Pass Medicine Flashcards
Features
- target lesions
- initially seen on the back of the hands / feet before spreading to the torso
- upper limbs are more commonly affected than the lower limbs
- pruritus is occasionally seen and is usually mild
Causes
- viruses: herpes simplex virus (the most common cause), Orf*
- idiopathic
- bacteria: Mycoplasma, Streptococcus
- drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, oral contraceptive pill, nevirapine
- connective tissue disease e.g. Systemic lupus erythematosus
- sarcoidosis
- malignancy
Erythema multiforme major is more severe form, erythema multiforme major is associated with mucosal involvement. (below)
Fungal nail infections
Onychomycosis is fungal infection of the nails. This may be caused by
- dermatophytes - mainly Trichophyton rubrum, accounts for 90% of cases
- yeasts - such as Candida
- non-dermatophyte moulds
Risk factors include for fungal nail infections include diabetes mellitus andincreasing age.
Features
- ‘unsightly’ nails are a common reason for presentation
- thickened, rough, opaque nails are the most common finding
Differential diagnosis
- psoriasis
- repeated trauma
- lichen planus
- yellow nail syndrome
Investigation
- nail clippings
- scrapings of the affected nail
- the false negative rate for cultures are around 30%, so repeat samples may need to be sent if the clinical suspicion is high
Management
- treatment is successful in around 50-80% of people
- diagnosis should be confirmed by microbiology before starting treatment
- dermatophyte infection: oral terbinafine is currently recommended first-line with oral itraconazole as an alternative. Six weeks - 3 months therapy is needed for fingernail infections whilst toenails should be treated for 3 - 6 months
- Candida infection: mild disease should be treated with topical antifungals (e.g. Amorolfine) whilst more severe infections should be treated with oral itraconazole for a period of 12 weeks
Cherry haemangiomas (Campbell de Morgan spots) are benign skin lesions which contain an abnormal proliferation of capillaries. They are more common with advancing age and affect men and women equally.
Features
- erythematous, papular lesions
- typically 1-3 mm in size
- non-blanching
- not found on the mucous membranes
As they are benign no treatment is usually required.
History of Epistaxis
Hereditary haemorrhagic telangiectasia
Also known as Osler-Weber-Rendu syndrome, hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant condition characterised by (as the name suggests) multiple telangiectasia over the skin and mucous membranes. Twenty percent of cases occur spontaneously without prior family history.
There are 4 main diagnostic criteria. If the patient has 2 then they are said to have a possible diagnosis of HHT. If they meet 3 or more of the criteria they are said to have a definite diagnosis of HHT:
- epistaxis : spontaneous, recurrent nosebleeds
- telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
- visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
- family history: a first-degree relative with HHT
Managment of plaque psoriasis
- regular emollients may help to reduce scale loss and reduce pruritus
- first-line: NICE recommend a potent corticosteroid applied once daily plus vitamin D analogue applied once daily (applied separately, one in the morning and the other in the evening) for up to 4 weeks as initial treatment
- second-line: if no improvement after 8 weeks then offer a vitamin D analogue twice daily
- third-line: if no improvement after 8-12 weeks then offer either: a potent corticosteroid applied twice daily for up to 4 weeks or a coal tar preparation applied once or twice daily
- short-acting dithranol can also be used
Psoriasis Secondary Care Management
Phototherapy
- narrow band ultraviolet B light is now the treatment of choice. If possible this should be given 3 times a week
- photochemotherapy is also used - psoralen + ultraviolet A light (PUVA)
- adverse effects: skin ageing, squamous cell cancer (not melanoma)
Systemic therapy
- oral methotrexate is used first-line. It is particularly useful if there is associated joint disease
- ciclosporin
- systemic retinoids
- biological agents: infliximab, etanercept and adalimumab
- ustekinumab (IL-12 and IL-23 blocker) is showing promise in early trials
Mechanism of action of commonly used drugs:
- coal tar: probably inhibit DNA synthesis
- calcipotriol: vitamin D analogue which reduces epidermal proliferation and restores a normal horny layer
- dithranol: inhibits DNA synthesis, wash off after 30 mins, SE: burning, staining
Hutchinson’s Sign
Acral lentiginous melanoma: Pigmentation of nail bedaffecting proximal nail fold suggests melanoma
Bacteria that contributes to the development of Acne
The bacteria responsible is Propionibacterium acnes which is an anaerobic rod. This is important because it means traditional beta-lactam antibiotics are ineffective in treating infections caused by this and so tetracyclines, macrolides or trimethoprim must be used in managing acne.
Scabies
Scabies is caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. It typically affects children and young adults.
The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.
Features
- widespread pruritus
- linear burrows on the side of fingers, interdigital webs and flexor aspects of the wrist
- in infants the face and scalp may also be affected
- secondary features are seen due to scratching: excoriation, infection
Management
- permethrin 5% is first-line
- malathion 0.5% is second-line
- give appropriate guidance on use (see below)
- pruritus persists for up to 4-6 weeks post eradication
Patient guidance on treatment (from Clinical Knowledge Summaries)
- avoid close physical contact with others until treatment is complete
- all household and close physical contacts should be treated at the same time, even if asymptomatic
- launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill off mites.
Bowen’s Disease
Bowen’s disease is a type of intraepidermal squamous cell carcinoma. More common in elderly females. There is around a 3% chance of developing invasive skin cancer
Features
- red, scaly patches
- often occur on sun-exposed areas such as the lower limbs
Management options:
- topical 5-fluorouracil or imiquimod
- cryotherapy
- excision
Venous Ulceration
Venous ulceration is typically seen above the medial malleolus
Investigations
- ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing
- a ‘normal’ ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease. Interestingly, values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)
Management
- compression bandaging, usually four layer (only treatment shown to be of real benefit)
- oral pentoxifylline, a peripheral vasodilator, improves healing rate
- small evidence base supporting use of flavinoids
- little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression
no mucosal involvment
Bullous pemphigoid is an autoimmune condition causing sub-epidermal blistering of the skin. This is secondary to the development of antibodies against hemidesmosomal proteins BP180 and BP230
Bullous pemphigoid is more common in elderly patients. Features include
- itchy, tense blisters typically around flexures
- the blisters usually heal without scarring
- mouth is usually spared*
Skin biopsy
- immunofluorescence shows IgG and C3 at the dermoepidermal junction
Management
- referral to dermatologist for biopsy and confirmation of diagnosis
- oral corticosteroids are the mainstay of treatment
- topical corticosteroids, immunosuppressants and antibiotics are also used
mucosal involvement: pemphigus vulgaris
TEN
Toxic epidermal necrolysis (TEN) is a potentially life-threatening skin disorder that is most commonly seen secondary to a drug reaction. In this condition the skin develops a scalded appearance over an extensive area. Some authors consider TEN to be the severe end of a spectrum of skin disorders which includes erythema multiforme and Stevens-Johnson syndrome
Features
- systemically unwell e.g. pyrexia, tachycardic
- positive Nikolsky’s sign: the epidermis separates with mild lateral pressure
Drugs known to induce TEN
- phenytoin
- sulphonamides
- allopurinol
- penicillins
- carbamazepine
- NSAIDs
Management
- stop precipitating factor
- supportive care, often in intensive care unit
- intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
- other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis
Lichen planus is a skin disorder of unknown aetiology, most probably being immune mediated.
Features
- itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
- rash often polygonal in shape, ‘white-lace’ pattern on the surface (Wickham’s striae)
- Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
- oral involvement in around 50% of patients
- nails: thinning of nail plate, longitudinal ridging
Lichenoid drug eruptions - causes:
- gold
- quinine
- thiazides
Management
- topical steroids are the mainstay of treatment
- benzydamine mouthwash or spray is recommended for oral lichen planus
- extensive lichen planus may require oral steroids or immunosuppression
Guttate psoriasis is more common in children and adolescents. It may be precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing.
Features
- tear drop papules on the trunk and limbs
Management
- most cases resolve spontaneously within 2-3 months
- there is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
- topical agents as per psoriasis
- UVB phototherapy
- tonsillectomy may be necessary with recurrent episodes
blistering skin disorder associated with coeliac
Dermatitis herpetiformis is an autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis.
Features
- itchy, vesicular skin lesions on the extensor surfaces (e.g. elbows, knees, buttocks)
Diagnosis
- skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis
Management
- gluten-free diet
- dapsone
Pityriasis rosea
Pityriasis rosea describes an acute, self-limiting rash which tends to affect young adults. The aetiology is not fully understood but is thought that herpes hominis virus 7 (HHV-7) may play a role.
