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HAEM/IMMUNOLOGY > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the acute phase response following recognition of pathogens?

A
  1. Innate immunity sense non self
  2. Cytokines produced
  3. Acute phase reactants produced
  4. Measures to localise the spread of infection and enhance systemic resistance
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2
Q

What do PRPs recognise in infections and tissue damage?

A

Infections: pathogens associated molecular patterns (PAMPS)

Tissue damage: danger/damage associated molecular patterns

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3
Q

Where are TLR-like and NOD-like receptors located?

A

TLR - on cell surface

NOD - cytosolic

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4
Q

What are pro-inflammatory cytokines?

A

IL-1B, IL-18, IL-6, TNF-alpha - all induced by TLR activation

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5
Q

What do pro-inflammatory cytokines lead to? 4

A

1/ activation of complement opsonisation
2/ phagocytosis
3/ decreased viral/bacterial activation
4/ initiate adaptive immune response

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6
Q

How do steroids suppress pro-inflammatory genes?

A

In nucleus - steroids induce expression of anti-inflammatory genes and suppress pro-inflammatory genes

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7
Q

Why is C reactive protein the best marker for an acute phase response?

A
  • it is pro-inflammatory

- important opsonin

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8
Q

What are the 3 pathways in complement system?

A
  1. alternative - activated by microbe
  2. Classical - activated by Ab-Ag immune complexes
  3. Lectin - activated by MBL
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9
Q

What are the physiologic activities of complement once it recognises pathogens?

A
  1. host defence: opsonisation for phagocytosis, chemotaxis and lysis of bacteria and cells (MAC)
    2 interface between innate and adaptive immune systems
  2. Disposal of waste
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10
Q

How can abnormalities in complement be detected?

A

Assessmemt of C3 and C4 serum levels

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11
Q

What is classical complement deficiency associated with?

A

Pyogenic infection and SLE

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12
Q

What are the 3 major classes of innate phagocytes?

A
  • Granuloctyes
  • Macrophages
  • immature D.C’s
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13
Q

What cells are involved in cell-mediated immunity and what do they do?

A

Intracellular organisms
T helper cells (CD4+) - activate macrophages to kill phagocytksed microbes

Cytotoxic T cells (CD8+) - bind infected cells and kill them directly

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14
Q

What is central and peripheral tolerance?

A

Central - Self antigens are presented to T cells in the thymus before they are released into periphery

Peripheral - T cells with self recognition are killed in the periphery

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15
Q

What cells are involved in humoral mediated immunity?

A

B cells - recognise extracellular

Follicular b cells: T cell dependent and produce a/b
Marginal zone B cells and B1 B-cells: T independent (IgM and short lived plasma cells) and they are important in polysaccharide and lipid responses

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16
Q

What are the 2 types of immunodeficiency?

A

Primary: inherent defect
Secondary: acquired problems as a result of another disorder (infection, drugs, haematological)

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17
Q

When should a Primary immunodeficiency disorder be suspected?

A
  1. Patients with infections - recurrent, opportunistic
  2. Family history of PID
  3. Other complications associated with immune deficiency - failure to thrive, facial features, cardiac abnormalities
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18
Q

How can PID’s be categorised?

A

B cell defects:

  1. XLA
  2. CVID

Combined immunodeficiencies
1. SCID

Phagocyte defects
1. CGD

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19
Q

What is X-linked agammaglobulinaemia?

A

Disorder of defective B cell development

  • No B cells due to mutation in BTK
  • usually present at 6months when maternal IgG disappears
  • commonly get pneumonia and otitis media
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20
Q

What is common variable immunodeficiency?

A

Defective B cell differentiation
- sinopulmonary and GI infections
Diagnosis: low Ig’s of at least 2 isotopes
Treatment: Ig replacement therapy/prophylactic antibiotics

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21
Q

What is severe combined immunodeficiency?

A

Defect of T and B cells characterised by absence of T cells.

- proofed susceptibility to infection

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22
Q

What are the groups of genetic defects that can cause SCID?

A
  1. cytokines not signalling properly
  2. recombination of antigen receptors
  3. premature lymphocytic death
  4. defects in TCR
  5. defects affecting thymus development
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23
Q

What is chronic granulomatous disease?

A

Disordered phagocyte killing

  • defective killing mechanism allows the microbe to survive causing granuloma formation and ongoing sterile inflammation
  • skin, bone, liver, GI tract most susceptible
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24
Q

What are 4 unwanted immune responses and examples?

A
  1. Autoimmune - SLE, RA
  2. Alloimmune - rejection of transplants
  3. Immune-mediated inflammatory disorders - sarcoidosis
  4. Allergic - asthma, atopic excema
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25
Q

What do these drugs have in common: cyclosporine, tacrolimus, sirolimus, everolimus

A

Inhibit lymphocyte signalling

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26
Q

What are some cytotoxic agents?

A

Anti-metabolite: MTX, AZA, mycophenolate

Alkylating: cyclophosphamide

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27
Q

What are patient considerations when choosing an immunosuppressant?

A

Age, gender, comorbidities, fertility status, genetics, medications

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28
Q

How do steroids act as immunosuppressants?

A

Bind to cystolic receptors, enter nucleus, alter gene expression of lymphocytes (inhibit NFkB)

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29
Q

Why is stopping steroids a slow process?

A

Steroids are adrenal suppressors so the body may take time to produce its own again

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30
Q

How does azathioprine act?and what are the side effects?

A

Inhibits DNA production and lymphocyte proliferation

Side effects: hypersensitivity, GI upset, hepatotoxicity, BM toxicity and infection

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31
Q

How does methotrexate act as an immunosuppressant? side effects

A

MTX inhibits folic acid metabolism, which is needed for DNA replication
Side effects: teratogen, BM suppression and infection, nausea, mouth ulcers, hepatotoxicity

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32
Q

How does mycophenolate act? and side effects

A

Inhibits the enzyme needed for production guanosine in lymphocytes
side effects - GIT upset, BM suppression, infection, teratogenic

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33
Q

How does cyclophosphamide act?

A

Potent alkylating agent - cross links DNA helix preventing division and replication= SEVERE drug

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34
Q

What is an example of a mono-clonal antibody and how does this class act?

A

Rituximab - antiCD20 antibody causes B cell depletion as it is a marker on B cells
May also stop T reactive responses as CD20 is on APCs that present to T cells

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35
Q

What are some TNF-alpha inhibitors? and their side effects?

A

Infliximab, etanercept, adalimumab

Side effects - infection, HF, Demyelinating disorders, infection, cytopenias

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36
Q

What are some hallmarks of endocrine autoimmunity?

A
  • auto reactive T cells

- chronic inflammatory infiltrate (lymphocytes, plasma cells, macrophages, germinal centres)

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37
Q

What are autoimmune diseases of the thyroid?

A

Hyperthyroidism - thyrotoxicosis

  1. Grave’s disease
  2. Toxic multi nodular goitre
  3. Toxic adenoma

Hypothyroidism - thyroiditis

  1. Hashimoto’s thyroiditis
  2. Atrophic thyroiditis
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38
Q

What is the disease process in Grave’s disease?

A
  • Autoantibodies to TSH receptor
  • stimulate hypertrophy and hyperplasia
  • auto-antibody binds TSH receptor and mimics TSH
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39
Q

What are signs of Grave’s disease?

A
  • weight loss
  • nervous
  • weakness
  • sweating
  • heat intolerance
  • enlarged thyroid
  • fast pulse
  • tremor
  • exophthalmos and periorbital myxoedema
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40
Q

What are the eye signs of Grave’s?

A

Stare and lid-lag

Exophthalmous - swelling of eye tissue = bulge

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41
Q

What is the laboratory diagnosis of Grave’s?

A

High T4
Low TSH
Diffuse increase in radio iodine uptake
- anti-thyroid peroxidase TPO and anti-thyroglobulin TG confirms autoimmunity and predicts eventual thyroid failure
- anti-TSH receptor antibodies confirm Grave’s

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42
Q

What is the treatment for Grave’s?

A

If it does not resolve - Ablative = surgery or large dose of radio iodine

Anti-thryoid drugs - most cases remit in 1-2yrs so these drugs can help in the meantime (neomercazole, propylthiouracil)

43
Q

What is hashimoto’s thyroiditis?

