Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immunology Block 4 > Organ-Specific Autoimmune Diseases > Flashcards

Organ-Specific Autoimmune Diseases Flashcards

1
Q

organ specific autoimmune diseases, symptoms are confined to

A

single organ

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

why are there organ specific autoimune disease

A

Cells of target organ are damaged directly, or

Autoantibodies may overstimulate or block the normal function of the target organ

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

there are no type ____ HSR for organ specific autoimmune disease

A

III

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

organ specific autoimmune disease are mediated by what HSR

A

type II or IV

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

autoimmune hemolytic anemia caused by

A

autoantibody against antigens on RBC

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

what are most susceptible to complement mediated lysis

A

RBC

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

Autoimmune Hemolytic Anemia antigen is on surface of

A

RBC

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

why do we have antibodies against RBC?

A

we don’t know 100%, think they might be cross reactive antibodies (molecular mimicry)

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

what are other forms of hemolytic anemia

A

anti-RhD (alloantigen incompatibility)

drugs that alter RBC glycoprotein structure (drug induced)

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

draw out mechanism of anti-RBC autoantibodies

A

pg 5

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

RBC are removed by what in spleen and liver

A

phagocytes

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

clincal features of autoimmune hemolytic anemia

A

Anemia, thrombocytopenia, hepatosplenomegaly

either Cold agglutinins (IgM) or Warm agglutinins (IgG)

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

IgM is referred to as what in hemolytic anemia

A

cold

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

IgG are referred toa s what in hemolytic anemia

A

warm agglutinin

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

how do you diagnose autoimmune hemolytic anemia

A

spherocytes in blood smear

coombs test

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

if individual has the autoimmune hemolytic anemia RBC will be coated with

A

autoantibody

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

if you take RBC from pts with what wil already be bound to RBC

A

autoantibody

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

to do coombs test:

A

use coombs reagant and if there is autoantibody it will bind, agglutination.

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

what is coombs reagant

A

anti human Ig

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

look at results of direct coombs test

A

pg 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what test is used to see if mom has antibody against Rh

A

indirect coombs test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why don’t you use direct coombs test to see if mom has antibody for Rh

A

b/c then you would need to take blood from baby :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

indirect coombs test:

A

take serum from mom, add to RBC with recess G antigen, add mom’s serum, if mother has antibody against it, it will bind to the positive RBC so when you come back with coombs reagant, it will lead to agglutination of the RBC if the mother has antibody that has bound

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

direct coombs test for Rh

A

just need fetal RBC and add anti human antibody

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

indirect coombs test for Rh

A

maternal serum Abs, add Rh+ then add anti-human antibody (so one extra setep)

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

if there is antibody bound to antigen on surface of RBC you will do what to clls with coombs reagant

A

agglutiante

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

exxample of drug to induce hemolytic anemia

A

penicillin

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

how do drugs cause autoimmune response

A

they modifiy RBC platelet and induce antibody production

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

once you stop taking drug, what happens to antibodies against blood

A

they will no longer bind, it is jsust b/c they are modified by the drug

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

Goodpasture’s Syndrome isn’t exclusively organ specific b/c epitope is shared b/w

A

glomerular basmenet membrane of kidney and alveolar basement membrane (lung)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

autoantibody in lung with Goodpasture’s Syndrome are pretty much

A

not accessible in lungs - until there is infection, once ther is infection the autoantibody will get access to the thing in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what happens in Goodpasture’s Syndrome

A

phagocyte/complement activation, neutrophils undergo frustrated phagocytosis, to attempt to engulf, but they can’t b/c it’s too big so they release their stuff at glomerular basement membrane resulting in tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Goodpasture’s Syndrome is it direct or indirect immunofluorescence (pg 12) take biopsy and add immunofluorescent IgG

A

direct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Goodpasture’s Syndrome is unusual b/c it is more common in

A

males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

two forms of Pemphigus

A

Pemphigus folaceous

Pemphigus vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pemphigus folaceus

