1. Approach to the patient with electrolyte disorders Hypokalemia-Hyperkalemia
Zehra Eren, M.D.

2. LEARNING OBJECTIVES recall potassium distribution
recall etiology of hypokalemia and hyperkalemia
describe sing and symptoms of hypokalemia and hyperkalemia
describe laboratory findings of hypokalemia and hyperkalemia
explane treatment of hypokalemia and hyperkalemia

3. POTASSİUM DİSTRİBUTİON
Gastrointestinal absorption→
%98 intracellular
%2 extracellular
NA+K+ ATPase → transports
two K+ into cell
three Na+ out cell

6. Hypokalemia 
Serum K+ < 3.5 mEq/L (mmol/L)

8. Causes of Hypokalemia Pseudohypokalemia -Extreme leukocytosis
Decreased K intake
Increased K losses
-Nonrenal (skin, gastrointestinal)
-Renal

9. RENAL POTASSİUM LOSS 1. Increased distal flow and distal Na+ delivery
-diuretics
-osmotic diuresis
-salt-wasting nephropathies
2. Increased secretion of potassium
- Mineralocorticoid excess: primary hyperaldosteronism [aldosterone-producing adenomas (APAs)], primary or unilateral adrenal hyperplasia (PAH), idiopathic hyperaldosteronism (IHA) due to bilateral adrenal hyperplasia, and adrenal carcinoma], familial hyperaldosteronism (FH-I, FH-II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignanthypertension, renin-secreting tumors, renal arterystenosis, hypovolemia), Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome

10. RENAL POTASSİUM LOSS
-Apparent mineralocorticoid excess: genetic deficiency of 11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice, food products, drugs), Liddle's syndrome [genetic activation of epithelial Na+ channels (ENaC)]
-Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin,oxacillin and carbenicillin)

11. Causes of Hypokalemia Redistribution (increased entry into cell)
-Insulin excess
-Alkalemia
-“Stress” [β2 adrenergic sympathetic activityꜛ: asthma attack, acute coronary syndrome, trauma, drug intoxication (cocaine) or alcohol withdrawal, B2 adrenergic drugs ]
-α-adrenergic antagonists
-Hypokalemic periodic paralysis
-Thyrotoxicosis
-Barium, Cesium
-Hypothermia
-Downstream stimulation of NA+/K+ ATPase: theophyline, cafferine

12. DİAGNOSİS Rule out -pseudohypokalemia -redistribution
Potassium deplettion
-renal
-gastrointestinal
-skin

13. Clinical manifestations
Cardiovascular:
-Hypertansion (↑BP 5-10mmHg )
-Arrhythmias
-Digitalis toxicity
Neuromuscular:
1.Smooth muscle:
-Ileus
2.Skeletal muscle:
-Weakness
-Paralysis
-Rhabdomyolysis

14. Clinical manifestations
Endocrine:
-Glucose intolerance (↓insulin release and sensitivity)
Renal: ↓blood flow,↑vascular resistance
-Vasopressin resistance
-Increased ammonia production
-Metabolic alkalosis (retention of Na, Cl, HCO3)
-Polyuria, phosphaturia, hypocitraturia
Structural changes:
Renal cysts
Interstitial changes
PT dilation, vacuolization

15. TREATMENT GOALS prevent life-threatening and/or chronic consequences
replace the associated K+ deficit
correct the underlying cause and/or mitigate future hypokalemia

16. TREATMENT
Urgency of therapy depends on -the severity of hypokalemia -associated clinical factors (cardiac disease,digoxin therapy, etc.) -rate of decline in serum K+ Cautions -severe redistributive hypokalemia -concomitant Mg2+ deficiency

17. TREATMENT Oral İntravenous Safely at a rate of 10 mmol/h
20mmol KCL →↑serum K + ~ 0.25 mmol/L
↑20mmol/h replacement →
central venous catheter

18. Hyperkalemia 
Serum K ≥5.0 mEq/L (mmol/L)

19. Causes of Hyperkalemia
Pseudohyperkalemia
-Thrombocytosis
-Leukocytosis
-Ischemic blood draw
Redistibution (increased K release from cells)
-Exercise, especially in setting of β adrenergic receptor blockade and mineral acidosis
-Hyperchloremic metabolic acidosis
-Insulin deficiency
-Hypertonicity
-α adrenergic receptor stimulation

20. Causes of Hyperkalemia
Excessive intake: rare as sole cause
Impeared renal K+ excretion
GFR <20 mL/min:
-Endogenous or exogenous K+
-Drugs that impair K+ excretion

23. Clinical manifestations
May be disproportionately greater than level of serum K
Cardiovascular
-T-wave abnormalities
-Bradyarrhythmias
Neuromuscular
-Ileus
-Paresthesias
-Weakness
-Paralysis
Renal/electrolyte
-Decreased ammonia production
-Metabolic acidosis

26. Case1
A 70-year-old man with advanced prostate cancer develops bilateral ureteral obstruction and acute on chronic renal failure. His potassium rises to 7.7 mEq/L with peaked T-waves on electrocardiogram. His medications include digoxin.

27. Case2
A 72 year old male found collapsed at home on floor of his bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. His family last had contact with him 3 days prior to his collapse.
Medical History:CCF , Hypertension , Type 2 DM, Osteoarthritis
Medication History:His is taking  enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis.His diabetes is diet controlled.