Vessel Pathology
·
Arteries
o 3 layers:
§ Intima: thin, includes endothelium, underlying thin layer of connective
tissue containing smooth muscle, and elastic interna – elastic fibre layer
§ Media: thick, smooth muscle and collagen. Large arteries have elastic fibres as well
§ Adventitia: thin layer containing elastic fibres in loose connective
tissue
o 3 sizes: large (elastic), medium (muscular), small
·
Veins: thin wall, large lumen,
IEL intact only in large vessels, scant media, contain valves
Atherosclerosis
Epidemiology
·
Causes 50% of all deaths in US –
including coronary, cerebral and peripheral vascular disease
·
A disease of Western
civilisation. Absent in certain 3rd world ethnic groups
Aetiology
·
Multifactorial
·
Endothelial damage ® permeability,
monocyte adhesion and endothelial proliferation ® intimal
hyperlipidaemia with invasion of foamy macrophages ®
cytokines (IL1 and TNF) and growth factors (PDGF and FGF) cause inflammatory
response and proliferation of smooth muscle with sclerosis; plaque thickened by
organisation of superimposed thrombi
Gross Morphology
·
Lesions appear in childhood as
fatty streaks
·
Adult plaques: discrete, yellow
white random elevations, more prominent around ostia of large branches
·
Plaques may have sclerotic firm
surfaces or ulcerate exposing soft cholesterol laden material
·
Severity increases with age
Microscopic Morphology
·
Plaque: intimal lesion –
deposition of cholesterol esters, necrotic debris, smooth muscle and foam
cells. Chronic fibrotic inflammatory response forming a superficial fibrous cap
·
Complications are ulcers with
thrombi, bleeding into plaque, embolisation, calcifications, atrophy of media ®
aneurysms
·
Reduplication of internal elastic
lamina: shows with Elastin Van Geesen (EVG) stain
·
Adventitial fibrosis and chronic
inflammation
Complications
·
Calcification ® rigid
pipe ® pulse pressure ® distal atherosclerosis. (NB Calcium laid down in two ways: dystrophic
calcification – Ca laid down in necrotic tissue – and metastatic calcification
- serum Ca ® Ca laid down abnormally
·
Ulceration: fibrous cap cracks –
debris discharged into lumen ® embolisation/thrombis
·
Thrombis: can embolise, or
occlude artery. Cause of majority of myocardial infarcts and cases of unstable
angina pectoris. If collateral circulation, can recannalise thrombis
·
Haemorrhage: a weak little new
artery in the plaque bursts ® pushes plaque against opposite wall
Aortic Aneurysm
·
Severe arteriosclerosis
·
20% familial incidence ® defect
in connective tissue component (?type III procollagen)
·
Syphilis and other bacterial
infections
·
Cystic medial necrosis ®
denudation of elastic layer
·
Trauma
·
Common in Marfan's syndrome (eg
Abraham Lincoln). Long ulnar, femur, weak aorta, and high arched pallet
·
75% occur in abdominal
aorta. Easy to repair cf thoracic and
thoraco-abdominal cases
·
Often asymptomatic ®
incidental finding
·
Can cause back pain (due to
retroperitoneal blood). Differential ®
pancreatitis
·
44% of symptomatic aneurysms
rupture. Distension
® inevitable rupture (Law of La Place)
·
Arteriosclerosis ® gradual
destruction of media ® focal weakening of wall ® distensibility ® ¯w + r ®tension +
¯blood velocity (T µ Pr/W)
·
Pressure ® radius ® tension ® radius, etc
·
Fusiform dilatation of severely
atherosclerotic aorta with sharp superior and inferior margins
·
Typically abdominal aorta, from
just below ostia of renal arteries to bifurcation of aorta
·
Larger aneurysms contain thick
old laminated thrombus reducing patent luminal size
·
Aneurysmal thrombus does not
organise due to the paucity of functioning vasa vasorum in fibrotic wall
·
Aneurysm wall: barely
identifiable media, fibrotic lesions with focal aggregates of mononuclear cells
·
Adventitia is fibrotic with
chronic inflammation
Complications
·
Thrombus ® distal
gangrene, calcification, bacterial infection (salmonella, shigella), rupture,
dissection, fistula (eg aorta-vena cava)
·
Usually involves the aorta
·
Fatal in 75 – 90% of cases
·
Causes: atherosclerosis, also
hypertension, Marfan‟s syndrome, trauma, inflammation of media
·
Pathogenesis:
o Cystic medial necrosis: mucoid cysts in the media, elastic fragmentation
and fibrosis
o Commences as a transverse intimal tear, 90% in ascending aorta
o Splits the media between the mid and outer 1/3
o Proceeds down occluding branches
·
Outcomes:
o Acute perforation ® sudden death
o Subacute progression ® perforation in several days
o Chronic ® rupture back into the lumen ® double barrel aorta
·
Diverse group of diseases
classified by aetiology, vessel size or histologic changes
Infectious arteritis
·
Wide range of organisms,
pyogenic, TB, parasites, viruses, fungi, syphilis
·
Vessel infected by septic emboli
(® lodges and forms mycotic aneurysm) or direct extension from adjacent
abscesses
·
Histology: oedema, fibrin, dense
neutrophilic infiltrate
·
Outcome: scarring, obliteration
of lumen ® distal infarction
·
Syphilis: occludes vasa vasorum ®
ischaemic damage to artery, small vessel occlusion ®
obliterative end arteritis, perivascular lymphocyte and plasma cell cuffing.
Famous for causing proximal aortic aneurysms
Physical/Chemical Agents
·
Irradiation, trauma, vascular
toxins, sulphonamides, penicillin
·
Arteritis syndromes
· See Vasculitis
·
Arteriosclerosis:
o = Thickening and loss of elasticity of arterial walls. Seen in chronic
hypertension, and to a lesser degree with ageing
o Hyaline arteriosclerosis: blood vessel takes on glassy „hyaline‟
appearance. Reflects mild or „benign‟ hypertension. Particularly seen in
kidneys
o Hyperplastic arteriosclerosis: concentric rings of increased connective
tissue and smooth muscle give arteries an onion skin appearance. Signifies
acceleration/malignancy of the hypertension
·
Fibromuscular dysplasia:
non-inflammatory thickening of large and medium sized muscular arteries causing
stenosis. Most significant in renal arteries ®
secondary hypertension
·
Thrombophlebitis: inflammation
and secondary thrombosis of veins, usually small veins as part of a local
reaction to bacterial infection
·
Varicose veins: enlarged,
dilated, tortuous blood veins and incompetent venous valves – mainly in legs.
Predisposing factors include older age, female, heredity, posture and obesity.
Varicose veins at other sites include haemorrhoids (rectal), oesophageal
varices and varicocoele (scrotum)
·
Vasculitis: inflammation and
necrosis of blood vessels – including arteries, veins and capillaries. May be
due to infection, trauma, radiation, toxins or immune (eg disposition of immune
complexes)
·
Leukocytoclastic vasculitis: a
form of hypersensitivity angiitis in the skin presenting as purpura
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