Dermatology Flashcards by Emily -

What is the differential diagnosis for scarring alopecia?

Discoid lupus
Lichen planus
Tinea capitus

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If a patient with DLE has negative autoantibodies what is their chance of developing SLE?

5% whereas 25% patients with systemic disease develop discoid lupus at some point

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What are the potential side effects of chronic topical steroid applications

Telangiectasia
Skin breakdown
Ulceration

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What is the management of discoid lupus?

Avoid sun
Sun protection
Stop smoking
Topical steroids
Topical tacrolimus
Antimalarials
Prednisolone
Azathioprine/mycophenolate/cyclophosphamide

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How do you treat psoriasis?

Topical

soap substitutes eg aqueous cream
emollient
vitamin d analogues
salicylic acid
topical steroids
coal tar
dithranol

Photo (chemo) therapy

Narrow band UVB given for 6 weeks
Psoralen plas UVA (PUVA)- psoralen is applied topically or orally at time
Risk of carcinogenesis is a long term side effect

Systemic

methotrexate
retinoids
ciclosporin

Biologics
- etanercept/adalimumab/infliximab

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What are the 6 clinical presentations of psoriasis?

chronic plaque psoriasis
Guttate psoriasis
Hyperkeratotic palmo-plantar psoriasis
flexural psoriasis
erythrodermic psoriasis (risk of sepsis and CV compromise)
Pustular psoriasis

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What are the precipitating factors in psoriasis?

Physical trauma (Koebner phenomonen)
Infections (classically beta haemolytic strep)
Drugs (beta blockers, antimalarials, lithium, NSAIDs, steroids)
Stress
Alcohol
Tobacco
Climate

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What are the two characteristic histological features seen in psoriasis?

Epidermal hyperplasia with squared off rete ridges

Inflammatory cell infiltrate in dermis and epidermis

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How can you establish severity and functional status of patients with psoriasis?

PASI: The Psoriasis Area Severity Index: objective assessment of severity- looking at redness, scaling, thickness and area involved Max score 72

DLQI: Dermatology Life Quality Index- patient questionaire, subjective measures

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How is neurofibromatosis inherited?

Autosomal dominant

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WHat is the diagnostic criteria for neurofibromatosis type 1?

Presence of 2 or more of:

> 6 cafe au lait macules (>15mm in adult)
neurofibromas
Freckling in axilla or inguinal regions
> 2 Lisch nodules (eye brown spots)
Optic glioma
Distinctive osseus lesion- sphenoid dysplasia
1st degree relative with NF1

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What are the symptoms with NF1?

Skin lesions- neurofibromas can undergo sarcomatous changes- exicsions

Neurological

radicular pain (nerve compression due to neuromas)
Visual problems (secondary to optic gliomas)
Epilepsy (secondary CNS tumours)
History of brain tumours
Previous surgery (skin, nerves, spine, brain)
Learning difficulties

Bones
- lordosis, kyphosis, dislocations

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How does type 2 neurofibromatosis classically present?

Hearing loss
Tinnitus
Balance problems

Result of unilateral or bilateral acoustic neuromas
Cutaneous features far less prominent

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What are the diagnostic criteria of NF2?

Bilateral 8th CN masses
or 1st degree relative with NF2 and either unilateral 8th nerve mass or 2 of: neurofibroma, meningioma, glioma, schwannoma or juvenile posterior subcapsular lenticular opacity

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Name 3 causes of hypertension associated with neurofibromatosis?

Renal artery stenosis
Phaeochromocytoma
Coarctation of aorta

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On which chromosomes are the genes responsible for neurofibromatosis type 1 and 2?

NF1: chromosome 17
NF2: chromosome 22

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What is the most common CNS tumour occuring in NF1?

OPtic glioma

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What is Crowes sign?

Axillary freckling

What is tuberous sclerosis?

Multisystem disorder characterised by the formation of harmartomas in many organs commonly the brain, skin and kidneys.

How is tuberous sclerosis inherited and how does it present?

Commonly presents in childhood with epilepsy and skin changes

What are the features of tuberous sclerosis?

Ash leaf macules
Adenoma sebaceum (facial angiofibromas)
Shagreen patches over sacrum and back
Ungual fibromas
Skin tags
Cafe au lait spots

Renal

Renal angiomyolipoma- multiple benign
polycystic kidneys

Cognitive and behavioural problems

What is vitiligo?

