Cardiovascular system and disease II Flashcards

1
Q

What is Atherosclerosis?

A
  • “hardening of the arteries”
  • Is a generic term for thickening and loss of elasticity of arterial walls
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2
Q

What is Atherosclerosis characterised by

A
  • Characterised by intimal lesions which protrude into an obstruct vascular lumens
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3
Q

Where does Atherosclerotic develop?

A
  • Atherosclerotic plaques develop primarily in elastic arteries (e.g. aorta, carotid) and large and medium sized muscular arteries (e.g. coronary arteries)
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4
Q

What is Atherosclerosis associated with

A
  • Associated with increased LDL-cholesterol and reduced HDL-cholesterol
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5
Q

What are the causes of Atherosclerosis

A
  • Causes are still unclear
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6
Q

What are the NON MODIFIABLE risk factors for Atherosclerosis

A
  • Age
  • Gender M>F
  • Positive family history
  • Genetic abnormality (eg ACE gene)
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7
Q

What are the MODIFIABLE risk factors for Atherosclerosis

A
  • Hyperlipidemia
  • Hypertension
  • Smoking
  • Diabetes
  • Obesity
  • Physical inactivity
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8
Q

What is Atherosclerotic plaques

A

build up of fats, cholesterol and other substances in and on the artery walls

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9
Q

How does plaques slow blood flow

A
  • The plaques protrude into the vessel lumens and
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10
Q

What does plaque consists of

A
  • The plaque consists of a raised lesion with a soft yellow, grumous core of lipid (mainly cholesterol and cholesterol esters) covered by a white fibrous cap
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11
Q

What are the structure of atherosclerotic plaques

A
  • A superficial FIBROUS CAP - SM cells, relatively dense collagen
  • Beneath and to the side of the cap (“shoulder”) - a more cellular area containing macrophages, T cells, SM cells
  • NECROTIC CORE (deep to the fibrous cap, containing lipid, debris from dead cells, foam cells, fibrin, variably organised thrombus, and other plasma proteins)
  • The CHOLESTEROL, frequently present as crystalline aggregates or “clefts”
  • NEOVASCULARISATION at the periphery of the lesions
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12
Q

What are the 3 principal components of Atherosclerosis

A
  • CELLS: SMCs, macrophages and other leukocytes
  • EXTRACELLULAR MATRICES: collagen, elastin, proteoglycans
  • INTRACELLULAR AND EXTRACELLULAR LIPID
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13
Q

What are the morphology of the lesions of Atherosclerosis

A
  • Earliest aortic atherosclerosis: fatty streaks:
    • lipid-filled foamy macrophages
    • begin as multiple minute flat yellow spots
  • Advanced complicated atherosclerosis in abdominal aorta
    • many of the lesions have ruptured
    • become thrombosed
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14
Q

Explain Endothelial injury as a key pathological event

A
  • Endothelial injury will do two things:
  • increases vascular permeability due to damage endothelium
  • any damaged endothelium will express adhesion proteins, in normal conditions they will not be expressed
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15
Q

Explain the key pathogenic events

A
  • Endothelial injury: increase vascular permeability, leukocyte adhesion, and thrombosis
  • Accumulation of lipoproteins: (mainly LDL) in the vessel wall
  • Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
  • ## Platelet adhesion
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16
Q

describe the consequences of Rupture, ulceration or erosion of the intimal surface

A
  • rupture, ulceration or erosion of the intimal surface -> highly thrombogenic substances -> thrombosis
17
Q

Describe the consequences of Haemorrhage into a plaque

A
  • Haemorrhage/bleeding into a plaque. Rupture of the fibrous cap -> intra-plaque haemorrhage -> plaque rupture
18
Q

Describe the consequences of Atheroembolism

A
  • Plaque rupture -> atherosclerotic debris into bloodstream -> microemboli
19
Q

Describe the consequences of Aneurysm formation

A
  • Atherosclerosis-induced pressure, ischemic atrophy, loss of elastic tissue -> weakness -> aneurysmal dilation and potential rupture
20
Q

What does the clinical outcome of atherosclerotic depend on

A
  • Size of the involved vessels
  • Relative stability of the plaque itself
  • Degree of degeneration (underlying arterial wall)
21
Q

What are the major consequences of atherosclerotic diseases

A
  • Myocardial infraction (heart attack)
  • Cerebral infraction (stroke)
  • Aortic aneurysms
  • Peripheral vascular disease (gangrene of the legs)
22
Q

What is Ischemic heart disease and what is its cause

A
  • Leading cause of death WORLDWIDE for both men and women
  • the cause of myocardial ischemia is reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries
23
Q

what are the clinical manifestations of ischemic heart disease

A
  • Angina pectoris
  • Myocardial infraction , the most important form of IHD
  • Heart failure
  • Sudden cardiac death
24
Q

What is chest pain also known as

A
  • Angina pectoris
25
Q

What is chest pain/angina pectoris characterised by

A
  • paroxysmal and usually recurrent attacks
  • substernal or precordial chest discomfort
  • variously described as constricting, squeezing, choking, knifelike
  • caused by transient (15 seconds to 15 minutes) myocardial ischemia
26
Q

What are the 3 overlapping patterns of angina pectoris

A

1) Stable or typical angina
2) Variant (Prinzmetal, vasospastic) angina
3) Unstable (crescendo) angina

27
Q

What is heart attack also known as

A
  • Myocardial infraction
28
Q

What is Myocardial infraction

A
  • also known as heart attack, is the death of cardiac muscle due to prolonged severe ischemia
29
Q

What is the pathogenesis of Myocardial infraction

A
  • Pathogenesis: Coronary arterial occlusion
30
Q

What is the causes of coronary arterial occlusion

A
  • Coronary atherosclerosis (90%)
  • Vasospasm with or without coronary atherosclerosis
  • Emboli from the left atrium in association with atrial fibrillation
  • Others
31
Q
A