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NURS 350 patho neur3

neruo alterations part 2

QuestionAnswer
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