Dermatology Flashcards
what is a plaque?
a raised flat-topped lesion, usually more than 2cm in diameter
what is pityriasis alba?
hypopigmentation of skin, commonly seen on children’s faces, especially asian
often resolves spontaneously
appearance of basal cell carcinoma?
pearly (translucent, shiny) papule, often skin coloured, and central ulcer/depression, rolled telangiectatic edge, usually on face in sun exposed site
telangiectatic vessels of surface account for common symptom of contact bleeding
metastases rare
can spread along bony passages into the skull
slowly causes local destruction if left untreated
excision is best
skin signs of coeliac disease?
dermatitis herpetiformis-very itchy/burning blisters on elbows, scalp, shoulders, ankles.
causes of pyoderma gangrenosum?
IBD myeloma neoplasia AI hepatitis wegener's granulomatosis
signs of psoriasis?
symmetrical, well-defined red plaques with silvery scale on extensor aspects of elbows, knees, scalp and sacrum.
flexures e.g. axillae, groin and umbilicus also frequently affected, but lesions non-scaly.
why might diet be important to ask about in suspected eczema?
some atopic children have food allergies e.g. dairy products and/or eggs which exacerbate eczema. rarely true intolerance-actual immune response.
role of emollients in eczema and psoriasis?
treat dryness and act as a barrier
greasy emollients are best in severe eczema
require frequent application-8-10 times daily!!
how can absorption of emollients in eczema be increased?
wearing of stockinette suits at night
or paste bandaging?
classification of eczema?
exogenous and endogenous endogenous: atopic discoid hand seborrhoeic venous-erythematous scaly, flaky skin over and above ankle medial malleolus, alongside skin pigmentation, lipodermatosclerosis, varicose veins, venous ulceration and atrophie blanche endogenous eczema of palms and soles, can be episodic acute pompholyx asteatotic exogenous: contact-irritant and allergic photosensitive (?photocontact) lichen simplex/nodular prurigo
aetiology of atopic eczema?
familial disease, strong maternal influence
often +ve FH of atopic disease e.g. asthma, hayfever
TH2 CD4+ T cell activation in skin drives inflammatory process, thought to be secondary to some break in skin barrier function
genetically complex, may be link to filaggrin gene-epidermal barrier protein where may be loss of function mutation
atopic eczema exacerbating factors?
infection (?superantigen effect) and non-infection in infancy (hygiene hypothesis) strong detergents woolen clothes severe stress or anxiety cat and dog fur dairy products and eggs
clinical features of atopic eczema?
itchy erythematous scaly patches, usually symmetrical and often in flexures-in front of elbows, behind the knees, in front on ankles and around the neck
often starts on face in infants before spreading elsewhere
very acute lesions can weep or exude, and can show small vesicles
scratching can produce excoriations (marks from skin picking)
rpted rubbing produces skin thickening (lichenification) with exaggerated skin markings
often reverse pattern of extensor involvement e.g. back of elbows, front of knees, in people with pigmented skin, and can cause hyper-or hypo-pigmentation in these people post-inflammation
skin of upper arms and thighs may feel roughened due to follicular hyperkeratosis
palms may show very prominent skin creases
may be assoc. ichthyosis vulgaris-‘fish like scaling’ of skin which is non-inflammatory and often prominent on lower legs
another name for fungal skin disease?
mycosis
3 groups of pathogenic fungi that commonly affect the outer skin layer?
dermatophytes-cause ‘ringworm’ type of rash
candida albicans
pityrosporum (malassezia genus)-pityriasis versicolor
how do fungal skin infections typically respond to steroid treatment?
hx of rash improving with treatment (due to suppression of inflammation), but worsening and spreading each time it is stopped
pityrosporum is a yeast part of normal skin flora, common in scalp, upper trunk and flexures. in what 3 dermatoses with overgrowth has it been implicated in?
pityriasis versicolor-presents most commonly on trunk in young people with reddish brown scaly macules (flat, circumscribed, non palpable lesion) which are asymptomatic, in darker skin more commonly presents as hypopigmented macular areas
seborrhoeic eczema
pityrosporum folliculitis
complications of atopic eczema?
secondary infection: staph aureus-impetigo, folliculitis
HSV-eczema herpeticum-multiple small vesicles or punched-out crusted papules and erosions assoc. with malaise and pyrexia, needs rapid tment with oral (if apyrexial) or IV aciclovir, give Abx for bacterial secondary infection (can also give BS as routine prophylaxis), complications=herpes hepatitis, encephalitis, DIC and rarely death. need early opthalm r/v if any evidence of ocular involvement-*risk of HSV keratitis and corneal ulcers.
conjunctival irritation
retarded growth
eczema treatment?
educate and explain
avoid irritants/allergens e.g. pet fur
emollients e.g. diprobase cream-can use as soap substitute, zeroderm, zerodouble, aveeno, zerobase, hydromol, eczmol, dermol, regular use may lessen the need for steroid use, creams and ointments to moisturise skin to reduce dryness-ointments best as stay on skin for longer but very greasy so may be used at night and something else during the day
bath oils and soap substitutes e.g. dermol-emollient and can be used as soap substitute and in the bath, as can eczmol and both antibacterial, hydromol can be used as moisturiser and soap substitute, shouldn’t wash just with water
topical therapies: steroids-1% hydrocortisone, eumovate, betnovate, dermovate, immunomodulators e.g. tacrolimus ointment-calicneurin inhibitor-calcineurin required for activation of T cells
adjuncts-oral Abx, antihistamines-sedating before bed e.g. Chlorphenamine or hydroxyzine in children, bandaging e.g. Icthopaste
phototherapy
oral pred, ciclosporin, MTX, azathioprine, mycophenolate mofetil
clinical features of seborrhoeic eczema (also called seborrhoeic dermatitis)?
in young adults presents as erythematous scaling along sides of nose in NL folds, in eyebrows, around eyes and extending into scalp
due to overgrowth of fungus pityrosporum ovale
tment=mild steroid ointment-prescribed for 1-3wks to reduce inflammation of an acute flare, and topical antifungal cream, which is suppressive rather than curative
keratolytics e.g. salicyclic acid can be used to remove scale where necessary
what type of eczema can often be confused with psoriasis?
discoid eczema-well-demarcated scaly patches, espec. on limbs
follows acute/subacute pattern
often an infection component-S.aureus
skin proliferation rate in psoriasis?
skin regeneration takes 4 days in comparison to normal 28 days
so 7 FOLD INCREASE!
psoriasis aetiology?
autoimmune condition, T lymphocyte mediated inflammatory process to particular antigens
Th1 lymphocytes involved, role of ILs and TNF-alpha
genetic component, gene loci involved some same as for RA, crohn’s disease and atopic eczema
clinical features of chronic plaque psoriasis?
pinkish red scaly plaques, with silver scale, on extensor surfaces e.g. knees, back of elbows, also lower back, ears and scalp.
new plaques occur at sites of skin trauma-kobner phenomenon, lesions can become itchy or sore
psoriasis treatment?
educate and explain, PASI score-assess severity
emollients-zeroderm, epiderm
purified coal tar products e.g. polytar shampoo, good for reducing scaling, especially with scalp psoriasis
dithranol-stains skin purple
Vit D analogues e.g. calcipotriol
topical corticosteroids e.g. eumovate (moderate), caution as can cause tachyphylaxis and cause pustular psoriasis
calcineurin inhibitors e.g. tacrolimus
for moderate to severe psoriasis, need systemic agent and/or phototherapy
topical therapy in combo with UVB or PUVA, PUVA-photochemotherapy, psoralens taken to sensitise skin to UVA before skin exposure to it, narrow band UVB-3 times a week for 16 weeks
systemic therapy-MTX, ciclosporin, acitretin-synthetic Vit A analogue
6-MP and azathioprine also considered, and cytokine modulators e.g. etanercept, infliximab, adalimumab-for conventional tment-resistant severe psoriasis.
