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Immunology Flashcards

1
Q

What are the main clinical features suggestive of immunodeficiency?

A
  • SPURS infections:
      • Serious (unresponsive to antibiotics)
      • Persistent
      • Unusual
      • Recurrent
  • Weight loss or failure to thrive
  • Severe skin rash (eczema)
  • Chronic diarrhoea
  • Mouth ulceration
  • Unusual autoimmune disease
  • Family history
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2
Q

What conditions are associated with secondary immunodeficiency?

A
  • Premature birth and elderly
  • Infection – HIV, Measles
  • Treatment interventions – Immunosuppressive therapy, anti-cancer agents, corticosteroids
  • Malignancy – Cancer of the immune system – lymphoma, leukaemia, myeloma
  • Biochemical and nutritional disorders – malnutrition, renal insufficiencies, diabetes, mineral deficiencies
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3
Q

What are the cells of the innate immune system?

A
  • Macrophages
  • Neutrophils
  • Mast cells
  • Natural Killer cells
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4
Q

What are the proteins of the innate immune system?

A
  • Complement
  • Acute phase proteins
  • Cytokines
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5
Q

What is the function of the innate immune system?

A
  • Rapid clearance of microorganisms
  • Stimulates the acquired immune response
  • Buys time while the acquired immune system is mobilised
  • Important in the first 72 hours after infection
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6
Q

What are the cells of the acquired immune response?

A

B lymphocytes and T lymphocytes

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7
Q

What are the proteins of the acquired immune response?

A

Antibodies

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8
Q

What are the functions of phagocytes?

A
  • Initiation and amplification of the inflammatory response
  • Scavenging of cellular and infectious debris
  • Ingest and kill microorganisms
  • Produce inflammatory molecules which regulate other components of the immune system
  • Resolution and repair
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9
Q

What is the prognosis of defects of phagocyte production, mobilisation and recruitment?

A

Patients rarely survive the first week if untreated

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10
Q

Kotsmann Syndrome (Congential neutropenia)

A

Rare autosomal recessive disorder where the defect is unknown but is somewhere that affects maturation of monocyte lineage. Present with sever infection early in life. Severe chronic neutropenia (lack of neutrophils).

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11
Q

What is the management of Kotsmann’s syndrome?

A
  • Stem cell transplantation: Defect is in the neutrophil precursor, so strategy is to replace all precursors with allogeneic stem cells and start again
  • Supportive treatment:
    • Prophylactic antibiotics
    • Prophylactic antifungals
    • Mortality 70% in first year of life without definitive treatment
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12
Q

Chronic Granulomatous Disease

A

X-linked disease causing deficiency of the intracellular killing mechanism of phagocytes and production of free radicals for killing

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13
Q

What test would you do for chronic granulomatous disease?

A

NBT (“nitroblue tetrazolium”) test

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14
Q

What are the different clinical features of primary immune deficiency disorders: congenital neutropenia, leukocyte adhesion defect and chronic granulomatous disease?

A

.

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15
Q

When does the acquired immune system activated?

A

After 96hrs

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16
Q

What are the 2 main types of T lymphocytes?

A

CD4+ and CD8+

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17
Q

Reticular dysgenesis

A

Failure of production of:

  • Neutrophils
  • Lymphocytes
  • Monocyte/macrophages
  • Platelets

Essentially no immune system

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18
Q

Severe Combined Immunodeficiency (SCID)

A

Failure to produce lymphocytes - Stem cells become lymphoid progenitors but stop there

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19
Q

What is the clinical presentation of SCID?

A
  • Unwell by 3 months of age
  • Persistent diarrhoea
  • Failure to thrive
  • Infections of all types
  • Unusual skin disease
    • Graft versus host disease
    • Colonisation of infant’s “empty” bone marrow by maternal lymphocytes and will attack the baby from within
  • Family history of early infant death
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20
Q

Why are patients with SCID only affected after 3 months of age?

A

Protected in part by mothers antibody in the first 3 months as babies cannot make its own antibody until 2-3months. So only notice deficiencies when they are relying on their own immune system.

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21
Q

What is the common form and mutation of SCID?

