بسم اهلل الرمحن الرحيم

In your hands are notes that I have taken from the book “Clinical

Dermatology” by Rona M. Mackie ( Fifth Edition ). I have found them very

helpful and time efficient for revision before the exam while some others

have found them helpful for studying.

I have tried my best to note down the most important information found

in the text, then adding a few extra notes after the exam for it to be more

useful for others.

If you decide to read these notes I suggest, at least, reading these

chapters once in the book to be more oriented and familiar with what you read

here.

These notes were typed by my Mother, reviewed by me, and

formatted by Yousef T. Khoja, all I ask is for your prayers for whomever has

worked on these notes and the doctors and professors who have worked hard

to prepare the lectures given.

I wish you all the best of luck ,,,

Bittawfeeg ,,,

Tareq A. Al-Salamah

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IInnttrroodduuccttiioonn ttoo DDeerrmmaattoollooggyy

Some notes taken during the introduction lecture: Primary Lesions: ‐ Macule:

• Less than 1 cm in size. • Flat. • Could be dark or light.

‐ Patch: • More than 1 cm in size. • Flat. • Could be dark or light. • It's like a large ' Macule '.

‐ Papule: • Less than 1 cm. • Elevated.

‐ Planus: • More than 1 cm.

‐ Verrucas: • More than 1 cm. • Elevated. • Sharp and rough edges.

‐ Plaque: • More than 1 cm. • Solid. • Elevated. • Like a large ' Papule '.

‐ Nodule: • Any size. • Solid. • Deep ( part of the lesion is below the skin ). • Epidermal, Dermal. • Could be flat, but still it's under the skin.

‐ Vesicle: • Less than 1 cm. • Elevated. • Containing fluid. • E.g. Herpes, Eczema, Pox virus.

‐ Bulla: • More than 1 cm. • Large. • Containing fluid. • Like a large ' Vesicle '.

‐ Pustule: • Elevated. • Containing purulent fluid.

‐ Wheal ( like patch but evanescent ): • Any size. • Evanescent. • Elevated.

‐ Cyst: • Soft ( Nodule is solid ). • Containing fluid ( abscess contains pus ). • Epidermal, dermal.

Secondary Lesions: ‐ Ulcer:

• It's a deep erosion. • Part of dermis is lost. • Causes scarring.

‐ Erosion: • Doesn't cause scarring.

‐ Scale: • It's an abnormal shedding of the stratum corneum.

‐ Crust: • Dried exudate ( serum, blood, pus ).

‐ Excoriation: • It's a superficial excavation. • Due to scratching.

‐ Fissures: • These are linear cracks in skin.

‐ Sclerosis • Lesions are circumscribed and hardened.

‐ Atrophy: • This is a thinning of a specific part of skin. • Epidermal atrophy. • Dermal atrophy ( Striae ).

‐ Lichenification: • Increased pigmentation. • Increased skin margin. • Increased thickening.

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Some notes from the third chapter of the book: ‐ Mutation in Laminin 5 ( important part of hemidesmosome ) leads to “ Junctional

Epidermolysis Bullosa ”, a congenital blistering disease. ‐ Connexin 26 ( important part of gap junctions ) mutation leads to or is found

in “ Palmoplantar keratoderma ” and deafness. ‐ In inflammation or keratinization conditions, transit time of a differentiating

keratinocyte from basal layer to outer surface is less ( normal = 28 days ). ‐ Normal epidermis maturation = “ Orthokeratosis ”. ‐ Normal mucosal maturation pattern = “Physiologic parakeratosis” ( No

granular layer but an outer layer of nucleated squamous cells ). ‐ “ Pathological parakeratosis ” = some diseases, Ps MC ( Imperfect

development of stratum corneum ). ‐ Keratin 5 and 14 expressed in basal layer, mutation leads to “ Epidermolysis

Bullosa Simplex ”. ‐ Keratin 1 and 10 expressed in supranasal layer, mutations lead to “ Bullous

Icthyosiform Erythroderma ” or “ Epidermolytic Hyperkeratosis ”. ‐ Integrin: Bullous Pemphigoid ( auto antibodies ) against lamina Lucida. ‐ Cadherin: Adhesion between supranasal keratinocytes ( with desmosomes ). ‐ Desmolegein is a family member of cadherin and problems lead to the

“ Pemphigus Group ” of blistering disorders. ‐ Abnormal Langerhans cell proliferation seen in Histiocytosis X. ‐ Expression of TGF2 is abnormal in Ps and also associated with overactivity of

dermal fibroblasts in dermal Hyperproliferative conditions, such as “ Keloid scarring ” and ” Scleroderma ”.

‐ Fibroblast Growth Factor is very important for melanocytes and is released in intact skin after exposure to UV light.

‐ IL-1 is increased in epidermis during sunburn. ‐ IL-10 is over-expressed in non-melanoma skin cancer and AD. ‐ IFN-γ abnormal amounts in ACD. ‐ Collagen 7 is deficient in the “ dystrophic ” type of “ epidermolysis bullosa ”.

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PPssoorriiaassiiss aanndd ootthheerr

DDiissoorrddeerrss ooff KKeerraattiinniizzaattiioonn

Psoriasis ( Ps )Psoriasis ( Ps ) Definitions: ‐ Chronic, ‐ Relapsing and remitting, ‐ Scaling, ‐ Any age, any body part.

Prevalences: ‐ Sexes affected equally. ‐ Two peaks: ‐ Second decade ( more common ) - ( Type 1 ) ( this type has a stronger family

history ). ‐ Fourth and fifth decades ( Type 2 ).

 

Etiology ( Not yet known ) : Genetics: ‐ Multifactorial inheritance. ‐ Chromosome 16q, “ nod2 ” associated with Chron’s Disease & PS. ‐ Psors1 is part of the major histocompatibility complex.

TNF: ‐ Increased in skin and joints of patient’s with cutaneous psoriasis and

psoriatic arthropathy. ‐ Maybe plays major role in clinical expression of Ps. ‐ TNF receptors up-regulated in synovial fluid in psoriatic arthropathy.

Immunological aspects: ‐ Lesions attract neutrophils and lymphocytes. ‐ CD8 +ve in epidermis, CD4 +ve in dermis. ‐ TNF, INF-y, IL-2 and IL-12 are increased in lesions. ‐ Th1 or cytotoxic pattern ( T-cell targeted approach to treatment ).

 

Epidermal keratinocyte proliferations: ‐ Plaques have an increased epidermal cell proliferation rate; ( normally =

50 - 75 days, in Ps = 8 - 10 days). ‐ Germinative component comprises the lower 3 layers of epidermal cells

( normally is confined to the basal layer ). ‐ Rapid turnover in Ps is due to:

• An increase in the number of actively dividing cells. • Acceleration in the rate of reproduction of psoriatic cells.

‐ Persisting keratin 5 and 1 above basal layer. ‐ Keratin 6 and 16 are seen.

+ve Koebner phenomenon

Systemic drugs and Ps: ‐ May be aggravated and precipitated by them ( even for the first time ): ‐ Include:

• Lithium, • β-blockers, • NSAIDS, • Anti-malarials.

‐ Beware Ps patients on tropical holidays ( DON'T give anti-malarials ) • Alternatives:

1. Paludrine. 2. Mefloquine.

Infection and Ps: ‐ Sore throat by streptococcus is a well-recognized precipitator in Guttate Ps. ‐ Development of Guttate Ps is in association with presence of HLA-CW6

antigen.

