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From Flashcardlet > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the four clinical features that form the SPUR checklist for diagnosing immunodeficiency?

A

Severe infection, Persistent infection, Unusual causative organism, Recurrent infection.

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2
Q

What causes chronic granulomatous disease (CGD)?

A

Defective neutrophils and monocytes are unable to destroy ingested bacteria.

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3
Q

What does LAD stand for?

A

Leukocyte Adhesion Disorder.

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4
Q

Name the two targets of autoantibodies produced in pernicious anaemia.

A

Parietal cells and intrinsic factor (IF).

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5
Q

What causes SLE?

A

Autoantibodies to nuclear antigens, such as DNA and histones.

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6
Q

What term is used to describe the reduced blood flow to the extremities often seen in connective tissue disorders such as SLE and scleroderma?

A

Raynaud’s phenomenon.

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7
Q

In what syndrome are autoantibodies directed against exocrine glands, in particular the salivary and lacrimal glands?

A

Sjogren’s syndrome.

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8
Q

Which Ig is produced in acute infection ?

A

IgM

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9
Q

Which Ig is for long term immunity ?

A

IgG

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10
Q

What is meant by pattern recognition receptors ?

A

It is an inclusive term for antigen recognition receptors in the INNATE immune system

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11
Q

What is the function if pattern recognition receptors ?

A
  • First line defense- interact with and facilitate removal of groups of organisms of similar structure
  • primes adaptive immune system
  • able to recognise self components - clearance of apoptosis and dying cells
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12
Q

Name two types of pattern recognition receptors

A
  1. Pathogen-associated molecular patterns (PAMPs)

2. Danger associated molecular patterns (DAMPs)

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13
Q

Name two GROUPS of pattern recognition receptors

A
  1. Cell surface receptors e.g. TLRs, mannose receptors (structures attached to cell membranes which engulf pathogens and then the cell releases lysosomal content to destroy it)
  2. Fluid phase soluble molecules e.g. when pathogen is in blood. Collectins (mannose binding lectin and surfactant protein A&D). Complement system
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14
Q

Mannose receptors:

  1. What are they ?
  2. Function
A
  1. C-type lectins receptors (cell surface) that recognise carbohydrates
  2. Mediate phagocytosis
    - processing and presentation of microbial peptides to MHC II
    - Induction of specific T and B responses
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15
Q

Which cells are TLRs expressed in ?

A

Sentinel cells (first line defense)

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16
Q

The cooperation of TLRs and NLRs regulate what responses ?

A

Regulate inflammatory and apoptotic responses

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17
Q

What is the range of estimated antigenic variability ?

A

10^9

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18
Q

How is genetic diversity produced in T cells ?

A

Gene rearrangement of multiple germ line genes

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19
Q

How is diversity of antibodies (B cells) generated?

A

Rearrange (genes) during pro-B stage to create unique cell surface receptors that define antigenic specificity

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20
Q

What is the relationship of bndng between T cell receptors (TCR) and antigens ?

A

Low affinity and degenerate

Many TCRs recognise the same molecules

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21
Q

Which has the highest affinity antigens, B or T cells ?

A

B cell

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22
Q

Which Ig is involved in the majority of blood Bourne infected ?

A

IgG

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23
Q

Which Ig crosses the placenta ?

A

IgG

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24
Q

Which Ig is the first line defence against pathogens crossing mucosal surfaces ?

A

IgA

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25
Q

Which Ig is an antigen receptor on B cells ?

A

IgM, IgD

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26
Q

What characteristic of IgM gives it high avidity and efficiency ?

A

Has a pentameric structure with 10 combining sites

V. Useful in early response before enough IgG produced

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27
Q

Which Ig primarily regulates B cell function ?

A

IgD

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28
Q

Which Ig is involved in allergic responses ?

A

IgE

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29
Q

Define avidity

A

Firmness of association between multideterminant antigen and the antibodies produced against it

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30
Q

Define valence

A

No. Of antigenic determinants it can react with

E.g. IgG antibodies have two fab regions and so can bind 2 molecules of same antigen, I.e. Valence = 2

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31
Q

Will antibodies produced by a memory relapse have higher or lower affinity for antigens than primary response ?

