Electrolyte Balance/Imbalance Flashcards by Francesca Polino

sodium

floats around the cell-major cation in ECF
-largely responsible for osmotic pressure
-combines with chloride (NaCl)
-normal levels=135-145 mEq/L
-followed by water

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sodium regulation

dietary intake, ADH&aldosterone, excretion

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hyponatremia

sodium<135 mEq/L
-water comes out of ECF into cells

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hypernatremia

sodium>145 mEq/L
-water comes out of the cells into the ECF

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hyponatremia causes

excessive Na+ loss
-in the kidneys, excess diuretics, GI tract, skin
excessive H20 intake
-polydipsia, tap water enema, NG irrigation
excessive hypotonic IV fluid
SIADH

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hyponatremia manifestations

cellular swelling-brain cells
-lethargy, confusion, nausea, coma
-similar to hypochloremia
-same as hyperkalemia

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syndrome of inappropriate antidiuretic hormone (SIADH)

excess release of ADH hormone
-release, inhibition of ADH fails
-dilutes blood and Na+ concentration
-low serum osmolarity, high urine osmolarity
-causes hyponatremia

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hypernatremia causes

excessive Na+ intake
-too much hypertonic solutions
excessive H20 loss
-GI loss
-hypertonic tube feedings
-DI
-hyperventilation
-near-drownings in salt water
decreased H20 intake
-NPO status, loss of thirst
diabetes mellitus

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hypernatremia manifestations

cellular shrinking-brain cells
-confusion, lethargy, coma, seizures
decreased vascular volume
-tachycardia, weak pulse, decreased BP
-similar to hyperchloremia
-same as hypokalemia

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diabetes insipidus (DI)

deficiency or decreased response to ADH
-central DI: defect in release of ADH in posterior pituitary
-nephrogenic DI: kidneys don’t respond (shut off) to ADH
manifestations
-increased serum osmolarity, polyuria, excessive thirst

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hyponatremia treatment

restrict fluid intake (further dilution), hypertonic solution 3% NaCl slowly

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hypernatremia treatment

hypotonic solution 0.3% NaCl slowly, vasopressin for DI

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potassium

inside of the cell-major cation inside cells
-normal: 3.5-5.0 mEq/L
-responsible for resting membrane potential (repolarization)
-makes carbs into energy
-changes glucose to glycogen
-builds amino acids to proteins

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potassium regulation

dietary intake, excretion
-kidneys-reabsorbed in proximal tubules>competes with H+ in distal tubule for reabsorption
-corticoids (aldosterone) make kidneys retain Na+ and excrete K+

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hypokalemia

potassium<3.5 mEq/L

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hyperkalemia

potassium>5.0 mEq/L

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hypokalemia causes

decreased intake
-NPO, anorexia
excessive loss
-diuretics, high aldosterone, GI loss, NG suctioning
shifts into body cells
-alkalosis, glucose/insulin transfusion

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hypokalemia manifestations

negative resting membrane potential, hyperpolarized, far from threshold, harder to make action potentials
-muscle weakness, cramps, paralytic ileus, polyuria, polydypsia, cardiac dysrhythmia
-flat T-wave, long PR interval, large U-wave
-same as hypernatremia

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hypokalemia treatment

replacement therapy-PO or IV, high potassium foods

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hyperkalemia cause

decreased excretion
-low aldosterone levels
-renal failure
shifts from body cells
-crushing injuries, acidosis, chemotherapy, burns
increased intake
-IV bolus, salt substitutes
insulin deficiency

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hyperkalemia manifestations

hyperpolerization, prolongs depolarization, closer to threshold
-eventually leads to stopped action potentials
-cardiac arrest, dysrhythmias
-muscle weakness, cramping
-paralysis
-peaked T-wave, wide QRS complex
-same as hyponatremia

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hyperkalemia treatment

reduce K+ intake, stop K+ diuretics, 50% glucose insulin IV, kayexalate PO

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chloride

normal: 95-105 mEq/L
-major anion of ECF
-maintains acid-base balance
-acidity of gastric solutions
-stops action potentials when in cell
-HCL

