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Alya Cards Pathology Robbins basis > Ch 6 > Flashcards

Ch 6 Flashcards

1
Q

Type 1 hypersensitivity mediated by which cell?

A

Mast cells

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2
Q

Type II hypersensitivity is mediated by which mediator?

A

Antibody

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3
Q

What is an example of Type II hypersensitivity?

A

Mismatched blood transfusion haemolysis

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4
Q

The process of which humans recognise self vs non self cells is called?

A

Self tolerance

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5
Q

The leading cause of death in HIV patients is

A

Opportunistic TB

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6
Q

What is the definition of ‘Window Period of HIV infection’?

A

The time between HIV infection and seroconversion (usually 2-3 weeks post infection)

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7
Q

Immunotherapy: how does this treatment achieve its effect?

A

Stimulates IgG to combine with antigens

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8
Q

Which cells are involved in rejection of an organ transplant?

A

T cells

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9
Q

What is the most useful marker in determining severity of HIV infection?

A

CD4+ counts

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10
Q

What is the role of HAART therapy in HIV?

A

Slows progression of disease

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11
Q

What are the components of the innate immune system?

A
  1. Epithelial barrier eg skin
  2. Monocytes/macrophages
  3. Phagocytes and dendritic cells, NK cells
  4. Complement
    5.plasma cells
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12
Q

What is the function of dendritic cells?

A

They phagocytose antigens and present the peptides to be recognised by T cells

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13
Q

What is the difference between TOLL like receptors vs NOD like receptors (location, function)?

A
  1. TOLL: located on plasma membrane, detect microbial molecules
  2. NOD: in the cytosol, detects molecules associated with necrotic cells, microbes
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14
Q

What is the role of TOLL like receptors?

A

Recruit leukocytes

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15
Q

Which pathways do TLR are able to recruit leukocytes?

A
  1. NF-KB (cytokine secretion and exp of adhesion molecules)
  2. IRF (Interferon regulatory factors) - produce Type 1 interferon/cytokines
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16
Q

What is the role of RIG-like receptors?

A

Detect viral nucleic acids–> produce antiviral cytokines (IFN A)

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17
Q

What is an interferonopathy?

A

Excessive production of IFN, leads to systemic inflammation (STING: stimulator of interferon genes)

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18
Q

Flare up associated with gout is an example of which receptor activation?

A

NOD like receptor

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19
Q

What is the function of NK cells? 2

A
  1. Detect IgG coated targets and destroy them
  2. Secrete cytokines eg IFN G to activate macrophages
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20
Q

What receptor does NK cells express?

A

CD16 (an IgG receptor)

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21
Q

How is NK cells regulated (self tolerance)? 2

A
  1. Type I MHC molecules on healthy cells
  2. Interleukins
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22
Q

Which interleukin activates NK cells to kill?

A

IL-12

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23
Q

Which interleukins stimulate proliferation of NK cells? 2

A

IL2 and IL15

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24
Q

What are the 2 types of adaptive immunity?

A
  1. Humoral immunity (extra cellular, B cell)
  2. Cellular immunity (Intracellular, T cells)
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25
Q

What are the components of adaptive immunity?

A

Lymphocytes and their cytokines
Antibodies/immunoglobulins

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26
Q

What is the role of Helper T cells?

A

Activate B cells to make antibodies and activate other leukocytes eg phagocytes

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27
Q

CD8+ cells recognise antigens presented by MHC ___ cells

A

I

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28
Q

CD4+ cells respond to antigen presented on MHC ___cells

A

II

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29
Q

What proteins do at cells express to assist their functional responses?

A

CD3, CD4, CD8, CD28

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30
Q

What is the role of CD4+ T cells?

A

Secrete cytokines to assist macrophages and B lymphocytes to fight infection

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31
Q

What is the role of CD8+ T cells?

A

Cytotoxic: they directly kill host cells

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32
Q

What Ig (2) do all B cells express to bind antigen?

A

IgM and IgD

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33
Q

Active B cells that produce antibodies are called ___

A

Plasma cells

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34
Q

What are the primary lymphoid organs? 2

A

Thymus (T cells)
Bone marrow (B cells)

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35
Q

What are the secondary lymphoid organs?

A

LN
Spleen
Mucosal and cutaneous lymphoid tissues

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36
Q

The primary co stimulators (2) for T cells that is recognised by CD28 receptor?

A

CD80 and CD86

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37
Q

CD4+ T cells differentiate to effector cells known as (2)

A

Th1 and Th2

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38
Q

What do Th1 secrete?