A
  • antibodies may stimulate TSH receptor but don’t cause increase in TH production
  • enlarged thyroid with inflammatory infiltrate + high levels of autoantibodies TG and TPO
  • Inevitably progress to thyroid failure = require TH replacement
44
Q

What is atrophic thyroiditis?

A
  • autoimmune disease that may result in thyroid failure

- antibodies to TPO and TG

45
Q

How is thyroid autoimmunity detected?

A

Presence of thyroid peroxidase antibodies = anti-TPO via:

  1. immunofluorescence on human thyroid tissue
  2. haemagglutination
    - proportion of ‘healthy people’ with these a/b progress to thyroid failure
46
Q

What is predictive of IDDM?

A

Autoantibodies to pancreatic islet cells:

  • islet cell antibodies
  • anti-glutamic acid decarboxylase
  • anti-tyrosine phosphatase
47
Q

What is addisonian pernicious anaemia?

A

Autoimmune disease - malabsorption of B12 due to autoimmunity to parietal cells = gastric atrophy = lack of intrinsic factor

48
Q

How is addisonian pernicious anaemia diagnosed and treated?

A

Diagnosis:

  • malabsorption of B12
  • Anti-parietal cell a/b
  • intrinsic factor antibody

Treatment - B12 injections

49
Q

What is coeliac disease?

A

Hypersensitivity to food protein (gluten) and autoimmunity to enzyme (trans glutamase) in the gut
Ingestion of gluten = atrophy of small bowel = malabsorption

50
Q

What is the mechanism of hypersensitivity in coeliac disease?

A
  1. Gliadin is rich in glutamine and proline and resists digestion
  2. tissue transglutaminase tTg removes amine from glutamine in the peptide
  3. peptide can now bind groove of HLA-DQ2 or 8
  4. this antigen is presented to a non-tolerant immune system, eliciting strong T cell and antibody response
  5. vigorous T cell response damages mucosa
51
Q

What is the revised ARA criteria for classification of SLE?

A

Skin and mouth: malar rash, discoid rash, photosensitivity, oral ulcers
Joints: arthritis
Lungs and heart: pleuritis or pericarditis
Kidney: proteinuria or casts
Nervous system: seizures or psychosis
Blood: low WBC/platelets/lymphocytes or haemolytic anaemia
Immune system: anti ds DNA/Sm/cardiolipin/anticoagulant and antinuclear antibody

52
Q

How does SLE affect the skin and joints?

A

Skin - malar/butterfly rash (photosensitivity), discoid rash and lesions
Joints - arthritis and tenosynovitis

53
Q

How does SLE affect the lungs and heart?

A

Lungs - fibrinoid effusions and adhesions, infections, interstitial pneumonitis, embolism/infarction
Heart - pericarditis, myocarditis

54
Q

How does SLE affect the kidneys, blood vessels and CNS?

A

Kidneys - immune complexes trapped in capillary walls, glomerulonephritis, renal failure (blood/protein in urine)
BV - micro thrombi and thromboembolism
CNS - micro infarcts, immune complexes deposited in choroid plexus

55
Q

What is Sjrogen’s and Sicca syndrome?

A

Sicca - dry eyes and mouth

Sjrogen - SICCA + connective tissue disease (arthritis and photosensitive rashes, lymphadenopathy, lymphoma, vasculitis)

56
Q

What is scleroderma (systemic sclerosis) characterised by?

A
  1. chronic inflammation thought to be result of autoimmunity
  2. widespread damage to small blood vessels
  3. progressive interstitial and perivascular fibrosis in the skin and multiple organs
57
Q

What is diffuse and limited scleroderma?

A

Diffuse - widespread skin involvement, rapid progression and early visceral involvement, presence of Raynaud’s, renal failure, GI and myocardial involvement (autoantibodies target nucleolus and RNA polymerase)
Limited - skin involved is on hands fingers, arm and face, visceral involved late and sometimes CREST syndrome (calcinosis, raynauds, esophageal dysmotility, sclerodactylyl, telangietasia) and antibody against centromere

58
Q

What is Raynaud’s phenomenon?

