USMLE CK - Electrolytes

- check lytes for met acidosis 2/2 bowel ischemia causing increased lactic acidosis

- poor marker for pancreatitis, lipase is better; can be elevated for multiple reasons
- can be used as red herring as false positive

- generation phase: vomit ==> lose HCL ==> HCO3 is kept in blood instead of secreted into the now non-acidic stomach
- maintenance phase: vomit ==> volume loss ==> decreased kidney perfusion ==> RAA activation ==> increased aldosterone ==> retain water, lose H+, K+ in urine ==> hypoK+ and contraction alkalosis
-tx: give H2O and K+ to deactivate RAA

- adrenal failure
- non specific complaints: n/v, diarrhea, constipation, weight loss, **hyperpigmentation (e.g. in palmar creases)
- decreased adrenals ==> decreased MC, increased vasopression (2/2 no cortisol suppression) => hypoNa+
- decreased aldo receptor activation = hyperK+
- note hyperK+ is associated with hyperCl-
- also see hyperCa2+

- opposite of addison's dz
- hyperNa+, hypoK+
- if severe hypoK+ tx with spironolactone

- poor nutrition, malabsorption, alcohol, diuretics

- d abuse: serum: hypoNa+, K+; urine: increased K+ and Na+ excretion (kidneys are not correctly compensating b/c of diuretic)
- bulemia: serum: hypoNa+, K+, urine: decreased K+ and Na+ (kidneys are correctly trying to compensate)

- chronic: must be corrected slowly, no more than 0.5 Na ml/hr
- acute: if symptomatic with seizures then must be corrected quickly with hypertonic saline (3% saline)

- give lorazepam

based on serum osm, extravascular fluid status (it pt looks euvolemic, hypervolemic (edema, JVP), and urine Na+
** see chart

- path: ADH affects distal tubule and collecting ducts ==> incrases free water reabsorption from urine
- criteria: serum osm < 270, urine osm >50, Urine Na >20
- essentially urine osm is increased and greater than serum osm; see hypoNa+ 2/2 increased fluid but don't see signs of extracellular volume increased e.g. edema, JVP else it would be CHF or cirrhosis
- if you give H2O then serum Na barely goes up but urine Na goes up alot because kidneys cont to inappropriately retain H2O and secrete Na

- see volume overload 2/2 hypoalbuminemia (decreased synthesis)
- see edema ==> causes depletion of intravascular volume ==> kidneys retain water, retain Na2+ ==> low urine Na

- used for depolarizing neuromuscular blocker (pt that will be intubated)
- causes increased K+ release, thus C/I in burn injuries > 8hrs ago, demyelinating dz e.g. GBS, tumor lysis syndrome
- use vecuronium or rocuronium nstead

pH = 6.1 + log (HCO3/(0.03xPaC2))

- pt vomiting ==> kidney retain H+, lose K+
- volume contraction ==> increased aldo ==> lose K+

- weakness, flaccid paralysis, rep insufficiency, cardiac toxicity, sine wave on EEG
- give K+ binding resin = Na polystyrene sulfonate

- ABG will show met acidosis 2/2 increased lactate from decreased tissue perfusion
- tx: tx underlying causes and restore tissue perfusion with IV normal saline

- controversial, only if v severe, pH <7.2

= 0.9% saline

1. chloride sensitive = hypoCl- and saline responsive, signs of volume depletion
-- etiology = thiazide, loss of gastric secretion, purging
-- path = volume contraction ==> increased MC ==> increased bicarb retention, H+ loss, K+ loss
-- tx: give saline

2. chloride resistance alkalosis = urine cl > 20 and ECF volume expansion
- etiology: primary hyperaldo, bartter, gitelman, black liorice
- tx: not corrected by fluid

- met acidosis

- was most likely give loop diuretic to tx volume overload

- loop diuretic ==> increased Na secretion, K+ excretion ==> incrases distal solute delivery, increases aldosterone ==> increasesd H+ excertion => met alk

- increased pH and bicarb

- check for frank uremia
- if not present then calculate osmolar gap to assess for ethanol, methanol, ethylene glycol intoxication
- serum osm = [2Na+glu/18 + GUN/2-8]
Gap = observed osm - calc osm

- calcium oxalate = ethylene glycol poisoning

- pt has visual changes, acute pancreatitis

- anion gap met acidosis

1. hypoCa2+ seen in pts with blood transfusion
2. hypoK+
3. hyperK+

- met acidosis, don't need pH to suggest
- calc anion gap to check if +AG or -AG

- seen in diabetic nephropathy I or II and worsened by ACE-I or ARB
- 2/2 aldo insufficiencity or insensitivity ==> don't secrete NH4, retain K+

- RTA
- low bicarb = met acidosis, non anion gap

- AG met acidosis

- GERD, HA, peripheral edema

- met alkalosis with resp compensation
- e.g. pt vomiting => increased HCO3 => pt compensates by decreased ventilation => increased PaCO2

- normla phenom of pregnancy ==> increased progesterone ==> increased respiration ==> resp alk w/ compensation of decreased HCO3
- not PE b/c PaO2 is perfect

7.23 = acidosis ==> decreased HCO3 = primary met acidosis ==> expect increased resp with decreased CO2 to compensation but since PaCO2 is normal you have primary resp acidosis too! = mixed met and resp acidosis
- can check w/ Winter's formula = PaCO2 = 1.5(HCO3) + 8 = expected CO2 for compensation

- normal = either primary hyperPTH or familial hypocalciuric hypercalemia. If urine excretion is increased then hyper PTH, if decreased urine excretion then FHH
- decreased PTH = vit D tox, MM, RCC, sarcoid 2/2 feedback

- beta agonist ==> drives K+ into cells
- calcium gluconate
etc

- in low albumin, usually do not have sx of hypoCa2+ b/c ionized Ca2+ is unchanged

- when you have normal anion gap met acidosis, use urine AG to ddx acidosis 2/2 renal or intestinal bicarb losses
- renal: RTA, carbonic anhydrase inhibitor
- intestinal: diarrhea

- resp alkalosis

- low aldo ==> low Na, high K+, high H+ = normal anion gap acidosis

- check corrected Ca2+ levels esp if low albumin
- corrected Ca2+ = 0.8(4-measured albumin) + measured Ca2+

- increased lactate

1. isotonic 0.9% NS. Once volume is restored, 0.45% saline to better replace free water deficit
- if less severe then start with D51/2NS
2. D5W

- sx: tinnitus, fever, tachypnea
- ASA => CNS => tachypnea
- ASA => oxidative phosphoylation uncoupling => hyperemia
- ASA => met acidosis by 1. increased O2 consumption in tissues from oxidative phosphoylation uncoupling; 2. renal damage can't excrete organic acids
- thus see resp alk and met acidosis mixed!; can check via Winter's fomula

- inherited, defective bicarb absorption, associated with Fanconi's
- or drugs: carbconic anhydrase inhibitor

- low tubular ammonium production
- can't excrete sufficient H+ in urine ==> thus can't produce ammonium

- exchange for bicarb
- thus increase Cl in urine => increase bicarb into plasma and increase H+ into urine