Endocrinology Practice Questions

Q: Which hormone acts on intracellular receptors?

Thyroxine. **Explanation:** Hormone receptors are classified based on their location, which is determined by the hormone's chemical nature (solubility). **1. Why Thyroxine is Correct:** Thyroxine ($T_4$) and Triiodothyronine ($T_3$) are lipid-soluble hormones. Unlike most amino acid-derived hormones, thyroid hormones enter the cell via carrier-mediated transport and bind to **intracellular receptors** (specifically **nuclear receptors**). Once bound, they act as transcription factors to alter gene expression. Other hormones using intracellular receptors include Steroids (Cortisol, Aldosterone, Estrogen, Progesterone, Testosterone), Vitamin D, and Retinoic acid. **2. Why the Other Options are Incorrect:** * **Glucagon:** A peptide hormone that binds to **G-Protein Coupled Receptors (GPCR)** on the cell membrane, utilizing the cAMP second messenger system. * **Insulin:** A peptide hormone that binds to a transmembrane **Enzyme-linked receptor** (specifically **Receptor Tyrosine Kinase**). * **PDGF (Platelet-Derived Growth Factor):** Like insulin, this growth factor binds to membrane-bound **Receptor Tyrosine Kinase** to trigger cellular proliferation. **Clinical Pearls for NEET-PG:** * **Mnemonic for Intracellular Receptors:** **"PET TV"** – **P**rogesterone, **E**strogen, **T**estosterone, **T**hyroid hormones ($T_3/T_4$), and **V**itamin D/A. * **Location Nuance:** While Steroids (like Cortisol) often bind to **cytoplasmic** receptors before translocating to the nucleus, Thyroid hormones bind directly to receptors already located on the **chromatin in the nucleus**. * **Speed of Action:** Hormones acting on intracellular receptors have a **slow onset** (hours to days) because they require protein synthesis, whereas membrane-bound receptors (like Glucagon) trigger rapid enzymatic cascades.

Q: What happens to FSH and LH concentrations at birth?

They rise abruptly.. **Explanation:** The correct answer is **A. They rise abruptly.** **1. Why the correct answer is right:** During intrauterine life, the fetal hypothalamus-pituitary-gonadal (HPG) axis is functional but remains profoundly suppressed. This suppression is due to the **negative feedback** exerted by high levels of maternal and placental hormones (estrogen and progesterone) crossing the placenta. At birth, the sudden removal of the placenta leads to a sharp decline in these circulating maternal steroids. This "withdrawal" relieves the negative feedback on the infant's pituitary, causing an **abrupt rise** in the secretion of Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH). This phenomenon is often referred to as **"Mini-puberty."** **2. Why the incorrect options are wrong:** * **Option B:** FSH and LH do not fall; rather, it is the *maternal steroids* that fall, which triggers the rise in gonadotropins. * **Option C:** A "no change" status is incorrect because the hormonal environment transitions from a suppressed state to an active state immediately post-delivery. * **Option D:** While gonadotropin levels remain elevated for several months (peaking around 1–3 months), the initial surge occurs **at birth** due to the loss of placental inhibition. **3. NEET-PG High-Yield Pearls:** * **Mini-puberty:** In males, the LH surge stimulates Leydig cells, leading to a testosterone peak between 1–3 months of age (essential for genital development). In females, FSH remains elevated longer (up to 2–3 years of age). * **Juvenile Pause:** After the initial postnatal surge, gonadotropin levels fall and remain low until the onset of true puberty (due to high sensitivity of the gonadostat to low steroid levels). * **Clinical Correlation:** This postnatal surge is why some neonates may show transient breast engorgement or "witch’s milk" (though this is primarily due to prolactin and steroid withdrawal).

Q: Which hormone secretion is increased if the pituitary stalk is transected?

Prolactin. ### Explanation **1. Why Prolactin is the Correct Answer:** The secretion of most anterior pituitary hormones is primarily regulated by **releasing hormones** from the hypothalamus. However, **Prolactin (PRL)** is unique because its primary hypothalamic control is **tonic inhibition**. The hypothalamus secretes **Dopamine**, which travels through the hypothalamic-hypophyseal portal system to the anterior pituitary to inhibit prolactin release. When the **pituitary stalk is transected**, the delivery of dopamine is interrupted. This "removal of the inhibitory brake" leads to an autonomous, unregulated increase in prolactin secretion. This phenomenon is known as **Stalk Effect hyperprolactinemia**. **2. Why the Other Options are Incorrect:** * **B (ACTH) and C (GH):** These hormones depend on **stimulatory** signals from the hypothalamus (CRH for ACTH; GHRH for GH). If the stalk is transected, these stimulatory signals cannot reach the pituitary, leading to a **decrease** or cessation of their secretion. * **D (None):** This is incorrect because Prolactin levels consistently rise following stalk interruption. **3. High-Yield NEET-PG Clinical Pearls:** * **Dopamine = Prolactin Inhibiting Hormone (PIH):** It acts on **D2 receptors** located on lactotrophs. * **Posterior Pituitary Hormones:** Stalk transection also leads to **Diabetes Insipidus** because ADH and Oxytocin (synthesized in the hypothalamus) can no longer be transported to the posterior pituitary for storage and release. * **Clinical Correlation:** Any mass lesion (like a Craniopharyngioma) compressing the pituitary stalk can cause mild elevations in Prolactin (usually <100 ng/mL), mimicking a small prolactinoma. * **Rule of Thumb:** In pituitary stalk injury, **all** anterior pituitary hormones decrease **EXCEPT** Prolactin, which increases.

