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Immunology Flashcards

0
Q

Clinical features of phagocyte deficiency?

A 
Recurrent infections effecting common or unusual sites:
Staph aureus - common
Burkholderia cepacia - unusual
Mycobacteria - TB
fungi - candida, aspergillus
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1
Q

What are the clinical features suggestive of immunodeficiency?

A

S - serious infection
P - persistent infection
U - unusual infection
R - recurrent infections

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2
Q

What is reticular dysgenesis?

A

Rare genetic disorder of the bone marrow resulting in complete absence of granulocytes and decreased no. Of lymphocytes.
Caused by haemopoetic stem cell defect that causes failure of production of immune cells so prevents thymus from growing

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3
Q

What is Kostmann’s syndrome?

A

rare autosomal recessive disorder.
Absolute neutrophil count drops to extreme low (<200/ul)
Presents as infections usually within 2 weeks of birth - recurrent then on.
Fever, irritability, oral ulceration and failure to thrive

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4
Q

How do you treat Kostmann’s syndrome?

A

Prophylactic antibiotics/antifungals
Mortality of 70% in first year

Definitive treatment:
Stem cell transplantation
Granulocyte colony stimulating factor

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5
Q

What is leukocyte adhesion deficiency?

A

Rare primary immunodeficiency caused by genetic defect in CD18. Results in failure of neutrophil adhesion and migration.
Clinically characterised by leukocytosis and localised bacterial infection

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6
Q

How do phagocytes recognise pathogens?

A

Pathogen recognition receptors
- toll like, scavenger and lectin
Recognise microbial specific structures. - bacterial sugars, lipopolysaccharides
Indirect recognition - opsonins

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7
Q

How can pathogen detection by phagocytes go wrong?

A

Defect in opsonin receptors

Any defect in complement or antibody production will also cause opsonin defect - a functional defect

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8
Q

What is chronic granulomatous disease?

A

Deficiency of the intracellular killing mechanism I phagocytes - oxidative killing
Unable to make oxygen free radicals
Impaired killing of intracellular micro-organisms
Inability to clear organisms leads to excessive inflammation and granulomatous formation

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9
Q

What are the features of chronic granulomatous disease?

A 
Recurrent deep bacterial infections
Recurrent fungal infections 
Failure to thrive
Lymphadenopathy and hepatosplenomegaly
Granulomatous formation
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10
Q

What investigations are done for chronic granulomatous disease?

A

NBT (nitroblue tetrazolium) test:

Check if neutrophils can kill through production of oxygen free radicals.
Feed patient neutrophils source of E.coli and add dye that is sensitive to H2O2. If produced by neutrophils dye changes colour

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11
Q

How do you treat chronic granulomatous disease?

A

Supportive:
Prophylactic antibiotics/antifungals

Definitive:
Stem cell transplant
Gene therapy - gamma interferon therapy

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12
Q

What are the intracellular pathogens and what do they do?

A

Salmonella, chlamydia and rickettsia all hide from immune system by locating within cells.
Mycobacteria hide with macrophages l.
They all need specific strategies to be cleared

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13
Q

How do macrophages defend against TB?

A

Activates IL12-gIFN network.
Infected macrophages stimulated to produce IL12 which induces T cells to produce gIFN. gIFN stimulates production of TNF by macrophages and neutrophils which activates NADPH oxidase stimulating oxidative pathways

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14
Q

What are defects in IL12-gIFN network associated with?

A

Single gene defects:
- gIFN receptor deficiency, IL12 deficiency and IL12 receptor deficiency

Mycobacterial infection:
- TB, salmonella

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15
Q

What is an important side effect of anti-TFN drugs?

A

Re activation of latent diseases such as latent TB.

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16
Q

How are T cell produced?

A

Pre T-cells produced in bone marrow and then transported to the thymus where proliferation and maturation occurs. Mature T cells then enter the circulation and reside in lymph nodes and secondary lymphoid follicles

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17
Q

What is the function of CD4+ T cells?

A

Immunoregulatory functions:
- stimulate activation of CD8+ T cells and B cells
- produce cytokines
Regulate other lymphocytes and phagocytes

Recognize peptides presented by HLA class II molecules (genes that encode MHC molecules)

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18
Q

What is the function of CD8+?

