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83 Cards in this Set

  • Front
  • Back
Name 6 major electrolytes/minerals
Sodium, Chloride, Potassium, Calcium, Phosphate, Magnesium
What are 3 functions of Sodium
maintains osmotic pressure,
balances acid/base,
transmits nerve impulses
What is the most abundant cation
What is the normal range for Na
135-145 mEq/L
Etiologies of Hyponatremia
gain of more water than salt:excess water,
loss of more salt than water,
diuretic usage,
excessive sweating,
renal dz,
excess ADH,
excessive IV infusion,
tap water enemas,
replacement of water after v/d/burns, but not salt
Neurological Clinical Manifestations of Hyponatremia
neuronal swelling, H/A, confusion, behavioral change, seizures, hallucinations
Cardiovascular manifestations of Hyponatremia
orthostatic hypotension, weak and/or thready pulse
Respiratory manifestations of hyponatremia
crackles, tachypnea, dyspnea, orthopnea
GI manifestations of hyponatremia
N/V, hyperactive bowel sounds, abdominal cramping, diarrhea
How to assess for hyponatremia
CNS sx, BP, HR (tachy), dry mucous membranes, fluid i/o, sodium below 135, cl below 97
Tx Goals for hyponatremia
correct body water osmolality,
restore cell volume,
raising ratio of na/h2o
Interventions for hyponatremia
reduce na loss in high risk patients,
restore sodium imbalance,
Etiologies of Hypernatremia
gain of more salt than water
loss of more water than salt: excess water loss,
overuse of IV saline solutions,
cushing's syndrome,
uncontrolled dm,
tube feeding
IV hypertonic solution,
inability to respond to thirst,
decreased ADH (diabetes insipidus),
diarrhea or sweating without water replacement,
difficulty swallowing fluids
neuro sx of hypernatremia
increased osmolality of ECF causes neurons to shrivel because water moves from cells to interstitial fluid causing confusion, seizures, coma and death
gi sx of hypernatremia
polyuria, nausea, vomiting
CV 6 sx of hypernatremia
HTN, jugular venous distention, S3 gallop, generalized weight gain and edema, dysrythmias
3 respiratory sx of hypernatremia
crackles, dyspnea, fluid effusion
tx goals for hypernatremia
correct body water osmolality,
restore cell volume,
decrease ratio of na/water
interventions for hypernatremia
monitor i/o,
oral care
name elements in extracellular fluid
sodium, bicarb HCO3, chloride, calcium

low in K, Mg, Phosphate
name elements in intracellular fluid
K, Mg, Phosphate, Protein

