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Potassium normal concentration 3.5-5 meq/L, must be maintained within its normal range or else serious complications
hypokalemia K <3.5 meq/L, caused by diuretics, vomiting, NG suctioning,diarrhea,liver failure, alkalosis, decreased intake and increased output, steroids, and B-agonist drugs
signs and symptoms of hypokalemia muscle weakness and cramps, fatigue, confusion, cardia arrhythmias, and metabolic alkalosis
hyperkalemia causes: too rapid IV administration of K+, anything that inhibits K+ excretion (renal failure)
signs and symptoms of hyperkalemia metabolic acidosis, muscle weakness, cardiac arrhythmias,nausea/vomit
treatment of hyperkalemia diuretics, IV glucose and insulin (increased K+ uptake by cells, CaCl or Ca+
Calcium 50% of Ca in blood is bound to protein and is affected by blood pH( increased PH=more Ca binds to protein)
hypocalcemia causes: renal failure, vitamin D deficiency, hyperthyroidism, dificiency in magnesium
signs and symptoms of hypocalcemia muscle craps and weakness, tetany, arrhythmias
function of Ca+ initiates muscular contraction, maintains neuromuscular irritability, normal blood coagulation, and maintains integrity of bones, Ca present in equal amounts ionized and nonionized
Treatment of hypocalcemia treat underlying cause, vitamin D
Hypercalcemia causes: renal failure, some malignancies, hyperthyroidism
signs and symptoms of hypercalcemia arrhytmias, neuromuscular weakness/fatigue, nausea/ vomiting
treatment of hypercalcemia treat underlying problem, diuretics, administer phosphate
magnesium predominately found intracellulary
hypomagnesium causes: renal failure, decrease in dietary intake, GI disturbances, alcoholism
signs and symptoms of hypomagnesium muscle craps, weakness, tetany, nausea/vomiting, arrhythmias
hypermagnosemia causes causes: renal failure, diabetes mellitis, adrenal insufficiency, and high magnesium diet+
hypermagnosemia signs and symptoms muscle weakness, cramps, arrhythmias
treatment of hypermagnosemia diuretics, dialysis if caused by renal failure
sodium regulation via NaCL mechanism sodium to maintain neutrality is accompanied by active transport with CL from the glomerular filtrate and into the renal tubular cell, both Na+ and Cl- are transported to the ECF and ultimately to the plasma (blood)
Sodium regulation via NaHCO3 mechanism 1) recaptures Na+2)HCO3 are reabsorbed(100% of HCO3 in tubules reabsorbed)
3 things that will increase the HCO3 production/reabsorption 1. increase in PCO2 (stimulates renal compensation)2.decrease in blood volume (renin-angiotensin system)3. decrease in K+ concentration in blood
Angiotensin II causes: systemic vasoconstriction which increases BP
Angiotensin II stimulates the production of: Aldosterone
Aldosterone stimulates NaHCO3 reabsorption because water reabsorption follows Na+ reabsorption, blood volume increases and improves perfusion to the kidneys
hyperaldosterone can result in metabolic acidosis and hypokalemia
Diaretics can interfere with either___________or___________reabsorption NaCl, or NaHCO3
Urinary buffers 2 main functions 1. excrete daily acid load( esp. fixed acids)2. regenerate bicarb that's lost during extracellular buffering
3 main urinary buffers 1.amonia2.phosphate3.HCO3
amonia works by: combining with H+ ions to form NH3 which minimizes the fall in pH
phosphate enhances excretion of H+
anion gap used with metabolic acidosishelps diagnosing causes of met.acidosis
high anion gap= increased amount of fixed acids
MUDPILERS methanol,uremia,diabetes/diabetic ketoacidosis,propylene glycol, Inhaled drugs used to treat TB, lactic acidosis, etholyene glycol, Renal failure, salicylates
Created by: qccrespiratory