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Immunology Spring 2 > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

What is the treatment of Wegner’s Granulomatosis (WG)?

A

Plasmapheresis and anti-inflammatory drugs.

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2
Q

What are the other symptoms of WG?

A

Conjunctivitis, lung infiltrates, rapidly progressing glomerulonephritis, granulomas found in all affected tissues (usually but not always).

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3
Q

What is the first symptom of WG?

A

Rhinitis: pain, stuffiness, and nose bleeds.

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4
Q

The vasculitis seen in WG is caused by what?

A

The activated neutrophils degranulate causing damage to the vasculature.

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5
Q

ANCAs bind to what elicting them to what?

A

Neutrophils. Activates them to upregulate adhesion molecules allowing them to bind to vascular endothelial cells.

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6
Q

T or F. The onset of WG typically follows bacterial or viral infection and the response to the pathogen elicits production of IgG that cross reacts with neutrophil determinants.

A

True

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7
Q

What type of Ig is the Ab that mediates WG?

A

IgG

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8
Q

What Ab mediates Wg?

A

Anti-neutrophil cytoplasmic antibodies (ANCAs).

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9
Q

WG uses what mechanism to elicit the autoimmune condition?

A

Molecular mimicry

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10
Q

Wegener’s Granulomatosis is what type?

A

Type II

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11
Q

What is the treatment for GBS?

A

Plasmapheresis and immunosuppressants.

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12
Q

What are the symptoms for GBS?

A

Symmetrical weakness of lower limbs that rapidly ascends to upper limbs and face. Difficulty swallowing and breathing. Drooling. Partial paralysis often occurs.

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13
Q

What is the results of the binding of the IgG in GBS?

A

Demyelination of nerves.

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14
Q

What is the Ig in GBS specific for?

A

Gangliosides: common components of human nerve tissue.

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15
Q

What Ig mediates GBS?

A

IgG

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16
Q

GBS uses what mechanism to elicit the autoimmune condition?

A

Molecular Mimicry

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17
Q

Guillain Barre Syndrome is what type?

A

Type II

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18
Q

T or F. Campylobacter jejuni induces autoimmune conditions via the action of molecular mimicry and is a diarrheal pathogen.

A

True

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19
Q

An infection of Campylobacter jejuni carries an associated risk to what autoimmune disease?

A

Reactive Arthritis

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20
Q

Is there an associated risk to autoimmune disease with certain bacterial, viral, and fungal infections?

A

Yes

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21
Q

T or F. Trauma to one eye can elicit effector T cells upon return to attack Ag in both eyes.

A

True

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22
Q

What are the 3 immunologically privileged sites of the body?

A

Eyes, testes, placenta/fetus

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23
Q

T or F. Position 57 of the HLA-DQbeta chain affects susceptibility to type I diabetes mellitus.

A

True

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24
Q

T or F. There is an increased risk of autoimmune disease in certain HLA haplotypes of MHC molecules.

A

True

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25
Q

T or F. An increased number of shared HLA haplotypes is directly related to incidence of diabetes in sibling pairs.

A

True

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26
Q

In general, do autoimmune diseases typically affect women or men?

A

Women

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27
Q

What does the diagnostic lab test result show for MS?

A

Presence of oligoclonal bands of IgG in CSF

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28
Q

What is the treatment for MS?

A

Immunosuppressants. IFN-beta1: reduces incidence of disease attacks.

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29
Q

T or F. MS is a highly variable progressive disease?

A

True

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30
Q

What are the symptoms of MS?

A

Motor weakness, impaired vision, lack of coordination, spasticity.

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31
Q

What does the destruction of myelin sheaths of nerve cells cause in MS?

A

Causes demyelination of white matter in the CNS forming sclerotic plaques.

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32
Q

In MS, the immune response is directed at what?

A

The myelin sheath of nerve cells.

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33
Q

What cell mediates MS?

A

Th1 Cells

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34
Q

Multiple Sclerosis is what type?

A

Type IV

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35
Q

What is the treatment for SjS?

A

No known cure. Artificial tears. Some pt’s wear goggles to increase humidity in the eyes. Punctal plugs: prevents tears from draining out of eye.

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36
Q

What tests are used to diagnose SjS?

A

Schirmer test: measures tear output. ANA and rheumatoid factor tests (bc SjS often occurs secondary to rheumatic fever and SLE).

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37
Q

T or F. SjS pt’s oftgen have serious dental problems?

A

T: caused by the dry mouth.

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38
Q

Is rhematoid factor required for SjS?

A

no

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39
Q

What are the symptoms of SjS?

A

dry eyes and dry mouth. sometimes skin, nose and vaginal dryness

40
Q

Are women or men more likely to suffer from SjS?

41
Q

T or F. SjS is the second most common rheumatic disease?

42
Q

What other organs are affected by SjS?

A

Kidneys, blood vessels liver, brain

43
Q

What cell initiates the inflammation in SjS?

A

autoreactive T cells

44
Q

Inflammation in SjS destroys what?

A

Exocrine glands that produce tears and saliva

45
Q

Sjogren’s Syndrome is what type?

46
Q

What is the treatment for RA?

A

Infliximab: an anti-TNF Ab. Rituximab: an anti-CD20 Ab uses ADCC to deplete B cells.

47
Q

What is the first symptom of RA?

