Disorders of K Metabolism Flashcards
Plasma K+ rises with ________ and falls with _______
(name that blood pH state)
↓↑→
acidemia, alkalemia
- in acidemia, K+ moves from ICF → ECF
- alkalemia increases K+ secretion
Effects of alkalosis on K+ secretion
- High pH causes movement of K+ into the all the cells from ECF
- enhances electrochemical gradient for K+ secretion
- Hypokalemic state
*note that alkalosis lowers H+ state, thus relieving their inhibitory effect on apical K channels→ faster flow of K+ into tubules
Difference between mild and severe acidosis on K+ secretion
Acidosis should normally ↓ K+ secretion due to:
- inhibiting apical K+ channels
- stimulate K+ movement from the cells into ECF (away from lumen)
Severe acidosis should normally ↑ K+ secretion due to:
- inhibiting Na+ R → inhibiting H2O R → increasing tubular flow → ↑ K+ secretion
Major determinants of urinary K+ excretion
- Normal distal tubule function
- Aldosterone activity
- Urinary flow rate
- Delivery of non-reabsorbed anions to distal nephron
Aldosterone stimulates the distal part of the nephron, stimulating K+ secretion or reabsorption?
aldosterone stimulates the distal nephron secretion of K+
(it upregulates Na reabsorption→ K into the cell → K+ out of the cell)
*absence of aldosterone increases body K and plasma K, which in turn increases aldosterone secretion
Increase in urinary flow rate does what to K+ excretion?
it should increase K+ excretion, by creating a favorable electrochemical gradient for tubular secretion
Delivery of non-reabsorbed anions to distal nephron does what to K+ excretion?
It should increase.
Anions should “drag” K+ along as an obligate cation.
Compare suddenly giving K+ to individuals who are maintained on a strictly low/moderate K+ intake vs giving low K+ diet with supplemental K+ .on the side
Low K+ diet + suddenly given K+ = severe hyperkalemia
Low K+ diet w/ supplemental K+ suddenly given K+ = harmless bc animal has adapted to high K+ loads and secrete K+ faster
why is hyperkalemia a problem in acute renal failure but not usually in chronic renal failure?
K+ adaptation, in contrast to Na+ reabsorption is a slow process to turn on/off.
Hyperkalemia is a bigger problem in ARF than CRF unless GFR is extremly depressed.
3 ways to evaluate ↓ Serum K+
Is the cause of low Serum K+ due to:
- Spurious (fake) causes
- Decreased TB K+
- Transcellular shift
Spurious(fake) causes of ↓ Serum K+
Extreme Leukocytosis WBC >100k
note that massively increased WBC also can lead to pseudohyperkalemia
Decreased TB K+ leading to ↓ Serum K+ are due to which 2 things?
Renal 101:
- decreased K+ intake
- increased K+ loss
- Renal or extrarenally
Transcellular shifts leading to ↓ Serum K+ (5)
- alkalosis
- insulin excess (acute)
- B2 adrenergic agonist excess (acute)
- Hypokalemic periodic paralysis
- Hypothermia
Treatment of hypokalemia/K+ deficiency
Restore plasma and TB K+ to normal:
- intravenously during emergency (cardiac arrythmia or paralysis)
- orally
- diuretics that are K+ sparing (spirinolactone, triamterone, amiloride)
(very limited, scary to treat, bc you have to do these slow)
Consequences of Hypokalemia/K+ deficiency
- Metabolic
- cardiovascular effects
- Neuromuscular effects
- Renal effects
Metabolic effects of Hypokalemia
- suppresses insulin release → glucose intolerance (high)
- retards growth
- intracellular acidosis
- increase renal ammonia production → make it worse
what do you have to worry about in pts on digitalis?
hypokalemia can enhance development of atrial/ventricular arrythmias in pts on digitalis
Both hyper and hypokalemia have which neuromuscular effects?
muscle weakness
paralysis
renal effects of hypokalemia
increased thirst
renal concentration defect → polyuria
Hyperkalemia progression on EKG
if pt has >6.0, do an EKG
peaked T waves → Wide QRS complex w. flattened P waves → sine waves (more severe)
EKG of hypokalemia
u waves after repolarization of T waves → artia/ventricular arrythmias in pts on digitalis
Types of hyperkalemia and their causes
- pseudohyperkalemia (spurious)
- hemolysis of drawn blood (tight torniquet)
- massively incrased WBC - True hyperkalemia
- transcellular shift from ICF to ECF
- decreased excretion
- increased input
Causes of transcellular shifts that result in true hyperkalemia (5)
reversible shift from ICF to ECF
- acidosis
- digitalis intoxication
- beta adrenergic blocker
- alpha 2 adrenergic agonist
- hyperglycemia!/hyperosmolar
Causes of decreased excretion that result in true hyperkalemia
Acute renal failure
K+ sparing diuretics
hypoaldosteronism (low adrenal steroids)
Causes of increased input that result in true hyperkalemia
endogenous ( hemolysis, rhabdo)
exogenous (K+ rich foods >300 mEq/d)
(note that diabetes/inadequate insulin response can also cause acute hyperkalemia) - acute
Treatment of Hyperkalemia with ECG changes present
- reverse the depolarization - stabilize membrane
- calcium infusion - move K+ from ECF to ICF:
- Sodium Bicarb
- Glucose/insulin
- beta agonist - remove K+ from body
- diuretics
- hemodialysis
insulin deficiency, acidosis, beta blockers may result in hyper or hypokalemia?
hyperkalemia
-
Vomiting, diarrhea, and anorexia could result in hyper or hypokalemia?
Hypokalemia (met acidosis)
- extrarenal cause
How does K+ affect insulin?
K+ is a stimulus for insulin secretion
- insulin moves K+ from ECF to ICF
What 3 hormones regulate internal K+ balance?
- insulin
- catecholamines
- aldosterone
How do catecholamines regulate K+
it moves K+ from ECF to ICF (just like insulin does), especially during stress via B2 receptor
what plays key roles in regulating external K+ balance (very imp)
- Kidney (reabsorption + SECRETION (unlike Na, water, ca, where there are just R)
- Cortical collecting tubule
- GFR (minor player)
Chronic hypokalemia what should you assess? What do you expect to find?
Look at urine K+
- low (40 Meq/L) - renal
low urine K
could be due to what?
Met acidosis
- diarrhea (GI losses)
Low K+ intake
high Urine K (>40 Meq/L) - renal causes of hypokalemia
look at that cortical collecting duct K secretion
no acid base disorder: Mg depletion
metabolic alkalosis: aldosterone drives K+ and H+ secretion
metabolic acidosis: DKA
What is the first test you would order in a pt with hyperkalemia?
repeat ECG
- if normal: work up first, treat second
- if not normal: treat now, work up second
Low aldosterone would cause hyper or Hypokalemia?
Hyper: leads to less Na+ R and thus less K+ excretion
