L8 Pathology of vessels Flashcards
(48 cards)
Clinical presentations of atherosclerosis depend on the end-organ ischemia. Which of the following are possible clinical presentations of atherosclerosis?
A. Claudication (pain on exertion) B. Cold dry skin C. Toe gangrene D. Pulseless E. Bruit
All of the above,
also with acute persistent pain e.g. acute myocardial infection.
What are the changeable risk factors for atherosclerosis? (4)
三高一吸
- Hyperglycemia
- Hyperlidpidemia
- Hypertension
- Smoking
Atherosclerotic plague complications? (3)
- Significant stenosis (80%) > symptoms
- Thrombotic occlusion > infarcts
- Aneurysmal mural thrombosis > embolism
What is the definition of atherosclerosis?
Focal accumulation of lipid (1) and proliferation of smooth muscle cells (1) within tunica intima (1) of arteries
Risk factors of atherosclerosis can be divided into non-modifiable and modifiable risk factors. Name a few non-modifiable risk factors.
- Fx
- Age
- Male and post-menopausal F
What are the 3 different stages of morphology/ types of atherosclerotic plaques?
- Fatty streaks
- Atheroma (atheromatous plaque)
- Complicated atheroma
Fatty streaks are foamy ____________(Cell type) that can be presented as slightly raised yellow deposits within the tunica intima (TI).
There are formed in virtually all children > 10 years old and develops into atheroma progressively.
macrophages
What is an atheroma/ atheromatous plaque?
What are the components? (memorise!)
Fibrous cap + Necrotic center
- Fibrous cap: smooth muscle cells, macrophages, foam cells, collagen..
- Necrotic center: cell debris, cholesterol crystals, foam cells
Components:
- Cells: smooth muscle cell, foam cells (lipid-laden macrophages + SMC)
- Extracellular matrix (ECM): collagen + elastic fibers
- Lipids: cholesterol cleft/crystal + calcification if old enough
What are the most common sites for atheroma to deposit onto? (4) List them in descending order.
- Infra-renal abdominal aorta
- Coronary arteries
- Popliteal arteries
- Internal carotid arteries
Complicated atheroma is the latest stage of morphology of atherosclerosis. What is it?
Unstable plagues
- with thinner fibrous cap, larger lipid core, more inflammation
What will complicated atheroma cause? (3As!)
- Acute plague changes
- rupture/ ulceration/fissuring: expose underlying necrotic centre (thrombogenic subendothelial basement membrane) to endothelial surface > induce thrombus formation > occlusion > ischemia, infarction
- Hemorrhage into a plague: plaque volume expansion
2. Atheroembolism: ruptured plague discharges debris into blood - micro emboli
3. Aneurysm: atherosclerosis-induced pressure or ischemic atrophy of tunica-media (TM) > loss of elastic tissue and structural weakening > aneurysmal dilation and rupture
Pathogenesis of atherosclerosis?
- Chronic endothelial injury (e.g. HTN, hypercholesterolemia) + Accumulation of lipoproteins (e.g. oxidised LDL and cholesterol crystals) in vessel wall
- Monocytes (become tissue macrophage) and other inflammatory cells migrate to subendothelial space
- Platelets adhere to endothelium
- Release cytokines and growth factors
- SMC proliferates and migrates to tunica intima from tunica media***
- Foam cells are formed as cholesterol enters SMC and macrophages
- SMC and macrophages release cytokines > produce Extra-cellular matrix
* ** SMC proliferation and ECM deposition are irreversible process converting fatty streak into atheroma
Hypertension can be essential or secondary.
How many of each type of hypertension is benign?
What is the significance of defining benign/malignant?
Essential: 90% benign, 10% malignant
Secondary: 80% benign, 20% malignant
- Benign: gradual increase in BP
- Malignant: rapid elevation of BP, associated with direct end-organ damage
What end organ damage can malignant hypertension cause (can be seen in PE)? (2)
- Papilloedema
- Retinal hemorrhage (& exudate)
* Fundoscopy can reflect severity of malignant hypertension
Type of atherosclerosis in elastic and large vessels?
What are the 2 main complications
Hypertensive atherosclerosis
1. Aneurysm: HT more commonly associated with aortic aneurysm
- Acute dissection (due to acute tearing off of the intima) - in long standing HT
Tunica media hyperplasia and hypertrophy occurs in _________ blood vessels. Fibroelastic hyperplasia is the reduplicate of internal elastic lamina + fibrous thickening of tunica media.
Muscular
Arteriole hypertension causes __________ arteriosclerosis in benign hypertension and _____________ arteriosclerosis in malignant hypertension.
Hyaline;
Hyperplastic
What is hyaline arteriosclerosis?
- caused by benign hypertension
- arterioles hardening due to subendothelial deposits of the glassy pink materials (exudative materials including fibrin), also found in ageing and DM
What does hyperplastic arteriosclerosis look like?
Onion-skin like;
concentric muscular thickening (tunica media) +/- wall thickening (tunica intima)
- Fibrinoid necrosis: increased permeability of small vessels to fibrinogen
What is the type of kidney disease caused by hypertension?
Nephrosclerosis
- sclerosis of small renal arteries and arterioles that is strongly associated with hypertension
Pathogenesis of benign nephrosclerosis?
- Hyaline atherosclerosis of renal arterioles > ischemia > necrosis, fibrosis and sclerosis of glomeruli > symmetrically renal atrophy + finely granular cortical surface with retention cysts
Malignant nephrosclerosis:
- Fibrinoid necrosis of arterioles causing ____________
- Hyperplastic arteriolosclerosis: “onion skin” lesion
petechiae hemorrhage
__________ is a localised, permanent dilatation of artery/vein.
Aneurysm
What is true and pseudo aneurysm?
True: involves all 3 layers of the artery (intima, media, adventitia)
Pseudoaneurysm (false aneurysm): involves only tunica media and adventitia with ruptured vessel wall creating a collection of blood bounded externally by adherent extravascular tissues
