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NURS 350 patho neur3
neruo alterations part 2
| Question | Answer |
|---|---|
| those at risk for head injury | young (learning to walk), adolescents (more daring), elderly (falls), high crime areas |
| two types of head injury | blunt/closed trauma-----open/penetrating trauma |
| which type of head injury category most common | blunt/closed trauma more common |
| blunt/closed trauma MOA | hard object hits head --> dura in tact, brain not exposed --> focal AND diffuse axonal injuries |
| open/penetrating trauma MOA | trauma --> break in dura, exposure of cranium --> FOCAL injury |
| clinical manifestations of head injury | Battle's sign (ecchymosis of mastoid process), raccoon eyes, CSF rhinorrhea, cranial nerve palsy, bleeding from nose, ears |
| What is the most common type of traumatic head injury? | concussion - which is cause by BLUNT trauma exceeding CSFs ability to protect brain |
| mild concussion | temporary axonal disturbance WIHOUT LOC. no physical damage seen on scan, only microscopic |
| cerebral contusion | traumatic injury --> bvessels leak into brain tissue (bruising). may involve intracerebral hemorrhage. monitor ICP/herniation |
| coup injury | injury at site of impact --> shearing of subdural veins --> trauma to skull base |
| contrecoup injury | injury OPPOSITE SIDE of impact--> shearing forces THROUGH brain |
| coup and contrecoup occur as continuous motion | head strikes fixed object (coup) and rebounds (contrecoup) |
| intracerebral hemorrhage | bleeding within brain itself bwo trauma, fall or hemorrhagic stroke |
| compound fractures occur when | all layers protecting brain have been breached. risk of infection most serious complication |
| Damage to the body after sustaining head injury occurs by 3 mechanisms | primary, secondary and tertiary mechanisms |
| What is primary head injury damage | caused by impact involving neronal/glial injury with vascular response |
| What is secondary head injury damage MOA | injury resulting from reduced circulation/brainshift. can manifest as cerebral edema, hemorraghe, infection, high ICP |
| What is tertiary head injury damage MOA | pt didn't get to hospital in time. NOw has increased ICP. Decreased BP and cerebral perfusion. |
| What causes tertiary head injury | apnea, hypoTN, lung/cardiac problems |
| what clinical intervention may be used in minimize impact of secondary/tertiary injury | brain cooling may be used |
| What are two categories of traumatic brain injury | focal and diffuse are two categories of BRAIN injury |
| Which type of traumatic BRAIN injury accounts for 2/3 of all head injury DEATHS | focal injury most frequent cause of deaths |
| MOA focal brain injury | compression of skull at point of impact and rebound effect. may be coupe/contrecoup. grossly observable brain lesions. |
| In focal brain injury, what are 3 grossly observable brain lesions | cortical contusion (bleeding from small vessels) ---- epidural hemorrhage ----subdural hematoma |
| in focal injury monitor for | brain edema --> high ICP. Bleeding/edema account for maximum effects of injury and peak 18-36 hours after injury |
| With focal injury, there are contused areas, which could lead to | contused areas could lead to infarction/necrosis, multiple hemorrhages and edema |
| ONCE AGAIN, name 3 types of focal injury | 1- epidural hematoma or epidermal hemorrhage 2- subdural hematoma 3 - intracerebral hematoma |
| Focal-epidural hematoma MOA | often ARTERIAL blood (middle meningeal artery). minimal hypoxia/ischemia. |
| Pt signs for focal-epidural hematoma | pt has LOC in field ----wakes up --- an hour later LOC again. pt generally does well as there is limited hypoxia/ischemia. |
| Focal - subdural hematoma | VENOUS bleed --> increased ICP. These bleeds often slow allowing body to compensate asymptomatic until bleed is significant. |
| cerebral hemorrhage MOA | when vessel breaks within brain (subdural or intracerebral) --> cerebral edema. Again, bleeding peaks within 18-36 hours, maybe aslong as 72 hours. If blood sits 2-3 days, can suction out liquefactive necrosis |
| Diffuse (axonal) brain injuries in general | in general are widespread damage to white matter |
| Major causes diffuse axonal brain injuries | most common in acceleration/deceleartion injury then physical trauma. |
| Other causes of diffuse axonal brain injury | hypoxia, meningitis, damaged blood vessels also contribute |
