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MK - (LUSUMA) Immune System > S1) Hypersensitivity > Flashcards

S1) Hypersensitivity Flashcards

1
Q

Define the term hypersensitivity

A

Hypersensitivity describes the antigen-specific immune responses that are either inappropriate or excessive and result in harm to host

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2
Q

What is the main similarity between hypersensitive immune response and the normal immune response?

A

The mechanisms underlying hypersensitive immune responses are the same as those employed by the host to fight infections

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3
Q

What are the two types of triggers for hypersensitivity?

A
  • Hypersensitivity to exogenous antigens
  • Hypersensitivity to intrinsic antigens
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4
Q

Identify the types of exogenous antigens which trigger the immune system

A
  • Non-infectious substance (innocuous)
  • Infectious microbes
  • Drugs e.g. penicillin
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5
Q

Identify the types of intrinsic antigens which trigger the immune system

A
  • Infectious microbes (mimicry)
  • Self antigens (auto-immunity)
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6
Q

Identify the type if hypersensitivity reactions

A
  • Type I / immediate (Allergy)
  • Type II / antiBody mediated
  • Type III / immune Complexes mediated
  • Type IV / cell mediated (Delayed)
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7
Q

What are the two phases that occur in hypersensitvity reactions

A
  • Sensitisation phase
  • Effector phase
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8
Q

What is the sensitisation phase?

A
  • First encounter with the antigen.
  • Activation of APCs and memory effector cells.
  • A previously exposed individual to the antigen is said to be “sensitized”
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9
Q

What is the effector phase?

A

Pathologic reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity

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10
Q

Which antigens are involved in Type I hypersensitivity?

A

Environmental non infectious antigens

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11
Q

How long does it take for type II hypersensitivity to be triggered?

Which antibodies are involved?

A
  • Usually develops within 5-12 hr
  • Involves IgG or IgM antibodies
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12
Q

Identify the targets of type II hypersensitivity reactions

A

Targets cell bound antigens:

  • Exogenous - Blood group antigens, Rhesus D antigens
  • Endogenous - self antigens
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13
Q

Identify the outcomes of type II hypersensitivity reactions

A

Induces different outcomes:

  • Tissue/cell damage
  • Physiological change
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14
Q

Which two mechanisms lead to tissue/cell damage in type II hypersensitivity?

What are examples of clinical diseases for each of these mechanisms of type II hypersensitivity?

A
  • Complement activation (cell lysis, neutrophil recruitment activation, opsonisation) -> examples:
    1. Haemolytic disease of the newborn (antigen = Rhesus D)
    2. Transfusion reactions (antigen = ABO system)
  • Antibody-dependent cell cytotoxicity (Natural Killer cells)
    1. Autoimmune haemolytic anaemia
    2. Immune thrombocytopenic purpura
    3. Goodpasture’s syndrome
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15
Q

Briefly, describe the processes involved in complement activation

A
  • Cell lysis (MAC - Membrane attack complex)
  • Neutrophil recruitment/activation (C3a/C5a) 
  • Opsonisation (C3b)
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16
Q

Haemolytic transfusion reaction is an example of disease caused by type II hypersensitivity. What happens in this condition?

A
  • Incompatibility in the ABO group or rhesus D antigens
  • Donor RBC destroyed by recipient’s immune system
  • RBC lysis induced by type II hypersensitivity (IgM)
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17
Q

What are the outcomes of the haemolytic transfusion reaction

A
  • Shock
  • Kidney failure
  • Circulatory collapse
  • Death
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18
Q

Haemolytic disease of the newborn (HDN) is another example of disease caused by type II hypersensitivity. What happens?

A
  • Involves Rhesus D antigen
  • Mismatch between mother(Rh-) and child (Rh+)
  • Rh+ antigens from the fetus enter the mother’s blood during delivery
  • Anti-Rh Antibodies are produced by mother against Rh+ antigen
  • After 2nd pregnancy, IgG antibodies cross placenta and cause HDN - damage the red blood cells of her second Rh+ fetus
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19
Q

Which three mechanisms lead to physiological damage in type II hypersensitivity?

Give examples of resulting diseases for each mechanism

A
  • Receptor stimulation
  • Receptor blockade
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20
Q

Identify and describe two conditions resulting in induced physiological change in type II hypersensitivity?

