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Disease, diagnostics and therapeutics > Skin diseases > Flashcards

Skin diseases Flashcards

1
Q

psoriasis

A

a complex, chronic and multi-factorial inflammatory disease which involves hyper proliferation of the keratinocytes in the epidermis. Thought to be the result of interplay between genetic predisposition and environmental factors

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2
Q

what can trigger psoriasis

A

infection, injury, allergy, extreme tips, alcohol, stress resulting in an inflammatory response

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3
Q

psoriasis occurs due to an increased

A

production of skin cells- long lasting chronic disorder.

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4
Q

process which causes psoriasis

A

1) trigger e.g. injury, infection, allergy, chemical, stress
2) langerhans cells waiting for engulfment
3) these triggers (sometimes PAMPs) will then trigger langerhans - engulfment - antigen presentation
4) langerhans migrate to the lymph nodes –> antigens presented to naive t helper cells (CD4+ cells)
5) langerhans secrete TGF-B, IL-6 and IL-23 –> stimulate T cells to turn into Th17 cells
6) Th17 cells produce IL-17 –> psoriatic skin

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5
Q

what can also trigger an inflammatory response

A

commensal bacteria

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6
Q

layers of the skin

A

outside –> inside

Stratum corneum 
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale
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7
Q

how does psoriasis affect the layers of the skin

A
  • stratum granulosum reduced or absent
  • stratum basel becomes obsessively proliferative
  • quick replication of keratinocytes (no differentiated cells due to lack of apoptosis)
  • nucleated undifferentiated cells one to the top layer of the skin
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8
Q

why is psoriasis red

A

due to blood vessel growth needed to satisfy vascular need of quickly reproducing cells

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9
Q

cells in psoriasis

A

dont stack very well due to being cuboidal

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10
Q

summary of psoriasis

A

auto-immune disease which involves the over activation of keratinocytes which live in the statute basal by cytokines which leads to them becoming excessively proliferative

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11
Q

what are SNPs

A

single nucleotide polymorphisms

  • subsitutions
  • deletion
  • insertion
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12
Q

SNPs can be used as

A

biological markers

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13
Q

some SNPs can help predict

A

responses to drug or risk of developing a disease e.g. skin cancer

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14
Q

to find SNPs

A

primers extending from SNPs used

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15
Q

which three genes are significantly associated with psoriasis

A

HLA-C
IL12B
IL24R

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16
Q

which cytokines are produced in excess in psoriasis

A

TNF, IL which trigger inflammation in the skin and other organs

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17
Q

what effect do cytokines have

A
  • widened blood vessels
  • accumulation of WBC
  • rapid multiplication of keratinocytes
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18
Q

normal keratinocytes

A

take a month to divide, mature and migrate to the skin surface and be shet

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19
Q

psoriatic keratinocytes

A

process takes 3 to 5 days, resulting in thickened, red skin, that sheds silvery scales of keratinocytes which have matured too qucikly

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20
Q

skin cancers

A

develop from abnormal cells in the skin which have he ability to spread to other parts of the body

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21
Q

three types of skin cancer

A

1) basal-cell skin cancer
2) squamous-cell skin cancer
3) melanoma

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22
Q

basal-cell skin cancer

A

arises from basal cells- slow growing and unlikely to spread to distant areas

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23
Q

squamous cell

A

more likely to spread. Uncontrolled growth of abnormal cells arising in squamous cells

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24
Q

melanoma

A

most aggressive. begins in melanocytes and is much more likely to spread to other parts of the body

25
Q

TNM system

A

described the stage of a cancer which originates from a solid tumour

26
Q

T

A

describes the size of the tumour and whether is has invaded nearby tissue

27
Q

N

A

describes nearby lymph nodes which may be involved

28
Q

M

A

describes distant metastases- if it has spread to other parts of the body

29
Q

Imiquimod

A

topical cream immune-modualtory used to treat precancerous and cancerous sun damaged skin (basal cell carcinoma)
-also viral warts and other cancerous skin

