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Y1 RESPIRATORY > Immunology > Flashcards

Immunology Flashcards

1
Q

What are SPUR infections? What do they indicate?

A

Serious, Persistent, Unusual, Recurrent

Indicate immune deficiency

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2
Q

What is the main hallmark of immune deficiency?

A

Recurrent infections

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3
Q

Primary immune deficiencies are common. True/False?

A

False

Rare! Secondary immune deficiencies are common

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4
Q

Risk of infection ______ as neutrophil count increases

A

Decreases

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5
Q

How can failure to produce neutrophils arise?

A

Failure of stem cell differentiation

Failure of neutrophil maturation

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6
Q

What is Kostmann syndrome?

A

Rare autosomal recessive disorder; congenital neutropenia

Clinically presents as (recurrent) infections 2 weeks after birth

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7
Q

What is leukocyte adhesion deficiency?

A

Rare primary immune deficiency where neutrophils fail to bind to endothelial markers - cannot find where infection is!
Genetic defect in CD18

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8
Q

What is chronic granulomatous disease? How do you test for it?

A

Failure of oxidative killing due to inability to generate oxygen free radicals
NBT test

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9
Q

Name an important related side effect of anti-TNF therapy

A

Reactivation of latent TB

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10
Q

In congenital neutropenia, neutrophil count is normal. True/False?

A

False

Low or absent

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11
Q

Is there pus formation in congenital neutropenia?

A

No

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12
Q

In leukocyte adhesion deficiency, neutrophil count is low during infection. True/False?

A

False

It is high

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13
Q

Is there pus formation in leukocyte adhesion deficiency?

A

No

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14
Q

In chronic granulomatous disease, neutrophil count is normal. True/False?

A

True

Would be raised in the acute stage but not once granuloma has formed

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15
Q

Is there pus formation in chronic granulomatous disease?

A

Yes

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16
Q

Give examples of definitive management of phagocyte deficiencies

A

Bone marrow transplant, gene therapy

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17
Q

What cells do T cells arise from?

A

Haemopoetic stem cells in bone marrow

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18
Q

Defects in stem cell differentiation in haemopoetic cells causes which fatal condition?

A

Reticular dysgenesis

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19
Q

What is Severe Combined Immunodeficiency (SCID)? How is it treated?

A

Failure of production of lymphocytes

Stem cell transplantation

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20
Q

What are some key clinical phenotypes of SCID?

A

Unwell by 3 months
Diarrhoea
Failure to thrive
Early death

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21
Q

Why does SCID present only after 3 months of age?

A

Maternal IgG protects the infant up to this point

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22
Q

In X-linked SCID, which receptor is mutated?

A

IL2 receptor

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23
Q

What is DiGeorge syndrome?

A

Failed development of the thymus

“Funny looking kid”

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24
Q

Which chromosome is deleted in DiG syndrome?

A

22q11

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25
Q

In DiG syndrome, the thymus fails to develop. What is the consequence of this?

A

Low/no T cells can mature (thus low T cell numbers)

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26
Q

What is hypogammaglobulinaemia?

A

Failure to produce mature B cells

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27
Q

What is common variable immunodeficiency?

A

Low IgG, IgA and IgE

Leads to recurrent infections, often autoimmune

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28
Q

Which type of hypersensitivity reaction do allergic diseases come under?

A

Type 1

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29
Q

Define what is meant by allergy

A

IgE-mediated response to an external antigen

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30
Q

Describe the hygiene hypothesis

A

Decrease in infectious exposure in early life predisposes to increased sensitivity/predisposition to allergic stimuli

31
Q

Allergic reactions typically take a few hours to develop. True/False?

A

False

Can be from within minutes to a couple hours

32
Q

What is the role of B lymphocytes in the allergic response?

A

Recognise antigen and produce IgE

33
Q

What is the role of T lymphocytes in the allergic response?

A

Aid B cells in producing IgE

34
Q

What is the role of mast cells in the allergic response?

A

Express Fc receptors for IgE

Produce inflammatory mediators upon degranulation

35
Q

Allergic reactions occur on first exposure to the allergen. True/False?

A

False
First encounter produces circulatory IgE, which then binds to mast cell; when second encounter occurs, the IgE is activated, causing mast cell degranulation, leading to allergy

36
Q

What is the clinical effect of histamine and other inflammatory mediators in the lung?

A 
Bronchoconstriction
Vasodilation
Increased vascular permeability 
Mucosal oedema, mucus secretion
Yellow sputum
37
Q

What is urticaria? How long does it last?

What is angiodema?

A

Hives/rash
Lasts typically 6 hrs

Self-limited localised swelling of subcutaneous tissues/mucous membranes

38
Q

Name some elective investigations for identifying allergic disease

A 
Skin prick test
RAST test (allergen specific IgE test)
Challenge testing (supervised exposure to antigen)
39
Q

What would be measured in an acute anaphylactic episode?

