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Cardiovascular II > Drugs for Angina and Ischemic Heart Disease > Flashcards

Drugs for Angina and Ischemic Heart Disease Flashcards

1
Q

Chronic ischemic heart disease is characterized by`

A

the partial occlusion of coronary artery

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2
Q

Classic angina

A
  • angina of effort, stable angina
  • occlusion of the coronary arteries resulting from the formation of atherosclerotic plaque
  • Most common form of angina
  • Symptoms occur during exertion or stress
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3
Q

Variant (Prinzmetal) angina:

A
  • episodes of vasoconstriction of coronary arteries
  • vasospastic
  • Genetic in origin
  • symptoms at rest
  • Less common than classic angina
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4
Q

Angina is the imbalance between

A
  • O2 demand of the heart and oxygen supply via the coronary arteries
  • Heart’s demand for O2>>O2 supply due to partially blocked coronary artery
  • Especially during exertion, stress
  • results in chest pain
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5
Q

Approaches to treat Angina

A
  • Reduce O2 demand by decreasing cardiac work OR
  • increase O2 supply by increasing blood flow through coronary arteries
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6
Q

Ways to increase coronary blood flow to treat angina–surgical and non-surgical approaches

A
  • Coronary artery bypass grafting (most radical)
  • Percutaneous transluminal coronary angioplasty (PTCA)
  • Atherectomy–tip of catheter shears off the plaque–risk of reocclusion
  • Stent–expandable tube used as scafforlding to keep vessel open (drug eluting stents–antiproliferative drugs–cause cell cycle arrest)
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7
Q

To increase coronary blood flow using vasodilators

A
  • useful in vasospastic (Prinzmetal–variant) angina
  • to relieve coronary spasm -to restore blood flow into ischemic area
  • NOT useful in atherosclerotic (classic) angina–can make it worse– due to coronary steal phenomenon
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8
Q

Coronary steal phemomenonen

A
  • redistribution of blood to non-ischemic areas–associated with the dilation of small arterioles
  • Ex: potent arteriolar vasodilators like Dipyridamole
  • vasodilation prevents adjacent arteries from providing collateral blood flow exacerbating symptoms in classic angina!! But vasodilator useful for variant angina!
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9
Q

Determinants of myocardial oxygen demand (targets for treatment)

A
  • Heart rate
  • Contractility
  • Preload
  • Afterload
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10
Q

Tachycardia increases HR and can be harmful. Why?

A
  • Tachycardia affects diastole more than systole
  • decreased length of diastole so blood flow through coronary artery is impeded
  • explains why tachycardia is harmful especially in angina patients
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11
Q

Vasodilator that lacks direct effect on autonomic receptors but may provoke angina attacks

A
  • Hydralazine
  • peripheral vasodilator
  • releases NO
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12
Q

Drug classes used in chronic ischemic heart disease

A
  • Nitrates (nitrovasodilators)
  • Calcium channel blockers
  • Beta-blockers
  • Newer agent: Ranolazine
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13
Q

Nitrovasodilators

A
  • Nitrogylcerin
  • isosorbide dinitrate
  • Isosorbide mononitrate (active metabolite of dinatrate)
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14
Q

Endothelium dependent vascular relaxation

A
  • Release of endothelium-derived relaxing factor (EDRF) by Ach leads to relaxation IF endothelium is present
  • endothelial NOS produces NO, an endogenous vasorelaxing agent
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15
Q

Endothelial Nitric Oxide Synthase

A
  • activated by Ca2+-calmodulin complex
  • then it activates arginine to make citrilline and NO
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16
Q

NO acts on

A

-Guanylyl cyclase–>act cGMP–>act Protein kinase G–> causes relaxation by dephosphorylating myosin light chain or by opening potassium channels and causing hyperpolarization and reduced calcium entry

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17
Q

MOA of nitrates in Variant angina

A

1) Nitrate–>NO via ADH2 (frequently thiols)–>
2) Vascular smooth muscle relaxation–>
3) Coronary artery dilation–>
4) Coronary spasm relief

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18
Q

MOA of nitrates in Classic angina

A

1) 1) Nitrate–>NO via ADH2 (frequently thiols)–>
2) Vascular smooth muscle relaxation–>
3) VENOUS dilation–>
4) Reduced preload–>
5) decreased O2 demand

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19
Q

Multiple effects of NO

A
  • vasodilation
  • Prevents platelet aggregation
  • inhibits interaction of endothelial cells with blood derived cells (leukocytes)–prevents rolling and transmigration and inflammation by leukocytes
  • inhibits smooth muscle proliferation (intimal thickening and reocclusion)
  • prevents oxidation damage -prevents LDL oxidation (protects against atherosclerosis)
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20
Q

Sensitivity of vasculature to nitrate induced vasodilation

A

-veins>large arteries>small arteries and arterioles

21
Q

Nitrovasodilator beneficial action in angina

A
  • decreased myocardial oxygen demand
  • relaxation of vascular smooth muscle
  • dilation of veins (major effect): increased venous capacitance, reduced ventricular preload
  • dilation of arterioles–higher concentrations of nitrates are needed compared to venous dilation
22
Q

Dilation of arteries leads to

A
  • reduced arterial pressure and after load
  • may dilate large epicardial coronary arteries
  • no significant increase in coronary blood flow into the ischemic area in atherosclerotic angina
23
Q

