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Nimna's Flash Cards > Immunology > Flashcards

Immunology Flashcards

1
Q

Types of IgA

A

IgA1- Found in serum and airways

IgA2- Found in mucous and gut

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2
Q

Cryoglobulinemia types

A

Type 1 - Monoclonal - usual related to MGUS/Myelomas
Type 2 - Monoclonal IgG/IgM + Polyclonal - usually infections
Type 3- Polyclonal - Usually auto-immune and some infections.

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3
Q

MOA of PD1/PDL1 inhibitors

A

prevents the signalling for programmed apoptosis

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4
Q

MOA of CTLA4 inhibitors

A

enhances APC activation of T cells by stopping the inhibitor receptor and ligand connection of CTLA4 to CD80, allowing CD28 and CD80 to connect and allow T cell differentiation

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5
Q

PAMPs stands for

A

Pathogen associated molecular patterns.

These are detected by toll like receptors which are a type of pattern recognition receptor.

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6
Q

Role of CRP in immune system

A

Can activate the classical complement pathway

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7
Q

What is CH50

A

A test of complement activity by testing the capacity to lyse foreign erythrocytes.

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8
Q

What is AH50

A

Tests the alternative complement pathway functioning

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9
Q

Activation of classical pathway

A

antigen-antibody reaction.

1x IgM or 6x IgG

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10
Q

Activation of Alternative pathway

A

microbial cell surfaces

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11
Q

Activation of Mannose binding Lectin pathway

A

plasma lectin that binds to mannose residues on microbes

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12
Q

Classical pathway cascade

A

C1 -> C4b -> C4bC2a (C3)-> C4bC2aC3b (C5)

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13
Q

Alternative pathway cascade

A

C3 -> spontaneous C3a, C3b -> C3bBb (C3)

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14
Q

Mannose binding lectin pathway cascade

A

MBL -> MSAP1, MSAP2 -> C4b -> C4bC2a (C3) -> C4bC2aC3b (C5)

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15
Q

Test used for anaphylactic reactions

A

Tryptase

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16
Q

Management of fever + neutropenia + organ dysfunction post CAR-T T cell therapy

A

This is Cytokine release syndrome.

Mx - Tocilizumab (IL-6R antagonist)

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17
Q

Role of Basilixumab

A

CD25 inhibitor.

Prevents T cell medicated rejection

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18
Q

Hypersensitivity types

A

Type 1: Immediate reaction. Mast cell degranulation causing histamine release. IgE mediated. Eg asthma, anaphylaxis.

Type 2: IgG mediated direct attack on cells. Eg haemolytic transfusion reactions.

Type 3: Immune complex deposition disease, activates complement causing inflammation in that tissue. Eg lupus, GN, serum sickness, Arthus reaction.

Type 4: Delayed reaction from T-cell mediated response. Eg contact dermatitis, chronic graft rejection.

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19
Q

FOX P3 mutation

A

FOX P3 is a gene involved in regulatory T cells.
Loss of CD4 and CD25 suppression.

Causes IPEX syndrome- Immune dysregulation, polyendocrinopathy, enteropathy, X-linked

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20
Q

mucocutaneous candidiasis, hypoparathyroidism, and adrenal failure triad

A

AIRE deficiency (autoimmune regulatory enzyme)/autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)

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21
Q

Castleman’s disease cause and symptoms.

A

Lymphoproliferative disorder with IL-6 overactivation.
Can be associated with HHV8
Can be associated with POEMS (polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal protein, Skin changes)

Mx - IL6 inhibitors - Siltuximab, Tocilizumab.

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22
Q

In what part of the immune system are Toll-like receptors

A

Innate immune system

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23
Q

Where is CRP produced and what stimulates it

A

In liver, stimulated by IL-6

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24
Q

Treatment for hereditary angioedema

A

Icatibant - Bradykinin antagonist

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25
Q

Receptors in the innate immune system

A

Toll-like receptors

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26
Q

Cytokines released by damaged cells

A

IL-1beta
TNF- alpha
IL-12
IL-6

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27
Q

MOA Natalizumab

A

Blocks VLA-4 (alpha 4), so white cells cannot cross blood vessel walls into organs

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28
Q

MOA Fingolimod

A

Inhibits SIP-1. Stops lymphocytes leaving the lymph nodes

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29
Q

Role of C3a

A

inflammatory mediator

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30
Q

Role of C3b

A

Opsonisation

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31
Q

Deficiency of C1-esterase inhibitor causes:

A

High levels of C1 - Hereditary angio-oedema

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32
Q

Immunosuppressive cytokines

A

IL-10, TGF-beta

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33
Q

T cell for extracellular pathogens - eg fungi

A

TH17

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34
Q

T help cell subtypes and roles

A

TH1 - macrophage activation and opsonisation antibodies for intracellular pathogens
TH2 - B cell activation, neutralizing antibodies. for parasites. Allergy.
TH17 - Neutrophil recruitment + extracellular pathogens
T reg - Anti-inflammatory

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35
Q

Role of IL 1

A

Promotes inflammation

Inhibitor Drug - Anakinra

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36
Q

Role of IL 2

A

Promotes T cell growth

Inhibitor drug - Basilixumab

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37
Q

Role of IL 3

A

Stimulates haematopoiesis.

