Common Dermatological Problems Flashcards

1
Q

Describe derm history taking

A

Open question: Ask patient to describe their skin problem
o Location/Distribution
o Onset/duration
o Associated symptoms: Itch, bleeding
o Changes/Progression
o Triggering factors
o Treatments they have tried
o Family history
o Impact on patient’s life

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2
Q

How would you conduct a skin exam?

A
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3
Q

What is the skin lesion ref guide?

A

Macules - small flat lesions, differently coloured to the surrounding area, less than 1cm in size
If larger than 1cm, you describe them as a patch.

If you have a small lesion that is raised, less than 0.5cm or 1cm= papule
Larger than 1cm = nodule
Excoriation - break in skin caused by scratching
Lichenification - thickening of skin caused by chronic rubbing

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4
Q

What is a dermascope?

A

You can also use a dematoscope tool that uses surface microscopy to look at skin lesions. we look at: colour, pattern

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5
Q

Describe atopic eczema

A

Most common eczema -15% of population
Majority onset is <5years, about 60% will clear by adolescence
Skin barrier defect- more easily irritated by soap and contact irritants, weather, temp, etc.
Chronic or acute flares
Atopic eczema=part of a triad w allergic rhinitis (hay fever) and asthma (so ask about these in history!!)

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6
Q

What is the presentation of atopic eczema?

A
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7
Q

Describe the histology of atopic eczema

A

Acute stage: epidermis oedema (spongiosis). Intraepidermal vesicles (fluid filled) which form blisters which can rupture

chronic stage: loss of vescicles. Epidermis thickens:
stratum spinosum - acanthosis
stratum corneum - hyperkeratosis

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8
Q

What is the presentation of atopic eczema in diff age groups?

A

Infantile atopic eczema
- widespread dry scaly skin
- can be weeping (exuding liquid)
- often cheeks= first area affected
- nappy area spared - moisture-effect

Toddler/school-age children: more localised (flexural), thickened, leathery (lichenified) lesions. Scratch marks

Adults: commonly persistent localised eczema
Recurrent secondary staphylo infection
Major factor for irritant contact dermatitiis

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9
Q

What is the treatment for atopic eczema?

A

Trigger avoidance
Break the itch-scratch-itch cycle (role of histamine)
Emollients: lotion (oil in higher water content). Cream (oil in lower water content). Ointment (oil-based)
Soap substitutes - aqueous cream, emulsifying ointment
Bath preparations
IF NOT WORKING
Topical steroids: mild, moderate, potent, v potent
Other: topical calcineurin inhibitors (Tacrolimus), antibiotics, antihistamines
Derm referral if poor response or diagnostic uncertainty

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10
Q

Secondary Care Atopic Eczema Management?

A

Phototherapy: UVA/UVB light helps to settle the inflammation. 2,3 x a week for 3 weeks

Systemic immunosuppresants: azanthioprine, methotrexate, ciclosporin, which dampen down overactive inflammatory cells

Biologics: Must have trialed other systemic(s) and have high disease severity. eg Dupilumab= monoclonal Ab that blocks IL-4 and IL-13

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11
Q

What are complications of atopic eczema?

A

Impetiginisation: co-infection w bacteria
E.g. Staph aureus, strep pyogenes. Patients present w honey yellow coloured crust as well as pustules

If they have co-infection with a virus, usually herpes simplex= eczema herpeticum - pouched out vesicles

PIH/Scarring
Striae/skin atrophy from steroid use
Depression

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11
Q

Describe the distribution of psoriasis

A

Distribution:
o Variety of size and shapes
o Symmetrical
o Extensor surfaces
o Sacrum, scalp, ears, palms, soles
o Nails
o Environmental, genetic, immunologic factors

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12
Q

What is the difference between psoriasis and eczema?
Inc the differences in secondary treatment

A

Opposite to eczema, its on the EXTENSOR surfaces. Backs of the arms, fronts of the knees, the sacrum
In psoriasis, epidermal thickening/scale is caused by reduced epidermal transit time of keratinocytes from 30 to 6 days

Both use phototherapy but UVB more common in psorasis
Systemics: acitretin for psoriasis, azanthioprine for eczema
biologics: Monoclonal Abs against TNF/IL for psoriasis, Dupilumab for eczema

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13
Q

What does this show?

A

Guttate psoriasis (raindrops)
Small plaques
Appear quickly
Comes in a week or two after a streptococcal throat infection (trigger)
Self resolves after three or four months
Topical treatment is tricky - hard to put it on each spot
Phototherapy is better

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14
Q

What does this show?

