Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1441: Polyuria in adults is commonly defined as urine output exceeding:

A. 50 ml/ kg / day
B. 30 ml / Kg/ day
C. 60 ml/ kg / day
D. 40 ml / Kg/ day (Correct Answer)

Explanation: ***40 ml / Kg/ day*** - **Polyuria** is clinically defined as urine output exceeding 3 liters per 24 hours (L/day) in adults. - Converting this to a weight-based measurement for an average 75 kg adult, 3 L/day equates to approximately **40 ml/kg/day**. *50 ml/ kg / day* - This value represents a significantly higher urine output than the standard clinical definition of **polyuria**, making it an unlikely threshold. - While excessive, it would indicate a more severe and less common degree of diuresis, not the general definition. *30 ml / Kg/ day* - This value is below the typical threshold for **polyuria** and is closer to what might be considered normal or slightly elevated urine output. - Normal urine output is typically between **0.5-1 ml/kg/hour**, which translates to 12-24 ml/kg/day. *60 ml/ kg / day* - This is a substantially high urine output, indicating a profound level of **diuresis**, well beyond the standard definition of polyuria. - While possible in extreme cases, it is not the common cutoff used for defining polyuria.

Question 1442: A patient undergoes bilateral adrenalectomy in view of bilateral pheochromocytoma. A day after surgery patient develops lethargy, fatigue and loss of appetite. On examination BP is 90/ 60 mmHg, pulse rate of 74 beats/min. No evidence of loss of volume. The likely cause is?

A. Cardiogenic shock
B. Septic shock
C. Cortisol deficiency (Correct Answer)
D. Hypovolemic shock

Explanation: ***Cortisol deficiency*** - Following **bilateral adrenalectomy**, the body loses its primary source of **cortisol**, a critical hormone for maintaining blood pressure and energy levels. [1] - The symptoms of **lethargy, fatigue, loss of appetite, and hypotension** are classic signs of **acute adrenal insufficiency** or **adrenal crisis** due to cortisol deficiency. [1] *Cardiogenic shock* - This condition involves severe pump failure of the heart, leading to **reduced cardiac output**. - While hypotension is present, the symptom complex of fatigue and loss of appetite shortly after adrenal surgery points away from primary cardiac dysfunction in the absence of preceding cardiac events. *Septic shock* - Characterized by hypotension, signs of infection, and organ dysfunction due to a systemic inflammatory response. - There is no mention of fever, leukocytosis, or other signs of infection in the patient's presentation. *Hypovolemic shock* - Caused by a significant reduction in circulating blood volume, often due to hemorrhage or severe dehydration. - The question explicitly states "No evidence of loss of volume," ruling out hypovolemic shock.

Question 1443: Which of the following is NOT the feature of secondary ACTH deficiency?

A. Anorexia
B. Fatigue
C. Hypotension
D. Hyperpigmentation (Correct Answer)

Explanation: ***Hyperpigmentation*** - **Hyperpigmentation** occurs in **primary adrenal insufficiency** (Addison's disease) due to high levels of **ACTH** and co-secreted **melanocyte-stimulating hormone (MSH)** [1]. - In **secondary ACTH deficiency**, ACTH levels are low, so there is no increased stimulation of melanocytes, and thus **hyperpigmentation is absent** [2]. *Anorexia* - **Anorexia** can be a feature of both **primary** and **secondary adrenal insufficiency** due to the general catabolic effects of **cortisol deficiency** and overall endocrine dysfunction. - Reduced cortisol can lead to altered metabolism and appetite, contributing to loss of appetite [2]. *Fatigue* - **Fatigue** is a common and prominent symptom in both **primary** and **secondary adrenal insufficiency** due to **cortisol deficiency** [2]. - Lack of adequate cortisol affects energy metabolism, muscle function, and overall well-being, leading to profound tiredness. *Hypotension* - **Hypotension** is more characteristic of **primary adrenal insufficiency** due to both **cortisol** and **aldosterone deficiency** [1]. - In **secondary ACTH deficiency**, aldosterone secretion is typically preserved (as it's regulated by the **renin-angiotensin system**), but severe **cortisol deficiency** can still contribute to mild hypotension [2].

Question 1444: A 36 year old female is found to have a large pituitary mass on MRI imaging. She underwent transsphenoidal hypophysectomy. Postop replacement of which of the following hormone is not needed?

