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Lecture 15

Cerebrovascular Pathology

QuestionAnswer
Acute loss of neurologic function, lasting greater than 24 hours. Stroke
Two types of storkes (1)Ischemic/hypoxia (2)Hemorrhagic
Etiology of ischemic strokes (1)Atherosclerosis/thrombosis (2)Embolism (3)Hypertension (4)Vasculitis
Abrupt loss of neurologic function lasting less than 24 hours. Symptoms are typically visual or focal motor dysfunction. Transient ischemic attack (TIA)
(T or F) Ischemic/infarction strokes are much more common than hemorrhagic strokes. True. Ischemic/infarction strokes are 7x more common than hemorrhagic strokes.
Risk factors for ischemic/occlusive cerebrovascular disease (1)Hypertension (2)Smoking (3)Diabetes (4)Atherosclerotic heart disease (5)Atrial fibrillation (6)Vasculitis
What percentage of cardiac output is used by the brain? The brain is only 2% of total body mass, but consumes 20% of cardiac output.
How long does cerebral function continue after prolonged ischemia? 10 seconds. The brain requires constant blood supply for oxygen and glucose.
(T or F) Irreversible CNS damage occurs after 30 minutes of ischemia. False. Irreversible damage occurs after 6-8 minutes of ischemia.
(T or F) Global ischemia is almost always due to hypotensive episodes True. Watershed areas are most sensitive to hypotensive events. The area of infarction is usally bilateral.
What is the leading cause of thrombosis-associated CNS infarction? Majority are due to atherosclerosis of carotid system.
What is the leading cause of emboli to the brain? Cardiac (mural or valvular thrombi)
Common sources of emboli to the brain (1) heart (2) carotids
(T or F) Emboli to the brain causes non-hemorrhagic infarction. False. Emboli cause infarction with secondary hemorrhage, presumed secondary to reperfusion through damaged vessels distal to embolus.
Most common causes of thromotic CNS disease (1) Atherosclerotic vascular disease (2) Endothelial damage
Lines of Zahn On microscopic examination, lines of Zahn are the alternating pale pink bands of platelets with fibrin and red bands of RBC's forming a true thrombus.
Sites of cerebral venous thromboses (1)Superior saggital sinus (2)Lateral sinuses (3)Straight sinus
Etiologies of cerebral venous thromboses (1)Infection (2)Hypercoagulable states (3)Stagnation of blood flow
(T or F) Glial cells are more sensitive to ischemic injury than neurons. False. Order of sensitivity to ischemic injury: neurons>glia>vascular cells
A rare non-inflammatory hereditary cause of strokes. It is characterized by thickened penetrating arteries due to deposition of granular substance in intimal smooth muscle basal lamina. CADASIL (Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)
A rare cause of strokes most commonly found in children<15 with a characteristic "puff of smoke" appearance on radiographic imaging. Moyamoya disease
Lacunar infarcts Infarcts of small arteries and arterioles affecting especially deep perforating arteries of deep white matter, basal ganglia, thalami, and pons. This is caused by long-standing hypertension.
Molecular mechanism of neuronal death due to excitoxicity Ischemia results in depolarization of the neuron. The neuron releases excessive glutamate. The glutamate binds to postsynaptic NMDA and AMPA-type receptor causing an influx of soduium and calcium ions, resulting in activation of proteases and apoptosis.
Molecular mechanisms of ischemic brain injury (1)Excitotoxicity (2)Oxidative stress (3)Nitric oxide (4)Acidosis (5)Inflammation
Acute protective responses aganist cerebral ischemia/hypoxia (1)NO-mediated vasodilation (2)Activation of GABAergic interneurons (3)Depletion of extracellular Na+ and Ca++ (4)Activation of anti-apoptotic signaling pathways
A protective response of the brain aganist ischemia/hypoxia where brief sublethal ischemic insults render resistance to more severe ischemic insults. Ischemic tolerance of the brain
Treatment for acute ischemic strokes Thrombolytic therapy
How does subarachnoid blood cause secondary ischemic injury? Subarachnoid blood causes secondary arterial vasospasm, leading to secondary ischemic injury.
Charcot-Bouchard Aneurysms Small aneurysms of that occur in small vessels of the cerebral vasculature that are prone to bleeding. Typically associated with long-standing hypertension.
A cause of intraparenchymal cerebral hemorrhage due to the deposition of beta-4 amyloid in the walls of small vessels. Amyloid anigopathy
Most common cause of subarachnoid hemorrhage Rupture of berry (saccular) aneurysm
(T or F) The annual risk of subarachnoid hemorrhage in a person with a cerebral aneurysm is about 50%. False. The risk is 0.05%/yr for aneurysms that are less than 1/2 inch and if no other aneurysm has bleed. The risk is 0.5%/yr for aneurysms larger than 1/2 inch or if another aneurysm has bleed and has been repaired.
Congenital malformations consisting of tortuous tangle of vessels in the brain with histologic features of both arteries and veins with intervening gliotic brain Arteriovenous malformations
Mass of greatly distended vessels with thin walls in the brain and no intervening brain tissue. Cavernous angiomas
Common locations of cavernous angiomas (1)Cerebellum (2)Pons (3)Deep white matter
Typical presentation of arteriovenous malformations (1)Seizures (2)Cerebral hemorrhage
What protein is mutated in cerebral amyloid angiopathy, hemorrhagic stroke? Mutations in amyloid precursor protein (APP)
Gene mutated in CADASIL Mutations in NOTCH 3, resulting in cerebral vessels showing fibrosis and media replaced by eosinophilic granular material
Mutation associated with MELAS(Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) Mitochondrial tRNA mutation
Mutation associated with cerebral cavernous malformation Mutation of KRIT1 gene on chromosome 7
Created by: UVAPATH2
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