Electrolyte Disorders - Potassium Flashcards
(38 cards)
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
