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Mechanisms of Disease > Lecture 6.1: Atherosclerosis > Flashcards

Lecture 6.1: Atherosclerosis Flashcards

1
Q

What is Atherosclerosis?

A

The thickening, narrowing and hardening of the walls of large and medium sized arteries as a consequence of atheroma and arteries become clogged with fatty substances called plaques, or atheroma

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2
Q

What Arteries are affected by Atherosclerosis?

A

Large Arteries (Aortas)
Medium Arteries (Coronary, Renal, Cerebral, Mesenteric, Popliteal)

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3
Q

What is Atheroma?

A

An accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

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4
Q

What is Arteriosclerosis?

A

The thickening and hardening of the walls of arteries and arterioles, from ANY CAUSE

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5
Q

What is the Macroscopic Appearance of Atherosclerosis?

A

• Fundamental lesion is the plaque

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6
Q

What are the 3 Stages of Plaque Developments?

A

1) Fatty streak
2) Simple plaque
3) Complicated plaque

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7
Q

3 Stages of Plaque Developments: Features of Fatty Streak (4)

A

• Can be seen in children
• Lipid deposits in intima
• Yellow, slightly raised
• No disturbance to blood flow

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8
Q

3 Stages of Plaque Developments: Features of Simple Plaque (8)

A

• Raised yellow/white
• Approximately 1cm in diameter
• Irregular outline
• Widely distributed
• Often occur around ostia
• Turbulent blood flow
• Enlarge and coalesce
• Impinge on vessel lumen

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9
Q

3 Stages of Plaque Developments: Features of Complicated Plaque (5)

A

• Calcification
• Thrombosis
• Haemorrhage into plaque
• Weakening of the wall
• Aneurysm formation

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10
Q

What is the Early Microscopic Appearance of Atherosclerosis? (4)

A

• Accumulation of foam cells
• Proliferation of smooth muscle cells
• Extracellular lipid deposition
• Scattered T lymphocytes

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11
Q

What is the Later Microscopic Appearance of Atherosclerosis? (8)

A

• Fibrosis
• Necrosis
• Cholesterol clefts
• Calcification
• Disruption of internal elastic lamina
• Damage extends into media
• Ingrowth of blood vessels
• Plaque fissuring & rupture

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12
Q

What are the Most Common Sites for Atherosclerosis?

A

• Aorta - especially abdominal aorta
• Coronary arteries
• Carotid arteries
• Cerebral arteries
• Arteries of the legs

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13
Q

Damage to Heart in Atherosclerosis Disease: Where? Effects?

A

• Coronary Arteries
• Ischaemic Damage/ Ischaemic Heart Disease
• Myocardial Infarction
• Angina Pectoris
• Chronic Congestive Cardiac Failure (CHF)
• Sudden death from Arrythmia

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14
Q

Damage to Brain in Atherosclerosis Disease: Where? Effects? How?

A

• Cerebral Arteries
• Atherosclerosis of carotid arteries
• Thrombus forms over plaque
• Thromboembolism to cerebral arteries
• Stroke (Cerebral Infarction)
• Transient Ischaemic Attack
• Multi-Infarct Dementia

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15
Q

Damage to Aorta in Atherosclerosis Disease: Where? Effects?

A

• Subdiaphragmatic Part
• Aneurysm Rupture

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16
Q

Damage to Peripheral Arteries in Atherosclerosis Disease: Where? Effects?

A

• Mainly the legs
• Distal Gangrene

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17
Q

Mechanism of IHD in Acute Myocardial Infarction

A

Acute severe coronary obstruction

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18
Q

Mechanism of IHD in Angina Pectoris

A

Chronic obstruction plus excess demand on heart causes, attacks of chest pain caused by reduced blood flow to your heart

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19
Q

Mechanism of IHD in Chronic Heart Failure

A

Chronic obstruction with multiple small infarct damage accumulation

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20
Q

Mechanism of IHD in Sudden Cardiac Death

A

Old infarct scar triggering acute LV arrhythmia

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21
Q

When is flow in an artery considered ‘significantly reduced’?

A

Until lumen is reduced by 70- 80% = <1mm diameter

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22
Q

What is an AAA? Structure?

A

• Abdominal Aortic Aneurysm
• A bulge or swelling in the aorta, the main blood vessel that runs from the
heart down through the chest and tummy
• It can rupture and cause fatal bleeding
• Lined/filled by thrombus

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23
Q

What is the size of an AAA?

