Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards
share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Neuro-McCance

Ch 16, 17

QuestionAnswer
arousal state of awakeness that an individual exhibits, attentional system, mediated by reticular activating system in conjunction with cerebral cortex
Structural causes of alt arousal 1-supratentorial, 2-infratentorial, 3-subdural, 4-extracerebral, 5- intracerebral
supratentorial above the tentorium cerebella; < LOC from encephalitis (diffuse); brainstem trauma, CVA(bilateral); impairment of hypthalamic activating system by mass/CVA (localized)
infratentorial below the tentorium cerebella by direct destruction of RAS/pathways or impairment of blood supply to RAS. < arousal by CVA, myelination disease, neoplasm, granulomas, ascessess, destruction of brainstem from head trauma
most common cause of direct destruction of RAS CVA (causes intratentorial disorder)
Extracerebral disorders "diffuse" bilateral cortical dysfunction, neoplasm, closed-head trauma w/bleeding; subdural empyema
Intracerebral disorders within the brain, primarily masses-include bleeding, infarcts, emboli, tumor
Metabolic causes of < arousal encephalopathy, interference with neuronal metabolism, liver failure, renal failure. interruption of energy-hypoglycemia, hypoxia, ischemia. alt. excitability: drugs, ETOH, anesthesia, epilepsy
Psychogenic unresponsiveness apparent unconsciousness, but physiologically awake and neurologic exam normal
confusion loss of ability to thin rapid/clearly; impaired judgement, decision making
disorientation beginning LOC, disorient to 1-time, then place, last self
lethargy limited spontaneous speech, easy arousal with speech/touch, may not be oriented, but usually are
obtunded mild to moderate reduction in arousal, fall asleep unless stimulated, answers question minimally
stupor deep sleep-eye open with vigorous stimulation. withdrawal or grab at pain
coma no verbal/stimuli response. deep pain, suction yield motor response
light coma purposeful mvt on stimuli
coma nonpurposeful mvt only on stimuli
deep coma unresponsiveness
brain death irreversible brain damage, destruction of brainstem, cerebellum
cerebral death irreversible coma, death of cerebral hemisphere, but intact brainstem-maintain homeostasis
central reflex hyperpnea sustained, deep rapid regular respirations, midbrain damage, > ICP, blunt head trauma
apneusis prolonged ispiratory cramp, alt end-inspiratory/expiratory pause, pontine level damage. hypoglycemia, anoxia, menengitis
cluster breathing lower pontine/upper medulla, disordered breathing
ataxic breathing irregular, lower pon, upper medulla
gasping failing medulla
assympetric reflexes, posturing, babinski structural induced coma
PERRL, symmetric motor/tone, no babinski metabolic induced coma
oculvestibular abnormalities with sudden onset coma, bizarre respirations infratentorial mass of destruction
supraventricular mass compressing of diencephalon or brainstem initiating signs of cerebral dysfunction, progress from rostral to caudal,assymetric motor signs
rostral to caudal LOC changes see p. 105 of study guide
seizure abnormal hypersynchronous discharge of CNS neurons, sudden transient alt in brain function
decorticate flexion of arms and fingers with extension of lower extremities (diencephalon)
decerebrate all 4 extremities in extension, worsening sign-brainstem
partial seizure unilateral, no LOC unless it spreads to other hemisphere (secondary generalization). focal onset
generalized seizure both hemisphere, LOC c postictal state. subcortical, deeper brain focus-usually no local onset
status epileptic repeat seizure before person regains full consciousness (still postictal)
epilepsy no correctable cause of seizures
dysphagia impairment of comprehension or production of language., written or verbal. CVA middle cerebral artery, left cerebral hemisphere, frontotemperal region. nonfluent-cant find the right word. or fluent-meaningless/wrong words
aphasia loss of comprehension or production of language
normal ICP 5-15mmHg or 60-180cm H2)
cerebral edema increased fluid content in brain. intra/extracellular. net accumlation of water. >ICP
vasogenic cerebral edema increased permeability of capillary endothelium of brain after injury to vascular structure-disrupt blood/brain barrier. focal neurologic deficit. change in LOC, resolve by slow diffusion
cytotoxic edema metabolic cerebral edema. not blood-brain barrier but failure of transport system. cells loss K/gain Na (H20 follows Na), occurs in gray matter
interstitial edema noncommunicating hydrocephalus. brain fluid volume > around ventricles, increase hydrostatic pressure of white matter
hydrocephalus excess fluid in cranial vault and/or subarachnoid space. interference with CSF flow by > fluid vol, obstruct of ventricle, defective reabsorption.
