Common Dermatological Problems Flashcards
Describe derm history taking
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
How would you conduct a skin exam?
What is the skin lesion ref guide?
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
What is a dermascope?
You can also use a dematoscope tool that uses surface microscopy to look at skin lesions. we look at: colour, pattern
Describe atopic eczema
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!!)
What is the presentation of atopic eczema?
Describe the histology of atopic eczema
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
What is the presentation of atopic eczema in diff age groups?
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
What is the treatment for atopic eczema?
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
Secondary Care Atopic Eczema Management?
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
What are complications of atopic eczema?
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
Describe the distribution of psoriasis
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
What is the difference between psoriasis and eczema?
Inc the differences in secondary treatment
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
What does this show?
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
What does this show?
Palmo plantar psoriasis
Just affects palms/soles/acral surfaces
Thickening, crusting
Topical treatment tricky cause skin is so thick
Describe the histology of psoriasis
Outline the treatments for psoriasis
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
Outline the secondary management for psoriasis
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)
What are the different types of acne lesions?
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.
Describe impetigo and viral warts
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)
Describe other skin conditions such as tinea, urticaria, vitiligo and keloid scar
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
What is erythroderma?
What is the management of Erythroderma?
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
What does this show?
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
What is SJS and TEN?
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.
What do the skin lesions on SJS and TEN look like?
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.
how is SJS and TEN classified?
Management of SJS/TEN?
What is this and what does it show?
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
Bullous pemphigoid?
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
What are the types of lesions in bullous pemphigoid?
complete the table
