Dermatology Flashcards
What occurs in psoriasis?
hyperproliferation of keratinocytes and inflammatory cell infiltration
T-cell mediated
What are the different types of psoriasis?
Guttate - raindrop lesions (usually following strep infection)
Scalp/seborrheic
Flexural
Pustular
Peak ages of psoriasis onset and common ethnicity?
15-25
50-60
Caucasians
What are the contributing factors/possible cause of psoriasis? Phenomenom?
Genetic, immunological and environmental factors
May be precipitated by infection, drugs, stress, alcohol, trauma (Koebner
Phenomenom – plaques are more common at sites of skin injury, often linear lesions)
What is Auspitz sign?
Scratching of the lesions removes scales and causes capillary bleeding
What percentage of patients with psoriasis also have nail changes and what are these?
50% have associated nail changes – pitting, onycholysis
Conditions associated with psoriasis?
- Psoriatic arthritis
- IBD
- Coeliac disease
- Uveitis
Management of psoriasis in primary care?
General – avoid precipitating factors
Topical (for mild) – emollients
First-line – corticosteroids OD + vit D analogues OD e.g. calcipotriol, calcitriol -> reduces cell division and differentiation, can be used longterm
Second-line – vit D analogue BD
Third-line – corticosteroid BD or coal tar preparations (used for scalps sometimes e.g. shampoos, inhibits DNA synthesis)
What are the maximum lengths of time to use steroids in psoriasis?
Very potent steroids – max 4 weeks at a time
Potent – max 8 weeks
Management of psoriasis in secondary care?
Phototherapy (for extensive disease) e.g. UV-B and photochemotherapy (psoralen + UV-A)
Oral therapies (for severe/systemic) – methotrexate, retinoids (vit A derivative), ciclosporin, biologics
Complications of psoriasis?
Erythroderma (red skin over 90% of body) – risk of infection, loss of heat and dehydration, dermatological emergency
Psoriatic arthropathy
Psychological and social impact
Where is eczema most common?
More common on the face and flexor aspects in children
On the extensors in infants
What causes eczema?
Not fully understood
Likely to be a primary genetic defect in skin barrier function
A mixture of type 1 and type 4 hypersensitivity
Triggers for eczema?
infection, allergens (detergents, house dust), sweating, heat, stress
Investigations for eczema?
RAST test – blood test to detect specific IgE Abs
Patch test – placed on the back
Management of eczema?
General measures – avoid exacerbating agents, use emollients +/- bandages and bath oil/soap substitute
Topical therapies – topical steroids for flare-ups, topical immunomodulators can be used as steroid-sparing agents
Oral therapies – antihistamines (not just for itch, may help with hayfever season etc), abx (flucloxacillin) for secondary bacterial infections and antivirals (aciclovir) for secondary herpes infection
Phototherapy and immunosuppressants (pred, azathioprine, ciclosporin) for severe non-responsive cases
Risks of topical steroids?
skin thinning, systemic absorption
What is eczema herpeticum and how to treat?
Describes a severe primary skin infection by HSV1 or HSV2
More common in children with atopic eczema
LIFE-THREATENING
Admit, IV aciclovir
What causes acne?
Hormones
Contributing factors - sebum production, follicular keratinisation, bacterial colonisation
Treatment of acne?
Minimum 6 week treatment
• Topical therapies – benzoyl peroxide + abx, topical retinoids
• Oral therapies (should always be co-prescribed with a topical retinoid or BP) – oral abx (e.g. tetracyclines, erythromycin (preg), minocycline – SE: irreversible skin pigmentation), anti-androgens e.g. cOCP (for females)
• Oral retinoids
Complications of acne?
Post-inflammatory hyperpigmentation, scarring, deformity, psychological and social effects
What causes acne rosacea?
Unknown cause
Presentation of acne rosacea?
Affects nose, cheeks, forehead
Flushing
Telangiectasia
Later, persistent erythema with papules + pustules
Rhinophyma (cauliflower like nose – my words)
Management of acne rosacea?
Topical metronidazole
Systemic abx for more severe disease – oral tetracyclines
Laser therapy for prominent telangiectasia
Steroid ranking in terms of strength?
1) Hydrocortisone
2) Eumovate
3) Betnovate
4) Dermovate
Cause of seborrhoea dermatitis?
Caused by inflammatory reaction to normal skin fungus called Malassezia furfur
Presentation of seborrhoea dermatitis?
Eczematous lesions on scalp, periorbital, auricular and nasolabial folds
Otitis externa + blepharitis
Management of seborrhoea dermatitis?
For scalp
First-line: OTC shampoos containing zinc pyrithione (head + shoulders) and tar (Neutrogena T/Gel)
Second-line: Ketoconazole
Elsewhere
Ketoconazole, potentially topical steroids
What is the name of the mite that causes scabies?
Sarcoptes scabei
How many mites live in a host on average in scabies? And in crusted scabies?
5-15
Crusted - may be hundreds
How long after scabies infection does the itch start?
30 days
Investigations for scabies?
Can extract mites from burrows using a sharp needle
Ink test – to show burrow
Skin scrapings can be taken with a blunt scalpel blade
Management of scabies? And crusted scabies?
Permethrin (applied all over at bedtime, repeat after one week, can remain itchy as mite debris has been burrowed quite deep into skin)
Malathion cream 2nd line
Wash all clothing/bed linin, treat close contacts
Pruritis persists for 4-6wks post eradication
Crusted scabies - Mx = ivermectin
Three main groups of fungal infections?
Dermatophytes (tinea/ringworm)
Yeasts (candidiasis)
Moulds (aspergillus)
Four types of dermatophytosis?
Tinea corporis - ringworm (infection on the trunk/limbs) Tinea cruris (infection of the groin/natal cleft) Tinea pedis (athlete’s foot) Tinea capitis (scalp ringworm)
Investigations for dermatophytosis?
Skin scrapings
Hair/nail clippings
Management of dermatophytosis?
Topical antifungal agent e.g. terbinafine cream
Oral antifungals e.g. itraconazole for severe/widespread/nail infections
Avoid topical steroids
Tx tinea corporis = fluconazole
If not responsive to ketoconazole, how to treat pityriasis versicolour?
PO itraconazole
What is a BCC?
A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes, normally in older individuals
Risk factors for a BCC?
UV exposure/Hx of frequent/severe sunburn in childhood Skin type 1 (always burns, never tans) Elderly males Immunosuppression Genetic predisposition
Four different types of BCC?
Nodular ©
Superficial - most common in young adults
Morphoeic - wax scar like plaques with instinguishable borders
Keratotic
Features of nodular BCC?
small, skin-coloured papule/nodule with surface telangiectasia, and a pearly rolled edge, the lesion may have a necrotic or ulcerated centre (rodent ulcer)
Management of BCC?
Surgical excision – this allows histological examination of the tumour and margins
o (Mohs micrographically controlled excision – carefully examining the excised tissue under the microscope to ensure complete excision)
Curettage and cautery/cryotherapy – suitable for small superficial BCCs
Topical treatment (e.g. imiquimod cream) for small/low-risk lesions
Radiotherapy – where surgery is not appropriate
Topical photodynamic therapy – for small, low-risk BCCs
What is a SCC?
A locally invasive malignant tumour of the epidermal keratinocytes
RFs of SCC?
Pre-malignant skin conditions Chronic inflammation e.g. leg ulcers Immunosuppression Genetic predisposition Exposure to psoralen UV-A
What to do if patient with organ transplant develop new lesions?
NICE advises all patients who have received organ transplants are referred urgently to a dermatologist if they present with any new or growing skin lesions
Presentation of SCC?
Keratotic, ill-defined nodules which may ulcerate They grow over weeks – months Often tender May be ‘non-healing ulcers’ Located on sun-exposed sites
Types of SCC?
