Dermatology Flashcards

Question

squamous cell carcinoma (skin) - cancer of what cell type, 5 risk factors, 3 appearance features, 2 mx, 2 features making prognosis worse

Answer 1

A locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has the potential to metastasise Causes ● Risk factors include excessive UV exposure, pre-malignant skin conditions (e.g. actinic keratoses/bowens disease), chronic inflammation (e.g. leg ulcers, wound scars), immunosuppression (eg HIV or post renal transplant) and genetic predisposition Presentation ● Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate Management ● Surgical excision - treatment of choice ● Mohs micrographic surgery – may be necessary for ill-defined, large, recurrent tumours ● Radiotherapy - for large, non-resectable tumours prognosis worse if immunosup'd, >20mm in diameter (this will need 6mm margins rather than 4)

Answer 2

invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise Causes ● Risk factors include excessive UV exposure, skin type I (always burns, never tans), history of multiple moles or atypical moles, and family history or previous history of melanoma Presentation ● The ‘ABCDE Symptoms’ rule (*major suspicious features): Asymmetrical shape* Border irregularity Colour irregularity* Diameter > 6mm Evolution of lesion (e.g. change in size and/or shape)* Symptoms (e.g. bleeding, itching) ● More common on the legs in women and trunk in men Types ● Superficial spreading melanoma – 70% of all cases,common on the lower limbs, in young and middle-aged adults; related to intermittent high- intensity UV exposure ● Nodular melanoma - common on the trunk, in young and middle- aged adults; related to intermittent high-intensity UV exposure ● Lentigo maligna melanoma - common on the face, in elderly population; related to long-term cumulative UV exposure ● Acral lentiginous melanoma - common on the palms, soles and nail beds (subungual pigmentation), in elderly population; no clear relation with UV exposure Management ● Surgical excision - definitive treatment ● Radiotherapy may sometimes be useful ● Chemotherapy for metastatic disease invasion depth is most important prognostic factor

Answer 3

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

Answer 4

benign epithelial tumour. They are more common with advancing age and rare in young people. Features - said to look like a volcano or crater initially a smooth dome-shaped papule rapidly grows to become a crater centrally-filled with keratin Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar. Such lesions should however be urgently excised as it is difficult clinically to exclude squamous cell carcinoma

Answer 5

common benign fibrous nodule usually found on the skin of the lower legs, composed of proliferating fibroblasts, sometimes forms in response to injuries eg injections, thorn injury, insect bite etc size varies from 0.5–1.5 cm diameter; tethered to skin surface and mobile over subcut tissue, dimples on pinching the skin around the lesion; if many erupt this can be sign of immunosuppression inc eg HIV; does not give rise to cancer sebaceous/dermoid cyst, lipoma, BCC, warts, xanthomas, skin tags, SCC, melanoma, pyogenic granuloma, keratoacanthoma, rheumatoid nodule, gouty tophi, keloid scar, NF lesion, skin met, or infection (leprosy, leishmaniasis, syphilis) epidermoid/sebaceous cyst: benign, derived from hair follicle, filled with keratin/lipid, generally due to occluded pilosebaceous unit, firm flesh coloured nodule fixed to skin but mobile over deeper layers, 1-3cm, with central punctum that may discharge, may become infected/inflamed

Answer 6

itchy red plaques, a little like psoriasis, but tend to vary in colour around the plaque and from lesion to lesion; or may be hypopigmented in kids but it is rare in kids, it's a rare form of T cell lymphoma

Answer 7

benign epidermal skin lesions seen in older people. Features large variation in colour from flesh to light-brown to black have a 'stuck-on' appearance keratotic plugs may be seen on the surface Management reassurance about the benign nature of the lesion is an option options for removal include curettage, cryosurgery and shave biopsy

Answer 8

perioral pigmentation/freckles, abdo pain +/- GI bleed due to hamartomatous polyps usually in small bowel AD inheritance inc'd risk of cancers of breast, colon (40%), panc, stomach (30%), ovaries, lung (15%), small intestine, cervix, uterus, testes if have then upper endoscopy, colonoscopy beginning at age 8, repeat at 18 or every 2-3yrs if polyps seen; every 2-3yrs after 18yo mammogram every 2-3yrs beginning at age 20; yearly testicular exam for boys; pancreas MRI or endu USS beginning at 30-35yo

Answer 9

- usually develops by early childhood and resolves during teenage years (but may recur) Epidemiology ● 20% prevalence in <12 years old in the UK Causes ● Not fully understood, but a positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present ● A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin) appears to underlie atopic eczema Presentation ● Commonly present as itchy, erythematous dry scaly patches ● More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults ● Acute lesions are erythematous, vesicular and weepy (exudative) ● Chronic scratching/rubbing can lead to excoriations and lichenification ● May show nail pitting and ridging of the nails Management ● General measures - avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute ● Topical therapies – topical steroids for flare-ups; topical immunomodulators (e.g. tacrolimus, pimecrolimus) can be used as steroid-sparing agents ● Oral therapies - antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. aciclovir) for secondary herpes infection ● Phototherapy and immunosuppressants (e.g. oral prednisolone, azathioprine, ciclosporin) for severe non- responsive cases Complications ● Secondary bacterial infection (crusted weepy lesions) ● Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum 1 fingertip unit of steroid cream good to cover one hand rubbed in

Answer 10

also known as dyshidrotic eczema. Pompholyx eczema may be precipitated by humidity (e.g. sweating) and high temperatures. Features small blisters on the palms and soles often intensely itchy sometimes burning sensation once blisters burst skin may become dry and crack Management cool compresses emollients topical steroids

Answer 11

condition typically seen in women aged 20-45 years old. Topical corticosteroids, and to a lesser extent, inhaled corticosteroids are often implicated in the development of the condition. Features clustered erythematous papules, papulovesicles and papulopustules most commonly in the perioral region but also the perinasal and periocular region skin immediately adjacent to the vermilion border of the lip is typically spared Management steroids may worsen symptoms should be treated with topical or oral antibiotics

Answer 12

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 if site of exposure rather than flexural, and in adult rather than young child (esp <5yo) then contact derm more likely than atopic eczema

Answer 13

● Widespread eruption - serious complication of atopic eczema or less commonly other skin conditions Cause ● Herpes simplex virus Presentation ● Extensive crusted papules, blisters and erosions ● Systemically unwell with fever and malaise Management ● Antivirals (e.g. aciclovir) ● Antibiotics for bacterial secondary infection Complications ● Herpes hepatitis, encephalitis, disseminated intravascular coagulation (DIC) and rarely, death

Answer 14

An inflammatory disease of the pilosebaceous follicle Epidemiology ● Over 80% of teenagers aged 13- 18 years Causes ● Hormonal (androgen) ● Contributing factors include increased sebum production, abnormal follicular keratinization, bacterial colonization (Propionibacterium acnes) and inflammation Presentation ● Non-inflammatory lesions (mild acne) - open and closed comedones (blackheads and whiteheads) ● Inflammatory lesions (moderate and severe acne) - papules, pustules, nodules, and cysts ● Commonly affects the face, chest and upper back Management ● General measures - no specific food has been identified to cause acne, treatment needs to be continued for at least 6 weeks to produce effect ● Topical therapies (for mild acne) - benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties) ● Oral therapies (for moderate to severe acne) - oral antibiotics, and anti-androgens ie COCP as alt to oral antibiotics (in females) ● Oral retinoids (for severe acne); oral abx of choice are tetracyclines like doxy or lemy but shold be avoided if preg, breastfeeding, <12yo; erythromycin can be used in pregnancy; alongside oral abx topical retinoid should be used unless contra'd; pregnancy is contra to oral and topical retinoids Complications ● Post-inflammatory hyperpigmentation, scarring, psychological and social effects

Answer 15

Topical Treatments - Most suitable for facial acne. - Use at night to affected areas to prevent new spots from developing. - Tell patients that it will take 4 to 6 weeks to start to work and they should have a 3-month trial. Topical retinoids (contraindicated in pregnancy): have anticomedonal properties - Counsel women of childbearing age to use effective contraceptive - Warn regarding irritancy, photosensitivity (wash off before direct sunlight) peeling / dryness and need to moisturise. Benzoyl peroxide: has keratolytic and antimicrobial properties (can be purchased from community pharmacy) - Start at 5% and increase to 10% if necessary. - Warn patients that it can bleach bedding and clothing and advise using a white towel Single topical treatment - Topical retinoid (if comedomal element) OR benzoyl peroxide (can be purchased from a community pharmacy) Combination topical treatments for example: - Duac® gel (benzoyl peroxide + clindamycin), once daily when not responding to above or widely distributed involving neck/back/chest use tetracycline or macrolide (note stop any topical abx before starting oral) If inadequate response after 3-4 months with oral antibiotic OR if there are other reasons to take COCP such as contraception and menstrual control, then consider adding COCP to treatment. Refer to dermatology: - All patients with severe acne (nodulocystic acne or systemically unwell, please refer urgently). - Inadequate response to above treatment. - Acne causing significant scarring. - Severe psychological distress regardless of physical sign. Please ensure women who are sexually active are on a reliable form of contraception (COCP or LARC) in addition to a barrier method before referral for consideration of oral isotretinoin treatment. Oral isotretinoin (contraindicated in pregnancy) To be initiated & prescribed by consultant dermatologist due to serious side effects including teratogenic & possible psychiatric effects

Answer 16

chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration Types ● Chronic plaque psoriasis is the most common type ● Other types include guttate (raindrop lesions), seborrhoeic (naso-labial and retro-auricular), flexural (body folds), pustular (palmar-plantar), and erythrodermic (total body redness) Epidemiology ● Affects about 2% of the population in the UK Causes ● Complex interaction between genetic, immunological and environmental factors ● Precipitating factors include trauma (which may produce a Köebner phenomenon), infection (e.g. tonsillitis), drugs, stress, and alcohol drug exacerbaters inc: beta blockers, lithium, antimalarials, ACEi, NSAIDs, inflixmab; strep infection can trigger guttate

