Endocrinology Practice Questions

Q: Which is least likely to be elevated in patients with a pheochromocytoma?

Intravascular volume. **Explanation:** **Why Intravascular Volume is the Correct Answer:** In patients with pheochromocytoma, chronic and excessive secretion of catecholamines (epinephrine and norepinephrine) leads to persistent **alpha-1 adrenergic stimulation**. This causes profound, generalized vasoconstriction. Over time, this "tightening" of the vascular bed, combined with pressure natriuresis (loss of sodium and water due to high blood pressure), results in a **contraction of the intravascular volume**. This is why these patients are often volume-depleted and can develop profound orthostatic hypotension despite being hypertensive. **Analysis of Incorrect Options:** * **A & B (Systolic and Diastolic Pressure):** Catecholamines increase peripheral vascular resistance (via alpha-receptors) and cardiac output/heart rate (via beta-receptors). This typically results in sustained or paroxysmal elevations of both systolic and diastolic blood pressure. * **C (Serum Norepinephrine):** Pheochromocytomas are catecholamine-secreting tumors of the chromaffin cells [1]. Elevated levels of norepinephrine (and its metabolite normetanephrine) are the biochemical hallmark of the disease. **NEET-PG High-Yield Pearls:** * **The Rule of 10s:** 10% are bilateral, 10% are extra-adrenal (Paragangliomas), 10% are malignant, and 10% occur in children. * **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia. * **Pre-operative Management:** Always follow the **"Alpha before Beta"** rule. Start alpha-blockers (e.g., Phenoxybenzamine) first to expand the contracted intravascular volume [1]. Giving beta-blockers first can lead to an unopposed alpha-agonistic crisis, causing a fatal spike in blood pressure. * **Diagnosis:** Best initial screening test is **Plasma free metanephrines**; most specific is 24-hour urinary metanephrines.

Q: Which of the following is associated with A-V block?

Hypothyroidism. **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.

Q: Jod-Basedow phenomenon refers to which of the following?

Iodine excess causing hyperthyroidism. **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].

Q: Which of the following is NOT a feature of hypercalcemia?

Diarrhea. 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.

Q: Lamina dura is lost or partially lost in which of the following conditions?

Hyperparathyroidism. 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).

Q: Angiofibromas are seen in which of the following conditions?

MEN 1. 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 1

Which is least likely to be elevated in patients with a pheochromocytoma?

Accepted Answer

Intravascular volume

Answer

Systemic arterial diastolic pressure

Answer

Systemic arterial systolic pressure

Answer

Serum norepinephrine

Question 2

A 60-year-old male with a history of diabetes and hypertension is found unconscious. On examination, pulse is 120/min, BP is 160/100 mm Hg, and bilateral extensor plantars are elicited. What is the next step in management?

Accepted Answer

Check blood glucose

Answer

Order CT scan

Answer

Administer intravenous mannitol

Answer

Immediately reduce blood pressure with antihypertensives

Question 3

Which of the following is associated with A-V block?

Accepted Answer

Hypothyroidism

Answer

Hyperthyroidism

Answer

Cushing disease

Answer

Pheochromocytoma

Question 4

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?

Accepted Answer

Low serum sodium

Answer

Low serum calcium

Answer

Low serum potassium

Answer

Normal serum potassium

Question 5

Jod-Basedow phenomenon refers to which of the following?

Accepted Answer

Iodine excess causing hyperthyroidism

Answer

Iodine excess causing suppression of TSH

Answer

Iodine excess causing transient decrease in thyroid hormone production

Answer

Iodine excess causing regression of Multinodular Goiter (MNG)

Question 6

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?

Accepted Answer

Addison's disease

Answer

Cushing's syndrome

Answer

Primary hyperaldosteronism

Answer

Secondary hyperaldosteronism

Question 7

Which of the following is NOT a feature of hypercalcemia?

Accepted Answer

Diarrhea

Answer

Polyuria

Answer

Depression

Answer

Vomiting

Question 8

Lamina dura is lost or partially lost in which of the following conditions?

Accepted Answer

Hyperparathyroidism

Answer

Hypothyroidism

Answer

Hyperthyroidism

Answer

Hypoparathyroidism

Question 9

What is true about thyroid storm?

Accepted Answer

Hyperthermia

Answer

Bradycardia

Answer

Hypercalcemia

Answer

Hypotension

Question 10

Angiofibromas are seen in which of the following conditions?

Accepted Answer

MEN 1

Answer

MEN 2

Answer

MEN 3

Answer

MEN 4

Endocrinology — MCQs

Endocrinology — MCQs

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