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Immunology block 2 > Chapter 17 > Flashcards

Chapter 17 Flashcards

1
Q

Type II autoimmunity is mediated by?

A

Antibodies

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2
Q

The antibodies in type II autoimmunity are specific for?

A

Cell surface & ECM

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3
Q

Type III autoimmunities are mediated by?

A

Antibodies

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4
Q

Type III autoimmunities are caused by?

A

Immune complexes deposited in tissues

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5
Q

Type IV autoimmunity is mediated by?

A

T cells

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6
Q

Are there immune diseases mediated by IgE?

A

No

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7
Q

5 ways in which we tolerate our own self?

A
  1. Negative selection in BM and thymus
  2. Expression of tissue specific proteins in thymus
  3. No lymphocyte access to some tissues
  4. Suppression of autoimmune responses by Treg cells
  5. Induction of anergy in auto reactive B and T cells
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8
Q

In this disease, a patient makes autoantibodies for their own erythrocytes

A

Autoimmune hemolytic anemia

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9
Q

What happens to the RBC’s in someone with autoimmune hemolytic anemia?

A

They are covered in antibodies or complement and are phagocytosed (in spleen)

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10
Q

Result of autoimmune hemolytic anemia?

A

Anemia (duh!!)

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11
Q

Test for autoimmune hemolytic anemia?

A

Direct Coomb’s test

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12
Q

What would you see in a direct coombs test that was positive for autoimmune hemolytic anemia?

A

Hemagglutination

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13
Q

IgG inhibition of an enzyme responsible for cleaving vWF?

A

Autoimmune (Idiopathic) Thrombocytopenic Purpura

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14
Q

Clinical presentation of ITP?

A

Bleeding. vWF is not properly cleaved. It is too big so it clots up small vessels. You use up all your platelets and clotting factors in these small clots so you bleed

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15
Q

Organs effected in ITP?

A

liver, kidneys, blood vessels, brain

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16
Q

Symptoms of ITP?

A
  1. Thrombocytopenia
  2. Purpura (bruising)
  3. Neurological symptoms
  4. Microangioplastic hemolytic anemia
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17
Q

Why do you get anemia in ITP?

A

RBCs are damaged as they are pushed through clots

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18
Q

What is microangioplastic hemolytic anemia?

A

Hemolytic anemia (low RBCs due to RBC destruction) microangioplastic (because it is due to clotting in small blood vessels)

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19
Q

In ITP, patient would present with?

A

Purpura (bruises), thrombocytopenia (low platelets), anemia (low RBCs), bleeding (due to using up platelets and clotting factors in small blood vessels)

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20
Q

Treatment of ITP?

A

Plasmapheresis with plasma from healthy donors

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21
Q

Pathogenesis of Goodpasture’s.. What do you make antibodies against?

A

Type IV collagen

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22
Q

Where is type IV collagen found?

A

Lines basement membranes throughout the body

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23
Q

Clinical presentation of Goodpasture’s?

A

Hemoptysis and hematuria (from Immunopath). When you think Goodpasture, think bloody lungs and bloody kidneys

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24
Q

Miller’s notes say that “kidney damage” results from Goodpasture’s. What does this imply?

A

Glomerulonephritis

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25
Q

Treatment of Goodpasture?

A

Plasma exchange and anti-inflammatory drugs

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26
Q

Goodpasture is autoimmunity type II, III, or IV?

A

II

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27
Q

Inflammatory destruction of vascular endothelial cells of arterioles and smooth muscle cells; replacement with collagen and other fibrous tissue

A

Systemic sclerosis (scleroderma)

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28
Q

Main symptom?

A

Hardening/thickening of skin

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29
Q

Is rheumatoid factor required for Scleroderma?

A

No

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30
Q

What test do you use to diagnose scleroderma?

A
  1. Anti-Scl70 (anti-DNA topoisomerase)
  2. Anti-nuclear
  3. Anti-centromere
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31
Q

Treatment for Scleroderma?

A

No cure, no standard treatment. Can only give drugs that increase blood flow to periphery

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32
Q

Scleroderma is what type of autoimmune disease?

A

II

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33
Q

This autoimmune disease is caused by antibodies produced from Streptococcus pyogenes doing molecular mimicry and attacking heart cells

A

Acute rheumatic fever

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34
Q

Result of acute rheumatic fever?

A

Heart valve scarring, myocarditis

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35
Q

Acute rheumatic fever is what type of autoimmune disease?

A

Type II

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36
Q

Acute rheumatic fever occurs after?

A

Strep throat!

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37
Q

This autoimmune disease is mediated by IgG specific antibodies for two proteins (desmoglein 1 and 3); results in loss of cohesion of keratinocytes in epidermis

A

Pemphigus vulgaris

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38
Q

Symptom of pemphigus vulgaris?

