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CP - JL > Core Immunology - Part 2 > Flashcards

Core Immunology - Part 2 Flashcards

1
Q

What does immunocompromised mean

A

disruption of specific defence of an organ/system

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2
Q

What disease do we worry about with burns

A

Pseudomonas and group A streptococcal infections

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3
Q

What can alter defence to make us more immunocompromised

A

Extremes of age, malnutrition or pregnant

Markedly immune compromised in neonates at 20 weeks and towards the end of pregnancy

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4
Q

What are the type of qualitative defects you can get in neutrophils

A

Reduced chemotaxis - rare, congenital - due to inadequate signalling/receptors and movement

Reduced killing power

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5
Q

how is killing power reduced in neutrophils

A

Inherited Chronic Granulomatous Disease
Defecient in NADPH Oxidase - can’t make H2O2 - can’t kill bacteria
Can’t mount a phagocytic response
Susceptible to Staph. Aureus infections

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6
Q

What is the quantitative defect in neutrophils

A

Neutropenic - especially severe if less than 0.5x10^9

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7
Q

What can make you neutropenic

A

cancer treatment
bone marrow malignancy
aplastic anaemia

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8
Q

What infections are you particularly susceptible in neutropenic patients

A

Pseudomonal - over 50% will die from these within 24 hours

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9
Q

What bacteria are you susceptible if you are neutropenic

A

Gram -ve e.g. E. coli
Gram +ve e.g. Staph aurues
Coagulase negative staph - when you put a line in

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10
Q

What fungal infections are you susceptible if you are neutropenic

A

Candida albicans and aspergillus

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11
Q

How to prevent infection in neutropenic patients

A

Broad spectrum antibiotics - amino glycoside and antipseudomonal penicillin

2nd line is carbapenems and then antifungals

Also give GCSF (granulocyte colony stimulating factors) - try to get the immune system working

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12
Q

Discuss types of T cell deficiencies

A

Congenital: Rare - T helper dysfunction +/- hypogammaglobulinaemias
Acquired: Drugs (cyclosporin after transplantation as decreases change of rejection)
Also through viruses

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13
Q

What pathogens usually infect you in T cell deficiencies

A

Opportunistic pathogens that tend to be intracellular

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14
Q

What bacteria are you susceptible to in T cell defeciency

A

Listeria (in cheese and pate so pregnant women should avoid)

TB

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15
Q

What viral infections are you susceptible to in T cell deficiency

A

HSV, CMV, VZV

Receive appropriate aciclovir and ganciclovir treatment and prophylaxis

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16
Q

What fungal infections are you susceptible to in T cell deficiencies

A

Candida albicans and cryptococcus

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17
Q

What Protozoa and parasitic infections are you susceptible to in T cell deficiencies

A

1) Cryptosporidium parvum (sporozoa)
2) Toxoplasmos Gondii (sporozoa)
3) Strongyloides stercolis (nematode)

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18
Q

Describe cryptosporidium infection

A 
Often in T cell deficiencies 
Spread by faecal/oral route - can be spread in water
Get severe diarrhoea - unto 3 weeks 
Immunocompromised may not recover
Only symptomatic treatment
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19
Q

Descrive Toxoplasma Gondii infection

A

Humans infected with cat faeces or transplanted heart or liver
May get lesion in brains or neurological signs
Most immunocompetent patients are asymptomatic - only get infected with T cell deficiencies

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20
Q

Describe strongyloides stercolis infection

A

Nematode
Get when worm enters your bare feet in the tropics - can be asymptomatic for a long time until immunocompromised
Worm can move from gut to bloodstream - infects blood with GI flora get gram negative septicaemia
Normal patients asymptomatic or rash of larva currens

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21
Q

Who do we suspect strongyloides stercolis infection

A

Patients from tropical countries or old prisoners of war

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22
Q

What are hypogammaglobulinaemias

A

Antibody problems/deficiences

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23
Q

Congenital causes of hypogammaglobulinaemias

A

X-linked agammaglobulinaemias

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24
Q

Acquired causes of hypogammaglobulinaemias

A

Multiple myeloma
Chronic lymphocytic leukaemia
Burns

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25
Q

What disease are you susceptible to in hypogammaglobulinaemias

A

Usually encapsulated bacteria in the respiratory tract (pneumoniae)
Or Giardia lamblia/cryptosporidium in the GIT

