Immunology 5: Inflammatory dermatoses Flashcards

1
Q

what are the 3 layers of skin?

A

epi dermis
dermis
subcutaneous tissues

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2
Q

hairy skin -

A

hair follicles

apocrine glands

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3
Q

describe the layout of the epidermis

A
  • base memb
  • on top = keratinocytes –> moves up as they proliferate –> form stratum cornea = important barrier function
  • contains melanocytes, merle cells, langherans cells
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4
Q

describe how keratinocytes changes as they move upwards

A
  • basal cells –> prickle cell –> granular cell –> (nuclei lost) –> keratin
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5
Q

describe the structure of the stratum corneum

A

contains keratinocytes

- in nbtw =glue = consisting of lipid + protein e.g filagrin –> aids integrity of stratum corneum

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6
Q

gene mutation in filagrin =

A

gene mutation in filagrin = pre disposed to be dry –> more likely to lead to eczema

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7
Q

what is atopy?

A

tendency to develop hypersensitivity

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8
Q

What are the 3 main atopic disease?

A
  • eczema, asthma, hay fever
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9
Q

What is a key characteristic of atopic eczema?

A

common, relapsing, remitting

–> defecting barrier function in skin

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10
Q

what is the atopic march

A

people with atopic disease tend to develop eczema first –> sensitizes inviduals to environmental allergens (in skin) –> which then manifests as other atopic diseases e.g rhinitis, asthma etc. later on in their life

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11
Q

What changes when atopic eczema becomes acute –> chronic?

A

Th2 immune response –> becomes Th1 immune response

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12
Q

What are some signs of having a filagrin mutation?

A
  • palmar hyperlinearity
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13
Q

Infantile atopic eczema –> e.g eczema on face –> food on face –> allergic to food later on

A

-

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14
Q

How does the pattern of atopic eczema change as they grow?

A

baby = back of head, arms, cheeks, below neck

adult = flexure of arms + legs, popliteal fossa, antecubital fossa

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15
Q

what is visual difference between acute and chronic eczema?

A
  • acute eczema = red, weepy + sore

- chronic eczema = less red + lichenification

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16
Q

what is eczema herpeticum

A
  • eczema = skin inflamed –> predisposed of herpes simplex

- -> spreads on skin surface –> presents as blisters + ulcers

17
Q

what is seborrheic eczema

what is treated with

A
  • nasal fold, scalp, eye lids
  • overgrowth of yeast

treatment = topical anti fungals, topical steroids

18
Q

what is allergic contact dermatitis

A
  • allergy to specific product
    e. g eye drops, makeup

-

19
Q

what is discoid eczema

A

-disc shapes around the body
esp in elderly / those who over wash

–> topical steroid + reduce use of soap/ wash gel

20
Q

What is psoriasis

A
  • immune related
  • inflammatory dermatosis
  • presents w skin lesions
  • plaques of skin (salmon pink)
  • with silver scale
21
Q

pathogenesis of psoriasis:

A
  • genetic suspectpibility required
    • env trigger e.g infection, drug, stress
  • immune réponse –> psoriasis
    t cells predominate in dermis –> stimulate cytokine release (TNF-a) –> neutrophils go into epidermins–> over production of keratinocytes –> causes thickening of epidermis

top layer = immature –> not lost neutrophils = scaling
red = blood vessel dilated

22
Q

what would be the characteristics of a histology of psoriasis

A
  • hyperkeratosis (thickening of outer skin layer)
  • parakeratosis (retention of nuclei in stratum corneum)
  • acanthosis (thickening of epidermis)
  • inflammation
  • dilated blood vessels
23
Q

describe the distribution of skin lesion in psoriasis

A
  • scalp
  • trunk
  • elbows (outside)
  • knees (outside)
  • groin + genitals
  • armpit
  • psoriasis soles (symmetrical)

–> tends occur in

24
Q

what are other signs of psoriasis ?

A
  • loss of nail cuticles
  • subungal hyperkeratosis
  • roughening of nails
  • pitting of nails
  • onycholysis
25
Q

What is guttate psoriasis

A
  • subtype of psoriasis
  • rain drop patches of psoriasis
  • in young people often after streptococcal infection
26
Q

NOTE: recurrent tonsillitis w psoriasis –> remove tonsils –> psoriasis improves

A

-

27
Q

palmoplantar psorasis

A

on hands

28
Q

3 causes of pustules

A
  • infections
  • psoriasis
  • drug reaction
29
Q

describe the development of acne

A
  • disorder of pilosebaceous unit
  • -> genetic factors + hormonal factors
  1. development of comedones ( due to hyperkeratonisation of neck of follicle)
  2. androgen stimulate –> increases sebum prolducito n
  3. overgrowth of propionibacteria acnes
  4. forms cystic rupture
30
Q

NOTE:
white head = closed comedones with covering
black head = come dome = open –> can see dead keratin
pustule
nodule –> thickened
papule –> raised inflammatory region

A
  • early treatment is important
    topical
    contraceptive pill
31
Q

what is bullous pemphigoid

A
  • autoimmune condition
  • esp in edlerly
  • autoantibody produced against component in basement membrane
    (BP antigen 1, BP antigen 2)

BM splits –> tense blisters form below epidermis

32
Q

how is bullous pemphigoid different to epidermolysis bullosa ?

A

epidermolysis bullosa –> genetically abnormal

33
Q

What is pemphigus vulgaris

A
  • autoantibodies produced against desmosome
    split in epidermis –> superficial blisters + erosion

treatments= steroids