Week 2:Disorders of Potassium balance Flashcards Preview

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

Define hyperkalemia and hypokalemia.

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


Describe pseudohyperkalemia.

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


What are 3 major general causes of hyperkalemia?

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
-hyperkalemic periodic paralysis


What is hyperkalemic periodic paralysis?

-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)


What are causes of decreased urinary K+ excretion?

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


Describe Type IV Renal Tubular Acidosis.

hyporeninemic hypoaldosternosism (deficiency of renin and aldosterone)
-non gap metabolic acidosis with normal urine acidifying ability
-mimicked by NSAIDS and COX2 inhibitors
-often underlying tubulointerstitial disease: DM, SLE, obstruction, HIV, myeloma


What are symptoms of hyperkalemia?

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


What is the treatment for hyperkalemia?

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
3. Removal of excess K+ (slow but definitive)
-cation exchange resin (Kayexalate-intestinal necrosis is complication)
4. Dietary K+ restriction (chronically helpful)


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

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


What is the main cause of pseudohypokalemia?

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


What are major causes of hypokalemia?

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


Describe familial hypokalemic periodic paralysis.

-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


What is thyrotoxic hypokalemic periodic paralysis?

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


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

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


What is the differential diagnosis of hyperaldosteronism?

W/ hypokalemia and HTN
1. High Aldosterone, High renin
-Renal artery stenosis
2. High aldosterone, low renin
-Primary hyperaldosteronism
-glucocorticoid-remediable aldosteronism
3. Low aldosterone
-Syndrome of apparent mineralocorticoid excess


What are the symptoms of hypokalemia?

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


How do you treat hypokalemia?

-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