Cause lipid material to coat the small cerebral arteries within deep structures

Cause lipid material to coat the small cerebral

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Cause lipid material to coat the small cerebral arteries within deep structures of the brain. This process leads to a thickening of the arterial walls, decreased blood flow, and ultimately a stroke. Cryptogenic stroke – Stroke of unknown origin o Hemorrhagic Stroke Accounts for approximately 15% of all strokes in the United States. Intraparenchymal hemorrhage About 10% of strokes in the United States are intraparenchymal hemorrhage (bleeding into the brain substance), usually caused by uncontrolled hypertension. Another cause is cerebral amyloid angiopathy. This condition is the result of abnormal amyloid protein deposits in the cerebral blood vessels. As a result, the cerebral blood vessels become friable and
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therefore prone to spontaneous rupture, even in patients without hypertension. When blood vessel ruptures, the escaped blood forms a mass that displaces and compresses brain tissue. The severity of the symptoms is dependent on the location and amount of hemorrhage. If the hemorrhage is large enough, herniation may result. Ruptured cerebral aneurysm Localized dilation of the cerebral artery wall that causes the artery to weaken and become susceptible to rupture. Patients with cerebral aneurysms are asymptomatic before the rupture unless they experience a warning “leak” or sentinel bleeding. The aneurysm commonly ruptures into the subarachnoid space of the basal cisterns and causes a subarachnoid hemorrhage (SAH). Bleeding into the subarachnoid space causes increased ICP, impaired cerebral autoregulation, reduced CBF, and irritation of the meninges. Hydrocephalus can occur after SAH through two mechanisms. Seizures occurring within the first 12 hours after rupture are attributed to increased ICP or rebleeding of the aneurysm. Central vasospasm is a narrowing of arteries adjacent to the aneurysm that results in ischemia and infaraction of brain tissues if it progresses. It is the leading cause of death after aneurismal SAH Arteriovenous malformation Congenital abnormality forming an abnormal communication between arterial and venous systems in the brain. Arterial blood is shunted into the venous system without a capillary network. This predisposes the vessels to rupture into the ventricular system or subarachnoid space, causing SAH, or into the brain parenchyma, causing intracranial hemorrhage ICH. o Interventions o Hemorrhagic Stroke Interventions ( ask professor if there’s more detail needed than what I have down here) Control of BP is important to prevent recurrent hemorrhage. MAP less than 130 mmHg is an important goal to help prevent continued bleeding. Glycemic management Diagnostic exams: CT Evaluation, Laboratory tests Medications: IV antihypertensives, and manage ICP with osmotic diuretics o Ischemic Stroke Interventions ( ask professor if there’s more detail needed than what I have down here) Goal: BP less than 220 mmHg, diastolic less than 120 mmHg Glycemic management
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