Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1011: Which of the following is NOT true regarding Polyglandular Autoimmune Syndrome Type I?

A. It is inherited in an autosomal recessive pattern.
B. It is caused by mutations in the APECED gene.
C. It is associated with chronic active hepatitis.
D. It is associated with celiac disease. (Correct Answer)

Explanation: Polyglandular Autoimmune Syndrome Type I (APS-1), also known as **APECED** (Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy), is a rare genetic disorder characterized by a classic clinical triad [1]. **Why Option D is the correct answer:** Celiac disease is **not** a characteristic component of APS-1. Instead, it is strongly associated with **APS-2** (Schmidt Syndrome), which also includes Type 1 Diabetes Mellitus and Graves' disease/Hashimoto's thyroiditis [2]. **Analysis of other options:** * **Option A & B:** APS-1 is inherited in an **autosomal recessive** pattern. It is caused by a mutation in the **AIRE** (Autoimmune Regulator) gene, located on chromosome 21. This gene is crucial for the negative selection of self-reactive T-cells in the thymus; its defect leads to widespread autoimmunity. * **Option C:** APS-1 has several minor associations beyond the classic triad, including **chronic active hepatitis**, pernicious anemia, vitiligo, and asplenism. **Clinical Pearls for NEET-PG:** * **The Classic Triad (Must-know):** 1. Chronic Mucocutaneous Candidiasis (usually the first sign). 2. Hypoparathyroidism. 3. Addison’s Disease (Adrenal insufficiency) [1]. * **Diagnosis:** Requires at least 2 out of the 3 classic features (or only 1 if a sibling is affected). * **Ectodermal Dystrophy:** Look for enamel hypoplasia, nail pitting, and alopecia in the clinical vignette. * **Contrast with APS-2:** APS-2 is more common, occurs in adults, is polygenic (HLA-linked), and lacks candidiasis/hypoparathyroidism.

Question 1012: Central diabetes insipidus is characterized by which of the following?

A. Low plasma and low urine osmolality
B. High plasma and high urine osmolality
C. Low plasma and high urine osmolality
D. Low urine osmolality and high plasma osmolality (Correct Answer)

Explanation: Central Diabetes Insipidus (DI) is caused by a deficiency in the synthesis or release of **Antidiuretic Hormone (ADH)** from the posterior pituitary. ADH normally acts on the V2 receptors in the renal collecting ducts to reabsorb water [1]. 1. **Why Option D is Correct:** In the absence of ADH, the kidneys cannot reabsorb water, leading to the excretion of large volumes of dilute urine. This results in **low urine osmolality** (typically <300 mOsm/kg). The excessive loss of free water leads to hemoconcentration, causing an increase in serum sodium and **high plasma osmolality** (>295 mOsm/kg). 2. **Why Other Options are Incorrect:** * **Option A & C:** Low plasma osmolality is characteristic of **Primary Polydipsia**, where excessive water intake suppresses ADH and dilutes the blood [2]. * **Option B:** High urine osmolality occurs in states of dehydration where ADH is functioning normally to conserve water. **NEET-PG High-Yield Pearls:** * **Water Deprivation Test:** The gold standard for diagnosis. In Central DI, urine osmolality remains low after dehydration but **increases by >50%** following the administration of exogenous desmopressin (dDAVP). * **Nephrogenic DI:** Unlike Central DI, there is **no response** to desmopressin because the defect lies in the renal receptors [2]. * **Most Common Cause:** Idiopathic is most common, followed by trauma/surgery to the pituitary-hypothalamic region [3]. * **MRI Finding:** Loss of the normal "posterior pituitary bright spot" on T1-weighted images is a classic sign of Central DI.

Question 1013: Syndrome of inappropriate ADH secretion is commonly associated with which of the following malignancies?

