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Pathology (Guide) > Immunology - Immune Modulation > Flashcards

Immunology - Immune Modulation Flashcards

1
Q

What 4 immune modulators boost the immune response?

A
  1. Vaccination
  2. Replacement of missing components
  3. Cytokine therapy
  4. Blocking immune checkpoints (for advanced melanoma)
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2
Q

What 6 immune modulators suppress the immune response?

A
  1. Steroids
  2. Anti-proliferative agents
  3. Plasmapharesis
  4. Inhibitors of cell signalling
  5. Agents directed at cell surface antigens
  6. Agents directed at cytokines
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3
Q

What is the mechanism of vaccination?

A
  • APCs present peptide to T cells (CD4 + CD8)
  • Clonal expansion: T cells with appropriate specificity proliferate + differentiate
  • CD4 cells: release cytokines + activate other cells (B cells)
  • CD8 cells: kill infected cells
  • Effector T cells then die by apoptosis OR surive as memory cells
  • B cells differentate to T cells independent (IgM) memory cells, OR undergo germinal centre reaction (T-cell dependent plasma cells ((IgA/IgG/IgE))
  • End result = immune memory (infection remembered + individuals remain protected)
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4
Q

How is immune memory achieved in vaccination?

A
  • Residual specific T + B cells with enhance capacity to respond to re-infection
  • Pre-formed pool of high affinity Abs
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5
Q

What are the 3 ideal vaccine requirements?

A
  1. Generates immunological memory
  2. Practical - single injection, easy storage, inexpensive
  3. No adverse effects
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6
Q

What is passive vaccination and how long does it last for?

A
  • Directly administering pre-formed antibodies/immunoglobulins
  • ~3 wks
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7
Q

What are some examples of passive vaccination?

A
  • HNIG (Human Normal Ig) = Hep A + Measles
  • HBIG (Hep B Immunoglobulin) + Hep B
  • HRIG (Human Rabies Immunoglobulin) = Rabies
  • VZIG (Varicella Zoster Immunoglobulin) = Varicella
  • Paviluzimab (monoclonal Ab to RSV) = RSV
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8
Q

What is herd immunity?

A

When enough people in the community are immunised against a disease, it makes it more difficult for the disease to get passed between those who aren’t immunised

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9
Q

Why is vaccination less effective in the elderly?

A
  1. Immune senescence
  2. Nutrition (insufficient energy due to poor nutrition; reduced availability of trace elements + minerals (reduced gut absorption))
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10
Q

What is immune senescence?

A

The process of remodelling lymphoid organs - happens in the elderly
1. Increased frequency of terminally differentiated effector memory T cells
2. Increased expression of senescence markers
3. Much reduced production of recent thymic emigrants which drive the naiive T-cell repertoire

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11
Q

What is the evidence and concept behind dendritic cell/cancer vaccines?

A

Evidence:
- Acquired defects in DC maturation/function seen in some malignancies allows cancer to evade immune recognition

Concept:
- Pt WBCs harvested + cultured with target “tumour” antigen
- WBCs re-infused back into pt to stimulate immune response

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12
Q

What is an example of a dendritic cell/cancer vaccine?

A

Provenge (Sipuleucel-T) = Prostate cancer

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13
Q

What vaccinations are received at 2 months of age?

A
  • 6-in-1
  • Men B
  • Rotavirus
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14
Q

What vaccinations are received at 3 months of age?

A
  • 6-in-1
  • Rotavirus
  • PCV (pneumococcal conjugate)
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15
Q

What vaccinations are received at 4 months of age?

A
  • 6-in-1
  • Men B
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16
Q

What vaccinations are received at 1 year?

A
  • Hib/Men C
  • Men B
  • PCV (pneumococcal conjugate)
  • MMR
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17
Q

What vaccination can be given between 2-10yrs?

A

Flu (annually) = Sept/Oct

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18
Q

What vaccinations are received at 3yrs 4 months of age?

A
  • DTaP/IPV (4-in-1 booster)
  • MMR
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19
Q

What vaccination is given at 12-13yrs of age?

A
  • HPV (6, 11, 16 + 18)
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20
Q

What vaccination is given at 14yrs of age?

A
  • Men ACWY
  • T/D/aP (3-in-1 booster)
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21
Q

What conditions make up the 6-in-1 injection?