5 types of nail change in psoriasis?
nail pitting onycholysis yellow-brown discolouration subungual hyperkeratosis-excessive proliferation of nail bed damaged nail matrix and lost nail plate
what do we want to know in hx of skin disease?
time course of rash distribution of lesions symptoms e.g. pain ,itch FH-atopy, psoriasis drug/allergy hx PMH provoking factors-sunlight or diet previous skin treatments
what is a seborrhoeic keratosis?
also known as basal cell papilloma/senile wart
benign growth of skin cells
no malignant potential
more common with advancing age
become more numerous as time goes by
thought to be degenerative
can occur anywhere except palms and soles
may be grouped in certain areas, look like stick to the skin surface
differing colours, flat or raised papule or plaque
can develop from a solar lentigo-these occur in relation high sun exposure and phototherapy
may be removed if desired due to itchy, catching on clothing or unsightly or if become inflamed-may be crusting and bleeding which necessitate biopsy for histology. may use cryotherapy, curettage and cautery, shave biopsy, all have disadvantages, espec. loss of pigmentation in dark-skinned people.
complications of removal also include scarring and lesion recurrence.
what is a solar keratosis?
(actinic keratosis)
a pre-cancerous skin lesion occurring on sun damaged skin
scaly spot, appearance varies:
flat or thickened papule or plaque
white or yellow; scaly, warty or horny surface
skin coloured, red or pigmented
tender or asymptomatic
main concern of a solar keratosis?
predisposition to squamous cell carcinoma
a tender, thickened, ulcerated or enlarging actinic keratosis is suspicious
treatment of a solar keratosis?
cryotherapy-intermittent bursts given over 10 seconds, gets rid of lesion but likely to return as not treating area of sun damaged skin, if multiple lesions e.g. over the head, then using topical treatment e.g. Effudix-5-FU better, but does initially cause an inflammatory reaction where skin erythematous.
shave, curettage and electrocautery
creams-used to treat areas of sun damage and flat keratoses, often after physical tments been carried out, e.g. 5-FU cream or diclofenac or imiquimod, all cause local inflammtory reaction e.g. redness and blistering, for varying length of time apart from diclofenac.
also new drug-picato gel-chemotherapeutic
what is bowen’s disease?
also known as intraepidermal squamous cell carcinoma (carcinoma-in-situ-not progressed through the basement membrane)
presents as 1 or more slow-growing red/brown irregular scaly plaques up to several cm in diameter, most often red but can be pigmented
often on sun exposed areas-ears, face, hands and lower legs
when multiple plaques, NOT symmetrical as in psoriasis
may rarely grow under the nail and destroy the nail plate
lesion can progress to SCC (infrequently, only 5%)
penile bowen’s disease=queyrat’s erythroplasia
tment=5-FU topical, cryotherapy, photodynamic therapy
what benign condition may a SCC be confused with?*
keratoacanthoma-a fast growing, benign, self-limiting papule plugged with keratin
*clinically disease is classified in some places as form of SCC, and requires surgical excision
SCC appearance?
ulcerated lesion, with hard raised edges, in sun-exposed sites
may begin in solar keratoses, or be found in long-standing venous ulcers (marjolin’s ulcer)
metastasise to LNs (rare)
tment=excision and radiotherapy
factors to consider in hx which may initiate rash development?
different food-?allergic reaction spicy foods alcohol sunlight stress change in temperature change in socks/shoes,tights walking through long grass, ?where pt has been walking
who gets lichen planus?
about 1 in 100 people worldwide
mostly adult over 40yrs
about 50% of those affected have oral lichen planus-more common in women
about 10% of lichen planus of the nails
contributing factors: physical or emotional stress
injury-where skin scratched
drugs e.g. gold, quinine
genetic predisposition
localised skin disease e.g. herpes zoster (shingles)
systemic viral infection e.g. Hep C
how does lichen planus occur?
T cell mediated AI disease in which inflammatory cells attack and unknown protein within skin and mucosal keratinocytes
presentation of cutaneous lichen planus?
small number or many skin or mucosal lesions
Papules and polygonal plaques are shiny, flat-topped and firm on palpation.
The plaques are crossed by fine white lines called Wickham striae.
Hypertrophic lichen planus can be scaly.
Size ranges from pinpoint to larger than a cm
Distribution may be scattered, clustered, linear, annular or actinic (sun-exposed sites such as face, neck and backs of the hands).
Location can be anywhere, but most often front of the wrists, lower back, and ankles.
Colour depends on the patient’s skin type. New papules and plaques often have a purple or violet hue, except on palms and soles where they are yellowish brown.
Plaques resolve after some months to leave greyish-brown post-inflammatory macules that can take a year or longer to fade
can be VERY ITCHY
presentation of oral lichen planus, and lichen planus of the nails?
oral: painless white streaks on inside of cheeks and sides of tongue
may also be painful and persistent erosions and ulcers (erosive lichen planus), diffuse redness and peeling of the gums (desquamative gingivitis) and localised inflammation of the gums adjacent to amalgam filling
nails: thins the nail plate, which may become grooved and ridged. The nail may darken, thicken or lift off the nail bed (onycholysis). Sometimes the cuticle is destroyed and forms a scar (pterygium). The nails may shed or stop growing altogether, and they may rarely, completely disappear (anonychia)
presentation of pytyriasis rosea?
possibly mild prodromal illness
Discrete circular or oval pink lesions
Scaling on most lesions
Peripheral collarette scaling with central clearance on more than 2 lesions-scale peels from centre towards edge
at least 1 of following should be present:
Truncal and proximal limb distribution (less than 10% of lesions distal to mid-upper-arm and mid-thigh)
trunk lesions lie with their long axes in lines sweeping from back to front-inverted Christmas tree appearance
Most lesions along skin cleavage lines
Herald patch 2 or more days before other lesions-a red or pink single oval and scaly plaque, often on trunk or upper arm
what is ptyriasis rosea?
a viral rash that last 6-12 weeks and characterised by herald patch ( a single plaque) appearance before similar smaller oval red patches appear afterwards mainly on chest and back
self-limiting disorder, predominantly affecting children and young adults
can treat with 7 day cause of high dose aciclovir (off licence), and recommend moisturising dry skin
mild topical steroids can help relieve irritation.
what is rosacea?
chronic rash affecting central face, patients in their 30s-60s, common in those with fair skin, blue eyes and celtic origins, and more common in females
features: frequent blushing or flushing
red face due to persistent redness and/or prominent blood vessels – telangiectasia (the first stage or erythematotelangiectatic rosacea)
red papules and pustules on the nose, forehead, cheeks and chin often follow (inflammatory or papulopustular rosacea); rarely, the trunk and upper limbs may also be affected
dry and flaky facial skin
aggravation by sun exposure and hot and spicy food or drink (anything that reddens the face)
may be soreness and burning sensation
can be rhinophyma (enlarged swollen nose), swollen forehead, eyelids, earlobes and chin, with sebaceous gland hyperplasia.
can involve eyes-blepharitis, conjunctivitis, episcleritis.
characteristic feature of acne?
blackhead
overall treatment for acne?
treatment at least 6 wks to produce effect
mild-topical anti-acne preparations e.g. benzoyl-peroxide-antiseptic and keratolytic, can give epiduo-combination of benzoyl peroxide and adapalene
then topical Abx e.g. clindamycin
?topical retinoids-comedolytic and anti-inflammatory
moderate-Abx e.g. tetracyclines (PO) e.g. lymecycline-may be better compliance as OD application, doxycycline or oxytetracycline, or erythromycin 500mg BD e.g. in children under 12 years of age and in pregnancy, and continue for at least 3-6mnths before reassessment, and/or antiandrogens e.g. COCP, combine oral treatment with topical treatment (retinoid or antibacterial) e.g. adapalene-anti-inflammatory, keratolytic (exfolients-peel off surface scale) and bactericidal
*note tetracyclines CI in children under 12yrs due to deposition in growing bone and teeth-risk of growth problems and teeth staining.
severe-may need course of oral isotretinoin (retinoid)-derived from Vit A, course often for 4-7 months. 1st choice tment in secondary care. *note can cause mood changes-?about previous anxiety or depression, also any intention to get pregnant-drug is teratogenic so pregnancy testing done during treatment-female pts put on pregnancy prevention programme-2 forms of contraception and monthly pregnancy tests, and pt must wait 5 weeks post stopping treatment before trying for a pregnancy (so programme continued until then).
what is molluscum contagiosum?
common viral skin infection seen in children under 10 yrs of age (although also seen adults, espec immunocompromised e.g. HIV where more likely widespread and atypical pres. e.g. larger lesions)
features pink, pearly papules which are umbilicated (dimples in the middle)
caused by DNA virus of pox family
NOT found on soles or palms
no specific med tment found to kill virus
can take up to 18mnths to resolve
can try cryotherapy, topical podophyllotoxin 0.5%, imiquimod 5% cream, can also try squeezing after bathing.
can be spread using same bath towels so avoid sharing towels!
what is alopecia areata?
