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Immunology Flashcards

1
Q

What drug may be given along side corticosteroids to decrease the need for large doses of steroid

A

Azathioprine

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2
Q

Action of azathioprine

A

Inhibits DNA synthesis, inhibits T and natural killer cel functions and is anti-inflammatory

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3
Q

Action of cyclophosphamides

A

Interferes with DNA synthesis but has little anti-inflammatory activity and is therefore generally given in combination with steroid.

Useful in supressing B cell activity and antibody production (autoantibody in particular)

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4
Q

Actions of tacrolimus and cyclosporin

A

Involved in modulation and down-regulation of various genes, particularly transcription of interleukin 2; as a result major immune suppressive effects are on T cells and natural killer cells

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5
Q

Principal role of mycophenolic acid

A

Transplant rejection, crohn’s, and some systemic autoimmune diseases such as SLA, ITP, wegener’s

Prevents T cell proliferation, antibody production and leucocyte migration

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6
Q

What is cytokine receptor therapy designed to do

A

Inhibit the activity of harmful cytokines or enhance the activity of beneficial cytokines

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7
Q

How does plasma exchange work

A

Patient’s plasma is filtered off ex-vivo in a special cenrifycge apparatus; at the same time normal donor plasma is given back to the patient to replace what has been taken off.

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8
Q

When is immunoglobulin therapy appropriate

A

As replacement therapy in patients with primary or secondary antibody deficiency

As immune modulating therapy in certain inflammatory or autoimmune disorders e.g. Kawasaki’s, allergic disorders, vasculitis, myaesthenia, SLE, ITP, neuropathies

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9
Q

What are the adverse reactions associated with immunoglobulin therapy

A

Adverse reactions during infusions

Transmission of infection - particularly hep C

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10
Q

What kinds of transplant are available

A

Autograft - from same organism
Isograft - transfer from genetically identical members
Allograft - genetically non-identical members of the same species
Xenograft - transfer between species

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11
Q

What must donor and recipient share in order for a graft to survive

A

ABO blood group antigen and major histocompatability antigens (differing organs need different closeness)

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12
Q

Give an example of a priveledged site

A

Cornea

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13
Q

Why are grafts rejected

A

Histocompatability differences between donor and recipient

ABO mismatches are rare and usually due to human error; most are due to incomplete HLA matching

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14
Q

Which cells are part of the innate immunity

A

Phagocytes, eosinophils, basophils, mast cells, natural killer cells, actions of complement system

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15
Q

What are the markers of tissue inflammation

A

Red
Swollen
Heat
Pain

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16
Q

Cell mediated immunity

A

T cells are responsible

T helper cells and cytotoxic T cells

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17
Q

Which cells are responsible for humoral immunity

A

Antibodies/immunoglobulins secreted by plasma cells (formed from B cells)

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18
Q

What are the primary lymphoid tissues

A

Thymus

Bone marrow

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19
Q

What are the secondary lymphoid tissues

A

Lymph nodes, spleen, tonsils, adenoids, intestines/peyer’s patches, bone marrow

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20
Q

Which cells present class 1 HLA molecules

A

All nucleated cells - all except RBC

They present to cytotoxic t cells

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21
Q

Which cells present class 2 HLA molecules

A

Macrophages, b cells and macrophage like cells

They present to t helper cells

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22
Q

What makes CRP levels increase

A

Plasma concentrations are markedly increased during inflammation

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23
Q

What are interferons

A

A family of cytokines that non-specifically inhibit viral replication in host cells. In response to viral infection most cells secrete interferon

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24
Q

What is tolerance

A

The process whereby the immune system avoids producing damaging reactions against self antigens. It arises through deletion of autoreactive T and B cells during cell maturation (central tolerance) or by inhibiting the action which escape the central tolerance process

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25
Q

Which immunoglobulins do babies gain from mothers

A

IgG from placenta

IgA from milk

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26
Q

Aetiology of autoimmunity

A

Interaction of aetiological factors (genetic predisposition, immune regulatory factors, hormonal factors, environmental factors, aging, malignant disease, trauma…) in association with disordered and dysregulated immune effector mechanisms