Cutaneous horn – d/t excessive keratin production
Keratoacanthoma
Carcinoma cuniculatum – slow-growing warty tumour on the sole of the foot
Management of SCC?
Surgical excision
Mohs micrographic surgery
Radiotherapy – for large non-resectable tumours
What is a malignant melanoma?
invasive malignant tumour of the epidermal melanocytes which can metastasise
RFs for malignant melanoma?
UV exposure
Skin type 1
Hx of moles/atypical moles
FH of melanoma
Features of malignant melanomas?
ABCDE symptoms Asymmetrical shape Border irregularity Colour irregularity Diameter >6mm Evolution of lesion (change in size/shape) Symptoms – bleeding, itching
More common on the legs in women and trunk in men
Four types of malignant melanoma?
o Superficial spreading melanoma (70%) – common on trunk/
- limbs in young/middle-aged adults, related to intermittent high-intensity UV exposure
o Nodular melanoma – common on sun exposed skin in young/middle-aged adults, related to intermittent high-intensity UV
- aggressive, mets early
o Lentigo maligna melanoma – common on the face in the elderly, related to long-term cumulative UV exposure
o Acral lentiginous melanoma – common on the palms, soles and nail beds in elderly population, no clear relation to UV
Management of malignant melanoma?
Surgical excision
Radiotherapy may sometimes be useful
Chemo for metastatic disease
Prognosis of malignant melanoma?
Recurrence of melanoma based on Breslow thickness (thickness of tumour) – the thicker it is, the more likely to recur
5 year survival based on TNM classification
What is bullous pemphigoid?
A blistering skin disorder affecting the elderly
Cause of bullous pemphigoid?
AutoAbs against hemidesmosomal protein BP180 and BP230 between the epidermis and the dermis causing a sub-epidermal split in the skin
Presentation of bulllous pemphigoid?
Tense, fluid-filled blisters on a red base
Often itchy
Usually affects the trunk/limbs, flexures
No mucosal involvement
Management of bullous pemphigoid?
Wound dressings where required, look out for signs of infection
Topical steroids for localised disease
Oral therapies for widespread disease e.g. oral steroids, combination of oral tetracycline + nicotinamide, immunosuppressive agents
What is pemphigus vulgaris?
A blistering skin disorder which usually affects the middle-aged
Cause of pemphigus vulgaris?
AutoAbs against desmoglein 3 within the epidermis causing an intra-epidermal split in the skin
Presentation of pemphigus vulgaris?
Flaccid, easily ruptured blisters forming erosions and crusts
Lesions are often painful, NOT itchy
Usually affects the mucosal areas
Management of pemphigus vulgaris?
Wound dressing where required, look out for signs of infection, good oral care
Oral therapies – high-dose oral steroids, immunosuppressive agents
Causes of lichen planus?
AI disorder – purple, pruritic, popular, polygonal rash
Genetic predisposition - FH association in 10% of cases
May be drug-induced e.g. quinine
Where is lichen planus most commonly found?
Forearms, wrists + legs
Can be found on oral mucosa
What is Whickham’s striae?
when the plaques are crossed by lacy white streaks in lichen planus
How to investigate for lichen planus?
Skin biopsy
Management of lichen planus?
Corticosteroids
Oral steroids or immunosuppression
Prognosis of lichen planus?
Cutaneous lichen planus tends to clear within a couple of years for most people
Mucosal can persist for longer
May recur at a later date
Scarring is permanent, including balding of the scalp
Who normally gets LS?
Most common in women >50
Often a FH of LS or another AI disease
What is molluscum contagiosum look like?
Pink/white pearly papules with central indention
Lesions appear in clusters
How is molluscum contagiosum transmitted?
Close contact/towels and flannels
How to treat molluscum contagiosum?
Self-limiting within 18 months
When does a strawberry naevus peak in size?
Usually 6-9 months
Potential complications of strawberry naevus?
mechanical e.g. obstructing visual fields/airway, bleeding, ulceration
Treatment (if needed) for strawberry naevus?
