Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1351: Most common cause of fulminant diabetes is?

A. Viruses
B. Non-ketotic hyperosmolar coma
C. Autoimmunity (Correct Answer)
D. Diabetic Ketoacidosis

Explanation: ***Autoimmunity*** - **Fulminant diabetes** is a distinct subtype of **Type 1 diabetes** with an acute onset and rapid, severe beta-cell destruction [1]. - This rapid destruction is primarily mediated by an **autoimmune process**, leading to profound insulin deficiency during the initial presentation [2]. *Viruses* - While certain **viral infections** (e.g., Coxsackievirus, enteroviruses) are implicated as potential triggers for **Type 1 diabetes**, they are not considered the direct and most common cause of the fulminant form itself [1]. - Viral infections might initiate or accelerate the **autoimmune process**, but autoimmunity is the direct mechanism of beta-cell destruction. *Non-ketotic hyperosmolar coma* - **Non-ketotic hyperosmolar coma (NKHC)** is a severe complication of **Type 2 diabetes**, characterized by extremely high blood glucose levels without significant ketosis [2]. - It is not a cause of fulminant diabetes but rather a distinct acute diabetic emergency. *Diabetic Ketoacidosis* - **Diabetic ketoacidosis (DKA)** is an acute, life-threatening complication of **Type 1 diabetes** (and sometimes Type 2), characterized by hyperglycemia, ketosis, and metabolic acidosis [3]. - DKA is a **result** of severe insulin deficiency, which can be seen in fulminant diabetes, but it is not the underlying cause of the fulminant condition itself.

Question 1352: Fatty liver with hepatomegaly is seen in:

A. Marasmus
B. Nutmeg liver
C. Metabolic syndrome (Correct Answer)
D. Wilson disease

Explanation: ***Metabolic syndrome*** - **Metabolic syndrome** is characterized by a cluster of conditions, including **insulin resistance**, obesity, hypertension, and dyslipidemia, which frequently lead to **non-alcoholic fatty liver disease (NAFLD)** and subsequent hepatomegaly [1]. - The accumulation of fat in the liver is a direct consequence of the metabolic derangements, leading to hepatic steatosis, inflammation, and potential fibrosis, with **hepatomegaly** often being a palpable clinical sign [1]. *Marasmus* - **Marasmus** is a form of severe protein-energy malnutrition characterized by significant **weight loss** and muscle wasting, but typically **does not involve fatty liver** or hepatomegaly. - In marasmus, caloric intake is severely deficient, leading to the mobilization of fat stores rather than accumulation in the liver [2]. *Nutmeg liver* - **Nutmeg liver** is a characteristic pathological finding in **congestive hepatopathy**, most often due to **right-sided heart failure**. - It results from chronic passive venous congestion, causing a mottled appearance with alternating areas of congestion and normal parenchyma, but not primarily **fatty infiltration**. *Wilson disease* - **Wilson disease** is a rare genetic disorder of **copper metabolism** that leads to excessive copper accumulation in various organs, including the liver, brain, and eyes. - While it can cause hepatomegaly and liver disease, the primary pathology is copper overload, not **fatty infiltration**, though steatosis can occur secondary to chronic liver injury. *Additional Note* - Enlargement of the liver due to fatty infiltration occurs when triacylglycerol accumulation exceeds the liver's capacity to secrete VLDL, a process seen in conditions like uncontrolled diabetes and certain metabolic stresses [2].

Question 1353: Central obesity is seen in;

A. Crohn's disease
B. Celiac disease
C. Cushing's disease (Correct Answer)
D. Conn's disease

Explanation: ***Cushing's disease*** - **Cushing's disease** is characterized by **excessive cortisol production**, leading to fat redistribution, including **central obesity** with a 'buffalo hump' and 'moon face' [1]. - **Cortisol's metabolic effects** promote increased visceral fat accumulation and breakdown of peripheral fat [1]. *Crohn's disease* - **Crohn's disease** is an **inflammatory bowel disease** that typically causes **weight loss**, abdominal pain, and diarrhea due to malabsorption and inflammation. - While patients can develop complications like **fistulas** and **abscesses**, central obesity is not a primary feature. *Celiac disease* - **Celiac disease** is an **autoimmune disorder** triggered by gluten, leading to **malabsorption** and usually presenting with **weight loss**, diarrhea, and nutrient deficiencies. - Central obesity is **not a typical presentation** and would be contradictory to the malabsorptive state. *Conn's disease* - **Conn's disease**, or primary aldosteronism, involves **excessive aldosterone** production, primarily causing **hypertension** and hypokalemia. - It **does not directly cause central obesity**; its metabolic effects are unrelated to fat distribution.

Question 1354: All of the following are the causes for hypercalcemia Except?