A

X-linkes SCIP occurring due to a mutation of a component of the IL2 receptor

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22
Q

What is the treatment for SCID?

A
  • Prophylactic:
    • Avoid infections
    • Antibiotics and antifungals
    • No vaccines
  • Definitive:
    • Stem cell transplant
      • Gene therapy
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23
Q

DiGeorge Syndrome

A

Development defect of 3rd/4th pharyngeal pouch - no thymus present

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24
Q

What is the clinical features of DiGeorge Syndrome?

A
  • Low set ears abnormally folded ears
  • High forehead
  • Cleft palate
  • Small mouth and jaw
  • Hypocalcaemia
  • Oesophageal atresia
  • T cell lymphopenia
  • Complex congenital heart disease
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25
Q

What are the genetics of DiGeorge Syndrome?

A

Deletion of 22q11. Key gene responsible is probably TBX1 which is critical for embryonic development of pharyngeal pouch

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26
Q

What will lab investigations show with DiGeorge Syndrome?

A
  • Absent or decreased number of T cells
  • Normal or increased B cells
  • Normal NK cells numbers
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27
Q

What is the management of DiGeorge syndrome?

A
  • Correct metabolic/cardiac abnormalities
  • Prophylactic antibiotics
  • Early and aggessive treatment of infection
  • Some patients require immunoglobulin replacement
  • T cell function improves with age
    • If they survive past 5 then they often do well
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28
Q

What are examples of B cell deficiencies - specifically maturation defects?

A
  • Bruton’s X-linked hypogammaglobulinaemia
  • Selective IgA deficiency
  • Common variable immune deficiency
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29
Q

What is the management for B cell deficiencies?

A
  • Aggressive treatment of infection
  • Immunoglobulin replacement
  • Treatment is life-long
  • Stem cell transplantation in some situations
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30
Q

Hypersensitivity reaction

A

Immune response that results in bystander damage to the self, usually exaggerates

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31
Q

Which classification system is used for hypersensitivity reactions?

A

Gell and Coomb’s classification.

  • Type I: Immediate hypersensitivity – Allergic diseases
  • Type II: Direct cell killing
  • Type III: Immune complex mediated
  • Type IV: Delayed type hypersensitivity
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32
Q

Allergy

A

IgE-mediated antibody response to external antigen

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33
Q

Which hypothesis is the main one underlying causes of allergies?

A

Hygiene hypothesis (combined with genetic contribution)

34
Q

What effect do mast cells have in allergies?

A

Orchestrate inflammatory cascade

  • Increase blood flow
  • Contraction of smooth muscle
  • Increase vascular permeability
  • Increase secretions at mucosal surfaces
35
Q

What happens in the initial and subsequent exposures to allergens?

A

Initial:

  • B cells produce antigen specific IgE antibody. These bind to the allergen and clear it, with no allergic reaction.
  • Residual IgE antibodies bind to circulating mast cells at the Fc receptors

Subsequent:

  • allergen binds to IgE- coated mast cells and disrupts cell membrane.
  • Crosslinking occurs where 2 of the IgE bound to the mast cells bind to the allergen, causing the mast cell to de-granulate and release inflammatory factors
36
Q

What effect does subsequent antigen exposure have in the lung and what are their clinical manifestations?

A

Release of histamine and other inflammatory mediators:

  • Muscle spasm causes bronchoconstriction
    • Clinical manifestation: wheeze
  • Mucosal inflammation causes mucosal oedema and increases secretions
    • Clinical manifestation: sputum production
  • Inflammatory cell infiltrate of lymphocytes and eosinophils into bronchioles
    • Clinical manifestation: sputum often yellow
37
Q

Urticaria

A

Hives; Wheals; Nettle rash; Blisters

38
Q

What are non-allergic causes of mast cell degranulation?

A
  • Drugs
    • Morphine and other opiates
    • Aspirin and non-steroidal anti-inflammatories
  • Thyroid disease
  • Idiopathic
  • Physical urticaria in response to pressure or heat
39
Q

Samter’s Triad:

A

Asthma, nasal polyps and aspirin sensitivity

40
Q

What specific investigations can be done for allergies?

