Physiology Review III Flashcards
bicarb buffering system
CO2 > H+ and HCO3-
acidosis
pH < 7.35
alkalosis
pH > 7.45
normal pH, HCO3, and PCO2
pH - 7.4
HCO3 - 24
PCO2 - 40
respiratory acidosis
too much CO2 - reaction to right
-increased bicarb
1: 0.1 ratio of CO2 increase to HCO3 increase
- acute uncompensated
metabolic acidosis
decreased bicarb
respiratory alkalosis
reduced CO2 - reaction to left
-decreased bicarb
1: 0.2 ration CO2 decreased to HCO3 decreased
- acute uncompensated
metabolic alkalosis
increased bicarb
compensated respiratory acidosis
kidney - days to complete - increased bicarb
1:0.35 CO2 increase to HCO3 increase
compensated metabolic acidosis
respiratory - rapid
winters equation - is resp compensating?
predicted PaCO2 = (1.5 x HCO3) + 8
should be +/- 2 of predicted value
-if so - compensation has occured
compensated respiratory alkalosis
1:0.5 ratio of CO2 decrease to HCO3 decrease
compensated metabolic alkalosis
decreased ventilation
equation to determine if compensation has occured:
predicted PaCO2 = (0.7 x rise in HCO3) + 40
within +/- 2 of predicted value - compensation occured
CO2 and bicarb in opposite direction
likely combined disturbance
plasma anion gap
PAG = Na - (Cl + HCO3)
to determine cause of metabolic acidosis
elevated anion gap acidosis
MUDPILES methanol uremia diabetic ketoacidosis paraldehyde iron lactic acidosis ethylene glycol salicylates
non-elevated anion gap acidosis
HARDUP hyperchloremic acetazolamide renal tubular acidosis diarrhea ureteral diversion pancreas fistula
respiratory vs. metabolic?
respiratory - H and HCO3 both increase/decrease
metabolic - H and HCO3 go opposite
hormones of posterior pituitary
ADH and oxytocin
-released from distal neuron terminals
ADH synthesis
in supraptic and paraventricular nuclei of hypothalamus
-released from posterior pituitary
ADH action
renal collecting duct - V2 receptors
- increased aquaporin channels
- more water reabsorption
- increases urea reabsorption
severe hemorrhage - on V1 receptors of vascular smooth m result in vasoconstriction
inhibition of ADH release
stretch receptors send constant (-) signals
normal osmolality
kept around 285
weightlessness
shift of blood centrally
-increases stretch receptor ADH inhibition
alcohol and ADH
inhibits ADH
ANP
atrial natriuretic peptide
- secreted by heart
- right atrium
- released with stretch, salt intake, CHF, fluid overload
increases sodium and water loss
natriuresis
sodium loss
diuresis
water loss
ANP action
dilates afferent arteriole
constriction efferent arteriole
increased GFR
also, inhibits aldosterone and CD reabsorption of water and Na
central diabetes insipidus
not enough ADH to affect renal CDs
nephrogenic diabetes insipidus
inability of kidney to respond to ADH
-with lithium
SIADH
syndrome of inappropriate ADH
-excessive secretion of ADH
- increase water retention
- volume expansion > increased renin > hyponatremia