Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Guyton 14e
Anterior pituitary (adenohypophysis)
Connected to the hypothalamus by the hypophyseal portal blood vessels. Hypothalamic releasing/inhibiting hormones (e.g. TRH, CRH, GnRH, GHRH, somatostatin, dopamine) travel in the portal blood to control secretion of the anterior-pituitary hormones: GH, TSH, ACTH, FSH, LH, prolactin.
Posterior pituitary (neurohypophysis)
An extension of the hypothalamus connected by direct neuronal axons. ADH and oxytocin are synthesised in the supraoptic and paraventricular nuclei, transported down the axons, and stored/released from the posterior lobe.
Control
Most axes operate by negative feedback — the target-gland hormone inhibits the hypothalamus and pituitary.
Synthesis and axis
Follicular cells make T₄ (and T₃) from iodine + thyroglobulin; T₄ → T₃ peripherally. Axis: TRH → TSH → T₃/T₄, with negative feedback.
Actions
- ↑Basal metabolic rate and heat production (calorigenic).
- Essential for normal growth and especially CNS development.
- Potentiate catecholamines (↑heart rate and contractility).
Hyperthyroidism (e.g. Graves)
↑BMR, weight loss, heat intolerance, tachycardia, tremor, exophthalmos.
Hypothyroidism
Child: cretinism (mental + growth retardation). Adult: myxoedema (cold intolerance, weight gain, slowness). Iodine deficiency → goitre.
Three cortical zones
- Zona glomerulosa → aldosterone (mineralocorticoid): ↑renal Na⁺ reabsorption + K⁺ secretion → controls volume/BP.
- Zona fasciculata → cortisol (glucocorticoid).
- Zona reticularis → adrenal androgens (DHEA).
Actions of cortisol
- Gluconeogenesis → raises blood glucose; promotes protein and fat catabolism (provides substrate).
- Anti-inflammatory and immunosuppressive.
- Central to the stress response; permissive for catecholamine action; controlled by the CRH → ACTH → cortisol (HPA) axis.
Clinical
Excess = Cushing syndrome; deficiency = Addison disease.
Insulin (β cell) — lowers glucose
Released when blood glucose rises. It increases glucose uptake into muscle and fat (GLUT4), and promotes glycogenesis, lipogenesis and protein synthesis (anabolic, fuel storage). It is the ONLY hypoglycaemic hormone.
Glucagon (α cell) — raises glucose
Released when blood glucose falls. It drives hepatic glycogenolysis and gluconeogenesis to release glucose.
Counter-regulation
Cortisol, growth hormone and adrenaline also raise glucose. The insulin:glucagon ratio sets the fed (storage) vs fasting (mobilisation) state.
Clinical
Insulin deficiency (type 1) or resistance (type 2) → diabetes mellitus: hyperglycaemia, glycosuria, osmotic diuresis, and in severe type 1, ketoacidosis.
Normal level
Plasma Ca²⁺ is held at 2.2–2.6 mmol/L because it controls nerve/muscle excitability, clotting and secretion.
PTH (raises Ca²⁺)
From the parathyroids in response to low Ca²⁺: ↑bone resorption, ↑renal Ca²⁺ reabsorption (with phosphate loss), and activation of vitamin D.
Calcitriol / active vitamin D (raises Ca²⁺)
↑Intestinal absorption of Ca²⁺ and phosphate.
Calcitonin (lowers Ca²⁺)
From thyroid C cells; inhibits osteoclasts (minor role in humans).
Disorders
Hypocalcaemia → tetany (↑excitability). Hyperparathyroidism → hypercalcaemia ('stones, bones, groans'). Vitamin D deficiency → rickets/osteomalacia.