A. Thiazides
B. Hyperparathyroidism
C. Acute pancreatitis (Correct Answer)
D. Hypervitaminosis of Vitamin D

Explanation: ***Acute pancreatitis*** - **Acute pancreatitis** is most commonly associated with **hypocalcemia**, not hypercalcemia [1]. - The likely mechanism for hypocalcemia in pancreatitis is the **saponification of calcium in necrotic fat** by free fatty acids released from local lipase activity [1]. *Thiazides* - **Thiazide diuretics** can cause a mild increase in calcium levels by **increasing calcium reabsorption in the distal renal tubule** [2]. - This effect is generally not severe enough to cause symptomatic hypercalcemia unless other underlying conditions are present. *Hyperparathyroidism* - **Primary hyperparathyroidism** is a common cause of hypercalcemia, due to the **overproduction of parathyroid hormone (PTH)** [2]. - PTH increases serum calcium by increasing **bone resorption**, renal calcium reabsorption, and intestinal calcium absorption [2]. *Hypervitaminosis of Vitamin D* - Excessive intake or production of **Vitamin D** leads to hypercalcemia by increasing **intestinal absorption of calcium** [2]. - It also enhances **bone resorption**, contributing to elevated serum calcium levels.

Question 1355: Pheochromocytoma produces all except?

A. Secretin (Correct Answer)
B. Vasoactive intestinal polypeptide
C. Norepinephrine
D. Calcitonin

Explanation: Secretin - **Secretin** is a hormone primarily produced by **S cells in the duodenum and jejunum** [3] in response to acidic chyme, stimulating pancreatic bicarbonate secretion. - Pheochromocytomas originate from **chromaffin cells** of the adrenal medulla and are known for producing catecholamines [2], not secretin. *Vasoactive intestinal polypeptide* - **Vasoactive intestinal polypeptide (VIP)** can be produced by some **neuroendocrine tumors** [1], including pheochromocytomas, though it's more commonly associated with VIPomas. - VIP acts as a **vasodilator** and can contribute to symptoms like flushing and diarrhea in rare cases of VIP-producing pheochromocytomas. *Calcitonin* - While calcitonin is primarily associated with **medullary thyroid carcinoma**, it can rarely be produced ectopically by **neuroendocrine tumors**, including some pheochromocytomas. - This ectopic production is part of the broader concept of **paraneoplastic syndromes** seen in various malignancies. *Norepinephrine* - **Norepinephrine** is a major catecholamine produced by pheochromocytomas, leading to classic symptoms such as **hypertension, palpitations, and sweating** [2]. - The tumor cells (chromaffin cells) are specialized to synthesize and release **catecholamines**, including norepinephrine and epinephrine [2].

Question 1356: Syndrome of inappropriate ADH secretion is characterized by all of the following EXCEPT:-

A. Expanded fluid volume
B. Hyponatremia
C. Hypo-osmolar urine (Correct Answer)
D. Water intoxication

Explanation: ***Hypo-osmolar urine*** - Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by the secretion of ADH in excess of what is appropriate for the plasma osmolality. This excess ADH causes the kidneys to retain water, leading to **concentrated (hyper-osmolar) urine** [1]. - Therefore, **hypo-osmolar urine** is not a characteristic of SIADH; rather, **hyper-osmolar urine** is expected as the body tries to excrete concentrated urine to compensate for water retention. *Expanded fluid volume* - The excess ADH in SIADH leads to increased **water reabsorption** by the kidneys [1]. - This increased water retention can result in an **expanded extracellular fluid volume**, although usually without significant peripheral edema due to natriuretic peptide release [2]. *Hyponatremia* - The retained water dilutes the plasma sodium concentration, causing **dilutional hyponatremia** [2]. - This is a hallmark feature of SIADH, as the body holds onto too much free water [2]. *Water intoxication* - The characteristic features of SIADH, including **hyponatremia** and **increased total body water**, directly lead to a state of **water intoxication** [1]. - Symptoms can range from mild (nausea, malaise) to severe (seizures, coma) depending on the severity and rapidity of hyponatremia.

Question 1357: Which of the following is best for diagnosis of pheochromocytoma?

A. 24-hour Urinary Hydroxy indole acetic acid
B. 24-hour urinary Vanillyl Mandelic acid
C. 24-hour Urinary Hydroxy tryptamine
D. 24-hour urinary Fractionated Metanephrine (Correct Answer)

Explanation: ***24-hour urinary Fractionated Metanephrine*** - This test measures the **metabolites of catecholamines** (epinephrine and norepinephrine), which are continuously produced by pheochromocytomas [1]. - As metanephrines are released continuously rather than episodically, their measurement in a 24-hour urine collection provides the **highest sensitivity and specificity** for diagnosing pheochromocytoma. *24-hour Urinary Hydroxy indole acetic acid* - This is a metabolite of **serotonin**, which is relevant to conditions like **carcinoid syndrome**, not pheochromocytoma. - Elevated levels would indicate a serotonin-producing tumor, not a catecholamine-producing tumor. *24-hour urinary Vanillyl Mandelic acid* - While VMA is a metabolite of both epinephrine and norepinephrine, it is a less specific and sensitive marker than fractionated metanephrines for pheochromocytoma. - Its measurement can be affected by various medications and dietary factors, leading to a higher rate of false positives and negatives compared to metanephrines. *24-hour Urinary Hydroxy tryptamine* - This refers to **serotonin**, which is not directly relevant to the diagnosis of pheochromocytoma. - Elevated levels would point towards conditions involving serotonin metabolism, such as carcinoid tumors.

