DERM Flashcards
What is acne rosacea? RF? Presentation? IX Treatment
Chronic relapsing/remitting inflammatory disorder of the hair follicles and blood vessels affecting the face
Women, middle aged, FHX, sun exposure, vasodialative drugs- ccb
Facial flushing Burning Dry skin Butterfly erythematous rash Telangiectasia Blepharitis, conjunctivitis, keratitis (in ‘ocular’ rosacea)
Clinical diagnosis
however if unsure- do a skin biopsy and ANA to exclude sle
Mild- Topical metronidazole + topical azealic acid
Moderate-severe- oral tetracycline/erythromycin
Brimonidine 0.5% gel: for patients with predominant flushing but limited telangiectasia
Oral isotretinoin or clonidine: for flushing
Lifestyle avoid sun, ccb and triggers
What is Acne vulgaris? Pathophysiology behind this how are comedones formed RF Presentation IX MX
Chronic inflammation of hair follicles and sebaceous glands
2 mechanisms
Hyperandrogenism- excess sebum production by sebaceous glands, causes excess production of keratin by keratinoycytes leading to blockage of the folicles leading to comedone formation
Propion bacterium acnes- colonisation of the folicles leading to inflammatory cytokines and lipases
Acne is characterised by the obstruction of the pilosebaceous follicle with keratin plugs, resulting in comedones, inflammations and pustules.
Open comedones- black heads
CLosed comedones- white heads
Teenagers and young adults: peaks at age 14 for girls and at age 16 for boys
Family history
Medications: androgens, corticosteroids
blackheads, white heads, pustules and papules all over the face and back
clinical diagnosis however can do Endocrine screen to exclude hyperandrogenism
Topical retinoid+ Benzoyl peroxide
TOpical abx- clindamycin alway coprescribe benzoyl peroxide to avoid abx resistance
Topical azealic acid
second line
Oral tetracycline + benzoyl peroxide
COCP
Oral isotretinoin- accutane vitamin a analogue
Pregnancy is a contraindication to both topical and oral retinoids- use erythromycin
What is actinic keratosis? Pathophysiology behind actinic keratosis Risk of forming RF IX MX
sun induced lesions
Ultra violet light b causes damage to p53 gene found on keratinocytes, so longer undergoes apoptosis and the keratinocytes turn into actinic keratoses
risk of turning into squamous cell carcinoma
large irregular scaly lesions with a pink colour and yellow tinge on sun exposed areas
CLinical diagnosis
however can use a dermoscope- straeberrry pattern
and skin biopsy
not usually treated but Lesion: Cryosurgery: liquid nitrogen Curettage Excision Field: Chemical peels Topical and systemic retinoids Lesion and field: Topical therapy: fluorouracil, imiquimod, diclofenac Photodynamic therap
What is alopecia areata? RF for alopecia? features IX Treatment
Autoimmune condition which leads to inflammation of the hair follicle leading to non scarring, patchy hairloss
Autoimmune disease: thyroid disease, vitiligo, type 1 diabetes, pernicious anaemia
Family history of autoimmune disease
patchy hairloss
non scarring
exclamation mark hairs- proximal thinner than distal
nail pitting
IX- clinicla but can do a hairpull test, skin biopsy
Treatment
camouflage
steroids
and minoxidil
WHat is basal cell carcinoma?
pathophysiology and likelihood of metastasis?