Q: Which of the following is NOT a function of oxytocin?

Galactopoiesis. **Explanation:** The correct answer is **D. Galactopoiesis**. To understand this, one must distinguish between the different stages of lactation. **Galactopoiesis** refers to the maintenance of milk secretion once it has been established. This process is primarily regulated by **Prolactin** (from the anterior pituitary) and growth hormone, not oxytocin. **Analysis of Options:** * **A. Galactokinesis:** This refers to the "milk-ejection reflex" or "let-down reflex." Oxytocin causes the contraction of **myoepithelial cells** surrounding the mammary alveoli, squeezing milk into the ducts. This is a classic function of oxytocin. * **B. Uterine contraction in a non-pregnant female:** While oxytocin is famous for labor, it also causes rhythmic uterine contractions during menstruation and coitus (to aid sperm transport) in non-pregnant females. * **C. Contraction of smooth muscle of vas deferens:** In males, oxytocin is released during ejaculation and facilitates sperm transport by stimulating the contraction of the smooth muscles in the vas deferens and epididymis. **High-Yield NEET-PG Pearls:** 1. **Synthesis vs. Storage:** Oxytocin is synthesized in the **Paraventricular nucleus (PVN)** of the hypothalamus but stored and released by the **Posterior Pituitary (Neurohypophysis)**. 2. **The "Love Hormone":** It plays a crucial role in maternal-infant bonding and social recognition. 3. **Positive Feedback:** The Ferguson reflex (vaginal/cervical stretch) and suckling are the primary triggers for oxytocin release, representing rare examples of positive feedback in physiology. 4. **Receptor Type:** Oxytocin acts via **G-protein coupled receptors (Gq)**, leading to increased intracellular calcium.

Q: All of the following steps in the synthesis of thyroid hormones are catalyzed by the thyroid peroxidase enzyme except?

Iodide trapping. **Explanation:** The synthesis of thyroid hormones is a multi-step process, most of which occurs within the follicular lumen and is mediated by the membrane-bound enzyme **Thyroid Peroxidase (TPO)**. **Why Iodide Trapping is the correct answer:** Iodide trapping is the first step in thyroid hormone synthesis, where inorganic iodide ($I^-$) is transported from the blood into the follicular cell against a chemical and electrical gradient. This process is mediated by the **Sodium-Iodide Symporter (NIS)**, a secondary active transporter located on the basolateral membrane. It is **not** catalyzed by TPO. **Analysis of incorrect options (Steps catalyzed by TPO):** * **Oxidation:** TPO uses hydrogen peroxide ($H_2O_2$) to oxidize iodide ($I^-$) into iodine ($I^0$ or $I^+$), the reactive form required for binding. * **Organification (Iodination):** TPO catalyzes the binding of oxidized iodine to tyrosine residues on the thyroglobulin molecule to form Monoiodotyrosine (MIT) and Diiodotyrosine (DIT). * **Coupling:** TPO facilitates the phenolic coupling of iodotyrosines. Two DIT molecules form $T_4$, while one MIT and one DIT form $T_3$. **High-Yield NEET-PG Pearls:** * **Wolff-Chaikoff Effect:** An autoregulatory phenomenon where high levels of circulating iodide inhibit TPO, leading to a transient decrease in thyroid hormone synthesis. * **Pendrin:** A chloride-iodide exchanger on the apical membrane that transports iodide into the follicle lumen. Mutations lead to **Pendred Syndrome** (goiter and sensorineural deafness). * **Clinical Correlation:** Propylthiouracil (PTU) and Methimazole act by inhibiting the TPO enzyme. PTU additionally inhibits peripheral conversion of $T_4$ to $T_3$.

Q: Glucose is transported in the pancreas through which receptor?

GLUT 2. **Explanation:** The correct answer is **GLUT 2**. In the pancreatic beta cells, GLUT 2 acts as the primary glucose sensor. It is a high-capacity, low-affinity bidirectional transporter. Because of its high $K_m$ (low affinity), the rate of glucose entry into the beta cell is proportional to the blood glucose concentration within the physiological range. Once inside, glucose is phosphorylated by **Glucokinase**, leading to ATP production, closure of ATP-sensitive $K^+$ channels, depolarization, and subsequent insulin release. **Analysis of Incorrect Options:** * **GLUT 1:** Found primarily in **RBCs** and the **Blood-Brain Barrier**. It provides basal glucose uptake required to sustain respiration in all cells. * **GLUT 3:** Primarily located in **Neurons** and the placenta. It has a very low $K_m$ (high affinity), ensuring glucose uptake even during hypoglycemia. * **GLUT 4:** The only **Insulin-dependent** glucose transporter. it is found in **Skeletal muscle** and **Adipose tissue**. Insulin triggers the translocation of GLUT 4 from intracellular vesicles to the plasma membrane. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT 2 Locations:** Remember the mnemonic **"KILP"** — **K**idney (PCT), **I**ntestine (basolateral membrane), **L**iver, and **P**ancreas. * **SGLT vs. GLUT:** SGLT (Sodium-Glucose Linked Transporters) are involved in *active* transport (secondary active), whereas GLUTs are involved in *facilitated diffusion*. * **Fanconi-Bickel Syndrome:** A rare glycogen storage disease caused by a congenital defect in the **GLUT 2** transporter. * **Glucokinase:** Often called the "Glucose Sensor" of the pancreas; mutations here can lead to MODY (Maturity-Onset Diabetes of the Young).

Q: Which of the following hormones is NOT released by the anterior pituitary gland?

Prolactin. **Explanation:** The anterior pituitary gland (adenohypophysis) synthesizes and secretes six major peptide hormones: Growth Hormone (GH), Thyroid-stimulating hormone (TSH), Adrenocorticotropic hormone (ACTH), Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), and Prolactin. **Wait! Re-evaluating the Question and Key:** There appears to be a technical error in the provided key. **All four options (TSH, Prolactin, ACTH, and FSH) are indeed released by the anterior pituitary.** In the context of NEET-PG, this type of question usually aims to distinguish between the **Anterior Pituitary** (Adenohypophysis) and the **Posterior Pituitary** (Neurohypophysis). The posterior pituitary does not synthesize hormones; it only stores and releases **Oxytocin** and **Antidiuretic Hormone (ADH/Vasopressin)**, which are produced in the hypothalamus. **Analysis of Options:** * **TSH (Option A):** Secreted by thyrotrophs in the anterior pituitary to stimulate the thyroid gland. * **Prolactin (Option B):** Secreted by lactotrophs in the anterior pituitary to stimulate milk production. * **ACTH (Option C):** Secreted by corticotrophs in the anterior pituitary to stimulate the adrenal cortex. * **FSH (Option D):** Secreted by gonadotrophs in the anterior pituitary to regulate gametogenesis. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypothalamic Control:** All anterior pituitary hormones are regulated by hypothalamic "releasing" or "inhibiting" hormones. 2. **The Prolactin Exception:** Unlike other hormones, Prolactin is under **predominant inhibitory control** by Dopamine. Therefore, any stalk injury or dopamine antagonist (like antipsychotics) leads to *increased* prolactin levels (Hyperprolactinemia). 3. **Embryology:** The anterior pituitary develops from **Rathke’s pouch** (oral ectoderm), while the posterior pituitary develops from **neuroectoderm**.

Q: Which of the following receptors mediate the release of ACTH by Vasopressin?

V3. **Explanation:** The release of Adrenocorticotropic Hormone (ACTH) from the anterior pituitary is primarily regulated by Corticotropin-Releasing Hormone (CRH). However, **Arginine Vasopressin (AVP)** acts as a potent synergistic secretagogue for ACTH. 1. **Why V3 is correct:** Vasopressin acts on the **V3 receptors** (also known as **V1b receptors**) located on the corticotroph cells of the anterior pituitary. These are G-protein coupled receptors (Gq) that activate the Phospholipase C pathway, leading to an increase in intracellular calcium and the subsequent release of ACTH. 2. **Why other options are incorrect:** * **V1a:** These receptors are primarily found on **vascular smooth muscle**, mediating vasoconstriction, and in the liver, mediating glycogenolysis. * **V2:** These receptors are located in the **principal cells of the renal collecting ducts**. They act via the Gs-cAMP pathway to insert Aquaporin-2 channels, mediating the antidiuretic effect. * **V4:** There is no clinically significant V4 receptor in human physiology; this is often used as a distractor in exams. **High-Yield Clinical Pearls for NEET-PG:** * **Synergy:** While CRH is the main stimulant, AVP (via V3) is crucial during the chronic stress response to sustain ACTH levels. * **Location Summary:** V1a (Vessels), V2 (Kidney), V3/V1b (Pituitary). * **Ectopic ACTH:** Some tumors (e.g., Small Cell Carcinoma of the Lung) may express V3 receptors, leading to paraneoplastic Cushing Syndrome. * **Desmopressin (dDAVP):** It is a selective V2 agonist, which is why it is used for Diabetes Insipidus without causing significant vasoconstriction (V1a) or ACTH release (V3).

Q: All of the following have a stimulatory action on glucagon secretion, EXCEPT:

Secretin. **Explanation:** Glucagon is a catabolic hormone secreted by the **alpha cells** of the pancreas. Its primary role is to increase blood glucose levels during states of energy deficiency or stress. **1. Why Secretin is the Correct Answer:** **Secretin** is a gastrointestinal hormone that primarily stimulates the secretion of bicarbonate-rich pancreatic juice. In the context of islet cell function, secretin (along with Somatostatin and Insulin) actually **inhibits** glucagon secretion. This is a physiological mechanism to prevent excessive glucose elevation during certain phases of digestion. **2. Analysis of Incorrect Options (Stimulators of Glucagon):** * **Beta-agonists (Option B):** Sympathetic stimulation via **Beta-2 adrenergic receptors** strongly stimulates glucagon release. This ensures adequate glucose availability for the "fight or flight" response. * **Exercise (Option C):** Exercise increases glucagon levels due to increased sympathetic activity and the body's demand for circulating glucose to fuel skeletal muscles. * **Amino Acids (Option D):** High levels of amino acids (especially Arginine and Alanine) stimulate glucagon. This is a protective mechanism: when a person eats a high-protein, low-carb meal, the insulin released (due to amino acids) could cause hypoglycemia. Glucagon is secreted simultaneously to maintain stable blood glucose. **High-Yield Clinical Pearls for NEET-PG:** * **Major Inhibitors:** Glucose, Insulin, Somatostatin, Secretin, and Free Fatty Acids (FFA). * **Major Stimulators:** Hypoglycemia, Amino acids (Arginine), Acetylcholine, Epinephrine (Beta-receptors), and CCK. * **The "Incretin" Distinction:** While **GLP-1** (Glucagon-like peptide-1) inhibits glucagon, **GIP** (Gastric Inhibitory Peptide) can actually stimulate it under certain conditions. * **Glucagonoma Clinical Triad:** Necrolytic migratory erythema (NME), Diabetes mellitus, and Anemia.

Question 1

Which hormone acts on intracellular receptors?

Accepted Answer

Thyroxine

Answer

Glucagon

Answer

Insulin

Answer

PDGF

Question 2

What happens to FSH and LH concentrations at birth?

Accepted Answer

They rise abruptly.

Answer

They fall abruptly.

Answer

There is no change.

Answer

They rise after 3 months of age.

Question 3

Which hormone secretion is increased if the pituitary stalk is transected?

Accepted Answer

Prolactin

Answer

ACTH

Answer

GH

Answer

None

Question 4

Which of the following is NOT a function of oxytocin?

Accepted Answer

Galactopoiesis

Answer

Galactokinesis

Answer

Uterine contraction in a non-pregnant female

Answer

Contraction of smooth muscle of vas deferens

Question 5

All of the following steps in the synthesis of thyroid hormones are catalyzed by the thyroid peroxidase enzyme except?

Accepted Answer

Iodide trapping

Answer

Coupling

Answer

Oxidation

Answer

Organification

Question 6

Glucose is transported in the pancreas through which receptor?

Accepted Answer

GLUT 2

Answer

GLUT 1

Answer

GLUT 3

Answer

GLUT 4

Question 7

Which of the following hormones is NOT released by the anterior pituitary gland?

Accepted Answer

Prolactin

Answer

Thyroid-stimulating hormone (TSH)

Answer

Adrenocorticotropic hormone (ACTH)

Answer

Follicle-stimulating hormone (FSH)

Question 8

Which of the following receptors mediate the release of ACTH by Vasopressin?

Accepted Answer

V3

Answer

V1a

Answer

V2

Answer

V4

Question 9

All of the following have a stimulatory action on glucagon secretion, EXCEPT:

Accepted Answer

Secretin

Answer

Beta agonist

Answer

Exercise

Answer

Amino acids

Question 10

A 30-year-old pregnant woman and her 2-year-old child reside in a high-altitude area. The child presents with short stature, a potbelly, an enlarged protruding tongue, and developmental delay. Iodine supplementation is initiated for both mother and child to prevent mental retardation in the developing fetus. All statements regarding iodide oxidation are true EXCEPT:

Accepted Answer

Iodide transported to the follicular lumen by Na-I symporter

Answer

Conversion of iodide to iodine

Answer

Promoted by the enzyme peroxidase

Answer

Propylthiouracil blocks this step

Endocrinology — MCQs

Endocrinology — MCQs

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