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Loco > Skin inflammation > Flashcards

Skin inflammation Flashcards

1
Q

What are the cardinal signs of acute inflammation? What are the causes of these signs?

A 
Heat
Redness
- both due to increased blood flow and vessels dilatation 
Swelling 
- due to accumulation of fluid 
Pain
- due to pressure on nerve endings 
Loss of function
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2
Q

Which cytokines + tcell mediate neutrophilic inflammation/are microbicidal? What organism(s) do they fight against?

A

IL-6, TGF-beta, stimulate IL-23, stimulates TH17

Fight against extracellular bacteria and fungi

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3
Q

Which cytokines + tcell mediate monocytic inflammation/intracellular killing? What organism(s) do they fight against?

A

IFN-gamma, stimulates IL-12, stimulates TH1

Fight against intracellular bacteria, protozoans and viruses

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4
Q

Which cytokines + tcell mediate eosinophilic, basophilic and mast cell inflammation/mucosal clearance? What organism(s) do they fight against?

A

IL-4 stimulates TH2

Fight against helminths

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5
Q

What type of inflammation causes:

  1. urticaria
  2. pemphigus
  3. vasculitis
  4. contact allergic dermatitis
  5. TB + sacroidosis
A
  1. Mast cell mediated
  2. Antibody mediated
  3. Immune complex mediated
  4. Delayed hypersensitivity
  5. Granuloma formation
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6
Q

What type of hypersensitivity is mast cell mediated inflammation?

A

Type 1

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7
Q

What occurs during mast cell mediated inflammation?

A

Exposed to allergen
antigen presented by APC to a TH2 cell
two things happen:
1. IL-5 and G-CSF is released from t cell to stimulate eosinophilic degranulation
2. IL-4 and IL-5 from T cell stimulate B cell to produce IgE
This IgE attaches to mast cell which stimulates the release of IL-3 and IL-5
IL-3 and IL-5 also stimulate eosinophilic degranulation

Degranulation of eosinophils + mast cells results in release of histamines, leukotrienes, prostaglandins and platelet aggregating factor

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8
Q

List a few mediators released by mast cells during a type I hypersensitivity reaction and their actions.

A
  1. Vasodilation and increased permeability:
    - histamine
    - PAF
    - Leukotriene C4, D4 and E4
    - Prostaglandin D2
    - Neutral proteases
  2. Smooth muscle spasm:
    - Histamine
    - PAF
    - Leukotriene C4, D4 and E4
    - Prostaglandin
  3. Leukocyte extravasation:
    - Cytokines (e.g. chemokines and TNF)
    - Leukotriene B4
    - Chemotactic factors for eosinophils and neutrophils
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9
Q

What are the different effects of histamine on the body?

A
  1. Stimulates sensory nerve: itchy flare
  2. Smooth muscle constriction: vessels leakage and oedema
  3. Arteriole dilatation: headache and hypotension
  4. Modulation of immune response via H2 receptors
  5. Bronchospasm
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10
Q

What is Der P1, and what does it do?

A

Der P1 = enzymes allergen from faecal pellets of dust mite

It cleaves occludin in tight junctions

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11
Q

Explain mast cell mediated inflammation using Der P1 as an example.

A

Der P1 is taken up by dendritic cells for antigen presentation and TH2 priming
Der P1-specific IgE binds to mast cells
Der P1 triggers mast cell degranulation

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12
Q

What are the local and generalised effects of mast cell degranulation?

A

Local: uritcaria, asthma and hayfever
Generalised: occurs when an antigen is released into the blood stream, binds to IgE on basophils –> MASSIVE release of inflammatory mediators and this causes bronchospasm and circulatory collapse, i.e. ANAPHYLAXIS

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13
Q

What is Omalizumab used to treat? What is the MOA of this drug?

A

Used for resistant urticaria and asthma
Binds to circulating IgE, reducing cell-bound IgE
Also reduces the expression of high-affinity receptors
This reduces tissue infiltration and mediator release which relieves symptoms

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14
Q

What type of hypersensitivity reaction is antibody-mediated inflammation? What type of immunoglobulin(s) is/are involved?