A

Specialised cytotoxic cells. Recognise peptides in association with HLA class I (MHC class I) and kills them directly.

It is particularly important in defence against viral infection and tumours

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19
Q

Where are B cells found and what is there function?

A

Arise from haemopoetic stem cells in bone marrow and mature B cells are found in bone marrow, lymphoid tissue and spleen.
There function is antibody production and antigen presentation

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20
Q

How do B cells develop?

A

Develop in bone marrow then become IgM B cells. These then become IgM plasma cells unless stimulated to proliferate by T cells.
CD4+ (Th cells) convert IgM to either IgG, IgE or IgA.
IgG is then turned into plasma cells

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21
Q

What is the function of antibodies?

A

Identification of pathogens
Recruitment of other components of the immune response to pathogens
-complement,phagocytes and NK cells
Neutralisation of toxins
Particularly important in defence against bacteria of all kinds

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22
Q

What is graft versus host disease in severe combined immunodeficiency?

A

When the baby fails to produce lymphocytes so lymphocytes in the babies blood are the mothers and colonise in infants empty bone marrow and begin to attack the host.

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23
Q

What is hypogammaglobuminaemia?

A

Low Immungloblins in the blood meaning the host gets more infections

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24
Q

What are the causes of SCID?

A

> 20 possible pathways identified
Presence of different lymphocyte subsets depend on exact mutations which may malfunction
X-linked - normally boys but not always.

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25
Q

What are the features of X-linked SCID?

A

Mainly boys and caused by mutation of IL2 receptor. Results in failure of T cell and NK cell development.
Therefore very low T cells, normal or increased B cells and a poorly developed thymus.

26
Q

Treatment of SCID?

A

Prophylactic treatment
Definitive treatment:
- put in lamina flow room (air flows out to prevent infection) until bone marrow stem cell transplant from HLA identical sibling or matched donor

27
Q

What is DiGeorge syndrome?

A

Developmental defect of 3rd/4th pharyngeal pouch leading to a child with no or impaired thymus.

28
Q

What is the phenotype of a child with DiGeorge syndrome?

A

Funny looking - low set ears, cleft palate, small mouth and jaw
Hypocalcaemia
Oesophageal atresia - oesophagus doesn’t join properly
Complex congenital heart defect

29
Q

What chromosome is effected by DiGeorge syndrome?

A

22q11

30
Q

What kind of infections are caught in DiGeorge syndrome and why?

A

Recurrent viral infection:
- CD8+ essential in killing infected T cells
Recurrent bacterial infection:
- T cells essential for helping B cells make antibodies
Frequent fungal infections:
- because T cells are essential for fungal defence

31
Q

How do you investigate DiGeorge syndrome?

A

Number of T cells-absent or decreased

Normal or increased B cells
- low IgG, IgA and IgE

Normal NK cell numbers

32
Q

What is the management of DiGeorge treatment?

A

Correct metabolic/cardiac abnormality
Prophylactic antibiotics
Early and aggressive treatment of infection
Some patients require immunoglobulin replacement
T cell function improves with age

33
Q

What is the presentation of antibody deficiencies?

A

Recurrent bacterial infections

  • U&L resp tract
  • recurrent GI infections
  • often common organisms

Antibody mediated autoimmune diseases - automimmune haemolytic anaemia, thrombocytopenia

34
Q

What is Bruton’s disease?

A

X-linked inherited leaving to hypogammaglobuminaemia (low Igs).

Failure to produce B cells leading to no plasma cells or circulating antibodies

35
Q

What are the features of a selective IgA deficiency?

A

2/3 Asymptomatic
1/3 have recurrent respiratory tract infections.
There is a genetic component but cause as yet unknown

36
Q

What are the features of common variable immune deficiency?

A 
Heterogenous group of disorders
- can be caused by many different 
gene problems 
Failure to produce antibodies 
Recurrent bacterial infections
Autoimmune disease
Granulomatous disease
37
Q

Management of B cell deficiencies?

A

Aggressive treatment of infection
Immunoglobulin treatment
Stem cell transplantation

38
Q

Outline each type of hypersensitivity.

A

Type I - immediate hypersensitivity
Type II - direct cell killing
Type III - immune complex mediated
Type IV - delayed type hypersensitivity

39
Q

define an allergy?

