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NURS 2200 FINAL EXAM 2025-2026|QUESTIONS AND CORRECT ANSWERS|A+ GRADED
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Parkinson's disease degenerative disorder of basal ganglia Parkinson's disease theoretical causes environment/injury, genetics, oxidative stress Parkinson's disease patho damage to basal ganglia, degeneration of neurons > decreased dopamine Parkinson's disease s/s TRAP (tremor, rigidity, akinesia/bradykinesia, postural/balance changes) multiple sclerosis
autoimmune demyelinating disease of CNS multiple sclerosis risk factors women, caucasian, colder climate multiple sclerosis s/s visual changes, numbness, paresthesia, pain, altered temp, foot drag, diplopia, ataxia, vertigo, fatigue, sexual dysfunction multiple sclerosis patio damage myelin sheath/oligodendrocytes, sclerosis of inflammatory lesions, axonal degeneration > permanent disability myasthenia gravis problem at neuromuscular junction myasthenia gravis patho
weakness/paralysis, spasticity, dysarthria/dysphagia, dyspnea/respiratory failure Gillian barre autoimmune destruction myelin sheath of peripheral nerves (includes cranial) Gillian barre trigger viral/bacterial infection; vaccination Gillian barre s/s ascending motor weakness/paralysis, areflexia SCI risk factors males aged 15- SCI causes
MCV, falls, sports, gunshot wounds concussion temporary loss of function contusion bruising hemorrhage bleeding into/around cord laceration tear mechanism of vertebral injury fracture/dislocation > compression, tearing, transection of spinal cord
neurogenic shock patho loss of brainstem and SNS control below level of injury > vasodilation neurogenic shock s/s hypotension, bradycardia, hypothermia C3 SCI vent dependent T1-12 SCI full arms/hands control; paraplegic S1/S5 SCI full leg movement; may have impaired bowel, bladder and sexual function
autonomic dysreflexia locations injuries at or above T autonomic dysreflexia definiton loss of SNS control below injury autonomic dysreflexia sudden onset BP, HA, bradycardia, sweating, lower vasoconstriction Back pain causes degenerative disc disease, spinal stenosis, fracture, herniated disc herniated disc causes trauma, degenerative disc disease herniated disc risk factors smoking, repetitive lifting
normal ICP 5 to 15 mmHg ICP causes tumor, increased CSF, intracranial hemorrhage, cerebral edema, infection monroe-kelli doctrine components brain, blood, css monroe-kelli doctrine compensatory mechanism (csf) displacement CSF and decreased production monroe-kelli doctrine compensatory mechanism (venous) compression of venous system
monroe-kelli doctrine compensatory mechanism (brain) vasoconstriction of blood vessels in brain monroe-kelli doctrine failure of compensatory mechanisms leads to ICP consequences of increased ICP decreased cerebral perfusion; ischemia and brain damage early s/s of ICP decreased LOC, sluggish pupils, ipsilateral pupil dilation, motor weakness, HA, diplopia, blurred vision late s/s of ICP severe HA, changes in VS (cushings triad), loss brain stem reflexes, pupils fixed and dilated, posturing flexor
subdural hematoma venous, slower deterioration epidural hematoma arterial bleed, loss of consciousness; may have lucid period, rapid deterioration diffuse TBI concussion, DAI concussion s/s temp LOC, neuro dysfunction, memory loss post concussion syndrome HA, cognitive impairment, psychological complains chronic traumatic encephalopathy
d/t repeated mild head injuries DAI shearing d/t rotational forces (injury/tearing of axons) glutamate TBI excitatory neurotransmitter, calcium influx calcium influx triggers release of cellular enzymes, breakdown cellular proteins/lipids, cell injury/death (can trigger apoptosis) TBI s/s change LOC, loss of reflexes, HA, N/V, focal injury (deficits change with LOC) CVD and stroke risk factors
lack of blood flow > ischemic cascade > amp pumps fail > release neurotransmitters > calcium builds up > activate cellular enzymes > breakdown of cell membrane/cell destruction hemorrhagic stroke cause HTN, AVM, aneurysm, trauma hemorrhagic stroke patho bleeding from vessel > expanding mass/hematoma > compression of brain tissue > ischemia > cerebral edema > increased ICP stroke s/s (motor/sensory) hemiparesis, flaccidity, spasticity, contractures, visual impairments stroke s/s (speech) expressive aphasia, receptive aphasia
stroke s/s (cognitive) memory, concentration, personality hydrocephalus abnormal increase in CSF d/t blockage or decreased reabsorption > enlargement ventricles and increased ICP hydrocephalus types noncommunicating, communicating, normopressure noncommunicating hydrocephalus obstructive; congenital, tumor communicating hydrocephalus absorption problem; SAH, meningitis normopressure hydrocephalus
LOC, seizures, HA, N/V, focal sx meningitis infection/inflammation of meninges me meningitis causes head trauma, sinusitis, otitis media, systemic infection, VP shunt meningitis patho pathogen enters through choroid plexus/blood vessels > exudate, can cause hydrocephalus meningitis s/s HA, fever, n/v, photophobia, stiff neck, brudzinski sign encephalitis acute febrile illness, usually viral
encephalitis patho organism enters brain tissue through blood or peripheral nerves > widespread damage/nerve cell degeneration > necrosis > cerebral edema and ICP encephalitis s/s fever, HA, paresis; focal paralysis; confusion, seizures encephalopathy altered brain function encephalopathy causes renal failure (uremia), liver failure, HIV, toxins, hypoxia, critical illness, trauma encephalopathy s/s
