Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV wk 3 & 4 > Ischemia 1 > Flashcards

Ischemia 1 Flashcards

1
Q

3 categories of risk factors for CAD

A
  1. Treatable with consequent reduced risk
  2. Treatable, but unclear if risk is reduced by treatment
  3. Not treatable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which risk factors reduce risk of CAD when treated?

A
  1. Smoking
  2. Hypertension
  3. Dyslipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which risk factors for CAD have no conclusive evidence if they reduce risk when treated?

A
  1. Diabetes/Insulin resistance
  2. Obesity
    3 Inflammation
  3. Psychological stress
  4. Sedentary lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which risk factors for CAD are untreatable?

A
  1. Male gender
  2. Age
  3. Most genetic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the mechanism of risk for smoking and CAD?

A
  • Thrombogenic tendency, platelet activation, increased fibrinogen
  • Aryl hydrocarbon compounds promote atherosclerosis
    endothelial dysfunction, vasospasm
  • CO decreases myocardial oxygen delivery
  • Adverse effect on lipoproteins (decreased HDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of risk for hypertension and CAD?

A
  • Increased shear stress on arterial wall causes direct endothelial cell injury
  • Increased arterial wall stress initiates pathologic cell signaling program causing oxidant stress, cellular proliferation
  • Circulating hormones increased in HTN (angiotensin, aldosterone, norepinephrine) exert adverse effects on arterial wall
  • A chronic increase in heart work causes left ventricular hypertrophy which may be an independent risk factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does hypertension represent health disparities in populations?

A

Far more prevalent in African Americans and Asians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

By how many fold does diabetes increase your lifetime risk of CAD?

A

1.5 to 2 fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the dyslipidemic triad

A
  1. High levels of LDL
  2. Low levels of HDL
  3. High triglycerides

All increase risk of atherosclerosis and coronary heart disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why is LDL cholesterol so bad?

A
  1. Can be oxidized
  2. When oxidized, becomes pro-inflammatory and atherogenic
    - foam cells = key role in atherosclerosis
  3. Deposited in arterial wall and taken up by macrophages, causing progressive increase in plaque volume.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is HDL beneficial?

A
  1. Garbage trucks, take lipid from places it shouldn’t be and move it to the liver. “Reverse cholesterol transport”
  2. Promotion of endothelial NO production
  3. Anti-thrombotic effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe how inflammation is key in coronary heart disease

A
  1. Lipid-laden macrophages are the bad actors. They are deposited in arterial wall plaque and are highly pro-inflammatory
  2. Extravascular inflammation may increase risk of atherosclerotic cardiovascular events
  3. Circulating markers of inflammation (CRP) provide information about CV risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can CRP predict future CV risk?

A
  1. Inflammatory cells secrete cytokines, one of which is IL-6
  2. IL-6 taken up by liver, liver amplifies signal
  3. CRP is created in response, and you can measure this increase in CRP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the “stable phase” of coronary artery disease?

A

When CAD becomes symptomatic and the cardinal symptom is angina pectoris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Myocardial ischemia

A

Imbalance between coronary oxygen delivery and myocardial oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 ways that coronary circulation is different

A
  1. Myocardium depends upon aerobic metabolism for energy supply (skeletal uses anaerobic)
  2. Under resting conditions, near maximal oxygen is extracted from coronary arterial blood. The only effective means of increasing myocardial O2 supply is to increase blood flow rate
  3. Left ventricle is perfused in diastole ONLY
17
Q

Myocardial O2 delivery

A

coronary blood flow rate X O2 content of arterial blood

18
Q

What 3 thing determine coronary blood flow rate

A
  1. Perfusion pressure
  2. Diastolic perfusion time
  3. Vascular resistance
19
Q

On what level does autoregulation occur?

A

Small arterioles

20
Q

What is autoregulation?

A

An adaptive mechanism to maintain perfusion in face of altered perfusion pressure. (via dilation of vessel)

21
Q

What is the role of autoregulation in CAD?

A
  1. Autoregulation will compensate for stenosis up to a point.
  2. Once the stenosis is too big, you can’t get autoregulation. As a result, you can get a drop in perfusion pressure
22
Q

Why is perfusion diastolic?

A
  • LV perfusion predominantly diastolic because of compression of intramural coronary vessels in systole
  • Increased heart rate shortens the cardiac cycle, predominantly by shortening diastole
  • Tachycardia can therefore compromise coronary flow
23
Q

NO are vasodilators, why do you use them to treat angina pectoris and myocardial ischemia?

A

If you introduce a vasodilator, then the obstruction won’t be as obvious and blood supply will be better.

24
Q

What can oxygen supply be compromised by?

A
  1. Anemia - less hemoglobin per ml of blood

2. Hypoxemia - incomplete saturation of hemoglobin

25
Q

What are the primary determinants of myocardial O2 demand

A
  1. Heart Rate
  2. Wall tension
  3. Inotropic state
26
Q

Tx to reduce O2 demand: systolic pressure

A

Antihypertensive drugs

27
Q

Tx to reduce O2 demand: HR

A
  1. B-blockers, CCBs
28
Q

Tx to reduce wall tes=jnsion

A
  1. Limit LV cavity size by limitinge preloa
29
Q

Tx to reduce O2: inotropic sate:

A
  1. Negative inotropes to attenduate contractile state
30
Q

Pathophysiology of unstable coronary sydnromes

A
  • Inflammation in arterial wall
    Weakening of fibromuscular cap
  • Abrupt plaque fissure or rupture
  • Thrombogenic components (lipids, tissue factor) exposed to blood
  • Thrombosis with partial or complete vessel occlusion
  • Myocardial injury and/or necrosis (serum markers)- - - Cardiac dysfunction, risk of arrhythmias, death
31
Q

How do you go from stable CAD to unstable CAD?

A

Via inflammation. Get unstable, ruptured plaque in unstable

32
Q

Why is someone who has had unstable angina at higher risk for another event?

A

Because if the inflammation has attacked and destroyed one plaque, it has probably already begun to attack and degrade the others

33
Q

Tx for MI?

A

Restore blood flow ASAP

CV wk 3 & 4 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions