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Disorders of CNS
patho exam 3
| Question | Answer |
|---|---|
| major components of central nervous system | brain and spinal cord |
| central nervous system | detect, transmit, analyze sensory information, generate signals to autonomic and motor pathways |
| what do the signals to autonomic and motor pathways generate by the CNS do? | orchestrate visceral and endocrine functions, coordination, and movement |
| what do the tissues of CNS rely heavily on? | receiving constant perfusion |
| why do the tissues of the CNS rely heavily on receiving constant perfusion? | cerebral auto regulation, blood-brain barrier |
| major disorders of the CNS | transient ischemic attack, stroke, subdural and spinal cord hemorrhage |
| what do disorders of circulation within brain revolve around? | lack of oxygen and increased pressure within skull |
| ischemia | obstructed blood vessels, drop in blood flow to brain |
| increased pressure within skull | hematoma, excessive production of cerebral spinal fluid, blockage of duct system conveying cerebral spinal fluid |
| vascular supply of brain | 2.5% of total body mass; receives 15% of cardiac output |
| vascular supply of white matter in brain | 60% of brain mass; uses 6% of cerebral oxygen |
| vascular supply of gray matter in brain | 84% of cerebral oxygen |
| maintenance of cerebral circulation | right and left carotid arteries, right and left vertebral arteries |
| arterial circulation of the CNS | anterior cerebral arteries, basilar artery, middle cerebral arteries, internal carotid arteries, vertebral arteries, common carotid arteries |
| circle of willis | anterior cerebral artery, anterior communicating arteries, posterior communicating artery, posterior cerebral artery, internal carotid artery |
| cerebral sinuses | drain blood from brain to systemic circulation, absorb CSF |
| what are the cerebral sinuses? | superior sagittal sinus, inferior sagittal sinus, straight sinus, vein of galen, confluence of sinuses, transverse sinus, sigmoid sinus, internal jugular vein |
| where is CSF produced? | in choroid plexi of ventricles |
| where does CSF flow through? | ventricular system of brain, through subarachnoid space surrounding brain and spinal cord |
| where is CSF resorbed? | into venous dural sinuses via arachnoid villi |
| hydrocephalus | blockage of flow of CSF through ventricles of brain or when can't be resorbed by arachnoid villi |
| blood-brain barrier | specialized endothelium present in brain capillaries |
| what does the blood-brain barrier do? | permits selective entry of substances |
| how does the blood brain barrier permit selective entry of substances? | tight junctions between endothelial cells, few pinocytotic vesicles, no fenestra, active transport |
| substances that cross blood-brain barrier | highly lipophilic substances cross directly, most nutrients cross barrier by facilitated diffusion |
| regions of brain lacking blood-brain barrier | subfornical organ and area postrema of brainstem, infundibulum of hypothalamus and pituitary gland |
| cerebral autoregulation | mechanisms that maintains steady flow of blood to brain and spinal cord |
| what do arteries respond to in cerebral blood flow? | pH, carbon dioxide, oxygen |
| increased blood pressure= | constricted cerebral capillaries |
| what do constricted cerebral capillaries do? | increase resistance so less blood to brain |
| decreased blood pressure= | dilated capillaries |
| decreased PaCO2 levels= | constricted cerebral vessels |
| increased PaCO2 levels rise= | dilated vessels |
| what is cerebral blood flow closely matched to? | metabolic needs |
| what happens when cerebral auto regulatory mechanisms fail? | loss of match between oxygen supply and demand of tissues |
| intracranial pressure | pressure exerted by contents of cranium |
| monro-kellie hypothesis | compensatory relationship maintaining cerebral compliance in response to changes in volume |
| injured brain tissue | cytotoxic edema, vasogenic edema, clearance of brain tissue swelling |
| vasogenic edema | when blood brain barrier breaks and fluid leaks into extracellular space |
| hydrocephalus | excessive accumulation of CSF in cranial vault, compresses surrounding structures |
| hydrocephalus causes | lesions that obstruct flow of CSF, problems with resorption |
| what percent of the body's oxygen consumption does the brain use? | 20% |
| cerebral blood flow | autoregulation, blood viscosity, cerebral vascular resistance, cerebral perfusion pressure |
| cbf= | cpp/cvr |
| concurrent ischemia and hypoxia | mitochondrial dysfunction, energy deprivation and loss of ion homeostasis, cerebral hemorrhage in sepsis |
