Lect 7 Flashcards
What causes diabetes insipidus
ADH is very low or ineffective
diabetes insipidus effect on plasma osmolality, urine osmolarity
-
plasma osmolality is high
- polydipsia: excessive thirst due to hyperosmotic plasma
-
urine osmolality is low
- polyuria (large volume of dilute urine)
explain neurogenic (central) diabetes insipidus
- plasma ADH is low due to hypothalamic-pituitary injury
- patient cannot secrete sufficient amounts of ADH
treatment of neurogenic (central) diabetes insipidus
will respond to exogenous ADH agonists (desmopressin)
explain nephrogenic diabetes insipidus
- renal is origin- kidney is unable to respond to ADH
- several causes
- defect in V2 receptor
- lithium toxicity
- hypercalcemia
- plasma ADH is high since pituitary is functioning normally
what is SIADH? what is caused by
syndrome of inappropriate ADH secretion
- head injury and some lung tumors can cause excessive amounts of ADH to be secreted
SIADH has what effect on sodium concentration? ECF volume? ICF volume
**excess free water retained -> hyposmotic volume expansion
- hyponatremia
- excess renal sodium loss
- expanded ECF volume
- hypervolemia -> low aldosterone
- dilution and expansion of the ISF
Na+ is the major cation of the ECF, it determines the volume of the ECF compartment. Therefore, Na+ loss is often what?
- isotonic : diarrhea, vomiting
- changes in Na+ concentration of ECF is generally caused by changes in body water content rather than changes in Na+ content
list the common causes of hyponatremia
- blood volume depletion
- high ADH
- thirst
- excessive free water conservation (SIADH)
- excessive water intake
what are common causes of hypernatremia? will these produce persistent hypernatremia in normal subjects?
- loss of water (Dehydration, diabetes insipidus)
- gain of sodium
- excess Na+ causes thirst; drinking water will quickly dilute the plasma sodium to normal
decreased sodium intake has what effect on sympathetic activity, ANP, renin-angiotensin-aldosterone?
- increased sympathetic activity -> constriction of afferent arterioles, increases Na+ reabsorption (proximal tubule)
- decreased ANP -> dilation of efferent arteriole, increases Na+ reabsorption (collecting ducts)
- increased RAAS -> increase Na+ reabsorption (proximal tubule and CD)
how is inherent pacemaker acitivity of kidney stimulated?
- renal calyxes and pelvis posses smooth muscle
- as urine collects, smooth muscle is stretched and pacemaker activity is stimulated
- peristaltic contraction forces urine into bladder
urge to void felt at what bladder volume? maximum bladder volume?
- 150 ml
- 500 ml
function of sympathetic fibers on detrusor muscle and internal sphincter (what receptors)
- relaxation of detrusor muscle during filling (inhibits contraction) (B2)
- contraction of internal sphincter during filling (a1)
- *dominates during bladder filling
function of parasympathetic fibers on detrusor muscle and internal sphincter? name receptors
- PNS causes detrusor to contract (M)
- relaxation of internal sphincter (M)
- *dominates during bladder emptying
