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HLSC 222 > Ch. 15 > Flashcards

Ch. 15 Flashcards

1
Q

Cognitive behavioral functional competence

A

integrated process of cognitive sensory, and motor systems

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2
Q

systems manifested through motor network

A

behaviors that are appropriate to human activity

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3
Q

full comsiousness

A

state of awareness of oneself and appropriate responses to environment

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4
Q

consciousness components

A

-arousal
-awareness

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5
Q

awareness

A

content of thought

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6
Q

arousal

A

state of awareness

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7
Q

alterations of arousal

A

-structural alterations
-metabolic alterations

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8
Q

structural alterations

A

divided according to their location of dysfunction
-supratenorial disorders
-infratentorial disorders

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9
Q

supratenorial disorders

A

disorders (above tentorium cerebelli) produce changes in arousal

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10
Q

infratentorial disorders

A

(below tentorial cerebelli) produce decline in arousal by dysfunction of reticular activating system or brain stem

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11
Q

metabolic alterations

A

disorders produce a decline in arousal by alterations in delivery of energy substrates

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12
Q

alterations in arousal manifestations

A

-level of consiousness
-pupillary reaction
-pattern of breathing
-oculomotor responses
-motor responses

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13
Q

level of consousness

A

-most critical index of neuro function
-changes indicate improvement or deterioration
-highest level of consousness
-normal state-confusion-disorientation-coma

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14
Q

highest level of cosiousness

A

person is a/o to onself, others, place, and time

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15
Q

patterns of breathing

A

-normal breathing= rhythmic pattern
-consiousness deminishes
-cheyne-stokes

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16
Q

diminished consiousness

A

breathing resopondes to changes in PaCO2 levels

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17
Q

Cheyne-stokes

A

altered peroid of tachypnea and apnea directly related to PaCO2

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18
Q

pnea

A

breathing

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19
Q

other related patterns to reduced arousal

A

-apneusis
-ataxic breathing

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20
Q

apneusis

A

prolonged insporatory time and a pause before expiration

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21
Q

ataxic breathing

A

complete irrefularity of breathing with increasing peroids of apnea

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22
Q

pupillary reaction

A

-indicate presence/level of brainstem dysfunction
-brainstem area controlling arousal is adjacent to area controlling pupils
-iscchema
-hypothermia/opiates cause pinpoint pupils

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23
Q

ischemia

A

dialated/fixed pupils

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24
Q

occulomotor responses

A

resting, spontaneous, and reflexive eye movements change at various levels of brain dysfunction
-a,b,c

