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roop/raja Flashcards

1
Q

___are proteins called immunoglobulins. The presence of these proteins indicate inflammation of CNS.

A

oligoclonal IgG band

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2
Q

what is oligoclonal IgG band useful in diagnosing?

A

MS, subacute sclerosing panencephalitis, herpes simplex encephalitis, bacterial meningitis, neurosyphilis, sarcoid and lupus

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3
Q

___is used to enhance brain lesions in scans

A

gadolinium

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4
Q

____is a contrast medium used in 1 in 3 MRI scans to improve the clarity of your bodys internal structures. This improves the diagnostic accuracy of MRI scan. For example it improves the visibility of inflammation, tumors, blood vessels and some organs blood supply

A

gadolinium

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5
Q

___is immune mediated inflammatory disease. It attacks the myelinated axons in the CNS.

A

MS

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6
Q

what is the hallmark for MS?

A

symptomatic episodes that occur months or years apart affecting different anatomic locations

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7
Q

MS commonly begins between ____years of age and is more common in _____.

A

20-40; women

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8
Q

in MS there is localized areas of demyelination called plaques with destruction of oligodendrocytes. Primarily in ____ Matter?

A

White

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9
Q

in MS there is perivascular inflammation and chemical changes in ___ and ___ components of myelin

A

lipid and protein

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10
Q

____ and ___ are damaged in MS

A

axons and cell bodies

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11
Q

____are hardened areas

A

scleroses

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12
Q

what happens to the speed of transmission in MS?

A

you would not have saltatory conduction

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13
Q

____ is potential jumping from nodes of ranvier and because of this we have synchronized movements like walking

A

saltatory conduction

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14
Q

in MS sensory loss occurs when?

A

early in disease

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15
Q

spinal cord symptoms (motor): muscle cramping secondary to _____

A

spasticity

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16
Q

what are spinal cord symptoms autonomic of MS?

A

bladder, bowel and sexual dysfunction

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17
Q

what are cerebellar symptoms of MS?

A

dysarthria, nystagmus and intention tremor

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18
Q

____inflammation of optic nerve

A

optic neuritis

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19
Q

what are other symptoms of MS?

A

trigeminal neuralgia, heat intolerance, fatigue (70% of cases), dizziness

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20
Q

episodes of acute exacerbations or relapses with recovery and stable course between relapses

A

relapsing remitting (RRMS)

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21
Q

gradual neurologic deterioration and worsening of symptoms with or without relapses in a previous RRMS patient.
-follows RRMS

A

secondary progressive (SPMS)

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22
Q

gradual, nearly continuous neurologic deterioration from onset of symptoms with no relapses or remissions

A

primary progressive (PPMS)

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23
Q

gradual neurologic deterioration from onset of symptoms with subsequent relapses and no remissions

A

progressive relapsing (PRMS)

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24
Q

what is the most common type of MS?

A

relapsing remitting (RRMS)

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25
Q

what are all the types of MS?

A

relapsing remitting (RRMS), secondary progressive (SPMS), primary progressive (PPMS) and progressive relapsing (PRMS)

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26
Q

what is the etiology of MS?

A

genetic and molecular factors

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27
Q

what is the etiology of viral infections have to do with MS?

A

EBV

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28
Q

low levels of vitamin ___ makes you at risk for developing MS

A

D

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29
Q

Histology of MS shows the ____as the myelin is destroyed

A

vacuolation

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30
Q

Histology of MS: the first step seems to be adhesion molecules interacting with ___, ___ and ____. Later the BBB endothelium is digested away and the cells enter.

A

T cells, B cells and macrophages

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31
Q

Histology of MS: ____ release immunoglobulins, ____ release inflammatory cytokines and chemokines; and ____ expose axons releasing NO, glutamate and oxygen free radicals

A
  1. B cells
  2. T cells
  3. macrophages
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32
Q

what are the three categories of acute demyelination in MS?

A
  1. phagocytic cells with perivascular and parenchymal T cell infiltration
  2. everything in category 1 plus the presence of complement and antibodies
  3. oligodendrocyte apoptosis
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33
Q

____responsible for myelin in CNS

A

oligodendrocyte

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34
Q

___responsible for myelin in PNS

A

schwann cell

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35
Q

-what determines remyelination or not, is not well understood
-remyelination with a thin myelin sheath
-chronic inactive
-smoldering

A

chronic MS

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36
Q

inflammation resolves without remyelination

A

chronic inactive

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37
Q

inflammation does not resolve and there is a slow demyelination

A

smoldering

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38
Q

what type of MS is smoldering most common?

