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16 Cards in this Set
- Front
- Back
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What is the no-reflow phenomenon? |
A short-lived period of hyperemia is quickly replaced by a longer lasting period of hypoperfusion at the level of the microcirculation after blood flow has been successfully restored |
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Reperfusion injury is characterized by? |
1. Excess free radical formation 2. Nitric oxide toxicity 3. Further glutamate release |
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The only clinically benficial intervention that has proved to be successful in cases of anoxic-ischemic brain injury? |
Hypothermia, which inhibits apoptosis and reduces free radical formation and excitatory neurotransmitters |
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Areas most susceptible to anoxic-ischemic damage? |
1. Area CA1 of hippocampus (Sommer sector) 2. Basal ganglia 3. Thalami 4. Cerebellar Purkinje cells 5. Cortex |
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Why are the aforementioned areas most susceptible to damage? |
1. Presence of receptors for excitatory neurotransmitters 2. High metabolic demands of these neurons |
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Microscopic evaluation of anoxic-ischemic damage may show what? |
Neuronal loss and gliosis of vulnerable areas |
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Clinical signs that may be promising in a comatose patient after CPR? |
1. Localization of a pain stimulus 2. Visual fixation and tracking |
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Mortality rate for patients who do not receive hypothermic treatment and do not awaken within the first 24 hours? |
80% to 90% |
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Clinical findings that are invariably indicators of a poor prognosis in a comatose patient after anoxic-ischemic damage? |
1. Absent pupil responses or corneal reflexes within days 1 to 3 2. Eye movement abnormalities such as sustained upward gaze 3. Myoclonus status epilepticus |
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Man in the barrel syndrome? |
Lack of motor response in the upper extremities after bilateral border zone infarction in the anterior and middle cerebral watershed regions; better outcomes than others with anoxic-ischemic injury |
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Anoxic injury that affects the watershed region between MCA-PCA, the result may be? |
Balint syndrome - asimultagnosia, optic ataxia, ocular apraxia and a transcortical sensory aphasia |
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Two important factors indicating a very poor prognosis in patients not receiving therapeutic hypothermia? |
1. Absent or extensor motor response on day 3 2. Absent pupillary or corneal reflexes on day 3 May be counfounded by multiorgan failure and caution must be advised |
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Neuroimaging that may be helpful in anoxic-ischemic injury? |
MRI with DWI sequences; disappearance of the gray-white junction is associated with failure to awaken |
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"Malignant patterns" on EEG in anoxic-ischemic injury? |
1. Burst suppression 2. Alpha coma with periodic sharp waves and spikes 3. Isoelectric or a markedly suppressed EEG |
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When would you consider somatosensory evoked potentials in a comatose patient? |
Between days 1 and 3 after cardiopulmonary resuscitation; they require stimulation of the median nerve that then results in a potential at the brachial plexus, cervical spinal cord, and bilateral cortex potentials (N20); if both N20 components are absent, the prognosis is poor and will likely never regain consciousness |
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Possible serum marker for poor outcome in comatose patients after anoxic-ischemic injury? |
Serum neuron-specific enolase of >33u/L at days 1 to 3 |
