Popham- Kalemic Flashcards
How much K is normally stored in an adult?
3000-4000 mEq
What is the daily intake and excretion of K?
4-120 mEq
Excretion min= 15-25 mEq
What percent of K is intracellular?
98%
How much K is extracellular?
4-5 mEq/L
How much K is normally in the serum?
4-5 mEq/L
What defines a body deficit vs. excess of K?
Deficet: decrease by 1 mEq/L = 200-400 mEq
Excess: increase by 1 mEq/L = 100-200 mEq
What are the functions of K?
Prot and glycogen synthesis
Maintains RMP via Na/K ATPase
Determines membrane excitability
Allows AP generation
What are sxs of LOW or HIGH K?
Unable to get an AP in muscles
Cramps
Muscle weakness/paralysis
EKG changes and arrythmias
How does hypercalcemia affect AP?
increases threshold potential and protects against hyperkalemia, which has decreased resting potential
What exacerbates hyperkalemia?
Metabolic acidosis
Causes K to be released form cells as HCl is buffered into cells
What drug potentiates risk of hypokalemia?
Digoxin
What can potentiate the risk of hyperkalemia?
Hyponatremia
What effects K distribution into cells and ECF?
- concentration dependent
2. Acid-base dependent
What happens if you drink 40 meq of OJ?
40 meq> 17 ECF > increase K by 2.4 meq/l
What increases K distribution into cells?
- Catecholamines and insulin increase Na/KATPase activity> uptake K into skeletal muscle and liver
- HIGH CONC causes passive movement of K into cells
What happens to K in acidemia vs alkalosis?
Acidemia: K+ moves OUT of cells as H+ is buffered into cells
Alkalosis: K+ moves INTO cells as H+ is buffered into the extracellular fluid
What determines excretion of K by the kidney?
- Plasma K+ concentration
- Urine flow in distal tubule (permissive)
- Aldosterone: causes K+ secretion by principal cells of collecting tubule
- Outer medulla, cortical & inner medulla
What influences K handling in the renal tubule?
- K is filtered at glomerulus
- Reabsorbed proximal tubule, following water and sodium
- Reabsorbed loop of Henle (thick ascending limb), via NaK2Cl carrier in luminal membrane
- Secreted distally: distal tubule, collecting tubule via principal cells
Where can K be reabsorbed in cases of severe hypokalemia?
Collecting duct by intercalated cells
How is K secreted in the distal tubule?
Principal cells
• Luminal membrane: Na+ & K+ channels
• Basolateral membrane: Na-K ATPase
Aldosterone
• Released in response to 0.1 meq/l increase in K+
• Increases # of open Na+ & K+ channels
• Increases activity of Na-K ATPase
K concentration in blood: gradient
Distal flow is permissive
What usually causes hypo/hyperkalemia?
adrenal glands or kidneys
NOT diet
What shifts K from extracellular to intracellular?
– Insulin
– Catecholamines
– Concentration gradient
– Acid-base status
What are the major determinants of K excretion by the kidney?
– K concentration
– Aldosterone
– Distal tubular urine flow (permissive)
What is a MAJOR toxicity of both hypo and hyperkalemia?
cardiac arrythmias
What causes hypokalemia?
- Decreased intake (rare)
- Increased entry into cells – met alk, hyperinsulinemia,
- catechol/β-agonists
- Increased GI losses
- Increased urinary losses – impaired H20/salt reabsorp, hypercalcemia, mineralcorticoid excess (aldosterone), hypomagnesemia
- Increased sweat losses
- Dialysis
How do you evaluate hypokalemia?
- Determine if loss is GI or renal
- GI losses should be obvious, except in cases of anorexia/bulemia/laxative abuse
- 24 hour urine K+ when hypokalemic
a. Kidney can decrease urine excretion of K+ to 25-30 meq in 24 hours
b. If urine K is low, then loss is not from kidney - Acid/base status: acidosis or alkalosis
What can cause LOW urinary K and acidosis?