A

progressive MS

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39
Q

what type of MS?
-recurrent attacks that resolve or almost completely resolve
-remission can last for month to years
-there is very little residual deficit. however, today it is theorized that there is progressive neuronal degeneration continuing even during periods of remission

A

RRMS

40
Q

today treatment modalities slow progress of ___, but within 10-15 years of the onset of the disease, 50% of patients will convert to ___

A
  1. RRMS
  2. SPMS
41
Q

____increasing disability with little response to todays drugs

A

SPMS

42
Q

____ 10-15% of cases there is a steady decline in function. No remissions and no clear exacerbations

A

PPMS

43
Q

___progressive decline with occasional relapses. Rare.

A

PRMS

44
Q

methylprednisolone is used in MS for ____

A

acute exacerbations

45
Q

disease modifying agents for MS (DMAMS)
-primarily for ____
-reduces frequency and severity of clinical attacks
-includes ____

A
  1. RRMS
  2. interferons, monoclonal antibodies
46
Q

____ reduce the frequency of clinical exacerbations, decreases lesion volume and number

A

interferons

47
Q

Frequency of disease: common
latitude gradient: present
female sex%: 70
ethnic variation: white people
age of onset: 20-40
progressive course: common
coexistent autoimmune disease: rare

A

multiple sclerosis (MS)

48
Q

Frequency of disease: rare
latitude gradient: not proven
female sex%: 90
ethnic variation: africans and asians
age of onset: 40-60
progressive course: rare
coexistent autoimmune disease: MG, SLE, sjorens, thyroid, APL

A

neuromyelitis optica spectrum disorder (NMOSD)

49
Q

NMOSD causes ____ (sometimes bilateral) resulting in loss of vision in the horizontal half of the visual field

A

optic neuritis

50
Q

NMOSD causes demyelination of the _____ or _____

A

cervical or thoracic spinal cord

51
Q

NMOSD causes muscle spasms, incontinence and ____ or ___

A

paraparesis or quadriparesis

52
Q

___ is direct demyelination (primary)

A

MS

53
Q

____ indirectly demyelinates myelin (secondary to astrocytic damage)

A

NMOSD

54
Q

the pathophysiology of NMOSD: body produces antibodies against ____

A

aquaporin 4

55
Q

aquaporin 4 is the most widely expresses water channel in the ___, ____ and ____ (also present in collecting ducts of kidney, parietal cells of the stomach, airways, secretory glands and skeletal muscles

A

brain, spinal cord and optic nerves

56
Q

in the CNS aquporin 4 is found primarily in the ___

A

foot processes of astrocytes

57
Q

in NMOSD antibodys get through BBB, bind to ____ on the astrocytes and intiate complement and inflammation

A

aquaporin 4 receptors

58
Q

in _____
-neutrophils and eosinophils are abundant
-damaged astrocytes can no longer support neurons or oligodendrocytes and demyelination occurs

A

NMOSD

59
Q

unlike MS, in NMOSD demyelination is secondary to ____

A

astrocytic damage

60
Q

what is the target in NMOSD?
what is the NMOSD mediated by?

A
  1. astrocytes
  2. complement
61
Q

-never fully recovers from relapses
-relapses accumulate in disability

A

NMOSD

62
Q

-older onset than MS-primarily
-5:1 female to male ratio
-no cognitive changes

A

NMOSD

63
Q

what is the target in MS?

A

oligodendrocytes and myelin

64
Q

-can fully recover from relapses
-disability not always correlate with relapses

A

MS

65
Q

-younger onset
-2:1 female to male ratio
-cognitive change over time

A

MS

66
Q

-treatment for?
1. high dose steriods for acute attacks
2. immunosupressives
3. untreated, approximately 50% of NMOSD patients will be in wheelchair and blind

A

NMOSD

67
Q

if untreated, 1/3 of ___patients die within 5 years of their first attack

A

NMOSD

68
Q

In MS
1. unknown trigger sets up intitial focus of inflammation in brain and BB becomes locally permeable to ____ and ____
2. T cells specific for cns antigen and activated in peripheral lymphoid tissues reencounter antigen presented on ___ or ___ in brain
3. Inflammatory reaction occurs in brain due to ____, ___, ___ and ___
4. demyelination of neurons occurs

A
  1. leukocytes and blood proteins
  2. microglia or dendritic cells
  3. mast cell activation, complement activation, antibodies and cytokines
69
Q

risk factors for MS
- _____ and _____
-in pateints, increased serum levels of antibodies targeting EBV nuclear antigen 1 (EBNA1) strongly correlate with MS onset, and relapses are reported to associate with defective CD8 T cell mediated control of EBV reactivation
-high levels of IgG against HHV-6 are observed in patients with certain stages of MS

