potassium Flashcards
typical intake of potassium
100
after a meal, potassium is rapidly taken up into cells by
Na/K ATPase
extracellular K+
4
principal cells contain what for potassium to flow into tubular fluid
K+ channel
increased Na delivery to principal cells
lumenal membrane becomes less lumenal positive which causes an increase in K+ secretion
furosemide
loop diuretic and inhibits the Na/K/Cl co-transporter and increases Na delivery to the CT
- K+ wasting
thiazide diuretic
inhibits the Na/Cl in DT which again causes increase in Na delivery to principal cells
- K+ wasting
gitelmans syndrome
characterized by hypotension (increased excretion of NaCl) and hypokalemia
amiloride
INHIBITS Na channels leading to a positive lumen and this K+ secretion decreases
- K+ sparing
defect in luminal Na/Cl co transporter
Gitelmans
potassium shifting into ICF
- insulin
- B-agonists
- catecholamines
- alkalemia
potassium shift our of ICF
- hyperosmolarity
- exercise
- cell lysis
- acedemia
- glucagon
transcellular shifts:
- sensitive to
- common in
- paralysis
- alkalemia or acidosis
- associated drugs
- sensitive to catecholamines
- hypokalemic periodic paralysis
- acute alkalemia
- associated with albuterol and insulin
clinical manifestations of hypokalemia
- muscle weakness and paralysis
- impaired urinary concentration
- arrhythmias- increased U wave
treatment of hypokalemia
- underlying cause
- cautious replacement by oral rout– not overshoot
- IV replacement with slower administration and not exceed 20 mEq/hr
etiologies of hyperkalemia
- pseudohyperkalemia
- increased intake
- decreased urinary excretion
- transcellular shift/cell lysis
pseudohyperkalemia
- hemolysis (think about blood draws)
- leukocytosis
- thrombocytosis
decreased excretory capacity of potassium can be from
- reduced GFR
- tubular secretory defect with preserved GFR
- drugs
what drugs are associated with hyperkalemia
ACEi, ARBs, K+ sparing, Heparin, NSAIDS
reduced GFR and hyperkalemia can be from
- Acute kidney injury
2. chronic kidney disease
tubular secretory defect with preserved GFR that leads to hyperkalemia (3)
- hyporeninemic hypoaldosteronism
- addison’s disease
- tubular dysfunction associated with lupus, sickle cell
what type of drug can cause a transcellular shift of K out of cells
Beta blockers
clinical manifestations of hyperkalemia
- muscle weakness and paralysis
- renal tubular acidosis due to impaired ammoniagenesis
- EKG abnormality- T wake is peaked
treatment of hyperkalemia
- stabilization of cardiac membranes- giving calcium
- transfer of potassium into cells
- removal of potassium from the body
