DERMATOLOGY ON-LINE RESOURCE FOR PRIMARY CARE

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INFLAMMATORY SKIN DISORDERS

PSORIASIS

DEFINITION
Psoriasis is an immune-mediated, inflammatory disease characterized by increased
epidermal cell turnover rate, mainly involving the skin and joints.

AETIOLOGY/PATHOGENESIS
 Multifactorial - immunological, genetic susceptibility, environmental factors
 Triggers in susceptible persons:
o drugs (beta blockers, lithium, chloroquine, rapid withdrawal of systemic
steroids)
o Streptococcus infection
o psychological and physical stress

EPIDEMIOLOGY
Bimodal distribution, peaking between ages 20 – 30 years and 50 – 60 years. But psoriasis
can occur at any age.

CLINICAL
 Pink to red papules or plaques with silvery scale. Figure 1
 Scratch with orange stick to illicit scale. Figure 1
 Auspitz sign: appearance of small bleeding points after scratching off scale.
 May occur at any site. Most commonly affects extensor surfaces (elbows, knees,
lower back); scalp and ear canal. In moist body folds the lesions appear as macerated
intertrigo. Palms and soles may also be affected. Due to the thickness of these areas,
it presents as pustules, thick scale and fissures.
 Genitalia are often affected: in males the head of the penis. In women, usually
undiagnosed and often a source of relationship and psychological stress.
 Nails: pitting, oil spots, onycholysis, subungual hyperkeratosis. Figure 2
 On the scalp, may have well-demarcated erythema with silvery scale, extending to
the hairline. Figure 3
 Psoriatic arthritis occurs in 5-10% of psoriatics. However, joint disease may precede
skin lesions. Clinical types include mono-arthritis; polyarthritis, spondyloarthropathy,
arthritis mutilans, involvement distal interphalangeal joints and enthesitis.

TYPES:
 Plaque psoriasis: papules and plaques
 Inverse psoriasis: intertriginous sites (axilla, sub-mammary, inguinal)

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  Pustular: pustules. May be systemically unwell
 Erythrodermic: more than 90% BSA erythema and scale
 Guttate psoriasis: small teardrop shaped papules. Described post Streptococcus
infection
 Nail psoriasis

ASSOCIATIONS
 Metabolic syndrome
 Obesity
 Depression
 Uveitis

COMPLICATIONS
 Erythroderma
 Pustular psoriasis
 Psychological
 Those associated with metabolic syndrome

MANAGEMENT

AVOIDANCE OF TRIGGERS

TOPICAL
 Face: 1% hydrocortisone
 Body:
o 5% liquor picis carbonis (LPC)
o 5% salicylic acid as keratolytic
o calcipotriol/betamethasone ointment (DovobetTM) to localized psoriasis. Do
not exceed 100g per week to avoid hypercalcemia
o potent topical steroid to stubborn plaques. Watch out for rebound on
withdrawal
o emollients such as soft paraffin or emulsifying ointment
o body folds: Topical steroid creams. Wean quickly to avoid atrophy and striae
distensae
 Scalp:
o 5-10% salicylic acid/HEB overnight to remove scale
o wash with tar shampoo
o potent topical steroid gel/lotion e.g. Fluocinolone gel
o calcipotriol/ betamethasone gel (XamiolTM)
 Failure to respond to standard topicals:
o REFER TO A DERMATOLOGIST
o dithranol/anthralin
o phototherapy
o systemics: methotrexate, acitretin, cyclosporin A, biologics

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Figure 1. Erythematous scaly papules and plaques

Figure 2. Pitting Figure 3. Profuse silvery scale on the scalp in psoriasis

ATOPIC ECZEMA

DEFINITION
Atopic eczema is a chronic relapsing pruritic inflammatory skin condition that is often
associated with elevated serum immunoglobulin (IgE) levels and occurs in families with
atopy (asthma, eczema, hay fever and food allergies).

AETIOLOGY/ PATHOGENESIS
Multifactorial. Mainly dysfunctional skin barrier resulting from immunological responses
that are influenced by genetic and environmental factors.

EPIDEMIOLOGY
 Most commonly develops between 3-6 months of age
 60% of cases developing in the first year of life
 90% before the age of 5 years
 10 - 30% persist into adulthood

CLINICAL FEATURES
 A clinical diagnosis
 Acute eczema: erythema, weeping, vesicles, crusting. Figure 4

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  Chronic eczema: thickening, increased skin markings, colour change= lichenification.
Figure 5
 Age dependent variation in distribution:
o infantile (<2 years): face and extensors
o childhood (2-12 years): flexures
o adult: face, flexors, hands
 Signs of atopy/atopic diathesis:
o infra-orbital folds (Denny-Morgan lines)- extra infra orbital fold Figure 6
o allergic salute sign - nasal crease from rubbing
o headlamp sign – nasal sparing (only if face is involved) Figure 6, 8
o post-auricular fissure Figure 7
o allergic shiners – dark rings around the eyes Figure 8
o hyperlinear palms
o muddy sclera
o keratosis pilaris

COMPLICATIONS
 Infections with Staphylococcus aureus (impetigo), Herpes simplex (eczema
herpeticum) Figure X, molluscum contagiosum
 Erythroderma >90% body surface area erythematous

TREATMENT

BASIC MEASURES
 Avoid irritants
 Soap substitutes such as aqueous cream, cetamacrogol, emulsifying ointment, liquid
paraffin

TOPICALS
 Moisturizers: cetomacrogol, emulsifying ointment, white soft paraffin, liquid paraffin
 Topical steroids
Use correct potency for site
o face: 1% hydrocortisone
o body: ultrapotent (clobetasol) or potent (fluocinolone). Wean to potent
steroid twice a week or diluted steroid (e.g. 10% fluocinolone/cetomacrogol).
o Scalp: wash with tar shampoo and apply potent steroid gel.
Use correct base/vehicle
o cream for wet eczema, body folds
o ointments for dry eczema
o gels or lotions for hair bearing sites
Side effects
o skin thinning, stretch marks, steroid-induced acne and rosacea, systemic
absorption
 Topical calcineurin inhibitors
o indicated for moderate to severe facial or periorbital eczema as steroid
sparing agents to prolong remissions. Not optimum for acute flares

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  Wet wraps useful for short term flare management
 If failed topical treatment/ recalcitrant:
o REFER TO A DERMATOLOGIST
o phototherapy
o systemics: cyclosporine, azathioprine, methotrexate

Figure 4. Acute eczema Figure 5. Chronic eczema

Figure Nasal sparing, Denny Morgan lines, headlamp sign

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Figure 7. Fissure beneath the ear

Figure 8. Nasal sparing, allergic shiners

SEBORRHEIC ECZEMA/DERMATITIS

DEFINITION

A chronic inflammatory condition characterized by recurrent erythema and greasy scale in

areas with terminal hairs and large sebaceous glands.

AETIOLOGY/PATHOGENESIS
 Thought to be due to overgrowth or exaggerated immune response to Malassezia
furfur (Pityrosporum ovale)

EPIDEMIOLOGY
Occurs in infants in first few months of life and is self-limiting. The adult type occurs at
puberty. Increased prevalence in HIV infected individuals and patients with neurological
conditions.

CLINICAL
 Erythematous patches with greasy scale, that is not well demarcated

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  In infants, greasy scale on scalp commonly referred to as “cradle cap “Figure 9, The
face and body folds can also be affected. Figure 10-11 In the groin the fold is
involved.
 In adolescents and adults, it affects scalp, central face, nasolabial folds, eyebrows,
body folds. In severe cases the male chest is involved. Figure 12-13

COMPLICATIONS
Secondary infection

TREATMENT
 Infants:
o face: 1% hydrocortisone ointment
o body folds: 1% hydrocortisone cream
o scalp: 2% salicylic acid/ 2% sulphur/HEB left on overnight to remove greasy
scale. Wash with selenium sulphide shampoo. Apply fluocinolone gel.
 Adults
o Face: 1% hydrocortisone ointment to face
o Scalp: Wash with Selenium sulphide shampoo. Apply Fluocinolone gel.
o Body folds: Potent topical steroid cream. Avoid using potent topical steroids
for prolonged periods.

Figure 9. Greasy scale on the scalp of an infant

Figure 10. Erythema in axilla

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Figure 11. Seborrheic dermatitis affecting the napkin area. The fold is involved.

Figure 12. Greasy scale on scalp

Figure 13. Erythema and scale in axilla

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STASIS ECZEMA

DEFINITION
An eczema of the lower legs due to venous hypertension.

