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SEPT 10 Built from the handwritten pages you uploaded on 10 September 2026.

Adrenal, pituitary & steroids

The anatomy of hormone production, Cushing versus Addison versus Conn, and the steroid equivalency table.

The adrenal gland

ADRENAL CORTEX MEDULLA catecholamines adrenaline ~80% noradrenaline · dopamine Reticularis androgens Fasciculata cortisol Glomerulosa aldosterone Outside in: Glomerulosa · Fasciculata · Reticularis "Salt, Sugar, Sex — the deeper you go, the sweeter it gets." The medulla is innervated by PREganglionic sympathetic fibres — modified postganglionic cells.

Pituitary hormones

Anterior (adenohypophysis)Posterior (neurohypophysis)
GH · Prolactin · LH · FSH · ACTH · TSH
Rathke's pouch — glandular. Releasing hormones arrive via the hypophyseal portal system.		Oxytocin · Vasopressin (ADH)
A neural downgrowth. Both are made in the hypothalamus (supraoptic and paraventricular nuclei) and transported down axons.

Consequence of the two different origins

  • Stalk section causes anterior pituitary failure but a RISE in prolactin — because prolactin is the only anterior hormone under tonic inhibition (by dopamine).
  • Posterior hormones are still made in the hypothalamus, so a lesion must be high to abolish ADH — hence diabetes insipidus after pituitary surgery or head injury.

What increases ADH

  • Physiological: rise in plasma osmolality (the primary stimulus, threshold about 280 mOsm/kg) · fall in blood volume or pressure via atrial and arterial baroreceptors.
  • Perioperative: surgical stress · pain · anxiety · nausea · positive pressure ventilation · raised PaCO₂ · hypoxia · exercise.
  • Drugs: morphine · nicotine · histamine · carbamazepine · SSRIs · cyclophosphamide.
  • Decreased by: alcohol · a rise in blood volume or atrial stretch (via ANP) · cold · hypo-osmolality.
  • Surgery is a potent ADH stimulus — one of the reasons postoperative patients retain water and become hyponatraemic on hypotonic fluid.

Cushing vs Addison — the mirror image

Cushing's (↑ cortisol)Addison's (↓ cortisol & aldosterone)
Sodium↑↓
Potassium↓↑
H⁺↓↑
Acid–baseMetabolic alkalosisMetabolic acidosis
Blood pressure↑↓
Volume↑↓
Glucose↑↓

Where the lesion is — ACTH tells you

  • Cushing's with ↑ ACTH → pituitary (Cushing's disease) or ectopic ACTH.
  • Cushing's with ↓ ACTH → adrenal source, or exogenous steroid (much the commonest cause overall).
  • Addison's with ↑ ACTH → primary adrenal failure, and therefore HYPERPIGMENTATION (ACTH shares a precursor with MSH).
  • Addison's with ↓ ACTH → secondary, pituitary in origin, and NO hyperpigmentation. Aldosterone is largely preserved, so hyperkalaemia is less marked.

Addisonian crisis

  • Fever · abdominal pain · vomiting · hypotension · hypovolaemia · shock, with hypoglycaemia.
  • Precipitated by surgery, sepsis, or abrupt withdrawal of long-term steroid.
  • Treatment: hydrocortisone 100 mg IV and aggressive fluid. Do not wait for a cortisol result to treat.

Conn's syndrome

  • Primary hyperaldosteronism — adenoma or bilateral hyperplasia.
  • ↑ Na⁺ · ↑ BP · ↓ K⁺ · ↓ H⁺ → hypokalaemic metabolic alkalosis.
  • Primary → renin is SUPPRESSED (low renin, high aldosterone). Secondary → renin is HIGH (renal artery stenosis, heart failure, cirrhosis, diuretics).
  • The aldosterone-to-renin ratio is the screening test. Treat with spironolactone or eplerenone, or adrenalectomy.
  • Anaesthetic relevance: correct potassium and blood pressure preoperatively; expect resistance to neuromuscular blockade reversal if profoundly hypokalaemic.

Steroid equivalency

SteroidEquivalent dose (mg)Gluco : Mineralo potency · half-life
Dexamethasone0.7525 : 0 · 36–54 h (long)
Methylprednisolone45 : 0.5 · 12–36 h
Prednisolone54 : 0.8 · 12–36 h
Hydrocortisone201 : 1 · 8–12 h (short)
Cortisone acetate250.8 : 0.8 · 8–12 h
FludrocortisoneNot used for glucocorticoid effect10 : 125 · 18–36 h

The mnemonic

  • D-1, M-4, P-5, H-20, Cortisone-25 — dexamethasone 1 (strictly 0.75), methylprednisolone 4, prednisolone 5, hydrocortisone 20, cortisone acetate 25.
  • Dexamethasone has NO mineralocorticoid activity — which is why it is the choice for cerebral oedema and as an antiemetic, and why it is useless as replacement in Addison's.
  • Fludrocortisone is the opposite: chosen entirely for its mineralocorticoid effect.
  • Hydrocortisone is 1:1 — the reference against which the others are measured, and the correct drug in an adrenal crisis.

A caveat on your table

  • The upper chart on your page gives hydrocortisone an equivalent dose of 25 mg, while the lower table gives 20 mg. 20 mg is the standard figure, and it is the one consistent with dexamethasone 0.75 mg and prednisolone 5 mg. The 25 belongs to cortisone acetate.

Quick recall

GFR Salt · Sugar · Sex
Medulla preganglionic supply
↑ACTH Addison pigmented
Conn's ↓K, ↓renin, alkalosis
D1 M4 P5 H20 C25
Dex zero mineralocorticoid
Stalk section prolactin RISES

Built from your adrenal, pituitary, cortisol and steroid equivalency pages. See also Autonomic & adrenoceptors.