A. Breast carcinoma
B. Ovarian carcinoma
C. Lung carcinoma (Correct Answer)
D. Hepatocellular carcinoma

Explanation: Explanation: Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a common paraneoplastic syndrome characterized by the autonomous, non-physiological secretion of ADH, leading to water retention and dilutional hyponatremia. Why Lung Carcinoma is Correct: Among all malignancies, Small Cell Lung Carcinoma (SCLC) is the most frequent cause of SIADH [1]. Approximately 7–10% of patients with SCLC develop SIADH because the neuroendocrine tumor cells ectopically produce and secrete arginine vasopressin (ADH) [1]. It is a classic high-yield association in clinical medicine. Analysis of Incorrect Options: * Breast and Ovarian Carcinoma: While these can occasionally be associated with paraneoplastic syndromes (like hypercalcemia of malignancy due to PTHrP), they are not classically or commonly associated with SIADH [1]. * Hepatocellular Carcinoma: This is more frequently associated with paraneoplastic erythrocytosis (due to EPO production) or hypoglycemia, but rarely SIADH [1]. NEET-PG High-Yield Pearls: * Most common cause of SIADH overall: Small Cell Lung Cancer (SCLC) [1]. * Diagnosis: Characterized by hyponatremia, low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg) in a euvolemic patient. * Management: The mainstay of treatment for chronic SIADH is fluid restriction. For symptomatic/severe hyponatremia, hypertonic saline (3%) is used. Vaptans (Vasopressin receptor antagonists) are pharmacological options. * Complication: Rapid correction of hyponatremia can lead to Osmotic Demyelination Syndrome (Central Pontine Myelinolysis). Remember: "Low to High, your Pons will die."

Question 1014: In a woman with polyuria of 6L/day, which are the 2 most important investigations to be done?

A. Plasma and urine osmolality
B. Water loading test
C. Water deprivation test (Correct Answer)
D. Plasma osmolality

Explanation: ### Explanation The primary goal in evaluating a patient with polyuria (defined as >3L/day) is to differentiate between **Solute Diuresis** (e.g., Diabetes Mellitus) and **Water Diuresis**. Once solute diuresis is ruled out, the clinician must distinguish between the three causes of water diuresis: Central Diabetes Insipidus (DI), Nephrogenic DI, and Primary Polydipsia [1]. **Why the Water Deprivation Test is correct:** The **Water Deprivation Test (Miller-Moses Test)** is the gold standard investigation for polyuria [1]. It assesses the body's ability to concentrate urine in response to dehydration. By withholding fluids, we stimulate the release of endogenous Vasopressin (ADH) [2]. If the urine fails to concentrate, the second phase involves administering exogenous Desmopressin to differentiate between Central DI (where urine osmolality increases) and Nephrogenic DI (where it remains low) [1]. **Analysis of Incorrect Options:** * **A & D (Plasma and Urine Osmolality):** While these are initial screening tests, they are often inconclusive on their own. In many cases of polyuria, baseline osmolality remains within the normal range due to compensatory mechanisms. They are *components* of the diagnostic workup but do not provide a definitive diagnosis like the deprivation test. * **B (Water Loading Test):** This test is used to assess the body's ability to *dilute* urine, typically used in the evaluation of SIADH or adrenal insufficiency, not polyuria. **Clinical Pearls for NEET-PG:** * **Initial Step:** Always rule out Diabetes Mellitus (check blood glucose) and hypercalcemia/hypokalemia before starting a water deprivation test [1]. * **Primary Polydipsia:** In this condition, the patient *can* concentrate urine during water deprivation (Urine Osmolality >600 mOsm/kg) because the ADH mechanism is intact [1]. * **Safety Tip:** Stop the water deprivation test if the patient loses >3% of body weight or if plasma osmolality exceeds 300 mOsm/kg to prevent severe dehydration [1].

Question 1015: Which type of diabetes is HLA associated?

