Posterior pituitary (neurohypophysis)

What it normally does

• It is not a glandular tissue. It is the far end of nerve cells whose bodies sit in the hypothalamus (supraoptic and paraventricular nuclei). They make ADH (vasopressin) and oxytocin, carry them down their own axons through the stalk, and release them into capillaries here.

  Explains central diabetes insipidus: a head injury, pituitary surgery or a stalk lesion can wipe out ADH by cutting the axons above the gland, and it can happen with anterior pituitary function intact. Do not assume it always is — a stalk or hypothalamic lesion commonly knocks out anterior hormones too, and untreated cortisol deficiency can mask the polyuria until glucocorticoid is replaced.

• ADH is released when the blood becomes too concentrated — hypothalamic osmoreceptors start firing above about 280-285 mOsm/kg. ADH binds V2 receptors on the last stretch of the nephron (collecting duct) and pushes water channels (aquaporin-2) into the membrane facing the urine. Water is pulled back and the urine ends up small and concentrated.

  Explains both diabetes insipidus (no channels, litres of dilute urine) and SIADH (channels left in place, water retained and sodium diluted).

• ADH's main job is to move water, not salt — so the plasma sodium is really a measure of body water. And a big fall in blood volume or pressure overrides osmolality: baroreceptors drive ADH out even when the plasma is already dilute.

  Explains why hyponatraemia turns up in vomiting, diuretics, heart failure and cirrhosis, and why the fluid state must be judged at the bedside before anyone says SIADH.

• Oxytocin contracts smooth muscle in two places: the muscle of the uterus (myometrium) and the basket cells wrapped around the milk glands (myoepithelial cells). Suckling and cervical stretch drive more release — positive feedback, not negative.

  Explains milk let-down, the progress of labour, and why the uterus must clamp down after delivery or the mother bleeds.

What goes wrong

• Central diabetes insipidus (arginine vasopressin deficiency, AVP-D)← from “It is not a glandular tissue. It is the far en…”

  The hypothalamic neurons or the stalk are destroyed — head injury, pituitary surgery, tumour, sarcoidosis. No ADH reaches the blood, so no aquaporin-2 goes into the collecting duct, so the duct is a waterproof pipe. The dilute fluid generated by the diluting segments runs straight out.

  Polyuria with dilute urine and a rising sodium after neurosurgery or head trauma is central DI until proved otherwise; the response to desmopressin settles it.

  You would find: Three to twenty litres of pale urine a day, nocturia every night, craving for iced water. Urine osmolality under 300 mOsm/kg while plasma osmolality sits high-normal. Sodium stays normal while the patient can drink, and climbs fast when they cannot — unconscious, nil by mouth, elderly, or nobody bringing the water. Urine concentrates after desmopressin.

• Nephrogenic diabetes insipidus (AVP resistance, AVP-R)← from “ADH is released when the blood becomes too con…”

  ADH is present in normal amounts but the collecting duct cannot hear it. Lithium is the common cause: it enters principal cells through the sodium channel ENaC and disrupts signalling downstream of the V2 receptor, so aquaporin-2 is never inserted. Long-standing hypercalcaemia and hypokalaemia do the same thing.

  Same picture, opposite site. The fault is in the kidney, not the pituitary, and the failure to concentrate after desmopressin is what separates them.

  You would find: Polyuria and dilute urine that looks like central DI — but there is little or no response to desmopressin. Ask about lithium, often taken for years. Check calcium and potassium.

• SIADH (syndrome of inappropriate ADH)← from “ADH is released when the blood becomes too con…”

  ADH is released when it should be switched off — a small cell lung cancer secreting it, pneumonia or a stroke driving it, drugs pushing it (SSRIs, carbamazepine, MDMA). Aquaporins stay in the membrane, water is retained, and the retained water dilutes the sodium. This is primarily water excess; total body sodium is normal or only slightly reduced.

  Hyponatraemia is the commonest electrolyte problem on any Australian ward. In SIADH do not reach for normal saline first — the kidney holds the water and excretes the salt, and the sodium can fall further.

  You would find: Low plasma sodium with low plasma osmolality, and urine that is inappropriately concentrated (>100 mOsm/kg) with urine sodium above 30 mmol/L, in someone who looks neither dry nor oedematous and is not on diuretics. Thyroid and adrenal failure must be excluded — it is a diagnosis of exclusion. A low serum urate supports it. Nausea and headache, then confusion; seizures if the sodium fell quickly.

• Hyponatraemia from low effective circulating volume← from “ADH's main job is to move water, not salt — so…”

  Vomiting, diarrhoea, diuretics, heart failure or cirrhosis all reduce the volume the baroreceptors sense. That signal overrides osmolality, ADH stays switched on, and water is held on top of a sodium that is already low or normal.

  Before diagnosing SIADH, decide whether the patient is dry, wet or neither, and check whether they are on a diuretic. That single assessment splits the causes of hyponatraemia and changes the treatment completely.

  You would find: Dry patient: postural drop, tachycardia, dry axillae, urine sodium under 20 mmol/L. Wet patient: oedema, ascites, raised JVP — and still urine sodium under 20 mmol/L, because the kidney is clinging to salt. Two traps: on a current thiazide or loop diuretic the urine sodium is high despite hypovolaemia, and in vomiting bicarbonaturia drags sodium into the urine — so urine sodium cannot be read in isolation. Either way the bedside fluid state separates them from SIADH.

• Uterine atony and postpartum haemorrhage← from “Oxytocin contracts smooth muscle in two places…”

  Once the placenta separates the spiral arteries are open holes. Nothing but the criss-cross myometrium contracting around them stops the flow. Overdistension (twins, big baby, polyhydramnios), long labour, or infection leaves the muscle slack, so the vessels are never clamped.

  PPH is a leading cause of severe maternal morbidity in Australia, and outcomes are worse for Aboriginal and Torres Strait Islander women, who more often birth far from a referral hospital. Routine prophylactic oxytocin in the third stage is among the cheapest effective preventions in medicine.

  You would find: Heavy bleeding after delivery with a soft, boggy uterus sitting high in the abdomen. It firms up when you rub the fundus. Conventionally 500 mL or more after vaginal birth and 1000 mL or more after caesarean, though any blood loss causing haemodynamic compromise counts.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.