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chloride regulation

diet, excretion
-kidneys-acid-base balance

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hypochloremia

chloride<95 mEq/L

hyperchloremia

chloride>105 mEq/L

hypochloremia causes

excessive vomiting, GI suctioning

hypochloremia manifestations

metabolic alkalosis -kidneys retain bicarbonate -hypertonicity of muscles -decreased respiration (body holds onto CO2) -tetanus-not enough to stop APs -similar to hyponatremia

hyperchloremia causes

excessive injestion, decreased excretion

hyperchloremia manifestations

metabolic acidosis -deep, rapid breathing (body tries to get rid of CO2) -weakness-from non-stop AP -coma -unconsciousness/stupor -similar to hypernatremia

hyperchloremia treatment

treat metabolic acidosis, sodium bicarbonate IV, LR solution IV

hypochloremia treatment

replacement therapy

calcium, phosphorus, magnesium balance

major in the body -Vit D keeps normal levels of Ca2+, PO by increasing absorption from intestine -calcitonin makes kidneys/bone remove calcium from ECF -PTH regulation

3 forms of ECF calcium

protein bound, complexed, ionized

calcium

essential cation for life -widely distributed in body -normal: 8.5-10.5 mg/dL -neuromuscular function, nerve impulses, muscle contraction -allows Na+ to go in cell, K+ out -blood clotting -bone/teeth strength -maintains normal cell permeability -inverse relationship with PO

calcium regulation

diet -Vit D PTH -absorption, excretion calcitonin -opposes bones -works inversely with PO

hypercalcemia

calcium>10.5 mg/dL

hypocalcemia

calcium<8.5 mg/dL

PTH regulation with calcium

releases when Ca2+ levels are low -pulls Ca2+ out of bone and into blood -makes kidneys get rid of PO, reabsorb Ca2+ -increases Vit D in intestine for reabsorption

hypocalcemia causes

hypoparathyroidism decreased intake/absorption -malabsorption, Vit D deficiency increased excretion -renal insufficiency, hyperphosphatemia shifts out of blood -blood transfusions

hypocalcemia manifestations

hyperactivity of muscle since K+ can't leave cell -muscle cramping, twitching, tetany - +Chvostek, +Trousseau -soft bones, teeth

hypercalcemia causes

increased intake -excessive antacids, Vit D shift from cells -hyperparathyroidism -immobility

hypercalcemia manifestations

decreased muscle excitability -constipation, GI issues -decreased reflexes, muscle weakness CNS depression -lethargy -coma kidney stones

hypocalcemia treatment

oral replacement, Vit D supplements, IV calcium

hypercalcemia treatment

IV diuretics

phosphorus

major intracellular anion -normal: 2.5-4.5 mg/dL -essential part of bone -carbs, lipids, protein metabolism component of ATP and 2,3 DPG -controls O2 in RBC major buffer in acid-base balance inverse relationship with Ca2+

phosphorus regulation

diet (usually proteins) excretion -kidneys, PTH secretion

hypophosphatemia

phosphorus<2.5 mg/dL

hyperphosphatemia

phosphorus>4.5 mg/dL

hypophosphatemia causes

alcoholism, refeeding after starvation, high glucose solutions, excessive antacids, hyperparathyroidism

hypophosphatemia manifestations

same as hypercalcemia -cell energy failure

hyperphosphatemia causes

renal failure, CaPO4 salt accumulation

hyperphosphatemia manifestations

same as hypocalcemia

hyperphosphatemia treatment

restrict intake, Ca2+ binders

hypophosphatemia treatment

replacement therapy

mangesium

major intracellular cation -normal: 1.8-3.0 mg/dL -enzyme activity -carbs, protein metabolism -protein, DNA synthesis -muscle excitability

magnesium regulation

diet PTH -absorption+excretion inflenced by calcium absorption+excretion in the kidneys

hypomagnesemia

magnesium<1.8 mg/dL

hypermagnesemia

magnesium>3.0 mg/dL

hypomagnesemia causes

impaired intake/absorption -alcoholism, malabsorption, malnutrition increased loss -ketoacidosis -diuretics, SIADH similar to hypocalcemia

hypomagnesemia manifestations

same as hypocalcemia -extreme muscle excitability

hypermagnesemia causes

renal failure, excessive antacids, IVs for pregnancy-induced hypertension, tissue trauma, hypovolemic shock -similar to hypercalcemia

hypermagnesemia manifestations

same as hypercalcemia -decreased muscle excitability

hypomagnesemia treatment

replacement therapy

hypermagnesemia treatment

increased calcium, eliminate ingestion