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145 Cards in this Set
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Pemphigus vulgaris |
IgG attack Dsg 3 +/- Dsg 1 (present throughout skin) If have antibodies to Dsg 3 only - little/no cutaneous blistering; if have both no compensation. Mucosal dominant/mucocutaneous (Dsg 1 + 3) Mucosal involvement may include eyes, mouth, pharynx, larynx, oesophagus, genitalia |
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Pemphigus foliaceous |
Disease confined to skin (Dsg 1 only) - superficial blisters Superficial blisters - break easily so can look like cuts Nikolsky sign +ve - rub normal skin blister develops |
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Management Pemphigus |
More common in middle age; certain Jewish groups Ix: Biopsy blister - acantholysis (separation of kertinocytes) Peri-lesional biopsy will confirm IgG intercellular staining within the epidermis Indirect immunofluorescence - antibodies Mx: high dose systemic steroids and immunosuppressant (azathioprine/mycophenolate 2nd: IVIG; anti CD20 antibodies, cyclophosphamide Unresponsive - consider paraneoplastic syndrome |
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Pemphigoid |
Antibodies against hemidesmosomes (anchor keratinocytes to BM (deep) Most common in elderly Itchy urticated lesions may proceed blister onset - large and more tense than pemphigus |
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Pemphigoid management |
Ix:Biopsies show an eosinophil rich inflammatory infiltrate and subepidermal blisters with IgG stainingalong the basement membrane visible on peri-lesional skin. Mx: systemic prednisolone +/- azathioprine 2nd - IVIG, anti CD20 antibodies, cyclophosphamide |
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Dermatitis Herpetiformis |
IgA antibodies against skin and tissue transglutaminases Associated with coeliac disease - usually asymp Intense burning itch; clusters of vesicles on extensor surface, wrists, sacrum and buttocks; no mucosal involvement |
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Dermatitis Herpetiformis management |
Biopsy - Small polymorph abscesses in the upper dermis are visible, and direct immunofluorescence showsgranular deposition of IgA in the papillary tips of the dermis. Mx: gluten free diet; Dapsone (sulphonamide antibiotic) - can cause angranulocytosis and haemolytic anaemia |
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Erythema Multiforme |
Target annular lesions with red or dusky cyanotic centre with bright red ring on outside; initially macular but becomes raised. Starts on hands & feet but can spread Can effect mucosa Most common <40; M>F Due to herpes or mycoplasma; rarely drugs. |
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Erythema multiforme management |
Clinical diagnosis but might biopsy (keratinocyte death and some dermal inflam) Mx: repeated episodes (HS) - chronic aciclovir Acute- no treatment/topical steroids Mucosal - IV fluids (uncommon) |
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Toxic Epidermal Necrolysis (TEN) |
Medical emergency most common in elderly. Result of adverse drug response - 7-28 days after start Sudden onset diffuse erythema; sheets of skin undergo necrosis (sloughing); Nikolsky +ve; pyrexia, malaise, dysurai, sore eyes can precede rash Worse on trunk |
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TEN management |
Biopsy - full thickness epidermal damage Mx: HDU/ITU care (fluids, analgesia etc); derm nursing; stop all non-essential drugs - Allopurinol, carbamazepine,sulphonamides are high risk. - ACE inhibitors, betablockers and calcium channel blockers areunlikely to cause TEN. -No good RCT of effective treatment - IVIG, anti-TNF and cyclosporin all been used. -40% mortality |
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Steven Johnson's syndrome |
Somewhere between TEN and erythema multiform May be sue to infection or adverse drug reaction See target lesions and skin peeling (less than in TENs); mucosal involvement Sore mouth and eyes |
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SJS management |
Admit for care of blisters and fluid management Opthamology inout needed for eye disease - scarring may occur. |
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Staphylococcal Scalded Skin Syndrome (SSSS) |
Results from circulating toxin produced by some types of staph - protease inhibits Dsg 1 (like pemphigus foliaceous but circulating). See in children <5; rarely in immunosuppressed adults or ITU pts Doesn't effect mucosae Onset with scarlet fever type rash around mouth and nappy areas; pyrexia; initially well Intense pain with separation og skin in sheets from red base; within 48hrs widespread flaccid blisters; nikolsky sign +ve |
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Management SSSS |
Clinical diagnosis +/- supporting biopsy. Culture swabs from throat and eyes (skin not site of infection) Mx: IV anti-staphylococcal drugs (flucloxacillin, vanc); barrier nursing -Low mortality with treatment |
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Leucocytoclastic Vasculitis |
