Endocrinology Practice Questions

Q: All of the following are known effects of corticosteroids on the skin and connective tissue except?

Hyperpigmentation. **Explanation:** The correct answer is **Hyperpigmentation**. Corticosteroids actually cause **hypopigmentation** (skin lightening) by inhibiting the activity of melanocytes and reducing the production of melanocyte-stimulating hormone (MSH). Hyperpigmentation is typically seen in conditions of corticosteroid *deficiency* (like Addison’s disease) due to the compensatory increase in ACTH, which shares a precursor with MSH. **Analysis of Options:** * **A & B (Antiproliferative effects):** Glucocorticoids inhibit the mitotic activity of both **keratinocytes** (epidermis) and **fibroblasts** (dermis). This is the pharmacological basis for using topical steroids in hyperproliferative skin disorders like psoriasis. * **C (Loss of collagen):** By inhibiting fibroblasts, steroids decrease the synthesis of Type I and III collagen and glycosaminoglycans. This leads to the hallmark clinical features of steroid excess: skin thinning (atrophy), easy bruising, and the formation of wide, purple **striae**. **High-Yield Clinical Pearls for NEET-PG:** * **Iatrogenic Cushing Syndrome:** Prolonged steroid use leads to a "moon face," "buffalo hump," and truncal obesity, but the skin remains thin and fragile. * **Wound Healing:** Corticosteroids **delay wound healing** because they inhibit the inflammatory phase and reduce the fibroblastic repair required for wound contraction. * **Topical Potency:** Fluorinated steroids are more potent but carry a higher risk of causing irreversible skin atrophy and telangiectasia.

Q: ACTH levels are increased in all of the following conditions except:

Evening. The regulation of Adrenocorticotropic Hormone (ACTH) is governed by the hypothalamic-pituitary-adrenal (HPA) axis and is highly sensitive to stress and circadian rhythms. **Explanation of the Correct Answer:** **C. Evening:** ACTH secretion follows a distinct **diurnal (circadian) rhythm**. Levels are highest in the early morning (around 6:00 AM to 8:00 AM) and gradually decline throughout the day, reaching their **nadir (lowest point) in the evening** and early hours of sleep (around midnight). Therefore, ACTH levels are decreased, not increased, in the evening compared to morning levels. **Explanation of Incorrect Options:** * **A. Exercise:** Physical exertion is a potent physiological stressor that activates the HPA axis, leading to a significant increase in CRH and subsequent ACTH release to mobilize energy stores. * **B. Emotions:** Psychological stress (anxiety, fear, or emotional trauma) triggers the amygdala to stimulate the hypothalamus, resulting in elevated ACTH levels. * **C. Tumors:** Pathological increases occur in **Cushing’s Disease** (pituitary adenoma secreting ACTH) or **Ectopic ACTH Syndrome** (e.g., Small Cell Carcinoma of the lung). **High-Yield Clinical Pearls for NEET-PG:** * **Diurnal Variation:** To diagnose Cushing’s syndrome, the loss of this diurnal rhythm (elevated late-night cortisol/ACTH) is a key diagnostic finding. * **Primary vs. Secondary:** ACTH is **increased** in Addison’s disease (Primary Adrenal Insufficiency) due to loss of negative feedback, but **decreased** in Secondary Adrenal Insufficiency (Pituitary failure). * **Nelson’s Syndrome:** Rapid increase in ACTH levels and skin hyperpigmentation following bilateral adrenalectomy due to the growth of a pre-existing pituitary adenoma.

Q: Which of the following hormones exhibits genomic action?

All of these. ### Explanation The correct answer is **D. All of these**. **1. Underlying Medical Concept: Mechanism of Hormone Action** Hormones are generally classified into two groups based on their solubility and receptor location. **Genomic action** refers to the process where a hormone binds to an intracellular receptor (either in the cytoplasm or nucleus), acts as a ligand-activated transcription factor, and directly influences gene expression (mRNA synthesis). Lipid-soluble hormones can easily cross the cell membrane to exert these effects. These include: * **Steroid Hormones:** Cortisol, Aldosterone, Estrogen, Progesterone, Testosterone. * **Thyroid Hormones:** $T_3$ and $T_4$. * **Vitamin D:** 1,25-dihydroxycholecalciferol (Calcitriol). * **Retinoids:** Vitamin A. **2. Analysis of Options** * **Thyroid Hormone (A):** Binds to receptors already attached to DNA in the nucleus (TR-RXR complex). It is a classic example of genomic action. * **1,25-dihydroxycholecalciferol (B):** As a steroid-like hormone, it binds to the Vitamin D Receptor (VDR) in the nucleus to regulate calcium-binding protein synthesis. * **Cortisol (C):** A glucocorticoid that binds to cytoplasmic receptors, translocates to the nucleus, and binds to Glucocorticoid Response Elements (GRE) on DNA. **3. High-Yield Clinical Pearls for NEET-PG** * **Speed of Action:** Genomic actions are **slow** (minutes to hours) because they require protein synthesis. In contrast, peptide hormones (like Insulin or Epinephrine) use second messengers (cAMP, $IP_3/DAG$) for **fast** non-genomic actions. * **Exception:** Thyroid hormones are amino-acid derivatives but behave like steroids (intracellular receptors). * **Receptor Location:** * **Cytoplasmic:** Glucocorticoids, Mineralocorticoids. * **Nuclear:** Thyroid hormones, Retinoic acid, Estrogen, Vitamin D.