A

Thickening of walls of small blood vessels supplying hands

  1. white = sharp demarcation, artery spasm or narrowing
  2. Blue = slow flow in dilated venues
  3. Red = capillary dilation in anoxic tissue
59
Q

What are 5 features of polymyositis/dermatomyositis?

A

Idiopathic inflammatory myopathy:

  1. symmetrical weakness of limb girdle muscles
  2. muscle fibre necrosis, phagocytosis, regeneration
  3. muscle enzymes in serum
  4. EMG changes
  5. DM rash = Gottron’s papules
60
Q

What is vasculitis and what are the typical features?

A

Vasculitis - vessel wall inflammation causing narrowing, thrombosis, rupture and multi system involvement
Features - constitutional signs and fever, myalgia, arthralgia and malaise

61
Q

What is mixed cryoglobulinaemia?

A

Small vessel vasculitis affecting the skin, peripheral nerves and kidneys (Associated with HepC)
Serum proteins precipitate in the cold and solubilise when re-warmed
Diagnosis - cryoglobulins in serum and complement is low
Treat - underlying HCV infection and immunosuppressants

62
Q

What are immune complexes?

A

Small vessel vasculitis

  • antigen bound to a/b
  • form in slight antigen XS
  • deposit in sub endothelium in high concentrations
  • fix and activate complement
  • recruit, activate and degranulate neutrophils
63
Q

What do anti-neutrophil cytoplasmic antibodies (ANCA) do?

A

Small vessel vasculitis
- directed against enzymes in primary granules of neutrophils
- results from dysregulated T and B autoimmunity to these enzymes
- ANCA activate neutrophils causing degranulation, sequestering acute inflammatory cells and causing inflammation
Treatment: prednisolone, rituximab, cyclophosphamide

64
Q

What is a type of medium vessel vasculitis? what are the clinical features and investigations?

A

Polyarteritis nodosa - systemic disorder affecting all parts of the body
Investigations -
Biopsy: necrotising vasculitis
Angiography: stenoses and aneurysms of medium sized arterioles

65
Q

What is large vessel primary vasculitis?

A

Chronically persistent inflammatory infiltrates within arteries in the 3 layers of the walls
Results from dysregulated innate and adaptive
Results in occlusion or aneurysm

66
Q

What is giant cell arteritis?

A

Large vessel vasculitis

  • driving factor - IL6
  • Panarteritis with transmural T cell and macrophage infiltrates
  • macrophages in different layers produce pro-inflammatory cytokines, reactive oxygen intermediates or growth factors
  • multinucleate giant cells - provide growth and angiogenic factors that promote intimal hyperplasia and luminal occlusion
67
Q

What are clinical features of giant cell arteritis, investigations and treatment?

A

Clinical features - headache, jaw claudication, scalp tenderness, malaise, weight loss, ocular symptoms
Investigations:
- blood - acute phase response
- imaging - stenosis or aneurysm
- biopsy - diagnostic for GCA
Treatment: high dose corticosteroids over 18-24 months with low dose aspirin

68
Q

What are causes of secondary cellular immunodeficiencies?

A
  1. Diseases affecting T cells/cytokines
  2. Medications/procedures
  3. Organ transplantation
  4. Progressive multifocal leukoencephalopathy (PML)
    rare
  5. Idiopathic CD4 lymphopenia
  6. Autoantibodies to interferon gamma
69
Q

What is progressive multifocal leukoencephalopathy?

A
  • results from reactivation of JC virus during immunosuppression
  • gradually demyelinates nerves = loss of coordination and weakness
  • JC virus infection/previous immunosuppressant therapy = risk factors
70
Q

What are common causes of secondary antibody immunodeficiency?

A
  1. disease affecting b cells/plasma cells - lymphoproliferative, myeloma, thymoma associated immune defects
  2. medications/medical procedure - immunosuppressant/rituximab, HSC transplant
71
Q

What is secondary hypogammaglobulinaemia? and when is Ig therapy recommended?