UV and Ps: ‐ Majority improve on exposure to normal sunlight, 15% get aggravated by

it ( opposing responses ).

Stress, smoking and alcohol: ‐ Worsen, delay or develop Ps.

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Pathology: ‐ Parakeratosis ( Stratum corneum contains nuclei ). ‐ No granular layer. ‐ Prickle layer is expanded with bulbous downward projections. ‐ Mitotic figures in supra-basal keratinocytes. ‐ Large dilated thin-walled BV’s in papillary dermis, above which epidermis is thin. ‐ Munro micro-abscess (spongiform pustules) caused by clumping of leukocytes

in both dermis and epidermis. ‐ Sparse lymphocytic infiltrate in early lesion ( CD8 epidermis, CD4 dermis ).

Clinical Presentation: Plaque Ps: ‐ A.K.A. ( Ps Vulgaris ) Most common. ‐ Features include red and scaly plaques. ‐ Site:

• Extensors of knees and elbows. • Scalp. • Hands. • Sacral area.

‐ If untreated: • Raised. • Palpable.

‐ Topped by grayish-silvery scale. ‐ Auspitz sign ( Pin-point bleeding when scales removed ).

 

Guttate Ps: ‐ A.K.A. ( Raindrop Ps ). ‐ More common in children. ‐ Multiple, small, mainly on trunk. ‐ Frequently proceeded by streptococcal throat infection. ‐ Common to have ONLY ONE psoriatic episode of this type. ‐ All patients carry HLA-CW6 antigen.

Seborrhoeic Ps: ‐ A.K.A. ( Ps Inversus ) or Flexural Napkin in infants. ‐ Lesions in body folds. ‐ DDx Seborrhoeic Dermatitis ( Hard to differentiate both clinically and

histologically due to resemblance of erythema and scaling in both cases ). ‐ Napkin Ps has fine scaling rather than the classic more clearly demarcated plaque. ‐ Rx is difficult as topical Tars and Dithranol irritate them ( which happen to

be very effective in other body sites ).

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Erythrodermic Ps: ‐ Extensive erythema of entire body. ‐ At times very few scaling psoriatic lesions. ‐ May lead to loss of thermoregulation and high output cardiac failure.

Pustular Ps: ‐ Any Ps with sterile pustules. ‐ Pustules appear at advancing edge of lesions. ‐ Von Zumbusch pustular Ps.

• Combination of erythrodermic Ps with sterile pustules. • Serious, life-threatening due to:

o Fluid and electrolyte imbalance. o High output CF.

‐ Usually chronic on palms and soles, but not life-threatening. ‐ Responds poorly to Rx.

Scalp involvement: ‐ Features:

• Thick. • Obvious scaling. • Redness.

‐ Site: • Hairline ( where it’s most obvious ). • Behind ears.

‐ Complications: • Hair thinning ( from Ps or Rx? ).

Nail involvements: ‐ Features:

• Pits. • Onycholysis. • Sublingual hyperkeratosis. • Discoloration ( Grease spots ).

‐ These patients have a higher incidence of psoriatic arthropathy.

Psoriatic Arthropathy: ‐ Seronegative. ‐ Site:

• Sacro-iliac joint. • Distal inter-phalangeal joint. • Any joint.

Note: The first two are the most common sites.

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Notes: ‐ Many patients with actively developing lesions complain of pruritis; more

commonly, mild involvement of the scalp, knees and elbows persists with episodes of more widespread involvement. Childhood Ps is less prevalent than in adults and tends to be both persistent and hard to treat.

DDx: Eczema: ‐ Very pruritic. ‐ More inflammation than scaling. ‐ Tends to affect flexures.

Ichthyosis: ‐ Very little itch. ‐ A lot of scaling. ‐ Little inflammation.

Reiter’s Disease: ‐ Excluded in the absence of complaints in these systems:

• GIT. • GU. • Rheumatological.

Lichen Planus: ‐ Biopsy shows Lichenoid reactions.

Seborrhoeic Dermatitis, pityriasis Rosea, Pityriasis rubra pilaris: ‐ Differentiated by biopsy ( Histological exam ).

Bowen’s Disease: ‐ Biopsy. ‐ Be careful in diagnosing an isolated plaque on the trunk of an elderly

patient as Ps !!!, because it could be Bowen's Disease.

Investigations: ‐ Biopsy not indicated unless there’s clinical doubt. ‐ Scrapings for mycological exam ( especially when on palm ). ‐ X-ray and blood when Ps with joint pain ( to exclude RA ).

• Test for: o Rheumatoid factor. o ANA assessment.

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TREATMENT ‐ Always consider:

• Age. • General Health. • Pregnancy ( if planning also ). • Type of Ps. • Area involved and worst affected. • Previous Rx ( successful ? ). • Patient's life-style.

Notes: Including pros and cons of topical and systemic therapy. ‐ Mild emollients minimize scaling ( i.e. emulsifying ointment BP or white soft

paraffin ) . ‐ Topical therapy is relatively free of toxicity. ‐ Topical therapy ( see table 5.1 page 69 ):

Advantage Disadvantage

Dithranol based Long-term safety Staining and irritation common

Tar Long-term safety Carcinogenicity?

Salicylic Acid Useful for scalp and hyperkeratotic palms and soles Danger of salicylism

Topical steroids Clean and acceptable Only moderate potency acceptable

Calcipotriol Very useful in primary care - Of value only in mild-moderate

Ps. - Improves, NOT clears lesion!.

UV light Unknown future malignancy

UVB - Natural sunlight wavelengths. - Improvement associated with presence of some erythema.

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‐ Systemic therapy ( see table 5.1 page 69 ):

Advantage Disadvantage

PUVA - - - Risk of SCC in patients with > 500 treatments

Cytotoxic drugs ( Methotrexate,

Azathioprine, Hydroxyurea )

Rapidly effective Teratogenic & Toxic to: Liver, Marrow & Kidney

Retinoid group ( acitretin,

Neotigason )

- Effective in 50% of chronic plaque Ps.

- Effective in 80% of pustular Ps of palms and soles.

Teratogenic, Raised chelitis, Bony changes & Serum lipids

Cyclosporin ( Neoral ) - - -

- Rapid rebound on stopping. - Risk of permanent renal

damage.

Cytokine modulators Useful in both skin and joint - - -

Immune modulators - - - Little data on toxicity

Emollients ( cosmetic improvement ): ‐ Reduce scaling & prevent cracks ( especially on palms and soles ). ‐ Lighter preparation for trunk and limbs, heavier for palms and soles. ‐ Doesn’t affect erythema or prevent new plaque development.

Tars: ‐ Antimitotic activity. ‐ Cosmetically unacceptable. ‐ Maximum benefit with 5 % concentration. ‐ Sterile folliculitis when put on hair-baring areas ( some patients ). ‐ Goeckerman regime ( combination of Tar with UVB ).

Dithranol: ‐ Inhibits mitosis. ‐ Normal skin irritated ( apply white soft paraffin to prevent that ). ‐ Ingram regime ( combination of Tar baths, topical Dithranol and UVB ).

• Safe and effective. • Clears plaques in 2 - 3 weeks. • Staining wears off 7 - 10 days after stopping Rx.

