Antihypertensives Flashcards
Thiazide MOA
Diuretic, true mechanism unknown - blocks sodium retention, decreases plasma volume, reducing peripheral resistance and stimulates RAAS
Thiazide SE
Hypokalemia, hyponatremia, hypercalcemia, hyperuricemia, increased cholesterol, glucose, serum creatinine and triglycerides. Also causes skin rash and photosensitivity
Thiazide monitoring
Hypokalemia may increase risk for HTN and diabetes (reason for high potassium diet)
Monitor serum creatinine and potassium
Thiazide in therapy
Primary stroke prevention-helps decrease incidence/risk of stroke
Decrease in heart disease (has the same efficacy as calcium channel blockers and ACE inhibitors)
Thiazide contraindications
Pancreatitis (increased triglycerides)
Gout (increased uric acid)
If patient already has lower potassium levels
Should also be cautious in patients with DM because thiazide can cause increased glucose
Beta blocker MOA
Has B1 and B2 effects
B1: decreases HR, decreases CO, myocardial oxygen demand
Also blocks norepinephrine (which is responsible for vasoconstriction so this block results in vasodilation)
Norepinephrine triggers RAAS
B2: vascular changes blocks arterial vasodilation and bronchoconstriction
Beta blocker = negative inotrope
Beta blocker SE
Bradycardia, heart block Fatigue, SOB Insomnia, nightmares Exacerbation of raynauds and peripheral arterial disease Sexual dysfunction Masking symptoms of hypoglycemia: tremors, tachycardia, sweating Hyperglycemia Increase triglycerides, cholesterol Decrease HDL
Beta blockers in therapy
Use for CHF, post MI, diabetes, a-fib, angina (decrease CO by decreasing HR), ventricular tachycardia
Can use for migraines
Second line in renal protection
Beta blocker contraindications
COPD & asthma - bronchoconstriction!!
Peripheral vascular disease
2nd-3rd degree heart block
If using in CHF patients, start at a low dose and increase carefully
Calcium channel blocker MOA
Vasodilator
Dihydropyridines: vasodilator - blocks calcium which causes smooth muscle relaxation (calcium needed for muscle contraction)
Non-hydropyridines: decreases HR and contractility (is a negative inotrope)
Calcium channel blocker SE
Dihydropyridines: flushing, headache, postural dizziness, palpitations, tachycardia, ankle edema, gingival hyperplasia
Non-dihydropyridines: bradycardia, postural hypotension, headache, dizziness, constipation, gingival hyperplasia
Calcium channel blockers in therapy
Angina Claudication, peripheral vascular disease, raynauds Isolated diastolic LV dysfunction HTN in COPD or asthma Non-Q wave MI
Calcium channel blockers contraindications
Do not use non-dihydropyridines in systolic CHF patients
ACE inhibitors & ARBs MOA
Block conversion of angiotensinogen 1 to angiotensin 2
Angiotensin 2 is a potent vasoconstrictor and stimulates aldosterone production, which causes sodium retention
Decrease aldosterone and increase bradykinin and vasodilatory prostaglandins
Can decrease pressure in glomerulus, decreasing GFR which increases serum creatinine
ACE inhibitor & ARBs SE
Hyperkalemia Increased serum creatinine - renal impairment Dry persistent cough Angioedema Macular rash
ARBs have less angioedema and less cough
ARBS: postural hypotension, tachycardia, dizziness, GI effects
