Dermatology Flashcards
(14 cards)
Investigation for contact dermatitis?
Skin patch testing
Two types of contact dermatitis?
Irritant and allergic
What type of hypersensitivity reaction is allergic contact dermatitis?
Type IV
Management of contact dermatitis?
Avoidance of trigger
Topical steroids
Oral antihistamines to reduce pruritus
When to refer to dermatology for contact dermatitis?
Severe, chronic, recurrent, persistent
Previously stable, now worse
Allergic to prescribed topical treatments
Dermatitis is associated with occupation
Unresponsive to treatment
Management of head lice?
Wet combing or 4% dimeticone lotion for breastfeeding, pregnant women, asthmatics and eczema patients, and 6 months -2 yo children
Malathion 0.5% for everyone else
What is sebhorreic dermatitis?
Features of it?
Management of sebhorreic dermatitis?
Complications of it?
Inflammatory skin reaction to Malassezia furfur, a yeast normally found on the skin.
Greasy, flaky scales on an erythematous background in sebum rich areas of skin - nasiolabial folds, scalp, posterior auricular skin
1st line: ketoconazole
2nd line: zinc pyrothine shampoo
3rd line: topical corticosteroids if severe inflammation
Complications of sebhorreic dermatitis: otitis externa and blepharitis
SCABIES
- What is scabies
- What hypersensitivity reaction is it
- What are the features?
- What type of scabies is seen in immunocompromised patients?
- Management of scabies?
- Contagious skin infection caused by Sarcoptes scabei mites
- Delayed Type IV, symptoms appear 30 days after exposure to mites
- VERY itchy papular/vesicular rash with superficial burrows on inter web spaces, wrist flexures, axilla, abdomen, groin (folds of the body)
WORSE AT NIGHT - Norweigan/Crusted scabies
- 1st line: topical permethrin applied to cool dry skin, on the whole body incl. face and scalp.
Crotamiton cream for itch relief
2nd line: Malathion 0.5%
TREAT ALL CONTACTS IN HOUSEHOLD ON THE SAME DAY
PEMPHIGUS VULGARIS
- What is it?
- Which population is it more common in?
- What type of hypersensitivity reaction is it?
- Features?
- Management of it?
- Autoimmune disease caused by antibodies against desmoglein 3 (epithelial adhesion molecule).
- Ashkenazi Jewish
- Type II
- MUCOSAL ULCERATION
Few months later, skin blistering - flaccid, easily ruptured vesicles and bullae. Nikolskys positive
Acantholysis on biopsy - 1st line: steroids
2nd line: immunosuppressants
BULLOUS PEMPHIGOID
- What is it?
- What type of hypersensitivity reaction is it?
- Features?
- Diagnosis of it?
- Management of it?
- Autoimmune disorder caused by antibodies against hemidesmosomal molecules BP180/BP230. Leading to SUB EPIERMAL BLISTERING
- Type II
- Elderly person with itchy tense blisters on flexures, healing without scarring.
Usu. NO mucosal involvement (unlike Pemphigus vulgaris) - Skin biopsy - immunoflorescence shows IgG and and C3 at demoepidermal junction
- Refer to dermatology
1st line: oral corticosteroids
with topical steroids, immunosuppressants, and/or abx
VITILIGO
1. What is it?
2. Associated conditions?
3. Features?
4. Management?
- Autoimmune condition causing melanocyte destruction
- T1DM
Pernicious anaemia
Addison’s
Autoimmune thyroid pathologies
Alopecia areata
AKA OTHER AUTOIMMUNE DISORDERS - Well dermacated patches of skin depigmentation particularly the peripheries, Koebner phenomenon (new depigmentation after skin trauma)
- Sunscreen
Makeup
Topical steroids
Topical tacrolimus
Phototherapy
SHINGLES
1. What is it?
2. Risk factors?
3. Which dermatomes are commonly affected?
4. Features
5. When is the patient infectious?
6. What people should the patient avoid whilst they are infectious?
7. How to reduce risk of infection?
8. Management
9. What is the most common complication?
- Acute, painful, blistering rash caused by Herpes Zoster virus which lies dormant in dorsal root/cranial nerve ganglia
- HIV!! Increased age, immunosuppressed
- T1 to L2
- Prodrome - burning pain over dermatome, fever, headache, lethargy
Initially erythematous macular rash that becomes vesicular, well demarcated and doesn’t cross midline - Infectious until vesicles have crusted over (after 5-7 days)
- Pregnant women, immunosuppressed
- Cover lesions
- Antivirals e.g. aciclovir, within 72h of rash. Don’t need to give in pts under 50 with mild rash and pain.
- Post herpetic neuralgia
CELLULITIS
- What is the most common causative organisms of cellulitis?
- What classification system do you use to categorise severity of cellulitis? What are the signs of class III and IV
- When would you admit patients with cellulitis?
- Management?
- Most common: Strep pyogenes
2nd common: Staph aureus - Eron
Class III and IV - systemically unwell, confusion, vascular compromise, necrotising fasciitis, sepsis - Eron III or IV
Rapidly deterorating cellulitis
Immunocompromised
Under 1 year old or frail
Significant lymphoedema
Facial/periorbital cellulitis - Eron I and II - oral flucloxacillin/clairithromycin/erythromycin
Eron III/IV - admit, IV/oral co-amoxiclav, clindamycin, or IV ceftriaxone
Which condition is associated with a ‘herald patch’?
Pityriasis rosea
Think of Herald holding a rose