BIOM1060 Lecture Notes - Lecture 6: Calcium Channel Blocker, Ace Inhibitor, Peripheral Edema
Document Summary
A: ace inhibitors, ang ii receptor antagonists and -antagonists. B: -blockers: slow responsiveness of heart muscle (decrease hr) Thresholds to commence treatment vary (dependant on patient and co-morbidities) Uncomplicated treatment: single drug commenced ace inhibitor, at1r antagonist, calcium channel blocker or thiazide diuretic (>65yrs) If control inadequate: additional drug added (dose not increased) Adverse reactions: peripheral oedema, flushing, headache, bradycardia. Antagonise vsm adrenoceptors vasodilation = reduce tpr and arterial bp. Oral tablet 1-3x/day peak plasma concentration 3hrs. Adverse effects: hypotension, nasal congestion, increased peristalsis (diarrhoea), pupillary constriction and urinary tract relaxation (treatment on bph) Block angiotensin converting enzyme (ace) active site prevent ang i conversion to ang ii: reduce ang ii-induced vasoconstriction, sodium retention and aldosterone release, and increases bradykinin levels vasodilation. Oral rapidly absorbed, peak plasma levels 1hr: food in gastrointestinal tract reduces absorption (-40%) take before meals, bp reductions max 60-90minsmo. 90% absorbed dose eliminated in urine (24hrs) First line therapy for hypertension, heart failure and diabetic nephropathy.