A. Estradiol
B. Glucocorticoids
C. L-Thyroxine
D. Mineralocorticoids (Correct Answer)

Explanation: ***Mineralocorticoids*** - **Mineralocorticoid** production (primarily aldosterone) is regulated by the **renin-angiotensin-aldosterone system** (RAAS) in the kidneys, not directly by the pituitary gland [1]. - Therefore, pituitary surgery generally does not affect **aldosterone secretion**, and replacement is typically not required unless the adrenal glands themselves are compromised [1][2]. *Estradiol* - **Estradiol** production by the ovaries is stimulated by **follicle-stimulating hormone (FSH)** and **luteinizing hormone (LH)**, which are pituitary hormones. - Pituitary surgery can disrupt the production of FSH and LH, leading to **secondary hypogonadism** and requiring estrogen replacement, especially in pre-menopausal women [2]. *Glucocorticoids* - The adrenal glands produce **glucocorticoids** (e.g., cortisol) under the stimulation of **adrenocorticotropic hormone (ACTH)** from the pituitary [1]. - Damage to the pituitary during surgery can reduce ACTH secretion, leading to **secondary adrenal insufficiency** and necessitating **glucocorticoid replacement** [1]. *L-Thyroxine* - The thyroid gland produces **thyroid hormones** (T3 and T4) under the influence of **thyroid-stimulating hormone (TSH)**, a pituitary hormone [1]. - Post-hypophysectomy, a patient may develop **secondary hypothyroidism** due to impaired TSH production, requiring **L-thyroxine replacement** [1].

Question 1445: Which of the following is not true regarding estrogen use in postmenopausal osteoporosis management?

A. Improves bone density
B. Lowers breast cancer risk (Correct Answer)
C. Increases thromboembolism risk
D. May cause endometrial hyperplasia

Explanation: ***Lowers breast cancer risk*** - Estrogen use, particularly **combined estrogen-progestin therapy**, actually **increases** the risk of breast cancer, rather than lowering it [1]. - This increased risk is a significant concern and a primary reason why estrogen therapy is not a first-line treatment for osteoporosis [1]. *Improves bone density* - Estrogen therapy is known to **prevent bone loss** and **increase bone mineral density** in postmenopausal women by inhibiting osteoclast activity [1]. - This effect is beneficial in reducing the risk of osteoporotic fractures [1], [2]. *Increases thromboembolism risk* - Estrogen therapy significantly **increases the risk of venous thromboembolism (VTE)**, including deep vein thrombosis and pulmonary embolism. - This is a well-established adverse effect and a contraindication in women with a history of thrombotic events. *May cause endometrial hyperplasia* - Unopposed estrogen therapy can **stimulate endometrial proliferation**, leading to **endometrial hyperplasia** and an increased risk of endometrial cancer. - This is why progestin is typically added to estrogen therapy in women with an intact uterus.

Question 1446: A 60-year-old diabetic presents with painless swelling of foot joints. X-ray shows bone fragmentation. What is the most likely diagnosis?

A. Osteoarthritis
B. Charcot Arthropathy (Correct Answer)
C. Gouty Arthritis
D. Rheumatoid Arthritis

Explanation: ***Charcot Arthropathy*** - **Painless swelling** of foot joints with **bone fragmentation** in a diabetic patient is highly characteristic of Charcot arthropathy, a degenerative joint disease resulting from neuropathy [1]. - The neuropathy prevents the patient from feeling pain, leading to repetitive trauma and progressive joint destruction, often presenting as a **warm, swollen, and sometimes deformed foot** [1]. *Osteoarthritis* - Osteoarthritis typically involves **painful joints** and is characterized by cartilaginous degeneration, not significant bone fragmentation resulting from neuropathy [2]. - While X-rays show joint space narrowing and osteophytes, the absence of pain and presence of bone fragmentation in a diabetic points away from this diagnosis [2]. *Gouty Arthritis* - Gout presents with **acute, exquisitely painful** inflammation of joints, often the great toe, due to uric acid crystal deposition. - The key features here are **painless swelling** and **bone fragmentation**, which are inconsistent with gout. *Rheumatoid Arthritis* - Rheumatoid arthritis is a **symmetric polyarthritis** involving smaller joints, leading to pain, stiffness, and eventual joint destruction, often accompanied by systemic symptoms [2]. - The presentation of a **painless, unilateral foot swelling** with bone fragmentation in a diabetic is not typical for rheumatoid arthritis [2].

Question 1447: A patient has hyperaldosteronism. Which lab finding is expected?

A. Metabolic acidosis
B. Hyperkalemia
C. Hypokalemia (Correct Answer)
D. Hyponatremia

Explanation: ***Hypokalemia*** - **Aldosterone** increases the excretion of **potassium** in the kidneys, leading to decreased serum potassium levels [1]. - This effect is mediated by aldosterone's action on the principal cells of the collecting duct, promoting potassium secretion into the urine [1]. *Metabolic acidosis* - **Hyperaldosteronism** typically causes **metabolic alkalosis** due to increased hydrogen ion excretion by the kidneys [1]. - Aldosterone promotes the reabsorption of sodium and water, and the excretion of potassium and hydrogen ions, leading to alkalosis [2]. *Hyperkalemia* - **Aldosterone's primary role** is to promote **potassium excretion** in the kidneys [1]. - Therefore, **excessive aldosterone** production would lead to **hypokalemia**, not hyperkalemia. *Hyponatremia* - **Aldosterone** promotes **sodium reabsorption** in the kidneys, which usually leads to normal or even slightly elevated serum sodium levels [1]. - **Hyponatremia** would be an unexpected finding in hyperaldosteronism [3].