Immune complex in post-capillary vessels Palpable purpura most commonly on legs - may be mm-2cm +/-blisters/pustules Aetiology: Hep A-C, strep, mycobacterium; BB, penicillin, thiazide diuretics; CLL, lymphoma, myeloma; small vessel vasculitides; IBD, SLE, Behcet's |
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Management leucocytoclastic vasculitis |
Clinical diagnosis + biopsy to confirm Search for cause - must exclude infection Mx: bed rest, elevation, compression bandaging, potent topical steroids/systemic steroids (MUST EXCLUDE SEPTIC vasculitis) -Resolves over 2-6 weeks |
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Henoch-Schonlein purpura |
Sub-type of leucocytoclastic vasculitis seen in <10s. IgA in skin lesions and kidney Preceded by URTI prev 2-3 weeks Rash, joint pain, abdo pain, 50% renal disease Many resolve spontaneously with rest & support, progressive kidney disease needs treated aggressively. |
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Septic Vasculitis |
Fatal if untreated Lesions like leuco vasc but often pustular with blistering and necrosis +/- pyrexia Aetiology: gonococcus, sub-acute bacterial endocarditis See Janeway spots (on palms) and Osler nodes on tips of fingers and toes in SBE Staph, meningococci, fungi must be considered in immunosuppressed |
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Pyodermic Gangrenosum |
Neutrophilic dermatosis with vasculitis Commonly see inflammatory lesion on legs (v small & sore) that looks like a bite. Then becomes pustular and breaks down - ulcer with red/purple edge grows in size with pain. May be systemically unwell May show pathergy - develop lesions at sites of minor trauma |
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Pyoderma Gangrenosum management |
Assos with IBD, RA, AS, myeloma, IgA gammopathy, diabetes, chronic active hepatitis, PBC Biopsy - large neutrophilic infiltrate with fibrin deposition in vessels and evidence of vasculitits Mx: systemic corticosteroids + treat underlying disease |
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Sweet's syndrome (acute febrile neutrophilic dermatosis) |
Patients present acutely with plaques or nodules, that may look blistered & may be pustular. Associated arthralgia & pyrexia Assos with AML Responds to prednisolone given over a few weeks |
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Erythema Nodosum |
self-limiting panniculitis (inflammation of the fat) withpainful red raised or indurated lesions most commonly on the lower legs in young adults. F>M. Assos with pill, penicillin, strep/mycobac, sarcoidosis, brucellosis, lymphoma, leukaemia, IBD, Behcet's, 50% unknown NSAIDs with rest and compression stockings may help; systemic steroids needed occassionally |
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Polymorphic light eruption (PLE) |
Affects 10-20% of population (heat rash) - looks different in different people Itching and erythema hours to days after sun exposure - may be raised with individual lesions like urticaria or large red plaques Can last several days Most common on shoulders, upper arm, neck and sides of face Avoidance of sun or graded exposure with phototherapy early in year; sedative antihistamine |
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Discoid lupus erythematosus |
May be precipitated by UVR Most often on face Epidermis and all of dermis and adnexal structures are involved Scarring occurs - can lead to alopecia 5-10% go on to develop SLE |
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SLE |
Rarer than discoid. Photosensitive butterfly rash on face Appears after ~2 days Affects epidermis and high dermis - no scarring |
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Subacute lupus erythematosus (LE) |
Strongly assos with UVR and anti-Ro/SSA antibodies Scaly lesions appear on sun exposed regions Scarring uncommon but depigmentation may occur Focussed on epidermis - need serology and biopsy to diagnose |
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Solar urticaria |
Widespread sheets of urticaria and itch within 5-10 mins of UVR or visible light exposure Transmissable - inject serum into individual from someone with disease it develops Phototesting is confirmatory - must also test sensitivity to visible light Mx: UVR/visible light avoidance; omit new drugs (can precipitate); H1 blockade limited effects |
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Porphyrias |
Rare groups of disorders resulting from various enzymatic defect sin haem biosynthesis - build up of substrates of which some are photosensitisers. Exposure to blue visible light #400nm causes release of free radicals and inflam Diagnose by measuring particular porphyria levels in blood, plasma or stool |
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Porphyria cutanea Tarda (PCT) |
Most common porphyria usually resulting from liver damage plus inherited predisposition Most obvious on back of hands and face - doesn't follow UVR exposure immediately. Erosions, blisters and crusts on back of hands; milia (keratin entrapped beneath epidermis to form tiny cyst); hyperpigmentation & hypertrichosis (increased hair growth) esp at temples Ix: biopsy & porphyrin levels Mx: treat liver disease; bimonthly phleb to normalise haem biosynthesis; chloroquine (anti-photosensitising) |
