Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1051: What is true about Cushing's syndrome?

A. The most common cause is excess ACTH.
B. There are high plasma levels of ACTH and cortisol.
C. It is also referred to as hyperadrenalism.
D. All of the above. (Correct Answer)

Explanation: **Explanation:** Cushing’s syndrome is a clinical state resulting from chronic exposure to excessive levels of glucocorticoids. Understanding the pathophysiology is crucial for NEET-PG. * **Option A (Most common cause):** While the most common cause of *exogenous* Cushing’s is iatrogenic steroid use [2], the most common cause of *endogenous* Cushing’s syndrome (approx. 70%) is **Cushing’s Disease**, which is caused by an ACTH-secreting pituitary adenoma [1]. Therefore, excess ACTH (either pituitary or ectopic) is the most frequent driver of the syndrome. * **Option B (High ACTH and Cortisol):** In ACTH-dependent Cushing’s (the most common variety), the pituitary overproduces ACTH, which chronically stimulates the adrenal cortex to overproduce cortisol [2]. Thus, both levels are elevated in the plasma [3]. * **Option C (Hyperadrenalism):** Cushing’s syndrome is the classic manifestation of hyperadrenalism specifically involving the zona fasciculata of the adrenal cortex. It represents a state of adrenal overactivity. **Clinical Pearls for NEET-PG:** 1. **Cushing’s Syndrome vs. Disease:** "Syndrome" is the broad clinical state; "Disease" specifically refers to a **pituitary adenoma** [1]. 2. **Screening Tests:** The best initial screening tests are the Overnight Dexamethasone Suppression Test (ONDST), 24-hour urinary free cortisol, or Late-night salivary cortisol [3]. 3. **Ectopic ACTH:** Classically associated with Small Cell Carcinoma of the Lung; these patients often present with profound hypokalemia and hyperpigmentation [2]. 4. **Low ACTH:** If cortisol is high but ACTH is suppressed (low), look for an adrenal adenoma or carcinoma (ACTH-independent) [3].

Question 1052: Galactorrhea can be seen in all of the following conditions except?

A. Prolactinoma
B. Acromegaly
C. Secondary hypothyroidism (Correct Answer)
D. Chronic renal failure

Explanation: The correct answer is **Secondary Hypothyroidism**. To understand why, we must look at the hypothalamic-pituitary-thyroid axis. **1. Why Secondary Hypothyroidism is the exception:** In **Primary Hypothyroidism**, the thyroid gland fails, leading to low T3/T4 [1]. This triggers a compensatory increase in **Thyrotropin-Releasing Hormone (TRH)** from the hypothalamus. TRH acts as a potent prolactin secretagogue; thus, high TRH levels lead to hyperprolactinemia and galactorrhea. [1] In **Secondary Hypothyroidism**, the defect is in the pituitary or hypothalamus [2, 5]. Consequently, TRH levels are low or inappropriately normal, and there is no stimulus to increase prolactin. Therefore, galactorrhea is not a feature. **2. Analysis of other options:** * **Prolactinoma (A):** The most common cause of pathological galactorrhea [1]. These are prolactin-secreting pituitary adenomas [4]. * **Acromegaly (B):** Growth Hormone (GH) and Prolactin share structural similarities [3]. Furthermore, many somatotroph tumors are "mammosomatotroph" (secreting both GH and Prolactin), or the large GH tumor causes "stalk effect," blocking dopamine (the prolactin inhibitor) [1]. * **Chronic Renal Failure (D):** Hyperprolactinemia occurs due to decreased renal clearance of prolactin and altered dopaminergic tone in uremia [1]. **NEET-PG High-Yield Pearls:** * **Dopamine** is the primary physiological inhibitor of prolactin (Prolactin Inhibiting Factor) [1]. * **Stalk Effect:** Any lesion compressing the pituitary stalk prevents dopamine from reaching the lactotrophs, causing mild-to-moderate elevations in prolactin (<200 ng/mL) [1]. * **Drugs:** Antipsychotics (D2 blockers), Metoclopramide, and Methyldopa are common pharmacological causes of galactorrhea [1].

