Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
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
Normal Size Small Size show me how
NURS 350 patho neur2
neuro alterations first section
| Question | Answer |
|---|---|
| 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
Popular Nursing sets