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scc nursing

cell body contains cell nucleus. center of cell metabolism
dendrites short unsheathed processes that transmit impulses to cell body.
axons longer process that transmit impulses away from cell body
myelin sheath covering for most axons. insulates nerve fiber. made up of fat cells
saltatory conduction nodes of ranvier, intermittent gaps in myelin shealth. provide for smooth nerve conduction.
cervical nerve plexus c1-c4, sends motor impulses to neck muscles, sends out phrenic nerve activating diaphragm, recieves sensory impulses from neck and back of head.
brachial plexus c5-t1, innervates shoulder, arm, forearm, wrist, and hand.
lumbosacral plexus t2-s4, innervates lower extremites. sends out large sciatic nerve
Lower motor neurons outside CNS, goes to skeletal muscles of the body. lesions cause weakness paralysis, muscle atrophy, and decrease muscle tone (flacidity) hyporeflexia
Upper motor neurons inside CNS lesions cause weakness/paralysis, hyperreflexia, increased muscle tone spastic
anosognosia inability to recognize bodily defect or disease. Lesions in r pariental cortex.
aphasia, dysphagia loss or impaired language comprehension,expression, both. l cerebral cortex lesion
dysarthria lack of coordination in articulating speech. cerebellar or cranial nerve lesion.
anisocoria inequality of pupil size. optic nerve inj
diplopia double vision. lesions affecting nerves of extaocular muscles, cerbellar damage.
homonymous hemianopsia loss of vision in one side of visual field. lesions in the contraleteral occipital lobe
dysphagia difficulty swallowing Lesions involving motor pathways of Cn IX X including lower brainstem
ophthalmoplegia paralysis of eye muscle lesions in brainstem
papilledema choked disc swelling of opic nerve head increase in intracranial pressure
Apraxia inability to perform learned movements despite having desire and physical ability to perform them cerebral cortex lesion
ataxia lack of coordination of movement lesions of sensory or motor pathway, cerebellum, antiseizure drugs, sedatives, hypnotic drug toxicity
dyskinesia impairment of voluntary movement resulting in fragmentary of incomplete movements disorder of basal ganglia, idosyncratic reaction to psychotropic drugs
hemiplegia paralysis on one side stroke and other lesions involving motor cortex
nystagmus jerking or bobbing of eyes as they track moving object lesions in cerebellum, brainstem, vestibular system
analgesia loss of pain sensation lesion in spinothalmic tract or thalamus
anesthesia abesence of sensation. lesions in spinal cord thalamus, sensory cortex, peripheral sensory nerve
paresthesia alteration in sensation lesions in the posterior column or sensory cortex
astereognosis inability to recognize form of object by touch lesions in parietal cortex
extensor plantar response (babinski) upgoing toes with plantar stimulation upper motor neuron lesion
deep tendon reflexes deminished or absent motor response lower motor neuron lesions
paraplegia paralysis of lower extremities spinal cord transection or mass lesion thoracolumbar region
tetraplegia paralysis of all extremities spinal cord transection or mass lesion cervical lesion
monro kellie principal any increase of volume of one component (brain tissue, blood, csf)changes the volume of other two.
fx that influence ICP b/p (a+v) intraabdominal/intrathroacic pressure posture temperature blood gases (acidosis dialation)
Normal ICP 0-15mmhg
Initial adaption of ICP csf absorption displacement of csf through brainstem, collapse of cerebral veins and sinuses
secondary adaption of ICP decreased production of csf change in intracranial blood volume venous outflow slight compression of brain tissue
cerebral perfusion pressure pressure needed to ensure blood flow to brain. norm 70-100mmhg.
CCP equation CCP=MAP-ICP
ccp below 60 ischemia
ccp below 30 not compatible with life
CCP changes Stage One autoregulation is occuring.
CCP changes Stage Two compliance is beginning to lessen. increase in volume places patient at risk
CCP changes Stage Three IICP with Cushing Triad
Cushings Triad widening pulse pressure, bradycardia, changes in respirations.
CCP Stage Four hernation is occuring IICP causes cerebral edemia and anoxia.
Factors affecting cerebral blood flow Pao2 levels <50=cerebral vasodialation paco2 acidotic state potent vasodialtor
Blood pressure should be maintained to: 100-140 systolic
O2 should be maintained to: 95%
IICP any increase in the brains three components
Vasogenic cerebral edema change in white matter and blood brain barrier. Leakage of proteins from capillaries causing change in osmotic force.
Causes of vasogenic cerebral edema brain tumor ingested toxins hemorrhages
cytotoxic cerebral edema local distruption of cell membrane (gray matter) Fluid moves from intravascular space into cells.
Causes of cytotoxic cerebral edema any hypoxic inj sodium depletion SIADH
interstitial cerebral edema Increased CSF pushed into interstitial space
Causes of interstitial edema hydrocephalus water overload
Conciousness awareness of self and surroundings
altered conciousness change in normal loc
unconsciousness unaware of self and surroundings
arousal state of wakefullness dependent on FAS
content ability to think, reason, feel and react purposefully
unconcious state does not respond to pain or corneal/gag/swallow pupillary reflexes
Cheyne Stokes respirations cycles of hyperventilation and apnea Abg decrease co2 slight decrease o2
central neurogenic hyperventilation sustained regaular rapid and deep breathing abg respiratory alkalosis brain stem dysfx lower midbrain/upper pons
apneustic apneustic center deep and prolong inspiration dysfx in pons
cluster breathing clusters of breaths follow each other with irregular pauses between dysfx of pons or medulla
ataxic (biots) completely irregular breathing pattern with some dep and some irregular pauses. slow rate medulla dx
Created by: 1161798020