Autoimmunity

Question 1

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

Answer 1

Plasmapheresis and anti-inflammatory drugs.

Question 2

What are the other symptoms of WG?

Answer 2

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

Question 3

What is the first symptom of WG?

Answer 3

Rhinitis: pain, stuffiness, and nose bleeds.

Question 4

The vasculitis seen in WG is caused by what?

Answer 4

The activated neutrophils degranulate causing damage to the vasculature.

Question 5

ANCAs bind to what elicting them to what?

Answer 5

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

Question 6

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.

Answer 6

True

Question 7

What type of Ig is the Ab that mediates WG?

Answer 7

IgG

Question 8

What Ab mediates Wg?

Answer 8

Anti-neutrophil cytoplasmic antibodies (ANCAs).

Question 9

WG uses what mechanism to elicit the autoimmune condition?

Answer 9

Molecular mimicry

Question 10

Wegener’s Granulomatosis is what type?

Answer 10

Type II

Question 11

What is the treatment for GBS?

Answer 11

Plasmapheresis and immunosuppressants.

Question 12

What are the symptoms for GBS?

Answer 12

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

Question 13

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

Answer 13

Demyelination of nerves.

Question 14

What is the Ig in GBS specific for?

Answer 14

Gangliosides: common components of human nerve tissue.

Question 15

What Ig mediates GBS?

Answer 15

IgG

Question 16

GBS uses what mechanism to elicit the autoimmune condition?

Answer 16

Molecular Mimicry

Question 17

Guillain Barre Syndrome is what type?

Answer 17

Type II

Question 18

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

Answer 18

True

Question 19

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

Answer 19

Reactive Arthritis

Question 20

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

Answer 20

Yes

Question 21

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

Answer 21

True

Question 22

What are the 3 immunologically privileged sites of the body?

Answer 22

Eyes, testes, placenta/fetus

Question 23

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

Answer 23

True

Question 24

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

Answer 24

True

Question 25

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

Answer 25

True

Question 26

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

Answer 26

Women

Question 27

What does the diagnostic lab test result show for MS?

Answer 27

Presence of oligoclonal bands of IgG in CSF

Question 28

What is the treatment for MS?

Answer 28

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

Question 29

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

Answer 29

True

Question 30

What are the symptoms of MS?

Answer 30

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

Question 31

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

Answer 31

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

Question 32

In MS, the immune response is directed at what?

Answer 32

The myelin sheath of nerve cells.

Question 33

What cell mediates MS?

Answer 33

Th1 Cells

Question 34

Multiple Sclerosis is what type?

Answer 34

Type IV

Question 35

What is the treatment for SjS?

Answer 35

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.

Question 36

What tests are used to diagnose SjS?

Answer 36

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

Question 37

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

Answer 37

T: caused by the dry mouth.

Question 38

Is rhematoid factor required for SjS?

Answer 38

no

Question 39

What are the symptoms of SjS?

Answer 39

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

Question 40

Are women or men more likely to suffer from SjS?

Answer 40

Women 9:1

Question 41

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

Answer 41

True

Question 42

What other organs are affected by SjS?

Answer 42

Kidneys, blood vessels liver, brain

Question 43

What cell initiates the inflammation in SjS?

Answer 43

autoreactive T cells

Question 44

Inflammation in SjS destroys what?

Answer 44

Exocrine glands that produce tears and saliva

Question 45

Sjogren's Syndrome is what type?

Answer 45

Type IV

Question 46

What is the treatment for RA?

Answer 46

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

Question 47

What is the first symptom of RA?

Answer 47

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

Question 48

Is rheumatoid factor required for RA?

Answer 48

no

Question 49

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

Answer 49

IgG, IgM, and IgA

Question 50

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

Answer 50

Women 3:1

Question 51

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

Answer 51

True

Question 52

Inflammation in RA damages what?

Answer 52

Cartilage and ligament tissue of joints

Question 53

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

Answer 53

Autoreactive T cells

Question 54

Rheumatoid Arthritis is what type?

Answer 54

Type IV

Question 55

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

Answer 55

it is more expensive

Question 56

What is the alternative therapy for patients w/ IDDM?

Answer 56

the use of human recombinant insulin

Question 57

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

Answer 57

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

Question 58

What is the treatment for IDDM?

Answer 58

Daily injections of pig or bovine insulin

Question 59

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

Answer 59

coma and death

Question 60

What ethnic group does IDDM primarily affect?

Answer 60

people of european descent

Question 61

T or F. Lymphocytic inflammation is characteristic of IDDM.

Answer 61

True

Question 62

The answer to #104 has specificity for what?

Answer 62

An unknown component of the Beta cells

Question 63

What are the effector cells of IDDM?

Answer 63

CTL's

Question 64

IDDM results in destruction of what cell type?

Answer 64

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

Question 65

Insulin-Dependent Diabetes Mellitus is what type?

Answer 65

Type IV

Question 66

What is the treatment for SLE?

Answer 66

Anti-inflammatory drugs

Question 67

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.

Answer 67

True

Question 68

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.

Answer 68

True

Question 69

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

Answer 69

shows the presence of autoAb's

Question 70

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

Answer 70

They thicken due to immune complex deposition

Question 71

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

Answer 71

True

Question 72

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

Answer 72

True

Question 73

The initial sign, characteristic rash of SLE forms where?

Answer 73

Butterfly rash on the face

Question 74

Where are immune complexes deposited in SLE?

Answer 74

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

Question 75

The damaged cells in SLE release what? Forming what?

Answer 75

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

Question 76

What leads to tissue destruction in SLE?

Answer 76

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

Question 77

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

Answer 77

DNA, histones, ribosomes.

Question 78

SLE is mediated by autoAb’s specific for what?

Answer 78

Many self macromolecules.

Question 79

Systemic Lupus Erythematosis is what type?

Answer 79

type III

Question 80

What are the symptoms of MEC?

Answer 80

Purpura, arthralgia, myalgia= Meltzer’s triad.

Question 81

What causes the immune complex disorder seen in MEC?

Answer 81

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

Question 82

MEC often follows what infection?

Answer 82

Hep C

Question 83

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

Answer 83

T: such as multiple myeloma or Waldenstrom macroglobulinemia.

Question 84

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

Answer 84

Bence Jones Proteins

Question 85

What is a cryoglobulin?

Answer 85

An Ig that becomes insoluble at reduced temperature

Question 86

Mixed Essential Cryoglobulinemia is what type?

Answer 86

Type III

Question 87

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

Answer 87

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

Question 88

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

Answer 88

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

Question 89

Which Ig mediates SBE?

Answer 89

IgG

Question 90

Subacute Bacterial Endocarditis is what type?

Answer 90

Type III

Question 91

What is an alternative treatment to MG?

Answer 91

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

Question 92

How do you treat MG?

Answer 92

Anti-inflammatory drugs.

Question 93

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

Answer 93

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

Question 94

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

Answer 94

73. The binding causes the receptors to be endocytosed and degraded. Antagonism

Question 95

The Ab’s in MG are specific for what?

Answer 95

72. The IgG binds to acetylcholine receptors on muscle cells.

Question 96

What Ig mediates MG?

Answer 96

IgG

Question 97

Myasthenia gravis is what type?

Answer 97

Type II