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Stage 2 Cheat sheets > IAH > Flashcards

IAH Flashcards

1
Q

Name an autoimmune disease affecting

a) Kidneys
b) IgE on basement membrane
c) Thyroid
d) B cells
e) Salivary glands

A

a) Goodpastures syndrome
b) Bullous pemphigoid
c) Graves disease
d) SLE, MS
e) Sjogren’s

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2
Q

What type of disease is Bruton’s X-linked agammaglobulinemia?

A

Immunodeficiency

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3
Q

What causes Bruton’s?

A

Defect in B cell receptor signalling so B cell deficiency resulting in decreased Ig

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4
Q

How does Bruton’s affect Ig levels?

A

B cell deficiency so low Ig

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5
Q

Why is Bruton’s more common in boys?

A

Girls have 2 copies of the X chromosome so can be a carrier, boys only have one X chromosome from the mother so if the mother is a carrier the boy will have it

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6
Q

What surface molecule is expressed on T helper cells only?

A

CD4

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7
Q

What surface molecule is expressed on all T cells?

A

CD3

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8
Q

What microorganism causes Karposi’s sarcoma, pneumonia and B cell lymphoma?

A

Characteristic of AIDS

HIV1 (HIV2 but less severe)

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9
Q

What bacteria causes pneumonia in AIDS?

A

P. Jirovecci

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10
Q

How do commensal bacteria help prevent infections?

A

Prevent pathogen from gaining an ecological foothold

Stimulate colonic epithelial cells to from a balanced state = physiological inflammation
Compete with pathogens for nutrients, attachment sites and living space
Secrete bactericidal products e.g. FA from propionibacterium and lactic acid from lactobacilli

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11
Q

What bacteria causes infection at burns?

A

P. aeruginosa

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12
Q

What makes burns susceptible to infection?

A

Opportunistic infection
Moist surface
Vascular damage
Lots of nutrients like haem

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13
Q

Function of CD4 on actual membrane?

A

Binds antigen presented on MHC II
If activated by BCR it an activate B cell differentiation
Co-stimulatory factor - activates CD8 cells

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14
Q

Describe structure of granuloma

A

Central area of infected macrophages surrounded by outer layer of CD4 TH1 cells

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15
Q

What cytokine is secreted by lymphocytes in the granuloma, what is the effect?

A

Th1 cells secrete IL-2 to promote T cell proliferation and IFN gamma to activate macrophages

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16
Q

What causes granulomas to form?

A

Mycobacterium resisting bactericidal attempts of macrophages

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17
Q

Function of CD8 Tc cells

A

Control infection by directly killing infected cells

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18
Q

How do Tc cells cause cell death?

A

Release of cytotoxins to induce apoptosis

Interaction of FasL and Fas on target - apoptosis

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19
Q

What cells form from the myeloid and lymphoid lineage?

A

WBC
Myeloid = granulocytes (neutrophils, basophils, eosinophils, monocyte, mast cell)
Lymphoid = B cell, T cell, NK cell, ILC

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20
Q

Acute rejection

A 
Type IV (T cell mediated) hypersensitivity reaction
Alloreactions in transplant rejection (recipients T cells attack the transplant alloantigen (HLA) or graft vs host disease (when T cells transplanted they react to host alloantgien (HLA))
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21
Q

Hyperacute rejection

A

Type II hypersensitivity caused by ABO or HLA mismatch

Pre-existing antibodies bind to graft = endothelial damage

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22
Q

What can increase the risk of hyper acute rejection?

A

Pre-existing anti-HLA antibodies e.g. pregnancy, multiple blood transfusion, past transplantation

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23
Q

How is hyper acute rejection circumvented?

A

Serological testing and antigen cross matching

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24
Q

Chronic rejection

A

Type III hypersensitivity reaction (immune complexes)
Donor-specific alloantibodies bind HLA not he surface on the graft, recruit inflammatory cells
Arteriosclerosis, fibrosis, hypo perfusion, loss of function

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25
Q

Other than HIV what causes karposis Sarcoma

A

HHV8

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26
Q

Use of monoclonal antibodies?

A

Target specific antigens
target cancer molecules
target host immune response to boost performance
identify size and location of tumour

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27
Q

Function of CD3 receptor on T cells?

A

Generates signal to activate signal transduction pathways once the binding has occurred

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28
Q

Function of CD28 receptor on T cells?

A

On surface of T cells interact with co-stimulatory molecules

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29
Q

What activates TLR4?

Where is it found?

A

LPS

Membrane bound

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30
Q

What activates TLR3?

Where is it found?

