Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1331: Insulin Resistance Syndrome (Syndrome X) is associated with which of the following? 1. Type 2 Diabetes Mellitus 2. Hyperinsulinaemia 3. Dyslipidaemia 4. Hypercalcaemia

A. 1, 3 and 4
B. 1, 2 and 3 (Correct Answer)
C. 2, 3 and 4
D. 1, 2 and 4

Explanation: ***1, 2 and 3*** - **Insulin Resistance Syndrome** (metabolic syndrome) is characterized by a cluster of conditions including **insulin resistance**, **type 2 diabetes mellitus**, **hyperinsulinemia**, and **dyslipidemia** [1], [2]. - **Hyperinsulinemia** results from the pancreas overproducing insulin to compensate for tissue insensitivity, and **dyslipidemia** (abnormal lipid levels) is a common component [1]. *1, 3 and 4* - This option correctly identifies **type 2 diabetes mellitus** and **dyslipidemia** as components of insulin resistance syndrome but incorrectly includes **hypercalcemia**. - **Hypercalcemia** (high calcium levels) is not a defining feature or direct consequence of insulin resistance syndrome. *2, 3 and 4* - This option includes **hyperinsulinemia** and **dyslipidemia**, which are core features, but incorrectly includes **hypercalcemia**. - It also omits **type 2 diabetes mellitus**, which is a significant clinical manifestation of prolonged insulin resistance [1]. *1, 2 and 4* - This option correctly identifies **type 2 diabetes mellitus** and **hyperinsulinemia** as associated conditions but incorrectly includes **hypercalcemia**. - This option omits **dyslipidemia**, which is a very common and important component of the metabolic syndrome, contributing to cardiovascular risk.

Question 1332: Which of the following are causes of GnRH dependent precocious puberty? 1. Constitutional 2. Tubercular Encephalitis 3. McCune-Albright syndrome 4. Primary hypothyroidism

A. 1 and 2 only
B. 1, 2 and 3 (Correct Answer)
C. 2, 3 and 4
D. 1, 3 and 4

Explanation: ***1, 2 and 3*** - **Constitutional precocious puberty** is the most common form of central (GnRH-dependent) precocious puberty, where the hypothalamic-pituitary-gonadal axis matures prematurely without an underlying organic cause [1]. - **Tubercular encephalitis** can cause CNS lesions that stimulate the hypothalamus, leading to premature GnRH release and subsequent central precocious puberty [1]. - **McCune-Albright syndrome** is primarily associated with GnRH-independent precocious puberty, but in a small percentage of cases, chronic stimulation of the ovaries (due to activating GNAS mutations) can eventually lead to secondary central (GnRH-dependent) precocious puberty via an exhausted feedback mechanism. *1 and 2 only* - This option is incorrect because while constitutional precocious puberty and tubercular encephalitis are causes of GnRH-dependent precocious puberty, McCune-Albright syndrome can also lead to GnRH-dependent precocious puberty secondarily. - It omits a valid cause, making it an incomplete answer. *2, 3 and 4* - This option incorrectly includes **primary hypothyroidism** as a cause of GnRH-dependent precocious puberty. Primary hypothyroidism is associated with GnRH-independent (peripheral) precocious puberty due to elevated TSH cross-reacting with FSH receptors. - It also omits **constitutional precocious puberty**, which is the most common cause of GnRH-dependent precocious puberty [1]. *1, 3 and 4* - This option incorrectly includes **primary hypothyroidism** as a cause of GnRH-dependent precocious puberty; it is a cause of GnRH-independent precocity. - While constitutional precocious puberty is a correct inclusion, the presence of primary hypothyroidism makes this option incorrect for GnRH-dependent causes.

