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pharm II exam 2 > vasodilators and angina treatment > Flashcards

vasodilators and angina treatment Flashcards

1
Q

etiology of classic or atherosclerotic angina

A

atheromatous obstruction of large coronary vessels especially with exercise

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2
Q

etiology of Variant/angiospastic/Prinzmetal’s angina

A

spasm or constriction in atherosclerotic coronary vessels

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3
Q

treatment if Variant/angiospastic/Prinzmetal’s angina

A
  • reversed by nitrates or calcium channel blockers
    • Nifedipine bc it will cause vasodilation
    • B-blockers could be harmful
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4
Q

why is using medications to increase oxygen supply ineffective in atherosclerotic angina

A
  • “coronary steal phenomenon”
  • atherosclerosis causes calcified vessels -> vasodilation from this vessel is minimum so vessel and surrounding tissue being perfused by that vessel doesn’t really get affected by the medication because healthier BV react and steal blood flow
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5
Q

drugs aimed at reducing what are the major mechanism to treat angina

A

oxygen demand

  • decrease
    • HR
    • cardiac contractility
    • myocardial wall tension
      • decrease preload and afterload
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6
Q

describe the process from calcium entry into a muscle cell to contraction

A
  1. Ca2+ enters via L type channels
  2. Ca2+ binds with calmodulin
    1. complex activates myosin light chain kinase
    2. activated MLCK phosphorylates myosin light chains
      1. phosphorylated Myosin-LC joins with actin -> contraction
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7
Q

describe the process from nitrates/nitrites to relaxation

A
  1. nitrates/nitrites -> NO -> activated guanylyl cyclase
    1. activated guanylyl cyclase => GTP -> cGMP ->
    2. cGMP => dephosphorylation of myosin light chains -> relaxation
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8
Q

Nitrates and Nitrites cause uneven vasodilation. what does this mean?

A
  • large veins are markedly dilated -> increased venous capacitance and decreased preload
  • arterioles and precapillary spincters are dilated less but will still decrease afterload
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9
Q

What is the DOC for any acute anginal attack

A
  • Nitrates and Nitrites
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10
Q

what is the predominant and secondary mechanism of nitrates/nitrites

A
  • predominant mechanism: decrease myocardial O2 requirement
  • secondary mechanism: redistribution of regional coronary blood flow from normal to ischemic areas even though total flow remains unchanged
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11
Q

do nitrates/nitrites affect baroflex?

A
  • yes
  • cause decreased cardiac output -> decreased preload and afterload
    • decreased BP -> increases baroreflex -> increases HR and contractility -> deceases diastolic perfusion time
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12
Q

what is the problem with takes nitrates orally

A
  • rapid hepatic metabolization (high first pass)
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13
Q

route of administration of amyl nitrite

A

inhaled

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14
Q

route of administration of nitroprusside

A

IV

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15
Q

the sublingual route is preferred for nitrates due to

A
  • avoid hepatic destruction (first pass metabolism)
  • rapid absorption
  • immediate anginal relief (1-3 minutes) and lasting 10-30 minutes
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16
Q

route of administration of Isosorbide dinitrate

A
  • solid form
  • sublingual or oral tablets
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17
Q

adverse effects of nitrates/nitrites

A
  • throbbing HA
  • frequent repeated exposure -> tolerance or marked reduction of most effects
    • not suitable for long term treatment
  • “Monday’s disease” caused by chronic exposure to nitrate
    • Mond: HA and dizziness
    • by Friday, symptoms dissappear
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18
Q

MOA of calcium channel blockers

A

relax all smooth muscles that depend on Ca2+ for normal resting tone and contraction

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19
Q

differentiate Nifedipine and Verapamil in terms on effect on HR

A
  • Nifedipine: inc HR
  • Verapamil: dec HR
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20
Q

slow release Nifedipine is indicated only in

A

HTN

  • may provoke angina pectoris
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21
Q

in general, are CCBs used for chronic or acute tx

A

chronic

22
Q

What is the beneficial effects of Nifepdipine and other dihydropyridines

A
  • coronary vasodilation -> increases myocardial O2 supply and decreases afterload
23
Q

what is the harmful effects of Nifepdipine and other dihydropyridines

A
  • enhanced development of MI
    • rapid hypotension -> baroreflex -> increased cardiac workload
24
Q

What is the beneficial effects of Verapamil and Diltiazem

A
  • decreased myocardial contractility
  • bradycardia caused by decreased SA node automaticity and AV node conduction
25
Q

What is the harmful effects of Verapamil and Diltiazem

A
  • potential to cause serious cardiac depression that could end in cardiac arrest, A-V block, or CHF
26
Q

which CCB is the most likely to produce reflex tachycardia

A

Nifedipine

27
Q

B-blockers have CV effects on what 3 organs? effect?