30
Q

mechanism of action of Imiquimod

A

binds TLR-7 and TLR-8

  • -> triggers inflammation and the immune system destroys cancerous cells
  • -> chemokine
  • -> vasodilation= more permeable to WBCs
31
Q

side effect of imiquimod

A

induces psoriasis like inflammation in susceptible mice and humans : IL23, IL17, Th17

32
Q

where are langerhans most adapted to live

A

stratum spinosum

33
Q

phototherapy is used to treat

A

psoriasis

34
Q

what does phototherapy use

A

PUVA

35
Q

PUVA

A

psoralen and UVA

36
Q

psoralen

A

drug given orally- makes skin more sensitive to UV light

37
Q

why is psoralen use important

A

means a lower dose of UV light can be given- less chance of bruning

38
Q

how can psoralen be given

A

topically (i.e. in a bath- dosage issue and not very localised)
- usually given orally

39
Q

what can phototherapy for psoriasis also be called

A

photochemotherpay

40
Q

concerns of phototherapy

A

it could cause skin cancer

41
Q

which are the wavelengths used in phototherapy and how high frequency are they

A

UVA and UVB

42
Q

frequency of UVB

A

290-320 nm

43
Q

frequency of UVA

A

340-400nm

44
Q

which UV penetrates furtherest?

A

UVA- penetrates into the dermis (dermal fibroblasts, dermal dendritic cells, endothelia cells, T cels, mast cells, granulocytes)

45
Q

how far does UVB penetrate

A

short penetration into epidermis (langerhans and keratinocytes)

46
Q

how does phototherapy treat psoriasis

A

1) increased keratinocytes derived expression of anti-inflammatory cytokines
- increase in IL-10 (anti-inflammatory)
- increase in prostaglandins
2) Suppression of cytokine induced upregulation of ICAM-1 = less adhesion molecules = keratinocyte links restored
3) modulate keratinocyte cytokine sand growth receptor expression and function

47
Q

Increase release of IL-10 because of phototherapy causes

A

Anti-inflammatory cytokine
Suppresses IFN-𝛄 from CD4-T cells
Decreases immune response

48
Q

increase in prostaglandins because of photothepray

A

PGE2: immunosuppressive impact

Effects expression of co-stimulatory molecules on antigen presenting cells (APCs)

49
Q

end result of phototherapy

A

apoptosis of T cells (Th17)

- psoriasis subsided

50
Q

what is photodynamic therapies used to treat

A

skin cancers

51
Q

photodynamic therapy simple

A

uses singlet oxygen to kill tumour cells and treat certain non melanoma skin cancers including basal cell carcinoma

52
Q

3 essential component of PDT

A

photosensitiser: 5-ALA
light
oxygen

53
Q

photosensitised used

A

5-ALA

54
Q

5-ALA

A

selectively accumulates in tumour cells because they have:

  • a higher expressionn of membrane transporters
  • more iron availability
  • overespression of Haem biosynthesis
  • more cytosolic and mochdonrial enzymes for harm biosynthesis pathway
  • leaky blood vessels
  • absence of lympathic dranage
55
Q

Absence of lymphatic drainage

A

increases permeability and retention of 5-ALA

56
Q

why is singlet oxygen used in photodynamic therapy

A

singlet oxygen has a localised damaging effect because:

  • it has a short lifespan
  • only diffuses a short distance
57
Q

anti tumour effect of singlet oxygen

A
  • apoptosis- necrosis and autophage
  • damage to tumour vasculature
  • robust inflammtory reaction
58
Q

step by step process of photodynamic therpay

A
  1. apply 5-ALA to skin
  2. cream is systemically distributed through the skin layers
  3. 5-ALA selectivelyaccuumulates in tumour cells
  4. tumour cells convert 5-ALA into photoporphyrin IX
  5. affect skin is irradiated with RED light from the visible part of the EM spectrum
  6. red light activates photoporphyrin IX. raises it from ground state to excited state
  7. excited photoporphyrin IX transfers its energy to oxygen. Causes singlets to be produced
  8. Singlet oxygen is cytotoxic and has many mechanisms of killing tumour cells
59
Q

why use red light

A
  • wave length of 600-800nm
  • penetrates skin between 10-20mm
  • enough energy to initiate photodynamic reactions

Disease, diagnostics and therapeutics (53 decks)

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