Dermatology Flashcards
Give an example of each of the following strengths of steroid cream
- Mild
- Moderate
- Potent
- Very potent
What is clobetasol propionate?
What is clobetasone butyrate?
What is betamethasone valerate?
Hydrocortisone
Eumovate
Betnovate
Dermovate
“He Buys donuts”
Explain what causes the following;
- Erythema
- Scale
- Lichenification
- Exudate
- Vesicle
Name the condition
Cause?
Treatment?
Seborrhoeic eczema
What is the treatment for eczema?
- Emollients
- Mild steroids
- antibiotics / antifungals / antivirals if relevant
- PUVA
- Oral altretinoin
- Oral azathioprine, ciclosporin
What is PUVA?
PUVA is a combination treatment consisting of taking a drug PSORALEN (P) and then exposing the skin to long-wave ultra- violet light (UVA) – hence the term PUVA. Psoralen is a drug that makes the skin temporarily sensitive to UVA. It may be taken as pills by mouth or by applying it directly to the skin.
Also called phototherapy, photo chemotherapy, or UVradiation treatment.
Treatment for eczema
What are some risk factors for allergies / atopy?
Name 5 different types of eczema
Name the 8 functions of the skin
What are the two types of skin and where are they located on the body? Differences?
Thin/hairy - everywhere else. Hair.
Thick/hairless - palms and soles. No hair. Epidermis is thicker. Stratum lucidum present. Doesn’t tan.
What conditions are highly responsive to corticosteroids?
Psoriasis
Atopic dermatitis (eczema)
Seborrhoeic dermatitis
Intertrigo
Eczema - differential diagnoses? What can present like eczema?
Scabies, Psoriasis, Tinea, drug erruption, bullous pemphigoid
What colours can melanoma present as?
Black, brown, red, dark blue and grey
What is the condition?
Describe the lesion.
Prognosis?
Basal Cell Carcinoma
Pearly, well-circumscribed, elevated, pigmented (pink), ulcerated in middle (sometimes)
Prognosis - Slow-growing, rarely metastasises
What is the condition?
What type of cells are involved?
Describe the lesion.
Prognosis?
Malignant melanoma
Involves melanocytes
Asymmetrically shaped
Borders - irregular
Colours - multiple
Diameter - over 6mm
Evolving rapidly
Metastasises easily
Most aggressive / deadly
What is the condition?
Describe the lesion.
Prognosis?
Squamous cell carcinoma
Involves squamous keratinocytes
Well circumscribed. Red/flesh coloured.
Can metastasise. Less severe than MM.
What is the pre-cancerous stage of malignant melanoma?
What does it look like?
Lentigo maligna
Brown patch, usually on face or other sun exposed area.
Lentigo maligna is a type of growth that develops in areas of long-term sun exposure, such as your face, arms or legs. Lentigo maligna starts as a brown flat spot with an irregular shape that slowly gets bigger.
What is the pre-cancerous stage / early stages of squamous cell carcinoma called?
Solar / actinic keratosis - pre-cancerous lesion (this is FLAT whereas SCC is RAISED).
Bowen’s disease or squamous cell carcinoma in situ - early stage
Name the three skin cancers from most to least deadly?
Diagnosis?
Treatment?
What is this called?
Can turn into what?
Melanocytic naevus
Melanoma
What is this called?
Can turn into what?
Pre-cancerous lesion - SCC
(SCC is raised, AK is flat)
What is the scale called to assess different skin types?
What is a skin type 1?
Skin type 6?
Fitzpatrick
Skin type 1 - pale
Skin type 6 - darkest
What things do you have to ask for a skin cancer history?
eg. a patient has booked a GP appointment with you to discuss a lesion they’ve found on their skin.
Things I forget
- Rate of growth / change
- Surgical considerations: pacemaker, anticoagulants, level of independence, home situation
- Site. Where is it?
- Duration. How long has it been there?
- Rate of growth/change. Is it growing / changing? How quickly?
- What does it look like? ABCD(E).
- Associated symptoms - pain? Itch? Affecting nearby structures eg eye?
- UV exposure
- PMH of cancer, FH of skin cancer
- Relevant surgical considerations in case excision is needed eg anticoagulation
What questions to ask for history of rash?
eg. a patient books a GP appointment with you to discuss a rash.
- Where
- When
- Better / worse
- Itch, pain?