A

Higher

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32
Q

What type of bond are the polypeptide chains of antibodies held together by ?

A

Covalent disulphides bridges

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33
Q

What type of chains are the basic unit of antigen made up of ?

A

2 identical pairs of heavy and light chains

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34
Q

What part of the structure of an antibody determines it’s class ?

A

The type of heavy chain

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35
Q

Which part of the antibody is the variable region ?

A

The ends of the heavy and light chains (tips of the ‘Y’) (these parts of amino acid sequence have higher variability)
-This is the antigen binding part

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36
Q

What is a FAB fragment (of antibody) ?

A

The variable region that Has been proteolytically cleaved from the rest of the antibody structure

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37
Q

Function of the castanet region (antibody) ?

A

Determines fate of antigen

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38
Q

What do plasma and memory cells mature from ?

A

B lymphocytes

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39
Q

Name the 3 types of T lymphocyte

A

Killer/cytotoxic
Helper (1&2)
Suppressor

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40
Q

What is the function of cytotoxic T cells ?

A

Kill virally infected cells (cellular immunity)

Express CD8

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41
Q

Which T cells secrete cytokines which control immune response & help B cells ?

A

Helper T cells

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42
Q

T helper cells are CD8+ or CD4+ ?

A

CD4+

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43
Q

Which cells express MHC class I ?

A

All nucleated cells

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44
Q

Is the processing pathway of MHC class I endogenous or exogenous ?

A

Endogenous

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45
Q

Which cells recognise molecules presented by MHC class I ?

A

CD8+ cytotoxic T cells

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46
Q

Which cells express MHC class II ?

A

All antigen presenting cells

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47
Q

Do CD4+ helper T cells recognise peptides presented by MHC class I or II ?

A

Class II

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48
Q

Genes coding MHC are closely linked to which chromosome ?

A

6

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49
Q

Name the 3 loci for MHC class I (alpha chain and Beta2 micro globulin)

A

HLA A, B, C

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50
Q

Name the 4 loci of MHC class II (alpha chain and Beta chain)

A

HLA-DP
HLA-DQ
HLA-DR
HLA-DM

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51
Q

Give examples of causes of secondary immunodeficiency

A 
Surgery 
Malignancies
Malnutrition
TB, HIV
irradiation 
Protein loss e.g. Proteinuria
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52
Q

Infections With intracellular microbes suggest what kind of immunodeficiency ?

A

Deficiency in T cells

E.g. Mycobacterium, Trichomonas vaginalis, E. Coli

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53
Q

What does recurrent infections with capsulated organisms (e.g. Pneumococcus, streptococcus, neisseria) suggest ?

A

Deficiency in complement

Opsonization essential for their removal by phagocytosis

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54
Q

Recurrent infections with extra cellular bacteria suggest what ?

A

Primary antibody deficiency

E.g. Campylobacter, enterococcus, staphylococcus etc

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55
Q

Name 3 conditions associated with deficits in humoral immunity:

A

SCID
Hyper IgM syndrome
CVIID

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56
Q

What age are own antibodies produced ?

A

5-6 months

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57
Q

What is severe combined immunodeficiency (SCID) ? What is it characterised by ?

A

Primary immunodeficiency:
Absence of functional T cells - defective antibody response. Both arms of adaptive immune system impaired
Characterised by common infections that are prolonged/ more serious symptoms than normal

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58
Q

What is the clinical presentation of a neonate with SCID ?

A

Interstitial lung disease
Chronic diarrhoea
Failure to thrive
Profuse oral candidiasis

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59
Q

Treatment for SCID ?

A

Haemopoietic Stem cell transplantation

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60
Q

What is omenn’s syndrome ?

A

A subtype of SCID:
Babies present with consequence of T cell dysfunction (rather than absence)
E.g. Eczema, splenomegaly, NOT recurrent infection

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61
Q

What is Wiskott-Aldrich syndrome ?

Characterised by ?