‐ Short contact regime: • Avoids need for dressing and staining of clothing. • Takes longer time to clear lesions.

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Salicylic Acid ( SA ): ‐ Most commonly used on scalp and hyperkeratotic areas on palms and soles. ‐ Keratolytic. ‐ Higher concentration on scalp ( 10 – 20% ).

Topical steroids: ‐ Best not to use strong steroids as mainstay of treatment ( unstable or

causes erythrodermic Ps ). ‐ Moderate potency steroids for Flexural Ps ( useful ). ‐ Stronger potency steroids for pustular Ps of palms and soles

( beclomethasone dipropionate or fluocinolone acetonide ). ‐ Combination of steroid with SA as a lotion for stubborn scalp Ps.

Vitamin D derivatives ( e.g. Calcipotriol ): ‐ Very little effect on mobilizing Ca+ stores. ‐ Act by promoting normal epidermal differentiation. ‐ As effective and more cosmetically acceptable ( clean and odor free ). ‐ Rapid reduction of scaling and slow, usually incomplete, reduction of erythema. ‐ To avoid hypercalcaemia, don't give > 100g weekly. ‐ Alternate topical Vit. D and topical steroids to:

• Reduce irritant effect of Vit. D. • Minimize undesirable anthropogenic effect of steroid.

Topical Retinoids, e.g. Tazarotene: ‐ Help promote psoriatic skin dedifferentiation. ‐ Some irritation of normal skin. ‐ Possible percutaneous absorption ( Teratogenicity ).

UVB: ‐ 280 – 315 nm is found in natural sunlight. ‐ 310 – 312 nm range is more effective ( alone or in combination ).

Shampoos: ‐ Tar-based and SA containing for mild Ps ( little proof of efficacy ).

Systemic Rx Notes: ‐ Only given or considered when a very adequate trial of topical Rx has failed. ‐ None are safe during child-bearing years without adequate contraception. ‐ Initially effective then doses have to increase, increasing side effects. ‐ Immunomodulators in trial for:

• Psoriatic Arthropathy. • Severe cutaneous Ps.

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PUVA: ‐ Contains an oral photosensitizing agent ( Psoralen ). ‐ UVA range = 320 – 365 nm. ‐ Only for clearing psoriasis – Induction Therapy. ‐ Future risk of skin cancer ( melanoma and non-melanoma ). ‐ 1000 J/m2 = maximum safe dose. ‐ Psoralen is deposited in lens of the eye ( must wear dark glasses ).

Retinoids: ‐ Vit. A-like derivatives. ‐ Heavier patients require slightly higher doses. ‐ Can be used relatively long-term. ‐ Minor side effects:

• Dry lips and nasal mucosa. • Increase serum cholesterol and triglycerides.

‐ Teratogenic ( until after 2 years of therapy cessation ). ‐ Combination with PUVA reduces dose requirement of other.

Methotrexate: ‐ Control of severe Ps with small doses at weekly intervals. ‐ Particular advantage speed of action ( within 48 hours ). ‐ Oral, IM, IV. ‐ Hematological and hepatic function monitoring is essential. ‐ SE:

• Marrow depression. • Hepatic fibrosis.

‐ Minimize or avoid alcohol intake. ‐ Drug interactions:

• NSAIDs. • Trimethoprim / sulphonamides. • Systemic steroids.

Cyclosporine: ‐ Control of severe Ps. ‐ Plaques clear rapidly ( within a week of starting ), but may return just as

rapidly when withdrawn. ‐ By inhibition of Calcineurin Phosphate. ‐ Mainly used to achieve short-term control of severe Ps, ( toxicity with

long-term use ). ‐ Main toxicity Renal damage. ‐ Dose of cyclosporine reduced or withdrawn, when creatinine > 25 %

above base-line values, and/or Diastolic BP > 95 mmHg.

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‐ Drug interactions: • Aminoglycosides. • Trimethoprim. • Ketoconazole. • Phenytoin. • Rifampicin. • Isoniazid. • NSAIDs.

Hydroxyurea: ‐ Last resort drug ( my words! ). ‐ Main toxicities:

• Bone Marrow depression. • Teratogenicity ( till 6 months after stopping ).

Mycophenolate Mofetil ( Cellcept ) ( usually used for graft rejection): ‐ Severe nausea.

Immune modulators: ‐ Reduce the number of pathogenic T-cells:

• Alefacept and Denileukin diftitox. • They work by fusing with proteins ( they are fusion proteins ). • Alefacept ( antigen 3 with Fc of IgG ). • Denileukin ( IL-2 with subunit of diphtheria toxin ).

‐ Inhibit T-cell migration and activation: • Efalizumab. • Humanized anti-CD11a monoclonal Ab. • Affects T-cell adhesion.

‐ Divert immune system: • Recombinant IL-10. • IL-10 down-regulates the excessive TH1 response in Ps.

‐ Cytokine-modulating agents: • Etanercept and infliximab ( 1st SC injection, 2nd IV infusion ). • TNF-alpha inhibitors in severe Ps. • For:

o Psoriatic arthropathy. o Severe cutaneous Ps.

• Concerns about: o Serious infection. o Sepsis. o TB reactivation.

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Mx of nail Ps: ‐ Severe involvement impossible Rx. ‐ Systemic Rx for short-term improvement.

Mx of Psoriatic arthropathy: ‐ May respond to systemic methotrexate or cyclosporine. ‐ For psoriatic arthropathy and severe cutaneous Ps, use:

• Anti-cytokine or, • Immune modulators.

Lichen Planus ( LP )Lichen Planus ( LP ) Definition: ‐ Cutaneous disorder, ‐ Itchy, ‐ Flat-topped papules. ‐ Site:

• Inner surfaces of wrists and lower legs ( Most common ). • Mucous membranes usually affected.

‐ Spontaneous resolution in 3 months – 2 years.

Etiology: ‐ Unknown ( immunological ? ). ‐ Drugs. ‐ Koebner phenomenon. ‐ There's an association between LP and Primary Biliary Cirrhosis.

Clinical Features: ‐ Acute onset papules. ‐ Intensely itchy. ‐ Shiny. ‐ Flat-topped. ‐ Mucous membrane lesions are:

• White. • Spongy. • Slightly raised. • Trabecular or lacey appearance . • Usually asymptomatic. • Important for Dx. • Similar lesions could be found on genitalia.

‐ Fine, white network may develop on lesion surface ( Wickham’s Striae ). ‐ Rare variants ( persistent and resistant to Rx ):

• Annular or linear pattern. • Atrophic. • Ulcerative. • Hypertrophic.

‐ Nail changes in 10%: • Fine ridging or growing. • Severe dystrophy. • Complete destruction of nail bed.

Pathology: ‐ That of ( Lichenoid tissue reaction ). ‐ ‘ Liquefaction degeneration ’ or selective destruction of basal layer of

epidermis dermo-epidermal junction ragged, ( saw-toothed ) outline. ‐ Mixed cell infiltrate in papillary dermis:

• Tends to be in close contact with epidermis. • Contains some free melanin.

‐ ‘ Colloid bodies ’ in papillary dermis. ‐ Epidermis:

• Thinned in Atrophic LP. • Thickened in Hypertrophic LP.

‐ Immunofluorescence shows many immunoglobulins on colloid body surfaces ( mostly IgM ), but this is NOT diagnostic.