- TRIGGERS eg new medication, pet, occupation, travel
- PMH atopy? Eczema, asthma, hay fever, allergies.
- Family hx - anyone else itchy in the household? genetic - eczema.
- Effect on life
What things to ask for eczema history?
Things I forget - better/worse, triggers, effect on life
- Where did it first appear? Where did it subsequently spread to?
- When did it first start.
- Does anything make it Better / worse.
- Itch, pain?
- TRIGGERS Does anything seem to trigger it?
- PMH atopy? Eczema, asthma, hay fever, allergies.
- Family hx - anyone else had eczema, asthma, hay fever, allergies?
- Effect on life
What things to ask for history of psoriasis?
Remember to ask about nail changes and joint pain
FH of psoriasis
What things to ask for in history of acne?
What I forget
- psychological impact
- Severity
Site - face, chest, back
Note the severity.
Triggers - hormonal?
Treatments tried - hormonal eg. pill. Topical
Ask about psychological impact
What things to ask for in history of urticaria?
Ask about lip swelling, mouth swelling / tingling, (worried about angioedema, airway compromise, anaphylaxis).
How to take a history for ‘disfiguring rashes’ eg. vitiligo, alopecia
Make sure to ask patient how they feel about the problem - don’t assume.
Ask about effect on their life - social, occupational, psychological
What to ask for in history of fungal infections?
Check for
- Spreading
- Immunosupporession
- Drugs eg steroids
- FH of fungal infections (current household members)
What is the difference between erysipelas and cellulitis? Describe erysipelas.
Most common causative organism?
Treatment? Give examples.
Erysipelas - SUPERFICIAL, well defined. Shiny, red, raised tender plaques, usually legs or face.
Cellulitis - DEEP.
Most common cause of both -
1. Group A streptococcus
2. Staphylococcus aureus.
Both - oral or IVABX.
1. Flucloxacillin
2. Doxycycline
3. Erythromycin
Scabies!
Symptoms?
What questions to ask in a history?
Treatment?
Itching ++ particularly in webspace between fingers
Permethrin, twice, 7 days apart. Applied to skin as a cream.
Change bedding etc, treat close contacts.
Name three syndromes that are related to drug reactions in the skin. Name from less to most severe.
What area of the body should you always check in these patients?
Usual cause of these syndromes?
Erythema multiforme
Stevens-Johnson syndrome - milder version of TEN
Toxic epidermal necrolysis (TEN)
SJS and TEN can be fatal
*MUST check mucosa (eyes/mouth also genitals) on examination. Use pen torch
Usually drug reaction eg antibiotics, NSAIDS, anti-epileptics, allopurinol
History for skin infections
- Triggers? How did the bacteria/virus etc get there?
- Predisposing factors? Is the host vulnerable
.
What are the names for
- Cold sores
- Chicken pox
- Shingles
- Eczema + herpes
What are these?
Treatment?
Benign moles (naevi)
If no change - no action needed.
If mole has recently been changing - monitor.
Have pigment network
What are these?
Nodular Basal Cell Carcinoma
(Differential diagnosis for 117 is malignant melanoma, but note how it is translucent/pearly)
BCC is a locally invasive skin tumour
- Slow growing
- Skin coloured, pink or pigmented
- Varies in size from a few millimetres to several centimetres in diameter
- Spontaneous bleeding or ulceration.
Nodular BCC
- Most common type of facial BCC
- Shiny or PEARLY nodule with a smooth surface. May be translucent.
- May have central depression or ulceration, so its edges appear rolled
- Blood vessels cross its surface
- Usually firm nodule, growing within the skin and below it, rather than on the surface
- Cystic variant is soft, with jelly-like contents
What are these?
How to describe this type of lesion?
Infiltrative Basal Cell Carcinoma
- Scar like
- Shiny
- Difficult to define edges of lesion
- Telangiectasia
NB. The patient with two arrows - infiltrative BCC on cheek, nodular BCC on eyelid
What is this?
Superficial BCC
Differential diagnosis - Patch of Bowen’s disease.
Localised red plaque on trunk, scaly.
Usually occurs by itself or few - asymptomatic
Slowly enlarge - shiny surface and narrow raised border
What are these?
