Dr. Tann Flashcards

1
Q

What are some important risk factors for coronary artery disease?

A
1st degree relatives w/ CAD
High Cholesterol
HTN
Older age
Smoking
Obesity
Stress Diabetes
Metabolic Syndrome--collection of risk factors.
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2
Q

What are the options for treating athersclerosis?

A

Meds or insertion of a stent. Basically–we don’t want a blood clot!!

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3
Q

What are the options for treating athersclerosis with a blood clot?

A

This needs to be physically removed.

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4
Q

What can mimic athersclerosis?

A

Vasospasms.

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5
Q

How does the blood vessel appear on imaging? Ultrasound in particular.

A

Adventitia–with a lot of collagen will appear gray or white.
Media–with a lot of smooth muscle cells–doesn’t reflect waves & appears dark.
Intima–If there is plaque it will appear different shades of white or gray.

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6
Q

What is the purpose of imaging?

A

To confirm your suspicion.

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7
Q

What is the artery’s response to plaque buildup?

A

It remodels itself to protect the lumen. It first expands outward. Then eventually it succumbs & the lumen narrows.

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8
Q

T/F if there is plaque buildup the flow will necessarily be bad.

A

False. Even with plaque buildup the artery can sometimes compensate & create good flow.

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9
Q

What is your fear with plaque?

A

So there is this nasty thrombogenic stuff trapped in the plaque buildup. A fibrous cap keeps it form contacting the blood in the lumen. Your fear is that if it ruptures there will be fast blood clot formation.

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10
Q

Which additions to the intima are dangerous & indicate unstable plaque & dangerous intimal thickening?

A

Lipid pool

Microcalcifications

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11
Q

Which cells are thought to destabilize a plaque & fibrous cap?

A

Inflammatory cells

activated macrophages

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12
Q

What is it that causes plaque growth?

A

Hemorrhage & rupture.

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13
Q

What is a thin cap fibro-atheroma? What are its characteristics?

A
Vulnerable Plaque
Large necrotic core
thin fibrous cap
presence of macrophages & lymphocytes
presence of type I collagen
absence of many smooth muscle cells
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14
Q

What is stable angina? How do you treat it?

A

Heart pain during exertion. Relieved w/ rest. Pressure or tightness.
Indicates improper O2 flow to the heart.
Modify risk factors
Beta blockers
ACE inhibitors
Statins
Calcium channel blockers

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15
Q

What is unstable angina? How is it treated?

A

Chest pain when at rest or with higher frequency.
This could indicate a partially occluding platelet-rich thrombus.
This causes no permanent damage.
You will sometimes see ST depression with this.
Treated aggressively, with meds, with diagnostic catheter, hemodynamic support & IV fluids

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16
Q

If the thrombus of unstable angina grows, what may happen?

A

Complete occlusion! Emergency! ST elevation.

17
Q

What is NSTEMI?

A

Non ST elevation MI.

Note, an MI with ST elevation is more easy to localize where the damage is.

18
Q

What was the new treatment for MI in 1979 that was considered crazy talk?

A

Angioplasty

19
Q

What were two other types of therapy for MI that were developed in the late 1980s & early 1990s?

A

Thrombolytic & Fibrinolytic therapy.

20
Q

What does aspirin try to do vs. what warfarin & heparin try to do?

A

Aspirin-anti-platelet

Warfarin & heparin–anti-thrombin

21
Q

What was one of the major dangers of fibrinolytic therapy?

A

Ischemia
Reinfarction
Brain hemorrhage

22
Q

What are most patients who go to the ER with chest pain treated with?

A

anti-coagulants

23
Q

Which coronary artery when messed with is called the widowmaker?

A

LAD

24
Q

What are 3 possible post-MI problems?

A

Ventricular Septal Rupture
Free Wall Rupture
Mitral regurgitation (b/c of papillary muscle dysfunction)