AI disease in which 1 or more round bald patches appear suddenly, onset may be triggered by a viral infection, emotional or physical stressors, trauma or hormonal change.
may be assoc. with atopic diseases e.g. atopic eczema, asthma, hayfever, and other specific AI diseases e.g. thyroiditis, type 1 DM, vitiligo
*atopy is an adverse prognostic factor
regrowing hair often initially coloured white or grey
exclamation mark hairs-2-3mm in length broken or tapered hairs which are narrower closer to the scalp
may be nail changes-pitting, onycholysis, brittle nails with vertical ridging and splitting
can apply topical very potent and intralesional potent steroids, *skin atrophy is a risk with prolonged or extensive use
may require counselling and advice on products used to cover up hair loss e.g. hair pieces, psychological support essential
often complete recovery with spontaneous regrowth within 6-12mnths, reassurance important, but must also stress possibility that disease can recur
may be future promising tment with biologic agents-monoclonal AB tments
diphencyprone topical immunotherapy may be considered in longstanding (more than 6 months) and extensive disease of scalp and/or eyebrows.
can be forms where more hair loss:
alopecia totalis-all scalp hair
alopecia universalis-all hair on entire body lost
if a patient was to present with recurrent episodes of angioedema without urticaria (hives=wheals), why might we want to assess their drug history?
angioedema is an ADR of ACEIs-this is a non allergic reaction mediated by bradykinin rather than histamine.
what is urticaria?
characterised by wheals (hives) or angioedema (swellings, in 10%) or both (in 40%). wheal=superficial skin-coloured or pale skin swelling, usually surrounded by erythema lasts from a few minutes to 24 hours. result of superficial dermis swelling raising the epidermis. Usually very itchy, it may have a burning sensation. Angioedema= deeper swelling within the skin or mucous membranes, and can be skin-coloured or red. It resolves within 72 hours. Angioedema often asymptomatic.
acute=less than 6 weeks
local increase in capillary permeability, due mainly to histamine release
more common in atopics e.g. asthma, hayfever, eczema
each wheal may last a few mins or several hrs
histamine, platelet-activating factor and cytokine release. bradykinin release causes angioedema. food and drug allergies=IgE mediated, type 1 hypersensitivity-CD4+ T helper 2 cells IL-4 and 5 release.
skin prick testing can be done
main tment= oral 2nd generation antihistamine e.g. cetirizine, should also avoid part triggering allergens, can also cool affected area.
if severe and non-sedating antihistamines not effective, consider 4-5 day course oral prednisolone
IM adrenaline for life threatening anaphylaxis or throat swelling-0.5mg IM every 5min as needed
drugs which most commonly cause stevens johnson syndrome and toxic epidermal necrolysis?
antibiotics: sulfonamides-co-trimoxazole-used in treatment of pneumocystis jiroveci pneumonia*caution as this pneumonia common in immunocompromised patients e.g.HIV patients, and SJS/TEN 100 times more common in patients with HIV infection.
beta-lactam: penicillins and cephalosporins
with ABx, symptoms occur within 1st week of starting treatment
anticonvulsants e.g. lamotrigine, phenytoin, carbamazapine, symptoms can develop up to 2 mnths after starting treatment
paracetamol
NSAIDs
how is damage mediated in stevens johnson syndrome/toxic epidermal necrolysis?
CD8+ cytotoxic T cells can directly kill keratinocytes
presentation of stevens johnson syndrome/toxic epidermal necrolysis?
rash preceded by prodromal flu like illness-fever more than 39 degrees C, sore throat, dysphagia, runny nose, cough, sore red eyes, conjunctivitis, general aches and pains
SJS characterised by at least 2 mucosal sites affected by mucocutaneous necrosis, in general SJS restricted to mucous membranes e.g. perineum, mouth, nose, with mild bullous disorder on skin (rash), less than 10% surface involvement
TEN=full thickness epidermal necrosis, skin detachment more than 10% of body surface area, with subepidermal detachment on histopathology.
then abrupt onset tender/painful red skin rash-burning sensation, may be itch, starts on trunk and extends rapidly to involve face and limbs over hrs to days, but spares palms, scalp and soles. skin lesions:
macules-flat smooth area of colour change less than 1.5cm diameter, appears as erythematous and diffuse or purple (purpuric) spots
diffuse erythema
targetoid-concentric zones, seen in urticaria
blisters-flaccid, these merge to form sheets of skin detachment, exposing red oozing dermis.
areas of skin redness +ve Nikolsky sign=blisters and erosions appear when skin rubbed gently
extensive epidermal loss causes severe dehydration and protein depletion.
prominent and severe mucosal involvement-conjunctivitis, cheilitis, angular stomatitis, pharynx and oesophagus-dyspagia, genital tract and UT-ulcers, diarrhoea, RT-cough and resp distress.
complications of acute phase of SJS and TEN?
dehydration and acute malnutrition
infection skin, mucous membranes, septicaemia, pneumonia
ARDS
thromboembolism and DIC
shock and multiple organ failure
GI ulceration, perforation and intussusception
treatment for SJD and TEN?
stop causative drug hosp admission for general supportive treatment: IV fluid and nutritional replacement temp maintenance analgesia non adherent dressings topical antiseptics e.g. silver nitrate poss. IV immunoglobulin and ciclosporin
name given to phenomenon where skin rash occurs within a scar?
koebner’s phenomenon (koerbnerisation)
skin conditions which cause koebner’s phenomenon?
psoriasis lichen planus warts SLE vitiligo
define a vesicle
small clear fluid containing blisters less than 0.5cm in diameter
approach to describing a pigmented lesion?
A, B, C, D, E asymmetry borders-irregular? well defined? colour-uniformity? diameter-more than 7mm? extra/evolution-ulceration, itch, has it changed over time?
how do we describe a lesion based on how it looks?
site e.g. face, trunk, limbs, consider if sun exposed area, photosensitive rashes
number e.g. single, multiple, rash
extent e.g. localised, regionalised, generalised, widespread
distribution-symmetrical, asymmetrical, sun exposed, flexures, extensors
arrangement e.g. discrete, coalescing, annular e.g. fungal skin infections, grouped, linear
individual lesion: SCAM shape, size-widest diameter colour assoc. secondary change morphology, margin (border) palpate lesion: surface consistency mobility tenderness temperature
then systematic check: hair, scalp, nails, mucous membranes
what is erythema nodosum?
a hypersensitivity response to a variety of stimuli
causes of erythema nodosum?
NODOSUM
idiopathic
drugs-sulfonamide antibiotics e.g. co-trimoxazole
OCP
sarcoidosis
IBD
TB, malignancy, group A beta-haemolytic streptococcus, chalmydia, leprosy
presentation of erythema nodosum?
discrete erythematous/blue tender nodules, which may become confluent, most commonly on the shins
continue to appear for 1-2wks and leave bruise like discolouration as resolve
do not ulcerate and resolve without atrophy or scarring
reassure patient that they resolve on their own
may prescribe analgesia to cope with pain
define angioedema
deeper swelling than urticaria, involving the dermis and subcutaneous tissues and mucosa, presents as swelling of the tongue and lips
*hereditary angioedema-rare autosomal dominant condition where patients lack the C1 esterase inhibitor protein or it is non-functioning, resulting in increased capillary permeability, mainly mediated by bradykinin, so increase fluid leak into interstitium producing oedema, which can involve face, hands, feet and airway, and intestinal wall swelling which can present as acute abdomen with severe abdo pain, nausea and vomiting.
must avoid ACEIs and oestrogen containing med.s e.g. OCP as increased risk of angioedema episodes.
laryngeal oedema=life-threatening-features include sore, tight, itchy throat or dysphagia, hoarse voice, barking, unable to speak, dyspnoea, stridor, anxiety, grasping their neck with thumb and index fingers. can die with asphyxiation-choke to death from lack of oxygen.
can treat by giving patients a C1 esterase inhibitor.
what is erythema multiforme?
