Endocrinology Practice Questions

Q: Which of the following is not an effect of insulin?

Increased glycogenolysis. ***Increased glycogenolysis*** - Insulin primarily **inhibits glycogenolysis** (the breakdown of glycogen) and promotes glycogen synthesis to lower blood glucose levels. - Thus, increased glycogenolysis is the opposite of an insulin effect. *Increased transport of glucose into cells* - Insulin **facilitates the uptake of glucose** into insulin-sensitive cells (muscle and adipose tissue) by promoting the translocation of GLUT4 transporters to the cell membrane. - This action helps to remove glucose from the bloodstream and reduce blood sugar. *Induction of lipoprotein lipase* - Insulin **activates lipoprotein lipase (LPL)**, an enzyme that breaks down triglycerides in chylomicrons and VLDL into free fatty acids for storage in adipose tissue. - This promotes energy storage after a meal. *Decreased gluconeogenesis* - Insulin **suppresses hepatic gluconeogenesis**, the process by which the liver synthesizes glucose from non-carbohydrate precursors. - This helps to reduce the liver's glucose output and lower blood glucose levels.

Q: Acidophilic cells of anterior pituitary secrete?

GH. ***GH*** - **Growth Hormone (GH)** is secreted by **somatotrophs**, which are a type of acidophilic cell in the anterior pituitary. - These cells stain readily with **acidic dyes** due to their abundant secretory granules. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is secreted by **corticotrophs**, which are **basophilic cells** in the anterior pituitary. - Corticotrophs stain with basic dyes due to different intracellular granule content. *TSH* - **Thyroid-stimulating hormone (TSH)** is secreted by **thyrotrophs**, which are a type of **basophilic cell** in the anterior pituitary. - Basophilic cells are characterized by their affinity for basic dyes. *ADH* - **Antidiuretic hormone (ADH)**, also known as vasopressin, is produced by the **hypothalamus** and released from the **posterior pituitary**, not the anterior pituitary. - It is not secreted by acidophilic cells.

Q: Which hormone is converted into its active form in the liver?

Thyroid hormone. ***Thyroid hormone*** - The liver is a major site for the conversion of **thyroxine (T4)**, the primary hormone secreted by the thyroid gland, into its more active form, **triiodothyronine (T3)**. - This conversion, primarily through **deiodination**, is critical for thyroid hormone action in target tissues throughout the body. *Corticosteroid* - **Cortisol**, the main human corticosteroid, is directly secreted by the **adrenal cortex** in its active form. - While the liver metabolizes cortisol for excretion, it does not convert an inactive form into an active corticosteroid. *Estradiol* - **Estradiol** is primarily produced and secreted in its active form by the **ovaries** in premenopausal women. - The liver is involved in the metabolism and conjugation of estradiol for excretion, not its activation. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is secreted by the **anterior pituitary gland** in its active form. - Its primary role is to stimulate the adrenal cortex to produce cortisol; it does not undergo activation in the liver.

Q: Insulin acts by which pathway-

Tyrosine kinase. ***Tyrosine kinase*** - Insulin binds to its receptor, a **receptor tyrosine kinase**, activating the intracellular tyrosine kinase domain. - This activation leads to the **autophosphorylation** of the receptor and subsequent phosphorylation of various intracellular substrates, initiating a signaling cascade. *Intrinsic ion channel* - This mechanism involves a receptor that is itself an **ion channel**, opening or closing to allow ions to pass through the cell membrane upon ligand binding. - Insulin's primary action is not to alter membrane permeability via direct ion channel modulation but rather to initiate an intracellular signaling cascade. *JAK-STAT-Kinase* - The **JAK-STAT pathway** is typically utilized by cytokine receptors (e.g., growth hormone, interleukins) that do not possess intrinsic kinase activity but activate associated soluble kinases like JAK. - Insulin signaling primarily utilizes its intrinsic tyrosine kinase activity rather than recruiting JAK kinases. *Transcription factor* - While insulin ultimately influences gene expression and thus the activity of **transcription factors**, it is not a transcription factor itself. - Insulin's initial binding and signaling occur at the cell surface via its receptor, leading to downstream events that *regulate* transcription factor activity.

Q: Which hormone is NOT increased in stress?

