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pathophysiology > ch15: alterations in cognitive systems, cerebral hemodynamic, and motor functions > Flashcards

ch15: alterations in cognitive systems, cerebral hemodynamic, and motor functions Flashcards

1
Q

what is consciousness?

A

awareness of oneself and the environment

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2
Q

what are three types of responses a pt can exhibit when faced with a stimuli?

A
  • no response
  • appropriate response
  • inappropriate response
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3
Q

what is arousal?

A

a state of awakeness and the ability to respond to stimuli

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4
Q

vegetative state

A

opposite of dormant; cells are functioning but pt can’t respond to stimuli

“quasi waking state”

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5
Q

what maintains a vegetative state?

A

the reticular activating system (RAS)

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6
Q

what is awareness/content of thought?

A

awareness of self, environment, moods…

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7
Q

what controls awareness and conscious mind?

A

the cerebrum (supratentorially)

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8
Q

what controls unconscious homeostatic functions?

A

brainstem

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9
Q

what are structural alterations of arousals?

A
  • supratentorial dysfunction
  • infratentorial dysfunction
  • metabolic dysfunction
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10
Q

supratentorial dysfunction

A

issue is at cerebrum above tentorial plate

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11
Q

infratentorial dysfunction

A

issue is below tentorial plate and affects the brainstem and cerebellum

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12
Q

metabolic dysfunction

A

alcohol, drugs –> affect state of arousal in different ways
- can affect ion concentrations that affect the brain

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13
Q

what is a psychogenic alteration of arousal?

A

not easy to assess clinically; psychology affects the state of arousal (mental illness) but pt can be “faking it”

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14
Q

6 steps when assessing arousal state

A
  1. LOC
  2. breathing pattern
  3. size/reactivity of pupils
  4. eye position/reflexive responses
  5. vomiting (yawning, hiccups)
  6. skeletal muscle motor responses
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15
Q 
posthyperventilation apnea (PHVA)
- explain
A

goes hand in hand with cheyne strokes respirations

hyperventilating → blowing off too much CO2 → pH goes up → stop breathing → start hyperventilating again bc of CO2 accumulation

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16
Q

oculocephalic test

A

turn head from center, left, right –> eyes should be able to focus on one object

abnormal: eyes follow head direction

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17
Q

oculovestibular test

A

inject cold water into patient’s ear, eyes should look in the direction of the water

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18
Q

what are 3 outcomes of alterations of arousal?

A
  • brain death
  • cerebral death
  • cognitive disorders
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19
Q

what happens with brain death?

- what are signs of it?

A

brain can’t maintain homeostasis –> irreversible autolysis of brain

  • no spontaneous respirations
  • pupils dilated and fixed with no response
  • flat EEG
  • persistence 6-12hrs after onset
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20
Q

what is a symptom usually associated after pt has a seizure and why?

A

fatige: cells in brain consume A LOT of O2 –> rest of the body feels deprived

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21
Q

what happens with cerebral death?

A

death of cerebrum (NOT cerebellum or brainstem); could possibly have spontaneous muscle movements

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22
Q

what can a survivor of a coma progress to?

A
  • vegetative state
  • minimally conscious state
  • locked in syndrome
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23
Q

vegetative state (VS)

A

maintain homeostasis, but higher level responsiveness is gone

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24
Q

minimally conscious state (MCS)

A

some part of the cerebrum still functions, only some response to some stimuli meant to target the cerebrum