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25
A- Normal response
eyes move together to side opposite from turn of head
26
B- abnormal response
eyes don't turn together
27
C- Absent response
eyes move indirection of head movement
28
Caloric ice water test
ice is injected into ear canal
29
Ice water test normal response
eyes turn together to side of head where ice is injected
30
Ice water test abnormal response
eyes don't move together
31
Ice water test absent response
no eye movement
32
motor responses
determon brain dysfunction and indicates most severly damaged side of the brain
33
patterns of response to motor responses
1. purposful 2. inappropriate, generalized movement 3. not present
34
motor signs indicating loss of cotrical inhibition
-decreased consciousness associated with the performane of primitive reflexes and rigidity (paratonia)
35
vomiting, yawning, and hiccups
complex refles-like motor reaponse integrated in brainstem (medulla oblongotta)
36
dysfunction of the medulla oblongata
compulsive/repetitive production of these responses
37
outcomes of alterations in arousal
-disability (morbitity) + mortality
38
disability + mortality
-outcomes depend on cause and duration of coma -some individuals never retain consiousness (neurological death)
39
two forms of neurological death
-brain death -cerebral death
40
Brain death (total brain)
-neurological determonation of death (NDD) -brain damage/can't recover/cant maintain homeostasis
41
Canadian criteria for NDD
-unresponsive coma -no brainstem functions -no spontaneous respiration (apnea)
42
cerebral death (irreversable coma)
-death of cerebral hemispheres except brainstem and cerebellum -perminant brain damage/individual doesn't respond a certain way -brain may continue to maintain homeostasis
43
cerebral death states
-persistant vegitative state -minimally consious state -locked in syndrome
44
Persistant vegitative state
-complete unawareness of self or environment/no speaking/ sleep wake cycle/cerebral function is absent
45
Minimally consious state (MSC)
-follow simple commanda, manipulate objects, give Y/n responses
46
Locked in syndrome
-complete paralysis of voluntary muscles except eye movement -content of thought and level of arousal are intact/fully consous -blinking as communication
47
awareness is
-all cognitive function -mediated by attention networks (EAN)
48
Exective attention networks
networks include selective attention and memory involve abstract reasoning, planning, decisionmaking, judgement, and self-control
49
selective attention (orienting)
-ability to select specific information and focus on related specific task -also includes selective visual and auditory attention
50
Executive attention deficits
-intial detection -mild deficit -severe deficit
51
initial detection
person fails to stay alert and oriented to stimuli
52
mild deficit
grooming and social graces are lacking
53
severe deficit
motionless/lack of respose/ doesn't react to surroundings
54
characteristics of executive attention deficits
inability to maintain sustained attention and ability to set goals and recognize when goal is achieved
55
memory
recording, retention and retrieval of information
56
amnisa
loss of memory
57
retrograde amnsia
difficulty rerieving past memories
58
anterograde amnesia
inability to form new memories
59
Data processing deficits
-problems associated with recognizing and processing sensory information -5 stages
60
5 stages of data processing deficits
1. agnosia 2. Dysphasia 3. Acute confusional states and delirium 4. dementia 5. frontotemporal dementia
61
Angosia
-defect of pattern recognition -failure to recognize form and nature of objects -usually only one sense effected -associated with cerebrovascular accidents ot specific brain areas
62
dysphasia
impairment of comprehensionor production of language
63
types of dysphasia
-expressive dysphasia -receptive dysphasia
64
expressive dysphasia (broca dysphasia)
-loss of ability to produce spoken or written language -can comprehend verbal
65
receptive dysphasia (wernicke dysphasia)
-inability to understand written or spoken language -speech is fluent, but no words and phrases have meaning
66
dysphasia cause
occlusion of middle cerebral artery
67
middle cerebral artery
1/3 major arteries supplying blood to brain
68
Acute confusional states and delirium
-transient disorders of awareness and may have sudden or gradual onset
69
causes of acute confusional states and delirium
drug intoxication, alcohom withdrawl, post anesthesia, electrolyte imblalnce
70
pathophysiology of acute confusional states and delerium
-disruption of reticular system, thalamus, cortex,and limbic system
71
delirium
-hyperactive acute confusional state -common in critical care unity >2-3 days causes sisruption of neurotransmitters Acetylcholine and dopamine
72
excited delerium syndrome
-hyperkineric delerium that can lead to sudden death -rapid breathing,high tolerance to pain, superhuman strength
73
manifestations of acute confusional states and delierium
-terrifying dreams -hallucinations -gross alteration of perception -individual can't sleep
74
evaluation of acute confusional states and delierium
-CAM-ICU
75
CAM-ICU
confusion assesment method for intensive care unit
76
Dementia
deterioration/progressive failure of many cerebral functions
77
causes of dementia
-cerebral neuron degeneration -atherosclerosis -genetics
78
manifestations of dementia
-no specific cure -maximix remaning capacities -helping family to understand
79
Alzhemiers disease
leading cause of severe cognitive dysfunction in older adults -unknown cause
80
forms of alzheimers
-Nonheditary sporadic late onset AD -early onset familial AD -early onset AD
81
Nonheriditary sporadic late onset AD
-most common form - no specific genetic association
82
early onset familial AD
linked to chromosome 21 mutations
83
early onset AD
-rare -inked to chromosomal 19 mutations
84
pathophysiology of AD
-all alterations for types of AD are the same -accumulation of toxic fragments of amyloid plagues -loss of acetylcholine in forbrain choliergic neurons = death of neurons
85
key components of alzheimers disease

HLSC 222 (9 decks)

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