Hypothalamic-Pituitary-Growth Axis and Related Disorders

Practice flashcards created for reviewing key concepts related to the hypothalamic-pituitary-growth axis and associated growth disorders.

What does the growth axis (hypothalamic–pituitary–somatotropic axis) regulate?

It regulates somatic growth, metabolism, and body composition.

Which hormones are released by the hypothalamus that affect growth hormone secretion?

GHRH (Growth Hormone-Releasing Hormone) which is stimulatory, and Somatostatin (GHIH; Growth Hormone-Inhibiting Hormone) which is inhibitory.

What is the primary target tissue for Growth Hormone (GH)?

The Liver.

What is IGF-1 also known as?

Insulin-like Growth Factor-1; formerly somatomedin C.

What stimulates the secretion of Growth Hormone?

GHRH, Ghrelin, deep sleep, exercise, stress, hypoglycemia, and amino acids.

What inhibits Growth Hormone secretion?

Somatostatin, negative feedback from IGF-1, hyperglycemia, and chronic stress.

What are the two main types of feedback regulation in the growth axis?

Long-loop feedback and short-loop feedback.

How does GH exert its effects?

Directly through metabolic effects like lipolysis and insulin resistance, and indirectly via IGF-1 for anabolic growth promotion.

What is the main result of dysregulation in the growth axis?

Disorders like growth hormone deficiency (short stature) or excess (gigantism/acromegaly).

What historical hypothesis was revised concerning growth hormone and its effects on growth?

The Somatomedin Hypothesis was revised to recognize IGF-1 as the primary mediator of postnatal growth.

What are the effects of IGF-1 on chondrocytes?

It stimulates chondrocyte proliferation and differentiation in the growth plate.

What is the primary mediator of growth hormone effects after postnatal growth?

IGF-1 (Insulin-like Growth Factor-1).

What are the types of dwarfism related to the growth axis?

Hypothalamic Insufficiency, Congenital or Acquired GH Deficiency, congenital or acquired IGF-1 Deficiency, and GH/IGF-1 Insensitivity.

What is Laron syndrome?

A condition of GH resistance resulting from mutations in the growth hormone receptor gene.

What differentiates gigantism from acromegaly?

Gigantism occurs before epiphyseal fusion, causing excessive linear bone growth, while acromegaly occurs after epiphyseal fusion, resulting in soft tissue overgrowth and bone deformity.

What are the main treatments for acromegaly?

Transsphenoidal surgery, somatostatin receptor ligands, GH receptor antagonists, and radiation therapy.

What is the function of somatostatin analogs in the treatment of acromegaly?

They suppress GH and IGF-1 secretion by binding to somatostatin receptors.

How does GH affect carbohydrate metabolism?

GH induces insulin resistance and impairs glucose utilization, acting predominantly as an anti-insulin hormone.

What is a key physiological effect of IGF-1 on bone?

It stimulates osteoblast proliferation and increases bone matrix synthesis.

What factors can affect GH secretion pulsatility?

Deep sleep, exercise, stress, and nutritional status.

What is the impact of GH during catabolic states like fasting?

It has a protein-sparing effect, reducing reliance on amino acids for gluconeogenesis.

What are the key differences in biological functions between IGF-1 and IGF-2?

IGF-1 is GH-dependent and promotes postnatal growth, while IGF-2 is less GH-dependent and primarily plays a role in fetal growth.