A

X-linked recessive
Clinical triad of by eczema, thrombocytopenia, recurrent infections.immunodeficiency first (antibody deficiency)
Then cellular immunity deficiency - recurrent infections, splenomegaly etc

complications include inc risk of non-hogkin lymphoma

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62
Q

Typical lab results in Wiskott-Aldrich ?

A

Low IgM
Elevated IgA
Elevated IgE ~

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63
Q

What is X-linked hyper IgM syndrome ?

A 
Condition where B cells don't class switch from IgM > IgG 
Due to defect in CD40 - no effective T or B immunity (IgM producing little effect)
Patients present SEVERELY
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64
Q

What are XL and AR hypogammaglobulinaemia ?

A

Type of primary immunodeficiency characterised by reduction in gamma globulins (including immunoglobulins)
- can’t manage effective antibody response
(Presented later in life as has maternal antibodies for first few weeks)

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65
Q

What is common variable immunodeficiency (CVID)?

A

IgG/IgA deficiency
Can present at any age with recurrent infections due to progressive inability to form Igs

Hypogammaglobulinaemia is a characteristic of this condition

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66
Q

Immune effects of 22q11 deletion syndrome (DiGeorge syndrome) ?

A

Generally have weak immune system due to problems with the thymus, susceptible to recurrent infections such as oral thrush and pneumonia.

  • cardiac malformations
  • hypocalcaemia
  • T lymphopenia
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67
Q

A deficiency in which immune component results in chronic granulomatous disease ?

A

Neutrophils

(Neutrophils unable to make superoxides- the mechanism by which they kill bacteria, so produce radicals- tissue damage- granulation)

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68
Q

Difference between effects of deficiencies in early (C1-3) and late (C5-9) components of the complement cascade ?

A

Early: recurrent infections and autoimmune disease
Late: neisseria meningitidis

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69
Q

Which innate immunodeficiency is highly susceptible to the early phases of herpes virus ?

A

NK cell deficiency

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70
Q

Defects in TLR signalling are susceptible to infections by which bacteria ?

A

Mycobacterium

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71
Q

Explain the autoimmune mechanism causing Hashimoto’s thyroiditis

A

Destruction of the thyroid follicles by autoantibodies to thyroglobulin and thyroid peroxidase
- leads to hypothyroidism, thyroid becomes firm, large and lobular

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72
Q

Outline the autoimmune basis of grave’s disease

A

Inappropriate stimulation of thyroid gland by anti-TSH antibody > hyperthyroidism

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73
Q

Outline the autoimmune basis of myasthenia gravis

A

Circulating antibodies blocking Ach receptors at posy synaptic NMJ Inhibiting excitory effect

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74
Q

What is auto inflammation characterised by ?

A

Spontaneous attack of systemic inflammation
No sign of infection
Absence of high titre autoantibodies
No evidence of auto antigenic exposure

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75
Q

Is auto inflammation involving the innate or adaptive immune system ?

A

Innate

Autoimmunity = adaptive

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76
Q

Name 2 examples of auto inflammatory diseases

A

Monogenic hereditary periodic fevers

Polygenic Crohn’s disease

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77
Q

What treatments are used to boost the immune system in primary immunodeficiency ?

A

Immunoglobulin therapy
Gamma interferon therapy (chronic granulomatous disease)
Growth factors - used when a lack of certain WBC

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78
Q

Types of diagnostic tests used in autoimmune disease:

A

Non-specific: ESR, CRP, Ferritin, complement etc

Specific: autoantibody testing, HLA typing

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79
Q

What are antinuclear antibodies (ANA)?

A

Test to detect autoantibodies in blood serum
Also used in cancer and infection
Quantified using ELISA

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80
Q

Which test is more specific for rheumatoid arthritis than rheumatoid factor ?

A

ACPA

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81
Q

Which an antibodies are tested for in association with vasculitis ?

A

Anti-neutrophil cytoplasmic antibodies (ANCA)

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82
Q

Antibodies found in autoimmune hepatitis ?

A

Anti-LKS

Liver, kidney,smooth muscle

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83
Q

Antibody specific for primary biliary sclerosis ?

