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Immunology Flashcards

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1
Q

Graves disease:

a) What type of autoantibody is produced? (class of Ig)
b) What is the target?
c) What type of hypersensitivity is it?

A

a) IgG
b) TSH receptor
c) II

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2
Q

What antibodies are found in Hashimoto’s thyroiditis, and what class of hypersensitivity is it?

A

Anti-TPO and anti-thyroglobulin

Type II and IV

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3
Q

Which auto antigens are present in T1DM and what type of hypersensitivity is it?

A

Glutamid acid dehydrogenase (GAD), islet antigen 2

Type IV hypersensitivity

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4
Q

What is the consequence of vitamin B12 deficiency?

A

Subacute degeneration of the spinal cord (lateral and dorsal columns), peripheral neuropathy, optic neuropathy.

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5
Q

What are the antibodies found in pernicious anaemia, and what type of hypersensitivity reaction is it?

A

Anti-IF, anti-gastric parietal cell

Type II

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6
Q

What are the antibodies found in myasthenia gravis, and what type of hypersensitivity reaction is it?

A

Anti-acetylcholine receptor

Type II

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7
Q

What unique test is used to confirm myasthenia gravis?

A

tensilon test - inject edrophonium (anticholinesterase) to prolong Ach life to act on residual receptors

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8
Q

What is the antibody seen in goodpasture disease and what is its pattern of deposition?

A

Anti-GBM

Smooth linear deposition

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9
Q

What type of nephritis is seen in good pastures, and what type of hypersensitivity reaction is it?

A

Crescentic nephritis

Type II

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10
Q

Is ANCA positive or negative in Goodpastures disease?

A

Negative

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11
Q

Which HLA type is associated with rheumatoid arthritis?

A

HLA DR4 and DR1

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12
Q

What is the pathophysiology of RA?

A
  • peptidylarginine deiminases (PAD) type 2 and 4 convert arginine to citrulline
  • polymorphisms associated with increased citrullination
  • HLA DR4/DR1 present citrullinated peptides
  • Antibodies against citrullinated proteins (loss of tolerance)
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13
Q

Which antibodies are found in RA, and what type of hypersensitivity reaction does it involve?

A

Anti-CCP (cyclic citrullinated peptide)
Anti-RF
Type II, III and IV

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14
Q

What is Anti-RF?

A

IgM against IgG (RF)

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15
Q

Which conditions are associated with anti nuclear antibodies?

A

SLE, sjogren’s syndrome, systemic sclerosis, dermato/polymyositis

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16
Q

Which antibodies are found in SLE, and what type of hypersensitivity reaction does it involve?

A

Anti-dsDNA

Type III hypersensitivity

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17
Q

What are anti-ENA antibodies and give some examples

A

Anti-extractable nuclear antigens:

  • Ribonucleoproteins (Ro, La, Sm, RNP)
  • Enzymes (RNA polymerase, topoisomerase)
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18
Q

Which complement components are affected during active and severe SLE?

A

Active: reduced C4

Severe active: reduced C4 and C3

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19
Q

Which antibodies are present in sjogren’s syndrome?

A

Anti-Ro, anti-La

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20
Q

Which antibodies to test for in antiphopholipid syndrome?

A

Anticardiolipid

Lupus anticoagulant

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21
Q

What is the difference between limited cutaneous systemic sclerosis and diffuse?

A

Limited: anticentromere antibodies, skin involvement not past forearms (but can involve personal)
Diffuse: antitopoisomerase (Scl70) antibodies, more extensive GI disease, interstitial pulmonary disease, scleroderma kidney

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22
Q

What type of hypersensitivity reactions are dermatomyositis and polymyositis?

A

Dermato: III
Poly: IV

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23
Q

Which antibody is associated with idiopathic inflammatory myopathy?

A

Anti-Jo1

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24
Q

What size vessels are affected in ANCA-associated vasculitis?

