Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 861: In a person who has fasted for 5 days, all are seen except:

A. Immunoreactive insulin decreased
B. GH levels decreased (Correct Answer)
C. Glucose tolerance decreased
D. Free fatty acids (plasma) increased

Explanation: ***GH levels decreased*** - During **prolonged fasting**, **growth hormone (GH) levels** typically **increase** to help spare glucose and promote lipolysis, not decrease. - GH's role in counter-regulation means it helps maintain blood glucose by decreasing glucose utilization and increasing liver glucose production. *Glucose tolerance decreased* - **Prolonged fasting** leads to **decreased glucose tolerance** due to **insulin resistance** in peripheral tissues. - This resistance is a physiological adaptation to conserve glucose for the brain and to utilize fatty acids as primary fuel. *Immunoreactive insulin decreased* - Fasting, particularly for an extended duration, results in significantly **decreased insulin secretion** due to the absence of glucose intake. - Lower insulin levels facilitate the mobilization of stored energy, such as fatty acids and amino acids. *Free fatty acids (plasma) increased* - During extended fasting, **lipolysis** is significantly upregulated, leading to a substantial **increase in plasma free fatty acids**. - These fatty acids become the primary fuel source for many tissues, sparing glucose for organs like the brain.

Question 862: What is the effect of insulin administration on the respiratory quotient (RQ) in diabetes?

A. RQ remains unchanged in Diabetes.
B. RQ decreases in Diabetes and increases with insulin administration. (Correct Answer)
C. In diabetes, RQ increases with insulin administration.
D. RQ increases in Diabetes and decreases with insulin administration

Explanation: ***RQ decreases in Diabetes and increases with insulin administration.*** - In uncontrolled diabetes, the body primarily metabolizes **fats for energy** due to insufficient insulin, leading to a lower **Respiratory Quotient (RQ)** (closer to 0.7). - Insulin administration shifts metabolism towards **carbohydrate utilization**, which has an RQ of 1.0, thereby **increasing the overall RQ**. *RQ remains unchanged in Diabetes.* - This is incorrect because the metabolic state in diabetes, particularly the shift to **fat metabolism**, directly impacts the RQ. - The RQ in uncontrolled diabetes is typically **lower than normal**, not unchanged. *In diabetes, RQ increases with insulin administration.* - While this statement is partially correct (RQ does increase with insulin), it is **incomplete** as it fails to mention that RQ is **decreased in the untreated diabetic state**. - The complete picture requires understanding that **RQ decreases in diabetes** due to fat metabolism, and then **increases with insulin** as glucose utilization is restored. *RQ increases in Diabetes and decreases with insulin administration* - This is completely incorrect as **RQ decreases** (not increases) in untreated diabetes due to predominant fat metabolism. - Insulin administration leads to an **increase** (not decrease) in RQ as carbohydrate utilization is favored.

Question 863: Wolf Chaikoff effect:

A. Iodine induced hyperthyroidism
B. Drug induced hyperthyroidism
C. Iodine induced hypothyroidism (Correct Answer)
D. Thyrotoxicosis due to excessive amount of thyroid hormone ingestion

Explanation: ***Iodine induced hypothyroidism*** - The **Wolf-Chaikoff effect** describes the phenomenon where a high concentration of **iodide** temporarily inhibits the synthesis and release of thyroid hormones. - This transient effect leads to a short period of **hypothyroidism** in response to excess iodine. *Iodine induced hyperthyroidism* - This describes **Jod-Basedow phenomenon**, which is distinct from the Wolf-Chaikoff effect. - **Jod-Basedow** occurs when iodine administration in an iodine-deficient individual or someone with pre-existing thyroid abnormalities leads to **hyperthyroidism**. *Drug induced hyperthyroidism* - This is a broad category referring to hyperthyroidism caused by various medications, such as **amiodarone**, but does not specifically define the Wolf-Chaikoff effect. - The Wolf-Chaikoff effect specifically relates to the direct inhibitory action of high **iodine** concentrations on the thyroid gland. *Thyrotoxicosis due to excessive amount of thyroid hormone ingestion* - This condition is known as **thyrotoxicosis factitia** or **exogenous thyrotoxicosis**. - It is distinct from the Wolf-Chaikoff effect, which involves the thyroid gland's self-regulatory response to **iodine** overload rather than external hormone intake.

Question 864: All of the following statements about insulin-like growth factor (IGF) are true, except which of the following?