A

Anti-mitochondrial

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84
Q

What is the most common inherited auto inflammatory disease ?

A

Familial Mediterranean fever

  • short episodes of fever, abdo. Pain, serotitis, usually lasting 72 hrs
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85
Q

What cell types are involved in acute inflammation mediated by the innate immune system?

A

Neutrophils and macrophages

86
Q

Name the 3 types of immunomodulators

A
  1. Those almost identical to body’s own key signalling proteins
  2. Myoclonic antibodies
  3. Fusion proteins
87
Q

Name the monoclonal antibody approved for use in psoriasis, chrohns and rheumatoid arthritis

A

Alimumab

Infliximab

88
Q

Name the mouse-human chimeric mAB that targets TNF-alpha

A

Infliximab

89
Q

How does Etanercept work and what are its uses ?

A

Fusion protein - TNF-a receptor fused to Fc region of human IgG1
Binds and inhibits TNF-a- decreases inflam.
Approved for: ankolysing spondylitis, RA and juvenile idiopathic arthritis

90
Q

A common example of immunostimulation:

A

Immunisations : stimulate development of protective immune response and immunological memory

91
Q

Which type of immunisation (active or passive) gives immediate but transient protection ?

A

Passive

92
Q

What is serum sickness ?

A

Complication of passive immunisation, induces a type III hypersensitivity reaction

93
Q

3 problems with active vaccinations:

A
  1. Allergy to vaccine component
  2. Limited usefulness in immunocompromised
  3. Delay in achieving protection
94
Q

Antivenins for snakebites are an example of which type of vaccine ?

A

Passive

95
Q

Use of pooled human Ig in replacement therapy ?

A

Used in antibody deficiency state

E.g. X linked immunoglobinaemia

96
Q

Function of G-CSF/GM-CSF

A

Act on bone marrow to increase production of mature neutrophils (by action of cytokines)

97
Q

Role of IL-2 in replacement therapy

A

Stimulates T cell activation
Cytokines produced by T cells then further stimulate immune response

rarely used in immunodeficiency, treats malignant melanoma & (only drug for) metastatic renal cell cancer

98
Q

Interferon used to treat hep C ?

A

A-interferon

99
Q

Uses of y-interferon ?

A

Intracellular infections e.g. Atypical mycobacteria
Chronic granulomatous disease
IL-12 deficiency

100
Q

How do anti inflammatory drugs (NSAIDs, hydroxychlorquine) affect immunomodulation ?

A

Interferes with production of cytokines

101
Q

Immunomodulation in dapsone (antibacterial drug)

A

Inhibits neutrophil adherence to endothelium

used to treat dermatitis herpetiforms

102
Q

Which drugs may cause haemolytic in G6PD deficiency ?

A

Dapsone

Hydroxychlorquine

103
Q

Immunomodulation exhibited by thalidomide ?

A

Anti-TNF, decreases expression of adhesion molecules, favours Th2 cell responses

used in myeloma

104
Q

Immunomodulation in corticosteroid action ?

A
  • Decreased neutrophil margination
  • Reduced production of inflam cytokines
  • Inhibition of Phospholipase A2
  • Lymphopenia
  • Decreases T cell proliferation.
  • Reduced Ig production
105
Q

List drugs targeting lymphocytes (immunosuppressants):

A
  • Antimetabolites e.g. Azathioprine(AZA) - inhibits purine synthesis, methotrexate (folate agonist)
  • calcineurin inhibitors (prevents T cell proliferation)
  • M-TOR inhibitors (cell cycle arrest)
  • IL-2 receptor mABs e.g. Basiliximab
106
Q

Role of immunosupression:

A
  • transplantation- allograft rejection

- autoimmune disease

107
Q

Cytotoxic effects of immunosupression:

A
  • Bone marrow suppression
  • Gastric upset
  • Hepatitis
  • Susceptibility to infections
108
Q

Treatment for vasculitis ?

