Electrolytes Flashcards
Body water distribution
intracellular fluid - 2/3 body water
extracellular fluid - 1/3 body water
Osmolality
measures the dissolved particles in a solution
osmoles/kg of water
Na+= 90%
275-295 mOsm/kg
ADH effect on Osmolality
osmole receptors in hypothalamus releases ADH if Osmolality is too concentrated
Calculated Osmolality
2[Na+] + [glucose/20] + [BUN/3]
gap between calculated osmole & measured osmole >20 is significant
other substances: ethanol, methanol, ethylene glycol, lactate etc etc
Blood Volume regulation
Renin-angiotensin-aldosterone
atrial natuiretic peptide- BNP tries to regulate blood pressure
volume receptors independent of osmolality- will stimulate ADH release
GFR- increase or decrease w/ volume
sodium concentration - its reabsorption brings kidney filtrate back into blood
Renin-angiotensin-aldosterone (RAA)
renin- hormone from kidney once released it acts on angiotensinogen to make angiotensinogen 1 (from liver) to go to angiotensinogen 2 which acts on blood pressure: acts on adrenal gland for aldosterone, constrict blood vessels, ADH secretion, H2O retention
aldosterone is a major hormone in the conservation of Na+ by the kidney, increase blood pressure
ADH- conserves water, decreases blood pressure
Major electrolytes
Na+, K+, Cl-, tCO2
function of major electrolytes
maintain osmotic pressure & hydration maintain pH regulate heart rate & muscle action involved in ox-reduc reactions essential co-factors for some enzymes
Na+ general characteristics
major cation in ECF
renal threshold 110-130 mmoles/L
aldosterone, angio II, ADH regulate Na+ levels
renal mechanims fosters Na+ retention (!) & excretion of H+, Cl- ion
Na+K+ ATPase
Na+ K+ ATPase
3 Na+ out of cell & 2 K+ into cell
Na+ regulation depends on :
intake of water, due to thirst & plasma osmoles
excretion of water affected by ADH response to blood volume or osmolality
blood volume status, affects Na+ excretion via ADH, aldosterone & Angio II
Hyponatremia
decreased Na+ <135 mmol/L
dilutional due to water retention (acute/chronic renal failure)
vomiting/ diarrhea
Nephrotic syndrome
SIADH (syndrome of inappropriate ADH) - increased ADH = increased water retention & decreased Na+
Hypernatremia
increased Na+
intake is high
dehydration
Na+ methods of analysis
ion selective electrodes that use Na+ sensitive glass
Slide ISE - uses potential difference
serum range - 136-145 mmol/L
Potassium K+
major intracellular cation ( 20x K+ inside vs in plasma)
increase serum K+ w/ exercise (cell break down)
excreted by kidney
K+ functions
regulate neuromuscular excitability
contraction of heart, ICF volume, H+ concentration
Hypokalemia
decreased K+
GI loss - vomiting, diarrhea, malabsorption
renal loss- nephritis, cushings, ^ aldosterone
decreased intake
cellular shift - alkalosis (!)
Hyperkalemia
^^ K+ decreased renal excretion - renal insufficiency , DM cellular shift - acidosis (!) increased intake platelet ruptures/ transfusions
Potassium methodology & range
ion selective electrode using valinomycin impregnanted membrane
3.5-5.1 mmol/L serum
Chloride Cl- characteristics & function
major extracellular anion
important in osmotic pressure, blood volume & electrical neutrality (chloride shift)
Chloride shift
Cl- ions exchange w/ HCO- ions as CO2 is transported in/ouit of RBC
maintains electrical neutrality within the RBC
Hypochloridemia
salt losing renal disease adlosterone deficiency: not absorbing Na+ prolonged vomiting diabetic Ketoacidosis (!): too much H+ being formed & Cl- is being used to neutralize pH
Hyperchloridemia
excess HCO3- loss
GI losses
renal tubular acidosis: kidney damage that prevents exchange
metabolic acidosis (!)
Chloride analyzer methods
titration methods
ion selective electrodes - chloride will bind w/ silver ions Ag1_
tCO2 general
90% HCO3-
important as part of CO2 buffer system in the body
buffers acids formed during normal metabolism
regulated by kidneys - almost all reabsorbed bc its such an efficient buffer
CO2 buffer reaction
CO2 + H2O H2CO3 H+ + HCO3-
tissues: give up CO2
lungs: breath out CO2
enzyme: carbonic anhydrase
Hypocapnia
low tCO2 (<23) metabolic ACIDOSIS - loss of CO2 from blood buffer system
Hypercapnia
high tCO2 (>30) metabolic ALKALOSIS - increased CO2 in the blood
total CO2 enzymatic method
substrate: patient HCO3-
enzymes: PEP carboxylase, malate dehydrogenase
read: NAD
specimens must be handled correctly to avoid losing CO2 (aka loose cap)
Anion gap
Na+ - (Cl+tCO2) = 7-16 range
>16 : uremia, renal failure, ketoacidosis (+>-)
<7: hypoalbuminemia, hypercalcemia
