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Block 6 Week 2 > AutoImmune Diseases- Hypersensitivity types II, III, IV > Flashcards

AutoImmune Diseases- Hypersensitivity types II, III, IV Flashcards

1
Q

What do you need to have autoimmunity?

A

T cells with receptors for self
susceptibility genes like MHC that allow self peptides to be presented
A trigger that upregulates co-stimulatory molecules on the APC (infection or tissue damage)

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2
Q

What 2 costimulatory moecules are needed to make a T cell reaction?

A

B7 and CD28

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3
Q

What is molecular mimicry?

A

when a microbe resembles a self antigen and thus you get a self-reactive T cell

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4
Q 
Which MHC class defect will cause suscpetiblity to:
 ankylosing spondylitits or acute anterior uveitis?
A

MHC 1

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5
Q 
Which MHC class defect will cause suscpetibility to:
good pasture's syndrome
MS
Graves' disease
Myasthenia Gravs
Systemic lupus erythematosus
Type I insulin-dependent diabetes mellitus
Rheumatoid arthritis
pemphigus vulgaris
hashimotos thryoiditis
A

MHC II

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6
Q

What kind of hypersensitivity reaction is this:

autoantibodies against surface antigens on blood cells

A

Autoimmune Type II hypersensitvity disease

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7
Q

What diseases are associated with autoantibodies aginst surface antigens on blood cells?

A

autoimmune hemolytic anemia

autoimmune (idiopathic) thrombocytopenic purpura

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8
Q

What kind of hypersensitivity reaction is this:

autoantibodies against cell surface antigens on fixed tissues

A

autoimmune type II hypersensitivity diseases

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9
Q

What diseases are associated with autoantibodies against cell surface antigens on fixed tissues?

A

good pasture syndrome
acute rheumatic fever
pemphigus vulgaris

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10
Q

What kind of hypersensitivity reaction is this:

autoantibodies against cellular receptors?

A

autoimmune type II hypersensitivity diseases

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11
Q

What diseases are associated with autoantibodies against cellular receptors?

A

myasthenia gravis

graves’ disease (hyperthyroidism)

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12
Q

In autoimmune thrombocytopenia, autoantibodies are formed against the (blank), a plasma membrane integrin

A

gpIIb:iiia

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13
Q

In thrombocytopenia, autoantibodies are formed against the gpIIb:IIIa, a platelet plasma membrane integrin
Antibody-coated platelets are destroyed by phagocytic cells in the (blank) and (blank).
How do you treat this?

A

liver and spleen

corticosteroids

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14
Q

WHat is this:
biopsy of early skin lesions show epidermal disruption and blister formation. There are deposits of IgG4 and antibodies to desmoglein 3.

A

Pemphigus vulgaris

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15
Q

How do you treat pemphigus vulgaris?

A

prednisone and cyclophosphamide

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16
Q

What antibodies do you find in good pasture syndrome?

A

alpha 3 chain of type IV collagen found in the glomerulus and alveolar basement membranes

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17
Q

What does good pasture syndrome cause?

A

causes a proliferative, rapidly progressive glomerulonephritis and a necrotizing hemorrhagic interstitial pneumonitis

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18
Q

How do you treate good pastures syndrome?

A

plasmapheresis (removes pathogenic circulating antibodies)

and immune suppression

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19
Q

How does graves’ disease work?

A

Antibodys mimic TSH and bind to TSH receptor to induce hyperthyroidism and thus pathophysiology

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20
Q

How does myasthenia gravis work?

A

antibodies bind to ACh receptors and inhibits acetycholine binding resulting in paralysis

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21
Q

(blank) is rare autoimmune disease that is usually associated with antagonistic autoantibodies directed against acetylcholine receptors

A

myasthenia gravis

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22
Q

How do you treat myasthenia gravis?

A

acetylcholinesterase inhibitors
and
plasmapheresis, immunosuppressants

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23
Q

Who are affected more with graves disease, men or women?

A

women

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24
Q

Graves hyperthyroidism has been linked to polymorphisms in immune-function genes like (blank) and (blank) alleles.

A

CTLA4 and HLA-DR3 allele

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25
Q

What is this:
Thyroid-stimulating IgG autoantibody binds to the TSH receptor and mimics the action of TSH (agonist), stimulating the release of thyroid hormones; no feedback inhibition to the pituitary.

A

Graves disease

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26
Q

What is this:

Pathology includes diffuse hyperplasia of the thyroid, ophthalmopathy (exophthalmos), and dermopathy.

A

graves disease

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27
Q

What are the lab findings in graves disease?

