Pathology - Vascular Flashcards
What is the pathogenesis, risks and clinical consequences of abdominal aortic aneurysms
- atherosclerotic plaque in intima compresses the media, causing ischaemia and degeneration
- local inflammation
- MMP further degrades medial ECM
- loss of medial SMC
risks: male, smoking, age > 50 years, atherosclerosis, familial history, connective tissue disease, HTN, diabetes
consequences: occlusion of branch vessel, atheroembolism, compression, rupture (25% if > 6cm)
What are the risks of rupture of AAA
0% if ≤ 4cm
1%/yr if 4-5cm
11%/yr if 5-6cm
25%/yr if > 6cm
What are the morphological features of AAA and the causes
- an aneurysm is a localised attenuation but intact portion of an arterial wall
- usually below the renal arteries and above the iliac bifurcation
- often contains atheromatous ulcers covered with mural thrombi with thinning and destruction of the media
causes: male, age, smoking, htn, ctd, atherosclerosis, congenital, syphilis, trauma, immunological
What are the signs and symptoms of aortic dissection?
symptoms: tearing chest pain radiating into the back, SOB, limb paraesthesia/weakness
signs: shock, ALOC, limb weakness, limb pulse discrepancy, inferior STE on ECG, widened mediastinum on XR, rarely SVC syndrome
What is the pathogenesis of an aortic dissection, what are the risk factors, classification and consequences?
- Occurs when blood separates the intima from the media due to weakness of media (intimal tear) and creates a false lumen, via 3 possibilities:
1) Atherosclerotic ulcer leading to intimal tear
2) Disruption of vasa vasorum causing intramural haematoma
3) De novo intimal tear
Risks: men 40-60, HTN, connective tissue disease (marfan syndrome), iatrogenic (cath lab), pregnancy
Classification: -Stanford A = proximal lesion in ascending aorta DeBakey 1 = ascending and descending aorta DeBakey 2 = ascending aorta only -Stanford B = distal lesion, does not involve ascending aorta DeBakey 3 = distal to subclavian artery
Consequences:
rupture back into intima or through adventitia/rupture out
into pericardial or pleural cavities
clinically causing = cardiac tamponade, aortic insufficiency, AMI, distal ischaemia, spinal cord ischaemia
What factors lead to atherosclerosis and what arteries are mostly affected
1) constitutional = genetics (fhx), age, men, post-menopausal women
2) modifiable = hyperlipidaemia, HTN, smoking, diabetes
3) additional = inflammation, metabolic syndrome
4) local = local flow disturbances (turbulence at branch points)
common sites: posterior wall of lower abdominal aorta, coronary arteries, popliteal arteries, internal carotids, COW
Describe the pathogenesis of atherosclerosis
1) endothelial injury and dysfunction leads to increased vascular permeability, leukocyte adhesion and thrombosis
2) accumulation of lipoproteins in vessel walls
3) monocyte adhesion and migration into intima, becoming macrophages and engulfing LDL
4) macrophage become foam cell, release cytokines that recruit more macrophages and accumulate in fatty streak
5) fatty streak is thrombogenic and attracts platelets, leading to platelet adhesion and release of PDGF
6) factors released from activated platelets and macrophages induce SMC recruitment into the intima
7) SMC secrete collagen and other products that form a fibrous cap
8) fatty streak + fibrous cap = plaque
How does an atherosclerotic plaque suddenly cause symptoms (pathological consequences)
- rupture of intima exposes blood to thrombogenic substances and induces thrombosis, leading to occlusion
- dislodging atheroembolism to distal site
- dissection, aneurysm formation and potential rupture
- stenosis of expanding plaque causing ischaemia
What is the difference between a stable and vulnerable atherosclerotic plaque
- stable plaque: dense collagenous and thickened fibrous cap with minimum inflammation and small lipid core
- vulnerable plaque: thin fibrous cap with large lipid core and increased inflammation, prone to rupture
What are the pathological changes that occur in atheromatous plaques and the consequences?
Changes and consequences: - rupture and fissuring -> thrombus formation, small vessel occlusion - erosion and ulceration -> embolus formation, distal occlusion - haemorrhage into atheroma -> aneurysm or dissection
Pathogenesis:
- accumulation of LDL cholesterol, engulfed by macrophages, forming fatty streaks
- plaque formation, with lipid core, covered by a fibrous cap made of smc and ct
- inflammation triggered by oxidised LDL, infiltration of inflammatory cells, contributing to growth and instability
- calcification, making plaque more rigid and brittle
How is hypertension classified
1) primary HTN (essential) = no one identifiable cause, 95% of all cases
causes:
genetics = familial, multi-gene foci and single gene errors
vasoconstrictive influences = structural changes in vessel wall
environmental = stress, obesity, smoking
2) secondary HTN = underlying pathology understood
causes:
renal = glomerulonephropathies, PKD, renal artery stenosis, renin-producing tumours
endocrine = cushing syndrome, primary hyperaldosteronism, pheochromocytoma, thyroid disorders
CVS = coarctation, polyarteritis nodosa
neurologic = increased intracranial pressure, sleep apnea
psychogenic = acute stress, surgery, pain
What are the long term consequences of HTN
atherosclerosis CAD CVD aortic aneurysm aortic dissection renal failure cardiac failure
What are the clinical features of malignant hypertension?
SBP > 200, DBP > 120 CNS: headache, ALOC, encephalopathy Chest pain/dyspnoea/nausea/vomiting Renal failure Eye changes: retinal haemorrhage, papilloedema, blurred vision LV hypertrophy