A

Cyclophosphamide

109
Q

Types of biologic DMARDs

A
  • Anti-cytokines: -TNF, IL-6, IL-1
  • anti-B cell
  • anti T cell
  • anti adhesion molecules
  • anti complement
110
Q

Which biologic DMARD also used to treat auto inflammatory syndromes ?

A

Anti IL-1

111
Q

What is the mechanism by which allergic-specific immunotherapy works ?

A

Switching of immune response from Th2 (allergic) to Th1 (non-allergic)
Development of T regulatory cells and tolerance

112
Q

Which mAB is used against IgE ?

A

Omalizumab

113
Q

What is farmer’s lung ?

A

A form of type III hypersensitivity reaction in the lung following inhalation of dust or mould spores. Causes immune complexes to do rm in the alveolar walls, reducing gas exchange

114
Q

Describe the immunopathology of type IV hypersensitivity reactions

A

Antigen specific T cell mediated cytotoxicity

115
Q

Describe e immune response to parasitic disease:

A
  • Increased levels of IgE
  • Tissue inflammation, with: eosinophilia, mastocytosis & basophils infiltration
  • presence of CD4+ T cells secreting interleukines
116
Q

What response occurs the first time an allergen is encountered

A

Innate IgM response

117
Q

Which gives an allergic response, Th1 or Th2 ?

A

Th2

Causes multiple cytokines release, in ant inflammatory response and drives Ig production

118
Q

Tests used for diagnosis of allergy ?

A
  • Specific IgE
  • Skin prick test
  • Intra-dermal test (injection)
  • Oral challenge test (food allergies)
  • Basophil activation test
119
Q

Role of basophils in allergic reaction ?

A

Degranulation when activated by IgE, Release initial systemic histamine

120
Q

What is the atopic triad ?

A

Asthma, rhinitis, eczema

121
Q

What is the major histocompatibility complex ?

A

Set of genes encoding proteins which are expressed on cell surface (MHC antigens)

  • they present self or non self antigens to T cell antigen receptors
122
Q

How is the MHC inherited ?

A

Mendelian inheritance

Each individual inherited two antigens at a given locus

123
Q

Antigen inheritance is expressed co dominantly, what does this mean ?

A

That the alleles (variants) inherited from both parents are expressed in equivalent way I.e. ALL of inherited antigens are displayed on cell surface

124
Q

What is a xenograft?

A

Grafts between members of different species

125
Q

What is an allograft ?

A

Graft between two members of the same species

126
Q

What is an isograft ?

A

Grafts between members of the same species with identical genetic makeup

127
Q

What component plays the major role in rejection of a transplant?

A

MHC antigens

128
Q

What is graft-vs-host (GVH) reaction ?

A

When, although the lymphoid cells in the graft are accepted by immunocompromised host, the immunocompetent T cells among graft cells recognise the alloantigens and respond by proliferating and damaging host tissue

Often fatal

129
Q

What is host-vs-graft rejection (HVG)?

A

Reaction of host against allo-antigens

130
Q

List the immune privileged sites of the body

A 
Brain
Anterior chamber of the eyes
Testis
Renal tubule
Uterus
131
Q

Which diseases are associated with having certain MHC haplotypes ?

A
  • Ankolysing spondylitis
  • Coeliacs
  • Reiter’s syndrome
  • Diabetes mellitus
  • Dermatitis herpatiforms
132
Q

What is a tolerogen ?

A

When an antigen induces tolerance

E.g. Non reactivity to self-antigens or non-self antigens

133
Q

How can tolerance be induced ? E.g. In neonate a or severely immunocompromised ?

A

Injecting haemopoietic stem cells

Grafting allogeneic bone marrow or thymus in early life

134
Q

What is the function of clonal deletion ?

A

To kill lymphocytes which recognise self

135
Q

What is clonal anergy ?

A

Induction of peripheral tolerance:
Auto-reactive T cells, when exposed to antigenic peptides on APCs that do not possess co-stimulatory molecules (CD80 or CD28) become anergic (non-responsive) to the antigen

136
Q

How is tolerance terminated ?

A

By prolonged absence of exposure to the tolerogen (antigen)

Immunisation with cross reactive antigens

137
Q

Outline the role of somatic hypermutation ?

