Na Homeostasis and Edema Flashcards
how are ICF and ECF maintained
ECF by total body Na, ICF by Na concentration
when is edema clinically apparent
2.5-3 L
role of cellular Na/K ATPase
3 Na out, 2 K in- high ECF Na and high ICF K
outline the response to ingestion of Na+
increased ECF tonicity causes water to flow out of ICF, thirst, and ADH release
water ingestion and retention (ADH) return tonicity to baseline, water moves back to cells
outline response to isosmotic water retention
ECF expands, renal excretion of salt and isosmotic volume, ECF back down
outline response to intake of free water
absorption, retention of water causes decrease in plasma Na and tonicity
2/3 enters ICF, 1/3 ECF
ADH suppressed, water reuptake blocked, water diuresis occurs to restore baseline
2 steps required for edema
alteration in capillary hydrostatic/oncotic pressure (or capillary permeability) and retention of dietary Na and water by kidneys
cap pressure changes alone are not enough, the plasma would run out of volume and hypoperfuse
fluid expansion perceived in SIADH? w/ water retention alone?
no, 2/3 of the water would move into ICF and not cause edema, to get enough water retention to have high ECF would make you very hyponatremic
list some causes of increased hydrostatic pressure
CHF, cirrhosis, nephrosis would cause increased retention of Na and water
venous HTN (right heart failure) would also cause this
decreased oncotic pressure causes
low albumin- nephrotic syndrome, cirrhosis
increased cap permeability causes
sepsis, toxins, anaphylaxis, inflammation
lypmhatics role in edema
normally are able to clear the interstitial fluid (usually there is net filtration), w/o this clearance edema can form
lymphedema
edema formation in nephrotic syndrome
arterial underfilling w/ loss of albumin stimulates RAAS and ADH, also a primary increase in renal Na