Insulin. ***Insulin*** - Insulin levels generally **decrease** during acute stress. This allows for increased availability of glucose for tissues, such as the brain and muscles, during "fight or flight" responses. - The sympathetic nervous system activity during stress **inhibits insulin secretion** from pancreatic beta cells. *Glucagon* - **Glucagon levels increase** during stress to promote **hepatic glucose production** (glycogenolysis and gluconeogenesis), ensuring a readily available energy supply. - This rise in glucagon is part of the counter-regulatory response to maintain blood glucose stability during stressful conditions. *Cortisol* - **Cortisol levels significantly increase** during stress as part of the **hypothalamic-pituitary-adrenal (HPA) axis** activation. - Cortisol mobilizes energy stores, suppresses the immune system, and prepares the body for prolonged stress. *Epinephrine* - **Epinephrine (adrenaline) levels increase rapidly** during acute stress as part of the **sympathetic nervous system** response. - It triggers the "fight or flight" response, increasing heart rate, blood pressure, and diverting blood flow to essential organs, while also promoting glucose release.

Q: Which hormone acts on cytoplasmic membrane receptor?

TSH. ***TSH*** - **TSH** (**Thyroid-Stimulating Hormone**) is a **peptide hormone** that cannot pass through the lipid bilayer of the cell membrane due to its large, hydrophilic nature. - Therefore, TSH binds to specific **G protein-coupled receptors** located on the **cytoplasmic membrane** of thyroid follicular cells to exert its effects. *Thyroxine* - **Thyroxine** (T4) is a **thyroid hormone** derived from the amino acid tyrosine (an iodinated tyrosine derivative), which is **lipophilic** and can easily cross the cell membrane. - It primarily binds to **intracellular receptors** in the nucleus to regulate gene expression. *Androgen* - **Androgens** are **steroid hormones** (e.g., testosterone) that are **lipophilic** and readily diffuse across the cell membrane. - They act on **intracellular androgen receptors** located in the cytoplasm or nucleus. *Cortisol* - **Cortisol** is a **steroid hormone** that is **lipophilic** and can freely pass through the cell membrane. - It primarily binds to **intracellular glucocorticoid receptors** within the cytoplasm, forming a complex that translocates to the nucleus to modulate gene transcription.

Q: Hormone associated with satiety is

α-MSH. ***α-MSH*** - **Alpha-Melanocyte-stimulating hormone (α-MSH)** is a key neuropeptide involved in the **satiety pathway**. - It acts on **MC4 receptors** in the hypothalamus, leading to a decrease in food intake and an increase in energy expenditure. *Neuropeptide-Y* - **Neuropeptide-Y (NPY)** is a potent **orexigenic (appetite-stimulating)** peptide produced in the hypothalamus. - It promotes food intake and reduces energy expenditure, thereby **increasing hunger**. *Ghrelin* - **Ghrelin** is a hormone primarily produced in the stomach, often referred to as the "**hunger hormone**." - It stimulates appetite, increasing food intake and **promoting weight gain**. *Orexin* - **Orexin (also known as hypocretin)** is a neuropeptide produced in the hypothalamus that regulates **arousal, wakefulness, and appetite**. - While it has a role in regulating feeding, its primary function is more related to **increasing wakefulness and promoting food-seeking behavior** rather than directly signaling satiety.

Q: Which of the following hormones is mainly responsible for skeletal maturation of long bones during puberty?

Estrogen. ***Estrogen*** - Estrogen is crucial for **epiphyseal plate fusion** in both sexes, leading to the cessation of longitudinal bone growth. - While growth hormone initiates growth, estrogen is the primary signal for its **termination and skeletal maturation**. *Growth hormone* - **Growth hormone (GH)** is essential for stimulating longitudinal bone growth by promoting the proliferation of chondrocytes in the **epiphyseal plates**. - However, GH primarily drives *growth*, not the final *maturation and closure* of the growth plates. *Testosterone/estrogen ratio* - The ratio itself is not the direct hormonal signal for **skeletal maturation**. - While testosterone is converted to estrogen in males, it is the **estrogen** produced that mediates epiphyseal fusion. *Testosterone* - In males, testosterone promotes bone growth and increased bone density, but its effect on skeletal maturation is largely mediated through its **aromatization to estrogen**. - **High levels of testosterone** in puberty lead to increased estrogen, which then signals the closure of the growth plates.