A
  • Diptheria
  • Tetanus
  • acellular Pertussis (Whooping Cough)
  • Inactivated Polio
  • Haemophilus influenza type B
  • Hepatitis B
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22
Q

What conditions make up the 4-in-1 booster vaccine?

A
  • Diptheria
  • Tetanus
  • acellular Pertussis
  • Inactivated Polio
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23
Q

What conditions make up the 3-in-1 booster vaccine?

A
  • Tetanus
  • Diptheria
  • acellular Pertussis
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24
Q

What adult vaccines are given and at what age groups?

A
  • Flu (annually) = 50yrs +
  • Pneumococcal (PPV) = 60yrs
  • Shingles = 70yrs
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25
Q

What vaccines are given during pregnancy?

A
  • Flu (during appropriate season)
  • DTaP/IPV from 16wks
    = Diptheria, Tetanus, acellular Pertussis, Inactivated Polio
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26
Q

At what age can you received the first and second covid vaccinations?

A

5 years

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27
Q

When can you receive a covid booster dose?

A
  • 16yrs +
  • 12-15yrs at high risk/living with an immunocompromised person
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28
Q

When can you receive an additional primary dose of the covid vaccine?

A

Severely weakened immune system at time of initial vaccine

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29
Q

When can you receive an additional seasonal booster dose of the covid vaccine?

A
  • 50yrs +
  • High risk
  • Pregnant
  • Frontline HCP
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30
Q

Which vaccinations are given for travel purposes?

A
  • Cholera
  • Hep A
  • Hep B
  • Jap Enceph
  • Tick-Bourne Enceph
  • Typhoid
  • Yellow Fever
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31
Q

How does the influenza vaccine work?

A
  • CD8 T cells control viral load but response relied on anti-haemagglutinin antibody
  • Protection begins within 7 days of immunisation
  • Protection lasts 6 months
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32
Q

How does the TB/BCG vaccine work?

A
  • BCG (Bacilli Calmette-Guerin) = attenuated strain of bovine TB
  • Relies on T cell response
  • Protects against primary infection (~20%) + progression to active TB (71%)
  • Protection lasts ~10-15yrs
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33
Q

What are the different types of vaccines and their differences?

A

Live attenuated:
- Live pathogen
- Modified to limit pathogenesis

Inactivated/Component:
- Destroyed pathogen OR Isolated Antigenic proteins

Conjugate:
- Polysaccharide
- Antigenic protein carrier to enhance response

DNA/RNA Vaccines:
- Pathogen’s genetic material delivered to host cells via viral vector/lipid complex
- Host cells produce + express protein (leading to immune response)

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34
Q

What are some advantages + disadvantages of Live Attenuated vaccines and some examples?

A

Advantages:
- Lifelong immunity possible (no boosters)
- Protection against different strains likely
- Activates all phases of immune system

Disadvantages:
- Reversion to virulence e.g. VAPP (polio vaccine)
- Risk for immunosuppressed/deficient
- Storage issues (requires refridgeration)

E.g. (MMR-VBOY):
- MMR
- VZV
- BCG
- Oral (polio/typhoid)
- Yellow fever
- Influenza 2-17yo

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35
Q

What are some advantages + disadvantages of inactivated/component vaccines and some examples?

A

Advantages:
- No reversion
- Safe in immunodeficiency
- Easier storage
- Low cost
- Can eliminate wild-type virus from community

Disadvantages:
- Poor response “immunogenicity”
- Repeated boosters or modifications needed
- Does not follow natural route of infection (e.g SC injection for flu)

Inactivated e.g.
- Influenza
- Polio
- Cholera
- Bubonic plague
- Hep A
- Rabies
- Pertussis

Component/Subunit e.g:
- Hep B
- HPV
- Influenza
- Toxoids: Diptheria + tetanus

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36
Q

What are some advantages + disadvantages of conjugate vaccines and some examples?

A

Advantages:
- Effective against encapsulated bacteria
- Used for children

Disadvantages:
- Similar to inactivated/components

E.g (NHS):
- N. meningitidis
- H. influenzae
- S. pneumoniae
- Tetanus

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37
Q

What are some advantages + disadvantages of DNA/RNA vaccines and some examples?