A

After solid organ transplant, some patients have IgG serum of <4g/L = 4x risk of infection
Therapy - if patient has recurrent or persistent infections with bacteria/enteroviruses

72
Q

What is asplenia-associated immunodeficiency?

A

Asplenic patients are predisposed to acute overwhelming post splenectomy infection (OPSI) - with encapsulated bacteria and blood borne parasites like malaria
- functional spleen required for maturation and differentiation of B cells (marginal zone)

73
Q

What is thymoma associated immune dysfunction?

A

Thymomas are associated with production of cytokine auto-antibodies, can cause:

  1. b cell deficiency
  2. cellular immunodeficiency
  3. autoimmune disease - myasthenia gravis, SLE
  4. lichen planus
74
Q

`What is an allergy?

A

Harmful, misguided and excessive immune response to antigens that causes tissue damage and disease

75
Q

What are the 4 types of hypersensitivity reactions?

A

Type I - immediate - IgE - mast cells - anaphylaxis
Type II - Cytotoxic - IgG - complement/phagocytes - AIHA
Type III - immune complex disease - IgG - immune complexes - SLE
Type IV - delayed - T cells (4 different types)

76
Q

What type of hypersensitivity is allergic rhinitis? and what is it mediated by?

A

Immediate hypersensitivity (type 1)

  • mediated by degranulation of mast cells and eosinophils
  • degranulation triggered by cross linking for IgE antibodies bound to mast cell by divalent hapten AND cross linking of IgE by anti-IgE
77
Q

What substances are released on degranulation of mast cells and eosinophils?

A

Preformed mediators - histamine, heparin, PAF, eosinophil and neutrophil chemotactic factors
Newly synthesised mediators - leukotrienes, PGD2, thromboxanes
TH2 cytokines - IL3, 4, 5, 6, GM-CSF

78
Q

What hypotheses explain the recent rise in allergy?

A
  1. Hygeine hypothesis
  2. Microbiota hypothesis
  3. Biodiversity hypothesis
79
Q

What type of hypersensitivity reaction is asthma?

A

Type 4b - TH2

80
Q

What are the 3 components of airway inflammation in asthma?

A
  1. cellular infiltration - eosinophils, TH2, IgE
  2. changes in resident cells
  3. changes in non-cellular components of airway wall
81
Q

What is the airflow limitation in asthma caused by?

A
  1. chronic mucous plug formation

2. airway remodelling - irreversible due to structural airway matrix changes

82
Q

What are the two phases of the allergic response in asthma?

A
  1. ACUTE: <1hour
    - binding of allergen to IgE pre bound to FcER1 on surface mast cells leads to degranulation and release of mediators such as histamine –> inflammation, redness, swelling
  2. CHRONIC
    - 6-12 hours after allergen exposure
    - recruitment of T cells, eosinophils and more mast cells to exposure site
    - recruited cells release enzymes, toxic proteins and more cytokines leading to increase inflammation
83
Q

How is the TH2 pathway involved in the allergic inflammatory response?

A

In allergy, a persons response is shifted towards the TH2 pathway (instead of TH1), which favours the development of IgE from B cells (class switching from IgM)

84
Q

What are regulatory T cells?

A
  • either thymic or induced in periphery
  • express FoxP3 transcription factor
  • control/inhibit proliferation of CD4/8 cells once they’ve done their job
  • maintain balance between immunity and tolerance
85
Q

What cells are involved in late allergic inflammation at:
6 hours
24 hours
>24 hours

A

6 hours - neutrophils
24 hours - eosinophils
>24 hours - lymphocytes, monocytes, DC, basophils, mast cells (result in altered epithelial and smooth muscle cells)

  • chemokine induce migrations of eosinophils which release granules that cause direct damage to bronchial tissue
86
Q

What happens in early inflammation in the allergic response (asthma)?

A
  • TH2 cells cause favouring of IgE to develop from B cells (class switching from IgM)
  • this is controlled by the cytokines they’re exposed to
87
Q

What is urticaria?

A

Red, raised, itchy rash from vasodilation, increased blood flow and vascular permeability

  • affects the superficial skin layers
  • wheals/hives can vary in size
  • usually spontaneous and resolve within 24hours
88
Q

What is angioedema?