Question 1053: Which is NOT a component of Wermer's syndrome?

A. Pituitary
B. Adrenal (Correct Answer)
C. Parathyroid
D. Pancreas

Explanation: **Explanation:** **Wermer’s Syndrome**, also known as **Multiple Endocrine Neoplasia Type 1 (MEN 1)**, is an autosomal dominant disorder caused by a mutation in the *MEN1* gene (encoding the protein Menin). It is characterized by the "3 Ps" rule, involving tumors of the **P**arathyroid, **P**ancreas, and **P**ituitary. * **Why Adrenal is the correct answer:** While adrenal cortical lesions (like adenomas or hyperplasia) can occasionally occur in MEN 1 patients, they are **not** considered a classic diagnostic component of the syndrome. Adrenal involvement is much more characteristic of **MEN 2** (specifically Pheochromocytoma). * **Why the other options are incorrect:** * **Parathyroid (Option C):** This is the most common feature (present in >95% of cases). It usually manifests as multiglandular hyperplasia leading to primary hyperparathyroidism. * **Pancreas (Option D):** Pancreatic neuroendocrine tumors (NETs) occur in about 40-70% of patients. Gastrinomas (leading to Zollinger-Ellison Syndrome) and Insulinomas are the most frequent. * **Pituitary (Option A):** Anterior pituitary adenomas occur in about 30-40% of cases, with Prolactinomas being the most common subtype. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for MEN 1 (Wermer’s):** **3 Ps** (Parathyroid, Pancreas, Pituitary). * **Mnemonic for MEN 2A (Sipple’s):** **1 P, 2 Ms** (Parathyroid, Medullary Thyroid Carcinoma, Pheochromocytoma). * **Mnemonic for MEN 2B:** **3 Ms, 1 P** (Medullary Thyroid Carcinoma, Marfanoid habitus, Mucosal neuromas, Pheochromocytoma). * **Most common initial presentation of MEN 1:** Hypercalcemia due to Hyperparathyroidism. * **Gene Mutation:** *MEN1* gene is located on Chromosome **11q13**.

Question 1054: Which of the following is true about empty sella syndrome?

A. Incidental finding (Correct Answer)
B. Visual defects
C. Anosmia
D. Hypogonadism

Explanation: **Explanation:** **Empty Sella Syndrome (ESS)** occurs when the subarachnoid space herniates into the sella turcica through a deficient diaphragma sellae, resulting in flattening of the pituitary gland against the sellar floor. On imaging (MRI/CT), the sella appears "empty" as it is filled with cerebrospinal fluid (CSF). **Why Option A is Correct:** Primary ESS is most commonly an **incidental finding** on neuroimaging performed for unrelated reasons (e.g., headache or minor head trauma) [1]. Most patients are asymptomatic middle-aged, obese, hypertensive females. Despite the radiological appearance of a "missing" gland, pituitary function is usually preserved because the thin rim of compressed tissue remains functionally adequate. **Why Other Options are Incorrect:** * **B. Visual defects:** Unlike pituitary adenomas, ESS rarely causes optic chiasm compression [2]. Visual field defects (like bitemporal hemianopsia) are not characteristic of ESS [1]. * **C. Anosmia:** This is associated with **Kallmann Syndrome** (hypogonadotropic hypogonadism with impaired smell) [3], not ESS. * **D. Hypogonadism:** While mild hyperprolactinemia (due to pituitary stalk stretching) can occur in <15% of cases, overt clinical hypogonadism or panhypopituitarism is rare in primary ESS. **High-Yield Pearls for NEET-PG:** * **Classic Patient Profile:** Obese, multiparous woman with chronic headaches [2]. * **Primary vs. Secondary:** Primary is due to a congenital defect in the diaphragma sellae; Secondary is due to surgery, radiation, or Sheehan syndrome [3]. * **Biochemical finding:** If any abnormality exists, **hyperprolactinemia** is the most common due to "stalk effect." * **Association:** Often associated with **Idiopathic Intracranial Hypertension (Pseudotumor cerebri)** [2].

