2/1 Potassium Disorders - Goldstein Flashcards
cellular fx of potassium
- major ion determining resting membrane potential
- imp for excitable tissues (ex. nerve, muscle)
- major intracellular osmotically active cation → cell volume regulation
- essential for enzyme activity, cell division, growth
- intracellular K participates in acid/base balance
- via exchange with extracellular protons and influence on ammoniagenesis
transcellular potassium distribution
factors that affect K movement to ECF
- incr acid (H/K exchange)
- hyperglycemic (ECF osmolality goes up → water moves, dragging potassium with it)
- low insulin state (insulin facilitates K uptake)
- digoxin (poisons pump)
- beta blockers (bc catecholamines have a role to play in K uptake)
- cell injury
factors that affect K movement into ICF
- insulin
- beta2 agonists
- alkalosis (pH v HCO3)
- Ba poisoning
- hypokalemic periodic paralysis
K dist and balance
only 2% of potassium is in ECF
meaning other 98% of K is intracellular!
- why important?*
- transcellular buffer allowing excess K to move into cells until enough can be excreted to accomodate it
see in pic: sigmoidal curve → magnitude of hypo/hyperK likely underestimates the magnitude of K depletion or overload respectively
filtration and reabs of K
92% of filtered K is reabs in proximal nephron
almost all of the K that is eventually excreted is secreted distally
factors influencing distal K secretion
- distal delivery of Na → impaired Na delivery means nothing to exchange for K
- tubular fluid flow rate → faster fluid moves, greater the conc gradient, so more secretion
- non-resorbable anions → need to be reabs with a cation (K is the most available in distal nephron)
- mineralocorticoid activity (aldosterone)
- ald stimulates K secretion
- ald def corrupts K secretion
K secretion and diet
enteric sensor increases K secretion after a protein-rich meal (bc also tend to be high K)
- incr in GFR and tubular fluid flow rate
- high flow → activation of maxi-K (“BK”) channel → incr K secretion
- incr flow also dilutes luminal K concentration → keeps gradient for K secretion optimal
- incr distal delivery of Na augments electrogenic K secretion through ROMK
inference: IV K replacement is more effective than oral K replacement bc your body is hardwired to get rid of “extra” K!
K and the acid base balance
acidosis
alkalosis
effects of K on acidbase homeostasis
acidosis DIRECTLY leads to hyperkalemia (primarily mineral acidoses vs. organic acidoses)
- see redist of K out of cells
- decr K secretion in distal tubule
- incr renal NH4 → decr in K secretion
- incr K reabs via incr H/K-ATPase
alkalosis leads to hypokalemia
- incr distal tubule apical K channel activity
- incr KCl secretion with low luminal Cl
direct effects of K on acid base homeostasis
- K depletion → intracellular acidosis → incr H secretion in prox and distal tubule with incr ammoniagenesis
- K depletion → incr H/K ATPase
- hyperK decreases ammoniagenesis and medullary thick asc limb ammonia transport
hypoK mech
disorders of internal balance
- hyperadrenergic states
* MI - periodic paralysis
- drugs
- insulin
- albuterol, terbutaline, theophylline
- metabolic alkalosis
- anabolism
- tx of pernicious anemia
- rapidly growing leukemias/lymphomas
- refeeding
hypoK mech
disorders of external balance
abnormal losses vs inadequate intake
LOSSES
- GI losses in emesis or diarrhea
- osmotic diuresis (ex. glycosuria)
- mineralocorticoid excess (primary/secondary)
- hypoMg
- types I and II RTA
- effects of dialysis or apheresis
- diuretics/laxatives
- Bartter’s Syndrome (mimic loop diuretic) → salt wasting, metabolic alk, hypercalciuria
- Gittleman’s Syndrome (mimic thiazide use)
- inactivating mutation of apical NaCl transporter
*
- inactivating mutation of apical NaCl transporter
keys for diagnosis
- WBC > 100k in acute leukemia → K uptake by cells → pseudohypoK
- urine K used to determine GI vs renal loss of K & estimate K replacement
- bp is a diagnostic discriminant in hypoK
- urine chloride divides hypokalemic metabolic alkaloses
hypokalemia
advanced?
- nephrogenic DI
- rhabdomyolysis
- acute kidney injury
treatment?
-
acute and sx
- IV KCl in glucose-free sol (bc dextrose will prompt K uptake)
- repair of hypomagnesemia (DO THIS SLOW)
- discontinue diuretics, laxatives
- careful surveilance
-
chronic or subacute/asymptomatic
- incr dietary K
- evaluate use of drugs leading to K wasting
- address underlying conds (ex. chronic diarrhea or malabs)
- oral K supplements
how does the human body protect against hyperkalemia?
- body responds to high protein/K meal by:
- incr GFR and tubular flow rate → incr distal delivery of Na → amplified K secretion
- high flow dilutes tubular fluid, increases K gradient between tubular epithelial cell and lumen →→ incr K secretion
- body has a large intracellular reservoir to hold K until secretion time
pseudohyperkalemia
- thrombocytosis (platelets > 500k-1M)
- leukocytosis (WBC> 70-100k)
- fist clenching during phlebotomy
- tourniquet effect
- small needle size with extracorp hemolysis
- specimen management (post phlebotomy hemolysis)
diseases and drugs that alter RAAS
- direct renin inhibitors
- ACE inhibitors
- ARBs
- Na channel blockers
- aldosterone receptor blockers
- impaired release of renin
- impaired aldosterone metabolism
hyperkalemia maintenance tx
