Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1701: Which of the following statements about factitious thyrotoxicosis is true?

A. TSH levels are typically elevated.
B. It can be seen in healthcare professionals.
C. It presents with features typical of thyrotoxicosis.
D. Radionuclide uptake is low. (Correct Answer)

Explanation: ***Radionuclide uptake is low.*** - In **factitious thyrotoxicosis**, the exogenous thyroid hormone suppresses the thyroid gland, leading to very low or absent **radionuclide uptake** on a scan [1]. - This differentiates it from other causes of thyrotoxicosis, like **Graves' disease** or **toxic multinodular goiter**, which show high uptake [1]. *It can be seen in healthcare professionals.* - While factitious thyrotoxicosis can occur in anyone, it is not uniquely or predominantly seen in **healthcare professionals**. - The behavior is linked to **deception** regarding illness or medication use, not profession. *TSH levels are typically elevated.* - In factitious thyrotoxicosis, the **exogenous thyroid hormone** suppresses endogenous thyroid stimulating hormone (TSH) production [1]. - Therefore, **TSH levels are typically suppressed or undetectable**, indicating the thyroid gland is not being stimulated to produce excess hormones. *It presents with features typical of thyrotoxicosis.* - While patients with factitious thyrotoxicosis may have symptoms of **thyrotoxicosis** due to excess thyroid hormone, the term refers to the *cause* being external (self-administered hormone) [1]. - The disease refers to the *self-administration* of thyroid hormones, which then leads to the symptoms [1].

Question 1702: All are seen in pheochromocytoma except which of the following?

A. Headaches
B. Weight loss
C. Sweating attacks
D. Hypotension (Correct Answer)

Explanation: ***Hypotension*** - Pheochromocytoma is characterized by the **overproduction of catecholamines** (epinephrine and norepinephrine), which typically cause **hypertension** rather than hypotension. - The classic symptoms of pheochromocytoma, often described as the "5 Ps," are **pain (headache)**, **palpitations**, **perspiration**, **pallor**, and **paroxysmal hypertension**. *Headaches* - **Severe, throbbing headaches** are a very common symptom in pheochromocytoma due to the **vasospastic effects** of high circulating catecholamines. - These headaches are often sudden in onset and can be debilitating. *Weight loss* - The **hypermetabolic state** induced by excessive catecholamines can lead to **increased caloric expenditure** and subsequently, **weight loss**. - Catecholamines increase **basal metabolic rate** and breakdown of fat stores. *Sweating attacks* - **Diaphoresis** or profuse sweating attacks are a hallmark symptom, caused by **sympathetic nervous system activation** due to high catecholamine levels. - These attacks are often paroxysmal and can be accompanied by an exacerbation of other symptoms.

Question 1703: What is the most common cause of hypercalcemic crisis?

A. Carcinoma of the breast
B. Parathyroid adenoma (Correct Answer)
C. Parathyroid hyperplasia
D. Paget's disease

Explanation: ***Parathyroid adenoma*** - **Primary hyperparathyroidism**, most often caused by a solitary parathyroid adenoma, is the leading cause of hypercalcemic crisis, though this is rare [1][2]. - The adenoma autonomously overproduces **parathyroid hormone (PTH)**, leading to increased calcium reabsorption from bone and kidneys, and enhanced intestinal calcium absorption [1]. *Carcinoma of the breast* - While breast carcinoma can lead to **hypercalcemia** through bony metastases or parathyroid hormone-related peptide (PTHrP) production, it's not the most common cause of hypercalcemic crisis. - Metastatic bone disease is a common cause of hypercalcemia in malignancy, but the extent of hypercalcemia varies. *Parathyroid hyperplasia* - **Parathyroid hyperplasia** is a rarer cause of primary hyperparathyroidism compared to adenoma, and thus less frequently causes hypercalcemic crisis [2]. - All four parathyroid glands are typically enlarged and overactive, leading to excessive PTH secretion. *Paget's disease* - **Paget's disease of bone** primarily causes localized areas of increased bone turnover and can lead to elevated **alkaline phosphatase** levels. - It rarely causes significant hypercalcemia, and even more rarely a hypercalcemic crisis, unless there is prolonged immobilization or coexisting hyperparathyroidism.