A

Ds viral RNA

Endoplasm

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31
Q

Function of

a) Th1
b) Th2
c) Treg
d) Th17
e) TFH

A

a) Activation of macrophage
b) Mast cell activation
c) Suppression of immune system
d) Re-enforcement of inflammation
e) activate B cells in lymph

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32
Q

How are CD8 cells activated?

A

Presentation of antigen on MHC class I molecule, CD3 then sends signal for signal transduction = release of cytotoxic release

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33
Q

What type of cell is MHC class I presented on?

A

Virally infected cells

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34
Q

Function of

a) IL1 and TNF
b) IL6
c) IL12
d) IL8
e) IL17

A

a) pro-inflammatory
b) Lymphocyte activation and increased Ig production
c) NK and T cell differentiation
d) chemokine release (neutrophil migration)
e) Th17 activation

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35
Q

Length of phases in HIV graph

a) symptomatic phase
b) non-symptomatic phase

A

a) 4-8 weeks (flu-like symptoms)

b) 2-12 years (reduction in CD4 equal to production of CD4 = fluctuations of virus in plasma

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36
Q

What disease results in the inability to class switch the Ig molecules, and what is the aetiology of this disease?

A

Common variable immune deficiency

Limited to IgA

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37
Q

What cells produce AMPs?

A 
Paneth cells
Neutrophils (alpha defensins)
Epithelial cells (beta defensins)
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38
Q

How do AMPs kill pathogens?

A

Ampipathetic properties = insert into membrane and disrupt pore formation = lysis

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39
Q

Name a virus that lays dormant in B cells? Which disease does this cause?

A

Epstein-Barr virus

In immunosuppressed individuals EBV can re-activate and cause B cell lymphoma

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40
Q

How does herpes simplex evade the immune response?

A 
Virally encoded Fc receptor blocks effector functions of antibodies bound to virally infected cells
Virally encoded complement receptor blocks effector functions of complement 
Blocks MHC class I presentation = no activation of Tc cells
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41
Q

How does p. gingivalis and mycobacterium tuberculosis evade the immune response

A

P. gingivalis = releases proteases that digest antibodies

Mycobacterium = phagocytosed but highly resistant to proteolysis/lysosome fusion = no MHC II presentation

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42
Q

Cause of cell necrosis in Granuloma formation?

A

Centre of granuloma cut off from blood supply, cells die through anoxia and excessive macrophage lytic enzymes = necrosis

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43
Q

2 disease caused by mycobacterium?

A

TB and leprosy

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44
Q

What tissue does HSV first infect?
Which tissue does it become latent in? Why?
Treatment?

A

Epithelial
Neurones (trigeminal ganglia) - very few MHC class I (so there isn’t an immune response within- = evade immune system
Aciclovir

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45
Q

Structure and function of Peyers patch?

A

Within the SI
M cell on surface which samples antigens
Antigens activate DC cells which present antigen to cells within the germinal centre of lymph nodes

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46
Q

Function of germinal centre of lymph node?

A

generate new cells - B and T cell activation

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47
Q

Mast cell

a) function
b) contents
c) activation

A

a) degranulation releases inflammatory mediators (histamine)
b) granules containing histamine
c) Cross linking of IgE (by antigen binding) causes degranulation

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48
Q

Identification of monocyte?
Function?
% of cells made up of monocytes

A

Large cell, kidney bean nucleus
Pre-cursor for macrophage. Circulates in the blood
2-10%

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49
Q

Candida albicans identification

A

Budding/hyphae form

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50
Q

Function of B cell antigen transport?

A

Present to T cells

Affinity mature

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51
Q

How do B cells change during life?

A

Somatic recombination
V region recombinase
Junctional diversity

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52
Q

Function of neutrophil?

A

Professional phagocyte
Release pro-inflammatory cytokines
Release AMP, ROS, NO

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53
Q

Function of MAC?

A

Form pits in membrane = lysis

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54
Q

Function of fibroblasts in inflammation?

A

Formation of scar tissue

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55
Q

Type I hypersensitivity?

A

Immediate

IgE mediated = Mast cells release pro-inflammatory cytokines

56
Q

3 causes of haemolytic anaemia (type II reaction)

A

Penicillin hypersensitivity
Autoimmune haemolytic anaemia
Blood group incompatibility

57
Q

Example of type II autoimmune reaction?

A

Pemphigus vulgaris

Autoimmune haemolytic anaemia

58
Q

Example of type III autoimmune reaction?

A

Rheumatoid arthiritis

59
Q

Example of type IV autoimmune reaction?

A

T1DM (autoantigens = beta cell antigen)

Chron’s (autoantigen = antigens of microbial microbiota)

60
Q

Atopy

A

Allergy with genetic predisposition (e.g. hay fever)

61
Q

Example of type I hypersensitivity?

