- oral (1/2-2/3) - kidney (excretion and conservation) - skin, lungs, GI = loss of water
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plasma water
- water phase with ions only (no proteins) - ions and chemical activity are normal (not affected by hyperproteinemia/hyperlipidemia)
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electrolyte exclusion effect
- exclusion of electrolytes from the fraction of the total plasma volume that is occupied by solids which leads to underestimation of electrolytes
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which has the highest conc of cation and anion inside the cell?
potassium and phosphate
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which has highest conc of cation and anion in interstitial and plasma?
sodium and chloride
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difference between plasma and interstitial solutes
practically no protein in interstitial fluid
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balance of water due to...?
- hydrostatic pressure from heart drives water into tissues - plasma proteins draw water into circulation from intracellular spaces - so low protein in vessels means most water will remain in tissues
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what can cause permeability b/w ISF and plasma to increase?
some disease states like bacterial sepsis leading to leakage of alb, reduced plasma volume (shock) and hypotension
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osmotic pressure def
- hydrostatic pressure that develops and is maintained when 2 solns of different concentrations exist on opposite sides of a semipermeable membrane - number of solid particles/unit volume or weight of soln - force that moves water from dilute solns to conc solns
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osmolarity
- weight to volume relationship in mOsmole/L - inaccurate if hyperlipidemia/hyperproteinemia is present
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osmolality
a weight to weight relationship in mOsmole/kg
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colligative properties
- related to number of total particles in soln and properties of those particles - includes BP, vapor pressure, osmotic pressure, FP
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uses of osmolality
- determines if serum water content deviates from normal - detects the presence of foreign lmw subs in blood - use of urine/serum ratios to determine concentrating ability of kidney - assess electrolytes and acid base disturbances
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serum osmolality equation
(Na)(1.86) + (BUN)/(2.8) + (glucose)/(18)
(Na)(2) + (BUN)/(3) + (glucose)/(20)
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osmolal gap
should be less than 10 mOsm/kg (6-10)
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causes of increased difference in osmolal gap
- attributed to other osmotically active cmpds other than sodium, glucose, urea - diabetic acidosis (ketones) - ethylene glycol poisoning - alcohol consumption (ethanol, methanol) - inc lipids inc proteins dec %water
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what is the specimen to measure osmolality?
- serum or random urine (cf if turbid) - plasma not recommended because it contains osmotically active ions (anticoag)
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osmometer
finds freezing point depression by supercooling sample and then begin warming under constant value
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what 3 mechanisms regulate water balance?
AVP, RAAS, thirst center
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what is AVP also known as?
ADH (antidiuretic hormone)
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thirst center
- inc in plasma osmolality (stimulates osmoreceptors in hypothalamus) - dec in intravascular volume - angiotensin II acts upon neurons in hypothalamus to produce sense of thirst - controls the balance of free water and output (without solute) by the kidney and free water intake
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arginine vasopressin hormone (AVP)
- stimulated by inc plasma osmolality and dec plasma volume - produced in posterior pituitary - increases water absorption in kidney (collecting ducts)
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renin angiotensin aldosterone system (RAAS)
- dec blood volume, BP, ECF - results in secretion of renin in kidney - renin activates plasma angiotensinogen to angiotensin I - angiotensin I(in lung) becomes angiotensin II (vasoconstrictor) via ACE - aldosterone (adrenal cortex) increases Na absorption and H and K excretion
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ACE inhibitors
- interfere with RAAS by stimulating dilation of vessels via blocking production of angiotensin II - leads to inc sodium and urine excreted, inc venous capacity, dec cardiac output
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natriuretic peptides
- released in response to intravascular volume expansion (reduces BP and plasma volume) - produced in heart and released when heart feels a volume expansion, pressure overload
- similar to ANP - used to measure stuff in ppl with congestive heart failure (chf)
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CNP
- function not understood - potent vasodilator, no natriuretic effects
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clinical significance - osmolality
water load, diabetes insipidus, SIADH, water deficit
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water load
- xs water intake (polydipsia) - dec osmol - no response from AVP (lose large volumes of water and it causes hyperosmolality and hyponatremia only in ppl with impaired renal excretion
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diabetes insipidus
urine osmol dec
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SIADH
- increase in AVP leading to in urine osm - secondary in asthma, pneumothorax, bacterial/viral pneumonia, copd, right side heart failure
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water deficit
- inc in plasma osmol - triggers AVP and thirst mechanism - not usually a concern unless pt is infant, unconscious, elderly, or dec mental status
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electrolyes
- important substances influencing distribution and retention of water - sum all all charges must equal zero between ECF/ICF
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anion gap
- difference between cations and anions - can include or exclude potassium - range w: 10-22 - range w/o: 6-18
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what are the measured electrolytes in the laboratory?
na, k, cl, hco3
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clinical significance of anion gap
- differential diagnosis of metabolic acidosis - QC indicator
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what could a dec AG mean as a QC indicator?