AETIOLOGY/PATHOGENESIS
Due to increased hydrostatic pressure in veins (venous hypertension) resulting in leakage of
serum and blood products into extravascular space. When the lymphatic drainage gets
overwhelmed pedal oedema and eczema result. Usually associated with varicose veins.
Other contributing factors include immobility of ankle or knee joints, previous DVT, obesity
and lower leg surgery (destroys fine lymphatic vessels).

EPIDEMIOLOGY
Common in obese, middle aged women.

CLINICAL
 Lower leg oedema
 Hyperpigmentation (haemosiderin deposition)
 Acute and/or chronic eczematous changes Figure 14

COMPLICATIONS
 Venous ulcers Figure 14
 Cellulitis
 Lipodermatosclerosis: Due to chronicity, the skin becomes bound down and sclerotic
and develops an inverted champagne bottle shape. Figure 14

TREATMENT
 Compression is the mainstay of treatment. Feel for pulses first. If diabetic, be careful
when using compression
 Elevate legs as frequently and for as long as possible daily
 Avoid irritants
 Use soap substitutes
 Moisturize frequently
 Apply ultrapotent/ potent topical corticosteroid

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Figure 14. Lipodermatosclerosis showing inverted champagne bottle sign and venous leg
ulcer

NUMMULAR (DISCOID) ECZEMA

DEFINITION
A relapsing, intensely itchy condition characterized by round, well demarcated ‘coin-like’
lesions.

AETIOLOGY/ PATHOGENESIS
Exact pathogenesis is unknown. Background of atopy, previous contact eczema, stasis
Eczema, xerosis and varicose veins have a strong association with nummular eczema.
.
CLINICAL
 Coin shaped or discoid plaques of eczema Figure 15
 Two forms are recognized:
o exudative acute form which presents with weepy blisters and plaques
o dry nummular eczema which is the subacute or chronic variant characterized by
dry plaques
 Darker skin is often associated hyperpigmentation
 Nummular eczema is most prevalent on the lower legs, although arms and trunk can
be affected

COMPLICATIONS
 Secondary impetigenization

TREATMENT
 Avoid irritants
 Use a soap substitute such aqueous cream or cetomacrogol or liquid paraffin
 Moisturize as much as possible
 Apply potent topical steroids
 May require potent/ ultra-potent topical steroids under occlusion, for short periods
of time

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Figure 15. Nummular eczema. Discoid/ coin shaped plaques with overlying crust

CONTACT DERMATITIS

DEFINITION
Refers to a group of disorders in which the skin reacts to a direct contact with the causative
agent.

PATHOGENESIS AND SUBTYPES

Contact eczema is classified into allergic, irritant, photo and systemic forms based on the
underlying mechanism and clinical appearance. There is often overlap between the different
forms. Figure 16
 Allergic contact eczema - the allergen induces a delayed type hypersensitivity
reaction only in susceptible people. Impaired barrier function of the skin as seen in
ulcers and atopy predisposes to allergic contact eczema. The reaction usually mirrors
the area of contact although it may extend beyond the margins. Common causes
include nickel, acrylates in glue, fragrances, rubber, hair dye, preservatives, topical
antibiotics and topical steroids.
 Irritant contact eczema occurs when exposure to chemicals (body fluids, water,
detergents) and physical agents (friction, heat, cold) damage the skin resulting in
impaired barrier function and subsequent inflammatory response. The speed of
onset and severity depends on the anatomical location, strength and quantity of
irritant, as well as frequency and duration of exposure. Unlike in allergic-contact
eczema, anyone with adequate exposure to the irritant can develop irritant-contact
eczema. The rash is usually confined to the area of contact with the irritant.
Common examples include napkin eczema, drool eczema and chemical burns.

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  Photo-contact eczema develops when a chemical applied to the skin interacts with
ultraviolet radiation. The reaction can either be photoallergic or phototoxic.
Photoallergic reaction is a delayed type hypersensitivity reaction to the UV-activated
chemical, whereas phototoxicity results from direct tissue damage by the UV-
activated chemical. Phototoxicity resembles severe sunburn, whereas photo allergy
presents as an eczematous eruption in sun-exposed areas

EPIDEMIOLOGY
Although common in the general population, allergic contact eczema clusters in certain
occupational groups such as hairdressers, cleaners and florists.

TREATMENT
 Try to identify cause
 Avoid exposure to irritants
 Treat with soap substitute
 Moisturize frequently
 Apply potent/ ultra-potent topical steroids, and wean
 Patch testing may be needed Figure 17

Figure 16. Acute severe contact dermatitis

Figure 17. Positive patch test

ACNE
DEFINITION
An inflammatory condition of the pilosebaceous unit.

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AETIOLOGY/PATHOGENESIS
 Increased sebum production secondary to increased androgens
 Impaired keratinization of hair follicle, leading to microcomedone formation
 Overgrowth of Propionobacterium acnes
 Immunological factors

EPIDEMIOLOGY
Affects 80-90% of adolescence. 20-30% are severe.

CLINICAL
 The comedone is the characteristic lesion of acne. Figure 18
o open comedones - blackheads
o closed comedones – whiteheads
 Other lesions: inflammatory papules, pustules Figure 19; nodules and cysts Figure 20
 Face, upper back, trunk

COMPLICATIONS
Scarring, depression, anxiety, poor self esteem

TREATMENT
 Noninflammatory (comedonal acne)
o topical retinoid at night
 Inflammatory acne
o mild papulopustular: Topical benzoyl peroxide morning/ topical retinoid
night.
o moderate papulopustular
 antibiotic (doxycycline for 3-4 months), benzoyl peroxide/topical
retinoid
 oral contraceptive plus benzoyl peroxide/topical retinoid
o severe papular/pustular/ OR nodulocystic acne
 REFER TO A DERMATOLOGIST for isotretinoin

Figure 18. Open and closed comedones, inflammatory papules and pustules.

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Figure 19. Inflammatory papules and pustules

Figure 20. Nodules and cysts

ROSACEA

DEFINITION
Chronic inflammatory disorder affecting the face predominantly

AETIOLOGY/PATHOGENESIS
Aetiology is unclear.
Factors include Demodex folliculorum, genetic predisposition and chronic use of steroids
Triggers include heat, drinking warm liquids, hot spicy foods and alcohol

EPIDEMIOLOGY
More commonly affects middle aged adults

CLINICAL
 History of flushing
 Erythematous papules and pustules on a background of erythema and telangiectasia
on the convex surfaces of the face Figure 21
 There are no comedones
 Long standing rosacea may be associated with phymatous swelling of the nose, chin
or forehead

COMPLICATIONS

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Phymatous change
Ocular rosacea

TREATMENT
 Avoidance of triggers including stopping all potent topical steroids
 Topical options
o 2% sulphur in calamine
o erythromycin
o metronidazole gel
o ivermectin cream
 Doxycycline 100mg a day for at least 6 weeks. May need to be repeated or treated
for longer periods
 Refer severe unresponsive cases to dermatologist for possible isotretinoin

Figure 21. Erythematous papules on a background of erythema and telangiectasia

PAPULAR URTICARIA

DEFINITION
Inflammatory disease caused by hypersensitivity to insect bites

AETIOLOGY/PATHOGENESIS
Hypersensitivity to insect bites

EPIDEMIOLOGY
Common in childhood

CLINICAL
 Erythematous papules, or vesicles. Intensely itchy
 Grouped or linear arrangement Figure 22
 “breakfast, lunch, supper”
 In a baby, the buttock is spared
 Heals with post inflammatory hyperpigmentation
 If severe and generalized, consider papular pruritic eruption (PPE) of HIV.

COMPLICATIONS
Secondary infection

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TREATMENT
 Potent topical steroid to fresh bites to minimize itch and inflammation
 5% LPC at night useful as anti-pruritic and insect repellant
Sedating antihistamines as required
 Deflea pets and spray home regularly. Fumigate if necessary

Figure 22. Erythematous papules (linear and grouped) with buttock sparing

URTICARIA

DEFINITION

AETIOLOGY/PATHOGENESIS
Type 1 hypersensitivity reaction characterized by raised total and specific IgE

EPIDEMIOLOGY
Affects up to 1% general population, typically begins in the 30s to 50s

CLINICAL
 Characterized by wheals or hives that usually last less than 24 hours Figure 23
 Leave no post inflammatory hyperpigmentation
 Acute urticaria: duration less than 6 weeks
 Chronic urticaria: duration more than 6 weeks

COMPLICATIONS
Psychological

TREATMENT
 Take good history
 Avoid aspirin and NSAIDS
 Non-sedating antihistamines up to four times daily dose

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Figure 23. Urticaria: Erythematous plaques (hives or wheals) that each last less than 24
hours. Some may be annular.