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26
Q

Why are you susceptible to parasites in hypogammaglobulinaemias

A

No IgA

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27
Q

How do we treat hypogammaglobulinaemias

A

Replace immunoglobulins

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28
Q

What are we at risk of in complement deficiencies

A

Encapsulated bacteria - we need complement activation to kill these organisms
The earlier the defect in the system the more susceptible we are

Also frequent S.pneumoniae infections due to poor opsonisation

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29
Q

What are we at risk of with C5-C8 deficiency

A

Neisseria meningitidis - MAC not formed so no lysis of bacteria

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30
Q

What does the spleen do

A

Source of complement and antibody producing B cells

Also removal of opsonised bacteria from blood

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31
Q

Why might we have a splenectomy

A

Trauma
Surgery
Functional e.g. sickle cell anaemia

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32
Q

What are we susceptible to in splenectomies

A

Strep pneumoniea, haemophilius influenza type B, neisseiria meningitidis, malaria

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33
Q

How to treat people with splectomies

A

Education
Vaccination
Prophylactic penicillin

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34
Q

What are biologics

A

Antibodies or other peptides that inhibit inflammatory cytokine signals

e.g. TNF inhibiting T cell activation or depleting B cells

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35
Q

What are you at risk of rheumatoid arthritis

A

TB, HZV, Legionalla Listeria etc. Due to biolgics Same as T cell deficiencies

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36
Q

What do we have liver transplants for

A

Hep C

Paracetamol overdose

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37
Q

What are the opportunistic infections after transplantation

A

CMV and aspergillus in the first 3 months

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38
Q

What are the later infections after transplantation

A

More T cell deficiency problems

E.g. listeria, VZV, candida

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39
Q

How do we prevent infection in immunocompromised infections

A

Hand washing
Aseptic techniques
Protectice isolation
Vaccinated patients - avoid live vaccines in T cell deficieincies
HEPA Air filtration removes aspergillus spores
Prophylaxis
Special diets e.g. avoid soft cheeses and pate

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40
Q

Who do we not give live vaccines to?

A

T cell deficient patients!

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41
Q

What do cytotoxic T cells do

A

Bind to infected cell
Perforin makes a hole in the membrane
Injects enzyme to cause apoptosis

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42
Q

How do Helper T cells work

A

Secrete cytokines to control immune response and help B and T lymphocytes

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43
Q

What is the target of HIV

A

Helper T cells

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44
Q

What do suppressor T cells do

A

Dampen down the immune response

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45
Q

How do antibodies promote phagocytosis

A

Neutrolization (blocks viral binding sites and coats bacteria)
Agglutination of microbes
Precipitation of dissolved antigens

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46
Q

What do antibodies activate

A

The complement system leading to cell lyiss

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47
Q

How does the innate system activate adaptive

A

They engulf micro-organisms and present them to cells

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48
Q

What are there common causes of immunodeficiency

A

Some are primary due to genetic defects - rare and often diagnosed early in childhood due to recurrent infection

Secondary - due to external factors e.g. stress, trauma, malnutrition, cancer, immunosuppressants, TB, HIV, AIDS, irradiation

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49
Q

What does IRAK do

A

It is a protein that causes the Nf-kb transcription factors to be produced

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50
Q

What is Nf-kb pathway essential for

A

Essential for the cell to produce inflammatory cytokines and cheekiness!

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51
Q

What happens in IRAK deficiency

A

Normally Toll Like Receptors (TLRs) recognise components of the cell wall and feed to the IRAK protein to activate the Nf-KB pathway

In deficiency have normal levels of WBC’s but much lower CRP in pneuomoccal pneumonia.
Would expect much larger response but no cytokines due to IRAK protein problems

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52
Q

What is chronic granulomatous disease

A

Mutation in NADPH Oxidase (gp91 most common and it is X-linked!!)

