PHARM: Angina Flashcards

1
Q

Sx of angina and how can it be different in females?

A
  • severe, crushing pain
  • SOB lasting a few mins
  • females often present w/ N&V, back/jaw pain, radiating to shoulder
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2
Q

3 types of angina (in terms of relative plaque/thrombi load)

A
  • stable: only on exertion, high plaque load only and no thrombi
  • unstable: @ rest, some plaque and some thrombi formation
  • variant (vasospastic) angina: no atherosclerosis, spasm of coronary artery
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3
Q

3 main drug classes to treat angina

A
  • nitrovasodilators (1st line)
  • beta blockers (2nd line)
  • DHP calcium channel blockers (3rd line, if B-blockers contraindicated)
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4
Q

4 MECHANISMS to treat angina

A
  • reduce contractility and heart rate = decreased oxygen demand AND increase coronary artery perfusion time = more sustained oxygen supply to the heart
  • decrease TPR to decrease afterload
  • reduce venous pressure to reduce preload/EDC
  • dilate coronary arteries to increase perfusion to cardiac tissue
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5
Q

inotropy, chronotropy, dromotropy

A
  • inotropy = effect on contractility of heart
  • chroNotropy = effect on SA node conduction and therefore HR
  • dromotropy = effect on AV node conduction
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6
Q

nitrovasodilators MOA, indications and example

A
  • cause NO release in SMOOTH MUSCLE = increased cGMP = decreased Ca2+ = vasodilation
  • reduces venous return, ultimately to decrease cardiac O2 demand
  • independent of endothelium so can function if its damaged
  • indications: angina (stable or unstable)
  • e.g. nitroglycerin (GTN), isosorbide dinitrate
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7
Q

contraindications and adverse effects of nitrovasodilators

A
  • contraindicated w/ viagra (severe hypotension)
  • AEs: hypotension, reflex tachycardia (therefore increased O2 consumption), headache (due to increased intracranial pressure), flushing, can develop tolerance after continual exposure
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8
Q

how is GTN administered?

A
  • sublingually
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9
Q

what makes nitrovasodilators better than other vasodilators

A
  • others only vasodilate the normal, functioning circuits = more blood flow to places that don’t need it
  • nitros also vasodilate collateral circuits to perfuse evenly
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10
Q

MOA and indications of B blockers

A
  • blocks B1 receptors = decreased rate (-ve chronotrope) and force of contraction (-ve inotrope) = prevent arrhythmias
  • leads to decreased BP (for HTN)
  • decreased O2 consumption and increased coronary artery perfusion time (for HFrEF + angina)
  • indications: HTN, HFrEF, angina, tachyarrhythmias
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11
Q

adverse effects and contraindication of B blockers

A
  • A/Es: cold extremities, bradycardia, bronchoconstriction
  • contraindicated in asthma, UNSTABLE heart failure and with class IV anti-arrhythmics (non-DHP Ca2+ channel blockers)
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12
Q

DHP Ca2+ channel blockers MOA + indications

A
  • MOA: inhibit L-type Ca2+ channels in blood vessels = vasodilation = decreased afterload = decreased BP (for HTN) and decreased O2 consumption (for angina)
  • indications: HTN, angina (stable + vasospastic)
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13
Q

adverse effects and contraindications of DHP Ca2+ channel blockers

A
  • AEs: cardiac depression, bradycardia, flushing, oedema, dizziness, headache, constipation, nausea
  • C/I: heart failure and aortic stenosis
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