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Immunology Block 4 > Systemic Autoimmune Diseases > Flashcards

Systemic Autoimmune Diseases Flashcards

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1
Q

SLE stands for

A

systemic lupus erythematsus

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2
Q

SLE mainly by what HSR

A

III

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3
Q

not a diagnostic autoantibody for

A

rheumatic diseases

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4
Q

SLE is most common

A

autoimmune rheumatic disease

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5
Q

why is complement pathway involved in SLE

A

they are involved in removing immune complexes

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6
Q

what is enviornmental trigger of SLE

A

UV light

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7
Q

deposition of immune complexes where in SLE

A

glomeruli & blood vessels

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8
Q

deposition of blood vessels in immune complexes are what give rise to

A

the rash (well known)

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9
Q

hemorrhaging of small blood vessels in skin give rise to what rash in SLE

A

butterfly/malar

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10
Q

what does SLE affect

A

everywehre - could eventually lead to organ failure and even death

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11
Q

symptoms of SLE

A

arthirtis, skin rashes (butterfly rash), pleurisy, kidney dysfunction, fever, weakness, anemia, thrombocytopenia, memory loss, headaches, confusion, seizures

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12
Q

treatment of SLE

A

immunosuppressive drugs, but SLE is a relapsing and remitting disease, so treatment is variable

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13
Q

what are triggers of SLE

A

UV

cigarette smoke

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14
Q

how can you diagnose SLE

A

ANA - antinuclear antibody (but most rheumatic diseases have this)
anti-SnRNP or smith antigen

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15
Q

ANA stand for

A

anti-nuclear antibody

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16
Q

most individuals with rheumatic disease will have

A

ANA

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17
Q

Rheumatoid Arthritis is chronic, episodic

A

joint inflammation

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18
Q

Rheumatoid Arthritis is due to what HSR

A

III and IV

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19
Q

what cells are responsible for inflammation in jionts in Rheumatoid Arthritis

A

neutrophils

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20
Q

what are the autoreactive cells in Rheumatoid Arthritis

A

CD4+ Th1 cells & Th17 cells

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21
Q

key cytokine in Rheumatoid Arthritis

A

TNF alpha

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22
Q

key cytokines in Rheumatoid Arthritis

A

IL-1
TNF alpha
prostaglandins
leukotrienes

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23
Q

Th17 cells will activate what that will be responsible for remodeling of bone in chronic Rheumatoid Arthritis

A

osteoclastst

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24
Q

what autoantibody is in Rheumatoid Arthritis

A

rheumatoid factor

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25
Q

rheumatoid factor is what isotype

A

IgM

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26
Q

rheumatoid factor not good for diagnosis b/c

A

only 70% pts with Rheumatoid Arthritis have it

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27
Q

detection of rheumatoid factor is useful in Rheumatoid Arthritis b/c it can be useful in

A

predicting outcome/prognosis of disease

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28
Q

pts who have rheumatoid factor in serum with Rheumatoid Arthritis tend to have (RF+)

A

more aggressive disease

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29
Q

test to detect RF is based on

A

agglutination

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30
Q

describe test to detect RF

A

latex particles that chemically coated with IgG
add pts serum
if pt has RF in serum it will bind to IgG and nbe very good at agglutination b/c IgM has 10 binding sites
so if pt does have RF in serum will see agglutination of serum

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31
Q

what is target antigen of RF

A

IgG

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32
Q

RF stands for

A

rheumatoid factor

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33
Q

test to detect RF and autoantibodies against any given autoantigen relies on activation of

A

complement

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34
Q

complement fixation test does what

A

detects if pt has antibody for particular antigen

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35
Q

fixation is old term for

A

ACTIVATION OF COMPLEMENT

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36
Q

describe complement fixation test

A

mix Ag with serum
add complement, a fixed amount
if antibody has bound to antigen complement will be activated
once complement is activated, will use up the fixed amount
to determine if complement is used up add indicator cells (RBC coated with antibody)
if antibody has not bound to the antigen the complement will not be used up and will be available to activation by cells that are coated with antibody (RBC) so in other words if in original tube there is not antibody specific for antigen, the complmeent is available for the RBC and will get lysis of RBC
if it is positive test and individual has antibody against antigen, the complement will b used up and no complement available to be activated on indicator cells (RBC) so no lysis of RBC

amount of erythrocyte lysis tell you if you have antibody specific for antigen

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37
Q

the important thing about the complement fixation test is that you add

A

limited amount of complement

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38
Q

negative result in complement fixation test, what is result

A

lysis of RBC

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39
Q

positive result of complement fixation test

A

no lysis of RBC, fixation of RBC

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40
Q

initiating factor of Rheumatoid Arthritis

A

don’t know :(

might be multiple things, different for different ppl

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41
Q

Rheumatoid Arthritis results in infltration f

A

Th1 and Th17 into joint

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42
Q

Th1 and Th17 activate what in Rheumatoid Arthritis

A

macrophages, fibroblasts, osteoclasts

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43
Q

during Rheumatoid Arthritis what happens to synovial membrane

A

thickened due to infiltration of inflammatory cells into membrane and into synovial fluid

44
Q

outgrowth from synovial membrane in Rheumatoid Arthritis what is it called

A

pannus

45
Q

what is in pannus* high yield

A

lots of neutrophils

46
Q

how do diagnose Rheumatoid Arthritis

A

no single test - based on clinical assessment, X-Ray
RF test
new test more specific than RF to test for cyclic citrullinated peptides

47
Q

treatments for Rheumatoid Arthritis

A

physiotherapy
immunosuppressive drugs
TNF alpha inhibitors
anti-CD20 mAb

48
Q

rewview pg 20

A

20

49
Q

CRP is ___ __ protein

A

acute phase

50
Q

CRP levels increase during

A

inflamamtion

51
Q

CRP decrease is consistent with decrease in

A

inflammation

52
Q

pts with Rheumatoid Arthritis that don’t respond to TNF alpha treatment will usually respond to

A

antiCD20 treatment

53
Q

Sjogren’s syndrome is probably what HSR

A

IV

54
Q

sjogren’s syndrome more common in women ormen

A

women

55
Q

what is most comon rheumatic disease besides SLE

A

sjogren’s

56
Q

what causes sjogren’s syndrome

A

autoimmune destruction of exocrine glands - often lacrimal and salivary glands

57
Q

parotid gland of pt with sjogren’s is full of

A

CD4+ T cells and b cells

58
Q

symptoms of sjogren’s syndrome depend on

A

exocrine glands affected

59
Q

symptoms of sjogren’s syndrome

A

Symptoms are highly variable
Dry eyes - decreased production of tears, red eyes
Dry mouth - decreased production of saliva, difficulty swallowing, cracking of lips and/or tongue
Dry skin, nose, throat, vagina
Joint pain, skin rash

60
Q

diagnosis for sjogren’s syndrome

A

Shirmer’s Test, to test tear production
Spit Test
Autoantibodies = ANA (anti-Ro, -La) and RF
Biopsy of enlarged gland

61
Q

RF is present in

A

many auto-rheumatic diseases

62
Q

autoantibodies most useful in detecting sjogren’s

A

anti-Ro, -La

63
Q

Granulomatosis with Polyangiitis is due to what response

A

Th1

64
Q

autoantibody associated with Granulomatosis with Polyangiitis

A

anti-neutrophil cytoplasmic autoantibodies (ANCA)

65
Q

antigen recognized by anti-neutrophil cytoplasmic autoantibodies (ANCA)

A

PR3 (proteinase 3)

66
Q

they think might have some disease/infection before Granulomatosis with Polyangiitis why

A

b/c of the granuloma that forms

67
Q

describe mechanism of Granulomatosis with Polyangiitis

A

uptake of autoantigen by dendritic cells
autoantigen seems to be proteinase 3
autoantigen taken to lymph which stimulates CD4 to differentiate into Th1
Th1 activate marophaegs at site of infection
formation of granuloma
T cells can provide help to b cells to make autoantibody

68
Q

proteinase 3 is released when

A

when neutrophils undergo netosis

69
Q

Vasculitis in GP what is initiating antigen

A

PR3

70
Q

in Vasculitis in GP autoantibodies stimulate the ___ of neutrophils

A

degranulation

71
Q

symptoms of Granulomatosis with Polyangiitis

A

Airway Symptoms: rhinitis, cough, chest pain,
sinusitis, congestion
Kidney disease, due to glomerulonephritis
Saddle nose, due to cartilage damage in bridge