Propranolol
Where do you normally get venous ulcers?
Common over medial malleolus
What may be in the PMH in someone who developed a venous ulcer?
Hx of venous disease e.g. varicose veins, DVT
What might you see in venous ulcers?
melanin deposits (brown pigment), lipodermatosclerosis and atrophie blanche (white scarring with dilated capillaries)
Investigations in venous ulcers?
Clinical Do ABPI (0.8-1) to make sure the patients arterial supply is good enough to allow compression
Management of venous ulcers?
Compression bandaging
Presentation fo arterial ulcer and where found?
Small, sharply defined deep ulcer
Necrotic base
Found on pressure/trauma sites e.g. pretibial, supramalleolar (usually lateral), distally (toes)
What makes the pain worse in arterial vs venous ulcers?
Venous - worse on standing
Arterial - worse at night when legs elevated
What may be in the PMH in someone who developed a arterial ulcer?
Atherosclerosis
Investigations for arterial ulcer?
ABPI <0.8 (presence of arterial insufficiency)
Doppler studies and angiography
Management of arterial ulcer?
Vascular reconstruction
Compression bandaging is CI
What dies a neuropathic ulcer look/feel like?
Variable size + depth
Granulating base
OFTEN PAINLESS
Abnormal sensation
Where neuropathic ulcers commonly found?
May be surrounded by or underneath a hyperkeratotic lesion (callus)
Common on pressure sites (soles, heel, toes, metatarsal heads)
Investigation in neuropathic ulcer?
ABPI <0.8 implies neuroischaemic ulcer
X-ray to exclude osteomyelitis
Management of neuropathic ulcer?
Wound debridement
Regular repositioning, appropriate footwear and good nutrition
Risk behaviour for PAD?
SMOKING
Three types of PAD?
Intermittent claudication
Critical limb ischaemia
Acute life-threatening ischaemia
What may occur as a complication of longterm abx use in acne? And how to Tx?
Gram-negative folliculitis - high-dose oral trimethoprim is effective if this occurs
Causes of lichenoid drug eruptions?
gold
quinine
thiazides
What is the SE of minocycline (used in acne)?
Irreversible skin pigmentation
When should you avoid giving tetracyclines as a treatment for acne?
avoided in pregnant or breastfeeding women and in children younger than 12 years of age
Which drugs can exacerbate psoriasis?
B-blockers, lithium, antimalarials, NSAIDs, ACEi
Which conditions might develop livedo reticularis?
idiopathic (most common) polyarteritis nodosa SLE/APS cryoglobulinaemia Ehlers-Danlos Syndrome homocystinuria
What is pyoderma gangrenosum?
Rare, non-infectious inflammatory disorder
Rapidly enlarging, very painful ulcer
Where do you most commonly see pyoderma gangrenosum?
Most commonly on the lower legs – often at site of minor injury (pathergy)
Cause of pyoderma gangrenosum?
Idiopathic (50%)
IBD (10-15%)
Rheumatological – RA, SLE
Haematological condition
Features of pyoderma gangrenosum?
Sudden formation of small pustule
Skin breaks down to form a painful deep ulcer (purple undermined edge)
May be systemic symptoms
May form around a stoma site in someone with IBD
Management of pyoderma gangrenosum?
Oral steroids
Immunosuppressive therapy – ciclosporin + infliximab
Postpone surgery to avoid risking more pathergy
What is scrofuloderma?
Breakdown of skin overlying a tuberculoid focus (usually infected LN)
What are necrobiosis lipoidica diabeticorum?
shiny, painless areas of yellow/red skin typically on the shin of diabetics
often associated with telangiectasia
Organism that causes erysipelas?
S. pyogenes
Features of erysipelas?
Abrupt onset painful erythema
Marked swelling
Systemic symptoms
Management of erysipelas?
Penicillin
Erythromycin if allergic
Usually for 10-14 days
Sedating antihistamine?
Chlorphenamine
Non-sedating antihistamines?
loratidine
cetirizine
LORRYtadine - LEAST sedating of the two
SE of retinoids?
