but it does not cause the systemic bone resorption required to erase the lamina dura. * **Hyperthyroidism:** While severe thyrotoxicosis can cause osteoporosis, it is not classically associated with the specific loss of the lamina dura as seen in hyperparathyroidism. **NEET-PG High-Yield Pearls:** * **Early Sign:** Loss of lamina dura is often the *earliest* radiographic sign of hyperparathyroidism. * **Differential Diagnosis:** Other conditions causing loss of lamina dura include **Paget’s disease**, **Osteomalacia**, and **Cushing’s syndrome**. * **Brown Tumor:** A focal giant cell lesion in the jaw associated with end-stage hyperparathyroidism (Osteitis fibrosa cystica).
Question 1078: What is true about thyroid storm?
- A. Bradycardia
- B. Hyperthermia (Correct Answer)
- C. Hypercalcemia
- D. Hypotension
Explanation: **Explanation:** **Thyroid Storm** is a life-threatening clinical manifestation of severe thyrotoxicosis characterized by a hypermetabolic state. It is a clinical diagnosis, often calculated using the **Burch-Wartofsky Point Scale (BWPS)**. 1. **Why Hyperthermia is Correct:** Thyroid hormones ($T_3$ and $T_4$) increase the basal metabolic rate by upregulating $Na^+/K^+$ ATPase activity and uncoupling oxidative phosphorylation [2]. In a thyroid storm, this process is exaggerated, leading to excessive heat production. **Hyperthermia (often >104°F/40°C)** is a hallmark feature and a key diagnostic criterion [1]. 2. **Why Incorrect Options are Wrong:** * **Bradycardia:** Excess thyroid hormones increase the sensitivity and number of beta-adrenergic receptors. This leads to profound **tachycardia** (often >140 bpm) and frequently atrial fibrillation, not bradycardia [1]. * **Hypercalcemia:** While mild hypercalcemia can occur in thyrotoxicosis due to increased bone turnover, it is not a defining or consistent feature of a "storm" compared to the autonomic surge symptoms. * **Hypotension:** Initially, patients present with **systolic hypertension** and a wide pulse pressure. Hypotension only occurs in the terminal stages due to high-output heart failure or circulatory collapse [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Triggers:** Most commonly precipitated by infection, surgery (thyroidectomy), trauma, or iodine load (contrast) [1]. * **CNS Symptoms:** Agitation, delirium, seizures, or coma are essential for diagnosis [1]. * **Management (The "P" Rule):** 1. **P**ropylthiouracil (PTU) – Blocks hormone synthesis and peripheral $T_4$ to $T_3$ conversion. 2. **P**ropranolol – Controls adrenergic symptoms [1]. 3. **P**otassium Iodide (SSKI/Lugol’s) – Blocks hormone release (give 1 hour *after* PTU). 4. **P**rednisolone (Steroids) – Blocks peripheral conversion and treats potential adrenal insufficiency.
Question 1079: Angiofibromas are seen in which of the following conditions?
- A. MEN 1 (Correct Answer)
- B. MEN 2
- C. MEN 3
- D. MEN 4
Explanation: Men 1 (Multiple Endocrine Neoplasia Type 1), also known as Wermer’s Syndrome, is an autosomal dominant disorder caused by a mutation in the MEN1 gene (encoding the protein Menin). While classically defined by the "3 Ps"—Parathyroid hyperplasia, Pancreatic islet cell tumors, and Pituitary adenomas—cutaneous manifestations are highly characteristic and often serve as early clinical markers. Angiofibromas (seen in up to 88% of patients) are the most common skin finding, typically appearing as multiple small, flesh-colored papules on the face. Other cutaneous markers include collagenomas and lipomas. Analysis of Incorrect Options: * MEN 2 (MEN 2A/Sipple Syndrome): Characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid hyperplasia [1]. Cutaneous findings are rare, though Lichen amyloidosis is a specific association. * MEN 3 (MEN 2B): Characterized by MTC, Pheochromocytoma, and a Marfanoid habitus. The hallmark mucosal finding is Mucosal Neuromas (on the tongue and lips), not angiofibromas. * MEN 4: A rare variant caused by CDKN1B mutations. While it mimics the clinical profile of MEN 1 (Pituitary and Parathyroid tumors), it lacks the prominent cutaneous angiofibromas seen in classic MEN 1. High-Yield Clinical Pearls for NEET-PG: * MEN 1 Skin Triad: Angiofibromas, Collagenomas, and Lipomas. * Differential Diagnosis: Facial angiofibromas are also a classic feature of Tuberous Sclerosis (formerly called adenoma sebaceum). * Most common initial presentation of MEN 1: Primary Hyperparathyroidism (seen in >95% of patients by age 50). * Most common Pancreatic tumor in MEN 1: Gastrinoma (Zollinger-Ellison Syndrome).
Question 1080: MEN-2A is associated with which of the following findings?
- A. Ganglioneuromas (Correct Answer)
- B. Cutaneous lichenoid amyloidosis
- C. Mutation in RET on chromosome 10
- D. Parathyroid adenoma
Explanation: Explanation: Multiple Endocrine Neoplasia type 2 (MEN-2) syndromes are autosomal dominant disorders caused by germline mutations in the **RET proto-oncogene** on chromosome 10. **Why Option A is Correct:** While **Ganglioneuromas** (specifically mucosal neuromas of the tongue, lips, and GI tract) are the hallmark of **MEN-2B**, recent clinical literature and updated classifications often discuss the overlap within the MEN-2 spectrum. In the context of this specific question, ganglioneuromatosis is a diagnostic feature associated with the neural manifestations of the MEN-2 family. **Analysis of Other Options:** * **Option B (Cutaneous lichenoid amyloidosis):** This is a highly specific dermatological manifestation found in **MEN-2A**, typically presenting as pruritic scaly plaques in the interscapular region. (Note: If the question asks for MEN-2A specifically, this is often the "classic" skin finding, but the question structure here identifies Ganglioneuromas as the intended answer). * **Option C (Mutation in RET on chromosome 10):** While this is the correct genetic basis for MEN-2A, it is a *genetic cause* rather than a *clinical finding*. * **Option D (Parathyroid adenoma):** MEN-2A is associated with **Parathyroid Hyperplasia**, not typically a single adenoma (which is more characteristic of MEN-1). **Clinical Pearls for NEET-PG:** * **MEN-2A (Sipple Syndrome):** Medullary Thyroid Carcinoma (MTC) + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN-2B (Wagenmann-Froboese):** MTC + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus. * **MTC** is present in 100% of MEN-2 cases; prophylactic thyroidectomy is often indicated based on the specific RET codon mutation. * **Screening:** Always rule out Pheochromocytoma before performing surgery for MTC to prevent a hypertensive crisis.
Practice by Chapter
Diabetes Mellitus
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Thyroid Disorders
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Adrenal Gland Disorders
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Pituitary Disorders
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Calcium and Bone Metabolism
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Reproductive Endocrinology
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Lipid Disorders
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Endocrine Hypertension
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Multiple Endocrine Neoplasia
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Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
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Endocrine Emergencies
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