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Immunology Flashcards

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1
Q

Hallmarks of immunodeficiency

A

Serious infections
Persistent infections
Unusual infections
Recurrent infections

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2
Q

Features suggestive of primary immune deficiency

A 
Weight loss or failure to thrive
Severe skin rash (eczema)
Chronic diarrhoea
Mouth ulceration
Unusual autoimmune disease
Family history
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3
Q

Primary immunodeficiency

A

Rare

Hereditary

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4
Q

Secondary

A

Common
Acquired
Often subtle
Often involves more than one component of immune system

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5
Q

Conditions associated with secondary immune deficiency

A 
Ageing, Prematurity
Infection
Treatment interventions
Malignancy
Biochemical and nutritional disorders
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6
Q

Phagocyte Deficiencies

A

Defects of phagocyte production, mobilisation and recruitment
Leukocyte Adhesion Deficiency
Defects of recognition
Failure of oxidative killing mechanisms

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7
Q

Failure of stem cells to differentiate into neutrophils

A

Primary defect: Recticular Dysgenesis

Secondary defect: After stem cell transplantation

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8
Q

Failure of neutrophil maturation

A

Kostmann syndrome

Cyclic neutropaenia

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9
Q

Recticular dysgenesis

A

Complete block in leukocyte development

Severe Combined Immuno Deficiency

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10
Q

Kostmann Syndrome

A

Defect in receptor or cytokine GCSF
Blocks neutrophil development
Autosomal recessive disorder
Severe chronic neutropaenia

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11
Q

Supportive treatments for kostmann syndrome

A

Prophylactic antifungals

Prophylactic antibiotics

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12
Q

Definite treatments for kostmann syndrome

A

Stem Cell transplantation

Granulocyte Colony Stimulating Factor

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13
Q

Leukocyte adhesion deficiency

A

Rare primary immunodeficiency
Caused by genetic defect in leukocyte integrins (CD18)
Failure to recognise activation markers expressed on endothelial cells

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14
Q

Markers of leukocyte adhesion deficiency

A

Localised deep tissue bacterial infections that are difficult to detect
Very high neutrophil count

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15
Q

Failure of oxidative killing mechanisms

A

Absent respiratory burst
Deficiency of the intracellular killing mechanism of phagocytes
Inability to generate oxygen free radicals
Failure to degrade chemoattractants and antigens
Persistent accumulation of neutrophils, activated macrophages and lymphocytes

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16
Q

Features of chronic granulomatous disease

A 
Recurrent deep bacterial infections
Recurrent fungal infections
Failure to thrive
Lymphadenopathy and hepatosplenomegaly
Granuloma formation
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17
Q

Laboratory investigation of chronic granulomatous disease

A

NBT Test

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18
Q

Treatment of chronic granulomatous disease

A

Prophylactic antibiotics
Prophylactic antifungals
Stem cell transplantation
Gene therapy

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19
Q

Investigations in phagocyte recruitment function

A

Full blood count & differential
Presence of pus
Expression of neutrophil adhesion molecules

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20
Q

Investigations in phagocyte recognition function

A

Chemotactic assays

Phagocytosis assays

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21
Q

Investigations in phagocyte killing function

A

NBT test of oxidative killing

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22
Q

What drives immunoglobulin class switching?

A

CD4 cell

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23
Q

What is the first antibody secreted from the bone marrow?

A

IgM

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24
Q

Antibody functions

A

Antigen receptors (IgM and IgD)
Opsonisation (IgG)
Neutralisation (IgA)
Mast cell activation (IgE)