Neutrophil activation.

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38
Q

Role of IFN gamma

A

Causes B cells to produce IgG subclasses for opsonisation and phagocytosis of intracellular pathogens.
Causes TH cells to become TH1 to activate macrophages and responds to intracellular pathogens.

39
Q

Role of IL 5

A

Stimulates Eosinophil growth

Inhibitor drug - Mepolizumab, Benralizumab

40
Q

Role of IL 6

A

Promotes fever and CRP production.

Inhibitor drug - Tocilizumab

41
Q

Role of IL 15

A

NK cell growth

42
Q

Role of TNF beta

A

Attacks malignant cells

43
Q

Role of TGF- beta

A

Stimulates IgA production for mucosal immunity

44
Q

IL 12/23 inhibitor

A

Ustekinumab

45
Q

IL 17 inhibitor

A

Secukinumab

46
Q

Drugs causing hypersensitivity vasculitis

A

PTU, Frusemide, Thiazides

47
Q

Polyarteritis Nodosa gene

A

ADA2

48
Q

SCID gene

A

ADA1

49
Q

Treatment for GPA

A
  1. Cyclophosphamide
  2. Azathioprine maintainence
  3. Prednisolone if flare
  4. Rituximab if poorly controlled
50
Q

How does immunotherapy work for allergy

A

High doses of the allergen switches pathway from TH2 to TH1.

51
Q

Most common immunodeficiency

A

IgA deficiency

52
Q

Disease with recurrent respiratory infections and bronchiectasis

A

CVID

53
Q

Infection type in complement deficiency

A

Neisserial infections

54
Q

Disease causing granulomas + recurrent infections.

A

Chronic granulomatous disease - a neutrophil disorder due to defective NADPH

55
Q

Defects in complement classical pathway cause

A

Autoimmune disease

56
Q

Defects in complement alternative pathway cause

A

Renal disease - aHUS + C3 glomerulopathy

57
Q

Defects in complement membrane attack complex cause

A

Immunodeficiency and Neiserrial infection

58
Q

Function of AIRE

A

Works in the thymus for T cell selection.

  • If high binding affinity to antigen - apoptosis occurs as likely self.
  • If low binding affinity occurs - positive selection as likely pathogen.
59
Q

Function of AIRE

A

Works in the thymus for T cell selection.

  • If high binding affinity to antigen - apoptosis occurs as likely self.
  • If low binding affinity occurs - positive selection as likely pathogen.
60
Q

How do IgA1 and IgA2 differ?

A

In their heavy chain components

61
Q

Where are the IgA subclasses found

A

IgA1 - airways and serum

IgA2 - mucosa + colon - can bind to got pathogens

62
Q

CD marker on NK cells

A

CD56, CD16, CD2, IL2

63
Q

Function of NK cells

A
  1. Direct cytotoxicity to infected and malignant cells - by release of perforins and granzymes.
  2. Mediate antibody mediated cytotoxicity through CD16.
  3. Mediate T cell responses by INF gamma.
64
Q

what is the trial for AERD (aspirin exacerbated respiratory disease)

A
  • aspirin intolerance
  • asthma
  • nasal polyps

Aspirin desensitisation can be used to treat AERD or if aspirin is required for another medical indication.
Once desensitized, patients must take at least 325 mg of aspirin daily to maintain the desensitized state.

65
Q

CD markers in Tregs

A

CD4 CD25

66
Q

Regulator gene of Tregs

A

FOXP3

67
Q

immune cell reliant on its release of mediators into
the extracellular fluid surrounding the organism in order to carry out its role in eradication of foreign
organisms.

A

Eosinophils

68
Q

What is the role of somatic hypermutation in B cells?

A

Where B-memory cells once encountered by the antigen under go a process of re-arrangement to find the antigen that binds with the highest affinity to that antigen. Allows for selection of high affinity B cells from the base B-cell.

69
Q

Genetic defect leading to increased Mycobacterial (TB and non-TB) infections

A

Defect in IFN-IL12 pathway = Mendelian susceptibility to mycobacterial diseases.
Includes GATA2 and STAT1 mutations, NEMO.