Answer 17

Well-demarcated erythematous scaly plaques ● Lesions can sometimes be itchy, burning or painful ● Common on the extensor surfaces of the body and over scalp ● Auspitz sign (scratch and gentle removal of scales cause capillary bleeding) ● 50% have associated nail changes (e.g. pitting, onycholysis) 5-8% suffer from associated psoriatic arthropathy - symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans - also dactylitis (ie swollen or sore, red finger) NICE recommend a step-wise approach for chronic 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 should be 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 Phototherapy (for extensive disease) - phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA ● Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement) - methotrexate, retinoids, ciclosporin, mycophenolate, infliximab scalp, face and flexures are particularly prone to steroid atrophy so topical steroids should not be used for more than 1-2 weeks/month systemic side-effects may be seen when potent corticosteroids are used on large areas e.g. > 10% of the body surface area NICE recommend that we aim for a 4-week break before starting another course of topical corticosteroids they also recommend using potent corticosteroids for no longer than 8 weeks at a time and very potent corticosteroids for no longer than 4 weeks at a time vit d analogues work by dec epidermal prolif, should be avoided in pregnancy

Answer 18

blistering skin disorder which usually affects the elderly Cause ● Autoantibodies against antigens between the epidermis and dermis causing a sub-epidermal split in the skin; blister is subepidermal and contains fibrin and large numbers of inflammatory cells including eosinophils; Direct immunofluorescence shows linear deposition of IgG (most often IgG4 subtype) and C3 along the basement membrane Presentation ● Tense, fluid-filled blisters on an erythematous base ● Lesions are often itchy ● May be preceded by a non-specific itchy rash ● Usually affects the trunk and limbs (mucosal involvement less common) Management ● General measures – wound dressings where required, monitor for signs of infection ● Topical therapies for localised disease - topical steroids ● Oral therapies for widespread disease and generally mainstay of tx after biopsy to confirm diagnosis – oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents there is usually no mucosal involvement

Answer 19

blistering skin disorder which usually affects the middle-aged Cause ● Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin;Early lesions of pemphigus vulgaris show suprabasal epidermal acantholysis, clefting and blister formation. The blister cavity may contain inflammatory cells including eosinophils; Direct immunofluorescence may be positive in perilesional skin with intercellular deposits of IgG and/or C3 in the epidermis Presentation ● Flaccid, easily ruptured blisters forming erosions and crusts ● Lesions are often painful ● Usually affects the mucosal areas (can precede skin involvement) Management ● General measures – wound dressings where required, monitor for signs of infection, good oral care (if oral mucosa is involved) ● Oral therapies – high-dose oral steroids, immunosuppressive agents (e.g. methotrexate, azathioprine, cyclophosphamide, mycophenolate)

Answer 20

v rare skin condition; simplex is AD, no scarring, in first year, esp over contact areas when crawling starts (knees/palms), generalised blistering in basal cell layer junctional is AR at birth w generalsied bullae/blisters at junction of derm and epiderm dystrophic form has AD form w less scarring, at onset of crawling; and AR form oft v severe w mucous membrane involvement, nail loss, syndactylyl, oesophageal strictures; in both blistering is in upper dermis

Answer 21

bullae uncommon in kids but can be caused by various reasons differential diagnosis for bullous skin lesions include infectious causes such as bullous impetigo, bullous tinea, eczema herpeticum, bullous scabies, mycoplasma pneumoniae, GAS, staph aureus/TSS, kawasaki disease, chickenpox, and herpes simplex infection; infection- and drug-associated causes such as erythema multiforme, DRESS, SJS and TEN; hereditary conditions such as epidermolysis bullosa, Kindler syndrome, and incontinenti pigmenti; and autoimmune conditions such as linear IgA bullous dermatitis, bullous pemphigoid, pemphigoid vulgaris, and fixed drug eruptions (type IV hypersens, mostly to abx or NSAIDs, always in same place in body, plaque or blister) treat cause and depending on severity +/- response escalate from oral pred to IV eg methylpred to IVIg approach 1. History Timeline of disease Prodromal symptoms ie symptoms that occurred before the rash started such as fever, difficulty eating, sore joints, New medications, including over-the-counter and natural products Previous reactions to drugs Family history of reactions to medications 2. General examination Is the patient well or sick? Check temperature, heart rate, blood pressure, respiratory rate Feel for enlargement of lymph nodes, liver or spleen 3. Blisters Localised or widespread? Appearance — tense or flaccid, clear or containing pus or blood Distribution on the skin Evolution — are new ones still developing and old ones resolving, or are all the blisters at the same stage of development? Involvement of mucous membranes (eg, inside mouth, eyes, vagina, etc.) Nikolsky sign — pressure applied to skin pulling sideways — positive if the skin detaches 4. Histopathology Often required to make the correct diagnosis Other ix inc mycoplasma IgM serology, + test for EBV, HHV6, HSV, CMV, Hep ABC, ASOT

Answer 22

extremely pruritic, chronic blisters usually >15yo symmetrical, small vesicles and papules on extensor surfaces - classically knees, elbows, scalp, sacrum dapsone and gluten free diet to treat linked to coeliac, biopsy to prove

Answer 23

rare autoimmune skin condition which results in clusters of blisters developing in rings often on the face or genitals also known as chronic bullous dermatosis or linear IgA dermatosis of childhood main feature is the development of clusters of blisters in specific areas of the body. These blisters are usually itchy and uncomfortable. Some children have many of these clusters, others have only a few. They tend to appear in phases, with new clusters of blisters appearing in the same area as previous ones Typically found in rings (annular lesions) in children — new blisters tend to arise in a ring around an existing blister known as the ‘string of beads’ sign skin biopsy is usually needed to confirm the diagnosis in biopsy will often show IgA antibodies as well which are arranged in a line serum IgA will be raised range of treatments are used, including dapsone mainly, +/- ciclosporin and topical or systemic steroids ddx Bullous impetigo Bullous pemphigoid Dermatitis herpetiformis — differentiated by its granular IgA deposition (not linear) Epidermolysis bullosa

Answer 24

behcets, lichen planus, SJS, sjogrens

Answer 25

50% idiopathic, may be herpes (think of this if rec), mycoplasma, EBV, histoplamosis, penicllines, sulphonamides, various CTDs remove causative agent

Answer 26

● Erythema multiforme, often of unknown cause, is an acute self- limiting inflammatory condition with herpes simplex virus being the main precipitating factor. Other infections and drugs are also causes. Mucosal involvement is absent or limited to only one mucosal surface. Stevens-Johnson syndrome is characterised by mucocutaneous necrosis with at least two mucosal sites involved. Skin involvement may be limited or extensive. Drugs or combinations of infections or drugs are the main associations. Epithelial necrosis with few inflammatory cells is seen on histopathology. The extensive necrosis distinguishes Stevens- Johnson syndrome from erythema multiforme. Stevens-Johnson syndrome may have features overlapping with toxic epidermal necrolysis including a prodromal illness. Toxic epidermal necrosis which is usually drug-induced, is an acute severe similar disease characterised by extensive skin and mucosal necrosis accompanied by systemic toxicity. On histopathology there is full thickness epidermal necrosis with subepidermal detachment. Management ● Early recognition and call for help ● Full supportive care to maintain haemodynamic equilibrium Complications ● Mortality rates are 5-12% with SJS and >30% with TEN with death often due to sepsis, electrolyte imbalance or multi-system organ failure

Answer 27

● Exfoliative dermatitis involving at least 90% of the skin surface Causes ● Previous skin disease (e.g. eczema, psoriasis), lymphoma, drugs (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) and idiopathic Presentation ● Skin appears inflamed, oedematous and scaly ● Systemically unwell with lymphadenopathy and malaise Management ● Treat the underlying cause, where known ● Emollients and wet-wraps to maintain skin moisture ● Topical steroids may help to relieve inflammation Complications ● Secondary infection, fluid loss and electrolyte imbalance, hypothermia, high-output cardiac failure and capillary leak syndrome (most severe) Prognosis ● Largely depends on the underlying cause ● Overall mortality rate ranges from 20 to 40%

Answer 28

pustules or vesicles on hand w history of similar on feet, or vesicles/ulcers in mouth mild erythema may surround the vesicles and child may be slightly unwell may be history of contact w others w similar lesions due to cocksackie virus, resolves spontaneously herpetic whitlow pustules may look similar, these found in children who suck their thumb or bite their nails a lot and so are in sites of expected paronychia; also consider pompholyx eczema for hand/feet lesions, and perioral lesions may be staph/strep infection eg bullous impetigo

Answer 29

Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur (formerly known as Pityrosporum ovale). It is common, affecting around 2% of the general population. Features eczematous lesions on the sebum-rich areas: scalp (may cause dandruff), periorbital, auricular and nasolabial folds otitis externa and blepharitis may develop Associated conditions include HIV Parkinson's disease Scalp disease management over the counter preparations containing zinc pyrithione ('Head & Shoulders') and tar ('Neutrogena T/Gel') are first-line the preferred second-line agent is ketoconazole selenium sulphide and topical corticosteroid may also be useful Face and body management topical antifungals: e.g. ketoconazole

Answer 30

itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms rash often polygonal in shape, with a 'white-lines' 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: typically a white-lace pattern on the buccal mucosa nails: thinning of nail plate, longitudinal ridging Lichenoid drug eruptions - causes: gold quinine thiazides Management potent 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

Answer 31

well defined flaky erythema with yellow/white scales, mild itching, symmetrical; scalp, face, upper chest/back, flexures and skin folds esp axilla, groin, anogenital, inframammary, umbilicus infantile form usually starts 3-8 weeks old continues until 6-12mo, oft cradle cap but can be in the other areas consider atopic eczema, psoriasis, scabies, contact derm, zinc def, pityriasis rosea (herald patch) or versicolor (sun exposed skin) reassure, topical emollient eg olive oil massage onto scalp, wash off with shampoo; clotrimazole if fails for up to 4 weeks; other areas bath daily with emollient instead of soap, maybe clotrimazole up to 4 weeks in adults use ketoconazole shampoo 2x week for 4 weeks then once every 1-2 weeks, cream for face and body; topical steroids can be used for flare of itching/inflam for 1-2 weeks derm referral if uncertainty or not responding

Answer 32

nappy rash - distressed child, itchy/painful rash; well defined erythema with scattered papules over convex surfaces with sparing of inguinal creases and gluteal cleft if bright red perianal patches or plaques, papules spreading into skin folds consider candida; exudate and pustules may be bacterial, and in this case swabs needed diffs inc contact dermatitis, eczema herpeticum (vesicles, fever), perianal streptococcal dermatitis (bright red, sharply demarcated perianal rash w/o satellite lesions (unlike thrush); seb derm; psoriasis (affecting clefts and folds not surface); lichen sclerosus (penile/vulval involvement, ivory coloured); scabies; tinea corporis manage: high absorb nappies, fit properly, leave off as long as poss; change every 3-4hrs and asap after soiling, washing skin between with water and dry after; if erythema then zinc, castor oil, paraffin ointment as barrier; inflamed and discomfort then topical hydrocort once a day for up to 7 days; doesnt resolve or otherwise suspect candida then topical clotrimazole (no barrier prep till after infection settles); if bacti then oral fluclox/clarithro for 7 days; microbiologst advice if not responded