A

IgE mediated antibody response to external antigen

40
Q

Clinical features of Type I hypersensitivity?

A

Occurs quickly after exposure
Same type of reaction each time
Presentation influence by site of contact

41
Q

What cells are involved in type 1 hypersensitive?

A

B lymphocytes - produce IgE
T lymphocytes - help B cells
Mast cells - inflammatory cells that release vasoactive substances (histamine, prostaglandins and interleukins)

42
Q

What is the Fc region?

A

The tail end of an antibody that interacts with cell surface receptors called Fc receptors. This property allows antibodies to activate the immune system

43
Q

What are the non-allergic causes of mast cell degranulation?

A

Drugs
- morphine, aspirin and NSAIDs
Thyroid disease
Idiopathic

44
Q

What specific investigations can be done to diagnosis a type I hypersensitive?

A

Elective:
- skin prick tests (gold standard) , quantative IgE check, challenged test (supervised exposure to antigen)

During acute anaphylactic episode there will be evidence of mast cell degranulation

45
Q

What is the management of IgE mediated allergic disorders?

A 
Avoid allergen
Block mast cell activation
Prevent effects of mast cells activation
Anti-inflammatory agents
Management of anaphylaxis
Immunotherapy
46
Q

What is a type II hypersensitivity?

A

Direct cell killing

Antibody binds to antigen on surface of target cell. Resulting in activation of phagocytes and compliment system

47
Q

What does activation of the complement system result in?

A

Formation of the membrane attack complex which punches holes I’m bacterial cell membranes

48
Q

How is the complement pathway stopped?

A

Fragments of pathway dissolve their own immune complex trigger switching off their activation.

(Negative feedback)

49
Q

Examples of type II hypersensitivity?

A

Blood transfusion with wrong blood type. For example:
Patient type A has anti-B antibodies. If donor blood is type B then anti-B antibodies stimulate complement pathway leading to haemolysis

50
Q

Management of type II hypersensitivity?

A

Plasmapheresis - removal of pathogenic antibody (patient blood removed via cell separator)

Immunosuppression

51
Q

What is a type III hypersensitivity reaction?

A

Immune complex mediated (antibody/antigen complexes)

52
Q

Give example of type III hypersensitivity

A

Acute extrinsic allergic alveolitis only!!!

53
Q

How do you diagnose a type III hypersensitivity?

A

Specific IgG to causative antigen

Complement

54
Q

Management of type III hypersensitivity reactions?

A

Avoidance
Decrease inflammation - corticosteroids
Decrease production of antibody - immunosuppression

55
Q

What is type IV hypersensitivity?

A

Delayed type hypersensitivity:

T cell mediated. Initial sensitisation to antigen generates primed T cells. Subsequent exposure leads to activation of primed T cells recruiting of macrophages, other lymphocytes and neutrophils - proteolytic enzymes cause inflammation

56
Q

Examples of type IV hypersensitivity?

A

Autoimmune
- type 1 diabetes, psoriasis, rheumatoid arthritis

Non-autoimmune - nickel, TB, sarcoidosis, organ transplant

57
Q

What is a granulomatous

A

An organised collection of activated macrophages and lymphocytes

58
Q

How is immunological memory created?

A

Long-lived memory B cells are generated during first contact and survive in a dormant state for many year after this until they are rapidly re-activated by a second encounter

59
Q

What are memory T cells?

A

Rare naive T cells stimulated by vaccine that induce a strong T cell response to antigen

60
Q

What is the difference between active and passive immunity?

A

Active - Produced by person’s own immune system (can be stimulated by vaccine or acquired infection)

Passive - transferred from another person and wanes with time

61
Q

Define immunisation and vaccination.

A

The process through which an individual develops immunity. (Natural infection)

Vaccination (deliberate administration of antigenic material)

62
Q

What are the four ways of generating memory against pathogens?

A

Exposure to the infection
Exposure to similar but less virulent pathogen
Exposure to inactivated pathogen
Exposure to a less virulent version of the same pathogen

63
Q

What is an adjuvant?

A

A substance which enhances the body’s immune response to an antigen. Given along with inactivated vaccine.

Respiratory (5 decks)

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