Question 1704: Which of the following best describes the hormonal profile in Cushing's disease?

A. Decreased ACTH and decreased cortisol levels
B. Increased ACTH and decreased cortisol levels
C. Increased catecholamines
D. Increased ACTH and increased cortisol levels (Correct Answer)

Explanation: ***Increased ACTH and increased cortisol levels*** - **Cushing's disease** is caused by an **ACTH-producing pituitary adenoma** [1], leading to excessive stimulation of the adrenal glands. - This results in **elevated ACTH** secretion, which then drives the adrenal glands to produce **excessive cortisol** [3]. *Decreased ACTH and decreased cortisol levels* - This profile typically indicates **adrenal insufficiency**, such as **Addison's disease**, where the adrenal glands fail to produce enough cortisol, and the pituitary tries to compensate (leading to high ACTH initially) or in central adrenal insufficiency where both ACTH and cortisol are low. - It describes a state of **cortisol deficiency**, which is the opposite of the hypercortisolism seen in Cushing's disease. *Increased ACTH and decreased cortisol levels* - This scenario suggests **primary adrenal insufficiency** (Addison's disease), where the adrenal glands cannot produce sufficient cortisol despite high stimulation from the pituitary gland. - The adrenal glands are unable to respond to the elevated ACTH by producing more cortisol. *Increased catecholamines* - **Elevated catecholamine levels** (epinephrine and norepinephrine) are characteristic of **pheochromocytoma** [2], a tumor of the adrenal medulla. - This condition is distinct from Cushing's disease, which involves excessive cortisol production, not catecholamines.

Question 1705: Which of the following factors contributes to the development of diabetic gangrene?

A. Ischemia due to reduced blood supply
B. Altered host defense mechanisms and neuropathy
C. Increased blood glucose levels leading to tissue damage
D. All of the options contribute to diabetic gangrene (Correct Answer)

Explanation: ***All of the options contribute to diabetic gangrene*** - Diabetic gangrene is a complex complication resulting from a combination of **vascular impairment**, **neuropathy**, and **immunological dysfunction** in diabetic patients [1]. - Each of the individual factors listed plays a significant and interconnected role in its pathogenesis, making a multifactorial etiology. *Ischemia due to reduced blood supply* - **Peripheral arterial disease (PAD)** is common in diabetes, leading to narrowed blood vessels and reduced blood flow to the extremities [1]. - This **ischemia** deprives tissues of oxygen and nutrients, making them vulnerable to injury and infection and impairing healing. *Altered host defense mechanisms and neuropathy* - **Diabetic neuropathy** can lead to loss of sensation, causing unnoticed injuries and breakdown of skin integrity [1]. - **Impaired immune function** in diabetes makes patients more susceptible to infections, which can rapidly progress and lead to gangrene. *Increased blood glucose levels leading to tissue damage* - **Hyperglycemia** directly contributes to macrovascular and microvascular complications, worsening **ischemia** and **neuropathy** [2]. - High glucose levels also impair **wound healing** and **immune responses**, facilitating infection and tissue destruction.

Question 1706: Which of the following statements about gynaecomastia is false?

