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Applied Pathophysiology > Coronary Artery Disease I > Flashcards

Coronary Artery Disease I Flashcards

1
Q

Simple definition of Coronary Artery Disease (CAD)

A

plaque builds up in an artery

(main BV in heart, uses glucose & fatty acid)

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2
Q

Coronary Artery Disease (CAD) can be…

A
  1. A buildup of plaque (ATHEROSCLEROSIS) can narrow coronary arteries, decreasing blood flow to the heart.
  2. The reduced blood flow may cause chest pain (ANGINA), shortness of breath, or other symptoms.
  3. A complete blockage can cause a heart attack (MYOCARDIAL INFARCTION; AKA Myocardial Ischemia)
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3
Q

A buildup of plaque (_______) can narrow coronary arteries, decreasing blood flow to the heart.

A

atherosclerosis

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4
Q

The reduced blood flow may cause chest pain (______), shortness of breath, or other symptoms.

A

angina

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5
Q

A complete blockage can cause a heart attack (_______).

A

myocardial infraction (aka myocardial ischemia)

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6
Q

What causes reduced coronary perfusion?

A

occlusion of the artery

(vasospasm; C.A. constricts or atherosclerosis (stable plaque); permanently decrease CA BF)

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7
Q

Which layer of the artery wall mostly controls the C.A.?

A

Smooth muscle
- b/c can constrict

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8
Q

Describe the mechanism of atherosclerosis

A

*check recording

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9
Q

What are the stages of atherosclerosis?

A
  1. HEALTHY
  2. FATTY STREAK
    - lipids
    - foam cell
  3. FIBROFATTY PLAQUE
    - core
    - smooth-muscle cell
  4. COMPLICATED PLAQUES
    - thrombus
    - calcification
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10
Q

What are the key points for the development of atherosclerosis?

A
  1. Endothelial cell injury or dysfunction leads to monocyte infiltration and these monocytes are further differentiated into macrophages.
  2. Oxidized LDLs are trapped in the extracellular matrix of sub-endothelial space.
  3. Uncontrolled uptake of oxidized lipids by macrophages triggers the formation of foam cells, which augments cytokine release and leads to the development of the fatty streak.
  4. Smooth muscle cells are proliferated and migrated into intima to induce plaque formation.
  5. The progression of the lesion induces calcification and changes the mechanical characteristics of the artery wall and predispose to plaque rupture at sites of monocytic infiltration.
  6. Plaque rupture exposes the flowing blood to tissue factor in the lesion, and this induces thrombosis.
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11
Q

What are the 3 major factors contributing to Atherosclerosis?

A
  • Metabolic dysfunction (hyperlipidemia - high cholesterol)
  • Inflammation
  • Thrombosis
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12
Q

What is metabolic dysfunction (hyperlipidemia)?

A
  • ↑ Low density lipoprotein (LDL) = bad cholesterol
  • ↓ High density lipoprotein (HDL) = good cholesterol

(hyperlipidemia = high cholesterol)

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13
Q

Which lipoprotein or cholesterol is involved in development of atherosclerosis/correlated?

A

↑ Low density lipoprotein (LDL) = bad cholesterol

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14
Q

Describe Treatment 1: Cholesterol medications

A
  • Aggressively LOWERING LDL cholesterol, the “bad” cholesterol, can slow, stop or even reverse the buildup of fatty deposits in coronary arteries.
  • BOOSTING HDL cholesterol, the “good” cholesterol.
  • Statins
    – Atorvastatin (Lipitor)
    – Simvastatin (Zocor)
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15
Q

Why are Statins used as cholesterol medication?

A

b/c it inhibits enzyme in liver & liver is main place where cholesterol is formed

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16
Q

What are the down sides of using Statins (Atorvastatin (Lipitor), Simvastatin (Zocor))

A
  1. Muscle damage if used long-term (measure/monitor)
  2. May get sclerosis if used for long-time
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17
Q

What is Inflammation?

A

Atherosclerosis is considered as an inflammatory disease based on the observations of immune activation and inflammatory signalling in human atherosclerotic lesions.

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18
Q

What is the pathology of Atherosclerosis (inflammation)?

A
  1. Healthy Artery
  2. Fatty Streak
  3. Atherosclerotic plaque
  4. Plaque rupture or erosion + thrombus formation

(increase Macrophages, T lymphocytes, Dendritic cells with each stage)

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19
Q

Describe Treatment 2: Anti-Inflammatory Therapies

A

New therapeutic targets:
- innate & adaptive immunity
- pro-inflammatory molecules

yield:
- current therapeutic approach: STATIN
- experimental approaches:
– chemokine antagonists
– TNF-alpha antagonists
– IL1Ra & IL6R antagonists
– regulatory T cell expansion
– CD4+ CD28null T-cell modulation

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20
Q

What is Thrombosis?

