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
The volume loss mechanism is well-documented
Some patients transition to a lower maintenance dose, while others stop completely and monitor for weight rebound
These mechanisms represent biologically plausible explanations, not established causal pathways, and should be interpreted as context for clinical vigilance rather than confirmed pharmacological certainty
AlCar also activates an enzyme that directs glucose away from storage as glycogen and into energy generating pathways
Less pronounced fullness after meals
