42 - Vascular Pathology Flashcards
Examples of vascular diseases 1) 2) 3) 4) 5)
1) Atherosclerosis 2) Arteriosclerosis 3) Arteriolosclerosis 4) Aneurysm 5) Dissection
Arteriosclerosis
Any thickening or hardening of arteries. EG: When a vascular wall is damaged, collagen is deposited in intima, and the wall fibroses.
Sequelae to fibrosis of arterial wall 1) 2)
1) Impairs artery’s role in controlling blood pressure 2) Can impair blood supply to downstream tissues
Hyaline arteriolosclerosis 1) 2) 3)
1) Smooth muscle in media produces too much ECM 2) Intimal damage and thickening 3) Proteins from blood can leak across damaged endothelium
Potential sequelae of hyaline arteriolosclerosis 1) 2)
1) Poor blood supply to tissues 2) Microaneurysms, haemorrhage.
Benign nephrosclerosis
Ischemia of kidney from narrowed arterioles. Gross pathology is shrunken kidney with bumpy surface.
Kidney disease from narrowed arterioles
Benign nephrosclerosis
Atherosclerosis
A build-up of inflammatory, fibrotic, necrotic, fatty material in arteries. Fibroinflammatory lipid plaque (Atheroma).
Potential effects of atherosclerosis 1) 2)
1) Can rupture 2) Can cause stenosis of artery
L= Lumen F= Fibrous plaque C= Necrotic, fatty core
Stages of atherosclerosis formation 1) 2) 3) 4)
- Fatty streaks 2. Damage, inflammation, cholesterol and fibrosis 3. Stable atherosclerotic plaque 4. Unstable atherosclerotic plaque
Fatty streaks 1) 2)
1) Collection of foam cells in intima 2) Clinically insignificant
If fatty streaks are clinically insignificant, why are they implicated in atherosclerosis?
Develop at ostia and branch points where atheroscleroses are common
Structure of atherosclerosis 1) 2) 3)
1) Fibrous cap 2) Necrotic, fatty core 3) Chronic inflammatory cells
Stable angina
Heart pain when exerting oneself. Often from reduced blood flow to heart
Potential cause of stable angina
Atherosclerotic plaque
Two ways in which pathologic calcification can arise
1) Dystrophic calcification 2) Metastatic calcification
Dystrophic calcification
Appears in areas of cell degeneration EG: TB, atherosclerosis
Metastatic calcification
When serum calcium and phosphate levels are too high. They reach precipitation threshold in blood, fall out of solution. Particularly implicated in kidney disease
Characteristics of unstable plaques 1) 2) 3) 4) 5)
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)
Effects of acute plaque events 1) 2) 3)
1) Thrombosis 2) Thromboembolism 3) Atheroembolism
When does chronic ischaemia occur with atherosclerosis?
When over 70% stenosed
Claudicaiton
Ischaemic leaking disease
Why is endothelium implicated in atherosclerosis? 1) 2) 3)
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
Important condition to start of atherosclerosis
Activated endothelium (leaky, expression of adhesion molecules, produce cytokines, growth factors, changes from anti-coagulant, pro-coagulant)
What does activated endothelium do in atherosclerosis? 1) 2) 3) 4)
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
Role of smooth muscle cells in atherosclerosis 1) 2)
1) Migrate into intima, change phenotype 2) Can proliferate, produce ECM (increases fibrous cap thickness, reduces risk of plaque rupture)
Aneurysm
Abnormal dilation of blood vessel or heart
What causes an aneurysm?
Weakness in tunica media
Types of aneurysm 1) 2) 3) 4)
1) Saccular (bulge on one side) 2) Fusiform (both sides bulge) 3) False aneurysm (hematoma) 4) False aneurysm (dissection)
Aneurysm associated with atherosclerosis
Abdominal aortic aneurysm
Abdominal aortic aneurysm 1) 2) 3) 4) 5)
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
Berry aneurysm 1) 2) 3)
1) Aneurysm in Circle of Willis in the brain. 2) Weakening attributed to a congenital defect 3) Major cause of subarachnoid haemorrhage
Dissection
Blood in the media under arterial pressure
Types of dissections
Type A or B determine whether base of aorta is involved or not
Association between hypertension and dissection
Over 90%
What is normally affected by a dissection
Aorta, especially ascending aorta
Possible sequelae of dissection 1) 2) 3)
1) Can involve or compress important arteries 2) Can rupture into pericardium (cardiac tamponade) 3) Can rupture into thorax (exsanguination)
If a patient has survived a thrombosis, what is likely to happen to the thrombus?
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.