Answer 33

prev called histiocytosis X may be a child w nappy rash that isn't responding to treatment, and a nappy area that looks like seb derm eosinophillic granuloma most benign, usually between 20-40yo w well defined lesions in skull, spine, ribs giving localised swelling and bone pain hand-schuller-christian disease in early childhood, with infiltration giving proptosis, central diabetes insipidus, lytic bone lesions, organomeg, otitis media, fibrosis lettere-siwe disease most severe, first couple of years with fever, anaemia, generalised lymphad, and seb derm like rash; skin, lumph node, bone biopsies and maybe skeletal survey high spont remission rate, <2yo worse pronosis and needs chemo

Answer 34

insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1) thus causes: type 2 diabetes mellitus gastrointestinal cancer obesity polycystic ovarian syndrome acromegaly Cushing's disease hypothyroidism familial Prader-Willi syndrome drugs combined oral contraceptive pill

Answer 35

smooth-surfaced, firm, dome-shaped and raised off skin, flesh-coloured or pearly white papules with a central umbilication. typically dev over weeks, normally 2-5mm but can be >1cm (normally if solitary lesion or immunocompromised) trunk, flexures, anogenital region most of all; rarely also feet, palms, eyelids, oral mucosa (and if immunocompromised maybe widespread across face) often asymp but may be itchy and look for surrounding eczema or bacti infection cause by molluscum contagiosum which is a poxvirus if on eyelid margin w red eye needs to see ophtho, if immunocomp or unsure of diagnosis then derm referral (or if extensive or painful lesions) mx is reassurance that will resolve but might take up to 18mo; treatment options exist for molluscum contagiosum, such as imiquimod 5% cream, podophyllotoxin 0.5% (off-label indication), and cryotherapy, but no convincing evidence for these lesions are contagious so no sharing towels, sheets etc, avoid squeezing, cover before using swimming pools; no need for exclusion from school

Answer 36

Herald patch followed 1-2 weeks later by multiple erythematous, slightly raised oval lesions with a fine scale confined to the outer aspects of the lesions. May 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. Normally on trunk, especially top down. Sometimes in eg axilla or proximal limbs many pts report recent resp infection self limiting, 6-12wks control itch with emollient, soap substitute like aqueous cream, and if abd then oral antihistamines or topical steroids (derm can do phototherapy)

Answer 37

multiple alternative names but perhaps 'eruptive haemangioma' is the most useful. The cause of pyogenic granuloma is not known but a number of factors are linked: trauma pregnancy more common in women and young adults Features most common sites are head/neck, upper trunk and hands. Lesions in the oral mucosa are common in pregnancy initially small red/brown spot rapidly progress within days to weeks forming raised, red/brown lesions which are often spherical in shape the lesions may bleed profusely or ulcerate Management lesions associated with pregnancy often resolve spontaneously post-partum other lesions usually persist. Removal methods include curettage and cauterisation, cryotherapy, excision

Answer 38

Drug Rash with Eosinophilia and Systemic Symptoms High fever Morbilliform eruption (aka rash that looks like measles) Haematological abnormalities Lymphadenopathy Inflammation of one or more internal organs (liver, kidney, lung, iris) most common drugs to cause this reaction are a number of anticonvulsant drugs (particularly carbamazepine, phenobarbital, and phenytoin), allopurinol, olanzapine, and the sulphonamide group of antibiotics. It’s a delayed T cell response diagnosis of drug hypersensitivity syndrome is based on the clinical triad of: High fever Extensive skin rash Organ involvement. It is supported by eosinophilia and abnormal liver function tests. As drug hypersensitivity syndrome can occur up to eight weeks after first exposure to the responsible drug, a great degree of care is required

Answer 39

most common in kids/teens/young adults might be a delayed hypersens reaction to infection, trauma, inflam etc skin coloured or red bumps form a ring in skin, esp over joints eg knuckles or back of hands, and the centre of the ring is smooth and a little depressed; also common on top of foot, on ankle, or over one or both elbows; they look a bit like ringworm but ringworm is scaly and itchy whereas GA is neither of these things (perhaps mildly itchy) it should clear by itself in a few months to a year (may take longer) but if persistent or visible/bothering them otherwise can refer for derm to consider topical steroids, topical calcineurin inhibs, cryotherapy etc in older ppl can generalise and need systemic steroids or other more complex treatments

Answer 40

red, raised, itchy, may burn/sting; usually last minutes to hours, <5% >6 weeks 50% idiopathic, else caused by infections (viruses including EBV, hepatitis, or URTI, bacti inc sinusitis or mycoplasma), may be allergic reaction (medication, bites/stings, food), or else stress, cold, vibrations, sweating or exercise, parasite infection can trigger beware and check for sx of anaphylaxis (inc wheezing, difficulty breathing) and angioedema (which occurs in deeper layer of dermis and often around face or throat) if lesions last over 24 hours, painful, palpable +/- sys upset consider vasculitic urticaria most common food allergies in adults are shellfish and nuts. The most common food allergies in children are shellfish, nuts, eggs, wheat, and soy ix not normally needed but if no clear cause after the history or if repeated episodes then can consider patch testing or RAST which identifies the allergy avoid trigger and consider antihistamines (fexofenadine or preferred cetirizine (can do/escalate to double dose if needed), can try piriton as alternative), steroids if more severe (eg angio-oedema), persisting or systemic sx inc fever - pred for 3 days; if recurrent or persist >6 weeks despite above can consider montelukast, omalizumab; can consider FBC (parasites, vasculitis), CRP/ESR, TFTs + coeliac screen (autoimmune chronic urticaria), urinalysis, viral swabs/tests

Answer 41

ddx for fever and urticaria: respiratory viruses, EBV, HIV, parasitic infection, HLH, macrophage activation syndrome, urticarial vasculitis, SLE, JIA (systemic onset), family Mediterranean fever, kawasaki disease, medication reaction (esp beta lactam abx), cyropyrin-associated periodic syndromes (CAPS), rarely may have underlying malignancy so take careful history and examination CRP, FBC, ESR, consider screen for infections above if febrile and not responding to antihistamines and second line measures (often steroid) then should biopsy the urticaria depending on results of biopsy can try measures such as IVIg, or anakinra note anakinra used for rheum arth, still's disease, CAPS, MAS, FMF, JIA, HLH; it is a recombinant interleukin 1 receptor antagonist protein thus blocking the pro-inflam activity of interleukin 1 alpha/beta; its use is currently off label in children and done under specialist advice, often starting 2mg/kg and uptitrating to eg 4mg/kg, maintenance dose may need to be given over a prolonged period

Answer 42

Causes ● Idiopathic, food (e.g. nuts, sesame seeds, shellfish, dairy products), drugs (e.g. penicillin, contrast media, non-steroidal antiinflammatory drugs (NSAIDs), morphine, angiotensin-converting enzyme inhibitors (ACE-i)), insect bites, contact (e.g. latex), viral or parasitic infections, autoimmune, and hereditary (in some cases of angioedema) Description ● Urticaria is due to a local increase in permeability of capillaries and small venules. A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic factors) play a role but histamine derived from skin mast cells appears to be the major mediator. Local mediator release from mast cells can be induced by immunological or non-immunological mechanisms. Presentation ● Urticaria (swelling involving the superficial dermis, raising the epidermis): itchy wheals ● Angioedema (deeper swelling involving the dermis and subcutaneous tissues): swelling of tongue and lips ● Anaphylaxis (also known as anaphylactic shock): bronchospasm, facial and laryngeal oedema, hypotension; can present initially with urticaria and angioedema Management ● Antihistamines for urticaria ● Corticosteroids for severe acute urticaria and angioedema ● Adrenaline, corticosteroids and antihistamines for anaphylaxis Complications ● Urticaria is normally uncomplicated ● Angioedema and anaphylaxis can lead to asphyxia, cardiac arrest and death

Answer 43

● A hypersensitivity response to a variety of stimuli Causes ● Group A beta-haemolytic streptococcus, primary tuberculosis, pregnancy, malignancy, sarcoidosis, inflammatory bowel disease (IBD), chlamydia and leprosy Presentation ● Discrete tender nodules which may become confluent ● Lesions continue to appear for 1-2 weeks and leave bruise-like discolouration as they resolve ● Lesions do not ulcerate and resolve without atrophy or scarring ● The shins are the most common site

Answer 44

bucket handle metaphyseal fractures of long bones, spiral fractures, mid-shaft fractures, fractures of various ages in x-ray or in ribs/skull/pelvis many sig bruises <1yo, or characteristic pattern like fingertip, hand slap, bite mark, or bruises in unusual places like perineum, ears also cig burns, scalds, retinal haemorrhages, SDH, torn frenulum, alert but anxious (frozen watchfulness), failure to thrive, underachievement at school, dev delay; vaginal bleeding/discharge, rec abdo pain, STIs or pregnancy; reflex anal dilatation (also in chronic constipation) other features in history: delay in seeking med attention, inconsistencies in history, either too much or too little parental concern, abnormal parental affect, anger from parent if admission wanted you should exclude bleeding/clotting problems and eg osteogenesis imperfecta, including doing a skeletal survey/bone scan as well as clotting studies detailed history and exam - document everything and treat injuries - admit child if suspicion high - look up at risk register and contact social services

Answer 45

ask about nosebleeds, gingivitis, menorrahgia, prolonged bleeding, joint swelling; tiredness, weight loss, fever, night sweats; nutritional status; FH; tendency to bruise easily examine for palpable purpura, pallor, jaundice, brittle hair/nails, hyperelast (EDS), organomegaly, lymphadenopathy urine dipstick, urgent FBC and film, clotting screen (INR if on warfarin); LFTs, U&Es, TFTs ITP can cause bruising etc as lowers plat count, autoimmune, usually follows viral infection or vaccination in children, self limiting in 8 weeks; life threatening intracranial H+ poss, up to 25% have nosebleeds, maybe menorrhagia; FBCs and film; avoid contact sports and nsaids in meantime; monitor, repeat FBC if remit or deteriorate; sec care may use steroids, IVIg; tranexamic acid for menorrhagia; 80% better by 6mo, some dev chronic form splenectomy if really needed