A

Advantages:
- mRNA/lipid complex noninfectious + non-integrating

Disadvantages:
- Relatively new technology
- DNA may theoretically integrate to host’s DNA
- Possible autoimmunity responses (e.g. SLE)
- Need target that invokes good imune response

E.g:
- mRNA = SARS-COV-2
- Adenoviral vector: AstraZeneca + Sputnik
- Ongoing research into other uses

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38
Q

What vaccinations can’t HIV patients receive?

A
  • BCG
  • Yellow fever
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39
Q

What are adjuvants?

A

Increase immune response without altering its specificity

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40
Q

What are three ways to ensure a good response + effective memory from a vaccine?

A
  1. Live vaccine
  2. More persistent antigen - depot adjuvant
  3. Assisted activation of immune response - stimulatory adjuvant
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41
Q

How does a depot adjuvant work?

A
  • Slows release of antigen
  • Injection of adjuvant + antigen mixture ensures steady stream of antigen leading to prolonged immune response
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42
Q

What are some features of the ALUM depot adjuvant and how does it work?

A
  • Most common
  • Primary adjuvant utilised in humans
  • Generally safe + mild

MoA:
- Antigens absorbed to alum so acts as means of slowly releasing antigen
- Activates Gr1+ cells to produce IL4
- This helps prime naiive B cells (mainly antibody mediated response)

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43
Q

How do stimulatory adjuvants work?

A
  • Mimic action of PAMPS on TLR/other PRRs
  • Leads to boosted immune response
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44
Q

How does the CpG stimulatory adjuvant work?

A
  • Immunostimulatory adjuvant activity linked to unmethylated DNA motif rish in CpG
  • CpG = DNA where a cytosine nucleotide is situated next to a guanine nucleotide
  • Activates TLRs on APCs stimulating expression of costimulatory molecules
45
Q

What are some features of the Complete Freund’s (stimulatory) adjuvant?

A
  • Water-in-oil emulsion containing mycobacterial cell wall components
  • Mainly for animals
  • Painful in humans
46
Q

What are some features of the ISCOMS (immune stimulating complex) stimulatory adjuvant?

A
  • Experimental
  • Multimeric antigen with adjuvant built in
  • Cell-mediated immune response + humoral response
  • With saponin results in strong serum antibody response
47
Q

What are some features of Interleukin-2 stimulatory adjuvant?

A
  • Used to achieve seroconversionin Hep B sA+ individuals
48
Q

What are some indications for a haematopoeitic SCT?

A

Life-threatening primary immunodeficiency:
- SCID
- Leukocyte defect

Haem malignancy

49
Q

What are the two types of Ab replacement?

A
  • Preformed IgG to wide range of unspecified organisms
  • High titres of IgG to specific pathogens
50
Q

What are some indications for Ab replacement (IgG to wide range)?

A

Primary Ab deficiency:
- Bruton’s X-linkde agammaglobulinaemia
- X-linked hyper IgM syndrome
- Common variable immune deficiency

Secondary acquired Ab deficiency:
- Haem malignancy
- Post BM transplant

Other:
- ITP, Kawasaki, GBS, Measles, Severe myasthenia gravis
- Toxic epidermal necrolysis
- CMV pneumonitis
- Dermatomyositis
- Chronic inflammatory demyelinating polyradiculopathy

51
Q

What are some indications for Ab replacement (IgG to specific)?

A

Passive immunisation post-exposure:
- Hep B
- Rabies
- VZV (pregnancy <20wks or immunocompromised)

52
Q

What are the different types of adoptive T cell transfer therapy and some indications of each?

A

Virus specific T cells:
- EBV-related B cell lymphoproliferative disease
- Severe viral infections in immunocompromised pts

Tumour infiltrating lymphocyte T cell therapy:
- Head + neck SCC
- Melanoma
- Lung + gynae Ca

TCR

CAR-T cell therapy:
- ALL
- Non-Hodgkin’s lymphoma

53
Q

What is recombinant cytokine therapy, its aims and some examples?

A

Recombinant cytokines = pro-inflammatory cytokines

Aim:
- Boost immune response to cancer + some pathogens

E.g:
- IL2 (increases T cell response) = Renal cancer
- Interferon α = Antiviral effect (Hep B + C), Anti-cancer, Kaposi sarcoma, hairy cell leukaemia, CML, melanoma
ABC = Interferon Alpha for hep B + C + Cml
- Interferon β = relapsing remitting MS
- Interferon gamma (increases macrophage function) = chronic Granulomatous disease

54
Q

What are some indications for immune checkpoint blockade?

