Exam 1 Electrolytes Flashcards
hyperkalemia range
more than 5.0 mEq/L potassium
causes of hyperkalemia
Renal failure, kidneys job to get of excess k+
Decreased aldosterone
Prolonged acidosis, k leaks out of cells and goes into blood
Tissue injury, more k inside cell than out, will leak from cells in blood
Rapid rate of administration of K+
hypokalemia ranges
less than 3.5 mEq/L potassium
hypokalemia causes
Inadequate intake
Diuresis associated with certain diuretics (lasix and hydrochlorothiazide - potassium wasting)
Treatment of diabetic ketoacidosis with insulin → increased extracellular shift in which k goes fro blood into cell, causing there to be less k in the blood
Beta 2 adrenergic agonists → intracellular shift
Metabolic alkalosis → excessive loss
Effects of hypokalemia
alters neuromuscular function - muscle weakness, fatigue, paresthesia, cardiac arrhythmias, decreases ability of excistble cells to develop AP
hypernatremia range
more than 145 mEq/L
hypernatremia causes
Insufficicient ADH (raises urine output, blood is more concentrated)
Loss of thirst mechanism/inability to communicate
Water diahrea
Excessive aldosterone (increases sodium retention)
Impaired ability of kidney to conserve water
High osmotic tube feeding without sufficient water
Effects of hypernatremia
increased thirst, increased ADH secretion, dry skin and mucous membranes, decreased skin turgor, decreased salivation, difficulty swallowing, confusion
treatment of hypernatremia
treat underlying cause, fluid replacement if due to fluid loss
extracellular osmotic pressure rises, causes shrinkage of cells/dehydration of cells
Hyponatremia range
less than 135 mEq/L, osmotic pressure is going down, causing fluid to go into cell
hyponatremia causes
Excessive sweating
Diahrrea
Certain diuretics
Insufficient aldosterone (no aldosterone means no holding onto sodium)
Deceased renal function/failure (holding onto fluid)
Excessive ADH secretion (SIADH) holding on to too much water, diluting the sodium
Excessive water intake
Diluting baby formula (babies can’t make concentrated urine so cells will swell)
effects of hyponatremia
muscle cramps, fatigue and weakness, nausea and vomiting, decreased osmotic pressure (cell swelling), confusion, seizures, headache/lethargy (brains cells shrink)
Treatment of hyponatremia
depends on cause - limiting water intake, discontinuing meds, IV saline, hypertonic saline with diuretic
Hypercalcemia ranges
above 10.5 mg/dL of calcium
hypercalcemia causes
Hyperparathyroidism
Increased increased intake of vitamin D or excess dietary calcium
Malignant bone tumors (breaks down bones and spreads CA)
Bronchogenic tumors → secrete pth (also paraneoplastic syndrome)
Demineralization of bone due to immobility or bone tumors
Acidosis (more h+ binding to neg charged oxygen, meaning clacium can’t bind to it
hypercalcemia effects
hyporeflexia: depressed neuromuscular activity, Loss of muscle tone, Polyuria (too much urine) due to decreased function of ADH in kidneys, Cardiac contraction increases in strength (more ca moving into heart cells), Bone pain, Renal stones (metastatic calcification)
Hypocalcemia range
below 8.5 mg/dL ca
hypocalcemia causes
Hypoparathyroidism (low pth)
Malabsorption
Vitamin d deficit/resistance
Elevated serum phosphate (phosphate has three neg charges, ca can bind to it, ionozied calcium goes down)
Increased serum pH (alkalosis): increased binding of calcium to protein
Renal failure (results in high phosphate, high phosphate = low calcium)
Increased urinary loss
hypocalcemia effects
increaesd excistability of nerve and muscle cells, hyperactive reflexes, weak heart contractions (less ca going into heart cells), cardiac arrhythmias, bp drops. Trousseau sign (carpopedal spasm) Chvostek sign (tap on facial nerve and see corner of mouth twitch)
Hypophosphatemia ranges
low phosphorus below 2.5 mg/dL
Hypophosphatemia causes
Malabsorption
Excessive use of antacids (phosphate binds to antacid)
Hyperparathyroidism (pth increases calcium and decreases phosphate)
Prolonged hyperventilation (intracellular shift to decrease phosphate
Refeeding syndrome (severely malnourished patient means low ATP, adenosine triphosphate. Refeeding them will cause the body to use the phosphate to make ATP and therefore lower phosphate)
Hypophosphatemia effects
blood cells function less efffectively, increased bleeding, impaired neurological function (tremors, confusion, parasthesias, dysphagia, anorxia, hyporeflexia
Hyperphosphatermia range
high phosphorus above 4.5
Hyperphosphatermia causes and symptoms
Results from renal failure
s/s same as hypo
Calcium is gonna bond to phosphate making the same symptoms of low calcium (high phosphate low calcium)
Hypomagnesemia
low mg
Hypomagnesemia causes
Limited intake and excessive loss (intestinal or renal)
Malnutrition
Starvation
Prolonged nasogastric suctioning
Decreased absorption
Diahrrea
diabetic ketoacidosis → increased renal loss
Hyperparathyroidism → increased renal loss
Loop diuretics → increased renal loss
Insulin → shifts Mg into cells
Hypermagnesia
high mg
Hypermagnesia causes
Renal insufficiency / kidney failure
Magnesium containing medications including laxatives, antacids
Hypervolemia
Excess fluid (isotonic)
Increased in interstitial and vascular volumes
Proportional increase socium and water
hypervolemia causes
increased consumption of sodium first followed by increased water, decreased excretion of sodium and water
Renal failure
Heart failure
Liver failure
Corticosteroid hormone excess
effects of hypervolemia
weight gain, edema, distended neck veins, bound pulse, increased BP, decreased hematocrit
results in circulatory overload
hypervolemia treatment
sodium restriction, diuretics
Potassium wasting diuretics (lose k)
Lasix and hydrochlorothiazide
Potassium sparing diuretics
Osmotic diuretics (IV)
hypovolemia
When output is greater than intake
Isotonic fluid volume deficit (causes: diahrrea, vomiting, excessive sweating, excessive urine loss → osmotic duresis or diuretic therapy, GI suction)
hypovolemia effects
increased thirst, wek pulse, increased heart rate, decreased BP (postural hypotension), constriction of cutaneous blood vessels, decreased urine output → concentrated urine, increased specific gravity (ADH), decreased skin turgor, increased hematocrit, dry mucous membranes, depressed fontanels in infants, sunken eyes
hypovolemia treatment
fluid replacement and physiological saline 0.9%
Compensatory mechanism hypovolemia
ADH increases
Renin angiotensin increases
Sympathetic increases
Aldosterone increases
ANP decreases
