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.