A

Small vessels

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25
Name the 3 ANCA-associated vasculitides
Microscopic polyangiitis Granulomatosis with polyangiitis (Wegener's) Eosinophilic granulomatosis with polyangiitis (Churg strauss)
26
Name 2 large-vessel systemic vasculitides.
Takayasu's arteritis | Giant cell arteritis/polymalgia rheumatica
27
Name 2 medium vessel systemic vasculitides
Polyarteritis nodosa | Kawasaki disease
28
Name 3 immune-complex associated small vessel systemic vasculitides
Anti-GBM disease (Goodpasture's) IgA disease Cryoglobulinaemia
29
What is the target of c-ANCA?
Proteinase 3
30
What is the target of p-ANCA?
Myeloperoxidase
31
Which of the 3 small-vessel ANCA is associated vasculitis is associated with c-ANCA (as opposed to p-ANCA)?
Granulomatosis with polyangiitis
32
Which antibody and other condition is associated with UC?
p-ANCA | PSC
33
Which HLA allele is most closely associated to coeliac disease?
HLA DQ2/8
34
Which is the 1 first-line immunological test for coeliac disease?
Anti-TTG
35
What type of antibodies are anti-TTG and anti-endomysial?
IgA
36
What are the histopathological features of coeliac disease?
Reduced/reversed villous:crypt ratio Villous atrophy Crypt hyperplasia >20 intraepithelial lymphocytes per 100 epithelial cells
37
What malignancy is coeliac associated with?
T cell lymphoma
38
Describe the pathway by which gluten causes epithelial damage.
- Gliadin deaminated by TTG and presented to APCs - CD4 T cells activated and produce IFNy - Leads to IL15 production - Activates intraepithelial lymphocytes which kill epithelial cells
39
What are the immune modulatory effects of corticosteroids?
- Inhibit phospholipase A2 (thus prostaglandin formation) - Reduce macrophage function - Reduce lymphocyte function and promote their apoptosis
40
Why do corticosteroids cause a transient increase in neutrophil counts?
* Decrease expression of adhesion molecules on endothelium | * Block signals involved in moving immune cells from blood to tissue
41
What is the relative proportions of white cells seen in someone soon after taking corticosteroids?
High neutrophils, low lymphocytes
42
What are some side effects of cyclophosphamide?
o Toxic to proliferating cells – BM depression, hair loss, sterility (M>F) o Haemorrhagic cystitis – toxic metabolic acrolein excreted via urine o Malignancy – bladder cancer, haematological malignancies, non-melanoma skin cancer o Infection – pneumocystis jiroveci
43
What to check before starting someone on azathioprine?
TPMT polymorphism
44
Which immunosuppressant is commonly used for systemic autoimmune conditions and vasculitis?
Cyclophosphamide
45
Which immunosuppressant increases the risk of infection with JC virus (multifocal leukoencephalopathy) and herpes virus reactivation?
Mycophenolate mofetil
46
What is the main limitation of plasmapheresis and how can this be overcome?
• Rebound antibody production | Give an anti proliferative agent.
47
Give examples of calcineurin inhibitors, their mechanism of action, and indications of use.
Ciclosporin, tacrolimus Block calcineurin, so less expression of IL2 in T cells, thus less T cell activation/differentiation Immunosuppresion
48
What are some cell signalling targets of immunosuppressants?
Calcineurin JAK PDE4
49
``` What are the cell surface targets of these immunosuppressants, and the resultant consequence/effect? • Basiliximab • Abatacept • Rituximab • Natalizumab • Tocilizumab ```
* Basiliximab – anti-CD25 (IL-2 receptor alpha chain). Prevent T cell activation. * Abatacept – CTLA4-Ig (binds to CD80 and 86 on APCs). Prevent T cell activation. * Rituximab – anti-CD20. Deplete mature B cells. * Natalizumab – anti-a4 integrin. Prevent T cell migration. * Tocilizumab – anti-IL-6 receptor. Reduce macrophage, T/B cell and neutrophil activation.
50
What is CD20 a marker of?
Mature B cells
51
Which biological agent targets CD20?
Rituximab
52
What is the function of IL-2?
Activates T cells
53
What is the mechanism of action of natalizumab?
Antibody against a2 integrin | Prevents leukocyte migration
54
What class of drugs are infliximab, adalimumab, certolizumab, golimumab?
Anti TNFa antibodies
55
``` What is: Etanercept? Ustekinumab? Secukinumab? Denosumab? ```
- TNFa antagonist, made of TNF receptor p65-Ig fusion protein - Antibody against p40 subunit of IL12 and IL23 - Antibody against IL17 - Antibody against RANK-Ligand
56
Which cells express RANK?
Osteoclasts
57
What is the risk of denosumab?
Avascular necrosis (of the jaw)
58
What cell type does JC virus infect, and what does infection put a patient at risk of?
Oligodendrocytes | Progressive multifocal leukoencephalopathy
59
What is the pathophysiology of anaphylaxis?
Cross-linking of IgE on surface of mast cells --> degranulation --> histamine, leukotrienes • Increase vascular permeability, smooth muscle contraction, inflammation, mucus production
60
What is the immediate management of anaphylaxis?
• Respiratory support may be required – intubation, tracheostomy • Oxygen by mask • Adrenaline IM 0.5mg, maybe repeat o Increase BP, limit vascular leakage, bronchodilate • Chlorpheniramine (antihistamine) IV 10mg • Nebulized bronchodilators • Hydrocortisone 200mg IV o Systemic anti-inflammatory agent o ~30 mins to take effect and doesn’t peak for several hours o Important in preventing rebound anaphylaxis • IV fluids
61
When is desensitisation (aka immunotherapy) useful?
insect venom and some aero-allergens (e.g. grass pollen)
62
What does complement deficiency put one at risk of?
Infection by encapsulated organisms: pneumococcus, meningococcus, gonococcus, haemophilus influenza B
63
What does antibody deficiency put one at risk of?
recurrent bacterial infections, esp upper and lower respiratory tract
64
Which immunological investigation to assess complement function?
C3 and C4, CH50, AP50
65
What does the CH50 test?
All components of the classical pathway of complement activation. C1,4,2 C3 C5-9
66
What does the AP50 test?
All components of the alternative pathway of complement activation. properdin, factor B/H/I C3 C5-9
67
How would you manage someone with a complement deficiency?
* Meningovax, pneumovax, HIB vaccines | * Daily prophylactic penicillin
68
Which serological markers reflect disease activity in SLE?
dsDNA antibody titre ESR Low levels of C4 and C3 (suggests active SLE)
69
Why is C4 and C3 low in active SLE?
* Immune complexes bind to C1q and activate classical pathway of complement activation * Complement is consumed
70
What pattern of nephritis is seen in SLE?
Diffuse proliferative nephritis
71
What does a low C3 and C4 generally indicate?
Activation of the classical complement pathway
72
How do lymphoproliferative disorders cause anaemia?
* Space limitation: expansion of malignant clone crowds out normal red and white cell precursors * Inhibitors: tumoru may produce local cytokines to inhibit normal bone marrow function
73
Which genetic factors predispose to RA?
``` HLA DR4 and HLA DR1 PADI (peptidylarginine deiminase) type 2 and type 4 PTPN 22 (Protein tyrosine phosphatase non-receptor 22) ```
74
What is the 1st line treatment for RA?
Methotrexate

Pathology (5 decks)

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