Blood Vessels Flashcards
Mutations in ENaC leading to inc tubular resorption by aldosterone
Liddle syndrome
Mechanisms of Essential Hypertension (4)
1 Reduced renal sodium ex
2 Inc vascular resistance
3 Genetics
4 Environment
Benign hypertension
Homo pink hyaline with thickening of arteriolar wall
Sometimes with nephrosclerosis
Hyaline arteriolosclerosis
Typical severe hypertension
Onionskin concentric laminated thickening and luminal narrowing
Necrotizing arteriolosclerosis
Hyperplastic arteriolosclerosis
Hardening of arteries
Arteriolosclerosis
Calcific deposits in muscular arteries
Older than 50
Do not encroach lumen not clinicially
significant
Monckeberg medial sclerosis
Presence of intimal lesions atheromas
Atherosclerosis
Strongly and independently predict risk of MI stroke PAD SCD even in healthy
CRP level
Atheroma development
Endothelial injury -> endothelial dysfunction and mac and smooth muscle activation ->mac and smooth ms engulf lipid -> smooth ms prolif collagen, ECM, lipid deposition
Minute yellow plaque macules that coalesce into elongated lesions made up of lipid filled foamy mac but do not cause significant flow disturbance
Forms as early as <1 yr
Fatty streak
Most involved vessels in atherosclerotic plaque formation:
Infrarenal abdominal aorta > coronary arteries > popliteal arteries > ICA > circle of Willis
Atherosclerotic plaque 3 principal components:
1 cells (smooth muscle or foam cell, mac and T lymphocytes) 2 ECM (collagen, elastic fibers, proteoglycan) 3 intracellular and extracellular lipid
When plaque exposes highly thrombogenic constituents
Plaque rupture/fissuring
Thrombogenic subendothelial membrane exposed to blood
Erosion/ulceration
Expansion of volume by plaque
Hemorrhage into atheroma
Plaque inflammation induces
collagen degradation
reduced collagen synthesis
True aneurysms
Involve all three layers of artery
False aneurysm
Pseudoaneurysm
Wall defect becoming extravascular hematoma communicating with intravascular space (pulsating)
Pressured blood enters arterial wall through defect and pushes apart underlying layers
Arterial dissection
Discrete outpouchings 5-20cm with thrombus
Saccular
Circumferential dilations up to 20cm involving aortic arch, abd aorta and iliac arteries
Fusiform
Aneurysms occur bec (4)
1 inadequate abnormal CT synthesis
2 excessive CT degradation
3 loss of smooth muscle cell or change in smooth muscle cell synthetic phenotype
Abnormal sequestration of tgf b in wall leading to dilation and dysregulating signalling and loss of elastic tissue
Marfan syndrome
scaffolding protein defective in Marfan
fibrillin
Mutation in tgf b result in
1 defective elastin
2 defective collagen synthesis
Type IV Ehrlos Danlos results fr
Defective Type III collagen synthesis with aneurysm
skin
ligament
blood vessel
Narrowing of aortic vasa vasorum fr sys HTN and ischemia Smooth muscle cell loss Aortic degenerative changes (fibrosis) Inadequate ECM synthesis Inc amorphous proteoglycan
Cystic medial degeneration
Most important causes of aneurysm (2)
1 atherosclerosis
2 hypertension
Factor in abdominal aneurysm
Atherosclerosis
Ascending aortic aneurysms
Hypertension
Embolization of septic embolus fr infective endocarditis
Extension of suppurative process
Direct infection of wall
Mycotic aneurysm
Tertiary syphilis has predilection for
Vasa vasorum of ascending THORACIC aorta
Immune response to spirochetes attacking thoracic aorta
Obliterative endarteritis
Men
Smokers
More than 50
Plaques compromising diffusion of nutrients and waste bet lumen and wall compressing media leading to necrosis and thinning
Abdominal Aortic Aneurysm AAA
Distinct subtype of with dense periaortic fibrosis with lymphoplasmacytic inflammation mac giant cell
Inflammatory AAA
Risk of aneurysm rupture is determined by
Size