A
  • involves submucosa, deeper reticular dermis and subcutaneous tissue
  • can persist for days
89
Q

What is the mechanism of urticaria and angioedema?

A
  • mast cells degranulate, releasing vasoactive mediators like histamine
  • leukotrienes and prostaglandins then released
  • extravasation of fluid into the superficial tissues
90
Q

What is the management of chronic and acute intermittent urticaria?

A

non sedating antihistamines leads to significant relief in about 45% of patients

91
Q

What is the aim of immunotherapy? and which form is recommended for asthma and allergic rhinitis?

A

Aim - shift from a TH2 response (IgE) to TH1 response (IgG4)
Asthma - Subcutaneous
Allergic rhinitis - sub lingual

92
Q

What are the pro’s and con’s of sublingual and subcutaneous immunotherapy?

A

Sublingual
Good - safe
? - long term benefits?, daily admin, more expensive, more difficult to treat multiple

Subcutaneous
Good - evidence, suited to multiple sensitisations, better compliance and cheap
? - systemic adverse reactions 2%, contraindicated in severe asthma

93
Q

What is the most common cause of contact dermatitis?

A

Nickel metal

94
Q

What is contact dermatitis?

A

Allergic contact dermatitis - allergen induces hypersensitivity immune reaction
Irritant contact dermatitis - substance directly damages skin

95
Q

What is the pathogenesis of type IV allergy? - dermatitis

A
  1. antigen engulfed by APC and presented to naive T cells in lymph node
  2. sensitised CD4/8 cells are produced and released
    (sensitisation process takes 10-14 days)
  3. re-exposure - antigen presented to sensitised lymphocytes which release cytokines and cause inflammation
  4. dermatitis in sensitised individual occurs within 12-48 hours after exposure
96
Q

What is the clinical presentation of contact dermatitis?

A

Typically a very itchy rash up to 2 weeks after exposure, papillary, erythematous, with indistinct margins

97
Q

What is the management of dermatitis?

A
  • avoid allergen/identify
  • alternative product
  • treat skin inflammation with topical steroids
  • restoration of skin barrier - emolient/moisturiser
  • skin protection
98
Q

How can drug hypersensitivities be classified?

A

type 1 drug reactions - IgE mediated
Immediate <1 hour
- anaphylaxis, hypotension, laryngeal edema, wheezing
Accelerated 1-72 hours
- urticaria, angioedema, laryngeal edema
Non-IgE mediated - late >72 hours,
- rash, fever, haemolytic anaemia, commonly T cell mediated

99
Q

What is a penicillin allergy? How is it tested for?

A
  • IgE molecules against the beta-lactam core or against R groups
    Testing - penicillin skin testing is gold standard for IgE mediated penicillin allergy but gives no info on non-IgE mediated allergy
100
Q

What are type IV drug reactions?

A

Delayed hypersensitivity - occurs days to 6/8 weeks after drug initiation
- often due to viral infections
Severe cutaneous drug reactions (SCAR)
- DRESS - drug reaction with eosinophilia and systemic symptoms
- DIHS - drug induced hypersensitivity - fever, rash, internal organ involvement
- Steven’s-johnson syndrome - <10% skin detachment
- toxic epidermal necrolysis - >30% skin detachment
- SJS-TEN together
- acute generalised exanthematous pustulosis

101
Q

How should Steven’s johnson syndrome and toxic epidermal necrolysis be identified and managed?

A

Identify - prick/intradermal WONT pick up, must use patch testing
MGMT - desensitisation is contraindicated, permanent drug discontinuation

102
Q 
What syndrome is associated with 
Abacivir
Flucloxacillin 
Carbamazepine
Allopurinol
A 
Abacivir - hypersensitivity syndrome - HLA-B-5701
Flucloxacillin - Hepatitis - HLA-B-5701
Carbamazepine
- SJS/TEN : through HLA-B-1502
-HLA-A-3101
Allopurinol - SJS, TEN, DRESS, DIHS
103
Q

What investigations would you do for SLE

A
  • C3 low
  • C4 low
  • +ve ANA
  • +ve Anti-dsDNA

HAEM/IMMUNOLOGY (5 decks)

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