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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
Q

Why are aneurysms caused in large arteries (most common reason)?

A

Due to Atherosclerosis

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26
Q

What is Peripheral Vascular Disease?

A

PVD is a common condition where a build-up of fatty deposits in the arteries restricts blood supply to leg muscles

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27
Q

Effects of PVD (4)

A

• Intermittent claudication
• Ischaemic rest pain
• Gangrene
• Leriche syndrome

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28
Q

What is Intermittent Claudication?

A

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

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29
Q

What is Ischaemic Rest Pain?

A

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
Q

What is Dry Gangrene?

A

A serious condition where a loss of blood supply causes body tissue to die

31
Q

What is Leriche Syndrome?

A

• 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
Q

Effects of Mesenteric Ischaemia & Bowel Infarction

A

• Superior Mesenteric Artery Disease
• Ischaemic Colitis
• Malabsorption
• Intestinal Infarction

33
Q

What is Superior Mesenteric Artery Disease?

A
34
Q

What is Ischaemic Colitis?

A
35
Q

What is Malabsorption?

A
36
Q

What is Intestinal Infarction?

A
37
Q

Pathogenesis of Atheroma: What is the Reaction to Injury Hypothesis?

A

Atherogenesis becomes an inflammatory, macrophage and smooth muscle cell
response process, involving both lipid and absorbed thrombus on the intima or arteries

38
Q

What are 5 Cellular Events that Lead to Atherosclerosis?

A

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
Q

What Cells are involved in Atherogenesis?

A

• Endothelial Cells
• Platelets
• Smooth Muscle Cells
• Macrophages
• Lymphocytes
• Neutrophils

40
Q

Process of Atherogenesis

A
41
Q

What happens when plaque ruptures?

A

Exposure of tissue triggers both the intrinsic & extrinsic coagulation pathways and a blood clot forms following plaque rupture, which limits blood flow

42
Q

Cells Involved in Atherogenesis: Endothelial Cells

A

• Key role in haemostasis
• Altered permeability to lipoproteins
• Secretion of collagen
• Stimulate proliferation and migration of smooth muscle cells

43
Q

Cells Involved in Atherogenesis: Platelets

A

• Key role in haemostasis
• Altered permeability to lipoproteins
• Secretion of collagen
• Stimulate proliferation and migration of smooth muscle cells

44
Q

Cells Involved in Atherogenesis: Smooth Muscle Cells

A

• Take up LDL and other lipids to become foam cells
• Synthesise collagen and proteoglycans

45
Q

Cells Involved in Atherogenesis: Macrophages

A

• Oxidise LDL
• Take up lipids to become foam cells
• Secrete proteases which modify matrix
• Stimulate proliferation and migration of smooth muscle cells

46
Q

Risk Factors for Atherosclerosis (12)

A

• 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
Q

Lipid Metabolism

A

• 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
Q

Chylomicrons in Lipid Metabolism

A

Transport lipid from intestine to liver

49
Q

VLDL in Lipid Metabolism

A

• Carry cholesterol and TG from liver to muscle and fat
• TG removed leaving LDL

50
Q

LDL in Lipid Metabolism

A

• Rich in cholesterol
• Carries cholesterol to non-liver cells

51
Q

HDL in Lipid Metabolism

A

Carry cholesterol from periphery back to liver

52
Q

What is the primary function of LDL?

A

The primary function of LDL is to provide cholesterol from liver to peripheral
tissues

53
Q

How is LDL absorbed by peripheral cells?

A

Peripheral cells express LDL receptor and take up LDL via process of receptor mediated endocytosis

54
Q

Why is LDL not efficiently cleared by the Liver?

A

• LDL do not have apoC or apoE
• Liver LDL-Receptor has a high affinity for apoE

55
Q

What clinic relevance of the half-life of LDL?

A

• Half life of LDL in blood is much longer than VLDL or IDL
• Making LDL more susceptible to oxidative damage

56
Q

How are Foam Cells formed? Clinic Relevance of Foam Cells?

A

• Oxidised LDL taken up by macrophages can transform to foam cells
• Contribute to formation of atherosclerotic plaques

57
Q

What is the function of HDL? Why is this important?

A

• 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
Q

What protein within cells facilitates transfer of cholesterol to HDL?

A

ABCA1

59
Q

What is cholesterol converted to after it is taken by HDL?

A

Cholesterol then converted to cholesterol ester by Lecithin–cholesterol acyltransferase (LCAT)

60
Q

Familial Hyperlipidaemia as a Risk Factor for Atherosclerosis

A

• Genetically determined abnormalities of lipoproteins
• Lead to early development of atherosclerosis

61
Q

Physical Signs associated with Hyperlipdaemia (3)

A

• Corneal Arcus
• Tendon Xanthomas
• Xanthelasma

62
Q

Smoking as a Risk Factor for Atherosclerosis

A

• 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
Q

Hypertension as a Risk Factor for Atherosclerosis

A

• Strong link between ischaemic heart disease and high systolic & diastolic
blood pressure
• Mechanism uncertain, perhaps endothelial damage caused by raised
pressure

64
Q

Impaired Glucose Tolerance/Diabetes Mellitus as a Risk Factor for Atherosclerosis

A

• 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
Q

Alcohol as a Risk Factor for Atherosclerosis

A

• More than 5units/day associated with increased risk of ischaemic heart
disease
• Smaller amounts of alcohol may be protective (increase HDL levels)

66
Q

Prevention of and Interventions in Atherosclerosis (8)

A

• 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
Q

Apolipoprotein E (Apo E) Genotype and Atherosclerosis

A

• 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
Q

Impaired Glucose Tolerance/DM and Atherosclerosis: AGEs

A

• 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
Q

Impaired Glucose Tolerance/DM and Atherosclerosis: Activation of Protein Kinase C

A

• Caused by intracellular hyperglycaemia
• Increases production of procoagulants (PAI-1) → ↓fibrinolysis
• Production of proinflammatory cytokines by vascular endothelium

70
Q

Lymphocytes in Atherosclerosis

A

• TNF (Tumor Necrosis Factor) may affect lipoprotein metabolism
• Stimulate proliferation and migration of smooth muscle cells

71
Q

Neutrophils in Atherosclerosis

A

• Secrete proteases leading to continued local damage and inflammation

Mechanisms of Disease (11 decks)

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