Module 2A - Dermatology Flashcards
Which cells predominantly make up the epidermis?
Keratinocytes –> migrate from lower epidermis (stratum basale)
- Once they reach the upper epidermis, they lose their nuclei and form tightly packed layers of keratin to form the stratum corneum
What is the top outer layer of the skin called –> what is it’s function
Epidermis –> barrier function
vicious cycle in eczema
Atopic eczema –> where does it usually affect + management
- Flexor surfaces
Management: - emollients –> regular use
- topical steroids –> acute flares
- phototherapy –> UVB
- DMARDs
- (if itchy –> antihistamines)
Emollients
Steroids and examples of use
- lower potentency for delicate areas such as face or genitals –> hydrocortisone 1%
- higher potency may be required for thicker skin areas like palm or soles –> betamethasone valerate 0.1%
Fingertip unit (FTU)
- 1 fingertip unit (FTU) covers area size of 2 hands
scoring tools –> EASI and DLQI –> what condition they used in
atopic eczema
What type of hypersensitivity reaction is allergic contact dermatitis?
Type IV delayed hypersensitivity reaction
–> reactions tend to happen 48-72hrs after contact with the allergen
Contact dermatitis
Why would patch testing be used?
If unknown allergen/trigger of contact dermatitis
Contact dermatitis –> management
- Avoid contact with allergen!
- Liberal emollients
- Topical steroids
- Treat any secondary infection
Skin anatomy –> label
time frame
Acute vs chronic urticaria
- Acute –> < 6 weeks
- Chronic –> > 6 weeks
Urticaria pathophysiology:
____ ____ degranulation
- type of hypersensitivity reaction
Mast cell
- Type I hypersensitivity immediate reaction due to allergen –> IgE mediated
4 types of hypersensitivity reactions
Type I –> reaction mediated by IgE antibodies
Type II –> cytotoxic reaction mediated by IgG or IgM antibodies
Type III –> reaction mediated by immune complexes
Type IV –> delayed reaction mediated by cellular response (48-72hrs)
All atopic diseases are what type of hypersensitivity reaction?
Type I –> IgE mediated immune repsonses
what to avoid + medications
Urticaria management
- Avoid trigger/allergen +/- treat infection + Avoid NSAIDs, aspirin, codeine
- 2nd-gen H1 antihistamine (non-sedating) up to QDS –> cetirizine, loratadine
- Sedating histamine at night –> eg. chlorphenamine
- Next step is prednisolone 30mg –> 5-6 days
Test for type I hypersensitivity
Skin prick testing
- Nodule
- Papule
- Pustule
- Vesicle
- Papule
- Nodule = larger
- Papule = smaller
- Pustule = blob has pus in it
- Vesicle = blob with fluid inside (clear)
- Papule = blob of skin with nothing inside it
Herpes simplex pathogens
- HSV-1 –> orofacial (80-90%)
- HSV-2 –> genital (70-90%)
Herpes simplex management
- Topical acyclovir 5% ointment
- If systemic –> acyclovir 200mg x5 a day for 5 days
- Prophylaxis –> acyclovir 200mg TDS for 6-12 months
Herpes zoster pathogen + aetiology
- Varicella zoster virus (VZV)
- reactivation of latent VZV in a sensory ganglia
Treatment for any herpes virus
Herpes zoster –> treatment
- Acyclovir
- can also give analgesia to relieve pain
treatment?
Viral warts pathogen
human papillomavirus (HPV)
–> benign condition no treatment
Molluscusm contagiosum pathogen
Molluscum contagiosum virus (MCV) –> poxvirus
Impetigo common pathogens
Staph. aureus and Strep. pyogenes
Impetigo –> treatment
- Clean –> hydrogen peroxide 1%
- Topical antibx –> fusidic acid
Folliculitis pathogens
Staph. aureus, Pseudomonas aeruginosa
2 bacteria that are infrequent resident flora of the skin
Staph. aureus and Strep. pyogenes
Cellulitis pathogens
Staph. aureus and Strep. pyogenes
Cellulitis –> treatment
beta-lactams –> penicillins and cephalosporins
Necrotising fascitis –> treatment
- surgical debridement, or amputation
- antibiotics –> gentamicin, clindamycin
Scabies pathogen
Sarcoptes scabiei var. hominis (human itch mite)
Scabies management
Skin lotions containing permethrin –> all family have to take
Tinea –> common organisms
- Tinea verrucosum
- Tinea rubrum
- Micosporum canis
Tinea treatment
topical antifungals –> imidazoles
Tinea…
- corporis
- capitis
- pedis
- cruris
- Tinea Corporis –> body
- Tine Capitis –> head (note: can get ringworm scab thing on scalp)
- Tinea Pedis –> feet
- Tinea Cruris –> groin
Candida intertrigo pathogen
Yeast –> usually candida albicans
Candida… treatment
topical antifungals
Pityriasis Versicolor and Seborrhoeic dermatitis pathogen
Yeast –> Malassezia furfur
Pityriasis versicolor treatment
- selenium sulphide shampoo (2.5%)
- ketoconazole shampoo
- or topical antifungals
A - HSV infection
B - Molluscum contagiosum
C - Folliculitis
D - Mucocutaneous leishmaniasis
A - HSV infection
B - Impetigo
C - Erysipelas/Cellulitis
D - Cutaneous leishmaniasis
IgE-mediated, Non-IgE-mediated, Non-allergic food hypersensitivity
Place into categories
- milk, egg, and peanut allergy
- Coeliac disease (gluten)
- Pollen related allergy
- lactose intolerance
- IgE-mediated –> milk, egg, and peanut allergy + pollen related allergy
- Non-IgE-mediated –> Coeliac disease (gluten)
- Non-allergic food hypersensitivty (food intolerance) –> Lactos (milk) intolerance
Which T-helper cell is involved in IgE production, mast cell activation, and allergic disease?