Nitrates in angina of effort

A
  • decreased preload
  • decreased oxygen demand
24
Q

Nitrates in vasospastic angina

A
  • relaxation of coronary artery vascular smooth muscle
  • relieving coronary spasm
25
Nitrate clinical use
- short acting formulations used to relieve the angina attack - long acting preparations may be used to prevent attacks
26
Development of nitrate tolerance
- depletion of thiol compounds -increased generation of oxygen radicals - reflex activation of sympathetic nervous system (tachycardia, decreased coronary blood supply) - retention of salt and water - increased generation of superoxide radical depletes tissues of NO
27
Reason to avoid oral administration of nitrates
-Rapid denitration by the liver enzymes
28
Adverse effects of nitrates
- headache (meningeal vasodilation) - orthostatic hypotension -increased sympathetic discharge - tachycardia, increased cardiac contractility - increased renal Na+ and H2O reabsorption
29
Nitrate drug interactions
- interaction of nitrates with drugs used for treatment of erectile dysfunction (sildenafil, vardenafil, tadalafil) - combination with nitrates causes severe increase in cGMP and a dramatic drop in BP - acute MI cases have been reported
30
-Calcium channel blockers
- non-cardioactive (DHP): - Amlodipine - Nifedipine - Nicardipine - Cardioactive: Diltiazem, Verapamil
31
CCB MOA
- Ca2+ mediates smooth muscle contraction; enters cells via voltage dependent calcium channels - CCBs block Ca2+ entry to relax vascular smooth muscle - vasculature does NOT have troponin so acts on Myosin-light chain kinase system (Ca2+-calmodulin sensitive)
32
Anti-anginal mechanisms of CCBs
- Decreased myocardial O2 demand (Classic angina) - Dilation of peripheral arterioles - Decreased PVR and after load, decreased BP - Arterioles more affected than veins (less orthostatic hypotension) - DHPs are more potent vasodilaters - Decreased cardiac contractility and heart rate (seen with non-DHPs) - increased blood supply (operates in variant angina)--dilation of coronary arteries relieves local spasm
33
Major adverse effects of CCBs
- cardiac depression, cardiac arrest, and acute heart failure (cardioactive CCBs) - bradyarrythmias, AV block (cardioactive CCBs) - short acting DHP CCBs--vasodilation triggers reflex sympathetic activation
34
Nifedipine adverse effects
- immediate release - increases risk of MI in patients with HTN--slow-release and long-acting DHPs are better tolerated - causes tachycardia due to hypotension and associated baroreflex
35
Minor adverse effects of CCBs
- flushing, headache, anorexia, dizziness - peripheral edema - constipation
36
Beta-blockers indicated in angina
- Propranolol - Nadolol - Metoprolol - Atenolol
37
MOA of B-blockers in angina
- decreased myocardial O2 demand - decrease HR leads to improved myocardial perfusion and reduced O2 demand at rest and during excercise - Decrease in contractility - Decrease in BP leads to reduced afterload
38
B-blockers adverse effects
- reduced CO - bronchoconstriction - impaired liver glucose mobilization - produce and unfavorable blood lipoprotein profile (increase VLDL and decrease HDL) - sedation, depression - withdrawl syndrome associated with sympathetic hyperresponsiveness
39
B-blocker contraindications
- asthma - peripheral vascular disease - Raynaud's syndrome - Type 1 diabetics on insulin - bradyarrhthmias and AV conduction abnormalities - severe depression of cardiac function
40
Effects of Nitrates alone in treatment of angina pectoris
- reflex increase in HR - decrease in arterial pressure - decrease EDV - reflex increase contractility - decrease in ejection time
41
Effects of B-blockers or CCBs alone in treatment of angina pectoris
- decreases HR, arterial pressure, contractility - increases EDV and ejection time
42
Effects of combined nitrates with B-blockers or CCBs in treatment of angina pectoris
- decrease HR, arterial pressure - no change or decrease in EDV - no change in contractility, ejection time
43
Ranolazine MOA
- inhibits late Na+ currents in cardiomyocytes - ischemic myocardium is often partially depolarized - Na+ channel in cardiomyocytes is voltage-gated - Late Na+ current is enhanced in ischemic myocardium and brings about Ca2+ overload and depolarization abnormalities - Ranolazine normalizes repolarization of cardiac myocytes and reduces mechanical dysfunction - reduce diastolic tension and compression of coronary vessels in diastole and reduces cardiac contractility and O2 demand
44
Ranolazine may reduce
- diastolic tension and compression of coronary vessels in diastole - may reduce cardiac contractility and oxygen demand
45
Ranalozaine does not affect
- heart rate - general ionotropic state of myocardium - coronary blood flow - peripheral hemodynamics
46
Ranolazine clinical use
- stable angina which is refractory to standard medications - decreases angina episodes and improves exercise tolerance in patients taking nitrates, or amlodipine, or atenolol
47
Ranolazine adverse effects
- QT interval prolongation--may trigger polymorphic ventricular arrhythmias - constipation - nausea - dizziness - headache
48
Ranolazine drug interactions
- metabolized by CYP3A4/5--interaction with drugs that modulate the activity of these enzymes - do not combine with strong CYP3A inhibitors: anti fungal azaleas, verapamil - inhibits CYP2D6--increases half life of Amitriptyline, Fluoxetine, metoprolol, opioid drugs - drugs that prolong QT interval--certain anti arrhythmic (Quinidine) and antipsychotic drugs (Thioridazine)--may trigger ventricular arrhythmias

Cardiovascular II (13 decks)

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