A. Seen in liver disease
B. There may be estrogen/testosterone imbalance
C. Can be drug induced
D. Subcutaneous mastectomy is the initial treatment of choice (Correct Answer)

Explanation: ***Subcutaneous mastectomy is the initial treatment of choice*** - **Subcutaneous mastectomy** is a surgical intervention, which is typically reserved for cases that are severe, persistent, or resistant to more conservative medical management. - The initial approach usually involves identifying and treating the underlying cause, or pharmacologic therapy if needed, before considering surgery. *Seen in liver disease* - **Liver disease**, particularly advanced states like cirrhosis, impairs the liver's ability to metabolize **estrogen**, leading to increased circulating levels. - This **estrogen excess**relative to **androgen** can stimulate breast tissue growth in males. *There may be estrogen/testosterone imbalance* - **Gynaecomastia** results from an imbalance between **estrogen** (which promotes breast tissue growth) and **androgen** (which inhibits it) [1]. - Conditions that increase **estrogen** levels, decrease **testosterone** levels, or block **androgen receptors** can cause this imbalance [1]. *Can be drug induced* - Many medications can cause **gynaecomastia** as a side effect, including **anti-androgens** (e.g., spironolactone, flutamide), **estrogens**, some **antidepressants**, and certain **cardiovascular drugs** (e.g., digoxin, calcium channel blockers) [1]. - These drugs can directly affect hormone levels or receptor activity, leading to breast tissue proliferation [1].

Question 1707: In which condition is pre-tibial myxedema most commonly observed?

A. Hypothyroid
B. Hyperthyroidism
C. Hashimoto
D. Graves' disease (Correct Answer)

Explanation: ***Graves' disease*** - **Pre-tibial myxedema** is a pathognomonic dermatological manifestation almost exclusively seen in **Graves' disease**, which is an autoimmune hyperthyroid condition [1]. - It involves the deposition of **glycosaminoglycans** and hyaluronic acid in the dermis, leading to non-pitting edema and thickened skin on the shins. *Hypothyroid* - While generalized **myxedema** (non-pitting edema) can occur in severe hypothyroidism, it is diffuse and not typically localized to the pre-tibial area as a distinct condition like pre-tibial myxedema. - The skin changes are usually more widespread, affecting the face, hands, and feet, and are due to widespread mucin deposition not specific to the shins. *Hyperthyroidism* - This is a general term for an overactive thyroid gland. While **Graves' disease** is a type of hyperthyroidism, pre-tibial myxedema is not a feature of all forms of hyperthyroidism (e.g., toxic multinodular goiter, thyroiditis) [1], [2]. - The presence of pre-tibial myxedema narrows the diagnosis specifically to Graves' disease among the hyperthyroid conditions [1]. *Hashimoto* - **Hashimoto's thyroiditis** is an autoimmune disease primarily causing hypothyroidism, though it may have a transient hyperthyroid phase. - It is not typically associated with **pre-tibial myxedema**; rather, patients often present with symptoms of hypothyroidism, such as fatigue, weight gain, and dry skin.

Question 1708: Which type of hypercholesterolemia is characterized by a genetic defect in the LDL receptor, leading to markedly elevated LDL levels?

A. Type I
B. Type IIa (Correct Answer)
C. Type IIb
D. Type III

Explanation: ***Type IIa*** - This type of hypercholesterolemia, also known as **familial hypercholesterolemia (FH)**, is caused by a genetic defect in the **LDL receptor gene**. - The dysfunctional or absent LDL receptors lead to impaired clearance of **LDL particles** from the blood, resulting in markedly elevated **LDL cholesterol levels**. *Type I* - Type I hypercholesterolemia (also called familial chylomicronemia syndrome) is characterized by a deficiency in **lipoprotein lipase (LPL)** or its cofactor **apoC-II**. - This leads to a severe accumulation of **chylomicrons** and **very-low-density lipoprotein (VLDL)**, causing extremely high triglyceride levels, not primarily elevated LDL. *Type IIb* - Type IIb hypercholesterolemia, or **familial combined hyperlipidemia**, involves elevated levels of both **LDL** and **VLDL**. - It is typically associated with overproduction of VLDL and impaired clearance of VLDL and LDL, but the primary defect is not specifically in the LDL receptor. *Type III* - Type III hypercholesterolemia, or **familial dysbetalipoproteinemia**, is characterized by a defect in **apoE**, leading to impaired clearance of **chylomicron remnants** and **VLDL remnants (IDL)**. - This results in elevated levels of both cholesterol and triglycerides, primarily due to the accumulation of these specific remnant lipoproteins, not a defect in LDL receptors.

