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IC > Drugs for Angina > Flashcards

Drugs for Angina Flashcards

1
Q

CAD

A

obstruction of coronaries by atheromatous plaques

-high risk, moderate risk, low risk (no, no risk class)

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2
Q

RF for CAD

A

high bp, high LDL cholesterol, smoking

also- diabetes, overweight, poor diet, inactivity, excessive alcohol use

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3
Q

Angina pectoris

A

chest discomfort when amt of blood delivered to heart annot supply enough oxygen to satisfy myocardial requirement
-chest pain resulting from myocardial ischemia

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4
Q

Nitroglycerin

A

immediately relieves angina pain

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5
Q

Classic or atherosclerotic angina

A

atheromatous obstruction of large coronaries
especially with exercise

-tx with drugs or bypass, angioplasty

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6
Q

Prinzmetal angina

A

spasm or constriction in atherosclerotic coronary vessels

-relived by nitrates of CCBs

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7
Q

MI pathophys

A

imbalance between oxygen supply and demand

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8
Q

oxygen demand depends on

A

cardiac workload which is determined by

-contractility, heart rate, wall stress

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9
Q

main energy source in heart

A

fatty acid oxidation (requires more oxygen than glycolysis)

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10
Q

Trimetazidine

A

shifts myocardial metabolism towards greater use of glucose- reduce oxygen demand
-pFOX inhibitors

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11
Q

Increase O2 delivery through coronary blood flow which is

A
  • related to perfusion pressure and duration of diastole
  • inversely proportional to coronary vascular bed resistance
  • damage to endothelium increases vascular resistance
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12
Q

agents decreasing O2 demand of heart

A

b adrenergic agonists, organic nitrates, CCB

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13
Q

agents increasing O2 supply

A

vasodilators, statins, anti thrombotics

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14
Q

drugs can relax vascular smooth muscles by

A

increasing cGMP

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15
Q

3 drug groups for use in angina

A

1) organic nitrates
2) CCB
3) b blockers

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16
Q

ranolazine

A

reduces intracellular calcium concentration and thus reduces cardiac contractility and work
-new drug recently approved for angina

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17
Q

trimetazidine

A

pFOX inhibitor- metabolic modulator inhibits fatty acid oxidation in myocardium

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18
Q

allopurinol

A

inhibits xanthine oxidase (contributes to oxidative stress and endothelial dysfunction)
-prolongs exercise time in pts with angina

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19
Q

ivabradine

A

direct bradycardic agents inhibit hyperpolarization activated sodium channel in SA node

20
Q

Fasudil

A

Rho kinase inhibitors reduce coronary vasospasm in experimental animals

21
Q

Nitrates in angina

A

Act on guanalyl cyclase to convert GTP–> cGMP which causes relaxation

22
Q

short acting nitrates

A

amyl nitrate inhaled, sublingual nitroglycerin or isosorbide dinitrate
-acute events

23
Q

long acting nitrate

A

nitroglycerine slow release or oral, isosorbide oral, isosorbide mononitrate oral (10 hrs)

  • chronic tx
  • can lead to tolerance; have 12 hrs every day w/o nitrate effect
24
Q

Nitrates act by releasing

A
  • NO
  • vascular smooth muscle ccells are relaxed, but vasodilation are uneven
  • Large veins markedly dilated, arterioles are dilated less
25
Q

Other effects of NO

A
  • erection req’s relaxation of smooth muscle (sildenafil)
  • inc cGMP in platelets–> decrease aggregation
  • nitrate ion reacts with hemoglobin- tx cyanide poisoning
26
Q

Anginal relief by nitrates

A

pronounced dilation of large veins- reduce preload, myocardial O2 demand, and cardiac work

  • redistribution of regional coronary blood flow from normal to ischemic areas
  • mild arteriolar dilation- reduced afterload
27
Q

IV sodium nitroprusside

A

dilates arteries and veins equally because does not need activation by enzyme

28
Q

harmful nitrate effects

A

reflex increases in hr and contractility leading to inc myocardial O2 demand (combine with beta blocker or CCB)
-reflex tachycardia leads to reduced perfusion due to shorter diastole

29
Q

nitrate absorption and metabolism

A

-oral nitrates metabolized by hepatic reductase
-routes are inhaled, sublingual, oral, transdermal
-sublingual nitro- immediate anginal relief, rapid action but short duration
-

30
Q

nitrate toxicity

A

acute- strong vasodilation- orthostatic hypotension, tachycardia, headaches
frequent repeated exposure- tolerance or marked reduction in magnitude of most effects

31
Q

Calcium- cardiovascular actions

A
  • triggers contraction in myocardium and vasc smooth muscles
  • req’d for pacemaker activity of SA node and conduction through AV node
  • Enters through calcium channel- L channel (long lasting) or T channel (transient)
  • opened by stimulation of b-receptors, closed by CCBs
32
Q

CCBs

A
  • block L type channels in myocardium and vasc smooth muscles
  • relax all smooth muscles that depend on calcium for normal resting tone and contraction
33
Q

Verapamil

A

CCB with strongest cardiac effects- decreased contractility, reduced SA node impulse generation, slowed AV node conduction–> reduced cardiac workload

  • no reflex tachycardia
  • can lead to serious cardiac depression- cardiac arrest, AV block, CHF
34
Q

Nifedipine

A

CCB dihydropyridine- vascular effect– vasodilation

  • most likely to produce reflex tachycardia
  • use with verapamil to address cardiac effects
35
Q

Diltiazem

A

in between with vascular and myocardial depression effects

- can cause serious cardiac depression

36
Q

reduction of digoxin renal clearance by

A

verapamil and diltiazem

-increases plasma digoxin and enhances toxicity

37
Q

b adrenergic antagonists

A

atenolol, metoproplol can be used to tx angina
-decreases sympathetic tone to decrease CO (decrease HR) –> dec cardiac workload and O2 demand
-may induce or worsen CHF when sympathetic activity is critical to support cardiac performance
-

38
Q

AE of b-adrenergic antagonists

A
  • in pts with CHF, exercise tolerance may be decreased by reduction of CO
  • potentially harmful in variant angina by slowing HR and prolonging ejection time will increase LV EDV
  • may inc plasma triglycerides and decrease HDL cholesterol–> atherogenesis
  • delays reccovery of normoglycemia
39
Q

most effective drug combinations

A
  • b adrenergic blocker and CCB or

- 2 CCBs (nifedipine and verapamil)

40
Q

reflex tachycardia of nitrates can be minimized by

A

combining with beta blocker or ccb

41
Q

Mechanism for nitrates

A

redistribution of flow leading to increased supply of O2

  • arteriodilation leads to reduced afterload and reduced demand
  • venodilation leads to reduced preload and reduced demand
42
Q

Mechanism for CCB

A

arteriodilation, coronary vasodilation (nifedipine) and reduced cardiac function (verapamil)

43
Q

Mechanism for b-adrenergic blockers

A

sympathetic inh, reduced vasoconstriction and reduced cardiac fxn

44
Q

effective antianginal therapy will

A

increase exercise tolerance and dec frequency and duration of MI

45
Q

b adrenergic antagonists used with caution in which pts

A
  • reduced myocardial reserve
  • asthma
  • peripheral vascular insuff
  • diabetes

IC (31 decks)

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