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Erythropoeitic protoprophyria (EPP) |
Exposure to sunshine present with immediate pain, erythema and oedema over several hour See in young children - screams within minutes of being put in sun then develops what looks like solar urticaria. Waxy plaques and scarring may develop Some pts develop liver disease Mx: sunblock/avoidance, betacarotene (scavenges free radicals) |
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Strimmer's disease |
Someone strimming grass in shorts an t-shirt. Cutting plants releases sap (photosensitiser) Next day covered in hundred of linear blisters (looks whipped) - UVR exposure has caused a photoxic rash |
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Solar elastosis |
Chronic UV exposure can result in alteration sin collagen causing fragmentation of fibres and apparent increase in volume - yellow appearnce. |
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Maculopapular Exanthema |
Most common cutaneous drug reaction - red, macular/papular. sometimes itchy, minimal scale Starts 4-21 days after taking medication No severe systemic involvement; no blisters; no mucosal involvement; no target lesions of erythema multiforme |
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DRESS - drug reaction with eosinophilia and systemic symptoms |
Widespread rash, may be eczematous +/- facial oedema; purpura esp on lower legs Rash occurs after ~2 weeks Other features: lymphadenopathy, pyrexia, hepatitis, nephritis Often due to carbamazepine, phenytoin, dapsone, allopurinol - looks like immunological response to reactivation of latenbt viral infection 10% mortality rate - due to hepatitis Stop causative drugs, supportive care, steroids |
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Fixed drug reaction |
Red, round plaques with erythema and sometimes blistering that resolve leaving hyperpigmented mark. Can effect single or multiple sites with re occurrence when drug used again |
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Acute generalised exanthematous pustulosis (AGEP) |
Fever, widespread pustular rash systemic steroids help |
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Vitiligo |
Acquired focal loss of pigmentation due to immunological attack on some melanocytes Occurs in 1% of pop but has biggest effect on those with high constitutional skin colour Sharply demarcated macular areas of depigmentation; symmetrical; loss hair pigment; may be dermatomal; genitalia, mouth and eyes affected most; can effect small to 100% body Assos with autoimmune disease DDx: piebaldism (KIT mutation). leprosy (raised lesion) |
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Vitiligo treatment |
Mx: resolve spontaneously; more extensive disease - worse prognosis; PUVA/UVB phototherapy in dark skin; camouflage make-up; |
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Albinism |
Collection of autosomal genetic disorders (commonly gene for tyrosinase - melanin biosynthesis) in which the amount of melaninproduced by melanocytes is reduced. The number of melanocytes is normal. Abnormal sensitivity to UVR - early onset skin cancer unless able to avoid sun Also loose pigment in iris and retina; poor visual acuity; nystagmus Mx: avoid sun; early treatment skin canceer |
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Melasma |
Brown/grey patches on cheeks and forehead commonly seen in pregnancy due to increased melanin hyperpigmentation Can also occur with COCP Sunblocks, azelaic acid and topical retinoids may help |
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Perioral dermatitis |
Papules, pustules and erythema +/- some scaling around the mouth Most common in young women. Commonly precipitated by topical use of steroids on the face Gradually reduce strength of steroids or treat with systemic tetracyclines |
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Seborrhoeic dermatitis/eczema |
Erythematous and scaly condition usually seen in areas rich in sebum. It is most commonlyseen in young and middle-aged adults. Concentrated around face, nasolabial fold, forehead, upper chest and back. Immune reaction to pityrosporum yeast which metabolises lipids on skin surface Dandruff is a milder form. May be severe in AIDs Mx: anti-yeast shampoos - ketoconazole |
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Lichen Planus |
Inflammatory disorder of unknown cause characterised by intense itch and violaceous polygonal plaques with frequent oral or mucosal involvement Commonly in middle age, tends to remit 6-12 months but can persist Can be assosc with Hep C Wickham striae - lace like pattern, diagnostic. Also see in mouth or genitalia (ulcers) If effect s scalp see scarring alopecia; nail LP causes thinning, longotudinal ridging and trachyonychia (v thin and pitted) |
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Management lichen planus |
Histology - T-cell infiltrate hugging epidermis with occasional apoptosed keratinocytes )cytoid bodies) Mx: stop any drugs it might be related to; sedative histamines (help itch) potent topical corticosteroids +/- systemic corticosteroids Get gynae or oral medical help Chronic LP is associated with SCC |
