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LR Dermatology > Skin Immunology > Flashcards

Skin Immunology Flashcards

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Dermatology Board Prep flashcards
1
Q

What factors contribute to the skin’s immune system?

A
  • Physical barrier (corneocytes in the keratin layer)

- Innate and adaptive immune cells

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2
Q

What are the key immune cells in the epidermis?

A
  • Keratinocytes

- Langerhans cells

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3
Q

How do keratinocytes aid the skin’s immune system (3)?

A
  • Sense pathogens via cell surface receptors and trigger an inflammatory response
  • Produce antimicrobial peptides (AMPs) that can directly kill pathogens
  • Produce cytokines and chemokines to recruit and regulate immune cells at the site
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4
Q

What are Langerhans cells?

A

A type of dendritic (antigen presenting) cell interspersed with keratinocytes in the epidermis

They are the main skin resident immune cell

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5
Q

How do Langerhans cells aid in the skin’s immune system?

A

They survey the environment with their dendrites, bind pathogens, and travel to lymph nodes to present the pathogens antigens to effector T cells

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6
Q

Which immune cells are found in both the dermis and epidermis?

A

T cells (mainly CD8+ cells in the epidermis)

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7
Q

Which immune cells are found in the dermis?

A

Dendritic cells, macrophages, T cells, natural killer cells, neutrophils, mast cells

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8
Q

How do CD4+ cells (helper T cells) aid in the skin’s immune system?

A

Th1: bind MHC II and produce cytokines that activate macrophages to destroy pathogens

Th2: bind MHC II and activate B cells to produce specific antibodies

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9
Q

How do CD8+ cells (cytotoxic T lymphocytes) aid in the skin’s immune system?

A

Bind MHC I and Fas death receptors, directly killing affected cells via apoptosis
(this is useful for infected cells or tumour cells)

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10
Q

How do neutrophils aid in the skin’s immune system?

A

They are the first responders to infection and attach pathogens by phagocytosis and degranulation of toxic substances

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11
Q

How do macrophages aid in the skin’s immune system?

A

Phagocytose pathogens and recruit more neutrophils to the site

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12
Q

How do mast cells aid in the skin’s immune system?

A

They are activated in response to IgE binding (allergic response), resulting in release of granules containing pro-inflammatory mediators

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13
Q

How do natural killer cells aid in the skin’s immune system?

A

They are activated by the release of interferons or other cytokines by macrophages

They bind MHC I and induce apoptosis

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14
Q

How does organ transplant damage the skin’s immune response?

A

Immunosuppressive treatments

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15
Q

How does sunlight damage the skin’s immune response?

A
  • Suppresses the immune system

- Damages skin structure

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16
Q

How does ageing damage the skin’s immune response?

A
  • Changes to skin structure
  • Decreased ability to detect malignant cells and foreign antigens
  • Decreased ability to recognise self from non-self (autoimmunity)
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17
Q

What are Birbeck granules?

A

Rod-shaped granules exclusive to epidermal langerhans cells

Their function is unknown

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18
Q

Which T helper cells are associated with psoriasis?

A

Th1 and Th17

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19
Q

Which T helper cells are associated with atopic eczema/dermatitis?

A

Th2 and Th17

20
Q

The epidermis contains mainly CD4+ T cells. True/false

A

False

Epidermis mainly contains CD8+ T cells

21
Q

What is the function of Th1 cells?

A

Activate macrophages to eliminate pathogens

22
Q

What is the function of Th2 cells?

A

Help B cells make antibodies

23
Q

Type 1 allergy is mediated by…

A

IgE

24
Q

How soon after exposure does a type 1 allergic reaction occur?

A

Within minutes -> up to 2 hours

25
Q

Type 1 allergies don’t always occur with every exposure. True/false?

A

False

Type 1 allergies have a reproducible reaction with every exposure. Intolerance is more likely if reactions do not occur with every exposure

26
Q

What are the 4 routes of exposure for type 1 allergy?

A

Ingestion (e.g., nuts, seafood)
Inhalation (e.g., pollen)
Skin contact (e.g., latex)
Injection (e.g., bee sting)

27
Q

Describe the mechanisms involved in a type 1 allergic reaction to peanuts

A

Sensitisation:

  • Peanut proteins taken up by dendritic cells
  • DC’s present antigen to T cells
  • Th2 secretes cytokines to activate B cells
  • B cells produce antibodies for peanut allergen
  • IgE bind to mast cells

Allergic reaction:

  • IgE re-encounters peanut antigen
  • IgE causes release of mediators from the mast cell they are bound to
  • These cause the allergic reaction
28
Q

What are the signs and symptoms of a type 1 allergic reaction?