A
  • Plaque rupture and superficial erosion typically cause localized, often occlusive thrombus formation.
  • The triggering of the coagulation system via factor XIIa, factor VIIa, tissue factor, and ultimately thrombin has a central role in mediating atherothrombosis.
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21
Q

Describe Treatment 3: Anticoagulants

A
  • The prevention of atherothrombotic events is an essential therapeutic goal in the treatment of patients with arteriosclerotic diseases.
  • Platelet inhibitors are the primary therapy used to prevent arterial thrombosis.
  • Aspirin
  • Clopidogrel
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22
Q

What is the primary therapy used to prevent arterial thrombosis?

A

Platelet inhibitors

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23
Q

What are the recommended Anticoagulants?

A
  • Aspirin
  • Clopidogrel
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24
Q

Why isn’t Warfarin a recommended Anticoagulant for this?

A

has side effects b/c will stimulate smooth muscle cell proliferation (will stimulate further dev. of atherosclerosis)
- trigger calcification in lumen

25
Q

What risk factors do we need to block to decrease development of atherosclerosis?

A
  • Metabolic dysfunction (hyperlipidemia - high cholesterol)
  • Inflammation
  • Thrombosis
26
Q

Describe the structure of the Coronary Arteries

A

Right Coronary Artery
- smaller branches & go to heart tissue

Left Coronary Artery
- BIGGER
- wall is thicker than right wall
- more imp. b/c contributes to ~70% ?

right supply to left & vice versa ?

*check recording

27
Q

The coronary blood flow supplies…

A

blood, oxygen and nutrients to the heart

Left Circumflex Artery - supplies the left atrium & left ventricle

Left Anterior Descending Artery - supplies the right ventricle, left ventricle & interventricular septum

Left Marginal Artery - supplies the left ventricle

Right Marginal Artery - supplies the right ventricle & the apex

Right Coronary Artery - supplies the right atrium & the right ventricle

28
Q

Describe Coronary blood flow

A

large EPIcardial arteries
(“ON” the surface of the heart)
LITTLE OR NO RESISTANCE to blood flow

INTRAmyocardial arteries
and arterioles
(“IN” the muscle of the heart) capillaries
HIGHER RESISTANCE to blood flow

29
Q

What are the Key Regulators of Coronary Blood Flow?

A
  • Autoregulation
  • Collateral blood flow
  • Metabolic regulation
  • Endothelial lining protection
  • Artery compression
30
Q

Autoregulation when stenosis < 70%:

A

— Autoregulation —>

arteriolar dilation that allows reserve coronary blood flow for exertion
- could regulate lower BF in C.A

31
Q

Autoregulation when stenosis > 70%

A

— Autoregulation —>

arteriolar dilation occurs but is INSUFFICIENT to allow reserve coronary blood flow for exertion

32
Q

Describe Collateral blood flow

A
  • Connections between smaller arteries trying to compensate for occlusions in the larger arteries
  • These connections allow for better flow to ischemic areas
  • Drawback is their presence can mask coronary heart disease until it is advanced
33
Q

What is the difference b/t Normal & Collateral circulation?

A

Normal circulation
- narrowed coronary artery

Collateral circulation
- collateral blood vessels

(dog’s heart has a lot of collateral BVs therefore never use)

34
Q

Describe Metabolic regulation

A
  • Changes in oxygen demand trigger metabolic mediators
  • adenosine (ATP → AMP) – vasodilation
  • nitric oxide - vasodilation
35
Q

Describe Endothelial lining protection

A
  • Protects the artery
  • physically
  • functionally
  • Damage has consequences
36
Q

Describe Artery compression

A
  • During diastole (relaxed), coronary arteries are perfused well (low pressure)
  • During systole (contracted - push BF forward), the coronary arteries are compressed (high pressure) and perfused less
  • Coronary inflow occurs mainly during diastole (relaxation phase) due to compression/pressure during systole
37
Q

What happens if all of the key regulators of coronary blood flow (autoregulation, collateral blood flow, metabolic regulation, endothelial lining protection, & artery compression) fail?

A

leads to Coronary Blood Flow

(which => myocardial ischemia/infraction)

38
Q

What is a Myocardial ischemia?

A
  • ISCHEMIA is insufficient blood flow to provide adequate oxygenation.
  • HYPOXIA: LACK OR DEFICIENCY OF OXYGEN in the myocardium.
  • Ischemia always results in hypoxia; however, *hypoxia can occur without ischemia if, for example, the oxygen content of the arterial blood decreases as occurs with anemia.
39
Q

Ischemia:

A

is insufficient blood flow to provide adequate oxygenation.

40
Q

Hypoxia:

A

LACK OR DEFICIENCY OF OXYGEN in the myocardium.

41
Q

_____ always results in hypoxia; however, _____ can occur without ischemia if, for example, the oxygen content of the arterial blood decreases as occurs with anemia.

