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Tp2. Pathological Processes > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What is atherosclerosis

A

The accumulation of intracellular and extracellular lipids in the intima of the medium and the large size artery’s

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2
Q

What are the stages that would form the atherosclerotic plaque

A

Damage to the endothelium
Platelet aggregation (Activation of the platelet derived growth factor)
Migration of the monocytes to the intima
Migration of the lipids
Macrophages and smooth muscle cells move from media
Fats engulfed by the smooth muscle cells and macrophages

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3
Q

What type of macrophages would be present

A

Foamy macrophages
(smooth muscle cells become when they engulf the lipids)

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4
Q

What areas of the blood vessels would be involved

A

Tunica intima
Tunica media

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5
Q

Where would the cells migrate from

A

The tunica media

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6
Q

What cells would be involved

A

Macrophages
Endothelial cells
Lymphocytes
Neutrophils
Smooth muscle cells

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7
Q

What is the fibrous cap

A

Layer of fibrous collagen
Would stabilise the plaque

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8
Q

What is he necrotic centre? Why would it be necrotic?

A

Necrotic as would have limited blood flow
Within: cholesterol crystals, calcium, cell debris, foam cells

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9
Q

What is a monkenbergs disease

A

Calcification of the medium artery’s

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10
Q

What is a vulnerable plaque

A

Whe would have a thin fibrous cap
The wall is easily ruptured
Lesion likely to move to the blood stream

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11
Q

What is a stable plaque

A

When would have a thick fibrous cap, so there would be a small chance of rupture

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12
Q

What are the most important causes of the endothelial dysfunction leading to atherosclerosis

A

Inflammation
Hypercholestrolemia
Hemodynamic disturbances (hypertension)

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13
Q

What is a complicated plaque

A

Late stage Plaques that would cause:
Aneurysms
Thrombosis
Haemorrhage
Calcification (due to necrosis leading to monkebergs disease)

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14
Q

What is a simple plaque

A

An early stage plaque:
Raised white and yellow
Enlarged and merged vessel
Widely distributed
Irregular outline

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15
Q

What are the clinical presentations

A

Progressive narrowing leading to stenosis
Acute atherosclerotic occlusion
Ruptured abdominal aneurysm

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16
Q

What can blockage of the abdominal aorta cause

A

Abdominal aneurysm
Haemorrhage of the abdominal organs (for example the intestines)

17
Q

What is peripheral vascular disease? what can it cause?

A

What: the build of the fatty deposits in the arteries, leading to the blockage of the blood vessel and so blood supply to lower limbs
Cause: the decreased blood flow to the lower limbs, gangrene (dry-coagulative)

18
Q

What is an aneurysm

A

Weak spots in the vessels would cause them to balloon and then rupture
If in the aorta, death

19
Q

What can familiar hyperlipidemia cause

A

Tendon Xanthomas (fatty deposits in the joints)
Arcus (corneal) fatty deposits in the cornea of the eye (forms a ring)
Xanthelasma (fatty deposits around the eyes)

20
Q

What are the modifying factors

A

Smoking
Hypertension
Infection
Hyperlipidaemia
Alcohol intake

21
Q

What are the non-modifying factors

A

Age
Genetics
Gender

22
Q

How can diabetes Mellitus lead to atherosclerosis

A

Increased risk hyperlipidaemia and hypertension

23
Q

What do endothelial cells do

A

Haemostasis
Collagen production
Proliferation and migration of the smooth muscle cells

24
Q

What do the platelets do

A

Haemostasis
Proliferation and migration of the smooth muscle cells

25
Q

What do the smooth muscle cells do

A

Take up the LDL and the other become foam cells
Synthesis of collagen and proteoglycans

26
Q

What do macrophages do

A

Oxidise LDL
Take up lipids
Proliferation of the smooth muscle cells

27
Q

What do the lymphocytes do

A

Proliferation of the smooth muscle cells

28
Q

What do the neutrophils do

A

Secrete proteases leading to continue local damage and inflammation

29
Q

What can cause the rupture an aneurysm

A

When the vessel would grown more then 6cm in length

30
Q

How does the normal vessels stop thrombus

A

Production of heparin like molecule
Prostacyclin production (produced in the artery walls - anticoagulant)
Thrombomodulin (integral membrane protein, cofactor to thrombin enzyme (protein c, stops procoagulant functions of thrombin)

31
Q

What are the infections that can cause atherosclerosis

A

Chlamydia pneumonia
Helicobacter pylori
Cytomegalovirus

32
Q

How do the smooth muscle cells become foam cells

A

Taking up LDL and other lipids

33
Q

What inflammatory mechanism would be stimulated

A

The chronic inflammatory

Tp2. Pathological Processes (9 decks)

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