Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1451: Which electrolyte disturbance is seen in primary hyperaldosteronism?

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

Explanation: ***Hypokalemia*** - **Aldosterone** normally promotes sodium reabsorption and potassium excretion in the renal tubules [1]. - In primary hyperaldosteronism, excessive aldosterone production leads to increased potassium excretion, resulting in **hypokalemia** [1], [2]. *Hyperkalemia* - **Hyperkalemia** (high potassium) is the opposite of what occurs in primary hyperaldosteronism [1]. - Aldosterone's primary action is to increase potassium secretion, so excess aldosterone would not cause potassium retention. *Hyponatremia* - **Hyponatremia** (low sodium) is not typical in primary hyperaldosteronism; instead, **hypernatremia** or normal sodium levels may be observed due to increased sodium reabsorption. - The increased sodium reabsorption also leads to increased water reabsorption which can lead to **hypervolemia** but **normonatremia** [3]. *Hypercalcemia* - **Hypercalcemia** (high calcium) is not directly associated with primary hyperaldosteronism. - Calcium regulation is primarily controlled by parathyroid hormone and vitamin D, not aldosterone.

Question 1452: A male with hyperpigmentation tanner stage 5 presents with hypertension & precocious puberty. The causative defect is:

A. 17 alpha hydroxylase deficiency
B. 17 beta hydroxylase deficiency
C. 11 beta hydroxylase deficiency (Correct Answer)
D. 21 beta hydroxylase deficiency

Explanation: ***11 beta hydroxylase deficiency*** - This deficiency leads to an accumulation of **11-deoxycortisol** and **deoxycorticosterone (DOC)**, a potent mineralocorticoid [1]. - **DOC excess** causes **hypertension** and **hypokalemia**, while the shunting of precursors to the androgen pathway results in **precocious puberty** in males and virilization in females, along with **hyperpigmentation** due to increased ACTH [1]. *17 alpha hydroxylase deficiency* - This deficiency impairs the synthesis of **cortisol** and **sex steroids**, leading to an accumulation of **mineralocorticoid precursors (DOC and corticosterone)**. - Patients typically present with **hypertension**, **hypokalemia**, and **absent or rudimentary secondary sexual characteristics** (delayed puberty/sexual infantilism) due to the lack of androgens/estrogens, not precocious puberty. *17 beta hydroxylase deficiency* - This enzyme is crucial for the final step in sex steroid synthesis (e.g., testosterone from androstenedione). - A deficiency would lead to **impaired sexual development** and **ambiguous genitalia or undervirilization** in males, along with delayed puberty, completely contradictory to precocious puberty. *21 beta hydroxylase deficiency* - This is the **most common cause of congenital adrenal hyperplasia (CAH)**, leading to a profound deficiency in cortisol and aldosterone, and an excess in androgens [1]. - Patients typically present with **salt-wasting crises** (due to aldosterone deficiency) or **virilization** (due to androgen excess), but usually **hypotension** (due to salt wasting) or normal blood pressure, not hypertension alongside precocious puberty in this specific manner [1].

Question 1453: A male patient with purple striae, thin skin, non-healing wound, and pedunculated abdomen, most probable cause?

A. Insulin resistance
B. Hypercortisolism (Correct Answer)
C. Hypothyroidism
D. Genetic connective tissue disorder

Explanation: Hypercortisolism - **Purple striae** are characteristic due to the breakdown of collagen and elastic fibers from excessive **cortisol**. - **Thin skin**, **non-healing wounds**, and a **pedunculated abdomen** (central obesity) are all classic signs of chronic high cortisol levels, as seen in **Cushing's syndrome** [1]. *Insulin resistance* - While insulin resistance can lead to conditions like **acanthosis nigricans** and **obesity**, it typically does not cause purple striae or thin skin directly. - It's often associated with **type 2 diabetes**, polycystic ovary syndrome, but not the specific dermatological features presented. *Hypothyroidism* - Hypothyroidism symptoms include **dry skin**, **coarse hair**, **fatigue**, and **weight gain**, but not typically purple striae or thin skin. - It can cause **non-pitting edema** (myxedema), which is distinct from the described skin changes. *Genetic connective tissue disorder* - Genetic connective tissue disorders like **Ehlers-Danlos syndrome** can cause thin, fragile skin and poor wound healing. - However, they do not typically present with the characteristic **purple striae** or **pedunculated abdomen** that point specifically to hypercortisolism.

Question 1454: Which condition results from hypersecretion of growth hormone in adults?