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27
Q

Aetiology of autoimmunity

A

Genetic factors - inheritence of HLA types, familial predisposition
Immune regulatory factors - defective tolerance induction, defective T cells, b cells
Hormonal factors - female, high incidence onset during pregnancy, puberty, after starting OCP
Environmental factors - infectious agents, solar radiation, drugs/chemicals, high fat diet,
Other - malignant disease, ageing, trauma

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28
Q

Where are IgA immunoglobulins secreted

A

Plasma cells lining the respiratory, genito-urinary and gastro-intestinal tract

And mammary glands

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29
Q

What are IgE antibodies mediated against

A

Allergy or multi-cellular parasites

30
Q

Effector mechanisms involved in autoimmunity

A

Antibody (B cell) or cellular (T cell) activity
Antibody and complement
Immune complex formation
Recruitment of innate components

31
Q

Therapeutic options for autoimmunity

A 
Immunosuppressive therapy
Anti-inflammatory therapy 
Plasmapheresis 
(Bone marrow transplant) 
Replacement of lost physiological factor 
Organ/tissue/mechanical graft
32
Q

What kind of hypersensitivity reaction is allergy

A

Type 1 - mediated by IgE

33
Q

What is atopy

A

A genetic tendency to produce IgE to normally innocuous environmental allergens

34
Q

What are the mast cell mediators

A

Preformed - histamine, heparin, tryptase…
–> early phase response

Newly synthesised - prostaglandins, leukotrienes
–> late phase response

35
Q

What is the effect of mast cells mediators

A 
Mucosal oedema
Capillary leakage 
Secretions 
Smooth muscle contraction 
Vasodilatation
36
Q

Diagnosis of allergy

A

History!!
Skin prick test
Laboratory investigations - IgE levels = RAST test; can also test histamine, leukotriene, and tryptase

37
Q

Treatment of allergy

A

Patient education and allergen avoidance
Antihistamines - local or systemic
Sodium cromoglycate - local (eye drops) or systemic
Steroids - local/systemic
Leukotriene antagonists
Adrenaline epipen for anaphylaxis

38
Q

Which immunoglobulins are implicated in type 2 hypersensitivity

A

IgG or IgM against self or exogenous

39
Q

Haemolytic reaction following blood transfusion is a type __ hypersensitivity reaction

A

2 - mediated by IgM and IgG

40
Q

Treatment of type 2 hypersensitivity

A

Prevention by cross matching of blood, tissue typing and detection of rhesus incompatibility in pregnancy

Immune suppression in autoimmune disease and transplant rejection

41
Q

Pathogenesis of type 2 hypersensitivity

A

Complement activation
Fc uptake and stimulation of phagocytes
Antibody dependent cellular cytotoxicity

42
Q

Which organ specific autoimmune diseases are type 2 hypersensitivity reactions

A

Graves (against TSH receptor)
Myaesthenia gravis (acetylcholine receptor)
Good pastures syndrome (type IV collagen)
Phemphigus (desmosomes)

43
Q

In type 3 hypersensitivity reactions clinical conditions arise as a result of..

A

Abnormal deposition of immune complexes in tissues - may be a self or exogenous antigen

Excessive or abnormal immune complex formation causes complement activation and recruitment and activation of inflammatory cells leading to tissue damage

44
Q

What kind of hypersensitivity reaction is anaphylaxis

A

Type 1

45
Q

What is serum sickness

A

A systemic illness where immune complexes form in the circulation and are deposited in a widespread fashion throughout many tissues

  • part of type 3 hypersensitivity
46
Q

What is an arthus reaction

A

A localised disorder where complexes are formed locally in tissues

47
Q

Precipitants of type 3 hypersensitivity reactions

A

Fungal antigens –> farmer’s lung
Avian antigens –> bird fancier’s lung
Complexes of streptococcal antigen and anti-strep antibody –> post streptococcal glomerulonephritis
Leprosy, malaria, hepatitis (chronic infections)
Tumours
SLE

48
Q

Treatment of type 3 hypersensitivity

A

Antigen elimination - infection or tumour
Removal of immune complexes via plasma exchange/plasmaphoresis
Immunosuppressive therapy

