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PY8.1-7 | Endocrine Physiology — SDL Guide (Part 4)

Growth Hormone (PY8.6)

GH (191 amino acids, from somatotrophs of anterior pituitary) promotes growth and has metabolic effects.

Regulation:
- GHRH (hypothalamus) → ↑ GH release
- Somatostatin → ↓ GH release
- Physiological stimuli for GH release: sleep (SWS), hypoglycaemia, exercise, stress, amino acids, puberty (oestrogen/testosterone)
- Negative feedback: IGF-1 (from liver) feeds back to both hypothalamus (↑ somatostatin) and pituitary (↓ GH release)

Actions — indirect (via IGF-1) and direct:
- IGF-1 mediated (anabolic): Linear bone growth (at open epiphyses), muscle mass ↑, organ growth
- Direct metabolic effects (anti-insulin / diabetogenic): ↑ Lipolysis, ↓ glucose uptake by peripheral tissues, ↑ gluconeogenesis

Disorders:
- GH deficiency in children: Proportionate dwarfism, delayed puberty, normal intelligence (unlike thyroid deficiency, which causes intellectual disability). Treatment: recombinant GH injections.
- GH excess in children (open epiphyses): Gigantism — linear growth up to 2.4 m
- GH excess in adults (fused epiphyses): Acromegaly — bones cannot lengthen, so they WIDEN: enlarged jaw (prognathism), hands (ring does not fit), feet (shoes too small), tongue (macroglossia), nose, forehead (frontal bossing). Also: carpal tunnel syndrome, hypertension, diabetes (GH is diabetogenic), cardiac complications.

Diagnosis of acromegaly: Serum IGF-1 (elevated, stable — unlike GH which pulsatile); GH suppression test — give oral glucose (should suppress GH to < 0.4 ng/mL; in acromegaly, GH does NOT suppress or paradoxically rises).
Treatment: Transsphenoidal adenomectomy; octreotide (somatostatin analogue) if surgery fails.

Growth Hormone (PY8.6) — Four-panel illustration showing GH regulation via GHRH/somatostatin and IGF-1 feedback, direct metabolic and indirect IGF-1-mediated growth effects, gigantism versus acromegaly from GH excess, and GH deficiency including Laron syndrome.

Summary

Key Endocrine Function Tests (PY8.7)

The principle behind endocrine testing: stimulation tests for suspected deficiency; suppression tests for suspected excess.

Thyroid:
- TSH: Screen first. ↑ in hypothyroidism (pituitary compensating); ↓ in hyperthyroidism (suppressed)
- Free T4, Free T3: Measure active hormone (not protein-bound)
- Anti-TPO antibodies: Hashimoto's; TSH receptor antibodies (TRAb): Graves'
- Radioiodine uptake scan: Diffuse ↑ uptake = Graves'; focal ↑ = toxic adenoma; ↓ uptake = thyroiditis (hormone leaking, not synthesised)

Diabetes:
- Fasting plasma glucose: ≥ 126 mg/dL × 2 = T2DM; 100–125 = impaired fasting glucose
- OGTT (75 g): 2-h glucose ≥ 200 mg/dL = diabetes; 140–199 = impaired glucose tolerance
- HbA1c: ≥ 6.5% = diabetes. Reflects average glucose over 2–3 months (RBC lifespan). Useful for monitoring control, not diagnosis in acute settings.
- C-peptide: Measures endogenous insulin secretion (equimolar with insulin, not degraded by liver). Low in T1DM; normal/high in T2DM; absent in exogenous insulin use.

Adrenal:
- Morning cortisol: Collected at 8 AM (peak). < 3 μg/dL = adrenal insufficiency; > 18 μg/dL = normal.
- ACTH stimulation test (Short Synacthen Test): Give synthetic ACTH; measure cortisol at 30 and 60 min. Normal: cortisol rises to > 18 μg/dL. Failure = adrenal insufficiency.
- 24-h urine free cortisol / overnight dexamethasone suppression test: For Cushing's syndrome diagnosis.

Calcium:
- Intact PTH (iPTH): ↑ in hyperparathyroidism; ↓ in hypoparathyroidism; ↓ in malignancy-associated hypercalcaemia (tumours suppress PTH)
- 25-OH Vitamin D: Reflects body stores (normal > 30 ng/mL; deficient < 20 ng/mL)
- 1,25-(OH)₂D₃: Not routinely measured; useful in sarcoidosis, CKD

Key Endocrine Function Tests (PY8.7) — Four-panel illustration showing endocrine function tests: thyroid function test algorithm with TSH screening, diabetes diagnostic criteria across four tests, adrenal function tests for Cushing's and Addison's, and calcium/GH function testing protocols.