A

mild

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pemphigus vulgaris

A

severe, can be fatal if not treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pemphigus folaceus, autoantigen is

A

demolglein 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pemphigus vulgaris, autoantigen is

A

desmoglein 3 (& 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

autoantibodies of Pemphigus are usually

A

IgG1 and IgG4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what do the autoantibodies of Pemphigus do

A

unqipping - blisters

splitting of keratonicyte sheets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

why is Pemphigus vulgaris so severe

A

can get lots of fluid loss through the blisters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

HOW DO YOU DIAGNOSE Pemphigus VULGARIS

A

Immunohistological demonstration of anti-desmoglein; detection of acantholysis
SHOULD BE ABLE TO DETECT AUTOANTIBODY HIGHLIGHTING THE DESMOSOMES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Myasthenia Gravis what kind of HSR

A

non-cytotoxic type II HSR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

non-cytotxic tyep II HSR mean

A

do not destroy the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Myasthenia Gravis ?

A

Produce blocking autoantibodies against  subunit of the nicotinic acetylcholine receptor (AchR), which is found at neuromuscular junctions in skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

in most common form of Myasthenia Gravis the Ach receptors are blocked by

A

antagonistic IgG autoantibody that prevents binding of Ach to AchR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

regardless of form of Myasthenia Gravis, they all have the same phenotype:

A

failure to transmit neoronal signal at neuromusclar junction: POOR MUSCLE CONTRACTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

similar to Myasthenia Gravis in presentation, but autoantiobody involved doesn’t block Ach binding, it prevents release of Ach at other side of junction

A

Lambert-Eaton Syndrome:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Lambert-Eaton Syndrome:

most common autoAbs

A

direct against voltage gated Ca2+ on neuron block release of Ach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

clinical features of Myasthenia Gravis

A

Progressive weakening of muscles

Facial muscles – drooping eyelids (ptosis), tongue, mouth
Chest muscles - impaired breathing, respiratory infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Myasthenia Gravis treated with

A

Acetylcholinesterase inhibitor, allows Ach to stay long enough to bind to residual receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how do you diagnose Myasthenia Gravis

A

Anti-AchR antibodies in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

most common form of hyperthyroidism

A

Graves’ Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Graves’ Disease:

A

Produce stimulating autoantibodies against thyroid-stimulating hormone receptor (TSH-R)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what normall y happens in Graves’ Disease

A

release of thyroid hormones is strictly controled (levels of T3 and T4 shut down production of TSH, negative feedback), in this disaese stimulation fo TSH-R is independent of TSH, it doesn’t prevent stimulation through TSH-R, so:
Anti-TSH-R autoAbs bind to and activate TSH-R on thyroid cells, leading to overproduction of T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is overproduced in grave’s disease

A

T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

symptoms of grave’s disease

A

Enlarged thyroid gland (goiter), heat intolerance, irritability, nervousness, warm moist skin, weight loss
Bulging eyes, stare (exophthalmos)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

enhanced appetite but still weight loss, what disease

A

grave’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

at initial presentation, ppl with graves disease don’t always present with

A

exophthalmos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is exophthalmos?

A

bulging eyes, stare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how do you diagnose graves disease

A

High T3/T4 levels in patient plasma, with no TSH

detection f antibody against TSH receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

how do you treat grave’s diseases?

A

Anti-thyroid drugs that inhibit thyroid function

Thyroid removal or destruction by radioiodine (131I), with synthetic thyroid hormone daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Plasmapheresis what is it

A

remove blood cells and filter to remove immunoglobulin and then reinfuse back into individual, to get rid of pathogenic autoantibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

unlike passive immunization, Intravenous immunoglobulins dose is much

A

higher than you’d give for passive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Intravenous immunoglobulins such high does b/c

A

injected high dose Intravenous immunoglobulins bind to low affinty Fc receptor on B clls (fc gamma recptor on b cells is negative co-receptor_ so you can force the injected IgG to bindt o the low affinity Fc receptor and shut down production of autoantibodies

67
Q

type II HSR are mediated by

A

IgG

68
Q

what can IgG do?