LICHEN PLANUS

DEFINITION
A group of inflammatory disorders which are intensely pruritic

AETIOLOGY/ PATHOGENESIS
Unknown

EPIDEMIOLOGY
Cutaneous variant estimated to occur <1% percent of the population

CLINICAL
 Clinical features can be characterized by 5 Ps: Purple, planar (flat topped), polygonal,
pruritic papules Figure 24-25
 In addition, may show fine lines in a lacy pattern on the surface (Wickham’s striae)
 Classic distribution is flexor surface of wrists, forearms, shins, lumbar back and
genitalia
 Oral involvement is common. There are many variants, the commonest is the lacy
reticular pattern
 Many drugs can cause lichenoid drug reactions, which can be indistinguishable from
the idiopathic form
 Hydrochlorothiazide commonly causes a photo lichenoid dermatitis which is photo
distributed Figure 26

COMPLICATIONS
Post inflammatory hyperpigmentation

TREATMENT
 If drug induced, stop drug if possible

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  Treat with potent topical steroids

Figure 24. Lichen planus

Figure 25. Purple plaques of lichen planus

Figure 26. Photolichenoid dermatitis/ eczema due to hydrochlorothiazide

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BACTERIAL INFECTIONS

IMPETIGO

DEFINITION
Impetigo is a superficial bacterial skin infection characterized by flaccid pustules and honey-
coloured crust

AETIOLOGY/PATHOGENESIS
Most commonly Staphylococcus aureus. Less commonly beta-haemolytic Streptococcus
pyogenes

EPIDEMIOLOGY
 Common in children aged 2-5
 Transmitted by direct contact with infected skin

CLINICAL PRESENTATION
 May be bullous or non-bullous
 Usually affects face and extremities
 Impetigo presents as erythematous plaques or thin walled vesicles that break down
leaving golden or honey-coloured crust. Figure 27-29.

COMPLICATIONS
 Cellulitis
 Osteomyelitis
 Staphylococcal scalded skin syndrome
 Acute post streptococcal glomerulonephritis

TREATMENT
 If mild, use antibacterials or topical antibiotics such as mupirocin, or fusidic acid
 Wash with povidone iodine
 If widespread or severe, treat with oral flucloxacillin or macrolides (erythromycin) if
penicillin-allergic, for 7-10 days

Figure 27. Honey-coloured crust in impetigo

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Figure 28. Child with secondarily impetiginized eczema peri-orally

Figure 29. Bullous impetigo of the face and trunk in a 3-month old child. Note the lesions in
varying stages of evolution ranging from intact blisters, to ruptured blisters and post
inflammatory hypopigmentation of healed lesions.

FOLLICULITIS
DEFINITION
Folliculitis is inflammation of the hair follicle.

AETIOLOGY/PATHOGENESIS
 Infective causes:
o Most frequent cause is Staphylococcus Aureus
o May also be less frequently caused by Malassezia furfur, Demodex mites, and
Candida albicans
 Occlusive causes
 Due to chemical irritation

EPIDEMIOLOGY
Common in childhood and adulthood

CLINICAL
 Itchy, painless or painful papules, or follicular pustules often with an erythematous
base Figure 30
 Predilection for scalp, extremities, occluded areas and areas prone to excessive
moisture or chafing

COMPLICATIONS
Furuncles
Carbuncles

TREATMENT
 Mild infection is self-limiting. Can be treated with topical mupirocin or antiseptics

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  Deep-seated infection may require flucloxacillin or macrolides or first generation
cephalosporins
 If recurrent, treat for staphylococcal carriage (patient and care-giver) with nasal
mupirocin or fusidic acid or half-strength chlorhexidine cream to nostrils twice daily
for 5 days of each month
 Advise on good hygiene, frequent showering and not sharing of personal
clothing/towels

Figure 30. Pustules with surrounding erythema

FURUNCLES

DEFINITION
Furunculosis (boils or abscess) is inflammation of the hair follicle, with deeper abscess
formation extending through the dermis and into the subcutis. A carbuncle occurs when
then are multiple furuncles aggregating to form deep, painful, swollen masses, that drain
through multiple sinus tracts.

AETIOLOGY/PATHOGENESIS
Most common aetiological agent is Staphylococcus aureus

EPIDEMIOLOGY
 Common skin infection
 Transmitted through contact with infected skin and fomites
 Predisposing factors: poor hygiene, overcrowding, malnutrition, immunodeficiency

CLINICAL
 Erythematous, tender fluctuant nodule with central purulence, which may point and
spontaneously drain Figure 31
 Most common on hair-bearing sites on neck, face, axilla and groin

COMPLICATIONS
 Carbuncles
 Septicaemia
 Osteomyelitis
 Scarring

TREATMENT
 If mild, may resolve spontaneously
 Surgical drainage is mainstay of treatment

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  Recurrent furunculosis requires anti- staphylococcal decolonization

Figure 31. Furuncle, erythematous fluctuant nodule, in the post-auricular area

CELLULITIS

DEFINITION
An infection of the dermis. The more superficial form is called erysipelas

AETIOLOGY/PATHOGENESIS
The aetiological agent is primarily beta-haemolytic Streptococcus pyogenes. Less commonly
Staphylococcus aureus.
Risk factors:
Disruption of skin barrier
Neglected wounds
Toe web intertrigo
Leg ulcers
Obesity

CLINICAL
 Patch that is erythematous, hot, tender, oedematus Figure 32
 May be associated with systemic signs and symptoms (malaise, fever, nausea and
vomiting)
 May be bullous or haemorraghic
 Most commonly affects the lower leg, but can also affect the face or other areas

COMPLICATIONS
 Recurrent infections can lead to lymphoedema
 Necrotizing fasciitis
 Phlebitis
 Osteomyelitis

TREATMENT
 If severe: intravenous antibiotics (penicillin)
 If mild: co-amoxyclav or clindamycin.
 If recurrent, consider monthly benzathine penicillin 1,2-2,4 mU.

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Figure 32. Cellulitis

SYPHILIS

DEFINITION
An infectious disorder caused by Treponema pallidum.

AETIOLOGY/PATHOGENESIS
Caused by the spirochete Treponema pallidum. Usually transmitted by sexual intercourse or
in-utero.

EPIDEMIOLOGY
Still common in Southern Africa.
May occur in conjunction with other STIs, including HIV.

CLINICAL
 Primary
o occurs 3-8 weeks after inoculation
o chancre = firm, painless ulcer
o may occur at any site
o may be asymptomatic and go undiagnosed especially on the cervix
o associated painless regional lymphadenopathy, occurs after the chancre
develops
 Secondary
o occurs 6-12 weeks after primary infection
o syphilis is known as the great mimic/imitator
o prodrome of sore throat, fever, malaise, myalgia
o skin lesions may be pink to brown (coppery) macules, scaly papules, nodules.
Figure 33-34. They may mimic psoriasis, pityriasis rosea, lichen planus etc.
o rash is usually not itchy
o may be annular, ulcerated (lues maligna) Figure 35, or crusted (rupioid
syphilis) Figure 36.
o palmar-plantar involvement is a useful clue Figure 37
o other signs include:
 condylomata lata - moist papules genitally or interdigitally
 split papules – same but at angles of mouth
 moth eaten alopecia – patchy non scarring hair loss Figure 38
 mucous patches on tongue

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  Tertiary
o cutaneous gumma
o cardiovascular
o neurosyphilis

COMPLICATIONS

TREATMENT
 Primary and secondary:
o single dose benzathine penicillin 2,4 mu IMI
 Late latent
o benzathine penicillin 2,4 mu IMI weekly x 3 weeks
 Tertiary / neuro syphilis
o procaine penicillin IV

Figure 33. Coppery brown nodules in secondary syphilis

Figure 34. Pink plaques in secondary syphilis

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Figure 35. Nodulo-ulcerative syphilis in secondary syphilis

Figure 36. Rupioid syphilis (like limpets stuck to a rock)

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Figure 37. Palmar involvement in secondary syphilis

Figure 38. Moth eaten alopecia

CUTANEOUS TUBERCULOSIS

DEFINITION

A group of cutaneous diseases due to infection with or hypersensitivity to Mycobacterium

tuberculosis.

AETIOLOGY/ PATHOGENESIS
Mycobacterium tuberculosis can infect the skin and the clinical presentation is determined
by the route of infection and immune status of the host. The route of infection may be
haematogenous, direct local spread, or exogenous. Tuberculids are hypersensitivity
reactions usually seen in people with good immunity.

EPIDEMIOLOGY

TB of the skin is relatively rare, but is more prevalent in TB endemic areas.