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53
Q

How does NADPH-oxidase mutation cause disease

A

Normally it transfers H+ across the membrane to produce free radicals and HOCL - makes the phagosome for more acidic to activate the proteolytic enzymes and kill bacteria

If theres a problem can’t transfer the protein
Cant acidify the phagosome
Cant kill the bacteria

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54
Q

Disease in chronic granulomatosus

A 
Osteromyelitis
Pneumonia
Swollen lymph nodes
Gingivitis
Non-malignant granulomas
IBD
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55
Q

How would we diagnose chronic granulomatosus

A

Nitroblue tetrazolium test (NBT)
Incubate neutrophils with NBT - they take in the dye
If NADPH-oxidase is working they make the blue dye a very dark colour –> in chronic granulomatous this doesn’t happen

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56
Q

Absent terminal complement pathway activity (C5-8) makes you susceptible to what

A

Meningococcal infections

But you would still have normal levels of immune molecules

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57
Q

How would we measure terminal complement pathway activity

A

Incubate sheep RBC with antibody to sheep RBC

Complement system should activate in this and should be lysis of the RBC

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58
Q

Presentation of absent terminal complement activity

A

Previous episodes of meningitis
No family history
Normal immune levels

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59
Q

Presentation of X-linked agammaglobulinaemias

A

history of recurrent sino-pulmonary infections
Maternal uncle/grandad has history of recurrent chest infections
Undetectable/low antibodies
Absent peripheral B cells, normal T cells
Bronchial dilation evident

60
Q

What is X-linked agammaglobulinaemia

A

Defects in B cells - loss of antibody secretion, get recurrent bacteria infections
Usually only diagnosed at 1/2 years as mothers antibodies protect you until then

61
Q

What is SCID

A

Severe combined immunodeficiency syndromes

When you have defects in T and B cells

62
Q

How to cure SCID

A

bone marrow transplant

Gene therapy

63
Q

Why are defects in T cells more dramatic

A

B cells need T cells help

Recurrent infection with opportunistic bacteria, viruses, fungi and protozoa

64
Q

Presentation of SCID

A

Severe herpes zoster infection and extensive oro-pharyngeal candida
Parents might be first cousing
Normal IgG but no IgA and reduced IgM

65
Q

Primary B-cell deficiencies

A 
agammaglobulinaemias
IgA deficieincy
Autosomal recessive hyper IgM syndrome
IgA deficiency
Transient hypogammaglobulinaemia of infacncy
66
Q

Primary T- cel deficiency

A 
SCID
Adenosine deaminate deficiency
Purine nucleoside phosphorylase deficiency
MHC Class II deficiency
Wiskott-Aldrich syndrome
67
Q

Deficiency of PRR’s makes you susceptible to?

A

HSV, Pneumococcus

68
Q

Deficiency of macrophages and neutrophils makes you susceptible to?

A

CGD, staphylococus, aspergillus

69
Q

Deficiency of T cell receptors makes you susceptible to?

A

SCID, opportunistic infections

70
Q

Deficiency of complement proteins makes you susceptible to?

A

Meningococcus

71
Q

Deficiency of cytokines makes you susceptible to?

A

Mycobacterium

72
Q

Deficiency of B cell makes you susceptible to?

A

Recurrent sino-pulmonary infections

73
Q

What is immunomodulation

A

The act of manipulating the immune system using immunomodulatory drugs to achieve a desired immune response

74
Q

What are immunomodulators

A

Mechanical products produced using molecular biology techniques including recombinant DNA technology

75
Q

What are the main classes of immunomodulators

A

Substances nearly identical to body own signalling
Monoclonal antibodies
Fusion proteins

76
Q

What is etranercept

A

Fusion protein between Fc-TNF receptor

77
Q

What is adalimumamb

A

Human IgG1 monoclonal antibody

78
Q

What is infliximab

A

Chimer human-mouse IgG1 monoclonal antibody

These antibodies detect TNF

79
Q

What is cetrolizuman

A

Humanised monovalent Fab-PEG

PEG (Polyethylene glycol) –> makes them more stable

80
Q

Problems with immunomodulator drugs

A

We create an immune response to them each time we inject them - they get less effective

81
Q

What is immunopotentiation

A

Essentially vaccination

82
Q

2 forms of immunopotentiation

A

Active and passive

83
Q

What is active immunopotentiation

A

Stimulates development of a protective immune response and immunological memory

84
Q

What material is used in active immunopotentiation

A

Weakened form of pathogens
Inactivated pathogens
Purified materials (proteins DNA)
Adjuvant - most work via TLR’s and PRR’s