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Pityriasis rosea |
Common rash characterised by an annular erythematous patch with a colarette ofscale. 7-10 days after herald patch see scaly red lesions on trunk and limbs - long axis of lesions tends to follow skin lines |
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Herald patch |
Initial lesion on upper chest in pityriasis rosea |
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Ichthyoses |
Widespread scaly disorder in which(usually) inflammation is not prominent (although occasionally inflammation is prominent) andwhich is not eczema, psoriasis, LP etc. Disease focus on epidermis |
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Icthyosis vulgaris |
Mutations in the filaggrin gene (tends to be in both alleles as opposed to one in atopic dermatitis) Diffuse polygonal scaling that tends to spare the flexures, keratosis pilaris, andhyperlinear palms. 1/3 have atopic dermatitis |
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Acquired ichthyosis |
An acquired ichthyosis may reflect an underlying malignancy, most commonly a lymphoma. Look forother symptoms (weight loss, night sweats). Patients need a full exam and work up. Occasionally thecause may be secondary to drugs or malnutrition |
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Keratosis pilaris |
Affects 50% of population. Commonly on back of triceps. See follicular plugging with rim of erythema around follicle Asymptomatic Assos with icthyosis and atopic eczema |
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Erythroderma |
Widespread erythema or papulosquamous rash. Commonly due to psoriasis, atopic dermatitis, drug reactions, cutaneous T-cell lymphoma Mx: Admit; fluid regulation; temperature reg (concealed hypothermia) Treatments include emollients, topical corticosteroids, systemic corticosteroids, cyclosporin, retinoidsor watchful waiting. |
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Necrobiosis Lipoidica |
Yellow or red patch with marked telangiectasia that looks like ‘lipid’. It is mostcommon on the shins. It may be raised, but also may be atrophic and even ulcerate. 20% of patients are diabetic Pathology shows necrobiosis Mx: topical steroids under occlusion or sometimes systemic steroids |
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Granuloma annulare |
Most commonly presents in children, or young adults, with annular lesions made up of lotsof individual papules, or nodules, with a smooth skin surface and no scale. Lesions may be multiple. Mx: tends to resolve spontaneously but can use topical steriods. |
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Lichen sclerosus et atrophicus (LSEA) |
Affects skin and mucosa. Presents as atrophic wrinkled skin that is v light. Atrophy of superficial dermis may led to blistering and bleeding. Can affect genitalia of men and women. If seen in children may be misdiagnosed as child abuse. Chronic LSEA increases chance of SCC. Mx: topical corticosteroids |
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Morphoea |
Presents initially as a violet macule, which develops central sclerosis within a lilac ring.Atrophy may develop with or without scarring. Underlying structures including fascia, muscles orbones may be involved Mx: top steroids, PUVA |
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Erythema Ab Igne |
Due to infrared damage to blood vessels from siting close to radiators or a fire. See blue/red reticular pattern that leaves hyperpigmentation. Tend to see on lateral aspect of one leg and medial aspect of the other. |
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Keloids |
Occur following surgery or inflammatory processes (such as acne), when there is overgrowth and excess production of collagen leading to a positive defect ratherthan a negative defect. Occur on upper 1/3 Injection with intralesional steroids - careful of over treatment as can cause atrophy |
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Impetigo |
Staph aureus skin infection commonly seen in children around mouth and nose Early lesions - small vesicles which may be clear, and rupture.Subsequently blisters (>1cm), which are pus filled then may be seen.Usually surrounding scabs and a characteristic golden / honey coloured exudate or crust. Lesions may itch, and scratching results in further inoculation of surrounding areas. Mx: Sample contents of blister/swab. Treat with fluclox or cephalosporin -If localised use topical Abx like mupirocin/fusidic acid +/- chlorhexidine |
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Folliculitis |
inflammation centred around the hair follicle, that may be infective – more commonly bacterial, or fungal – ornon-infective. Most folliculitis is bacterial in origin, self-limiting, and rarely requires medical attention. If around vellus hairs see pustule and surrounding erythema. A boil is a deeper, larger more painful focus of infective folliculitis. |
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Causes of folliculitis |
staphylococcal infection - candida folliculitis - herpes simplex folliculitis - gram-negative folliculitis (something seen occasionally in patients who have been treated withtetracyclines, or other antibiotics, for acne). - in dermatology patients, a non-infective folliculitis due to emollients or tar therapy |
