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Immunology Flashcards

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1
Q

Various responses to infection (3)

A

Resolution
Latent infection
Chronic infection

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2
Q

Resolution characteristics (3)

A

Normal immune response
Pathogen cleared
Tissue repaired

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3
Q

Latent infection characteristics (3)

A

Normal immune response
Pathogen controlled
Infection can reoccur

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4
Q

Chronic infection characteristics (2)

A

Defective immune response

Pathogen not cleared or controlled

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5
Q

Major hallmarks of immune deficiency and characteristics (SPUR) (4)

A

Serious infections - Unresponsive to oral antibiotics
Persistent infections - Early structural damage & chronic infections
Unusual infections - Unusual organisms in unusual sites
Recurrent infections - 2 major or 1 major and recurrent minor infections in 1 year

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6
Q

Primary immunodeficiency disorders (PID) characteristics (3)

A

Immune dysregulation
Autoinflammatory disorders
Defects in innate and adaptive immunity

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7
Q

Secondary immunodeficiency disorders (SID) characteristics (3)

A

Common
Subtle
Involves more than 1 component of immune system

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8
Q

Conditions associated with secondary immune deficiency (5)

A

Physiological immune deficiency - Extremes of life (Ageing, prematurity)
Infection - HIV, measles
Malignancy - Cancer of immune system, metastatic tumours
Treatment interventions - Immunosuppressive therapy, Anti-cancer agents, Corticosteroids
Biochemical disorders - Malnutrition, dialysis, type 1 & 2 diabetes

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9
Q

Upper respiratory complications of PIDs (3)

A

Sinusitis
Otitis media
Laryngeal angioedema

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10
Q

Lower respiratory complications of PIDs (4)

A

Malignancies
Interstitial lung disease
Pneumonia
Bronchitis/bronchietasis

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11
Q

Primary antibody deficiency (PAD) (3)

A

Associated with sinusitis and otitis media
Selective IgA deficiency
It is X-linked agammaglobulinemia (XLA)

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12
Q

Complement system disorders (4)

A

Considered in patients with laryngeal angioedema
C1 esterase inhibitor defect causes hereditary angioedema (HAE)
Can cause obstruction and asphyxiation
Not an allergic reaction

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13
Q

Pneumonia (2)

A

Inflammatory condition of the lung secondary to infection due to opportunistic organisms
Happens due to PAD, complement system disorders, congenital phagocytosis deficiency & combined immunodeficiencies

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14
Q

Most common PID associated with respiratory complications in children

A

Congenital neutropenia (abnormally low concentration of neutrophils in blood)

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15
Q

How can life cycle of a neutrophil go wrong (3)

A

Defects in Neutrophil development
Defects in Neutrophil trans-endothelial migration
Defects in Neutrophil killing

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16
Q

Defects in Neutrophil development (2)

A

Granulocyte-monocyte progenitor doesn’t respond to cytokine G-CSF causing severe congenital neutropenia
Example is Kostmann syndrome

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17
Q

Defects in Neutrophil trans-endothelial migration (3)

A

Due to Failure to recognise activation markers expressed on endothelial cells
Neutrophils are mobilized, but cannot exit bloodstream
Example is Leukocyte adhesion deficiency

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18
Q

Defects in Neutrophil killing (3)

A

Most common form is a lack of a NADPH oxidase complex component
This causes an inability to generate ROS and impaired killing of microorganisms
Example is Chronic granulomatous disease

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19
Q

Neutrophil count (3)

A

Absent in severe congenital neutropaenia
Increased in leukocyte adhesion defect during infection
Normal in chronic granulomatous disease

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20
Q

Pus formation (2)

A

None in Severe congenital neutropaenia & Leukocyte adhesion defect
Yes in Chronic granulomatous disease

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21
Q

Leukocyte adhesion markers (2)

A

Normal in Severe congenital neutropaenia & Chronic granulomatous disease
Absent in Leukocyte adhesion defect

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22
Q

Neutrophil ROS/RNS-dependent killing

3

A

Usually absent in Severe congenital neutropaenia
Normal in Leukocyte adhesion defect
Abnormal in Chronic granulomatous disease

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23
Q

Treatment of phagocyte deficiencies (3)

A

Immunoglobulin replacement therapy
Aggressive management of infection - Oral/IV antibiotics, anti-fungal and abscess draining
Definitive therapy - Gene therapy

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24
Q

Transient hypogammaglobulinaemia of infancy

A

Low amount of antibodies when sLgA is decreasing but neonatal production of IgG begins to rise

