Fluid and Electrolyte imbalances Flashcards
causes of extracellular edema
- increased capillary hydrostatic pressure
- decreased plasma proteins
- increased capillary permeability
- blockage of lymph return
factors that can increase capillary hydrostatic pressure
- excess kidney retention of salt and water (acute/chronic KI, mineralocorticoid excess)
- high venous pressure ( HF, venous obstruction, failure of venous pumps)
- decreased arteriolar resistance (excessive body heat, insufficiency of SNS, vasodilator drugs)
factors that can decrease plasma protein concentration
loss of protein in urine (nephrotic syndrome)
loss of proteins from denuded skin areas (burns/wounds)
failure to produce . proteins (such as in liver dz or severe protein or caloric malnutrition)
factors that can increase capillary permeability
immune rxns that cause release of histamine toxins bacterial infections vit deficiency (esp. c) prolonged ischemia burns
factors that can block lymph return
cancer
infections (filarial, nematodes )
surgery
congenital absence or abnormality of lymphatic vessels
factors working to prevent extracellular edema from occurring
interstitium normally has a low compliance
lymph flow has a capacitance to increase 10-50 fold
increased amounts of protein-poor capillary fluid flow wash proteins out from the interstitial space, thereby decreasing net capillary filtration pressure
causes of intracellular edema
- depression of metabolic systems of tissue
- lack of adequate nutrition to the cells
cells lack the resources to drive the NA/K ATPase so na accumulates in cells and they expand (water follows Na into cells) - too little extracellular Na
- too much water
increased RBF and GFR leads to
increased delivery of oslute to JG apparatus (senseed by macula densa )
increased resistance of afferent arterioles
decreased RBF, GFR
ECV sensors
low pressure . - cardiac atria and pulmonary vasculature
high pressure - carotid sinus, aortic arch, JG apparatus of kidney
regulatory hormones of the proximal tubule
angiotensin II, noreepinephrine and epinephrine
regulatory hormones of hte late distal tubuel and collecting ducts
aldosterone, atrial natriuretic peptide
increased Na intake leads to \_\_\_\_ ECF AND EABV \_\_\_\_ sympathetics \_\_\_\_\_ ANP \_\_\_\_\_\_ PIc \_\_\_\_\_\_ RAAS
increased ECF volume and increased effective arterial blood volume decreasing sympathetic (dilaiton of afferent arterioles, decreased na reabsorption in PT), increasing ANP (constricting efferent arterioles, decreased Na reabsorption) decreaseing PIc, decreased RAAS
clinical signs of hypovolemia
decreased skin turgor 9tenting) thirst dry mucous membranes sunken eyes oliguria progressing to tachycardia, hypotension, tachypnea, confusion
clinical signs of hypervolemia
weight gain
edema
bounding pulse
causes of absolute hypovolemia
extra-renal - bleeding, GI fluid loss, skin fluid loss, respiratory fluid loss, extracorproreal ultrafiltration
renal - diuretics, na wasting tubulopathies, genetic or acquired tubulointerstitial disease, obstructive uropathy/postobstructive diuresis, hormone deficiency, hypoaldosteronism adrenal insufficiency
causes of relative hypovolemia
extrarenal - edmatous states, HF, cirrhosis, anaphylaxis, drugs, spesis, pregnancy, third space loss
renal - severe nephrotic syndrome
causes of volume excess
primary renal na retention (increased effective circulating volume) d/t - oliguric acute renal failure acute glomerulonephritis sevrere chronic renal failure nephritic, nephrotic syndrome primary hyperaldsoteronism cushing syndrome early stages of severe liver dz conn syndrome gorndon syndrome liddle syndrome secondary renal Na retention (decreased ECV) HF, later stages of severe liver dz, nephrotic syn drome, pregnancy
hyper/hyponatremia is a problem with
WATER
hypo <135
hyper >145
normal plasma osmolality value
285-295
quick estimate = 2x [Na]
vasopressin is more responsive to changes in blood pressure or plasma osmolality
plasma osmolality
