6- Dermatology (Inflammatory conditions) Flashcards
Atopic Eczema
Background
- Inflammatory skin condition
- Chronic, relapsing atopic condition caused by defects in the normal continuity of the skin barrier, leading to inflammation in the skin
- Significant variation in the severity of the condition
- Can become infected e.g. cellulitis
Pathophysiology of eczema
The simplified pathophysiology is that eczema is caused by defects in the barrier that the skin provides. Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response, resulting in inflammation and the associated symptoms.
Causes/ risk factors for eczema
- Genetic influence
- Atopic- dust, fur
- Environmental triggers
o Cold
o Dietary products
o Washing powders
o Stress
presentation of eczema
Presentation
- Presents in infancy
- Acute: itchy papules and vesicles
- Dry, red, itchy and sore patches of skin
- Flexor surfaces e.g. elbow, knees, face and neck
- Nail signs- pitting and ridging
- Can appear as flares rather than being constant
management of eczema is split into
maintenance and management of flares
maintenance management of eczema
- Provoking factors avoided
- Emollients used to create an artificial barrier over the skin to compensate for the defective skin barrier
- Used as often as possible, particularly after washing and before bed (3-4 times a day)
AVOID
- Hot baths
- Scratching
- Soaps which remove natural oils
Management of Eczema Flares
- Thicker emollients and “wet wraps’ (applying a wrap to areas covered in emollient overnight)
- Topical steroids (oral if severe)
- Antibiotics to treat infections e.g. fluxcloxacillin
Specialist treatment for severe non responsive eczema
- Phototherapy
- Topical tacrolimus
- Oral corticosteroids
- Methotrexate
- Azathioprine
types of emollients
The thicker the more effective
- Ointments- has the highest oil content, therefor most effective at treating dry skin
- Creams- lighter and easier to leave on skin (less oil on skin)
o Lots of people use creams in the day and ointment at night
- Lotions (least oil content)- least effect on dry skin
examples of emollients
Thin creams:
* E45
* Diprobase cream
* Oilatum cream
* Aveeno cream
* Cetraben cream
* Epaderm cream
Thick, greasy emollients:
* 50:50 ointment (50% liquid paraffin)
* Hydromol ointment
* Diprobase ointment
* Cetraben ointment
* Epaderm ointment
How to use emollients?
- Always wash and dry hands first (best after a shower)
- Never use fingers to decant emollient from a tub (bacteria can get into ointment)- use spatula or clean spoon
- How much? Depends on condition of skin
o For adults with very dry skin use 500-1000g per week - Follow the direction the hair lies and apply emollients with stroking motion
- If using a steroid cream or another treatment for skin condition, wait at least 30 mins after putting emollient on before applying (avoids dilution)
- Can be applies as often as you like (3-4 times a day
o Esp hands and face - Can use before swimming
topical steroids rules
- use weakest steroid for shorted period of time to get the skin under control.
- Mild: for face and flexure
- Stronger: thicker skin
steroid ladder
- Mild: Hydrocortisone 0.5%, 1% and 2.5%
- Moderate: Eumovate (clobetasone butyrate 0.05%)
- Potent: Betnovate (betamethasone 0.1%)
- Very potent: Dermovate (clobetasol propionate 0.05%)
side effective of steroids
- Thinning of the skin
- Telangiectasia
Systemic absorption of steroid
- Slower growth
- Weight gain
- Roundness of face
- Mood changes
how to apply steroid creams
- Wash and dry hands
- Squeeze out about the same amount as the tip of your finger (this I enough for the same area as if you put your two hands flat together)
- Only apply to effected areas
- Avoid applying steroids with emollients (dilution)
- Dry and wash hands thoroughly after
Eczema and infections
Bacterial
- Most commonly staphylococcus aureus
- Oral antibiotics: flucloxacillin
- Severe cases may require admission and IV abx
Eczema herpeticum
- Viral skin infection cause by HSV or VZV
Eczema herpeticum
Background
- Widespread eruption
- Serious complication of atopic eczema
- Occurs in those with pre-existing skin conditions where the virus an enter the skin and cause infection
causes of eczema herpeticum
Causes
- Herpes simplex virus (HSV 1)
o May be associated with a coldsore
- Varicella zoster virus
Presentation of eczema herpeticum
- Extensive crusted papules, blisters and erosions
o Will burst - Systemically unwell with fever and malaise
- Lymphadenopathy
management of eczema herpticum
First line: Acyclovir
- Oral if moderate
- IV if severe (will need admitting)
Antibiotic for secondary bacterial infection
Complications of eczema herpeticum
- Herpetic hepatitis
- Encephalitis
- Bacterial superinfection
- DIC
- Death
Psoriasis
Background
- Psoriasis is a chronic, autoimmune skin condition that can also affect the nails and joints. It tends to flare up from time to time. (psoriatic arthritis- pitting, onycholysis = nail signs))
- Increases risk of arthritis and CVD- inflammation of vasc
pathophysiology of psoriasis
- Occurs due to increased production of skin cells- keratinocytes
- Skin cells normally replaced every 3-4 weeks, however in this chronic condition it only takes 3-7 days
- Underlying cause not fully understood- to do with immune system mistaking healthy cells
triggers for psoriasis
o Injury to skin- Koebner phenomenon
o Throat infection- step
o Medications
o Stress
o Infection
o Smoking and alcohol
risk factors for psoriasis
- fairer complections
- genetic risk
presentation of psoriasis
- Usually extensor e.g. elbows and knees and scalp region (as opposed to eczema)
- Erythematous, crusty skin covered with silvery scales
- Raised and rough plaques
- Guttate more common in children, my be preceded by strep throat infection
- Nail psoriasis e.g. pitting, thickening, oncolysis
- Psoriatic arthritis 10-20% (usually middle age starts)
- Auspitz sign – scratch and gentle removal of scales cause capillary bleeding
Auspitz sign
scratch and gentle removal of scales cause capillary bleeding
management of psoriasis
Management
- Emollient
- Topical corticosteroids
- Topical Vitamin D analogues (Calcipotriol)
- Second line
o Phototherapy (narrow band UV B)
- Unlicenced treatments for severe psoriasis
o Methotrexate, cyclosporine, retinoids, biologic medications such as DMARDs e.g. TNF antagonist adalimumab
- Psychosocial counselling
types of psoriasis
plaque
guttate
flexutal
pustular
erythroderma
Plaque psoriasis
the most common sub-type resulting in the typical well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
Guttate psoriasis:
transient psoriatic rash frequently triggered by a streptococcal infection.