Question 1709: Which of the following is not a clinical feature of hyperprolactinaemia?

A. Oligomenorrhea
B. Galactorrhea
C. Recurrent abortions
D. Ambiguous genitalia (Correct Answer)

Explanation: ***Ambiguous genitalia*** - **Ambiguous genitalia** refers to a condition where external genitalia do not clearly identify an infant as male or female [4]. This is usually due to **congenital adrenal hyperplasia (CAH)** or other developmental disorders, not hyperprolactinemia [3]. - Hyperprolactinemia primarily affects reproductive function and milk production, not the determination of sex characteristics during fetal development. *Oligomenorrhea* - **Oligomenorrhea** (infrequent menstruation) is a common clinical feature of hyperprolactinemia. Elevated prolactin levels can disrupt the **hypothalamic-pituitary-gonadal axis**, inhibiting GnRH pulsatility and subsequent ovarian function [2]. - This hormonal imbalance leads to irregular or absent menstrual periods [2]. *Galactorrhea* - **Galactorrhea** (inappropriate milk production) is a classic symptom of hyperprolactinemia [1]. Prolactin's primary physiological role is to stimulate milk synthesis [5]. - Pathologically high levels of prolactin result in milk discharge from the breast unrelated to childbirth or nursing [2]. *Recurrent abortions* - Hyperprolactinemia can lead to **recurrent miscarriages** or abortions due to its impact on the menstrual cycle and the potential for a **luteal phase defect**. - High prolactin can interfere with adequate progesterone production needed to maintain an early pregnancy by disrupting follicular development and corpus luteum function [2][5].

Question 1710: Diabetic ketoacidosis is said to be present if:

A. Hyperglycemia, glycosuria, hyperkalemia, and hypocalcemia are present.
B. Hypoglycemia, hypokalemia, hypercalcemia, and ketonemia are present.
C. Hypoglycemia, ketonemia, ketonuria, and hypokalemia are present.
D. Hyperglycemia, heavy glycosuria, ketonemia, ketonuria, and acidosis are present. (Correct Answer)

Explanation: ***Hyperglycemia, heavy glycosuria, ketonemia, ketonuria, and acidosis are present.*** [1], [3] - **Diabetic ketoacidosis (DKA)** is characterized by **uncontrolled hyperglycemia** (blood glucose > 250 mg/dL), metabolic acidosis (pH < 7.3, bicarbonate < 18 mEq/L), and the presence of **ketones** in the blood (ketonemia) and urine (ketonuria). - The heavy glycosuria reflects the body's attempt to excrete excess glucose through the kidneys. *Hyperglycemia, glycosuria, hyperkalemia, and hypocalcemia are present.* - While **hyperglycemia** and **glycosuria** are present in DKA, **hyperkalemia** is often seen due to the acidosis shifting potassium out of cells, but it is not a defining diagnostic criterion. [2] - **Hypocalcemia** is not a primary diagnostic feature of DKA; calcium levels are generally normal or may even be slightly elevated due to hemoconcentration. *Hypoglycemia, hypokalemia, hypercalcemia, and ketonemia are present.* - **Hypoglycemia** contradicts the definition of DKA, which is characterized by **hyperglycemia**. - While **ketonemia** is a feature, **hypokalemia** and **hypercalcemia** are not defining diagnostic criteria for DKA. Hypokalemia may develop during treatment, but patients often present with normal or high potassium. [2] *Hypoglycemia, ketonemia, ketonuria, and hypokalemia are present.* - **Hypoglycemia** is a direct contradiction to the diagnostic criteria of DKA, which requires **hyperglycemia**. - Although **ketonemia** and **ketonuria** are features of DKA, **hypokalemia** is not a defining characteristic at presentation and typically develops during insulin therapy. [2]

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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