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33 Cards in this Set

  • Front
  • Back
hyperosmolal state - 2 types
hyperglycemia
hypernatremia
hyperglycemia
occurs in patients with DM
loss of water from cells
loss of total body water - glycouria
hypernatremia
high level of Na
hypoosmolal state
*to much H2O in cells
hyponatremia (low Na)
water deficit - description
decrease volume of ECF & ICF
increase solute concentration
ADH released causing some water conservation
water deficit - etiologies
reduced intake
unusual losses (GI, diuretics, kidney disorders)
water excess - description
expansion of ECF & ICF
decrease solute concentration
reduced ADH
water excess - etiologies
decreased excretion of water
excessive renal Na & water retention
SIADH
sodium homeostasis
predominant ECF cation
est osmotic pressure relationship
hypernatremia
deficit of water rel to Na
-water loss thats not replaced
-water loss exceding Na loss (fever, burns,diahrrea)
-high NaCl ingestion
hypervolemic hyponatremia
excess body water relative to Na
decr blood volume w/ decr renal perfusion
caused by CHF, cirrhosis, nephrosis
hypovolemic hyponatremia
total body depletion of Na caused by excessive use of diuretics, chronic renal disease, mineralocorticoid deficiency
mineralocorticoid
a class of steroids characterised by their similarity to aldosterone and their influence on salt and water metabolism
euvolemic hyponatremia
normal ECF volume commonly caused by SIADH
potassium homeostasis
body stores - 45-55mEq/kg
major IC cation
involved in muscle contration, nerve impulse,enzymes,& cell membranes
hyperkalemia
diminished excretion
increased K+ supply
endocrine diseases
metabolic acidosis
cell lysis
drugs that cause hyperkalemia
K-Dur, NSAIDs
hypokalemia
poor intake
reduced absorption
increased loss (GI, renal, skin)
licorise abuse
drugs that cause hypokalemia
corticosteroids
amphotericin B
calcium homeostasis
present in ECF
complexed to bicarb,protein bound, or ionized
effect on cell membrane potential/permeability, muscle contraction
parathyroid hormone
released in response to low ionized Ca
incr absorption from intestine & renal
calcitonin
opposes PTH
from C cells of thyroid
released in response to high Ca level
inhibits osteoclasts (breaks down bones)
hypercalcemia - etiologies
incr intake or absorption
endocrine disease
neoplastic disorder (cancer)
drugs that cause hypercalcemia
tums
lithium
hypocalcemia - etiologies
decr intake or absorption
incr loss (vomiting, diahrrea)
endocrine disease
endocrine
glands that secrete hormones into the bloodstream
drugs that cause hypocalcemia
glucocordicoids
loop diuretics
magnesium homeostasis
2/3 free cation
excreted via kidney
involved with enzymes that transfer phosphates
alteration in Mg usually provokes alteration in Ca
hypermagnesemia -etiologies
renal insufficiency
hypomagnesemia - etiologies
diminished absorption or intake
increased loss
usually seen in alcoholics
phosphorus homeostasis
80% in bones
integral in eneergy transfer & metabolism
urinary buffer
hypophospatemia - etiologies
incr renal exrcretion
catabolic states / tissue destruction
IC shifting
hyperphosphatemia - etiologies
decr renal excretion
shift from IC to EC
incr intake of vit D or phosphate
laundry detergent ingestion