acute self-limiting inflammatory condition with HSV-so ?coldsore hx, being the main precipitating factor
other causes include drugs e.g. penicillins, NSAIDs, sulphonamides
and infections can cause it e.g. CMV, EBV, HIV, adenovirus, hepatitis, mumps, mycoplasma
radiotherapy
cancers
CT disease
limited mucosal involvement
pathology at dermoepidermal junction, may be delayed hypersensitivity reaction
characterised by target lesions-centre is dusky or dark red with a blister or crust, next ring is a paler pink and is raised due to oedema, bright red outermost ring.
pt may complain of itch or pain
distribution characteristically extensor surfaces of arms and legs, but more importantly is palm and sole involvement
lesions appear suddenly, enlarge over course of a few days, then fade, often leaving pigmentary disturbances
whole process settles in about 3 wks
self-limiting, but can treat underlying cause, and can always reduce rash duration with topical steroid
rptd episodes can be triggered by HSV-could give LT low treatment dose aciclovir
can develop into TEN/SJS
rash of meningococcal septicaemia?
non-blanching pupuric rash on trunk and extremities, may be preceded by blanching maculopapular rash, and can rapidly progress to ecchymoses, haemorrhagic bullae and tissue necrosis.
complications= septic shock, DIC, multiorgan failure and death
give IV or IM benzylpenicillin
how does erythroderma present?
this is a state, rather than pathological diagnosis
this is an exfoliative dermatitis involving at least 90% of the skin surface (so essentially clinical state of inflammation of all skin), where skin appears erythematous, inflamed, scaly and oedematous, and pt is systemically unwell with lymphadenopathy and malaise.
must treat underlying cause e.g. stop causative drugs e.g. penicillins, sulfonamides previous skin disease-eczema, psoriasis, use emollients, and wet-wraps to maintain moisture of skin, and topical steroids can be given to relieve inflammation e.g. betnovate (betamethasone) or dermovate
complications include secondary infection, high output heart failure, central hypothermia from heat loss which can cause sudden death, fluid loss and electrolyte imbalance, renal failure, hypoalbuminaemia and capillary leak syndrome-can cause ARDS requiring ITU management.
define necrotising fasciitis
rapidly spreading infection of the deep fascia with secondary tissue necrosis
2 types: 1=often seen post op, caused by both aerobic and anaerobic bacteria
2=group A haemolytic streptococcus, and can arise spontaneously in healthy people
patients at risk include those with diabetes and abdominal surgery
appears as erythematous, blistering and necrotic skin, with fever, tachycardia and crepitus (SC emphysema)
soft tissue gas may be seen on X-ray
must do rapid extensive surgical debridement, and give high dose post op IV antibiotics e.g. benzylpenicillin.
IV Abx alone are ineffective as compromised blood supply to necrotic tissues
important risk factor for melanoma recurrence?
Breslow thickness
=depth of the tumour, measure in mm on histology from the granular cell layer to the deepest point of the tumour
types of melanoma?
superficial spreading melanoma
nodular melanoma
lentigo maligna melanoma
acral lentiginous melanoma
RFs for melanoma development?
more than 5 episodes of sunburn under age of 10 years
more than 100 naevi
atypical naevus syndrome
personal or FH of melanoma
skin type 1-burns easily and doesn’t tan in the sun
guttate psoriasis is often preceeded by what?
sore throat-streptococcal URTI
topical treatment of pityriasis versicolor?
topical anti-fungals-azole creams e.g. miconazole-which is combined with hydrocortisone in daktacort, ketoconazole.
ketoconazole shampoo
how can the severity of psoriasis be assessed?
use a PASI score-psoriasis area and severity index
a representative area of psoriasis is selected for each body region, and a score out of 4 given for each of the following:
redness
thickness
scaling
4=very severe
these are each multiplied by body surface area represented by that region
name given to thickening of skin that occurs with chronic eczema?
lichenification
how does allergic contact dermatitis contrast with allergic contact urticaria e.g. that seen with latex allergy?
allergic contact dermatitis-arises some hrs after contact with causative material, urticaria-rash appears within mins of exposure and disappears within mins to hrs.
define anaphylaxis
systemic allergic response which is life threatening
symptoms of anaphylaxis?
urticaria itch angioedema-laryngeal oedema-dysphagia, sore, tight, itch throat, unable to speak flushing stridor wheeze nausea and vomiting dizziness syncope fear of impeding doom-due to high circulating adrenaline abdo pain diarrhoea loss of consciousness
treatment of anaphylaxis?
get help!-must contact senior doctors including anaesthetist
remove trigger, maintain airway, give 100% oxygen
IM adrenaline 0.5mg, rpt every 5mins as needed to support CVS
IV hydrocortisone 200mg
IV chlorpheniramine 10mg-anti-histamine
if hypotensive lay flat and fluid resuscitate, can elevate legs but not if SOB
treat bronchospasm-wheeze and chest tightness-with neb salbutamol
laryngeal oedema-neb adrenaline
how does IgE mediated hypersensitivity develop?
for an allergy, must be previous asymptomatic exposure to allergen-here sensitisation occurs with allergen specific IgE formed which binds to mast cells.
when subsequent allergen exposure, allergic reaction occurs with allergen cross linking of at least 2 adjacent IgE allergen specific molecules on mast cells, causing mast cell degranulation.
IgE mediated hypersensitivity reactions=type 1 hypersensitivity, immediate hypersensitivty
types of psoriasis?
chronic plaque psoriasis
guttate psoriasis-younger people post viral infection
flexural psoriasis
pustular psoriasis (palmoplantar or generalised)-note may result from topical steroid use for chronic plaque psoriasis
erythrodermic
features that may help distinguish eczema from psoriasis?
location-eczema flexor surfaces, psoriasis extensor surfaces
pruritus-lack would favour psoriasis over eczema
plaques-well demarcated in psoriasis, poorly demarcated in eczema unless discoid type
koebnerization-not seen with eczema
nail changes of psoriasis
joint problems in psoriasis
FH of psoriasis
personal and FH of atopy in eczema
how can an objective assessment be made of the impact of skin disease e.g. psoriasis, on a patient’s everyday life?
Dermatology Life Quality Index (DLQI)-10 item questionnaire completed by pt, can be used to monitor effectiveness of treatment.
medical name for moles?
melanocytic naevi-a benign proliferation of melanocytes
*more than 100 is a risk factor for melanoma
what 3 types of melanocytic naevi (benign proliferation of melanocytes) are commonly seen?
junctional naevus-brown, evenly pigmented macule
compound naevus-raised pigmented lesion with regular border, and symmetry of shape and colour. pigment colour may vary from pale to very dark brown, surface may be cobblestoned or cerebriform
intradermal naevus-dome-shaped, skin-coloured papule or nodule, often with overlying telangiectatic vessels.
what changes should be asked about in the hx of a pt with melanocytic naevi that might suggest development of malignant melanoma?
duration of the naevi, and any recent hx of change-size, shape or colour?
any bleeding or itching?
how is a suspicious looking mole managed by a GP?
urgent r/f to dermatology via 2ww cancer pathway
dermatologist will organise excision biopsy with a 2mm clinical margin for a suspicious pigmented lesion
areas of skin part. close attention should be made in suspected scabies?
web spaces of fingers and toes thenar and hypothenar eminences wrists and ankles axillae genitalia-papules on the penis
what cutaneous signs are being examined for in scabies?
burrow-short, wavy, scaly, grey line on skin surface
papules, nodules, pustules, vesicles
excoriations-scabies VERY ITCHY!
eczema-scabies can cause widespread eczema, and this can become secondarily infected with staph, strep or both. prescribe emollients and topical corticosteroids for eczema.
note rash can take up to 6 weeks to manifest after infection
how is definitive diagnosis of scabies made?
burrow skin scrapings looked at under microscopy where mites or eggs are identified.
treatment of scabies?
1st line-permethrin 5% dermal cream (parasiticidal)
2nd line-malthion
give aq preparations in children as alcoholic lotions sting and can cause wheeze.