Features
- herald patch (usually on trunk)
- followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance
Management
- self-limitingm - usually disappears after 6-12 weeks
Actinic, or solar, keratoses (AK) is a common premalignant skin lesion that develops as a consequence of chronic sun exposure
Features
- small, crusty or scaly, lesions
- may be pink, red, brown or the same colour as the skin
- typically on sun-exposed areas e.g. temples of head
- multiple lesions may be present
Management options include
- prevention of further risk: e.g. sun avoidance, sun cream
- fluorouracil cream: typically a 2 to 3 week course. The skin will become red and inflamed - sometimes topical hydrocortisone is given following fluorouracil to help settle the inflammation
- topical diclofenac: may be used for mild AKs. Moderate efficacy but much fewer side-effects
- topical imiquimod: trials have shown good efficacy
- cryotherapy
- curettage and cautery
Hair growth
Hirsutism is often used to describe androgen-dependent hair growth in women, with hypertrichosis being used for androgen-independent hair growth
Polycystic ovarian syndrome is the most common causes of hirsutism. Other causes include:
- Cushing’s syndrome
- congenital adrenal hyperplasia
- androgen therapy
- obesity: thought to be due to insulin resistance
- adrenal tumour
- androgen secreting ovarian tumour
- drugs: phenytoin, corticosteroids
Assessment of hirsutism
- Ferriman-Gallwey scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism
Management of hirsutism
- advise weight loss if overweight
- cosmetic techniques such as waxing/bleaching - not available on the NHS
- consider using combined oral contraceptive pills such as co-cyprindiol (Dianette) or ethinylestradiol and drospirenone (Yasmin). Co-cyprindiol should not be used long-term due to the increased risk of venous thromboembolism
- facial hirsutism: topical eflornithine - contraindicated in pregnancy and breast-feeding
Causes of hypertrichosis
- drugs: minoxidil, ciclosporin, diazoxide
- congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
- porphyria cutanea tarda
- anorexia nervosa
Vitalgo
Vitiligo is an autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin. It is thought to affect around 1% of the population and symptoms typically develop by the age of 20-30 years.
Features
- well-demarcated patches of depigmented skin
- the peripheries tend to be most affected
- trauma may precipitate new lesions (Koebner phenomenon)
Associated conditions
- type 1 diabetes mellitus
- Addison’s disease
- autoimmune thyroid disorders
- pernicious anaemia
- alopecia areata
Management
- sunblock for affected areas of skin
- camouflage make-up
- topical corticosteroids may reverse the changes if applied early
- there may also be a role for topical tacrolimus and phototherapy, although caution needs to be exercised with light-skinned patients
Keratoacanthoma is a skin lesion that erupts in sun-damaged skin, rather like a little volcano. It grows for a few months; then it may shrink and resolve by itself.
Impetigo Management
Limited, localised disease
- topical fusidic acid is first-line
- topical retapamulin is used second-line if fusidic acid has been ineffective or is not tolerated
- MRSA is not susceptible to either fusidic acid or retapamulin. Topical mupirocin (Bactroban) should therefore be used in this situation
Extensive disease
- oral flucloxacillin
- oral erythromycin if penicillin allergic
- children should be excluded from school until the lesions are crusted and healed or 48 hours after commencing antibiotic treatment
Contact Dermatitis
There are two main types of contact dermatitis
- irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare
- allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated
Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis whilst the dichromates in cement also can cause an allergic contact dermatitis
acne vulgaris managment
Acne vulgaris is a common skin disorder which usually occurs in adolescence. It typically affects the face, neck and upper trunk and is characterised by the obstruction of the pilosebaceous follicles with keratin plugs which results in comedones, inflammation and pustules.
Acne may be classified into mild, moderate or severe:
- mild: open and closed comedones with or without sparse inflammatory lesions
- moderate acne: widespread non-inflammatory lesions and numerous papules and pustules
- severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring
A simple step-up management scheme often used in the treatment of acne is as follows:
- single topical therapy (topical retinoids, benzoyl peroxide)
- topical combination therapy (topical antibiotic, benzoyl peroxide, topical retinoid)
- oral antibiotics: e.g. Oxytetracycline, doxycycline. Improvement may not be seen for 3-4 months. Minocycline is now considered less appropriate due to the possibility of irreversible pigmentation. Gram negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim is effective if this occurs
- oral isotretinoin: only under specialist supervision
Skin Disorders of Pregnancy
Polymorphic eruption of pregnancy
- pruritic condition associated with last trimester
- lesions often first appear in abdominal striae
- management depends on severity: emollients, mild potency topical steroids and oral steroids may be used
Pemphigoid gestationis
- pruritic blistering lesions
- often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
- usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
- oral corticosteroids are usually required
Skin signs of Diabetes Mellitis
- necrobiosis lipoidica, usually affecting pretibial skin
- rubeosis (chronic flushed face)
- diabetic dermopathy (atrophic hyperpigmented lesions on lower legs – an under-diagnosed entity probably present to some degree in 50% diabetics; male > female)
- generalised granuloma annulare
- vitiligo
- acanthosis nigricans
- lipodystrophy
- vascular changes
- xanthomata (eruptive in uncontrolled diabetes)
- yellow skin (increased serum carotene)
- dry and wet gangrene
- candidiasis
- necrotising fasciitis
- foot ulcers
Diabetes Herpetiformis Treatment
- Dapsone, the treatment of choice, is highly effective and symptoms resolve in days.
- Rare early adverse reactions with dapsone are haemolysis and agranulocytosis.
- The condition improves slowly with a gluten-free diet which is recommended to continue life-long.
Drugs that cause drug rashes
- Penicillins/ sulphonamides
- Anticonvulsants
- NSAIDS
- Thiazide diuretics
- Allopurinol
- Gold and penicillamine