A

elevated free T4 and T3, depressed TSH levels

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28
Q

What is scary about have an autoantibody disease when pregnant?

A

the autoantibodies can cross the placent and cause disease in the fetus and newborn infant

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29
Q

What is the symptom of myasthenia gravis?

A

muscle weakness

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30
Q

What is the symptom of graves’ disease?

A

hyperthyroidism

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31
Q

What is the symptom of thrombocytopenic purpura?

A

bruising and hemorrhage

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32
Q

What is the symptom of neonatal lupus rash and/or congenital heart block?

A

photosensitive rash and/or bradycardia

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33
Q

What is the symptom of pemphigus vulgaris?

A

blistering rash

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34
Q

How long do autoimmune type III immune complex diseases usually last?

A

they persist for life

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35
Q

How prevalent is systemic lupus erythematosis (SLE)?

A

1 in 200 with a predilection for females of childbearing age

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36
Q

Is there a genetic component associated with SLE?

A

yes HLA-DR3

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37
Q

What system does SLE attack?

A

all of them

38
Q

What are the clinical findings of SLE?

A

photosensitive rash, polyarthritis, serositis, fatigue

39
Q

What usually leads to death in SLE?

A

lupus nephritis and CNS involvement

40
Q

What laboratory finding can you find in systemic lupus and how?

A

presence of ANA via anti-double-strandd DNA and anti-Smith ribonucleoprotein

41
Q

(blank) deficiency is an important risk factor for SLE

A

complement (hypocomplementemia may occur during flares)

42
Q

explain how one gets systemic lupus erythematosis (SLE)

A

-something caues apoptosis of cells and inflammation
-nuclei of cells are inadequately cleared and large amount of nuclear antigens are around
-linked recognition causes self-reactive T and B cells to interact and make nuclear antibodies
-complexes of the antigens and antibodies bind to Fc receptors on B cells and dendritic cells and are endocytosed
- endosomal TLR stimulate B cells to produce more antibodies and activate dendritic cells to produce interferons and cytokines which further enhances immune response and causes more apoptosis.
Net results in a cycle of antigen release and immune activation resulting in production of high affinity autoantibodies

43
Q

anti-DNA antibodies are generated by (blank)

A

linked recognition

44
Q

Explain linked recognition

A

T and B cells specifc for histone proteins are floating aroun. B cell internalizes some self DNA pieces (histones) and then acts as an APC to T cells which will bind to it and become stimulated and release cytokines and CD40L to bind to CD40 on B cells and activate more B cells

45
Q

Which organ systems are most affected by systemic lupus erythematosus?

A
  • consititutional symptoms (fatigue, fever, weight loss)
  • mucocutaneous involvement (malar rash, alopecia, mucosal ulcers, discoid lesions)
  • musculoskeletal involvement
  • serositis
  • glomerulonephritis
  • neuropsychiatric involvement
  • autoimmne cytopenia
46
Q

Why are peope that have SLE so at risk to have renal failure?

A

because there DNA immune complexes get stuck in the kidneys and cant be removed and make sort of a clot that results in renal failure.

47
Q

How can you tell whether you have drug induced LE or SLE?

A

drug induced has high amount of antihistone and SLE has high amounts of anti-double stranded DNA and anti-SM and nuclear RNP

48
Q

What does sjogren syndrom have high levesl of ?

A

RNP

49
Q

What does scleroderma have high levels of?

A

centromeric proteins

50
Q

WHat does systemic sclerosis have high levels of?

A

DNA topoisomerase

51
Q

What does inflammatory myopathy have high levels of?

A

histidyl-tRNA synthetase

52
Q

Type IV hypersensitivity is mediated by (blank)

A

T cells

53
Q

What are the 2 ways you can get Type IV hypersensitivity via T cells?

A

Cytokine-mediatd inflammation which is where APC connect with CD4 T ells to release cytokines and infammation
OR
T Cell-mediated cytolysis which is where APC connect with CD8 and these cells kill tissue

54
Q

What are 2 organ-specific autoimmune diseases mediated by T cells?

A

Multiple sclerosis and hashimoto thyroiditis

55
Q

What are 2 systemic autoimmune diseases mediated by T cells?

A

systemic sclerosis

sjogren syndrome

56
Q

How do you get MS?

A

T cells with receptors for many neuroantigens dont get destroyed in the thymus, an unknown trigger causes inflammation n the CNS and ten you get diruption of BBB that allows these neuroantigen specific T ells into the CNS and microglial cells activate these T cells to release mediators and demyelinate axons

57
Q

What are the 3 mediators in MS that promote demyleination?

A

CF
ROS
IL-1beta

58
Q

What are 2 frequent presentations of symptoms in MS?

A

visual compromise and stiffness/weakness

59
Q

What do oligoclonal bands of IgG in the CSF indicate?

A

clonal expansion of B-cell clones

60
Q

HOw do you typically treat MS acutely? what about chronically?

A

IV corticosteroids

Alpha and Beta interferons and glatiramer acetate

61
Q

What is the prevalence of MS, and what gender do you find it in most? is there a genetic component?

A

females (10x more likely)

yes HLA DR2

62
Q

What do CD8 cells need to mess up tissues?

A

FASL and FAS

63
Q

What is the prevalence of hashimoto thyroiditis?

A

1 in 200

64
Q

How does hashimoto thyroiditis work?

A

make autoantibodies agaoins thyroglobulin and thyroid peroxidase

65
Q

In Hashmimoto thyroidits, what will you see in a thyroid?

A

infiltration of parenchyma by a mononuclear inflammatory infiltrate contain small lymphocytes, plasma cells and well-deveoped germinal centers

66
Q

What are the lab values of hashimoto thyroiditis?

A

low T3 and T4 levels and high levels of TSH

67
Q

Hashimoto thyroiditis increases the risk for what other disease?

A

B cell non-hodgkin lymphomas

68
Q

(blank) is characterized by excessive fibrosis in a variety of tissues from collagen deposition by activated fibroblasts.

A

Systemic sclerosis (SS)

69
Q

What is the benign form of systemic sclerosis?

A

limitd scleroderma OR

CREST syndrome

70
Q

How can you tell if you have limited scerleroderma or CREST syndrome?

A

via the presence of anti-centrome antibody

71
Q

What does CREST stand for?

A

C = Calcinosis in skin and elsewhere
R = Raynaud’s phenomenon, sensitivity to cold
E = Esophageal dysmotility from submucosal fibrosis S = Sclerodactyly from dermal fibrosis
T = Telangiectasias

72
Q

What is diffuse scleroderma? How do you diagnosis this?

A

the worst form of SS

anti-DNA topoisomerase I antibody (Scl-70)

73
Q

(blank) presents with CREST findings and arterial intimal thickening and proliferation (hyperplastic arteriosclerosis “onion skin” lesion) leading to malignant hypertension with arterial fibrinoid necrosis, thrombosis, and renal infarction.

A

Diffuse scleroderma

74
Q

What do half of Systemic Sclerosis patients die of?

A

renal disease

75
Q

What is the mechanism behind systemic sclerosis (scleroderma)?

A

CD4 t cells respond to an antigen that accumulates in the tissues and release cytokines that activate inflammatory cells and fibroblasts

76
Q

Systemic sclerosis is a rare disorder with a female-to-male ratio of (blank) to (blank)

A

3:1

77
Q

What age do most people get systemic sclerosis?

A

50 to 60 years old

78
Q

What is raynauds phenomenon?

A

episodic vasoconstriction of the arteries and arterioles of the extremities. (it is seen in al patient and preceds other symptoms in 70% of patients)

79
Q

How often do you see dysphagia in SS patients?

A

50% of the time

80
Q

What is this disease:

decrease in tears and saliva (sicca syndrome)

A

sjogren syndrome

81
Q

Why do you get decrease in tears and saliva in sjogren syndrome?

A

you get lymphocytic infiltration and fibrosis of lacrimal and salivary glands

82
Q

What is the mechanism of action behind sjogren syndrome?

A

an initial trigger-> local cell death-> release of self-antigens-> CD4 cell and B cells react-> inflammation, tissue damage, fibrosis-> antibodies come -> rheumatoid factor, 2 antibodies which are SS-A(Ro) and SS-B(La)

83
Q

What are the 2 antibodies found in sjogren syndrome?

A

SS-A(Ro) and SS-B (La)

84
Q

What is the prevalence of sjogren syndrome? Female to male ratio?

A

1 in 300

9:1

85
Q

What age is sjogren syndrome most prevalent?

A

40-60 year old females

86
Q

What is the dry eyes and dry mouth sjorgen syndrome caused by

A

T cell-mediated destruction of lacrimal and salivary glands

87
Q

What is found in 70% of cases of sjogren syndrome?

A

rheumatoid factor

88
Q

What are diagnostic for sjogren syndrome?

A

SS-A(Ro) and SS-B(La)

89
Q

What is a schirmer test?

A

measures quantity of tears secreted

90
Q

What will a lip biospy show us if someone has sjogren syndrome?

A

lymphoid foci

91
Q

WHat drugs will you use to relieve symptoms?

A

pilocarpine (relieves dryness) an artificial tears

Block 6 Week 2 (7 decks)

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