A

cross placenta

69
Q

if women suffering from type II HSR it can be

A

transferred to child by crossing plaecnta

70
Q

list diseases that can be transferred to mother through IgG in placenta

A

Myasthenia gravis
graves
thrombocytopenic purpura
pemphigus vulgaris

71
Q

pernicious anemia is what type of HSR

A

type IV

72
Q

Pernicious Anemia is characterized by presecens of

A

autoantibody

73
Q

we don’t think autoantibody in Pernicious Anemia is

A

pathogenic antibody

74
Q

why do we think autoantibodies in Pernicious Anemia are not pathogenic

A

unless parietal cell si damaged, there is no way the autoantibody can get ti autoantigen, b/c parietal cel autoantigen is proton potassium ATPase which exclusivelly localized in luminal side of cell, not availble on basal lateral surface of cell so antibody can’t get to it

75
Q

IF is entirely ____ until secreted into lumen

A

intracellular

76
Q

what do they think happens in pernicious anemia

A

some inflammatory process damges parietal cell which reveals ATPas and IF to B cells so autoantibody is useful for diagnosis but not pathogenic

77
Q

what deficiency is in pernicious anemia

A

vitamin B12

78
Q

what is not accessible to autoantibody in Pernicious Anemia

A

IF and ATPase

79
Q

what do they think causes pernicious anemia

A

Evidence for Type IV HSR response against H+/K+-ATPase leading to parietal cell destruction (by Th1 cells and macrophages) and release of autoantigens.

80
Q

some evidence that what two diseases might be involved in development of pernicious anemia

A

Autoimmune Gastritis

Role of Helicobacter pylori infection??

81
Q

destruction of parietal cell leads to decreased production of

A

intrinsic factor

82
Q

less intrinsic factor means there is less absorption of

A

vitamin B12

83
Q

Type 1 Diabetes mediated by what HSR

A

type IV

84
Q

describe Type 1 Diabetes

A

specific destruction f insulin producing beta cells in panreatic islets by autoreactive T cells

85
Q

what is killed in Type 1 Diabetes

A

insulin producing beta cells in pancreas

86
Q

Type 1 Diabetes can be associated with prior infections of

A

coxsackie virus proteins

87
Q

most important players in destruction of beta cells in Type 1 Diabetes

A

Th1 cells and macrophages

88
Q

Th1 cells make what that harm beta cells

A

IFN gamma

89
Q

clinical features of Type 1 Diabetes

A

Symptoms due to disruption of glucose metabolism
Atherosclerotic vascular lesions; gangrene in extremities; renal failure; blindness
beta-cell damage precedes symptoms
Increased appetite, increased urinary frequency/micturition

90
Q

diagnoseis of type 1 diabetes

A

Increased blood glucose levels

Autoantibodies against GAD65 and insulin

91
Q

type 1 diabetes treatment

A

daily insulin jections

beta cell transplantation

92
Q

downside of beta ell transplanataion

A

need two pancreas to get enough beta cells for transplantation

93
Q

Hashimoto’s Thyroiditis

is example of

A

hypothyroidism

94
Q

hypothyroidism:

A

decreased thrydoif fucntion

95
Q

goiter of Hashimoto’s Thyroiditis is result of

A

infiltration f CD4, CD8 and B cells

96
Q

Hashimoto’s Thyroiditis get malignancy in

A

thyroid

97
Q

Hashimoto’s Thyroiditis more common in

A

women

98
Q

autoantibodies in Hashimoto’s Thyroiditis are against

A

products, they are not pathogenic

99
Q

Th1 cells in individuals with Hashimoto’s Thyroiditis are against

A

thyroglobulin

100
Q

what is treatment for Hashimoto’s Thyroiditis

A

synthetic thyroid hormone daily

101
Q

diagnosis of Hashimoto’s Thyroiditis

A

Thyroid histology (well-developed germinal centers) antibodies to TPO & thyroglobulin are epiphenomena and not pathogenic

can detect inappropriate expression of MHC II

102
Q

what disease can you detect inappropriate expression of MHC II

A

Hashimotos’s thyroiditis (can detect them on thyroid cells)