A. Gigantism
B. Growth hormone deficiency
C. Cushing's syndrome
D. Acromegaly (Correct Answer)

Explanation: ***Acromegaly*** - **Acromegaly** is the clinical syndrome that results from **hypersecretion of growth hormone (GH)** in adults, after the growth plates have fused [1], [3]. - This leads to characteristic symptoms such as the **enlargement of hands, feet, and facial features**, as well as various systemic complications [1]. *Gigantism* - **Gigantism** results from **hypersecretion of GH during childhood or adolescence**, before the epiphyseal growth plates have fused [1]. - This condition leads to **excessive linear growth** and an abnormally tall stature [1]. *Growth hormone deficiency* - **Growth hormone deficiency** is caused by the **underproduction** or lack of growth hormone secretion. - In children, it leads to **delayed growth and short stature**, while in adults, it can cause changes in body composition and metabolism. *Cushing's syndrome* - **Cushing's syndrome** is caused by prolonged exposure to **high levels of cortisol**, not growth hormone [2]. - Its symptoms include central obesity, a "moon face," "buffalo hump," and skin thinning, which are distinct from those of excess growth hormone [2].

Question 1455: A 40F presents with double vision, headaches, and a progressively enlarging thyroid mass. She has proptosis and limited eye movement. TSH is suppressed. Likely cause of her symptoms?

A. Pituitary adenoma
B. Orbital cellulitis
C. Graves' orbitopathy (Correct Answer)
D. Thyroid carcinoma

Explanation: Graves' orbitopathy - The combination of **proptosis**, **limited eye movement (ophthalmoplegia)** causing double vision, and a suppressed TSH (indicating hyperthyroidism) is highly characteristic of **Graves' disease** with orbital involvement [1]. - An **enlarging thyroid mass** further supports Graves' disease, as it often presents with goiter and hyperthyroidism, leading to the autoimmune sequelae in the orbit [1]. *Pituitary adenoma* - While it can cause **headaches** and **double vision** due to oculomotor nerve compression, a pituitary adenoma would not typically cause a progressively **enlarging thyroid mass** or **proptosis** with suppressed TSH. - Hypersecreting pituitary adenomas (e.g., ACTH, GH) affect other endocrine axes, and non-secreting ones primarily cause mass effect. *Orbital cellulitis* - This is an **acute infection** of the orbital tissues, usually presenting with **pain, fever, rapidly progressing proptosis**, and erythema, which is not suggested by the chronic and progressive nature of this patient's symptoms. - It would not be associated with a suppressed TSH or an enlarged thyroid gland. *Thyroid carcinoma* - A thyroid carcinoma can present as an **enlarging thyroid mass** and may cause local symptoms like dysphagia or hoarseness if advanced, but it does not directly cause **proptosis**, **double vision**, or suppressed TSH. - Although some rare thyroid cancers can metastasize to the orbit, primary presentation with bilateral proptosis and ophthalmoplegia is not typical.

Question 1456: Which hormone is primarily elevated in hyperthyroidism?

A. Thyroxine (T4) (Correct Answer)
B. Thyroid-stimulating hormone (TSH)
C. Triiodothyronine (T3)
D. Reverse T3

Explanation: ***Thyroxine (T4)*** - In **hyperthyroidism**, the thyroid gland overproduces thyroid hormones, leading to elevated levels of **free T4** in the blood [1][2]. - An elevated **free T4** level is a primary diagnostic indicator of hyperthyroidism. *Thyroid-stimulating hormone (TSH)* - **TSH** levels are typically *suppressed* in hyperthyroidism due to the negative feedback mechanism from high circulating thyroid hormones [1][2]. - The elevated T4 and T3 signal the pituitary gland to reduce TSH secretion, so a *low TSH* is often observed [1]. *Triiodothyronine (T3)* - While **T3** levels are also elevated in hyperthyroidism, **T4** is the primary hormone secreted by the thyroid gland and is often measured first [2]. - T3 can be preferentially elevated in some forms of hyperthyroidism, but T4 is generally the most common initial indicator. *Reverse T3* - **Reverse T3** often increases in response to illness or stress, and its role in diagnosing overt hyperthyroidism is limited. - High **rT3** usually indicates impaired peripheral conversion of T4 to T3, not necessarily overproduction by the thyroid gland.

Question 1457: In a 25-year-old male diagnosed with decreased bone density, which hormone should be assessed first?

A. Testosterone level (Correct Answer)
B. Insulin level
C. Estrogen level
D. Parathyroid hormone level

Explanation: Detailed Explanation: ***Testosterone level*** - In a young male with **decreased bone density**, an underlying cause like **hypogonadism** (low testosterone) should be investigated as testosterone plays a crucial role in bone formation and maintenance [1]. - **Androgens** (like testosterone) are important for achieving peak bone mass and preventing bone loss in men [1]. In hypogonadism, the pathogenesis of bone loss is similar to post-menopausal osteoporosis, as testosterone deficiency results in an increase in bone turnover and uncoupling of bone resorption from bone formation [1]. *Insulin level* - Poorly controlled **diabetes** can negatively affect bone health, but assessing insulin levels directly is not typically the first step in investigating decreased bone density. - **Insulin resistance** or Type 1 diabetes can indirectly impact bone through inflammation or metabolic imbalances, but it's not the primary hormonal deficiency directly linked to reduced bone density in a young male. *Estrogen level* - While estrogen is crucial for bone health in both sexes, in a young male, **estrogen levels** are usually assessed secondary to testosterone, as testosterone is aromatized to estrogen and is the primary sex hormone [1]. - Significant **estrogen deficiency** in males is rare and usually indicates severe hypogonadism where testosterone would be low too. *Parathyroid hormone level* - **Parathyroid hormone (PTH)** regulates calcium and phosphate levels and is assessed to rule out hyperparathyroidism or hypoparathyroidism, which can affect bone density. - However, in a young male, **PTH** would typically be considered after initial evaluation of sex hormones and other more common causes of osteoporosis.

Question 1458: A 62-year-old woman with type 2 diabetes presents with persistent hyperglycemia despite the maximum use of oral hypoglycemic agents. What is the next best step in management?

A. Increase oral hypoglycemics
B. Start insulin therapy (Correct Answer)
C. Add GLP-1 receptor agonist
D. Diet and lifestyle modification

Explanation: ***Start insulin therapy*** - When **maximum doses** of oral hypoglycemic agents (OHAs) fail to achieve glycemic targets in type 2 diabetes, **insulin therapy** is generally the next recommended step. - This ensures effective glucose control and prevents long-term complications associated with **persistent hyperglycemia** [1]. *Increase oral hypoglycemics* - The patient is already on the **maximum use of oral hypoglycemic agents**, meaning further increases are unlikely to be effective and could increase side effects. - Continued escalation of OHAs beyond their maximum effective dose is not a standard or safe practice for glycemic control. *Add GLP-1 receptor agonist* - While **GLP-1 receptor agonists** can be beneficial, they are often considered *before* reaching maximal OHA therapy or in conjunction with insulin, not necessarily as the *next best step* when maximal OHAs have already failed. - In cases of **persistent hyperglycemia** despite maximal OHA use, insulin is typically the most potent and effective option for immediate and sustained glycemic control [1]. *Diet and lifestyle modification* - Diet and lifestyle modifications are **fundamental** for all diabetic patients and should always be emphasized, but in this scenario, they have likely already been implemented. - For **persistent hyperglycemia** despite maximal pharmacotherapy, lifestyle changes alone are insufficient to achieve adequate glycemic targets.

Question 1459: A patient presents with severe abdominal pain and hyperglycemia. Imaging reveals a mass in the pancreas. Which pancreatic cell type's dysfunction most likely explains the hyperglycemia?

A. Alpha cells
B. Beta cells (Correct Answer)
C. Delta cells
D. Acinar cells

Explanation: ***Beta cells*** - **Beta cells** produce **insulin**, a hormone vital for lowering blood glucose by promoting glucose uptake into cells [1]. - Dysfunction or destruction of **beta cells** leads to insufficient insulin production, resulting in **hyperglycemia** (high blood sugar) [2]. *Alpha cells* - **Alpha cells** produce **glucagon**, a hormone that increases blood glucose levels by promoting **glycogenolysis** and **gluconeogenesis** in the liver [1]. - While glucagon excess can cause hyperglycemia, the primary cell type linked to the pancreatic mass and hyperglycemia in this context points to insulin deficiency. *Delta cells* - **Delta cells** produce **somatostatin**, which inhibits the secretion of both insulin and glucagon, as well as other gastrointestinal hormones [1]. - Dysfunction of delta cells is not typically associated with severe hyperglycemia as a primary symptom. *Acinar cells* - **Acinar cells** constitute the majority of the exocrine pancreas and produce **digestive enzymes** like amylase and lipase. - While a pancreatic mass could involve acinar cells, their primary role is in digestion, and their dysfunction alone does not directly cause hyperglycemia, although severe pancreatitis can secondarily affect islet cells.

Question 1460: A 35-year-old female with palpitations and diaphoresis who has a thyroid mass is most likely to be diagnosed with what condition?

A. Thyroid carcinoma
B. Thyroid cyst
C. Toxic adenoma (Correct Answer)
D. Hashimoto's thyroiditis

Explanation: ***Toxic adenoma*** - **Palpitations** and **diaphoresis** are symptoms of **hyperthyroidism**, which can be caused by a toxic adenoma, a benign nodule that autonomously produces thyroid hormones [1]. - A palpable **thyroid mass** (nodule) in conjunction with hyperthyroid symptoms is highly suggestive of a toxic adenoma. *Thyroid carcinoma* - While a thyroid mass is present, **thyroid carcinoma** is typically **non-functional** and does not cause symptoms of hyperthyroidism like palpitations and diaphoresis. - Symptoms of thyroid cancer usually include a rapidly growing mass, hoarseness, dysphagia, or lymphadenopathy. *Thyroid cyst* - A **thyroid cyst** is a fluid-filled sac and is usually non-functional, meaning it does not produce thyroid hormones. - Therefore, it would not cause symptoms of **hyperthyroidism** such as palpitations and diaphoresis. *Hashimoto's thyroiditis* - **Hashimoto's thyroiditis** is an autoimmune condition that typically causes **hypothyroidism**, not hyperthyroidism [2]. - While it can present with a goiter or nodules, the associated symptoms would be fatigue, weight gain, and cold intolerance, not palpitations and diaphoresis [1].

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

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Neuroendocrine Tumors

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Endocrine Emergencies

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