A

Palmo plantar psoriasis
Just affects palms/soles/acral surfaces
Thickening, crusting
Topical treatment tricky cause skin is so thick

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15
Q

Describe the histology of psoriasis

A
16
Q

Outline the treatments for psoriasis

A

Topical:
o Emollients
o Topical steroids
o Coal tar
o Salicylic acid
o Vitamin D analogues (Calcipotriol)
o Combination of above
o Dithranol

Refer to Dermatologist if: Diagnostic uncertainty, severe psoriasis or poor response to topical therapy

17
Q

Outline the secondary management for psoriasis

A

phototherapy - commonly use UVB, which again suppresses major components of cell-mediated immune function.
Systemics: ciclosporin, methotrexate, acitretin
Biologics: Monoclonal Abs against TNF/IL. Must meet specific criteria based on disease severity/quality of life. Must have trialed other systemic(s)

18
Q

What are the different types of acne lesions?

A

Papules (small, tender red bumps)
Pustules (white or yellow “squeezable” spots)
Nodules (large painful erythematous lumps)
Pseudocysts (cyst-like fluctuant swellings)
Individual acne lesions usually last less than 2 weeks but the deeper papules and nodules may persist for months.

19
Q

Describe impetigo and viral warts

A

Usually bacterial infection with staph aureus
Golden crust on the surface
Starts as one spot which erupts and then the rash spreads
Treatment: either topical antibiotics (fusidic acid), or oral antibiotic if more widespread (oral flucloxacillin)

20
Q

Describe other skin conditions such as tinea, urticaria, vitiligo and keloid scar

A

Tinea= fungal infection, typically affects warmer skin areas. Unlike psoriasis, this has asymmetric presentation
Urticaria= allergic skin reaction, thickened itchy lesions. Last for about 24hr. Can look like tinea, look at pt history!
Vitiligo= immune condition, skin loses pigment
Keloid scar= post surgical scarring process has been over-active. Scar extends beyond original incision

21
Q

What is erythroderma?

A
22
Q

What is the management of Erythroderma?

A

Discontinue all unnecessary medications
Monitor fluid balance; loss of fluid from skin= electrolyte disturbance and dehydration
Maintain skin moisture and body temp w wet wraps & greasy emollients
Antibiotics if superimposed bacterial infection
Antihistamines if itch
Identify underlying cause and start specific treatment

23
Q

What does this show?

A

Erythema Multiforme. 2 types (both have classic targetoid lesions)
1. Major: Mucosal erosions and blisters, target lesions, bullae. Cause: medications
2. Minor: No erosions/blisters. Targetoid lesions on extremities. Cause: infections

Management: Stop offending drug if its major
- Treat underlying cause
- Supportive/symptomatic

24
Q

What is SJS and TEN?

A

Stevens-johnson (SJS) and Toxic epidermal necrosis (TEN) MEDICAL EMERGENCY
Severe, immune complex medicated, drug hypersensitivity eruptions that affect the skin and mucous membranes
Nearly always caused by meds- type B reaction
Anyone on medication can develop SJS/TEN unpredictably - 40% caused by antibiotics.

25
Q

What do the skin lesions on SJS and TEN look like?

A

Skin lesions may be:
- Flat, red and diffuse macules (measles-like spots) or purple (purpuric) spots
- Diffuseerythema
- Targetoid lesions
- Flaccid blisters
- Sheets of skin detachment
- Nikolsky sign positive → blisters and erosions appear when skin is rubbed gently.

26
Q

how is SJS and TEN classified?

A
27
Q

Management of SJS/TEN?

A
28
Q

What is this and what does it show?

A

Pemphigus vulgaris=AI blistering skin condition
Painful blisters and erosions on skin and mucous membranes
IgG binds to Desmoglein 3 protein in the epidermis–> keratinocytes separate from eachother and replaced by fluid
Diagnosis: skin biopsy for direct immunofluorescence → IgG antibodies on the surface of keratinocytes in epidermis
Management: symptom control + topicals + systemic immunosuppression

29
Q

Bullous pemphigoid?

A

Subepidermal autoimmune disease
Risk factors: neurological conditions, psoriasis, medications
Attack on collagen (BP180) in the basement membrane of the epidermis by IgG +/- IgE, which form blisters

Diagnosis: direct immunofluorescence of askin biopsy→ linear deposition of IgG along the basement membrane (between the epidermis and dermis)
Management: emollients, potent topical steroids+ systemic steroids/ doxycycline/ immunosuppressants

30
Q

What are the types of lesions in bullous pemphigoid?

A
31
Q

complete the table

A