Kalemic - Popham

Question 1

What are the normal body stores of Potassium?

Answer 1

• Normal body stores (70 kg adult) are 3000 to 4000 meq K+ (50-55 meq/kg)
• 98% of K+ is INTRACELLULAR
  
  • Maintains gradient

Question 2

What is the intracellular concentration of K+?

Answer 2

140 mEq/L

Question 3

What is the extracellular concentration of K+?

Answer 3

4-5 mEq/L

Question 4

What is the average daily intake of K+? What if you are not getting enough?

Answer 4

• 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

Question 5

What is the reflected total body deficit if K+ decreased by 1 mEq/L?

(normal serum/plasma K+ 4-5 mEq/L)

Answer 5

200-400 mEq

Question 6

What is the reflected total body excess if K+ increased by 1 mEq/L?

(normal serum/plasma K+ 4-5 mEq/L)

Answer 6

100-200 mEq

Question 7

What is the function of K+?

Answer 7

• 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

Question 8

What are symptoms of low or high K+?

Answer 8

• 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+

Question 9

What EKG changes are present in Hypokalemia?

Answer 9

• PR interval prolongation
• ST depression
• Flattened or inverted T waves
• U-waves
• QRS widening

Question 10

What EKG changes are present in Hyperkalemia?

Answer 10

• PR interval prolongation
• Elevated T waves
• Widened QRS interv

Question 11

How does calcium modify the K+ effects on action potentials?

Answer 11

• 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)

Question 12

How does metabolic acidosis modify the K+ effects on action potentials?

Answer 12

• Exacerbates hyperkalemia by causing K+ to be released from cells as HCl is buffered into cells
  
  • Correct with bicarb

Question 13

How does Potassium effect digoxin levels?

Answer 13

• CLINICAL TIP:
  
  • HYPOkalemia increases digoxin toxicity
  • digoxin toxicity causes HYPERkalemia
    
    • Digoxin disables Na+/K+ ATPase

Question 14

How is the balance between intracellular and extracellular K+ regulated?

Answer 14

• 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

Question 15

How does the K+ that you drink in a glass of Orange Juice distribute between the cells and extracellular fluid?

Answer 15

• 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

Question 16

How does potassium shift during states of acidemia and alkalosis?

Answer 16

• 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

Question 17

What determines K+ secretion in the kidney?

Answer 17

• Plasma K+ concentration
• Urine flow in distal tubule (permissive)
• Aldosterone:
  
  • causes K+ secretion by principal cells of collecting tubule – outer medulla, cortical & inner medulla

Question 18

What are the causes of Hypokalemia?

Answer 18

• 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 sweat losses
• Dialysis

Question 19

How do you evaluate hypokalemia if the cause is not obvious by history and physical?

Answer 19

• 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

Question 20

What are the possible acid-base etiologies for hypokalemia with low urinary K+?

Answer 20

• Low urinary K+ (therefore GI losses)
  
  • Acidosis: lower GI losses
    
    • laxatives/villous adenoma
  • Alkalosis: upper GI losses
    
    • Vomiting

Question 21

What are the possible acid-base etiologies for hypokalemia with high urinary K+?

Answer 21

• 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

Question 22

What are the major complications of Hypokalemia?

Answer 22

• 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+

Question 23

What is the treatment for Hypokalemia?

Answer 23

• 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

Question 24

What are the three causes of hyperkalemia?

Answer 24

1. Increased Intake: oral or IV
2. Shift: Movement from cells into extracellular fluid
3. Decreased urinary excretion

Question 25

How does the body adapt to increase K+?

Answer 25

• 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

Question 26

How can serum K+ be elevated even when total body K+ is normal?

Answer 26

• 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

Question 27

What three things cause Hyperkalemia due to decreased urinary excretion?

Answer 27

• Renal failure: most common cause
• Effective circulating volume depletion
  
  • Decreased distal flow
• Hypoaldosteronism
  
  • decreased adrenal synthesis (Addison’s)
  • decreased RAAS

Question 28

What is the best way to treat Hyperkalemia?

Answer 28

• 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

Question 29

When trying to figure out the underlying cause of Hypokalemia/Hyperkalemia, where should you look first?

Answer 29

Look primarily to adrenal glands (mineralcorticoids) and kidneys for causes: not usually dietary cause

Question 30

What mechanisms control distal tubule secretion of K+?

Answer 30

• 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+