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25
Severe combined immunodeficiency (SCID) (2)
Failure to produce lymphocytes | Due to cytokine receptors and signalling molecules deficiency, metabolic defects, defective receptor rearrangements
26
Clinical phenotype of SCID (6)
``` Unwell by 3 months of age Persistent diarrhoea Failure to thrive Infections of all types Unusual skin disease Family history of early infant death ```
27
Common form of SCID
X-linked SCID | caused by mutation of IL-2 receptor
28
Treatment of SCID (5)
``` Avoid infections Aggressive treatment of existing infections Antibody replacement Stem cell transplant Gene therapy ```
29
The IL-12 : IFNɣ network (4)
Defense against intracellular mycobacteria Infected macrophages produces IL-12 that stimulates NK TH1 cells to secrete IFNɣ IFNɣ feeds back into macrophages and neutrophils Causes stimulation of TNFα production and NADPH oxidase complex activation
30
Hypersensitivity reaction definition (2)
Immune response resulting in bystander damage to the self | Pathophysiological basis for many chronic diseases, including allergy and autoimmunity
31
Types of hypersensitivity - Gel and Coomb’s classification (4)
Type I: Immediate hypersensitivity Type II: Direct cell effects (cytotoxic or stimulatory) Type III: Immune complex mediated Type IV: Delayed type hypersensitivity
32
Type 1 hypersensitivity definition
IgE-mediated antibody response to external antigen (allergen)
33
Type 1 hypersensitivity conditions (9)
Asthma, diarrhoea, vomiting, urticaria (rashes), angioedema, atopic eczema, conjunctivitis, anaphylaxis, allergic rhinitis
34
Prevalence of Type 1 hypersensitivity
Increasing due to 'hygiene hypothesis'
35
Type 1 hypersensitivity allergens (3)
Examples are dust mites, foods, drugs, latex, insect venom Many are soluble proteins that function as enzymes NOTE: Not all adverse reactions are allergic reactions
36
Spontaneous Mast cell degranulation (3)
Causes physical urticarial Example is Aspirin-induced asthma Affects 20% of asthmatics
37
The 'Hygiene Hypothesis' (2)
Changes in microbial stimuli influences the maturation of immune response Results in increased predisposition to allergic conditions during childhood
38
TH2 effector cells roles (3)
Secrete cytokines activating and proliferating B cells Causes IgE production and secretion Causes mast cell activation, killing of parasites and allergic responses
39
Stages of allergic disease (2)
Sensitisation stage | Allergic stage
40
Stimulation of allergen-specific T cells by allergen-derived peptides in the context of class II MHC molecules results in
Differentiation of CD4+ T cells into effector TH2 cytokine-producing cells
41
TH2 cells produce what chemicals which causes (3)
IL-4, IL-5, IL-13 | Regulates allergic response
42
Regulation of allergic response processes (3)
Regulate synthesis and secretion of IgE by plasma cells Stimulates differentiation and egress of eosinophils from bone marrow into the blood Helps activate mast cells and eosinophils at sites of allergen exposure
43
Pathophysiology of sensitisation stage (4)
Mast cells and eosinophils express receptors for Fc region of IgE antibody on their surface On first encounter with allergen, B cells produce antigen-specific IgE antibody Allergen is then cleared Residual IgE antibodies bind to circulating mast cells via Fce receptors
44
Pathophysiology of allergic stage (4)
Due to re-encounter of allergen Allergen binds to IgE-coated mast cells & disrupts cell membrane Immediate release of vasoactive mediators (histamine, tryptase) Increased expression of pro-inflammatory cytokines and leukotrienes
45
Clinical features of allergic disease (3)
Muscle spasm - Bronchoconstriction and wheezing due to leukotrienes Mucosal inflammation - Increase mucus secretion and oedema Inflammatory cell infiltrate - Yellow sputum due to lymphocyte and eosinophil infiltration into bronchioles
46
Management of IgE mediated allergic disorders (6)
``` Avoidance of allergen Block mast cell activation Prevent effects of mast cell activation Anti-inflammatory agents Management of anaphylaxis Immunotherapy ```
47
Type II hypersensitivity reactions involve
IgM or IgG antibodies to cell surface or extracellular-matrix antigens
48
Adaptive immune responses produces IgG/M antibodies that target (4)
Self antigens - Autoimmune disease Cross reactive antigens - Autoimmune disease Foreign antigens - Blood transfusion reactions Penicillin - Haemolytic anaemia
49
Goodpasture's Syndrome (4)
A type 2 hypersensitivity An autoimmune disease affecting lungs (alveolar haemorrhage) and kidneys (glomerulonephritis) Defined by presence of auto-reactive antibodies to the α3 chain of type IV collagen present in basement membrane Caused by smoking or drugs in a person with genetic susceptibility
50
Goodpasture's Syndrome Treatment (4)
Stop smoking Corticosteriods - Immunosuppresion Plasmapheresis - Remove antibodies Remove offending agents
51
Type 3 hypersensitivity pathophysiology (4)
In presence of excess antigens, antibodies bind forming small immune complexes These are trapped in blood vessels, joints and glomeruli This results in complement activation, opsonisation, infiltration and activation of neutrophils and macrophages Enzymes released from neutrophils causes damage to endothelial cells of basement membrane
52
Clinical example of type 3 hypersensitivity
Acute hypersensitivity pneumonitis
53
Acute hypersensitivity pneumonitis formation (4)
