Clinical Chemistry: Fluid Balance and Electrolytes Flashcards

percent of body weight made up of water

water found in intracellular fluid

water found in extracellular fluid

detect change in concentration of solutes in blood

signals thirst response and hormone release by signaling osmoreceptors to drink more fluids and the pituitary to release ADH/vasopressin

reflects the status of hydration of the intracellular and extracellular compartments as part of the total body hydration; measures amount of dissolved particles per unit of water; reflects changes in properties of a solution in relation to water

excess water seen as low plasma osmolality

AVP and thirst activated; kidneys respond to ADH signal to retain water and reabsorb in the collecting ducts

the response to decreased blood volume; blood pressure decreased, heart signaled to increase contraction strength, kidneys signaled to secrete hormones to stimulate thirst (angiotensin II) and stimulate hormone secretion to reabsorb sodium in DCT, adrenal glands stimulated to release aldosterone

controls amount of water reabsorbed from kidney; produced in hypothalamus delivered to posterior pituitary; constricts arterioles in peripheral circulation

enzyme produced, stored, and secreted by kidney (glomerulus) in response to low sodium; acts on angiotensinogen to produce angiotensin I

hormones; I becomes II by ACE causing vasoconstriction to help increase blood pressure; acts on hypothalamus to increase thirst and kidneys to increase sodium reabsorption; stimulates release of aldosterone

hormone from adrenal cortex; acts on distal tubule and collecting duct in nephron to reabsorb Na and excrete K; regulates blood pressure through sodium diffusion in ECF; as it increases K decreases through excretion by renal tubule into urine

diagnose renal concentration disorders (concentration ability, electrolyte balance, and polyuria) as well as patient hydration status; increased in hypovolemia, SIADH; decreased in diabetes insipidus, polydipsia

diagnose renal concentration disorders as well as patient hydration status; increased in dehydration, hyperglycemia, DKA, diabetes insipidus, ingestion of alcohols; decreased in overhydration, hyponatremia, SIADH

three main analytes that affect osmolality

normal serum osmolality

normal 24 hour urine osmolality

normal random urine osmolality

calculated osmolality equation

calculated difference between measured and calculated osmo; shows presence of substances other than Na, urea, and glucose such as alcohols, lactate, beta-hydroxybutyrate

reference range for osmolal gap

electrolytes that regulate fluid volume and osmotic pressure

electrolytes that regulate myocardial rhythm and contractility

electrolytes that activate enzymatic reactions/cofactors

electrolytes that activate coagulation cascade

electrolytes that regulate ATPase ion pumps

electrolytes that maintain acid base balance

electrolytes that aid in neuromuscular excitability

cofactors necessary for coagulation

electrolytes that produce ATP from glucose

largely determines plasma osmolality; major extracellular cation in ECF (90%); active transport systems maintain correct ICF/ECF concentrations; 60-75% reabsorbed in PCT; kidneys can conserve of excrete large amounts; regulated by water intake, excretion, and blood volume (RAAS)

low plasma sodium <135 leading to nausea, vomiting, lethargy, and ataxia; caused by increased sodium loss (dehydration, burns, K deficiency, decreased aldosterone), increased water retention (renal tubal disorders, nephrotic syndrome, hepatic cirrhosis, CHF), and water imbalance (polydipsia, SIADH)

high plasma sodium >145 leading to altered mental status, lethargy, irritability, seizures; hyperosmolar due to water imbalance (water problem, not sodium problem); caused by excess water loss (sweating, prolonged diarrhea, burns, diabetes insipidus), decreased water intake, increased sodium intake

major intracellular cation; regulates neuromuscular excitability, heart contraction, regulation of ICF volume, pH regulation; reabsorbed by PCT in kidney, excreted and exchanged in DCT and collecting ducts for Na; released by muscles during exercise, hyperosmolality gradually depletes as it leaves with water

promotes potassium entry into skeletal muscle and liver increasing Na/K ATPase pump

promote cellular entry of potassium

impair cellular entry of potassium

low plasma potassium <3.5 due to increased renal or GI loss, alkalosis, or insulin use leading to weakness, fatigue, paralysis, and arrhythmia

high plasma potassium >5.1 caused by another disorder such as decreased excretion in renal failure, cellular shift caused by acidosis, loss of cellular potassium due to insulin insufficiency, hyperosmolality due to water and K being pulled from cells into plasma, tissue breakdown/injury, drugs such as diuretics that increase urine output, ACE inhibitors, digoxin, and collection issues causing false increase; leads to muscle weakness, cramps, mental confusion, tingling or numbness, cardiac arrest

major extracellular anion that maintains osmolality and blood volume; almost completely absorbed through diet by intestinal tract-reabsorbed by renal tubules with Na and excess excreted in urine and sweat; maintains electrical neutrality; aids in Na reabsorption in kidney, loss of HCO3 from cell causes diffusion of Cl from plasma into RBC to maintain neutrality

low plasma chloride <98 caused by excess loss (vomiting and ketoacidosis), DKA, or renal disease

high plasma chloride >107 caused by dehydration, excess HCO3 loss (diarrhea, renal tubular acidosis, metabolic acidosis

coulometry to generate silver ions which combine with Cl ions to quantitate

gold standard for cystic fibrosis diagnosis; CFTR gene mutation on chromosome 7

second most abundant anion in ECF; major component of buffering system in blood; measured as TCO2 in plasma/serum electrolyte panel- bicarb ion HCO3, carbonic acid H2CO3, and dissolved CO2