Answer 46

suggests that adenoma sebaceum has been misdiagnosed as acne, and this condition is actually tuberous sclerosis it is usually onset between 2-5yo they are angiofibromas (red or brown papules, often in butterfly distribution around nose) could look for ash-leaf spots (hypopig macules from birth), shagreen patches (leathery, lumbosacral, 2-5yo), subungual fibromas (usually from puberty)

Answer 47

flat red/purple macular vascular lesions due to dilated caps, growth in prop with child, may fade over time but usually don't and might become bumpy may have sturge-weber if in opthalmic diision of trigem- in ipsi cortex will see vascular abnorm may overly hypertrophy of soft tissue and bone, most often the limbs; this is klippel-trenaunay syndrome treat w laser therapy

Answer 48

first split into strawberry naevus and cavernous haemangiomas (deeper) former bright red, raised, lobulated w distinct borders, in 10% of infants, grow in first few weeks of life until 6mo-1yo then involute, completely disappearing by 6-7yo; cav haem may be skin coloured or bluish, and have ireg borders complications inc bleeding or ulceration, infection, functional impairment if around orbit, platelet sequestration giving thrombocyto, and high output heart failure due to AV shunting (last 2 only in large lesions) conservative unless function impaired (risk of amblyopia), near airway, or large having sx as above or appearance troubling; propanolol or laser/surg; if one present look for others, consider internal/visceral ones too; consider laryngoscopy if skin one + stridor mongolian blue spot - grey/blue macule usually in lumbosacral region but maybe limbs/buttocks, in 10% white babies but 80% asian/black babies, usually fades over years; wonder about NAI too pigmented naevi - giant if >20cm, grow in prop to child's growth; main concern is 7% lifetime risk of melanoma in larger lesions so reg exam and f/u, maybe full thickness excision and graft for cosmetic reasons

Answer 49

acute mucocutaneous perioral/anal rash (eczematous w pustules or bullae) soon after weaning AR disease causing defective intestinal zinc absorption may also have diarrhoea, failure to thrive, and hair loss and due to low levels of serum zinc oral zn supplements

Answer 50

bluish mottling/marbling of skin, may be normal in neonates as skin cools or else in babies who are periph shutdown - check CRT, if <2s you dont have to worry also see in down/edward syndrome, congen hypothyroid, cornelia de Lange syndrome

Answer 51

caused by papilloma virus flesh coloured papules - verrucas in hands/feet, verrucae plantaris in soles; there are also genital warts (be alert to sexual abuse, but may be transmitted at birth)

Answer 52

v rare xld condition affecting only females (in utero fatal for males) in first weeks of life get bullae/vesicles on trunk + extremities, then papular rash w streaks of irregular red papules, then hyperpig stage with whorling/streaks of blue-grey pigment on trunk and extremities, lasting several years and resolving leaving hypopig areas 1/3 get cns involvement (seizures, umn signs), 2/3 delayed dentition or pegged teeth, and maybe also cataracts, blindness, cardiac/skeletel abnorms

Answer 53

AR inherited white skin/hair, blue/pink eyes and commonly nystagmus, photophobia, refractive errors due to defect in tyr metab blonde hair, blue eyes and mental retardation could be angelmans

Answer 54

Normal skin is continuously shed and re-grown to form an effective barrier against infection and other damage. In ichthyosis, this mechanism does not work properly, so the skin does not shed properly, so builds up as thick, rough areas. 4 kinds: icthyosis vulgaris is AD w fine white scales on skin, esp back and extensor surfaces; xlr ichythosis has collodion membrane around baby, then dark scales over body except palm/soles, maybe corneal opacitis and poor uterine contraction; lamellar icthyosis is AR with collodion membrane at birth, later thick dark plate like scales and oft absent nails, AR patterns also include harlequin type ichthyosis; epidermolytic hyperkeratosis is AD at birth w generalised erythroderma, later thick warty scales and rec bullae main symptom of all types of ichthyosis is rough, scaly skin that is very dry. The specific areas affected and how severely will vary depending on the type of ichthyosis All types of ichthyosis have a characteristic appearance but as it is a rare condition, diagnosis of the precise type of ichthyosis will usually only be possible at a specialist centre. With the more severe types of ichthyosis, a baby may be transferred to a specialist centre soon after birth both for diagnosis and the more intensive support needed dermatologist treats, emollients generally v important + use as soap substitute; soak skin once a day and rinse with antiseptic to remove scale; In moderate-severe disease specialists use systemic retinoids; at risk of heat loss and infection if v severe, hence need to be at a specialist centre

Answer 55

AR form of icthyosis, an inborn error of metabolism resulting in the deficiency of an enzyme, fatty aldehyde dehydrogenase (FALDH) Children with Sjögren-Larsson syndrome have red, dry skin from birth. Scaling more usually develops after infancy. The neck, lower abdomen and large folds are most involved. Thick skin of the palms and soles (palmoplantar keratoderma) affects 70% of patients Itching and scratching is common. Heat intolerance may arise Glistening white dots on the retina are often detectable in the first year of life. Delayed motor development (muscles) of legs and/or arms is noted in childhood. It results in: Abnormal gait Paresis (weak muscles) Spasticity (muscle stiffness and spasms). Children may have speech delay and intellectual impairment. Seizures (epilepsy) affect 40% of children Learning disability Photophobia Alteration of posture and gait leads to: Kyphoscoliosis (abnormal curvature of the spine) Hip dislocation Short stature diagnosis usually made clinically. It may be confirmed in some centres by measurement of fatty aldehyde dehydrogenase in white blood cells or cultured fibroblasts collected by skin biopsy; genetic testing can be performed multidisciplinary mx with input from speech and language therapy, physiotherapy, occupational therapy, dermatology, neurology, ophthalmology and orthopaedic services. Skin hydration is important; emollients and moisturisers should be applied to dry skin regularly. Topical keratolytics such as urea and lactic acid can reduce scale and skin thickening. Severe ichthyosis is sometimes treated with oral retinoids

Answer 56

congen - may be sec to syndrome like ellis van creveld, or on its own; consultation w dentist and removal may be needed if risk of them falling out (then aspirating) or if interfering w breast feeding brown discoloration due to excess fluoride exposure; brown-yellow if tetracyclines (dont use these before 8yo where permanent dentition fully enamelled

Answer 57

vitiligo, piebaldism, pityriasis versiclor, leprosy, post-burns, albinism, phenylketonuria, chediak-higashi syndrome, hypopitu (last 4 cases are more generalised)

Answer 58

insidious onset of oval macules and confluent patches that can be fawn, pink, red, brown, or almost white — the surface of patches usually has a fine scale; caused by malassazia furfur In people with lighter skin tone lesions may be more noticeable in the summer months if patches fail to tan; in people with darker skin tone affected skin is commonly paler most commonly occurs on sebum-rich areas of the skin, particularly the upper trunk, often with spread to the upper arms, neck, and abdomen. Other areas that may be affected include the face (especially in children), axillae, groin, thighs, scalp, and genitalia Skin scrapings may be considered if the diagnosis is uncertain or initial treatment has failed not contagious as the yeast that causes it is normally present on human skin Treatment is usually highly effective, but may need to be repeated, as recurrence is common and skin discolouration may take several weeks or months to fully resolve large areas - use ketoconazole 2% shampoo, small areas use clotrimazole or ketoconazole cream BD for 2-3 weeks treat relapse as the original If episodes of pityriasis versicolor recur on exposure to warm, humid environments or sunshine, prophylactic treatment prior to exposure eg ketoconazole 2% shampoo once daily for a maximum of 3 days prior to sun exposure if treatment failure then skin scrapings +/- derm referral for eg oral antifungals

Answer 59

NF, russell-silver syndrome, turner syndrome, TS, mccune-albright syndrome

Answer 60

idiopathic self limiting vasculitis in children 6mo-5yo, mainly in east asian people but also affects other races; peak incidence 18-24mo assess any children with fever for 5days+ for this, ask about symptoms not just now but also from when fever started as may have resolved by presentation abrupt onset fever (39deg+), often irritable out of prop with fever; must also have 4+ of: oropharyngeal inflam (cracked lips, strawberry tongue, inflamed mucosa), erythema/oedema or desquam of extremities, bilat dry conjunctivitis, widespread non-vescicular rash (ot start with erythema of palms/soles/perineum, itchy and takes various forms), cervical lymphadenopathy; also maybe lethargy, diarrhoea, vomiting, urethritis, myalgia, arthralgia risk of coronary artery aneurysms, MI, pancarditis, aortic or mitral incompetence aseptic meningitis and sterile pyuria may occur; gallbladder may be distended FBCs, LFTs, urinalysis; echo is essential to assess for aneurysms and heart function inpatient bed rest during acute 2 week due to risk of cardiac events; aspiring (yes really) and IVIg to protect heart and reduce fever, follow up echoes; PCI or CABG may be needed

Answer 61

Roseola infantum (also known as exanthem subitum, occasionally sixth disease) is a common disease of infancy caused by the human herpes virus 6 (HHV6). It has an incubation period of 5-15 days and typically affects children aged 6 months to 2 years. Features high fever: lasting a few days, followed later by a maculopapular rash - classically 3 days fever then rash on the 4th Nagayama spots: papular enanthem on the uvula and soft palate febrile convulsions occur in around 10-15% diarrhoea and cough are also commonly seen Other possible consequences of HHV6 infection aseptic meningitis hepatitis School exclusion is not needed. Rash typically starts on the trunk and limbs (this is different to chickenpox which is typically a central rash). HHV6 is neurotropic (attacks the nervous system) and thus a rare complication is encephalitis and febrile fits (after cessation of the fever)

Answer 62

An umbilical granuloma is an overgrowth of tissue which occurs during the healing process of the umbilicus. It is most common in the first few weeks of life. On examination, a small, red growth of tissue is seen in the centre of the umbilicus. It is usually wet and leaks small amounts of clear or yellow fluid. It is treated by regular application of salt to the wound, if this does not help then the granuloma can be cauterised with silver nitrate. Omphalitis or umbilical cellulitis is a bacterial infection of the umbilical stump which presents as a superficial cellulitis, usually a few days after birth. Umbilical hernias occur in 1 in 5 newborn children and usually resolves by 2 years.

