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 deathâ€, 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