Potassium: Hyperkalemia and Hypokalemia Flashcards
Where is most of the K in our body?
98% is intracellular
What is the intracellular K concentration and what is the extracellular K concentration?
intracellular = 140 mM
extracellular -= 4 mM
A decrease of K by 1 mM reflects what in total body?
a 200-400 meq total body deficit - huge!
What are the main symptoms of low and high K+ and how does this relate to K;s function in the cell?
they relate to an inability to generate action potentials in the muscles - muscle weakness/paralysis starting in the legs, along with EKG changes and cardiac arrhythmias
What are the EKG changes in hypokalemia?
PR interval prolongation ST depression Flattened or inverted T waves U waves QRS widening
What are the EKG changes in hyperkalemia?
PR interval prolongation
Elevated T waves
Widened QRS interval
What protects against hyperkalemia: hypercalcemia or hypocalcamie?
hypercalcemia - it increases threshold potential and protects against hyperkalemia (which has a decreased resting potential)
Is hyperkalemia exacerbated by metabolic acidosis or alkalosis?
acidosis - K+ is released from cells as HCl is buffered into cells
Which is tolerated better - chronic or acute hyper/hypokalemia?
chronic
What is potassium’s relationship with digoxin?
a bad one…
digoxin toxicity is worse with hypokalemia, but digoxin can cause hyperkalemia
The risk of hyperkalmia is potentiated by hyponatremia or hypernatremia?
hyponatremia - less action of the Na/K ATPase
What are the three conditions/states that influence the distribution of K_ between cells and the extracellular fluid?
- concentration of K
- acid-base status
- insulin/catecholamine presence - they’ll move K into the cells
HOw is K excreted?
almost entirely by the kidneys
There’s a butt load of K in a glass of OJ. Why don’t we keep over during breakfast?
Because K+ will rapidly distribute into the cells because of catecholamine and insulin release and the newly high K concentration - this brings the extracellular K concentration back to normal very quickly
How do insulin and catecholamines get K into the cells?
they upregulate the Na/K ATPase
What direction will K move in acidemia? alkalosis?
acidosis = K will move out of the cells as H is buffered into cells (hyperkalemia) alkalosis = K will move into cells as H is buffered into the extracellular fluid (hypokalemia)
What are hte major controls on K secretion by the kidneys?
- plasma K concentration = more K, more secretion
- urin flow in distal tubule = more flow, more secretion
- aldosterone = released during times of hyperkalemia to cause K secretion by principal cells of collecting tubule
In general, describe K handling by the renal tubule?
- filtered at glomerulus
- reabosrbed in proximal tubule, following water and sodium
- reabsorbed in LOH via NaK2Cl carrier
- Secreted in distal tubule and collecting tubule via principal cells
- can be reabsorbed in collecting duct by beta intercalated cells during severe hypokalemia
What are the main causes of hypokalemia?
decreased intake (rare) increaesd entry to cells GI losses increased urinary losses increased sweat losses dialysis
What are some ways to get hypokalemia fro inadequate diet?
poverty - no fruits and veggies
exacerbated by diuretics
clay ingestion
What are three ways to have hypokalemia from an increased K entry into cells?
metabolic alkalosis
hyperinsulinemia
increased catecholamines/beta agonists
What are some ways you can get hypokalemia due to increased GI losses?
- nasea/vomiting
- nasogastric tube suction
- diarrhea/intestinal fistulas
How can you get kypokalemia due to increased urinary losses?
- increased distal flow with impaired salt and water reabsorption from diuretics, salt wasting or polydipsia
- hypercalcemia (increased distal flow)
- mineralcorticoid excess - aldosterone mediated secretion
- hypomagnesemia (affects K channels)
What lab can you do to determine if K loss is from the GI tract or renal?
do a 24-hr urine K
the kidneys can decrease urine excretion ot K to 25-30 meg in 24 hours if the patient is hypokealmic.
if the urine K is appropriately low, the loss is somehwere other than th ekidney
If you have low urinary K and acidosis, where is the loss? How about low urinary K and alkalosis?
acidosis = lower GI loss (laxatives, villous adenoma)
alkalosis = upper GI loss (vomiting)
What are the complications of hypokalemia?
muscle weakness, cramps, cardiac arrhythmias
rhabdomyolysis
renal dysfunciton
hypertension (low K causes uptake of Na)
What is the treatment for hypokalemia?
replace to get them out of danger initialy and then more gradually replace entire K deficit (either orally or IV)
treat underlying cause
What are the general causes of hyperkalemia?
- increased intake
- shifting from inside cells to extracellular fluid
- decreased urinary excretion
What are some things that can cause the K to shift from the cells to the extracellular compartment?
muscle/tissue breakdown
insulin deficiency with hyperglycemia
metabolic acidosis
What is the most common cause of hyperkalemia?
renal failure
What effect will hypoaldosteronism have on K?
you’ll get hyperkalemia.
can be a syndrome, can be from drugs like ACEI or NSAIDS, can be from aldosterone resistance like with the K sparing diuretics, etc.
How do you determine whether you should treat a hyperkalemia?
check for EKG changes
if K is 6.5 to 7 meq/l and EKG shows no changes, check for pseudohyperkalemia
If EKG changes - treat immediately
How do you treat hyperkalemia?
- antagonist K effects with calcium IV
- shift K into the cells with glucose, insulin, bicarb and beta agonists. Give 3% NaCl is hyponatremia still present
- remove excess K in the long run with diuretics, kayexalate and hemodialysis as last resort