A. Type I diabetes (Correct Answer)
B. Type II diabetes
C. Malnutrition-related diabetes
D. Pregnancy-related diabetes

Explanation: **Explanation:** **Type 1 Diabetes Mellitus (T1DM)** is an autoimmune disorder characterized by the destruction of pancreatic beta cells [1]. Its pathogenesis is strongly linked to the **Major Histocompatibility Complex (MHC)**, specifically the **HLA class II genes** located on chromosome 6p21 [2]. * **Why Option A is correct:** Approximately 90–95% of children with T1DM carry the high-risk haplotypes **HLA-DR3-DQ2** or **HLA-DR4-DQ8**. These HLA molecules are responsible for presenting islet autoantigens to T-lymphocytes, triggering the autoimmune cascade [1]. Heterozygosity for both (DR3/DR4) confers the highest genetic risk. * **Why other options are incorrect:** * **Type 2 Diabetes (B):** This is primarily a metabolic disorder characterized by insulin resistance and relative insulin deficiency. While it has a stronger overall genetic component (higher concordance in identical twins) than T1DM, it is **polygenic** and not associated with HLA or autoimmune markers [1]. * **Malnutrition-related Diabetes (C):** Now largely classified under "Other specific types," this is associated with environmental factors (protein deficiency/cassava toxins) and pancreatic calcification, not HLA-mediated autoimmunity [3]. * **Pregnancy-related Diabetes (D):** Gestational Diabetes (GDM) is driven by placental hormones (like Human Placental Lactogen) causing insulin resistance; it does not have an HLA association. **High-Yield Clinical Pearls for NEET-PG:** 1. **Strongest Association:** HLA-DR3 and HLA-DR4 [1]. 2. **Protective Allele:** HLA-DQB1*0602 is known to provide protection against T1DM. 3. **Autoantibodies:** The presence of GAD65, IA-2, and Zinc Transporter 8 (ZnT8) antibodies confirms the autoimmune nature of T1DM [2]. 4. **LADA:** Latent Autoimmune Diabetes in Adults also shows HLA associations similar to T1DM.

Question 1016: Brown tumour is seen in which of the following conditions?

A. Increased parathyroid hormone (Correct Answer)
B. Increased thyroxine
C. Increased thyroid hormone
D. Increased calcitonin

Explanation: **Explanation:** **Brown tumors** (also known as osteitis fibrosa cystica) are non-neoplastic bone lesions that occur as a direct complication of **Hyperparathyroidism** (specifically primary or tertiary) [1]. 1. **Why Option A is Correct:** Increased Parathyroid Hormone (PTH) stimulates excessive osteoclast activity [1]. This leads to rapid bone resorption and the replacement of normal marrow with vascular fibrous tissue [1]. Micro-hemorrhages occur within these cystic spaces; the subsequent breakdown of hemoglobin leaves behind **hemosiderin** deposits. This pigment gives the lesion its characteristic "brown" appearance under the microscope. 2. **Why Other Options are Incorrect:** * **Options B & C (Thyroxine/Thyroid Hormone):** While hyperthyroidism can cause increased bone turnover and osteoporosis, it does not lead to the formation of localized fibro-cystic brown tumors. * **Option D (Calcitonin):** Calcitonin is secreted by the parafollicular C-cells of the thyroid and acts to *inhibit* osteoclast activity (lowering blood calcium) [1]. High levels (often seen in Medullary Thyroid Carcinoma) do not cause bone resorption or brown tumors. **High-Yield Clinical Pearls for NEET-PG:** * **Radiological Hallmark:** Brown tumors appear as well-demarcated, expansile lytic lesions on X-ray. * **Classic Description:** "Salt and pepper" appearance of the skull and subperiosteal resorption of the phalanges (radial aspect of middle phalanges) are pathognomonic for hyperparathyroidism. * **Von Recklinghausen's Disease of Bone:** This is the historical name for the skeletal manifestations of severe hyperparathyroidism (not to be confused with NF-1). * **Management:** The primary treatment is surgical removal of the offending parathyroid gland; the bone lesions often regress spontaneously once PTH levels normalize.

Question 1017: What is the treatment for lithium-induced diabetes insipidus?

