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Pathophysiology Spring 16 > Chronic disorder of neurologic function > Flashcards

Chronic disorder of neurologic function Flashcards

1
Q

characterized by excessive cortical electrical discharges and spontaneous positive potentials r/t Na+

A

Seizure disorder

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2
Q

neurons are hyperactive and hypersensitive to their environment

A

seizure disorder pathogenesis

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3
Q

decreased distance between membrane and threshold potential

A

neurons hypersensitive

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4
Q

Anticonvulsants target

A
  1. Positive ions, Na+ and Ca++ (depolarization of the cell)

2. Enhance GABA- inhibitory (hyper polarize cell- Cl-)

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5
Q

PROGRESSIVE deterioration and CONTINUING decline of memory and cognitive changes

A

Dementia

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6
Q

two types of dementia

A

Alzheimers and Vascular

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7
Q

degeneration of CORTICAL neurons in temporal and frontal lobes

A

dementia

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8
Q

brain atrophy around TEMPORAL

amyloid plaques

neurofibulary tangles

A

Alzheimers

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9
Q

Characterized by a LOSS of function

A

Alzheimers disease

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10
Q

mild cognitive impairment

A

NOT Alzheimers

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11
Q

plaques and tangles

A

proteinopathies

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12
Q

extracellular space

A

plaques

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13
Q

intracellular space

A

tanagles

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14
Q

B- amyloid deposits

A

Plaques

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15
Q

Tau Protein

A

Tangles

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16
Q

dense central AB core with inflammatory cells and DYSTROPHIC neurites in periphery

A

plaques

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17
Q

high potential for aggregation and accumulation

A

plaques

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18
Q

paired helical filament configuration

A

tangles

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19
Q

disassociates from microtubule and begins to fold

A

tangles

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20
Q

AB peptide gets clever into

A

AB42

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21
Q

B-amaeyloid is a byproduct that exists EXTRACELLULARLY and gets cleared in 3 ways normally

A
  1. Uptake by another neuron
  2. Macrophages
  3. enzymes
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22
Q

INCREASED in alzheimers

A

CSF Tou

normally stays in neuron membrane, if it has increased in CSF it has LEAKED out of the neuron and their is an accumulation.

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23
Q

DECREASED in alzheimers

A
  1. AB42 normally in CSF, if it is decreased it has accumulated somewhere else (extracellular space)
  2. FDG PET - glucose metabolism ahs decreased indicating decreased neuronal function (neurodegerative disease)
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24
Q

most common byproduct of alzheimers

A

AB42

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25
Q

risk factor for alzheimerw

A

E4 allele of APOE has a higher affinity for B-Amyloid

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26
Q

INCREASES metabolism, INCREASES aggregation and DECREASES clearance of AB peptide

A

E4 allele of APOE

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27
Q

how do we increase or cognitive reserve

A

exercise your brain and start with a higher baseline

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28
Q

syndrome with evidence of CLINICAL STROKE or VASCULAR BRAIN INJURY

A

dementia; vascular cognitive impairment

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29
Q

cognitive impairment r/t cerebrovascular injuries

A

vascular dementia

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30
Q

communication with WHITE MATTER degrades

A

vascular dementia

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31
Q

vascular dementia from ______________ more so than ____________.

A

cumulative tissue damage

large cerebral infarcts

32
Q

atherosclerosis is often associated

A

hyaline substance in vessel wall- yellow lipid deposits

33
Q

acute state of brain dysfunction, abrupt onset

A

delerium

34
Q

Leukoaraiosis

A

confluent white matter lesions

35
Q

Lacunar Infarcts

A

small, white mater infarcts

36
Q

CAA

A

Cerebral amyloid angiopathy

37
Q

micro infarcts

A

leading cause of vascular dimentia

38
Q

progressive failure of cerebral functions, onset is gradual

A

dementia

39
Q

hyperkinetic confusional state

A

delirium with sympathetic NS overactivity

40
Q

hypokinetic confusional state

A

delirium with parasympathetic NS Confusional states

41
Q

degeneration of dopaminergic neurons in basal ganglia and development of LEWY bodies

