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Phase 2a > Dermatology > Flashcards

Dermatology Flashcards

1
Q

In older children and adults what part of the body does atopic dermatitis commonly affect?

A

extremities

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2
Q

In infants which part of the body does atopic dermatitis most commonly affect?

A

Generalised: cheeks, forehead and scalp

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3
Q

In children which part of the body does atopic dermatitis most commonly affect?

A

Becomes more localised: flexor regions of the body: elbows, behind knees, ankles, wrists

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4
Q

What test is used for diagnosing the specific antigen that might cause atopic dermatitis?

A

The patch test

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5
Q

How would you define the lesion in atopic dermatitis?

A

pruritic, oozing lesion

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6
Q

How does early exposure to the various environmental antigens affect the chance of developing atopic dermatitis?

A

decreases the chance of getting atopic dermatitis

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7
Q

Which type of hypersensitivity is atopic dermatitis associated with?

A

Type I hypersensitivity (Allergic)

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8
Q

Does living in a dry climate affect atopic dermatitis?

A

increases chance of developing atopic dermatitis

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9
Q

Who is most commonly affected with atopic dermatitis?

A

Children (15-30%)

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10
Q

Describe atopic dermatitis (eczema)….

A

superficial skin inflammation + vesicles (when acute), redness, oedema, oozing, scaling and usually pruritis

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11
Q

Give some causes of atopic dermatitis….

A

GENETICS

- filaggrin def (caucasians)&raquo_space; poor barrier func and dry skin&raquo_space; allows antigen penetration into epidermis

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12
Q

What is the atopic triad?

A
  1. Atopic dermatitis
  2. Asthma
  3. Allergic rhinitis
    - if have one of these likely to have experience others
    - eczema first to appear&raquo_space; asthma&raquo_space; hayfever
    - all caused by hypersensitivity reaction to certain allergens
    - conditions of atopic triad tend to be passed on through genetics
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13
Q

Give some triggers of atopic dermatitis…

A

cigarette smoke, pet fur, dust mites, hygiene hypothesis, strong detergents, dietary antigens

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14
Q

What forms the mainstay of atopic dermatitis treatment?

A

Topical corticosteroids

  • weak steroids = hydrocortisone for face
  • stronger steroids = betamethasone for body and soles
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15
Q

What forms the mainstay of atopic dermatitis treatment?

A

Topical corticosteroids

  • weak steroids = hydrocortisone for face
  • stronger steroids = betamethasone for body and soles
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16
Q

In what type of eczema would you see round, oval, and erythematous lesions on both legs. There is noticeable xerosis of the affected skin.

A

Nummular (meaning round or “coin shaped”) dermatitis or eczema (NE) is an inflammatory skin condition characterized by the presence of well-demarcated round-to-oval erythematous plaques

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17
Q

Chronic scratching or rubbing in atopic dermatitis may lead to….

A

Lichenification = leather skin

  • skin thickens due to inflammation
  • see thickened skin plaques + scaling
  • skin lines exaggerated
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18
Q

If both parents have atopic dermatitis what is the chance of their offspring having it?

A

70%

STRONG GENETIC DISPOSITION

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19
Q

Name one of the most common triggers of a flare up of atopic dermatitis…

A

Staph Aureus invasion&raquo_space; stimulates Tcell responses + produces IgE&raquo_space; exacerbations

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20
Q

Which dermatological condition is associated with coeliac disease?

A

Dermatitis hepetiformis

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21
Q

How is atopic dermatitis seen histologically?

A
  • epidermal vesicles (spongiosis)
  • hyperkeratosis (or scalyness)
  • acanthosis (an enlargement of the stratum spinosum layer).
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22
Q

Name the 5 layers of the skin….

A 
Stratum Basale
Stratum Spinosum
Stratum Granulosum
Stratum Lucidum
Stratum Corneum
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23
Q

Who does acne affect?