RFs for catching scabies?
spread by close personal contact-common in infants and children, and in elderly people in nusring homes and can be transmitted to nursing staff
between adults transmission often by sexual contact
how long does scabies take to resolve following successful treatment?
can take at least 6 weeks
how is permethrin applied for scabies treatment?
over whole body (except head and neck) twice, with applications 1 week apart, should be left on for 12 hours before washing off.
in children aged up to 2yr, and in elderly and immunocompromised, application should extend to scalp, neck, face and ears
may need mittens or socks for thumb or toe sucking infants and toddlers
treat all members of affected household at same time, and sexual contacts of adults
clothes and bed linen should be machine washed at temp.s above 50 degrees C
how does allergic contact dermatitis differ from irritant contact dermatitis?
allergic-an itchy skin condition occurs as a result of an allergic reaction to a particular allergen the patient has been sensitised to, and this allergen would not cause this allergic reaction in everyone, in contrast to irritant-which may affect anyone who has had enough exposure to the irritant e.g. hand soaps, water, detergents, acids, alkalis and friction.
how does scabies tend to present in children in comparison to adults?
very young children often have widespread eczematous erythema, part. on trunk, which is sometimes more symptomatic than lesions on typical sites
very young babies don’t scratch, may just be miserable or feed poorly, pinkish brown scabetic nodules and involvement of palms and soles part. characteristic of scabies in babies.
clinical features of allergic contact dermatitis?
dermatitis generally confined to site of contact with allergen, but severe cases can extend outside contact area and may be generalised
unexpected places may be affected due to allergen spread from fingers e.g. eyelids and genitalia
skin appearance-erythema, dry, swollen, blistered and bumpy
past medical history to be interested in pt with suspected hand dermatitis?
?allergic contact dermatitis, want to know medical hx of atopy-eczema, hayfever, asthma
advice to patients with contact hand dermatitis?
protect hands with gloves (but remember latex or rubber allergy can occur)
use soap substitutes
avoid direct contact with irritating chemicals e.g. detergents, soaps, but also foods-citrus fruits, potato peeling-can irritate hands!
regular emollient use, and use of potent topical steroid for dermatitis flares
typical examples of allergic contact dermatitis?
An eczema of the wrist underlying a watch strap due to contact allergy to nickel
An eczema of the lower leg when ankle strapping has been removed due to contact allergy to rosin in the adhesive plaster
Hand dermatitis caused by rubber accelerator chemicals used in the manufacture of rubber gloves
Itchy red face due to contact allergy with methylisothiazolinone, a preservative in wash-off hair products and baby wipes
what is a photocontact dermatitis?
rash confined to sun exposed areas although allergen may have been in contact with covered up areas, contact allergy arises only after skin exposure to UV light.
may be due to a sunscreen chemical, and occurs on top of arm but not under surface
face, neck, hands and arms dermatitis due to antibacterial soap
investigation of choice for contact dermatitis?
patch testing-decide if contact allergy
done on the back over 1 week, type IV delayed hypersensitivity reaction
treatment of active allergic contact dermatitis?
emollients
topical steroids e.g. betnovate for 1 week
topical or oral Abx for secondary infection
oral steroids, usually short courses, for severe cases
photochemotherapy
immunosuppressant e.g. azathioprine, ciclosporin
tacrolimus ointment and pimecrolimus cream (calcineurin inhibitors)
indications for use of PUVA (psoralens-temporarily skin made sensitive to UVA, plus UVA exposure)-photochemotherapy?
psoriasis dermatitis vitiligo cutaneous T cell lymphoma polymorphic light eruption
risks and side effects of PUVA?
burning itching nausea eye damage skin Ca
what can be used as a guide to how much product to apply to a given area of skin?
fingertip unit
how might topical steroid treatment be used in eczema if a patient is suffering recurrent flares?
may use topical steroid on 2 consecutive days each week (weekend therapy) on problem areas to treat subclinical inflammation before it becomes apparent.
*normally, steroid tment in eczema should be to the area of acute inflammation and emollient use for surrounding skin to reduce dryness, and when acute inflammation settles, must encourage pt to continue regular emollient use, as chronic disease with no cure.
features of discoid eczema?
circular, thick and well circumscribed erythematous lesions
plaques usually very itchy
may be misdiagnosed as ringworm-fungal infection (tinea corporis), but this is annular (clearer centrally), with scaly plaques with a characteristic active edge. could do skin scrapings to look for fungal infection (mycology).
in males over 50yrs, what is discoid eczema associated with?
chronic alcoholism
what order should emollients and topical steroids be applied in eczema?
steroids better absorbed if skin been moisturised or washed with a moisturiser beforehand, but can be flexible with regards to pt preference
if moisturise 1st, should leave 30mins before applying steroid so steroid not diluted.
what could be used to treat the itch of eczema?
sedating antihistamines before bed e.g. chlorphenamine
give 2 hrs before go to bed so patient isn’t itching as they go to bed!
treatment of rosacea?
avoid triggers e.g. spicy foods, alcohol, keep face cool, protect face from sun-use high sun protection factor sunscreen
bland emollients to moisturise and wash with, avoid oil-based facial creams
new gel for flushing and red face-mirvaso gel
topical Abx e.g. metronidazole
oral Abx, usually tetracyclines e.g. doxycycline,limacycline, usually for 6-12wks, Abx used for papulopustular rosacea
oral isotretinoin when Abx ineffective or poorly tolerated
laser for fixed erythema (permanent), but erythema may recur a few yrs later
surgery or laser ablation for rhinophyma, need resurfacing of enlarged nose
what advice regarding mediation should be made to patients with atopic eczema who develop a cold sore?
if on topical tacrolimus should be advised to stop it as more at risk of eczema herpeticum and cold sores caused by HSV.
characteristics of eczema herpeticum?
clusters of itchy blisters or punched out erosions and crusting, blisters are monomorphic-all appear similar, may weep or bleed
fever, malaise, lympahdenopathy
eczema herpeticum treatment?
oral aciclovir 5 times daily if apyrexial
IV aciclovir if severe
systemic Abx for secondary bacterial infection and as prophylaxis-BS antibiotic
general supportive measures-IV fluids and antipyretics
ensure early ophthalmological r/v if worried about eye involvement
stop any non essential treatment including topical corticosteroids
treatment of BCC?
surgical excision, with 4mm margin of surrounding normal skin, or with narrower margin using Mohs surgery (uses frozen histological sections at time of surgery)
complete surgical removal is curative, but there is increased risk of other separate BCCs developing in future. should advise pt sun protection with at least SPF 30 sunscreen with high UVA star rating, avoid prolonged sun exposure between 11am and 3pm, wear hat and sunglasses in sunshine and seek shaded areas where can.
potential complications of excising a BCC?
bruising, minor bleeding, swelling, black eye post op
minor discomfort requiring paracetamol
scar-can contract as it heals which can pull on lower eyelid (ectropion) causing a watery eye
risk of more significant bleeding, wound infection, localised numbness around scar and incomplete surgical removal causing a local recurrence.
presentation of bullous pemphigoid?
this is an AI subepidermal blistering disease, which causes a severe itch and usually large, tense bullae (raised clear fluid filled lesion more than 0.5cm in diameter) which rupture forming crusted erosions
bullae appear on erythematous, oedematous plaques rather than normal skin
often in people over 80yrs
how is bullous pemphigoid diagnosis confirmed?
skin biopsy-specimens to be sent for histology and direct immunofluorescence-visble IgG antibodies along basement membrane zone (dermo-epidermal junction).
treatment of bullous pemphigoid?
non-adherent dressings to eroded skin from burst blisters
large intact blisters deflated with sterile needle
topical very potent corticosteroids e.g. dermovate (clobetasol proprionate)
systemic corticosteroids-oral prednisolone
other immunosuppressants e.g. MTX, azathioprine, as steroid sparing.
name given to a fungal infection of the nails?
onychomycosis
dermatological conditions that commonly cause nail changes?
psoriasis
lichen planus
eczema
alopecia areata-nail pitting
what can alopecia areata cause other than hair loss?
nail changes
most commonly=pitting
also brittle nails with vertical ridging and splitting
and onycholysis
RFs for acne?
FH of severe acne
hx suggestive of PCOS e.g. irregular periods, increased BMI, hirsutism
med. hx e.g. anabolic steroid use
frequent use of sauna/steam rooms, or working in hot humid environments e.g. kitchens
ADRs of oral isotretinoin?
dry skin and lips, sometimes eyes and nose-epistaxis
severe birth defects
elevated blood lipids and LFTs
mood disturbance
what advice needs to be given to a pt with SCC?
check for lumps as SCC spreads via lymphatics
checking for new nodule or sores and report them as pt at higher risk of developing subsequent new primary tumours
sun protection
common bacterial cause of infection that precedes guttate psoriasis?
streptococcal-strep throat
how does rosacea progress?