A

Anaphylactic shock
Eczama
Asthma

62
Q

Type III reaction

A

Formation of immune complex that invade tissues and causes inflammation and destruction

63
Q

Pus?

A

Dead/dying neutrophils

64
Q

Polymorphism?

Example?

A

Genetic variation = different forms within the population

MHC

65
Q

Which receptor has holotypes associated with autoimmune disease?

A

TCR

If they don’t have central tolerance

66
Q

Hypermutation effect

A

Mutations in B cells to produce Ig with higher affinty

67
Q

SCID?

Causes?

A

Severe combined immunodeficiency
Defects in T cell development = no T cells, antibodies, memory
Caused by mutations in genes for cytokine signalling e.g. Il2 receptor

68
Q

HHV8

Consequence

A

Herpes simplex virus 8

Highly prevalent in HIV patient = enlargement of lymph nodes

69
Q

What Ig component recognises LPS?

A

Constant region (Fc)

70
Q

What Ig component is most polymorphic?

A

Antigen binding site

71
Q

What cell surface molecule recognises LPS?

A

TLR4

72
Q

What is rearranged after a primary immune response?

A

Random recombination of gene segments to produce diversity in the antigen binding sites

73
Q

Consequence of excessive tissue exudates

A

Neutrophils

Chronic inflammation and tissue destruction

74
Q

What cells secrete performs?

A

NK

75
Q

Most abundant WBC in healthy peripheral tissue?

A

Neutrophil

76
Q

What WBC is low in chemotherapy patients?

A

Neutrophil

77
Q

What is the consequence of S. pyogenes infection?

A

Strep throat = sore throat

78
Q

What component of the immune response is mostly involved in S. pyogenes infection?

A

IgA

79
Q

What is the general consequence of pyogenic bacterial?

A

Production of pus

80
Q

How do streptococci evade the immune system?

A

Polysaccharide capsule

81
Q

What cell surface receptor helps distinguish between active and naive T cells?

A

IL2 receptors

82
Q

Cytokine associated with

a) TH1
b) TFH
c) Treg
d) Th17

A

a) IFN gamma
b) IL4
c) IL-10
d) IL-17

83
Q

Example of

a) type IV hypersensitivity
b) type III
c) type II
d) type I

A

a) Chronic asthma
b) serum sickness
c) blood group incompatibility
d) allergic rhinitis (hay fever)

84
Q

Anatomical structure tonsils protect?

A

Larynx and back of throat

85
Q

What cell synthesise IgA in the mouth and where are they located?

A

Plasma cells

Salivary glands

86
Q

Where are the antigens that stimulate the production of IgA taken up in the body and where have they likely originated?

A

In the gut (M cells of peyer’s patch)

Antigens probably come form mother

87
Q

Difference between classical and alternative pathway

A 
classic = C-reactive protein or antibody presentation
Alternative = pathogen surface causes activation
88
Q

Clinical consequence of complement deficiency?

A

More infections from extracellular bacteria like staphylococcus or pyogenic bacteria

89
Q

2 cytokines that induce vascular changes associated with inflammation and their target?

A

IL1 and TNF

Endothelial cells of BV

90
Q

3 social and/or demographic factors influencing the pattern of infectious disease?

A 
Availability and infrastructure to healthcare
Travel availability
Poverty
Porous borders
Insolation/heirachy
91
Q

Genetic basis fro antigenic shift and drift and how the outbreaks differ?

A 
Drift = point mutation (gradual) = seasonal variation and limited epidemics
Shift = recombination between strains = widespread infection (pandemics), jump between species = no immune response
92
Q

Other than herpes simplex name another disease caused by re-actiavtion of latent herpes virus and name the virus responsible.
What 2 locations of the body are the lesions commonly manifested?

A

Herpes Zoster = shingles

Skin of torso and head and neck

93
Q

How does T. palladium evade antibody recognition?

A

Coated in fibronectin

94
Q

Function of staphylococcal enterotoxins on T cells?

A

Superantigens = bind MHC and TCR independent of antigen specificity = polyclonal T cell response = excessive release of cytokines = toxic shock syndrome = apoptosis

95
Q

Aetiology of primary immunodeficiencies>

A

Genetic mutation

96
Q

Clinical consequence of B cells deficiency?

A

Increase infections from extracellular bacteria e.g. S/ pneumonia

97
Q

Causes fo secondary immunodeficiency?

A 
Immune senecence (age and nutrition)
Trauma (burns, surgery)
Drugs (immunosuppressants)
Tumours (CLL)
Infection (HIV)
98
Q

Why is it difficult to gauge true extent of HIV infection?

