SM 193a - Potassium

Question 1

Why is insulin an effective treatment for hyperkalemia?

Answer 1

Insulin increases Na+ entry into the cell

• -> Increased activity of the Na+/K+ ATPase
  
  • Pumps Na+ out of the cell and K+ in
• -> Removal of K+ from the serum

Note: you need to also give glucose when you give insulin for hyperkalemia to prevent hypoglycemia!

Question 2

How can electrolyte levels help you determine whether a patient has Barter’s syndrome, or bulimia?

Answer 2

Urine analysis: Cl- is the key

• Barrter’s syndrome
  
  • High Na+, K+ and Cl- in the urine
    
    • The Na+/K+/2Cl- cotransporter is blocked, so none of these are reabsorbed
• Bulemia (vomiting)
  
  • Variable Na+
  • High K+
  • Low Cl-
    
    • Alkyosis is responsive to saline

Question 3

If a patient has low cortisol and high plasma renin activity, what kind of aldsoterone deficiency do they have?

Answer 3

Aldosterone + Glucocorticoid deficiency

Ex: Addison’s disease

Question 4

What are the most common causes of depletional hypokalemia?

Answer 4

• Extrarenal losses
  
  • GI tract losses
    
    • Vomiting, diarrhea, intestinal fistula, tube drainage
• Renal losses
  
  • Mineralcorticoid excess
  • Diuretics
  • Bartter syndrome
  • Gitelman syndrome
  • Renal tubular acidosis
• Low intake

Question 5

What is the first EKG manifestation of hyperkalemia?

Answer 5

High T wave

Question 6

What stimulus drives K+ secretion through Maxi-K?

Answer 6

Increased flow in the lumen creates a chemical gradient

• Flow removes K+ in the lumen
• K+ flows down its concentration gradient through Maxi-K

Question 7

What causes of hypokalemia are associated with metabolic alkalosis?

Answer 7

• Vomiting
• Diuretics
  
  • Thiazide and loop
• Bartter’s syndrome
• Gitelman’s syndrome

Question 8

What are the common etiologies of hypokalemia associated with normal or low blood pressure?

Answer 8

• Diuretics
  
  • Thiazides and loop diuretics
  • These might be prescribed for HTN, but over-use -> hypovolemia -> hypotension
• Proximal & distal tubular acidosis
• Bartter’s syndrome
• Gitelman’s syndrome
• Drug-induced

Question 9

What cause of hypokalemia are associated with metabolic acidosis?

Answer 9

Diarrhea (Low serum K+, low urine K+

Renal tubular acidosis (Low serum K+, High urine K+)

Question 10

What are the renal causes of hyperkalemia?

Answer 10

• Decreased GFR
• Aldosterone deficiency
• Decreased distal Na+ delivery
• Blockade of Na+ channels in the cortical collecting tubule
  
  • Amiloride
  • Spironolactone

Question 11

Which hormones upregulate activity of the Na+/K+ ATPase?

Answer 11

• Insulin
  
  • -> Na+ entry into the cell
  • -> stimulation of the Na+/K+ ATPase
• Epinephrine (Beta-2 agonist)
  
  • -> Formation of cAMP
  • -> Stimulation of Na+/K+ ATPase
  • Also causes a minor release of K+ into cells via alpha-1 stimulation

Question 12

Describe the mechanism for K+ reabsorption in the proximal tubule

Answer 12

Paracellular pathway

H2O is reabsorbed and K+ comes with ti

This reabsorbs about 67% of filtered K+

Question 13

What are the EKG effects of hypokalemia?

Answer 13

As hypokalemia worsens, the following EKG changes appear:

• Low T wave
• High U wave
• Low ST segment

Question 14

What diseases might produce hypokalemia associated with hypertension?

Answer 14

• Primary hyperaldosteronism
• Cushings syndrome

Question 15

What is the first EKG manifestation of hypokalemia?

Answer 15

Low T wave

Question 16

What causes Gitelman’s syndrome?

What is the effect on K+ homeostasis?

Answer 16

LOF mutation in the Na+/Cl- cotransporter in the distal tubule leads to hypokalemia (but less severe than Bartter’s)

• K+ and Na+ stays in the lumen (not reabsorbed)-> Increased Na+ delivery to the cortical collecting duct
  
  • -> Increased Na+ reabsorption through ENaC
  • -> Increased K+ secretion through ROMK
  • -> Hypokalemia
• Na+ wasting
  
  • -> Increased aldosterone
  • -> Further promotes Na+ reabsortion through ENaC
  • -> Further increases K+ secretion through ROMK

Question 17

What causes Bartter’s syndrome?

How does it affect K+ homeostasis?

Answer 17

Defect the K+/Na+/2Cl co-transporter in the thick ascending limb that leads to hypokalemia

• K+ and Na+ stays in the lumen (not reabsorbed)
  
  • -> Increased Na+ delivery to the cortical collecting duct
    
    • -> Increased Na+ reabsorption through ENaC
    • -> Increased K+ secretion through ROMK
    • -> Hypokalemia
• Na+ wasting
  
  • -> Increased aldosterone
  • -> Further promotes Na+ reabsortion through ENaC
  • -> Further increases K+ secretion through ROMK
• Also causes volume depletion due to wasting of Na+ and Cl-

Question 18

What are the EKG effects of hyperkalemia?

Answer 18

As hyperkalemia progresses, the following ECG chagnes appear:

• High T wave
• Prolonged PR interval, depressed ST segment
• Ventricular fibrillation