42 - Vascular Pathology

Question 1

Examples of vascular diseases 1) 2) 3) 4) 5)

Answer 1

1) Atherosclerosis 2) Arteriosclerosis 3) Arteriolosclerosis 4) Aneurysm 5) Dissection

Question 2

Arteriosclerosis

Answer 2

Any thickening or hardening of arteries. EG: When a vascular wall is damaged, collagen is deposited in intima, and the wall fibroses.

Question 3

Sequelae to fibrosis of arterial wall 1) 2)

Answer 3

1) Impairs artery’s role in controlling blood pressure 2) Can impair blood supply to downstream tissues

Question 4

Hyaline arteriolosclerosis 1) 2) 3)

Answer 4

1) Smooth muscle in media produces too much ECM 2) Intimal damage and thickening 3) Proteins from blood can leak across damaged endothelium

Question 5

Potential sequelae of hyaline arteriolosclerosis 1) 2)

Answer 5

1) Poor blood supply to tissues 2) Microaneurysms, haemorrhage.

Question 6

Benign nephrosclerosis

Answer 6

Ischemia of kidney from narrowed arterioles. Gross pathology is shrunken kidney with bumpy surface.

Question 7

Kidney disease from narrowed arterioles

Answer 7

Benign nephrosclerosis

Question 8

Atherosclerosis

Answer 8

A build-up of inflammatory, fibrotic, necrotic, fatty material in arteries. Fibroinflammatory lipid plaque (Atheroma).

Question 9

Potential effects of atherosclerosis 1) 2)

Answer 9

1) Can rupture 2) Can cause stenosis of artery

Question 10

Answer 10

L= Lumen F= Fibrous plaque C= Necrotic, fatty core

Question 11

Stages of atherosclerosis formation 1) 2) 3) 4)

Answer 11

1. Fatty streaks 2. Damage, inflammation, cholesterol and fibrosis 3. Stable atherosclerotic plaque 4. Unstable atherosclerotic plaque

Question 12

Fatty streaks 1) 2)

Answer 12

1) Collection of foam cells in intima 2) Clinically insignificant

Question 13

If fatty streaks are clinically insignificant, why are they implicated in atherosclerosis?

Answer 13

Develop at ostia and branch points where atheroscleroses are common

Question 14

Structure of atherosclerosis 1) 2) 3)

Answer 14

1) Fibrous cap 2) Necrotic, fatty core 3) Chronic inflammatory cells

Question 15

Stable angina

Answer 15

Heart pain when exerting oneself. Often from reduced blood flow to heart

Question 16

Potential cause of stable angina

Answer 16

Atherosclerotic plaque

Question 17

Two ways in which pathologic calcification can arise

Answer 17

1) Dystrophic calcification 2) Metastatic calcification

Question 18

Dystrophic calcification

Answer 18

Appears in areas of cell degeneration EG: TB, atherosclerosis

Question 19

Metastatic calcification

Answer 19

When serum calcium and phosphate levels are too high. They reach precipitation threshold in blood, fall out of solution. Particularly implicated in kidney disease

Question 20

Characteristics of unstable plaques 1) 2) 3) 4) 5)

Answer 20

1) Prone to rupture 2) Thinner fibrous cap or ulceration 3) Larger necrotic core 4) More inflammatory cells 5) Less than 50% stenosis (makes them harder to detect)

Question 21

Effects of acute plaque events 1) 2) 3)

Answer 21

1) Thrombosis 2) Thromboembolism 3) Atheroembolism

Question 22

When does chronic ischaemia occur with atherosclerosis?

Answer 22

When over 70% stenosed

Question 23

Claudicaiton

Answer 23

Ischaemic leaking disease

Question 24

Why is endothelium implicated in atherosclerosis? 1) 2) 3)

Answer 24

Several risk factors involve endothelium 1) Hypertension has a low-grade shear effect 2) Smoking has toxic and pro-inflammatory effects 3) High blood sugar, lipids can damage endothelial wall

Question 25

Important condition to start of atherosclerosis

Answer 25

Activated endothelium (leaky, expression of adhesion molecules, produce cytokines, growth factors, changes from anti-coagulant, pro-coagulant)

Question 26

What does activated endothelium do in atherosclerosis? 1) 2) 3) 4)

Answer 26

1) Takes up LDL more avidly into the intima 2) Allows monocytes into intima, which phagocytose LDL and become foam cells 3) Macrophages release inflammatory cytokines, which forms a kind of positive feedback loop (EG: matrix metalloproteases degrade ECM) 4) LDL oxidises, forms ROS in intima, becomes actively toxic

Question 27

Role of smooth muscle cells in atherosclerosis 1) 2)

Answer 27

1) Migrate into intima, change phenotype 2) Can proliferate, produce ECM (increases fibrous cap thickness, reduces risk of plaque rupture)

Question 28

Aneurysm

Answer 28

Abnormal dilation of blood vessel or heart

Question 29

What causes an aneurysm?

Answer 29

Weakness in tunica media

Question 30

Types of aneurysm 1) 2) 3) 4)

Answer 30

1) Saccular (bulge on one side) 2) Fusiform (both sides bulge) 3) False aneurysm (hematoma) 4) False aneurysm (dissection)

Question 31

Aneurysm associated with atherosclerosis

Answer 31

Abdominal aortic aneurysm

Question 32

Abdominal aortic aneurysm 1) 2) 3) 4) 5)

Answer 32

1) Associated with atherosclerosis 2) Inflammatory environment weakens SCM (MMPs) 3) Intimal thickening interferes with wall perfusion 4) Risk of rupture increases above 5cm diameter 5) Often contains thrombus, which can embolise

Question 33

Berry aneurysm 1) 2) 3)

Answer 33

1) Aneurysm in Circle of Willis in the brain. 2) Weakening attributed to a congenital defect 3) Major cause of subarachnoid haemorrhage

Question 34

Dissection

Answer 34

Blood in the media under arterial pressure

Question 35

Types of dissections

Answer 35

Type A or B determine whether base of aorta is involved or not

Question 36

Association between hypertension and dissection

Answer 36

Over 90%

Question 37

What is normally affected by a dissection

Answer 37

Aorta, especially ascending aorta

Question 38

Possible sequelae of dissection 1) 2) 3)

Answer 38

1) Can involve or compress important arteries 2) Can rupture into pericardium (cardiac tamponade) 3) Can rupture into thorax (exsanguination)

Question 39

If a patient has survived a thrombosis, what is likely to happen to the thrombus?

Answer 39

Over time, a thrombus will undergo organisation and recanalisation. That is, macrophages will migrate in and fibroblasts and small blood vessels will grow into the thrombus from the wall of the artery i.e. forming granulation tissue. Macrophages will phagocytose dead cells and fibroblasts will form extracellular matrix. Ultimately scar tissue will form. New vessels may persist in the scar tissue, joining the proximal and distal lumina across the scar.

N.B. Organisation is the process of the formation of scar tissue via the formation of granulation tissue, which in this case will replace the thrombus. Recanalisation refers to the formation of new vessels in the granulation (and later scar) tissue through the occluded lumen. Passage of blood will be limited, however, and in the case of occluded arteries, the tissue supplied will already be dead.