Pathology: circulatory disorders Flashcards
describe artery structure
Three layer structure
Inner layer- tunica intima
Middle layer- tunica media
Outer layer- tunica adventitia
what is atherosclerosis
A slow progressive intimal disease of large to medium sized muscular and elastic arteries
It results in elevated or occlusive intimal based lesions
The lesions or plaques are composed of lipids, smooth muscle cells and ECM
what are some non modifiable risk factors for atherosclerosis
genetic abnormalities
family history
increasing age
male gender
what are some modifiable risk factors for atherosclerosis
Hyperlipidaemia Hypertension Smoking Diabetes Inflammation
what is the pathogenesis of atherosclerosis
1) In the first response we get monocyte/platelet adhesion
2) The monocytes-> macrophages and secret cytokines and take up lipids in the blood stream
3) The macrophage now continues to take up lipids and smooth muscle leading to the formation of a atheromatous plaque
what is the sequence of atherosclerosis
Normal artery Fatty streak Fibrofatty artery Advanced vulnerable plaque Clinical stenosis- about 70% bloackage
what can atherosclerosis lead to
gradual mechanical obstruction to flow
plaque rupture
weakening of the vessel
what are major consequences in atherosclerosis
if in the coronary heart arteries- ischameic heart disease, angina
if in the aorta- aortic aneurysm
if in the mesenteric artery’s- bowel ischamia
if we get atherosclerosis in the coronary arteries what can it lead to
angina, MI
ischaemic heart disease
if we get atherosclerosis in the aorta what can it lead to
aortic aneurysm
if we get atherosclerosis in the mesenteric arteries what can it lead to
bowel ischaemia
what is age related vascular changes called
arteriosclerosis
what do we see as a patient ages in the arteries
thickening of the intimate
scarring of the media
fragmentation of the lamina
calcification
how can hyperglycaemia damage the vessel
• ROS formed
• Decreased NO
• Formation of advanced glycation end products
• Activation of inflammatory pathways
Promotion of thrombosis and atherosclerosis
what are the consequences of diabetic vascular disease
Microangiopathy Haemorrhage Hypertension Atherosclerosis MI Nephrosclerosis Islet cell loss Gangrene Peripheral vascular atherosclerosis
what is giant cell arteritis
it is also known as temporal/cranial arteritis depending on the vessel
chronic vasculitis of large/medium sized vessels
when do we see giant cell arteritis
hardly ever occurs in someone less than 50
what are the clinical signs and symptoms of giant cell arteritis
new headache- temporal tenderness, enlarged artery
jaw claudication
visual symptoms- amaurosis fugax
non descriptive eg flu, body ache
what is amaurosis fugax
blindness like curtains coming down on the eyes
what should the GDP do if we suspect GCA
seek advice
treat with oral steroids glucocorticoids
40-60mg prednisolone daily
what are tests we can do if we suspect giant cell arteritis
ESR- raised over >100mm/hr
CRP raised
haematology- normochromic normocytic anaemia
temporal artery biopsy- at least 1cm or longer within 7 days of treatment
what can giant cell arteritis lead to
retinal arterial occlusion- permanent partial/complete loss of vision in one or both eyes
if other branches are affected what can giant cell arteritis lead to
cerebral ischameia
mesenteric ischaemia
aneurysms
what is an aneurysm
localised, permanent abnormal dilations of a blood vessel