Multiple red, teardrop lesions appear on the body-> especially trunk
o second most common
o children
o small raised papules
Flexural psoriasis
in contrast to plaque psoriasis the skin is smooth
Pustular psoriasis
commonly occurs on the palms and soles
o Rare
o Pustules form under erythematous skin
o Not infectious
o Medical emergency and usually require hospital admission
Erythroderma psoriasis
- Rare form of psoriasis with extensive erythematous inflamed areas covering most of the surface area of the skin
- Skin falls away in large patches resulting in raw exposed areas
- Medical emergency
Koebner phenomenon
refers to the development of psoriatic lesions to areas of skin affected by trauma
Residual pigmentation
of the skin after the psoriatic lesions resolve
Acne vulgaris
Background
- Very common condition
- Acne – comedowns
- Open comedowns- blackheads
- Closed comedowns- whiteheads
pathophysiology of acne vulgaris
Pathophysiology
- Caused by chronic inflammation, with or without localised infection, in pockets of skin known as pilosebaceous unit
- Acne results from increased production of sebum, trapping keratin and blocking the pilosebaceous unit
- Leads to swelling and inflammation
- Androgenic hormones increase production of sebum- therefore exacerbated by puberty and improves with anti-androgenic hormonal contraception
- Bacteria: Propionibacterium acnes – bacteria which colonises the skin and can contribute to acne
sk factors for acne vulgaris
Risk factors
- Puberty and adolescence
- Family history
Presentation of acne vulgaris
- Significant variation in severity of acne
- Red, inflamed and sore spots on the skin
- Typically distributed
o Face
o Upper chest
o Upper back - In darker skin -> hyperpigmented lesiosn
Management of acne vulgaris
Stepwise
- No treatment if mild
- Psychosocial counselling
- Topical benzoyl peroxide
- Topical retinoids (chemicals related to vitamin A)- slows production of sebum
- Topical antibiotics – clindamycin (prescribed with benzoyl peroxide t reduce bacterial resistance
- Oral antibiotics such as lymecycline (make sure not pregnant- tetracycline is a teratogen)
- Oral contraceptive pill e.g. Co-cyprindiol (Dianette)- COCP)
- Oral retinoids e.g. isotretinoin
Describing acne lesions
- Pustules are small lumps containing yellow pus
- Comedomes are skin coloured papules representing blocked pilosebaceous units
- Blackheads are open comedones with black pigmentation in the centre
- Ice pick scars are small indentations in the skin that remain after acne lesions heal
- Hypertrophic scars are small lumps in the skin that remain after acne lesions heal
- Rolling scars are irregular wave-like irregularities of the skin that remain after acne lesions heal
Oral retinoids
Isotretinoin i.e. Roaccutane
- Effective last line option
- Prescribed by specialist
- Highly teratogenic
- Women must have reliable contraception and do regular pregnancy tests
o And agree to termination if gets pregnant
o Stop a month before trying to get pregnant
retinoids MOA
- Reduce production of sebum, reducing inflammation and bacterial growth
Side effects of oral retinois
- Dry skin and lips
- Photosensitivity of the skin to sunlight
- Depression, anxiety, aggression and suicidal ideation. Patients should be screened for mental health issues prior to starting treatment.
- Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
Contact dermatitis
Background
- Itchy rash caused by direct contact with allergen
- Delayed Type 4 hypersensitivity reaction
- Types
o Chemical burns
o Irritant contact dermatitis
o Allergic contact dermatitis
Pathophysiology of contact dermatitis
Common in children because skin is easily sensitised:
- Thinner skin than adults
- Can absorb more applied substances
- More likely to have underlying atopic dermatitis which facilitates sensitisation due to impaired skin barrier
- Sensitization can occur in newborns from ages 0-3, prevalence of subsequent allergic contact dermatitis increases with age
common allergens which cause contact dermatitis
- Nickel (piercings, buttons, fasteners, clips, toys)
- Fragranced products
- Colophonium found in plasters
presentation of contact dermatitis
- Shows up on skin after direct contact e.g. face, hands, feet, arms, legs
- When allergen is removed, rash slowly resolves over several days to several weeks and will reappear with further contact
- Always itchy
- Erythematous blisters
- Oedema
- Dryness
- Fissuring
- Lichenification
- Pigmentation increase or decrease
investigations for contact dermatitis
- Patch testing
management of contact dermatitis
Management
- Once cause has been identified, avoid direct contact (lifelong)
- Avoid soap and dry skin carefully after washing
- Short course of topical corticosteroid cream
o Hydrocortisone for face
- Emollients frequently applies
- Severe: oral corticosteroids e.g. prednisone
- Second line: calcineurin inhibitor