Squamous Cell Carcinoma
Proliferation of epidermal keratinocytes in a deranged manner – with a visible degree of differentiation into epidermal cells
First change is thickening of the skin with scaling or hyperkeratosis of the surfaces. More differentiated tumours have warty, keratotic crust whereas others may be nodular.
Generally solitary. Fleshy, indurated base. May have moist or crusted surface rather than formed keratosis. Asymmetry of ulceration
What is the difference between actinic keratosis and squamous cell carcinoma?
Similarities?
Both can be rough and keratotic
Actinic keratosis is flat
SCC is raised
What are these?
Actinic Keratosis
What is this?
Bowen’s disease
Pre-cursor to SCC
Bowen’s –
superficial intra-epidermal tumour
Slow radial expansion. Localised erythematous, scaly or crusted plaque
Bowen’s is not usually ulcerated, moist or thickened. If it is consider ?SCCs
What are these? Give two options.
What is the difference?
- SCC
- Keratoacanthoma – Precise symmetry. Bolstered shoulder of skin stretched around tumour.. Formed central horn. Stop growing after 2-3 months
Keratoacanthomas will stop growing and then recede, whereas SCCs will keep on growing.
What is this?
What are these?
Actinic keratosis / solar keratosis
Sun exposed sites –face, back of hands, bald scalp Rough area of skin / raised, keratotic lesion Usually multiple, have a hard, spiky keratinous surface. Not indurated or thickened at the base
What are these?
What are the signs of this on dermoscopy?
Malignant melanoma. The bottom one is ‘nodular melanoma’.
Dermoscopy of melanoma
- dots
- globules
- branched streaks (brown steaks going outward)
- asymmetry
- blue veil
- milky red
- scar like
- disrupted pigment network
Malignant melanoma vs naevus
A clear history of an individually changing lesion is best discriminator in early melanoma
Increasing size, irregular edge and varied and asymmetric pigmentation
Many ordinary naevi have more than one shade of brown, but black colours are uncommon
Varied colours, if present are usually symmetrical about long or short axis
Change in elevation is a common and normal maturation change in naevi
Stands out amongst other moles
What are these?
How can you tell?
Seborrhoeic keratosis
- Seb K’s more rounded than moles, sharply defined rounded margin
- Fissured hyperketatotic plaque
- Karatin plugs.Seb Ks occur infrequently below 30 years of age, whereas most naevi develop below this age.
Typical crusted appearance of seborrheic keratosis / warty surface
Stuck on appearance. Common on trunk. Flat lesions on legs are not uncommon. Seb Ks have a more keratotic surface than solar lentigos – small white dots formed by pearls of keratin may be visible. Margin is usually sharply defined.
In lesions without significant keratinisation, there is typically a fairly uniform yellowish brown colour and a greasy cobblestoned surface, and small white (pearls ) of keratin are usually visible. Keratin plugs (with pseudofollicular appearance)
If naevi are elevated – rubbery or fleshy feel
What is this?
How would you describe it?
How to tell the difference between this and naevus?
Dermatofibroma - a benign tumour
Flesh-coloured papule (papule means raised and less than 0.5cm. Raised and > 0.5cm would be a nodule eg BCC).
Dermatofibroma vs naevus
Dermatofibromas are firmer than naevi
Dermatofibromas are tethered within the dermis (gives rise to dimple sign). mainly on limbs
What is a dermatofibroma? A dermatofibroma is the name we give to a common and harmless knot of fibrous tissue which occurs in the skin. Dermatofibromas are firm bumps which feel like small rubbery buttons lying just under the surface of the skin.
Sometimes a dermatofibroma is confused with a mole. The way to tell the difference between the two is to pinch the bump. If you pinch a dermatofibroma, it creates a dimple because it is attached to the underlying subcutaneous tissue.1 On the other hand, if you pinch a mole, it projects up away from the skin. Moles appear when skin cells grow in clusters.
While dermatofibromas are usually red, brown, or purplish, moles can be tan, black, blue or pink in addition to the typical dermatofibroma’s color. Moles can appear in both exposed and unexposed areas of the body, including the armpits or even under nails.
Benign - not normally excised
What are these?
Pyogenic granuloma
Contains no pus – it is vascular and grows rapidly. Tend to bleed. Fingers is a common site.
Top one could also be an ‘amelanotic melanoma’ - rapidly evolving friable nodule.
What are these?
Haemangioma - vascular.
Differ from melanoma in that their colour is more purple, pink and yellow.