Question 1333: Refeeding syndrome seen after enteral or parenteral nutrition is characterized by all EXCEPT:

A. Hypomagnesemia
B. Hypocalcemia
C. Hypophosphatemia
D. Hyponatremia (Correct Answer)

Explanation: ***Hyponatremia*** - **Hyponatremia** is not a characteristic feature of refeeding syndrome; rather, fluid retention can sometimes lead to dilutional hyponatremia, but it's not a direct electrolyte shift caused by refeeding. - The core biochemical derangements in refeeding syndrome involve shifts of potassium, magnesium, and phosphate intracellularly [1]. *Hypomagnesemia* - **Hypomagnesemia** is a common and characteristic feature of refeeding syndrome as magnesium is required for ATP generation and cell growth, leading to intracellular shift [1]. - This can contribute to various symptoms such as arrhythmias, weakness, and altered mental status. *Hypocalcemia* - While less direct than other electrolyte disturbances, **hypocalcemia** can occur in refeeding syndrome, partly due to the association with hypophosphatemia and hypomagnesemia. - It may also be exacerbated by vitamin D deficiency or increased parathyroid hormone resistance in malnourished states. *Hypophosphatemia* - **Hypophosphatemia** is the biochemical hallmark of refeeding syndrome, as phosphate is rapidly taken up by cells for ATP synthesis and other metabolic processes during refeeding [1]. - Severe hypophosphatemia can lead to **respiratory failure**, cardiac dysfunction, and rhabdomyolysis.

Question 1334: A few days following viral fever, a 50 year old female presented with pain in neck, fever, malaise and firm enlargement of both the lobes of thyroid. On investigation thyroid antibodies were normal & serum T4 was high normal. Probable diagnosis is:

A. Lymphoma of thyroid
B. Riedel's thyroiditis
C. Autoimmune thyroiditis
D. Granulomatous thyroiditis (Correct Answer)

Explanation: ***Granulomatous thyroiditis*** - The presentation of **neck pain**, **fever**, **malaise**, and **firm, enlarged thyroid lobes** following a viral fever, along with normal thyroid antibodies and high-normal T4, is highly characteristic of **subacute granulomatous thyroiditis (de Quervain's thyroiditis)** [1]. - This condition is typically **post-viral**, causes inflammation leading to temporary hyperthyroidism due to hormone release, and is often painful [1]. *Lymphoma of thyroid* - Thyroid lymphoma usually presents as a **rapidly growing neck mass** in older individuals and is not typically preceded by a viral illness. - It is less commonly associated with pain and fever in this manner, and thyroid function can be variable. *Riedel's thyroiditis* - **Riedel's thyroiditis** is a rare, invasive fibrosis of the thyroid and surrounding structures, leading to a **rock-hard, painless goiter**. - It does not typically follow a viral infection with acute pain and fever or present with high-normal T4. *Autoimmune thyroiditis* - **Autoimmune thyroiditis (Hashimoto's thyroiditis)** is characterized by elevated thyroid antibodies and typically presents with **hypothyroidism**, often with a **painless goiter**. - It does not usually follow a viral illness with acute pain and fever or cause temporary thyrotoxicosis with normal antibodies [1].

Question 1335: Which one of the following is NOT correct regarding MEN-1 syndrome?

A. It involves pancreas
B. It involves pituitary gland
C. It involves pineal gland (Correct Answer)
D. It involves parathyroid glands

Explanation: ***It involves pineal gland*** - MEN-1 syndrome, also known as Wermer's syndrome, is characterized by tumors of the **parathyroid glands**, **pituitary gland**, and **pancreatic islet cells** [1]. - The **pineal gland** is not typically associated with MEN-1 syndrome. *It involves pancreas* - **Pancreatic islet cell tumors** are a hallmark of MEN-1, often leading to diseases like **Zollinger-Ellison syndrome** (gastrinomas) or insulinomas [1]. - These tumors can cause significant endocrine dysfunction due to excessive hormone production [1]. *It involves pituitary gland* - **Pituitary adenomas**, particularly prolactinomas, are a common manifestation of MEN-1 syndrome [1]. - They can cause symptoms related to hormone excess (e.g., galactorrhea) or mass effects (e.g., visual disturbances) [1]. *It involves parathyroid glands* - **Hyperparathyroidism** due to parathyroid adenomas or hyperplasia is the most common manifestation of MEN-1 syndrome, affecting nearly all patients [2]. - This leads to elevated **calcium levels** and can cause symptoms like kidney stones, bone pain, and fatigue.

