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Path Pro > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Define Atheroma

A

Accumulation of Intracellular and extracellular lipid in the intima and media of large/ medium sized arteries

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2
Q

Define Atherosclerosis

A

The thickening and hardening of arterial walls as a consequence of Atheroma

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3
Q

Define Arteriosclerosis

A

The thickening of the walls of arteries and arterioles, due to hypertension or Diabetus Mellitus

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4
Q

What 2 conditions are causes by Atherosclerosis, making it the biggest killer in the world?

A

MI

Stroke

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5
Q

Describe the 3 stages/ Macroscopic features of Atherosclerosis

A
  1. Fatty streak (Early stages);
    - Lipid deposit in intima
    - Yellow, slightly raised
  2. Simple plaque;
    - Raised yellow/ white
    - Irregular outline
    - Widely distributed
    - Enlarge and coalesce
  3. Complicated plaque (Other things happen);
    - Ulceration (Fibrous cap eroded from underneath)
    - Thrombosis
    - Haemorrhage into plaque
    - Calcification
    - Aneurysm formation
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6
Q

Name the 5 most common sites of Atherosclerosis

A 
Aorta (Especially abdominal)
Coronary arteries 
Carotid arteries 
Cerebral arteries 
Leg arteries
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7
Q

What are the 3 early changes in Microscopic features of Atherosclerosis

A

Proliferation of smooth muscle cells
Accumulation of foam cells
Extracellular lipid deposition

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8
Q

What are the 6 later changes in Microscopic features of Atherosclerosis

A
  • Necrosis and fibrosis
  • Cholesterol clefts
  • Disruption of internal elastic lamina
  • Damage extends into media
  • Ingrowth of blood vessels from adventitia
  • Plaque fissuring
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9
Q

What are cholesterol clefts?

What are the 3 basic components of a plaque?

A

Needle shaped clefts left in the plaque, after cholesterol crystals have been dissolved by solvents used in microscopy

  • Cells (Macrophages, WBCs, smooth muscle cells)
  • Intra and Extracellular lipid
  • ECM (Collagen, Elastin, Proteoglycans)
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10
Q

What conditions are caused by Atherosclerosis at;

  1. Heart
  2. Brain
  3. Kidneys
  4. Legs
  5. Bowel
A
  1. Ischaemic heart disease
  2. Cerebral ischaemia
  3. kidneys- Abdominal Aortic Aneurysm
  4. Legs- Peripheral vascular disease
  5. Bowel- Mesenteric ischaemia
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11
Q

What are 5 outcomes of Ischaemic heart disease

A 
Sudden death
MI
Angina
Arrhythmia 
Cardiac failure
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12
Q

What are 3 outcomes of Cerebral Ischaemia

A
  • Transient ischaemic attack (Mini stroke, resolves in <24h)
  • Cerebral infarction (Stroke)
  • Multi-Infarct dementia
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13
Q

What are 3 outcomes of Mesenteric Ischaemia

A

Ischaemic colitis
Malabsorption
Intestinal infarction

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14
Q

What are 2 outcomes of Peripheral Vascular Disease

A

Gangrene

Intermittent claudication

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15
Q

What are 2 outcomes of Abdominal Aortic Aneurysm in Kidneys

A

Hypertension

Renal failure

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16
Q

Identify 11 risk factors for Atherosclerosis

A

DISHH GAFAAG

Diabetes (-> Hypercholesterolaemia)
Infection
Smoking 
Hyperlipidaemia (High LDL)
Hypertension

Gender
Age
Familial hyperlipidaemia
Alcohol consumption (Excess, small amounts protect)
Apolipoprotein E Genotype
Geography (Lower in Asia, South America, Africa)

17
Q

How is gender a risk factor for atherosclerosis

What 3 organisms cause infection which may lead to atherosclerosis

A

Women are relatively protected before menopause
(Hormones?)

Chlamidyia pneumoniae
Helicobater pylori
Cytomegalovirus

18
Q

Explain how genetics can make you more likely to get Atherosclerosis in 2 ways?

