Cerebrovascular Pathology
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| Acute loss of neurologic function, lasting greater than 24 hours. | Stroke
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| Two types of storkes | (1)Ischemic/hypoxia (2)Hemorrhagic
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| Etiology of ischemic strokes | (1)Atherosclerosis/thrombosis (2)Embolism (3)Hypertension (4)Vasculitis
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| Abrupt loss of neurologic function lasting less than 24 hours. Symptoms are typically visual or focal motor dysfunction. | Transient ischemic attack (TIA)
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| (T or F) Ischemic/infarction strokes are much more common than hemorrhagic strokes. | True. Ischemic/infarction strokes are 7x more common than hemorrhagic strokes.
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| Risk factors for ischemic/occlusive cerebrovascular disease | (1)Hypertension (2)Smoking (3)Diabetes (4)Atherosclerotic heart disease (5)Atrial fibrillation (6)Vasculitis
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| 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.
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| How long does cerebral function continue after prolonged ischemia? | 10 seconds. The brain requires constant blood supply for oxygen and glucose.
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| (T or F) Irreversible CNS damage occurs after 30 minutes of ischemia. | False. Irreversible damage occurs after 6-8 minutes of ischemia.
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| (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.
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| What is the leading cause of thrombosis-associated CNS infarction? | Majority are due to atherosclerosis of carotid system.
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| What is the leading cause of emboli to the brain? | Cardiac (mural or valvular thrombi)
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| Common sources of emboli to the brain | (1) heart (2) carotids
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| (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.
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| Most common causes of thromotic CNS disease | (1) Atherosclerotic vascular disease (2) Endothelial damage
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| 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.
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| Sites of cerebral venous thromboses | (1)Superior saggital sinus (2)Lateral sinuses (3)Straight sinus
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| Etiologies of cerebral venous thromboses | (1)Infection (2)Hypercoagulable states (3)Stagnation of blood flow
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| (T or F) Glial cells are more sensitive to ischemic injury than neurons. | False. Order of sensitivity to ischemic injury: neurons>glia>vascular cells
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| 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)
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| A rare cause of strokes most commonly found in children<15 with a characteristic "puff of smoke" appearance on radiographic imaging. | Moyamoya disease
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| 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.
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| 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.
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| Molecular mechanisms of ischemic brain injury | (1)Excitotoxicity (2)Oxidative stress (3)Nitric oxide (4)Acidosis (5)Inflammation
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| 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
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| 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
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| Treatment for acute ischemic strokes | Thrombolytic therapy
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| How does subarachnoid blood cause secondary ischemic injury? | Subarachnoid blood causes secondary arterial vasospasm, leading to secondary ischemic injury.
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| 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.
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| A cause of intraparenchymal cerebral hemorrhage due to the deposition of beta-4 amyloid in the walls of small vessels. | Amyloid anigopathy
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| Most common cause of subarachnoid hemorrhage | Rupture of berry (saccular) aneurysm
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| (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.
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| 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
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| Mass of greatly distended vessels with thin walls in the brain and no intervening brain tissue. | Cavernous angiomas
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| Common locations of cavernous angiomas | (1)Cerebellum (2)Pons (3)Deep white matter
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| Typical presentation of arteriovenous malformations | (1)Seizures (2)Cerebral hemorrhage
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| What protein is mutated in cerebral amyloid angiopathy, hemorrhagic stroke? | Mutations in amyloid precursor protein (APP)
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| Gene mutated in CADASIL | Mutations in NOTCH 3, resulting in cerebral vessels showing fibrosis and media replaced by eosinophilic granular material
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| Mutation associated with MELAS(Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) | Mitochondrial tRNA mutation
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| Mutation associated with cerebral cavernous malformation | Mutation of KRIT1 gene on chromosome 7
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