low in Cl and Na
what is major anion found predominantly in extracellular spaces
which mineral follows sodium
what is the function of chloride
maintains cellular integrity
What is the normal range for chloride
98-107 mEq/L
hypochloremia etiologies
loss via gi tract,
clinical manifestations of hypochloremia
weakness, muscle cramps, hyperactive reflexes
hyperchloremia etiologies
increased in na serum levels,
deficit of bicarb
clinical manifestations
metabolic acidosis
what is the principle cation of intracellular fluid and the primary buffer of the cell
what are 5 functions of potassium
nerve conduction,
muscle function,
acid/base balance,
osmotic pressure,
controls rate/force of contraction of heart and cardiac output
what is the normal range for potassium
3.5 - 5 mEq/L
hypokalemia: etiologies
decreased K intake (anorexia, fasting, NPO),
increased K loss (renal, fecal, sweating),
K redistribution from ECF into cells (excess insulin tx for DM),
debilitated patients,
gi sx of hypokalemia
anorexia, n/v, abdominal distention, decreased bowel sounds
cv sx of hypokalemia
r/t decreased conduction,
ECG/EKG changes,
dysrhythmias, hypotension, weak pulse,
slightly peaked p wave,
prominent u wave
neuro sx of hypokalemia
postural hypotension,
weakness, fatigue, irritability, confusion, a/v premature beats, v fib
respiratory sx of hypokalemia
shallow respirations, SOB, apnea
interventions for hypokalemia
cardiac monitor,
oral or iv potassium,
potassium rich foods,
hyperkalemia: etiologies
increased K intake (excessive or too rapid IV infusion),
impaired excretion of K (renal dz),
shift of K out of cells into ECF (24-72 hours after trauma, crushing injury, cytotoxic drugs, lack of insulin from untreated DM)
gi sx of hyperkalemia
abdominal cramps, diarrhea
cv sx of hyperkalemia
r/t increased conduction,
ecg/ekg changes, dysrythmias, hypotension, tachycardia, arrythmia, death by asystole or V fib, cardiac arrest
respiratory sx of hyperkalemia
muscle paralysis
neuro sx of hyperkalemia
nerve and muscle irritability,
renal sx of hyperkalemia
oliguria, anuria
hyperkalemia ecg changes
decreased r wave amplitude (not as high),
widened QRS,
narrow and peaked T wave
What is normal range for Calcium
4.5 - 5.5 mEq/L
what other lab values are affected by calcium
decreased albumin = decreased calcium
increased phosphorus = decreased calcium
3 types of calcium in the body
protein bound 50%,
citrate/salt form,
free/ionized (most active)50%
functions of ionized calcium
muscular contraction, cardiac function, nerve impulse transmission, blood clotting
hypocalcemia: etiologies
decreased ca intake or absorption (chronic diarrhea from laxative abuse or pancreatitis),
decreased physiologic availability of ca (hypoparathyroidism, hypomagnesmia),
increased ca excretion via renal or fecal routes,
inadequate vitamin D intake (lactose intolerance, gi disease, liver disease),
NPO status,
parathyroid disease
neuro sx of hypocalcemia
paresthesias in hands/feet/toes/lips,
chvostek's sign,
trousseau's sign,
muscular irritability,
muscle twitching,
cv sx of hypocalcemia
r/t abnormal conduction,
hypotension, dysrhythmia, prolonged QT interval
hematological sx of hypocalcemia
prolonged bleeding times
musculoskeletal sx of hypocalcemia
tetany, laryngospasm, muscle twitching and cramping, pathological fractures
interventions for hypocalcemia
cardiac monitor and
monitor for bleeding
hypercalcemia: etiologies
increased ca intake or absorption (antacids, vit. D overdose from shark cartilage),
mobilization of ca from bone into blood (hyperparathyroidism, malignant tumor, leukemia),
decreased ca excretion (thiazide diuretics)
gi sx of hypercalcemia
n/v, constipation, anorexia
neuro sx of hypercalcemia
r/t abnormal conduction,
fatigue, muscle weakness, decreased reflexes, h/a, confusion, lethargy, personality change, coma
renal sx of hypercalcemia
kidney stones
cv sx of hypercalcemia
r/t abnormal conduction,
shortened QT interval,
Widened T wave,
cardiac arrest
interventions for hypercalcemia
cardiac monitoring,
increase fluid intake,
safety precautions
functions of phosphate
generation of bony tissue,
metabolism of glucose and lipids,
maintanance of acid/base balance,
storage and transfer of energy
what is normal serum range for phosphate
2.7 - 4.5 mg/dL
hypophosphatemia: etiologies
decreased intake or absorption (alcoholism, chronic diarrhea, malabsorption),
shift from ECF into cells (insulin),
increased excretion through normal renal route (diabetes, ETOH withdrawal),
loss through abnormal route (excessive vomiting),
excessive antacid use,
lead poisoning
clinical findings in hypophosphatemia
r/t decreased energy source,
anorexia, malaise, paresthesias, hemolysis, decreased reflexes, muscle aches/weakness, confusion, stupor, seizures, coma, respiratory failure, impaired cardiac function
interventions for hypophosphatemia
mild: treat with diet,
severe: treat with TPN
hyperphosphatemia: etiologies
increased intake or absorption (iatrogenic),
redistribution from cells into ECF (tumor lysis, crushing injury),
decreased excretion (renal failure with oliguria),
excessive vitamin D,
addison's disease
gi sx of hyperphosphatemia
anorexia, n/v
neuro sx of hyperphosphatemia
cv sx of hyperphosphatemia
tachycardia, palpitations, dysrhythmia
renal sx of hyperphosphatemia
kidney obstruction
interventions for hyperphosphatemia
mild or asymptomatic: diet modification - limit high phosphate foods,
administer calcium or aluminum products
what is normal serum magnesium range
1.5 - 2.5 mEq/L
How is magnesium distributed in body
40-60% in bone,
20% in muscle,
30% in cells
Functions of magnesium
regulates neuromuscular irritability and clotting mechanism,
linked with calcium
hypomagnesemia: etiologies
decreased intake or absorption (alcoholics, malnutrition),
decreased availability of mg,
increased loss through normal routes,
loss thru abnormal routes
cv sx of hypomagnesemia
r/t increased neuromuscular activity,
premature ventricular contraction, atrial or ventricular fibrillation, ecg changes
neuro sx of hypomagnesemia
increased neuromuscular excitability,
insomnia, increased reflexes, muscle cramping/twitching, chvostek sign,
trousseau sign,
gi sx of hypomagnesemia
anorexia, nausea, abdominal distention
psychological sx of hypomagnesemia
depression, psychosis, confusion
hypermagnesemia: etiologies
increased intake or absorption (antacid tx, near drowning in salt water),
decreased excretion (renal failure with oliguria, decreased urine output),
severe dehydration,
iv administration,
cv sx of hypermagnesemia
r/t decreased neuromuscular activity,
ECG changes, heart block, premature ventricular contractions,
neuro sx of hypermagnesemia
decreased reflexes, lethargy, loss of deep tendon reflexes, respiratory paralysis, loss of consciousness, drowsiness