A

Variations in Apolipoprotein metabolism

Variations in Apolipoprotein receptors

19
Q

What are the 3 theories of of how Atherosclerosis comes about?

A
  • Thrombogenic Theory/ Encrustations Hypothesis
  • Monoclonal Hypothesis
  • Reaction to injury hypothesis/ Insudation Theory
20
Q

Describe the Monoclonal Hypothesis

A

Each plaque is monoclonal, so plaques could be benign

Possibly Induced by virus/ cholesterol

21
Q

Describe the Thrombogenic theory/ Encrustation hypothesis

A

Plaques are formed by repeated thrombi and lipid deposit is derived from the thrombi

22
Q

Describe Reaction to injury hypothesis/ Insudation Theory

A

Atherosclerosis is chronic inflammation due to endothelial injury

Increased Permeability leads to;

  • Monocytes penetrate endothelium
  • Extracellular lipid deposition + Foam cells
  • SMC proliferation
23
Q

What 4 processes are involved in atherosclerosis

A

Thrombosis
Lipid accumulation
Production of intercellular matrix
Interactions between cell types

24
Q

What 6 cells are involved in Atherosclerosis

A 
Endothelial cells
Platelets 
SMCs
Macrophages 
Lymphocytes 
Neutrophils
25
Q

What are 2 roles of Endothelial cells in Atherosclerosis?

A
  • Produce collagen

- Stimulate proliferation and migration of SMCs

26
Q

What are 2 roles of Smooth Muscle Cells in Atherosclerosis?

A
  • Take up lipid to become Foam Cells

- Make collagen + proteoglycans

27
Q

What are 3 roles of Macophages in Atherosclerosis?

A
  • Take up lipids and LDL to become foam cells
  • Stimulate Proliferation and migration of SMCs
  • Modify matrix by secreting proteases
28
Q

What is the role of Platelets in Atherosclerosis?

A
  • Stimulate Proliferation and migration of SMCs
29
Q

What is the role of Neutrophils in Atherosclerosis?

A
  • Secrete proteases leading to continued local damage and inflammation
30
Q

What are 2 roles of Lymphocytes in Atherosclerosis?

A
  • TNF affect lipoprotein metabolism

- Stimulate SMC proliferation and migration

31
Q

Outline Stage 1 of the Unifying Hypothesis

A

Endothelial injury due to;

  • Raised LDL
  • Toxins
  • Hypertension
  • Haemodynamic stress
32
Q

Outline Stage 2 of the Unifying Hypothesis

A

Endothelial injury causes;

  • Platelet adhesion
  • SMC proliferation and migration
  • Lipid insudation and LDL oxidation
  • Lipid uptake by SMCs and Macrophages
  • Monocyte accumulation in intima
33
Q

Outline Stage 3 of the Unifying Hypothesis

A
  • SMCs produce matrix material

- Foam cells secrete cytokines

34
Q

Suggest 7 methods of prevention/ intervention of Atherosclerosis

A
  • No smoking
  • Reduce fat intake
  • Treat hypertension
  • Reasonable alcohol Intake
  • Regular exercise/ weight control
  • Treat Diabetes Mellitus
  • Lipid lowering drugs (Statins)
35
Q

Describe the cellular events leading to Atherosclerosis, in 5 steps

A
  1. Chronic endothelial injury (Hyperlipidaemia, Hypertension, Smoking) leads to Endothelial dysfunction
  2. Lipid+monocytes accumulate in intima, macrophages ingest lipid-> Foam cells
  3. Fatty streak: Foam cells make endothelium bulge, SMCs migration and proliferation
  4. Plaque grows, SMCs take up lipid, SMCs form a ‘roof’ over plaque and secrete collagen, elastin-> ‘fibrous cap’. Endothelium stretches-> Gaps in plaque that are filled by platelets
  5. Necrosis in centre of plaque, cholesterol released-> Cholestrol crystals, Blood vessels grow into plaque, Calcification

6.

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