A

Clubbing of the hands. At least I think that’s what it’s called. Just big bumps in joints of the fingers.

48
Q

Is rheumatoid factor required for RA?

49
Q

RA pt’s produce what 3 Ig’s that are specific for the Fc region of Ab molecules?

A

IgG, IgM, and IgA

50
Q

Are women or men more likely to be affected by RA?

51
Q

T or F. RA is the most common of the rheumatic diseases

52
Q

Inflammation in RA damages what?

A

Cartilage and ligament tissue of joints

53
Q

The inflammatory disease of the joints seen in RA is initiated by what cell?

A

Autoreactive T cells

54
Q

Rheumatoid Arthritis is what type?

55
Q

What is the drawback for the use of human recombinant insulin in DM patients?

A

it is more expensive

56
Q

What is the alternative therapy for patients w/ IDDM?

A

the use of human recombinant insulin

57
Q

Can some patients make an immune response to the treatment for IDDM?

A

Yes. The immune response is directed against the “foreign” insulin and makes the disease much worse.

58
Q

What is the treatment for IDDM?

A

Daily injections of pig or bovine insulin

59
Q

If IDDM is left untreated, what can happen to the pt?

A

coma and death

60
Q

What ethnic group does IDDM primarily affect?

A

people of european descent

61
Q

T or F. Lymphocytic inflammation is characteristic of IDDM.

62
Q

The answer to #104 has specificity for what?

A

An unknown component of the Beta cells

63
Q

What are the effector cells of IDDM?

64
Q

IDDM results in destruction of what cell type?

A

Beta cells in the islets of Langerhan’s in the pancreas, the insulin-producing cells.

65
Q

Insulin-Dependent Diabetes Mellitus is what type?

66
Q

What is the treatment for SLE?

A

Anti-inflammatory drugs

67
Q

T or F. In SLE, a B cell that internalizes a macromolecular complex can present Ag’s to T cells specific for any of the proteins of that complex.

68
Q

T or F. In SLE, CD4+ T cells specific for one epitope of a macromolecular complex can provide help to B cells specific for other accessible epitopes of the complex.

69
Q

What does immunofluorescent staining with anti-IgG show in SLE pt’s?

A

shows the presence of autoAb’s

70
Q

What happens to the basement membranes of glomeruli in SLE pt’s?

A

They thicken due to immune complex deposition

71
Q

T or F. SLE is most common in women, especially Asian and African women.

72
Q

T or F. SLE is a progressive disease with episodic inflammation.

73
Q

The initial sign, characteristic rash of SLE forms where?

A

Butterfly rash on the face

74
Q

Where are immune complexes deposited in SLE?

A

Blood vessels, kidneys, joints. This deposition leads to even more inflammation.

75
Q

The damaged cells in SLE release what? Forming what?

A

They release soluble macromolecules forming immune complexes when autoAb’s bind.

76
Q

What leads to tissue destruction in SLE?

A

The autoAb’s bind to cell surface components and initiate inflammation that leads to the tissue destruction.

77
Q

What are some examples of the SLE autoAb’s specificity?

A

DNA, histones, ribosomes.

78
Q

SLE is mediated by autoAb’s specific for what?

A

Many self macromolecules.

79
Q

Systemic Lupus Erythematosis is what type?

80
Q

What are the symptoms of MEC?

A

Purpura, arthralgia, myalgia= Meltzer’s triad.

81
Q

What causes the immune complex disorder seen in MEC?

A

The cryoglobulins bound to Fc regions of Ab molecules. Note: cryoglobulins act similar to rheumatoid factor.

82
Q

MEC often follows what infection?

83
Q

T or F. Cryoglobulins are most often produced by patients that have a B cell proliferative disorder.

A

T: such as multiple myeloma or Waldenstrom macroglobulinemia.

84
Q

If the cryoglobulin is only composed of light chains, what name is it given?

A

Bence Jones Proteins

85
Q

What is a cryoglobulin?

A

An Ig that becomes insoluble at reduced temperature

86
Q

Mixed Essential Cryoglobulinemia is what type?

87
Q

What 2 things are responsible for the inflammation seen in SBE?

A

Phagocytes that recognize opsonized bacteria (IgG and complement) and anaphylatoxins produced as a result of complement cascade activation.

88
Q

The inflammation in SBE is initiated by Ab’s that bind to Strep viridans that have colonized what?

A

Damaged heart valves. Note that pt’s that get SBE have withstanding damaged heart valves.

89
Q

Which Ig mediates SBE?

90
Q

Subacute Bacterial Endocarditis is what type?

91
Q

What is an alternative treatment to MG?

A

Pyridostigmine: inhibits acetylcholinesterase  longer lived acetylcholine competes better for receptor binding

92
Q

How do you treat MG?

A

Anti-inflammatory drugs.

93
Q

When muscle cells lose receptors, are they less sensitive or more sensitive to neuronal stimulation?

A

Less sensitive: leads to the severe muscle weakness seen in MG.

94
Q

The binding of Ab’s in MG results in what? Antagonism or agnoism?

A
  1. The binding causes the receptors to be endocytosed and degraded. Antagonism
95
Q

The Ab’s in MG are specific for what?

A
  1. The IgG binds to acetylcholine receptors on muscle cells.
96
Q

What Ig mediates MG?

97
Q

Myasthenia gravis is what type?

Immunology Spring 2 (7 decks)

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