Q: Intracellular receptors are found in all except

Insulin. ***Insulin*** - **Insulin** is a **peptide hormone** that cannot easily cross the cell membrane. It binds to a specific **extracellular receptor** on the cell surface, initiating a signaling cascade. - Its receptor is a **transmembrane protein** with an extracellular ligand-binding domain and an intracellular tyrosine kinase domain. *Androgen* - **Androgens** are **steroid hormones** that are lipid-soluble and can readily diffuse across the cell membrane to bind to **intracellular receptors** in the cytoplasm or nucleus. - The androgen-receptor complex then translocates to the nucleus to regulate gene expression. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that, despite being an amine derivative, is lipophilic and can enter cells to bind to **intracellular receptors** located in the nucleus. - These nuclear receptors regulate gene transcription involved in metabolism, growth, and development. *Corticosteroids* - **Corticosteroids** are **steroid hormones** that are lipid-soluble and diffuse through the cell membrane to bind to **intracellular receptors**, primarily in the cytoplasm. - The activated receptor-hormone complex then moves into the nucleus to influence gene expression.

Q: An elderly hypothyroid patient with chronic gastrointestinal complaints is being treated with triiodothyronine (T3) rather than thyroxine replacement because the former drug has better gastrointestinal absorption. When compared with no medication, triiodothyronine should have which of the following effects on serum levels of TSH, T3, and T4?

Decreased TSH, increased T3, and decreased T4. ***Decreased TSH, increased T3, and decreased T4*** - Administration of exogenous **T3** directly increases serum **T3** levels, which then exerts negative feedback on the pituitary gland, leading to a **decrease in TSH** secretion [1]. - Reduced TSH stimulation of the thyroid gland, combined with the fact that T3 (rather than T4) is being provided, results in **decreased endogenous T4** production and release. *Decreased TSH, decreased T3, and decreased T4* - While TSH and T4 would decrease due to negative feedback and reduced thyroid stimulation, therapeutic administration of **T3** would lead to **increased T3** levels, not decreased. - This option incorrectly suggests a decrease in the directly administered hormone. *Increased TSH, decreased T3, and decreased T4* - **Increased TSH** is characteristic of untreated or under-treated hypothyroidism because of the lack of negative feedback from low thyroid hormones; exogenous T3 would correct this, leading to decreased TSH. - Therapeutically administered **T3** would cause an **increase in T3** levels, not a decrease. *Decreased TSH, increased T3, and increased T4* - While TSH would decrease and T3 would increase, **T4 levels would typically decrease** because the thyroid gland's endogenous production is suppressed by the decreased TSH, and no exogenous T4 is being provided. - This option incorrectly assumes that T4 levels would increase despite TSH suppression.

Question 1

Which of the following is not an effect of insulin?

Accepted Answer

Increased glycogenolysis

Answer

Increased transport of glucose into cells

Answer

Induction of lipoprotein lipase

Answer

Decreased gluconeogenesis

Question 2

Acidophilic cells of anterior pituitary secrete?

Accepted Answer

GH

Answer

ACTH

Answer

TSH

Answer

ADH

Question 3

Which hormone is converted into its active form in the liver?

Accepted Answer

Thyroid hormone

Answer

Corticosteroid

Answer

Estradiol

Answer

ACTH

Question 4

Insulin acts by which pathway-

Accepted Answer

Tyrosine kinase

Answer

Intrinsic ion channel

Answer

JAK-STAT-Kinase

Answer

Transcription factor

Question 5

Which hormone is NOT increased in stress?

Accepted Answer

Insulin

Answer

Glucagon

Answer

Cortisol

Answer

Epinephrine

Question 6

Which hormone acts on cytoplasmic membrane receptor?

Accepted Answer

TSH

Answer

Thyroxine

Answer

Androgen

Answer

Cortisol

Question 7

Hormone associated with satiety is

Accepted Answer

α-MSH

Answer

Neuropeptide-Y

Answer

Ghrelin

Answer

Orexin

Question 8

Which of the following hormones is mainly responsible for skeletal maturation of long bones during puberty?

Accepted Answer

Estrogen

Answer

Growth hormone

Answer

Testosterone/estrogen ratio

Answer

Testosterone

Question 9

Intracellular receptors are found in all except

Accepted Answer

Insulin

Answer

Androgen

Answer

Thyroxine

Answer

Corticosteroids

Question 10

An elderly hypothyroid patient with chronic gastrointestinal complaints is being treated with triiodothyronine (T3) rather than thyroxine replacement because the former drug has better gastrointestinal absorption. When compared with no medication, triiodothyronine should have which of the following effects on serum levels of TSH, T3, and T4?

Accepted Answer

Decreased TSH, increased T3, and decreased T4

Answer

Decreased TSH, decreased T3, and decreased T4

Answer

Increased TSH, decreased T3, and decreased T4

Answer

Decreased TSH, increased T3, and increased T4

Endocrinology — MCQs

Endocrinology — MCQs

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