Question 1055: What is the investigation of choice in a patient presenting with episodic hypertension, headache, and a thyroid nodule?

A. Urinary catecholamines and aspiration of nodule (Correct Answer)
B. Thyroid function tests only
C. Urinary basic amino acid metabolite
D. Urinary HIAA

Explanation: ### Explanation The clinical presentation of **episodic hypertension** and **headache** is a classic triad (along with palpitations and diaphoresis) suggestive of **Pheochromocytoma**. The presence of a **thyroid nodule** in this context strongly points towards **Multiple Endocrine Neoplasia Type 2 (MEN 2A or 2B)**, where Pheochromocytoma coexists with **Medullary Thyroid Carcinoma (MTC)**. **1. Why Option A is Correct:** In a suspected case of MEN 2, the priority is to screen for Pheochromocytoma before addressing the thyroid nodule. **Urinary catecholamines** (or metanephrines) are the initial biochemical screening tools to confirm catecholamine excess [1]. **Aspiration of the nodule** (Fine Needle Aspiration Cytology) is then required to evaluate the thyroid lesion for MTC. *Note:* In clinical practice, the Pheochromocytoma must be surgically removed *before* any thyroid surgery to prevent a fatal hypertensive crisis during anesthesia [1]. **2. Why Other Options are Incorrect:** * **Option B:** Thyroid function tests (TFTs) assess the metabolic status (hypo/hyperthyroidism) but do not diagnose MTC or Pheochromocytoma. * **Option C:** "Urinary basic amino acid metabolites" is a vague distractor and not a standard diagnostic test for these conditions. * **Option D:** **Urinary 5-HIAA** is the screening test for **Carcinoid Syndrome**, which presents with flushing and diarrhea, not episodic hypertension. **Clinical Pearls for NEET-PG:** * **MEN 2A:** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus. * **Rule of 10s for Pheochromocytoma:** 10% bilateral, 10% malignant, 10% extra-adrenal, 10% familial [1]. * **MTC Marker:** Serum **Calcitonin** is the specific tumor marker for Medullary Thyroid Carcinoma.

Question 1056: Which of the following is the most likely clinical feature for the causes of sexual dysfunction that rarely indicate organic disease?

A. loss of sexual desire
B. failure of erection with absent nocturnal penile tumescence (NPT)
C. absence of emission
D. absence of orgasm with normal libido and erectile function (Correct Answer)

Explanation: ### Explanation Sexual dysfunction can be broadly classified into **organic** (physical) and **psychogenic** (functional) causes [1]. Understanding the sequence of the male sexual response—libido, erection, emission, and orgasm—is crucial for diagnosis. **Why Option D is Correct:** The **absence of orgasm despite normal libido and erectile function** is a specific clinical scenario that rarely points to an organic disease. It is most commonly associated with **psychological factors** (such as performance anxiety or relationship issues) or the use of specific medications, notably **Selective Serotonin Reuptake Inhibitors (SSRIs)**. In these cases, the physiological machinery for arousal and erection is intact, but the neurological/psychological threshold for climax is not met [3]. **Analysis of Incorrect Options:** * **A. Loss of sexual desire:** This is frequently organic, often indicating **hypogonadism** (low testosterone) or **hyperprolactinemia** [2]. * **B. Failure of erection with absent NPT:** The presence of Nocturnal Penile Tumescence (NPT) is the "gold standard" to differentiate psychogenic from organic impotence [4]. If NPT is **absent**, it strongly indicates an **organic cause** (vascular disease, diabetes, or nerve damage). * **C. Absence of emission:** This is usually organic, often due to **retrograde ejaculation** (common in post-TURP patients or diabetics with autonomic neuropathy) or sympathetic nerve damage. **Clinical Pearls for NEET-PG:** * **Psychogenic Impotence:** Characterized by sudden onset, presence of morning erections (NPT), and situational dysfunction [3]. * **Organic Impotence:** Characterized by gradual onset, absence of NPT, and global dysfunction (occurs in all situations). * **Hyperprolactinemia:** Always check prolactin levels in patients with decreased libido and erectile dysfunction, as it inhibits GnRH secretion [2], [4]. * **Drug-induced:** Spironolactone and Cimetidine are classic causes of erectile dysfunction and gynecomastia due to anti-androgenic effects [2].