A
  • Advanced melanoma
  • Metastatic renal cancer
  • Other malignancies
55
Q

What is the biggests risk for immune checkpoint blockade?

A

Autoimmunity

56
Q

What are two examples of immune checkpoint blockade and how do they work?

A

Ipilimumab:
- Monoclonal Ab specific for CTLA4
- CTLA4 = inhibitory checkpoint found on T cells (competes with CD28 to bind CD86/B7 on APCS to block T cell activation)
- CTLA4 blockade leads to increased APC presentation to T cells, and increased T cell activation

Pembrolizumab/Vivolumab:
- Monoclonal Ab specific for PD-1
- PD-1 = programmed death receptor, found on regulatory T cells, binds PD-L1/2 on APCs/tumour cells leads to T cell inactivation + death
- PD-1 blockade leads to T cells remaining active and thus killing tumour cells

57
Q

What are adverse effects of immunosuppressive therapies?

A
  • Infusion reaction
  • Injection site reactions
  • Acute infection
  • Chronic infection
  • Malignancy
  • Autoimmunity
58
Q

How does an infusion reaction present as a result of immunosuppressive therapies?

A
  • IgE mediated = Urticaria, hypotension, tachycardia, wheeze
  • Not classical Type I hypersensitivity: headahce, fever, myalgia
  • Cytokine storm
59
Q

How does an injection site reaction present as a result of immunosuppressive therapies?

A
  • Peak reaction at ~48rs
  • ?Occurs at previous injection sites
  • Mixed cellular infiltrates, often CD8 T cells
  • Not generally IgE or immune-complex mediated
60
Q

How can an acute infection as a result of immunosuppressive therapies be prevented and treated?

A

Prevention:
- Vaccination (not live)
- Avoid contact

Tx:
- Stop immunosuppression
- Abx (cover for atypicals)

61
Q

How can a chronic infection as a result of immunosuppressive therapies be prevented + treated for patients with TB, HIV, Hepatitis + JCV infections?

A

TB:
- Check Hx/travel/contacts
- CXR/Elispot
- Give prophylaxis/Tx as needed

HIV:
- Check HIV status prior
- Consider risks vs benefits

Hep:
- B = check core Ab pre-treatment
- C = Check Ab pre-treatment
- Further Ix for active disease if positive serology

JCV (John Cunningham Virus):
- Polyoma virus that can reactivate
- Infects + destroys oligodendorcytes
- Causes progresive multifocal leucoencephalopathy (PML)
- Seen with +++ immunosuppressive agents

62
Q

What are some examples of malignancies that can arise from conditions having immunosuppressive therapies, and how can this be prevented?

A
  • EBV = lymphoma
  • Non-melanoma skin cancer = HPV
  • Melanoma = anti-TNF α

Prevention: Targeted immunosuppression lowers risk of cf. transplant regimes

63
Q

How can autoimmunity arise as a result of using immunosuppressive therapies and some examples?

A

Dysregulation of the immune system:
- SLE + lupus-like syndromes
- APLS
- Vasculitis
- Interstitial lung disease
- Sarcoidosis
- Uveitis
- AI hepatitis
- Demyelination

64
Q

What is the mode of action of steroids?

A

Prostaglandins:
- Inhibits phospholipase A2
- No breakdown of phospholipids to arachidonic acid
- Prostaglandin synthesis is blocked = reduced inflammation

Phagocytes:
- Inhibits phagocyte trafficking, phagocytosis + release of proteolytic enzymes
- Causes transient increases in neutrophil count

Lymphocytes:
- Lymphopenia (sequestered in lymphoid tissue)
- Blocks cytokine gene expression
- Decreased Ab production
- Promotes apoptosis

65
Q

What are some indications for steroid use?

A
  • Allergic disorders
  • Autoimmune + autoinflammatory disease prevention + Tx
  • Transplant rejection
  • Malignancy
66
Q

What are some side effects for steroid use?

A

Metabolic:
- Diabetes
- Central obesity
- Moon face
- Lipid abnormalities
- Osteoporosis
- Hirsutism
- Adrenal suppression
- HTN
- Immunosuppression = infection

Others:
- Cataracts
- Glaucoma
- Peptic ulceration
- Pancreatitis
- Avascular necrosis

67
Q

What do anti-proliferative agents do and what are four examples?

