BPS 334 Lecture Notes - Lecture 24: Distal Convoluted Tubule, Ace Inhibitor, Carbonic Anhydrase
Document Summary
Thiazides: inhibit na/cl co-transporter, encourage loss of sodium and increase urine volume. Decrease the loss of calcium and uric acid. Functional group: sulfonamide group at location 7 and r2 group must be electron withdrawing. Preferred o(cid:448)er loop(cid:859)s (cid:449)he(cid:374) crcl is greater tha(cid:374) (cid:1007)0(cid:373)l/(cid:373)i(cid:374). Digoxin toxicity, lithium levels can also go up. Elevated blood sugar, lipids, potassium and uric acid (gout) N double bond in the thiazides is reduced to form hydrothiazides replace ring-sulfamoyl group with other electronegative group. Loss of sodium, potassium, magnesium, and calcium in the urine. Preferred o(cid:448)er thiazide(cid:859)s (cid:449)he(cid:374) crcl is less tha(cid:374) (cid:1007)0(cid:373)l/(cid:373)i(cid:374) or if significant edema is present. Taken if the patient has a sulfa allergy. Sodium channel blockers (potassium sparing): inhibit sodium channels. Duration: greater than 24 hours because some metabolites are active. 50% excreted unchanged (un-metabolized) thus renal impairment can increase life. Aldosterone antagonists (potassium sparing): late distal tubule and collecting duct. Avoid use if crcl < 50 ml/min.