4 stages
initial transient facial flushing with red face and hot and/or burning sensation
permanent redness and later to papulopustular rosacea
permanent redness and swelling e.g. rhinophyma-espec. in men, due to sebaceous gland overgrowth with ongoing inflammation
ocular rosacea-red and sore eyes
what bacteriostatic treatment, also used in leprosy, can be used to treat dermatitis herpetiformis?
dapsone
treatment of female pattern hair loss (FPHL)?
no cure, tment aim to slow or stop progression
minoxidil can be used topically, this dilates small blood vessels which may increase cell proliferation
anti-androgens sometimes tried
hair wigs, hair transplantation
disease has strong genetic predisposition
may be related to androgens
presents with diffuse thinning of hair on scalp, due to increased shedding, reduction in volume, or both.
what is ehlers-danlos syndrome and what features may be apparent on patient examination?
group of inherited disorders, 6 subtypes, which involve a genetic defect in collagen, different collagen involved depending on type e.g. type III collagen reduced or absent in vascular EDS
overall fragile and hyperelastic skin, hypermobile and unstable joints *Beighton score, and fragile tissue and blood vessels.
skin hyperelasticity
skin fragility
epicanthic folds-skin folds between eyes make bridge of nose appear wide
molluscoid pseudotumours-small spongy lumps over pressure points e.g. knees and elbows
nodules
hypermobility
bruising and haematomas after trivial injuries
mitral valve prolapse, aortic regurgitation
eye features-epicanthic folds, blue sclera, lens subluxation, posterior staphyloma-abnormal uveal protrusion through weak point in eyeball due to inflammatory or degenerative weakening of the cornea or sclera, retinal detachments, keratoconus.
treatment options for sarcoidosis?
no treatment-often symptoms non disabling and resolve spontaneously
oral prednisolone
immune-modifying drugs e.g. MTX, azathioprine, hydroxychloroquine or tetracycline Abx which also have non antibiotic properties such as reducing inflammation
topical corticosteroids for eye and skin lesions
cutaneous presentation of sarcoidosis?
erythema nodosum discoid eczema erythema multiforme calcinosis cutis pruritus specific lesions=show granulomas on histology: lupus pernio skin plaques maculopapular eruptions SC nodules (Darier-Roussy disease) scar sarcoidosis
advantage of using immunosuppressive drugs tacrolimus and pimecrolimus as topical agents in atopic eczema over topical corticosteroids?
don’t cause skin atrophy
When might a SCC grow very rapidly in size and so make distinguishment from a keratoacanthoma even more difficult?
In a patient who is immunocompromised e.g. receiving chemotherapy
indications for imiquimod?
solar keratosis
BCC-small superficial
molluscum contagiosum-highly contagious viral infection
different skin types, and importance in management with regards to UV therapy?
type 1=always burns, never tans
2=always burns, sometimes tans
3=sometimes burns, always tans
4=never burns, always tans
in using UV therapy to treat dermatological conditions e.g. psoriasis, eczema, vitiligo, cutaneous T cell lymphoma, lichen planus, the duration a patient is exposed to the UV radiation for and so the amount of light energy they receive is based on their skin type, their response to treatment and the particular condition being treated.
management of lichen planus?
often self-resolving, but can take up to 18 months
tment aimed at keeping often intense pruritus under control, mainstay tment=potent or very potent topical steroids
oral steroid short course can be given if above fails
acitretin, ciclosporin or MTX may be considered for longer term control
phototherapy can also be useful
a patient with PMR is on oral prednisolone, but also suffers from psoriasis, why is it important for his oral steroid dose to be weaned down SLOWLY?
weaning down to quickly can precipitate a severe psoriasis exacerbation, including generalised pustular psoriasis that can cause serious illness and prolonged hospital admission.
management of scalp psoraisis?
de-scaling with emollients, tar based products and salicyclic acid part. good for surface scaling
can also use coconut-oil based compunds
washed off with tar shampoo
topical corticosteroid scalp application also useful, can be combined with a Vit D analogue e.g. as dovobet-calcipotriol and betamethasone, or with salicyclic acid-keratolytic.
what is a dermatofibroma, how does it present?
benign dermal tumour, consisting of a mixture of histiocytes, fibrous tissue and blood vessels, lesion made up of a proliferation of fibroblasts
may follow minor trauma, insect bite
can be itchy
often on lower legs
may appear as well circumscribed pink nodule, commonly central white area surrounded by faint pigment network
lesion firm on palpation and will demonstrate central dimpling when lateral edges are gently pressed
smooth surface-indicative of dermal pathology
treatment often not needed, but may consider excision under LA if itchy, tender or prone to bleeding on trauma
must distinguish from rare malignant variant=dermatofibrosarcoma protuberans-more likely if large size (more than 1cm), rapid enlargement, asymmetry or irregular shape. need wide excision of lesion, including deep fascia.
define an ulcer
break in skin epidermis and dermis
use of imiquimod in BCC treatment?
can be used for low risk superficial BCC as 5% topical cream, applied to lesion and 1cm margin 5 days per week for 6 weeks.
most common malignant skin tumor in white skin?
BCC, often known as ‘rodent ulcer’ due to destruction caused with local invasion if left to grow.
clinical variants of BCC?
nodular-nodule with central depression and rolled edge, surface telangiectasia
morphoeic-flat growth pattern which causes scar-like appearance, can be difficult to know where tumour begins and ends, local invasion more common
superficial-lesions usually solitary, grow for many yrs, can be many cm across, characterisitcally worm like edge, multiple tumours may indicate previous arsenic ingestion
pigmented-usually patchy pigmentation but may be very dark and dense.
can BCCs be hereditary?
yes-rare familial condition of Gorlin’s syndrome
what distinguishes rash of eczema herpeticum (HSV) from that of chickenpox (VSV)?
eczema herpeticum-monomorphic punched out erosions
chickenpox-polymorphic appearance
conditions associated with eczema herpeticum (Kaposi’s varicelliform eruption)?
atopic eczema pemphigus foliaceus Darier's disease cutaneous T cell lymphoma ichthyosis
skin diseases that result from herpes virus infection?
eczema herpeticum-HSV
chickenpox (varicella zoster) and shingles (herpes zoster)-VZV (human herpesvirus 3)
erythema multiforme-HSV
oral herpes-coldsores (herpes labialis if recurrent)-HSV-1 (human herpesvirus 1)
genital herpes-HSV-2
herpetic whitlow if virus inoculated into finger
pityriasis rosea-reactivation of herpes viruses 6 and 7
presentation and treatment of staphylococcal scalded skin syndrome (SSSS)?**
dermatological emergency
blistering disorder caused by exfoliative toxins produced by some types of staphylococci, causing epidermal split at level of stratum granulosum
skin peels away, leaving scalded/burned appearance
give IV Abx-flucloxacillin, IV fluids, good nursing and nutritional care
treatment of erythroderma?
general: keep pt warm-nurse them in warm room
swab skin for secondary bacterial infection
monitor vital signs, serum albumin, keep meticulous fluid balance charts
treat secondary medical problems e.g. heart failure, dehydration and infections
specific: simple emollients and mild topical steroids
biopsy skin to make definitive diagnosis
stop any causative drugs, treat as for underlying cause
e.g. if know psoriasis, start systemic anti-psoriasis treatment e.g oral ciclosporin
4 most important causes of erythroderma?
dermatitis, including allergic contact dermatitis
psoriasis
cutaneous T cell lymphoma
drugs e.g. sulphonamide Abx
examples of dermatological emergencies?
necrotising fasciitis meningococcal septicaemia toxic epidermal necrolysis and stevens-johnson syndrome erythroderma staphylococcal scalded skin syndrome eczema herpeticum anaphylaxis and angioedema
need hospital admission!!
treatment of granuloma annulare?*
usually spontaneous resolution
persistent lesions can be treated with cryotherapy or intralesional triamcinolone (synthetic corticosteroid long acting)
could also consider imiquimod or topical calicineurin inhibitors
localised tends to clear up within a few mnths or years
widespread may require systemic therapy e.g. oral steroids or MTX
cutaneous manifestations of diabetes?*
certain cutaneous infections neuropathic ulcer necrobiosis lipodica diabetic dermopathy acanthosis nigricans xanthomas diabetic bullae lipoatrophy cheiroarthropathy
acquired causes of scalp hair loss?