A
  • Skin prick tests (gold standard)
  • Quantitate specific IgE to putative allergen (RAST tests)
  • Challenge test - Supervised exposure to the putative antigen
41
Q

What is the management for IgE mediated allergic disorders?

A

1) Avoidance of allergens
2) Block mast cell activation via mast-cell stabilisers eg. sodium chromoglycate
3) Prevent effects of mast cell activation: antihistamines (H1 receptor antagonists) and leukotriene receptor antagonists
4) Anti-inflammatory agents: corticosteroids
5) Anaphylaxis management: self-injectable adrenaline
6) Immunotherapy: controlled exposure to increasing amounts of allergen

42
Q

What kind of reaction is asthma?

A

Type I hypersensitivity (allergic) reaction

43
Q

What are the key features of Type II hypersensitivity reaction: direct killing?

A

Antibody to cell surface antigens. Eg. in haemolytic anaemia:

  • B cells produce IgM or IgG antibody directed against cell membrane protein which can be expressed on red cells.
  • Binding of IgG or IgM antibody to cell surface antigen results in complement activation.
  • Complement then punches holes in the cell surface, causing them to lyse.
44
Q

What produces complement?

A

Liver

45
Q

What is the central component of the complement cascade?

A

C3

46
Q

What are examples of Type II Hypersensitivity reactions?

A
  • Autoimmune haemolytic anaemia
  • Goodpasture’s syndrome
  • Myasthenia gravis
  • Guilian barre syndrome
  • Graves disease
47
Q

What is the management for Type II hypersensitivity reactions?

A

Getting rid of pathogenic antibodies: -Plasmaphoresis and immunosuppression

48
Q

What is involved in Type II hypersensitivity reactions?

A

Reaction involves antibodies and circulating antigens, rather than those sitting on the cells, which come together to form immune complexes. These immune complexes can deposit themselves in small vessels, such as a glomerulus and causes complement activation. There is infiltration of macrophages and neutrophils.

49
Q

What are examples of Type III hypersensitivity reactions?

A

Farmer’s lung, bird fanciers lung or acute hypersensitivity pneumonititis

50
Q

What is the pathophysiology of farmers lung, as an example of Type III hypersensitivity reactions?

A

Inhaled fungal particles (from hay etc) deposited in lung. Stimulate antibody formation which form immune complexes with antigen by binding to the fungal particles. Results in complement activation, Inflammation and recruitment of other cells whenever exposed to the same antigen.

51
Q

What is the management of Type III hypersensitivity reactions?

A
  • Avoidance – just get rid of your pigeons mate, don’t be that guy
  • Decrease inflammation: Corticosteroids
  • Decrease production of antibody: Immunosuppression
52
Q

What is involved in Type IV Delayed Type Hypersensitivity?

A

T cell mediated

  • Initial sensitisation to antigen generates “primed” T cells
  • Subsequent exposure causes activation of previously primed T cells
  • Recruitment of macrophages, other lymphocytes, neutrophils
  • Release of proteolytic enzymes, persistent inflammation……
53
Q

What are examples of Type IV hypersensitivities?

A

Nickel hypersensitivity, Type I diabetes, rheumatoid arthritis, TB, sarcoidosis

54
Q

What is the underlying reaction of sarcoidosis?

A

Type IV Delayed type hypersensitivity

55
Q

Vaccination

A

Deliberate exposure to an antigen in order to induce immunologically mediated resistance to disease through the induction of immunological memory

56
Q

How is immunological memory generated?

A

Long-lived Memory B cells are generated during primary humoral immune responses. These memory B cells can survive in a dormant state for many years after the antigen has been eliminated. They then rapidly re-activate in response to a second encounter with that specific antigen

57
Q

Which antibody is primarily involved in immunological memory and how?

A

IgG - and the point is to have IgG react sooner to exposure so that you dont get the clinical symptoms

58
Q

Active immunity

A

Protection produced by the person’s own immune system (permanent)

59
Q

Passive immunity

A

Protection transferred from another person or animal (temporary)

60
Q

How does an active vaccine work?