Th-2
guttate psoriasis?
Psoriasis –> Management
- Vitamin D3 analogues –> calcipotriol
- Corticosteroids –> topical or oral
- Coal tar –> soothes
- Keratolytics (eg. salicylic acid) –> reduces scales –> enhances penetration of topical treatment
- Phototherapy –> UVB, PUVA –> narrow-band UVB is best
- Topical dithranol –> good for inflammation and over production of skin cells
- Biologics –> anti-TNFs
(Guttate psoriasis –> often spontaneously resolves within 2/3 months)
UVA vs UVB
- UVA –> causes ageing
- UVB –> main carcinogen –> damages DNA and inhibits DNA repair processes
Breslow thickness
- Breslow thickness –> predicts melanoma survival (5 yr survival)
- essentially how deep the cancer goes
Glasgow 7-point checklist for melanoma
Management of any suspected skin cancer
- Skin excision biopsy –> histopathology
Exclamation mark hair –> what condition
Alopecia areata
Alopecia Totalis vs Alopecia Universalis
- Alopecia Totalis –> total loss of scalp hair
- Alopecia Universalis –> total loss of body hair
Trichotillomania
Self-induced pulling of hair
Hirsutism –> what is it + if symptoms of deep voice, increased muscle bulk, or clitoromegaly, then what are your next steps
- Androgen-dependent hair growth in a female
- urgently referred to endocrine for possible ovarian or adrenal tumour –> can also check for abdominal mass
Nail problems:
- Clubbing –>
- Koilonychia –>
- Onycholysis –>
- Pitting –>
Management of nail psoriasis
- Potent topical steroid at base of nail/cuticle
- Steroid injection into base of nail
Hutchinson’s sign –> what condition?
Extension of pigmentation to nail fold –> acral lentiginous melanoma
size?
Papule vs pustule
- Papules = measuring <5mm in diameter
- Pustules = pus-filled spots
size?
Nodulocystic acne –> more severe
Nodules = inflamed, swollen lesions >5mm
2 skin changes seen in acne
Grading of severity of acne
Acne management
- Benzoyl peroxide (gel or face wash) –> antiseptic –> reduces no. bacteria on skin
- Topical retinoids (gel or cream) –> eg. tretinoin, adapalene –> works by keratinocyte proliferation –> removes dead skin cells from surface of skin (exfoliating) –> prevents building up within hair follicles
- Topical antibiotics –> eg. erythromycin, doxy, clarithro
- Combined oral contraceptive pill for females –> lowers androgen lvls –> less sebum and less severe acne
- +/- Oral antibiotics (doxy, erytrho, clarithro)
- Isotretinoin –> severe acne (specialist use)
Acne –> when to refer to dermatology
What pill that women sometimes take can make acne worse?
Progesterone only pills –> the lack of oestrogen may allow for higher lvls of androgen
Diagnostic features of rosacea
Rosacea management
- 1st line –> topical ivermectin and oral doxycycline
Pathogenesis of acne
- Keratinocyte proliferation - leading to follicular plugs
- Androgen-induced sebum production - usually occurs during puberty
Most common side effect of topical steroids
Skin thinning
Creams vs ointments
- Ointments are oil-based
- Creams are a mixture of oil and water
How long should you wait between emollient application and topical steroids application
30 mins
Name 3 pre-cancerous lesions and treatment for each
- Actinic keratoses, Bowen’s disease (SCC in situ), and lentigo maligna are all pre-cancerous lesions
- Actinic keratoses + Bowen’s –> Efudix cream or 5-fluorouracil (topical chemo.) + cryotherapy
(Curettage and cautery (C+C) can be used for Bowen’s) - Lentigo maligna –> imiquimod (immunosuppessive drug) or surgical excision
Risk factors associated with skin cancer
+ treatment
Erythema nodosum causes
- depends on cause –> eg. stopping causative drug, symptomatic treatment
- if no cause –> bed rest + fluids
Treatment of pyoderma gangrenosum
High-dose oral steroids
- Necrobiosis lipoidica –> associated with diabetes
- annular granuloma –> raised borders
- associated with autoimmune and diabetes
- usually self-limiting
most common trigger
- Erythema mulitforme - target lesions
- most common triggers - infections (Herpes simplex)
Treatment of a widespread erythematous rash
Moisturiser + topical steroid
- Fluid-filled blisters, erythematous patches
–> Bullous pemphigoid - Skin biopsy
- Management –> high dose oral prednisolone is mainstay, then can add potent topical steroids, azathioprine
- erythematous ulcerated patches from ruptured blisters
- pemphigus vulgaris
- skin biopsy
- potent topical steroids, high dose oral prednisolone, azathioprine