A

Can be 10-15cm in diameter

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24
Q

What is an Aneurysm?

A

• Local dilatation of an artery due to weakening of the wall
• May rupture
• Can produce emboli

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25
Why are aneurysms caused in large arteries (most common reason)?
Due to Atherosclerosis
26
What is Peripheral Vascular Disease?
PVD is a common condition where a build-up of fatty deposits in the arteries restricts blood supply to leg muscles
27
Effects of PVD (4)
• Intermittent claudication • Ischaemic rest pain • Gangrene • Leriche syndrome
28
What is Intermittent Claudication?
Pain affecting the calf, and less commonly the thigh and buttock, that is induced by exercise and relieved by rest Due to reduced blood flow to legs due to PAD/PVD
29
What is Ischaemic Rest Pain?
Severe pain in the legs and feet while a person is not moving, or non-healing sores on the feet or legs It is due to reduced blood flow to legs due to atherosclerosis of blood vessels in the legs
30
What is Dry Gangrene?
A serious condition where a loss of blood supply causes body tissue to die
31
What is Leriche Syndrome?
• Aka aortoiliac occlusive disease • Caused by severe atherosclerosis • Affects: distal abdominal aorta, iliac arteries, and femoro-popliteal vessel • Presents with triad of claudication, impotence & absence of femoral pulses
32
Effects of Mesenteric Ischaemia & Bowel Infarction
• Superior Mesenteric Artery Disease • Ischaemic Colitis • Malabsorption • Intestinal Infarction
33
What is Superior Mesenteric Artery Disease?
34
What is Ischaemic Colitis?
35
What is Malabsorption?
36
What is Intestinal Infarction?
37
Pathogenesis of Atheroma: What is the Reaction to Injury Hypothesis?
Atherogenesis becomes an inflammatory, macrophage and smooth muscle cell response process, involving both lipid and absorbed thrombus on the intima or arteries
38
What are 5 Cellular Events that Lead to Atherosclerosis?
1) Chronic Endothelial Injury (LDL, toxins, hypertension, haemodynamic stress) 2) Endothelial Dysfunction (T-Cell attraction to area, platelet adhesion, PDGF) 3) Smooth muscle emigration from media into intima 4) Macrophages & smooth muscle cells engulf accumulated, oxidised lipid and form foam cells 5) Smooth muscle proliferation in response to cytokines and growth factors, collagen and matrix deposition, neovascularistaion
39
What Cells are involved in Atherogenesis?
• Endothelial Cells • Platelets • Smooth Muscle Cells • Macrophages • Lymphocytes • Neutrophils
40
Process of Atherogenesis
41
What happens when plaque ruptures?
Exposure of tissue triggers both the intrinsic & extrinsic coagulation pathways and a blood clot forms following plaque rupture, which limits blood flow
42
Cells Involved in Atherogenesis: Endothelial Cells
• Key role in haemostasis • Altered permeability to lipoproteins • Secretion of collagen • Stimulate proliferation and migration of smooth muscle cells
43
Cells Involved in Atherogenesis: Platelets
• Key role in haemostasis • Altered permeability to lipoproteins • Secretion of collagen • Stimulate proliferation and migration of smooth muscle cells
44
Cells Involved in Atherogenesis: Smooth Muscle Cells
• Take up LDL and other lipids to become foam cells • Synthesise collagen and proteoglycans
45
Cells Involved in Atherogenesis: Macrophages
• Oxidise LDL • Take up lipids to become foam cells • Secrete proteases which modify matrix • Stimulate proliferation and migration of smooth muscle cells
46
Risk Factors for Atherosclerosis (12)
• Age (non-modifiable) • Gender (non-modifiable) • Hyperlipidaemia (increased LDL significant) • Smoking • Hypertension • Impaired glucose tolerance and diabetes mellitus • Alcohol • Geography – Civilisation & Diet • Lack of exercise/ Obesity • Soft water • Oral contraceptive pill • Possibly stress and personality type (type ‘A’)
47
Lipid Metabolism
• Lipid in the blood is carried in lipoproteins • Lipoproteins carry cholesterol and triglycerides (TG) • Hydrophobic lipid core • Hydrophilic outer layer of phospholipid and apolipoprotein (A-E)
48
Chylomicrons in Lipid Metabolism
Transport lipid from intestine to liver
49
VLDL in Lipid Metabolism
• Carry cholesterol and TG from liver to muscle and fat • TG removed leaving LDL
50
LDL in Lipid Metabolism
• Rich in cholesterol • Carries cholesterol to non-liver cells
51
HDL in Lipid Metabolism
