Posterior pituitary Flashcards
Source and targets of the post pituitary hormones
ADH: from supraoptic nucleus, target kidney and blood vessels; Oxytocin: paraventricular nucleus, target uterus and mammary glands
Fn of ADH
Kidney: increase permeability of collecting duct (bind G protein R, cAMP/PKA, (P)’s vesicles and release more aquaporins), Vasoconstriction reduces GFR; Pressor Action: Contraction of blood vessel smooth muscle (Only occurs at high concentrations (hemorrhage))
List the three stimuli for ADH release
Thirst Centre, Osmoreceptor (Dehydration -> shrinkage of the osmoreceptor neurons, more ADH, more thirst - much less ADH needed here), Baroreceptor (lower BP or BV, postural hypotension)
Describe the clinical manifestations of diabetes insipidus
Too little ADH (central diabetes insipidus) or abnormal ADHr in kidney (nephrogenic DI).
Causes of Central and nephrogenic diabetes insipidus
Central: Post-hypophysectomy, Post-trauma, Idiopathic, Suprasellar tumor, Infiltration, eg. sarcoidosis, histiocytosis, Familial. Nephrogenic: Congenital, Acquired (interstitial disease, lithium), Hypercalcemia
Differentiate between central diabetes insipidus, nephrogenic diabetes insipidus and primary polydipsia
Water deprivation test. Central DI: Uosm remains low after 8h but ↑ with vasopressin. Nephrogenic DI: Uosm remains low after 8h and no increase with vasopressin. Primary polydipsia: Uosm ↑ after 8 h of dehydration (>800 mOsm/l, urine output < 30 cc/hour). Graph.
Identify the diagnostic tests that may aid in diagnosis of diabetes insipidus
Serum Na, Serum and urine osmolality, Blood urea nitrogen and creatinine, Calcium and glucose, Water deprivation test (need close supervision), ADH measurement (expensive, not required to make the diagnosis), MRI (after confirmation)
Tx of Central DI
Desmopressin (DDAVP, nasal, oral or SC), Chlorpropamide (partial DI)
List the diagnostic criteria of SIADH
Syndrome of inappropriate ADH. Water retention. Common in the elderly and patients on anticonvulsants. Euvolemic hyponatremia. Mild hyponatremia, asymptomatic. Severe or rapid onset hyponatremia, confusion, lethargy, weakness, seizure, coma
Identify the common causes of SIADH
Increase hypothalamic production of ADH. CNS infection; CNS neoplasm; CNS trauma; CNS vascular events (stroke, hemorrhage); Drugs (antidepressant, narcotics); Pulmonary disease (pneumonia, TB); Ectopic production of ADH (Carcinoma (lung, pancreas)); Potentiation of ADH effect: Psychosis, Drugs (oral hypoglycemic agent, carbamazepine)
Classification of SIADH
Type A, erratic, unregulated release of ADH (no relation to plasma osmolality). Type B, modest and constant leak of ADH. Type C, downward resetting of osmostat (sodium 125 - 135 mmol/L). Type D, urine is concentrated even if ADH release is suppressed
Identify the medications that may be involved in SIADH
Water restriction (800 to 1200 cc depending on degree of hyponatremia). Hypertonic saline if severe (done with caution, aggressive treatment can lead to central pontine myelinolysis). Demeclocycline or lithium in chronic cases. Vasopressin antagonist
Fn of oxytocin
Uterus: Parturition, Clamping ruptured blood vessels, Restoration of uterine size. Mammary glands: Milk let-down. Bonding Behavior: Maternalism, Orgasm
Regulation of oxyctocin
Increase oxytocin from distention of the cervix at term of pregnancy and by uterine contraction during parturition. Positive feedback to PVN and SON for further oxytocin release