- lab error (overestimation of cl or underestimation of na) - MM: myeloma proteins act as cations
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what is an increase in the anion gap usually caused by?
- usually by unmeasured anions (cations have little effect) - inc organic acids - chronic renal disease - diabetes mellitus-ketoacidosis - salicylate, methanol, ethylene glycol poisoning
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sodium functions
- maintain osmotic pressure and water distribution - acid base balance exchange for hydrogen in renal tubes - responsible for 1/2 osmotic strength of plasma
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kidney control of sodium
- major route of excretion (glomerulus) - 80-90% reabsorbed in the proximal tubule
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hormonal control of sodium
- ADH lessens the filtration of na and GFR - aldosterone: inc na reabsorption in distal tubule and collecting duct
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hypernatremia symptoms/causes
- neurological (ataxia, irritability, fever, confusion, coma) - hypovolemia: xssive water loss/failure to replenish lost water - hypervolemia: inc in sodium intake
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hypovolemia - xs water loss causes
- diabetes insipidus (no ADH or no response to ADH) - renal disease (damaged glomerulus = dec na excretion) - nephrotic syndrome (loss of proteins in urine = low osmotic pressure so fluid shifts to interstitial space) - sweating, diarrhea
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hypovolemia - dec water intake
- seen in older persons, infants, and those with mental impairment - most ppl can respond to thirst mechanism so this rarely occurs
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extrarenal water loss
- urine osm >700 - Na >20 - GI/skin loss
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renal water loss
- urine osm low to normal - urine Na high - thiazides w/o water replacement
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hypervolemia - inc Na/retention
- hospitalized pts get hypertonic saline/bicarb - hyperaldosteronism: inc Na absorption and potassium excretion, more water retained - cushing's syndrome - chf: retention and more reabsorbed - liver disease: venous pressure in and forces fluid into peritoneal space (lowering plasma volume) - pregnancy (unknown interruption b/w sodium and body water)
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osmotic diuresis
- inc urination from large molecules in the kidneys that draw water from the bloodstream into the urine - urine osm 300-700
- GI loss - renal loss - cellular shift - dec intake
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hypokalemia - GI loss
- diarrhea - intestinal tumor - malabsorption - chemo/radiation therapy - large doses of laxative
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hypokalemia - renal loss
- nephritis, RTA - hyperaldosteronism (K excretion) - cushings syndrome (high cortisol = dec in potassium) - hypomagnesemia (promotes K excretion) - acute leukemia
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hypokalemia - cellular shift
- alkalosis (K shifts to ICF as H shifts to ECF) - insulin therapy
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chloride functions
- osmotic pressure regulation - production of HCl in gastric
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which cation does chloride follow?
sodium unless there is an acid base disturbance
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kidney control of chloride
- major route of excretion (glomerulus) - 97% reabsorbed by tubules
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hyperchloremia causes
- renal tubular acidosis (kidney unable to make bicarb) - metabolic acidosis (severe diarrhea) - prolonged vomiting - loss of nahco3 - dehydration - xssive reabsorption from GI tract
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hypochloremia causes
- loss of gastric juice (vomiting or pyloric obstruction) - inc urinary excretion (diuretics or chronic pyelonephritis - salt losing) - metabolic alkalosis (inc bicarb = chloride shift)
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specimen collection for measuring electrolytes
- plasma or serum - heparinized whole blood or arterial/venous specimens from ABG - serum for K can be elevated from clotting process
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interferences for sodium
- high lvl of macromoles (proteins/lipids) will give falsely dec results in indirect methods - hemolysis = dilutional effect
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potassium interferences
- tourniquet in place too long - hemolysis - leukocytosis/thrombocytosis will falsely inc
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chloride interferences
- inc with prolonged exposure bc CO2 lost so Cl moves to serum - once separated from the cells, the Cl is stable
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test methodologies
- atomic absorption - flame photometry - amperometry - ISE (direct and indirect)
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what does flame photometry measure?
Na and K
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what does amperometry measure?
Cl
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direct ISE
- measures free ion activity in plasma water and does not take into account total volume so other solids do not interfere - no dilution - blood gas analyzers, POCT, single use instruments
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indirect ISE
- based on sample dilution and based on total volume so solids are included and protein/lipids will interfere - measures total ion concentration - adv: large sample volume to adequately cover membrane surface - more common in lab instruments
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ion selective membranes
potential produced is proportional to the log of ionic activity or conc
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errors of ISE
- lack of analytical sensitivity - repeated protein coating of membrane - contam of the membrane or salt bridge
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ISEs
- used for Na, K, Cl, K - uses direct measurement of electrical potential due to acitivity of ion - Ag/AgCl: internal reference