16. Dermatological Systemic Disease Flashcards
Describe the pathophysiology of venous ulcers
Valvular incompetence/obstruction = impaired venous return = venous hypertension = “trapping” of WBC in capillaries = activated, release of inflammatory mediators = tissue injury, poor healing, necrosis
What are the symptoms of venous ulcers?
Shallow, irregular borders, granulating base
Characteristically located over the medial malleolus (gaiter region)
Prone to infection and can present with associated cellulitis
Painful - worse on standing
Venous insufficiency = oedema, varicose eczema or thrombophlebitis, haemosiderin skin staining, lipodermatosclerosis, or atrophie blanche
How should venous ulcers be investigated?
Duplex US
ABPI
Swab cultures
How should venous ulcers be managed?
Leg elevation
Lifestyle = increase exercise (promoting calf action), weight reduction, improved nutrition
Abx - Tx sec infection
Multicomponent compression bandaging with emollients
- Make sure ABPI is >0.6
Concurrent varicose veins = endovenous techniques or open surgery (improved venous return = healing)
Describe the pathophysiology of arterial ulcers
Reduction in arterial blood flow = decreased perfusion of the tissues = poor healing
Discuss the symptoms of arterial ulcers
Small deep lesions
Well-defined borders
Necrotic base with little granulation tissue
Occur at sites of trauma and pressure
Intermittent claudication
Critical limb ischemia (pain at night)
Pain - worse at night and when elevated
Limbs will be cold
Reduced/absent pulses
Sensation is maintained
What are the investigations for arterial ulcers?
ABPI >0.9 = normal 0.9-0.8 = mild 0.8-0.5 = moderate <0.5 = severe Duplex US
CT angiography
MR angiography
How should arterial ulcers be managed?
Urgent referral for vascular review
Lifestyle = smoking cessation, weight loss, increased exercise
Medical = statin, aspirin/clopidogrel, optimising BP and glucose
Surgical = angioplasty, bypass grafting, skin graft
Outline vitiligo
Ae = acquired depigmenting disorder, melanocytes lost
- induced by drugs: immune checkpoint inhibitors (pembrolizumab, nivolumab), BRAF inhibitors
- higher risk of having autoimmune diseases: DM, thyroid disease, pernicious anaemia (B12 def), Addison disease, SLE, RA, psoriasis, alopecia areata
S+S =
- well-defined milky-white patches of skin (leukoderma): face, neck, eyelids, nostrils, fingertips and toes), body folds (armpits, groin), nipples, navel, lips and genitalia
- white hair is called ‘leukotrichia’ or ‘poliosis’
- favours sites of injury (koebner phenomenon)
Ix = clinical Dx
Mx =
- Minimise skin injury, sunscreen
- Cosmetic camouflage
- Corticosteroid cream
- Calcineurin inhibitors (pimecrolimus cream and tacrolimus ointment
- Phototherapy (immune suppression, stim cytokines (growth factors)
What is alopecia areata
Ae/Path = autoimmune loss of hair
- histologically characterised by T cells around the hair follicles
- T cells release pro-inflam cytokines and chemokines that reject the hair
S+S =
- Patchy: often the scalp, eyebrows, eyelashes and beard
- Alopecia totalis: all/nearly all scalp hair is lost
- Alopecia universalis: all/nearly all hair on the entire body is lost
- Ophiasis: bald area on occipital and lateral scalp
- Nails: pitting, ridging, koilonychia, trachyonychia, Beau lines, onychorrhexis, onychomadesis, onycholysis and red spots
Mx =
- Injections of triamcinolone acetonide (hair growth)
- Oral/pulse IV steroids, high dose (temp regrowth)
Outline the aetiology of lupus
Ae = connective tissue disease and autoimmune disorder that can affect one or several organs
- UVB irradiation causes keratinocyte necrosis, immune system activation and antibody formation
- Drug induced
How does cutaneous lupus present?
S+S =
- Lesions may be localised or generalised
- Malar eruption or ‘butterfly rash’ (erythema and oedema of cheeks, sparing nasolabial folds)
- Erythematous papular rash on arms, sometimes forming large plaques and spreading widely
- Photosensitivity (a rash on all recently sun-exposed skin)
- Cheilitis and mouth ulcers
- Blisters (bullous SLE) and erosions
- Annular or polycyclic plaques that clear centrally
- Lupus profundus: firm deep and tender nodules (lesions resolve leaving dented, atrophic scars - lipoatrophy)
How is lupus Ix and Mx?
Ix = Anti Ro/La Abs, ANA, skin biopsy may show lichenoid tissue reaction (specific to cutaneous LE), direct immunofluorescence tests may show +ve Ab deposition along BM (lupus band test)
Mx =
- Topical steroids
- Calcineurin inhibitors, pimecrolimus cream or tacrolimus ointment
- Intralesional corticosteroid
- Topical/systemic retinoids
- Cosmetic camouflage
- Hydroxychloroquine
- Methotrexate
Discuss vasculitis
Ae/Path = injury by bacteria/viral, Ab, complement
- inflam blood vessels in the skin - capillaries, venules, arterioles, lymphatics.
S+S =
- painful lesions
- dependent areas (legs, buttocks, flanks)
- palpable purpura (often painful)
- haemosiderin deposition
- systemically unwell
Ix = bloods, urine analysis, skin biopsy
Mx = Tx underlying cause, steroids, immunosuppressants
What are the dermatologic manifestations of Paraneoplastic Syndromes
Metastasis = leukemia cutis, cutaneous T-cell lymphoma, and Paget disease of the breast
Nonspecific metabolic effects related to inanition = wasting, alopecia, and xerosis
Infections related to immunosuppression = herpes zoster
Signs resulting from compromise or dysfunction of the affected organ = jaundice
Paraneoplastic syndromes = diverse dermatologic entities that signal the presence of a remote malignancy
