Chapter 27: Vascular Flashcards
Most common congenital hyper coagulable disorder
Resistance to activated protein C (Leiden factor)
Most common acquired hyper coagulable disorder
Smoking
Atherosclerotic stages
- 1st
- 2nd
- 3rd
1) Foam cells (macrophages have absorbed fat and lipids in the vessel wall)
2) Smooth muscle cell proliferation (caused by growth factors released from macrophages; results in wall injury)
3) Intimal disruption (from smooth muscle cell proliferation)
What stage of athersclerosis causes thrombus formation?
Third - intimal disruption: leads to exposure of collagen in vessel wall and eventual thrombus formation -> fibrous plaques then form in these areas with underlying atheromas
Risk factors for atherosclerosis
Smoking, HTN, hypercholesterolemia, DM, hereditary factors
3rd most common cause of death in the United States
Stroke
Most important risk factor for stroke
HTN
Supple 85% of blood supply to the brain
Carotids
Most common site of stenosis in cerebrovascular disease
Carotid bifurcation
Type of flow from normal internal carotid artery
Continuous forward flow
1st branch off the internal carotid artery
Ophthalmic artery
Type of flow from external carotid artery
Triphasic flow
1st branch of the external carotid artery
Superior thyroid artery
Communication between the ICA and ECA
Ophthalmic artery (off ICA) and internal maxillary artery (off ECA)
Most commonly diseased intracranial artery
Middle cerebral artery
Most commonly from arterial embolization from the ICA (not thrombosis)
- Can also occur from a low-flow state through a severely stenotic lesion
Cerebral ischemic events
2nd most common source of cerebral emboli
Heart
Lesion: mental status changes, release, slowing
Anterior cerebral artery events
Lesion: contralateral motor and speech (if dominant side); contralateral facial droop
Middle cerebral artery events
Lesion: vertigo, tinnitus, drop attacks, incoordination
Posterior cerebral artery events
Occlusion of the ophthalmic branch of the ICA (visual changes -> shade coming down over eyes); visual changes are transient
Amaurosis fugax
What do you see on ophthalmologic exam in amaurosis fugax?
Hollenhorst plaques
Treatment: carotid traumatic injury with major fixed deficit:
- Occlusion
- Nonocclusion
- If occluded, do not repair -> can exacerbate injury with bleeding
- If not occluded -> repair with carotid stent or open procedure
Indications for CEA
Symptomatic > 70%, asymptomatic > 80%