noncommunicating hydrocephalus internal. ventricular obstruction, > CSF, often seen in children. atrophy of cerebral cortex, degenerate white matter tract, selective preservation of gray matter.
communicating hydrocephalus without obstruction, seen in adults
acute hydrocephalus rapid > ICP, without quick treatment, person becomes comatose.
stage 3 intracranial hypertension ICP approach aterial pressure, hypoxia, hypercapnia. Cheyne-Stokes respirations, pupils become sluggish and dilate. widen pulse pressure, bradycardia. severe hypoxia and acidosis of brain tissue
Stage 4 intracranial hypertension herniation. from compartment of greater pressure to lower pressure.
Stage 1 intracranial hypertension vasoconstriction/external compression of venous system to < ICP. subtle symptoms, confusion, drowsiness, slight pupil and respiratory changes
Stage 2 intracranial hypertension pressure compromising neuronal oxygenation. systemic blood pressure elevates to overcome > ICP.
focal brain injury specific, grossly observable brain lesion seen in cortical contusion, epidural hemorrhage, subdural hematoma, intracerebral hematoma, open-head trauma
contusion bruise on the brain. smaller the area of impact-greater severity of injury. can include immediate LOC, loss of reflexes, transient cessation of respirations, bradycardia, drop in BP- with stabilize VS, reflex return, regain consciousness (min.to days)
coup direct impact
countrecoup opposite line of force
Subdural hematoma tearing of bridging VEINS, subdural space fills with blood. Falls, MVA. elderly, alcoholics
acute subdural hematoma headache, drowsiness, restless-agitated...LOC change in respiration, pupils.
chronic subdural hematoma progressive dementia with generalize rigidity, gelatinous blood require surgical evacuation
extradural hematoma epidural hematoma. ARTERIAL bleed. may also have skull fx. assoc MVA, falls, sport accidents. LOC with lucid period (hrs/days). > h/a, vomiting, change in consciousness. good prognosis if intervene before bilat. dilation of pupils
Diffuse Brain injury DAI (diffuse axonal injury) shaking effect, high level of accel/decel. shearing, tearing, stretchin of nerv fibers.
mild DAI decerebrate/decorticate posturing, prolonged stupor or restlessness
moderate DAI prolonged coma; last days or weeks. recovery is often incomplete.
severe DAI immediate autonomic dysfunction-braistem sign. > ICP 4-6 days p injury. pulm complication. uncoordinated mvt, inability to learn/reason or modulate behavior
spinal cord injury usually at 1-2C, 4-7T, 12T-2L: most mobile portion of vertebrae. size makes injury to spinal cord easy. initial edema(swelling r/t degree of dysfunction) followed by meninge thickening/scarring with healing.
spinal shock complete loss of reflex function below level of lesion. skeletal muscles, bladder, bowel, sexual function, autonomic control. thermal regulation problems. last 7-20 days.
autonomic hyperreflexia sudden, dangerous HTN. stimulate below level of injury-ANS to > BP-baroreceptors conteract w/PNS to < HR, but lower level vessels don't dilate lesion T6 or above. distended bladder/bowel/sensory stimulation can cause.
neurogenic shock loss of sympathetic outflow, vasodilation, hypotension, bradycardia, hypothermia
meningitis infection of meninges, bacterial, fungi, parasites, viral, toxins p. 121, study guide
Created by: Sniffen group