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Hypokalemia and Hyperkalemia Dr Madhukar Mittal Medical Endocrinology.

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Presentation on theme: "Hypokalemia and Hyperkalemia Dr Madhukar Mittal Medical Endocrinology."— Presentation transcript:

1 Hypokalemia and Hyperkalemia Dr Madhukar Mittal Medical Endocrinology

2 Hypokalemia 1.Spurious −Extreme leukocytosis (WBC uptake of K+ in the test tube)

3 2.Transcellular shift –Stress induced catecholamine release Asthma, COPD exacerbation, CHF, MI/Angina, Drug withdrawal syndrome –Drugs Insulin Theophylline, β2 agonists –Anabolic state Vit B12 or Folate treatment GM-CSF TPN –Hypokalemic periodic paralysis 3.Decreased Total Body K+

4 Metabolic alkalosis – Mineralocorticoid excess Primary aldosteronism Secondary aldosteronism ↑ mineralocorticoid (Non-aldosterone) action – Normal/↓ BP, No edema, Secondary aldosteronism Bartter syndrome Gitelman syndrome Diuretic abuse Chronic vomiting Hypomagnesemia Metabolic acidosis – DKA – RTA type 1 & 2 – Ureterosigmoidostomy – Amphotericin B – Acetozolamide Normal pH – Decreased intake – GI losses Metaboic acidosis – Lower GI losses Diarrhea Laxative abuse Metabolic alkalosis – Villous adenoma – Congenital Cl- losing diarrhea – Remote vomiting – Remote diuretic use Variable pH – Postobstructive diuresis – Drugs Aminoglycosides Cisplatin Renal Loss (urinary K + >20meq/l) Extra-renal Loss (urinary K + <20meq/l)

5 Metabolic alkalosis –Mineralocorticoid excess Primary aldosteronism Secondary aldosteronism ↑ mineralocorticoid (Non-aldosterone) action –Normal/↓ BP, No edema, Secondary aldosteronism Bartter syndrome Gitelman syndrome Diuretic abuse Chronic vomiting Hypomagnesemia Metabolic acidosis –DKA –RTA type 1 & 2 –Ureterosigmoidostomy –Amphotericin B –Acetozolamide Normal pH –Decreased intake –GI losses Renal Loss (urinary K + >20meq/l)

6 Metaboic acidosis –Lower GI losses Diarrhea Laxative abuse Metabolic alkalosis –Villous adenoma –Congenital Cl- losing diarrhea –Remote vomiting –Remote diuretic use Variable pH –Postobstructive diuresis –Drugs Aminoglycosides Cisplatin Extra-renal Loss (urinary K + <20meq/l)

7 ↑Aldosterone, ↓PRA (Primary Aldosteronism) –Adrenal adenoma (Conn syndrome) –Idiopathic hyperplasia –Adrenal carcinoma –Glucocorticoid remediable aldosteronism (GRA)

8 Hypermineralocorticolism/Aldosteronism (Metabolic alkalosis, Hypokalemia, ↑BP) ↑↑Aldosterone, ↑PRA (Secondary Aldosteronism) –Edema states (Cirrhosis, CHF, Nephrosis) –Pregnancy (Normal physiologic response) –↑Renin d/t ↓Renal blood flow Renal artery stenosis Accelerated Hypertension (renal vasoconstriction) Malignant hypertension (arteriolar nephrosclerosis) –Primary reninism Renin producing tumors –↓/N BP, No edema Bartter syndrome Gitelman syndrome Chronic vomiting Diuretic abuse Hypomagnesemia Hypertensive States

9 Hypermineralocorticolism/Aldosteronism (Metabolic alkalosis, Hypokalemia, ↑BP) ↓/N Aldosterone, ↓PRA (↑ Mineralocorticoid action) –Liddle syndrome –Cushing syndrome –AME (apparent mineralocorticoid excess syndrome) –Licorice/Carbenoxolone ingestion (Glycyrrhizinic acid Ɵ 11-βHSD II enzyme) –CAH – 11β hydroxylase deficiency –DOC (deoxycorticosterone) secreting tumour

10 Hypermineralocorticolism/Aldosteronism (Metabolic alkalosis, ↓ K +, ↓/N BP) Bartter syndrome –Hypercalciuria Gitelman syndrome –↓Urinary Ca, ↓ serum Mg Diuretic abuse Hypomagnesemia Chronic vomiting –Urine Cl - <10meq/l Urine Cl - >20meq/l

11 CVS - ECG Flattening or inversion of T wave with ST depression Prominent U waves Prolonged QT (QU) interval + prolonged PR interval, wide QRS complex Atrial and ventricular arrhythmias Predisposition to digitalis toxicity