Question 1358: All of the following syndromes are seen with obesity except:

A. Laurence Moon - Biedl syndrome
B. Cohen syndrome
C. Prader - Willi syndrome
D. Carcinoid syndrome (Correct Answer)

Explanation: ***Carcinoid syndrome*** - Carcinoid syndrome is caused by **neuroendocrine tumors** that secrete **serotonin** and other vasoactive substances, leading to symptoms like flushing, diarrhea, and bronchospasm [2]. **Obesity is not a primary feature** of this syndrome. - The symptoms are directly related to the **hormonal effects** of the secreted substances, not to metabolic alterations associated with obesity. *Laurence Moon - Biedl syndrome* - This is a **rare genetic disorder** characterized by **obesity**, retinitis pigmentosa, polydactyly, intellectual disability, and hypogonadism [1]. - Obesity is a **consistent and prominent feature** of this syndrome, often present from childhood. *Cohen syndrome* - Cohen syndrome is a rare genetic disorder characterized by **obesity** (especially truncal obesity), intellectual disability, microcephaly, characteristic facial features, and hypotonia. - While not as universally severe as in some other syndromes, **obesity is a common clinical feature** of Cohen syndrome. *Prader - Willi syndrome* - Prader-Willi syndrome is a genetic disorder caused by a deletion on chromosome 15, leading to **insatiable hunger (hyperphagia)** and chronic overeating, which results in **severe obesity** [1]. - **Obesity is a cardinal feature** of this syndrome, developing in early childhood due to hypothalamic dysfunction affecting appetite control.

Question 1359: A girl presents with primary amenorrhea, grade V thelarche (mature breast), grade II pubarche (sparse growth of pubic hair) and no axillary hair. Likely diagnosis is:

A. Turner syndrome
B. Testicular feminization (Correct Answer)
C. Gonadal dysgenesis
D. Mullerian agenesis

Explanation: Androgen Insensitivity Syndrome (also known as testicular feminization) is characterized by a phenotype where primary amenorrhea occurs in a girl with mature (Grade V) breast development but sparse or absent pubic and axillary hair (Grade II pubarche). In this condition, androgens are produced but their receptors are non-functional, leading to normal breast development through the peripheral conversion of androgens to estrogens while inhibiting androgen-dependent hair growth [3]. *Turner syndrome* - Characterized by gonadal dysgenesis [1], leading to primary amenorrhea and absent or rudimentary breast development (grade I thelarche). Patients typically present with characteristic physical features such as short stature [1], webbed neck, and coarctation of the aorta, which are not mentioned here. *Gonadal dysgenesis* - This is a broader term for abnormal development of the gonads [2], often leading to primary amenorrhea and lack of secondary sexual characteristics [1]. Unlike the described case, individuals with gonadal dysgenesis would not have mature breast development. *Mullerian agenesis* - Presents with primary amenorrhea due to the absence or hypoplasia of the uterus and upper vagina, but normal ovarian function. Patients with Mullerian agenesis would typically have normal breast development and normal pubic and axillary hair growth, as their androgen receptors are functional.

Question 1360: Treatment of post menopausal osteoporosis are all EXCEPT

A. Estrogen
B. Magnesium and Zinc (Correct Answer)
C. Calcium, Vit D supplementation
D. Raloxifene

Explanation: ***Magnesium and Zinc*** - While **magnesium** and **zinc** are essential for overall health, their role as primary therapeutic agents for established postmenopausal osteoporosis is **unproven** and is not standard treatment. - They are considered **trace elements** and their deficiency can affect bone health, but supplementation alone is not sufficient to treat osteoporosis. *Estrogen* - **Estrogen replacement therapy** was historically used for postmenopausal osteoporosis due to its role in preventing bone loss, but its use is now limited due to **adverse effects** like increased risk of breast cancer and cardiovascular events [1]. - It is still considered in select cases for symptom relief and bone health, but generally at the lowest effective dose for the shortest duration [1]. *Calcium, Vit D supplementation* - **Calcium and Vitamin D supplementation** are fundamental components of osteoporosis management by supporting bone mineralization and calcium homeostasis [2]. - Adequate intake is critical for both **prevention** and **treatment**, often used in conjunction with other pharmacologic agents [2]. *Raloxifene* - **Raloxifene** is a **selective estrogen receptor modulator (SERM)** that acts as an estrogen agonist on bone, thereby reducing bone resorption and increasing bone mineral density [1]. - It is used in the treatment and prevention of postmenopausal osteoporosis, with the added benefit of reducing the risk of invasive breast cancer [1].

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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