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Y1 RESPIRATORY > Immunology > Flashcards

Immunology Flashcards

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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
In DiG syndrome, the thymus fails to develop. What is the consequence of this?
Low/no T cells can mature (thus low T cell numbers)
26
What is hypogammaglobulinaemia?
Failure to produce mature B cells
27
What is common variable immunodeficiency?
Low IgG, IgA and IgE | Leads to recurrent infections, often autoimmune
28
Which type of hypersensitivity reaction do allergic diseases come under?
Type 1
29
Define what is meant by allergy
IgE-mediated response to an external antigen
30
Describe the hygiene hypothesis
Decrease in infectious exposure in early life predisposes to increased sensitivity/predisposition to allergic stimuli
31
Allergic reactions typically take a few hours to develop. True/False?
False | Can be from within minutes to a couple hours
32
What is the role of B lymphocytes in the allergic response?
Recognise antigen and produce IgE
33
What is the role of T lymphocytes in the allergic response?
Aid B cells in producing IgE
34
What is the role of mast cells in the allergic response?
Express Fc receptors for IgE | Produce inflammatory mediators upon degranulation
35
Allergic reactions occur on first exposure to the allergen. True/False?
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
What is the clinical effect of histamine and other inflammatory mediators in the lung?
``` Bronchoconstriction Vasodilation Increased vascular permeability Mucosal oedema, mucus secretion Yellow sputum ```
37
What is urticaria? How long does it last? | What is angiodema?
Hives/rash Lasts typically 6 hrs Self-limited localised swelling of subcutaneous tissues/mucous membranes
38
Name some elective investigations for identifying allergic disease
``` Skin prick test RAST test (allergen specific IgE test) Challenge testing (supervised exposure to antigen) ```
39
What would be measured in an acute anaphylactic episode?
Serum tryptase
40
What is a skin prick test?
Expose patient to standardised solution of antigen through a prick to the forearm A positive test will yield a local flare
41
Why is measuring total IgE not useful in diagnosing allergic disease?
IgE can be raised by lots of things - allergy can also occur in the absence of IgE
42
Which drug supposedly blocks mast cell degranulation?
Sodium chromoglycate
43
What disease type is an example of Type I hypersensitivity?
Allergy | Anaphylaxis
44
Type II hypersensitivity involves direct cell killing through which main mechanism/process?
Complement pathway
45
What are the 4 main effects of Complement activation?
Direct killing (MAC) Opsonisation (C3b) Solubilisation of immune complexes Chemotaxis
46
Give clinical examples and description of Type II hypersensitivity
``` Blood transfusions Goodpastures syndrome of the kidney Myastheria gravis Guillan Barre syndrome Pemphigus vulgaris Graves disease Rhesus disease of the newborn ```
47
How are type II hypersensitivity reactions treated?
PLASMAPHARESIS: Remove pathogenic antibody from a patient's blood IMMUNOSUPPRESSION
48
What mediates Type III hypersensitivity?
Immune complexes
49
What happens in Type III hypersensitivity?
Immune complexes get stuck in areas and activate Complement in those areas, attracting macrophages and causing phagocytosis
50
Give clinical exampleS of Type III hypersensitivity
EAA | Lupus
51
Which cell type mediates Type IV hypersensitivity?
T cells
52
What happens in Type IV hypersensitivity?
T cells generated due to initial sensitisation of antigen; repeated exposure causes recruitment of inflammatory cells to the site
53
What term is given to a collection of activated macrophages and lymphocytes?
Granuloma
54
Give examples of non-autoimmune Type IV hypersensitivity conditions
Sarcoidosis Tuberculosis Leprosy Organ rejection
55
What are memory B cells?
Generated in primary humoral responses, they survive in a dormant state and rapidly reactivate in response to second encounter with same antigen
56
What are the 4 main ways of active vaccination?
Exposure to infectious organism Exposure to similar, less virulent pathogen Exposure to less virulent form of same organism Exposure to inactivated organism
57
What is the main danger of live attenuated vaccines?
Can cause disease particularly in immunosuppressed individuals
58
Give examples of live attenuated vaccines
Measles and mumps Chickenpox Rubella Smallpox
59
HLA Class II presents to which T cell?
CD4
60
HLA Class I presents to which T cell?
CD8
61
Why is HLA matching in transplantation important?
Minimise differences between donor and recipient to prevent transplant rejection
62
Mathcing HLA Class I is more important than matching HLA Class II. True/False?
False | Class II more important as CD4 cells are the main mediators of the immune response
63
What are the disadvantages of HLA matching?
``` Limited benefit if the donor pool is small Rare variants (ethnic groups) may not have good chances ```
64
What are the 2 situations where HLA matching is used to allocate donors?
Stem cell transplants | Kidney transplants
65
When is HLA matching not used to allocate donors?
Lung, heart and liver transplants
66
Which type of hypersensitivity reaction is acute cellular rejection?
Type IV
67
How is hypersensitivity classified?
1. Immediate hypersensitivity (Allergy, Anaphylaxis, Atopy) 2. Direct cell killing (antiBody) 3. Immune Complex mediated 4. Delayed type hypersensitivity
68
What drugs block the effects of mast cell activation?
Antihistamines - H1 receptor antagonists | Leukotriene receptor antagonists - montelukast
69
How is anaphylaxis managed?
Adrenaline Avoidance Immunotherapy
70
How are type III hypersensitivity reactions tested for?
Look for presence of specific IgG antibodies
71
How are type III hypersensitivity reactions managed?
Avoidance Immunosuppression CCS
72
How are type IV hypersensitivity reactions managed?
Waiting - spontaneous remission NSAIDs CCS
73
What is passaging?
Growing attenuated strains by repeated subculturing through cells/ live animals
74
List some sources of passive immunity
Transfer of maternal IgG in 3rd trimester Naturally acquired Therapeutic passive immunisation

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