Angina Flashcards

1
Q

What are the characteristics of these types of angina

  • stable
  • mixed
  • vasospastic (Prinzmetals)
  • microvascular (Syndrome X)
  • unstable
A

Stable

  • Stenosis >70%
  • tight crushing pain on physical/emotional exertion (supply demand mismatch => adenosine, bradykinin release => pain)

Mixed

  • stenosis + vasospasm
  • unpredictable exertion

Vasospastic (Prinzmetals)
-no stenosis, coronary spasm

Microvascular (Syndrome X)

  • can’t VD enough due to endothelial dysfunction
  • no stenosis, linked to post/perimenopause

Unstable
-transient thrombus => partial occlusion

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2
Q

What are the main aims of drug treatment

-2 reasons

A

Decrease future attacks

  • decrease coronary O2 demand
  • increase coronary flow

Protect against future CV events

  • decrease risk factors via
    • Bblockers
    • Statins
    • ACEi
    • Aspirin
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3
Q

Describe the mechanism behind B blockers
What are the SE and why
What are the CI

A

Decreased SNS => decreased contractility and renin release => increase flow, diastole

SE due to VD inhibition

  • cold extremities
  • hypoglyacaemia due to dampened SNS dominated adrenaline reaction
  • exercise intolerance
  • fatigue

CI due to VD inhibition

  • asthma
  • VS angina
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4
Q

Describe the mechanism behind Ca channel blockers

What are the 3 main drugs in this group

A

VD CORONARIES

Amilodipine
-increase VD arteries => decrease after load => decrease cardiac stress

Verapamil, Diltiazem
-decreased inotropy => increase diastole

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5
Q

Describe the mechanism behind organic nitrates
What are the SE and why
Why can you develop a tolerance to this

A

Decreased CVP (decreaseSM, depolarization => venous VD) => decrease wall stress => decrease O2 demand

Decrease TPR
VD of coronaries

SE due to VD

  • low BP, reflex tachycardia
  • headache, facial flush

Tolerance due to increased oxygen radicals

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6
Q

Describe the mechanism behind ranalazine

A

Ischemia => increased ROS => increased late Na I

Normally

  • APs more likely
  • afterdepolarization arrhythmias

-increased [Ca] I => myocardial stunning => decreased diastolic period => increased work, decreased coronary flow

Ranalazine inhibitions late Na I

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7
Q

Describe the mechanism behind ivabradine
What are the SE and why
What are the CI

A

Blocks If => decreased HR => increased diastole, decreased after load, O2 demand

SE due to reflex increases

  • headache, dizzy
  • bradycardia
  • luminous phenomena

CI
-renal, hepatic impairment

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8
Q

Describe the mechanism behind nicorandil
What are the SE and why
What are the CI

A

KATP channel activator => opens channels in SM => hyper polarization and Ca removal/desensitization
=> VD => decreased pre/afterload => decreased work/O2 demand

SE due to VD
-headache, dizzy, flushed

CI

  • hypotension
  • PDE5 inhibitor (synergistic VD)
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9
Q

What are the 2 physical treatments for angina

How would you do this

A

PCI

  • guide catheter via femoral/radial vein
  • balloon inflates stent open

CABG

  • saphenous/int mammary for serious cases
  • more invasive, increase survival
  • needs thoracotomy, CP bypass
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