A

adolescents to mid 20’s

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24
Q

What is the most common type of acne?

A

acne vulgaris

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25
Q

What are the psychological effects of acne?

A

affect self-esteem and mood

  • anxiety and depression
  • increased rates of suicide
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26
Q

Where on the body does acne present?

A

Face, back and chest (high number of sebaceous glands in these areas)

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27
Q

Name the different types of pimples…

A

whitehead, blackhead, papule, pustule, nodule and cyst

28
Q

What is the difference between open and closed comedones?

A

Closed comedome = white head (closed pore)

Open comedome = blackhead (open pore)

29
Q

When does inflammation occur in acne?

A

Inflammation occurs when the wall of the comedome ruptures

30
Q

Describe the 3 things that contribute to acne…

A
  1. hypercornification- blockage of pilosebaceous units (microplug formed)
  2. seborrhoea: hyper proliferation of sebaceous glands&raquo_space; increased sebum production
  3. infection and proliferation of bacterium (proprionibacterium)- secretes inflammatory molecules and chemotactic factors that initiate and perpetuate the local inflammatory response
31
Q

Why does acne occur specifically during puberty?

A

increased androgens in puberty&raquo_space; hyper proliferation of sebaceous glands

32
Q

What is post-inflammatory hyper-pigmentation?

A

the medical term used to describe discoloration of the skin that follows an inflammatory wound.
Common in patients with darker skin

33
Q

What is the difference between papule, pustules, nodules and cysts?

A 
papule = small red bumps
pustule = white/yellow spots
nodule = large red bumps
cyst = fluctuant nodules
34
Q

Name the two different types of scar in acne…

A
  1. Raised (hypertrophic)

2. depressed (pitting)

35
Q

What is the first line treatment in acne?

A

MILD ACNE
Topical treatments
- Benzoyl peroxide: antimicrobial (can combine with top Abx)
- topical antibiotics (if inflamm): erythromycin/clindamycin
- topical retinoids: tretinoin (re-establishes epithelial growth homeostasis)
- Nictotinamide: Vit3 dérivative with anti-inflamm action

36
Q

Wha is the second line treatment in acne?

A

MOD-SEVERE ACNE

a) oral antibiotics (in add to topical except Abx)
- tetracycline/doxycycline >6 months
- CI in preg: erythromycin + trimethoprim
b) hormone treatment
- anti-androgen treatment: co-cyprindiol

37
Q

What is the third line treatment in acne?

A

SEVERE = oral retinoids: isotretinoin (roaccutane)

  • given if Abx failed, nodular cystic acne + scarring or severe psych disturbance
  • synthetic vit A analogues modulating cell proliferation, differentiation, apoptosis and altering the immune response

The only therapy that impacts on all of the major aetiological factors implicated in acne.

38
Q

How effective are oral retinoids at treating acne?

A

> 90% response rate and 65% long term ‘cure’

39
Q

What are the side effects of oral retinoids?

A

teratogenic, alter mood, increased risk of suicide, depression, dry skin (especially lips)

40
Q

What is psoriasis?

A

a chronic hyper proliferative disorder

41
Q

What is the aetiology of psoriasis?

A

Polygenic BUT dependent on certain environmental triggers:
PSORS1 on Cr6
Triggers = infection, UV light, stress, drugs (lithium)

42
Q

What is the epidemiology of psoriasis?

A

2% of UK pop
Two peaks: 16-22 and 55-60yrs
UNUSUAL IN CHILDREN
M = F

43
Q

What is the pathophysiology of psoriasis?

A

T- lymphocyte driven
unidentified antigen&raquo_space; T cell activation&raquo_space; upset of Th1 cytokines
e.g. IF gamma, IL1, 2 & 8, TGF and TNF alpha
This causes kertainocyte hyper proliferation

44
Q

What is Koebners phenomenon?

A

It describes the formation of psoriatic skin lesions on parts of the body that aren’t typically where a person with psoriasis experiences lesions. This is also known as an isomorphic response.