A

Parkinsons

42
Q

TRAP

A

tremor

rigidity

akinesia/bradykinesia

postural instability

43
Q

treated with LEVADOPA

A

Parkinsons

Levadopa = precursor to dopamine

44
Q

breakdown the precursor to Dopamine

A

MAO - Parkinsons treated with MAOI

45
Q

Autoimmune, inflammatory, progressive demyelination of the CNS

A

Multiple Sclerosis

46
Q

demyelination often occurs at optic, oculomotor and spinal tracts

A

Multiple sclerosis

47
Q

exacerbated by heat, infection, trauma and stress

A

Multiple sclerosis

48
Q

MS: immune cells attacking meylin

A

Autoreactive T cells

49
Q

MS: activated to chew up myelin sheath

A

macrophages

50
Q

MS: these cells DIE, normally function to deposit myelin to cover axons

A

oligodendorcytes

51
Q

macrophage alone attacks myelin sheath

A

macrophage mediated

52
Q

macrophage works with helper t and b to create antibodies that destroy myelin

A

Antibody mediated

53
Q

attacking NERVE ENDING of ODC that is responsible for melioration causing demylination

A

Distal Oligodendropathy

54
Q

Macrophage is attacking Oligodendrocyte in General

A

Primary ODC damage with peripheral Secondary demyelination

55
Q

double vision, weakness, poor coordination, sensory deficits, bowel and bladder control may be lost memory impairment

A

Multiple sclerosis symptoms

56
Q

progressive, UPPER and LOWER motor neurons

A

ALS

57
Q

Pathogenesis of ALS

A
  1. Excitotoxicity (Glutamate, Ca++)
  2. Oxidative Stress
  3. Mitochondrial Dysfunction
  4. Neuorinflammation
58
Q

hyperrelexia in weak atrophied extremity

A

ALS

59
Q

neurons die in retrograde and anterograde fashin

A

ALS

60
Q

secondary injury from spinal cord injury from

A

swelling

hemorrhage

ischemia

inflammation

61
Q

temporary loss of reflexes below the spinal cord injury

A

Spinal Shock

62
Q

muscles flacid/skeletal and autonomic reflexes lost

A

spinal shock

63
Q

Cervical or upper thoracic injury

A

neurogenic shock

64
Q

loss of brainstem and higher control of SNS

A

neurogenic Shock

65
Q

hypotension, bradycardia, circulatory collapse

A

Neurogenic shock

66
Q

secondary complication due to injury of ANS at or above T6

A

Autonomic Dysreflexia

67
Q

visceral stimulus or activation of pain receptors BELOW the injury are common stimuli

A

Autonomic Dysreflexia

68
Q

manifests as: hypotension, headace, bradycardia, flushing ABOVE the level of injury and clammy BELOW level of injury

A

Autonomic Dysreflexia

69
Q

IN Autonomic Dysreflexia a stimulus generates ______________ which will cause widespread ______________ in splanchinc vasculature and an increase in peripheral resistance, where blood is then shunted to _____________ circulation. _______________ sense increased blood pressure and activate the __________________ to lower the blood pressure. with this activation theirs a loss of ____________ tone and increased peripheral ______________.

A

sympathetic response

vasoconstriction

general circulation

Baroreceptors

PSNS

sympathetic tone

vasodilation

70
Q

stablilization of vertebrae

A

treament for Autonomic Dysreflexia

71
Q

in neurogenic shock we want to

A

Maintain oxygenation and blood pressure

72
Q

neuropathic condition with progressive weakness and diminished or absent MYOTATIC reflexes

A

Guillian- Barre Syndrome

73
Q

inflammatory, demyelinating disease of the PERIPHERAL nervous system

A

Guillian- Barre Syndrome

74
Q

A lower motor neuron disorder

A

Guillian- Barre Syndrome

75
Q

AIDP

A

Guillian- Barre Syndrome

acute inflammatory demyelinating polyneuropathy

76
Q

muscle weakness that begins in lower extremities and speeds to proximal spinal neurons

A

Guillian- Barre Syndrome

77
Q

Treatment include plasmapheresis and immunoglobulin

A

Guillian- Barre Syndrome

Pathophysiology Spring 16 (9 decks)

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