Coronary Artery disease Flashcards

1
Q

coronary artery diseases (CADs) can be symptomless, true or false

A

true

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2
Q

ACS(acute coronary syndromes) mostly have symptoms, true or false

A

true

typically chest pain or discomfort, shortness of breath, nausea, sweating, or dizziness

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3
Q

CADs normally present as?

A

athelerosclerosis

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4
Q

what is athelerosclerosis

A

it is a disease of the large and medium sized elastic and muscular arteries, usually affecting the intima and the media

the intima is the innermost layer of the arteries, the media is the middle layer. the damage to the media is **secondary **

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5
Q

is the adventitia affected in athelerosclerosis

A

no it is generally uninvolved

it is the outermost layer of a blood vessel or organ

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6
Q

describe ATHEROSCLEROTIC LESIONS

note they are essentially the same as plaques

A

they are fibroinflammatory lipid plaques that occur over several decades, continually growing and encroaching the other layers of the arterial wall, thereby narrowing the lumen of the affected vessel

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7
Q

describe the stages of ATHEROSCLEROTIC plaque development

A

fatty streaks initially identified. note this may deteriorate(get worse) as the process advances .

the fatty streak is followed by the formation of an established plaque(aka intermediate lesion).

then there is a complicated plaque formation

Plaque rupture may occur after the fibrous cap has been weakened by the production of degradative enzymes, and reactive oxygen species, from the inflammatory cellular infiltrate

this exposes highly prothrombotic material, leading to formation of thrombus

this may then result in ACS

fatty streaks in the vessels are the earliest identifiable change in atherosclerosis

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8
Q

the intermediate lesion in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT is characterised by?

A

characterised by the accumulation of increasing numbers of;
* macrophages
* foam cells

these are local chronic inflammatory infiltrates in CADs

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9
Q

the complicated plaque in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT is characterised by?

A

smooth muscle cell migration

formation of;

a fibrous cap

a necrotic lipid core

an ever-lasting inflammatory infiltrate

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10
Q

the role of smooth cell migration in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT

A

initially contributing to the expansion of atherosclerotic lesions by moving into the intima from the media layer of the artery wall, and later by forming a protective fibrous cap that stabilizes the plaque

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11
Q

some signs and symptoms of chronic CAD

A

asymptomatic in some cases

chest pain

shorteness of breath

heart attack

fatigue…etc

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12
Q

what is angina and how is it experienced ?

A

it is chest pain or discomfort that occurs when the heart doesn’t get enough blood

it is experienced as squeezing or pressure, or heaviness in the chest.

these signs also radiate and then localise to the shoulders, neck, jaw and back

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13
Q

what is the cause of angina pectoris

note this is the same as angina

A

it IS DUE TO
MYOCARDIAL OXYGEN DEMAND
EXCEEDING MYOCARDIAL OXYGEN
SUPPLY

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14
Q

state the types of angina

A

stable
unstable
variant

the most common type is stable angina

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15
Q

how do the various types of angina compare, especially stable and unstable

variant is quite rare

A

stable angina has a common pattern, occurs during exercise, and decreases at rest. it is also treatable

while

unstable angina has no pattern, is not relieved by rest/medicine , and is a prelude to heart attack. treatable

variant angina is rare, occurs at rest between midnight and early morning, and is relieved by medicine

stable and unstable angina not curable but both treatable

prelude means an action or event serving as an introduction to something more important.

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16
Q

risk factors of angina

A

Unhealthy eating

Physical inactivity

Smoking

Alcohol

Stress

High blood pressure

High cholesterol

Diabetes

Heart conditions

Inflammation

family history

17
Q

the goal of treatment in chronic stable angina

A

To “restore” the balance between myocardial oxygen
supply (coronary blood flow) and myocardial oxygen
demand

18
Q

what does restoring the balance between myocaridal oxygen supply and myocardial oxygen demand depend on?

A

the heart rate:The most significant factor, as increasing heart rate directly increases oxygen consumption.

contractility: Higher contractility leads to increased oxygen demand.

afterload(wall tension): Increased afterload, like high blood pressure, increases oxygen demand.

19
Q

What does ᵦ-adrenoceptor stimulation in the heart do?

A
  1. Increased Heart Rate (Positive Chronotropy): β₁-receptor activation in the sinoatrial (SA) node increases firing rate, leading to tachycardia.
  2. Increased Contractility (Positive Inotropy): β₁-receptor stimulation enhances calcium influx into cardiomyocytes, leading to stronger myocardial contractions.
  3. Increased Conduction Velocity (Positive Dromotropy): β₁-receptors in the atrioventricular (AV) node increase conduction speed, reducing PR interval and improving impulse propagation.
20
Q

what does the use of β-ADRENOCEPTOR ANTAGONISTS lead to

A

leads to decreased:
o heart rate (sinus rate)
o contraction
o conduction velocity through the AV node
o Leads to reduced myocardial oxygen demand
o May also increase coronary blood flow by
prolonging the diastolic filling time

delays the onset of angina

21
Q

β-ADRENOCEPTOR ANTAGONISTS are used prophalactically, true or false?

means they are only used in the prevention of diseases

A

true

it is not used to treat acute angina

22
Q

the role of beta blockers during exercise

A

decrease the peak heart rate during exercise

Dose of drug is calibrated to maintain the
* resting HR at approx 50 bpm
* peak HR during exercise ≈ 110-120 bpm