Question 1057: Which of the following is NOT a treatment for Zollinger-Ellison syndrome?

A. Proton pump inhibitors
B. Octreotide
C. Streptozotocin
D. Diazoxide (Correct Answer)

Explanation: Explanation: Zollinger-Ellison Syndrome (ZES) is caused by a gastrin-secreting neuroendocrine tumor (gastrinoma), leading to massive gastric acid hypersecretion and severe peptic ulcer disease. **Why Diazoxide is the correct answer:** **Diazoxide** is used to treat **insulinomas**, not gastrinomas. It works by opening ATP-sensitive potassium channels in pancreatic beta cells, which inhibits insulin secretion and increases blood glucose levels. It has no role in inhibiting gastrin secretion or reducing gastric acid production, making it ineffective for ZES. **Analysis of incorrect options:** * **Proton Pump Inhibitors (PPIs):** These are the **first-line medical therapy** for ZES. High-dose PPIs (e.g., Omeprazole) effectively control gastric acid hypersecretion, preventing complications like perforation or strictures. * **Octreotide:** As a somatostatin analog, it inhibits the release of various hormones from neuroendocrine tumors. It can be used to decrease gastrin levels and provide symptomatic relief in metastatic or unresectable cases. * **Streptozotocin:** This is a nitrosourea chemotherapeutic agent specifically toxic to pancreatic islet cells. It is used in the management of **metastatic gastrinomas** to reduce tumor burden. **Clinical Pearls for NEET-PG:** * **Location:** Most gastrinomas are found in the **Passaro’s Triangle** (Gastrinoma Triangle). * **Association:** Approximately 25% of ZES cases are associated with **Multiple Endocrine Neoplasia type 1 (MEN1)**. * **Diagnosis:** The best initial test is a **fasting serum gastrin level** (>1000 pg/mL is diagnostic). The most sensitive provocative test is the **Secretin Stimulation Test** (gastrin levels rise in ZES, whereas they fall in normal individuals). * **Drug of Choice:** PPIs for symptom control; surgical resection for localized disease.

Question 1058: SIADH is associated with which type of lung malignancy?

A. Small cell carcinoma of the lung (Correct Answer)
B. Adenocarcinoma of the lung
C. Squamous cell carcinoma of the lung
D. Mixed cell tumor of the lung

Explanation: **Small cell carcinoma of the lung (SCLC)** is the correct answer because it is a neuroendocrine tumor derived from Kulchitsky cells. These cells have the metabolic machinery to produce ectopic hormones [1]. In approximately 7–10% of cases, SCLC cells secrete **Arginine Vasopressin (AVP/ADH)**, leading to the Syndrome of Inappropriate Antidiuretic Hormone (SIADH) [2]. This results in dilutional hyponatremia, concentrated urine, and euvolemic status. **Analysis of Incorrect Options:** * **Squamous cell carcinoma (SCC):** This is classically associated with the ectopic production of **Parathyroid Hormone-related Protein (PTHrP)**, leading to hypercalcemia [1]. A common mnemonic is "Squamous starts with S, and so does Stones (hypercalcemia)." * **Adenocarcinoma:** This is the most common lung cancer in non-smokers and is typically associated with **Hypertrophic Osteoarthropathy (HOA)** and digital clubbing rather than SIADH [2]. * **Mixed cell tumor:** While these can exhibit features of multiple cell types, they are not the primary or classic association for SIADH in medical examinations. **High-Yield Clinical Pearls for NEET-PG:** * **SCLC Associations:** SIADH, ACTH production (Cushing Syndrome), and Lambert-Eaton Myasthenic Syndrome (LEMS) [1], [3]. * **Diagnosis of SIADH:** Characterized by hyponatremia (Na <135 mEq/L), low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg). * **Management:** The mainstay of treatment for SIADH in SCLC is fluid restriction and treating the underlying malignancy. For refractory cases, Vasopressin receptor antagonists (Vaptans) may be used.