DDx: ‐ Lichenoid eruptions due to:

• Drugs ( thiazides, anti-malarials, gold ), or • External contact with photographic color developers.

‐ Ps: Biopsy to confirm ( biopsy also with persistent ulcerative or hypertrophic lesions ).

Rx: ‐ Control itch ( Most important ). ‐ Moderately potent topical steroids ( Most useful preparation ). ‐ Systemic sedating antihistamines for persistent itch. ‐ Intra-lesional steroid injection.

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Pityriasis Rosea ( PR )Pityriasis Rosea ( PR ) Definition ‐ Self-limiting, asymptomatic erythematous scaling macules, on trunk.

Incidence and etiology ‐ Most commonly seen in children and young adults. ‐ Increased in spring and autumn. ‐ Infective, maybe viral ( Herpes 6 and 7 ? ).

Clinical Features: ‐ Herald patch:

• First lesion. • Pink or red patch with peripheral collarets of scales. • Seen on trunk a week before main eruption. • Followed by oval macules ( also with peripheral scaling ) on trunk, thighs

and upper arms. ‐ Trunk lesions:

• Long axis parallel to ribs. • ‘ Christmas tree ’ distribution.

‐ Usually asymptomatic lesions ( may be mild pruritis ). ‐ Usually remits spontaneously in 4 - 8 weeks.

Pathology: ‐ Moderate dense infiltrate:

• Lymphocytic dermal ( mainly ). • Papillary edema. • Few extravasated RBC's.

‐ Spongiosis in epidermis ( at edge of developing lesion ). ‐ Histologic picture very similar to secondary syphilis ( differentiated by

serological tests ).

DDx & how to differentiate them from Pityriasis Rosea: ‐ Secondary syphilis serological tests. ‐ Drug eruptions history. ‐ Pityriasis versicolor -ve mycological exam. ‐ Guttate Ps biopsy.

Rx: ‐ Moderate potency topical steroid until clears spontaneously

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CCuuttaanneeoouuss IInnffeeccttiioonn

Bacterial InfectionsBacterial Infections Impetigo ( superficial cutaneous ): ‐ Etiology:

• Staph aureus, or • Strep Group A.

‐ More common in children. ‐ Clinical Features:

• Thin-roofed, quickly ruptured blisters ( esp. staph ). • Superficial lesion. • Covered with a heavy “ honey-colored crust ”. • Usually on face and hands.

‐ May complicate a pre-existing skin problem: • AD ( Atopic Dermatitis ). • Acne.

‐ Management: • Warm saline or olive oil to remove crust. • Topical Abx. • Systemic Abx only if strep to avoid post streptococcal glomerular

nephritis. ‐ Prognosis:

• Infection is extremely superficial Good healing with no scar.

Erysipelas: ‐ Cutaneous strep ( enters through abrasions and infects superficial lymph vessels ). ‐ Clinical Features:

• Bright red, brawny, edematous. • Sharply demarcated. • Usually on face. • Associated with leukocytosis and fever.

‐ Dx and Rx: • Responds to full doses of oral penicillin ( best Dx method ). • Should take swab ( but DON’T wait for results ). • Withhold topical steroids because it delays response to systemic Abx. • If recurrent Erysipelas at same site chronic lymphoedema.

Cellulitis ( Very similar to Erysipelas ): ‐ Cutaneous strep but deeper involvement of subcutis than Erysipelas. ‐ Clinical Features:

• Raised. • Hot and tender. • Erythematous. • Larger and more diffuse than Erysipelas. • Edges NOT well demarcated. • Associated with fever and leukocytosis. • Draining lymph nodes are palpable and tender.

‐ Dx and Rx: • Dx is straightforward. • Full doses of systemic Abx immediately (don’t wait for swab results!):

o Penicillin V for strep. • If Immunocompromised, blood cultures should return before starting Rx.

Erythrasma: ‐ Cutaneous Corynebacterium minutissimum ( CM ). ‐ Clinical Features:

• Asymptomatic. • Reddish-brown. • Commonly in body flexures, particularly the groin. • Not contagious. • If not treated, spreads with a well-demarcated advancing edge.

‐ Dx and Rx: • By bacterial identification of CM, or Coral-red fluorescence under

Wood's light ( To resolve confusion with fungal infections ). • Topical Imidazoles, or • Topical Erythromycin, or • Full doses of oral Erythromycin.

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Viral InfectionsViral Infections Warts ‐ Benign cutaneous tumors, caused by HPV. ‐ Transmitted by direct contact. ‐ Types:

1. Common Warts: • A.K.A Verruca Vulgaris. • Clinical Features:

o Multiple. o Raised. o Hyperkeratotic. o Found on hands commonly. o Painful ( when periungual ).

• Particularly common in children ( 5-10 yrs ). • Demonstrate Koebner Phenomenon.

2. Plane Warts: • Mostly on face and back of hands. • Clinical Features:

o Slightly raised plaque. o Circular or oval.

• Resistant to Rx. 3. Plantar Warts:

• A.K.A Verruca Plantaris. • Grow inwards towards dermis ( because constant pressure on soles

prevent outward expansion ). • Pain ( due to pressure on nerves ). • Risk when using communal showers.

4. Genital Warts: • Tend to develop in large clusters. • Re-infection is very common if Rx isn't right. • All patients with peri-anal warts should have a proctoscopic exam to

exclude rectal involvement. Notes:

1. Cutaneous warts ( 1,2,3 ) are caused by HPV 1, 3 and they’re not oncogenic. 2. Genital warts ( 4 ) are caused by HPV 16, 18 and may be oncogenic. 3. All warts are more persistent when cell-mediated immunity is low, e.g.

transplant patients.

‐ Pathology: • Page 143.

‐ Dx: • Periungual fibromata of tuberous sclerosis could be misdiagnosed as

periungual warts. • Plantar warts may be confused with either corns, or with invasive

malignant tumors ( if hemorrhage into lesion with discoloration ). • In plantar warts punctate bleeding occurs when scratched with a scalpel:

o In corns only thick epidermis. o In malignant tumors dark friable vascular tissue :

› If a malignant tumor is suspected, do an immediate excisional biopsy. • Genital warts may be confused with condylomata lata of syphilis:

o Full serological screening should be done for venereal diseases in all cases of genital warts.

‐ Rx:

• A lot of common warts resolve spontaneously, so no Rx is required for 3 - 4 months ( could use salicylic acid paint ).

• If persistent after 3 - 4 months Cryotherapy with liquid nitrogen or a slush of CO2 snow and acetone.

• If more persistent curettage or electrocautery or diathermy under local anesthesia.

• NO RADIOTHERAPY !!. • Plane warts:

o Bland non-scarring preparations. o Salicylic acid paints may speed clearance.

• Plantar warts: o 1st pare away as much overlying skin as possible. o 2nd apply salicylic acid or glutaraldehyde-containing paint. o 3rd cover with occlusive plaster. o These steps cause tissue necrosis with bandage on for 10 - 14 days,

remaining wart tissue can be curetted away. o Formalin soaks are also of value.

• Genital warts: o Can be persistent and difficult to treat. o Cryotherapy for as long as necessary ( best method of out-patient Mx ). o Daily podophyllum for 3-4 days in soft paraffin, but leads to

maceration and discomfort. o If pregnant or immunosuppressed lesions tend to become fungating

and cauliflower-like ( cryotherapy is the treatment of choice ) ( podophyllum is NOT recommended ).

