Atherosclerosis

Question 1

atherosclerosis is a _____ disease affecting ….

Answer 1

systemic, large and medium-sized arteries

Question 2

what is atherosclerosis characterized by? complications of atherosclerosis account for _______ of all deaths in the western worlds

Answer 2

by the formation of atheromas (fibrofatty plaques) which narrow (stenose) the artery lumens, resulting in blood-flow reduction (ischemia) and subsequent damage or necrosis to the “downstream” organs.

Complications of atherosclerosis account for more than half of all deaths in the Western world.

Question 3

pathogenesis of atherosclerosis

Answer 3

The earliest pathological lesion is called a fatty-streak. Some of these slowly progress and develop into the mature atherosclerotic lesion, the fibro-fatty plaque.

Question 4

what does the response to injury hypothesis explain

Answer 4

explains plaque development as a chronic inflammatory response resulting from injury to the endothelial lining of the artery

Question 5

Many of the atherosclerotic risk factors (subsequently discussed) act by contributing to….

• this results in…
• how do you get to the end result

Answer 5

some form of epithelial damage
-endothelial dysfunction, allowing for platelets and monocytes (macrophages) to adhere to the lining. These elements release various growth factors and cytokines, which cause recruitment and migration of smooth muscle cells and fibroblasts into the endothelium. Collagen is produced. Macrophages also engulf lipid and cholesterol derived from the blood. The end result is a raised plaque, with both fibrous and fatty elements, which narrows the vessel lumen.

Question 6

3 major risk factors for astherosclerosis

-what is an important feature of these?

Answer 6

smoking, hypertension, and elevated blood cholesterol. An important feature of all three is that they are potentially modifiable

Question 7

what is also a major risk factor for atherosclerosis that isnt considered the big 3

Answer 7

diabetes mellitus

Question 8

non-modifiable risk factors of atherosclerosis

Answer 8

age, sex (premenopausal women at lower risk but catch up to men after menopause), family history, ethnicity, obesity, lower socioeconomic class, type “A”
personality/stress, elevated blood homocysteine level

Question 9

protective factors

Answer 9

moderate alcohol consumption

Question 10

Major sites of atherosclerotic ischemic injury and therefore clinical disease are:

Answer 10

 Heart - causing angina pectoris, myocardial infarction, chronic heart failure, sudden cardiac death
 Brain - ischemic stroke
 Extremities - claudication, gangrene
 Kidneys - chronic kidney failure

Question 11

epidemiology of ischemic heart disease

Answer 11

mortality rate of IHD (ischemic heart disease) has been declining since the 1960s but it remains a leading cause of death. However, the rate has been steadily increasing in developing countries (due partly to increasing life expectancy and also to acquiring bad “Western” lifestyle habits) and therefore the overall global burden of IHD is on the rise.

Question 12

the heart receives its blood supply from

Answer 12

coronary arteries

Question 13

3 major branches of the coronary arteries and what they supply

Answer 13

the left anterior descending (LAD) branch and the left circumflex branch supply the anterior and lateral portions of the left ventricle respectively, and the right coronary artery (RCA) supplies the right ventricle and the posterior wall of the left ventricle.

Question 14

Coronary atherosclerosis begins _________ and is ______ progressive

Answer 14

early life (20s), slowly

Question 15

when does coronary atherosclerosis manifest clinically with symptoms? what is this due to?

Answer 15

until later in life when there is reduction in blood flow of a magnitude which can potentially cause ischemic damage (necrosis) of heart muscle

Question 16

the degree of flow reduction that causes ischemia of the heart muscles until there is about __% reduction in the…

Answer 16

70% area of the coronary artery lumen

Question 17

What is angina and what is it the result from

Answer 17

chest pain which is the result of myocardial ischemia, and this blood flow reduction is usually due to coronary atherosclerosis.

Question 18

what is stenosis

Answer 18

abnormal narrowing of a body channel

Question 19

in angina pectoris, what is there usually in terms of the arteries?

Answer 19

at least one coronary artery with a fixed severe stenosis although vasospasm (muscular constriction of the vessel wall) can further contribute to the narrowing

Question 20

the pain of angina is usually describes as

Answer 20

“crushing, tightness or heaviness”

Question 21

why cant angina result in necrosis of heart muscle

Answer 21

myocardial ischemia is of insufficient duration and magnitude to result in actual death (necrosis) of the
downstream heart muscle

Question 22

how is angina precipitated? how do episodes resolve?

Answer 22

by events that increase myocardial blood flow

demand such as exercise or stress. Episodes usually resolve with rest or medications (nitroglycerine).

Question 23

If myocardium is ischemic for about __________, it begins to die, and the result is a_________.

Answer 23

30-40 mins, myocardial infarction

Question 24

What are most MIs precipitated by?

What did awareness of this lead to

Answer 24

formation of a thrombus on the luminal surface of a coronary artery plaque, causing complete or near-complete occlusion of the vessel (the thrombus is the “straw that breaks the camel’s back”).
Awareness of this led to the development of thrombolytic drugs (“clotbusters”) which are highly effective in re-establishing coronary blood flow and either preventing or reducing infarction. These drugs must be administered promptly, again emphasizing the importance of early diagnosis & treatment.

