ACS and atherosclerosis Flashcards

(64 cards)

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
If left main closes more than 50%, then you have:
Obstructive CAD
26
If other coronary arteries close more than 50%, then you have:
Obstructive CAD
27
In moderate CAD, how much closure do you have?
>65%
28
In severe CAD, how much closure do you have?
Lumen is 90% closed -this is the time they have symptoms/ signs
29
If testing for luminal obstruction, is that a good predictor of CAD?
No
30
Stable Angina things to know:
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
When does type 1 lesions happen?
Within the first 10 years of life -silent 40-50 years old can still be silent
32
Type 5 and 6 lesions?
Can develop thrombosis and dislodge
33
What do statins do?
Stabilize endothelium membrane
34
What is so important about the endothelium?
It is resistant to thrombosis
35
Endothelium dysfunction/ injury means?
An thrombosis can occur
36
What happens when LDL is oxidized?
Inflammatory response -enters lumen and macrophages and monocytes go inside endothelium-this forms foam cells, making a lipid rich necrotic core plaque
37
What happens as endothelium thickens?
Forms fibroatheroma and now becomes vulnerable plaque
38
Vulnerable plaque can —— and —— thrombosis
Dislodge and activate They dislodge and cause platelet aggregation causing a thrombosis
39
The more thrombosis and platelet aggregation is you have ——
The more endothelium dysfunction you have
40
If plaque is stable you still have….
Some perfusion
41
Best treatment for CAD?
Management of lipids-statin
42
Endothelium is known as
Thrombo resistant barrier
43
In the arterial wall, what happens if endothelium is damaged?
Stops penetrating/ filtering to connective tissue and thickening of the intima
44
Thickening of the intima causes ?
Endothelium barrier to decrease and making it lose its thrombo resistant barrier
45
Patho of pre-atherosclerosis?
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
Increased intima thickening means
Closure of the lumen
47
What is the driving factor of atherosclerosis?
Inflammation
48
Can you develop atherosclerosis even if LDL is low?
Yes because in combo with other risk factors like smoking, lupus, RA, it still can develop
49
What is a cause of atherosclerosis?
Increased ApoB containing LDL
50
Endothelium functions as :
A barrier Decreased inflammation Prevents vessel remodeling and growth Lipoprotein ApoB does not penetrate Prevents platelet aggregation and adhesion of monocytes, thrombosis
51
atherosclerosis usually occurs in a ———
High pressure area
52
Where does atherosclerosis usually occur?
Left main (ostia can form here) and is most susceptible
53
Most of coronary perfusion comes from?
Left main
54
Where is it much harder to put a stent?
Left anterior descending (bifarctions) separation
55
Inner curvatures happen when?
When driving or making a sharp turn
56
The more turbulent flow you have , the more…..
Injury you have
57
What are focal lessons?
Abnormal shears with retracted cells
58
What causes cells to retract?
Smoking (vasoconstriction)
59
When retracted cells become smaller….?
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
What does the necrotic core do?
The matrix degrades, inflammation, and activates fibrin, thrombin and causes break down of endothelium—- expansive remodeling
61
What do you do if you think it is a heart attack?
Give aspirin (we have to stop the platelet activation)
62
What if the plaque hemorrhages?
More thrombin and platelet forms-> causes extravasation of plasma proteins and erythrocytes->inflammation So need heparin and aspirin
63
Thrombosis is from?
Mostly plaque ruptures, some erosion and calcifications
64
Vulnerable plaque has a
Thin capped fibroatheroma