Question 1336: Medical management of thyrotoxic crisis includes all of the following EXCEPT:

A. IV propanolol
B. IV antibiotics (Correct Answer)
C. IV hydrocortisone
D. IV fluids

Explanation: ***IV antibiotics*** - **Antibiotics** are not a primary treatment for **thyrotoxic crisis** itself unless there's an underlying infection triggering the crisis, which is not indicated as a universal management step [1]. - The crisis is caused by an acute exacerbation of **hyperthyroidism**, not bacterial infection, so antibiotics would not address the core pathophysiology. *IV propanolol* - **Propranolol** (or other beta-blockers) helps control the adrenergic symptoms of thyrotoxic crisis, such as **tachycardia**, **tremors**, and **anxiety** [1]. - It also inhibits the peripheral conversion of **T4 to T3**, providing an additional therapeutic effect. *IV hydrocortisone* - **Glucocorticoids** like **hydrocortisone** are crucial in thyrotoxic crisis to inhibit the peripheral conversion of **T4 to T3**, stabilize cell membranes, and provide adrenal support. - They also help manage potential adrenal insufficiency, which can be an exacerbating factor or complication. *IV fluids* - **Intravenous fluids** are essential for correcting **dehydration**, which is often present due to increased metabolic rate, fever, sweating, and vomiting in patients with thyrotoxic crisis [1]. - They also help address **electrolyte imbalances** and support cardiovascular stability.

Question 1337: A patient presents with headaches, palpitations, hypertension, and urine VMA positivity. The biopsy findings are shown in the image. Which of the following statements is correct?

A. Mostly malignant
B. Mostly in children
C. Mostly bilateral
D. Associated with MEN 2A (Correct Answer)

Explanation: ***Associated with MEN 2A*** - The clinical presentation (headaches, palpitations, hypertension) and positive **urine VMA (vanillylmandelic acid)** strongly suggest a **pheochromocytoma**. - Pheochromocytomas are tumors of the adrenal medulla that secrete catecholamines and are frequently associated with **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**, along with medullary thyroid carcinoma and primary hyperparathyroidism. *Mostly malignant* - Pheochromocytomas are generally benign, with approximately **10% being malignant** ("rule of 10s"). - Malignancy is difficult to predict based on histology alone and is usually defined by the presence of **metastases**. *Mostly in children* - While pheochromocytomas can occur at any age, they are **more common in adults**, typically between 30 and 50 years old. - When they do occur in children, they are more often bilateral, extra-adrenal, or associated with genetic syndromes. *Mostly bilateral* - The majority of pheochromocytomas (approximately **90%**) are **unilateral**. - Bilateral pheochromocytomas are often seen in genetic syndromes such as **MEN 2**, von Hippel-Lindau disease, and neurofibromatosis type 1.

Question 1338: A woman presents with altered sensorium, breathlessness, hypotension and bradycardia. Examination revealed non-pitting edema of the extremities. She has a long -standing history of weight gain, constipation, cold intolerance, and menorrhagia. What is the most likely diagnosis?

A. Myxedema coma (Correct Answer)
B. Hyperthyroidism
C. Cardiogenic shock
D. Septic shock

Explanation: ***Myxedema coma*** - The constellation of **altered sensorium**, **hypotension**, **bradycardia**, and **non-pitting edema** in a patient with a history of **weight gain**, **constipation**, **cold intolerance**, and **menorrhagia** (symptoms of hypothyroidism) is highly suggestive of myxedema coma [2]. - This is an **extreme manifestation of severe, untreated hypothyroidism**, characterized by decompensation of multiple organ systems. *Hyperthyroidism* - Hyperthyroidism usually presents with symptoms like **tachycardia**, **tremors**, **weight loss**, and **heat intolerance** [1], [3], which are contrary to the patient's presentation. - It would not explain the **bradycardia**, **non-pitting edema**, or chronic symptoms like **constipation** and **cold intolerance**. *Cardiogenic shock* - While cardiogenic shock can cause **hypotension** and **altered sensorium**, it is typically characterized by signs of **cardiac dysfunction** such as elevated JVP, crackles, and often **tachycardia** (reflexive or primary), not bradycardia [4]. - It does not account for the **long-standing hypothyroid symptoms** like weight gain, constipation, and cold intolerance. *Septic shock* - Septic shock is primarily due to a severe infection, leading to **fever** (though hypothermia can occur in severe cases), **leukocytosis**, and signs of systemic inflammatory response (SIRS), which are not mentioned. - The patient's chronic symptoms are inconsistent with an acute infectious process as the primary cause of shock.

