Week 2:Disorders of Potassium balance Flashcards
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?
- Increased intake
- excessive ingestion doesn’t lead to hyperkalemia without other contributing factors - Decreased urinary K+ excretion
- chronic hyperkalemia can’t occur unless you have this - Cell shift
- metabolic acidosis
- hyperglycemia
- b-blocker
- digitalis
- 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
- decreased CD [K] secretion rate
- ENac Block: amiloride, trimethoprim, pentamidine, cyclosporine
- Hypoaldosteronism: RTA type 4, NSAIDs, ACEI/ARB, heparin, spironolactone - 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
- hyperkalemia
- 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?
- Stabilize membrane excitability if there are EKG changes: Calcium chloride or gluconate
- Increase K+ entry into cells (rapid but transient)
- glucose and insulin
- beta adrenergic agonist
- NaHCO3 - Removal of excess K+ (slow but definitive)
- cation exchange resin (Kayexalate-intestinal necrosis is complication)
- diuretics
- dialysis - Dietary K+ restriction (chronically helpful)
What causes a fall in serum K and a increase in serum K?
- Fall in Serum K, moves into cell
- insulin
- beta agonists
- alkalosis
- alpha adrenoreceptor blockers - 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
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?
- cellular shift
- metabolic alkalosis
- increased B-agonist activity
- insulin
- hypokalemic periodic paralysis - Enhanced GI losses
- vomiting
- diarrhea - 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
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
- High Aldosterone, High renin
- Renal artery stenosis
- reninoma - High aldosterone, low renin
- Primary hyperaldosteronism
- glucocorticoid-remediable aldosteronism - Low aldosterone
- Cushings
- Liddles
- Syndrome of apparent mineralocorticoid excess