A

IFN G

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39
Q

What does Th2 secrete?

A

IL-4

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40
Q

What is the role of Th2 cells?

A

Secrete IL-4 to turn B cells into IgE secreting plasma cells

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41
Q

What is the mechanism of Immediate Type I hypersensitivity?

A

IgE antibody –> mast cell release of vasoactive amines

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42
Q

What are examples of Type I hypersensitivity?

A

Allergies
Asthma
Anaphylaxis

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43
Q

What is the mechanism of Type II Hypersensitivity?

A

Antibody mediated: production of IgG and IgM which binds to cell/tissues
This gets phagocytosed/lysis by activated complement

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44
Q

What are 2 examples of Type II hypersensitivity?

A
  1. Haemolytic anemia
  2. Good pastures syndrome
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45
Q

What is Type III hypersensitivity?

A

Deposition of antibody complexes onto target tissues

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46
Q

What is an example for Type III hypersensitivity? 3

A
  1. lupus
  2. Glomerulonephritis
  3. Serum sickness
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47
Q

Fibrinoid necrosis is likely associated with (type of hypersensitivity)

A

III

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48
Q

What is Type VI hypersensitivity?

A

Activated T cell lymphocytes: release of cytokines (CD4+) and T cell mediated cytotoxicity (CD8+)

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49
Q

Oedema and/or granuloma formation is part of (Type of Hypersensitivity)

A

VI

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50
Q

What are 4 examples of Type VI hypersensitivity?

A
  1. Type I diabetes
  2. Contact dermatitis
  3. TB
  4. Multiple sclerosis
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51
Q

The propensity to develop a hypersensitivity reaction is called?

A

Atopy

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52
Q

Graves disease is an example of (hypersensitivity type)

A

Type II

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53
Q

Myasthenia gravis is (type of hypersensitivity)

A

Type II

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54
Q

Post streptococcal glomerulonephritis is an example of (hypersensitivity)?

A

Type III

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55
Q

Type VI hypersensitivity involved which T cell?

A

CD4+ T cell

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56
Q

Delayed hypersensitivity is also known as

A

Type VI

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57
Q

Type VI hypersensitivity: which Th is involved?

A

Th1 (secrete IL-12) -primary
Th17 (IL-17 and IL-22)

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58
Q

What is the role of IL-12 in Type VI hypersensitivity?

A

To amplify Th1 response

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59
Q

Immune tests: diagnosis of fungal/bacterial or coccidioidomycosis

A

Complement fixation (IgM/IgG to detect titers of certain antigens)

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60
Q

Where does the acquired immune response begin for circulating antigens?

61
Q

Leukocytes that become inactive are called?

62
Q

What are the 2 types of tolerance in immunity?

A
  1. Central tolerance
  2. Peripheral tolerance
63
Q

What is Central tolerance?

A

Immature/naive lymphocytes that recognise self antigens undergo apoptosis. B cells undergo switching to new antigen receptors

64
Q

What is peripheral tolerance?

A

Mature lymphocytes that recognise self antigens become inactive (anergy) or suppressed by T cells

65
Q

What factors lead to failure of immune self tolerance? 2

A
  1. Inherit susceptibility genes
    2.infections/injury exposes self antigens and activate APCs
66
Q

Central tolerance occurs in (tissue sites 2)

A

Central tissues: thymus (T cells), Bone marrow (B cells)

67
Q

Autoimmune polyendocrine syndrome: what gene defect and what immune tolerance failed?

A

AIRE gene
Central tolerance

68
Q

What is the mechanism of which T cells will respond to an antigen?

A
  1. Need to be presented to T cell by APC
  2. Need co stimulators to activate response eg CD28
69
Q

Regulatory T cells are produced in response to ___

A

Recognition of self antigens

70
Q

What CD do regulatory T cells express?

A

CD4+ (have high levels of CD25)

71
Q

___ and ____(1 interleukin, 1 factor) are required to maintain regulatory T cells

A

IL-2 and FOXP3

72
Q

Immunosuppressive cytokines that inhibit leukocyte activation? 2

73
Q

What is the defective allele in ankylosing spondylitis?

A

HLA B27 (class I HLA allele)

74
Q

Myocarditis secondary to streptococcus is an example of which immune phenomenon?

A

Molecular mimicry

75
Q

What is molecular mimicry?

A

Immune response to microbes causes activation of leukocytes (microbes sharing similar amino acids as self antigen)

76
Q

What is epitope spreading?