103
Q

MHC II expression is usually limited to

A

APC & epithelial cells in thymus for positive and negative selection

104
Q

autoreactive Th1 cells promote differentiation into

A

cytotoxic t cells

105
Q

evidence that what is actually killing the thyroid cells in Hashimoto’s Thyroiditis

A

cytotoxic t cells

106
Q

Addison’s Disease like type I diabetes and celiac is associated with what

A

HLADQ2 and HLADQ8

107
Q

Addison’s Disease is risk for developing

A

type I diabetes & celiac disease

108
Q

Addison’s Disease mediated by what HSR

A

IV

109
Q

primary pathogenic cells of Addison’s Disease

A

CD8 T cells specific from peptide 21 hydroxylase

110
Q

Addison’s Disease following destruction of cells in adrenal cortex get production of

A

autoantibodies

111
Q

autoantibodies against 21 hydroxylase in Addison’s Disease are, they are useful for diagnsis

A

not pathogenic

112
Q

main mechanism of destruction of Addison’s Disease

A

killing of adrenocorticol cells by autoreactive cytotoxic t cells and macrophages

113
Q

review pg 38

A

38

114
Q

symptoms of Addison’s Disease

A

Tiredness, extreme weakness, weight loss, nausea/vomiting, abdominal pain

115
Q

treatments of addison’s disease mostly due to lack of

A

cortisol

116
Q

how to treat addison’s disease

A

Cortisone acetate
Hydrocortisone tablets
Fludrocortisone acetate

117
Q

MS is caused by destruction of

A

myelin sheath of nerve fibers in brain and spinal cord

118
Q

what causes destruction of myelin sheath in MS

A

autoreactive T cells

119
Q

MS is more common in women or men

A

women

120
Q

areas of demyelination seen in MS are often referred to as

A

plaques

121
Q

edge of plaques in MS contain:

A

CD4 and CD8 t cells, b cells, plasma cells

122
Q

cells responsible for destroying myelin sheath are

A

resident macrphages in brain - microglial cells activated by infiltrating Th1 cellse

123
Q

symptoms of MS

A

Muscle wasting - weakness
Progressive visual failure
Epilepsy
Disarthria (speech impairment)

124
Q

describe relapsing-remitting MS

A

unpredictable relapses followed by periods of months to years of remission

125
Q

describe secondary progressive MS

A

initially relapsing-remitting MS changing to progressive neurologic decline without remission

126
Q

describe primary progressive MS

A

Steady neurological decline with little or no remission

127
Q

describe progressive relapsing MS

A

Steady neurological decline with additional acute attacks of MS
combination of primary progressive and relapsing-remitting

128
Q

what form of MS never has relapsing phase to it

A

primary progressive

129
Q

progressive forms of MS can lead to total loss of mobility within

A

8-10 years of onset

130
Q

what cells do they think are activating the microglial cells that start MS

A

autoreactive Th1 cells

131
Q

Th17 are highly

A

inflammatory

132
Q

Th17 implicated in pathogenesis of

A

MS and rheumatoid arthritis

133
Q

candidate antigens in pathogenesis of MS

A

myelin basic protein (MBP)

myelin oligodendrocyte glycoprotein (MOG)

134
Q

can find cells reactive against what in MS

A

MBP nd MOG

135
Q

you can find autoreactive cells against MBP and MOG in ppl who do not have

A

MS - so something else is going on

136
Q

what happens to allow the autoreactive T cells to reach BBB and get into CNS and attack the demyelinated axons?

