Electrolyte Disorders - Potassium Flashcards
Primary regulator of serum K+
Kidney in the distal part of the nephron. Principle cells do secretion, and alpha-intercalated cells do reabsorption.
Difference between transcellular shift and renal excretion of K+
Shift is for immediate response and renal is for long-term
What drives K+ into cells?
B-adrenergic agonists: insulin, epi, aldosterone
What drives K+ out of cells
alpha-adrenergic agonists
Major intracellular cation is ___ and extracellular is ___
Intra: K
Extra: Na
What kind of K channel is in the thick ascending limb
NKCC2: K enters cell
ROMK: K leaves cell
What happens in the collecting duct in the principle cell?
Principle cells do K+ secretion
ENaC channel is here
Aldosterone acts here.
What happens in the collecting duct in the intercalated cell?
K+ reabsorption. K+/H+ antiporter is here.
What part of the nephron regulates urinary K+ secretion?
Distal part
Def. of hyperK and RFs
Serum K> 5 or 5.5 mEq/L
RFs: AKI, CKD, DM, Meds (NSAIDs, ARBs/ACEi, Aldosterone antags, heparin), malignancy, rhabdo, older pt, acidosis
Sx of hyperK
- Cardiac arrhythmia (vfib, bradycardia due to AVB, asystole)
- Skeletal muscle weakness (diaphragm!)
- Metabolic acidosis
1. too much K…K enters cells…so H+ leaves to try to keep neutrality…leads to ACIDOSIS!
2. HperK decreases ammoniagenesis –> decreased ammonium chloride excretion in kidneys –> less net acid excretion
What does too much K+ do to the RMP?
Raises the RMP i.e. makes it LESS negative will increase excitability. Over time though, long-term depol. leads to Na channel deactivation, causing a net decrease in excitability. This is what causes cardiac and muscle issues.
What are some EKG findings in hyperK
- Peaked T waves
- Depressed ST
- Prolonged QRS
- Sinusoidal wave pattern (suggests vfib!)
What are the 2 main reasons for hyperK?
- Transcellular shift (K+ leaving cells)
2. Decreased renal K excretion
HYPOK: What can cause transcellular shifts of K+?
- Insulin (DM, refeeding)
- B2 agoinist (albuterol, catecholamines)
- Metabolic alkalosis (lots of basic HCO3 in body so K+ leaves cells to maintain balance)
- Pseudohypok
HYPOK: What can cause extrarenal loss of K+?`
- Upper GI loss (vomiting, NG suction) due to assctd. urinary losses secondary to metabolic alkalosis and volume depletion (w/ volume depletion, aldosterone stimulates Na+ reabsorption and increases K+ secretion)
- Lower GI loss (diarrhea)
- Sweating
HYPOK: What can cause renal loss of K+?
- Diuretics (loop or thiazide)
- Increased mineralcorticoid activity (aldosterone increases Na+ reabsorption via ENaC, so lumen becomes more neg, so more K+ secreted by ROMK)
- Hypomagnesemia
- RTA 1 or 2
- Others
HYPOK: What kind of cilia leads to increased K+ secretion
BENT
HYPERK: What can cause transcellular shifts of K+?
- PseudohyperK
- Metabolic acidosis
- Insulin deficiency, hyperglycemia, hyperosmolality
- Increased tissue catabolism
- Meds
- Exercise
- Transfusions
How does insulin deficiency, hypergly, and hyperosmolality cause a transcellular shift leading to HYPERK?
- Insulin stims. Na/K/ATPase to drive K+ intracellulary…so if you’re deficient, you aren’t driving K+ into the cell.
- Hyperglycemia or hyperosmolality causes H2O to passively leave the cell and take K+ with it
What kinds of things lead to increased tissue catabolism leading to a transcellular shift in HYPERK
Trauma, burns, radiation, tumor lysis syndrome, rhabdo
What kinds of meds lead to transcellular shift in HYPERK
B2-blockers (remember, B2 helps drive K+ in…so if it’s blocked, get HYPERK)
aplha-1-adrenergic agonist (drives out; dopamine, phelyepherine, digoxin, succs, minoxidil)
What 3 things can lead to pseudohyperK
- RBC hemolysis
- Serum blood samples- in thrombocytopenia, when the platelets clot it releases K. R/O w/ a plasma K+ (not clotted)
- Leukocytosis (fragile WBCs can rupture and leak K)
HYPERK: What can lead to decreased renal K+ excretion/
- Low aldosterone secretion
- Aldosterone resistance (K+ sparing diuretics)
- AKI or CKD
- Hypovolemia
- Ureterojejunostomy
- Intrinsic renal defect
What kinds of specific meds cause aldosterone resistance leading to decreased renal K+ excretion?
K+ sparing diuretics!
- Aldosterone receptor blockers: spironolactone or eplerenone
- Na channel blockers: amiloride or triamterene or trimethoprim
How do you generally diagnose hyperK
- Clinically
- Labs guided by suspected cause given hx
- FEK (<10% renal etiology, >10% extrarenal etiology)
- DONT ORDER TTKG
How do you prevent a bad arrhythmia in hyperK?
Give IV calcium gluconate
How do you tx a transcellular shift in hyperK?
- Insulin & Dextrose
- B2 agonist: albuterol
- Bicarb infusion
How can you remove K+?
Slow: loop or thiazide diuretic or exhange resin (Kayexelate, zirconium, patiromer)
Fast: Hemodialysis
How else can you tx hyperK?
Low K+ diet. Remove meds that increase K+ (ACEi/ARB, aldosterone blockers, K+ supplements)
Def and RFs of HYPOK
Serum K<3.5 mEq/L
RFs: V/D, meds (diuretics, insulin, etc)
Sx of HYPOK
- Cardiac arrhytmia (PACs, PVCs, tachy, brady, vfib)
- Skeletal muscle weakness (diaphragm!)
- Rhabdo
- Metabolic alkalosis (H+ enters ICF b/c K+ is leaving ECF in efforts to bump up K+ levels –> leads to not enough H+ in the ECF –> alkalosis)
- Nephrogenic diabetes insipidus
How does HYPOK affect RMP
Lowers it and makes it more negative. So it’s harder for an AP to occur due to hyperpolarization.
WHat EKG changes are present in hypoK
- Low T wave
- Low T wave, high U wave
- Low T wave, high U wave, low ST
What are the 3 main reasons for HYPOK?
- Transcellular shift (cells uptake K)
- Extrarenal loss
- Renal loss
How do you diagnose HYPOK?
- Clinically
- Labs guided by suspected cause given hx
- Urinary K+ excretion to determine if it’s renal or extrarenal etiology
How do you determine urinary K+ excretion when diagnosing HYPOK
- 24 hr urine K+. If >25-30/day = renal K wasting
2. Urine K/Cr ration. If higher value = renal K wasting
How do you tx HYPOK
- Tx underlying cause
- Replace K+ deficit w/ KCL (K+ will increase by 0.1 for ever 10 mEq of KCl given)
- Replace Mg if low
- Repeat K+ labs