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25
locked in syndrome
mentally aware but cannon physically respond; communicate through blinking
26
what are some cognitive disorders (and what part of the brain do they affect)
affects the cerebrum - selective attention deficits - executive attention deficits - retrograde amnesia - anterograde amnesia
27
selective attention deficit
inability to preferentially attend to relevant aspects of a task and to ignore irrelevant information ex. not being able to listen to music while driving, not being able to talk to friend in a crowded place
28
executive attention deficits
when a person's brain has difficulty performing assorted important functions (ADHD, ADD) - ex. can't start or finish tasks, can't stay on track, can't follow multi-step instructions
29
retrograde amnesia
can't remember the distant past
30
anterograde amnesia
can't form new memories
31
what are cognitive disorders caused by?
- direct physical damage - hypoxic/ischemic damage (O2 deprivation) - chemical/toxic damage (drugs, alcohol, ion imbalances)
32
agnosia | - who is it more common in?
common in dementia pts: impaired detection, can't recognize common objects or ppl you used to know
33
dysphasia
difficulty sending or receiving verbal cues
34
what are three types of dysphasia?
1. expressive dysphasia 2. receptive dysphasia 3. global dysphasia
35
dementia
loss of more than one cognitive function
36
primary dementia
usually idiopathic; easily mistaken for alzheimers
37
how detect true alzheimer's in patients?
need autopsy of the brain
38
secondary dementia
obvious defined cause for dementia | - stroke, neurodegenerative disease
39
progressive dementia
often irreversible; possible infection of prions
40
acute confusional states (ACS) | - what is the most common feature
precursor to diagnosis of agnosia, dysphasia | - impaired detection is the most common feature
41
what can ACS lead to
delirium
42
key feature of delirium
hyperactivity/agitation with impaired detection
43
developments of ACS
1. physical injury to nervous tissue 2. ischemic/hypoxic damage 3. chemical/toxin damage 4. "activation" of suppressed brain section
44
what are some degenerative disease?
- alzheimer's disease - pick's disease - parkinson's disease - huntington disease - multiple sclerosis - amytrophic lateral sclerosis (ALS) - myasthenia gravis
45
what can degenerative diseases lead to?
all may lead to various myopathies (disease condition of your muscle tissues)
46
____ can send multiple sclerosis into remission
pregnancy
47
alzheimer's disease
ability to recognize ppl/objects can be transient (come and go)
48
what are neurofibrillary tangles?
in alzheimer's disease: proteins begin to coagulate and polymerize and act as if they have been infected by prion
49
what proteins are involved in neurofibrillary tangles
misfolded tau proteins
50
senile plaques
see this in alzheimers disease patients | - one of the first thing noticed if autopsy in brain is done (NOT prion but BEHAVES like prion)
51
pick's disease | - who is it more common in
more rare than true alzheimers; more common in younger ppl - polymerization of tau proteins + neurons - signs and symptoms similar to alzheimers but in younger - possible progeria
52
progeria
condition where a kid ages quick
53
parkinson's disease
idiopathic; muscle spasms and tremors (involuntary spastic movements when pt is trying to do smth) - body has low amounts of dopamine - spastic movements
54
huntington's disease (chorea) | - what accumulates?
huntington protein accumulation --> due to genetic/heredity factors
55
what does it mean when huntington disease is an autosomal dominant condition
one bad huntington allele: you'll get this disease | HH: huntington, hh: no huntington
56
multiple sclerosis (ms)
immune system is attacking myelin sheaths in neurons
57
what happens when there's no myelin sheaths?
no myelin sheaths = nerve impulse less efficient or complete interruption
58
amyotrophic lateral sclerosis (ALS) "gehrig's disease"
progressive loss of muscle tone | - slow motor neuron wasting --> lose ability to innervate
59
myasthenia gravis
deficiency of the thymus (t cell quality control) | - flunky t cells --> start attacking neuromuscular junction
60
cerebral blood flow
how efficiently is blood being applied to the brain
61
cerebral blood volume
how much blood in brain
62
cerebral perfusion pressure
pressure that circulatory system is exerting in cranial vault can affect ability to effect provide those tissues with O2 and other nutrients
63
cerebral oxygenation
O2 in the cerebrum
64
explain the effects of increased intracranial pressure
increased icp --> vasoconstriction --> decreased O2 to brain = decreased perfusion
65
how to relieve increased intracranial pressure
drain some CSF (decrease overall pressure by compensating somewhere else)
66
where is CSF made
in the ventricles of the brain
67
what is spina bifida
breach in formation of neural tube during development → no proper closure = babies can’t create CSF
68
cerebral edema
increased fluid content in brain tissue
69
what are 4 types of cerebral edema
- vasogenic edema - cytotoxic (metabolic) edema - ischemic edema - interstitial edema (NCH)
70
vasogenic edema
problem with circulatory system that supplies blood to the brain
71
cytotoxic (metabolic) edema
imbalances in ion concentration at physiological level --> affect blood supply to brain
72
ischemic edema
problem with perfusion toward the brain (part of vasogenic family)
73
interstitial edema (NCH)
most rare; noncommunicable hydrocephalus - CSF build up in meninges - defect in replenishing CSF, ventricles keep making = accumulation
74
congenital hydrocephalus
rare; infectious disease (toxoplasmosis) --> mom passes onto kids
75
how does congenital hydrocephalus present in adulthood
asymmetry in facial features
76
noncommunicating hydrocephalus
old CSF not coming out = ventricles keep making CSF = impeding ability for old to come out
77
communicating hydrocephalus
old stuff can get out, ventricles keep making CSF and its overpowering release of old CSF
78
acute hydrocephalus
due to injury; rapidly developing
79
seizure
sudden discharge of cerebral neurons
80
convulsions (paroxysms)
random disordered muscle movements; eyes roll to back of head, drooling
81
epilepsy
usually idiopathic; a disorder in which nerve cell activity in the brain is disturbed, causing seizures
82
what can cause seizures?
1. cerebral lesions 2. biochemical disorders 3. cerebral trauma 4. epilepsy
83
epileptogenic focus
hypersensitive area of neurons, source area for seizure | - mirror foci development
84
phases of seizure?
1. preictal (prodromal) phase 2. tonic phase 3. clonic phase 4. postictal phase
85
preictal phase
signs that seizure may begin - aura - vision blurs
86
tonic phase
sudden stiffness or tension in the muscles of the arms, legs or trunk.
87
clonic phase
start to see alternating contracting and relaxing spasms of muscles (can be very subtle)
88
postictal phase
after seizure; extreme fatigue (bc O2 consumed is 60% above normal), headache, lousy mood
89
_____ provides temporary relief of seizure
pregnancy
90
hypotonia
decrease in muscle tone
91
hypertonia
tonic phase: increase in muscle tone
92
dystonia
certain postures, gaits; can tell you where issue may be in nervous system
93
hypokinesia
dysfunction of voluntary motor movement
94
akinesia
lack of voluntary motor movement
95
bradykinesia
slow voluntary movement
96
hyperkinesia
rapid and disorganized voluntary movement
97
what are 2 types of hyperkinesia
1. paroxysmal dyskinesia(s) | 2. tardive dyskinesia
98
paroxysmal dyskinesia(s)
tourette's syndrome; involuntary movements of muscles other than facial muscles
99
tardive dyskineisa
involuntary movement of facial muscles
100
dystonia
whole body rigidity
101
decorticate posture
whole body rigidity (hands to chest)
102
decerebrate posture
whole body rigidity (hands on sides)
103
dysparaxia/apraxia
lack of/impeded movements for fine motor tasks (handling utensils, writing)

pathophysiology (16 decks)

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