CLINICAL
 Scrofuloderma
o Direct local extension of infection from affected lymph node or bone (Figure
39)
o Presents as firm painless nodules that ulcerate and form draining sinuses
o Heals with scarring
 Lupus vulgaris
o Red brown plaques which may ulcerate and become crusted
 Miliary TB
o Haematogenously spread
o Miliary TB is so named because of a millet-like appearance of the TB bacilli in
the lung, as seen on a chest x-ray.
o Cutaneous miliary TB most often presents as vesiculo-papules, the size of a
pinhead, that become necrotic.
 Papulonecrotic TB
o A tuberculid
o Classically presents as papules, with central necrosis; that is distributed
predominantly on acral sites including elbows, knees, earlobes. Figure 40

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  Erythema induratum
o A tuberculid
o Subcutaneous nodules that occur on the posterior calf and often ulcerates
Figure 41(Compare this to erythema nodosum which occurs on the anterior
shin and does not ulcerate)

COMPLICATIONS
 Miliary TB has high mortality
 Scrofuloderma and lupus vulgaris is scarring

TREATMENT
 All forms of cutaneous TB are treated with 6 months of standard TB treatment

Figure 39. Scrofuloderma. Nodules which have ulcerated and crusted

Figure 40. Papulonecrotic TB

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Figure 41. Erythema induratum

SOUTH AFRICAN TICK BITE FEVER

DEFINITION
Rickettsial infection

AETIOLOGY/PATHOGENESIS
Causative organism is Rickettsia africae or Rickettsia conori

EPIDEMIOLOGY
This infection is endemic to Southern Africa.
Transmitted by a bite from an infected tick.
Incubation period 3-15 days after tick bite.

CLINICAL
 Will develop an eschar at site of tick bite Figure 42
 Fever, myalgia, headache
 Rash that may be morbilliform or purpuric Figure 42
 Palm and sole involvement is a characteristic feature

COMPLICATIONS
Renal or cardiac dysfunction

TREATMENT
 Doxycycline 100mg twice daily for 7 -10 days

28
Figure 42. Purpuric rash of South African tick bite fever and eschar

FUNGAL INFECTIONS
SUPERFICIAL FUNGAL INFECTION

DERMATOPHYTOSIS/ TINEA
DEFINITION
These are superficial skin infections caused by fungi called dermatophytes. They include
tinea capitis, tinea corporis, tinea unguium, tinea pedis etc.

AETIOLOGY/PATHOGENESIS
Caused by fungi called dermatophytes.

EPIDEMIOLOGY
Common infection worldwide. Fungal strains vary with geographical region.

CLINICAL
 Tinea corporis
o annular plaques with active edge and central clearing Figure 43-44
 Tinea capitis
o classically as non-scarring alopecia with scale and broken hairs
o other variants: favus, kerion (inflammatory tinea), black-dot tinea, seborrheic
dermatitis like tinea Figure 45
 Tinea pedis
o may present with scale on soles
o maceration between toes
 Tinea unguium
o discoloured, thickened and brittle nails Figure 46
o usually affects several, rarely all nails
o commonly asymmetrical
o “two foot and one hand”
o May have associated tinea pedis
 Tinea incognito

29
 o Refers to tinea corporis with an atypical appearance – most commonly after
inappropriate treatment with topical steroids

COMPLICATIONS
 Secondary bacterial infection
 ID reaction (auto-eczematization as a hypersensitivity reaction the fungus. Presents
with eczematous lesions at a distant site to the primary tinea

TREATMENT
 Topical azoles such as clotrimazole for localized or mild infections
 Systemic antifungals reserved for tinea capitis, unguium or extensive disease. These
include fluconazole, terbinafine, itraconazole. Griseofulvin may be used for tinea
capitis.
 Prevention by changing footwear frequently, adequate drying of feet, refraining
from sharing clothing

Figure 43. Tinea corporis in child

Figure 44. Multiple annular plaques with active edge

30
Figure 45. Tinea capitis showing non-scarring alopecia with scale

Figure 46. Tinea unguium. Note the asymmetry

TINEA VERSICOLOR
DEFINITION
A mild chronic superficial fungal infection caused by Malassezia furfur.

AETIOLOGY/PATHOGENESIS
Caused by Malassezia furfur, a commensal yeast on the skin.

EPIDEMIOLOGY
Very common.
Predisposing factors include high humidity and increased sweating

CLINICAL

 Hypopigmented macules with fine scale Figure 47

 Can be hyperpigmented in dark skin
 Scale can be accentuated by stretching the skin
 Inactive lesions, have no scale

COMPLICATIONS

Residual dyspigmentation may persist for many months

TREATMENT

 For mild cases, selenium sulphide shampoo applied to affected areas and left for ten
minutes or overnight before washing off. This can be done weekly for three weeks.
 Alternative includes ketoconazole shampoo.

31
  For extensive or recurrent cases, a stat dose of Fluconazole 6mg/kg monthly for 3
months may be used; or itraconazole 200mg daily for a week.
 For prevention, use of selenium sulphide shampoo once monthly is recommended

Figure 47. Tinea versicolor showing hypopigmented patches with scale

CANDIDA

DEFINITION
A yeast infection of the skin and mucosa.

AETIOLOGY/ PATHOGENESIS/ EPIDEMIOLOGY

Causative organism is Candida albicans
Risk factors:
 Impaired skin barrier
 Immunosuppression
 Diabetes
 Friction
 Humidity
 Wearing occlusive clothing
 Prolonged antibiotic use

CLINICAL
 Characteristic lesions are pink to red patches, with overlying white patch
 In skin folds include nappy area: erythematous patch, with satellite pustules or
patches Figure 48
 Oral: commonly white patch on erythematous base. The white patch is easily
scraped off
 Other common sites include anogenital, interdigital, angles of the mouth

32
TREATMENT
 Intertrigo:
o antifungal cream bd
o zinc and castor oil
 Oral:
o nystatin drops
o fluconazole 150 mg single dose in severe cases

Figure 48. Intertrigo due to Candida. Mote the beefy red colour and satellites

VIRAL INFECTIONS
HERPES SIMPLEX
DEFINITION
Common and recurrent viral infections caused by herpes simplex virus.

AETIOLOGY
Herpes simplex virus 1(HSV) usually causes oral herpes while HSV2 usually causes genital
herpes, however, HSV1 can infect genitalia and vice versa

EPIDEMIOLOGY
Acquired by direct contact
Sexual transmission in HSV2
Intrauterine and intrapartum transmission may occur.

33
CLINICAL

Oral
 The primary infection occurs in childhood and presents with fever, malaise, mouth
ulcers and difficulty drinking. Figure 49. It may be subclinical.
 Spontaneously subsides but remains latent on nerve ganglia
 Recurrent infections are triggered by stress, UV light, fever, menstruation
 Recurrent infections present as grouped vesicles on erythematous base which later
becomes crusted Figure 50
 Preceded by burning, itching or tingling
 Common sites: vermilion border, but may occur anywhere

Genital
 Usually HSVII
 Sexual transmission
 Painful vesicles leaving painful erosions

COMPLICATIONS
 Secondary impetigenization with streptococci or staphylococci
 In immunocompromised:
o systemic dissemination
o eczema herpeticum (also see section on atopic eczema) Figure 51
o large punched out ulcers

TREATMENT
 Topical antivirals have no role
 Treat with systemic antiviral e.g. acyclovir

Figure 49. Primary Herpes simplex in an immunocompromised child affecting the lips, angle
of the mouth and the tongue.

34
Figure 50. Herpes simplex: Grouped vesicles on an erythematous base

Figure 51. Punched out ulcers of eczema herpeticum in a plaque of eczema in a child with
atopic eczema

VARICELLA / CHICKEN POX

DEFINITION
A common viral infection due to a primary infection with varicella zoster virus (VZV)

AETIOLOGY/PATHOGENESIS
Caused by VZV.

EPIDEMIOLOGY
Mostly affects children
Spread by droplets as well direct contact with blister fluid
Incubation period 7-21 days

CLINICAL
 Itchy vesicles on erythematous base (“dew drops on a rose petal”) Figure 52
 Appear in crops, mainly on trunk, face, scalp, (often in mouth); they heal with crust
 Usually preceded by fever, loss of appetite

COMPLICATIONS

35
  In adults may be complicated by severe pneumonia
 Secondary bacterial infection

TREATMENT
 Treatment in healthy child is symptomatic (Paracetamol and Calamine)
 Acyclovir in severe infection, adults and immunocompromised
Prevention
Vaccine

Figure 52 Chicken pox

ZOSTER (SHINGLES)

DEFINITION
A dermatomal skin disease caused by reactivation of varicella zoster virus (VZV).

AETIOLOGY/PATHOGENESIS
VZV lies dormant on the sensory ganglion after primary chicken pox infection. Reactivation
in times of stress, immunocompromised state or waning immunity from the primary
childhood infection (> 50 years), leads to eruption of varicella zoster in the distribution of
the nerve root.

