The Posterior Pituitary: Dagogo-Jack Flashcards
Understand factors controlling the release of arginine vasopressin (AVP)/ADH
The release of AVP is influenced by:
1- Osmoregulation- primarily (receptors found in hypothalamus) incr. osmol. –> increased AVP
2- Volume regulation- volume decr–> AVP secretion
3- Baroreceptors- carotid and aortic baros sense v in pressure –> AVP secretion
4- Neuronal- Both cholinergic and beta adrenergic stimuli cause release of AVP. Also, stress, n/v, pain.
5- Aging. ^ age –> rising plasma osm –> ^ AVP
6- Pharm- EtOH inhibits. Nicotine ^ release of AVP
7- water deprivation
8- Effects of glucocorticoids- Cortisol has an antagonistic effect on AVP. Increases osm threshold for AVP release and also cause more excretion of solute free water in urine.
Know major causes of AVP/ADH deficiency (diabetes insipidus)
Familial
Acquired
::idiopathic 30% associated with Abs against AVP neurons
::Tumor
::Head Trauma- tubercullum sellae bisects stalk
::Granulomatous dz involving hypothalamic-pit area
::CNS infections
::Cerebrovascular disorders
Understand pathophysiology of polyuria and its clinical investigation.
Pathophysiology:
1) insufficiently osmoregulated AVP (neurogenic DI)
2) complete or partial renal resistance to antidiuretic action of AVP (nephrogenic DI)
3) Habitual fluid drinking or primary polydypsia
Investigation:
Dx rests on the results of endocrine investigations. Polyuria is >2.5L urine/24hrs
Severe neurogenic DI plasma osmo is high normal, urine is low (295mOsm/kg), while urine osm remains low. Admin of AVP returns urine osm to over 750mOsm/kg.
Plasma AVP will not change with admin of hypertonic saline IV.
Nephrogenic pts will not respond to admin of AVP. Hypertonic saline IV will increase their plasma AVP.
Primary polydypsia pts will have low plasma and urine osm.
Water deprivation yields increased urine osm and serum osm maintained in normal range. Pts respond to hypertonic saline IV by incr. AVP secretion.
Know major causes and pathophysiology of the syndrome of inappropriate secretion of ADH (SIADH).
Causes:
1) Malignant tumors with autonomous AVP release eg. small cell lung cancer (80% of malignancy SIADH)
2) Nonmalignant pulmonary dz eg. TB, PNA
::nontumerous mass either acquires ability to secrete ADH or reduces left atrial filling v CO, v BP, ^ ADH secretion.
3) CNS disorders eg. meningitis
4) Drugs eg. narcotics
Understand how to Dx SIADH
SIADH should be suspected in any pt w/ hyponatremia and hypertonic urine relative to the plasma.
Need to exclude:
1) hypovolemic or depletional hyponatremia, esp due to adrenal insufficiency, salt-losing nephropathy, diarrhea, and prev. antidiuretic tx.
2) hypervolemic hyponatremia associated with edematous states (congestive heart failure, cirrhosis, nephrotic syndrome)
3) pseudohyponatremia (associated with severe hyperlipidemia, hyperproteinemia, or severe hyperglycemia) as seen in debilitating dz.
:: osmoreceptors reset at a subnormal level. Thus, AVP is released at plasma osm below normal threshold –> SIADH
Know major actions of oxytocin and factors responsible for its release.
Cardinal actions:
stimulation of uterine contractions at parturition and augmentation of intramammary pressure during suckling by action on myoepithelial cells surrounding milk glands.
Factors responsible for release:
Mechanical distension of the female repro tract (vagina) and suckling on nipples. Both acting through neural pathways to effect oxytocin release from posterior pituitary.
Also, osmotic/hemodynamic factors similar to those responsible for the release of ADH. This is b/c at high concentrations, oxytocin has similar effects on vascular constriction and water retention as ADH due to their similar structures.
Define diabetes insipidus.
Failure to concentrate urine as a result of decreased secretion of osmoregulated AVP. Always peeing, always drinking. Majority of cases are acquired, but can be familial.
