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electrolytes
positive or negative electrically charged particles (ions) that are critical for cellular reactions: nerve impulse transmission, muscular contraction, water balance
sodium (Na+)
major electrolyte found in all bodily fluids; responsible for osmotic pressure and acid-base balance; regulates renal retention & excretion of H2O; stimulates neuromuscular reactions; maintains systemic BP; regulated by aldosterone and ADH; very closely related to water in body
hypernatremia
increased Na+ levels; associated with excessive water loss (dehydration, diabetes insipidus, diarrhea, vomiting, excessive sweating, fever) or abnormal retention of sodium (excessive saline therapy/sodium intake)
s/s of hypernatremia
extreme thirst, tachycardia, HTN, low-grade fever, dry, sticky mucous membranes, swollen tongue, high pitched cry, depressed fontanels (infants), restlessness, disorientation and hallucinations, oliguria
hyponatremia
decreased Na+ levels; reflects a relative excess of body water rather than low total-body sodium; associated with severe burns, HF/edema, diuretics, large amts of water by mouth or intravasation
s/s of hyponatremia
polyuria (when due to water excess), rapid pulse, hypotension, muscle cramps, weakness, diarrhea, lethargy, fluid retention, weight gain, edema, confusion, HA, seizures
potassium (K+)
freely excreted by the kidneys & not stored by the body (must be supplied in diet or IV to prevent levels from dropping rapidly), important role in nerve conduction, muscle function, acid-base balance, osmotic pressure; controls rate and force of contraction of the heart along with calcium and magnesium
hyperkalemia
increased K+ levels; K+ shifts from cells to intracellular fluids w/ inadequate kidney excretion and with excessive K+ intake: kidney disease, AKI, dehydration, obstruction, trauma, excessive K+ intake, massive cell destruction, use of K+ sparing diuretics, ACE inhibitors, metabolic acidosis (drives potassium out of cells)
s/s of hyperkalemia
oliguria, muscle irritability, nausea, diarrhea, abdominal cramping, skeletal muscle weakness, can progress to flaccid-type paralysis with difficulty speaking/breathing
hypokalemia
decreased K+ levels; associated with shifting of K+ into cells, K+ loss from GI and biliary tracts, kidney K+ excretion, reduced K+ intake: diarrhea, vomiting, sweating, starvation, malabsorption, diuretics
s/s of hypokalemia
cardiac arrythmias, muscle weakness (esp. legs), hypoactive bowel sounds, confusion, irritability, depression
magnesium (Mg+)
critical in nearly all metabolic processes (carb metabolism, protein synthesis, nucleic acid synthesis, muscular tissue contraction); esp important to monitor in cardiac pts; excreted primarily by kidneys; alterations in Mg tied to Ca, K, or P and regulates neuromuscular irritability and the clotting mechanism
hypermagnesemia
causes include acute kidney injury or reduced kidney function, dehydration, & use of antacids containing magnesium (ex: milk of magnesia)
s/s of hypermagnesemia
muscle weakness/fatigue (can progress to muscle paralysis), lethargy/slurred speech/depression; weak or absent DTRs, ECG changes/complete heart block, cardiac arrest
hypomagnesemia
causes include chronically low intake over a period of time (ex: alcoholic, drinking not eating), malnourished, toxemia of pregnancy, chronic pancreatitis, hypercalcemia of any cause, elderly (muscle/bone loss)
s/s of hypomagnesemia
tetany, tremors, muscle cramps, insomnia, cardiac arrythmias/increased cardiac irritability, delirium, convulsions
calcium (Ca+)
reflects parathyroid function, calcium metabolism and malignancy activity; used to monitor pts kidney disease, kidney transplantation, hemodialysis, hyper/hypoparathyroidism, pancreatitis, malignancy
hypercalcemia
causes include hyperparathyroidism, malignancy, bone fractures combined with bed rest/long-term immobilization, excessive intake of vitamin D, milk, antacids, paget disease of the bone
s/s of hypercalcemia
fatigue, cardiotoxicity/cardiac arrhythmias, coma
hypocalcemia
<9.0 mg/dL; most common cause is hypoalbuminemia
s/s of hypocalcemia
tetany, muscle spasm, carpopedal spasm, possible convulsions, irritability, depression, psychosis
anion gap (AG)
the difference between the cations and anions in the extracellular space; helps identify cause of metabolic acidosis and the presence of a mixed acid/base situation; most metabolic acidotic states are associated with an increased AG (diabetic ketoacidosis, fasting/starvation, ketogenic diets, poisoning, alcoholic ketoacidosis
lactic acid (lactate)
0.5-2.2 mEq/L; measured in cases of suspected septic shock; contributes to the knowledge of acid-base volume and is used to detect lactic acidosis in pts with underlying risk factors; increased by: metformin, sepsis, cardiac arrest, diabetes, shock, liver disease/alcoholism, ischemic tissue/trauma, hemorrhage, pulmonary failure
procalcitonin (PCT/Procal)
<0.1 ng/mL; a protein that is the precursor of calcitonin, a hormone that is synthesized by the parafollicular C cells of the thyroid and involved in calcium homeostasis; helps confirm sepsis in pt with elevated lactate
0.15-2 = localized mild to moderate bacterial infection
>2 = bacterial sepsis
blood glucose
majority of glucose comes from dietary intake of carbs and conversion of glycogen to glucose by the liver; diabetes, a group of metabolic disorders, is characterized by hyperglycemia and abnormal protein, fat, and carb metabolism due to defects in insulin secretions
fasting blood glucose (FBG)
70-100 mg/dL; if elevated, other tests will be performed; keep pt fasting at least 8 hours; withhold insulin or oral hypoglycemics until after blood is drawn; be sure pt receives meals/meds when test is completed; FBS of >126 mg/dL on two occasions indicates DM
postprandial blood sugar (PPBS)
<120 mg/dL = normal; purpose is to see how the body responds to the ingestion of carbs in a meal; time of blood specimen drawing must be accurate (usually 2 hr post prandial); instruct pt to eat entire meal and then not to eat anything else until blood is drawn; no smoking during testing
random blood sugar (RBS)
70-110 mg/dL; evaluate according to time of day performed; no special prep; usually fingerstick
oral glucose tolerance test (OGTT)
done in 2nd trimester of pregnancy to identify gestational diabetes; usually scheduled for early morning after the client has been fasting all night; procedure = draw FBS, 75g glucose dissolved in water, RBS collected at 1 and 2 hour intervals, results plotted on graph to see how long it takes the blood sugar to return to normal; potential complications (dizziness, tremors, anxiety, sweating, euphoria, fainting during testing)
hemoglobin A1C (glycosolated hemoglobin (GHB) or diabetic control index)
used to diagnose and monitor diabetes treatment; provides an accurate long-term index of patients average blood glucose level (past 2-3 months); looks at % of hgb that is glycosolated)
nondiabetic adult = 4.0-5.6%
prediabetes = 5.7%
diabetes = 6.5%
causes of hyperglycemia
diabetes, cushing disease, acute emotional or physical stress, pancreatitis, pancreatic tumors, advanced liver disease, chronic kidney disease
s/s of hyperglycemia
blurred vision, polydipsia, polyuria, polyphagia, loss of Na and K, weight loss, dehydration
causes of hypoglycemia
pancreatic islet cell carcinomas, addison disease, starvation, malabsorption, liver damage, insulin overdose, reactive hypoglycemia
s/s of hypoglycemia
diaphoresis, tachycardia, anxiety, weakness, hunger, irritability, confusion, behavioral changes, tremors or convulsions; many sx are due to release of epinephrine, also due to lack of sugar for CNS