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Patho Exam Pt. 3 - Neuro

Terms in this set (75)

what are CVA's caused by
thrombus, embolism, hemorrhage
thrombus
atherosclerosis or intracranial vessels, plaque causes blockage of blood flow- associated with HTN, smoking, DM
embolism
a thrombus which originates outside the brain and flows to brain - oral contraceptives, embolus after surgery, endocarditis
hemorrhage
rupture of cerebral vessel due to HTN, aneurysm, trauma
how quickly does cell change occur with a CVA
cell changes begins 4-5 minutes after decreased blood flow and O2. Permanent damage within 10 minutes
what is the trigger for an infarction
tissue injury (blood vessels swell, circulation is decreased, vasospasm results in the infarction)
what is the result of a CVA in one hemisphere
causes S&S on the opposite side of the body
what is the result of a CVA that damages cranial nerves
affects the same side of the body in which the infarction occurs
TIAs
"warning stroke" lasts from seconds to hours (clear within 24 hours), a sign for developing a CVA
CVA symptoms
weakness in lower face, arms, hands, fingers, legs, numbness and tingling of face, double vision, slurred speech
anterior cerebral artery
personality - confusion, weakness, numbness of affected side, paralysis of opposite side, incontinence, personality changes (flat, distractibility)
middle cerebral artery
speech - aphasia (can't speak), dysphasia (trouble speaking and swallowing), dyslexia, dysgraphia (can't write), hemiparesis on affected side
posterior cerebral artery
vision - visual field cuts, sensory impairment, dyslexia, coma, blindness
basilar artery
balance - dizziness, weakness on affected side, visual deficits, poor coordination, dysphagia, amnesia, ataxia (unsteady gait)
internal carotid artery
HA, weakness, paralysis, numbness, altered visual disturbances (blurring on affected side), altered LOC, bruits (murmur) over carotid artery, aphasia, dysphagia, ptosis (drooping eye lid)
diagnosis of CVA
cerebral angiography (detailed disruption of circulation), MRI, PET, Lumbar puncture (blood WBC)
best test for examining the entire cerebral artery
cerebral angiography
how quickly should you give thrombolytic therapy after a CVA
within the first 3 hours of stroke to restore circulation to affected brain tissue and limit brain injury
which should you use to decrease cerebral edema in a CVA
corticosteroids (dexamethasone)
what should you give to decrease the risk of a further stroke
anticoagulants (Heparin)
what does the brain need more of during a seizure?
the brains demand for O2 increases, hypoxia leads to brain damage
what can cause a seizure to stop?
inhibitory substances
secondary seizure disorder causes
birth trauma (anoxia), infectious disease (meningitis, encephalitis), ingestion of toxins (mercury, lead), brain tumors, head injury, metabolic disorders (hypo/hyperglycemia), CVA
simple partial seizure
lasts a few seconds, no alterations in consciousness, jacksonian march (motor involvement), flashing lights, smells, hearing hallucinations, sweating, pupil dilation
complex partial seizure
lasts for 1-3 minutes, amnesia occurs during and after, during seizure pt. can follow simple commands
absence seizure
lasts 1-10 seconds, seen in children, brief changes in LOC, blank stare, pt. maintains posture, can occur up to 100x/day
myoclonic seizures
single jerk of one or more muscle groups, involuntary jerks lasts a few seconds, consciousness is not lost
generalized tonic- clonic seizures
lasts 2-5 minutes, loud cry, body stiffens (tonic phase), then body relaxes (clonic phase), tongue biting, incontinence, labored breathing, apnea, cyanosis. After - confused, difficulty talking, may fall into deep sleep
atonic seizure
"drop attack" lost of postural tone, loss of consciousness, seen in young children
status epilepticus
most life treating, continuous tonic- clonic seizure, respiratory distress with hypoxia (trigger and result), results form withdrawal of anti seizure meds, head trauma, metabolic disorders (acidosis), septicemia, encephalitis
what chemical imbalances can an epileptic patient have?