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25
How can the adaptive immune system go wrong?
Defects of hematopoietic stem cells Defects of lymphoid precursors (SCID) Failure of Thymic development Disorders of T cell effector function
26
Clinical phenotype of severe combined immunodeficiency
``` Unwell by 3 months of age Persistent diarrhoea Failure to thrive Infection of all types Unusual skin disease Family history of early infant death ```
27
Causes of SCID
Deficiency of cytokine receptors Deficiency of signalling molecules Metabolic defects Defective receptor arrangements
28
X-linked SCID
Mutation of a component of the IL-2 Receptor Results in inability to respond to cytokines -Failure of T cell and NK cell development -Production of immature B cells
29
DiGeorge Syndrome
Failure of thymic development | Results in T cell immunodeficiency
30
Phenotype of DiGeorge Syndrome
``` Congenital heart defects Cleft palate Hypocalcaemia Developmental delay Psychiatric disorders Oesophageal atresia T cell lymphopaenia ```
31
Laboratory results for DiGeorge Syndrome
Absent or decreased number of T cells Normal or increased B cells Normal NK cells numbers
32
Disorders of T cell effector function
Cytokine production Cytotoxicity T-B cell communication (IFNy deficiency, IL-12 deficiency)
33
First line investigations of T cell deficiencies
Total white cell count and differential Quantitation of lymphocyte subpopulations Serum immunoglobulins
34
Second line investigations of T cell deficiencies
Functional tests of T cell activation and proliferation Additional tests of T lymphocyte lineage HIV test
35
Immune deficiencies affecting B lymphocytes
B cell maturation defects Failure of TFH cell co-stimulation Failure of IgA production (Selective IgA deficiency) Failure of production of IgG (Common variable immune deficiency, Selective antibody deficiency)
36
First line investigations of B cell deficiencies
Total white cell count and differential | Serum/ urine immunoglobulins
37
Second line investigations of B cell deficiencies
Quantitation of B and T lymphocytes | Specific antibody responses to known pathogens
38
Hypersensitivity Reaction
Immune response that results in bystander damage to the self Usually exaggeration of normal immune mechanisms
39
Type 1 Hypersensitivity reaction
Immediate hypersensitivity
40
Type 2 hypersensitivity reaction
Direct cell killing
41
Type 3 hypersensitivity reaction
Immune complex mediated
42
Type 4 hypersensitivity reaction
Delayed type hypersensitivity
43
What type of hypersensitivity reaction is allergic reaction?
Type 1: Immediate hypersensitivity
44
Allergy
IgE-mediated antibody response to external antigen
45
The 'Hygiene Hypothesis'
Changes in microbial stimuli influences the maturation of the immune response General decrease in infectious burden during early life results in increased predisposition to allergic conditions during childhood
46
Vasoactive substances produced by mast cells
Histamine, Tryptase, Heparin Leukotrienes, prostaglandins TNFa, IL-4
47
The role of mast cells in allergic reactions
Express receptors for Fc region of IgE antibody on their surface Release of vasoactive mediators (histamine, tryptase) Increased cytokine and leukotriene transcription
48
Mast cell stabilisers
Sodium cromoglycate Stabilises mast cell membranes Prevents release of inflammatory mediators
49
Anti-histamine
H1 Receptor antagonists | Block biological effects of histamines
50
Leukotriene receptor antagonists
Montelukast | Blocks effects of leukotrienes
51
Adrenaline
Acts on B2 adrenergic receptors to constrict arterial smooth muscle
52
Pathophysiology of direct cell killing (type 2)
Antibody binds to cell surface antigen | Results in activation of complement and opsonisation
53
Functions of antibody
Activates B lymphocytes Acts as opsonins Mast cell degranulation Causes antigen clumping and inactivation of bacterial toxins Activates antibody dependent cellular activity Activates complement
54
Effects of complement activation
Chemotaxis Solubilization of immune complexes MAC-direct killing of bacteria Opsonisation
55
Which fragments of complement proteins released after activation increase permeability of blood vessels
Anaphylotoxins (C3a and C5a)
56
Clinical examples of type 2 hypersensitivity
Acute haemolytic transfusion reaction | Drug induced haemolysis
57
Blood type A
Surface antigen A | Anti-B antibodies
58
Blood type B
Surface antigen B | Anti-A antibodies
59
Blood type AB
Surface antigen A and B | Neither anti-A or anti-B antibodies
60
Type O
Neither surface A or B antigens | Anti- A and anti-B antibodies
61
Type 2 hypersensitivity management
Plasmapheresis | Immunosuppression
62
Pathophysiology of type 3 hypersensitivity
Antibodies bind to soluble antigens forming small immune complexes These are trapped in small blood vessels, joints and glomeruli
63
Management of type 3 hypersensitivity reaction
(Avoidance) Corticosteroids to reduce inflammation Immunosuppression to decrease production of antibody
64
Autoimmune diseases associated with delayed hypersensitivity reaction
Type 1 diabetes Psoriasis Rheumatoid arthritis
65
Non-autoimmune diseases associated with delayed hypersensitivity reaction
``` Contact dermatitis Tuberculosis Leprosy Sarcoidosis Cellular rejection of organ transplant ```
66
Pathophysiology of type 4 hypersensitivity reaction
Initial sensitisation to antigen creates 'primed' generation of effector Th1 and memory T cells Subsequent exposure activates previously primed T cells Recruitment of macrophages, lymphocytes, neutrophils, proteolytic enzymes, inflammation...
67
Management of type 4 hypersensitivity reaction
Watchful waiting NSAIDS Systemic corticosteroids

Respiratory (19 decks)

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