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T2 Nishiyama Hypoxia Ischemia


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What are the results of ischemia?
Ischemia: transient, prolonged, or permanent. Results vary according to collateral circulation, duration, magnitude and anatomic area involved and rapidity of blood flow reduction.
Differentiate global vs. focal ischemia. What are three causes of global ischemia?
Global - Generalized reduction of cerebral blood flow (blood flow to entire brain is compromised). Causes: cardiac arrest, shock, severe hypotension. Focal Ischemia - Localized area of ischemia due to large-vessel disease (embolic or thrombotic occlusion) or to small-vessel disease (vasculitis)
Describe Global Cerebral Ischemia and impact on patients.
Widespread infarction; Severe impairment or in deep coma (persistent vegetative state); Other pts meet clinical criteria of “brain death”, flat EEGs; With maintenance of such patients, brain undergoes autolysis. Gross morphology described as respirator brain.
In focal cerebral ischemia, what are the causes and common sites of occlusive vascular disease?
Occlusive vascular disease of two types: thrombosis or embolism. Thrombosis: most due to atherosclerosis. Other sources: Arteritis (TB or syphilis in past; more common in immunosuppressed pts with Toxoplasmosis, Aspergillus and CMV infections), periarteritis nodosa, amyloid angiopathy Common sites: carotid arterial bifurcation, origin of middle meningeal artery, either end of basilar artery. Emboli: most from cardiac mural thrombi, atheromatous plaques of carotid arteries. Other sources: paradoxical emboli, cardiac surgery, fat emboli, atheromatous emboli, air emboli, bone marrow emboli. Most commonly affected structure: middle cerebral artery
What is the difference between the two types of brain infarcts?
Two types: hemorrhagic (emboli) or ischemic (thrombose). Hemorrhagic type: may be confluence of petechial hemorrhages, typical of emboli, due to reperfusion of damaged vessels and tissue. Ischemic type: usual result of thrombosis
What is the progression in morphology of ischemic infarcts and hemorrhagic infarcts?
First 6 hrs: nothing to be seen. By 48 hours: pale, soft, swollen tissue, poor corticomedullary demarcation. Two to 10 days: boundary between normal & abnormal tissue becomes distinct because edema lessens. 10 to 21 days: tissue liquefies, leaves fluid-filled cavity that enlarges as necrotic tissue is removed. Morphology of hemorrhagic infarcts: similar to ischemic infarcts with addition of extravasation and resorption of blood.
What would be seen in the microscopy of ischemic infarct?
After 12 hours: ischemic neurons (pyknotic nuclei and orange cytoplasm). Up to 48 hours: neutrophilic migration increases; phagocytic cells predominate later & filled with lipid, derived from myelin and blood breakdown. After several months: Network of glial fibers, derived from astrocytes, form glial network, mixed with new capillaries & perivascular fibrous tissue
Define and list causes of Intracranial Hemorrhage.
Intracerebral hemorrhage formed by ruptures of small parenchymal blood vessels. >50% assoc w/hypertension. Other causes include Charcot-Bouchard aneurysms, systemic coagulation disorders, open-heart surgery, amyloid angiopathy, vasculitis, vascular malformations
What are Charcot-Bouchard aneurysms?
Charcot-Bouchard aneurysms, in chronic hypertension, minute aneurysms, may rupture; aneurysms occur in vessels <300uM; usually in basal ganglia
For intracerebral hemorrhages, what is the origin in the brain? And also for ganglionic hemorrhage and lobar hemorrhage.
Morphology: may originate in putamen (50-60% of cases), thalamus, pons and cerebrum. Hypertensive hemorrhage classicaly seen in putamen and globus pallidus. Ganglionic hemorrhage: hemorrhage in basal ganglia. Lobar hemorrhage: in cerebral hemisphere
What are the most significant and other causes of Subarachnoid Hemorrhage?
Most significant cause: ruptured berry aneurysm. Other causes: Trauma, Hypertensive intracerebral hemorrhage, Vascular malformations, Hematologic disturbances, Tumors
What are examples of intracranial aneurysms?
Berry aneurysm, Atherosclerotic (mostly basilar artery), mycotic, traumatic, dissecting (commonly carotid a.)
What is a Berry aneurysm?
Berry aneurysm (congenital aneurysm: most common intracranial aneurysm)
What are the top 4 causes of cerebrovascular disorder?
Thrombosis, embolism, hypertensive encephalopathy, Berry aneurysm.
What is the epidemiology and pathogenesis of Berry aneurysms?
Found in 29% of autopsies. 90% in the anterior circulation of circle of Willis, near branching points. 10-20% of cases, multiple aneurysms. Pathogenesis: unknown. May be related to autosomal dominant polycystic kidneys, Ehler-Danlos syndrome, neurofibromatosis, coarctation of aorta, fibromuscular dysplasia of arteries
What are the Predisposing factors for Berry Aneurysm?
Hypertension related to rupture. Smoking is a factor. Described as “congenital” aneurysm: not identifiable at birth.
What are the Clinical features for Berry Aneurysm?
Rupture site: at apex of aneurysmal sac. 74% of pts with aneurysms, rupture found at autopsy. Age: 50yrs most common, predominantly females
What is the mortality related to first rupture of a Berry Aneurysm, and the presenting symptoms?
25-50% mortality, first rupture. Rebleeding common in survivors. No way to predict recurrence. Rupture related to increased intracranial pressure (straining at stool, sexual orgasm). Excruciating headache: usual presenting symptom (worst headache of life)
What are the four groups of Vascular Malformations?
Four groups: Arteriovenous malformation (AVM), cavernous angiomas, capillary teleangiectasis, venous angiomas
Describe epidemiology and common sites of AV Malformations?
Most common vascular malformation. More common in males. First episode of bleeding: between ages 10-20 years. Most common site: area supplied by middle meningeal artery. Large malformations: associated with heart failure in children
What is the most common site of Cavernous angiomas?
Cavernous angiomas: most common in cerebellum, pons, subcortical regions
What is the most common site of Capillary angiomas?
Capillary angiomas: most common in pons
What is the most common site of Venous angiomas?
Venous angiomas (varices): most common in pons
Describe the location and morphology of Lacunar Infarcts.
Lacunar infarct is a Hypertensive Cerebrovascular Disease: arteriolosclerosis with cavitary infracts, often multiple. Small spaces in lenticular nucleus, thalamus, internal capsule, deep white matter, pons. Morphology: small cavities containing fat-containing macrophages with adjacent gliosis
Describe Slit hemorrhages and Hypertensive encephalopathy.
Slit hemorrhages: small slit-like spaces; headache, artery shows fibrinoid necrosis. Hypertensive encephalopathy: acute syndrome with headache, etc.
Describe the chronic changes and autopsy findings.
Chronic changes: infarcts of gray matter (cortex, thalamus and basal ganglia) & white matter (centrum semiovale). At autopsy: heavy brains with petechiae & fibrinoid necrosis in walls of small arterioles in gray and white matter.
What are characteristic symptoms of Hypertensive Cerebrovascular Disease?
Characterized by: dementia, gait abnormalities & focal neurologic deficits.
What are the causes of vascular (multi-infarct) dementia?
Vascular (multi-infarct) dementia is caused by: Cerebral arterial atherosclerosis, Thrombosis or embolization from carotid arteries and heart, Cerebral arteriosclerosis, due to chronic hypertension

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