A

Serum tryptase

40
Q

What is a skin prick test?

A

Expose patient to standardised solution of antigen through a prick to the forearm
A positive test will yield a local flare

41
Q

Why is measuring total IgE not useful in diagnosing allergic disease?

A

IgE can be raised by lots of things - allergy can also occur in the absence of IgE

42
Q

Which drug supposedly blocks mast cell degranulation?

A

Sodium chromoglycate

43
Q

What disease type is an example of Type I hypersensitivity?

A

Allergy

Anaphylaxis

44
Q

Type II hypersensitivity involves direct cell killing through which main mechanism/process?

A

Complement pathway

45
Q

What are the 4 main effects of Complement activation?

A

Direct killing (MAC)
Opsonisation (C3b)
Solubilisation of immune complexes
Chemotaxis

46
Q

Give clinical examples and description of Type II hypersensitivity

A 
Blood transfusions
Goodpastures syndrome of the kidney
Myastheria gravis
Guillan Barre syndrome
Pemphigus vulgaris
Graves disease
Rhesus disease of the newborn
47
Q

How are type II hypersensitivity reactions treated?

A

PLASMAPHARESIS: Remove pathogenic antibody from a patient’s blood
IMMUNOSUPPRESSION

48
Q

What mediates Type III hypersensitivity?

A

Immune complexes

49
Q

What happens in Type III hypersensitivity?

A

Immune complexes get stuck in areas and activate Complement in those areas, attracting macrophages and causing phagocytosis

50
Q

Give clinical exampleS of Type III hypersensitivity

A

EAA

Lupus

51
Q

Which cell type mediates Type IV hypersensitivity?

A

T cells

52
Q

What happens in Type IV hypersensitivity?

A

T cells generated due to initial sensitisation of antigen; repeated exposure causes recruitment of inflammatory cells to the site

53
Q

What term is given to a collection of activated macrophages and lymphocytes?

A

Granuloma

54
Q

Give examples of non-autoimmune Type IV hypersensitivity conditions

A

Sarcoidosis
Tuberculosis
Leprosy
Organ rejection

55
Q

What are memory B cells?

A

Generated in primary humoral responses, they survive in a dormant state and rapidly reactivate in response to second encounter with same antigen

56
Q

What are the 4 main ways of active vaccination?

A

Exposure to infectious organism
Exposure to similar, less virulent pathogen
Exposure to less virulent form of same organism
Exposure to inactivated organism

57
Q

What is the main danger of live attenuated vaccines?

A

Can cause disease particularly in immunosuppressed individuals

58
Q

Give examples of live attenuated vaccines

A

Measles and mumps
Chickenpox
Rubella
Smallpox

59
Q

HLA Class II presents to which T cell?

A

CD4

60
Q

HLA Class I presents to which T cell?

A

CD8

61
Q

Why is HLA matching in transplantation important?

A

Minimise differences between donor and recipient to prevent transplant rejection

62
Q

Mathcing HLA Class I is more important than matching HLA Class II. True/False?

A

False

Class II more important as CD4 cells are the main mediators of the immune response

63
Q

What are the disadvantages of HLA matching?

A 
Limited benefit if the donor pool is small
Rare variants (ethnic groups) may not have good chances
64
Q

What are the 2 situations where HLA matching is used to allocate donors?

A

Stem cell transplants

Kidney transplants

65
Q

When is HLA matching not used to allocate donors?

A

Lung, heart and liver transplants

66
Q

Which type of hypersensitivity reaction is acute cellular rejection?

A

Type IV

67
Q

How is hypersensitivity classified?

A
  1. Immediate hypersensitivity (Allergy, Anaphylaxis, Atopy)
  2. Direct cell killing (antiBody)
  3. Immune Complex mediated
  4. Delayed type hypersensitivity
68
Q

What drugs block the effects of mast cell activation?

A

Antihistamines - H1 receptor antagonists

Leukotriene receptor antagonists - montelukast

69
Q

How is anaphylaxis managed?

A

Adrenaline
Avoidance
Immunotherapy

70
Q

How are type III hypersensitivity reactions tested for?

A

Look for presence of specific IgG antibodies

71
Q

How are type III hypersensitivity reactions managed?

A

Avoidance
Immunosuppression
CCS

72
Q

How are type IV hypersensitivity reactions managed?

A

Waiting - spontaneous remission
NSAIDs
CCS

73
Q

What is passaging?

A

Growing attenuated strains by repeated subculturing through cells/ live animals

74
Q

List some sources of passive immunity

A

Transfer of maternal IgG in 3rd trimester
Naturally acquired
Therapeutic passive immunisation

Y1 RESPIRATORY (12 decks)

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