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NURS 350 patho neur2

neuro alterations first section

QuestionAnswer
general causes of altered awareness 1. pathological/structural (vascular, inf) 2. metabolic (hypoxia, elytes) 3. psychogenic (fronat lobe maybe)
5 assessment parameters for arousal 1. LOC 2. Breathing - rate, rhythm, pattern 3. pupils 4. Eye position & reflex 5. sk musc response
confusion can't think fast or clearly. impaired judgement/decision making
disorientation beginning loss of consciousness; disorientation to place and impaired memory; loss of self recognition last
lethargy spontaneous speech, movement. arouses with speech or touch
obtundation mild-moderate reduction in arousal. asleep if not stimulated
stupor deep sleep or unresponsiveness. Aroused with VIGOROUS/REPEATED stimulation
coma no response to stimuli, even if its noxious
what causes Cheynes-stokes respirations these near-death resperations are in response to overbreathing-->low C02-->apnea til C02 restores
clinical manifestation Cheynes-stokes progressively deeper, sometimes faster breathing followed by apnea in 30 second - 2 minute cycles
pupil assessment for this region of brain brain stem areas that control arousal close to areas that control pupils
what does dilated/fixed pupils indicate indicates drug alteration like amphetamine, atropine, scopolamine
what does pinpoint pupils indicate indiactes opiate use
what do WIDE, FIXED pupils indicate ischemia, hypoxia
cerebral death irreversible coma. death of cerebral cortex EXCLUDING brainstem/cerebellum (homeostasis)
vegetative state - can occur with cerebral death BP/breathing DO NOT require artificial support. unaware of self, surroundings. no cerebral fxn. sleep/wake cycles present. spontaneous eye opening to stimuli
locked-in syndrome - permanent efferent pathways disrupted, CN 1-4 in tack so pt can move eyes vertically/blink/communicate.
What is one cause of locked-in syndrome admin Na too quickly tx for hyponatremia --> demyelination of pons --> locked in. content of thought/arousal present
brain death legally dead det by transcranial dopplers showing brain moving forward/backwards. brainstem and cerebellum destroyed.
decorticate posture manifests as arms to core. upper extremity flexion. may or may not have leg extensor responses
decorticate posturing indicates cortical damage with LESS severe hemispheric dysfunction
decebrate posturing extension, abduction and hyperpronation of arms. extension of legs.
decebrate posturing indicates severe hemispheric damage (and brain stem, midbrain, cerebellum lesions)
generalized seizures no focal onset, bilateral neurons from subcortical --> impaired or LOC
partial focal seizures cortical focus -->unilateral neuron--> local onset. depending on foci, consciousness may be maintained.
epilepsy seizure syndrome with unknown etiology
dysphasia impairment of comprehension/production of written/verbal language (CVA with MCA involvement = middle cerebral artery usually on left side
aphasia loss of comprehension/production of language
expressive dysphasia Broca's affected --> primary verbal expression deficits
receptive dysphasia Wernicke's affected --> impaired verbal comprehension/reception
dementia loss of global cognitive ability affecting memory, attention, language and problem solving
normal range of ICP 5-15 mmHG
4 causes of increased ICP --->cerebral edema 1. increased intracranial content (tumors) 2. edema 3. excess CSF 4. bleeding
Intractranial HTN Stage 1 body compensating well (vasoCON, venous) to reduce ICP. usually asymptomatic
Intracranial HTN Stage 2 ICP starts to exceed compensatory mechs. systemic vasoCON attempts to raise BP/MAP > ICP so as to perfuse brain. neronal oxygenation compromised --> subtle/transient manifestations (conf, drows, sl pupil/breathing changes)
Intracranial HTN Stage 3 ICP approaches MAP-->brain hypoxic/hyercapneic. Rapid deterioration (dec arousal, central neurogenic hypervent, wide pulse press, slow HR, small/sluggishly reactive pupils)
Intracranial HTN Stage 4 Very high ICP nealy equal/equal to MAP. brain herniates (from higher pressure to lower pressure compartment). Cerebral blood flow stops when MAP = ICP
cerebral edema increase in fluid content of brain. may involve ECF or ICF. distorts bvessels, displaces brain tissue
causes of cerebral edema infection, trauma, tumors, ischemia, infarction, hypoxia
brain herniation deadly side effect of very high ICP. Brain shifts across structures - falx cerebri, tentorium cerebelli, foramen magnum
causes of brain herniation anything increasing ICP (tramua, stroke, tumor, hematomas)
hemiparesis dysfunction in brain/brainstem (tumor, CVA) --> WEAKNESS on one side of body
hemiplegia dysfunction in brain/brainstem (tumor, CVA) --> PARALYSIS on one side of body
paraplegia dysfunction of spinal cord --> paralysis of lower extremities
quadriplegia dysfunction of spinal cord --> paralyses of all 4 extremities
paresis weakness with INCOMPLETE loss of muscle power
paralysis loss of motor function
Created by: lorrelaws