Question 1059: Phaeochromocytomas occur in all of the following syndromes except?

A. Multiple endocrine neoplasia type 1 (MEN 1) (Correct Answer)
B. Familial paraganglioma syndrome
C. Von Hippel-Lindau syndrome
D. Neurofibromatosis type 1

Explanation: **Explanation:** The correct answer is **A. Multiple endocrine neoplasia type 1 (MEN 1)**. Pheochromocytomas are catecholamine-secreting tumors of the adrenal medulla. While they are associated with several hereditary syndromes, **MEN 1 (Wermer’s Syndrome)** is characterized by the "3 Ps": **P**arathyroid hyperplasia, **P**ancreatic islet cell tumors (e.g., Gastrinoma, Insulinoma), and **P**ituitary adenomas (e.g., Prolactinoma). Pheochromocytoma is notably absent in MEN 1. **Analysis of other options:** * **MEN 2 (A and B):** Pheochromocytoma is a hallmark of MEN 2, occurring in approximately 50% of cases. * **Familial Paraganglioma Syndrome:** Caused by mutations in the Succinate Dehydrogenase (**SDH**) genes (SDHB, SDHD, etc.), these patients frequently develop both extra-adrenal paragangliomas and adrenal pheochromocytomas. * **Von Hippel-Lindau (VHL) Syndrome:** VHL type 2 is strongly associated with pheochromocytomas, alongside hemangioblastomas and renal cell carcinoma. * **Neurofibromatosis type 1 (NF1):** While rare (approx. 1-5% of NF1 patients), there is a well-established increased risk of pheochromocytoma in these individuals. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** Traditionally, 10% are bilateral, 10% are extra-adrenal, and 10% are malignant (though genetic cases often have higher rates of bilaterality). * **Most common site for extra-adrenal tumor:** Organ of Zuckerkandl (near the origin of the inferior mesenteric artery). * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. * **Pre-operative Management:** Always start an **alpha-blocker** (e.g., Phenoxybenzamine) *before* a beta-blocker to prevent a hypertensive crisis.

Question 1060: Which chromosome is involved in the pathogenesis of MEN 4?

A. 10
B. 11
C. 12 (Correct Answer)
D. 13

Explanation: **MEN 4 (Multiple Endocrine Neoplasia Type 4)** is a rare autosomal dominant syndrome characterized by a clinical phenotype similar to MEN 1 (parathyroid and pituitary tumors) but caused by a distinct genetic mutation. 1. **Why Option C is Correct:** MEN 4 is caused by a germline mutation in the **CDKN1B gene**, which is located on **Chromosome 12 (12p13)**. This gene encodes the protein **p27 (Kip1)**, a cyclin-dependent kinase inhibitor that acts as a negative regulator of the cell cycle. A loss-of-function mutation in *CDKN1B* leads to uncontrolled cell proliferation, resulting in endocrine neoplasia. 2. **Why Other Options are Incorrect:** * **Option A (Chromosome 10):** This is the location of the **RET proto-oncogene**, which is mutated in **MEN 2A and MEN 2B**. * **Option B (Chromosome 11):** This is the location of the **MEN1 gene** (encoding the protein Menin), which is mutated in **MEN 1 syndrome**. * **Option D (Chromosome 13):** This chromosome is associated with the *RB1* (Retinoblastoma) gene and *BRCA2*, but it is not involved in the primary pathogenesis of MEN syndromes. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 4 Phenotype:** Primarily involves primary hyperparathyroidism and pituitary adenomas. It may also include tumors of the adrenals, kidneys, and reproductive organs. * **Differential Diagnosis:** Always consider MEN 4 in patients who present with MEN 1-like symptoms but test negative for mutations in the *MEN1* gene. * **The "P" Rule for MEN 1:** Pituitary, Parathyroid, Pancreas (Chromosome 11). * **The "M" Rule for MEN 2:** Medullary Thyroid CA, Marfanoid habitus (2B), Mucosal Neuromas (2B), Pheochromocytoma (Chromosome 10).

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