EPIDEMIOLOGY
Peak age is 50-70
Exclude immunosuppression if in a younger person, if severe or multi-dermatomal.

CLINICAL
 Grouped vesicles or pustules on an erythematous base following a dermatome
Figure 53-54
 May be haemorrhagic or necrotic
 Lasts about 7 days
 Multi dermatomal or crossing of midline suggests immunosuppression
 May be preceded by pain or burning along the affected nerve

COMPLICATIONS
 Post herpetic neuralgia
 Secondary impetigenization
 Ocular involvement if first part of trigeminal nerve affected

36
  Disseminated disease
 Zoster encephalitis, pneumonitis etc.

TREATMENT
 Drying lotions such as calamine, zinc oxide
 Acyclovir at immunosuppressive doses
 Treat post herpetic neuralgia with amitriptyline, pregabalin, gabapentin

Figure 53. Vesicles and pustules in a dermatome

37
Figure 54. Zoster affecting V1 dermatome with ocular involvement and secondary infection

WARTS

DEFINITION
Different morphological variants caused by human papilloma virus (HPV)

AETIOLOGY
Causative agent is human papilloma virus (HPV).
Different types associated with different clinical patterns and oncogenic potential.

EPIDEMIOLOGY
Children commonly affected
Transmitted by direct contact and inoculation

CLINICAL
 Plane warts (verruca plana)
o smooth surface, slightly elevated (planar) above the surrounding skin Figure
55
o hypo or hyperpigmented
o more extensive in HIV
o caused by HPV 3
 Common warts (verruca vulgaris)
o flesh coloured hyperkeratotic nodules, plaques or tumours Figure 56
o common sites are fingers, hands, arms and face. Oral mucosal lesions may
also occur. Figure 57
o on paring with a blade, one sees punctate black haemorrhagic dots

38
  Genital warts (condylomata acuminata)
o may present as flat, dome-shaped, cauliflower-shaped, or pedunculated
lesions Figure 58
 Plantar warts
o occur on the sole of the foot
o papule or plaque with loss of skin markings, and overlying hyperkeratosis
o tender on side to side pressure
o paring with a blade reveals black haemorraghic dots. note callous does not
have punctate black dots on paring

TREATMENT

 Plane warts
o poor response to treatment
o trial of tretinoin cream, or salicylic acid
o extensive disfiguring disease sometimes warrants systemic retinoids
 Common warts (verrucae vulgaris)
o watchful waiting as most will resolve spontaneously
o encourage to soak in hot water, par with sandpaper, pumice stone or blade
followed by daily wart paint: (20% salicylic acid/20% lactic acid/60%
collodion)
o liquid nitrogen
o cautery
o cantharidin
 Genital warts
o podophyllin tincture 25% applied one or twice weekly until clear. Protect the
surrounding skin petroleum jelly ensuring that the warts remain exposed,
then apply a thin layer of podophyllin on the wart surface, followed by a
sprinkling of talc powder to cake the podophyllin and petroleum mixture. The
talc powder ensures that the mixture does not run to normal skin. Washed
off four hours after application. Podophyllin has to be applied by a health
care worker.
o podophyllotoxin 0,5% applied twice daily for 3-4 days followed by a 3-day
rest. Repeat this cycle until the warts are clear. Podophyllotoxin can be
applied by the patient.
o cryotherapy
o cautery. Wear a mask to prevent inhalation of fumes that may contain viable
wart particles.
o imiquimod. Apply thinly three times a week for 16 weeks
 Plantar warts
o soak in hot water. Par with blade, pumice stone or sandpaper. Apply
petrolium jelly to area surrounding wart. Apply wart paint (20% salicylic
acid/20% lactic acid/60% collodion) to affected area. Occlude with a plaster.
Repeat daily.
o cantharidin

39
Figure 55. Plane warts

Figure 56. Multiple common warts on the hand

Figure 57. Multiple oral warts

Figure 58. Perianal condylomata acuminata

40
MOLLUSCUM CONTAGIOSUM
DEFINITION
Molluscum contagiosum is a common viral infection of the skin

AETIOLOGY/PATHOGENESIS
Caused by poxvirus

EPIDEMIOLOGY
 Common in childhood
 Transmission is physical contact and auto-inoculation

CLINICAL
 Usually skin coloured pearly dome shaped papules with central umbilication Figure
59-60
 May be single or multiple
 Tend to spontaneously remit in 18-24 months
 More extensive and atypical in patients with HIV

COMPLICATIONS
Secondary infection, which may lead to scarring

TREATMENT
 Most are self-limiting, so may reassure and practice watchful waiting
 Various destructive and irritant methods may be used with varying success:
o benzoyl peroxide
o topical retinoids
o cryotherapy
o trichloroacetic acid
o curettage
o cautery
o cantharidin
o salicylic acid/lactic acid preparations

41
Figure 59. Molluscum contagiosum in a child. Multiple nodules with umbilicated centres

Figure 60. Extensive molluscum contagiosum

PARASITIC INFESTATIONS
SCABIES

DEFINITION
A very common highly contagious infestation.

AETIOLOGY/PATHOGENESIS
Caused by the Sarcoptes scabies mite. The female mite burrows into the epidermis and
deposits its eggs and faeces. The pruritus and skin lesions are a hypersensitivity reaction to
the mites, eggs and faeces.

EPIDEMIOLOGY

42
  Spread by close personal contact
 Usually affects multiple people in the home
 May lead to epidemics in old age homes

CLINICAL
 History of multiple people itching in the home
 Very itchy papules, vesicles, excoriations and burrows Figure 61-62
 Common sites are web spaces, wrists, axilla, umbilicus, groin. But may occur at any
site
 In infants, the palms and soles may be affected Figure 63
 May be crusted especially in old age homes, and immunosuppressed

COMPLICATIONS
 Secondary infection

TREATMENT
 All affected individuals and close contacts should be treated at the same time,
whether symptomatic or not
 Apply benzyl benzoate in a thin layer to the whole body. Wash off after 24 hours.
Repeat once after a week
 Children <6 months old: 5% sulphur twice a day for 3 days
 In children <2 years: 25% benzyl benzoate
 Children 2-12 years: 50% benzyl benzoate
 Wash all clothes and linen worn in the previous 24 hours in hot water. It should be
hung in the sun and ironed if possible
 Ivermectin is indicated for crusted scabies

Figure 61. Papules and vesicles

43
Figure 62. Excoriated papules, burrows. Note the interdigital involvement.

Figure 63. Papules, vesicles and burrows on the palms of an infant

PEDUCULOSIS CAPITIS
DEFINITION
Infestation if the scalp by lice

AETIOLOGY/PATHOGENESIS
 Pediculus humanus capitis
 Females lay eggs on the base of hair follicles called nits which mature after 8 days to
release nymphs that take further 8 days to mature
 Transmitted by direct contact

EPIDEMIOLOGY
 Worldwide
 All socioeconomic backgrounds
 People of African descent < those of European descent

CLINICAL
 Visualization of hatched eggs that are bigger than nits and adult lice even bigger (2-
3mm).
 Itch
 Dandruff

DIAGNOSIS
Visualization of live lice using fine comb (0.2mm), preferably wet. Nits can persist after
successful therapy

44
COMPLICATIONS
Secondary infection

TREATMENT
 Manual removal (wet combing)
 Permethrin
 Malathion
 Topical ivermectin
 Benzyl alcohol
 Resistant cases require oral ivermectin (section 21)

NEOPLASTIC DISORDERS

BASAL CELL CARCINOMA

DEFINITION
Malignant epidermal tumour arising from basal keratinocytes

AETIOLOGY/PATHOGENESIS
 Risk factors include fair skin, blue eyes, blonde-red hair (Fitzpatrick skin types I and
II), chronic intermittent sun exposure, genetic predisposition

EPIDEMIOLOGY
 Most common non-melanoma skin cancer
 More common in Fitzpatrick type I and II but can occur in other skin types less
frequently

CLINICAL
 May be an erythematous patch, or nodule Figure 64
 Slow growing
 Characteristic features include pearly shine or translucency, telangiectasia. May
develop ulcer or erosion
 Different subtypes including superficial spreading BCC, nodular BCC, morpheic BCC

COMPLICATIONS
 Has the potential to invade locally
 Tends to not metastasize

TREATMENT
 Refer to dermatologist
 Treatment options are dependent on whether low or high risk BCC
 These include curettage and cautery, wide local excision and Mohs surgery