| MOA of diffuse brain injury | injury to axons bwo shearing, tearing, stretching, shaking --> distortions of brain |
| diffuse-axonal injury - shaken baby syndrome | brain moving so fast axon shearing --> grey/white mixes together --> petichial hemorrhage throughout |
| general characteristics of CVA cerebrovascular disorder | pathological process of brain vessels. most common clinical manifestation |
| what is 4th leading cause of death in US leading to 50% of all neurological admissions | CVA is this statistic |
| Is it easier/harder to prevent secondary injury in CVAs | easier to prevent secondary injury in this class |
| definition of CVA | sudden, non-convulsive FOCAL neurological deficit |
| 3 classes of CVAs | 1-throbogenic 2-embolic/ischemic 3-hemorrhagic |
| 3 sub-classes of thrombogenic CVAs | 1-TIAs 2-stroke-in-evolution 3-completed stroke |
| CVA - thrombogenic stroke MOA | thrombi (atherosclerotic, inflamm arterial wall) -->arterial occlusion |
| what causes CVA-thrombogenic stroke | caused by increased coag, inadequate cerebral perfusion factors |
| CVA - embolic/ischemic stroke MOA | thrombus --> emboli --> travels to brain and obstructs bifurcation or small artery. most common in middle cerebral arter. can also be emboli of air, fat, tumors. |
| CVAs in general - range of outcomes | ranges from minimal damage/unnoticed - to severe with hemiplegia, coma or death. |
| CVA -hemorrhagic stroke MOA | blleding may displace/compress adjacent brain tissue, seep into ventricles. Caused by HTN, ruptured aneurysms, AV malformations |
| thrombogenic - TIA MOA | intermittent blockage by spasm or thrombi. preceeds 35% of strokes. NEURO DEFICITS CLEAR WITHIN 24 HOURS. NO RESIDUAL DEFICIT |
| thrombogenic - stroke in evolution | intermittent progression over minutes-hours-days. characteristic of thrombotic/slow hemorrhage stroke |
| thrombogenic - completed strokes | CVAs that reach max destructiveness and produce neuro deficit |
| what do we mean by 'time is brain' | best time to treat CVAs is within 6 hours (antithrombotics and metabolic protection therapy) |
| cerebral infarction defn | stroke due to disturbance in blood vessels supplying blood to brain - CAN BE ISCHEMIC OR HEMORRHAGIC |
| cerebral hemorrhage | primary cause is HTN --> walls of arterioles thicken. MICROANEYURSMS form and bleed --> ischemia/edema |
| intracranial aneurysms result from | vascular wall defects allow thinning/balooning of wall --> bleeding/rupture |
| AV malformations | AV = arteriovenous malformatons that are tangled masses of dilated vessels. may be congenital |
| what is the worst kind of stroke | subarachnoid hemorrhage, which is caused (95%) by cerebral aneurysms --> 50% mortality |
| what is MOA of subarachnoid hemorrhage stroke | blood blocks arachnoid villi granulations --> CSF circulation impaired -->hydrocephalus/ICP increases |
| clinical manifestation of subarachnoid hemorrhage stroke | ICP rises about 10 minute --> cerebral blood flow/perfusion reduced --> expanding hematoma that displaces brain |
| what are the early manifestations of cerebral hemorrhage | HA/altered mental motor weakness numbing/tingling |
| Alzheimer's definition | severe cognitive dysfunction in elderly. TOO LITTLE ACh |
| Alzheimer's causes | caused by early/late onsent (genetic) or idiopathic late onset |
| Alzheimer's theories | loss of ACh function, amyloid proteins, apopliprotein E binds Beta amyloid protein, activation of NMDA receptors with XS Ca++ influx, prions/autoimmune |
| Parkinson's Disease | disease of basal ganglia --> too little dopa, too much ACA -->tremor/rigidity. |
| Huntington's Disease | hereditary involving basal ganglia/cerebral cortex. Depletion of GABA --> fragmented movement |
| Multiple sclerosis | immunogenic-viral --> demyelination CNS --> hypersensitivitiy reactions. steroids shorten exacerbation. immunosuppresion may slow progression. |
| ALS = amyotrophic lateral sclerosis | genetic/SOD degeneration of upper/lower neurons --> flaccid paralysis. GLUTAMATE TOXICITY thought to cause neruon degeneration |
| myasthenia gravis | autoimmune prevents ACh binding ACh receptor at nm junction |
| myasthenia gravis | undermedicated, no ACh at nm junction --> respiratory crisis, quadriparesis or quadriplegia |
| cholinergic crisis | results from anticholinesterase toxicity |
Created by:
lorrelaws
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