72
Q

diagnosis of Granulomatosis with Polyangiitis

A

detect serum anti-PRS ANCA - the most specific

can also do x0ray, etc

73
Q

review pg 29

A

29

74
Q

Ankylosing Spondylitis is unusual b/c

A

ratio of males to females - 90% male

75
Q

Ankylosing Spondylitis has very strong association with

A

HLA-B27

76
Q

features of Ankylosing Spondylitis

A

fusion of vertebrae at base of spine - lose S shape curvature

77
Q

clinical freatures of Ankylosing Spondylitis

A

Pain and stiffness in lower back and hips
Chronic synovitis (esp. Achilles)
20% have other HLA-B27-associated arthritides: Reactive Arthritis or Reiter’s syndrome

78
Q

treatment of Pain and stiffness in lower back and hips
Chronic synovitis (esp. Achilles)
20% have other HLA-B27-associated arthritides: Reactive Arthritis or Reiter’s syndrome

A

anti-TNF mAbs (or drugs to inhibit activity of TNF)

79
Q

role of HLA-B27 in Ankylosing Spondylitis

A

4 different theories

presentation of disease associated peptides by B27 - proposes that disease associated B27 alleles present peptide and recogniztion of peptide is what leads to arthritis

disease associated alleles cannot present peptide, failure to respond against pathogen that leads to development of Ankylosing Spondylitis

misfolded HLA-B27 on cell surface and in ER
one theory says misfolded on cell surface reocnigzed by NK and T cells
other theory says misfolded on ER triggers secretion f proinflammatory cytokines (unfolded protein response)

they don’tk now how it contributes

80
Q

Scleroderma blood vessels involved look like

A

chronic graft rejection

81
Q

features of blood vessles in Scleroderma

A 
proliferation of smooth muscle cells
infiltration of B and T cells
imune complexes
fibrosis of blood vessels
just like chornic graft rejection
82
Q

features of Scleroderma

A

occlusion of blood vessels - called raynaud’s syndrome
tightening of skin - sclerodactyll
digital ulcers

83
Q

limited cutaneous form of Scleroderma

A

restricted to skin on hands, arms, face, feet

84
Q

diffuse cutaneous form of scleroderma

A

more servere:
extensive skin + internal organ(s)
lung, kidney, heart, GI diseases
complications: pulmonary fibrosis; pulmonary hypertension

85
Q

diagnosis of scleroderma

A

anti-nuclear autoantibodies (ANA)

RF+

86
Q

review slide 35

A

35

87
Q

omab means

A

only mouse

88
Q

ximab means

A

mouse/human chimera

89
Q

zumab means

A

humanized - almsot all human except CDR

90
Q

mumab means

A

fully human

91
Q

what is the target for SLE

A

skin
joints
kidneys
nervous system

92
Q

what type of HSR for SLE

A

III

93
Q

what are the autoantibodies for SLE

A

Anti-Sm
Anti-Ro
Anti-La

94
Q

what is the target for Rheumatoid arthritis

A

joints

blood vessels

95
Q

what is HSR for rheumatoid arthritis

A

III & IV

96
Q

autoantibodies for rheumatoid arthritis?

A

Anti-CCP

RF

97
Q

what is the target for scleroderma

A

skin
lungs
kidneys
heart

98
Q

what are the autoantibodies for scleroderma?

A

anti-centromere
anti-ro
anti-RNP

99
Q

what is the target for Ankylosing spondylitis

A

axial skeleton
peripheral joints
eye

100
Q

what is the HLA for Ankylosing spondylitis

A

B27

101
Q

what is the target for Granulomatosis with polyangiitis (WG)

A

kidneys
lungs
joints
skin

102
Q

what is HSR for Granulomatosis with polyangiitis (WG)

A

II

103
Q

what are autoantibodies for Granulomatosis with polyangiitis (WG)

A

anti-proteinase 3

104
Q

what is target for sjogren’s syndrome

A

exocrine glands

105
Q

what is HSR for sjogrens syndrome

A

IV

106
Q

what are autoantibodies for sjogrens syndrome

A

anti-Ro
Anti-La
RF

Immunology Block 4 (10 decks)

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