A

To increase or decrease the specificity and affinity of an antibody for the particular antigen that stimulated the activation in the first place

(If given a disadvantaged mutation, cannot make contact with Th cell -> -ve selection - apoptosis, increased affinity> class switching and differentiation)

138
Q

Are PAMPs found on pathogenic or non-pathogenic organisms or both?

A

Both

139
Q

Examples of PAMPs?

A

LPS, peptidoglycans, lipoteichoic acid, flagella, DNA/RNA of particular pathogen

140
Q

What is the central protein of the complement system?

A

C3

141
Q

Which complement protein is involved in chemotaxis?

A

C5a

142
Q

Which complement proteins are anaphylatoxins?

A

C2b, C3a, C4a

143
Q

Function of C3b in the complement system?

A

Cleavage of C5 along with C2a & C4b. Also opsonisation.

144
Q

Which pathway of the complement system is triggered by carbohydrates on micro-organism cell walls?

A

The lectin pathway/MBL

145
Q

Auto-activation of which protein in the alternative pathway of the complement system?

A

C3 into C3a & C3b

146
Q

The ability of immune cells to recognised self cells from non self cells is termed what?

A

Self tolerance

147
Q

Is the Fab region on an immunoglobulin the constant or variable region?

A

Variable region - Ag binding site

148
Q

Which Ig class is a pentamer?

A

IgM - largest Ig

149
Q

Which Ig class is a dimer?

A

IgA

150
Q

Which Ig classes are monomers?

A

IgG, IgE, IgD

151
Q

Most abundant Ig?

A

IgG - found mainly in blood and ECF

152
Q

Which Ig is produced in response to parasitic infections & allergic diseases?

A

IgE - binds to the high affinity Fc receptors of mast cells and basophils

153
Q

Which two classes of Ig test positive for complement fixation?

A

IgG & IgM

154
Q

Secondary lymphoid tissue? (3) allows for Ag encounter and post Ab proliferation and maturation

A

Spleen, lymph nodes and mucosal associated lymphoid tissue (MALT) - appendix and tonsils

155
Q

During class switching does the Ag specificity change?

A

No - Ab retains affinity for the same Ag but can interact with different effector molecules

156
Q

What recognises intracellular pathogens?

A

T cells recognise other cells which have MHC displayed on them indicating that there is a pathogen inside. T cell do NOT detect free or circulating Ag

157
Q

Where do T cells mature?

A

Thymus

158
Q

MHC class I or class II expressed only on APCs?

A

MHC class II

159
Q

MHC class I = CD4+ or CD8+ T cells?

A

CD8+ T cells

160
Q

MHC class I or class II are expressed on all nucleated cells?

A

MHC class I

161
Q

What is central tolerance?

A

Occurs during lymphocyte development. Negative selction of T or B cells if they are self-reactive

162
Q

Which type of T helper cells promote B cell activation?

A

Th2 - also involved in allergic disease and response to helminthic infections

163
Q

Which type of T helper cells are responsible for cell-mediated immunity reactions like delayed type hypersensitivity and cytotoxic T cell activation?

A

Th1 - also activate macrophages

164
Q

Term used if the immune response is inadequate to prevent infection progressing?

A

Immunodeficiency

165
Q

Term used if the immune response is not controlled sufficiently to prevent host damage?

A

hypersensitivity

166
Q

IgE Ab mediated mast cell and basophil degranulation is what type of hypersensitivity?

A

Type I

167
Q

Hay fever, allergic asthma, pollen, bee venom, animal dander, allergic rhinitis, atopic eczema all are which type of hypersensitivity?

A

Type IgE mediated

168
Q

Action of histamine and kallikrein (early phase pre-formed mediators) in hypersensitivity reactions?

A
  • stimulation of irritant nerve receptors
  • smooth muscle contraction
  • increase in vascular permeability
169
Q

List 5 examples of type II hypersensitivity reaction?