12 Clinical NeuroMs –Weakness, flaccid paralysis –Cramps, tetany, rhabdomyolysis –Ileus, constipation, urinary retention Endocrine –Glucose intolerance –Growth retardation, ↓ aldosterone Renal –↓ renal blood flow, ↓ GFR –Nephrogenic diabetes insipidus –Increased ammoniagenesis (hepatic encephalopathy) –Chloride wasting/metabolic alkalosis

13 Treatment Agent –KCl –Pot bicarbonate and citrate for hypokalemia associated with chronic diarrhea, RTA Max concentration –<40 mmol/l via peripheral vein –<60 mmol/l via central vein Infusing solution –NS –Mannitol Rate of infusion –<20mmol/hr unless paralysis, malignant ventr arrhythmias

14 Treatment Montoring –Clinical – NeuroMs –ECG –Plasma K conc. Hypokalemic periodic paralysis –Ca channel disorder –Oral KCl mmol/Kg every min –IV KCL in mannitol –Long term – Actazolamide mg/d, Triamterene mg/d, Spironolactone mg/d, Dichlorphenamide mg/d

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16 Hyperkalemia 1.Spurious (Pseudo) −Prolonged use of tourniquet −Ischemic blood draws −RBC hemolysis in test tubes −Marked thrombocytosis or leukocytosis

17 2.Transcellular shift –Metabolic acidosis –Drugs Insulin deficiency and hypertonicity β blockers –Tissue breakdown Rhabdomyolysis Tumor lysis syndrome Intravascular hemolysis –Hyperkalemic periodic paralysis –Drug toxicity Digitalis succinylchloline 3.Chronic Hyperkalemia

18 3. Chronic Hyperkalemia (Metabolic acidosis, Hypokalemia) ↓Aldosterone, ↑PRA (Hypoaldosteronism) –Primary adrenal insufficiency –Aldosterone bisynthetic defect Mutation in aldosterone synthase gene (cyp 11B2) CAH – Lipoid, 3β-HSD def, 21-OH-lase deficiency –Heparin –ACE Ɵ, ARBs (selective unresposivensess to angiotensin II) ↓Aldosterone, ↓PRA (Hyporeninemic Hypoaldosteronism) –NSAIDS –Chronic TIN, Diabetic Nephropathy, Mild renal failure

19 3. Chronic Hyperkalemia ↓Aldosterone, ↓PRA, ↑BP, (Cl- shunt/reabsorption in distal tubule) –PHA-II (Gordon’s syndrome) –Cyclosporine –Distal Type 4 RTA ↑Aldo, ↑PRA, ↓BP (Mineralocorticoid Resistant Hyperkalemia), Impaired distal Na+ reabsorption –PHA-I –Potassium sparing diuretics - Spironolactone, Eplerenone, Triamterene, Amiloride –Trimethoprim –Pentamidine

20 ↓Aldosterone, ↓PRA (Hypoaldosteronism) NSAIDS Chronic TIN Mild renal failure Cl- shunt/reabsorption in distal tubule (↑BP) –Cyclosporine –Type 4 RTA –Gordon syndrome (PHA-II)

21 ↑Aldosterone, ↑PRA (Mineralocorticoid Resistant Hyperkalemia) PHA-I Potassium sparing diuretics –Spironolactone, Eplerenone –Triamterene, Amiloride –Trimethoprim –Pentamidine –↓BP –Impaired distal Na+ reabsorption

22 CVS - ECG Tall peaked (tented) T waves (earliest change) Short QT interval Wide QRS, PR interval prolongs → 2 0 or 3 0 AV block ↓ P wave amplitude → complete loss of P waves with associated junctional rhythm QRS widens → sine wave (ventr. flutter-like) pattern Eventual asystole

23 Treatment 1.Restrict K intake to <40 mmol/day 2.Stop K supplements 3.Stop K sparing diuretics

24 Treatment 1.Ca gluconate (10%) –10 ml over 1 -3 min IV –Repeat if no change in ECG after 5-10 min U regular insulin g glucose IVI 3.NaHCO3 3 amp (50-150mmol) in 1L of 5%D 4.Nebulized β 2 agonist (albuterol 20mg in 4ml NS)

25 Treatment 5.Diuretics – furosemide mg/day 6.Resins (sodium polysterene sulfonate) –25-50g in 100ml of 20% sorbitol –Retention enema 50g in 50ml of 70% sorbitol in 150ml tap water 7.Dialysis –For patients with renal failure –Severe life-threatening hyperkalemia unresponsive to conservative treatment –Hemodialysis – most rapid and effective way –Peritoneal dialysis – only 15-20% as effective as hemodialysis

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27 Thank You


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