Tetrogenic Dry skin © Low mood Raised triglycerides Hair thinning Photosensitivity
Why should you not combine isotretinoin treatment with tetracyclines?
Intracranial HTN
What does hypertrichosis mean?
Androgen-independent hair growth
What can cause SJS?
SANA
Sulphonamides/penicillins
Anticonvulsants - lamotrigine, carbamazepine, phenytoin
NSAIDs
Allopurinol
How to manage SJS?
Admit to hospital for conservative management
First-line: IVIg if needed, then immunosuppressants
What is Toxic Epidermal Necrosis (TEN)?
Extreme version of SJS
Characterised by extensive skin and mucosal necrosis + systemic toxicity
What would you see on histology in TEN?
full-thickness epidermal necrosis with subepidermal detachment
What is Nikolsky’s sign?
epidermis separates with mild lateral pressure
Mortality in SJS and TEN?
Mortality – 5-12% with SJS
>30% with TEN
Which cell type is predominantly involved in SJS/TEN?
T cell
What causes acanthosis nigricans?
T2 DM, GI Ca, PCOS, obesity
Endocrine conditions – acromegaly, cushings, hypothyroidism
Drugs – cOCP, nicotinic acid
What is the pathophysiology of acanthosis nigricans?
Insulin resistance -> hyperinsulinaemia -> stimulation of keratinocytes/fibroblast proliferation via IGF-receptor 1
What are the symptoms of acanthosis nigricans?
Symmetrical, brown, velvety plaques – often found on neck, axilla + groin
Causes of erythema nodosum?
NODOSUM NO: NO causes in 80% of cases D : Drugs (sulfonamides; amoxicillin) O : Oral contraceptive pills S : Sarcoidosis/ Tuberculosis U : Ulcerative colitis; Crohn's disease; Behcet disease M: Micro Viral : HSV; EBV; Hep B; Hep C Bacterial: campylobacter; salmonella; streptococci; Brucellosis Parasite : Amoebiasis; Giardiasis
What is Erythema gyratum repens associated with?
Swirly lines across skin, gyrating - ‘wood-grain’ appearance
Paraneoplastic - associated with lung cancer
What type of hypersensitivity reaction is associated with scabies?
Delayed T4
In which conditions can you see Koebner’s phenomenon?
Psoriasis Vitiligo Warts Lichen planus + sclerosis Molluscum contagiosum
Causes of non-scarring alopecia?
Male pattern baldness Drugs: cytotoxic drugs, carbimazole, oral Con pill, colchicine, anti-Coagulant (heparin) Alopecia areata (autoimmune) Telogen effluvium (when stressed) Iron/zinc deficiency
What is hyperhidrosis?
Excessive sweating
How to treat hyperhidrosis?
Topical aluminium chloride SE: skin irritation
Iontophoresis (electrical current) - useful if palmar/plantar/axillary hyperhidrosis
Botox: axillary symptoms
Surgery - endoscopic transthoracic sympathectomy
What causes pityriasis rosea?
HHV-7
What are the features of pityriasis rosea?
May be history of recent viral illness
Herald patch (usually on trunk)
Erythematous, oval, scaly patches – ‘fir-tree’ appearance
Management of pityriasis rosea?
Self-limiting – disappears after 6-12 weeks
What are the features of zinc deficiency?
Perioral dermatitis Acrodermatitis Alopecia Short stature Hepatosplenomegaly Geophagia (ingesting clay) Cognitive impairment
What are the symptoms of selenium deficiency?
Fatigue, hair loss, weight gain, joint and muscle pain.
What is Onychomycosis and what causes it?
Fungal nail infection
dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
yeasts - such as Candida
non-dermatophyte moulds
Skin rashes associated with TB?
lupus vulgaris (accounts for 50% of cases) - seen in Indian, cutaneous TB
erythema nodosum
scarring alopecia
scrofuloderma
verrucosa cutis - can occur after second infection in a previously infected individual
gumma
What skin condition are patients at risk of after recurrent Erythema ab igne?
