Derm 2 (weblearn) Flashcards
What eponymous name is given to the rash over the knuckles?
Gottron’s papules (dermatomyositis)
How would you confirm a diagnosis of dermatomyositis?
Raised serum muscle enzymes: ALT, AST, CK, LDH
EMG shows fibrillation potentials
Muscle biopsy
Autoantibody associations: anti-Mi2, anti-Jo1
Which cancers are associated with dermatomyositis?
lung, ovary, breast, stomach or cervix.
How do you treat dermatomyositis?
Immunosuppression.
Start prednisolone. Consider azathioprine, methotrexate etc in resistant cases.
What treatments are available for psoriasis?
topical treatments including dithranol, steroids and vitamin D anologues
Enstilar foam (vit D analogue calcipotriene and betamethasone dipropionate) Dovobet gel (Calcipotriol, a derivative of vitamin D, works by reducing the production of skin cells. Betamethasone, a corticosteroid, helps reduce inflammation.) Exorex Lotion 1% contains 1% prepared coal tar in the bast of esterified fatty acids. OK to get on normal skin
PUVA (oral psoralens followed by UVA treatment two or three times a week)
UVB 311-312 nm 3 x weekly for 8 weeks
Methotrexate
Ciclosporin
Oral retinoids
A 3-year-old boy, who has suffered with eczema in the past, presents with a fever and an area of rapidly worsening, painful eczema on his face. There are extensive crusted papules, blisters and erosions. What’s the diagnosis?
Eczema herpeticum
Which pathogen is the likely cause for eczema herpeticum?
Herpes simplex virus
What are the complications of eczema herpeticum?
Herpes hepatitis
Herpes encephalitis
Disseminated intravascular coagulation (DIC)
What features would make you worry about malignant melanoma?
Asymmetry
Borders - irregular
Colour - more than 1
Diameter - > 6mm
Evolution - lesion has changed over time
What is the most important prognostic indicator for malignant melanoma?
Breslow thickness - the depth of local invasion (Breslow’s thickness = from granular cell layer to deepest part of invasion.)
Less than 1 mm : 5 year survival 95–100%
1–2 mm : 5 year survival 80–96%
2.1–4 mm : 5 year survival 60–75%
Greater than 4 mm : 5 year survival 50%
In Oxford any melanoma greater that 2mm would be referred for sentinel node lymph node biopsy. If this is positive then patients can be entered onto clinical trial.
What is a DLQI?
dermatology life quality index
What facts are key in determining a dermatological history?
Duration
How does it affect you? (Quality of life assessment)
How bad is it today?
What has been tried and for how long?
How are topical preparations being applied?
Occupation: history of long term sun exposure (e.g. lived abroad, gardening), exposure to chemicals at work
PMHx/medication
FHx of Atopy or Skin tumours if appropriate
What information must be specified when prescribing topical corticosteroids?
Base e.g. gel, cream, ointment
Size of tube e.g. 30g
Where to apply it
How often to apply it
How long to continue for
Discuss likely outcome of treatment reduce scale, redness and itch
Advice re side effects of inappropriate long term use
What are the differentials of itch?
Skin – Dermatitis, allergic or atopic, infection(fungal), scabies, other eg lichen planus
Renal – chronic renal failure
Liver – cirrhosis, any cause of cholestasis and increased bilirubin
Haematological – Fe deficiency anaemia, polycythaemia
Thyroid – hypo and hyperthyroid
Malignancy – lymphoma, leukaemia
Psychiatric – anxiety, depression, obsessive compulsive
Drug- eg ACE inhibitors
List the most important types of psoriasis. Briefly describe the morphology and/or distribution of each
- Chronic plaque psoriasis (most common) – well demarcated erythematous plaques with thick silvery scale. Common on extensor surfaces, and scalp
- Guttate: raindrop lesions- often reactive eg to streptococcal sore throat. Increased life time risk of chronic plaque
- Flexural/ inverse psoriasis
- Pustular: palmar plantar distribution. Generalised pustular Can be following inappropriate topical steroid use on plaque psoriasis
- Erythrodermic (complication of psoriasis): whole body redness
What key features distinguishes psoriasis from other dermatological conditions?