A

Type II

involves IgG and IgM

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15
Q

List the 4 different mechanisms of antibody-mediated inflammation.

A
  1. Complement mediated lysis –> antibody attaches to antigen
  2. Phagocytosis by extracellular macrophage
  3. Antibody-dependent cell-mediated cytotoxicity
  4. Receptor blockage
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16
Q

Explain what occurs in a type II hypersensitivity reaction, using Pemphigus Vulgaris as an example.

A

In this case the antigen = keratinocyte
IgG antibody-antigen complex binds to the surface of keratinocytes
Autoantibodies break down desmoglein, causing disruption to desmosomes between cells
Causes blistering of the skin

17
Q

What would a histology slide of pemphigus vulgaris show?

A

Suprabasal splitting
Acantholysis = loss of cohesion between epidermal keratinocytes
As the keratinocytes are still usually attached to the basement membrane the microscopic slide will often show a characteristic ‘tombstoning’ feature

18
Q

What are the treatment options for pemphigus vulgaris?

A

Oral steroids
Immunosuppression by c myophenolate mofetil or azathioprine
rituximab - target CD20 on B cells (inhibit acantholysis)

19
Q

What type of hypersensitivity reaction is immune complex mediated inflammation? What immunoglobulin(s) is/are sometimes involved?

A

Type III

IgG

20
Q

What occurs during immune complex mediated inflammation?

A

Antibody and antigen form an immune complex
there is production of complements, platelet aggregation (forming microthrombi) and release of lysosomal enzymes from neutrophils
this results in:
- leaky vessel extravasation (= oedema)
- proteases degrading BM
- necrosis of vessel wall due to microthrombi
- deposition of fibrin

21
Q

What are the early, established and severe manifestations of vasculitis?

A

Early: erythema and oedema
Established: palpable purpura
Severe: ulceration and necrosis (of skin)

*leukocytoclastic vasculitis is usually drug-induced and pts present with blistering and necrotic skin (histology: fibrin in blood vessel and nuclear dust)

22
Q

What antigens and antibodies are involved in:

  1. systemic lupus erythematous
  2. polyarteritis nodosa
A
  1. antigen = DNA
    antibody = anti-DNA
  2. antigen = Hep B surface antigen (HBsAg)
    antibody = Anti-HBsAg
23
Q

What type of hypersensitivity reaction is delayed hypersensitivity? Give the most common example of a delayed hypersensitivity reaction.

A

Type IV

Common example = allergic contact dermatitis

24
Q

Describe what occurs in a delayed hypersensitivity reaction.

A
  • CD4+ Th1 helper T cell recognised an antigen in a complex with MHC class II on the surface of an APC
  • These APCs can be macrophages that secrete IL-12 and stimulate the proliferation of further CD4+ Th1 helper cells
  • CD4+ T cells secrete IL-2 and IFN-gamma which:
    1. promote Th1 response = secretion of IL-2, IL-3, GM-CSF, IFN-gamma and TNF
    2. promote macrophage-rich response
  • CD8+ T cells kill target cells on contact, whereas macrophages release hydrolytic enzymes and can transform into multinucleated giant cells

**maximal response is 48-72h after exposure

25
Q

What type of hypersensitivity response is granuloma formation?

A

Type IV

26
Q

What occurs during granuloma formation? What causes granuloma formation?

A

antigen (e.g. mycobacterium TB) causes clonal T-cell expansion
induces secretion of TH1 cytokines = IL-2, IFN-gamma, TNF
stimulates macrophages
macrophages can:
1. fuse = GIANT cell
2. transform = HISTIOCYTE (epithelial macrophage)

Causes: TB, sarcoidosis, foreign body granuloma (tattoo)

27
Q

What are autoantibodies formed against in:

  1. alopecia areata
  2. vitiligo
A
  1. Hair follicle

2. Melanocytes

Loco (19 decks)

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