Question 1448: A patient with DKA has a pH of 7.1, Na 130, and K 5.5. What is the best initial treatment?

A. IV insulin
B. IV fluids (Correct Answer)
C. IV potassium
D. IV bicarbonate

Explanation: ***IV fluids*** - Initial management of **diabetic ketoacidosis (DKA)** prioritizes aggressive **intravenous fluid resuscitation** to correct dehydration and improve renal perfusion, thereby facilitating ketone and glucose excretion [1]. - This step is critical before insulin administration to prevent rapid drops in osmolality, which can lead to **cerebral edema** [2]. *IV insulin* - While critical for resolving DKA by stopping ketone production and lowering glucose, **insulin is typically started after initial fluid resuscitation** and only once potassium levels are stable or >3.3 mEq/L to prevent hypokalemia. - Early insulin without adequate fluid replacement can worsen dehydration and increase the risk of **cerebral edema**. *IV potassium* - Although DKA patients are typically **potassium-depleted**, despite what appears to be normal or high serum potassium due to extracellular shift, IV potassium replacement is usually initiated only once serum potassium falls below 5.3 mEq/L and after the start of insulin, which drives potassium into cells [1]. - Administering potassium too early without baseline potassium re-evaluation after initial fluid resuscitation could lead to **hyperkalemia** if the initial high level is truly representative. *IV bicarbonate* - Bicarbonate therapy for DKA is controversial and generally **not recommended** unless the pH is extremely low, typically < 6.9, or in cases of severe cardiovascular instability. - Rapid correction of acidosis can lead to **cerebral edema**, **rebound metabolic alkalosis**, paradoxical central nervous system acidosis, and worsening hypokalemia.

Question 1449: Which of the following is a component of the classic triad used for clinical diagnosis of pheochromocytoma?

A. Hyperkalemia
B. Hypertension
C. Headache (Correct Answer)
D. Bradycardia

Explanation: ***Headache*** - **Headache** is a key symptom in the classic triad for pheochromocytoma, caused by the **vasoconstrictive effects** of catecholamine surges. - The other two components of the classic triad are **palpitations** and **sweating**. *Hyperkalemia* - **Hyperkalemia** is not a typical manifestation of pheochromocytoma; rather, these tumors produce **catecholamines** that can lead to hyperglycemia. - Mineralocorticoid excess (e.g., in aldosteronism) is more commonly associated with electrolyte imbalances like hyperkalemia or hypokalemia. *Hypertension* - While **hypertension** is a hallmark feature of pheochromocytoma, it is a general sign rather than one of the specific three components of the classic clinical triad used for initial diagnostic suspicion. - The classic triad focuses on the most prominent and specific symptoms that suggest a **catecholamine-secreting tumor**. *Bradycardia* - **Bradycardia** is contrary to the expected cardiovascular effects of pheochromocytoma, which typically causes **tachycardia** (palpitations) due to excessive catecholamine release. - Catecholamines, such as **epinephrine** and **norepinephrine**, increase heart rate and myocardial contractility.

Question 1450: Which of the following is a classic feature of pheochromocytoma?

A. Hypoglycemia
B. Hyperkalemia
C. Bradycardia
D. Episodic hypertension (Correct Answer)

Explanation: Episodic hypertension - Episodic hypertension is a hallmark symptom of pheochromocytoma, caused by the intermittent release of large amounts of catecholamines (epinephrine and norepinephrine) from the tumor. - These episodes often manifest with a sudden onset of headache, palpitations, sweating, and anxiety, alongside a sharp rise in blood pressure. [1] Hypoglycemia - Pheochromocytoma typically causes hyperglycemia, not hypoglycemia, due to the catecholamine-induced breakdown of glycogen and inhibition of insulin release. - Catecholamines increase blood glucose levels by stimulating glycogenolysis and gluconeogenesis. [1] Hyperkalemia - Catecholamines, particularly epinephrine, can actually cause a shift of potassium into cells, potentially leading to hypokalemia in some situations, not hyperkalemia. [1] - Hyperkalemia is not a characteristic feature of pheochromocytoma and would suggest other underlying conditions. [1] Bradycardia - Patients with pheochromocytoma usually experience tachycardia and palpitations due to the direct chronotropic effects of excess catecholamines on the heart. - Bradycardia is contrary to the expected physiological response to high levels of circulating catecholamines, which stimulate beta-adrenergic receptors. [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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