What are these?
Top - blue naevus, uniform blue colour
Bottom two - Blue is not uniform colour, has black and pink areas also. metastatic malignant melanoma. Will have history of prior MM removal.
What are these? Describe.
Top = cyst. Often have central punctum. Stretched skin means blood vessels more visible. Site, size, shape - Single Round, raised, well demarcated. Surface - flesh coloured, some ?telangectasia / visible blood vessels from strethcing of the skin, warmth. Substance - consistency, translumination, reducability, pulsatile, fluctuation. Surrounbding structures: mobile - not tethered, no invasion (regular borders).
164 = Fungal infection. Was mistakenly sent through 2ww. See pus - swab it! Pustules, erythema, crusting.
What are these? Describe.
121= giant keratin plug. Whirls. Remove (squeeze out) or leave. Benign. Like big black head.
163 = keloid scar. Some people produce a big scar/ bump to trauma (ear piercing) probably wouldn’t remove as another keloid would form from surgery trauma.
What is this? Describe.
Infiltrative BCC
Scar like, can be depressed, pale, shiny.
Describing rashes/a lesion - what are the stages and some models you can use?
Distribution
Configuration
Colour
Morphology
What are different terms to describe the ‘distribution’ of a rash? and what does each term mean
- Generalised, widespread, localised
- Flexural, extensor, pressure areas
- Dermatomal (area of skin supplied by a single spinal nerve, eg. shingles)
- Photosensitive eg. face, neck, back of hands (eg. Lupus)
- Kuebner - at site of trauma
What are different terms to describe the ‘configuration’ (pattern) of a rash? and what does each term mean
Examples
Annular eg. Lyme disease
Discoid eg. discoid eczema, discoid lupus.
Name 5 terms you could use to describe ‘colour’ of a rash?
.
Describing rashes /lesions - morphology.
What do there terms mean? Papule, patch, macule, nodule? Give example of each type.
Describing rashes /lesions - morphology.
What do there terms mean? Plaque, wheal, bulla, vesicle? Give example of each type.
Describing rashes /lesions - morphology.
What do there terms mean? Pustule, cyst, ulcer, fissure, erosion? Give example of pustule and cyst.
And you can say well demarcated, poorly demarcated.
What are the types of ‘secondary lesions’ / secondary change?
Give example for each
.
What is bullous pemphigoid? How is it different to pemphigus vulgaris?
Treatment?
Bullous pemphigoid
- No Nikolsky’s sign (skin does not split with lateral pressure)
- Blisters between the dermis and epidermis
Pemphigous vulgaris
- Nikolsky’s sign present (skin splits with lateral pressure)
- Blisters within the epidermis
Nikolsky’s sign - lateral pressure causes split between laters of the epidermis
What are the 5 layers of the epidermis, from inner to outer?
+ Stratum basale at the base
When to refer a skin lesion to dermatology?
I forget
- Non-healing ulceration
- Personal hx of malignancy
- Family hx of malignancy
- Significant risk factors eg. UV exposure
Name these lesions
Name three examples of pigmented lesions, and three examples of non-pigmented lesions
Name some subtypes of melanoma
What is the most common location on
- men
- women?
Patient asks you, what causes acne?
(Pathogenesis of acne)
What are open and closed comedones?
Papule / pustule?
Hormonal change eg puberty →
increased production of sebum (oil) and keratin = blocked hair follicle. Increased bacteria on the skin also.
Open pore (comedone) = black head, oil and dirt gets trapped
Closed pore (comedones) = white head , pus gets trapped
Papule = inflammatory lump <5mm (less than nodule)
Pustule = yellow topped lump - accumulation of material and pus
How is acne assessed / graded?
Severe - cysts, scarring, inflammation.
Inflammatory - redness, swelling, pustules
Non-inflammatory - just blackheads
Suggest some treatments for
- Mild acne
- Moderate acne
- Severe acne
Name some prognostic factors for melanoma. Which is the most important?
Breslow thickness = most important prognostic factor.
The thicker the melanoma → more likely it will metastasise.
eg. Stage 1 normally means the melanoma is less than 1mm thick.
Breslow thickness is the measurement of the depth of the melanoma from the surface of your skin down through to the deepest point of the tumour. It’s measured in millimetres (mm) with a small ruler, called a micrometer.