A

EBV and human herpesvirus 6 (HHV-6)

70
Q

risk factors for MS
-____, ___ and ____: an individual immune system is strongly influenced by nutrition, both through the demand for engery and how nutrition shapes the gut microbiome
-obesity in adolescents and young adults, classified as having a body mass index of >30 kg/m2, is associated with the increase risk of MS

A

metabolism, diet and obesity

71
Q

______, are found in active MS lesions within the CNS

A

CD4 TH cell in MS pathogenesis, IFN gamma producing TH1 cells and IL17 producing TH17 cells

72
Q

____can weaken the integrity of the BBB and thereby, promote further neuroinflammation

A

TH17 cells

73
Q

___ which can migrate to and damge neurons directly within the grey matter have been associated with neuronal decline and neurodegeneration

A

CD4 T cells

74
Q

____ dominate the T cell infiltrates in active MS lesions and are reduced in criculation

A

CD8 T cells

75
Q

____ in MS lesions exhibit tissue resident memory phenotype and show markers of activation, as well as expresssion of pro-inflammatory cytokine IL17

A

CD8 T cells

76
Q

___ these clonally expanded and antigen experienced B cells recognize ubiquitos intracellular and seemingly non pathogenic self proteins

A

B cells

77
Q

recruitment of ____ into the CNS is controlled by the presence of the growth factor GM-CSF, which is produced by autoreactive T cells

A

monocytes

78
Q

conventional ___ show a dysregulated pro-inflammatory phenotype, enhanced production of IL12 and IL23, as well as increased expression of chemokine receptors CCR5 and CCR7, permitting their migration to the CNS

A

dendritic cells

79
Q

The role of IL12 production by ____ and other APCS is pivotal for the generation of TH1 cells and cytotoxic CD8 t cell expansion, and in promoting autoreactive TH1 cell and CD8+ T cell populations in MS

A

dendritic cells

80
Q

-targets for MS
_____ is generated against proteins of the CNS towards the myelin sheath that protects the axons of neurons

A

antigen specific immune response CD4 T cells

81
Q

targets for MS
-components of the myelin sheath for example ____ are the main targets for autoimmune attacks

A

myelin basic protein (MBP), myeline oligodendrocyte glycoprotein (MOG) or proteolipid protein (PLP)

82
Q

-targets for MS
________have been recognized to cross react with glial cell adhesion molecule (glialCAM), a protein expressed by CNS resident glial cells

A

antibodies against the Epstein Barr Virus (EBV) nuclear antigen 1 (EBNA1)

83
Q

-targets for MS
___release and autoimmune brain inflammation can be induced independently of specific antigens

A

cytokine

84
Q

unpredictable attacks which may or may not leave permanent deficits followed by periods of remission

A

relapsing remitting MS RRMS

85
Q

steady increase in disability without attacks

A

primary progressive MS PPMS

86
Q

intial relapsing remitting multiple sclerosis that begins to have decline without periods of remission

A

secondary progressive MS SPSM

87
Q

steady decline since onset with super imposed attacks

A

progressive relapsing MS (PRMS)

88
Q

-very early in disease
widespread inflammatory infiltrates, populations of ____
-the subsequent destruction of myelin producing oligodendrocytes by these cells leads to formation of acute lesions in early disease stages
-demyelinated axons and axonal damage occur and the neuronal body is affected. this indicates that neuronal loss, a defining feature of disease progression, is also present in early stages of disease

A

CD4 T cells, CD8 T cells, B cells and monocytes

89
Q

_____
-S1 preceptor modulators
-agents that stop T cell, B cell proliferation
-prevent entry of lymphocytes into CNS
-push T cell into T-reg state
-interferons

A

disease modifying therapies for MS

90
Q

what do S1 preceptor modulators do?

A

sequester lymphocytes in lymph nodes

91
Q

___ binds Cd20 B cells, inducing cell death

A

ocrelizumab

92
Q

____inhibits dihydro-orotate dehydrogenase, inducing cytostatis

A

teriflunomide

93
Q

____binds CD52 lymphocytes, inducing cell death

A

Alemtuzumab

94
Q

___affects proliferating lymphocytes DNA, inducing cell death

A

cladribine

95
Q

___ binds a4 integrin subunit on lymphocytes. inhibits lymphocyte entry into the CNS

A

Natalizumab

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