Growth Hormone and Growth Factors — MCQs

10 questions

A patient presents with large sweaty hands, macroglossia, and frontal bossing. What is the best test for confirmation of the diagnosis?

Which of the following actions of GH is mediated by IGF-1?

What is the initial treatment for most patients with growth hormone-secreting pituitary adenoma?

Laron dwarfism is due to:

All of the following statements about Insulin like Growth factor - 1 are true, except:

A middle aged man noticed that he can no longer fit in his shoes and that his jaw was protruding and phalanges were enlarged. These effects are likely to be mediated by

Which of the following is NOT true about ghrelin?

Which of the following compounds antagonizes the actions of insulin?

Intracranial Irradiation most commonly leads to deficiency of

Q10

Which of the following can cause an increase in growth hormone levels in blood?

Growth Hormone and Growth Factors Indian Medical PG Practice Questions and MCQs

Question 1: A patient presents with large sweaty hands, macroglossia, and frontal bossing. What is the best test for confirmation of the diagnosis?

A. GHRH levels
B. IGF-1 (Correct Answer)
C. IGF-2
D. GH levels after glucose suppression
E. Random GH level

Explanation: ***IGF-1*** - Elevated **IGF-1 (Insulin-like Growth Factor 1)** is the most reliable screening test for acromegaly, reflecting integrated GH secretion over time. - The clinical signs of **large sweaty hands**, **macroglossia**, and **frontal bossing** are classic symptoms of acromegaly, caused by excessive growth hormone (GH) production, which then stimulates IGF-1. *GHRH levels* - **Growth hormone-releasing hormone (GHRH)** levels are typically only measured when investigating ectopic GHRH production as a rare cause of acromegaly, which is not the primary diagnostic step. - While GHRH stimulates GH, its direct measurement is not the standard initial diagnostic test for suspected pituitary-driven acromegaly. *IGF-2* - **IGF-2 (Insulin-like Growth Factor 2)** plays a role in fetal growth and certain tumor-related syndromes, but it is not the primary mediator or diagnostic marker for acromegaly in adults. - IGF-1, not IGF-2, is the main growth factor responsible for the anabolic effects of growth hormone. *GH levels after glucose suppression* - Measuring **GH levels after glucose suppression** (oral glucose tolerance test with 75g glucose) is a confirmatory test for acromegaly, used when IGF-1 levels are equivocal or borderline. - In healthy individuals, glucose suppresses GH secretion to <1 ng/mL, but in acromegaly, GH levels remain elevated (failure to suppress), confirming autonomous GH hypersecretion. *Random GH level* - **Random GH levels** are unreliable for diagnosing acromegaly due to the pulsatile nature of GH secretion, with significant variation throughout the day. - A single normal GH level does not exclude acromegaly, and a single elevated level can occur in healthy individuals during normal secretory peaks, making it inadequate as a diagnostic test.

Question 2: Which of the following actions of GH is mediated by IGF-1?

A. Na+ retention
B. decreases insulin
C. Antilipolysis (Correct Answer)
D. Lipolysis

Explanation: ***Antilipolysis*** * **Insulin-like growth factor 1 (IGF-1)**, stimulated by GH, plays a role in reducing **lipolysis** indirectly. * IGF-1 promotes **anabolic processes** and nutrient storage, which can lead to decreased fat breakdown. *Na+ retention* * **Na+ retention** is more directly influenced by hormones like **aldosterone** and **ADH**, not IGF-1. * While GH can exert some influence on fluid and electrolyte balance, this specific action is not primarily mediated by IGF-1. *decreases insulin* * IGF-1 and GH generally tend to **increase insulin sensitivity** in some tissues or antagonize insulin effects indirectly. * IGF-1's primary metabolic role is not to decrease insulin itself directly. *Lipolysis* * **Growth hormone (GH)** directly promotes **lipolysis**, breaking down fat for energy. * However, the question specifically asks for actions mediated by **IGF-1**, which has an opposite, antilipolytic effect.

Question 3: What is the initial treatment for most patients with growth hormone-secreting pituitary adenoma?

A. Transphenoidal surgical resection (Correct Answer)
B. Somatostatin analogs
C. Dopamine agonists
D. GH receptor antagonists

Explanation: ***Transphenoidal surgical resection*** - This is the **preferred initial treatment** for most growth hormone (GH)-secreting pituitary adenomas, as it offers the best chance for **cure** and rapid reduction in GH levels [1]. - Success rates are high, especially for **smaller tumors** (microadenomas), and it can quickly relieve mass effect symptoms [1]. *Somatostatin analogs* - These are typically used as **second-line therapy** if surgery is unsuccessful or contraindicated, or in patients not surgical candidates. - They work by **inhibiting GH secretion** but do not usually achieve a complete cure like surgery. *GH receptor antagonists* - These medications, such as pegvisomant, **block the action of GH** at its receptor, normalizing IGF-1 levels. - They are primarily used when other treatments, including surgery and somatostatin analogs, have failed to control GH excess. *Dopamine agonists* - While dopamine agonists (e.g., cabergoline) can **sometimes reduce GH secretion** in a minority of patients, they are significantly less effective for GH-secreting tumors compared to prolactinomas [1]. - They are occasionally used as **adjunctive therapy** or in specific cases where the GH-secreting tumor also co-secretes prolactin [1].