RF
Types and features
IX
management
s the most common cutaneous malignancy and arises from basal cells (stratum basale) of the epidermis
SUn exposure leads to uv related dna damage and metastaiss are rare
Male
Ultraviolet (UV) exposure: e.g. sunbeds and sun exposure
Fair skin: Fitzpatrick skin types I and II
nodular- Most common type
Found on skin exposed to the sun
Most commonly affects the face, neck, ears and chest
Pearly, indurated flesh-coloured papule with rolled border and covered in telangiectasia
May ulcerate later, creating a central ‘crater’
Slow growing and rarely metastasises
superficial-Less common
Flat, scaly plaque
Usually on the trunk
clinical diagnosis but can do a biopsy if unsure
surgicla excision and chemo and radiotherapy
What is bullous phemigoid? pathophysiology
Features
IX
MX
autoimmune bullous disease. It is a type of sub-epidermal blistering skin disease and is thought to occur due to autoantibodies directed against 2 hemidesmosomal proteins, BP180 and BP230
itchy, tense blisters typically around flexures
the blisters usually heal without scarring
there is usually no mucosal involvement
Skin biopsy
immunofluorescence shows IgG and C3 at the dermoepidermal junction
Management
referral to a dermatologist for biopsy and confirmation of diagnosis
oral corticosteroids are the mainstay of treatment
topical corticosteroids, immunosuppressants and antibiotics are also
what is contact dermatitis? 2 types? how to differentiate RF and common allergens Symptoms IX Management
skin reaction caused by an external agent
Irritant contact dermatitis- within minutes to hours no prior exposure
Allergic contact dermatitis- requires prior exposure and takes days for rash to show up
occupation, history of atopic eczema, nickel sulfate, neomycin, formaldehyde, sodium gold thiosulfate
Erythema pruritus burnign vesicles affecting areas which have been touched Scaling and lichenification are signs of chronic contact dermatitis
IX- skin patch testing–> Skin biopsy
Avoid irritant, emoilients, topical corticosteroids
second line- topical calcineurin inhibitors
what is eczema? Types of eczema RF for eczema Features of eczema IX manegement life threatening complication
Inflammation of the epidermis
atopic dermatitis, contact dermatitis, discoid eczema, seborrheic dermatitis, venous dermatitis
devloped world, urban, atopy, fhx
pruritus, dry skin, erythema, vesicles
mainly clinical, can do allergy testing
Emoilients, corticosteroids, antihistamines
eczema herpeticum, due to infection with hsv treat with iv aciclovir
what is impetigo? 2 forms rf features IX management complication
superficial bacteria infection due to staph aureus or strep pyogenes
non bullous= more common and bullous
young, close contact with infected people, poor environement
honey crusted lesions, flacid dluid filled bullae and diarrhoea, fever lymphadenopathy
clinical diagnosis but can do a swab
school absitencne after crusted over or 48 hours after ABX
if localised hydrogen peroxide or topical fusidic acid
if widespread- topical fusidic acid or oral flucoxacillin
cellulitis and staphylococcal scalded skin syndrome
what is a malignant melanoma? RF Features Ix prognostic factors
Tumour arising from the melanocytes
age, fhx, pale, uv exposure, previous cancers
Asymmetry, border irregularity, colour changes, diamter over 6mm, evolution
dermoscopy, excision biopsy, sentinel lymph node biopsy, CTCAP- staging associated with BRAF mutations
Management- Excision, topical imiquimod, lymph node dissection, radiotherapy
the Breslow thickness. Other poor prognostic factors include lymph node involvement, ulceration and male sex .
What is pityriasis rosea
features
IX
Management
inflammatory skin condition associated with hhv 6 and hhv 7
Itchy rash, herald patch and then. generalised rash, urti precedes the rash
IX- clinical diagnosis
MX- self resolving can sue topical steroids and antihistamines
What is psoriatic arthiritis? Pathophysiology RF and associations features IX MX
Chronic systemic inflammatry skin disease with multifactorial aetiology
immune mediated condition t cell activation stimulates proliferation of keratinocytes leading to plaque formation
HLA b13 and b17
Psoriatic arthirtis, IBD, fh, obesit smoking ACE inhibitors
Beta-blockers
NSAIDs
Lithium
Hydroxychloroquine
Antibiotics: tetracycline, penicillin
Steroid withdrawal
Plaques, pruiritus, Pitting onchyolisis, nail loss
clinical diagnosis
TOpical corticosteroid and topical vit D
short acting diathrol
phototherapy
DMards and biologics
may need coal tar shampoo if scalp
What is scabies
feratures
itchy skin infestation caused by sarcoptes scabei
pruritus specifically at night
symemtrical erythematous papules
linear crroked burrows
INK burrow test
permithin cream and topical crotamiton cream
