(LUSUMA) Immune System > S1) Hypersensitivity > Flashcards

S1) Hypersensitivity Flashcards

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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?

A
  • Complement activation 
  • Ab-dependent cell cytotoxicity (ADCC, IgG)
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15
Q

Briefly, describe the processes involved in complement activation

A
  • Cell lysis (MAC)
  • 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+) and thus antibodies are produced against Rh+ antigen
  • After 2nd pregnancy, IgG antibodies cross placenta and cause HDN
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19
Q

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

A
  • Receptor stimulation
  • Receptor blockade
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20
Q

Identify and describe two conditions resulting for 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
  • Replacement therapy: receptor blockade
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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
What causes tissue damage in type III hypersensitivity?
Tissue damage caused by **immune complex deposition**
26
What are the 3 key factors in type III hypersensitivity pathogenesis?
- Complex size - Host response - Local tissue factors
27
Describe the role of complex size in immune complex pathogenesis
Complex size: - Small and large size immune complexes cleared - Intermediate size immune complexes
28
Describe which host responses in immune complex pathogenesis
Host response: - Low affinity antibody - Complement deficiency
29
Identify which local tissue factors are involved in immune complex pathogenesis
Local tissue factors: - Haemodynamic factors - Physicochemical factors
30
Rheumatoid arthritis is an example of a disease caused by type III hypersensitivity. What happens in this disease?
- Antigen = Anti-Rheumatoid factor IgG (75%) - Involves episodes of inflammation/remission
31
Glomerulonephritis is an example of a disease caused by type III hypersensitivity. What is this disease?
- Infectious disease - Bacterial endocarditis - Hepatitis B infection
32
Systemic lupus erythematosus is an example of a disease caused by type III hypersensitivity. What happens in this disease?
- Antigen = Ds-DNA - Most prevalent immune complexes disease - Affects mainly females
33
What is the immune mechanism involved in type III hypersensitivity?
- Intermediate-sized IC's deposited in tissue - Complement activated - Neutrophil chemotaxis, adherence then degranulation
34
How long does it take for type IV hypersensitivity to be triggered? Which antibodies are involved?
- Usually develops within 24-72hr - Involves lymphocytes and macrophages
35
Identify the three different subtypes of type IV hypersensitivity
- Contact hypersensitivity - Tuberculin hypersensitivity - Granulomatous hypersensitivity
36
State the duration of contact hypersensitivity and the reactions involved
**Contact hypersensitivity:** - 48-72 hr - Epidermal reaction (eczematous rash)
37
State the duration of tuberculin hypersensitivity and the reaction involved
**Tuberculin hypersensitivity:** - 48-72hr - Dermal reaction (induration and swelling)
38
State the duration of granulomatous hypersensitivity and the processes involved
**Granulomatous hypersensitivity:** - 21-48 days - Persistence of the antigens (tissue damage)
39
Identify 4 diseases caused by type IV granulomatous hypersensitivity (exogenous antigens)
- Tuberculosis - Leprosy (tuberculoid) - Schistosomiasis - Sarcoidosis
40
Identify 3 substances which trigger type IV contact hypersensitivity (exogenous antigens)
- Nickel - Poison ivy - Organic chemicals
41
Identify three diseases caused by Type IV hypersensitivity to endogenous antigens
- Insulin-dependent diabetes mellitus - Hashimoto’s thyroiditis - Rheumatoid arthritis
42
Identify types of anti-inflammatory drugs used in type III and IV hypersensitivity reactions
- Non-steroidals (NSAIDs) - Corticosteroids (oral prednisolone) - Second drugs as steroid-sparing agents (\<10 mg oral steroid)
43
Identify types of monoclonal antibodies used in type III and IV hypersensitivity reactions
- B Cells and T cells - Cytokine network - APCs
44
Type I hypersensitivity is called allergy. Describe the local and system reactions of this form.
Immediate reaction (\<30min): - **Local reaction** - ingested or inhaled allergen - **Systemic reaction** - insect sting or IV administration
45
What are the three types of exposure involved in type I hypersensitivity?
- Seasonal exposure - Perennial exposure - Accidental exposure
46
Which allergens are involved in seasonal exposure
Tree and grass pollens
47
Which allergens are involved in accidental exposure?
- Insect venom - Medicines *eg. penicillin* - Chemicals *eg. latex* - Foods *e.g. milk, peanuts, nuts*
48
Which allergens are involved in perennial exposure?
- House dust mite - Animal dander (cats and dogs) - Fungal spores
49
Identify and describe the 2 immune mechanisms involved in type I hypersensitivity?
- **Abnormal adaptive immune response against the allergens:** TH2 response, IgE production - **Mast cell activation:** sensitised individuals
50
Compare and contrast developed and developing lifestyles to explain why more people in developed countries have allergies
- **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
What are the two most notable factors associated with developed countries to explain the high incidence of allergies?
- **Reduced infectious burden:** animals, pets and microbes - **Microbial dysbiosis:** alteration of the symbiotic relationships with parasites and bacteria
52
Define dysbiosis
**Dysbiosis**: compositional and functional alterations of microbiome
53
Define microbiome
**Microbiome**: the complete genetic content of all the microorganisms that typically inhabit in the body, such as the skin or the GI tract
54
Describe the strategic location of mast cells
- Most mucosal and epithelial tissues - GI tract, skin, respiratory epithelium - Connective tissue (surrounding blood cells)
55
Identify 4 mast cell mediators
- Tryptase - Histamine - Leukotrienes C4, D4, E4 - Platelet-activating factor
56
Describe the biological effects of tryptase
Remodels connective tissue matrix
57
Describe the biological effects of histamine and leukotrienes
- Increase vascular permeability - Cause smooth muscle contraction
58
Describe the biological effects of platelet-activating factor
- Attracts leukocytes - Activates neutrophils, eosinophils and platelets
59
Outline the immune mechanism of an allergic reaction
- **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
Urticaria is a skin manifestation of allergic reactions. How is it caused?
- Mast cell activation within the epidermis - Mediators: histamine and leukotrienes/cytokines
61
What is the skin manifestation if the allergic exposure is chronic or prolonged?
- Atopic dermatitis - Eczema
62
Angioedema is a facial manifestation of allergic reactions. How is it caused?
- Mast cell activation in the deep dermis - Mediators = histamine and bradykinin
63
Anaphylaxis results from the systemic activation of mast cells. Identify some manifestations of this
- Hypotension - Cardiovascular collapse - Generalized urticaria - Angioedema - Breathing problems
64
Identify forms of therapy for the mast cell activation occurringin type I hypersensitivity?
- Anti-histamine - Leukotriene receptor antagonists  - Corticosteroids
65
Identify forms of therapy for the abnormal adaptive immune response seen in type I hypersensitivity
- Allergen desensitization (oral immunotherapy) - Anti-IgE monoclonal antibody
(LUSUMA) Immune System
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