Week 2:Disorders of Potassium balance Flashcards Preview

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Flashcards in Week 2:Disorders of Potassium balance Deck (17)
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1
Q

Define hyperkalemia and hypokalemia.

A

Hyperkalemia: Serum [K+]>5 mEq/L
Hypokalemia: Serum [K+]<3.5 mEq/L

2
Q

Describe pseudohyperkalemia.

A

Needs to be ruled out. Can be from:

  • hemolyzed blood sample
  • leukocytosis/thrombocytosis (release of K during lysis of cells)
  • ischemia from prolonged tourniquet time or exercise of the limb in the presence of tourniquet
3
Q

What are 3 major general causes of hyperkalemia?

A
  1. Increased intake
    - excessive ingestion doesn’t lead to hyperkalemia without other contributing factors
  2. Decreased urinary K+ excretion
    - chronic hyperkalemia can’t occur unless you have this
  3. Cell shift
    - metabolic acidosis
    - hyperglycemia
    - b-blocker
    - digitalis
    - hyperkalemic periodic paralysis
4
Q

What is hyperkalemic periodic paralysis?

A
  • autosomal dominant
  • muscle disease, onset in infancy or childhood
  • transient episodes of paralysis
  • recurrent attacks of muscle weakness lasting<1-2hr
  • precipitated by cold, rest after exercise, fasting
  • hyperkalemia usually mild
  • mutations that impair inactivation of voltage dependent Na+ channel SCN4A (depolarizing block-sustained depolarization)
  • made worse by hyperkalemia (b/c decreases gradient for K+ to leave cell and depolarize)
5
Q

What are causes of decreased urinary K+ excretion?

A

Defined as 24 hr urine K+<40mEq

  1. decreased CD [K] secretion rate
    - ENac Block: amiloride, trimethoprim, pentamidine, cyclosporine
    - Hypoaldosteronism: RTA type 4, NSAIDs, ACEI/ARB, heparin, spironolactone
  2. Decreased tubular flow rate
    - renal failure
    - decreased in ECV
6
Q

Describe Type IV Renal Tubular Acidosis.

A

hyporeninemic hypoaldosternosism (deficiency of renin and aldosterone)

  • non gap metabolic acidosis with normal urine acidifying ability
  • hyperkalemia
  • mimicked by NSAIDS and COX2 inhibitors
  • often underlying tubulointerstitial disease: DM, SLE, obstruction, HIV, myeloma
7
Q

What are symptoms of hyperkalemia?

A

-usually asymptomatic
-muscle uptake
-cardiac arrhythmias
EKG changes
-peaked T waves, widened QRS, shortened ST, loss of P wave, sine wave idioventricular rhythm

8
Q

What is the treatment for hyperkalemia?

A
  1. Stabilize membrane excitability if there are EKG changes: Calcium chloride or gluconate
  2. Increase K+ entry into cells (rapid but transient)
    - glucose and insulin
    - beta adrenergic agonist
    - NaHCO3
  3. Removal of excess K+ (slow but definitive)
    - cation exchange resin (Kayexalate-intestinal necrosis is complication)
    - diuretics
    - dialysis
  4. Dietary K+ restriction (chronically helpful)
9
Q

What causes a fall in serum K and a increase in serum K?

A
  1. Fall in Serum K, moves into cell
    - insulin
    - beta agonists
    - alkalosis
    - alpha adrenoreceptor blockers
  2. Increase in serum K, moves out of cell
    - acidosis
    - beta blockers
    - increased osmolality (causes water to shift out of cell, concentrating K+ inside, and it follows out too)
    - exercise
    - alpha adrenoreceptor agonists
10
Q

What is the main cause of pseudohypokalemia?

A

-acute myeloblastic leukemia, large numbers of abnormal leukocytes take up potassium when blood is stored in collection vial for prolonged periods at room temp

11
Q

What are major causes of hypokalemia?

A
  1. cellular shift
    - metabolic alkalosis
    - increased B-agonist activity
    - insulin
    - hypokalemic periodic paralysis
  2. Enhanced GI losses
    - vomiting
    - diarrhea
  3. Increased urinary losses (K wasting)
    - loop and thiazide diuretics
    - vomiting
    - mineralocorticoid excess, most often aldosterone producing adrenal adenoma
    - secondary hyperaldosteronism due to renal artery stenosis
    - renal tubular acidosis
12
Q

Describe familial hypokalemic periodic paralysis.

A
  • autosomal dominant, mutations in Ca and Na channels
  • precipitated by meal or exercise
  • repetitive episodes of acute profound hypokalemia and paralysis lasting hrs to days
  • recovery of serum K+ after each episode without repletion
13
Q

What is thyrotoxic hypokalemic periodic paralysis?

A
  • 20-40 yrs, predominantly Asians
  • mostly male
  • only with thyrotoxicosis, which may be asymptomatic
14
Q

How is increased urinary K+ excretion diagnosed? What are causes?

A

24 hr urine K+>40mEq
1. Decreased TALH/DCT NaCL reabsorption
-Bartter’s: inactivating mutations in TALH, can be in NaK2CL, ROM K, Cl channel
(loop diuretic mimics)
-Gitelman’s: inactivating mutations in Na-Cl cotransporter (thiazide diuretic mimics)
2. Delivery of Na+ w/ nonreabsorbable anion–>increases rate of K+ secretion
-HCO3- delivery due to vomiting, ketoanions
3. Hyperaldosteronism
-Liddle’s: activating mutation in ENac
-glucocorticoid remediable aldosteronism
-syndrome of apparent mineralocorticoid excess: inactivating mutation of B-HSD
4. Increased membrane permeability; amphotericin

15
Q

What is the differential diagnosis of hyperaldosteronism?

A

W/ hypokalemia and HTN

  1. High Aldosterone, High renin
    - Renal artery stenosis
    - reninoma
  2. High aldosterone, low renin
    - Primary hyperaldosteronism
    - glucocorticoid-remediable aldosteronism
  3. Low aldosterone
    - Cushings
    - Liddles
    - Syndrome of apparent mineralocorticoid excess
16
Q

What are the symptoms of hypokalemia?

A
  • usuallly asymptomatic
  • muscle weakness
  • polyuria/polydipsia- acquired nephrogenic DI
  • Rabdomyolysis
  • EKG changes (depressed ST segement, Flat T waves, prolonged QT, U waves)
  • Arrhythmias
17
Q

How do you treat hypokalemia?

A
  • Oral KCl supplements (K citrate if patient has metabolic acidosis)
  • IV KCl (no more than 10-20 mEq/hr)
  • Concomitant hypomagnesemia needs to be corrected (otherwise hypokalmia is refractory)
  • Amiloride or spironolactone may be useful in patients with hyperaldosteronism