Electrolytes and Body Water ppt

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Last updated 12:09 PM on 10/12/22
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102 Terms

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what percentage of our mass is water?
60%
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what are the three places water can be?
- ICF: all water within cell membranes
- ECF: intravascular and interstitial
- transcellular water (CSF and vitreous)
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what determines water distribution?
solutes (electrolytes) exert a pressure against water (osmotic pressure)
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osmolality
- measure of dissolved particles in a soln
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what affects water metabolism?
- activity levels
- environmental conditions (humid/dry)
- disease
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water balance
- 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
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ANP
- reduces venous pressure
- increases vascular permeability
- promotes natriuresis and diuresis
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BNP
- 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
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hyponatremia symptoms
- 120 = malaise, nausea
- 110-120 = generalized weakness, mental confusion
- 90-105 = mental impairment, seizures, coma, death
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what is the most common electrolyte disorder in hospitalized/non hospitalized pts?
hyponatremia
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hyposomotic causes of hyponatremia
- inc na los (depletional)
- inc water retention (dilutional)
- water imbalance
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hyposomotic - inc Na loss
- hypoaldosteronism (na excreted)
- diuretics (thiazides): lose na
- ketonuria: na loss with ketones
- renal disorder (salt wasting nephropathy )
- prolonged vomiting, diarrhea
- burns
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determining cause of Na loss
- urine na
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hyposomotic - inc water retention aka dilutional hyponatremia
- acute/chronic renal failure
- nephrotic syndrome
- hepatic cirrhosis
- chf
- detected by weight gain/edema
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hyposmotic - water imbalance
- normal volume but nacl deficit
- SIADH
- defect in AVP prod
- hypothyroidism
- adrenal insufficiency
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SIADH
- inc ADH release causes water to be retained
- urine osm > plasma osm by 100
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defect in AVP production causes
- pulmonary disease
- malignancies
- trauma
- infection
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hyperosmotic hyponatremia
- inc amts of other solutes
- caused by severe hyperglycemia
- causes shift of ECF or ICF shift of Na
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isosmotic hyponatremia
- pseudohyponatremia (hyperlipidemia/hyperproteinemia - MM)
- detected by osm (urine > plasma)
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pseudohyponatremia
- analytical error giving a false low sodium
- glucose, plasma osm and urea are normal
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potassium functions
- influences excitability of muscle
- influences osmotic pressure inside cell
- involved in cellular metabolism
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kidney control of potassium
- major route of excretion (glomerulus)
- almost completely reabsorbed in proximal tubule
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hormonal control of potassium
- aldosterone: secretion of K in distal tubule and collecting duct
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hyperkalemia causes
- decreased renal excretion (inc retention)
- inc K intake
- redistribution or cellular shift
- artifactual
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hyperkalemia symptoms
mental confusion, weakness, tingling, flaccid paralysis in limbs, weakness of the respiratory muscles, bradycardia
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>7 potassium
vascular collapse and cardiac arrest
(check for hemolysis before notifying floor)
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>10 potassium
incompatible with life
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hyperkalemia - dec renal excretion
- acute/chronic renal failure (most common)
- hypoaldosteronism (ace inhibs block aldo)
- addison's disease
- diuretics (potassium sparing)
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hyperkalemia - inc intake
oral or IV replacement therapy
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hyperkalemia - redistribution (cellular shift)
- acidosis: K shifts to ECF as H shift to ICF
- muscle/cellular injury
- hemolysis
- drugs: digoxin, beta blockers, nsaids, spironolactone, cyclosporine, heparin therapy
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hyperkalemia - artifactual
- sample hemolysis
- thrombocytosis/leukocytosis
- prolonged tourniquet/xssive fist clenching
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hypokalemia causes
- 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
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sodium ISE
glass membrane permeable to only Na
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potassium ISE
liquid ion exchange membrane with valinomycin