Carry cholesterol from periphery back to liver
52
What is the primary function of LDL?
The primary function of LDL is to provide cholesterol from liver to peripheral tissues
53
How is LDL absorbed by peripheral cells?
Peripheral cells express LDL receptor and take up LDL via process of receptor mediated endocytosis
54
Why is LDL not efficiently cleared by the Liver?
• LDL do not have apoC or apoE • Liver LDL-Receptor has a high affinity for apoE
55
What clinic relevance of the half-life of LDL?
• Half life of LDL in blood is much longer than VLDL or IDL • Making LDL more susceptible to oxidative damage
56
How are Foam Cells formed? Clinic Relevance of Foam Cells?
• Oxidised LDL taken up by macrophages can transform to foam cells • Contribute to formation of atherosclerotic plaques
57
What is the function of HDL? Why is this important?
• HDL can remove cholesterol from cholesterol laden cells & return it to liver • Important process for blood vessels as it reduces likelihood of foam cell and atherosclerotic plaque formation
58
What protein within cells facilitates transfer of cholesterol to HDL?
ABCA1
59
What is cholesterol converted to after it is taken by HDL?
Cholesterol then converted to cholesterol ester by Lecithin–cholesterol acyltransferase (LCAT)
60
Familial Hyperlipidaemia as a Risk Factor for Atherosclerosis
• Genetically determined abnormalities of lipoproteins • Lead to early development of atherosclerosis
61
Physical Signs associated with Hyperlipdaemia (3)
• Corneal Arcus • Tendon Xanthomas • Xanthelasma
62
Smoking as a Risk Factor for Atherosclerosis
• Powerful risk factor for ischaemic heart disease and atherosclerosis • Risk falls after giving up smoking • Mode of action uncertain but it is a procoagulant • Reduced prostacyclin (which is a platelet activation inhibitor) and therefore increased platelet aggregation
63
Hypertension as a Risk Factor for Atherosclerosis
• Strong link between ischaemic heart disease and high systolic & diastolic blood pressure • Mechanism uncertain, perhaps endothelial damage caused by raised pressure
64
Impaired Glucose Tolerance/Diabetes Mellitus as a Risk Factor for Atherosclerosis
• Cardiovascular disease accounts for 80% deaths in DM type 2 • DM patients have at least 3 times greater incidence of death from CVD compared to non-DM • Protective effect in premenopausal women is lost if they are diabetic • Diabetes mellitus associated with high risk of cerebrovascular and peripheral vascular disease
65
Alcohol as a Risk Factor for Atherosclerosis
• More than 5units/day associated with increased risk of ischaemic heart disease • Smaller amounts of alcohol may be protective (increase HDL levels)
66
Prevention of and Interventions in Atherosclerosis (8)
• No smoking • Decrease fat intake • Treat hypertension • Aspirin • Sensible alcohol intake • Regular exercise and control of weight control • Good glycaemic control in diabetes mellitus • Lipid lowering drugs, e.g., statins, where needed
67
Apolipoprotein E (Apo E) Genotype and Atherosclerosis
• Genetic variations in Apo E are associated with changes in LDL levels • Polymorphisms of the genes involved lead to at least 6 Apo E phenotypes • Polymorphisms can be used as risk markers for atherosclerosis
68
Impaired Glucose Tolerance/DM and Atherosclerosis: AGEs
• Formation of advanced glycation end products (AGE – amino acids of proteins which have reacted with glucose derivatives) • Crosslinks collagen in large vessels → ↓elasticity predisposes to endothelial injury • Changes protein properties which results in ↑LDL trapping and enhances cholesterol deposition in intima • React with plasma proteins, leading to interaction with endothelial cells and release of inflammatory markers • Increase procoagulant activity of endothelial cells
69
Impaired Glucose Tolerance/DM and Atherosclerosis: Activation of Protein Kinase C
• Caused by intracellular hyperglycaemia • Increases production of procoagulants (PAI-1) → ↓fibrinolysis • Production of proinflammatory cytokines by vascular endothelium
70
Lymphocytes in Atherosclerosis
• TNF (Tumor Necrosis Factor) may affect lipoprotein metabolism • Stimulate proliferation and migration of smooth muscle cells
71
Neutrophils in Atherosclerosis
• Secrete proteases leading to continued local damage and inflammation

Mechanisms of Disease (11 decks)

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