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3. Week 2 - General Pathological Mechanisms > Disorders of the immune system > Flashcards

Disorders of the immune system Flashcards

1
Q

What is the Coombes and Gell classification of type I hypersensitivity?

A
  • immediate, atopic

- IgE mediated

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2
Q

What is the Coombes and Gell classification of type II hypersensitivity?

A
  • Cytotoxic, antibody-dependent

- IgM or IgG bound to cell/matrix Ag

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3
Q

What is the Coombes and Gell classification of type III hypersensitivity?

A
  • Immune complex

- IgM or IgG bound to soluble Ag

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4
Q

What is the Coombes and Gell classification of type IV hypersensitivity?

A
  • Cell-mediated

- T cells (CD4 and CD8)

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5
Q

What is the Coombes and Gell classification of type V hypersensitivity?

A

Likely a subclass of type II

  • Receptor-mediated
  • IgM or IgG bound to receptors
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6
Q

What are the specific characteristics of type I hypersensitivity

A
  • response to challenge occurs immediately
  • tends to increase in severity with repeated challenge
  • predominantly mediated by IgE bound to mast cells
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7
Q

What is the process of mast cell activation?

A
  1. sensitisation
  2. mast cells primed with IgE
  3. re-exposure to antigen
  4. antigen binds to IgE associated with mast cells
  5. mast cells degranulate
  6. pro-inflammatory process stimulates and amplifies future responses
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8
Q

What substances are released when mast cells degranulate?

A
  • toxins (i.e. histamine)
  • tryptase
  • pro-inflammatory cytokines
  • chemokines
  • prostaglandins
  • leukotrienes
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9
Q

What is the result of histamine release?

A
  • in the skin: swelling and itching

- in the respiratory tract: bronchospasm and wheeze

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10
Q

What is the result of tryptase release?

A
  • a type of proteinase

- degradation

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11
Q

Which substances released from mast cells encourage the immune system to mount an inflammatory response?

A
  • pro inflammatory cytokines
  • chemokines
  • prostaglandins
  • leukotrienes
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12
Q

What are the tissue effects of an early phase type 1 hypersensitivity reaction?

A
  • occurs within minutes of exposure
  • largely as a result of histamine and prostaglandin exposure

> smooth muscle constriction
increased vascular permeability

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13
Q

What are the tissue effects of an late phase type 1 hypersensitivity reaction?

A
  • occurs over hours to days after exposure
  • principally mediated through recruitment of T cells and other immune cells to site

> sustained smooth muscle contraction/hypertrophy
tissue remodeling

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14
Q

What is anaphylaxis?

A

Severe, systemic type 1 hypersensitivity reaction

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15
Q

What causes anaphylaxis?

A

widespread mast cell degranulation caused by systemic exposure to antigen

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16
Q

What is the principle danger in anaphylaxis?

A

vascular permeability causing:

  • soft tissue swelling threatening airway
  • loss of circulatory volume causing shock
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17
Q

Give examples of type 1 hypersensitivity

A
  • asthma (although not true type 1)
  • penicillin allergy
  • hay-fever
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18
Q

What is the cause of type II hypersensitivity

A

caused by binding of antibodies directed against human cells

19
Q

What are the characteristics of type II hypersensitivity?

A
  • delayed - generally over days, weeks or months
  • uncommon cause of drug allergy
  • common cause of auto-immune disease
20
Q

Name a type II hypersensitivity drug allergy

A

Drug associated haemolysis

  • goes on to develop anaemia
  • pretty rare
21
Q

Name a type II hypersensitivity autoimmune disease

A

bullous pemphigoid

  • characterised by development of deep blisters on the skin
  • antibody found between the epridermis-dermis junction
22
Q

What is the process of type II hypersensitivity reaction

A
  1. sensitisation
  2. opsonisation of cells
  3. cytotoxicity
    - complement activation
    - inflammation
    - tissue destruction
23
Q

What is the process of type V hypersensitivity?

A
  1. sensitisation
  2. opsonisation of cells
  3. cytotoxicity
    - complement activation
    - inflammation
    - tissue destruction
  4. direct biological activation with antigen
    - Either through receptor activation (common) or receptor blocking (occasional)
24
Q

What is a common autoimmune example of type V hypersensitivity?

A

Graves’ disease

25
Q

What causes type III hypersensitivity?

A

Mediated by immune complexes bound to soluble antigen

- aggregates get stuck in small vessels, where they activate complement and cause inflammation around them

26
Q

Name examples of type III hypersensitivity reactions

A
  • SLE
  • RA
  • Post-strep glomerulonephritis
27
Q

Which hypersensitivity reaction presents delayed from time of exposure?

A
  • type II
  • type III
  • type IV
  • type V
28
Q

Name an example of type IV hypersensitivity reaction

A

contact dermatitis

29
Q

What causes type IV hypersensitivity reaction?

A
  • mediated by the action of lymphocytes infiltrating the area

N.B by definition, is delayed

30
Q

How may nickel cause a type IV hypersensitivity reaction?

A

Nickel is too basic in structure to trigger a response.

It binds to human proteins, altering the shape. This is what is recognized by the immune system.

31
Q

What is autoimmune disease?

A

harmful inflammatory response directed against ‘self’ tissue by the adaptive immune response

  • organ specific
  • systemic
32
Q

What hypersensitivity reaction is seen in T1DM?

A

selective, autoimmune destruction of the pancreatic beta cells
- often mix of type II and type IV

33
Q

What hypersensitivity reaction is seen in myasthenia gravis?

A

Classic example of type II(V) hypersensitivity

34
Q

What causes myasthenia gravis?

A

IgG against the acetylcholine receptor

- antibody blocks the receptor, preventing signal transduction

35
Q

What are the systemic effects of RA?

A
  • pulmonary nodules and fibrosis
  • pericarditis and valvular inflammation
  • small vessel vasculitis
  • soft tissue nodules
  • skin inflammation
  • weight loss, anaemia
36
Q

Describe rheumatoid factor in relation to RA

A
  • IgM and IgA directed against the Fc portion of IgG forming a large immune complex
  • high conc. in synovial fluid
  • also in other tissues
  • not specific to RA
37
Q

Describe the pathophysiology of RA

A
  • Inflammation leads to the release of PAD from inflammatory cells
  • alters proteins to citrulline
  • allows immune system to recognise as foreign
  • anti-citrullinated protein antibodies found in RA
38
Q

Describe the immune response in RA

A
  • loss of tolerance
  • activation of macrophages and lymphocytes
  • TNF alpha and IL1 produced
  • amplification of inflammatory cascade occurs
    etc.
39
Q

What are the main treatment methods for autoimmune disorders?

A
  • steroids
  • inhibitors of metabolism
  • inhibitors of T cell function
  • biological therapies
40
Q

What is the benefit of biological therapies in treating autoimmune disorders?

A

Neutralises a specific part of the immune system without significant side effects of other drugs

41
Q

What is molecular mimicry?

A
  • bacteria possesses an antigen that looks very similar to the human antigen
42
Q

Name an example of molecular mimicry

A

Rheumatic fever

  • caused by strep. which is similar to heart tissue
  • cellular infiltrate into the myocardium and you get inflammation of the heart valves, called a rheumatic valve
43
Q

What modifiable factors are linked with RA?

A

smoking - generates a lot of citrullinated proteins

3. Week 2 - General Pathological Mechanisms (12 decks)

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