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33 Cards in this Set
- Front
- Back
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what is within the closed space of the cranium and spine?
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brain and spinal cord
CSF blood vessels and blood volume associated with pathology |
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stage of compensation?
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increase in volume of one compartment may be tolerated by a corresponding decrease in the volume of other compartments;
limits may be quite abrupt |
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principle of CSF production?
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produced at constant rate;
reductions in absorption are not matched by reduction in production |
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CBF?
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usually luxuriant and matches by autoregulation;
first defense is to increase O2 extraction ration |
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true of CBF over 50-150 mmHg systemic BP?
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pretty constant
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effect of hypercapnia on CBF?
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increased CBF
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effect of hypocapnia on CBF?
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decreased CBF
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effect of hypertension on CBF?
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shifted to the right, takes higher pressure to reach constant flow
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why is hyperventilation a strategy to reduce cranial volume?
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produces hypocapnia and reduces CBF
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at what CBF is there EEG changes?
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25
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at what CBF is there reversible dysfunction?
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20
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how long does it take for infarction to occur due to in adequate CBF?
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at 0 only takes a couple of minutes;
under an hour when CBF <20 |
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calculate cerebral perfusion pressure?
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systemic pressure - intracranial pressure
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cycle of brain injury?
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increased ICP --> decreased CPP --> infarction --> edema --> increased ICP, etc
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progressional change in posturing seen by level?
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above the midbrain = flexor
below the midbrain at pons = mixed below midbrain = extensor (midbrain eliminated) |
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why is CN3 susceptible to compression?
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located on roof of cavernous sinus and is compressed by temporal lobe herniation
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unilateral vs bilateral dilated pupils?
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bilateral is concerning for midbrain infarction and is a point of no return
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signs of normal pressure hydrocephaly?
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ventriculomegaly
ataxia incontinence |
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mechanism of papilledema?
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constrict ligature
swell proximally from retina ganglion cells |
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signs of increased ICP?
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headache
nausea/vomiting papilledema 6th nerve palsy obscurations of vision |
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primary head injury?
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occurs at impact:
diffuse axonal injury contusion, intracerebral hemorrhage skull fracture cranial nerve injury arterial dissection dura/arachnoid injury with CSF leak |
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mechanism of secondary injury due to head injury?
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due to decreased CBF and O2:
inflammation inappropriate release of excitatory transmitters Ca2+ influx ion pump dysfunction free radicals |
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major role in therapy of head injury?
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prevent secondary injury to increase cell survival by preventing hypotension, maintaining CPP and CBF, and controlling ICP
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priorities with head injury?
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breathing
bleeding brain bowel bladder bone spine precautions |
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contents of mini neuro (GCS)?
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eye opening
verbal response best motor response |
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grading for eye opening?
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4 = spontaneous
3 = to speech 2 = to pain 1 = no response |
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grading for verbal response?
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5 = oriented
4 = confused 3 = inappropriate 2 = incomprehensible 1 = none |
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grading for best motor response?
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6 = obeys command
5 = localizes pain 4 = withdraws 3 = flexor posture 2 = extensor posture 1 = none |
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when monitor ICP based on GCS?
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8 or less
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strategies to lower ICP?
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drill hole on side of dilated pupil
hyperventilate administer mannitol |
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mannitol use?
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lower ICP
fluid moves from tissue to vascular compartment |
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common location for shear injury?
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brachium conjuctiva in superior cerebellar peduncle
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flexor > extensor response indicates?
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intact midbrain
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