A
  • Inhibit DNA synthesis
  • Cells with rapid turnover = most sensitive

E.g.:
- Cyclophosphamide
- Mycophenolate Mofetil
- Azathioprine
- Methotrexate

68
Q

What is the mechanism of action of Cyclophosphamide?

A
  • Alkylates guanine base of DNA
  • Damages DNA + prevents cell replication
  • Affects B cells > T Cells, but at high doses affects all cells with high turnover
69
Q

What are some indications for cyclophosphamide use and some side effects?

A

Indications:
- Connective tissue disease
- Vasculitis
- Anti-cancer agent

SEs:
- Bone marrow suppression
- Hair loss
- Sterility (M>F)
- Haemorrhagic cystitis
- Malignancy: bladder, haem, non-melanoma skin
- Infection: PCP

70
Q

What is the mechanism of action of Mycophenolate Mofetil?

A
  • Anti-metabolite
  • Inhibits IM PDH, prevents guanine synthesis
  • Blocks de novo nucleotide synthesis - prevents replication of DNA
  • Prevents T>B cell proliferation
71
Q

What are some indications for Mycophenolate Mofetil use and some side effects?

A

Indicators:
- Transplantation
- Auto-immune diseases
- Vasculitis

SEs:
- Bone marrow suppression
- Infection: HSV reactivation, progressive multifocal leukoencephalopathy (JC virus)

72
Q

What is the mechanism of action of azathioprine?

A
  • Anti-metabolite
  • Metabolised by liver to 6 mercaptopurine
  • Blocks de novo purine (e.g. adenine, guanine) synthesis
  • Prevents replication of DNA, preferentially inhibits T cell activation + proliferation > B cell
73
Q

What are the indications for azathioprine use and some side effects?

A

Indicators:
- Transplantation
- Auto-immune disease
- Auto-inflammatory diseases

SEs:
- Bone marrow suppression - TPMT polymorphism
- Infection
- Hepatotoxicity

74
Q

What is the mechanism of action of methotrexate?

A
  • Anti-folate
  • Inhibits dihydrofolate reductase (DHFR)
  • Decreases SNA synthesis
75
Q

What are the indications for methotrexate use and some side effects?

A

Indicators:
- RA
- Psoriasis
- Crohn’s
- Chemotherapy

SEs:
- Bone marrow suppression
- Infection
- Malignancy
- Teratogenic
- Pneumonitis
- Pulmonary fibrosis
- Hepatotoxicity
- Folate deficiency (macrocytic megaloblastic anaemia)

76
Q

What is the mechanism of action of plasmapharesis?

A
  • Removal of pathogenic antibody
  • Patient blood passes via separator
  • Plasma treated to remove immunoglobulins + reinfused (or replaced with albumin in plasma exchange)
77
Q

What are the indications for plasmapharesis and some side effects?

A

Indicators:
- Severe Ab-mediated Type II disease (Goodpasture syndrome, myasthenia gravis, Ab mediated transplant rejection/ABO incompatibility)

SEs:
- Rebound Ab production limits efficacy
- Given with anti-proliferative agent to reduce risk
- Anaphylaxis

78
Q

What are some examples of drugs that are inhibitors of cell signalling?

A
  • Tacrolimus
  • Cyclosporin
  • Sirolimus / Rapamycin
    Tofacitinib
  • Apremilast
79
Q

What is the mechanism of action of tacrolimus and cyclosporin?

A
  • Inhibits Calcineurin
  • Prevents T cell proliferation/function via reduced IL-2 expression
80
Q

What are some indications for Tacrolimus/Cyclosporin use and their side effects?

A

Indicators:
- Rejection prophylaxis (transplantation)
- SLE
- Psoriatic arthritis
- Can be used in pregnancy

Tacrolimus SEs:
- Nephrotoxic
- HTN
- Neurotoxic
- Diabetogenic

Cyclosporin SEs:
- Nephrotoxic
- HTN
- Neurotoxic
- Dysmorphism
- GINGIVAL (GUM) HYPERTROPHY

81
Q

What is the mechanism of action of Sirolimus + Rapamycin and their indications and side effects?

A

MoA:
- mTor inhibitor
- Inhibits T cell proliferation via IL-2 pathway

Indicators:
- Transplantation

SEs:
- HTN
- Less nephrotoxic

82
Q

What is the mechanism of action of Tofacitinib and its indications?

