Coronary Artery disease Flashcards
(80 cards)
coronary artery diseases (CADs) can be symptomless, true or false
true
ACS(acute coronary syndromes) mostly have symptoms, true or false
true
typically chest pain or discomfort, shortness of breath, nausea, sweating, or dizziness
CADs normally present as?
athelerosclerosis
what is athelerosclerosis
it is a disease of the large and medium sized elastic and muscular arteries, usually affecting the intima and the media. Causes the buildup of fats, cholesterol and other substances in and on the artery walls
the intima is the innermost layer of the arteries, the media is the middle layer. the damage to the media is **secondary **
is the adventitia affected in athelerosclerosis
no it is generally uninvolved
it is the outermost layer of a blood vessel or organ
describe ATHEROSCLEROTIC LESIONS
note they are essentially the same as plaques
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
describe the stages of ATHEROSCLEROTIC plaque development
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
the intermediate lesion in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT is characterised by?
characterised by the accumulation of increasing numbers of;
* macrophages
* foam cells
these are local chronic inflammatory infiltrates in CADs
the complicated plaque in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT is characterised by?
smooth muscle cell migration
formation of;
a fibrous cap
a necrotic lipid core
an ever-lasting inflammatory infiltrate
the role of smooth cell migration in ATHEROSCLEROTIC
PLAQUE DEVELOPMENT
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
some signs and symptoms of chronic CAD
asymptomatic in some cases
chest pain
shorteness of breath
heart attack
fatigue…etc
what is angina and how is it experienced ?
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
what is the cause of angina pectoris
note this is the same as angina
it IS DUE TO
MYOCARDIAL OXYGEN DEMAND
EXCEEDING MYOCARDIAL OXYGEN
SUPPLY
state the types of angina
stable
unstable
variant
the most common type is stable angina
how do the various types of angina compare, especially stable and unstable
variant is quite rare
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.
risk factors of angina
Unhealthy eating
Physical inactivity
Smoking
Alcohol
Stress
High blood pressure
High cholesterol
Diabetes
Heart conditions
Inflammation
family history
the goal of treatment in chronic stable angina
To “restore” the balance between myocardial oxygen
supply (coronary blood flow) and myocardial oxygen
demand
what does restoring the balance between myocaridal oxygen supply and myocardial oxygen demand depend on?
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.
What does ᵦ-adrenoceptor stimulation in the heart do?
- Increased Heart Rate (Positive Chronotropy): β₁-receptor activation in the sinoatrial (SA) node increases firing rate, leading to tachycardia.
- Increased Contractility (Positive Inotropy): β₁-receptor stimulation enhances calcium influx into cardiomyocytes, leading to stronger myocardial contractions.
- Increased Conduction Velocity (Positive Dromotropy): β₁-receptors in the atrioventricular (AV) node increase conduction speed, reducing PR interval and improving impulse propagation.
what does the use of β-ADRENOCEPTOR ANTAGONISTS lead to
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
β-ADRENOCEPTOR ANTAGONISTS are used prophalactically, true or false?
are they used in the treatment of acute angina ?
means they are only used in the prevention of diseases
true
it is not used to treat acute angina
the role of beta blockers during exercise
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
CCBs MoA
Decrease Ca2+ influx through voltage gated L-type Ca2+ channels. As a result, Intracellular Ca2+ conc decreases leads to reduced contraction of:
o cardiac myocytes
o vascular smooth muscle
why are CCBs effective especially in CAD
Effective because they:
o ↓ arteriolar pressure (afterload)
o ↓ myocardial O2 consumption