• In children about to receive chemotherapy for leukemia and such, make sure you treat warts before commencing chemo, same goes for transplant patients ( very persistent warts in transplant patients may require intralesional Bleomycin or systemic interferon) .

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Molluscum contagiosum ‐ Cutaneous, infectious, by Pox virus – benign but troublesome. ‐ Clinical Features:

• Usually in the under-fives. • Multiple in young children, isolated in adults. • Mostly on face and neck. • Elevated, smooth, reddish papules. • All have a small central punctum. • Troublesome if around eyelids and at vermilion border of lips.

‐ Pathology: • Page 147: • Histological hallmark:

o Molluscum bodies ( amorphous eosinophilic structures ). ‐ Rx

• Aim is to stimulate an inflammatory reaction in the dermis underlying the lesion, done by puncturing individual lesions ( curettage ) and applying iodine.

Herpes Simplex: ‐ Page 148 ( Sorry I didn't write notes on this topic ).

Herpes Zoster ( Shingles ): ‐ Cutaneous, by chicken pox virus, herpesvirus varicella ‐ Disease of adults and old age ‐ Patients with Hodgkin’s are particularly prone ‐ Direct immunofluorescence using antibodies specific for herpes simplex or zoster

will differentiate between them while infection is still in its early stage ( serology from about 14 days after infection ).

‐ Clinical Features: • Prodromal pain in a dermatome distribution . • Malaise and sometimes fever. • Linear erythematous band on dermatome. • Then small blisters on erythema ( some become secondarily infected). • Local lymphadenopathy is common. • If develops to post-herpetic neuralgia difficult Rx. • Special Mx if:

o Ophthalmic division of trigeminal is affected. o First and second sacral ganglia are involved. o More than one dermatome in elderly and immunosuppressed.

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‐ Rx: • Mild cases symptomatic:

o Simple analgesics. o Fluid balance. o Soothing ( drying ) topical.

• Do NOT give topical steroids. • Lesions clear in 7-10 days. • If more painful and widespread – full course Acyclovir. • Systemic corticosteroids MAY help in post-herpetic neuralgia.

Orf ‐ Rapidly growing solitary cutaneous lesion, by Pox virus. ‐ Clinical Features:

• Infection by contact with sheep. • Red papule after an incubation period of 7-10 days. • Rapidly growing. • Central necrotic or bullous area. • Lymphangitis, lymphadenopathy, fever ( not uncommon ). • One attack confers immunity. • Usually on sides of fingers. • Spontaneous recovery.

‐ Rx: • Broad Abx ( Flucloxacillin orally ). • Topical Abx could be used ( Aureomycin ).

Fungal InfectionsFungal Infections Candida Infections (Candidosis, thrush): ‐ C. Albicans is normal in GIT, could be a pathogen if disturbed ( very young,

elderly, if treated with Abx ). Can be a serious and resistant problem in HIV. ‐ Clinical Features:

• In children Napkin Candidosis. • In adults “ Intertrigo ” in submammary folds, Axillae, Groins. • Glazed brick-red. • Characterized by ‘satellite lesions’ and occasionally pustules around

involved areas. • Painful fissures in affected folds ( may be resistant to Rx ).

• Candidal Paronychia involved with wet-work occupations ( cuticle is lost ). Inflammation produces a ‘ bolstered ’ posterior nail fold where beads of pus can be expressed.

• Chronic candidal granuloma ( commonly on lips ) in patients with a long history of candidosis.

• Oral candidosis produces adherent white patches on tongue and inner cheek surfaces, if scraped off raw bleeding area.

• Irritable erythema with copious discharge in candidal vulvovaginitis: o Pregnant and diabetics are at more risk.

• In infants with napkin candidosis and persistent diarrhea, always keep in mind bronchial and GI mucous membrane candidosis.

• Generalized systemic infections due to candida are rare, usually with immunosuppression or Abx.

‐ Pathology: • Page 155. • PAS= Periodic Acid Schiff.

‐ Dx: • Swab and examine, but not necessarily caused by it when found! It may

also colonize a pre-existing skin condition and cause an opportunistic secondary infection.

‐ Rx: • Alter the damp, moist, warm microclimate in which Candida thrives. • In patients with intact immunity, choice of therapy is either:

o Nystatin: › Oral suspension, pessary, cream, gel, ointment. › Safe. › Best for infants.

o Imidazoles: › ”Ketoconazole” has greatest activity against candida ( better than other

Imidazoles ). o Candida paronychia responds slowly, but good results with working

Nystatin ointments into nail folds and keeping hands dry. o Infants with persistent napkin candida should be given oral nystatin

drops as a high proportion will have GI involvement. o Topical steroids are contraindicated. o Oral Fluconazole or Itraconazole:

› As prophylaxis in immunosuppressed patients. › Short courses for eradicating persistent genital candidosis in healthy

individuals.

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Dermatophytes: ‐ Presents commonly as athlete’s foot, nail infections, tinea corporis and scalp

ringworm. ‐ Clinical Features:

• Tinea Pedis ( athlete’s foot ): o With use of communal showers and such. o Usual site is the toe webs, especially the fourth. o Moist, white ‘blotting-paper' skin is seen. o Pruritis is common. o The instep of foot and nails may be involved in persistent cases. o Organisms T. rubrum, T. mentagrophytes, verinterdigitale E.

Floccosum. • Tinea Corporis ( ringworm ):

o Infection of trunk ( frequently begins in folds ). o Itchy, erythematous, raised advancing edge. o Scrapings have +ve results if taken from edge ( most likely ).

‐ Dx: • Not always straightforward. • Isolated lesions on trunk may resemble psoriasis. • Tinea corporis + topical steroids = Atypical presentation. • Persistent hand dermatitis may be due to dermatophytes ( mostly T.

rubrum ) in which palm is dry with itchy, scaly creases. In such cases Mycological exam should be routine.

‐ Infection of hair shafts: • Scalp or beard area. • Organisms: T. tonsurans, M. canis, T. rubrum, T. verrucosum. • 1st sign is a well-circumscribed pruritic scaling area of hair loss with

variable inflammatory response. • Suspected hair infection should always be examined under Wood’s light

( Diagnostic green fluorescence with M. canis and M. audouinii, T. schoenleinii gives dull green fluorescence which gives rise to a distinctive clinical entity called “Favus” ).

• Features of Favus: o Extensive or complete hair loss. o Scalp atrophy leading to permanent alopecia. o Adherent scales ( scutula ) on remaining hairs.

• Kerion: o Infection of hair shaft with T. verrucosum. o Very brisk inflammation. o Commonly in children after contact with cattle or domestic animals. o Acute folliculitis with pustules and swelling forming a boggy mass on

the scalp.

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o Hair loss and scarring alopecia are common. o One attack usually confers immunity.

‐ Pathology: • Inhabit keratinized tissue, they do NOT invade living tissue. • They grow down pilosebaceous follicles towards bulb but do NOT reach it

.and fan out to form multiple hyphal fronds known as Adamson’s fringe • Hair shaft is invaded. • They can be seen on direct examination by taking scrapings or nail

clippings and putting them on a slide with potassium hydroxide. • To identify type culture for 3 weeks on Sabouraud’s medium. • If biopsy is needed, histological section should be stained with PAS or

methamine silver to show them in the stratum corneum. ‐ Dx:

• Most cases: Direct microscopy of scrapings in potassium hydroxide and use of Wood’s light.

• Remainder: Culture of skin scrapings or nail clippings. • Atypical presentations could mimic Ps, seborrhoeic dermatitis, or mycosis

fungoides. ‐ Rx:

• Oral Griseofulvin ( should be given during a fatty meal ) and Terbinafine are effective against dermatophytes NOT candida, but should be reserved for severe cases in body sites other than inter-digital clefts.

• They’re the Rx of choice for widespread or persistent tinea corporis, tinea capitis and tinea unguium.

• Terbinafine is fungicidal. Good for finger and toenails. • Topical preparations include:

o Allylamines. o Miconazole. o Ketoconazole.

Pityriasis Versicolor: ‐ Persistent, often asymptomatic due to M. furfur. ‐ Clinical Features:

• Asymptomatic. • Mainly on trunk and proximal limbs. • Fine superficial scale. • In untanned white Caucasian skin ↑ pigmentation with yellowish-brown

scale. • Heavily tanned or dark skinned Depigmentation. • Overall effect is a dappled appearance.

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‐ Dx: • Skin scrapings for direct microscopy, and exam under Wood’s light for

pale yellow fluorescence. • Could be confused with Vitiligo. • Hyphae are found in horny layers, there is little underlying reaction.

‐ Rx: • Rx of choice Topical Imidazole. • In severe and persistent cases Monthly oral Itraconazole. • Recurrence is common.

Protozoal InfectionsProtozoal Infections Leishmaniasis ‐ Cutaneous or systemic transmitted by sand fly. ‐ Mostly seen as superficial granuloma. ‐ Search will reveal “ Leishman Donovan bodies ” in cells of granuloma. ‐ Clinical Features:

• Most likely presentation is a crusted sore on the face, hand or leg 6 - 8 weeks after being affected.

‐ Dx: • Based on history, histology and +ve Leishmania test ( if needed ):

o Leishmania test = intra-dermal injection of heat-killed organisms. ‐ Rx:

• In healthy people resolves spontaneously. Cryotherapy is also effective. • In persistent cases oral pentavalent antimony ( Pentostam ).

Cutaneous InfestationsCutaneous Infestations ‐ The commonest are due to lice or scabies.

Scabies: ‐ Persistent pruritic skin eruption by mites ( Sarcoptes scabiei ). ‐ Female inhabits a burrow in the stratum corneum then dies after laying eggs,

which hatch and mature in 14 days, the cycle is then repeated. ‐ Pathology:

• Local hypersensitivity reaction causing release of inflammatory mediators. • Occasionally, nodular lesions persist after successful therapy, associated

with a chronic inflammatory reaction with many lymphocytes in dermis.

‐ Clinical Features: • Severe persistent itch, worse at night and after bathing. • Classical sites:

o Finger webs. o Sides of fingers. o Flexor of wrists. o Penile or scrotal skin. o In infants not yet walking soles of feet. o Points of elbows. o Anterior axillary folds. o Periumbilical area. o Areola of nipples in females.

• The extent of burrows is known by painting the area with Indian ink then washing off excess skin on the surface.

• In long-standing infections, secondary infection with pustule formation and crusting is common.

• Nodular persistent lesions after successful therapy may be seen. Commoner on buttocks and male genitalia.

• A moist oozing, infected dermatitis may develop on top of scabietic burrows. ‐ Dx

• Cardinal diagnostic test demonstration of acarus ( mite ) by extracting it from burrow.

• Most common mistake is to misdiagnose is as Contact Dermatitis or Dermatitis Herpetiformis.

‐ Rx: • Most common acaricides are:

o 1% Gamma benzene hexachloride. o Malathion. o Permethrin.

• In infants: o Sulphur preparations ( due to less chance of percutaneous absorption ).

• It’s essential that the entire body from neck to soles be treated. • Boiling or fumigation of clothing and such is NOT required. • Pruritis may continue for a few days even after successful Rx and

Crotamiton cream will minimize this. • Others around patient in home should also be treated even if asymptomatic.

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Pediculosis Capitis: ‐ Relatively common in school children. ‐ Less in adults, usually vagrants and very poor. ‐ By nit (head-louse egg), stuck to scalp hair by capsule. ‐ No symptoms till louse hatches causing an irritant dermatitis. ‐ Scratching leads to secondary impetiginization, particularly on nape of neck

and behind ears. ‐ Dx:

• Identification of nit or adult head louse with naked eye. • Shaving NOT required, cutting hair short helps in Rx. • Comb with a fine comb. • Malathion and permethrin applied to entire scalp and left for 12-24 hours,

and then shampooed and dead nits combed out. • Rx may have to be repeated in 7-10 days. • Like scabies, treat family members too.

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DDeerrmmaattiittiiss aanndd EEcczzeemmaa

Terms ‐ Dermatitis: inflammation due to exogenous problems. ‐ Eczema: inflammation due to endogenous problems.

Notes: ‐ T lymphocyte is recruited into dermis and epidermis in the great majority of

cutaneous inflammatory processes. ‐ CD4+ helper is found in much larger quantity than CD8+ cytotoxic. ‐ In atopic dermatitis the majority of T-helper lymphocytes are of the Th2 subset. ‐ The predominating cells in the skin after inflammation stimulus by 4-6 hours

PMN leukocytes; by 24 hours virtually all are lymphocytes. ‐ Both LFA and IFN-γ are expressed in epidermis and papillary dermis early. ‐ Langerhans cell plays a role ( esp. in induction of contact allergic dermatitis ).

Acute, subacute and chronic dermatitis ‐ Each one has a distinct clinical and pathological appearance. ‐ Each one requires a different approach to Rx. Acute: ‐ Clinical:

• Redness, swelling, pain, heat, tenderness. • Oozing. • Edematous ( small blisters ).

‐ Pathological: • Dermal and epidermal edema ( spongiosis ). • Dilated congested dermal capillaries. • Infiltrate ( early leukocytes, later lymphocytes ).

Subacute: ‐ Clinical:

• Redness, swelling. • Crusting. • Scaling ( due to secondary infection ). • Itch.

‐ Pathological: • Crusting and parakeratosis. • Early acanthosis. • Perivascular lymphocyte infiltrate, few lymphocytes in dermis.

Chronic: ‐ Clinical:

• Scaling with thick skin. • ↑ skin markings ( Lichenification ). • Itch. • Purple or violaceous elevated plaque.

‐ Pathological: • Marked acanthosis. • Coarsening of papillary dermal collagen. • Lymphocytic infiltrate in papillary dermis.

Atopic Dermatitis ( AD ): Definition: ‐ Chronic. ‐ Extremely itchy. ‐ Strong genetic association ( FH ). ‐ Begins in infancy. ‐ Associated with asthma and rhinitis. ‐ Benign.

Prevalence and etiology: ‐ In adults, it’s less frequent but worse. ‐ Rarer in Chinese but more severe and persistent. ‐ Associated problems:

• HSV1 ( eczema herpeticum ). • Staph aureus in epidermis . • Dry skin. • Keratosis pilaris. • Juvenile planter dermatosis. • Nipple dermatitis in females. • Warts and molluscum contagiosum ( most common in children ). • Cataract and keratoconus. • Food allergy and intolerance.

Immune aspects: ‐ ↑ IgE in 80% ( this is neither necessary nor sufficient for Dx ). ‐ ↑ RAST ( radioallergosorbent testing ):

• Infants: to food. • At 1 year: to inhale allergens.

‐ Th2 overactivity produces IL-4 and 5 which stimulate IgE production by β lymphocytes.

‐ Th1 activity is low low IFN-γ.

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AD and bacterial or viral infections: ‐ In AD there are vascular abnormalities ( instead of a normal ‘weal and

flare’ response, firm rubbing elicits “white dermographism” as a simple white linear streak along the site of pressure with NO erythema ).

Clinical Features: ‐ Infants:

• As early as 6 weeks. • Scalp, face and trunk. • Sparing of the central panel of face.

‐ Toddlers and older children: • Elbow, knee, buttock flexures, ankles, dorsa of feet under shoe straps,

retroauricular fold, antecubital fossa. • When severe;

o Gross involvement of all four limbs. o Excoriation and secondary infection. o Some develop shiny hacked skin on soles ( juvenile plantar

dermatosis ). ‐ Adults:

• Generalized dry skin. • Diffuse itchy plaques. • Trunk and face. • Some have autosomal dominant ichthyosis vulgaris and keratosis pilaris.

Notes: ‐ A lot of children will clear spontaneously between 2-5 years of age. ‐ If not cleared and continues to adulthood it develops into the more chronic

type, with striking lichenification in the popliteal and antecubital fossae and on the nape of the neck. Prominent intra-orbital creases are also seen giving an aged expression.

‐ Thinning of the lateral part of the eyebrows ( Hertoghe’s sign ). ‐ Shiny fingernails from buffing rather than scratching is also seen.

AD and contact dermatitis: ‐ AD has a higher association with irritant contact dermatitis than

allergic contact dermatitis.

Investigations: ‐ Dx should be made on clinical grounds:

• Presence of itch for the past 12 months. • 2 or more flexural dermatitis. • Onset before 2 years of age.

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• Personal history of: o Asthma, or o Hay fever, or o Dry skin.

• IgE: o Not necessary nor sufficient. o Always normal in infants until after 6 months of age.

• Bacterial swabs from lesions: o Show heavy staph aureus. o Not specific!.

• Swab for HSV1: o Useful or therapeutically relevant. o If +ve, requires systemic anti-viral Rx.

Kaposi’s varicelliform eruption ( eczema herpeticum ): ‐ Most important complication of AD after exposure to HSV1. ‐ Clinical Features:

• Small blisters on lesions. • General malaise and fever.

‐ Keep AD patients away from children with simple cold sores !.

Rx: ‐ Explain nature of AD. ‐ Control rather than cure is the aim. ‐ Mild – moderate:

• Emollients. • Topical steroids. • Sedating antihistamines. • Wet-wrap dressings. • Ichthyol bandages. • UVB. • Environmental change.

‐ Severe: • Photochemotherapy ( UVB (narrow band) usually, PUVA rarely ). • Oral cyclosporine ( short periods ). • Azathioprine. • Mycophenolate mofetil. • Topical tacrolimus. • Alternatives; Chinese herbs and Hypnotherapy.

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‐ Emollients: • Reduces discomfort and itch. • Reduces quantity and potency of steroids needed. • White soft paraffin should be used in place of soap to prevent more drying. • Addition of urea may increase efficacy.

‐ Topical steroids: • Weak and moderately potent are of great value in regular management. • Overuse could lead to:

o Atrophy. o Telangiectasia. o This is why we don’t use more than 1% hydrocortisone longer than

1-2 weeks on thin skin ( face ). • Systemic side-effects due to absorption through inflamed skin.

‐ Antibiotics: • Combination of topical steroids with anti-staph Abx is often useful. • Abx could be given orally ( Flucloxacillin ). • Concerns about MRSA developing!.

‐ Antihistamines:

• Sedating type helps control itching and prevent night-time scratch. • Promethazine and hydroxyzine hydrochloride should be used alternately

as sedating effect is lost after 3-4 weeks ( patient gets used to it ).

‐ Wet-wraps: • Weak antiseptic such as Burrows solution ( aluminum acetate ). • Or a diluted topical steroid. • Beneficial effect due to:

o Good hydration of lesion. o Therapeutic effect. o Hard to scratch.

• Mainly used for short periods for small children and infants. • Care must be taken to avoid hypothermia.

‐ Occlusive bandaging: • Ichthyol bandages over a topical steroid. • Particularly useful for stubborn lesions on limbs. • Alternative 1% Ichthyol in zinc ointment over topical steroid.

‐ Photochemotherapy: • Narrow band UVB and PUVA. • UVB dose should be calculated. • PUVA should be used very rarely.

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‐ Cyclosporine: • Extremely effective in controlling severe AD. • However, high doses ( 2-5 mg/kg/day ) are needed renal toxicity. • A 6-8 week course of Rx that can be repeated is recommended. • Oral only in exceptional cases in childhood dermatitis, and only for

short periods.

‐ Azathioprine ( Imuran ): • 50-100 mg/day is usually effective. • Monitor carefully for:

o Marrow depression. o Hepatic damage.

‐ Mycophenolate mofetil ( Cellcept ): • In adult with severe AD. • Nausea is the main side effect.

‐ Tacrolimus: • Efficient and safe in both adults and children. • Sometimes irritation and burning sensation during 1st week.

‐ Pimecrolimus: • Topical ascomycin ( cream ). • For resistant AD. • Efficient with low toxicity. • Used in infants as young as 3 months old.

‐ Mx of eczema herpeticum: • Topical herpes simplex infection superimposed on AD. • Always suspect eczema herpeticum in a patient with AD who develops

vesicles or shows rapid deterioration, particularly if feverish and unwell. • Commence systemic acyclovir without waiting for lab results. • If febrile IV acyclovir for 1st 28 - 72 hours. • Topical steroids should not be given. • Once there’s obvious HSV infection, topical acyclovir is not effective.

‐ Dietary restriction: • Assistance of dietitian is important, particularly in children to make

sure they’re getting enough nutrients ( especially Ca+ ).  

Notes: ‐ To date there is no reliable, proven, effective and safe method of permanently

suppressing symptoms. ‐ In the great majority of patients, it’s self-limiting and clears spontaneously by

5 years of age.

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Nummular or Discoid Dermatitis ( DD ): Definitions: ‐ Chronic. ‐ Recurrent pattern. ‐ Discrete coin-shaped lesion. ‐ Tends to involve limbs.

Incidence and etiology: ‐ Usually adults with a past history of AD. ‐ Unknown etiology. ‐ Secondary infection is common, although primary infection has not been proven.

Clinical Features: ‐ Lesions are circular or oval. ‐ Symmetrical on legs. ‐ Dermatitis is usually subacute with erythema. ‐ Erythema. ‐ Sometimes surface vesiculation. ‐ Surface may be moist, -/+ pruritis.

Dx: ‐ Classical DD is easy to diagnose, unlike atypical cases:

• Primary infection. • Ps ( Psoriasis ). • ACD ( Allergic Contact Dermatitis ).

‐ Distribution of lesions is usually sparing: • Knees. • Elbows. unlike Ps • Scalp.

‐ ACD: • Discarded by -ve patch test ( not completely ).

  Rx: ‐ Topical corticosteroids ( most effective means of controlling ). ‐ Steroid-Abx combination since secondary infection is common. ‐ In persistent cases Tar or ichthyol in zinc paste. ‐ Rarely systemic anti-pruritics.

     

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Asteatotic Eczema ( AE ) ( Eczema Craquele ): ‐ Dry irritable skin. ‐ Mainly on limbs of elderly. ‐ Large scales with a ‘ crazy-paving ’ look. ‐ Cause:

• Loss of epidermal lubrication, together with inadequately removed soap. ‐ Rx:

• Replacing missing lubrication ( apply emollients and reduce bathing ). • Withdraw soap. • NO topical steroids ( because skin’s already thin and fragile ).

  

Seborrhoeic Dermatitis (SD): Definitions: ‐ Distinct age groups:

• Infants. • Young adults.

‐ Infantile: • Large yellowish scales. • Scalp, face, napkin area. • Self-limiting.

‐ Adult: • Face, scalp, anterior chest. • Itch and irritability ( out of proportion to mild scaling and

erythema ).

Prevalence and etiology: ‐ Infantile:

• Common. • May be confused with infantile AD. • No link between it and adult form.

‐ Adult: • Less common, but more persistent. • Mostly in young adult males, and often associated on the trunk with

involvement of hair follicles ( seborrhoeic folliculitis ). ‐ No quality or quantity changes in seborrhoeic secretion in either form. ‐ P.ovale is found in higher numbers in the lesions ( 10 or 20 ? ). ‐ Some respond to anti-fungals. ‐ Severe persistent SD is seen in a lot of HIV +ve patients.

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Clinical Features: ‐ Infantile:

• Presents in early infancy. • Large yellow scales on scalp extending down onto forehead. • Also usually on:

o Trunk. o Napkin area. o Axillae.

• No pruritis ( Diagnostic favour of SD and against AD ). ‐ Adults:

• Discrete. • Asymptomatic, or mildly pruritic. • Red-yellow, glazed looking. • Site:

o Trunk ( mainly ) ( circular, pale pink, sometimes difficult to see ). o Pre-sternal. o Axillae. o Submammary folds. o Groin. o External ear. o Facial lesions ( More common in men, may be more persistent in

nasolabial fold ). o Scalp ( presenting with severe persistent dandruff ). o Eyebrows and eyelids ( common with early morning stickiness;

blepharitis may be unresponsive to Rx ). • Mild erythema and fine scaling ( usual Clinical Feature ).

Dx: ‐ ACD Patch testing to differentiate. ‐ Ps:

• Lesions aren’t greasy yellow, and distribution differs. • In Ps, lesions are:

o Easily palpable. o Well delineated. o Large coarse silvery scales.

• Pityriasis versicolor: o Excluded by lesion scrapings.

• In SD: o More diffuse. o Smaller scales.

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Rx: ‐ Topical anti-fungals ( Imidazoles ). ‐ Oral anti-fungals when topicals fail ( should not be given continuously on

long-term basis. ‐ Seborrhoeic folliculitis is difficult to treat ( may only respond to systemic

imidazoles ). ‐ Weak potency topical steroids ( cream on face and flexures ). ‐ With any Rx, lesions still tend to recur.  

Contact Dermatitis: Types: ‐ Direct irritant action. ‐ Allergic contact dermatitis ( ACD ):

• Only when previously sensitized. • Reaction mediated by specifically sensitized T lymphocytes.

  Differences between both: ‐ Table 6.3 Page 115.  

Direct Irritant Contact Dermatitis ( DICD ): Definitions: ‐ Caused by exposure. ‐ Damages normal barrier function of epidermis.

Incidence and etiology: ‐ Acute:

• Seen after one single exposure ( usually accident ). • Rapid onset. • Lesions appear exactly at sites of contact.

‐ Subacute: • Seen as ongoing irritation. • E.g. Infantile Napkin Dermatitis.

‐ Chronic: • Cumulative exposure to mild irritants, ‘ barmaid’s hands ’. • Due to degreased skin and removal of protective layer. • Patients with AD are particularly susceptible.

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Clinical Features: ‐ Acute:

• Exposure to strong irritant. • Reddish-brown with vesicles. • Rapid appearance ( 6 - 12 hours ). • Well localized to site of contact. • Painful and itchy. • If no further contact rapid recovery. • Lesions don’t usually develop at distant sites.

‐ Subacute: • Erythema with crusting. • Sometimes blistering. • Maybe early acanthosis. • In infantile napkin dermatitis ( striking sparing of skin folds ) vs

napkin candidosis ( skin folds encourage candida overgrowth ). ‐ Chronic:

• Presents initially as: o Dry, or o Hacked, or o Fissured areas of skin.

• Substances tend to accumulate under rings, with added effect of local trauma, which may provoke severe reactions similar to those seen in ACD to metals.

Rx: ‐ Identification and avoidance ( cornerstone ). ‐ Patch testing to rule out ACD. ‐ For active phase removal of soap and replace with emollient ( Epaderm )

and a topical steroid. ‐ If acute with vesicles wet dressings as soaks or lotions until subacute

phase is reached then substitute with topical steroids. ‐ In napkin dermatitis:

• Remove napkin. • Warm, dry environment. • Skin exposed. • Improvement faster by mild steroid-antifungal combination.

‐ In chronic cases: • Protect area involved. • Liberal use of emollients to replace lipid barrier ( up to 6 months daily

use of emollients, and continuing avoidance of soap may be needed before skin regains its barrier function and can be considered normal ).

 

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Allergic Contact Dermatitis ( ACD ): Definition: ‐ Prior exposure to an allergen. ‐ Specific cell-mediated sensitization.

Prevalence and etiology: ‐ Certain groups are more susceptible, e.g.:

• Chronic skin conditions ( allergy to meds ). • Workers exposed to common sensitivities.

Clinical Features: ‐ Acute or subacute lesions at site of contact. ‐ Milder lesions distant from contact site. ‐ Common sites:

• Ear lobes. • Nape of neck. • Wrist. • Feet.

‐ Topical steroids may elicit ACD ( should be considered in dermatitis patients ).

‐ Early stages: • Inflamed. • Itchy. • Papules. • Vesicles.

‐ Continued exposure: • Dryness. • Scaling. • Fissuring.

‐ Picture is complicated when renewal exposure causes an acute or subacute exacerbation on a long-standing chronic dermatitis.

‐ In all cases of persistent hand dermatitis do: • Patch test to exclude an allergen. • Scrapings to exclude fungal infections.

‐ 80% of all Contact Dermatitis involves the hands and forearms.

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Rx ( 4 stages ): 1. Detection of likely sensitizing agent. 2. Preparation for valid patch testing:

‐ Clear any dermatitis with topical steroids BEFORE patch test is performed ‐ Pregnancy affects immune system which affects patch test results

( wait till after birth ). ‐ Recent sun exposure ( maybe causing erythema! ) will confuse results.

3. Patch testing for suspected substances: ‐ Patches are left for 48 hours. ‐ Check at 48 hours then again 48 hours later ( at 96 hours ). ‐ Make sure that result ( if present ) is an allergic reaction NOT irritant reaction.

4. Counseling on avoidance of responsible allergens.