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Y2 Immuno (MCD) > Inflammatory dermatoses > Flashcards

Inflammatory dermatoses Flashcards

1
Q

What is the pilo-sebaceous unit?

A

Erector pili muscle, hair follice and sebaceous gland

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2
Q

Label this

A
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3
Q

What is the keratinocyte differentiation pathway?

A

basal cell -> prickle cell -> granular cell -> keratin.

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4
Q

What is the structure of the stratum corneum?

A
  • Composed of corneocytes (differentiated keratinocytes)
  • Lipids and proteins in between each of them.
  • One of these proteins is filagrin
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5
Q

How are sweat glands different to eachother?

A

Ecrine:

  • located all over the body

Apocrine:

  • located in the axilla and groin
  • Produce a viscous smelly sweat
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6
Q

What is sebum?

A

Oil that lubricates hair

Contains chemicals to suppress bacterial and fungal growth

Produced by sebaceous glands

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7
Q

What is the distinguishing feature of the stratum spinosum?

A

Spinous processes between keratinocytes

These are desmosomes

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8
Q

What is the distinguishing feature of the stratum granulosum?

A

Keratin hyaline granules in the cells

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9
Q

Label this

A
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10
Q

What is the function of the stratum corneum?

A

Barrier function

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11
Q

What is atopy?

A

tendency to develop hypersensitivity

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12
Q

Give 3 examples of atopic diseases

A
  • eczema,
  • asthma,
  • hayfever
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13
Q

What predisposes patients to atopic eczema?

A

Gene mutation in filaggrin - one of the proteins between corneocytes in the stratum cornea important for its integrity

Causes dry skin

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14
Q

How does atopic eczema develop?

A
  • Intrinsic factors e.g. filagrin mutation lead to defects in the epidermal skin barrier
  • Extrinsic factors take advantage of this. Exogenous agents e.g. allergens and pathogens penetrate the epidermis
  • Acutely this leads to activation of CD4+ lymphocytes and the Th2 immune response
  • This causes B-lymphocyte IgE antibody production, mast cell degranulation and subsequent histamine release
  • Chronically this causes activation of CD4+ and CD8+ lymphocytes and activation of the Th1 response
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15
Q

What is a sign of a filagrin gene mutation?

A

Palmar hyperlinearity

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16
Q

What is atopic eczema?

A
  • Defective skin barrier
  • Defective barrier then allows entry of irritants, allergens and pathogens
  • These then cause inflammation.
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17
Q

Are the areas of skin inflammation well defined in psoriasis and atopic eczema?

A

Psoriasis - well defined

Atopic eczema - not well defined

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18
Q

Where do infants commonly get atopic eczema?

A
  • Face
  • Elbows
  • Knees
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19
Q

Where do adults commonly get atopic eczema?

A

Flexural areas:

Elbows

Knees

Hands

Neck

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20
Q

What are the signs of chronic atopic eczema?

A

Lichenification - skin markings more visible, thickened leathery skin

Due to chronic scratching and rubbing

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21
Q

What is erythrodermic eczema?

A

Eczema and redness all over the body

Patient systemically ill

Often due to Staphylococcus infection because of the eczema

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22
Q

What is Eczema herpeticum?

A
  • Eczema with HSV infection
  • The eczema allows the HSV to spread on the skin’s surface
  • Results in fever, malaise
  • Punched out vesicles where blisters have broken down to form ulcers
  • Can become septic or result in Herpes encephalitis
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23
Q

What causes Seborrhoeic Eczema?

A

Overgrowth of Malassezia yeast causing the same thing as dandruff just more severe

Causes inflammation and shedding of the upper skin layers

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24
Q

Where does Seborrhoeic Eczema effect?

A
  • nasolabial folds,
  • eyebrows,
  • scalp,
  • central chest,
  • axilla
  • groin
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25
Q

Is seborrhoeic eczema itchy?

A

No

26
Q

How do you treat Seborrhoeic Eczema?

A

Topical sterioids

Anti-fungals

27
Q

What are the types of eczema?

A
  • Atopic
  • Seborrhoeic
  • Allergic contact
  • discoid
28
Q

What is Allergic contact eczema?

A

Physical skin contact with a product causes inflammation

Atopic eczema pre-disposes

Nickel and rubber common

29
Q

What is discoid eczema?

A

Specific pattern of eczema - discs scattered around the body

30
Q

What causes discoid eczema?

A

Age

Overwashing - wash natural skin lipids away making the skin dry

31
Q

How does psoriasis present?

A

Plaques:

  • slightly raised
  • salmon pink
  • silvery scale
  • well defined
  • Sore and itchy
32
Q

What causes psoriasis?

A

Genetic susceptibility needed

Environmental trigger needed e.g. infection, drugs, stress, alcohol, smoking

33
Q

What is the pathophysiology of psoriasis?