Answer 63

common and benign condition seen in newborn infants. It affects as many as half of all full-term newborn infants but is less common in infants born prematurely Most cases of toxic erythema of the newborn begin in the first few days after birth, although onset can be as late as two weeks of age. Toxic erythema of the newborn is evident as white headed spots on erythematous skin. The eruption typically waxes and wanes over several days and it is unusual for an individual lesion to persist for more than a day. Toxic erythema of the newborn often begins on the face and spreads to affect the trunk and limbs. Palms and soles are not usually affected. The infant is otherwise well

Answer 64

Morning+/-Evening: · Bathe in luke-warm water for 10-20 minutes · Use eg cetraben, diprobase, or others as a soap substitute (an emollient soap sub, to avoid the drying + alkaline effect); Aqueous cream is no longer recommended, either as a leave-on emollient or as a soap substitute, as in addition to being a poor moisturiser it contains the ingredient sodium lauryl sulphate (SLS), which can irritate the skin and make eczema worse. · Pat child dry with a soft towel, do not rub the skin · Apply emollient (moisturizer) to the body in direction of hair growth. · Wait 10-20 minutes then apply steroid to inflamed areas on body and limbs (so steroid not diluted or spread by rubbing the cream off eczema area) During the day · Apply emollient (moisturizer) all over body as regularly as necessary Emollients: Lotions contain more water and less fat than creams. Because of their high water content, lotions need to contain preservatives, which people can become sensitised to, although this is rare; not good at moisturising v dry skin because they are not thick enough to repair the skin barrier. They are useful for hairy areas and weeping eczema Creams contain a mixture of fat and water, and feel light and cool on the skin. They are quite easy to spread over sore and weeping skin and are not greasy, so many people prefer them to ointments for daytime use. Like lotions, creams need to contain preservatives, which can cause sensitivity; apply every 6-8 hours Ointments are often stiff and greasy, and some people may find them cosmetically unacceptable. However, because they are very effective at holding water in the skin and repair the skin barrier well, they are useful for very dry and thickened areas, under wet wraps, or if a heavier emollient is required at night. They should be applied every 6–8 hours. Ointments should not be used on weeping eczema. so many emollients but some egs: cetraben, dermol, diprobase, E45

Answer 65

The greasier an emollient is the more effective it is at retaining hydration. Leave-on emollients should be prescribed in large quantities (250-500g weekly) for severe cases. Always use an emollient as a soap substitute. DO not use any other wash product that lathers/makes bubbles, as this will take away all the benefit of the emollient. * Bath or shower daily during flares of eczema. * Apply lots of emollient three to four times a day during flares of eczema and reduce application slowly once eczema clears, increasing again if eczema rebounds. * Apply emollient to whole body morning and night (as all skin is prone to eczema) and to dry or red areas on 1‐2 further occasions during the day, or whenever it is itching. * If the skin remains dry increase the grease content of the emollient or apply the emollient more regularly If the skin becomes spotty, reduce the grease content of the emollient choice. If there are yellow heads antimicrobial therapy such as the Dermol products may be required. * Patients may prefer to use lighter emollient during the day, with a greasier one for use at night. During hot weather/on holiday in hot climates use a Light or Creamy emollient in the morning. Leave at least half an hour and then apply the child’s sunscreen. Reapply sunscreen regularly throughout the day if out in the sun and use a Greasy or Very Greasy emollient at night if skin is dry. * If a child has eczema on the face then application of a thin layer of a Greasy or Very Greasy emollient before they eat or go outside into cold, windy weather may help as a barrier light: cetraben lotion, E45, dermol 500 (contains antiseptic so good if frequent skin infections) creamy: epimax cream, zerobase, cetraben cream greasy: cetraben ointment, diprobase ointment, zerodouble gel very greasy: hydromol/zeroderm ointment, white soft paraffin Be aware that washing clothing or fabric at a high temperature may reduce emollient build‐up but not totally remove it. Warn patients not to smoke or go near naked flames because clothing or fabric such as bedding or bandages that have been in contact with an emollient or emollient‐treated skin can rapidly ignite

Answer 66

patches of white hair and leukoderma caused by absent melanocytes can have cafe au lait macules AD inheritance also consider waardenburg sydrome (deafness, increased distance between eyes), vitiligo (different distribution and acquired) suncreams and sun exposure guidance needed as higher risk of cancer in the white areas

Answer 67

congen absence of skin inc sometimes also underlying structures which can inc bone, from mm to 10cm+ across small areas can heal by themselves, larger areas need dressing and referral to plastics, possibly also neurosurg if brain tissues/meninges exposed

Answer 68

derm emergency rapidly progressive and is often accompanied by disseminated intravascular coagulation and circulatory collapse. It occurs in neonates, children, and adults is a rapidly evolving syndrome of skin microvascular thrombosis and hemorrhagic necrosis. skin lesions may present early as petechial rashes. These rapidly progress to larger ecchymotic areas. Later in the course, hemorrhagic bullae may form which contribute to the classic hard eschars characteristic of purpura fulminans It is considered a sign of certain systemic diseases rather than a disease unto itself. The 3 types of purpura fulminans are neonatal, idiopathic, and acute infectious. Neonatal purpura fulminans is associated with a hereditary deficiency of the anticoagulants protein C, protein S, and antithrombin III. It manifests very early in life and treatment is aimed at these deficiencies Idiopathic purpura fulminans is thought to be a post-infectious autoimmune disorder often following an initiating febrile illness, which later leads to rapidly progressive purpura. In this form, a relative deficiency of protein S is believed to be causative. Acute infectious purpura fulminans is the third and most common type. It manifests as a skin finding in the most severe septic patients (DIC) as well as in necrotizing fasciitis caused by dermal vascular thrombosis

Answer 69

aka burning feet syndrome erythema, warmth, and burning pain affecting extremities (often feet, sometimes hands, very rarely face) - typically b/l but may be unilat 3 types - one due to thrombocythemia (esp in the 3 primary myeloprolif disorders), primary if idiopathic or inherited, secondary otherwise (to many conditions) primary usually in first two decades of life, secondary usually in forties/fifties generally triggered by exercise, warm climates, standing, and wearing tight-fitting shoes, which may last minutes to days, and the symptoms typically get relieved by cooling FBC (also exclude cellulitis), autoimmune + rheumatoid screen, HIV testing, uric acid (rule out gout)

Answer 70

necrosis of skin and subcut fat due to calcium deposition, usually related to CKD (about 1% of dialysis pts) but may also be related to other causes of hypercalc (measured blood Ca may be normal however), diabetes, hypoalbuminemia, warfarin it is bc the calcification of small vessels leads to (micro)thrombosis -> ischaemia; initially purple mottling then bleeding, necrosis, itching, severe pain skin biopsy often needed to tell from eg nec fasc, cryoglobulinemia, vasculitis, antiphospholipid syndrome etc when trigged by warfarin it is in the first few days due to pro-coag state (so heparin cover should prevent)

Answer 71

common viral infection that presents with localised blistering. It affects most people on one or more occasions during their lives caused by one of two types of herpes simplex virus (HSV), members of the Herpesvirales family of double-stranded DNA viruses. Type 1 HSV is mainly associated with oral and facial infections Type 2 HSV is mainly associated with genital and rectal infections However, either virus can affect almost any area of skin or mucous membrane. After the primary episode of infection, HSV resides in a latent state in spinal dorsal root nerves that supply sensation to the skin. During a recurrence, the virus follows the nerves onto the skin or mucous membranes, where it multiplies, causing the clinical lesion. After each attack and lifelong, it enters the resting state. During an attack, the virus can be inoculated into new sites of skin, which can then develop blisters as well

Answer 72

Primary Type 1 HSV most often presents as gingivostomatitis, in children between 1 and 5 years of age. Symptoms include fever, which may be high, restlessness and excessive dribbling. Drinking and eating are painful, and the breath is foul. The gums are swollen and red and bleed easily. Whitish vesicles evolve to yellowish ulcers on the tongue, throat, palate and inside the cheeks. Local lymph glands are enlarged and tender. The fever subsides after 3–5 days and recovery is usually complete within 2 weeks. Primary Type 2 HSV usually presents as genital herpes after the onset of sexual activity. Painful vesicles, ulcers, redness and swelling last for 2 to 3 weeks, if untreated, and are often accompanied by fever and tender inguinal lymphadenopathy. Recurrences can be triggered by: Minor trauma, surgery or procedures to the affected area Upper respiratory tract infections Sun exposure Hormonal factors (in women, flares are not uncommon prior to menstruation) Emotional stress In many cases, no reason for the eruption is evident. The vesicles tend to be smaller and more closely grouped in recurrent herpes Itching or burning is followed an hour or two later by an irregular cluster of small, closely grouped, often umbilicated vesicles on a red base. They normally heal in 7–10 days without scarring. The affected person may feel well or suffer from fever, pain and have enlarged local lymph nodes. Herpetic vesicles are sometimes arranged in a line rather like shingles If there is clinical doubt, HSV can be confirmed by culture or PCR of a viral swab taken from fresh vesicles. HSV serology is not very informative, as it’s positive in most individuals complications: conjunctivits, pharyngitis causing painful swallow, In patients with a history of atopic dermatitis or Darier disease, HSV may result in severe and widespread infection, known as eczema herpeticum ( Numerous blisters erupt on the face or elsewhere, associated with swollen lymph glands and fever), erythema multiforme (symmetrical plaques on hands, forearms, feet and lower legs. It is characterised by target lesions, which sometimes have central blisters. Mucosal lesions may be observed), Cranial/facial nerves may be infected by HSV, producing temporary paralysis of the affected muscles. Rarely, neuralgic pain may precede each recurrence of herpes by 1 or 2 days (Maurice syndrome). Meningitis is rare, Disseminated infection and/or persistent ulceration due to HSV can be serious in debilitated or immune deficient patients, for example in people with HIV Mild, uncomplicated eruptions of herpes simplex require no treatment. Blisters may be covered if desired, for example with a hydrocolloid patch. Severe infection may require treatment with an antiviral agent. High dose/longer course (get advice) if immunosuppressed, eczema herpeticum, or systemic

