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Pathophys Exam III > neuro mod 2 > Flashcards

neuro mod 2 Flashcards

(70 cards)

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1
Q

what is a stroke

A

interruption in blood flow to CNS

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2
Q

stroke rank among leading COD in US

A

3rd

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3
Q

common symptoms of stroke

A
  1. sudden numbness of face, arm or leg (one sided)
  2. sudden confusion, trouble speaking
  3. sudden trouble seeing in one or both eyes
  4. sudden trouble walking, dizziness, loss of balance
  5. sudden severe H/A with unknown cause
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4
Q

which stroke is more common - hemorrhagic or ischemic?

A

ischemic is more common

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5
Q

pathology of hemorrhagic stroke

A
  1. bleeding into brain parenchyma
  2. primary destruction of neurons from hemorrhage
  3. secondary destruction from potential rise in ICP
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6
Q

mechanism of injury of hemorrhagic stroke

A
  1. small vessel bleeding from HTN
  2. anticoagulation therapy
  3. cocaine use
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7
Q

cause of ischemic stroke

A

embolism/thrombus

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8
Q

what causes extra cranial embolism in ischemic stroke

A

most arise from heart

-valve, MI, afib, dilated myopathy, CHF

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9
Q

what causes intracranial thrombus in ischemic stroke

A

cerebral branches of circle of willis, internal carotid artery, small vessels of posterior circulation

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10
Q

intervention for ischemic stroke

A

thrombolytic intervention ASAP

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11
Q

what is the window of time for thrombolytic intervention of ischemic stroke

A

initial :

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12
Q

pathology of ischemic stroke - primary site

A

primary site of irreversible damage to neuron

  1. neuron becomes depolarized causing influx of Ca/ion channel dysfunction
  2. calcium influx leads to release of degradative enzymes
  3. neuron cell membrane destroyed releasing more substances to perpetuate inflammation/cell necrosis in the immediate area
  4. within hours/days - cytokines and other factors are released which promote additional inflammation/cell destruction
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13
Q

pathology of ischemic stroke - secondary site

A

Secondary site of reversible damage

Within hours the secondary site can be attacked by cascade of events in primary site

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14
Q

what is penumbra and what is it related to

A

“penumbra” = shadow

ischemic stroke - secondary site of reversible damage

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15
Q

which sites are reversible vs irreversible in the pathology of ischemic stroke

A
  1. primary site is irreversible damage to neuron

2. secondary site is reversible damage

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16
Q

what is the general pathology of ischemic stroke and how long does it take

A

cascade of inflammatory events occur within seconds to minutes

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17
Q

goal of tx for ischemic stroke

A

preserve neurons in the secondary site by

  1. restoring blood flow as soon as possible
  2. meds to block cascade of inflammation
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18
Q

risk factors for ischemic stroke

A
  1. family hx
  2. age >55
  3. HTN >140/90
  4. elevated chol/hyperlipidemia >200 total
  5. smoking
  6. diabetes
  7. obestiy BMI >30
  8. co-existing CV dz
  9. previous TIA
  10. high levels of homocysteine
  11. use of BC or hormone therapy
  12. heavy or binge drinking
  13. illicit drugs - cocaine
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19
Q

what is a TIA

A

transient ischemic attacks

-transient loss of blood flow

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20
Q

cause of TIA

A

numerous

atherosclerosis, emboli, arterial dissection, arteritis, cocaine, and other drug use

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21
Q

neurological symptoms usually last how long in TIA

A
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22
Q

TIA increases risk for what?

A

stroke

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23
Q

circle of willis receives blood from

A

ICA and VA (vertebral arteries/basilar artery)

