Antihypertensives Flashcards
(51 cards)
evidence based tx of systemic arterial HTN
Treat with the intent of reducing risk of CV events and thereby reducing CV morbidity and mortality.
BP goal (controversial)
< 150/90 mmHg for patients > 60 y.o. (<140/90? controversial)
< 140/90mmHg for most patients < 60 years of age
strategies for antihypertensive therapy
Reduce TPR
Reduce CO
Reduce body fluid volume (salt & water)
Adjust homeostatic regulatory reflexes
- reflex tachycardia (increased SANS)
- edema (increased renin activity)
MOA of clonidine and role in therapy?
increase a2 activity - alter SANS activity
Most commonly prescribed central alpha2-agonist
SE of clonidine
Can cause rebound hypertension if stopped abruptly
Optimally used with a diuretic to diminish fluid retention
Overdose can cause paradoxical hypertension
MOA of a-methyldopa
Stimulate central alpha2 receptors –> decreased release of NE
role of a methyldopa in therapy
gestational hypertension
chronic hypertension in pregnancy
MOA of reserpine
blocks transport of NE into storage granules
role of reserpine in therapy
the most effective use of reserpine is in combination with a thiazide diuretic, which can mitigate related sodium and water retention.
SE of resserpine
- *strong sympatholytic effect results in increased parasympathetic activity:**
- nasal stuffiness, increased gastric acid secretion, diarrhea, and bradycardia.
MOA of guanethidine
affect vesicle storage:
- Transported across the sympathetic nerve membrane via NET1 –> concentrated in transmitter vesicles & replaces NE –> gradual depletion of NE stores
name the ACE inhibitors
Captopril, Lisinopril, Fosinopril
role of ACE inhibitors in therapy (Captopril, Lisinopril, Fosinopril)
First-line or add-on therapy for uncomplicated HTN
First-line therapy for compelling indications of:
- diabetes
- chronic kidney disease
- coronary artery disease
- left ventricular dysfunction
- previous ischemic stroke
ACE inhibitors are cleared mostly by what?
when would you reduce the dose?
Cleared mostly by the kidney –> reduce dose in kidney failure
Elevated plasma renin activity causes hyperresponsive to ACEIs reduce doses in pts with high plasma renin levels (e.g., heart failure, Na+-depleted patients)
action of ACE?
Angiotensin I –> angiotensin II
SE of ACEI
coughing
who should avoid use of ACEI
pregnancy
what are the angiotensin receptor blockers (ARBs)
receptor = AT1
Losartan, Valsartan, Candesartan
effects of ARBs (Losartan, Valsartan, Candesartan)
- *Inhibit Ang II-induced:**
1) contraction of vascular smooth muscle
2) thirst
3) vasopressinrelease
4) aldosterone secretion
5) release of adrenal catecholamines
6) enhancement of noradrenergic neurotransmission
7) increases in sympathetic tone
8) changes in renal function
9) cellular hypertrophy and hyperplasia
role of ARBs (losartan, valsartan, candesartan) in therapy
First-line or add-on therapy for uncomplicated hypertension – as effective as ACEIs
First-line therapy for compelling indications of
- Diabetes
- Chronic kidney disease
- Coronary artery disease
- Left ventricular dysfunction
Commonly used as an alternative for patients with intolerance to ACE inhibitors
when should ARBs not be used
pregnancy
what is a direct renin inhibitor?
what is it preventing?
Aliskiren
Binds directly to the catalytic site of renin –> prevents it from cleaving angiotensinogen to generate angiotensin I
role of aliskiren in therapy
Approved as monotherapy or in combination therapy for HTN
Demonstrated efficacy in lowering BP when used in combination with a thiazide, ACE inhibitor, ARB, or CCB
SE of aliskiren
Can cause hyperkalemia in patients with CKD and diabetes or in those receiving a potassium-sparing diuretic, aldosterone antagonist, ACE inhibitor, or ARB