Q: Amylin is secreted by which cell of the pancreas?

Beta cells. **Explanation:** **Amylin (Islet Amyloid Polypeptide - IAPP)** is a 37-amino acid peptide hormone that is **co-secreted with insulin from the Beta (β) cells** of the pancreatic islets of Langerhans. It is stored in the same secretory granules as insulin and is released in response to the same stimuli (primarily glucose). Amylin functions as a synergistic partner to insulin by slowing gastric emptying, inhibiting glucagon secretion, and promoting satiety, thereby preventing postprandial glucose spikes. **Analysis of Options:** * **Option B (Correct):** Beta cells constitute about 60-75% of the islet cells and are the primary source of both Insulin and Amylin. * **Option A (Incorrect):** Alpha (α) cells secrete **Glucagon**, which increases blood glucose levels by stimulating glycogenolysis and gluconeogenesis. * **Option D (Incorrect):** Delta (δ) cells secrete **Somatostatin**, a universal inhibitor that suppresses the release of both insulin and glucagon. * **Option C (Incorrect):** Gamma (γ) cells, also known as PP cells, secrete **Pancreatic Polypeptide**, which regulates exocrine pancreatic secretions. **High-Yield Clinical Pearls for NEET-PG:** 1. **Pramlintide:** A synthetic analogue of amylin used as an adjunct treatment in both Type 1 and Type 2 Diabetes Mellitus. 2. **Amyloid Deposits:** In Type 2 Diabetes, amylin can aggregate to form amyloid deposits in the islets, which is a classic histopathological finding contributing to beta-cell dysfunction. 3. **Ratio:** Insulin and Amylin are secreted in a ratio of approximately 50:1 to 100:1.

Q: Which of the following hormones is secreted in response to TRH stimulation?

Prolactin and TSH. **Explanation:** The correct answer is **Prolactin and TSH (Option C)**. **Underlying Medical Concept:** Thyrotropin-Releasing Hormone (TRH) is a tripeptide synthesized in the paraventricular nucleus of the hypothalamus. While its primary physiological role is to stimulate the anterior pituitary to release **Thyroid Stimulating Hormone (TSH)**, it also acts as a potent **Prolactin-Releasing Factor (PRF)**. TRH binds to G-protein coupled receptors on both thyrotropes and lactotropes, leading to the secretion of both hormones. **Analysis of Options:** * **Option A (Prolactin):** While TRH does stimulate Prolactin, this option is incomplete because TSH is also secreted. * **Option B (TSH):** This is the primary target of TRH, but choosing this alone ignores the significant stimulatory effect TRH has on Prolactin. * **Option D (None):** Incorrect, as TRH has well-documented stimulatory effects on both hormones. **Clinical Pearls & High-Yield Facts for NEET-PG:** * **Primary Hypothyroidism Connection:** In patients with primary hypothyroidism (low T3/T4), there is a compensatory increase in TRH levels due to the loss of negative feedback. This elevated TRH can lead to **hyperprolactinemia**, which clinically manifests as galactorrhea, amenorrhea, or infertility. * **Dopamine's Role:** Remember that Dopamine is the primary *inhibitor* of both Prolactin (major) and TSH (minor). * **Diagnostic Use:** The TRH stimulation test was historically used to differentiate between secondary (pituitary) and tertiary (hypothalamic) hypothyroidism.

Q: Adrenal insufficiency is not associated with which of the following?

Metabolic alkalosis. **Explanation:** Adrenal insufficiency (Addison’s disease) is characterized by the deficiency of adrenal cortical hormones: **Aldosterone** and **Cortisol**. **Why Metabolic Alkalosis is the Correct Answer:** Aldosterone normally acts on the distal convoluted tubules and collecting ducts to reabsorb sodium and water while secreting Potassium ($K^+$) and Hydrogen ions ($H^+$). In adrenal insufficiency, the lack of aldosterone leads to decreased $H^+$ secretion. This results in the retention of $H^+$ ions, leading to **Metabolic Acidosis** (specifically Normal Anion Gap Metabolic Acidosis), not alkalosis. **Analysis of Incorrect Options:** * **A. Hyponatremia:** Lack of aldosterone leads to "salt wasting" (failure to reabsorb $Na^+$), resulting in low serum sodium levels. * **B. Hyperkalemia:** Without aldosterone, the kidney cannot effectively excrete potassium, leading to its accumulation in the blood. * **C. Hypoglycemia:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis and antagonizes insulin. Its deficiency leads to impaired glucose production and increased insulin sensitivity, causing low blood sugar. **High-Yield Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** Hyperpigmentation (due to high ACTH/POMC) and mineralocorticoid deficiency (electrolyte imbalances) are features of **Primary** Adrenal Insufficiency (Addison’s), but are absent in Secondary (Pituitary) insufficiency. * **The "Addisonian Triad":** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Eosinophilia:** A common but often overlooked hematological finding in adrenal insufficiency. * **Gold Standard Test:** ACTH Stimulation Test (Cosyntropin test).

