Electrolytes Flashcards

1
Q

Body water distribution

A

intracellular fluid - 2/3 body water

extracellular fluid - 1/3 body water

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2
Q

Osmolality

A

measures the dissolved particles in a solution
osmoles/kg of water
Na+= 90%
275-295 mOsm/kg

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3
Q

ADH effect on Osmolality

A

osmole receptors in hypothalamus releases ADH if Osmolality is too concentrated

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4
Q

Calculated Osmolality

A

2[Na+] + [glucose/20] + [BUN/3]
gap between calculated osmole & measured osmole >20 is significant
other substances: ethanol, methanol, ethylene glycol, lactate etc etc

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5
Q

Blood Volume regulation

A

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

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6
Q

Renin-angiotensin-aldosterone (RAA)

A

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

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7
Q

Major electrolytes

A

Na+, K+, Cl-, tCO2

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8
Q

function of major electrolytes

A
maintain osmotic pressure & hydration
maintain pH
regulate heart rate & muscle action
involved in ox-reduc reactions
essential co-factors for some enzymes
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9
Q

Na+ general characteristics

A

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

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10
Q

Na+ K+ ATPase

A

3 Na+ out of cell & 2 K+ into cell

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11
Q

Na+ regulation depends on :

A

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

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12
Q

Hyponatremia

A

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+

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13
Q

Hypernatremia

A

increased Na+
intake is high
dehydration

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14
Q

Na+ methods of analysis

A

ion selective electrodes that use Na+ sensitive glass
Slide ISE - uses potential difference
serum range - 136-145 mmol/L

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15
Q

Potassium K+

A

major intracellular cation ( 20x K+ inside vs in plasma)
increase serum K+ w/ exercise (cell break down)
excreted by kidney

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16
Q

K+ functions

A

regulate neuromuscular excitability

contraction of heart, ICF volume, H+ concentration

17
Q

Hypokalemia

A

decreased K+
GI loss - vomiting, diarrhea, malabsorption
renal loss- nephritis, cushings, ^ aldosterone
decreased intake
cellular shift - alkalosis (!)

18
Q

Hyperkalemia

A
^^ K+
decreased renal excretion - renal insufficiency , DM
cellular shift - acidosis (!)
increased intake
platelet ruptures/ transfusions
19
Q

Potassium methodology & range

A

ion selective electrode using valinomycin impregnanted membrane
3.5-5.1 mmol/L serum

20
Q

Chloride Cl- characteristics & function

A

major extracellular anion

important in osmotic pressure, blood volume & electrical neutrality (chloride shift)

21
Q

Chloride shift

A

Cl- ions exchange w/ HCO- ions as CO2 is transported in/ouit of RBC
maintains electrical neutrality within the RBC

22
Q

Hypochloridemia

A
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
23
Q

Hyperchloridemia

A

excess HCO3- loss
GI losses
renal tubular acidosis: kidney damage that prevents exchange
metabolic acidosis (!)

24
Q

Chloride analyzer methods

A

titration methods

ion selective electrodes - chloride will bind w/ silver ions Ag1_

25
Q

tCO2 general

A

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

26
Q

CO2 buffer reaction

A

CO2 + H2O H2CO3 H+ + HCO3-

tissues: give up CO2
lungs: breath out CO2
enzyme: carbonic anhydrase

27
Q

Hypocapnia

A
low tCO2 (<23)
metabolic ACIDOSIS - loss of CO2 from blood buffer system
28
Q

Hypercapnia

A
high tCO2 (>30)
metabolic ALKALOSIS - increased CO2 in the blood
29
Q

total CO2 enzymatic method

A

substrate: patient HCO3-
enzymes: PEP carboxylase, malate dehydrogenase
read: NAD
specimens must be handled correctly to avoid losing CO2 (aka loose cap)

30
Q

Anion gap

A

Na+ - (Cl+tCO2) = 7-16 range
>16 : uremia, renal failure, ketoacidosis (+>-)
<7: hypoalbuminemia, hypercalcemia