A

MoA:
- JAK1/3 inhibitor
- Influences gene transcription via JAK-STAT signalling pathway
- Inhibits production of inflammatory molecules

Indicators:
- RA
- Psoriatic arthritis
- Axial spondyloarthritis

83
Q

What is the mechanism of action of apremilast and its indications?

A

MoA:
- PDE4 inhibitor
- Increases cAMP
- Influences gene transcription via protein kinase A pathway

Indicators:
- Psoriasis
- Psoriatic arthritis

84
Q

What are some drug agents that are directed against cell surface antigens, block signalling + cell depletion?

A
  • Basiliximab
  • Abatacept
  • Rituximab
  • Vedolizumab
  • Natalizumab
  • Tocilizumab
  • Muromonab-CD3
  • Anti-thymocyte globulin (ATG)
  • Dacilizumab
  • Efalizumab
  • Alemtuzumab
85
Q

What is the mechanism of action of, indications for and side effects of basiliximab?

A

MoA:
- Anti-CD25 (α chain of IL-2 receptor)
- Inhibits T cell proliferation

Indicators:
- Allograft rejection (prophylaxis)

SEs:
- Infusion reactions
- Infection
- Malignancy
- GI disturbance

86
Q

What is the mechanism of action of, indications for and side effects of Abatacept?

A

MoA:
- Anti-CTLA4-Ig fusion protein
- Reduces co-stimulation of T cells via CD28

Indicators:
- RA

SEs:
- Infusion reactions
- Infections: TB, HBV, HCV
- Malignancy
- Cough

87
Q

What is the mechanism of action of, indications for and side effects of Rituximab?

A

MoA:
- Anti-CD20
- Depletes mature B cells (not plasma cells)

Indicators:
- Lymphoma
- RA
- SLE

SEs:
- Infusion reactions
- Infection: PML
- Exacerbation CV disease

88
Q

What is the mechanism of action of, indications for and side effects of Vedolizumab?

A

MoA:
- Anti-α-4-β-7integrin
- Inhibits cell migration (blocks integrin binding to MadCAM1)

Indicators:
- IBD

SEs:
- Infusion reactions
- Hepatotoxicity
- Infection
- Malignancy

89
Q

What is the mechanism of action of, indications for and side effects of Natalizumab?

A

MoA:
- Anti-α-4-β-1 integrin (binds to VCAM1 + MadCAM1 to mediate rolling/arrest of leukocytes)
- Inhibits T cell migration

Indicators:
- Relapsing-remitting MS
- Crohn’s disease

SEs:
- Infusion reactions
- Infection: PML
- Malignancy
- Hepatotoxicity

90
Q

What is the mechanism of action of, indications for and side effects of Tocilizumab?

A

MoA:
- Anti-IL6-receptor
- Reduces macrophage, T cell, B cell, neutrophil activation

Indicators:
- Castleman’s disease
- RA

SEs:
- Infusion reactions
- Infection
- Hepatotoxic
- Hyperlipidaemia
- Malignancy

91
Q

What is the mechanism of action of, indications for and side effects of Muromonab-CD3?

A

MoA:
- Blocks CD3 on T cells
- Mouse monoclonal antibody (OKT3)

Indicators:
- Active allograft transplant rejection

SEs:
- Fever
- Leucopenia

92
Q

What is the mechanism of action of, indications for and side effects of Anti-thymocyte globulin (ATG)?

A

MoA:
- Lymphocyte depletion
- Modulation of T cell activation + migration

Indicators:
- Allograft rejection (renal, heart)

SEs:
- Infusion reactions
- Leucopenia
- Infection
- Malignancy

93
Q

What is the mechanism of action of and indications for Dacilizumab?

A

MoA:
- IL-2 receptor antibody
- Targets CD25

Indicators:
- Organ transplant rejection prophylaxis

94
Q

What is the mechanism of action of Efalizumab?

A
  • Anti-CDIIa
  • Inhibits migration of T cells
95
Q

What is the mechanism of action of, indications for and side effects of Alemtuzumab?

A

MoA:
- Monoclonal Ab that binids to CD52 found on lymphocytes resulting in depletion

Indicators:
- CLL
- MS
- T cell rejection (transplant)

SEs:
- CMV infection

96
Q

What are some agents that are directed at cytokines/receptors?

