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Pathophysiology > Adult Cardio 3 (Coronary Artery Disease) > Flashcards

Adult Cardio 3 (Coronary Artery Disease) Flashcards

1
Q

Coronary artery disease is also known as…

A

Ischemic heart disease

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2
Q

Coronary artery disease is caused by a blocked ___ in a branch of the left coronary artery

A

Lumen

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3
Q

___ ___ ___ is the leading cause of death, with coronary artery disease being the largest percentage of that

A

Cardiovascular disease

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4
Q

The creation of ___ drugs started the decline in prevalence of coronary artery disease

A

CABG

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5
Q

____ is an aging process that happens over a long period of time

A

Atherscleorosis

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6
Q

Between ___-___ years of age is when you might start to see the thickening of the endothelium (beginning of the atherosclerosis process)

A

10-20

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7
Q

Massive occlusions caused by atherosclerosis happen between __-__ years of age, typically

A

50-60

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8
Q

Massive occlusions caused by atherosclerosis can cause…

A

-Myocardial infarction
-Ischemia, stroke, TIA
-UA
-Acute limb ischemia
-CV death

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9
Q

___ ___ ___ describes connections or anastomoses between 2 branches of the same coronary artery or connections/branches between the same right coronary artery and left coronary artery

A

Collateral coronary circulation

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10
Q

What is the functional importance of collateral coronary circulation?

A

Protects the heart

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11
Q

Gradual coronary artery ___ results in growth of collaterals

A

Occlusion

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12
Q

What two things will facilitate collateral growth?

A

-Nitric oxide
-Vascular endothelial growth factors

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13
Q

The degree of left ventricle deterioration is ____ related to the presence of collaterals

A

Inversely

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14
Q

The incidence of ventricular aneurysm formation after myocardial infarction is ___ when significant collaterals are present

A

Decreased

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15
Q

The risk for severe dysrhythmias after myocardial infarction is ____ when significant collaterals are present

A

Decreased

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16
Q

The presence of collaterals expands the “window of ___” in which reperfusion strategies are effective after myocardial infarction

A

Time

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17
Q

___ people are more likely to develop collateral circulation because they have more time

A

Older

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18
Q

___ people have more severe and more deadly occlusion (more severe symptoms like crushing chest pain)

A

Younger

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19
Q

Older people might have more ____ symptoms with MI

A

Atypical

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20
Q

Women might also have atypical symptoms because they usually have MI ___ years after men due to estrogen which slows down atherosclerotic process (they have more time for collateral circulation)

A

10

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21
Q

___ ___ is more common in elderly people

A

Unstable angiotensin (blood pressure)