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24
Q

function of circle of willis

A
  1. origin of major blood vessels of the brain
  2. anastomosis pathyways
  3. small perforating arteries
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25
small perforating arteries off the circle of willis contribute to what
blood supply to the subcortical regions of the brain
26
what areas do the small perforating arteries of circle of willis supply
1. diencephalon 2. internal capsule 3. limbic structures 4. pons
27
what is included in the diencephalon
1. thalamus 2. hypothalamus 3. subthalamus
28
what is the internal capsule
- pathway of myelinated axons leaving and entering the cerebral cortex - located between thalamus and basal ganglia
29
what are limbic structures
amygdale, hippocampus, etc
30
what is the ACA
anterior cerebral artery
31
what does the ACA supply
1. medial (saggital) regions of each hemisphere: - motor and sensory areas - lower body (distribution can be observed in homunculus diaphragm) - prefrontal lobe
32
what do the small perforating arteries of the ACA supply
portions of subcortical structures (internal capsule and basal ganglia)
33
motor function with infarction of ACA
1. LE contralateral hemiparesis (motor loss) 2. urinary incontinence 3. possible motor disorders associated with basal ganglia (Parkinson's)
34
sensory function with infarction of ACA
LE contralateral hemiparesthesia or hemianesthesia (loss of sensation)
35
behavioral/personality changes with infarction of ACA
1. apathy, poor motivation 2. perseverance 3. social inappropriateness
36
what is akinetic mutism
bilateral damage to frontal lobe Akinetic: lack of movement Mutism: lack of speech
37
what functions are lost with akinetic mutism in ACA infarction
1. conscious alert pt who retains ability to move/speak but fails to do so 2. damaged pathways inhibit motivation/increase apathy cause passiveness to interact or respond
38
what is the MCA
middle cerebral artery
39
what does the MCA supply
lateral aspect of each hemisphere: 1. motor and sensory areas (face, UEs, trunk) 2. association areas 3. prefrontal lobe 4. portion of optic tract
40
infarction of MCA will have what effects
depends on location
41
major trunk occlusion of MCA
everything of MCA stroke??
42
occlusion of superior branches of MCA (lateral frontal/parietal lobes)
global/broca's aphasia & most calssic MCA s/s
43
occlusion of inferior branches of MCA (lateral temporal and inferior parietal lobes)
Wernicke's and visual hemianopsia
44
motor changes with MCA infarct
1. contralateral hemiparesis or hemiplegia (area 4&6) 2. conjugate gaze (horizontal) 3. apraxia (inability to perform purposeful voluntary movement)
45
where is the contralateral hemiparesis or hemiplegia in MCA infarct
lower face/trunk and UE | LEs spared
46
where will the eyes deviate with conjugate gaze brought on by MCA stroke (vs normal)
eyes deviate toward side of lesion | Normal: area 8 provides conjugate game toward opposite side, CN6&3
47
apraxia with MCA infarct - common in which hemisphere - which areas affected
1. MC with dominant but may see in non dominant infarction | 2. pre-motor, motor or sensory association areas - UE apraxia, sensory apraxia (ideational apraxia, conceptual apraxia)
48
sensory changes with MCA infarct
1. contralateral hemiparaesthesia or hemianesthesia 2. contralateral astereoagnosis 3. Visual & auditory or smell
49
where do the contralateral hemiparaesthesia or hemianesthesia occur in MCA infarct
Lower face/trunk and UE | LE spared
50
what is contralateral astereoagnosis in MCA infarct
tactile agnosis: inability to judge/interpret object by touch
51
visual losses with infarct in MCA
visual: hemianopia - half of visual field loss, MCA supplies portion of optic tract
52
potential behavioral/personality changes with MCA infarct
1. apathy, poor motivation 2. perseverance 3. social inappropriateness
53
dominant hemisphere loss with MCA infarction
1. apraxia | 2. language/communication loss - aphasia
54
types of aphasia in dominant hemisphere loss with MCA infarction
1. Broca's aphasia (non fluent or motor aphasia) - comprehend but can't speak - area 44,45 2. Wernicke's aphasia (fluent or sensory aphasia) - speak but can't comprehend, word salad - area 22 3. Global aphasia - sensory and motor language loss, combo of fluent (sensory) and non fluent (motor), global damage to dominant hemisphere (massive infarct) - involve both parietal/temporal and frontal lobes
55
non dominant hemisphere with MCA infarction
1. anosognosia 2. construct apraxia 3. dressing apraxia 4. dysprosodia 5. confusion 6. extinction 7. unintentional fabrication of info
56
what is anosognosia in MCA infarction non dominant hemisphere loss
neglect, denial of injury, won't turn head to contralateral side
57
what is construct apraxia in non dominant loss of MCA infarction
ex. can't draw a clock
58
what is dressing apraxia in non dominant hemisphere loss of MCA infarction
not actual motor area but occurs b/c of inability to connect motor to purpose/meaning
59
what is dysprosodia
language/communication loss
60
motor dysprosodia in non dominant hemisphere loss of MCA infarction
difficulty of speech in producing the normal pitch, rhythm and variation of stress/tone in speech (musical aspects of speech)
61
what is sensory dysprosodia in non dominant hemisphere loss of MCA infarction
difficulty of speech in interpreting the normal pitch, rhythm and variation of stress/tone in speech (musical aspects of speech)
62
what is the PCA
posterior cerebral artery
63
what does the PCA supply
occipital lobe | inferior regions of temporal lobe
64
infarction of PCA
1. hemianopia (loss of same side in each eye - area 17) - contralateral to lesion 2. visual changes 3. possible memory impairments (temporal lobe involvement)
65
visual association loss with infarction of PCA
1. visual agnosia 2. prosopagnosia 3. alexia
66
what is visual agnosia that occurs with PCA infarction
inability to recognize an object by site | lesion in secondary visual cortex of occipital lobe (areas 18,19)
67
what is prosopagnosia with PCA infarction
difficulty recognizing familiar faces | occipital lobe secondary area, and association areas temporal/parietal lobes
68
what is alexia with PCA infarction
can't read
69
small branches of PCA supply
some of thalamus and midbrain
70
potential loss in PCA infarction with small branches
potential for sensory or motor symptoms in addition to visual changes -thalamic damage = chorea, hemiballismus

Pathophys Exam III (1 decks)

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