Question 25

other treatments for MI

Answer 25

Other treatments include percutaneous transluminal coronary angioplasty (dilatation of a stenosis by inflation of a balloon catheter) or coronary artery bypass surgery. (both of these treatments can also be given for unstable angina to prevent infarction)

Question 26

clinical symptoms of MI

Answer 26

- prolonged “angina-like” chest pain, often radiating to jaw or left arm, associated nausea and sweating (diaphoresis).

Question 27

other ways to diagnose MI

Answer 27

- changes on the electrocardiogram (ECG) which can indicate heart muscle injury - measuring elevated levels of cardiac enzymes such as troponins and cardiac muscle creatine kinase (CK-MB). These substances are specific to heart muscle and they leak into the blood when heart muscle cells are injured and dying

Question 28

MIs most often involve the _____ _________

Answer 28

left ventricle

Question 29

what does transmural mean? what does subendocardial mean?

Answer 29

If an infarct involves the full thickness of the wall | If it involves only the inner half of the wall

Question 30

how do infarcts heal

Answer 30

heal by a process of scarring; muscle does not regenerate. Therefore, infarcted muscle is “lost” to the heart which has to rely on its remaining muscle to keep it functioning - Healing starts with removal of the dead muscle. This requires the digestive proteolytic and phagocytic action of neutrophils and macrophages. - This is followed by ingrowth of fibroblasts which produce and lay down collagen which forms the bulk of the scar - Scar is usually well-developed after 2 months

Question 31

early complications of MI

Answer 31

Dysrythmias - disturbances in the electrical rhythm of the heart. Infarcted muscle can interfere with the normal conduction of electrical impulses through the heart. These can be serious and potentially fatal and often require either drugs or electrical pacemakers. Congestive heart failure/cardiogenic shock - if too much muscle is infarcted and the remaining living muscle cannot meet the demands required of the heart, the result is “back-up” congestion of blood in the lungs (congestive heart failure) and inadequate forward flow of blood to the body (cardiogenic shock) Ventricular rupture - sometimes the infarcted zone cannot hold together and the heart wall ruptures, causing acute hemorrhage into the sac around the heart which in turn compresses the heart (cardiac tamponade) and is almost always fatal Pericarditis (inflammation of the heart surface) can be either an early or late complication

Question 32

late complications of MI

Answer 32

- An end-stage scar from a large transmural infarct can weaken and bulge, forming an aneurysm of the LV wall - Congestive heart failure can be a chronic condition

Question 33

Hypertension is generally accepted as __ / __ or greater

Answer 33

140 / 90

Question 34

about ___% of the population is hypertensive

Answer 34

25

Question 35

only about ___% of hypertensive Canadians know they are hypertensive only ___% of hypertensive Canadians have adequate blood pressure control

Answer 35

50 , 16

Question 36

BP = _______ x _________

Answer 36

BP = cardiac output x peripheral vascular resistance

Question 37

cardiac output depends on what 2 things

Answer 37

heart rate and stroke volume

Question 38

what is peripheral resistance controlled by?

Answer 38

d by the balance of constricting and dilating humoral and neural factors on blood vessels (e.g. epinephrine is a vasoconstrictor)

Question 39

how does the kidney play an important role in BP regulation

Answer 39

o Sensing a drop in BP, the kidney will release the hormone renin which in turn activates the vasoconstrictor angiotensin o The kidney also controls the body’s sodium balance which in turn influences the blood volume

Question 40

primary hypertension is also called

Answer 40

essential or idiopathic

Question 41

___% of cases are primary hypertension

Answer 41

90

Question 42

almost any renal disease can result in ....? why?

Answer 42

Because the kidney is so important for BP regulation, almost any renal disease can result in HTN

Question 43

how can endocrine disease result in hypertension

Answer 43

can result in elevated hormone levels which can increase BP via their vascular constricting influence. (e.g. an epinephrine-secreting tumour of the adrenal gland). Hyperthyroidism is another example of an endocrine cause of HTN

Question 44

what is white coat HTN

Answer 44

A patient may get nervous and stressed when having their BP measured in a medical setting, but when checked in a relaxed setting it is normal.

Question 45

why has HTN been labelled the silent killer

Answer 45

because it doesn’t cause symptoms until damage occurs in vital organs

Question 46

What damage does HTN result in

Answer 46

the consequence of the effects that HTN has on arteries, both large and small. In small arteries (arterioles), HTN causes hyaline arteriosclerosis-their walls become thickened and their lumens narrowed. In larger arteries, the stresses of HTN cause accelerated atherosclerosis (recall from prior notes that HTN is a major risk factor for atherosclerosis).

Question 47

What 3 major organs does HTN cause vascular damage

Answer 47

Kidney -HTN results in nephrosclerosis, a major cause of renal failure, because it damages the main functioning unit of the kidney, the glomerulus (a specialized small arterial/capillary structure which filters urine). Heart - HTN affects the heart in two ways. Firstly, it contributes to coronary atherosclerosis and all of its ischemic heart complications. Secondly, increased blood pressure increases the workload of the heart which adapts by undergoing hypertrophy (ie. Increases its muscle mass). Eventually, the heart may be unable to compensate and the end result may be congestive heart failure. Brain - HTN-induced arteriosclerosis also affects small arteries supplying the base of the brain. These damaged vessels can rupture, resulting in hemorrhagic strokes. HTN also accelerates atherosclerosis of large arteries supplying the brain and the result can be an ischemic stroke if these vessels are sufficiently