A

Immune response to one self antigen, leads to tissue damage and release of more self antigens

77
Q

What phenomenon explains the chronicity of autoimmune disease?

A

Epitope spreading

78
Q

Double stranded DNA and sm ab are found in which proportion of lupus patients?

A

DNA (40-60%)
Smith (20-30%)

79
Q

Which autoantibody is specific for rheumatoid arthritis?

A

CCP (cyclic citrulinaged peptides)

80
Q

Which antibody is specific for systemic sclerosis?

A

DNA topoisomerase I (30-70% patients have positive)

81
Q

Nephritis in lupus are associated with which antibody?

82
Q

Congenital SLE/congenital heart block is associated with which antibody?

A

Anti Ro (SSA)

83
Q

Which antigen determines rejection of donor organ?

A

HLA antigen on donor

84
Q

What are the classifications for graft rejection? 3

A
  1. Hyperacute
  2. Acute
  3. Chronic
85
Q

What is hyperacute rejection?

A

Preformed antibodies specific for antigens on graft endothelial cells

86
Q

What is acute graft rejection?

A

T cells and antibodies react to graft alloantigens (CD8 direct damage, or CD4 inflammatory cytokines)

87
Q

What pathway does acute rejection use when antibodies bind to vascular endothelium?

A

Classical pathway

88
Q

What is chronic graft rejection?

A

Same as acute but gradual sclerosis and takes months to years

89
Q

What are primary immunodeficiencies?

A

Genetically determined defects in innate immune system eg NK cells, phagocytes, complement, T/B cells

Usually manifest 6mo age -2 years

90
Q

What defects can occur in primary immunodeficiency? 4

A
  1. Defective leukocyte adhesion eg leukocyte adhesion deficiency I/II
  2. Defects to phagolysosome function/cannot fuse with lysosomes eg chediak-higashi SX
  3. Defects to microbicidal activity (phagocyte oxidase) eg chronic granulomatous disease
    4.Defective TLR signalling herplex simplex encephalitis (TLR3)
91
Q

What is the most common complement deficiency?

A

C2 deficiency (classic pathway)

92
Q

X-linked SCID: what is the defect?

A

Common gamma chain of cytokine receptor (leads to failure of IL7 signalling, defective lymphopoisis)

93
Q

What is the mutation in autosomal recessive SCID?

A

Adenosine deaminase

94
Q

SCID is mainly caused by defect in which immune cell type?

A

T cells mostly
B cell can also be affected

They get bacterial, viral and fungal infections

95
Q

What is the mutation of X linked Agammaglobulinemia/Bruton?

A

Failure of pre B cells and pro B cells to become mature B cells (tyrosine kinase mutation)

96
Q

What are the characteristics of Brutons disease? 5

A

B cells are low or absent in circulation
Low serum Ig (all types)
CD19 expressed (pre B cell marker)
LN, Peyer’s patches, appendix, tonsils underdeveloped
Normal T cells

97
Q

What is Digeorge syndrome?

A

Thymic hypoplasia: failure of T cell development in the thymus (failure of development of 3&4th pharyngeal pouches)

Loss of chromosome 22q11

98
Q

What do the 3&4th pharyngeal pouches give rise to? 4

A

Thymus
Thyroid (C cells)
Ultimobrachial body
Parathyroid

99
Q

What is hyper IgM syndrome?

A

Too much IgM, low IgE/G/A: B cells cannot undergo class switching

B cell defect or CD4 Th cell defect (CD40 or cytidine deaminase)

100
Q

What is seen in patient blood count in hyper IgM syndrome?

A

Normal B and T cells
High IgM
Low IgE/G/A

101
Q

What is common variable immunodeficiency?

A

Hypogammaglobinemia (low all Ig, sometimes just low IgG)

BAFF mutation (B cells cannot survive or differentiate)

Presents similar to Brutons (can have hyper proliferation of lymphoid tissues)

102
Q

What is X linked lymphoproliferative disease?

A

SAP (SLAM associated protein) deficiency
Recurrent EBV infections (cannot activate NK/T cells)

103
Q

What are the clinical features of AIDS?

A

Fever >1 mo
High viral load
Fatigue
Weightloss
Diarrhoea
Lymphadenopathy
Neurological
Secondary tumours
Opportunistic infections eg TB

104
Q

What are the type of progressors (AIDS)?

A
  1. Rapid progressors
  2. Long term non progressors (VL <500)
  3. Elite controllers (VL 50-70)

Able to control as have high CD4 and CD8 T cells responses

105
Q

Which test is most sensitive/best screening method for HIV?

