Ezcema Flashcards

1
Q

Eczema vs dermatitis

A

Skin lesions with similar clinical & pathological features
but different pathogenetic mechanisms (ie different causes)

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2
Q

Describe the acute phase of eczema

A

papulovesicular
erthematous (red) lesions
oedema (spongiosis)
ooze or scaling & crusting

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3
Q

Describe the chronic phase of eczema

A

thickening (lichenification)
elevated plaques
Increased scaling

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4
Q

Contact allergic dermatitis pathogenesis & histology

A

Pathogenesis - Delayed type (type 4) h/s reaction
Histology Spongiotic dermatitis

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5
Q

Contact irritant dermatitis pathogenesis & histology

A

Pathogenesis - Trauma eg soap, water
Histology - spongiotic dermatitis

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6
Q

Atopic dermatitis (eczema) pathogenesis & histology

A

Pathogenesis - Genetic & environmental factors resulting in inflammation
Histology - spongiotic dermatitis

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7
Q

Drug related dermatitis pathogenesis & histology

A

Pathogenesis - Type 1 or 4 h/s reaction
Histology - spongiotic dermatitis & eosinophils

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8
Q

Photo-induced dermatitis pathogenesis & histology

A
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9
Q

Lichen simplex dermatitis pathogenesis & histology

A
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10
Q

Stasis dermatitis pathogenesis & histology

A
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11
Q

Contact allergic dermatitis pathophysiology

A
  • Langerhans cells in the epidermis are exposed to an allergy on the skin & express the antigen on their MHC II molecules
  • They then present the antigen to Th cells in the dermis
  • The sensitised Th cells migrate into lymphatics and then to regional nodes where antigen presentation is amplified
  • When exposed to the allergen again, they migrate & infiltrate the dermis & cause inflammatory cytokine release & cell mediated cytotoxicity
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12
Q

Contact allergic dermatitis clinical features

A

Itchy, eczematous rash (vesicles, fissures, erythema), typically 24-48 hours after exposure that may extend beyond the boundaries of the immediate contact

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13
Q

Contact allergic dermatitis diagnosis

A

Patch testing - allergens prepared onto Finn chambers which are applied on the back and removed after 48 hours, readings at 48 and 96 hours

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14
Q

How is the clinical presentation of allergic vs irritant contact dermatitis different

A
  • In allergic, the rash may extend beyond the boundaries of immediate contact…
  • In allergic, there is a sensitisation phase & so they may have never had the problem in the past…
  • In allergic, there is a specific allergen…

This is not the case in irritant contact dermatitis

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15
Q

What is irritant contact dermatitis

A

Non specific physical irritation causing eczema/dermatitis

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16
Q

What occupations are commonly associated with irritant contact dermatitis

A

hairdressers, health care staff, builders and cleaners

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17
Q

Irritant contact dermatitis clinical features

A
  • Eczematous rash localised to the direct area of contact
  • There may be burning, pain, and stinging
  • May have coexisting allergic contact/ atopic dermatitis
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18
Q

A nappy rash is an example of irritant contact dermatitis. What are of the skin would be spared

A

Flexure will be spared (due to urine)

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19
Q

Irritant contact dermatitis investigations

A
  • Clinical diagnosis, attempt to identify triggers from history
  • If trigger can’t be identified, patch testing may be required
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20
Q

What would cause irritant contact dermatitis around the lips

A

Lip lick chelitis

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21
Q

What is the main feature of atopic eczema

A

Pruritus

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22
Q

What other conditions are associated with atopic dermatitis/ eczema

A

other atopic diseases e.g. asthma, allergic rhinitis, food allergy

23
Q

Describe atopic dermatitis/ eczema

A
  • Chronic inflammatory disorder of the skin
  • Characterised by dermal inflammation (dermatitis) with resultant spongiotic change in the epidermis histologically
  • Chronic features including epidermal acanthosis, hyperkeratosis, and parakeratosis
24
Q

What three factors occur in combination with atopic dermatitis/ eczema

A

Eczema is a combination of decreased skin barrier function, environmental factors and immunology

25
Q

What mutation that affects skin barrier function is associated with atopic dermatitis/ eczema

A

mutations in fillagrin gene that result in severe/early onset disease (ichthyosis vulgaris)

26
Q

What is the relevance of the defective skin barrier in eczema

A

The defective skin barrier allows access/sensitisation to allergen and promotes colonisation by microorganisms

27
Q

What happens to the dermatitis in atopic dermatitis

A
  • The normal dermis has a small amount of lymphocytes and other immune cells but in skin with eczema there is a vast infiltrate visible
  • TH2 cells, DC, macrophages and mast cells are involved (probably attracted to lesions by stressed keratinocytes)
28
Q

What happens to keratinocytes in eczema

A

Keratinocytes in the epidermis start detaching from one another, becoming rounder and the intercellular spaces widening between them

29
Q

What causes the histological spongiotic change in eczema

A
  • If the eczema has come on acutely, this separation may be so severe that vesicles form
  • Under the microscope, this makes the epidermis look like a sponge, hence ‘spongiotic’ change
30
Q

How does eczema change with age

A

Childhood predominance: symptoms tend to become less severe with age

31
Q

What areas are commonly affected in eczema of infants vs teens

A

Infants - face is common site
Older kids/adults - flexor distribution (antecubital fossa and posterior knee)

32
Q

Atopic dermatitis/ eczema clinical features

A
  • The skin is itchy, erythematous, and oozing
  • May be vesicles, which may have crusted over (infections)
  • Eventually, the skin becomes dry and flaky
  • Repeated scratching causes lichenification (thick, leathery skin, also called lichen simplex et chronicus)
33
Q

Eczema can present differently in different skin colours. What is a common presentation in black people

A

Nodular Pruigo (well define itchy, lichenified nodules)

34
Q

Secondary infection can occur in patients with atopic dermatitis/ eczema. What would indicate this? name 2 examples

A
  • Crusting => Staph aureus
  • Monomorphic punched-out lesions => Herpes simplex virus (eczema herpeticum)
35
Q

What is eczema herpeticum

A

Herpes simplex virus infection in patients with eczema, presenting as monomorphic punched-out lesions

36
Q

Atopic dermatitis/ eczema diagnosis

A

Clinical diagnosis, diagnostic criteria…

Itching plus 3 or more of:
- Visible of flexural rash (cheeks/extensor surfaces in infants)
- History of flexural rash (cheeks/extensor surfaces in infants)
- Personal history of atopy (or first degree relative if <4 years)
- Generally dry skin
- Onset before age 2

37
Q

Atopic dermatitis/ eczema conservative management

A

Break the itch-scratch cycle!
- Avoid allergens & triggers e.g. soap substitutes
- Keep the area cool & dry
- Sedating antihistamine can reduce itching and aid sleep
- Liberal emollients should be applied frequently
- Psychological support may be needed

38
Q

Mild atopic dermatitis/ eczema topical management

A

Mild Topical steroid

39
Q

Moderate atopic dermatitis/ eczema topical management

A
  • Moderate topical steroid e.g. betamethasone valerate 0.025% or clobetasone butyrate 0.05%
  • If face affected start with mild steroid in that area
40
Q

Severe atopic dermatitis/ eczema topical management

A
  • Potent topical steroid e.g. betamethasone valerate 0.1% on inflamed areas
  • For more sensitive areas moderate potency e.g. betamethasone valerate 0.025% or clobetasone butyrate 0.05% max 5 days use
  • Consider occlusive dressings
41
Q

Last line/ secondary care atopic dermatitis/ eczema management

A
  • Phototherapy UVB - mainly
  • Systemic immunosuppression
  • Biological agents (for atopic - target IL-4/IL-13)
42
Q

What is discoid eczema

A
  • Eczema occuring in circular or oval patches (well-defined)
  • Patients are often atopic
  • Very often infected
43
Q

What are the two different causes of photo-induced/ sensitive eczema

A
  • Reaction to UV light (Well defined edge e.g. cut-off collar)
  • Patients often atopic
  • Can also occur secondary to photosensitising drugs
44
Q

What is lichen simplex dermatitis

A

Caused by chronic itching & is characterised by well demarcated, erythematous patches, and plaques of thickened leathery skin

45
Q

What causes stasis (varicose) dermatitis

A
  • This is eczema associated with chronic venous insufficiency (venous hypertension), usually affecting the gaiter area
  • Increased hydrostatic pressure of the blood results in extravasion of RBCs
46
Q

what clinical features would you expect in stasis dermatitis

A

Associated skin change include venous ulcers, lipodermatosclerosis, and hemasiderosis

47
Q

Stasis dermatitis management

A

Compression stockings

48
Q

What is dyshidriotic eczema (pompholyx eczema)

A
  • Occurs when there is a very sudden acute flare up of eczema and the spongiotic vesicles join together
  • Dermatological emergency and may complicate atopic eczema
49
Q

Dyshidriotic eczema (pompholyx eczema) presentation

A
  • There will be widespread redness (90%)
  • Tiny blisters develop in hands (classically sides of fingers) and feet
  • Intensely itchy
50
Q

Seborrheic eczema clinical features

A
  • The skin is flakey with a fine scale, oily, and erythematous
  • There is usually minimal pain or stinging or itch
  • The scale may coalesce into thicker plaques
  • It tends to affect the face (especially hairline, nasolabial fold, and brow area) in adults
51
Q

What is dandruff

A

Dandruff is the common term used to describe a mild, non-inflamed form of seborrheic dermatitis

52
Q

What is cradle cap

A

Infantile seborrheic dermatitis

53
Q

How does cradle cap appear

A

diffuse, yellow, greasy scale, coalescing into plaques on the scalp/groin/armpit

54
Q

Cradle cap treatment

A
  • Emollients (such as olive oil) loosen the scales, which can then be brushed off
  • Antifungal shampoos may be used if the issue persists
  • Tends to resolve with age