Question 4: Laron dwarfism is due to:

A. GH deficiency
B. GHRH deficiency
C. GH receptor resistance (Correct Answer)
D. IGF-1 deficiency

Explanation: ***GH receptor resistance*** - **Laron dwarfism** is caused by a genetic defect in the **growth hormone (GH) receptor**, leading to cellular insensitivity to GH. - Despite normal or elevated GH levels, the body cannot respond to GH, resulting in impaired **insulin-like growth factor 1 (IGF-1)** production and stunted growth. *GH deficiency* - This would involve insufficient production of **growth hormone** from the pituitary gland. - In such cases, administration of exogenous GH would typically be effective, which is not the case in Laron dwarfism due to receptor resistance. *GHRH deficiency* - A deficiency in **growth hormone-releasing hormone (GHRH)** from the hypothalamus would lead to decreased GH secretion. - This would ultimately result in **GH deficiency**, but the primary defect in Laron syndrome is at the receptor level, not in GHRH or GH production. *IGF-1 deficiency* - While Laron dwarfism does result in functionally low **IGF-1** levels due to GH insensitivity, the primary defect is in the GH receptor, which *prevents* GH from stimulating IGF-1 production. - True primary **IGF-1 deficiency** (apart from GH resistance) is a less common cause of dwarfism and would not involve high GH levels.

Question 5: All of the following statements about Insulin like Growth factor - 1 are true, except:

A. Mainly secreted by the pancreas (Correct Answer)
B. Required for skeletal and cartilage growth
C. Secretion is stimulated by Growth Hormone
D. Also known as Somatomedin C

Explanation: ***Mainly secreted by the pancreas*** - **Insulin-like Growth Factor-1 (IGF-1)** is primarily produced by the **liver** in response to **growth hormone (GH)** stimulation, not the pancreas. - While the pancreas does produce some growth factors and hormones, IGF-1 synthesis is predominantly hepatic. *Required for skeletal and cartilage growth* - IGF-1 is a crucial mediator of **growth hormone's effects**, playing a significant role in **linear growth, bone formation**, and **cartilage maintenance**. - It promotes **cell proliferation** and differentiation in various tissues, including bone and cartilage. *Secretion is stimulated by Growth Hormone* - **Growth hormone (GH)** from the pituitary gland stimulates the liver and other tissues to produce IGF-1. - IGF-1 then mediates many of the growth-promoting actions of GH. *Also known as Somatomedin C* - **Somatomedin C** is an older name for **Insulin-like Growth Factor-1 (IGF-1)**. - This term reflects its **growth-promoting actions** and its similarity in structure to **insulin**.

Question 6: A middle aged man noticed that he can no longer fit in his shoes and that his jaw was protruding and phalanges were enlarged. These effects are likely to be mediated by

A. TRH
B. ACTH
C. TGF Beta
D. IGF-1 (Correct Answer)

Explanation: ***IGF-1*** - The described symptoms (increased shoe size, jaw protrusion, enlarged phalanges) are characteristic of **acromegaly**, a condition caused by excessive growth hormone (GH) secretion in adults. - **Insulin-like Growth Factor 1 (IGF-1)** is primarily responsible for mediating the growth-promoting effects of GH on various tissues, leading to the clinical manifestations seen in this patient. *TRH* - **Thyrotropin-releasing hormone (TRH)** stimulates the release of thyroid-stimulating hormone (TSH) from the pituitary, which in turn regulates thyroid hormone production. - Excess TRH would lead to hyperthyroidism symptoms like weight loss, heat intolerance, and tachycardia, not acromegalic features. *ACTH* - **Adrenocorticotropic hormone (ACTH)** stimulates the adrenal glands to produce cortisol. - Excessive ACTH causes **Cushing's syndrome**, characterized by central obesity, moon facies, striae, and muscle weakness, which are different from the presented symptoms. *TGF Beta* - **Transforming growth factor beta (TGF-beta)** is a pleiotropic cytokine involved in cell growth, differentiation, apoptosis, and immune regulation. - While it plays a role in tissue remodeling and fibrosis, it is not the direct mediator of the generalized growth and skeletal changes seen in acromegaly.

Question 7: Which of the following is NOT true about ghrelin?