LOWER GI losses
from laxatives/villous adenoma
What can cause low urinary K and Alkalosis?
Upper GI loss
vomiting
What causes high urinary K and acidosis?
Ketoacidosis, type I or II RTA
What causes high urinary K and alkalosis?
Normotensive: vomiting (GI loss, but high urinary K due to urinary bicarb excretion with metabolic alkalosis) diuretics (early), Bartter’s syndrome (Inherited)
Hypertension
- High renin: diuretics,renovascular disease, reninoma, Cushings
- Low renin: measure aldosterone
What does low vs high aldosterone indicate in situations when there is low renin?
low- exogenous mineralcorticoid
high- adrenal adenoma or hyperplasia
What complications can occur with hypokalemia?
- Muscle weakness, cramps, cardiac arrhythmias
- Rhadomyolysis (K+ < 2.5 meq/l)
- Renal dysfunction:
a. loss of urinary concentrating ability
b. Increase in urinary NH3 and NH4+ production/excretion
c. Hypokalemic nephropathy/Interstitial fibrosis - Hypertension: low K+ diet causes uptake of Na+
How do you treat hypokalemia?
- Replace to get patient out of danger initially, then more gradually replace entire K deficit
- K+ deficit can only be approximated:
a. Roughtly 200-400 meq for each 1 meq/l drop in K+
b. Below 2, K+ deficit can be much greater due to shifts out of cells to compensate - Treat underlying cause of low potassium
- Potassium replaced orally or intravenously
What causes hyperkalemia?
- Increased Intake: oral or IV
- Shift: Movement from cells into extracellular fluid – muscle/tissue breakdown, insulin deficiency w/ hyperglycemia, met acidosis
- Decreased urinary excretion – MCC = renal failure, hypoaldosteronism
What causes hypoaldosteronism?
- Secondary decrease in aldosterone due to decreased activity of renin-angiotensin system
- Primary decrease in adrenal synthesis of aldosterone
- Aldosterone resistance
What causes secondary decreases in aldosterone?
i. Hyporeninemic hypoaldosteronism (diabetics with CKD)
ii. Drugs: ACEi, NSAID’s, cyclosporine
iii. HIV disease/clinical AIDS
What causes aldosterone resistance?
Drugs: K+ sparing diuretics, Trimethoprim
Pseudohypoaldosteronism
How do you diagnose hyperkalemia?
DX = Transtubular K Gradient (TTKG) <7
How do you calculate TTKG?
[Urine K+ / (Uosm/Posm]
/Plasma K+
What should you do if K is 6.5-7 meq/l and there are no EKG changes?
check for pseudohyperkalemia
What should you do if there are EKG changes and you suspect hyperkalemia?
Start treatment immediately
*Monitor on telemetry
What can potentiate K toxicity?
Concomitant acidemia or hyponatremia
How do you treat hyperkalemia?
Antagonize K+ effects (seconds/minutes)
a. Calcium IV
Shift K+ into cells (minutes)
a. Glucose & insulin
b. NaHCO3
c. Beta-agonists: albuterol nebs
d. 3% NaCl if hyponatremia present
Remove excess K+ (hours)
a. Loop diuretics if patient makes urine
b. Cation-exchange resins (kayexalate): avoid rectal use
c. Hemodialysis/peritoneal dialysis
What EKG changes are associated with hypokalemia?
- PR interval prolongation
- ST depression
- Flattened/ inverted T waves
- U-waves
- QRS widening
What ST changes are associated with hyperkalemia?
- PR interval prolongation
- Elevated T waves
- Widened QRS
How should you treat EKG changes seen with hypokalemia?
- Concomitant digoxin use increases risk
- Treat to get out of danger, replace losses, and prevent further losses
- Check for hypomagnesemia
How should you treat EKG changes seen with hyperkalemia?
- Antagonize membrane effects: Calcium IV
- Shift K+: insulin/glucose/NaHCO3
- Remove K+: diuretics, Kayexylate, dialysis