Answer 73

chickenpox is a highly contagious viral infection that causes an acute fever and blistered rash, mainly in children. Once a person has had the chickenpox infection, it is unlikely he or she will get it again, as it confers lifelong immunity caused by primary infection with the varicella-zoster virus aka herpesvirus type 3 usually begins as itchy red papules progressing to vesicles on the stomach, back and face, and then spreading to other parts of the body. Blisters can also arise inside the mouth The spread pattern can vary from child to child. There may be only a scattering of vesicles, or the entire body may be covered with up to 500 vesicles. The vesicles tend to be very itchy and uncomfortable. Some children may also experience additional symptoms such as high fever, headache, cold-like symptoms, vomiting and diarrhoea. Chickenpox is usually more severe in adults and can be life-threatening in complicated cases. Most adults who get chickenpox experience prodromal symptoms for up to 48 hours before breaking out in the rash. These include fever, malaise, headache, loss of appetite and abdominal pain blisters clear up within one to three weeks but may leave a few scars. Diagnosis of chickenpox is usually made on the presence of its characteristic rash and the presence of different stages of lesions simultaneously. A clue to the diagnosis is in knowing that the patient has been exposed to an infected contact within the 10–21 day incubation period PCR detects the varicella virus in skin lesions and is the most accurate method for diagnosis. The culture of blister fluid is time-consuming and is less frequently performed. Serology (IgM and IgG) is most useful in pregnant women, or before prescribing immune suppression medication to determine the need for pre-treatment immunisation usually uncomplicated/self limiting Secondary bacterial infection of skin lesions caused by scratching Infection may lead to abscess, cellulitis, necrotising fasciitis and gangrene Dehydration from vomiting and diarrhoea Exacerbation of asthma Viral pneumonia Chickenpox lesions may heal with scarring. Some complications are more commonly seen in immunocompromised and adult patients with chickenpox. Disseminated primary varicella infection; this carries high morbidity Central nervous system complications such as Reye syndrome, Guillain-Barré syndrome and encephalitis Thrombocytopenia and purpura

Answer 74

Exposure to varicella virus in pregnancy may cause viral pneumonia, premature labour and delivery and rarely maternal death. Approximately 25% of fetuses of mothers with chickenpox become infected. It is harmless to most of them. Offspring may remain asymptomatic, or develop herpes zoster at a young age without a previous history of primary chickenpox infection. They may also develop congenital varicella syndrome, one of the TORCH infections. Congenital varicella syndrome occurs in up to 2% of fetuses exposed to varicella in the first 20 weeks of gestation. It can result in spontaneous abortion, fetal chorioretinitis, cataracts, limb atrophy, cerebral cortical atrophy and microcephaly, cutaneous scars, and neurological disability. Mortality in newborns infected with varicella is up to 30%. If a mother develops chickenpox just before delivery or during the 28 days after delivery, her baby is at risk of severe infection. Trim children's fingernails to minimise scratching. Take a warm bath and apply moisturising cream. Paracetamol can reduce fever and pain Avoid NSAID use outside of hospital settings due to the increased risk of severe cutaneous complications such as invasive group A streptococcal superinfections. Do not use aspirin in children as this is associated with Reye syndrome. Calamine lotion and oral antihistamines may relieve itching. Consider oral aciclovir (antiviral agent) in people older than 12 years, which reduces the number of days with a fever. Immunocompromised patients with chickenpox need intravenous treatment with the antiviral aciclovir. In cases of inadvertent exposure to the virus, varicella-zoster immune globulin if given within 96 hours of initial contact can reduce the severity of the disease though not prevent it. This is used where there is no previous history of chickenpox (or the patient has no antibodies to the varicella-zoster virus on blood testing) in pregnancy, in the first 28 days after delivery, and in immune deficient or immune-suppressed patients. A person with chickenpox is contagious 1–2 days before the rash appears and until all the blisters have formed scabs. This may take 5–10 days. Children should stay away from school or childcare facilities throughout this contagious period

Answer 75

Herpes zoster is a localised, blistering and painful rash caused by reactivation of varicella-zoster virus (VZV). Herpes zoster is also called shingles. can occur in childhood but is much more common in adults, especially older people - chance of then getting shingles a second time is 1% characterised by dermatomal distribution, usually unilateral with sharp cut-off first sign of herpes zoster is usually localised pain without tenderness or any visible skin change. It may be severe, relating to one or more sensory nerves. The pain may be just in one spot, or it may spread out. The patient may feel quite unwell with fever and headache. The lymph nodes draining the affected area are often enlarged and tender. Within one to three days of the onset of pain, a blistering rash appears in the painful area of skin. It starts as a crop of red papules. New lesions continue to erupt for several days within the distribution of the affected nerve, each blistering or becoming pustular then crusting over Pain and general symptoms subside gradually as the eruption disappears. In uncomplicated cases, recovery is complete within 2–3 weeks in children and young adults complications: Eye complications when the ophthalmic division of the fifth cranial nerve is involved Deep blisters that take weeks to heal followed by scarring Muscle weakness in about one in 20 patients. Facial nerve palsy is the most common result (Ramsay Hunt syndrome). There is a 50% chance of complete recovery, but some improvement can be expected in nearly all cases Infection of internal organs, including the gastrointestinal tract, lungs, and brain (encephalitis) Herpes zoster is infectious to people who have not previously had chickenpox. Shingles in late pregnancy can cause chickenpox in the fetus or newborn. Post-herpetic neuralgia is defined as persistence or recurrence of pain in the same area, more than a month after the onset of herpes zoster. It becomes increasingly common with age, affecting about a third of patients over 40. It is particularly likely if there is facial infection. Post-herpetic neuralgia may be a continuous burning sensation with increased sensitivity in the affected areas or spasmodic shooting pain. The overlying skin is often numb or exquisitely sensitive; instead of pain may have persisting itch Antiviral treatment can reduce pain and the duration of symptoms if started within one to three days after the onset of herpes zoster; rest, analgesia, abx if 2ndry bacti infection for neuralgia: Local anaesthetic applications Topical capsaicin Neuropathic painkillers

Answer 76

the most common ulcerative condition of the oral mucosa, and presents as a painful punched-out sore on oral or genital mucous membranes. 20% of ppl get, often start in childhood/adolescence can be an early manifestation of a systemic disease such as Behçet disease, or gastrointestinal disorders including coeliac disease, Crohn disease, and ulcerative colitis and smoking may be protective against them 40% of people who get aphthous ulcers have a family history of aphthous ulcers triggers may inc stress, lack of sleep, foods, medications, toothpaste, viral infection, menstruation typically a solitary round or oval punched-out sore or ulcer inside the mouth on an area where the mucosa is not tightly bound to the underlying bone, such as on the inside of the lips and cheeks or underneath the tongue can be painful nvestigations are rarely required, but are undertaken if there are recurrent attacks of multiple or severe oral ulcers or complex aphthosis. Blood tests may include: Blood count, iron, vitamin B12, and folate studies Gluten antibody tests for coeliac disease Faecal calprotectin test for Crohn disease. Swabs for microbiology evaluate the presence of Candida albicans, Herpes simplex virus Other causes of mouth ulcer should be considered, including: Herpes simplex, hand foot and mouth disease, and other viral infections Herpangina Erythema multiforme Fixed drug eruption SJS/TENS Local anaesthetics benzocaine and lignocaine (lidocaine) to reduce pain. Antibacterial mouthwash to prevent superadded infection Avoid triggers

Answer 77

neutrophilic dermatosis that may develop de novo or, more commonly, in the clinical setting of an underlying inflammatory or neoplastic disease, eg rheumatoid arthritis, autoimmune hepatitis, behcets, GPA, or IBD (esp UC) and malignancies esp leukaemias; 50% may be idiopathic lesion’s characteristics include a deep, extremely painful, papulopustular, necrotic cutaneous ulcer with an undermined and violaceous border that frequently heals with cribiform scarring; most commonly on legs in adults, in children, it frequently appears on the head and in the genital, peristomal, and perianal regions dev acutely or over months-years (see incorrect diagnosis of eg venous ulcer) small lesions eg topical steroid/tacrolimus larger or more aggressive systemic steroid eg methylpred pulse (risk of relapse and often extra rx needed), ciclosporin and tacrolimus, then infliximab or adalimumab

Answer 78

highly contagious infection caused by a morbillivirus of the paramyxovirus family typical incubation period of about 10 days (with a range of 7 to 21 days), with a further 2–4 days of prodromal symptoms (including malaise, fever, and cough) before the characteristic skin rash develops person is infectious from when symptoms first appear (around four days before the rash appears) to four days after the onset of the rash. Measles is spread by direct contact with infectious droplets or by airborne transmission from breathing, coughing or sneezing Susceptibility to opportunistic infection is increased for a period of several weeks to months, and this effect may last up to three years after the person has recovered from measles, as the measles virus suppresses the reaction of the immune system to other pathogens Secondary infections of the respiratory tract include: Otitis media (7–9% of cases). Pneumonitis. Tracheobronchitis. Pneumonia Convulsions and encephalitis may occur acutely, and years later rarely may see SSPE Blindness can result from measles keratoconjunctivitis or other ocular complications, and occurs mainly in children with vitamin A deficiency Most people with measles make a full recovery with symptomatic management after around seven days of symptoms; 1-5 deaths a year in UK, all in unvaccinated children

Answer 79

typical measles presents with fever, usually of 39ºC or more without antipyretics, maculopapular rash, and at least one (and usually all three) of cough, coryzal symptoms, and conjunctivitis. The prodromal phase occurs 10–12 days after contracting the infection and lasts for 2–4 days before the rash becomes apparent. Symptoms include increasing fever, malaise, cough, rhinorrhoea, and conjunctivitis. This latter symptom may help differentiate measles from other flu-like illnesses. Fever increases during the prodromal phase to around 39ºC at about the time the rash appears, and then gradually decreases. Koplik's spots may appear on the buccal mucosa at the end of the prodromal phase, a day or so before, or around the same time as the rash, and disappear over the next 2-3 days. These consist of 2–3 mm red spots with white or blue-white centres. These are pathognomonic for measles but can easily be confused with other mouth lesions. The rash is erythematous and maculopapular and may become confluent as it progresses. It appears on the face and behind the ears first (when other symptoms tend to be at their most severe), before descending down the body to the trunk and limbs, and forming on the hands and feet last, over the course of about 3–4 days. The rash fades after it has been present on an area for about 5 days, with the total duration of rash being up to 1 week Consider a different cause for the rash if the person is likely to have immunity to measles, clinical features are atypical, there is no history of contact with measles or travel to measles-endemic countries, and there are no local outbreaks If there is any suspicion of measles infection, immediately notify the local HPT. Measles is a notifiable disease. Clinical diagnosis alone is unreliable, infection must be confirmed by laboratory investigation (but notification should not await laboratory confirmation) - HPT will send an oral fluid testing kit to the affected person for IgM/IgG and/or viral RNA testing ddx: parvovirus, roseola, strep, EBV, kawasaki, zika/dengue/chikungunya, drug reaction, and rubella In children without fever, other causes of florid rash including erythema multiforme and viral or allergic urticaria should be considered rubella: rash usually starts behind the ears and on the face, and then spreads down the body (similar to measles). However, the infection is generally mild, and if fever is present it rarely occurs after the first day of the rash. There may be post-auricular and sub-occipital lymphadenopathy. Koplik's spots are not visible low threshold for admission of infants under the age of 1 years, children who are immunosuppressed and pregnant young people with suspected measles, due to the higher risk of complications in these groups - keep in negative pressure cubicle until 4 days after rash onset Children and young people with mild or moderate disease and no risk factors for severe complications (high risk - infants under the age of 1 years, children who are immunosuppressed) can be managed in the community with the usual advice on antipyretics and self-care for febrile viral illnesses - isolate at home until 4 days after rash onset supportive mx, abx if secondary infection eg pneumonia, IVIg or high dose vitamin A based on infectious diseases team advice if severe/immunosuppressed