45
Q

Give some D/D’s for psoriasis?

A
  • dermatitis
  • SLE
  • Reactive arthritis
  • Lichen planes
  • Pitynasis Rosea
  • 2nd stage of syphilis
46
Q

What nail changes can you see in psoriases?

A
  • pitting
  • onycholysis (nail lifts off bed)
  • Beaus lines
  • subungal hyperkeratosis
47
Q

What can you see on histology in psoriasis?

A
  • parakeratosis (retain nucleus)
  • acanthuses (thickening of epidermis)
  • NO granular layer
  • lengthened Rete ridges
  • Munro’s micro abscesses
48
Q

What findings on histology reflect the increases in turnover of the skin in psoriasis?

A

parakeratosis- retained nuclei of cells

acanthosis- thickened epidermis

49
Q

Name 5 types of psoriasis…

A
  1. classical
  2. gluttate
  3. palmoplantar pustular
  4. flexural
  5. erythrodermic
50
Q

Which type of psoriasis is most common?

A

Classical

51
Q

Describe classical psoriasis… its features, distribution and features

A 
plaques = well circumscribed, erythematous, silver scaling
distribution = extensor surfaces, scalp or sacral
features = pain/itch (less than eczema)
52
Q

What is Auspitz sign?

A

bleeding when the scale is removed

- seen in classical psoriasis

53
Q

Describe gluttate psoriasis….

A

RAINDROP LIKE

  • young age
  • onset = after streptococcal infection
  • clears with treatment
  • plaques = v.small, circular, discoid erythematous
  • seen on trunk, upper arms and legs
54
Q

Describe palmoplantar pustular psoriasis…

A
  • on palms of hands and feet
  • get thickening of palms and soles + yellow-brown pustules
  • heavy smokers
  • X severe systemic symptoms
55
Q

Describe flexural psoriasis….

A

ELDERLY

  • localised to skin folds + genitals
  • NOT SCALY (glazed and red plaques)
56
Q

Describe erythrodermic psoriasis…

A

EMERGENCY
- ACUTE onset of erythroderma and pustular plaques
- systemically unwell
METHOTREXATE

57
Q

What is the 1st line treatment for typical psoriasis?

A

Dithranol

58
Q

What is the 2nd line treatment for typical psoriasis?

A 
Vit D analogues e.g. calcitriol (decrease cell proliferation)
\+
salycylic acid
\+-
UVB
59
Q

What is the third line treatment for typical psoriasis

A

Retinoids
or
PUVA + immunosuppressants

60
Q

Name some topical treatments for psoriasis…

A
  1. emollients
  2. Vit D-analogues e.g. calcitriol (decreases cell prolif)
  3. Coal tar: inhibits DNA synthesis
  4. Dithranol: inhibits DNA synthesis
  5. Keratolytics = salycylic acid (scalp psoriasis)
  6. Corticosteroids (ONLY IN COMBINATION)
  7. Retinoids e.g Tazarotene
61
Q

Name some systemic treatments for psoriasis…

A
  1. immunosuppressants e.g. methotrexate
  2. Retinoids e.g. acitretin (teratogenic for <3 years)
  3. phototherapy- UVB for classic & glutamate
    • PUVA for palmoplantar
  4. Biological agents e.g. efalizumab
62
Q

What is the Goekerman regime in psoriasis treatment?

A

TAR + UVB

63
Q

What us the Ingram regime in psoriasis treatment?

A

Goekerman regime + dithranol

64
Q

How does the migration time of skin cells differ in psoriasis?

A

Increases to ~4 days (normal = 4 weeks)

65
Q

Give some side effects of Vit D analogues…

A

hypercalacaemia if overdose

66
Q

Give some disadvantages of using coal tar

A

Smelly and messy

67
Q

What does dithranol do to clothes?

A

stains them purple

Phase 2a (7 decks)

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