A. Secretion is stimulated by insulin
B. Also known as somatomedin A (Correct Answer)
C. Required for skeletal and cartilage growth
D. Mainly secreted by the liver

Explanation: ***Also known as somatomedin A*** - This statement is **imprecise and potentially incorrect** when referring to IGF in general. - **IGF-1** (the predominant form) is known as **somatomedin C**, not somatomedin A. - **IGF-2** is known as somatomedin A, but IGF-2 is less physiologically significant in postnatal growth. - In standard physiological discussions, "IGF" typically refers to IGF-1, making this statement the exception (false/imprecise). *Secretion is stimulated by insulin* - This statement is **TRUE** - insulin does stimulate IGF-1 secretion. - While **growth hormone (GH)** is the primary stimulator of hepatic IGF-1 production, **insulin acts permissively and directly** to enable IGF-1 synthesis. - **Insulin deficiency** (e.g., Type 1 diabetes) results in **low IGF-1 levels** despite elevated GH, demonstrating insulin's essential role. - Insulin enhances GH receptor expression and directly stimulates IGF-1 gene transcription in hepatocytes. *Required for skeletal and cartilage growth* - This statement is **TRUE** - IGF-1 is crucial for **postnatal skeletal and cartilage growth**. - IGF-1 mediates most of **GH's growth-promoting effects** through its anabolic actions on bone and cartilage. - It promotes **chondrocyte proliferation and differentiation**, essential for linear bone growth. *Mainly secreted by the liver* - This statement is **TRUE** - the **liver produces approximately 75%** of circulating IGF-1. - Hepatic IGF-1 production occurs in response to **growth hormone stimulation** via the GH receptor. - While other tissues produce IGF-1 for local (paracrine) effects, the liver is responsible for most **endocrine IGF-1**.

Question 865: What is the primary function of the paraventricular and supraoptic nuclei?

A. All of the options.
B. Regulate water balance. (Correct Answer)
C. Destruction can lead to diabetes insipidus.
D. Are located in the anterior pituitary.

Explanation: ***Regulate water balance*** - The **paraventricular** and **supraoptic nuclei** of the hypothalamus synthesize **antidiuretic hormone (ADH)**, also known as **vasopressin**. - ADH plays a crucial role in **regulating water balance** by increasing water reabsorption in the kidneys. - This is the **primary and most fundamental function** of these nuclei. *Destruction can lead to diabetes insipidus* - While this statement is factually true, it describes a **pathological consequence** rather than the primary function. - Destruction of these nuclei impairs ADH synthesis, resulting in **central diabetes insipidus** with polyuria and polydipsia. - However, the question asks for the primary function, not the consequence of destruction. *Are located in the anterior pituitary* - The **paraventricular** and **supraoptic nuclei** are located in the **hypothalamus**, not the anterior pituitary. - These nuclei synthesize hormones that are stored and released by the **posterior pituitary**. *All of the options* - This is incorrect because the anterior pituitary location statement is false. - Additionally, only one option represents the primary function being asked for in the question.

Question 866: In uncomplicated cases, cortisol levels typically return to normal within how many days after acute hemorrhage?

A. 3 days (Correct Answer)
B. 2 weeks
C. 10 days
D. 7 days

Explanation: ***3 days*** - In uncomplicated cases of acute hemorrhage, the normal physiological response involves a rapid stress-induced rise in **cortisol**, which typically **returns to baseline within 3 days**. - This quick normalization reflects the body's efficient ability to restore **homeostasis** after a transient stressor. *2 weeks* - A two-week period for cortisol normalization is unusually long for an **uncomplicated acute hemorrhage**. - Such a prolonged elevation might suggest ongoing stress, a more severe or **complicated hemorrhage**, or a different underlying pathology affecting the **hypothalamic-pituitary-adrenal (HPA) axis**. *10 days* - A 10-day period is still longer than typically expected for **uncomplicated cases**, indicating a more sustained stress response than usual. - While stress can prolong cortisol elevation, for a simple acute hemorrhage, this duration would be uncommon without other complicating factors. *7 days* - While cortisol levels can remain elevated for several days after significant stress, in **uncomplicated acute hemorrhage**, a 7-day period for normalization would be on the longer side. - The initial surge usually subsides more quickly as the acute physiological stress resolves.

Question 867: Osteoclasts are inhibited by:

A. 1,25-dihydroxycholecalciferol (Activated Vitamin D)
B. Tumor Necrosis Factor (TNF)
C. Calcitonin (Correct Answer)
D. Parathyroid Hormone (PTH)