diffuse hair loss with normal scalp skin: thyroid disease Fe deficiency drugs e.g. chemotherapy SLE alopecia totalis
androgenetic alopecia
circumscribed hair loss with normal scalp skin:
alopecia areata
traction
trichotillomania-compulsive plucking of hair
hair loss with abnormal scalp skin:
without scarring-seborrhoeic dermatitis, severe psoriasis, tinea capitis
with scarring-discoid lupus erythematosus
lichen planus
lupus vulgaris
tment of tinea capitis?
fungal infection of scalp
always treat with oral antifungals-terbinafine tablets for adults/older children, griseofulvin suspension for younger children
consider combining with topical antifungal shampoos and creams
management of impetigo?
swab crusted plaques for microbiology
topical fusidic acid (fucidin), or mupirocin, or retapamulin if localised infection
oral flucloxacillin or erythromycin indicated in treatment of more extensive infection
regular greasy ointment application to soften crusted lesions
ensure good personal hygiene measures to prevent cross infection to other body sites or people e.g. use separate towels and antiseptic containing soap substitute.
factors predisposing to impetigo?
immunocompromised atopic eczema scabies head louse infection skin trauma-insect bite, thermal burn, chickenpox, abrasion, surgical wound
what feature is highly characteristic of pemphigus, and what is the only other disease in which this occurs?
nikolsky sign: skin at edge of blister slides off when pushed with a finger or picked up with forceps
also occurs in toxic epidermal necrolysis
commonly 1st used treatment in acne vulgaris?
Benzoyl peroxide-topical application, keratolytic and antibacterial
2 clinical forms of impetigo?
bullous and non-bullous
non-bullous= caused by s.aureus, streptococci or both
bullous=s.aureus
what might streptococcal impetigo be associated with?
poststreptococcal acute glomerulonephritis
what can be said about the pathology of a skin lesion if there is scaling present?
disease involves the epidermis
name given to a skin lesion that has been self-inflicted?
dermatitis artefacta
co-morbid conditions associated with psoriasis?
metabolic syndrome, CVD-psoriasis is an independent RF for CVD
chronic alcoholism
psychological implications, more susceptible to depression
complications of psoriasis?
erythroderma-more than 90% of skin surface inflamed
acute pustular psoriasis
why is erythroderma (although not a disease entity in itself) a dermatological emergency?
risk to life from fluid imbalance that can cause pulmonary oedema and ARDS, loss of ability to thermoregulate and susceptibility to infection
fluid imbalance: massive blood flow to the skin plus loss of water from skin surface so systemic hypotension and reflex tachycardia, presents like sepsis
thermoregulation: disruption due to loss of skin barrier
infection: again due to loss of skin barrier functioning
role of Vit D analogues in psoriasis?
indicated following emollient use-regular daily moisturising, salicylic acid containing products
examples-dovonex (calcipotriol)
good for long term use in psoriasis but can worsen severe psoriasis and erythroderma
can be combined with topical steroid e.g. dovobet ointment-calcipotriol and betamethasone
why are ointments generally preferred as topical treatment in dermatology?
they stay on the skin for longer
what other than strep throat can precipitate guttate psoriasis?
stress
features on examination of a patient suggestive of treatment with oral ciclosporin?
resting tremor
gum hypertrophy
hirsutism (androgen dependent hair growth)
which patients should oral acitretin (retinoid) e.g. in treatment of chronic plaque and palmoplantar pustular psoriasis, NOT be given to?
pre-menopausal women as patients must wait at least 3 years post stopping oral acitretin before safe to become pregnant
causes of atopic eczema exacerbations?
infection allergens-chemicals, food, dust, pet fur cold weather-skin dry heat sweating stress
what advice should be given to parents regarding emollient use and general treatment measures for a child with atopic eczema?
in scooping emollient out from tub e.g. hydromol, use a spatula rather than their own hands as we are colonised with staph. bacteria so this could cause stap skin infection e.g. impetigo in the child
cut the child’s fingernails to stop excoriations occurring when the child is sleeping
topical corticosteroid can be applied, even to the face, safely, although should be used for a shorter duration than in psoriasis, may consider eumovate for the face, or 1% hydrocortisone once it improves, and betnovate for the body, may use for 5 days, then slowly reduce the steroid use, or if recurrent flares can consider maintenance therapy where topical steroid just givn twice a week at the weekend
sedating antihistamine e.g. hydroxyzine or chlorphenamine to stop child scratching eczema at night
may then consider topical calcineurin inhibitor e.g. tacrolimus or pimecrolimus-should warn that this will initially sting for 1st few days up to a week, use BD for 6 weeks, then OD and then consider maintenance dosing
LT risk associated with topical calcineurin inhibitors?
skin cancer
what ADRs should be examined for in patients using regular topical corticosteroids?
skin bruising striae telangiectasia atrophy especially in the flexures
what would a pustule swab reveal in pustular psoriasis?
sterile pustules
how can cellulitis be differentiated from erysipelas?*
cellulitis=bacterial infection of subcutaneous tissues, so 360 degrees involvement and poorly circumscribed
erysipelas-superficial streptococcal cellulitis, involves superficial dermis, well circumscribed
treatment of viral warts?
cryotherapy
topical salicyclic acid
topical imiquimod if multiple
describe the appearance of viral warts
piloform (follicular)?
Plantar warts-thickened skin with black dots-thrombosed capillaries, frequently painful, contrast to uniform thickened patches seen with calluses and painful central keratin plug seen with corns.
treatment required if nail involvement in tinea pedis?
oral antifungal e.g. terbinafine, topical antifungal will not treat nail involvement
what blood monitoring is required with terbinafine treatment (oral antifungal)?
LFTs-can become deranged
name given to an abscess formed by a fungal infection, that can present as an inflamed, thickened, pus filled area, commonly on the scalp?
kerion
what part of the body should always be inspected in case of suspected fungal infection?
feet!-espec. in between 4th and 5th toes
usual bacterial cause of cellulitis?
streptococcus pyogenes
RFs for cellulitis?
break in skin barrier e.g. dermatitis, minor abrasion, fissures in between toes assoc. with tinea pedis, trauma, surgical wounds, radiotherapy leg ulcers leg oedema previous cellulitis episodes obesity DM alcoholism pregnancy
tment of choice in presumed streptococcal cellulitis?
IV benzylpenicillin
when might cellulitis prophylaxis be considered?
in patients with recurrent episodes of cellulitis, each damaging lymphatics and causing further oedema
treat with oral phenoxymethylpenicillin (penicillin V)
or oral erythromycin
how does folliculitis differ from furunculosis (boils) and carbuncles?
folliculitis=superficial infection of hair follicle, vs. deep infection in furunculosis vs. deep infection of group of adjacent hair follicles in a carbuncle
all S.aureus infection
if recurrent boils, should swab nose for culture, and if found to be staph carrier, given topical Abx e.g. mupirocin, could also have antibacterial bath additive, and prolonged flucloxacillin course.
carbuncles often nape of neck, associated with DM and debility in middle aged and elderly men, treat with flucloxacillin
cause of warts?
HPV
characteristic appearance of shingles (herpes zoster)?
unilateral band of grouped vesicles on an erythematous base, in a dermatomal distribution most commonly on thorax or abdomen
may affectany branch of trigeminal nerve, most commonly ophthalmic
vesicles on side of nose (Hutchinson’s sign) indicate nasociliary branch of ophthalmic involvement, causing conjunctivitis, keratitis and/or iridocyclitis
due to reactivation of VSV in dorsal root ganglia
eruption may be preceded by pain in region of dermatome
vesicles dry up within a few days and form crusts
what is most problematic about shingles?
persistence of pain after lesions have healed (postherpatic neuralgia)
management of vitiligo?
phototherapy-probably carries best chance of success in case of vitiligo of the hands
topical treatment with potent/very potent corticosteroids, or tacrolimus ointment
offer skin camouflage cream to disguise the changes
management of fungal infection of a nail (onychomycosis/tinea unguium)?
prolonged ORAL antifungal treatment-terbinafine 6 wks for fingernails and 12 wks for toenails
name given to fungal infection of hand?
tinea manuum
name for fingal infection of foot?
tinea pedis
most likely allergen in allergic contact dermatitis due to hair dye?