A

they don’t know what the trigger is

they can do it in animals with neurotrpic viruses

137
Q

describe cells involved in MS

A

Th1 activate microglial cells and microglial cells are responsible for the demyelination
in add’n to Th1 cells will also detect B cells and sometimes will see what looks like secondary lymphoid tissue in the CNS

138
Q

treatment of MS

A

IFN beta - they dn’t know why really but many pts benefit

139
Q

downside of IFN beta treatmen tof MS

A

need to give a strong dose

140
Q

about 40% of ppl who take IFN beta for MS develop

A

antibodies against the IFN beta

141
Q

where is crohn’s disease

A

any part alng GI tract

142
Q

where is ulcerative colitis

A

usually just in colon/rectum

143
Q

NOD1 and NOD2 detect

A

bacterial products in cytoplasm of cells

144
Q

IL 23 binding to IL23-R promotes

A

proliferation and stabilizes phenotype of Th17 cells

145
Q

result of polymorphsm in IL23 receptor in crohns and ulcerative colitis it may promote

A

generation fo Th17 cells at expense of Treg cells

146
Q

essential balance b/w Th17 and

A

Treg in gut

147
Q

Th17 role in inflammation

A

highly pro-inflammatory cytokine

148
Q

review pg 50

A

50

149
Q

IL 22 is important for maintaining barrier in

A

gut

150
Q

IL 22 induces production of

A

antimicrobial petpdies and prmotes colonization of gut by microflora at expense of pathogenic flora

151
Q

in inflammatory bowel diseases balance b/w what is thrown off

A

Th17 and Treg

too any Th17 abd nt enough Treg

152
Q

experimental evidence that restoration of Treg/Th7 balacne can resolve IBD:

A

inflammatory lesions entirely clear up

153
Q

celiac disease is associated with

A

MHC II

HLA-DQ2 and HLA-D8

154
Q

what HSR is celiac disease

A

IV

155
Q

80% of individuals with celiac disease is

A

undiagnosed

156
Q

many people with celiac disease have silent celiac disease:

A

no real symptoms, but intestine still looks bad

157
Q

symptoms of celiac disease

A

Symptoms associated with malabsorption due to villus atrophy
Iron-deficiency anemia
Osteoporosis (Calcium, Vitamins D and K)
Stunted growth
Fatigue
Silent celiac disease
Overtly asymtomatic but have mucosal damage
Can present with other autoimmune diseases
1:20 celiacs have Type I diabetes (HLA-DQ2/DQ8)

158
Q

co-presentations of ppl with celiac disease

A

dental enamel defects & dermatitis herpetiformis

159
Q

dental enamel defects may be the only symptom of

A

celiac disease

160
Q

dermatitis herpetiformis with celiac disease, will find what if you look at contents

A

lots of IgA anti-epidermal translutaminase

161
Q

what gives rise to rash and blister in skin for celiac disease

A

tissue transtaminase in gut is one recgnized in gut, they cross react with epidermal form

162
Q

describe mechanism of celiac (also on pg 57)

A

enterocytes in gut become stressed and induce stress response and the stressed eneerocytes release zonulin which acts on enterocytes to make epithelial barrier more leaky. that allows stuff to penetrate. stressed enterocytes express MICA and MICB which are recognized by intraepithelial lymphocytes which kill the enterocytes. when the enterocytes are killed get released of tissue transcataminase (one substrate is alpha gliadin itself) and modifies the apha gliadin, you get t cell response against this and get antibodies against it. so get alpha glidin specific Th1 cells. some evidence for enterocyte lysis by actiated CTL. T cells help B cells make antibodies and main antigen they rcognize are antigens releaed from enterocytes including tissue transcaatminase as wella s alpha gliadin. IgA against the tissue transcataminase that cross reats with epiderm and gives rise to rashes.

163
Q

diagnosis for celiac disease

A

Serological tests
Antiendomysial antibodies
Anti tissue transglutaminase antibodies
Tissue biopsy of symptomatic seropositive individuals

164
Q

treatment for celiac disease

A

strict gluten-free diet for life

Immunology Block 4 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions