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Respiratory > Immunology > Flashcards

Immunology Flashcards

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
Q

Severe combined immunodeficiency (SCID) (2)

A

Failure to produce lymphocytes

Due to cytokine receptors and signalling molecules deficiency, metabolic defects, defective receptor rearrangements

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26
Q

Clinical phenotype of SCID (6)

A 
Unwell by 3 months of age
Persistent diarrhoea
Failure to thrive
Infections of all types
Unusual skin disease
Family history of early infant death
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27
Q

Common form of SCID

A

X-linked SCID

caused by mutation of IL-2 receptor

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28
Q

Treatment of SCID (5)

A 
Avoid infections
Aggressive treatment of existing infections
Antibody replacement
Stem cell transplant
Gene therapy
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29
Q

The IL-12 : IFNɣ network (4)

A

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

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30
Q

Hypersensitivity reaction definition (2)

A

Immune response resulting in bystander damage to the self

Pathophysiological basis for many chronic diseases, including allergy and autoimmunity

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31
Q

Types of hypersensitivity - Gel and Coomb’s classification (4)

A

Type I: Immediate hypersensitivity
Type II: Direct cell effects (cytotoxic or stimulatory)
Type III: Immune complex mediated
Type IV: Delayed type hypersensitivity

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32
Q

Type 1 hypersensitivity definition

A

IgE-mediated antibody response to external antigen (allergen)

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33
Q

Type 1 hypersensitivity conditions (9)

A

Asthma, diarrhoea, vomiting, urticaria (rashes), angioedema, atopic eczema, conjunctivitis, anaphylaxis, allergic rhinitis

34
Q

Prevalence of Type 1 hypersensitivity

A

Increasing due to ‘hygiene hypothesis’

35
Q

Type 1 hypersensitivity allergens (3)

A

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
Q

Spontaneous Mast cell degranulation (3)

A

Causes physical urticarial
Example is Aspirin-induced asthma
Affects 20% of asthmatics

37
Q

The ‘Hygiene Hypothesis’ (2)

A

Changes in microbial stimuli influences the maturation of immune response
Results in increased predisposition to allergic conditions during childhood

38
Q

TH2 effector cells roles (3)

A

Secrete cytokines activating and proliferating B cells
Causes IgE production and secretion
Causes mast cell activation, killing of parasites and allergic responses

39
Q

Stages of allergic disease (2)

A

Sensitisation stage

Allergic stage

40
Q

Stimulation of allergen-specific T cells by allergen-derived peptides in the context of class II MHC molecules results in

A

Differentiation of CD4+T cells into effector TH2 cytokine-producing cells

41
Q

TH2 cells produce what chemicals which causes (3)

A

IL-4, IL-5, IL-13

Regulates allergic response

42
Q

Regulation of allergic response processes (3)

A

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
Q

Pathophysiology of sensitisation stage (4)

A

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
Q

Pathophysiology of allergic stage (4)

A

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
Q

Clinical features of allergic disease (3)

A

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
Q

Management of IgE mediated allergic disorders (6)

A 
Avoidance of allergen
Block mast cell activation
Prevent effects of mast cell activation
Anti-inflammatory agents
Management of anaphylaxis
Immunotherapy
47
Q

Type II hypersensitivity reactions involve

A

IgM or IgG antibodies to cell surface or extracellular-matrix antigens

48
Q

Adaptive immune responses produces IgG/M antibodies that target (4)

A

Self antigens - Autoimmune disease
Cross reactive antigens - Autoimmune disease
Foreign antigens - Blood transfusion reactions
Penicillin - Haemolytic anaemia

49
Q

Goodpasture’s Syndrome (4)

A

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
Q

Goodpasture’s Syndrome Treatment (4)

A

Stop smoking
Corticosteriods - Immunosuppresion
Plasmapheresis - Remove antibodies
Remove offending agents

51
Q

Type 3 hypersensitivity pathophysiology (4)

A

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
Q

Clinical example of type 3 hypersensitivity

A

Acute hypersensitivity pneumonitis

53
Q

Acute hypersensitivity pneumonitis formation (4)

A

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
Q

Acute hypersensitivity pneumonitis examples (3)

A

Farmers lung, bird fanciers lung, malt workers lung

55
Q

Clinical features of acute hypersensitivity pneumonitis (2)

A

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
Q

Type 3 hypersensitivity management (3)

A

Avoidance
Decrease inflammation - corticosteroids
Decrease antibody production - Immunosuppresion

57
Q

Type 4 hypersensitivity disease types and examples (2)

A

Autoimmune - Type 1 diabetes, rheumatoid arthritis

Non-autoimmune - TB, sarcoidosis

58
Q

Sarcoidosis

A

Multisystem non-caseating granulomatous disease of unknown aetiology in lungs and skin

59
Q

Management of sarcoidosis (3)

A

Watchful watching
Nonsteroidal anti-inflammatory drugs
Systemic corticosteroids - Block T cell and macrophage activation

60
Q

Autoimmunity definition

A

Presence of immune responses against self-tissue/cells

61
Q

Autoimmunity causes

A

Generation of autoreactive T and B cells in primary lymphoid tissues that remain alive and activated

62
Q

How does the immune system deal with autoreactive T and B cells (3)

A

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
Q

Presence and function of Regulatory T cells (3)

A

5-10% of CD4+ T cell population
Inactivation of lymphocytes
Suppresses hype-reactive or autoreactive T cells via anti-inflammatory cytokine production

64
Q

Pathogenesis of autoimmune diseases

A

Genetic susceptibility leads to breakdown of immune tolerance to self-antigens

65
Q

Genetic influences in autoimmune disease (2)

A

Monogenic disorder - Single gene defects causing autoimmune diseases are rare
Complex genetic interplay

66
Q

Monogenic disorder example

A

Immune dysregulation, Polyendocrinopathy, Enteropathy and X-linked inheritance syndrome (IPEX) syndrome

67
Q

IPEX syndrome (4)

A

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
Q

IPEX syndrome pathogenesis (3)

A

X-linked
Due to mutation in FOXP3 gene - responsible for development of regulatory T cells
It is failure of peripheral tolerance mechanisms

69
Q

HLA/MHC class 1 and 2 genes (3)

A

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
Q

Why is polymorphism vital in HLA molecules (2)

A

Maintains diversity of antigen responsiveness at population and individual level via different peptide binding
Functionally significant in terms of disease susceptibility and progression

71
Q

Do HLA genes have a high prediction level

A

No it is limited so not useful in determining disease risk

72
Q

Which type of people have a higher risk of getting autoimmune diseases (4)

A

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
Q

Environmental influences on autoimmune disease mechanisms (4)

A

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
Q

Toxic shock syndrome

A

Reactivates T cells that have been inactivated by regulatory T cells

75
Q

Classification of autoimmune diseases (2)

A

Clinical - Organ specific or multisystem

Pathological - Gel and Coombs

76
Q

Graves disease (3)

A

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
Q

Systemic lupus erythematosus (SLE) (3)

A

Mediated by type 3 hypersensitivity
Auto-antibodies targets nuclear antigens
Causes skin rashes, nephritis, alveolitis and increased risk of CVD

78
Q

Pathonogenesis of SLE (4)

A

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
Q

Rheumatoid arthritis (3)

A

Mediated by type 4 hypersensitivity
Due to inflammatory reactions initiated by T cells and macrophages
Complications are inflammation in lungs and heart

80
Q

Lung issues linked to Rheumatoid arthritis (3)

A

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
Q

Role of TH17 effector cells (2)

A

Associated defense against extracellular bacteria and fungi and development of autoimmune diseases
Highly pro-inflammatory

Respiratory (8 decks)

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