PPD-paraphenylenediamine
what is auspitz sign?
in psoriasis, name for scratch and gentle removal of scales causing capillary bleeding
complications of acne vulgaris?
post-inflammatory hyperpigmentation
scarring
deformity
psychological and social effects
characteristic name for lesions seen in guttate psoriasis?
raindrop/teardrop lesions
precipitating factors in psoriasis?
trauma-*koebner phenomenon infection e.g. tonsillitis-strep throat-guttate psoriasis stress alcohol drugs e.g. lithium, antimalarials
aetiology of acne vulgaris?
androgens
contributing factors-increased sebum production, abnormal follicular keratinisation, bacterial colonisation (propionibacterium acnes) and inflammation
most common dermatophyte infection?
tinea pedis (athlete’s foot)
clinical picture of tinea cruris, and what location of the body should always be examined?
scaly, erythematous margin spreading gradually down medial aspects of thighs, commonly in men
may extend backwards to involve buttocks and perineum
patient’s feet to be examined: nearly always infection source!
what can fungal scrapings be examined for under microscopy?
hyphae, which form a branching network in vegetative phase of dermatophyte fungi
how can tinea capitis be diagnostically confirmed from seborrhoeic dermatitis?**
microsporum canis, the most usual cause, fluoresces yellow-green under long wavelength UV light (Wood’s light
oral antifungals available for treating nail fungal infections, and tinea capitis?
terbinafine
itraconazole
how can severity of an itch be assessed in hx?
does it affect sleep?
does it interfere with work or school?
how is a skin surface described if it appears softened due to constant wetting?
maceration
clinical features of a seborrhoeic keratosis?
appears 'stuck on' white warty surface, white dots under dermatoscope-milia like cysts often pigmented, can be pink cerebriform appearance greasy surface small surface pits and irregularities follicular plugging papillomatous appearance-elevated and bumpy surface
can be left but can treat with cryotherapy e.g. if itchy or catching on clothing or becomes inflamed
how are freckles (ephelides) different from lentigines?
both benign melanocytic tumours
freckles=normal number of melanocytes but hyperresponsive to UV radiation, fade in winter mnths
lentigines=flat pigmented areas composed of increased numbers of melanocytes
most common location of a dermatofibroma (benign dermal tumour comprising proliferation of fibroblasts)?
skin of lower legs
what is an angioma e.g. Campbell de morgan spot?
collection of aberrant blood vessels within the dermis and/or SC tissues
presentation and tment of a pyogenic granuloma?
this is a benign reactive inflammatory mass composed of b.vessels and fibroblasts
erupts rapidly, usually polypoid appearance and a ‘collar’ around base
profuse contact bleeding common
often on site of an injury or infection, often digit
removal by curettage or excision, follow with histology as must distinguish from SCCs and amelanotic melanomas
common location of granuloma annulare?
dorsum of hands and feet
presentation of granuloma annulare?
smooth, discoloured, often annular plaques
occur in children, teenagers or young adults more commonly
SC granuloma annulare presents as rubbery lumps that appear similar to rheumatoid nodules but occur commonly in children without RA
result of delayed hypersensitivity reaction to some component of the dermis
localised disease assoc. with AI thyroiditis although does not clear up with thyroid replacement, extensive disease can be assoc. with HIV, lymphoma, solid tumours, DM and hyperlipidaemia.
most common cutaneous drug reactions?
exanthematic eruptions=itchy widespread, symmetrical erythematous and maculopapular, most often begins a few days after starting the drug e.g. NSAIDs, Abx part. ampicillin, other semisynthetic penicillins, sulphonamides and gentamicin.
drugs that can exacerbate psoriasis?
lithium
antimalarials
LT problems of SJS/TEN?
pigment change
skin scarring
nail loss with permanent scarring (pterygium) and failure to regrow
scarred genitalia-phimosis and vaginal adhesions
joint contractures
lung disease-bronchiolitis, bronchiectasis, obstructive disorders
eye problems-conjunctivitis, corneal ulcers, opacities and scarring, trichiasis, synechiae-iris sticks to cornea. can cause blindness.
how is a distinction made between SJS and TEN?
SJS=less than 10% of body skin surface involvement
TEN=more than 30% of body’s skin surface involved
differences between bullous pemphigoid and pemphigus?
pemphigoid=subepidermal blisters, IgG deposition on immunofluorescence at dermo-epidermal junction, more common, typically adults over 50, commonly over 80yrs
importance of a gluten free diet in dermatitis herpetiformis?
reduce risk of developing non-hodkin’s lymphoma
maximum wkly dose of methotrexate in treatment of psoriasis?
30mg
how can liver fibrosis be monitored for in patients taking methotrexate for psoriasis?
blood test-serum type III procollagen peptide (PIIINP)
fibroscan of the liver
what medical management is good for patients with excessive scaling psoriatic disease?
salicylic acid- can be combined with potent steroid betnovate in diprosalic treatment
tar based products including tar based shampoos, and the use of dithranol, are good for excessive scaling, but tar is messy and stains, and dithranol stains and causes burning, these are less commonly used now
Treatment of pityriasis versicolor?
Topical antifungals e.g. imidazaole antifungal creams, topical terbinafine, ketoconazole shampoo
Can use selenium sulfide in form of shampoo left on skin for few mins during bathing
Oral itraconazole alternative
Tment may need repeating as tends to recur
Hypo pigmented areas can take a while to repigment
why does the term versicolor fit with the clinical presentation of pityriasis versicolor?
presents differently in people of different skin colour: often as brown macules in fair skinned individuals, and as hypopigmented areas in dark skinned individuals.
what are cherry angiomas also known as?
Campbell de Morgan spots
drugs which can cause lichen-planus like skin eruptions?
gold
hydroxychloroquine
some beta blockers
sulfonylureas
what is acitretin, how does it work?
acitretin is a retinoid-a synthetic analogue of Vit A
it brings about normalisation of epidermal cell proliferation, differentiation and keratinisation, without suppressing immune system function.
what oral retinoid can be given for the treatment of severe chronic hand eczema following failed treatment with potent topical corticosteroids?
alitretinoin
if eczema has predominantly hyperkeratotic features than more likely to respond than if frequent presentation with pompholyx-rapid bullae development.
what is hidradenitis suppurativa, how is it treated?
chronic, relapsing inflammatory disease affecting apocrine gland bearing skin in axillae, groins, and sub mammary area
recurrent boil like nodules, abscesses, sinus tracts
often concurrent severe acne, or had acne in the past
smoking, obesity, metabolic syndrome, FH, crohn’s disease are all RFs
medical management: topical Abx e.g. clindamycin, with benzoyl peroxide, oral Abx-short course for acute staph abscesses e.g. flucloxacillin, and prolonged courses e.g. tetracyclines. also antiandrogens, and/or isotretinoin, but may require plastic surgery.
what drug use is associated with perioral dermatitis?
topical steroid abuse
ichthyosis, a disorder of keratinization presenting with extremely dry and scaly skin, is often inherited but if acquired, what disease might we be worried about?
lymphoma
acquired ichthyosis can also be a manifestation of AIDS, renal failure, sarcoidosis, malnutrition and leprosy.
characteristic presentation of neurofibromatosis 1 (von Recklinghausen’s disease), a form of neurofibromatosis, both of which autosomal dominant inheritance?
multiple café au lait patches
axillary freckling (crowe’s sign)
numerous neurofibromas
lisch nodules-pigmented iris hamartomas
also assoc with scoliosis, increased risk of IC neoplasms e.g. optic nerve glioma, increased HTN risk assoc with phaeochromcytoma or fibromuscular hyperplasia of renal arteries.
in contrast NF 2 does not have significant cutaneous manifestations, but is characterised by bilateral acoustic neuromas/vestibular schwannomas, and other CNS tumours.
presentation of dermatitis herpetiformis?
symmetrical distribution of VERY itchy papules (prurigo) and vesicles on normal or erythematous skin, so often presents as erosions and crusting due to immediate scratching, found on elbows, knees, scalp, shoulders and buttocks.
what is as true sebaceous cyst?
a fluid collection due to blocked sebaceous gland, producing a cyst with a central punctum-sebum collection.
removed surgically if very large, prone to infection, causing the patient irritation.
define the pathology of erythema nodosum
inflammation of the SC fat