106
Q

Which is the most specific test for HIV?

A

Western blot

107
Q

Which test is best to detect HIV in the Window period?

A

P24 Ag assay

108
Q

What is the most common AIDS pneumonia infection?

A

Pneumocystis pneumonia (TB is the most opportunistic overall, not pneumonia)

109
Q

Most common cancer in AIDS/HIV?

110
Q

The most common fungal infection in AIDS/HIV?

A

Candidiasis

111
Q

What is the most neuro disease in AIDS?

A

AIDs dementia complex

112
Q

Most common organism to cause pneumonia in HIV?

A

Streptococcus

113
Q

The most common haemolytic manifestation in AIDS?

A

Autoimmune haemolytic anemia

114
Q

The most common space occupying lesion in HIV/AID?

A

Toxoplasmosis (‘tumor’ = primary CNS lymphoma)

115
Q

Urethritis is characteristic of (syndrome)

116
Q

Xerostomia is classically associated with (syndrome)

117
Q

Difficulty swallowing is classically associated with (syndrome)

A

Scleroderma

118
Q

Which immune syndrome classically has positive syphilis result?

A

Lupus (anticardiolipin antibodies)

119
Q

What is the effect of lupus anticoagulant in VIVO?

A

Thrombosis

120
Q

Which CD molecule HIV binds to enter cells?

121
Q

What are the co-receptors that allow HIV to infiltrate T cells/Lymphocytes

A

Chemokines receptor (CCR5, CXCR4)

122
Q

Elevated anti-streptolysin titre (ASO) is suggests (condition)

A

Previous Group A strep infection

123
Q

In most people with SLE, which Ig is increased?

124
Q

Treatment of graft vs host disease?

A

Methotrexate

125
Q

Which medication is used to minimise risk of transplant rejection?

A

Cyclosporin

126
Q

What is the effect of anti-red cell ab in SLE?

A

Pancytopenias
Anemias
Thrombocytopenia

127
Q

What is the common infection in slsective IgA deficiency?

A

Sinopulmonary infections and diarrhoea (strep/bacteria causing)

128
Q

Which organisms (class) do T cells defend against?

A

Viral and fungal

129
Q

HIV patient with red/purple skin lesions probably has (cancer)

A

Kaposi sarcoma

130
Q

Kaposi sarcoma is classically associated with (virus)

A

Human Herpes virus 8

131
Q

Anti-histone antibodies are associated with (immune disease)

A

Drug induced SLE

132
Q

Anti-U1 ribonucleoprotein antibodies suggest (disease)

A

Mixed connective tissue disease

133
Q

Glomerulus looks like this. Disease?

A

‘wire loop’ capillaries suggest SLE

134
Q

Wiskott-Aldrich presentation?

A

Eczema
Thrombocytopenia
Viral and bacterial infections
Lymphoma risk

135
Q

Late phase hypersensitivity Type I: what are the involved inmune cells? 3

A

Neutrophils
Eosinophils
CD4+

136
Q

What is an Arthus reaction?

A

Localised immune-complex reaction (eg from vasculitis).

Causes decreased C3 and C4 complements

137
Q

Congo red stain gives this appearance on BX. Suggests?

A

Amyloid ‘apple green’

138
Q

Amyloid is seen in which kinds of diseases?

A

Chronic inflammatory eg rheumatoid

139
Q

Limited vs diffuse scleroderma: differences?

A

Diffuse involves lung

140
Q

Polymyositis mechanism?

A

Muscle lysis from CD8+ T cells

141
Q

Digeorge syndrome presentation

A

Thymic/parathyroids/aorta/heart involvement
Hypocalcemic tetany
T cell dysfunction: viral and fungal infections

142
Q

Which immune cell participates in dermal fibrosis (scleroderma)?

143
Q

Which CD cell is involved in polymyositis?

144
Q

Which WBC expresses MHC II?

145
Q

What are the 3 major symptoms of Reiter syndrome?

A

Urethritis
Arthritis
Conjunctivitis

146
Q

What is the mechanism of Good pastures syndrome?

A

Antibody directed to Type VI collagen (anti basement membrane)

147
Q

Delayed type hypersensitivity (Type VI) involves which immune cell?

148
Q

Inheritance of Wiskott-Aldrich?

149
Q

Which marker is associated with amyloid associated heart failure in elderly?

A

Transthyretin

Alya Cards Pathology Robbins basis (12 decks)

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