70
Q

People at high risk for latex allergy

A
  • Health care workers - exposure to gloves.

- Patients with spina bifida - exposure to latex from recurrent catheterisations.

71
Q

What cells have CD20

A

CD20 is highly expressed on B cells but not on stem cells or mature plasma cells

72
Q

Survival prognosis for solid organ transplants - heart, lungs, kidney, liver.

A

Lung - 6.5 years

  • higher in double lung transplant
  • lowest 1 yr survival is in IPAH
  • highest 1 yr survival is in COPD (but decreases with time)
  • lowest 10 yr survival is ILD.

Cardiac - 11 years
Kidney - 90% 5 year survival
Liver - 75% 5 year survival

73
Q

Red meat allergy cause

A

Tick bite - alpha gal allergy

74
Q

Reaction in serum sickness

A

Type 3 hypersensitivity reaction.

An antigen which has antibodies directed against causing antigen-antibody or immune complexes. Normally cleared by phagocyte system, but excess immune complexes may deposit in tissues or form directly in the involved tissues.
Deposition of immune complexes causes complement activation and/or recruitment of neutrophils by interaction of immune complexes with Fc IgG receptors.

75
Q

Functions and clinical relevance of beta 2 microglobulin

A
  1. It is a component of MHC1 markers on all cells.
  2. Regulates Hepcidin expression in the liver (with HFE protein)
  3. Can cause dialysis associated amyloidosis
  4. Can be a marker in multiple myeloma.
76
Q

Which cell type destroys cells with MHC1 downregulation

A

NK cells

77
Q

Mutation and type of mutation in Mastocytosis

A

KIT - gain of function (receptor)

Stem cell factor (ligand)

78
Q

Function of plasmacytoid dendritic cells.

A

Cells which recognise viruses and produce interferrons.

Are NOT phagocytic APC’s like classical dendritic cells.

79
Q

Pathogens associated with each toll-like receptor

A

TLR1 - Mycoplasma
TLR2 - Gram Positive, viruses, Parasites, self.
TLR3 - Viruses. Work through NFkB
TLR4 - Gram Negative , viruses, self
TLR5 - Flagella. Work through NFkB
Others - TLR6 - mycoplasma TLR7/8 - ssRNA viruses TLR9/11 - protozoa.

“My pink vagina never fakes orgasms” which takes a TOLL on our relationship.

80
Q

Staph decolonisation procedure

A

Mucopuricin and chlorhex antiseptic wash

Do this AFTER all acute lesions have healed

81
Q

Contra-indications to the varicella vaccine

A
  • Anaphylaxis to varicella vaccine
  • Pregnancy + 28 days before - but CAN have vaccine when breastfeeding
  • People who have received an immunoglobulin-containing product should wait 3–11 months before receiving varicella vaccine
  • People who have received a varicella-containing vaccine should not receive immunoglobulin-containing products for 3 weeks after vaccination
  • HIV if CD4 <200
  • People on steroids >1mg/kg (must stop for atleast 1m before vaccine)
  • 6 months after blood product transfusion
  • people on bDMARDs and tsDMARDs

NOTE: People ≥50 years of age with mild immunocompromising conditions may receive zoster vaccine.

82
Q

tsDMARDs and MOA

A

barcitinib
tofacitinib

MOA: Jakus kinase inhibition

83
Q

Uses and SE of tsDMARDs

A

barcitinib
tofacitinib

SE: Infection: Infection (20% to 22%)
Respiratory: Nasopharyngitis (3% to 14%)
Increased serum cholesterol (5% to 9%)

84
Q

NK cell activating receptor and ligand

A

ligand - MIC A

receptor - G2G

85
Q

NK cell inhibiting receptor and ligand

A

ligand - MHC 1

receptor - KIR

86
Q

SCID mutations

A

Zap 70
JAK3 - autosomal recessive
ILR2 mutation - X-linked

87
Q

recurrent infections + bad teeth + fine hair + no sweating

A

NF-Kappa-B mutation in receptor NEMO

88
Q

Cytokine which triggers B cells to produce IgA

A

TNF- beta

89
Q

Cytokine which triggers B cell to produce IgG

A

IFN- gamma

90
Q

Cytokine which triggers B cell to produce IgE and IgG4

A

IL4

91
Q

Cytokine which activates neutrophils

A

IL 17

- also activates TH17

92
Q

Which cell type mediates SJS

A

T cells - SJS is not an IgE reaction

93
Q

Methods of T cell activation by drugs

A
  1. Hapten - reactive drugs are a direct T cell target and cell is attacked when it is bound to cell protein.
  2. Prohapten - drug only becomes reactive when bound to cell protein
  3. Pi concept - drug directly activates receptor on t cell.

Nimna's Flash Cards (15 decks)

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