85
Q

What are adjuvants

A

Work via TLR’s and PRR’s

They stimulate different receptors to create the required response

86
Q

Problems with active immunopotentation

A

Allergies
Limited usefulness in immunocompromised
Delay in achieving protection

87
Q

What is passive immunopotentation

A

Transfer of specific high titre antibodies from nor to recipient
Provide immediate but transient protection

88
Q

Problems with passive immunopotentation

A

Risk of virus transmission
transient protection
Can cause serum sickness - IgG can be pro-inflammatory

89
Q

What are the uses of passive immunopotentation

A

Hep B - prophylaxis and treatment

Botulism, VZV (in pregnancy), diphtheria and snake bites

90
Q

What can we use for passive immunopotentiation

A 
Pooled human immunoglobulins
Animal sera (antitoxins and antivenins)
91
Q

What does GCSF do

A

Acts on the bone marrow to increase the production of mature neutrophils

92
Q

What does Il-2 do?

A

Stimulates T cell activation

93
Q

What does alpha interferon treat?

A

Treats hepatitis C

94
Q

What does beta interferon treat?

A

Multiple sclerosis

95
Q

What does gamma interferon treat?

A

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

96
Q

What do interferons do?

A

cause protein synthesis in cells to make the cell less susceptible to viral infection

97
Q

Problems with interferons

A

Makes you feel awful

98
Q

What are DMARD’s

A

Type of immunosuppressant

Disease modifying anti rheumatic drugs - contain gold!

99
Q

How do corticosteroids work

A 
Decrease neutrophil margination
Reduces proliferation of inflammatory cytokines - as they INHIBIT PHOSPHOLIPASE A2 (this reduces arachidonic acid metabolites production)
Lymphonpenia
Reduced T cell proliferation
Reduced immunoglobulin production
100
Q

Side of effects of corticosteroids

A

Carbohydrate and lipid metabolism affected - can cause diabetes and hyperlipidaemia
Reduced protein synthesis - poor wound healing
Osteoporosis
Glaucoma and cataracts
Psychiatric complications

101
Q

Use of corticosteroids

A

Autoimmune diseases e.g. vasculitis and RA
Crohns, sarcoid, GCA, lymphoma, allograft rejection (initially)

BUT we don not want people on steroids long term - usually just give as part of an induction therapy

102
Q

How are T cells activated

A

Interaction with an APC

The T cell then produces IL-2 to increase transcription factors

103
Q

What does IL-2 stimulate

A

Other signals such as m-Tor which allows the cell to go into proliferation

104
Q

What do antimetabolites stop

A 
Inhibit nucleoside (purine) synthesis
Stops the proliferation of T & B cells

Stops DNA synthesis

105
Q

Examples of antimetabolites

A 
azathioprine
mycophenolate mofetil (MMF)
106
Q

What do Calcineurin inhibitor do

A

Inhibit initial T cell activation

107
Q

Examples of calcineurin inhibitors

A

Ciclosprorin A

Tacrolimus

108
Q

What do M-tor inhibitor do?

A

Interfere with T cell proliferation

109
Q

Examples of M-tor inhibitors?

A

Sirolimus

110
Q

What do IL-2 Receptor Monoclonal antibodies do?

A

Block Il-2 binding as iL-2 stimulates other signals such as m-Tor which causes the T cell to proliferate

111
Q

Examples of IL-2 Receptor Monoclonal antibodies

A

Basiliximab

Daclizumab

112
Q

What does ciclosporin A bind to?

A

Intracellular protein cyclophilin

Prevent NFAT activation

113
Q

What does tacrolimus bind to?

A

Intracellular protein FKBP-12

Prevents NFAT activation

114
Q

How do Calcineurin inhibitors prevent T cell activation?

A

Prevents NFAT activation

NFAT normally stimulates cytokines (IL-2 and INF) and gene transcription

115
Q

Is calcineurin reversible or irreversinle

A

Reversible
Have more of a targeted effect than steroids
Initially used for organ transplatation

116
Q

What is siromilus

A

A macrolide antibiotic that inhibits T cell proliferation

117
Q

How does sirolmilus (rapamycin) work?

A

Binds to FKBP-12
Inhibits mammalian target of rapamycin (mTOR)
Inhibits the response to IL-2
Cell cycle arrests at the G1-S phase hence stops proliferation

118
Q

Is sirolmillus reversible?

A

Yes

119
Q

Where does siromilus stop the T cell cycle?