45
Figure 64. Nodular BCC

SQUAMOUS CELL CARCINOMA

DEFINITION
Malignant epidermal tumour arising from keratinocytes

AETIOLOGY/ PATHOGENESIS
 Multifactorial
 Usually due to chronic intermittent sun exposure in fair skinned individuals (blue
eyes, blonde-red hair, burns easily)
 Other factors include:
o HPV subtypes, especially types 16 and 18
o immunosuppression (HIV or iatrogenic)
o radiation
o areas of chronic inflammation
o arsenic
o tar

EPIDEMIOLOGY
Second commonest non melanoma skin cancer

CLINICAL
 Ulcerated nodule or crusted plaque on sun damaged skin Figure 65
 Does not have distinguishing features such as BCC
 Grows more rapidly than BCC

COMPLICATIONS
Metastasize to regional lymph nodes

TREATMENT

46
  Refer urgently to dermatologist
 Wide local excision is treatment of choice

Figure 65. Squamous cell carcinoma

MELANOMA

DEFINITION
Malignant tumour of melanocytes

AETIOLOGY/ PATHOGENESIS
 Risk factors include
o genetic predisposition
o excessive sun exposure, including sunburns
o Fitzpatrick skin types I and II (fair skin, blue eyes, always burns, never tans)
o presence of familial atypical naevus syndrome- multiple atypical naevi
o family history or personal history of melanoma
o presence of large numbers of melanocytic naevi (>100)
o giant congenital melanocytic naevi
 2/3 arise de novo, 1/3 arise in pre-existing melanocytic naevi

EPIDEMIOLOGY
Least common of the skin cancers but most dangerous

CLINICAL
 The clinical diagnosis is based on the A, B, C (D, E) of melanoma
o A= asymmetry of lesion
o B= irregular or notched border
o C= multiple colours. A blue-grey “veil” is highly suspicious
o D= diameter > 6mm
o E= enlarging or elevating or evolving
 Four main subtypes
o Superficial spreading melanoma
 Most common type
 Age 40-60 years

47
  Trunk of men, legs of women
o Lentigo maligna melanoma
 >60 years
 Most often on face
 Better prognosis, prolonged radial growth phase
o Nodular melanomas lack a radial growth phase, and invade rapidly, hence
have a worse prognosis
o Acral lentiginous melanoma: Fig 66
 Most common melanoma in dark skinned individuals.
 The subungual variant may present as a dark streak on the nail
(longitudinal melanonychia). Suspect melanoma if there is widening,
irregularity, or spilling of pigment on to the nail fold (Hutchinson sign)
 Poor prognosis as often diagnosed late

COMPLICATIONS
 Metastasis
 Prognosis is inversely proportional to the depth of invasion (Breslow/s depth)

TREATMENT
 If suspect melanoma, refer urgently to dermatologist
 Will need excision biopsy, followed by wide local excision depending on Breslow’s
depth
 Long-term follow-up with an oncologist

Figure 66. Malignant melanoma

KAPOSI’S SARCOMA

DEFINITION
A multifocal proliferative disorder of lymphatic and endothelial cells

AETIOLOGY/ PATHOGENESIS
All forms of KS are caused by the aetiological agent, Human herpes virus 8 (HHV8)

EPIDEMIOLOGY
 Most common neoplasm in HIV infected
 There are 4 variants:
o AIDS-KS: commonest

48
 o classic KS: occurs in Mediterranean; HIV non infected; elderly males
o African endemic KS: occurs in HIV non infected. Less common than AIDS=KS
o immunosuppressive/ Iatrogenic KS: HIV non infected; commonly organ
transplant patients on immunosuppression

CLINICAL
 Violaceous/ purple patches, plaques or nodules Figure 67-68
 Often associated with lymphoedema Figure 69
 Mucosal disease is a useful clue

COMPLICATIONS
May disseminate to lungs, GIT etc

TREATMENT
 Check HIV status
 If AIDS-KS, start ART
 If not respond to ART, or disseminated disease refer to oncology for chemotherapy.

Figure 67Purple patches, plaques and nodules in KS

49
Figure 68. Purple nodules in KS

Figure 69. Purple nodules with lymphoedema in KS

50
INFANTILE HAEMANGIOMA

DEFINITION
A benign vascular neoplasm of childhood, also known as “strawberry naevus”

AETIOLOGY/ PATHOGENESIS
Unknown

EPIDEMIOLOGY
4-5% of infants

CLINICAL
 A precursor lesion may be present at birth
 Rapid growth which leads to a red, or purple nodule Figure 70-71, which may
ulcerate
 Natural history is rapid growth phase in the first year, followed by an involution
phase (involutes by 10% per year)

COMPLICATIONS
 Ulceration is the most common
 Higher risk of complications:
o haemangiomas in the beard area likely to cause airway obstruction
o may be function threatening: those overlying vital structure such as eyes,
ears, mouth
o if multiple may be associated with liver haemangiomas
o large facial segmental haemangiomas associated with multiple systemic
abnormalities (PHACES)

TREATMENT
 Refer to dermatologist
 Uncomplicated, low risk – treat with ultra-potent topical steroids
 Complicated or high risk areas – treat with beta-blockers

51
Figure 70. Infantile haemagioma

Figure 71. Infantile haemangioma

MELANOCYTIC NAEVUS
DEFINITION
A benign proliferation of melanocyte nests

CLINICAL
 Well circumscribed brown, flesh coloured or black macule, papule or nodule Figure
72
 Regular borders, one or two colours, and symmetrical

TREATMENT
 Melanocytic naevi do not need removal

52
  Refer if sudden change in A, B, C, D, E or looks different to rest “ugly duckling sign”
to exclude dysplastic naevus or melanoma

Figure 72. Melanocytic naevus

DERMATOFIBROMA
DEFINITION
Benign spindled cell neoplasm

AETIOLOGY/ PATHOGENESIS
Unknown, thought to be a reaction to an insect bite

CLINICAL
 Well circumscribed firm papule or nodule Figure 73
 Usually flesh coloured, pink or brown
 May be tender
 When compressed from the sides it becomes depressed – Dimple sign (melanocytic
naevus will protrude outward)

TREATMENT
 Reassure
 Resolve spontaneously over years

53
Figure 73. Dermatofibroma

SEBORRHEIC KERATOSIS

DEFINITION
A common benign epidermal neoplasm

AETIOLOGY/PATHOGENESIS
Unknown aetiology

EPIDEMIOLOGY
Common with increasing age.

CLINICAL
 May be flesh-coloured, pink or brown
 “Stuck on” papule or plaque Figure 74
 Have a greasy or warty surface

COMPLICATIONS
May become irritated or inflamed
Often confused with melanoma

TREATMENT
 Treatment is for cosmetic reasons
 Do not over treat
 Cryotherapy
 Cautery with or without curettage

54
Figure 74. Seborrheic keratosis

ACTINIC KERATOSIS

DEFINITION
A pre-malignant condition with partial dysplasia of the epidermis

AETIOLOGY/ PATHOGENESIS
UV exposure

EPIDEMIOLOGY
Fair skinned individuals

CLINICAL
 Scaly patches or hyperkeratotic papule or plaque Figure 75
 Always in sun exposed areas

COMPLICATIONS
1% chance per year of individual lesions becoming a squamous cell carcinoma

TREATMENT
 Advise on sun protection
 Cryotherapy
 Curettage and cautery
 5-fluorouracil

Figure 75. Actinic keratosis

DRUG REACTIONS

55
STEVENS JOHNSON SYNDROME/TOXIC EPIDERMAL NECROLYSIS (SJS/TEN)

DEFINITION
SJS/ TEN represents a spectrum of severe cutaneous adverse drug reactions, characterized
by widespread epidermal necrosis and mucosal involvement

AETIOLOGY/ PATHOGENESIS
Immunologically mediated
In HIV-infected, most common drugs implicated are nevirapine, cotrimoxazole and TB drugs.
Other common offenders are allopurinol and antiepileptic drugs

EPIDEMIOLOGY
Rare, but increased in HIV-infected persons

CLINICAL
 Occurs 7-14 days after initiation of the drug
 Preceded by a prodrome of headache, fever, malaise, myalgia, arthralgia
 Mucocutaneous lesions start as dusky macules that progress to papules, vesicles,
bullae and epidermal necrosis and detachment Figure 76
 2 or more mucosae have to be affected Figure 77
 SJS <10% epidermal necrosis
 SJS/ TEN overlap 10-30%
 TEN> 30% epidermal necrosis

COMPLICATIONS
 Eye complications including corneal erosions, pseudomembranes, and corneal ulcers
 Sepsis
 Hypovolaemia
 Death (mortality rate for SJS is 1-5%; and TEN 25-30%)

TREATMENT
 Refer early
 Identify and withdraw suspected offending agent(s)
 Supportive care involves analgesia and maintenance of adequate fluid and
electrolyte balance
 Encourage oral fluids
 Eye care: needs ophthalmology review and frequent lubrication with liquid tears and
lubricants
 Mouth care: Open and close mouth to prevent adhesions with frequent gargling and
paraffin gauze to eroded lips and mouth angles
 Genital care: retract foreskin and open the labia to avoid adhesions
 Apply non adherent dressings such as paraffin gauze, Telfir, or in resource poor
settings use sterile sheets with liquid paraffin
 Good nursing care is essential

56
Figure 76. Epidermal necrosis and detachment (stripping) in TEN

Figure 77. Severe oral involvement in SJS/TEN with chelitis and mucosal erosions

FIXED DRUG ERUPTION (FDE)

DEFINITION
A fixed drug eruption characteristically recurring in the same site or sites each time the drug
is administered

AETIOLOGY/PATHOGENESIS
Immunologically mediated
Caused by many drugs

EPIDEMIOLOGY

57
CLINICAL
 Acute lesions usually develop 30 minutes to 8 hours after drug administration
 They start as round or oval itchy plaques of erythema and oedema, becoming dusky
violaceous or brown, sometimes blistering Figure 78
 Resolves with post inflammatory hyperpigmentation in darker skin types
 With subsequent exposure to the drug, it reoccurs in the same site sometimes other
sites

COMPLICATIONS
 May be extensive
 Bullous types are confused with SJS/TEN but usually do not affect three mucosal
surfaces Figure 79

TREATMENT
 Identify and stop the offending drug

Figure 78. Fixed drug eruption

58
Figure 79. Extensive Bullous Fixed Drug Eruption

DRUG REACTION WITH EOSINOPHILIA AND SYSTEMIC SYMPTOMS (DRESS)

DEFINITION
A severe cutaneous adverse drug eruption characterized by a long latency period, a rash and
systemic involvement

AETIOLOGY/ PATHOGENESIS
Immunologically mediated

EPIDEMIOLOGY
More common in HIV-infected persons

CLINICAL
 Occurs 3 - 8weeks after drug initiation
 The rash is urticaria-like or indurated erythema Figure 80
 Associated features are fever, oedema, lymphadenopathy, eosinophilia and hepatitis
 Leukocytosis or atypical lymphocytes may occur

COMPLICATIONS
 Severe liver failure, pancreatitis, pneumonitis, renal failure, myocarditis
 Mortality rate of 10%

59
TREATMENT
 Identify and stop the offending drug
 Monitor LFTS and eosinophils frequently depending on severity
 Topical steroids may be helpful
 Oral steroids may be needed in severe cases

Figure 80. Indurated erythema of DRESS

ERYTHEMA MULTIFORME (EM)

DEFINITION
While EM used to be thought of as part of the SJS/TEN spectrum, it is now considered to be
a separate entity.

AETIOLOGY/ PATHOGENESIS
The most common aetiology is due to infection, usually recurrent herpes simplex or
Mycoplasma pneumoniae. Compare this to SJS/TEN where the most common aetiology is
drugs.

EPIDEMIOLOGY
More common in children.

CLINICAL
 The classic feature is the target lesion which consists of three concentric rings: A
central erythematous or purple plaque, that may blister; a pale ring; and a red halo.
Figure 81-2
 Distribution – may occur at any site, but involvement of palms and soles is
characteristic
 Mucosal involvement is usually milder than in SJS/TEN
 Resolves in 7-14 days
 May recur

TREATMENT

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  Symptomatic
 Encourage oral fluids
 Gargle frequently with glycothymol or saline
 Use non adherent dressings on eroded skin
 Prevent adhesions if mucosal lesions present
 Treat underlying cause

Figure 81. Target lesions

Figure 82. Target lesions

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ABNORMALITIES OF PIGMENTATION

VITILIGO

DEFINITION
A cutaneous disorder that causes complete loss of melanin in affected areas

AETIOLOGY/PATHOGENESIS
Considered to be an autoimmune disorder leading eventually to complete destruction of
melanocytes in affected skin

CLINICAL
 Characterized by depigmented patches, which are commonly symmetrical. Figure 83
However focal or segmental distribution may also occur
 Loss of hair colour (poliosis) may occur
 Natural history and extent is variable
 Spontaneous repigmentation may occur
 Acrofacial vitiligo (lips and hands and feet) tend not to repigment.

TREATMENT
 Potent topical steroids for 3-4 months, then wean
 Recommend natural UV exposure, 10-15 minutes in early morning or late afternoon
 Counsel about use of camouflage / make up to cover affected areas
 Refer to dermatologist for phototherapy or other treatments if extensive

Figure 83. Vitiligo

PITYRIASIS ALBA

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DEFINITION
A mild self-limiting form of eczema

AETIOLOGY/ PATHOGENESIS
Unknown

EPIDEMIOLOGY
Occurs most commonly in children, and may be associated with atopy

CLINICAL
 Hypopigmented patches with fine scale Figure 84
 May have central hyperpigmentation.
 Commonly seen on the face
 It is self-limiting

TREATMENT
 Mild steroid to face (1% hydrocortisone)
 Emollients
 Soap substitute

Figure 84. Pityriasis alba

ALBINISM

DEFINITION
A group of inherited disorders characterized by the partial or complete reduction in melanin
synthesis.

AETIOLOGY/ PATHOGENESIS
Abnormal activity or levels of tyrosinase

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EPIDEMIOLOGY
 Variable around the world
 Oculocutaneous albinism type 2 most common in sub-Saharan Africa

CLINICAL
 Different types of albinism have varying degrees of pigmentary dilution Figure 85
 Solar lentigines and keratosis occur at a young age
 Associated with eye changes: nystagmus, photophobia, severe myopia, blindness

COMPLICATIONS
 Develop non-melanoma skin cancers and melanomas at an early age Figure 86
 Photo aging

TREATMENT
 Counsel
 Advise on sun avoidance and sun protection from birth (They may need up to six
sunscreens per month, sun protective clothing and wide brimmed hats)
 Continuous surveillance for the development of skin cancers
 Refer for eye testing

Figure 85. Albinism

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Figure 86. Squamous cell carcinomas in a patient with albinism

MELASMA

DEFINITION
A common form of localized hyperpigmentation

AETIOLOGY/ PATHOGENESIS
Interplay between hormonal factors and UV light

EPIDEMIOLOGY
 More common in women, but may occur in men
 More common in pregnancy, those on oral contraceptive and menopausal women

CLINICAL
 Tan, brown hyperpigmented macules and patches Figure 87
 Common sites are cheeks, forehead and upper lip

TREATMENT
 Advise sunscreen use
 Topical retinoid at night
 Some response to hydroquinone combinations for short periods only
 Refer to dermatologist

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Figure 87. Brown hyperpigmented patches

ACANTHOSIS NIGRICANS

DEFINITION

AETIOLOGY/ PATHOGENESIS
Associated with weight and insulin resistance
Can be familial
Rare association with other endocrine disorders

CLINICAL
 Characterized by brown velvety plaques, commonly in the body folds Figure 88
 More extensive disease should alert one to other rarer causes

TREATMENT
 Treat the underlying cause
 Topical retinoids or calcipotriol or salicylic acid may be helpful

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Figure 88. Brown velvety plaques of acanthosis nigricans in the neck

HAIR DISORDERS

ALOPECIA AREATA

DEFINITION
A non-scarring alopecia considered to be auto immune.

AETIOLOGY/ PATHOGENESIS
Auto immune disease targeting the hair follicle.

CLINICAL
 Commonest type presents with patches of non-scarring alopecia, with underlying
normal skin surface Figure 89
 Alopecia totalis refers to alopecia affecting the entire scalp
 Alopecia universalis refers to alopecia affecting hair on the entire body
 Ophiasis refers to involvement of the hair margins

TREATMENT
 Mild patchy disease can be treated with ultra-potent topical steroid cream to the
scalp
 Extensive disease needs referral to dermatologist for possible Dithranol or
immunosuppression.

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Figure 89. Patchy alopecia areata

TRACTION ALOPECIA

DEFINITION
A non-scarring alopecia secondary to persistent pulling of hair

AETIOLOGY/PATHOGENESIS/EPIDEMIOLOGY
 More common in women
 Tight braiding, weaves, twisted dreadlocks, ponytails. Use of relaxers with these
hairstyles contribute to traction alopecia

CLINICAL
 Non-scarring alopecia commonly of the fronto temporal area and vertex Figure 90
 Can affect any area subjected to traction
 Clue is fringe sign
 Initially it is reversible, but may become scarring.