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Predisposing factors in folliculitis |
excess sweating - occlusion and maceration - obesity and diabetes - topical or systemic corticosteroids (as in Cushing’s syndrome) - oily skin care preparations (make-up etc), greasy emollients or tars applied to the skin Mx: topical antiseptic or topical chemotherapy (fusidic acid or mupirocin; anti-staph for boils; drain boils with bus. |
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Cellulitis |
Inflam of dermis and subcut tissues -Typically elderly pt with unilat erythema on lower leg with oedema, pain and local warmth -May be systemically unwell -May be obvious point of entry; may be strep or staph (others after surgery or immunosuppression) -Can see lymphangitis |
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Erysipelas |
Streptococcal infection of deep dermis Tends to affect face and has sharper palpable border than cellulitis. |
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Managing cellulutis |
Clinical diagnosis DDX: contact allergic eczema; necrotising fasciitis; pseudocellulitis; erythema nodosum; carcinomatous infiltration Mx: IV benpen or flucloxacillin (may use oral Abx) |
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Ringworm/tinea corporis |
-Dermatophyte infection. Annular erythematous scaly eruption with or without pustules,with an apparently more active edge -Scrape lesion for mycological confirmation -Treat with azole creams or topical terbinafine -Scalp and nail often require systemic azoles or terbinafine. |
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Cutaneous candida |
Seen on warm, moist skin e.g. under breast or in folds of skin (right into depths) -See bright red demarcated red areas with a little bit of scaling and satellite lesions |
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Pityriasis versicolor |
Yeast infection caused by malassezia. -Most commonly seen in young people after a summer holiday (swimming) - dull, red/light brown scaly plaques on upper chest and back -When scratch release abundant scale (see yeast in scale) -Use imidazole shampoo |
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Verrucae vulgaris/common wart |
Most commonly seen in children. -Hyperkeratotic papules that when pared back with a blade show a point like dermal vessel. More papillomatous in flexures. -More common in immunosuppressed -Treat with salicylic acid preps, paring with blade or cryotherapy |
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Verrucae vulgaris |
On the foot can cause problems due to pressure forcing them inwards causing pain. |
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Molluscum contagiosum |
Pox virus spread by direct contact in children - if see in adults think immunosuppression (HIV). -Papules/nodules have shiny white centre and central umbilication - often see eczema surrounding lesions. -Child should use separate towel. Take ~6mths until immunity develops. |
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Herpes simplex |
Cold sores: tingling sensation, papule formation, clustering of lesions, blister formation -Reoccurence precipitated by UVR exposure or other illnesses -Treat with topical acyclovir to shorten duration |
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Herpes Varicella Zoster |
Chickenpox: 90% have had by mid-teens; spread via droplets (incubation ~3 wks); red macules turn to blisters; tend to itch & can heal leaving punched out scars; latent virus remains in dorsal root ganglion -In adults can cause severe illness - pyrexia, malaise and potentially varicella pneumonia |
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Varicella in pregnancy |
In 1st trimester can cause - |
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Shingles - herpes zoster |
10-20% of people get in lifetime; follows dermatomal pattern; vesicles on red base that pustulate, crust and scar; pain before rash comes -Dangerous if 1st branch of trigeminal effected - ocular complications including keratitis. -2nd branch trigeminal effected - can cause blisters on 1/2 tongue or palate. -Treat with acyclovir to shorten course (IV if immunocomp) -Post-herpetic neuralgia -Now vaccinate |
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Scabies |
Infestation with sarcoptes scabiei mite (see under dermatoscope) -Delayed type hypersensitivity reaction to mite eggs & faeces (only see 3 wks post-infestation) -Effects 30-40% children; intensely itchy (worse night); burrows seen on palms/soles; nodules on nipples and genitalia -Only spreads by close physical contact (not towels etc) -Crusted scabies - hyperkeratotic - looks like severe psoriasis. -Intense itch and involvement of other family members - examine whole patient - follow burrow & show pt under microscope Mx: permethrin or malathion treat all in close contact |
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Pediculosis capitis (head lice) |
Infestation with lice that attach to hairs and feed on blood - itchy eruption on scalp and nape of neck with secondary excoriation Mx: Malathion or permethrin - kills nits (eggs) not the mites so may retreat one week later |
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Pediculosis Corporis |
Lice infestation resulting in itching, scratching and excoriation - usually in those with poor personal hygiene. -Examine clothes as well - treat clothes not person. Hot wash & ironing. |
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Dermatitis Artefacta |
Skin lesions self inflicted without any obvious cause - pt may not admit they are causing lesions. -Rash appears bizarre & pt denies involvement in causation. -Usually not sensible to confront patients. |
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Cutaneous dysmorphobia |
Patients present with a mark on their skin which appears trivial, but which the patient claims is severely impacting on their life, and therefore wishes tobe treated. |
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Parasitophobia |
Delusions of infestation. Ask psych |
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Pregnancy induced hyperpigmentation |
Hyperpigmentation of the nipples, labia and the linea nigra; melasma (deep brown/grey pigmentation of skin on cheeks & forehead) -Can also see on COCP |
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Pemphigoid Gestationis |
pregnancy-specific / post-partum pemphigoid in which it is likely that theplacenta precipitates an autoimmune response, which clinically, and immunologically, resemblespemphigoid. -Starts as intense pruritic itch in 3rd trimester then flares/starts post-partum -Most commonly starts around umbilicus - small number of children will be effected -Confirm by pathology -Mx: topical/systemic steroids & sedative antihistamine -Increased risk SGA and prematurity -Rash likely to recur and worsed in future pregnancies if father the same |
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Polymorphic Eruption of Pregnancy (PEP) |
Much more common that pemphigoid gestationis (10-20 times) -Itchy red papules at end 3rd trimester; +/- widespread erythema, small vesicles, target-like lesions, plaques look like eczema -Lesions preferentially effect striae, spare umbilicus, spreads from abdomen -More common in 1st pregnancies Mx: topical corticosteroids & antihistamines -Systemic steroids - ask O&G |
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Intrahepatic Cholestasis of Pregnancy |
Intense pruritus usually in late second or third trimester - usually see no primary skin lesions, just scratches -Serum bile acids raised - diagnostic -Increased risk of foetal loss, prematurity & foetal distress |
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Atopic eruption of pregnancy |
Most common itchy disorder of pregnancy and can either occur in those who are known tohave atopic dermatitis, or those who are atopic, but without previous skin disease. It is eczematous andpapular, with or without xerosis. -See in 1st trimester -Manage like atopic eczema |
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Genital herpes simplex |
Indication for c-section if present at time of delivery |
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Erythema Infectiosum (slapped cheek/fifth disease) |
Parovirus B19 infection. -Classically in children this rash presents with a livedo / lace-likerash on the cheek and arms, that develops on the cheeks to look as though the child has had his or herface slapped. The disease is often asymptomatic, and school outbreaks common in spring. - In pregnancy if mother has no immunity - 2-5% foetal loss - hydrops foetalis. |
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Causes hirsutism |
Congenital adrenal hyperplasia; adrenal tumour; cushing's syndrome; PCOS -If have clear sign of virilisation - enlarged clitoris, hirsutism, and acne vulgaris require investigation ismerited. |
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Causes of hypertrichosis |
Growth of hairs that are longer, thicker, or more obvious than you would expect at aparticular site. -Malnutrition, anorexia nervosa, dermatomyositis, porphyria cutanea tarda (PCT) |
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Androgenic alopecia |
Male pattern baldness - Develops in up to 50% of men reflecting sensitivity to androgens resulting in a change fromterminal hairs to vellus hairs and then loss of hairs. Mx: minoxidil (appliedtopically) and systemic finasteride (a 5-alpha reductase inhibitor) - pretty rubbish; hair transplant. |
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Telogen effluvium |
Hair loss several months after a major life event - The ‘insult’ causes many hairs to exit anagen simultaneously into catagen.Several months later they then fall out in telogen synchronously. -Hair will returnn |
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Alopecia Areata |
Common, of unknown aetiology, and is characterised by sharply demarcated coin shaped areasof hair loss, and is common on the scalp or the beard area. -Common in early adulthood or childhood -Exclamation mark hairs (bulb of follicle becomes dot of exclamation mark) -Non-scarring -normally regrows -See nail pitting -Normally patches but can be diffuse Mx: wait, topical steroid injection; induce contact allergic sensitivity; short burst systemic steroids at start |
