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ACS and atherosclerosis Flashcards

1
Q

Young people have positive or negative troponin?

A

Negative

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2
Q

What does it mean when troponin increases?

A

Heart injuries

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3
Q

For CAD what tests do you do?

A

Troponin test or EKG

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4
Q

Does the presentation need to match the labs?

A

Yes !!

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5
Q

ST elevations mean?

A

Poor prognostic—full MI-> can develop cardiomyopathy

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6
Q

Death is much higher in westernized or developing countries?

A

Death is much higher in developing countries but incidence is lower

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7
Q

What are the non modifiable risk factors?

A

Genes, age, gender, family history

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8
Q

What are the modifiable risk factors?

A

Smoking, high cholesterol, HTN, DM, physical inactivity-do 300 min per week

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9
Q

Majority of patients with CAD are ?

A

Obese and HTN

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10
Q

Which artery provides the majority of O2 blood supply?

A

Left main artery provides 70-80%

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11
Q

What happens when the left anterior descending artery is obstructed?

A

Significant decrease in O2 for the rest of the body

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12
Q

What are the characteristics of stable angina?

A

Chest pain with exertion (physical activity)
EKG normal but can have ST changes
It is a precursor to unstable angina

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13
Q

What are the characteristics of unstable angina?

A

Chest pain at rest (sitting/ talking) - no exertion
Troponin -
EKG changes may happen to show St depression or T wave inversion or may not

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14
Q

What are the characteristics of NSTEMI?

A

Troponin +
No elevation of ST waves
ST depression
T-waves can be inverted
Looks like unstable

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15
Q

What are the characteristics of STEMI?

A

ST elevations (full thickness injury)
Troponin +
Have all the symptoms

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16
Q

In stable angina what type of plaque do you have?

A

Stable plaque - hard plaque and won’t rupture

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17
Q

What happens if the plaque ruptured?

A

Can cause acute coronary syndrome

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18
Q

What are the characteristics of vasospastic disease?

A

Usually young women, anxiety can cause the spasm->focal/transient vasospasm

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19
Q

How do you treat vasopastic disease?

A

Need vasodilator (ccb)
Not BB

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20
Q

What is microvascular dysfunction?

A

When collateral circulations start closing -> can develop long term ischemic cardiomyopathy or takotsubo syndrome

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21
Q

What is takotsubo?

A

Broken heart syndrome

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22
Q

If <20% coronary stenosis , then you have:

A

No significant CAD

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23
Q

If left main closes 20-50%, then you have:

A

Non-obstructive CAD

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24
Q

If other coronary arteries close 20-70%, then you have:

A

Non-obstructive CAD

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25
Q

If left main closes more than 50%, then you have:

A

Obstructive CAD

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26
Q

If other coronary arteries close more than 50%, then you have:

A

Obstructive CAD

27
Q

In moderate CAD, how much closure do you have?

A

> 65%

28
Q

In severe CAD, how much closure do you have?

A

Lumen is 90% closed -this is the time they have symptoms/ signs

29
Q

If testing for luminal obstruction, is that a good predictor of CAD?

A

No

30
Q

Stable Angina things to know:

A

Smooth muscle over plaque is strong enough still.
Can start a stent especially if in left main—-Aggressive treatment
Narrow arteries
EKG usually shows acute MI instead of silent MI

31
Q

When does type 1 lesions happen?

A

Within the first 10 years of life -silent
40-50 years old can still be silent

32
Q

Type 5 and 6 lesions?

A

Can develop thrombosis and dislodge

33
Q

What do statins do?

A

Stabilize endothelium membrane

34
Q

What is so important about the endothelium?

A

It is resistant to thrombosis

35
Q

Endothelium dysfunction/ injury means?

A

An thrombosis can occur

36
Q

What happens when LDL is oxidized?

A

Inflammatory response -enters lumen and macrophages and monocytes go inside endothelium-this forms foam cells, making a lipid rich necrotic core plaque

37
Q

What happens as endothelium thickens?

A

Forms fibroatheroma and now becomes vulnerable plaque

38
Q

Vulnerable plaque can —— and —— thrombosis

A

Dislodge and activate
They dislodge and cause platelet aggregation causing a thrombosis

39
Q

The more thrombosis and platelet aggregation is you have ——

A

The more endothelium dysfunction you have

40
Q

If plaque is stable you still have….

A

Some perfusion

41
Q

Best treatment for CAD?

A

Management of lipids-statin

42
Q

Endothelium is known as

A

Thrombo resistant barrier

43
Q

In the arterial wall, what happens if endothelium is damaged?

A

Stops penetrating/ filtering to connective tissue and thickening of the intima

44
Q

Thickening of the intima causes ?

A

Endothelium barrier to decrease and making it lose its thrombo resistant barrier

45
Q

Patho of pre-atherosclerosis?

A

Overtime calcifications increase
Replaces smooth muscle in intima with core plaques-more lipids penetrate and arteriosclerosis gets bigger
Starts the minute you’re born

46
Q

Increased intima thickening means

A

Closure of the lumen

47
Q

What is the driving factor of atherosclerosis?

A

Inflammation

48
Q

Can you develop atherosclerosis even if LDL is low?

A

Yes because in combo with other risk factors like smoking, lupus, RA, it still can develop

49
Q

What is a cause of atherosclerosis?

A

Increased ApoB containing LDL

50
Q

Endothelium functions as :

A

A barrier
Decreased inflammation
Prevents vessel remodeling and growth
Lipoprotein ApoB does not penetrate
Prevents platelet aggregation and adhesion of monocytes, thrombosis

51
Q

atherosclerosis usually occurs in a ———

A

High pressure area

52
Q

Where does atherosclerosis usually occur?

A

Left main (ostia can form here) and is most susceptible

53
Q

Most of coronary perfusion comes from?

A

Left main

54
Q

Where is it much harder to put a stent?

A

Left anterior descending (bifarctions) separation

55
Q

Inner curvatures happen when?

A

When driving or making a sharp turn

56
Q

The more turbulent flow you have , the more…..

A

Injury you have

57
Q

What are focal lessons?

A

Abnormal shears with retracted cells

58
Q

What causes cells to retract?

A

Smoking (vasoconstriction)

59
Q

When retracted cells become smaller….?

A

It is easier for LDL to penetrate and start the activation process -> once entered macrophages kick in and foam cells are created -> pick up all cholesterol and form fatty streaks in vasculatures

60
Q

What does the necrotic core do?

A

The matrix degrades, inflammation, and activates fibrin, thrombin and causes break down of endothelium—- expansive remodeling

61
Q

What do you do if you think it is a heart attack?

A

Give aspirin (we have to stop the platelet activation)

62
Q

What if the plaque hemorrhages?

A

More thrombin and platelet forms-> causes extravasation of plasma proteins and erythrocytes->inflammation
So need heparin and aspirin

63
Q

Thrombosis is from?

A

Mostly plaque ruptures, some erosion and calcifications

64
Q

Vulnerable plaque has a

A

Thin capped fibroatheroma

Isbp (4 decks)

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