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The first category reflects operational growing pains

Hyperkalemia Drugs That Cause Hypokalemia (Low Potassium) These drugs increase potassium loss from the kidneys or shift potassium into cells: Diuretics (most common cause): Loop diuretics: Furosemide, Torsemide Thiazide diuretics: Hydrochlorothiazide, Chlorthalidone Corticosteroids: Prednisolone, Dexamethasone (mineralocorticoid effect) Beta-2 Agonists: Salbutamol (Albuterol), Terbutaline Insulin (in high doses): Drives potassium into cells Amphotericin B High-dose Penicillins (e.g., Carbenicillin, Piperacillin) act as non-reabsorbable anions Theophylline Laxative abuse / diarrhea-causing drugs Clinical signs: Muscle weakness, cramps, arrhythmias (e.g., U-waves on ECG) Drugs That Cause Hyperkalemia (High Potassium) These drugs reduce potassium excretion or increase potassium retention: Potassium-sparing diuretics: Spironolactone, Eplerenone (Aldosterone antagonists) Amiloride, Triamterene ACE Inhibitors: Enalapril, Ramipril, Lisinopril ARBs: Losartan, Telmisartan, Valsartan Direct Renin Inhibitor: Aliskiren NSAIDs: Indomethacin, Ibuprofen (reduce renal perfusion) Heparin (including low molecular weight) Trimethoprim Beta-blockers (especially non-selective): Propranolol Digoxin (in toxicity) Cyclosporine, Tacrolimus Clinical signs: Peaked T-waves, muscle weakness, risk of cardiac arrest Key Tip for Memory | Potassium (Hypo) Think Diuretics & -Agonists | Potassium (Hyper) Think RAAS Blockers & K-Sparing Drugs | To view or add a comment, sign in WHY NASAL DELIVERY OF GLP-1 PEPTIDES? In contrast to the oral and subcutaneous routes of administration, nasal delivery of GLP-1 peptide drugs provides unique advantages: The nasal mucosal environment is less acidic, less digestive, and simpler to use than the oral delivery route

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