CVS - Angiotensin Antagonists, CCBs, Vasodilators - Drugs affecting vascular tone Flashcards Preview

systemic pharmaco > CVS - Angiotensin Antagonists, CCBs, Vasodilators - Drugs affecting vascular tone > Flashcards

Flashcards in CVS - Angiotensin Antagonists, CCBs, Vasodilators - Drugs affecting vascular tone Deck (24):
1

Classes of angiotensin antagonists & examples

1. ACE Inhibitors - Captopril, Enalipril
2. AT1 Receptor Antagonists - Losartan, Valsartan
3. Renin Inhibitors - Aliskiren

2

Actions of angiotensin II (5)

1. Arteriolar vasoconstriction - increases bp
2. NaCl reabsorption, K+ excretion, H2O retention
3. Increased sympathetic activity
4. Post pit - ADH secretion - CD H2O absorption
5. Aldosterone secretion

3

Mechanism of action of ACEI

1. Inhibits converting enzyme peptidyl dipeptidase (ATI to ATII) - inhibits RAAS - hypotension
2. Inhibits bradykinin (potent vasodilator) degradation - stimulation of kallikrein-kinin system - hypotension

4

Uses of ACEI (3)

1. Hypertension - by decreasing PVR, CO & HR unchanged
2. Chronic Renal Failure - diminish proteinuria, stabilize fn
3. Heart Failure, after MI

5

Toxicity of ACEI (4) + Contraindications (1)

1. Severe Hypotension
2. Acute Renal Failure - esp in bilat renal stenosis
3. Hyperkalemia - esp in renal insufficiency/diabetes
4. Dry Cough +/- wheezing & angioedema - due to bradykinin & substance P

1. Pregnancy - 1st trimester - increased teratogenicity, 2nd/3rd trimester - fetal hypotension, anuria, renal failure

6

Mechanism of action of AT1R antagonist

1. Antagonizes angiotensin II type 1 receptors - no effect on bradykinin, more selective, more complete effects
2. Prolonged inhibition of AT1 - disinhibits renin secretion + increases circulating AII - increases ATIIR activation (vasodilation)

7

Mechanism of action of renin inhibitors

1. Inhibits renin - involved in the rate limiting step for AII production
2. Produces dose dependent reduction in plasma renin activity, AI, AII and aldosterone concentrations

8

Uses of renin inhibitors (2)

1. Reduces BP - similar to ACEI/diuretics in safety, tolerability
2. Prevents rise in renin activity - produced by ACEI/ARBs/diuretics

9

Compare Verapamil, Diltiazem, Nifedipine
(A) Lowering BP
(B) Vasodilator
(C) Cardiac Depressant

(A) V = D = N
(B) N > D > V
(C) V > D > N

10

Mechanism of action of CCBs

- L-type channel blockers, predominant type in cardiac/smooth muscle
- Blocks Ca channels on the inner side of membrane (binds more effectively to open and inactivated channels) - decreases frequency of opening in response to depolarization - reduced transmembrane calcium current

11

Uses of CCBs (4)

1. Anti-HTN - sustained relaxation in smooth muscle - decreasd muscle tone - reduced bp
2. Anti-angina - reduced cardiac contractility - decreases O2 requirements in patients with angina
3. Anti-arrhythmia - slowed/blocked SAN & AVN conduction (Verapamil, Diltiazem)
4. Cerebral Vasospasm following subarachnoid hemorrhage (Nimodipine)

12

Toxicity of CCBs (2) + Contraindications (1)

1. Cardiac Depression (cardiac arrest, bradycardia, AV block, heart failure) - due to excessive inhibition of Ca influx - but rare
2. Minor effects - flushing, dizziness, nausea, constipation (esp verapamil), peripheral edema

1. Congestive Heart Failure

13

Mechanism of α-1 blockers

Prazosin, terazosin, doxazosin

Selectively blocks α-1 receptors in arterioles & venules - dilates both resistance & capacitance vessels - anti-HTN

14

Uses of α-1 blockers (3)

1. Hypertension
2. Prostate Hyperplasia
3. Bladder Obstruction (urinary hesitancy)

15

Considerations when using α-1 blockers (3)

1. Has 1st dose effect - marked postural hypotension - Give small first dose at bedtime
2. Increased salt/water retention - Use with diuretics/β-blockers
3. Mild, infrequent toxicities - dizziness, palpitations, headache, lassitude

16

Mechanism of hydralazine

1. Increases cGMP + is a NO donor
2. leading to smooth muscle dilation (arterioles, not veins)

17

Uses of hydralazine (2)

1. Hypertension - combination therapy, 2nd line with diuretics/β-blockers
2. Heart Failure - in combination with nitrates

18

Toxicity of hydralazine (2)

1. Headaches, nausea, anorexia, palpitations, sweating, flushing
2. In IHD: reflex tachycardia & sympathetic stimulation may provoke angina/ischemia arrhythmias

19

Mechanism of minoxidil

Opens K+ channels in smooth muscle stabilizing membranes - makes contractions less likely - dilates arterioles, not veins

20

Uses of minoxidil (2)

1. Hypertension associated with reflex sympathetic stimulation & Na/fluid retention, use with loop diuretic/β-blocker
2. Stimulant for hair growth in male pattern baldness (topical)

21

Toxicity of minoxidil (3)

1. Sweating
2. Hypertrichosis
3. With inadequate diuretics/β-blockers - tachycardia, palpitations, angina, edema

22

Mechanism of smooth muscle relaxants

Sildenafil, Tadalafil, Vardenafil

Increases cGMP by inhibiting PDE5 breakdown (primarily in arterial walls of smooth muscle of lungs, penis)

23

Uses of smooth muscle relaxants (2)

1. Erectile Dysfunction - relaxes intimal cushions in helicine arteries - vasodilation + increases blood flow to corpus cavernosum
2. Pulmonary Hypertension - relaxes pulmonary arteries - reduces PR & workload of right ventricle

24

Toxicity of smooth muscle relaxants + Contraindications (3+4)

1. Headache
2. Flushing
3. Nasal congestion

1. If taking nitrates
2. Hepatic impairment
3. Renal dysfunction
4. Hypotension