Hypokalemia and Hyperkalemia Management PDF
Document Details

Uploaded by CleanlyBoston
Mansoura
Tags
Related
- Hypokalemia and Hyperkalemia Management PDF
- Hypokalemia & Hyperkalemia - Clinical Pharmacology PDF
- Potassium PDF - Biology
- Clinical ECG: Conduction Blocks, Pacemakers, and Electrolyte Disturbances PDF
- Regulation and Disorders of Potassium Balance PDF
- CapÃtulo 25.5 Trastornos HidroelectrolÃticos PDF
Summary
This document provides a discussion of hypokalemia and hyperkalemia, two conditions related to potassium levels in the body. It covers causes, symptoms, and management strategies, including pharmacological approaches. The information is presented in a factual manner with clear explanations, suitable for clinical and medical reference.
Full Transcript
█ Hypo okalemia a  Potassium is the major intracellula ar cation. 98% of K+ in the bo dy is found in the intra acellular co ompartment, leaving g 2% in exttracellular fluid spacees.  Ren + nal K excrretion occu urs from thhe DCT...
â–ˆ Hypo okalemia a  Potassium is the major intracellula ar cation. 98% of K+ in the bo dy is found in the intra acellular co ompartment, leaving g 2% in exttracellular fluid spacees.  Ren + nal K excrretion occu urs from thhe DCT and d is mediated by ald a Na+ dosterone and delivery to thee distal nep phron.  Hyppokalemia is defined as serum K+ 5 mEq/L. m It can c result ffrom trans scellular + + shifft of K , or decreased d renal exc cretion of K (as in chhronic renaal failure).  Thee most co ommon manifestati m ions are muscle paralysis, p palpitations, high peaaked T wavve and sho ort QT interrval in the ECG.  Beccause K is + i usually exchange ed with H+ at the DCT,D hypeerkalemia is i often linkeed to meta abolic acid dosis. Druugs cause transcellu of K+ (from ular shift o m tissue to o plasma):: Insu ency and β-blockers: they ↓ transmembra ulin deficie ane Na+/K++-ATPase activity. a ugs that ↓ renal excrretion of K +: Dru K+ sparing diu uretics, AC CEIs, NSAIIDs, cyclos sporins. 101 Management  Mild hyperkalemia: could be corrected by diuretics and oral cation exchange resins (Polystyrene sulfonate) to promote the exchange of Na+ for K+ in the GIT.  Severe hyperkalemia with ECG changes: ï€ Intravenous calcium gluconate to reduce cardiac toxicity (↓ membrane excitability). The usual dose is 10 mL of a 10% solution infused over 2 to 3 minutes. ï€ Intravenous insulin with glucose: 20 U regular insulin mixed with 500 ml D5W. ï€ Correct metabolic acidosis with i.v. NaHCO3 solution. ï€ Hemodialysis is reserved for patients with renal failure or with life-threatening hyperkalemia resistant to other treatment. Part 6: Pharmacological manipulation of the urine pH Normal urine pH is 5.2-6.5. It is possible, by the use of pharmacological agents, to produce urinary pH values ranging from ~ 5 to 8.5. â–ˆ Alkalinization of the urine  Indications: ï€ To enhance excretion of acidic drugs and organic compounds e.g. aspirin, sulfonamides, and uric acid. ï€ To enhance dissolution of uric acid and cystine stones. ï€ To relieve dysuria (burning micturition) in some cases of bladder infection.  Alkalinizing agents: ï€ Oral: sodium and potassium citrate salts: citrate is metabolized into bicarbonate which is excreted in urine. ï€ Intravenous bicarbonate solution: contains 5% NaHCO3. â–ˆ Acidification of the urine  Indications: ï€ It is rarely used clinically except in a specialized test to discriminate between different kinds of renal tubular acidosis. ï€ It can be very dangerous in cases of renal or hepatic impairment.  Acidifying agents: ï€ Oral: ascorbic acid > 2 g/d. ï€ Intravenous ammonium chloride (NH4Cl) solution. 102