A. Vasopressin
B. Mineralocorticoid antagonist
C. Amiloride (Correct Answer)
D. Loop diuretic

Explanation: Lithium-induced Diabetes Insipidus (DI) is the most common cause of drug-induced **Nephrogenic Diabetes Insipidus**. **Why Amiloride is the Correct Answer:** Lithium enters the principal cells of the collecting duct through **ENaC (Epithelial Sodium Channels)**. Once inside, lithium inhibits glycogen synthase kinase-3β (GSK-3β), which interferes with the action of ADH (Vasopressin) on its V2 receptors. This prevents the insertion of Aquaporin-2 channels, leading to polyuria. **Amiloride** is a potassium-sparing diuretic that specifically **blocks ENaC**. By blocking these channels, amiloride prevents lithium from entering the principal cells, thereby restoring the kidney's sensitivity to ADH and reducing polyuria. **Analysis of Incorrect Options:** * **A. Vasopressin:** This is the treatment for *Central* DI [1]. In lithium-induced DI, the kidneys are resistant to vasopressin; therefore, giving more will not resolve the issue [1]. * **B. Mineralocorticoid antagonist (e.g., Spironolactone):** These act on the aldosterone receptor but do not specifically block the entry of lithium through ENaC as effectively as amiloride. * **D. Loop diuretic (e.g., Furosemide):** These inhibit the Na-K-2Cl symporter in the Loop of Henle and would actually worsen dehydration and polyuria. **High-Yield Clinical Pearls for NEET-PG:** 1. **First-line management:** If possible, discontinue lithium. If lithium must be continued (e.g., for bipolar stability), **Amiloride** is the drug of choice. 2. **Thiazide Diuretics:** Paradoxically, Thiazides can also be used in Nephrogenic DI. They cause mild volume depletion, which increases proximal tubule reabsorption of water, reducing the volume delivered to the distal nephron. 3. **Monitoring:** Always monitor serum lithium levels, as diuretics can alter lithium clearance and potentially lead to toxicity.

Question 1018: All are true regarding SIADH except:

A. Increased level of ADH
B. Urine hypoosmolar (Correct Answer)
C. Hyponatremia
D. Adequate hydration status

Explanation: **Explanation:** **SIADH (Syndrome of Inappropriate Antidiuretic Hormone)** is characterized by the autonomous, non-physiological release of ADH, leading to excessive water reabsorption in the collecting ducts of the kidney [1]. **Why Option B is the correct answer (The "Except"):** In SIADH, the excess ADH causes maximum water retention, which results in highly concentrated urine [1]. Therefore, the urine is **hyperosmolar** (typically >100 mOsm/kg, and often > plasma osmolality), not hypoosmolar [1]. Finding dilute (hypoosmolar) urine in the presence of hyponatremia would instead point toward diagnoses like primary polydipsia [2]. **Analysis of Incorrect Options:** * **A. Increased level of ADH:** This is the primary pathophysiology. ADH levels are inappropriately high relative to low plasma osmolality [3]. * **C. Hyponatremia:** This is a hallmark feature. It is a **dilutional hyponatremia** caused by excessive water retention, not a true sodium deficiency [1]. * **D. Adequate hydration status:** SIADH patients are clinically **euvolemic** [2]. While there is water retention, the body compensates via pressure natriuresis (atrial natriuretic peptide release), which excretes sodium and water to prevent overt edema or hypertension. **NEET-PG High-Yield Pearls:** 1. **Diagnostic Criteria:** Hyponatremia + Low plasma osmolality (<270 mOsm/kg) + High urine osmolality (>100 mOsm/kg) + High urine sodium (>40 mEq/L) [2]. 2. **Common Causes:** Small cell carcinoma of the lung (ectopic production), CNS disorders (stroke, trauma), and drugs (SSRIs, Carbamazepine, Cyclophosphamide). 3. **Management:** Fluid restriction is the first-line treatment. For refractory cases, use **Vaptans** (Vasopressin receptor antagonists) or Demeclocycline [3]. 4. **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis).

Question 1019: Which of the following is NOT true about autonomic neuropathy?