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22
Q

Chest pain is also known as ____

A

Angina

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23
Q

People may have __-__% occlusion before they are symptomatic

A

50-75%

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24
Q

___% what patients have chest pain plus one or more other symptoms

A

90

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25
___-___% may be symptomatic during increased myocardial oxygen demand
50-75
26
Symptoms and outcomes are dependent upon ___ vs ___
Ischemia (reduced blood flow); infarction (no blood flow)
27
Infarction causes ____ activation, aggregation, and adherence
Platelet
28
Common symptoms other than angina:
-Dyspnea -Diaphoresis -N/V (due to vagus nerve innervation) -Syncope (due to systolic dysfunction)
29
The continuum of ischemic heart disease:
-Coronary artery disease -Ischemia -Myocardial infarction
30
Definition of coronary artery disease:
Any vascular disorder that causes narrowing/occlusion of coronary arteries
31
Definition of ischemia (angina):
Local state in which myocardial O2 supply is diminished to the extent that myocardial cellular metabolism is impaired
32
What are four types of ischemia?
-Stable -Variant (Prinzmetal's) (Vasospasm) -Silent -Unstable (acute coronary syndrome)
33
Myocardial infarction is the ___ of acute coronary syndrome
Endpoint
34
Myocardial infarction causes ___ necrosis
Myocyte
35
What are the two types of MI?
-ST elevation MI -Non-ST elevation MI
36
Within the progression of coronary artery disease, is systolic or diastolic function impaired first?
Diastolic
37
If someone has a normal ___, it does not mean that they definitely don't have heart issues
EKG
38
Ischemia is an imbalance between ___ and ___
Supply and demand
39
What can cause increased O2 demand?
-Hyperthermia -Hyperthyroidism -Sympathomimetic toxicity -Hypertension -Anxiety -AV fistula -Hypertrophic CMP -Aortic stenosis -Dilated CMP -Tachycardia
40
What can cause decreased O2 supply?
-Anemia -Hypoxemia (pneumonia, asthma, COPD, sleep apnea) -Sickle cell -Sympathomimetic toxicity -Hyperviscosity (polythemia, leukemia) -Aortic stenosis -Hypertrophic CMP
41
Acute coronary syndrome starts when atherosclerotic ___ with a lipid-rich core and thin fibrous cap forms
Plaque
42
What may cause rupture of this plaque?
-Shear force -Inflammation -Apoptosis -Macrophage-derived degradative enzymes
43
After the plaque has ruptured, what may cause thrombus formation over the lesion, plus vasoconstriction of the vessel?
-Increased inflammation with release of multiple cytokines -Platelet activation -Production of thrombin and vasoconstrictors
44
Acute decrease in coronary blood flow then leads to...
-Unstable angina -Myocardial infarction
45
Mitochondria needs ___ to generate ATP
Oxygen
46
When O2 is reduced, there is not enough ___ being produced
Energy
47
What are some major users of ATP?
-Actin -Myosin -Sodium-potassium pump
48
Since actin and myosin are ___ in proximity than the sodium-potassium pump, they will get most of the oxygen (the sodium-potassium pump suffers more)
Closer
49
Without the sodium-potassium pump, the ___ of the cell is messed up and the cell will remain in repolarization for longer periods of time
Polarity
50
___ would then start and this would indicate ischemia
Hypokenesis (smaller range of motion of body)
51
The dysfunction of the sodium-potassium pump cause too much ___ to get into the cells, causing the cell to swell
Sodium
52
With too much sodium in the cell, you might go into ____ because energy is being used to get sodium into the cell
Acidosis
53
Severe acidosis leads to ___ and lots of damage to nearby cells; you would be able to detect troponin in the blood
Necrosis
54
If there is less severe acidosis, you might see ____which would not damage nearby cells (no troponin in the blood)
Apoptosis
55
Less severe acidosis might cause problems since it is less symptomatic and might go ____
Undetected
56
Characteristics of an unstable plaque:
-Inflammatory cells -Thin fibrous cap -Few smooth muscle cells -Eroded endothelium -Activated macrophages
57
Characteristics of a stable plaque:
-Lack of inflammatory cells -Thick fibrous cao -More smooth muscle cells -Intact endothelium -Foam cells
58
Local risk factors for plaque rupture:
-Cap fatigue -Atheromatous core (size/consistency) -Coronary hemodynamics -Cap thickness/consistency -Mechanical injury -Cap inflammation
59
Systemic risk factors for plaque rupture:
-Smoking -Cholesterol -Diabetes Mellitus -Homocysteine -Impaired fibrinolysis
60
____ use their membrane to form clots
Platelets
61
Platelets are activated because they think there is a ___ in the artery, but there is really just a crack in the endothelial layer of the heart
Cut
62
____ is the first line therapy for MI because it is anti-platelet (we want to get rid of the clot)
Aspirin
63
If patient has unstable angina, after doing a history, physical exam, ECG, and looking at cardiac markers, you can determine if there is ___ elevation or not
ST
64
If someone has ST elevation, is is presumed an ___ ___
Acute MI
65
If someone has no ST elevation, look at ___ __ ___ and ECGs
Serial marker sampling
66
If someone has positive markers, it is presumed __ __
Acute MI
67
If someone has negative markers, it could indicate one of what two things?
-Unstable angina -Noncardiac chest pain
68
____ infarction, also known as (STEMI), involves all 3 muscle layers of the heart
Transmural
69
A non-transmural (non-STEMI) infarction can be classified as one of what two things?
-Subendocardial -Subepicardial
70
Subendocardial non-STEMIs involve what two muscle layers?
-Endocardium -Myocardium
71
Subendocardial non-STEMIs are more ____ because blood supply to the endocardium is at greater risk due to the mechanics of systolic compression on these vessels
Common
72
Subepicardial non-STEMIs involve what two muscle layers?
-Epicardium -Myocardium
73
STEMI MIs have ___ ___, which is more concerning
Full occlusion
74
Non-STEMIs are problematic because they might not be ____
Detected
75
What should we look for when diagnosing STEMI vs non-STEMI?
-Patient's story -Physical exam -Electrocardiogram -Cardiac markers
76
What should we look for during history and physical exam?
-Precipitating factors -Chest pain (differentials) -N/V -Diarrhea -Weakness -Dizziness -Palpations -Cold perspiration
77
Pain in the lungs might indicate....
-Pneumothorax -Pulmonary embolism
78
Main in the musculoskeletal regions might indicate...
-Non-specific pain -Cocaine abuse
79
Pain in the heart might indicate...
-MI -Aortic dissection -Pleural effusion -Heart failure -Coronary artery disease -Heart valve diseases -Atrial fibrilation
80
GI pain might indicate...
-Acid reflux disease -Esophageal rupture
81
CPK is a cardiac biomarker which would rise 4-8 hours after MI, peak ___-___ hours after, and normalize in 3-4 days
12-24
82
CK-MB is a cardiac biomarker which would rise 4-6 hours after MI, peak ___-___ hours after, and normalize 2-3 days after
12-24
83
Troponin is a cardiac biomarker that would rise 3-12 hours after MI, peak __-__ days after, and normalize 1-2 weeks after
1-2
84
The goal is for EMS to balloon time to be within ___ minutes after the onset of symptoms
90
85
Total ischemia time should be less than ___ minutes from time of symptom onset to balloon
120
86
Sending a patient to the cath lab __-__ hours after symptoms might be deadly due to reperfusion injury
3-4
87
If it has been 304 hours since onset of MI symptoms, sending the patient to the cath lab causes creation of ___ ___ ___ (if the mitochondria does not deactivate the ROS, it goes to the DNA and causes cell death)
Reactive oxygen species
88
Reperfusion injury causes ____ levels to skyrocket and cause widespread necrosis which could cause death
Troponin
89
___ ___ happens in 50-70% of cases and causes sudden death
Ventricular fibrilation
90
With ventricular fibrillation, the heart starts fibrillating instead of ____ (causes death)
Contracting
91
____ ___ is another mechanism of how occlusion can lead to death; it causes multiorgan failure
Cardiogenic shock
92
With ___ ___, the left ventricle fails, so blood backs up into the lungs and causes breathing problems and death
Pulmonary edema

Pathophysiology (18 decks)

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