A

Painful, chronic blistering of skin

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39
Q

Which IgG (1,2,3,4) is thought to be the pathogenic one in the case of pemphigus vulgaris?

A

IgG4

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40
Q

How do you diagnose pemphigus vulgaris?

A

Punch biopsy of a lesion (skin blister) and immunofluourescent staining

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41
Q

How do you treat pemphigus vulgaris?

A

Corticosteroids and other anti-inflammatory drugs, rituximab

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42
Q

Hashimoto’s thyroiditis, Grave’s disease, Subacute thyroiditis, Idiopathic hypothyroidism are all diseases of what endocrine gland?

A

Thyroid gland

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43
Q

Type I diabetes and type II diabetes are autoimmune diseases of which endocrine gland?

A

Islets of Langerhans (pancreas)

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44
Q

Addison’s disease is a disease of which endocrine gland?

A

Adrenal gland

45
Q

This disease is caused by antibodies specific for self thyroid stimulating hormone (TSH) receptors. The antibody acts as an agonist and stimulates the receptor as if it were binding to its actual ligand

A

Grave’s disease

46
Q

Graves disease- what type?

A

Type II autoimmue disease

47
Q

Symptoms of graves disease?

A

Bulging eyes, heat/cold intolerance, irritability, weight loss

48
Q

Treatment of Grave’s disease?

A

Plasmapheresis

49
Q

Antibodies in this disease are specific for Acetylcholine receptors

A

Myasthenia gravis

50
Q

Clinical presentation with myasthenia gravis?

A

Muscle weakness

51
Q

Treatment of myasthenia gravis?

A

Anti-inflammatory drugs and pyridostigimine

52
Q

How does pyridostigimine work?

A

Inhibits cholinesterase (which degrades acetylcholine) so acetylcholine “lives longer” and has more of a chance to bind to its receptor

53
Q

This disease is mediated by antibodies that bind normal flora (Streptococcus viridans), but are now binding to damaged heart valves

A

Subacute bacterial endocarditis

54
Q

Which antibody mediates subacute bacterial endocarditis?

A

IgG

55
Q

T/F This disease usually only occurs after someone has already had damage to their heart valves?

A

True, typically patient has previously had rheumatic fever or a congenital heart condition

56
Q

How is inflammation mediated in subacute bacterial endocarditis?

A

Inflammation is mediated by phagocytes that recognize opsonized bacteria; and anaphylatoxins that are produced as a result of the complement cascade

57
Q

Subacute bacterial endocarditis is which type of autoimmune disease?

A

Type III (immune complex mediated)

58
Q

This disease is characterized by the production of cryoglobulins

A

Mixed essential cryoglobulinemia

59
Q

What are cryoglobulins?

A

Immunoglobulins that become insoluble at reduced temperatures

60
Q

What are cryoglobulins called when only the light chain is present?

A

Bence-Jones proteins

61
Q

Characteristic trait of people with mixed essential cryoglobulinemia?

A

They usually have a B cell proliferative disorder

62
Q

Along with B cell proliferative disorder, what other infection is common in conjunction with Mixed essential cryoglobulinemia?

A

Hepatitis C

63
Q

What do cryoglobulins do?

A

Act like rheumatoid factor and bind to Fc regions of Ig’s causing immune complex disorder

64
Q

Symptoms of mixed essential cryoglobulinemia?

A

Meltzer’s triad: purpura, arthalgia, myalgia

65
Q

Mixed essential cryoglobulinemia is what type of autoimmune disease?

A

Type III (immune complex)

66
Q

The prototypical systemic autoimmune disease. Patient makes autoantibodies for DNA, histones, ribosomes, etc…

A

Systemic Lupus Erythmatosis

67
Q

How is inflammation initially initiated in SLE?

A

Auto-antibodies bind to cell surface components which initiates inflammation leading to tissue destruction

68
Q

The damaged cells release macromolecules; immune complexes form and are deposited in blood vessels, kidneys, and joints. What does this lead to?

A

Further inflammation

69
Q

Treatment of Lupus?

A

Anti-inflammatory drugs

70
Q

Lupus is what type of autoimmune disease?

A

Type III (immune complex mediated)

71
Q

This autoimmune disease results in destruction of insulin-producing cells in the pancreas

A

Insulin dependent diabetes mellitus (type I diabetes)

72
Q

What cells are the effectors of type I diabetes?

A

CTL’s; that makes type I diabetes a type IV autoimmune disease

73
Q

What produces insulin?

A

Beta cells in islets of Langerhans in the pancreas

74
Q

Treatment for insulin dependent diabetes?