A
  • Infliximab
  • Adalimumab
  • Certolizumab
  • Golimuab
  • Etanercept
  • Ustekinumab
  • Guselkumab
  • Secukinumab
  • Denosumab
  • Tocilizumab
  • Sarilumab
  • IL-1 blockade
  • IL-4/5/13 blockade
97
Q

What is the mechanism of action of, indications for and side effects of infliximab, adalimumab, certolizumab + golimumab?

A

MoA:
- Anti-TNFa

Indicators:
- RA
- Ankylosing spondylitis
- Psoriasis
- Psoriatic arthritis
- IBD
- Familial Mediterranean Fever

SEs:
- Infusion/injection site reactions
- Infection: TB, HCV, HBV
- Lupus-like conditions
- Demyelination
- Malignancy (Lymphoma)

98
Q

What is the mechanism of action of, indications for and side effects of Etanercept?

A

MoA:
- TNFalpha/TNFbeta receptor p75-IgG fusion protein
- Inhibits both cytokines

Indicators:
- RA
- Ankylosing spondylitis
- Psoriasis
- Psoriatic arthritis
- JIA

SEs:
- Infusion/injection site reactions
- Infection: TB, HCV, HBV
- Lupus-like conditions
- Demyelination
- Malignancy (Lymphoma)

99
Q

What is the mechanism of action of, indications for and side effects of Ustekinumab?

A

Moa:
- Anti-IL-12 + IL-23
- Binds to p40 subunit

Indicators:
- Psoriasis
- Psoriatic arthritis

SEs:
- Injection site reactions
- Infection: TB
- Malignancy
- Cough

100
Q

What is the mechanism of action of, indications for and side effects of Guselkumab?

A

MoA:
- Anti-IL-23
- p19 alpha subunit

Indicators:
- Psoriasis
- Psoriatic arthritis

SEs:
- Injection site reactions
- Infection: TB
- Malignancy

101
Q

What is the mechanism of action of, indications for and side effects of Secukinumab?

A

MoA:
- Anti-IL-17A

Indicators:
- Psoriasis
- Psoriatic arthritis
- Ankylosing spondylitis

SEs:
- Infection: TB

102
Q

What is the mechanism of action of, indications for and side effects of Denosumab?

A

MoA:
- Anti-RANK ligand
- Inhibits RANK mediated osteoclast differentiation + function

Indicators:
- OSTEOPOROSIS
- Multiple myeloma
- Bone mets

SEs:
- Injection site reactions
- Infection
- Avascular necrosis of jaw

103
Q

What is the mechanism of action of, indications for and side effects of Tocilizumb + Sarilumab?

A

MoA:
- Anti-IL-6
- Reduce macrophage, T + B cell, + neutrophil activation

Indicators:
- RA
- Castleman’s disease

SEs:
- Infusion reactions
- Infection
- Hepatotoxicity
- Liid abnormalities
- Malignancy

104
Q

What is the mechanism of action of and indications for IL-1 blockade?

A

MoA:
- Anti-IL-1

Indicators:
- Familial Mediterranean Fever
- Gout
- Adult-onset Still’s disease

105
Q

What is the mechanism of action of and indications for IL-4/5/13 blockade?

A

MoA:
- IL-4R α subunit antibody
- Anti-IL13 Ab
- Anti-IL5 Ab

Indicators:
- Eczema
- Asthma
- Eosinophilic asthma

106
Q

What is an allergic disorder?

A

An immunological process resulting in immediate + reproducible symptoms after allergen exposure
- Usually IgE mediated Type 1
- Allergen normally an otherwise harmless substance

107
Q

What is allergen sensitisation?

A

Detection of specific IgE (skin prick/blood test) to allergen

108
Q

What is the process of allergen desensitisation?

A

Supervised administration of allergen
1. Start with tiny dose every week until maximal dose reached
2. Maintenance dose given monthly for 3-5yrs

109
Q

What are some features of allergen desensitisation?

A
  • Reduces clinical Sx of monoallergic disorders
  • Good for: bee/wasp venom, grass pollen, house dust mite
  • Not good for: food, latex
  • Costly, laborious + risk of severe adverse reaction
  • Only Tx that alters natural course of disease

Pathology (Guide) (84 decks)

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