| concurrent ischemia and hypoxia: mitochondrial dysfunction | leads to infarction and tissue death, anaerobic and glycolytic pathways initiated |
| concurrent ischemia and hypoxia: energy deprivation and loss of ion homeostasis | cells unable to maintain negative membrane potentional, excitatory amino acids in extracellular space, glutamate and influx of calcium ions, apoptosis |
| concurrent ischemia and hypoxia: cerebral hemorrhage in sepsis | immune cells activated, leukocytes enter the brain, inflammatory agents contribute to brain inflammation, nitric oxide/ nitric oxide synthetase pathway, mitochondrial dysfunction and apoptosis |
| transient ischemic attack | temporary episode of neurologic dysfunction, partial blockage of any vasculature that takes blood to the brain |
| first sign of stroke | transient ischemic attack |
| what is a transient ischemic attack caused by? | focal brain, spinal cord, or retinal ischemia without acute infarction |
| transient ischemic attack etiology and pathogenesis | same as ischemic stroke, clot blocking blood supply to region of brain, atherosclerosis |
| nonmodifiable risk factors of transient ischemic attack | age, family history, prior tia or stroke, race (african american), sex, sickle cell disease |
| modifiable risk factors of transient ischemic attack | cardiovascular disease, carotid artery disease, diabetes, excess weight, high blood pressure, high cholesterol, cigarette smoking, heavy drinking, physical inactivity, poor nutrition, use of birth control pills |
| transient ischemic attack clinical manifestations | facial drooping, arm or leg weakness on one side of body, speech difficulty, sudden trouble seeing in one or both eyes, difficulty walking with dizziness, lack of balance or coordination, severe headache |
| transient ischemic attack diagnosis and treatment | exclusion of conditions that mimic TIA, blood glucose and other blood tests, electrocardiography, noncontrast CT, MRI with diffusion-weighted imaging, CT angiography or magnetic resonance angiography, carotid doppler |
| stroke | interruption in blood supply to region of brain or bleeding of vessel resulting in brain tissue damage or infarction |
| types of strokes | ischemic, hemorrhagic |
| what percent of strokes are ischemic | 87% |
| what percent of strokes are hemorrhagic | 13% |
| etiology and pathogenesis of ischemic stroke | partial or complete occlusion of cerebral blood flow due to thrombus or embolus; atherosclerosis, cardiac disorders, thrombotic strokes |
| thrombotic strokes | internal carotid artery, middle cerebral artery, basilar artery |
| etiology and pathogenesis: hemorrhagic stroke | bleeding into brain from blood vessel (intracerebral, intraventricular, extracerebral), subarachnoid hemorrhage, cerebral aneurysm, arteriovenous malformation |
| ischemic and hemorrhagic stroke clinical manifestations | sudden onset of focal neurologic deficit persisting for at least 24 hours due to reduction or occlusion of cerebral circulation or rupture of blood vessels |
| what do other signs and symptoms of ischemic and hemorrhagic strokes depend on? | area of the brain or spinal cord affected |
| treatment of ischemic stroke | restoration of blood flow and reducing area of infarction, supplemental oxygen, glycemic control, fibrinolytic therapy, antihypertensive therapy, aspiring 325mg, hypothermia |
| penumbra | tissue surrounding infarction |
| treatment of hemorrhagic stroke | osmotic diuretics, surgical evacuation, craniotomy with aneurysm clipping, endovascular therapy with coil embolization, delayed cerebral ischemia |
| subdural hematoma | bleeding from bridging veins between dura mater and arachnoid membrane |
| subdural hematoma etiology and pathogenesis | trauma from high speed impact to skull, spontaneous |
| acute subdural hematoma | bleeding identified immediately after an injury |
| chronic subdural hematoma | brain atrophy |
| subdural hematoma clinical manifestations | headache, confusion, changes in behavior, dizziness, nausea, vomiting, lethargy or excessive drowsiness, weakness, apathy, seizures |
| subdural hematome treatment | surgery |
| hemorrhage of spinal cord | rare |
| spinal cord hemorrhage etiology and pathogenesis | trauma, vascular malformation, bleeding disorders, epidural, subdural, or intramedullary |
| intramedullary hemorrhae | hematomyelia |
| spinal cord hemorrhage clinical manifestations | sudden, severe back pain with or without radiculopathy, headache, neck stiffness, photosensitivity, irreversible sensory loss below level of bleed |
| spinal subdural hemorrhage treatment | surgical decompression |
| spinal subarachnoid hemorrhage treatment | surgical resection, catheter-based interventional techniques, focal radiation therapy with gamma knife, cold photon knife |
Created by:
camrynfoster