A
  • Graves’ disease: increased thyroid activity, antigen is TSH receptor
  • Myasthenia gravis: impaired neuromuscular signalling, antigen is ACh receptor
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21
Q

Identify and describe 4 therapeutic approaches used for tissue/cell damage induced by type II hypersensitivity

A
  • Immune suppression for complement activation
  • Plasmapheresis for circulating antibodies and inflammatory mediators
  • Splenectomy for opsonisation/Phagocytosis
  • Intravenous immunoglobulin (IVIG) for IgG degradation
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22
Q

Identify and describe 2 therapeutic approaches used for physiological damage induced by type II hypersensitivity

A
  • Correct metabolism: receptor stimulation -> therefore give anti-thyroid drugs in Graves’ disease, or thyroidectomy
  • Replacement therapy: receptor blockade. Give pyridostigmine in Myasthenia gravis, or Vit B12 in pernicious anaemia
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23
Q

How long does it take for type III hypersensitivity to be triggered?

Which antibodies are involved?

A
  • Usually develops within 3-8hr
  • Involves immune complexes between IgG or IgM antibodies
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24
Q

What are the targets of type III hypersensitivity?

A

Targets soluble antigens:

  • Foreign (Infection)
  • Endogenous (self antigens)
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25
Q

What causes tissue damage in type III hypersensitivity?

A

Tissue damage caused by immune complex deposition

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26
Q

What are the 4 key factors in type III hypersensitivity pathogenesis?

A
  • Complex size
  • Host response
  • Local tissue factors
  • Persistence of antigen
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27
Q

Describe the role of complex size in immune complex pathogenesis

A

Complex size:

  • Small and large size immune complexes cleared
  • Intermediate size immune complexes
28
Q

Describe which host responses in immune complex pathogenesis

A

Host response:

  • Low affinity antibody
  • Complement deficiency
29
Q

Identify which local tissue factors are involved in immune complex pathogenesis

A

Local tissue factors:

  • Haemodynamic factors
  • Physicochemical factors
30
Q

Rheumatoid arthritis is an example of a disease caused by type III hypersensitivity. What happens in this disease?

A
  • Antigen = Anti-Rheumatoid factor IgG (75%)
  • Involves episodes of inflammation/remission
31
Q

Glomerulonephritis is an example of a disease caused by type III hypersensitivity. What is this disease?

A
  • Infectious disease
  • Bacterial endocarditis
  • Hepatitis B infection
32
Q

Systemic lupus erythematosus is an example of a disease caused by type III hypersensitivity. What happens in this disease?

A
  • Antigens (there are two for lupus) = Ds-DNA- most specific Ab, positive ANA - most sensitive Ab for lupus
  • Most prevalent immune complexes disease
  • Affects mainly females
33
Q

What is the immune mechanism involved in type III hypersensitivity?

A
  • Intermediate-sized IC’s deposited in tissue
  • Complement activated
  • Neutrophil chemotaxis, adherence then degranulation
34
Q

How long does it take for type IV hypersensitivity to be triggered?

Which antibodies are involved?

A
  • Usually develops within 24-72hr
  • Involves lymphocytes and macrophages
35
Q

Identify the three different subtypes of type IV hypersensitivity

A
  • Contact hypersensitivity
  • Tuberculin hypersensitivity
  • Granulomatous hypersensitivity
36
Q

State the duration of contact hypersensitivity and the reactions involved

A

Contact hypersensitivity:

  • 48-72 hr
  • Epidermal reaction (eczematous rash)
37
Q

State the duration of tuberculin hypersensitivity and the reaction involved

A

Tuberculin hypersensitivity:

  • 48-72hr
  • Dermal reaction (induration and swelling)
38
Q

State the duration of granulomatous hypersensitivity and the processes involved

A

Granulomatous hypersensitivity:

  • 21-48 days
  • Persistence of the antigens (tissue damage)
39
Q

Identify 4 diseases caused by type IV granulomatous hypersensitivity (exogenous antigens)

A
  • Tuberculosis
  • Leprosy (tuberculoid)
  • Schistosomiasis
  • Sarcoidosis
40
Q

Identify 3 substances which trigger type IV contact hypersensitivity (exogenous antigens)

A
  • Nickel
  • Poison ivy
  • Organic chemicals
41
Q

Identify three diseases caused by Type IV hypersensitivity to endogenous antigens

A
  • Insulin-dependent diabetes mellitus
  • Hashimoto’s thyroiditis
42
Q

Identify types of anti-inflammatory drugs used in type III and IV hypersensitivity reactions

A
  • Non-steroidals (NSAIDs)
  • Corticosteroids (oral prednisolone)
  • Second drugs as steroid-sparing agents (<10 mg oral steroid)

Anti-proliferative: Azathioprine, mycophenolate mofetil
Cytotoxic drugs: Cyclophosphamide
Anti-metabolite drugs: Methotrexate
Anti-T cell drugs: Cyclosporin

43
Q

Identify types of monoclonal antibodies used in type III and IV hypersensitivity reactions

A
  • B Cells and T cells
  • Cytokine network
  • APCs
44
Q

Type I hypersensitivity is called allergy. Describe the local and system reactions of this form.