A

Urticaria (raised, itchy rash on the skin)

Angioedema

Rhinorrhoea/sneezing

Wheeze

Abdominal pain

Nausea/vomiting

Diarrhoea

29
Q

What are the signs and symptoms of anaphylaxis?

A

Urticaria, flushing, angioedema, throat tightening, SOB, wheeze, hypotension, tachycardia, chest pain, fainting, abdominal pain, nauseam vomiting

30
Q

List investigations involved in suspected type 1 allergy

A
  • History (most important)
  • Specific IgE testing (RAST)
  • Skin prick test
  • Challenge test
  • Serum mast cell tryptase level (during anaphylaxis)
31
Q

What are the advantages and disadvantages of skin prick testing?

A

Advantages:

  • Quick (results in 15-20mins) and cheap
  • Higher specificity & sensitivity than IgE testing (90+% compared to 70-75%)

Disadvantages:
- Anaphylaxis risk

32
Q

How is challenge testing carried out to avoid anaphylaxis?

A

The allergen is presented a little bit at a time e.g., touch lips -> chew and spit -> swallow

33
Q

Why would you carry out challenge testing for type 1 allergy?

A

If the skin prick test came back negative

34
Q

What is the gold standard management for type 1 allergy?

A

Allergen avoidance

35
Q

What is the step-up management plan for a patient with a type 1 allergy?

A
  • Anti-histamines
  • Anti-inflammatory e.g., corticosteroid (if antihistamine doesn’t work within 30 mins)
  • Adrenaline autoinjector (for anaphylaxis)
36
Q

What dose of pre-loaded adrenaline is given to…
- adults
- children
… from an epi-pen?

A

Adults - 300 micrograms

Children - 150 micrograms

37
Q

List some non-allergic reactions that can mimic the symptoms of a type 1 allergic reaction

A
  • Coeliac disease
  • Esosinophilic gastroenteritis
  • Use of morphine/aspirin/NSAIDs
  • Lactose intolerance
  • Scombroid fish toxin
38
Q

Type 4 allergy is mediated by…

A

T cells

39
Q

Type 4 allergic reactions of the skin are called…

A

Allergic contact dermatitis/ allergic contact allergy

40
Q

How soon after exposure does a type 4 allergic reaction occur?

A

After 12-24 hours

41
Q

What are the 3 main routes of exposure for allergic contact dermatitis?

A

Direct skin contact (e.g., preservatives in makeup)

Airborne contact (e.g., perfume, plants)

Injection (e.g., tattoo)

42
Q

Describe the sensitisation phase of allergic contact dermatitis

A
  • Allergen penetrates the epidermis and is taken up by Langerhan cells
  • These migrate to lymph nodes and present the antigen to CD4+ and CD8+ cells
  • These T cells clonally expand in the lymph nodes then travel through the blood to affected tissues
43
Q

Describe the elicitation phase of allergic contact dermatitis

A
  • On re-exposure, APC’s present the antigen to antigen-specific T cells
  • T cells are activated and recruit more T cells
  • T cella release chemokine and cytokines that lead to the reaction seen in allergic contact dermatitis
44
Q

What is the gold-standard test for allergic contact dermatitis?

A

Patch testing

45
Q

What are the steps of Patch testing for allergic contact dermatitis?

A
  • Allergens are prepared on Finn chambers
  • Finn chambers are applied to the back
  • Chambers are removed after 48 hours
  • Readings are taken at days 2 and 4 (48 and 96 hours)
46
Q

What factors, other than allergic, can cause dermatitis?

A
  • Irritant contact e.g., abrasion causing nappy rash
  • Endogenous factors from underlying skin disorder e.g., dry eczema, scaly psoriasis
  • Infection
47
Q

What are the management options for allergic contact dermatitis?

A
  • Allergen avoidance/ minimisation
  • Emollients (moisturiser)
  • Topical steroids
  • UV phototherapy
  • Immunosuppressants (not used often)

LR Dermatology (11 decks)

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