Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

neurons are hyperactive and hypersensitive to their environment

A

seizure disorder pathogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

decreased distance between membrane and threshold potential

A

neurons hypersensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anticonvulsants target

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PROGRESSIVE deterioration and CONTINUING decline of memory and cognitive changes

A

Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

two types of dementia

A

Alzheimers and Vascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

degeneration of CORTICAL neurons in temporal and frontal lobes

A

dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

brain atrophy around TEMPORAL

amyloid plaques

neurofibulary tangles

A

Alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Characterized by a LOSS of function

A

Alzheimers disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

mild cognitive impairment

A

NOT Alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

plaques and tangles

A

proteinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

extracellular space

A

plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

intracellular space

A

tanagles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

B- amyloid deposits

A

Plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Tau Protein

A

Tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

high potential for aggregation and accumulation

A

plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

paired helical filament configuration

A

tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

disassociates from microtubule and begins to fold

A

tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AB peptide gets clever into

A

AB42

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

most common byproduct of alzheimers

A

AB42

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

risk factor for alzheimerw

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

INCREASES metabolism, INCREASES aggregation and DECREASES clearance of AB peptide

A

E4 allele of APOE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how do we increase or cognitive reserve

A

exercise your brain and start with a higher baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

syndrome with evidence of CLINICAL STROKE or VASCULAR BRAIN INJURY

A

dementia; vascular cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cognitive impairment r/t cerebrovascular injuries

A

vascular dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

communication with WHITE MATTER degrades

A

vascular dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

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

59
Q

neurons die in retrograde and anterograde fashin

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions