9630942363 Genuine Call Girls In Ahmedabad Gujarat Call Girls Service
Dermatology revision book
1. Dermatology 101
A dermatology revision guide for Birmingham medical students
Dr. Kalaprapa Asavisanu (FY1)
University of Birmingham
MBChB
Updated: February 2018
1
2. 2
Green boxes--‐ TIPS
Text in red/in red boxes --‐ common themes for OSCES
and MCQs
About this guideline
This booklet is aimed at 4th year medical students at the
university of Birmingham as a summary of the dermatology
curriculum.
The purpose is to prepare students for the MCQs, OSCEs and
work as junior doctors.
Disclaimer: This booklet does not represent the University of
Birmingham,any of the west midlands foundation trusts or the
British association of dermatologists. The views expressed in
these lectures are of the author only.
4. 4
History taking
Presenting complaint:
--‐ Site
--‐ Symptom
--‐ Duration
--‐ Associated symptoms e.g. pain, swelling, discharge, itch
--‐ Evolution of Sx – was it like this at the start?
Past medical history:
--‐ Past skin problems
--‐ Atopic triad: hay fever, eczema, asthma
Family history:
--‐ Skin cancer
Drug history:
--‐ Current meds
--‐ What have they tried
Social history
--‐ How isthis affecting their QoLe.g. confidence, clothes they wear,wherethey
go.
--‐ Sun bed, do they burn
--‐ Job – skin better whenaway?
Examination (Inspect, palpate, systematic
check)
Inspect
‘SSCAMM’
Site, Size, color, associated secondary features, morphology,
margins.
Palpate
‘Skin conditions must be touched tenderly’
Surface, consistency, mobility, tenderness, temperature
Systematic check: hair, nails, mucous membranes
If lesion pigmented:
ABCDE: Asymmetry, irregular border, ≥2 colors, diameters > 6 mm
Just describe
what you
see/feel!
And fill the gaps
with SSCAMM/Skin
conditions must be
touched tenderly--‐
Because sometimes
it takes longer to
remember the
pneumonic!
Dermatology
OSCE’s tend to
be history
taking stations.
Get a good
STORY.
And don’t forget
your ICE!
History and examination
5. 5
General terms
• Puritis– itchy (scabies, eczema, urticaria, lichen planus)
• Lesion – area of alteredskin
• Rash--‐ eruption (drug rash)
• Naevus – localized malformation of skin tissue
• Comedone – sebaceous follicle plug with sebum, bacteria + cellular debris.
(Can be open or closed = open: blackheads, closed: whiteheads)
Site
• Generalized--‐ all over body (scabies, chickenpox)
• Widespread--‐ extensive (drug eruption)
• Localized--‐ just one area of skin (burns)
• Flexural – body fold e.g. groin, popliteal, antecubital fossa (eczema)
• Extensor– knees, elbows, shins (psoriasis)
• Pressure areas – sacrum, buttocks, ankles, heels (pressure sores)
• Dermatome--‐ area supplied by a spinal nerve (shingles)
• Photosensitive--‐ sun--‐exposed areas e.g. face, neck (sunburn)
• Koebner--‐ linear eruption at site of trauma
(psoriasis)
Morphology
• Discrete--‐ separate lesions
• Confluent--‐ lesions merged
• Linear--‐ in line (scabies)
• Target--‐ dartboard rings (erythema multiforme)
• Annular--‐ circles (tinea)
• Discoid/nummular--‐ coin shaped (discoid eczema)
Color
• Erythema--‐ red – blanches on pressure – due to inflammation + vasodilation
(palmar erythema)
• Purpura--‐ red due to bleeding into skin/mucous membrane – DOES NOT
blanch on pressure (can be petechiae – small pinpoint macules or
ecchymoses--‐ larger bruise--‐like patch) –HSP, meningococcal septicaemia
• Hypopigmentation--‐ area of paler skin (pityriasis versicolor)
• De--‐pigmentation--‐ white skin due to no melanin (vitiligo)
• Hyper--‐ pigmentation – darker skin (post--‐ inflammatory changes in acne,
malaema )
Dermatology terminology
6. 6
Morphology
• Macule – small flat area < 5 mm (freckle)
• Patch – large flat area > 5 mm (port--‐wine stain)
• Papule--‐ small raised lesion < 5mm (xanthomata)
• Nodule – large raised round lesion > 5 mm (pyogenic granuloma)
• Plaque--‐ large raised area with flat top > 5 mm (psoriasis)
• Vesicle– small clear fluid filled lesion < 5 mm (chickenpox, pompholyx)
• Bulla – large fluid filled lesion > 5 mm (bullous pemphigoid, insect bites)
• Pustule– small pus filled bubble < 5 mm (acne)
• Abscess--‐ localized area of pus (paronychia)
• Wheal – raised area of dermal oedema
• Boil/furuncle – staph infection within a hair follicle
• Carbuncle--‐ multiple boils/furuncles
• Excoriation– loss of epidermis from trauma (scratching in eczema)
• Lichenification – well--‐defined toughened skin with accentuation of skin
markings
• Scales--‐ thick flakes of the top layer of the skin (psoriasis)
• Crust--‐ rough area of dried serum, blood, bacteria + cellular debris (impetigo)
• Scar--‐ new fibrous tissue can be: atrophic (thinning), hypertrophic
(hyperproliferation WITHIN wound boundary), keloid (hyperproliferation
BEYOND wound margin)
• Ulcer--‐ loss of epidermis and dermis, heals with scar (leg ulcers)
• Fissure – epidermal crack (eczema)
• Striae – linear areas which change from purple--‐ pink--‐ white (pregnancy,
growth spurts, steroid side effects)
Hair
• Alopecia--‐ hair loss (apolecia areata)
• Hirsutism – androgen--‐ dependent hair growth in a female (PCOS)
• Hypertrichosis--‐ non--‐androgen dependent pattern of excess hair
(hypertrichosis)
Nails
• Clubbing--‐ loss of angle between nail fold and nail plate (CF, bronchiectasis,
SBE, cyanotic heart diseases,IBD)
• Koilonychia – spoon--‐ shaped nail (iron def, congenital, idiopathic)
• Onycholysis--‐ nail separating from nail bed (trauma, psoriasis, fungal nail
infection, hyperthyroidism)
• Pitting--‐ depressions in nail plate (psoriasis, eczema, alopecia areata)
7. 7
Common MCQ
questions about side
effects/monitoring
of treatment
1) ECZEMA
1) Atopic eczema
Risk factor: family history (atopic triad: eczema,
asthma, hay fever).
Strong genetic cause. 90% +ve for family history.
Symptoms: itch, weep/crust/scaling lesion that is not well demarcated, sleep
disturbance/bleeding/ lichenification (prominent skinmarkingsduetochronic
scratching) on flexural areas.
Diagnosis: clinical
Treatment:
Eczema patient education:
1) Education: explain to patients that the natural
history is relapse--‐ remission. It will come and
goanditisnottheirfault.Complications:
infection + what to do (Abx). Prognosis: for
childhood eczema--‐ most people will grow out of it.
90% by teens.
2) Explain: that treatment is a control not a cure. Show
the two--‐tier approach.
3) Empathy: psychologicalsupport.
Avoid exacerbating agents.
Atopic eczema
Source: DermNet NZ
Liberalemollients. Soap substitutes,bathoils. –regular treatment whetherskinis
good/bad.
Topical therapies: topical steroids for flares, topical
immunomodulators (e.g. tacrolimus, pimecrolimus)--‐ steroid
sparing agents.
Oral therapy--‐ oral steroids, oral immunomodulators e.g.
ciclosporin (Monitor BP and renal function), azathioprine (Check TPMT and
LFT).
Other:antihistamine foritch, antibiotics e.g.flucloxacillin for secondarybacterial
infection,
Eczema: common OSCE
history taking station
which involves patient
counseling
Inflammatory skin conditions
8. 8
Emollients (Try to use as greasy as possible):
V greasy: epaderm
Greasy: hydrous ointment
Moderate: diprobase, double base.
Light: aveeno, E45.
Steroid (use for flares--‐ try to use as low potency as possible)
Mild: 1--‐2.5% hydrocortisone
Moderate:eumovate
potent: betnovate, elocon
v potent:dermovate.
Complication: infection (crusty/weeping lesions), eczema herpeticum (tx: aciclovir)
Oralsteroidss/e:HTN,growthsuppression, osteoporosis, GIulceration,mood
swings. Insomnia, acne, weight gain, DM, cushing’s syndrome.
Topical steroids s/e: skin thinning, infections, telangiectasia, straie, easy bruising
2) Discoid eczema--‐ a nummular dermatitis.
Discoid eczema
Source: DermNet NZ
3) Seborrheic eczema/dermatitis--‐ esp
young adults. M>F. diagnosis is based on
characteristicdistribution: sideof nose,forehead,
eyebrows,scalp, behind ears. (classic is red,flaky
lesions on side of nose)
Tx: anti--‐yeast e.g. ketoconazole
Seborrhiec dermatitis
Source: DermNet NZ
9. 4) Contact dermatitis – 2 types: 1) allergic 2)
irritant
I) Allergiccontact dermatitise.g.nickelisthe
most common causee.g. ear rings,watches.Ifthe
eczema is in a strangedistribution e.g. shape of a
belt,watch think allergic contact dermatitis.
Diagnosis: patchtesting.(type4hypersensitivity reaction).
NOT skin prick. Skin pricksarefor type1 hypersensitivity
reaction for things like food allergies.
II) Irritant contact dermatitis--‐ e.g. constantly
washing hands. No test,diagnosis basedon
history e.g. hair dressers,surgeons, chefs.
5) Venous eczema – usually elderly lower leg
due to venoushypertension.
Treatment: compression stockings.
6) Pompholyx eczema--‐ blisters in hands and
feet that is intensely itchy usually in summer +
winter months.
Allergic contact dermatitis
Source: DermNet NZ
Irritant contact dermatitis
Source: DermNet NZ
7) Asteatotic eczema--‐ in elderly people in lower legs, looks like a
cracked riverbed. Tx:moisturizer.
Treatment: moisturizer.
8) Photosensitive eczema--‐ sun induced
eczema.Only seein sunexposedareas.Sparing
under neck, under nose.
Venous eczema +
lipodermatosclerosis
Source: DermNet NZ
Pompholyx eczema
Source: DermNet NZ
Asteatotic eczema
Source: DermNet NZ
9
11. 11
3) Psoriasis
Chronic inflammatory skin disease due to keratinocyte hyperproliferation.
1) Chronicplaquepsoriasis (mostcommon type)–
Symptoms: symmetrical red, well circumscribed, scaly plaques.
Treatment:
Topicaltherapy:vitamindanalogue (calcipotriol, calcitriol), topical corticosteroids,
coal tar, topical retinoids
Phototherapy (extensive disease)--‐ e.g. PUVA
Oral therapy (extensive, severe psoriasis)--‐ methotrexate, ciclosporin.
Biologics--‐ infliximab, etanercept
50% of patients have nail changes. 15% have arthritis.
Auspitz sign--‐ scratch--‐ get pinpoint bleed.
Extra--‐dermatological signs: nails: pitting, onycholysis, subungal hyperkeratosis, oil
drop sign,
S/E of treatment:
Methotrexate: hepatotoxicity, neutropenia
Ciclosporin; HTN, nephrotoxicity
PUVA: skin cancer, photoaging
Acitretin: hyperlipidaemia, dry skin, teratogenic
Scoring for severity of psoriasis: PASI
Other types of psoriasis:
2)Guttate psoriasis(raindrop lesions usually
on the back)
Salmon colored paint drop. 2 weeks post--‐
streptoccoccal throat infection. In children it is
usually self--‐limiting. 40% will go on to develop
chronic plaque psoriasis. Tx: can use UV light,.
Guttate psoriasis
Source: DermNet NZ
Common MCQ
questions about side
effects of treatment
12. 12
3)Erythrodermic psoriasis--‐ derm emergency--‐ skin extensively red. Get
high output cardiac failure +dehydration (moredetail see‘erythroderma’ section).
4) Palmoplantar pustular psoriasis--‐ yellow sterile
pustules on palmes and soles.
Tx: Bed rest. Bland emollients e.g. 50:50.
Other types:Seborrheic(usually onnasolabial fold, behind ears),flexural.
Psoriasis is associated with:
--‐ ocular inflammation: iritis/episcleritis
--‐ IBD
--‐ Psoriatic arthritis (classically DIP)
--‐ Nail psoriasis (40--‐50%)
--‐ Metabolic syndrome: DN, hyperlipidaemia, HTN, high BMI, MI.
--‐
Patient counseling: control not cure. Lesions are not contagious.
Chronic plaque psoriasis
Source: DermNet NZ
Chronic plaque psoriasis
Source: DermNet NZ
Chronic plaque psoriasis on the
elbow
Source: DermNet NZ
Palmoplantar pustulosis
Source: DermNet NZ
13. 13
Epidermis lesions
1) Seborrheic
keratosis--‐
--‐ often trunk. After 40 years. Often
multiple. Stuck on cornflake
appearance.
Treatment: leave it alone. Can
remove for cosmetic reasons but
not available on NHS.
Seborrhoiec keratosis
Source: DermNet NZ
Seborrhoiec keratosis
Source: DermNet NZ
Melanocyte lesions
2) Melanocytic naevi akamoles--‐ most common benign skin lesion.
Generally after puberty + early life.
3types:1)junctional (flat pigmented macule) 2)compound (warty pigmented
papule/nodule) 3) Intradermal: skin colored papule
Other types of nevi: blue naevi, halo naevi.
If any doubt about moles it should be excised for histology.
Junctional naevi--‐ flat mole
Source: DermNet NZ
Intradermal naevi--‐ skin
colored papule/nodule
Source: DermNet NZ
Compound naevi--‐ warty--‐
pigmented
papule/nodule
Source: DermNet NZ
Benign skin tumors
14. 14
Hair follicle lesions
3) Epidermoid cyst--‐ central punctum. Can be excised
under LA for cosmetic reasons.
Blood vessel lesions
4) Angioma--‐ aka campbell de morgan spots aka
cherry angioma–acquiredovergrowthofcapillaries.
No tx neededbut can belasered off or cauterized.
5) Pyogenic granuloma – lobular proliferation of
BV.Localized traumaoftenatrigger.Surgical removal
usually by curettage and cautery. Sample must be
submitted for histology as appearance can mimic a
melanocytic and non--‐pigmented melanoma.
6) Telangiectasia – dilated BV of central arteriole and
surrounding capillary network. Increase in pregnancy.
Treat: laser for cosmetic reasons.
7) Capillary hemangioma (strawberry
naevus) – most common benign tumor in infancy.
Nearly all resolve over severalyears.
Epidermoid cyst--‐ note the
characteristic central punctum
Source: DermNet NZ
Cherry angioma (can mimic
nodule melanoma)
Source: DermNet NZ
Pyogenic granuloma
Source: DermNet NZ Telangiectasia
Source: DermNet NZ
Capillary hemangioma
Source: DermNet NZ
15. 15
Fibroblast lesions:
8) Dermatofibroma--‐ firm nodule in dermis.
Most often occur after insect bite. Treatment:
none--‐ needed if diagnosis in doubt can do excision
biopsy. (theskin dimples on pinching thelesion)
9) Keloid--‐ fibrous tissue overgrowth BEYOND the
site of trauma. Treatment: occlusive dressing
with silicone, steroid cream/tape/injection. E.g.
triamcinolone.
10) Hypertrophic scar--‐ fibrous
overgrowth WITHIN the scar boundaries.
Dermatofibroma
Source: DermNet NZ
Pinching of a dermatofibroma causes
skin to dimple
Source: DermNet NZ
Hypertrophic scar--‐
hypertrophy stays within
wound margins
Source: DermNet NZ
Fat lesions
11) Lipomas--‐ v common, slowly growing,
doughy feeling subcutaneous nodules.
Commonly in: shoulder, neck, trunk, arms.
Can be surgically excised under LA.
Sebaceous gland lesions
12) Sebaceous adenoma – benign
overgrowth of sebaceous glands.
13) Sebaceous gland hyperplasia--‐
common in middle age/elderly people--‐ soft yellow,
domed papulesusually on theface.Treatment:none
needed but can be flattened with gentle cautery.
Keloid scar--‐ hypertrophy
extends beyond wound margins
Source: DermNet NZ
Sebaceous gland hyperplasia
Source: DermNet NZ
16. 16
1) BCC(most common type of skin cancer)
Most common skin cancer. Mets is v rare.
Risk factors: UV exposure, sunburn, family history,
immunosuppression.
Presentation/types
Nodular (most common)--‐ pearly nodule with telangiectasia.
On temple, nose.
Superficial (plaque--‐ like)--‐ esp on back + limbs e.g. radiotherapy to spine for
lymphoma can get lesions on back.
Cystic, morphoeic , keratotic, pigmented.
Classical presentation: pearly nodulewith telangiectasia. (but may benecroticor
ulcerated with a pearly rollededge).
Treatment
Surgical (mainstay)--‐ excision margin 4 mm (if tumor ≥2 cm then 6 mm margin)
MoHs – for high risk recurrent tumors.
Radiotherapy when surgery not appropriate e.g. frail, elderly.
Small, low risk lesions – cryotherapy, curettage, cautery, imiquimod cream.
Curettage + cautery/ topical therapy like imiquimod--‐ only in small + superficial
lesions.
High risk tumors: on eye, nose, lips, nasolabial fold, ear, ≥2 cm diameter, ill--‐defined,
immunosuppressed, infiltrative, recurrent/incompletely excised.
Follow up: low risk tumors don’t need to be followed--‐ up. Follow up tailored to
clinical picture.
Nodular BCC
Source: DermNet NZ
Nodular BCC
Source: DermNet NZ
Nodular BCC
Source: DermNet NZ
Skin cancers:
common OSCE
stations
Skin cancers
17. 17
Superficial BCC
Source: DermNet NZ Morphoeic BCC
Source: DermNet NZ
2) Solar keratosis/actinic keratosis (pre--‐cancerous
lesion) – 10% becomeSCC
Risk factors: fair skin, outdoor job, old age.
Presentation:scaly rough patches on aredbackground often on head,tip of
ear, back of hands. Feels like sandpaper.
Treatment: prevention: hats, sunscreen.
Cryotherapy, 5--‐ fluorouracil cream, imiquimod, curettage + cautery and
excision.
Actinic keratosis
Source: DermNet NZ
Actinic keratosis
Source: DermNet NZ
18. 18
3) Bowen’s disease (SCC insitu)
Fixed, non--‐itchy erythematous patch of skin often slightly
scaly on the lower legs of elderly women. Can be
mistaken for patches of eczema/psoriasis.
Treatment: 5--‐ fluorouracil, cryotherapy,
imiquimod.
Actinic keratosis
Source: DermNet NZ
4)Keratoacanthoma
Variant of SCC.
Fleshy basewithkeratinplug. Treatedthesameway asSCCs.
(see below)
Actinic keratosis
Source: DermNet NZ
Common MCQ
question
19. 19
5) SCC(secondmost common typeof skin ca)
Risk factors: UV exposure, pre--‐malignant conditions (e.g. AKs),
immunosuppression, family history, chronic inflammation (e.g. leg ulcers).
Presentation: ill defined nodule, ulceration, keratotic.
Mets uncommon but highest in poorly differentiated tumors esp on high risk sites
e.g. lip, tongue, ear, or if it occurs in areas of chronic ulceration/scarring.
Important topalpate how deepthe lesion is becausemay extenddownwards.
Management
Surgery (mainstay)--‐ 4 mm margin (if tumor ≥2 cm then 6 mm margin)
MOHs--‐ for high risk lesions--‐ large, recurrent/ or where margins may be technically
difficult to achieve or are indistinct.
Radiotherapy--‐ for those not suitable for surgery e.g non--‐resectable tumors.
High risk:perineuralinvasion, >20mm,vertex,ears, backgroundofbowens.
SCC follow--‐up:
Low risk at 3months and discharge if no signs of recurrence.
High risk: follow up for 2 years at 3--‐month intervals
SCC
Source: DermNet NZ
High risk SCC
Source: DermNet NZ
SCC
Source: DermNet NZ
20. 2
0
6)Mycosis fungoides
T cell lymphoma of skin.
Presentation; scaly, erythematous, atrophic
skin +/--‐ depigmentation.
Prognosis: very good. The majority of
patients have normal life expectancy.
Stagedaccording todegreeofskin,LN+
haematological involvement.
Treatment: moisturizer, topical steroids,
phototherapy (lesions very sensitive to
light).
For more extensive disease may need radiotherapy or chemo.
Mycosis fungoides
7) Malignant melanoma Source: DermNet NZ
Riskfactors:UVexposure,peoplewhoeasily burn(skintypeIandII),multiple
moles, family history.Phenotype:think red/blonde hair/freckleswithfair skin.
Presentations: ABCDE (asymmetry, irregular borders, more than 2 colors,
diameters>6mm,quick growth/evolutionoflesion). NEW andCHANGINGarekey
features.
*old moles tend not to become melanomas.
Types
Superficial spreading melanoma--‐ usually lower limbs. [most common type)
Nodular melanoma--‐ usually in trunk. Round, asymmetrical, deeply pigmented,
irregular shape often with inflamed (red) edge.
Lentigo maligna melaenoma – usually face in the elderly.
Acral lentiginous melanoma--‐ nail, palms, soles, often in the elderly
Subungal melanoma: melanoma from nail matrix. Hutchinson’s sign (pigmentation
through nail fold--‐ important sign of subungal melanoma)
Treatment
Surgery(mainstaydefinitivetreatment)
Radiotherapy
Chemotherapy (for metastatic disease).
21. 21
Breslows thickness + ulceration are main prognostic factors. 20% of patients
will relapse. Main pattern of spread: lymphatics [so in follow up clinic feel the
lymph nodes).
Follow up: anything more than stageIais high risk follow up for 5 years.Lowrisk 1
year.
How does melanoma kill? Through spread via BV, lymphatics to vital organs.
Superficial spreading melanoma
Source: DermNet NZ
Acral melanoma
Source: DermNet NZ
Lentigo maligna melanoma
Source: DermNet NZ
Nodular melanoma
Source: DermNet NZ
22. 22
1) Erysipelas/cellulitis
Bacterial infection of the skin
Erysipelas--‐ superficial form of cellulitis (dermis and upper sc)
Cellulitis--‐ dermis and sc infection.
Symptoms:
Cellulitis--‐ often lower limbs, swelling erythema, warmth. Systemically
unwell: fever, malaise. Lymphangitis (seen as red streaky marks)
Erysipelas--‐ often on face well--‐defined, red border (cellulitis is less well
defined).
Treatment: Antibiotics e.g. flucloxacillin.
Skin infections
Cellulitis of the left
leg
Sou rce: Waikato district
health board, DermNet NZ
Erysipelas of the face
Sou rce: D@nderm
23. 23
2) Staphylococcalscaldedskinsyndrome
Blistering condition caused by exotoxins from certain strains of Staph Aureus. Often in
children.
Presentation: scald--‐like appearance, bullae, perioral crusting. V painful.
Treatment: Antibiotics (e.g. flucloxacillin), analgesia
Severe SSS
Source: DermNet NZ
3) Fungal skin infections
3 main groups: 1) Dermatophytes (tinea/ringworm), years (e.g. malassezia fur
fur, candidiasis), 3) moulds (e.g.aspergillosis)
Tinea: exactly what it is called depends on location of infection.
Tinea corporis (trunk/limbs)--‐ annular sessions, itchy, scaly edges.
Tinea cruris (groin/natal cleft) – similar to tinea corporis
Tinea pedis (feet aka atheletes foot)--‐ scaling and dryness of palms.
Tinea manuum (hand)--‐ scaling and dry palmar creases.
Tinea unguium (nail)--‐ yellow crumbly, thick nails
Tinea capitis (scalp)--‐ patches of baldness, scales.
Tinea incognito (when tinea infections are incorrectly treated with corticosteroids)--‐
ill defined (not as scaly as the above lesions).
Very severe SSS
Source: Dr. Raimo
Suhone n. DermNet NZ
25. 25
Candidiasis – white plaques on mucous membranes,
erythema with satellite lesions esp in nappy area.
Pityriasis versicolor – infection with malassezia
furfur--‐ pale brown patches usually on upper back that
fail to tan.
Diagnosis
Samplese.g.hair, skinscrapings, nail clippings for tinea
and swabs for yeasts likecandidiasis
Treatment
Ifsmallskinlesion: topical antifungal e.g.terbinafine
cream
Widespread lesions or nail infections e.g. oral
itraconazole., oral terbinafine
NO CORTICOSTEROIDS--‐ can cause tinea incognito.
4)Impetigo
Pityriasis versicolor
Source: DermNet NZ
Pityriasis versicolor
Source: DermNet NZ
Golden crust usually around mouth in children. Takeswabfor
culture.
Tx:localized:mupirocin topical therapy.Widespread:oral
flucloxacillin
5) Folliculitis--‐ pustule centered hair follicles usually beard,
groin, mustache.95%staph.aureus.Tx:oralflucloxacillin.
6) Viral warts--‐ HPV 6,11 – genital warts. HPV 16,18 – cervical
cancer.
Folliculitis
Source: DermNet NZ
Viral wart
Source: DermNet NZ
26. 26
7) Pityriasis rosea--‐ rash thought to be related to HHV 6/7. Starts as a herald
patch and then get red/pink patches all over body in a characteristic
‘Christmas tree; distribution). URTI symptoms preceded 70% of the time.
Treatment: none needed self--‐limiting.
Pityriasis rosea--‐ herald patch
Source: DermNet NZ
Pityriasis rosea
Source: DermNet NZ
27. 27
What causes blisters? Trauma, infection, drugs, autoantibodies + genetic diseases.
1) Bullous pemphigoid
Blistering condition caused by antibodies against type 17 collagen.
Presentation: tense blisters. Often lesions are itchy. Mucosal involvement less
common.
Treatment:
General:wounddressing, septicprecautions
localized disease: topical steroids
Widespread disease--‐ oral steroids, immunosuppressive agents e.g. azathioprine,
mycophenolate mofetil, methotrexate.
Bullous pemphigoid
Source: DermNet NZ
Bullous pemphigoid
Source: DermNet NZ
Blistering skin disorders
29. Always whatever the emergency:
1) A--‐E assessment
2) Withdrawal ofcause
3) Manage complications e.g. infection,
fluid loss, hypothermia
4) Consider any specifictreatments
1) Urticaria,angioedema,anaphylaxis
Uriticaria/Anphylaxis--‐ oedema from leaky capillaries in layers
of skin (urticarial) and mucosa (angioedema)
Anaphylaxis--‐ life threatening systemic hypersentivity reaction
Symptoms
Uritcaria--‐ itchy wheals
Angioedema--‐ swelling of lips, tongue, larynx (larynx swelling
manifests as stridor, hoarseness, respiratory distress)
Anaphylaxis--‐ bronchospasm, hypotension, stridor, facial
oedema.
Common causes: food e.g. nuts, shellfish, drugs e.g NSAIDs,
ACEi,, contrast, idiopathic, autoimmune, hereditary.
Treatment:
Urticaria: antihistamine
Angioedema: antihistamine, if severe e.g. noisy breathing,
difficulty talking, hypotension--‐ treat as anaphylaxis
Anaphylaxis:IMAdrenaline (0.5 mg,0.5mlof1:1000),oxygen,
steroids(200mgIVhydrocortisone),antihistamine e.g.10mg
IV chlorphenamine + admit for observation for 6--‐12 hrs.
Know the doses for
anaphylaxis--‐ 5th year
MCQ/OSCES
Angioedema2
o9
f the hands
Sou rce: DermNet NZ
Urticaria
Source: DermNet NZ
Angioedema of the lips
Sou rce: DermNet NZ
Angioedema of the face
Sou rce: DermNet NZ
Dermatological emergencies
30. 30
2) Erythema multiforme (EM), Stevens--‐Johnson
syndrome (SJS), Toxic epidermal necrolysis (TENS)
Hypersensitivity reactions causing death and detachment of epidermis
Symptoms
EM--‐ typically target lesions
Cause often unknown, HSV main known cause. Mucosal involvement absent/limited
to one mucosal surface.
SJS and TENS is a continuum of each other--‐ both involves mucocutanous necrosis.
The main difference is the TBSA involved.
SJS <10% TBSA
Maincauses:drugsandinfection.
10--‐30% TBSA –SJS/TENS overlap
TENS > 30% TBSA
Main causes: drugs e.g.
Sulfonamides: co--‐trimoxazole,
beta--‐lactam: penicillin, cephalosporins,
anticonvulsants: lamotrigine, carbamazepine, phenytoin, phenobarbitone,
allopurinol, paracetamol, nevirapine, NSAIDS
Treatment:
EM: most need no treatment--‐ self--‐limiting. Consider e.g. aciclovir for herpes labialis
SJS/TENS: Removecausee.g.stopdrug.Supportivetreatment e.g.skincarethe
sameasburns,fluidbalance, analgesia, treatment secondary infection,temperature
control. ITU for TENS.
Predictive mortality scale: SCORETEN
33. 33
4)Erythroderma
Exfoliative dermatitis involving > 90% of skin
Symptoms: whole skin, red, hot, flaky, patients are systemically unwell: malaise,
lymphadenopathy.
Causes: psoriasis, eczema, drug (penicillin, sulphonylurea, allopurinol),
malignancies (lymphoma)
Treatment: Removal of cause e.g. stop drug, supportive treatment; bed rest,
emollients (50/50),wetwraps,fluidresuscitation,temperature control,treatment
secondary infection.
Erythroderma
Source: D@nderm
Erythroderma
Source: D@nderm
Erythroderma
Source: D@nderm
34. 34
5)Eczema herpeticum
Infection of an eczematous area with HSV.
Symptoms: extensive crusted blisters, erosions.
Treatment:aciclovir andantibiotic cover e.g.flucloxacillin +withhold steroidsin
eczematous areas.
Less severe eczema herpeticum on the
flexural aspects of the wrists and hands
Source: D@nderm
Severe eczema herpeticum
on theface
Source: D@nderm
Severe eczema
herpeticum on the face
Source: D@nderm
Very severe eczema herpeticum on
the face
Source: D@nderm
Very severe eczema herpeticum on
the face
Source: D@nderm
35. 35
6) Necrotisingfasciitis
Surgical emergency! Infection of deep fascia usually polymicrobial in
diabetes/immunosuppressed patients but in healthy people usually Strep pyogenes
(Group A strep).
Symptoms:severepainoutofproportion ofclinical appearance,blisters,necrotic
skin, systemically unwell (tachycardia,fever).
Treatment: IV antibiotics, urgent surgical debridement
Necrotising fasciitis –
dusky, cyanotic and
gangrenous
Source: DermNet NZ
Necrotising fasciitis –
necrotic
Source: DermNet NZ
Necrotising fasciitis – a
rapidly destructive infection
Source: DermNet NZ
36. Diabetes mellitus:
Skin manifestation: candidiasis, granuloma annulare (self--‐
limiting, topical/oral steroid, steroid injections), necrobiosis
lipoidica (PUVA), diabetic shin spots and gangrene.
Drug photosensitivity--‐ severe erythema of sun exposed
area--‐ drug induced photosensitivity e.g. doxycycline,
amiodarone,
Hypercholesterolemia: xanthomata (cholesterol deposit
anywhere in the body)
Endocrine:
Addison’s disease--‐ generalized hyperpigmentation.
Haemochromatosis--‐ hyperpigmentation of skin. (bronze
skin)
Thyroid--‐ pre--‐tibial myxoedema.
Erythema nodosum: sarcoidosis, IBD, TB, pregnancy (self--‐
limiting, tx cause)
Systemic sclerosis: sclerodactyly, microstomia,
telangiectasia.
Sub--‐acute endocarditis: splinter
haemorrhage.
Heliotrope sign--‐ purple violaceous
erythema around eyes: dermatomyostiis.
(in dermatomysositis--‐ hunt for malignancy
in elderly people there is usually an
underlying malignancy--‐ esp breast, lung,
ovarian,gastriccancer)Tx:corticosteroids,
azathioprine, methotrexate
Necrobiosis Lipoidica
Source: DermNet NZ
Granuloma annulare
Source: DermNet NZ
Pyoderma gangrenosum
(IBD/rheumatoid arthritis). Acutely
inflamed +ulceratedskin,dusky,blue
edge to lesion. Despite looking
purulent it is sterile. Treatment:
topical/systemic steroids
Pyoderma gangrenosum
Source: DermNet NZ
Heliotrope rash
Source: DermNet NZ
Erythema nodosum
Source: DermNet NZ
36
Skin signs insystemic disease
37. 37
Too much hair: PCOS, idiopathic, ovarian tumor, adrenal
tumor, congenital adrenal hyperplasia, obesity
Too little hair:
1) Telogen effluvium--‐ scalp condition characterized
by early entry of hair in the telogen phase
(resting/shedding phase) e.g. eating disorder,
childbirth, chronic illness and major surgery.
2) Anagen effluvium--‐ scalp condition where you get
hair falling out in itsgrowthphase/pathologic loss
of anagen or growthphase hair e.g. radiotherapy,
chemotherapy.
3) Alopecia areata--‐ autoimmune condition where you
get discrete areas of scalp hair loss.
4) Alopecia universalis--‐ hair loss of all hair including
eyebrow,pubic hair, eyelashand scalp hair.
5) Alopecia with fungal infections e.g. tinea capitis--‐
can potentially cause scarring
Anagen effluvium
Source: DermNet NZ
Hair
38. 38
1) Delusionalparasitosis
Patient has fixeddelusions that thereareinsects,mites,bacteriain their skin
despite evidence to suggest otherwise.
‘Matchbox’ sign--‐ patients will bring things which they believe to be the parasite,
bacteria to doctors e.g. in matchboxes, on celotape, bring bits of hair, fluff, carpet.
Differentials ofdelusional parasitosis:organic disease (e.g.dementia,alcohol, drugs,
thyroid,trueinfestation), psychiatriccondition e.g.hypochondria, schizophrenia,
paranoia.
Examination, appropriate blood tests (e.g FBC,
U&E, LFT, TFT, B12, folate,), skin sample
(whatever the patient brings) and very rarely
skin biopsy.
Management: joint consultation with
dermatologist and psychiatrist.May usenew
atypical antipsychotic e.g. risperidone,
olanzapine, quetiapine.
Manage co--‐morbidities: e.g. depression with
SSRI
Manage skin e.g. emollients, antibiotics for
secondary infection.
2) Folie--‐a--‐deux
Excoriations due to delusional parasitosis
Source: DermNet NZ
--‐ when theindex casethinks they havetheparasite family membersthink they
have it too.
--‐ Treatment for index caseisantipsychotics but family just treat their skine.g.
moisturizers, abx for secondary infection.
Skinandthemind
39. 39
References:
Backgroundinfo
Dermatology: A handbook for medical students & junior doctors
Dr. Nicole Chiang
Professor Julian Verbov
Dermatology e--‐learning modules
University of Birmingham
Illustrations
DermNet NZ
https://www.dermnetnz.org/
D@nderm
http://www.danderm--‐ pdv.is.kkh.dk/atlas/index.htmll