- Dermatitis herpetiformis
- Check TTG (tissue transglutaminase) –> coeliac blood test
- Skin biopsy –> IgA deposition
- Management –> gluten-free diet and topical steroids
- Dapcin if coeliac diet doesn’t work
Causes + investigations + management
Wound healing video
Dr Matt and Dr Mike video:
https://www.youtube.com/watch?v=1VBLmyDjC0w
Vitiligo is associated with…
Autoimmune diseases –> Addison’s, Type 1 diabetes
Serious condition that eczema can develop into –> pt has red, rash, and outbreak of spots/inflammation + management
- Eczema herpeticum
- IV antivirals (aciclovir)
Acne vulgaris drugs that are contraindicated in pregnancy
Tetracyclines and retinoids –> teratogenic
Sebhorroeic dermatitis treatment
- Corticosteroids
- Scalp –> ketaconazole shampoo
- Face/body –> topical antifungal (ketoconazole)
Pityriasis rosea often follows a…
Viral infection
Drugs known to exacerbate psoriasis
- Lithium
- Anti-malarials
- Beta-blockers
- ACEi
- anti-TNF-alpha
- NSAIDs
TEN (toxic epidermal necrolysis) –> 4 classes of drugs that can cause crossreactions leading to TENs
- Beta-lactam antibiotics –> penicillin, cephalosporin and carbapenem (penicillins –> co-amoxiclav)
- Sulph- drugs
- Anticonvulsants –> carbamazepine, phenytoin
- NSAIDs
SJS vs TEN
- SJS –> < 10% of body affected by rash
- TEN –> > 30% of body affected by rash
(overlap in between)
A 62-year-old female is referred to dermatology by her GP due to a lesion over her shin. It initially started as a small red papule which later became a deep, red, necrotic ulcer with a violaceous border. What is the likely diagnosis?
Pyoderma gangrenosum
Shingles (herpes zoster) –> treatment + timeline to start treatment within
Oral antivirals –> within 72hrs onset
Vitamin D (Calcitriol) –> functions + how is it acquired
- Important for bones –> increases dietary calcium and phosphate absorption
- Acquired from UV skin exposure (up to 15 mins per day) and Diet
- Vitamin D deficiency common –> it is important to give people advice about sun protection but also advise vit D supplements
Why are transplant patients at an increased risk of skin cancer?
- due to immunosuppression
What are the two main types of albinism?
Oculocutaneous albinism:
- Type 1: more severe - no melanin
- Type 2: some melanin
- Ocular albinism: normal, or slightly paler than normal eyes for their ethnicity, skin, and hair
Actinic keratoses –> pathology + aetiology + location on body
- Proliferation of cytologically aberrant epidermal keratinocytes
- UV-induced + very common in bald white men over 75yrs
- Sun-exposed areas –> scalp
BCC –> pathogenesis + mutations in what gene predispose to BCC
- Basal Cell Carcinoma (aka. rodent ulcer) is the most common cancer in humans, derived from non-keratinising cells originating in the basal layer of the epidermis
- mutations in the PTCH gene
Erythema migrans –> what disease + management
- Lyme disease
- Antibiotics (doxy, amox)
Impetigo –> most common causative pathogen + management
- Staph. A or Strep. pyogenes
1. Clean –> hydrogen peroxide 1% cream
2. Topical antibiotics –> fusidic acid
Gorlin’s syndrome predisposes to what skin cancer?
BCC
Alopecia ariata management
- 80-90% will spontaneously regrow
- consider –> topical corticosteroids, topical minoxidil
Dermatitis herpetiformis –> underlying pathophysiological process + skin biopsy finding
Formation of IgA antibodies –> skin biopsy shows a granular pattern of IgA deposition
Impetigo vs Measles –> isolation periods
- Impetigo –> isolate until 48hrs after starting treatment (fusidic acid) and should have crusted over
- Measles –> isolate for 4 days after rash appears
Most common side effect of oral isotretinoin
Dry skin
What drug type is known to exacerbate plaque psoriasis?
Beta-blockers
What gene is associated with eczema?
Filaggrin gene
Biopsy and immunofluorescence showing IgG auto-antibody deposits within the epidermis
VS
Biopsy and immunofluorescence would show IgG auto-antibodies deposited on the basement membrane
- Pemphigus vulgaris vs bullous pemphigoid
- Pemphigus –> deposits within epidermis
- Bullous pemphigoid –> deposits on basement membrane
Nikolsky sign positive suggests
Pemphigus Vulgaris
Psoriasis –> which drug may be used long term
Calcipotriol (vit D3 analogue)
–> reduces epidermal proliferation, reduces scale and thickness of plaques, but doesn’t help with erythema