Question 1339: A diabetic patient's fasting blood glucose level is found to be $160 \mathrm{mg} / \mathrm{dL}$. What will you advise the patient regarding non-pharmacological management?

A. At least 25-35 g of dietary fibre
B. <30 % of the calories should come from fat (Correct Answer)
C. Dietary cholesterol <300 mg per day
D. <2.3 g sodium intake every day

Explanation: ***<30 % of the calories should come from fat*** - Reducing dietary fat intake to less than 30% of total calories is a crucial non-pharmacological strategy for diabetic patients to manage blood glucose levels and prevent cardiovascular complications [1]. - Excess dietary fat, especially saturated and trans fats, can contribute to insulin resistance and weight gain, both of which negatively impact glycemic control [1]. *At least 25-35 g of dietary fibre* - While adequate dietary fiber (typically 25-30g for adults, sometimes up to 35g for men) is beneficial for managing blood glucose, it is generally recommended as a baseline for healthy eating and not the primary or most impactful intervention to address a fasting glucose of 160 mg/dL [1]. - Fiber helps slow glucose absorption and can improve insulin sensitivity, but a specific "at least 25-35g" statement without further context on total caloric intake or other macronutrient distribution might not be the most targeted advice for this specific glucose level [1]. *Dietary cholesterol <300 mg per day* - Limiting dietary cholesterol to less than 300 mg per day is a general recommendation for cardiovascular health, which is particularly important for diabetic patients due to their increased risk of atherosclerosis [2]. - However, for directly addressing a fasting blood glucose of 160 mg/dL, focusing on overall fat intake and carbohydrate quality would have a more immediate impact on glucose control than dietary cholesterol alone. *<2.3 g sodium intake every day* - Restricting sodium intake to less than 2.3 g per day is recommended for managing hypertension and reducing cardiovascular risk, which is often comorbid with diabetes [2]. - While important for overall health in diabetic patients, this recommendation does not directly target blood glucose control and would not be the primary non-pharmacological advice for a fasting glucose of 160 mg/dL.

Question 1340: A patient with a pituitary tumor demonstrates elevated prolactin levels. Which of the following changes in dopamine signaling best explains the hyperprolactinemia?

A. Increased D1 receptor activation
B. Enhanced dopamine reuptake
C. Increased dopamine synthesis
D. Decreased tuberoinfundibular dopamine release (Correct Answer)
E. Increased D2 receptor activation

Explanation: ***Decreased tuberoinfundibular dopamine release*** - **Dopamine** acts as a **prolactin-inhibiting hormone (PIH)**, primarily through the **tuberoinfundibular pathway** from the hypothalamus to the pituitary [1]. - A **pituitary tumor** can compress or damage the pituitary stalk or the hypothalamus, leading to decreased dopamine delivery to the pituitary and thus **hyperprolactinemia** [1]. *Increased D1 receptor activation* - **D1 receptors** are generally associated with **excitatory effects** and are not the primary receptors mediating dopamine's inhibitory effect on prolactin. - **Dopamine's inhibitory action** on prolactin secretion is predominantly mediated by **D2 receptors**. *Enhanced dopamine reuptake* - Enhanced reuptake would lead to **less dopamine availability** at the receptor site, which would indeed cause hyperprolactinemia. - However, this is not the most direct or specific consequence of a **pituitary tumor's mechanical effects** on dopamine signaling [1]. *Increased dopamine synthesis* - **Increased dopamine synthesis** would lead to higher dopamine levels and thus **inhibit prolactin secretion**, which is contrary to the hyperprolactinemia observed in the patient. - This option would result in **hypoprolactinemia**. *Increased D2 receptor activation* - **D2 receptor activation** by dopamine **inhibits prolactin release** from lactotrophs in the pituitary [1]. - Therefore, increased D2 receptor activation would lead to **decreased prolactin levels**, not hyperprolactinemia.

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

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