Kalemic - Popham Flashcards
What are the normal body stores of Potassium?
- Normal body stores (70 kg adult) are 3000 to 4000 meq K+ (50-55 meq/kg)
- 98% of K+ is INTRACELLULAR
- Maintains gradient
What is the intracellular concentration of K+?
140 mEq/L
What is the extracellular concentration of K+?
4-5 mEq/L
What is the average daily intake of K+? What if you are not getting enough?
- Daily intake averages 40-120 meq
- If you’re not getting enough K+ in → kidney can reduce K+ excretion to less than 15-25 meq/day
What is the reflected total body deficit if K+ decreased by 1 mEq/L?
(normal serum/plasma K+ 4-5 mEq/L)
200-400 mEq
What is the reflected total body excess if K+ increased by 1 mEq/L?
(normal serum/plasma K+ 4-5 mEq/L)
100-200 mEq
What is the function of K+?
- Cellular function: role in protein & glycogen synthesis
- Maintains RMP in muscle cells and neurons
- via 3:2 Na+/K+ ATPase
- Determines membrane excitability;
- allows actions potentials to be generated
What are symptoms of low or high K+?
- Relates to inability to generate action potentials in muscles
- Cramps, Muscle weakness/paralysis: starts in legs
- Clinical pearl: “My legs are weak” (esp. if CKD) → K+ is high
- EKG changes & Cardiac Arrhythmias
- PAC’s, PVC’s, bradycardia, atrial or junctional tachycardia, AV block, v-tach/v-fib
- Low K+ can look same as high K+
What EKG changes are present in Hypokalemia?
- PR interval prolongation
- ST depression
- Flattened or inverted T waves
- U-waves
- QRS widening
What EKG changes are present in Hyperkalemia?
- PR interval prolongation
- Elevated T waves
- Widened QRS interv
How does calcium modify the K+ effects on action potentials?
- Hypercalcemia increases threshold potential and protects against hyperkalemia
- which has decreased resting potential
- “Every time you see the QRS widen, give an amp of calcium” → prevents cardiac arrest (lasts 10-15 min)
How does metabolic acidosis modify the K+ effects on action potentials?
- Exacerbates hyperkalemia by causing K+ to be released from cells as HCl is buffered into cells
- Correct with bicarb
How does Potassium effect digoxin levels?
- CLINICAL TIP:
- HYPOkalemia increases digoxin toxicity
- digoxin toxicity causes HYPERkalemia
- Digoxin disables Na+/K+ ATPase
How is the balance between intracellular and extracellular K+ regulated?
- Distribution of K+ between cells and extracellular fluid
- concentration dependent
- The higher the K+, the more K+ is going to shift into the cells
- Acid-base status dependent
- Insulin/catecholamines move K into cells
- concentration dependent
How does the K+ that you drink in a glass of Orange Juice distribute between the cells and extracellular fluid?
- Glass of OJ: 40 mEq K+ → 40 meq distributed in 17 L (EC volume of 70 kg male) K+ would increase 2.4 mEq/L
- K+ distributed rapidly into cells
- Catecholamines & insulin increase activity of Na+/K+ ATPase → uptake of K+ into skeletal muscle & liver
- High K+ concentration causes passive movement of K+ into cells
How does potassium shift during states of acidemia and 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 K+ secretion in 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 are the causes of Hypokalemia?
-
Decreased K+ intake (rare)
- Poverty
- Hypocaloric liquid protein diet supplements
- Exacerbated by diuretics for HTN
- Clay ingestion (a southern phenomenon)
-
Increased K+ entry into cells
- Metabolic alkalosis, hyperinsulinemia, increased catecholamines/beta agonists
-
Increased GI losses
- Nausea/vomiting →exacerbated by metabolic alkalosis & urinary K+ losses
- Nasogastric (NG) tube suction
- Diarrhea/intestinal fistulas/tube drainage
-
Increased urinary losses
-
Increased distal flow d/t impaired salt & water reabsorption
- Diuretics
- Salt wasting nephropathies
- Polydipsia/polyuria
- Hypercalcemia → increased distal flow
- Mineralcorticoid excess – aldosterone producing tumor
- Hypomagnesemia – affects # K channels
-
Increased distal flow d/t impaired salt & water reabsorption
- Increased sweat losses
- Dialysis
How do you evaluate hypokalemia if the cause is not obvious by history and physical?