- Symmetric
- Affects extensor surfaces
- Non-pruritic, unlike eczema
- Auspitz sign: gentle scratching of scale causes capillary bleeding
- Koebener phenomenon seen on trauma
- 50% have nail pitting
- May have associated arthropathies due to HLA association of psoriasis
What is known of the pathophysiology underlying psoriasis?
- Chronic inflammatory skin disease due to keratinocyte hyperproliferation and inflammatory cell infiltration.
- Cause unknown. Complex interaction of genetic, immunological and environmental factors.
- Triggers: trauma (friction, inflammation), infection esp streptococcal, drugs (lithium, antimalarials, ACEi, beta blockers), stress and alcohol and UV light in 6%.
How is psoriasis managed?
- General avoidance of triggers
- Regular emollients, soap substitutes
- Topical: vitamin D analogues (calcipitriol), corticosteroids, retinoids (tazarotene), keratinolytics (coal tar) and scalp preparations
- Phototherapy for extensive disease e.g. UVB, and photochemotherapy (PUVA – psoralen and UVA)
- Oral therapies for extensive and severe psoriasis: methotrexate, oral retinoids, cyclosporin, mycophenolate mofetil, fumaric acid esters, biological agents if PASI >= 10 (infliximab (anti-TNF), etanercept, efalizumab, ustekinumab (anti-IL12/23))
PASI = Psoriasis area and severityindex
What are the main risk factors associated with the development of squamous cell carcinomas?
SHIT
Sunlight Scars, burns,venous ulcers Human papilloma virus Immunosuppression Ionising radiation Industrial carcinogens – pitch, tar, creosote, crude paraffin oil, fuel oil Toxins- Arsenic
What is the management for SCC?
- Surgical excision is the treatment of choice
- Moh’s micrographic surgery is indicated in high risk, recurrent tumours and involves excision of the lesion and tissue borders until specimens are microscopically free of tumour
- Radiotherapy may be indicated for large, non-resectable tumours
- Chemotherapy may be appropriate for metastatic disease
What are the characteristic features of a BCC?
- A nodule or ulcer on an exposed site with a rolled pearly edge and telangiectasia.
- It can expand to cause necrosis and ulceration causing local destruction of tissues but does not metastasise.
Which 4 clinical types of BCC exist?
Nodulo-cystic
Superficial
Pigmented
Morphoeic
What treatments are available for BCC?
MOHS surgery
Radiotherapy
Cryotherapy and curettage and cautery can be used for small and low risk lesions.
What are the risk factors that are particularly associated with the development of melanoma?
- Atypical moles
- Having numerous moles and naevi (>100)
- Skin phototypes I and II (red hair and freckling)
- Sunburn – especially severe burning during childhood
- Family history of MM
- Previous cutaneous MM
- Immunosuppression
What are the’red flag’ characteristics of moles that suggest malignancy?
Asymmetry Border irregularity Colour heterogeneity Diameter >7mm Evolution over time, incl symptoms such as bleeding, itching
What types of benign melanocytic naevi are there?
- Benign moles that can either be intradermal, compound or junctional
- Congenital naevi
- Halo naevi (have an area of surrounding depigmentation)
- Spitz naevi (found on Children’s faces)
- Blue naevi (e.g. Mongolian blue spots)
- Clinically atypical or dysplastic naevi – these are concerning as there is an increased risk of melanoma
What is a keratoacanthoma?
It is a common, benign, non-melanocytic tumour. It is a well-differentiated SCC. The normal progression is intially a period of rapid growth, followed by persistance for 2-3 mo, then involution over 4-6 mo. They may be removed surgically.
What is Bowen’s disease and how does it present?
Bowen’s disease is full thickness dysplasia and is an SCC in situ. It presents as a solitary scaly plaque, usually on a light exposed site and is asymmetrical. It rarely develops into SCC.
What is the differential diagnosis for Bowen’s disease?
Superficial BCC
Fungal infection
Psoriasis
How is Bowen’s disease treated?