49
Q

Which cells mediate type 4 hypersensitivity

A

Th1 cells and cytokine products

50
Q

What do the cells mediating type 4 hypersensitivity react to

A

Inert environmental substances or as a reaction to infection with certain micro-organisms

Reactions take place because immune system finds it difficult to destroy these environmental agents

51
Q

Which hypersensitivity reaction is often delayed

A

Type 4

Takes 48-72 hours

52
Q

Clinical features of type 4 hypersensitivity

A

Tissue damage which occurs during microbial infections
Mantoux test
Contact dermatitis in response to metals, drugs, plastics, rubber, plants, cosmetics

53
Q

Treatment of type 4 hypersensitivity (delayed type)

A

Avoidance or prevention of contact with antigens
Corticosteroids
Antimicrobial therapy as indicated by microorganisms

54
Q

Cause of secondary immune deficiency

A 
Malnutrition 
Malignant disease
Splenectomy
Infection 
Diabetes 
Burns/surgery
Immunosuppressive therapy
Chronic renal failure
55
Q

Clinical presentation of phagocyte disorders

A

Pneumonia, osteomyelitis, skin/mucous membrane infection, liver abscesses, suppurating lymph nodes

56
Q

What is hereditary angioedema

A

An autosomal dominant condition characterised by recurrent attacks of painless, non-pruritic, non-erythematous swellings in subcutaneous tissues, intestinal wall and larynx (due to deficiency f complement factor1)

57
Q

Functions of the complement system

A

Inflammatory and chemotactic mediators
Opsonins
Membrane lysing complexes

And maintaining solubility of circulating immune complexes

58
Q

Clinical features of severe combines immune deficiency

A 
Usually well for first 3 months of life
Persistent superficial candida
Diarrhoea and failure to thrive 
Chronic bronchiolitis 
Interstitial pneumonitis 
Overwhelming bacterial sepsis
59
Q

Defects in____________ cause severe combines immune deficiency

A

Pluripotent stem cells
Lymphoid stem cells
T and B cells themselves

60
Q

Management of severe combined immune deficiency

A

Intensive supportive therapy and nutritional support, prophylactic and therapeutic antibiotics, anti-fungal and anti-viral therapy prn and immunoglobulin replacement therapy

Bone marrow transplant is curative

61
Q

Presentation of IgA deficiency

A

Recurrent sinus and respiratory tract infections, GI disease, allergic symptoms and autoimmune disease

62
Q

How could IgA deficiency be induced

A

Secondary to phenytoin, penicillamine, gold or sulphasalazine

63
Q

Presentation of adaptive immune deficiency

A 
Unexplained failure to thrive 
Excessive infections
Abnormal lymphoid tissue
Unexplained enlargement of liver or spleen 
Unexplained joint symptoms
64
Q

Complications of adaptive immune deficiency

A 
Infection - opportunistic, serious, persistent, unusual, recurrent
Malignant disease
Autoimmune disease
Hypersensitivity disorders
Iatrogenic problems
65
Q

Infectious complications of antibody defects

A

Staph, strep, haemophilus,

Giardia

Echo and poliovirus

66
Q

Infectious complications of T cell defects (e.g. In AIDS)

A

CMV, herpes, measles

Mycobacteria, listeria

Candida, aspergillus

Pneumocystis, cryptosporidiosis, toxoplasma

67
Q

General principles of treatment for immune deficiencies

A 
Treat underlying cause if any 
Antimicrobial therapy 
AVOID IMMUNISATION WITH LIVE VACCINES 
AVOID BLOOD TRANSFUSION IN CELL MEDIATED DEFECTS 
Genetic counselling

Immunoglobulin replacement
Thymic hormones
Transplantation - bone marrow, fetal liver, fetal thymus

Gene therapy
Cytokine therapy

68
Q

Main tests of humoral immunity

A

Immunoglobulin levels - serum/plasma of IgG,A,M,E

69
Q

Main test for cell mediated immunity

A

T cell numbers

Skin tests - should produce positive skin test in presence of normal T cell immunity against candida, tetanus, diptheria, mumps…

70
Q

Effect of corticosteroids

A

Affect both T and B cell function.
Major affects are on: cytokine networks, inflammation, T cell and monocyte function and transit and circulation of immunologically active cells.

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