A

Insulin injections (either from pig or human recombinant insulin)

75
Q

Inflammatory disease of the joints mediated by auto-reactive T cells

A

Rheumatoid arthritis

76
Q

Describe rheumatoid factor

A

The production of IgM, IgG, and IgA specific for the Fc region of antibodies

77
Q

Is rheumatoid factor required for rheumatoid arthritis?

A

No

78
Q

Treatment of rheumatoid arthritis?

A

Infliximab (anti-TNF Ab)

Rituximab (uses anti-CD20 ADCC to deplete B cells)

79
Q

Rheumatoid arthritis is what type of autoimmune disease?

A

Type IV

80
Q

This disease is a T cell mediated auto-reactivity against the exocrine glands that produce tears and saliva

A

Sjogren’s syndrome

81
Q

Symptoms of Sjogrens?

A

Dry eyes and mouth

82
Q

Is rheumatoid factor required for Sjogrens?

A

No

83
Q

How do you diagnose Sjogrens syndrome?

A

Schirmer test to measure tear output; also ANA and rheumatoid factor test (often occurs secondary to rheumatic fever and SLE)

84
Q

Treatment of Sjogrens?

A

No cure; use artificial tears, wear goggles

85
Q

Sjogrens syndrome is what type of autoimmune disease?

A

Type IV

86
Q

This autoimmune disease is mediated by Th1 CD4 T cells that are directed towards the myelin sheath of nerve cells

A

Multiple sclerosis

87
Q

Causes demyelination of white matter in CNS?

A

MS

88
Q

Symptoms of MS?

A

motor weakness, impaired vision, lack of coordination, spasticity

89
Q

Is MS early onset, sudden onset, progressive?

A

Progressive, and the progression is highly variable

90
Q

Treatment of MS?

A

Immunosuppressive drugs and IFN-beta1

91
Q

This malady occurs in 85% of MS patients

A

Oligoclonal bands of IgG

92
Q

Do HLA allotypes play a role in autoimmune diseases?

A

You betcha, for some diseases, if you have a specific haplotype you have an increased risk of getting the disease

93
Q

Position 57 of the DQ-beta chain affects susceptibility to?

A

Type 1 diabetes

94
Q

Name 3 immunologically privileged sites?

A

Eyes, testes, placenta/fetus

95
Q

Molecular mimicry- Group A Strep could lead to?

A

Acute rheumatic fever

96
Q

Chlamydia trachomatis infection can lead to what autoimmune disease?

A

Reiter’s syndrome (arthritis)

97
Q

Shigella flexneri, Salmonella typhimurium, Salmonella enteritidis, Yersinia enterocolitica, Campylobacter jejuni can lead to?

A

Reactive arthritis

98
Q

Borrelia burgdorferi can lead to?

A

Chronic arthritis in Lyme disease

99
Q

Coxsackie A virus, Coxsackie B virus, echoviruses, rubella can lead to?

A

Type 1 diabetes

100
Q

In molecular mimicry, is it the same or a different MHC molecule that presents the self antigen?

A

The same MHC molecule presents both the infectious antigen and the similar self antigen

101
Q

What 3 diseases from this lecture are diseases of molecular mimicry?

A
  1. Acute rheumatic fever
  2. Guillain Barre Syndrome
  3. Wegener’s Granulomatosis
102
Q

This is a type II autoimmune disease mediated by IgG specific for gangliosides. It results in demyelination of nerve cells

A

Guillain Barre syndrome

103
Q

Guillain Barre is a disease of molecular mimicry. What infection leads to this disease?

A

Campylobacter jejuni

104
Q

Symptoms of Guillain Barre?

A

Symmetrical weakness of lower limbs ascending to upper limbs and face; difficulty swallowing and breathing; drooling; partial paralysis often occurs

105
Q

Treatment for Guillain Barre?

A

plasma exchange; immunosuppressive drug treatment

106
Q

A disease of molecular mimicry mediated by anti-neutrophil cytoplasmic antibodies (ANCA); it is IgG mediated; most common determinant is proteinase-3

A

Wegener’s Granulomatosis

107
Q

Pathology of Wegener’s?

A

ANCA’s bind to neutrophils activating them; the neutrophils up regulate adhesion molecules allowing them to bind to vascular endothelial cells; then the neutrophils degranulate causing damage to the vasculature (vasculitis)

108
Q

Symptoms of Wegener’s?

A
  1. Rhinitis & conjunctivitis
  2. Lung infiltrates
  3. Rapidly progressive glomerulonephritis
  4. Granulomas usually found in all affected tissues
109
Q

Treatment of Wegener’s?

A

Plasma exchange; anti-inflammatory

Immunology block 2 (5 decks)

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