A
  • transfusion reactions
  • glomerulonephritis
  • organ rejection
  • antibody mediated cellular dysfunction (myasthenia gravis & graves disease)
  • AI disease (haemolytic anaemia & thrombocytopenic purport)
170
Q

Antibody mediated cytotoxic reactions are a type of which hypersensitivity reaction?

A

Type II - binding of Ab to target Ag on cell membrane results in activation of complement cascade, opsonisation and phagocytosis.

171
Q

Which antibodies are usually implicated in Type II hypersensitivity reaction?

A

IgG & IgM

172
Q

What is the arthrus reaction an example of?

A

Type III hypersensitivity reaction

173
Q

Type III hypersensitivity is caused by what w.r.t immune system?

A

Immune complex reaction

1) AgAb complex
2) FcR in complex binds C1
3) complement activation leads to generation of activated complement fragments
4) C5a = chemtactic and C3b = opsonin
5) phagocytosis of complexes release oxygen radicals which damage tissue

174
Q

Examples of Type III hypersensitivity reaction?

A

SLE, Polyarteritis nodosa, serum sickness, arthrus reaction, post strep glomerulonephritis, Henoch–Schönlein purpura

175
Q

What is delayed type hypersensitivity?

A

Type IV - T cell mediated (CD4+ MHC class II) Ag-specific T cell releases cytokines to recruit macrophages. Requires previous exposure to Ag (TB)

176
Q

Examples of Type IV hypersensitivity?

A

Type I DM, MS, RA, response to microbial infection (TB, viruses, fungi, parasites). Contact dermatitis.

177
Q

What is X-linked agammaglobuilemia? mutation? Who it affects? What happens as a result?

A

Failure to produce mature B cells and plasma cells so results in agammaglobulinaemia.
Genetics: mutation of B cell bruton tyrosine kinase.
Male infants, recurrent infections of the pharynx and lungs from h.influenzae, s.pneumococcus, s.aureus.

178
Q

What is CVID?

A

Common variable immunodeficiency. Group of disorders of B cell maturation defect and hypogammaglobulinaemia.
Both sexes affected. Recurrent bacterial infections, increased frequency of AI disease (ITP, Pernicious anaemia) and inc risk of non-hodgkins lymphoma and gastric cancer.

179
Q

Modes of inheritance of SCID?

A

X-linked or AR.

180
Q

What is sensitisation?

A

Any event which elicits an HLA directed immune response

  • preggo
  • blood transfusion
  • transplantation
  • serum screening
  • crossmatching
181
Q

What happens in a parasitic infection?

A

Tissue inflammation - eosinophilia & mastocytosis, basophil infiltration. Presence of CD4+ T cells secreting IL4,5,13

182
Q

What is the major trigger in atopic dermatitis?

A

HOUSE DUST MITES

183
Q

What is autoimmune sympathetic opthalmia?

A

Damage to one eye, exposes eye antigens to the immune systems and therefore mounts a response against this ‘foreign’ antigen and can cause blindness in the other eye

184
Q

Autoimmunity restricted to auto antigens of a specific organ - examples of such autoimmune diseases?

A
  • thyroid (hashimoto’s thyroiditis, graves disease)
  • adrenals,
  • stomach (pernicious anaemia)
  • pancreas (type I diabetes)
185
Q

Examples of systemic autoimmune conditions?

A

Scleroderma (skin), SLE (kidney), RA (joints)

186
Q

Three types of autoimmune mechanisms? + examples

A

1) Direct Ab mediated effects (AI thyroid diseases, myasthenia gravis, rheumatic fever, pernicious anaemia)
2) Immune complex mediated effects (SLE & vasculitis)
3) T-cell mediated (RA, Type I diabetes, MS)

187
Q

What AI disease presents with a butterfly rash?

A

SLE

188
Q

What AI syndrome results from an auto antigen against type IV collagen resulting in glomerulonephritis?

A

Good pasture’s syndrome

189
Q

Autoimmunity or auto-inflammation; innate immunity affected?

A

auto-inflammation

190
Q

Autoimmunity or auto-inflammation; B&T cells involved rather than neutrophils and macrophages?

