Endocrinology Practice Questions

Q: What is the function of incretin?

Increased insulin secretion. **Explanation:** **Incretins** are gut-derived hormones, primarily **Glucagon-like peptide-1 (GLP-1)** and **Glucose-dependent insulinotropic polypeptide (GIP)**. They are secreted by the enteroendocrine cells (L-cells and K-cells) of the small intestine in response to nutrient ingestion. 1. **Why Option B is Correct:** The "Incretin Effect" describes the phenomenon where oral glucose triggers a significantly higher insulin response compared to an equivalent dose of intravenous glucose. Incretins bind to receptors on pancreatic beta cells, stimulating **glucose-dependent insulin secretion**. They also suppress glucagon release and slow gastric emptying, helping to maintain postprandial glycemic control. 2. **Why Incorrect Options are Wrong:** * **Option A & C:** Heart rate and respiratory rate are primarily regulated by the autonomic nervous system and chemoreceptors. Incretins do not have a primary physiological role in cardiorespiratory stimulation. * **Option D:** Erythropoiesis is stimulated by Erythropoietin (EPO), produced mainly by the peritubular interstitial cells of the kidneys in response to hypoxia. **High-Yield Clinical Pearls for NEET-PG:** * **DPP-4 Inhibitors (e.g., Sitagliptin):** These drugs prevent the breakdown of endogenous GLP-1, prolonging its half-life. * **GLP-1 Agonists (e.g., Liraglutide, Exenatide):** These are injectable analogs used in Type 2 Diabetes that also promote weight loss. * **Key Difference:** Unlike sulfonylureas, the insulinotropic action of incretins is **glucose-dependent**, meaning they carry a much lower risk of hypoglycemia. * **Site of Secretion:** GLP-1 (L-cells of ileum/colon); GIP (K-cells of duodenum/jejunum).

Q: Insulin secretion is inhibited by which of the following substances?

Epinephrine. **Explanation:** Insulin secretion is primarily regulated by the autonomic nervous system and gastrointestinal hormones. **Why Epinephrine is correct:** Epinephrine (and Norepinephrine) acts as a potent inhibitor of insulin secretion. This occurs via the activation of **$\alpha_2$-adrenergic receptors** on the pancreatic beta cells. During "fight or flight" situations or exercise, the body needs to maintain high blood glucose levels for the brain and muscles. By inhibiting insulin, epinephrine prevents glucose storage and promotes hyperglycemia. While catecholamines can also bind to $\beta_2$ receptors (which stimulate insulin), the **$\alpha_2$ inhibitory effect is dominant.** **Why the other options are incorrect:** * **Secretin & Gastrin (Options A & D):** These are gastrointestinal hormones (Incretins). The "Incretin effect" explains why oral glucose causes a greater insulin spike than intravenous glucose. Both Secretin and Gastrin, along with GIP and GLP-1, **stimulate** insulin secretion in anticipation of rising blood glucose. * **Growth Hormone (Option C):** While GH is a counter-regulatory hormone that causes insulin resistance in peripheral tissues (diabetogenic effect), it actually **stimulates** the synthesis and secretion of insulin from the pancreas to compensate for the rising blood sugar. **High-Yield Clinical Pearls for NEET-PG:** * **Dominant Stimulus:** The most potent stimulator of insulin is **Glucose**. * **Receptor Logic:** * $\alpha_2$ stimulation = **Inhibition** of insulin. * $\beta_2$ stimulation / Parasympathetic (Vagus/ACh) = **Stimulation** of insulin. * **Somatostatin:** Produced by Delta cells, it is a potent universal inhibitor of both insulin and glucagon. * **Potassium Channels:** Insulin release is triggered by the **closure** of ATP-sensitive $K^+$ channels, leading to depolarization and $Ca^{2+}$ influx.

Q: Insulin decreases:

Lipolysis. **Explanation:** Insulin is the body’s primary **anabolic hormone**, secreted by the beta cells of the Islets of Langerhans. Its fundamental role is to promote energy storage and inhibit the breakdown of stored fuels (catabolism). **Why Lipolysis is the correct answer:** Insulin is a potent **anti-lipolytic** hormone. It inhibits the enzyme **Hormone-Sensitive Lipase (HSL)** in adipose tissue. HSL is responsible for breaking down stored triglycerides into free fatty acids and glycerol. By inhibiting HSL, insulin decreases the concentration of circulating free fatty acids, thereby promoting fat storage and preventing ketogenesis. **Analysis of Incorrect Options:** * **A. Glucose uptake:** Insulin **increases** glucose uptake in peripheral tissues (skeletal muscle and adipose tissue) by inducing the translocation of **GLUT-4** transporters to the cell membrane. * **B. Glycogen synthesis:** Insulin **increases** glycogenesis by activating the enzyme **Glycogen Synthase**, ensuring excess glucose is stored in the liver and muscles. * **C. Protein synthesis:** Insulin is anabolic for proteins; it **increases** amino acid uptake and protein synthesis while inhibiting proteolysis. **NEET-PG High-Yield Pearls:** * **GLUT-4** is the only insulin-dependent glucose transporter (found in heart, skeletal muscle, and adipose tissue). * Insulin stimulates **Lipoprotein Lipase (LPL)** in capillary walls to clear chylomicrons from the blood, but inhibits **Hormone-Sensitive Lipase (HSL)** inside adipocytes. * **Key Enzyme Regulation:** Insulin activates Phosphofructokinase (Glycolysis) and Glycogen Synthase (Glycogenesis), while inhibiting Fructose-1,6-bisphosphatase (Gluconeogenesis).

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.

Question 1

What is the function of incretin?

Accepted Answer

Increased insulin secretion

Answer

Increased heart rate

Answer

Increased respiratory rate

Answer

Stimulate erythropoiesis

Question 2

Insulin secretion is inhibited by which of the following substances?

Accepted Answer

Epinephrine

Answer

Secretin

Answer

Growth hormone

Answer

Gastrin

Question 3

In a seriously ill patient, the addition of amino acids to the diet results in a positive nitrogen balance. What is the primary mechanism for this?

Accepted Answer

Increased secretion of insulin

Answer

Increased growth hormone secretion

Answer

Enhanced rate of gluconeogenesis

Answer

Increased absorption of amino acids from the diet

Question 4

Insulin decreases:

Accepted Answer

Lipolysis

Answer

Glucose uptake

Answer

Glycogen synthesis

Answer

Protein synthesis

Question 5

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 6

Axillary hair growth is stimulated by which hormone?

Accepted Answer

Testosterone

Answer

Estrogen

Answer

Prolactin

Answer

Androgens

Question 7

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

Accepted Answer

Evening

Answer

Exercise

Answer

Emotions

Answer

Tumors

Question 8

Which of the following hormones exhibits genomic action?

Accepted Answer

All of these

Answer

Thyroid hormone

Answer

1,25-dihydroxycholecalciferol

Answer

Cortisol

Question 9

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 10

Amylin is secreted by which cell of the pancreas?

Accepted Answer

Beta cells

Answer

Alpha cells

Answer

Gamma cells

Answer

Delta cells

Endocrinology — MCQs

Endocrinology — MCQs

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