Q: Osteoclasts have a specific receptor for which hormone?

Calcitonin. **Explanation:** The correct answer is **Calcitonin**. This is a classic high-yield concept in bone physiology. **1. Why Calcitonin is Correct:** Osteoclasts are the primary target cells for calcitonin. Calcitonin receptors are G-protein coupled receptors located directly on the cell membrane of **osteoclasts**. When calcitonin binds to these receptors, it rapidly inhibits the resorptive activity of osteoclasts and decreases their number, leading to a reduction in bone resorption and a decrease in serum calcium levels. **2. Why the Other Options are Incorrect:** * **Parathyroid Hormone (PTH):** Contrary to popular belief, osteoclasts do **not** have PTH receptors. PTH acts primarily on **osteoblasts**. When PTH binds to osteoblasts, it triggers the release of **RANKL** (Receptor Activator of Nuclear Factor kappa-B Ligand), which then binds to RANK receptors on osteoclast precursors to stimulate bone resorption. * **Vitamin D3 (Calcitriol):** Like PTH, Vitamin D3 receptors (VDR) are primarily found on **osteoblasts**. Vitamin D3 promotes osteoclast differentiation indirectly via the RANKL pathway. * **Thyroxin:** While thyroid hormones influence bone turnover, they do not have specific, primary regulatory receptors on osteoclasts that govern calcium homeostasis in the same direct manner as calcitonin. **Clinical Pearls for NEET-PG:** * **The "Indirect" Rule:** Remember that most bone-resorbing factors (PTH, Vitamin D3, IL-1, TNF) act **indirectly** on osteoclasts via osteoblasts. Calcitonin is the major exception that acts **directly**. * **Marker of Osteoclasts:** Tartrate-resistant acid phosphatase (TRAP) is a key histological marker for osteoclasts. * **Therapeutic Use:** Due to its direct inhibitory effect on osteoclasts, synthetic calcitonin (Salmon calcitonin) is used clinically to treat Paget’s disease and severe hypercalcemia.

Question 1

All of the following are known effects of corticosteroids on the skin and connective tissue except?

Accepted Answer

Hyperpigmentation

Answer

Antiproliferative effect on fibroblasts

Answer

Antiproliferative effect on keratinocytes

Answer

Loss of collagen

Question 2

Axillary hair growth is stimulated by which hormone?

Accepted Answer

Testosterone

Answer

Estrogen

Answer

Prolactin

Answer

Androgens

Question 3

ACTH levels are increased in all of the following conditions except:

Accepted Answer

Evening

Answer

Exercise

Answer

Emotions

Answer

Tumors

Question 4

Which of the following hormones exhibits genomic action?

Accepted Answer

All of these

Answer

Thyroid hormone

Answer

1,25-dihydroxycholecalciferol

Answer

Cortisol

Question 5

Chvostek’s sign is elicited by:

Accepted Answer

Stimulating the facial nerve by tapping over the parotid gland

Answer

Inflating a blood pressure cuff in the arm for 5 minutes

Answer

Tapping over the extensor pollicis brevis tendon

Answer

Tapping over the flexor retinaculum

Question 6

Amylin is secreted by which cell of the pancreas?

Accepted Answer

Beta cells

Answer

Alpha cells

Answer

Gamma cells

Answer

Delta cells

Question 7

Which of the following hormones is secreted in response to TRH stimulation?

Accepted Answer

Prolactin and TSH

Answer

Prolactin

Answer

TSH

Answer

None of the above

Question 8

What is true about insulin action?

Accepted Answer

Required for the transport of glucose, amino acids, K+, and Na+

Answer

Causes gluconeogenesis

Answer

Not useful for growth and development

Answer

Catabolic hormone

Question 9

Adrenal insufficiency is not associated with which of the following?

Accepted Answer

Metabolic alkalosis

Answer

Hyponatremia

Answer

Hyperkalemia

Answer

Hypoglycemia

Question 10

Osteoclasts have a specific receptor for which hormone?

Accepted Answer

Calcitonin

Answer

Parathyroid hormone

Answer

Thyroxin

Answer

Vitamin D3

Endocrinology — MCQs

Endocrinology — MCQs

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