CO2 enters RBC, combines with H2O to form carbonic acid H2CO3, H+ dissociates to form HCO3 which leaves the cell and chloride enters

leads to urinary increase in HCO3 excretion

leads to urinary increase in tubular reabsorption of HCO3

caused by respiratory alkalosis and metabolic acidosis; inhibition of carbonic anhydrase by diuretics causing renal loss of bicarb

caused by respiratory acidosis and metabolic alkalosis

measures total carbon dioxide content-bicarb, carbonic acid, and associated CO2 with proteins; measured by ISE for pCO2 and enzymatic methods

reference range for TCO2

calculated subtracting anions from the cations to indicate an increase in 1 or more unmeasured anions in serum-QC for analyzer; increase caused by renal failure, ketoacidosis, glycol poisoning, lactic acidosis, MeOH intoxication, ASA OD

cofactor for >300 enzymes included in glycolysis, transcellular ion transport, neuromuscular transmission, energy production, oxidative phosphorylation, carb, protein, lipid, and nucleic acid synthesis, and release and response to certain hormones; 4th most abundant cation in body, 2nd intracellularly; mostly found in bone and tissue, but also bound to albumin in serum and RBC; found in diet, absorbed through GI tract; regulated by kidneys, aldosterone increases renal excretion, and affected by PTH (enhanced renal and intestinal absorption)

low plasma magnesium <0.63; rare in healthy, depletion due to severe illness, reduced intake, malabsorption, increased renal excretion, endocrine PTH malfunction, drugs/diuretics; leads to cardiac arrhythmias, tetany, tremors, paralysis, coma; treated with oral supplements, antacids, and injections

high plasma magnesium >1.0; rarely seen, caused by decreased renal excretion (renal failure), increased antacids, dehydration, and bone carcinoma; leads to hypotension, flushing, nausea, vomiting; treated by D/C Mg products

intracellular found everywhere in living cells; found in bone, soft tissue, and 1% in serum; component of phospholipids, DNA, RNA, and ATP-reservoirs are ATP, creatine phosphate; obtained through diet and intestinally absorbed, lost from bone and excreted in kidney; PTH increases renal excretion, vitamin D increases intestinal and renal absorption; diurnal variation

phosphate >1.42 seen in acute and chronic renal failure, ALL, and neonates

phosphate <0.78 caused by increased renal excretion, decreased intestinal absorption (vit D deficiency or antacid use); enhanced in patients with DKA, COPD, asthma, malignancy, anorexia, alcoholism, and irritable bowel

essential for myocardial and skeletal muscle contraction; needed for hemostasis and bone development; 99% found in bone, 1% in ECF (45% ionized in ECF, others bound to albumin, bicarb, citrate, lactate); regulated by PTH (stimulates osteoclast breakdown to release calcium when low), vitamin D (increases intestinal absorption), and calcitonin (inhibitor)

free biologically active form of calcium used to assess renal function, parathyroid function, and bone disease

gold standard for calcium measurement along with ISE for ionized

low plasma calcium <1.03 caused by hypomagnesemia (inhibits PTH and impairs its action with bone, causes vit D resistance), hypoparathyroidism (No PTH, little vit D, decreased calcium absorption) decreased albumin, renal disease; present in critically ill, septic, burned, cardiopulmonary insufficiency, renal failure; monitored during open heart to measure cardiac output; leads to neuromuscular irritability, tetany, cramps, and arrhythmia

present in excess PTH and malignancy; nonspecific symptoms such as weakness, lethargy, constipation, nausea, and vomiting; treated with estrogen replacement and parathyroidectomy

increases serum Ca bone resorption, decreases serum Phos by increasing renal excretion, increases D3, regulated by ionized Ca

increases Ca and Phos absorption in intestines, increases osteoclast activity with PTH, and increases renal absorption of Ca and Phos

decreases Ca and Phos by inhibiting osteoclast bone reabsorption

inadequate dietary calcium and vitamin D; most prevalent metabolic bone disease in adults; DEXA scan to diagnose

caused by abnormal bone mineralization, calcium, phosphate, vit D deficiency; occurs in growing bone leading to deformity of long bones and soft weak bones

caused by abnormal bone mineralization, calcium, phosphate, vit D deficiency; occurs in adults after closure of epiphyseal plates so no deformities

produced by most tissues in the body, highest in muscle, cleared by the liver in gluconeogenesis; measures hypoxia in shock, MI, CHF, PE, blood loss; may be present in metabolic situations, leukemia, liver or renal disease, salicylate or alcohol poisoning; identifies severity of sepsis and effectiveness of treatment

reabsorb phos, Ca, Mg, Na, Cl, K, and HCO3

tests included in electrolyte panel

tests included in basic metabolic panel

tests included in comprehensive metabolic panel