A

G1-S phase

120
Q

Side effects of calcineurin and mTOR inhibits?

A 
Hypertension
Nephrotxocitiy
Hepatoxicity
Lymphones
Hirsutism
Opportunistic infections
Neurotoxicity
Drug interactions
121
Q

What was a main problem of ciclosproin

A

Nephrotoxicity as commonly used in kidney transplantatinos

122
Q

What Azathioprine (AZA)

A

Anti-metabolite
Guanine anti-metabolite
Rapidly coverted to 6-mercarptopurine
Inhibits nucleotide (purine) synthesis

123
Q

What is mycophenolate mofetil (MMF)

A

Anti-metabolite
Non-competitive inhibitor of IMPDH
Prevents production of guanosine triphosphate

124
Q

What is the only T cell targeted immunosuppression that targets B & T cells

A

Anti-metabolites
As causes impaired DNA production
Prevents early stages of active cell proliferation
But can target any rapidly dividing cell

125
Q

What is methotrexate

A

Anti-metabolite

Folate antagonist

126
Q

What is cyclophopsphamide

A

Cross-links DNA (CYTOTOXIC DRUG)

127
Q

Side effects of T cell suppression deugs

A

Gastric upset
Bone marrow suppression
Heptatitis
Susceptibility to infection

128
Q

Specific side effect of cyclophosphamide

A

Cystitis

129
Q

Uses of AZA and MMF

A

Both antimetabolites
Used for autoimmune diseases and allograft rejection
(Vasculitis, SLE, IBD)

130
Q

Methotrexate uses

A

Rheumatoid arthritis Vasculitis, GvHD, Polymyositis, PsA

131
Q

Cyclophosphagmide use

A

Vasculitis (Wegeners, CSS) SLE

132
Q

What are biologic DMARDS

A 
Can target specific cell types
E.g. Anti-cytokines
Anti-B cell
Anti -T cell activation
Anti-adhesion molecules
Complement Inhibitiors
133
Q

Treatment of Rheumatoid Arthritis

A

Anti-TNF
Anti-IL-6 (Tocilizumab)
Anti IL-1 (Anakinara, rilonacept, canakinumab)
Rituximab

134
Q

What is Anti-TNF

A

TNF important for macrophage activation
Use anti-TNF to prevent full activation and treat rheumatoid arthritis

Can also be used in Crohns, psoriasis and ankylosing spondylitis

BUT Susceptible to TB as macrophages not fully primed

135
Q

What does anti IL-6 (toclizumab) do?

A

Blocks IL-6 receptor
Treats rheumatoid arthritis and AOSD

But may cause problems with control of serum lipids

136
Q

What does anti-IL-1 treat?

A

AOSD and auth inflammatory responses

137
Q

What is rituximab

A

A chimeric monoclonal antibody to CD-20 on B cell surface

Only cells in blood express CD-20 not the ones in the bone marrow hence rituximab can target these cells

138
Q

What does rituximab treat?

A 
Chemo resistant DLCL
Lymphomas
Leukaemias
Transplant rejections
Autoimmune disorders
139
Q

What is adoptive immunotherapy

A

Bone marrow transplant and stem cell transplant

140
Q

what is adoptive immunotherapy used for

A 
Immunodeficiency (SCID)
Lymphomas
Leuaemias
Inherited metabolic disorders (osteoporosis)
Autoimmune diseases
141
Q

What is allergen specific immunotherapy

A

Take something you are allergic to in a controlled manner
Start small and build up dose
Develop a tolerance

142
Q

How does allergen specific immunotherapy work?

A

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

143
Q

What is omalizumab

A

Monoclonal antibody against IgE
Treats asthma, urticarial and angiodema

BUT may cause sever systemic anaphylaxis

144
Q

What is mepolizumab

A

Monoclonal antibody against IL-5
Prevents eosinophil recruitment and activaton
Limited effect on asthma
No clinical efficay in hypereosinophil syndrome

145
Q

What does IL-5 do?

A

Eosinophilic recruitment and activation

146
Q

What do allergy immunomodulators target

A

Can use immunosuppressants e.g. steroids but not good for long term use
Allergen specific immunotherapy
Anti-IgE therapy (omalizumab)
Anti IL-5 Monoclonal treatment (mepolizumab)

CP - JL (14 decks)

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