A. Resting tachycardia
B. Silent myocardial infarction
C. Orthostatic hypotension
D. Bradycardia (Correct Answer)

Explanation: **Explanation:** Autonomic neuropathy, most commonly seen in Diabetes Mellitus, involves damage to the nerves regulating involuntary body functions [1]. The correct answer is **Bradycardia** because autonomic dysfunction typically leads to the loss of vagal (parasympathetic) tone, which normally slows the heart rate [2]. **1. Why Bradycardia is NOT true:** In early cardiac autonomic neuropathy (CAN), there is a preferential loss of parasympathetic (vagal) innervation. This results in unopposed sympathetic activity, leading to **resting tachycardia** rather than bradycardia [2]. Furthermore, the heart rate becomes "fixed," meaning it does not respond normally to exercise, stress, or the Valsalva maneuver [2]. **2. Analysis of Incorrect Options:** * **Resting Tachycardia:** This is one of the earliest signs of CAN due to the withdrawal of vagal inhibition on the SA node [2]. * **Silent Myocardial Infarction:** Denervation of sensory afferent fibers in the myocardium prevents the transmission of pain signals. Consequently, patients may present with dyspnea or heart failure rather than classic angina. * **Orthostatic Hypotension:** This occurs due to the failure of the sympathetic nervous system to cause peripheral vasoconstriction and increase heart rate upon standing [2]. It is defined as a fall in systolic BP >20 mmHg or diastolic BP >10 mmHg upon standing. **High-Yield Clinical Pearls for NEET-PG:** * **Gastroparesis:** Another manifestation of autonomic neuropathy, leading to delayed gastric emptying and postprandial fullness [2]. * **Gustatory Sweating:** Excessive sweating while eating, often involving the face and neck [2]. * **Erectile Dysfunction:** Often the earliest clinical sign of autonomic neuropathy in men [2]. * **Bladder Dysfunction:** Leads to "cystopathy" (painless urinary retention and overflow incontinence) [2].

Question 1020: Which of the following is the most likely clinical feature associated with high prolactin levels causing sexual dysfunction?

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

Explanation: Hyperprolactinemia is a common cause of secondary hypogonadism. High prolactin levels inhibit the pulsatile secretion of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus, leading to decreased LH and FSH, and subsequently, low testosterone levels [1]. ### **Explanation of the Correct Option** **B. Failure of erection with absent nocturnal penile tumescence (NPT):** In males, hyperprolactinemia leads to **hypogonadotropic hypogonadism**. Low testosterone levels result in organic erectile dysfunction [2]. A hallmark of organic (hormonal or neurovascular) impotence is the **absence of Nocturnal Penile Tumescence (NPT)**. In contrast, psychogenic impotence typically maintains normal NPT. Hyperprolactinemia is a recognized endocrine cause of impotence and sterility [3]. ### **Explanation of Incorrect Options** * **A. Loss of sexual desire:** While decreased libido is a common symptom of high prolactin, it is a subjective symptom. The question asks for the "clinical feature" specifically associated with the physiological dysfunction (erectile failure) caused by the hormonal axis disruption. * **C. Absence of emission:** Emission is primarily mediated by the sympathetic nervous system and is usually preserved unless there is significant autonomic neuropathy (e.g. Diabetes) or surgical trauma. * **D. Absence of orgasm with normal libido:** Hyperprolactinemia typically affects the "arousal" and "desire" phases due to low testosterone; it does not cause isolated anorgasmia while leaving libido intact. ### **NEET-PG High-Yield Pearls** * **Mechanism:** Prolactin $\uparrow$ $\rightarrow$ GnRH $\downarrow$ $\rightarrow$ LH/FSH $\downarrow$ $\rightarrow$ Testosterone $\downarrow$ [1]. * **Clinical Triad in Men:** Erectile dysfunction, decreased libido, and infertility (oligospermia). Galactorrhea is rare in men (<10%) [1]. * **Drug-Induced:** Antipsychotics (Risperidone) and Metoclopramide are common causes due to D2 receptor antagonism [1]. * **Gold Standard Test for NPT:** Rigiscan (helps differentiate organic from psychogenic ED).

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