Jan9 M2-Potassium Pathophysiology Flashcards
hyperK and hypoK effect on resting potential
hyperK: depol (resting potential more positive)
hypoK: hyperpol (resting potential more negative)
electrical effects of hyperK on the heart + ultimate effect (less or more excitable)
- sustained gradual depolarization
- inactivation of Na channels
- *less excitable even though closer to threshold bc Na channels inactivated
hyperK on ECG (step by step)
peaked T wave, widened QRS, loss of P wave, sine wave, V fib
3 causes of hyperkalemia
impaired cell entry, increased cell release, reduced urinary excretion
key points in hyperK
almost all cases involve decreased GFR and are multifactorial
why can have hyperK in heart failure
volume contraction with decreased GFR
hormonal problem that can cause hyperK and 3 causes to that
hypoaldosteronism (1. primary adrenal insufficiency 2. ACEi 3. NSAIDs bc inhibit PGs’ effect on renin release)
drug that can cause hyperK
K sparing diuretics
can high K diet cause hyperK? yes no and why
no bc aldo turned on and K excreted normally
why does high K diet not cause high Na reabso
when euvolemic, RAAS is off (aldo is on because detects K but renin and therefore AT2 are off so AT2 doesn’t promote Na reabso at PCT)
hyperK cause related to not enough cell entry
insulin deficiency in hyperglycemia or uncontrolled diabetes
hyperK cause related to too much excretion from cells
rhabdomyolysis (muscle breakdown so K from these cells is released)
why can have false positive hyperK
when blood sample is hemolyzed (cells in it lysed)
history of patient with hyperK
- ask for CKD!!! (GFR!!), diabetes, adrenal insufficiency
- drugs taken (ACEi, ARB, K-sparing like spironolactone)
labs in hyperK patient
Cr, urea (GFR!!), glucose, electrolytes, bicarb