hypoglycemia (give them dextrose), electrolyte imbalances
drug therapy for epilepsy
Dilantin (phenytoin), phenobarbital, gabapentin (neuron tin)
status epilepticus treatment
IV diazepam (valium), phenytoin (Dilantin), phenobarbital
what is the inflammatory reaction of spinal chord injuries
phagocytes and macrophages come within 48 hours of injury
C1-C3
no control of head, neck, diaphragm, dependent care, respirator, no bladder or bowel control, wheelchair
C4
sensation in head, neck, and some control of head and neck, diaphragm movement, dependent care
C6
use of shoulder, extension of wrists, dependent care - can transfer themselves to wheelchair
C7-C8
extends elbows, flexes wrists, use of some fingers, dependent care, manual wheelchair
T1-T5
paraplegia with use of diaphragm, arm function, bladder and bowel
T6-T12
paraplegia, no abdominal reflexes present, no bladder or bowel control, sensation to groin
L1-L5
bowel and bladder dysfunction, lower leg weakness, hip and knee movement
S1-S5
loss of bladder, bowel, sex function, no paralysis of legs, loss of sensation to scrotum, perineum, anus, anal area, and upper inner aspect of thigh
spinal chord injury: respiratory
decreased cough reflex, limited chest expansion, decreased vital capacity
spinal chord injury: cardiovascular
orthostatic hypotension, decreased venous return, paroxysmal HTN, hypercalcemia
spinal chord injury: GU
urinary retention or incontinence, neurogenic bladder, impotence, decreased vaginal lubrication
spinal chord injury: musculoskeletal
contractures, bone demineralization, muscle spasms, pathological fracture
spinal chord injury: integument
decub ulcers
spinal chord injury: psychosocial
loss of body functions, change in self-image, dependent role, financial debt, thoughts of suicide
spinal shock
begins within one hour of injury and can last for 6 weeks, parasympathetic dominates - hypotension, bradycardia, flaccid muscles, loss of sensation, pain, tough, and temp, loss of ability to perspire
autonomic dysreflexia
exaggerated sympathetic response in patients with a T6 injury or above. abnormal triggers such as a full bladder or bowel causes following: bradycardia, HTN, severe HA, goose flesh skin below injury
neurogenic shock
most frequent in cervical injury, results form loss of autonomic function and result in orthostatic hypotension, bradycardia, hypothermia, can't sweat below level of injury
which chemical decreases in parkinson's disease
dopamine, which is responsible for control of movement
parkinson's disease symptoms
decrease in speed of movement to carry out tasks, masked face and monotonous tone, tremors at rest (pill rolling), legs suffering gait, bradykinesia (slowing of voluntary movement)
Parkinson's treatment
levodopa - restores dopamine levels
Multiple Sclerosis
myelin sheath of the brain and spinal column are destroyed, which causes an interruption of nerve conduction. Plaque formation occurs in white matter of brain and spinal column which are surrounded by inflammation. Astrocytes appear and form scar tissue replacing the nerve axons with scar tissue
MS risk factors
family history, 20-40 years old, cool and cold environments, recent viral infection
what does an MS pattern mean?
exacerbations and remissions
MS motor:
fatigue, tremor, ataxia
MS eyes:
diplopia (double vision), blurred vision, nystagmus (horizontal movement of eye involuntary
MS: head
slurred speech, dysphagia
MS: sensory
decreased response to touch, vibration, pain, temperature, numbness, tingling "pins and needles" sensation, hyperesthesia
MS: emotional
irritability/hyperexcitability, apathy/depression, can change rapidly
MS: cognitive
memory loss, poor judgement, inappropriate responses
MS diagnosis
cerebrospinal fluid, increase mononuclear cells and IgG, positive myelin basic protein (MBP), MRI
MS treatment
immunosuppressants, antivirals, corticosteroids, interferon -alpha, antibiotics, antispasmodics
myathenia gravis
destruction of acetylcholine receptor sites in the muscle, lack of receptor sites for acetylcholine, results in muscle's inability to contract
where is myasthenia graves first seen?
muscles of eye - ptosis (drooping of eyelid), diplopia (double vision), incomplete closure of eyelid
how do you diagnose myathenia gravis
tonsil test - stimulate muscle receptor sites temporarily so muscles contract
myathenia gravis treatment
anticholinesterase (neostigmine) - restores muscle function; corticosteriods - relieves symptoms
alzheimers disease
loss of blood perfusion to the brain, amyloid (starch -like proteins accumulate in brain tissue), loss of nerve cells
what do patients with alzheimers have a deficit of?
neurotransmitter - acetylcholine
what is the end result of alzheimers disease
memory impairment and deterioration of intellect
first stage alzheimers
2-4 years - forgetfulness, recent memory loss, decreases ability to concentrate, lack of spontaneity, social withdrawal
second stage alzheimers
may last several years - inability to recognize family/friends, incontinence, inability to eat
Alzheimers diagnosis
EEG, CT scan (brain atrophy), MRI (brain atrophy), PET Scan (decreased metabolic activity of brain, can be used to diagnose early disease)
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