Answer 80

a common adverse drug reaction resulting in a cutaneous eruption after exposure to visible or ultraviolet (UV) radiation in patients taking topical or systemic photosensitising medications. drug or its metabolites present within the skin absorbs UV radiation and triggers a chemical photosensitivity reaction cipro, doxy, sulphonamides, dapsone ketoconazole, itraconazole Amiodarone Atorvastatin Diltiazem Furosemide Most NSAIDs Retinoids Chlorpromazine affected skin may look like sunburn or eczema discontinue the med, oral antihistamine if itchy, and topical steroid (oral if severe)

Answer 81

bloom syndrome (short stature; photosensitive rash most prominently on the cheeks, nose, and around the lips; a long, narrow face; prominent nose, cheeks, and ears; and micrognathism or undersized jaw; immunodef; cancer predisposition) cockayne syndrome (photosensitive rash, short stature, premature ageing, microcephaly, visual and hearing decline and neurodegen) hartnup disease (failure to thrive, photosensitive rash, intermittent ataxia, nystagmus, and tremor; due to impaired non-polar aa absorption particularly tryptophan that can be, in turn, converted into serotonin, melatonin, and niacin (deficiency of this last one a common pathway with pellagra hence similar rashes) xeroderma pigmentosum - Severe sunburn when exposed to only small amounts of sunlight. These often occur during a child's first exposure to sunlight. Development of many freckles at an early age. Rough-surfaced growths (solar keratoses), and skin cancers. Eyes that are painfully sensitive to the sun and may easily become irritated, bloodshot and clouded; due to defect in nucleotide excision repair; 20% have neuro sx: include spasticity, poor coordination, developmental delay, deafness, and short stature juvenile spring eruption - itchy red small lumps which evolve into blisters and crusts and heal with minimal or no scarring, appearing on one or both ears; appearance of the rash is delayed 8–24 hours after sun exposure and heals in about 2 weeks; give potent topical steroid and emollient, antihistamines for itch, and protect affected area from the sun (eg hat) porphyria cutanea tarda - Excess porphyrin in the skin results in photosensitive rash, esp hands and forearms, with erosions and blisters; urine often dark/tea coloured drug induced: NSAIDs, thiazides, tetracyclines, quinine SLE, rosacea, psoriasis, dermatomyositis

Answer 82

‘allergy testing’, in general, refers to evaluation for suspected type I or type IV hypersensitivity reactions that occur because of exogenous allergens. On the contrary, type II hypersensitivity reactions occur because of the presence of endogenous IgM or IgG antibodies, for example, in acute haemolytic transfusion reaction, rheumatic fever and pemphigus vulgaris. Type III reactions, in turn, are due to antigen-antibody complexes that result in hypersensitivity reactions, as in systemic lupus erythematosus, serum sickness, reactive arthritis, IgA vasculitis and nephropathy. Type II and III reactions are not evaluated via allergy testing. type I reaction, also known as the immediate hypersensitivity reaction, occurs because of IgE activation of mast cells in the skin as well as the gastrointestinal and respiratory mucosal linings. Food (e.g. seafood), drugs, transfusion products, insect venom, and environmental or inhaled allergens such as pollen, animal dander and house dust mites are common triggers. Previous exposure to the allergen is necessary for this reaction to manifest. The first exposure produces sensitization, and subsequent exposure to the same allergen triggers a cascade of events that produces a reaction within minutes (immediate reaction) and up to 1 to 3 days afterward (late phase reaction). type IV reaction, also known as the delayed hypersensitivity reaction, is T-cell mediated and also involves two phases. The initial sensitization phase occurs when contact is made with the allergen, which penetrates the skin. Repeated exposure to the same allergen triggers an inflammatory reaction manifesting as cutaneous lesions, usually within 12 to 48 hours of exposure, for weak allergens. This reaction commonly presents on the contact area (localized) as pruritic and erythematous papules, macules or vesicles that may spread through the systemic immune response and become generalized. This phenomenon is known as contact dermatitis with secondary generalization (or id reaction). Contact dermatitis, drug reactions (e.g. Stevens— Johnson syndrome), and allergic reactions to implants (e.g. joint or dental implants) are some examples prick test works on the principle of activating IgE antibodies on the skin’s mast cells. Allergens in the form of liquid droplets are placed on the skin surface least 2 cm apart on the flexor aspect of the forearm. A sterile needle or lancet is introduced into the skin through the droplet, and the needle then pushes the allergen into the dermis. test area is examined after 15 to 20 minutes to evaluate the skin reaction. Presence of a wheal with a diameter of 3 mm or greater is considered as indicative of a positive reaction. Larger wheals indicate higher sensitivity to the allergen but not necessarily more severe allergic symptoms. patch test is the gold standard test used to detect type IV reaction; Common allergens acquired through contact include fragrances, vehicles and preservatives in cosmetics, latex, plants, topical medications (e.g. topical antibiotics and corticosteroids), metals (e.g., nickel), adhesives, textiles and hair dyes; Indications for the patch test: Suspected contact or occupational dermatitis where the lesion is isolated in the area of contact. Worsening of existing atopic dermatitis despite adequate treatment. Recurrent dermatitis affecting the lips, face, hands, feet and perineum

Answer 83

lupus vulgaris results from skin infection with Mycobacterium tuberculosis; it is very rare Direct inoculation of the skin or mucous membranes with tubercle bacilli from an outside source results in a tuberculous chancre - infection may follow piercings, tattooing, or other penetrating skin injury tuberculous chancre appears 1-4 weeks after inoculation, presenting initially as a firm reddish brown papule which becomes a painless shallow ulcer with a granular base and undermined edge. Sporotrichoid lesions and enlarged regional lymph nodes can develop; may persist for years Scrofuloderma follows the direct invasion of the skin from tuberculosis in an underlying lymph node or bone; Firm, painless lesions that eventually ulcerate with a granular base. May heal even without treatment but this takes years and leaves unsightly scars if widely disseminated TB can get miliary TB with skin lesions that are small (millet-sized) red spots that become necrotic, developing into ulcers and abscesses; The patient is generally sick and prognosis is poor Tuberculoid (TT) leprosy is the paucibacillary form defined clinically by: A few (1–2) sharply defined red patches with raised borders or a single larger hypopigmented patch less than 10 cm in diameter Loss of sweating with rough dry hairless skin in the patches Loss of sensation in lesions Borderline tuberculoid (BT) leprosy presents with: Similar lesions to TT but larger in size, more numerous (5-20), and can be less well-defined Asymmetrical distribution Satellite lesions Anaesthesia over the lesions is less pronounced Borderline borderline (BB) leprosy is a rarely seen, transient, unstable form of leprosy defined by: Multiple lesions of varying size, shape, and distribution Skin-coloured or erythematous lesions Characteristic, but rare, inverted saucer-shaped lesions with sloping edges and punched out centre Borderline lepromatous (BL) leprosy is characterised by: Widespread bilaterally symmetrical lesions Macules, papules, and nodules of variable size and shape Sensation and hair growth remain normal within a lesion Characteristic glove and stocking numbness Lepromatous (LL) leprosy is the multibacillary form defined by: Early symptoms of nasal stuffiness, discharge, and bleeding Swelling and thickening of limbs, especially ankles and legs with subsequent ulceration Widespread poorly defined hypopigmented and erythematous macules with a shiny surface and normal sensation Progression to widespread infiltration of skin forming nodules and plaques Characteristic leonine facies with thickening of the forehead, loss of eyebrows and eyelashes (madarosis), distortion of the nose, and thickening of the earlobes cutaneous leishmaniasis: parasitic disease transmitted by sandflies infected with the protozoa Leishmania Cutaneous leishmaniasis typically occurs at the site of inoculation. The presentation and prognosis will vary depending on the species involved Solitary lesions are typical, but multiple lesions do occur The initial lesion is a small red papule, which gradually enlarges up to 2 cm in diameter Central ulceration is typical Ulcers can be moist and exude pus or dry with a crusted scab Incubation time between an infected sandfly bite and lesion development is ranges from 2 weeks to 6 months Lesions are usually painless, and most resolve spontaneously often leaving residual atrophic scarring Time to resolution varies between 2 months to more than a year Sporotrichoid spread with lymphocutaneous nodules may occur

Answer 84

Suspect a diagnosis of fungal infection clinically if: The nail looks abnormal and is discoloured. A single nail, several nails, or rarely all nails may be affected. The first and fifth toenails are most commonly involved. May be white, yellow, flaky. Send clippings/scrapings for microscopy and culture consider also psoriasis, lichen planus, yellow nail syndrome, eczema, trauma, bacterial infection antifungal treatment is not needed if: The person is not troubled by the appearance of the nail(s), and/or infection is asymptomatic Topical rx only if very early and very superficial Offer treatment with an oral antifungal agent if an adult has confirmed fungal nail infection and self-care measures alone and/or topical treatment are not successful or appropriate for dermatophytes: terbinafine (2mo for fingers and 3 for toes) for candida: itraconazole