Acquired idiopathic disorder characterised by circumscribed de-pigmented macules and pacthcs. Functional melanocytes disappear from skin

How do you manage vitiligo?

Psychological support
Camouflage
Suncream
Reversal: UVB, PUVA, tacrolimus, potent steroids
Depigmentation with bleaching creams

What disorders are associated with vitiligo?

Autoimmune disorders
Strongest is thyroid disorders
- Pernicious anaemia
- Addisons disease
- Diabetes
- Alopecia
- Coeliac disease

Is vitiligo familial?

Around 36% have a positive FH so a genetic component

WHat is the histology of vitiligo?

Marked absence of melanocytes and melanin in epidermis

Can you suggest any theories for the aetiology of vitiligo?

Autoimmune destruction due to antibodies against melanocytes - intrinsic defect in melanocytes - reduced melanocyte survival and dysregulation of melanocyte apoptosis - destruction of melanocytes by neurochemical substances

What is pyoderma gangrenosum?

Uncommon, recurrent condition causing skin ulceration frequently assoc with underlying disease

How do you treat pyoderma gangrenosum?

``` Bed rest Topical steroids High dose systemic steroids systemic therapy eg ciclosporin or dapsone Inflixumab ```

What systemic disease are assoc with pyoderma gangrenosum?

around 50% have assoc condition - IBD - Crohns disease - Arthritis- RA - Haematological disease: AML, CML, hairy cell leukaemia, myelodysplasia, monoclonal gammopathy

Apart from cutaneous sites, what other sites can be affected?

Mucous membranes and peristomal sites- sites of ileostomy and colostomy in UC and Crohns Less commonly- vulva, penis, scrotum

What are the four major clinical forms of pyoderma gangrenosum?

Ulcerative Bullous Pustular Superficial granulomatous

Is the histology in pyoderma gangrenosum specific?

No, non specific neutrophilic infiltration, haemorrhage and necrosis of epidermis

What is necrobiosis lipodica?

Rare, chronic skin condition associated with diabetes mellitus. Granulomatous inflammation and fibrosis appears as yellow, atrophic skin lesions almost exclusively on shins.

What proportion of patients with necrobiosis lipoidica have diabetes

Around 60%, occurs in both type 1 and type 2 but only 0.5% of patients with diabetes develop it.

What are the other skin changes assoc with diabetes mellitus?

Infections: bacterial, fungal Ulcers: arterial, neuropathic Diabetic dermopathy: brown, scaly indented patches in skin Diabetic bullae: blisters which heal spontaneously Granuloma annular

What are the signs of HHT?

Mutiple telangiectasia present on face and mouth Pallor- anaemia Nails- telangiectasia in nail bed Visceral AVMs- pulmonary and hepatic bruits - signs of high output cardiac failure due to left to right shunting between hepatic arteries and veins due to large AVM - neurological sequalae

What are the clinical criteria for diagnosis of HHT?

Curacao criteria: - epistaxis- spontaneous and recurrent - Telangiectasia: multiple and in characteristic sites - Visceral lesions: GI telangiectasia, pulmonary, hepatic, cerebral, spinal AVM - FH: 1st degree relative with HHT 3 criteria definite, 2 criteria=possible

What are the complications of HHT?

``` GI haemorrhage: AVMs, angiodysplasia, telangiectasia Epistaxis Pulmonary AVM: haemoptysis Iron def anaemia Headache SAH ```

What is porphyria cutanea tarda?

Caused by a deficiency of enzyme uroporphyrinogen decarboxylase (UROD) leading to accumulation of porphyrins in skin and resultant photo-induced dermatitis. Characterised by bullae, milia and scarring over sun exposed sites.

What are the pre-disposing factors in porphyria cutanea tarda?

Alcohol intake: high intake worsens conditions History of hepatitis often assoc History of liver problems eg haemochromatosis Oestrogens that reduce UROD activity

How do you diagnose porphyria cutanea tarda?

Urine examination: fluresces pink/coral under woods light 24hr urine uroporphyrins skin biopsy If diagnosis made then consider investigating for hepatitis, iron/ferritin levels and AFP

How would you treat porphyria cutanea tarda?

Removal of contributing agents eg alcohol, oestrogen containing med Sun avoidance Phelbotomy (iron stores in liver inhibit UROD enzyme) Anti-malarials- chloroquine