A
  • T cells in the dermis stimulate cytokine release of TNF alpha
  • Neutrophil infiltration into the epidermis
  • Overproduction of keratinocytes
  • Stiffening and thickening of the epidermis
  • Top layer of epidermis has neutrophils - abnormal
  • Blood vessels become dilated
34
Q

How would you describe the histology of psoriasis?

A
  • Hyperkeratosis - overproduction of keratinocytes
  • Parakeratosis - Stratum corneum retains neutrophils
  • Acanthosis - Epidermal thickening
  • Inflammation
  • Dilated blood vessels
35
Q

Where are you likley to get psoriasis?

A
  • Scalp
  • Face
  • Armpits
  • Elbows
  • Trunk
  • Buttocks
  • Groin and genitals
  • Nails
  • Knees
36
Q

How can you tell the difference between psoriasis soles and fungal foot infection?

A

Fungal infections usually asymetircal whereas this can be symmetrical

37
Q
A
38
Q

Where do the plaques appear in psoriasis of the soles?

A

On sites of pressure

39
Q

What are the features of nail psoriasis?

A
  • Subungual hyperkeratosis
  • Dystrophic nail and loss of cuticle
  • Onycholysis (nail lifted away from the nail bed)
  • Pitting
40
Q

What is the difference between psoriasis of the nails and a fungal infection of the nail?

A

Fungal infections only involve some of the nails whereas psoriasis effects all the nails

41
Q

What is palmoplantar pustulosis?

A
  • Psoriasis of the hands and feet
  • Often dont have psoriasis in other places
  • Being a smoker pre disposes
42
Q

What can cause pustules?

A

Infection

Psoriasis

Drug reaction

43
Q

What are the different types of psoriasis?

A
  • Soles psoriasis
  • Nail psoriasis
  • Guttate psoriasis
  • Palmoplantar pustulosis
  • Generalised pustular psoriasis
44
Q

What are the side effects of Roaccutane?

A
  • Depressant
  • Teratogenic
  • Hypercholesterolaemia
45
Q

How does acne develop?

A
  • Hyperkeratinisation of the follicle neck (comedone formation)
  • Increased androgen production - stimulation increases sebum production
  • Accumulation of dead cells and sebum
  • ‘Propionibacteria acnes’ proliferate - pimple forms
  • Inflammation
  • Cyst forms
  • Rupture of follicle canal cyst
  • More inflammation
46
Q

What are the skin changes in psoriasis?

A

Scales and plaques that flake off

Inflamed upper skin layer

Thickening of epidermis

47
Q

How is psoriasis treated?

A

Topical corticosteroids

Immunosupressants

48
Q

What is guttate psoriasis?

A

Small raindrop like pattern of papular psoriasis plaques

49
Q

Who is more likley to develop guttate psoriasis?

A

Young people

Often following a streptococcal infection (after tonsillitis)

50
Q

What are the different acne lesions?

A
  • Whitehead - comedome covered with skin
  • Blackhead - comedome open, can see dead keratin within it
  • Papule - raised inflammatory lesion
  • Pustule - pus filled comedome
  • Nodule - inflammatory thickening of the skin
51
Q

How is acne treated?

A

Topical antibiotics - benzoyl peroxide

Systemic antibiotics - erythromycin, clindomycin

Contraceptive pill - Yasmin, dianette

Isotretinoin (Roaccutane)

52
Q

What is bullous pemphigoid?

A

Autoantibody is produced against a component of the basement membrane

Causes the basement membrane to split

Subepidermal tense blister

53
Q

How does the basement membrane attach the dermis to the epidermis?

A

Tonofilaments attach the epidermis to the basement membrane

Anchoring fibrils attach the basement membrane to the dermis

54
Q

Why does the basement membrane need to have specialised attachment methods?

A

Epidermis is derived from the ectoderm

Dermis is derived from the mesoderm

Dont naturally stick together

55
Q

What proteins are targetted in bullous pemphigoid?

A

BPAg1 and/or BPAg2

These are components of hemidesmosomes attaching epidermis to BM

56
Q

What conditions develop when there is a genetic defect in BM proteins vs when an autoantibody is produced against BM proteins?

A

Genetic defect - Epidermolysis bullosa

Autoantibody - Bullous pemphigoid

57
Q

How does Pempigus vulgaris present?

A

Superficial blisters that break easily leading to skin erosions

58
Q

What is pempigus vulgaris?

A

Autoantibody produced against desmosome connecting keratinocytes to eachother in the epidermis

Attack desmoglein 1 & 3 -components of desmosomes

59
Q

What is the difference in histology of pemphigus vulgaris and bullous pemphigoid?

A

Pemphigus Vulgaris splits more superficially above the basement membrane

60
Q

How do you treat Pempigus vulgaris and bullous pemphigoid?

A

Topical corticosteroids

Systemic immunosupressants

Y2 Immuno (MCD) (5 decks)

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