Explanation: ***Correct Option: Calcitonin*** - **Calcitonin** is a hormone primarily produced by the **C-cells of the thyroid gland** that acts to lower blood calcium levels. - It **directly inhibits the activity of osteoclasts**, the cells responsible for bone resorption. - This is the primary mechanism by which calcitonin reduces serum calcium levels. *Incorrect Option: 1,25-dihydroxycholecalciferol (Activated Vitamin D)* - **Activated vitamin D** (calcitriol) primarily promotes **calcium absorption** in the intestines and kidney. - While it can indirectly affect osteoclasts by increasing calcium availability, it does not directly inhibit their activity. - In fact, chronic high levels can promote bone resorption by stimulating osteoclast activity. *Incorrect Option: Tumor Necrosis Factor (TNF)* - **Tumor Necrosis Factor (TNF)** is a pro-inflammatory cytokine that **stimulates osteoclast activity** and bone resorption. - It plays a significant role in **inflammatory bone loss**, such as in rheumatoid arthritis. - TNF promotes, rather than inhibits, osteoclast function. *Incorrect Option: Parathyroid Hormone (PTH)* - **Parathyroid hormone (PTH)** primarily increases blood calcium levels by stimulating bone resorption through **activating osteoclasts**. - It also promotes **calcium reabsorption** in the kidneys and the conversion of vitamin D to its active form. - PTH has the opposite effect of calcitonin on osteoclasts.

Question 868: Which of the following is NOT true about vasopressin?

A. It is released in response to increased plasma osmolality
B. It increases peripheral vascular resistance
C. It is structurally similar to insulin (Correct Answer)
D. It acts on V2 receptors in renal collecting ducts

Explanation: ***It is structurally similar to insulin*** - **Vasopressin** (arginine vasopressin or ADH) is a **nonapeptide** (9 amino acids), whereas **insulin** is a larger protein composed of 51 amino acids in two chains. Their structures are distinct and not similar. - While both are peptide hormones, their primary amino acid sequences and overall three-dimensional structures differ significantly, leading to distinct receptor interactions and physiological roles. *It increases peripheral vascular resistance* - Vasopressin acts on **V1 receptors** located on vascular smooth muscle, causing **vasoconstriction**. - This vasoconstriction leads to an increase in **peripheral vascular resistance** and, consequently, an elevation in **blood pressure**. *It is released in response to increased plasma osmolality* - **Osmoreceptors** in the hypothalamus detect increased **plasma osmolality** (due to dehydration or high solute concentration). - This triggers the release of vasopressin from the **posterior pituitary**, promoting water reabsorption to dilute the plasma. *It acts on V2 receptors in renal collecting ducts* - Vasopressin binds to **V2 receptors** on the basolateral membrane of principal cells in the **renal collecting ducts**. - This binding leads to the insertion of **aquaporin-2 channels** into the apical membrane, increasing water permeability and reabsorption.

Question 869: Disruption of the hypothalamic-pituitary portal system will lead to

A. Increased follicular development due to elevated circulating levels of PRL.
B. Ovulation with subsequent increase in circulating progesterone levels.
C. Increased FSH levels due to reduced ovarian inhibin levels.
D. High circulating levels of PRL, low levels of LH and FSH, leading to ovarian atrophy. (Correct Answer)

Explanation: ***High circulating levels of PRL, low levels of LH and FSH, leading to ovarian atrophy.*** - Disruption of the **hypothalamic-pituitary portal system** impairs the transport of **gonadotropin-releasing hormone (GnRH)** to the anterior pituitary, leading to decreased **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)**. - This disruption also prevents **dopamine** from reaching the anterior pituitary, leading to uncontrolled **prolactin (PRL)** secretion (disinhibition), which suppresses GnRH and **gonadotropin** release, contributing to **ovarian atrophy**. *Increased follicular development due to elevated circulating levels of PRL.* - Elevated **prolactin (PRL)** levels typically **inhibit** ovarian function and **suppress follicular development**, rather than promoting it. - **Hyperprolactinemia** causes **hypogonadism** by interfering with **GnRH** pulsatility and directly affecting ovarian responsiveness to **gonadotropins**. *Ovulation with subsequent increase in circulating progesterone levels.* - Disruption of the portal system leads to decreased **LH** and **FSH**, which are essential for **follicular development** and **ovulation**. - Without ovulation, a **corpus luteum** cannot form, and therefore, there will be no significant increase in **progesterone** levels. *Increased FSH levels due to reduced ovarian inhibin levels.* - Reduced **FSH** and **LH** levels, resulting from the disruption, would lead to impaired **follicular development** and thus **reduced estrogen** and **inhibin** production by the ovaries. - While reduced inhibin usually leads to increased FSH (negative feedback), the primary impairment in this scenario is at the **hypothalamic-pituitary axis**, directly causing low **gonadotropin** levels, overriding the inhibin effect.

Practice by Chapter

Principles of Endocrine Regulation

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Hypothalamus and Pituitary Gland

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Thyroid Physiology

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Adrenal Cortex and Medulla

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Pancreatic Hormones and Glucose Metabolism

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Calcium and Phosphate Homeostasis

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Growth Hormone and Growth Factors

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Endocrine Regulation of Metabolism

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Hormone Receptors and Signaling

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Assessment of Endocrine Function

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