A
  • Stimulates immune response to antigen through same pathways as natural infection
  • Generates immunity and immunologic memory similar to natural infection
61
Q

What are methods of generating immunological memory?

A

1) Exposure of an individual to the infectious organism itself - variolation and swine flu parties
2) Exposure to a similar but less virulent pathogen eg. Jenner and vaccinia vaccine- exposure to cowpox prevents smallpox
3) Exposure to inactivated vaccine eg. killed/attenuated vaccines
4) Exposure to a less virulent version of the same pathogen e.g. live attenuated vaccine

62
Q

Variolation

A

The same organism is being administered as the one that can cause disease, but the route of administration is different. Eg. Exposure of an individual to the contents of dried smallpox pustules from infected patient

63
Q

How does exposure to a similar but less virulent pathogen create immunological memory?

A

One disease is being induced to generate cross-reactive immunity against another disease

64
Q

What are inactivated viruses (killed or attenuated vaccines)?

A

Consists of virus particles, bacteria, or other pathogens which are grown in culture and then killed using a method such as heat or formaldehyde. These viruses are grown under controlled conditions and are rendered non-infectious as a means to reduce infectivity of the virus and prevent infection from the vaccine

65
Q

What are the key features of inactivated vaccines?

A
  • Cannot replicate
  • Generally not as effective as live vaccines
  • Immune response primarily antibody based (not T cells)
  • Antibody titer may diminish with time so need to re-immunised regularly
  • Require multiple doses to stimulate immune response
66
Q

Adjuvants

A

Mixture of inflammatory substances required to stimulate immune responses to coadministered peptides, proteins or carbohydrates. To get optimum immune response, often give vaccines mixed with adjuvants.

67
Q

What types of inactivated vaccines are there?

A
  • Whole cell (whole organism used)
  • Fractional (only part of the organism used) - eg. Hep B vaccine is a subunit vaccine
68
Q

Live attenuated vaccines

A
  • Attenuated (weakened) form of the “wild” virus or bacterium
  • Immune response similar to natural infection
  • Organism must replicate to be effective
  • Usually generate immunity with single dose
69
Q

What are the 2 types of polio vaccine?

A

Salk (inactivated) Sabin (live attenuated)

70
Q

What are sources of passive immunity?

A

1) Naturally acquired passive immunity - Tranplacental transfer of antibody
2) Therapeutic passive immunisation eg. pooled immunoglobin

71
Q

What is in the future for vaccines?

A

Cancer and addiction vaccines

72
Q

Which antigen/gene is involved in transplant rejection?

A

Human leukocyte antigen (HLA) - MHC is the overall type of gene

73
Q

What is a main ways in minimising transplant rejection?

A

Minimise the stimulus - minimise the difference between the donor and recipient via HLA matching

74
Q

Which transplants use HLA matching?

A

Stem cell and kidney, not lung, heart or kidney

75
Q

Which kind of reaction is associated with transplant rejection?

A

Type IV hypersensitivity response

76
Q

**What are the different types of transplant rejection?

A

.

77
Q

Hyper acute rejection

A

Rapid destruction of graft within minutes-hours - once the clamp is released in the organ, it appears pink and begins to be perfused – but then becomes black and ischaemic suddenly. Mediated by pre-formed antibodies that react with donor cell.

78
Q

Why would an individual have preformed antibodies against donor cells such as in hyperacute rejection?

A

1) If it is their second transplant
2) If they are different blood types

79
Q

Acute vascular rejection

A

Rejection mediated predominantly by antibody - can happen in the first week

80
Q

What are the risk factors for chronic Allograft Rejection (“chronic rejection”)?

A
  • Immune
    • More prevalent if HLA mismatch
    • Associated with previous acute rejection episodes
  • Non-immune
    • Initial delayed graft function
    • Non compliance with medication
    • Hypertension
    • Hyperlipidaemia
    • Older donor age
    • Recipient infection eg Cytomegalovirus
    • Calcineurin inhibitors (Ciclosporin, Tacrolimus)
81
Q
A

RW Respiratory (17 decks)

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