Answer 85

if paronychia present then soak in warm water for 20 mins then use blunt needle to drain cover with fluclox if recurrent then swab the lesion (to confirm the causative organism and antibiotic sensitivities) and treat the person with the appropriate antibiotics, consider herpetic whitlow, XR for osteomyelitis, check for nail biting and eg working as a dishwasher (they need to wear gloves) in trauma: subungual haematoma forms when blood collects between the nail and nail bed Compression of the nail bed between the distal phalanx and nail can result in a simple or complex laceration. A nail bed laceration is usually present with an intact nail and a subungual haematoma greater than 50% of the nail surface area A nail bed avulsion is when the nail and part of the nail bed are pulled away from the rest of the finger. Often associated with fracture. plain film radiographs of the injured finger should be taken to rule out fractures, dislocations, and foreign bodies. Anteroposterior, lateral, and oblique views of the injured finger are commonly used to rule out distal phalanx fractures (and Seymour growth plate fractures in children) will need abx to cover following the injury; seymour fractures will need urgent repair Following injuries should be referred to Orthopaedics for surgical repair in an operating theatre: < 12 months old Contraindication to ED procedural sedation Ischaemic fingertip (CRT > 2 seconds) Partial amputation (>50% of the lateral height) Any fracture other than an isolated tuft fracture Isolated subungal haematomas should be treated conservatively with nail trephination only if pain is significant Soft tissue lacerations can be repaired with Dermabond in most cases Conservative management can be considered for nail plate injuries especially if nail plate is firmly attached at the proximal nail fold If the nail plate is partially avulsed and intact, replace the nail into the fold If the nail plate is very damaged or completely avulsed, it should be removed and the nail inspected chlorhexidine, digital ring block, irrigate, replace nail if possible, dermabond for lacerations, if nail plate must be removed then dissect it away; place back under nail fold if possible; cover with abx and GP review in one week

Answer 86

former is a proliferation of benign melanocytes that are present at birth or develop shortly after birth A small congenital melanocytic naevus is < 1.5 cm in diameter. A medium congenital melanocytic naevi is 1.5–19.9 cm. A large or giant congenital melanocytic naevus is ≥ 20 cm in diameter. They usually grow proportionally with the child They may have increased hair growth (hypertrichosis). The surface may be slightly rough or bumpy. Giant melanocytic naevi, and to a lesser degree small lesions, are associated with increased risk of melanoma - 70% of melanomas associated with giant congenital melanocytic naevi are diagnosed by the age of ten years only definite indication for surgery in a giant congenital melanocytic naevus is when melanoma develops within it; if a small congenital naevus is growing at the same rate as the child and is not changing in any other way, the usual practice is not to remove it until the child is old enough to co-operate with a local anaesthetic injection, usually around the age of 10 to 12 years Lumbosacral dermal melanocytosis or Mongolian spot or slate grey naevus is a blue-grey marking of the skin that usually affects the lower back and buttock region of newborn babies; normally a few cm in diameter but can be larger thought to be due to entrapment of melanocytes (pigment cells) in the dermis of the developing embryo, when the cells have failed to reach their proper location in the epidermis, then appearing blue due to the tyndall effect benign and does not require treatment. Usually the discolouration spontaneously disappears by the time the child reaches 4 years old

Answer 87

consider safeguarding need to pop blisters and scrub off slough (after adequate analgesia given) and take photos before applying jelonet or similar dressing and discussing with your local burns centre ensure all burns cooled for 20 minutes (effective up to 3 hours post-injury) with running water or serial wet cloths Keep all children with facial burns sitting upright Anticipate airway problems and move to early intubation if any of: 1) Airway burn &/ or Inhalation injury: history of exposure, burns involving face or neck, singed nasal hair, carbonaceous debris in/ around mouth or nose & in sputum, stridor, wheeze, change in voice, respiratory distress 2) Reduced or falling level of consciousness 3) Large burn ~25% 4) Electrical burns Respiratory failure can be due to chest trauma, inhalational injury or restrictive chest wall eschar formation Early access - 2x large bore cannulae or intraosseous  Blood Gas (lactate, O2Hb, COHb, MetHb), x-match, glucose, U&Es, CK; urine b-HCG if female adolescent  Burns fluid resuscitation using Parkland Formula  If shocked: 10mL/kg balanced crystalloid bolus’ titrated to cardiovascular response  Refractory hypotension, consider other causes e.g. trauma (may require additional resuscitation inc. blood products)  Electrical burn: Baseline 12 lead ECG & monitor for arrhythmias  Maintain urine output >1mL/kg/h (early catheterisation) Parkland Formula  Applicable to burns > 10% TBSA  Fluid requirement starts at time of burn  Aim to replace fluid lost from burned surface in first 24 hours  Total volume (first 24hrs) of balanced crystalloid solution 4ml x weight (kg) x %TBSA 50% volume in first 8 hrs Use Lund & Browder chart to document percentage + depth of burn Cover burn area with longitudinal cling film (avoid circumferential dressings) Carbon Monoxide (CO) poisoning:  Pulse oximetry unreliable (false high SpO2 despite arterial hypoxia)  Arterial blood gas (normal COHb levels 1-3%)  Use 100% O2 - CO clears in 3-5 hrs  CO Hb level >20% may benefit from Hyperbaric Oxygen Therapy Cyanide poisoning: (aerosolisation of upholstery and fabrics)  Features: metabolic acidosis (esp. if lactate >10mmol/L) despite 100% O2 & adequate fluid resuscitation in first 2 hours of presentation; arteriovenous saturation difference <5%  Treatment: Hydroxycobalamin (Cyanokit) 70mg/kg IVI (max 5g) or 50% sodium thiosulphate 0.5mL/kg over 10mins* (max 50ml/12.5g)  Discuss with burns centre & on-call consultant toxicologist Intranasal diamorphine can be given (use local guideline)  IV morphine infusion preferred to obtain baseline control of pain & boluses as required  IV ketamine for procedures with anaesthetic support

Answer 88

epidermis develops from a single layer of cells to three layers by 11 weeks gestation, and to 4–5 layers by 23 weeks. The stratum corneum layer of the epidermis begins to develop at 15 weeks gestation and forms a functional barrier at 34 weeks’ gestation. Compared to a baby born at term, the epidermis of a preterm infant has fewer cell layers making it vulnerable to injury and heat loss, and with increased permeability Compared to mature infants and adults, the dermis in premature infants has less structural protein connecting to the epidermis. Collagen fibre bundles are small and elastic fibres are sparse and immature. This leaves premature infants susceptible to skin injuries, including those caused by medical adhesives therefore use of adhesives on newborn skin and their removal necessitates particular care, especially in preterm newborns Vernix caseosa coats the skin of a fetus, with synthesis beginning from 28 weeks gestation. The vernix is a mix of water, lipids, and proteins. vernix is usually absent in extremely preterm ultra-low weight infants. Babies born at term have less vernix coverage than those born at 32–37 weeks gestation. If vernix is present, it should be retained and allowed to absorb naturally as it improves skin hydration, includes antimicrobial peptides active against common pathogens, has wound-healing properties, and lowers skin acidity Extremely preterm infants have a lower total microbial diversity than full-term infants. Staphylococcus and Escherichia species predominate on their skin, reflecting the infant's environment. Premature skin develops to resemble the skin of a full-term infant by 2 to 4 weeks of age, although this may take longer in ultra-low weight neonates A premature infant's skin should be examined all over daily or more frequently as required. Staff in the NICU use tools such as the neonatal skin condition score (NSCS) to assess the skin integrity. Bathing may start at 12–24 hours of age depending on the gestational age of the baby, and can occur at least every fourth day without increasing skin bacterial colonisation or the risk of skin infection.

Answer 89

Advise to wash daily with lukewarm water and to keep the foreskin retracted until the glans penis is dry, where possible. Do not attempt to retract the foreskin to clean under it, if it is still fixed. Avoid irritants such as soap, bubble bath, or baby wipes. Consider use of an emollient as a soap substitute. If there is suspected non-specific dermatitis: Prescribe topical hydrocortisone 1% cream or ointment once a day, until symptoms settle or for up to 14 days +/- imidazole cream, the frequency depending on the preparation used, until symptoms settle or for up to 14 days there is suspected or confirmed bacterial balanitis: If there is mild infection, consider use of a topical antibiotic preparation such as mupirocin 2% ointment 2–3 times a day for 7–10 days. If there is severe infection, consider prescribing oral phenoxymethylpenicillin for 10 days while awaiting swab results if balanitis is severe, persistent, or recurrent (especially if candida infection is present) consider HbA1c for DM and consider if further immunosuppresion workup indicated At birth, there are adhesions between the prepuce and the glans of the penis. Over time these gradually break down. Mean age of 1st foreskin retraction is 10.4 years Around 95% of pathological phimosis is due to the process ‘Balanitis xerotica obliterans’ (BXO); where keratinisation of the tip of the foreskin causes scaring and the prepuce remains non-retractile. Ballooning of the foreskin during micturition is a common presentation, but it is normal phenomenona non-retractile foreskin aged 2-4 years. This is self-resolving as the prepuce becomes more mobile with age; BXO presents with scaring of the urethral meatus presents with irritation, dysuria, haematuria and local infection. If the meatus involved BXO or the prepucial scarring is very extensive, then the patient can present with episodes of urinary obstruction; BXO-affected prepuce will appear as a white, fibrotic and scarred preputial tip mainstay of management of BXO is circumcision. It is important to send the foreskin off to histopathology in order to confirm the diagnosis Post operatively expect a degree of swelling and some serous discharge around the penis for around a week post operatively. If there are still concerns about infection, this can be treated with antibiotics.

Answer 90

a characteristic response of the skin to viral infection in which there is a papular rash that lasts for several weeks specific viruses causing papular acrodermatitis of childhood may include: Hepatitis B infection Epstein-Barr virus (EBV) Cytomegalovirus (CMV) Enterovirus infections Echoviruses Respiratory syncytial virus SARS-CoV-2 it is often seen following an URTI, EBV being the commonest association profuse eruption of dull red spots develops first on the thighs and buttocks, then on the outer aspects of the arms, and finally on the face. The rash is usually symmetrical. The individual spots are 5–10 mm in diameter and are a deep red colour. Later they often look purple, especially on the legs, due to leakage of blood from the capillaries. They may develop fluid-filled blisters (vesicles). not usually itchy may feel quite well or have a mild temperature. Mildly enlarged lymph nodes in the armpits and groins may persist for months A mild topical steroid cream or emollient may be prescribed if any itch. fades in 2–8 weeks with mild scaling

Dermatology Flashcards

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