The deeper the tumour, the worse is the prognosis. Patients with a melanoma of 0.76–1.49 mm Breslow depth have a 5-year survival rate of 80–95 %, whereas at a Breslow depth of 1.50–4.00 mm the corresponding rate is 60–75 % and at > 4.00 mm less than 50 %.
What would you need to ask in a hair history? - what questions would you ask someone with a complaint of hair loss
Things I forget
- Pattern of hair loss
- Increase shedding?
- Pain / itching ?
- other sites other than scalp
Name and describe these nail changes. What disorders are they associated with?
.
What investigations would you do for hair loss?
What are the signs of allopecia arreata?
Allopecia arreata
- Oval patches of hair loss occipitally
- Exclamation mark hairs
- Nail pitting
Treatment: None (often self limiting), steroids, PUVA, immunosuppression, wigs.
Name and describe the two main types of cause of excess hair. Give a few examples of causes of each.
Hirsuitism
- PCOS
- Cushing’s syndrome
Hypertrichosis
- Spina bifida
- Chronic liver disease
What are some causes of hirsutism?
Hirsuitism
- Investigation
- Treatment
Treatment
- Treat underlying cause
- Hair removal
- Lifestyle advice eg. diet and exercise
- Anti-androgens eg spironolactone
- COCP
What is this?
Normally occurs in?
Treatment?
Guttate psoriasis.
Little lesions all over body, usually torso. Common in children, presentation post strep / viral infection.
Topical steroids, usual treatments. Resolves over several months.
What is this?
Differential diagnoses?
Palmoplantar psoriasis
DD - Tinea, scabies
Differential diagnoses for chronic plaque psoriasis?
DD for scalp psoriasis?
Treatment for psoriasis - describe the stages of the treatment ladder and some options for the stages.
- what is the criteria for using step 4?
- Topical treatments eg. corticosteroids
- Phototherapy
- Oral treatments eg. methotrexate
- Biologics - if severe, who have failed to respond to steps 1+2+3. (Severe psoriasis is PASI>10 AND DLQI>10)
Name three oral treatments for psoriasis, explain how they work
Methotrexate - Methotrexate treats psoriasis by slowing the growth of skin cells to stop scales from forming. Methotrexate may treat rheumatoid arthritis by decreasing the activity of the immune system.
Ciclosporin
Systemic retinoid eg. acitretin
Name some of the different types of psoriasis.
What is the effect on people’s life?
Name two local anaesthetics and describe the difference between them
.
Suggest the names of different types of sutures?
What are the steps to performing interrupted sutures?
What are four key questions to ask/consider to diagnose a skin infection?
In Stevens-Johnson syndrome what surface area % of epidermis is detached? and TEN?
Usual cause of these conditions?
What scale/score is used to measure the severity?
SJS < 10%
overlap 10-30
TEN > 30%
Prodromal illness (systemic symptoms eg fever)
Nikolsky sign +ve
Usually drug reaction
SCORTEN scale - higher the score the worse the mortality
Name five drug classes / drugs associated with causing SJS / TEN
Most important part of management?
Antibiotics eg. penicillins
Antifungals
Antivirals
Allopurinol
NSAIDS eg ibuprofen
Anti-convulsants eg phenytoin
Management
- stop the drug!
- sedating antihistamine
- steroids topical / oral
- anaphylaxis
What are the 4 subtypes of melanoma?
Which is most common?
Which is worst prognosis?
Most common - superficial spreading
Worst prognosis - nodular
What are the differences between atopic eczema and psoriasis on examination? (how to tell the difference).
How to tell difference between eczema and psoriasis in the history taking?
What are the 5 layers of the epidermis?
What structures are found within the dermis?
What is the most common site for a BCC?
BCC originates from what layer of the epidermis?
BCC - Upper lip, stratum basale
Where in the skin does a keratoacanthoma originate from?
What things to ask for in the history for anaemia?
Name three anaemias of
- microcytic
- Normocytic
- macrocytic
Investigations for back pain?
Malignant haematology - Name three myeloid and three lymphoid disorders
UV irradiation of skin
- Name three positive effects
- Name three negative effects
What cells make up the
- Innate
- Adaptive immunity
What is an endotoxin?
What is an exotoxin?
What are the 6 P’s of lichen planus?
What are Wickham’s striae?
What does QALY stand for and what does it mean?
What is a DALY?
What is the difference between DALYs and QALYs?