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Causes chronic diffuse alopecia |
Systemic malignancy- Renal / liver failure- Hypo / hyperthyroidism or hypopituitarism- Iron deficiency (said to occur even in the absence of any anaemia)- Drugs ( antithyroid drugs, retinoids, azathioprine) |
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Trichotillomania |
Hair is pulled out often following twisting around finger |
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Neurofibromatosis |
Mutations of neurofibromin 1(NF1) or 2 (NF2) areassociated with neurofibromatosis, but ‘peripheral’ NF is due to mutations of NF1. Features: -Cafe au lait macules (more than 5 is abnormal); axillary freckling; neurofibromas (with a characteristic soft, almost ‘negative’, pressure sensation); flexiform large sub-cutaneous neurofibromas; lisch nodule (iris hamartoma); CNS tumours (e.g. gliomas) and tumours elsewhere |
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Tuberous sclerosis |
Autosomal dominant. Features: - Ash-leaf macules, oval areas of depigmentation, present at birth. - Connective tissue nevi, known as shagreen patches; Angiofibromas, commonly seen on the face (referred to incorrectly as adenoma sebaceum, asthough they were sebaceous tumours) -Periungual fibromas - Seizures and mental retardation |
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Acanthosis nigricans |
Brown hyperkeratotic velvety / warty areas in the axillae, neck and thegroins, and at other skin friction sites -multiple superimposed skin tags, andhistologically resemble seborrhoeic keratoses. -Paraneoplastic phenomenon- especially if see in thin patient -Also assos with excessive insulin growth factor - seen in obesity and DMII |
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Dermatomyositis |
Autoimmune disorder, F>M, characterised by a range ofskin changes, and myositis. - 50% ofcases (but not in children) paraneoplastic. Skin findings: violet/heliotrope rash round eyes; erythematous rash (sometimes photosensitive; Gottron's papules (violaceous lichenoid rash along the dorsal surface of the hands and fingers); painful cuticles & prominent nail fold capillaries -Proximal muscle weakness - difficulty rising from chair Biopsy and draised serum CK, 50% ANA +ve Mx: high dose pred & look for malig |
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Hereditary haemorrhagic telangiectasia/ Osler-Rendu-Weber disease |
Autosomal dominant disorder, characterised bysmall AV malformations that look like 1-3mm flat red spots. -Lesions are common on the lips, oral and nasal mucosae, skin (especially hands), and GI tract. -Frequently presents with nose bleeds and epistaxis. May lead to anaemia. In a patient with GIbleeding, look at the lips and hands! |
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Nail destruction |
Psoriasis, lichen planus, tumours |
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Oncholysis |
Separation of the distal nail from the nail bed. It is frequently a useful diagnostic sign. Causes include: psoriasis, dermatophyte infection, trauma- thyroid disease (rare) |
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Pitting |
Focal depressions in nail. Causes: psoriasis, eczema, lichen planus, alopecia areata |
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Horizontal lines (Mee's lines) |
Changes to nail growth that have in common interruption ordisturbance of the growth of the nail in the nail matrix. The common result is one or more ‘tidy’ convexbands of disturbance. -Multiple lines may reflect chemo |
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Koilonychia |
Spoon-like nails seen in iron deficiency/normal |
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Green nail |
Colonisation by pseudomonas aeruginosa |
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Melanonychia |
Presence of a brown longitudinal streak in the nail. -Common in people withdark skin and the lesions are often multiple. -In lighter skinned individuals the concern is whether thepigmentation reflects either a benign nevus or a melanoma in the dorsal nail matrix. If there ispigmentation in the nail fold (Hutchinson’s sign) the likely cause is a melanoma |
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Blue black nail |
-Usually due to haematoma but could be melanoma - Hutchinson’s sign (pigmentation of skin aroundthe nail) strongly points towards melanoma. |
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Paronychia |
Inflammation around the nail. - Usually the result of acute or chronicinfection gaining access via an abnormal cuticle, such as you see in eczema, or in individuals whosehands are frequently exposed to water or solvents. Acute - pain, swelling, erythema - treat with anti-staph if severe. Chronic - atopic or continual industrial exposure; may relate to chronic candida - topical steroids +/- anticandida. |
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Melanoma |
Asymmetry of shape; border irregularity; colour variation; diameter >1cm/Ugly duckling sign |
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Actinic keratoses |
Erythema and scale on sun exposed areas |
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Bowen's disease |