A

ISCHEMIA

HYPOXIA

42
Q

Stable Angina (Pectoris - chest pain) (vs. unstable)

A

Stable atherosclerotic plaque impairs perfusion

–> Ischemia reduces production of ATP, increases production of chemicals and results in acidosis
(inhibit O2 supply CO2 is imp. for fatty acid & glucose to produce ATP)

–> ANAEROBIC METABOLISM (LACK OF OXYGEN): lactic acid
MYOCYTES: serotonin, bradykinin, histamine, reactive oxygen species, and adenosine
PLATELETS: serotonin, thromboxane A2 and 5-hydroxytryptamine

–> BUILDUP OF CHEMICALS: no washout of acidic/chemical substances

–> PAIN (in chest)

43
Q

What is the angina pain distribution?

A
  • chest
  • back
  • maybe arm and mouth
44
Q

What are triggers of an angina attack?

A
  • PHYSICAL EXERTION. This can precipitate an attack by increasing myocardial oxygen demand.
  • EXPOSURE TO COLD. This can cause vasoconstriction and elevated blood pressure, with increased oxygen demand.
  • EATING A HEAVY MEAL. A heavy meal increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle; in a severely compromised heart, shunting of the blood for digestion can be sufficient to induce anginal pain.
    (*b/c most blood go to stomach for digestion so less blood in heart)
  • STRESS. Stress causes the release of catecholamines, which increase blood pressure, heart rate, and myocardial workload.
45
Q

What are symptoms of Stable Angina?

A
  • Pain
  • Radiation of pain
  • Shortness of breath
  • Bradycardia
  • Tachycardia
  • Nausea/vomiting
46
Q

Describe the pain of Stable Angina

A
  • often described as discomfort
  • squeezing, pressure, burning, tightness, heavy weight on chest (elephant)
  • Levine sign “fist in the center of the chest”
  • gradual in onset; intensity increases over minutes (non-cardiac pain is
    usually the opposite)
  • resolves with REST and SHORT DURATION (usually 2-5 minutes, but not more than 20 minutes)
  • **THIS IS A KEY FEATURE OF STABLE ANGINA
47
Q

Describe the radiation of pain of Stable Angina

A
  • arms, shoulders, neck, jaw, back, throat, teeth, upper abdomen (C7-
    T4)
  • tend to have the same quality of chest discomfort with recurrent ischemic episodes (i.e. same location and intensity); increase in severity is a warning sign of unstable angina/acute coronary syndromes
48
Q

Describe the Shortness of breath of Stable Angina

A
  • dysfunction of the heart leads to mild pulmonary congestion
49
Q

Describe the Bradycardia of Stable Angina

A
  • slow heart rate <60 bpm
  • less common
  • blood supply to AV node impaired

(b/c C.A. BF isn’t enough to supply blood to AV node; contraction decrease)

50
Q

Describe the Tachycardia of Stable Angina

A
  • stress/panic and release of catecholamines (to try and compensate for reduced oxygen supply)
51
Q

Describe the Nausea/vomiting of Stable Angina

A
  • vagus nerve stimulation
52
Q

What are the Diagnostic Tests used for Stable Angina?

A

Electrocardiogram (ECG)
- electrical activity of the heart by monitoring electrical changes in the skin
- ST segment elevation/depression, T wave inversion

Stress or Exercise Tolerance Test (ETT) (trigger chest pain & then do ECG)
- ECG combined with physical exertion (e.g. treadmill)

Angiogram (popular worldwide)
* catheter inserted via femoral artery
* inject dye to illuminate coronary vessels
* TIMI – Thrombolysis in Myocardial Infarction
- TIMI 0 = zero perfusion/flow
- TIMI 3 = normal perfusion/flow

53
Q

What are the risk factors for CAD?

A

Modifiable:
* Smoking
* Dyslipidemia
* Hypertension
* Obesity/sedentary lifestyle
* Stress
* Chronic kidney disease
* Illicit drugs

Non-Modifiable:
* Male (estrogen/has protecting effect on females ?)
* Age (>40 years)
* Genetics/Family history * Ethnicity
* Environmental factors
* Diabetes

54
Q

What is the management of CHD?

A

“myocardial oxygen demand” > “myocardial oxygen supply”

Nitrates (NO imp. for vasodilation)
Determinants:
* heart rate
* systolic blood pressure (afterload)
* myocardial contractility
* myocardial wall tension or stress* *considered to be the most important

Determinants:
* oxygen carrying capacity of the blood
* oxygen tension
* hemoglobin (Hb) concentration
* degree of oxygen unloading from Hb
* coronary artery blood flow

1 – dilate arteries to improve blood flow and/or reduce blood pressure 2 – dilate veins to reduce preload (return of blood to the heart)

55
Q

Beta-blockers act on…

A

HR, systolic BP (afterload) & myocardial contractility)
- 1st line for preventing myocardial infraction & cardiac death

56
Q

Calcium channel blockers act on…

A

HR, systolic BP (afterload) & myocardial contractility, myocardial wall tension or stress & C.A. BF

Reduce conduction velocity through SA and AV nodes Reduce blood pressure by dilating arteries
Reduce contractility

dilate coronary arteries
prevent coronary artery vasospasm

57
Q

Lipid-lowering medications can…

A

help manage CHD (ex: Statin)

58
Q

Anti-platelet medications act on…

A

C.A. BF

Applied Pathophysiology (34 decks)

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