A

Immediate reaction (<30min):

  • Local reaction - ingested or inhaled allergen
  • Systemic reaction - insect sting or IV administration
45
Q

What are the three types of exposure involved in type I hypersensitivity?

A
  • Seasonal exposure
  • Perennial exposure
  • Accidental exposure
46
Q

Which allergens are involved in seasonal exposure

A

Tree and grass pollens

47
Q

Which allergens are involved in accidental exposure?

A
  • Insect venom
  • Medicines eg. penicillin
  • Chemicals eg. latex
  • Foods e.g. milk, peanuts, nuts
48
Q

Which allergens are involved in perennial exposure?

A
  • House dust mite
  • Animal dander (cats and dogs)
  • Fungal spores
49
Q

Identify and describe the 2 immune mechanisms involved in type I hypersensitivity?

A
  • Abnormal adaptive immune response against the allergens: TH2 response, IgE production
  • Mast cell activation: sensitised individuals
50
Q

Compare and contrast developed and developing lifestyles to explain why more people in developed countries have allergies

A
  • Developed: good sanitation, high antibiotic use, low orofecal burden, low helminth burden, stable intestinal microflora
  • Developing: poor sanitation, low antibiotic use, high orofecal burden, high helminth burden, variable intestinal microflora
51
Q

What are the two most notable factors associated with developed countries to explain the high incidence of allergies?

A
  • Reduced infectious burden: animals, pets and microbes
  • Microbial dysbiosis: alteration of the symbiotic relationships with parasites and bacteria
52
Q

Define dysbiosis

A

Dysbiosis: compositional and functional alterations of microbiome

53
Q

Define microbiome

A

Microbiome: the complete genetic content of all the microorganisms that typically inhabit in the body, such as the skin or the GI tract

54
Q

Describe the strategic location of mast cells

A
  • Most mucosal and epithelial tissues - GI tract, skin, respiratory epithelium
  • Connective tissue (surrounding blood cells)
55
Q

Identify 4 mast cell mediators

A
  • Tryptase
  • Histamine
  • Leukotrienes C4, D4, E4
  • Platelet-activating factor
56
Q

Describe the biological effects of tryptase

A

Remodels connective tissue matrix

57
Q

Describe the biological effects of histamine and leukotrienes

A
  • Increase vascular permeability
  • Cause smooth muscle contraction
58
Q

Describe the biological effects of platelet-activating factor

A
  • Attracts leukocytes
  • Activates neutrophils, eosinophils and platelets
59
Q

Outline the immune mechanism of an allergic reaction

A
  • Allergen 1st exposure: TH2 response
  • Allergen 2nd exposure: IgE cross-linking
  • Mast cell degranulation
  • Release of histamine and leukotriene: vasodilation and increased vascular permeability
60
Q

Urticaria is a skin manifestation of allergic reactions. How is it caused?

A
  • Mast cell activation within the epidermis
  • Mediators: histamine and leukotrienes/cytokines
61
Q

What is the skin manifestation if the allergic exposure is chronic or prolonged?

A
  • Atopic dermatitis
  • Eczema
62
Q

Angioedema is a facial manifestation of allergic reactions. How is it caused?

A
  • Mast cell activation in the deep dermis
  • Mediators = histamine and bradykinin
63
Q

Anaphylaxis results from the systemic activation of mast cells. Identify some manifestations of this

A
  • Hypotension
  • Cardiovascular collapse
  • Generalized urticaria
  • Angioedema
  • Breathing problems
64
Q

Identify forms of therapy for the mast cell activation occurringin type I hypersensitivity?

A
  • Anti-histamine
  • Leukotriene receptor antagonists 
  • Corticosteroids
65
Q

Identify forms of therapy for the abnormal adaptive immune response seen in type I hypersensitivity

A
  • Allergen desensitization (oral immunotherapy)

- Anti-IgE monoclonal antibody

MK - (LUSUMA) Immune System (4 decks)

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