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SIADH and Diabetes Insipidus


POSTERIOR PITUITARY
axons originate from nerve cell bodies in hypothalamus
stalk = "infundibulum"
no vascular connection to hypoathalamus
adjacent to anterior pituitary which has no neuronal connection to hypothal
axons of post pit are storage site for two peptide hormones synthesized by hypothalamus:
ADH regulates water balance
oxytocin regulates lactation and uterine contraction

ADH = ANTI-DIURETIC HORMONE AKA VASOPRESSIN
*created tag: vasopressin
main regulator of body fluid osmolarity
ADH concentrates urine, decreases urine volume, builds blood volume
ADH low in central DI, high in nephrogenic, and normal or low in psychogenic

ADH MOA
increases permeability of renal collecting duct-->more H20 resorbed-->less urine
secretion regulated by hypothalamic osmoreceptors which sense concentration of blood (plasma osmolarity)
blood too thick-->stimulate vasopressin secretion and thirst
ADH also secreted in response to cholecystokinin from small intestine (mediated by ? unknown)
not enough blood volume-->baroreceptors in carotids, atria, veins-->renal angiotensin 2 from kidneys
just right osmolarity and vascular volume-->atria release atrial natriuretic peptide (ANP)
ANP-->negative feedback inhibits further release of angiogtensin II and ADH

*nausea stimulates release of ADH
*use BNP (ANP?) to discriminate between CHF and pneumonia: BNP increased in CHF, not in pneumonia
*coffee and alcohol interfere with ADH receptor, decreasing response and increasing urine output

SIADH
syndrome of "inappropriate" antidiuretic hormone (too much ADH, should be "indiscriminate")
ETIO: usudt trauma incl CNS infx, MVA, Sheehan's syndrome
ETIO: functional CA of lung(small cell/oat), prostate, breast)
ETIO: persistent nausea
SX: low serum osmolality, concentrated urine, hyponatremia (or normal Na early)
SX of hyponatremia: n/v, headache, malaise, disorientation/confusion, decr DTRs, convulsions, stupor, coma
DX: must rule out adrenal and renal dysfx
DDX: low serum osmolality mbdt too much water or not enough sodium dt other causes
DDX: low Na+ mbdt Addisons<--sudden d/c of prednisone
DDX: barbiturates and narcotic analgesics may stimulate or potentiate effects of ADH
COMPLIC: very low Na+-->seizures, coma (low Na+ can stim thirst-->even lower Na)
TX: deal with cause: injury or tumor
TX: water restriction (1.0-1.5L/day) to prevent fatally low Na
TX: if water restriction fails, drugs ie: demeclocycline which blunts renal response to ADH
TX: IV saline 3%, very gradual or risk complication
COMPLIC: too fast incr in Na+-->central pontine myelinolysis or heart failure


DIABETES INSIPIDUS
not enough ADH (central/neurogenic) or renal resistance to ADH (nephrogenic
or psychogenic polydipsia
SX: polyuria (>2500ml/day), polydipsia (mb>10L/d, tends to want COLD water or ice)
SX: dehydration (not retaining fluids)
LAB: very dilute urine, serum osmolality mb normal or high (incr Na, gluc, urea)

CENTRAL DI
ETIO 1 CENTRAL: mc is trauma: trauma to pit stalk, hypothalamic or pit surgery, radiation, tumor, CNS infx
ETIO 1: Sheehan's (ischemia of pit), CNS granulomatous dz (TB, sarc), CNS AI dz
DX CENTRAL: test other pit hormones, MRI to see if prolactinoma, other tumor
LABS: ADH low
DX: water restriction-->no change in urine osmolarity
DX: give synthetic ADH-->incr urine osmolarity
TX: synthetic ADH via nasal spray

NEPHROGENIC DI
ETIO 2 NEPRHOGENIC: chronic renal dz destroys medullary architecture, also pyelonephritis
no function renal tissue, or no receptors?
ETIO 2: sickle cell dz, hereditary dz affecting receptors, and lithium
LITHIUM: mc drug assoc w/ iatrogenic DI, cofactor for neurotransmitters, poisons receptors sites
pt may or may not recover after drug is removed
(what dose is dangerous?)
LABS: ADH high
DX: water restriction-->no change in urine osmolarity
DX: give synthetic ADH-->no change in urine
CONVENTIONAL TX: thiazide diuretic-->incr diuresis but also feedback causes the rest of nephron to conserve
TX: free access to plenty of water

PSYCHOGENIC DI
ETIO 3: psychogenic water intoxication, binging dt psych or other factors
may have no detectable psych disorder
may be schizoid
IMAGE: MRI may reveal enlarged ventricles, shrunken cortex
LABS: ADH mb low (dt flushing) or normal
DX: water restriction in highly controlled environment (they might drink from toilet)-->incr serum osmolarity
DX: give synthetic ADH-->increase in urine osmlarity
TX: a cage with a water dropper (joke)

*synthetic ADH also given to pts with von Willebrands dz prior to surgery to improve clotting fx

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