SCC carcinoma in situ; well defined psoriatic like plaque commonly on legs or trunk in elderly women |
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Keratoacanthomas |
Mimic of SCC - assume SCC until proven otherwise. -Volcano like with central keratin plug -Excise 4-6 mm margin |
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SCC |
Ugly/untidy looking; may be ulcerated or eruptions -Found areas more sun exposure |
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BCC |
Ulcerated with pearly border; telangectasia; middle third of face. -Don't metastasise |
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Kaposi's sarcoma |
Multiple purple papules on skin and mucosa; haemoptysis and pleural effusion; due to HSV 8; seen in HIV |
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Paget's disease of breast |
unilateral eczema nipple; reflect adenocarcinoma underlying |
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Freckles |
Flat focal areas of overproduction of melanin (no increase in melanocyte number) from UV exposure in sensitive skin. |
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Seborrhoeic keratosis |
Benign keratinocyte tumours -Stuck on appearance; warty irregular surface; plugged follicles; most commonly on trunk but can occur on face & limbs (not palms or soles); often multiple; increase with age. |
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Solar lentigines |
Flattish brown marks on back of hands, forearms and face; reflect sun exposure |
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Melanocytic nevi |
Focal collection of melanocyte clusters; develop up to mid 30s; change from flat and dark to raised with less pigment |
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Blue nevi |
Melanocytic nevi deep in dermis appear blue; appear in childhood (suspicious in middle/older age); increased in asian populations |
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Halo nevi |
Melanocytic nevi under immune attack with destruction of melanocytes; appear in adults with MM elsewhere - check whole body |
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Spitz nevi |
Reddish brown nodule in child or young adult on upper arms and face. Benign |
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Haemangioma |
Collection small blood vessels that form lump under skin; can remove blood by pressure (not always possible) |
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Pyogenic granuloma |
Vascular proliferation in response to wound in which vascular proliferation tissue continues to grow inappropriately; commonly on fingers in young people |
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Sebaceous hyperplasia |
Clusters of sebaceous glands on face; translucent and yellow rosette shape around central follicle; mimic BCC |
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Urticaria |
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Comedonal Acne |
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Acne congloblata |
Severe acne with burrowing & interconnecting abscesses and irregular scars |
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Acne inversa/hidradenitis suppurativa |
Effects apocrine bearing areas (axillae, groin, perineum and perianal areas) -Rupture of follicle and dispersion of contents in to surrounding dermis - inflam. -Sterile abscess formation and sinus tracts with excesive scarring -More common in women and young adults -Antibiotics, isotretinion, steroid (Acute); surgical excision |
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Lichenification |
Chronic eczema - exaggeration of skin markings |
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Contact allergic eczema |
Period of sensitization |
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Varicose eczema |
Due to venous incompetence |
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Discoid eczema |
Seen in middle age. Treat with steroids |
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Dennie-Morgan folds |
Double fold of skin over lower eyelid from rubbing -Atopic eczema |
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Pityriasis alba |
White slightly scaly areas on arms and face of children with atopic eczema |
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Papular eczema |
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Eczema herpeticum |
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Plaque psoriasis |
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Guttate psoriasis |
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Erythrodermic psoriasis |
Covers 90% body |
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Pustular psoriasis |
Sterile pustules; systemic upset; can occur in anyone with psoriasis |
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Nail psoriasis |
Pitting; oncholysis (separation distal nail bed); oily spots |
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Onychomycosis |
Caused by: -dermatophytes -mainly Trichophyton rubrum (accounts for 90% of cases yeasts) - Yeasts - Candida - non-dermatophyte moulds -Confirm diagnosis via clippings/scraping then treat with oral terbinafine or itraconazole |