A

Autoimmunity

191
Q

Autoimmunity or auto-inflammation; recurrent often seemingly unprovoked attacks rather than continuous progression?

A

Autoinflammation

192
Q

Autoimmunity or auto-inflammation; use of anti-cytokine therapy instead of anti-b and t cell?

A

Autoinflammation

193
Q

Examples of auto inflammatory disorders?

A

Monogenic hereditary periodic fevers, polygenic crohn’s disease, spondylarthropathies

194
Q

Diagnostic tests; What is more specific for RA than RF?

A

ACPA (anti CCP) - autoABs that are frequently detected in blood of RA patients

195
Q

The therapeutic effect of immunomodulation may lead to 3 things…?

A

Immunopotentiation, immunosuppression or induction of immunological tolerance

196
Q

Main classes of immunomodulators?

A

1) substances that are nearly identical to the body’s own key signalling proteins
2) mAb
3) fusion proteins

197
Q

Uses of passive immunisation?

A

Hep B prophylaxis and treatment, botulism, VZV preggo, diphtheria, snake bites

198
Q

Beta interferon used in the treatment of?

A

MS

199
Q

Alpha interferon mainly used in the treatment of?

A

Hep C

200
Q

Gamma interferon mainly used in the treatment of?

A

Intracellular infections (atypical mycobacteria) and chronic granulomatous disease and IL-12 deficiency

201
Q

Main groups of immunosuppressives?

A

1) Anti-inflammatory drugs
2) cytotoxic agents
3) anti-proliferative agents
4) DMARD’s
5) biologic DMARD’s

202
Q

Examples of anti-inflammatory drugs used as immunosuppressives? Action? Used for? adverse effects? (6)

A

1) NSAIDs - inhibit COXs
2) Hydroxycloroquine - interferes with cytokine productions. Joint and skin problems. Can cause haemolytic anaemia in G6PD
3) Sulphasalazine - IBD & RA, regualar FBC monitoring
4) Colchicine - interferes with microtubule assembly. Used if Familial Mediterranean fever and behcet’s/ Causes Gi problems
5) Dapsone - inhibits neutrophil adherence to endothelium. Dermatitis herpetiformis. Haemolysis in G6PD
6) Thalidomide - anti TNF. Used in Behcet’s disease and myeloma. Birth defects and peripheral neuropathy.

203
Q

Examples of cytotoxic drugs?

A

1) Azathioprine - inhibition of purine synthesis
2) Methotrexate - folate antagonists
3) Cyclophosphamide - cross link DNA

204
Q

What is azathioprine used to treat? + adverse effects?

A

AI disease (SLE, vasculitis, IBD), allograft rejection.

Bone marrow suppression, GI upset hepatitis, susceptibility to infection

205
Q

Uses of corticosteroids?

A

1) AI disease - vasculitis, RA, SLE, Scleroderma
2) Inflam disease - crohns, sarcoid, rheumatic
3) Lymphoma
4) Allograft rejection

206
Q

Side effects of corticosteroids?

A

Diabetes, hyperlipidaemia, poor wound healing, osteoporosis, glaucoma and cataracts

207
Q

3 examples of anti proliferative/activation agents?

A

1) Ciclosporin - inhibits T cell activation by preventing IL-2 transcription. Prevents graft rejection.
2) Tacrolimus - similar to ciclosporin. Calcineurin inhibitor
3) Sirolimus -M-tor inhibitor

208
Q

Side effects of anti proliferative drugs?

A

Hypertension, hirsutism, nephro, neuro & hepatotoxicity, lymphomas, opportunistic infections.

209
Q

Examples of biologic DMARD’s?

A

1) anti-cytokines (anti TNF, IL-6, IL-1)
2) anti-B cell therapies
3) anti-T cell activation
4) anti-adhesion molecules
5) complement inhibitors

210
Q

Example of an anti-B cell therapy?

A

Rituximab - used in lymphomas, leukaemia, transplant rejection and AI

211
Q

Use of omalizumab?

A

Asthma, chronic uticaria, angioedema. But can cause severe systemic anaphylaxis

From Flashcardlet (22 decks)

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