A. Has anorexic effect (Correct Answer)
B. Stimulates growth hormone release
C. Secreted by gastric fundus cells
D. Increases gastric motility

Explanation: ***Has anorexic effect*** - Ghrelin is known as the **"hunger hormone"** because it stimulates appetite and has an **orexigenic effect**, meaning it increases food intake. - Therefore, stating that it has an **anorexic effect** (reduces appetite) is incorrect. *Stimulates growth hormone release* - Ghrelin is a **natural ligand** for the **growth hormone secretagogue receptor (GHSR)**. - This binding leads to the stimulation of **growth hormone (GH)** release from the pituitary gland. *Secreted by gastric fundus cells* - The primary source of ghrelin in the body is the **P/D1 cells** found in the mucosa of the **gastric fundus**. - Smaller amounts are also produced in the small intestine, pancreas, and hypothalamus. *Increases gastric motility* - Ghrelin is involved in regulating stomach function and can **increase gastric motility** and acid secretion. - This action helps to prepare the digestive system for incoming food.

Question 8: Which of the following compounds antagonizes the actions of insulin?

A. Substance P
B. Growth hormone (Correct Answer)
C. Neuropeptide Y
D. Vasoactive intestinal peptide

Explanation: ***Growth hormone*** - **Growth hormone (GH)** is a potent **anti-insulin hormone** that raises blood glucose by promoting **gluconeogenesis** and reducing glucose utilization by peripheral tissues. - It decreases **insulin sensitivity** in target tissues like muscle and adipose tissue, often leading to a temporary state of **insulin resistance**. *Substance P* - **Substance P** is a **neuropeptide** involved in pain transmission and inflammation, and its primary actions do not directly involve glucose metabolism or insulin antagonism. - While it can influence local metabolic processes, it does not exert systemic effects on insulin action. *Neuropeptide Y* - **Neuropeptide Y (NPY)** is a **neurotransmitter** primarily involved in stimulating appetite and reducing energy expenditure, playing a role in weight regulation. - Although it affects metabolic balance, NPY does not directly antagonize insulin's actions on glucose uptake or utilization. *Vasoactive intestinal peptide* - **Vasoactive intestinal peptide (VIP)** is a **neurotransmitter** and hormone that primarily affects smooth muscle relaxation, exocrine and endocrine secretions, and local blood flow. - It does not directly antagonize insulin's effects on glucose metabolism or directly impact insulin sensitivity in a significant way.

Question 9: Intracranial Irradiation most commonly leads to deficiency of

A. ACTH
B. PROLACTIN
C. GROWTH HORMONE (Correct Answer)
D. TSH

Explanation: ***GROWTH HORMONE*** - **Growth hormone (GH)** deficiency is the most common endocrine complication following **intracranial irradiation**, particularly affecting children and adolescents due to the sensitivity of somatotrophs. - The somatotrophs, responsible for GH production, are highly vulnerable to radiation damage, often manifesting as GH deficiency even at lower radiation doses or earlier after treatment. *ACTH* - **ACTH deficiency** (leading to secondary adrenal insufficiency) can occur after intracranial irradiation but is less common and typically appears later or at higher radiation doses than GH deficiency. - The corticotrophs, which produce ACTH, are generally more resilient to radiation compared to somatotrophs. *PROLACTIN* - **Prolactin deficiency** is relatively rare following intracranial irradiation, as lactotrophs (prolactin-producing cells) are among the most radioresistant pituitary cells. - Conversely, hyperprolactinemia due to damage to the dopamine inhibitory pathways is more frequently observed than prolactin deficiency. *TSH* - **TSH deficiency** (central hypothyroidism) can occur after intracranial irradiation but is less common than GH deficiency and tends to manifest later. - Thyrotrophs, which produce TSH, are more radiosensitive than lactotrophs and corticotrophs but less so than somatotrophs.

Question 10: Which of the following can cause an increase in growth hormone levels in blood?

A. Cortisol
B. Glucose
C. Hypoglycemia (Correct Answer)
D. Methylprednisolone

Explanation: ***Hypoglycemia*** - **Hypoglycemia** is a potent stimulus for **growth hormone (GH) secretion**, as GH acts to raise blood glucose levels, serving as a counter-regulatory hormone. - The body perceives low blood glucose as a stressor, activating the **hypothalamic-pituitary-adrenal axis** and stimulating GH release to mobilize energy stores. *Cortisol* - **Cortisol** (a glucocorticoid) generally has an **inhibitory effect** on GH secretion at the hypothalamic and pituitary levels. - High levels of cortisol can lead to **suppression of GH pulsatility** and overall lower GH release. *Glucose* - An increase in **blood glucose** levels typically **suppresses growth hormone (GH) release**, as GH tends to increase blood glucose. - This negative feedback mechanism helps maintain **glucose homeostasis** within the body. *Methylprednisolone* - **Methylprednisolone** is a synthetic **glucocorticoid** that mimics the actions of cortisol. - Like cortisol, it suppresses GH secretion and can lead to **growth retardation** in children with chronic use.

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