Intro to Antihypertensive Agents IV

Question 1

amlodipine

Answer 1

calcium channel blocker

Question 2

clevidipine

Answer 2

calcium channel blocker

-DHP

Question 3

felodipine

Answer 3

calcium channel blocker

-DHP

Question 4

isradipidine

Answer 4

calcium channel blocker

-DHP

Question 5

nicardipine

Answer 5

calcium channel blocker

-DHP

Question 6

nifedipine

Answer 6

calcium channel blocker

-DHP

Question 7

nisoldipine

Answer 7

calcium channel blocker

-DHP

Question 8

diltiazem

Answer 8

calcium channel blocker

-non-DHP

Question 9

verapamil

Answer 9

calcium channel blocker

-non-DHP

Question 10

diazoxide

Answer 10

K channel opener

Question 11

minoxidil

Answer 11

K channel opener

Question 12

fenoldopam

Answer 12

dopamine agonist

Question 13

hydralaine

Answer 13

NO donor

Question 14

nitroprusside

Answer 14

NO donor

-nitropress

Question 15

nitroglycerin

Answer 15

NO donor

-organic nitrate

Question 16

isosorbide dinitrate

Answer 16

NO donor

-organic nitrate

Question 17

calcium channel blocker mechanism

Answer 17

block L-type Ca channels
-cardiac myocyte and SA and AV nodal cells

decreased vascular smooth m contraction

Question 18

dihydropyridine mechanism

Answer 18

• bind L-type Ca channels
• arteriolar vasodilation predominant

**more vascular effect

Question 19

non-dihydropyridine mechanism

Answer 19

• bind L-type Ca channels
• predominant cardiac effects, but also act at vascular tissues

verapamil > diltiazem

Question 20

hemodynamics of CCBs

Answer 20

• reduced TPR
• reduced afterload
• reduced O2 demand
• non-DHPs reduce CO
• decreased coronary vascular resistance and increased coronary blood flow

Question 21

CCBs and cardiac muscle

Answer 21

negative inotropic effect

• Na fast channel primary depolarization, but Ca slow channels is additional
• Ca entry - induce Ca release from SR
• Ca binds troponin - allows contraction

verapamil > diltiazem > DHPs (inotropic effects)

Question 22

DHPs

Answer 22

relax vascular smooth m at lower concentration than required for direct action on heart

Question 23

DHPs and cardiac muscle

Answer 23

greater vasodilatory effect

-reflex increased sympathetic tone that overcomes negative inotropic effect

Question 24

CCB effect on cardiac nodal cells

Answer 24

SA and AV node - depolarization L-type Ca channels

DHPs block channel - but don’t effect recovery of channel and ARE NOT frequency dependent

Question 25

verapamil and diltiazem

Answer 25

non-DHP CCB -block channel, delay recovery of channel, and ARE frequency dependent - decreased rate of SA node depolarization and slow AV nodal conduction - useful for Tx of supraventricular tachyarrhythmias but dangerous for patients with slow nodal conduction

Question 26

non-DHPs

Answer 26

more cardiac effect | -decreased contractility, suppress SA automaticity, and AV conduction

Question 27

CCB pharmacokinetics

Answer 27

high 1st pass effect

Question 28

long half life CCBs

Answer 28

amlodipine, felodipine, isradipine

Question 29

DHP with long plasma half lives **

Answer 29

preferred to minimize reflex cardiac effects - **decreased reflex tachycardia - release preparations are available

Question 30

CCBs sometimes used IV

Answer 30

nifedipine, clevidipine, verapamil, diltiazem

Question 31

CCB adverse effects

Answer 31

generally very well tolerated - excessive vasodilation - dizzy, hypotension, HA, nausea - constipation** (verapamil), peripheral edema, coughing, wheezing, pulmonary edema

Question 32

non-DHP with beta blocker**

Answer 32

contraindicated | -risk for potential AV block

Question 33

non-DHP contraindications

Answer 33

- ventricular dysfunction - SA or AV nodal conduction defects - systolic BP < 90

Question 34

CCB clinical uses

Answer 34

HTN (with other agent to counteract reflex CV response), hypertensive emergency, angina (reduced O2 demand)

Question 35

potassium channel opener mechanism

Answer 35

increased K permeability > hyperpolarizes smooth m. membrane > reduce probability of contraction

Question 36

diazoxide adverse effects

Answer 36

- excessive hypotension can cause stroke/MI | - hyperglycemia

Question 37

minoxidil adverse effects

Answer 37

-HA, sweating, hypertrichosis, reflex tachycardia, edema

Question 38

with minoxidil

Answer 38

use beta-blocker and diuretic

Question 39

topical minoxidil

Answer 39

baldness

Question 40

potassium channel openers

Answer 40

arteriolar vasodilation | -diazoxide and minoxidil

Question 41

fenoldopam

Answer 41

D1 dopamine receptor agonist -renal afferent arteries contain dopamine receptors >increased blood flow to kidney

Question 42

clinical use fenoldopam

Answer 42

HTN emergency and post op HTN

Question 43

adverse effects of fenoldopam

Answer 43

tachycardia, headache, flushing

Question 44

avoid in patients with glaucoma

Answer 44

fenoldopam | -increased IOP

Question 45

hydralazine mechanism

Answer 45

released NO from endothelium | >dilates arterioles (not veins)

Question 46

clinical for hydralazine

Answer 46

first line for HTN in pregnancy (with methyldopa) combine with nitrates -heart failure pts

Question 47

adverse effects of hydralazine

Answer 47

fluid and Na retention - HA, nausea, anorexia, sweating, flushing, palpitations - reflex tachycardia - provoke angina - lupus like syndrome (reversible on drug withdrawal)

Question 48

effect of organic nitrates

Answer 48

``` dilate arterial and venous vessels >decreased TPR and venous return >decreased preload and afterload >main relaxation of large veins (decreased venous return/preload) >also decreased O2 demand >smaller decreased afterload ```

Question 49

adverse effects of nitroprusside

Answer 49

excessive hypotension, CN poisoning

Question 50

adverse effects of nitrates

Answer 50

orthostatic hypotension, syncope, throbbing HA

Question 51

compensatory response to vasodilators

Answer 51

- increased RAAS system | - increased sympathetic outflow