TREATMENT
 Address hair grooming practices
 Encourage wearing the hair in looser style
 Advise against tight braids or weaves

Figure 90. Severe traction alopecia

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ANDROGENETIC ALOPECIA

DEFINITION
Hair loss due to androgenic hormones in genetically susceptible individuals

AETIOLOGY/PATHOGENESIS
Thought to be related to conversion of testosterone to dihydrotestosterone

EPIDEMIOLOGY
Males >>>> Females
Age of onset is variable
Early onset may occur in some

CLINICAL
 Male pattern baldness affects the frontal and temporal margins and vertex
 Female pattern tends to give you thinning over the vertex, with a widened frontal
path. Note females have retention of frontal margin Figure 91

TREATMENT
 Reassurance
 Topical 5% Minoxidil
 Consider finasteride in men
 Hair transplant

Figure 91. Female pattern alopecia

TELOGEN EFFLUVIUM

DEFINITION
A diffuse non scarring alopecia.

AETIOLOGY/PATHOGENESIS
Due to changes in the hair cycle as a result of stressful events, such as trauma, pregnancy,
illness, psychological stress, iron deficiency, thyroid dysfunction, drugs
This is usually transient, and hair loss occurs 3-6 months after an event
In some it becomes chronic.

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CLINICAL
 Diffuse hair thinning Figure 92
 Widened path from frontal area to occiput
 Patient often complain of a decrease in size of their pony tail

COMPLICATIONS
Psychological distress

TREATMENT
 Ascertain and treat cause
 Do iron studies, or thyroid functions if clinically indicated
 Reassure
 Consider 5% Minoxidil

Figure 92. Telogen effluvium

FOLLICULITIS (FORMERLY ACNE) KELOIDALIS NUCHAE

DEFINITION
A scarring alopecia.

AETIOLOGY/PATHOGENESIS
Postulated to be mainly related to close shaving hairstyles

EPIDEMIOLOGY
Predominantly males with curly hair, but can occur in straight hair and in females

CLINICAL
 Keloid-like papules, plaques or nodules Figure 93
 Erythema, pustules, scale or crust if active
 Usually affects the occiput, but can affect the vertex (if occiput involved)

70
TREATMENT
 Advise on grooming practices
 If active, Doxycycline 100mg daily
 Potent steroid gel or cream
 Ultra-potent steroid cream if severe

Figure 93. Folliculitis keloidalis nuchae

OTHER
DISCOID LUPUS

DEFINITION
A form of chronic cutaneous lupus erythematosus

AETIOLOGY/PATHOGENESIS
Postulated to be an autoimmune condition

EPIDEMIOLOGY
More common in women

CLINICAL
 Well-demarcated erythematous plaques with peripheral hyperpigmentation and
central hypopigmentation, follicular plugging, atrophy and telangiectasia Figure 94-
95
 It is scarring, and may also be associated with a scarring alopecia on the scalp
 Most commonly distributed in sun exposed areas, but occur at any site if extensive

COMPLICATIONS
Less than 10% of patients will develop systemic lupus

TREATMENT
 Sunscreen

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  Topical steroids, moderate to potent
 If severe, chloroquine 2,3 mg/kg/day
 At baseline, do urine, ANA, systemic enquiry and exam to rule out SLE

Figure 94. Discoid lupus of face and scalp

Figure 95. Discoid lupus

SYSTEMIC DISEASE

SYSTEMIC LUPUS

DEFINITION
A multi system connective tissue disorder characterized by auto antibodies to nuclear
antigens

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AETIOLOGY/PATHOGENESIS
Unknown, but postulated to be autoimmunity in genetically predisposed.

EPIDEMIOLOGY
Women>men

CLINICAL
 Cutaneous (may have any of the following)
o malar / butterfly rash: erythema over the malar area (does not scar) Figure
96
o acute cutaneous lupus- may involve the area between the knuckles Figure 97
o discoid lupus
o subacute lupus
o alopecia
o bullous lesions
o painless oral ulcers
o photosensitivity
o vasculitic lesions
o Raynaud’s phenomenon
 Systemic manifestations
o Lupus nephritis
o Serositis (pleuritic, pericarditis)
o Neurological disease (seizures or psychosis)
o Arthritis
 Laboratory abnormalities
o proteinuria
o haemolytic anaemia
o leukopaenia
o lymphopaenia
o thrombocytopaenia
 Serology
o ANA usually positive
o anti dsDNA is specific for SLE
o anti SM, antiphospholipid antibodies may be positive

TREATMENT
 Refer to rheumatologist for treatment
 Cutaneous lupus treated as for discoid lupus

73
Figure 96. Butterfly rash of systemic lupus

Figure 97. Acute cutaneous lupus in SLE. It affects the area between the knuckles.

DERMATOMYOSITIS

DEFINITION
An autoimmune connective tissue disease affecting skin and muscle

AETIOLOGY/ PATHOGENESIS
Autoimmunity

EPIDEMIOLOGY
 Affects children
 Women> men
 Age >50 suggests paraneoplasia

CLINICAL
 Cutaneous

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 o violaceous periorbital oedema – heliotrope Figure 98
o sign
o violaceous lichenoid papules over knuckles – Gottrens papules Figure 99
o erythema over knuckles, knees or elbows- Gottrens sign
o nail fold capillary changes Figure 100
o erythematous to violaceous patches over V of neck/ shoulders – shawl Figure
101
o erythematous to violaceous patches over hips – holster sign
o mechanics hands – rough skin on sides of fingers
 Proximal muscle weakness
o will have raised CK
o muscle weakness, respiratory muscle involvement most serious

TREATMENT
 For skin: chloroquine 2,3mg/kg/day and potent topical steroids
 For myopathy and systemic involvement: refer to Rheumatologist for systemic
steroids and immunosuppression.

Figure 98. Heliotrope in patient with dermatomyositis

75
Figure 99. Resolved Gottrens papules over knuckles

Figure 100. Nail fold capillary changes of dermatomyositis

Figure 101. Shawl sign

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SARCOIDOSIS

DEFINITION
A chronic granulomatous disease characterized by a reaction to an unknown antigen.

AETIOLOGY/ PATHOGENESIS
Granulomatous reaction to unknown antigen

EPIDEMIOLOGY
25% of patients with sarcoidosis have skin lesion

CLINICAL
 Red brown papules, nodules or plaques Figure 102
 May be annular or hypopigmented Figure 103
 Commonly on face
 May affect multiple systems, most commonly eyes and lungs

COMPLICATIONS
Multisystem disease

TREATMENT
 Refer for biopsy
 Refer to ophthalmology for assessment
 Refer for CXR to exclude lung involvement
 Treat cutaneous lesions with potent topical steroid and chloroquine 2,3 mg/kg/day

Figure 102. Red brown nodules of sarcoidosis

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Figure 103. Annular plaques of sarcoidosis

PORPHYRIA CUTANEA TARDA (PCT)

DEFINITION
A metabolic disorder of haem biosynthesis

AETIOLOGY/PATHOGENESIS
 Due to enzymatic defects in haem synthesis
 Can be genetic or acquired
 PCT is often associated with liver disease, alcohol, HIV and drugs

CLINICAL
 Photo distributed blisters that heal with post-inflammatory hypo/depigmentation,
scarring and milia Figure 104-105
 Associated facial hyperpigmentation and hypertrichosis

DIAGNOSIS
 Send for porphyrin screen (blood and stools)

TREATMENT
 Advise to stop alcohol offending drugs
 Sunscreen
 Chloroquine
 Phlebotomy
 Refer to dermatologist or porphyria clinic for initial diagnosis and treatment plan

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Figure 104. Erosions and scars with post inflammatory depigmentation on dorsum of hands
and extensor arms

Figure 105. Blisters, erosions, with scarring in PCT

79
PELLAGRA

DEFINITION
A nutritional disorder due to lack of nicotinic acid

CLINICAL
 Characterized by the 4 Ds: dermatitis, diarrhea, dementia and death
 The skin changes are characterized by a hyperpigmented scaly lesions
 Photo distributed affecting V of neck, back of hands, upper back
 In neck described as Casals necklace Figure 106

TREATMENT
 Dietary supplementation

Figure 106. Casals necklace

VASCULITIS
DEFINITION
Inflammation of post capillary venules

AETIOLOGY/ PATHOGENESIS

80
  Immune complex mediated leading to fibrinoid necrosis of vessels
 Triggers
o infection
o drugs
o autoimmune disorders
o neoplasia
o other

CLINICAL
 Palpable purpura which do not blanch Figure 107
 They can be bullous, annular, urticarial
 Often distributed on lower legs, acral sites such as ear lobes
 Ulceration if severe
 May have systemic involvement especially if severe and above the waist

TREATMENT
 Treat the cause
 Rule out systemic involvement. Do urine dipstix.
 Refer to specialist

Figure 107. Palpable purpura and bullae

81