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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
Q

locked in syndrome

A

mentally aware but cannon physically respond; communicate through blinking

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26
Q

what are some cognitive disorders (and what part of the brain do they affect)

A

affects the cerebrum

  • selective attention deficits
  • executive attention deficits
  • retrograde amnesia
  • anterograde amnesia
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27
Q

selective attention deficit

A

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

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28
Q

executive attention deficits

A

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
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29
Q

retrograde amnesia

A

can’t remember the distant past

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30
Q

anterograde amnesia

A

can’t form new memories

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31
Q

what are cognitive disorders caused by?

A
  • direct physical damage
  • hypoxic/ischemic damage (O2 deprivation)
  • chemical/toxic damage (drugs, alcohol, ion imbalances)
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32
Q

agnosia

- who is it more common in?

A

common in dementia pts: impaired detection, can’t recognize common objects or ppl you used to know

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33
Q

dysphasia

A

difficulty sending or receiving verbal cues

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34
Q

what are three types of dysphasia?

A
  1. expressive dysphasia
  2. receptive dysphasia
  3. global dysphasia
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35
Q

dementia

A

loss of more than one cognitive function

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36
Q

primary dementia

A

usually idiopathic; easily mistaken for alzheimers

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37
Q

how detect true alzheimer’s in patients?

A

need autopsy of the brain

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38
Q

secondary dementia

A

obvious defined cause for dementia

- stroke, neurodegenerative disease

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39
Q

progressive dementia

A

often irreversible; possible infection of prions

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40
Q

acute confusional states (ACS)

- what is the most common feature

A

precursor to diagnosis of agnosia, dysphasia

- impaired detection is the most common feature

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41
Q

what can ACS lead to

A

delirium

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42
Q

key feature of delirium

A

hyperactivity/agitation with impaired detection

43
Q

developments of ACS

A
  1. physical injury to nervous tissue
  2. ischemic/hypoxic damage
  3. chemical/toxin damage
  4. “activation” of suppressed brain section
44
Q

what are some degenerative disease?

A
  • alzheimer’s disease
  • pick’s disease
  • parkinson’s disease
  • huntington disease
  • multiple sclerosis
  • amytrophic lateral sclerosis (ALS)
  • myasthenia gravis
45
Q

what can degenerative diseases lead to?

A

all may lead to various myopathies (disease condition of your muscle tissues)

46
Q

____ can send multiple sclerosis into remission

A

pregnancy

47
Q

alzheimer’s disease

A

ability to recognize ppl/objects can be transient (come and go)

48
Q

what are neurofibrillary tangles?

A

in alzheimer’s disease: proteins begin to coagulate and polymerize and act as if they have been infected by prion

49
Q

what proteins are involved in neurofibrillary tangles

A

misfolded tau proteins

50
Q

senile plaques

A

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
Q

pick’s disease

- who is it more common in

A

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
Q

progeria

A

condition where a kid ages quick

53
Q

parkinson’s disease

A

idiopathic; muscle spasms and tremors (involuntary spastic movements when pt is trying to do smth)

  • body has low amounts of dopamine
  • spastic movements
54
Q

huntington’s disease (chorea)

- what accumulates?

A

huntington protein accumulation –> due to genetic/heredity factors

55
Q

what does it mean when huntington disease is an autosomal dominant condition

A

one bad huntington allele: you’ll get this disease

HH: huntington, hh: no huntington

56
Q

multiple sclerosis (ms)

A

immune system is attacking myelin sheaths in neurons

57
Q

what happens when there’s no myelin sheaths?

A

no myelin sheaths = nerve impulse less efficient or complete interruption

58
Q

amyotrophic lateral sclerosis (ALS) “gehrig’s disease”

A

progressive loss of muscle tone

- slow motor neuron wasting –> lose ability to innervate

59
Q

myasthenia gravis

A

deficiency of the thymus (t cell quality control)

- flunky t cells –> start attacking neuromuscular junction

60
Q

cerebral blood flow

A

how efficiently is blood being applied to the brain

61
Q

cerebral blood volume

A

how much blood in brain

62
Q

cerebral perfusion pressure

A

pressure that circulatory system is exerting in cranial vault can affect ability to effect provide those tissues with O2 and other nutrients

63
Q

cerebral oxygenation

A

O2 in the cerebrum

64
Q

explain the effects of increased intracranial pressure

A

increased icp –> vasoconstriction –> decreased O2 to brain = decreased perfusion

65
Q

how to relieve increased intracranial pressure

A

drain some CSF (decrease overall pressure by compensating somewhere else)

66
Q

where is CSF made

A

in the ventricles of the brain

67
Q

what is spina bifida

A

breach in formation of neural tube during development → no proper closure = babies can’t create CSF

68
Q

cerebral edema

A

increased fluid content in brain tissue

69
Q

what are 4 types of cerebral edema

A
  • vasogenic edema
  • cytotoxic (metabolic) edema
  • ischemic edema
  • interstitial edema (NCH)
70
Q

vasogenic edema

A

problem with circulatory system that supplies blood to the brain

71
Q

cytotoxic (metabolic) edema

A

imbalances in ion concentration at physiological level –> affect blood supply to brain

72
Q

ischemic edema

A

problem with perfusion toward the brain (part of vasogenic family)

73
Q

interstitial edema (NCH)

A

most rare; noncommunicable hydrocephalus

  • CSF build up in meninges
  • defect in replenishing CSF, ventricles keep making = accumulation
74
Q

congenital hydrocephalus

A

rare; infectious disease (toxoplasmosis) –> mom passes onto kids

75
Q

how does congenital hydrocephalus present in adulthood

A

asymmetry in facial features

76
Q

noncommunicating hydrocephalus

A

old CSF not coming out = ventricles keep making CSF = impeding ability for old to come out

77
Q

communicating hydrocephalus

A

old stuff can get out, ventricles keep making CSF and its overpowering release of old CSF

78
Q

acute hydrocephalus

A

due to injury; rapidly developing

79
Q

seizure

A

sudden discharge of cerebral neurons

80
Q

convulsions (paroxysms)

A

random disordered muscle movements; eyes roll to back of head, drooling

81
Q

epilepsy

A

usually idiopathic; a disorder in which nerve cell activity in the brain is disturbed, causing seizures

82
Q

what can cause seizures?

A
  1. cerebral lesions
  2. biochemical disorders
  3. cerebral trauma
  4. epilepsy
83
Q

epileptogenic focus

A

hypersensitive area of neurons, source area for seizure

- mirror foci development

84
Q

phases of seizure?

A
  1. preictal (prodromal) phase
  2. tonic phase
  3. clonic phase
  4. postictal phase
85
Q

preictal phase

A

signs that seizure may begin

  • aura
  • vision blurs
86
Q

tonic phase

A

sudden stiffness or tension in the muscles of the arms, legs or trunk.

87
Q

clonic phase

A

start to see alternating contracting and relaxing spasms of muscles (can be very subtle)

88
Q

postictal phase

A

after seizure; extreme fatigue (bc O2 consumed is 60% above normal), headache, lousy mood

89
Q

_____ provides temporary relief of seizure

A

pregnancy

90
Q

hypotonia

A

decrease in muscle tone

91
Q

hypertonia

A

tonic phase: increase in muscle tone

92
Q

dystonia

A

certain postures, gaits; can tell you where issue may be in nervous system

93
Q

hypokinesia

A

dysfunction of voluntary motor movement

94
Q

akinesia

A

lack of voluntary motor movement

95
Q

bradykinesia

A

slow voluntary movement

96
Q

hyperkinesia

A

rapid and disorganized voluntary movement

97
Q

what are 2 types of hyperkinesia

A
  1. paroxysmal dyskinesia(s)

2. tardive dyskinesia

98
Q

paroxysmal dyskinesia(s)

A

tourette’s syndrome; involuntary movements of muscles other than facial muscles

99
Q

tardive dyskineisa

A

involuntary movement of facial muscles

100
Q

dystonia

A

whole body rigidity

101
Q

decorticate posture

A

whole body rigidity (hands to chest)

102
Q

decerebrate posture

A

whole body rigidity (hands on sides)

103
Q

dysparaxia/apraxia

A

lack of/impeded movements for fine motor tasks (handling utensils, writing)

pathophysiology (16 decks)

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