- 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
- Kidney can decrease urine excretion of K+ to 25-30 meq in 24 hours
- If urine K is low, then loss is not from kidney
- Acid/base status: acidosis or alkalosis
What are the possible acid-base etiologies for hypokalemia with low urinary K+?
- Low urinary K+ (therefore GI losses)
- Acidosis: lower GI losses
- laxatives/villous adenoma
- Alkalosis: upper GI losses
- Vomiting
- Acidosis: lower GI losses
What are the possible acid-base etiologies for hypokalemia with high urinary K+?
- High urinary K+ (therefore kidney losses)
- Acidosis = ketoacidosis, type I or II renal tubular acidosis
- 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
- Low aldosterone = exogenous mineralcorticoid (real licorice)
- High aldosterone = adrenal adenoma or hyperplasia
What are the major complications of Hypokalemia?
- Muscle weakness, cramps, cardiac arrhythmias, rhabdomyolysis (K+ < 2.5 mEq/L)
-
Renal dysfunction – common in someone w/ anorexia/bulimia or somebody who is abusing diuretics or Bartter’s
- Loss of urinary concentrating ability
- Increase in urinary NH3 and NH4+ production/excretion
- Hypokalemic nephropathy/Interstitial fibrosis
- Hypertension – low K+ diet causes uptake of Na+
What is the treatment for Hypokalemia?
- Replace K+ → get patient out of danger initially
- then more gradually replace entire K deficit
- K+ deficit can only be approximated
- 200-400 mEq for each 1 mEq/L drop in K+
- 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 IV
What are the three causes of hyperkalemia?
- Increased Intake: oral or IV
- Shift: Movement from cells into extracellular fluid
- Decreased urinary excretion
How does the body adapt to increase K+?
- Normal kidney function – kidneys can adapt to excrete as much as 5x the normal K+ intake (400 meq/day)
- Chronic Kidney Disease (CKD) = reduced nephron mass, each nephron works harder
- Increased K+ excretion per nephron as long as distal urine flow is maintained and aldosterone secretion occurs
How can serum K+ be elevated even when total body K+ is normal?
- Potassium shifts from IC → EC
- Muscle/tissue breakdown
- rhabdomyolysis
- necrotic tissue from gangrene
- Insulin deficiency with hyperglycemia
- Metabolic acidosis (K+ moves out of cells)
- Drugs:
- Succinylcholine (paralytic agent)
- Beta-blockers (anti-catecholamines)
- Digoxin
- Muscle/tissue breakdown
What three things cause Hyperkalemia due to decreased urinary excretion?
- Renal failure: most common cause
- Effective circulating volume depletion
- Decreased distal flow
- Hypoaldosteronism
- decreased adrenal synthesis (Addison’s)
- decreased RAAS
What is the best way to treat Hyperkalemia?
- Antagonize K+ effects (seconds/minutes)
- Calcium IV
- Shift K+ into cells (minutes)
- Glucose & insulin
- NaHCO3 (make them alkalemic)
- Beta-agonists: albuterol nebs
- 3% NaCl if hyponatremia present
- Remove excess K+ (hours)
- Loop diuretics if patient makes urine (Lasix)
- Cation-exchange resins (kayexalate): avoid rectal use
- Can cause ischemic bowel
- Hemodialysis/peritoneal dialysis
When trying to figure out the underlying cause of Hypokalemia/Hyperkalemia, where should you look first?
Look primarily to adrenal glands (mineralcorticoids) and kidneys for causes: not usually dietary cause
What mechanisms control distal tubule secretion of K+?
- 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 and increases activity of Na-K ATPase
- K+ concentration in blood – gradient
- Distal urine flow is permissive to excretion of K+