SCC
What malignancy is associated with necrolytic migratory erythema?
Glucagonoma
What is the most common malignancy to affect the lower lip?
SCC
What is associated with yellow nail syndrome?
congenital lymphoedema
pleural effusions
bronchiectasis
chronic sinus infections
How to treat vitiligo?
Sun cream + make-up
Steroids early, may be a role for topical tacrolimus and phototherapy
Which cells are lost in vitiligo?
Melanocytes
Which Ig would you see on biopsy in dermatitis herpetiformis?
IgA deposition in the dermis
What are actinic keratoses?
Premalignant skin lesions that develops as a consequence of chronic sun exposure
What is the management of actinic keratoses?
Sun cream Fluorouracil cream – 2-3 weeks Topical diclofenac – if mild Cryotherapy Curettage and cautery
What is a polymorphous light eruption?
A rash that develops when skin is exposed to sun
Causes of Porphyria cutanea tarda?
Can be hereditary or occur in people with liver disease (excessive alcohol, hep B and C, haemochromatosis)
Due to defect in uroporphyrinogen decarboxylase
Features of Porphyria cutanea tarda?
Photosensitive rash with blistering + skin fragility on face + dorsal aspect of hands
Hypertrichosis (hair growth)
Hyperpigmentation
Investigations in Porphyria cutanea tarda?
Urine – elevated uroporphyrinogen + pink fluorescence of urine under Wood’s lamp
Serum iron ferritin level is used to guide therapy
Management of Porphyria cutanea tarda?
Chloroquine
Venesection – if iron levels ok
Drugs that cause hypertrichosis?
minoxidil, ciclosporin, diazoxide
Which conditions are associated with seborrhoeic dermatitis?
Associated with HIV and parkinsons
In who are keloid scars more common?
young, black, male adults
What sort of incisions decrease the chance of keloid scarring?
Keloid scars are less likely if incisions are made along relaxed skin tension lines
Treatment of keloid scarring?
early keloids may be treated with intra-lesional steroids e.g. triamcinolone
excision is sometimes required
Inheritance pattern of hereditary haemorrhagic telangiectasia?
AD
Features of hereditary haemorrhagic telangiectasia?
Epistaxis: spontaneous, recurrent Telangiectasis: Multiple Visceral lesions: GI telangiectasia, pulmonary/hepatic/cerebral/spinal AV malformation \+ FH 'Family VET'
What is Necrobiosis lipoidica and what is it associated with?
Assoc with DM
shiny, painless areas of yellow/red/brown skin typically on the shin
often associated with surrounding telangiectasia
What is Sweet’s syndrome associated with?
AML
Skin conditions associated with DM?
Granuloma annulare
Necrobiosis lipoidica
Vitiligo
Lipatrophy
Skin rxns in DM are LOVINNG:
LipOatrophy
Vitiligo
Infectious (strep, candida)
Necrobiosis lipoidica diabeticorum (shiny, painless, yellow/brown, surrounding telangiectasia)
Neuropathic ulcers
Granuloma annulare (hyperpigmented, centrally depressed)
What do the following fungus lead to?
Trichophyton rubrum
Trichophyton verrucosum
Trichophyton tonsurans
Trichophyton rubrum -> fungal nail and tinea corporis
Trichophyton verrucosum -> tinea corporis
Trichophyton tonsurans -> tinea capitis
Which type of melanoma is the most aggressive and metastasises early?
Nodular
What is systemic mastocytosis?
A neoplastic proliferation of mast cells
What is produced in systemic mastocytosis and what does this lead to?
Associated with increased histamine production -> leads to increased gastric acid production
What are the features of systemic mastocytosis?
Urticaria pigmentosa (red-brown papules) – produces a wheal on irritation (Darier’s sign)
Flushing
Abdo pain
Monocytosis on blood film
Diagnosis of systemic mastocytosis?
Raised serum tryptase levels
Urinary histamine