Inhaled antigens deposited in lung Stimulate antibody formation (7-10 days) Antibodies form immune complexes with antigen Results in complement activation, Inflammation and recruitment of leukocytes
54
Acute hypersensitivity pneumonitis examples (3)
Farmers lung, bird fanciers lung, malt workers lung
55
Clinical features of acute hypersensitivity pneumonitis (2)
Wheeze & Breathlessness - Inflammation of terminal bronchioles and alveoli caused by activated phagocytes and complement impairing gas exchange Malaise, pyrexia - Systemic manifestation of inflammatory response
56
Type 3 hypersensitivity management (3)
Avoidance Decrease inflammation - corticosteroids Decrease antibody production - Immunosuppresion
57
Type 4 hypersensitivity disease types and examples (2)
Autoimmune - Type 1 diabetes, rheumatoid arthritis | Non-autoimmune - TB, sarcoidosis
58
Sarcoidosis
Multisystem non-caseating granulomatous disease of unknown aetiology in lungs and skin
59
Management of sarcoidosis (3)
Watchful watching Nonsteroidal anti-inflammatory drugs Systemic corticosteroids - Block T cell and macrophage activation
60
Autoimmunity definition
Presence of immune responses against self-tissue/cells
61
Autoimmunity causes
Generation of autoreactive T and B cells in primary lymphoid tissues that remain alive and activated
62
How does the immune system deal with autoreactive T and B cells (3)
Via tolerance mechanisms Central tolerance - Deletion of self-reactive lymphocytes in primary lymphoid tissues Peripheral tolerance - Inactivation of self-reactive lymphocytes in peripheral tissues that escape central tolerance
63
Presence and function of Regulatory T cells (3)
5-10% of CD4+ T cell population Inactivation of lymphocytes Suppresses hype-reactive or autoreactive T cells via anti-inflammatory cytokine production
64
Pathogenesis of autoimmune diseases
Genetic susceptibility leads to breakdown of immune tolerance to self-antigens
65
Genetic influences in autoimmune disease (2)
Monogenic disorder - Single gene defects causing autoimmune diseases are rare Complex genetic interplay
66
Monogenic disorder example
Immune dysregulation, Polyendocrinopathy, Enteropathy and X-linked inheritance syndrome (IPEX) syndrome
67
IPEX syndrome (4)
Presents in early childhood Characterized by overwhelming systemic autoimmunity Symptoms are severe infections, intractable diarrhoea, eczema, early onset of insulin dependent diabetes mellitus, autoimmune manifestations Treatment is hematopoietic stem cell transplantation, immunosuppressive drugs, parental nutrition
68
IPEX syndrome pathogenesis (3)
X-linked Due to mutation in FOXP3 gene - responsible for development of regulatory T cells It is failure of peripheral tolerance mechanisms
69
HLA/MHC class 1 and 2 genes (3)
Both are highly polymorphic All nucleated cells express several types of Class I molecules - HLA-A, HLA-B and HLA-C Specialized antigen-presenting cells express additional Class II molecules - HLA-DR, HLA-DQ and HLA-DP
70
Why is polymorphism vital in HLA molecules (2)
Maintains diversity of antigen responsiveness at population and individual level via different peptide binding Functionally significant in terms of disease susceptibility and progression
71
Do HLA genes have a high prediction level
No it is limited so not useful in determining disease risk
72
Which type of people have a higher risk of getting autoimmune diseases (4)
Women mostly of childbearing age - Hormone levels People with a family history - Multiple sclerosis People exposed to certain environments - Smoking, infections People of certain races and ethnic backgrounds - Type 1 diabetes more common in white people
73
Environmental influences on autoimmune disease mechanisms (4)
Altered self-antigens Antigen sequestration - Tissues don't communicate with blood or lymph Molecular mimicry - Cross-reactivity between antigens expressed by pathogen and self during infection Super antigens - Toxic shock syndrome
74
Toxic shock syndrome
Reactivates T cells that have been inactivated by regulatory T cells
75
Classification of autoimmune diseases (2)
Clinical - Organ specific or multisystem | Pathological - Gel and Coombs
76
Graves disease (3)
Involves type 2 and 4 hypersensitivity (since target cells are stimulated and not killed) Leading cause of hyperthyroidism Auto-antibodies are generated that bind to the thyroid stimulating hormone receptor (TSHR)
77
Systemic lupus erythematosus (SLE) (3)
Mediated by type 3 hypersensitivity Auto-antibodies targets nuclear antigens Causes skin rashes, nephritis, alveolitis and increased risk of CVD
78
Pathonogenesis of SLE (4)
Increased apoptosis Decreased phagocytosis of apoptotic bodies Decreased solubilisation and clearance of immune-complexes Loss of tolerance - No suppression of auto-reactive B cells increasing production of auto-antibodies
79
Rheumatoid arthritis (3)
Mediated by type 4 hypersensitivity Due to inflammatory reactions initiated by T cells and macrophages Complications are inflammation in lungs and heart
80
Lung issues linked to Rheumatoid arthritis (3)
Scarring - Related to long term inflammation Lung nodules - Carries no sign and symptoms but if nodule ruptures it can cause lung collapse Pleural disease - Pleural inflammation causes build up of fluid in pleural cavity leading to pleural effusion
81
Role of TH17 effector cells (2)
Associated defense against extracellular bacteria and fungi and development of autoimmune diseases Highly pro-inflammatory

Respiratory (8 decks)

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