A
  1. Heart: decreased CO
  2. kidneys: decreased renin
  3. CNS: decreased sympathetic tone
28
Q

how do B-blockers provide anginal relief

A
  • dec sympathetic activation -> dec cardiac activity and dec vasoconstriction -> hypotension and bradycardia -> dec cardiac workload -> dec myocardial O2 demand
  • bradycardia -> increased in myocardial perfusion time
29
Q

can B-blockers produce coronary vasodilation?

A

No

30
Q

adverse effects of beta blockers

A
  1. bronchoconstriction
  2. plasma triglycerides may increase
  3. recovery from insulin-induced hypolgycemia is delayed
  4. CNS side effects -> fatigue, depression
31
Q

why should beta blockers not be used to treat variant angina

A
  • can potentially be harmful in variant angina
  • by slowing HR and prolonging ejection time -> increased left ventricular end-diastolic volume -> increased myocardial O2 requirement
32
Q

MOA of Ranolazine (Ranexa)

A
  • partial fatty acid oxidation inhibitor
    • decreases O2 consumption in ischemic tissue
  • also inhibits late inward sodium current
    • decreases contractility
33
Q

indications/theraputic effects of Ranolazine (Ranexa)

A
  • used to decreased left ventricular wall stiffness, improves coronary circulation
  • used when other anti-anginal medications do not work
34
Q

What is the most effective drug combination for tx of classic angina pectoris

A
  • B-blockers + a vasodilator
    • ex: nitrate
35
Q

reflex tachycardia from nitrates can be minimized by

A
  • combining with CCB or B-blockers
36
Q

What drug class is Sildenafil (viagra) in

A

Phosphodiesterse type 5 inhibitors

  • orginally developed as an antianginal agents, was found to be more effective in tx of ED
37
Q

Phosphodiesterse type 5 inhibitors MOA

A
  • PDE5 is a selective inhibitor of cyclic guanosine monophosphate (cGMP)
  • so inhibiting it -> increased cGMP -> relaxation
38
Q

List the Nitrates/Nitrites

A
  • Nitroglycerin
  • Isosorbide dinitrate (Isordil®)
  • Amyl nitrite (Aspirols)
  • Nitroprusside
39
Q

List the Calcium Channel Blockers Dihydropiridines

A

Nifedipine (Procardia®) Nimodipine (Nimotop®)

40
Q

List the CCB that are not Dihydropiridines:

A
  • Verapamil (Calan®)
  • Diltiazem (Cardizem®)
41
Q

List the Phosphodiesterase type 5 (PDE5) inhibitors

A
  • Sildenafil (Viagra®)
  • Vardenafil (Levitra®)
  • Tadalafil (Cialis®)
42
Q

indications/theraputic use of Sildenafil

A
  • treatment of male erectile dysfunction
  • also pulmonary HTN
43
Q

Sildenafil

  • route of administration
  • half-life
  • metabolized by
A
  • oral
  • half-life 4 hours
  • metabolized by CYP3A4
44
Q

adverse effects of Sildenafil

A
  • transient and mild/moderate in nature
    • HA, flushing
    • visual impairment including blue color tinge, photophobia, or blurred vision
45
Q

contraindications to taking Sildenafil

A
  • pregnant, lactating women
  • patients taking nitrates or nitrites in any form
  • patients taking alpha blockers
46
Q

why are there many drug interactions with Sildenafil

A
  • any drug that is an inhibitor of CYP3A4 will reduce Sildenafil clearance and lead to adverse side effects
    • ex: cimetidine, quinidine, ketoconazole, macrolides
47
Q

What differentiates Vardenafil and Tadalafil from Sildenafil

A

Vardenafil and Tadalafil: more selective for PDE5 than PDE6 -> less visual disturbances

48
Q

differentiate between Vardenafil and Tadalafil

A
  • Vardenafil => very soon
    • achieves maximum plasma concentration sooner which may result in a faster onset of action
  • Tadalafil => tomorrow
    • duration of action is 24-36 hours appears to be longer than that of the other drugs
49
Q

Most preferred drug combo to treat classic angina pectoris in patients with asthma or DM

A
  • CCB + nitrate/nitrite
50
Q

Most preferred drug combo to treat classic angina pectoris in patients with HTN

A
  • B-blocker or CCB
51
Q

Most preferred drug combo to treat classic angina pectoris in patients with heart failure

A
  • only a nitrite/nitrate

pharm II exam 2 (9 decks)

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