A

Many asymptotic carriers that don’t know they are HIV +

99
Q

3 properties that compromise host immune response giants HIV?

A

High mutation rate, genetic variability, latency

100
Q

Mode of anti-viral nucleoside analogues?

A

Interfere with viral transcription from viral RNA to viral cDNA

101
Q

Other than nucleoside analogue, 2 other anti-HIV drugs?

A

Reverse transcription inhibitors and protease inhibitors

102
Q

HAART?
Advantages?
Disadvantages?

A

highly active antiretroviral therapy
Combination of anti-viral drugs = good when some viruses have resistance to some drugs

Lifelong treatment (need gets rid of viral load), expensive, serious side effects

103
Q

What elements of immune response mediate autoimmune disease?

A

Autoantibodies and autoimmune T cells

104
Q

2 autoimmune disease involving CNS

A

MS

Myasthenia gravis

105
Q

3 autoimmune disease of endocrine system

A

Graves
T1DM
Addisons

106
Q

Autoimmune disease effecting exocrine gland

A

Sjogrens

107
Q

3 lines of evidence that autoimmune disease have heritable element

A

Association with HLA genotype
Run in families
Different susceptibility of mice with different genetics
High concordance in twin studies

108
Q

Why are autoimmune disease often characterised by deficiency disorder to compromised function?

A

Often involve tissue destruction

109
Q

3 autoimmune disease with oral manifestations?

A

Sjogrens, SLE, pemphigus vulgaris

110
Q

Why are autoimmune diseases unequally distributed between sexes?

A

Endocrine effect

Imprinting

111
Q

Allergen encountered through

a) inhalation
b) injection
c) ingested
d) contacted

A

a) pollen
b) drugs
c) food
d) plants/synthetics

112
Q

Immune mediators of

a) Type I hypersensitivity
b) Type II
c) Type III
d) Type IV

A

a) IgE
b) IgG
c) IgG
d) T cells

113
Q

Red patch often associated with wheal and flare?

A

Erythema

114
Q

2 cells involved in type I hypersensitivity?

A

Mast cell

Plasma cell

115
Q

Another name for atopic dermatitis?

A

Eczema

116
Q

Management of type I hypersensitivity?

A

Anti-histamines
Avoidance
Desensitisation

117
Q

Properties of Ig produced by memory B cells?

A

Class switched and high affinity to antigen

118
Q

Properties of good vaccine preventing viruses entering cells of vaccinated individuals?

A

Induce neutralising antibodies

119
Q

Properties of good vaccine helping responses against intra-cellular pathogens in vaccinated individuals?

A

Induce protective T cells

120
Q

3 Practical difficulties with vaccinations by injection?

A

Needs a professional
Expensive
Equipment disposal problems

121
Q

Reasons many populations remain unvaccinated?

A

Need for refrigeration

Need for skilled workers

122
Q

3 manufacturing processes for antigen element of vaccine?

A

Killed
Live attenuated
Recombinated
Purified

123
Q

What is the challenge in developing vaccines against encapsulated bacteria?

A

By themselves they only provide and inadequate thymus independent immune response so a conjugated capsular vaccine is need to provide an environment for T cell differentiation

124
Q

What 2 vaccines administered by mucosal route?

A

Polia and influenza

125
Q

Why are adjuvants needed?

A

Purified antigens don’t elicit an innate immune response, adjuvants promote a better immune response

126
Q

Possible consequence of endocrine function of developing child of mother with Graves?

A

Hyperthyroidism as autoantibodies are passively transferred through placenta. Stimulate TSH receptor = more thyroid hormones release

127
Q

Why does London have a higher incidence of certain infectious disease than other parts of the country?

A

Varied and dynamic population
Variable disease exposure
Variable immunity

128
Q

Factors that may compromise the effectiveness of vaccination programmes?

A

Reduced uptake (fear, apathy)
Expense
Mutation of live attenuated viruses
Shift in herd immunity

129
Q

Other than organ transplantation, identify 4 further tissues commonly transplanted?

A

Cornea, blood, bone marrow, heart valves

130
Q

Organ least likely to be rejected as a result of imperfect tissue matching?

A

Liver

131
Q

Allotransplantation
Xenotransplatation
Autotransplatation

A

Between same species
Between different species
Within individual

132
Q

Universal donor and universal recipient, why?

A 
O = donor = no ABO antigens so cannot be recognised as non-self
AB = no A or B antibodies so will not mount an immune response
133
Q

Visible symptom of graft vs host disease?

A

Skin rash

134
Q

3 features of rejected organ?

A

Swollen
Hameorrhage
Necrosis

135
Q

Whta function of T cells do immunosuppressants target?

A

Cytokine secretion

Stage 2 Cheat sheets (9 decks)

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