Give an example of
- Gram positive cocci (aerobic)
- Gram negative rods (aerobic)
- Anaerobes (negative/positive)
.
What are the primary lymphoid organs?
What are the secondary lymphoid organs?
What drugs cause photosensitive drug reaction?
What inflammation cells can move?
What does the drug Dapsone do?
Used to treat?
Neutrophils and macrophages
Dapsone decreases activity of neutrophils.
Used for leprosy and Dermatitis herpetiformis (also Pneumocystis jirovecii (Pneumocystis carinii) pneumonia)
Name two large vessel vasculitis, two medium vessel vasculitis, two small vessel vasculitis.
What are the three ANCA-associated small cell vasculitides?
What is purpura?
What are petechiae?
What are ecchymoses?
Think - is it palpable. Usually cause of macular purpura? (non-palpable)
Usual cause of papular purpura? (palpable)
Macular - usually non-inflammatory eg ITP.
Petechiae - thrombocytopenia
Ecchymoses - DIC, trauma
Papular - usually inflammatory eg vasculitis. (or septic emboli)
Vasculitis - Purple Painful Purpura
What are some causes of purpura?
Trauma
Platelet disorders
Vasculitis
Coagulation disorder eg. DIC
What are the 5 causes of vasculitis?
Idiopathic
Infection (eg. HSP)
Inflammatory and autoimmune disease
Drugs
Neoplastic
What is this?
Associated with?
Diagnosis?
Treatment?
DD?
Dermatitis herpetiformis. Age onset 20-60. Itchy +++ rash. Extensors.
Blisters (herpetiformis) usually already ruptured through itching.
Coeliac disease
Diagnosis - Skin biopsy, from uninvolved skin - IgA deposits, immunofluorescence
- Duodenal biopsy
- TTG
Treatment - gluten free diet (takes 2-3 years for rash to resolve)
- Dapsone (anti-leprosy, controls the skin, check for G6PD first).
- Sulphonamides
DD - scabies (important to exclude), psoriasis
What is this?
Pathology?
What age presents?
Presents as?
Nikolsky sign?
Mucocutaneous blisters present?
Investigation?
Treatment?
Pemphigus vulgaris (vulgarIS in the epidermIS)
Acquired autoimmune disease. Oral ulcers and preceding rash. ‘Sore’ rather than itchy.
Disruption within the epidermis. Desmoglein.
Younger people: 40-60
Presents as erosions (superficial blisters have burst). Fragile, flaccid blisters.
Nikolsky +ve
High involvement mucocutaneous blisters - mouth, nose, genitals
Investigation
Biopsy - histology shows intra-epidermal split
- Immunofluorescence shows IgG +- C3
Treatment
1. Very high dose oral steroids eg 2-3mg/kg → 140-210mg.
2. Azathioprine
Other - plasmapheresis, Iv Ig.
Mortality 5-15%. Problems - infection, fluid and electrolyte imbalance.
What factors are involved in this extrinsic pathway of the clotting cascade?
Which of PT or aPTT measures extrinsic pathway?
Normal measurement value?
Tissue factor (factor III) and factor VII.
PT - prothrombin time
Play Tennis OUTSIDE
PT - 12 seconds.
What factors are involved in this intrinsic pathway of the clotting cascade?
Which of PT or aPTT measures intrinsic pathway?
Normal value?
Factreos 12, 11, 9 & 8.
XII, XI, IX & VIII.
aPTT = activated partial thromboplastin time
Play Table Tennis INSIDE.
https://www.youtube.com/watch?v=xY3sspj_E0I
What is this?
Pathology?
What age presents?
Presents as?
Nikolsky sign?
Mucocutaneous blisters present?
Investigation?
Treatment?
Bullous Pemphigoid (More common than PV)
Disruption in basement membrane between dermis and epidermis
Older people
Deep, tense blisters. First sign : red, itchy rash (can be misdiagnosed as eczema/acne/urticaria). Relapsing/remitting, up to 5 years duration.
Nikolsky -ve
Less/no mucocutaneous blisters than PV
Investigation: Ellipse biopsy over edge of blister. Perilesional area (normal skin) for direct immunofluorescence (IgG, C3 deposits), and blister base for histology.
Treatment: Steroids eg. prednisolone 30mg OD (1/2mg/kg) or doxycycline.
3rd choice - azathioprine.