- surgery
- topical 5-fluorouracil or imiquimod
What are the risks associated with solar keratoses and subsequently, what is the management strategy?
They are premalignant tumours which arise from dysplasia in the epidermal basal cell layer. They are an indicator that a patient is at risk of skin cancer. About 20% regress spontaneously, and progression to SCC is rare.
Treatment is only required if they are troublesome, otherwise advice should be for patients to be vigilant for the development of cancers, and to take necessary precautions e.g. sun protection.
What are seborrhoeic keratoses?
They are a benign proliferation of epidermal keratinocytes of unknown aetiology
What are the clinical features of seborrhoeic keratoses?
- These are benign, warty lesions that can be solitary or multiple.
- They are pigmented and flat-topped with surface pits and irregularities.
- They have a “stuck-on” appearance.
What are the side effects of methotrexate that must be discussed with patients and what must be monitored in patients taking this drug?
Taken once weekly for psoriasis. Avoid alcohol
- Anorexia, nausea
- Low WBC: regularly check FBC. Need to monitor for infection
- Hepatitis, liver fibrosis, rarely cirrhosis (urea and electrolytes and LFTs done pre treatment, then weekly until therapy stabilised, then monthly)
- Interstitial pneumonitis/pulmondary fibrosis (seen in rheumatoid arthritic not psoriasis) – SOB, cough, fever
- Teratogenic – males and females should avoid conception for at least 3 months after stopping
When is isotretinoin used? What are the side effects of isotretinoin and what monitoring is required?
Isotretinoin is a drug used to treat severe acne vulgaris. Give for at least 16 weeks
Minor side effects: dry skin and mucous membranes, nose bleeds, cheilitis, temporary elevation of serum lipids (reverts to normal at end of course), headache, arthragia, hairloss
Reports of depression and suicide but causal link never proved.
Major side effects: teratogenic (written consent form, continue contraceptive treatment for 1 month after stopping), liver dysfunction (raised liver enzymes)
Monitoring: pregnancy test before starting therapy and also start patient on oral contraceptives. Pre-treatment test liver function and fasting lipids. Recheck liver function tests and fasting lipids during treatment.
What is the main use for ciclosporin in dermatology?
Ciclosporin is effective for treating severe psoriasis
What requires monitoring in patients on ciclosporin and why?
The main problem is renal toxicity and so blood pressure and renal function should be measured. Ciclosporin interacts with a number of drugs (e.g. trimethoprim, NSAIDs).
When are antihistamines used in dermatology?
- Management of Urticaria. Chlorpheniramine can also be used alongside adrenaline and hydrocortisone in the management of anaphylaxis and angioedema.
- Sedating antihistamines e.g. chlorpheniramine may also be used to therefore stop night time scratching. e.g. atopic dermatitis. Care must be taken in the elderly due to falls risk.
What are the different types of topical steroid available?
Mildly potent – hydrocortisone acetate
Moderately potent (2-25 times stronger than hydrocortisone)
– clobetasone butyrate (eumovate)
– triamicinolone acetonide
Potent (100-150 times stronger than hydrocortisone)
– betamethasone valerate (betnovate)
– hydrocortisone 17-butyrate
– methylprednisolone aceponate
Very potent (600 times stronger than hydrocortisone)
– clobetasone propionate (dermovate)
– betamethasone dipropionate
What are the side effects of topical steroids that patients must be warned about?
Skin atrophy, telangiectasia, striae
They may mask, cause or exacerbate skin infections, acne or perioral dermatitis and allergic contact dermatitis
What are the different types of eczema/dermatitis?
Primarily exogenous
- Irritant contact (e.g. occupational)
- Allergic contact (type IV hypersensitivity)
Primarily endogenous
- Atopic (often in childhood, resolves in teenage years)
- Seborrheoic
- Discoid
- Pompholyx
- Asteototic
- Stasis (venous)
What are key questions in a history of atopic eczema?
Duration?
Triggers/exacerbants (infections, allergens, heat, stress)?
Sites affected?
How does it affect your life?
What has been tried already? Has it worked?
Personal or Fhx of atopy e.g. hayfever, asthma, allergic rhinitis?
