Macule: Flat lesion < 1 cm in diameter
Papule: Solid elevated < 1 cm in diameter
Vesicle: Fluid-filled elevated lesion < 0.5 cm diameter
Patch: Flat lesion > 1 cm in diameter
Nodule: Solid circumscribed palpable lesion > 1 cm in diameter
Plaque: Solid elevated lesion > 1cm with a mesa-like or disc-like shape
Bulla: Fluid-filled elevated lesion > 0.5 cm in diameter
Blisters: Refers to both vesicles and bullae
Erosion: Area of skin in which there is partial loss of epidermis
Ulcer: Area of skin in which there is complete loss of epidermis

Commonest complaint is a rash.

History of presenting complaint:
What did it look like at the beginning?
Does it itch?
If it itches when is the itching worse?
Relieving or aggravating factors?
Is the rash intermittent or persistent?
What has the patient been putting on it and with what effect?

Past medical history:
Past history of skin disease
History of atopy
Other medical problems

Atopy is said to exist when there is a personal or family history of eczema of a particular distribution,
asthma and hay fever. It is a genetically determined disorder in which there is an increased liability to form
IgE (reagin) antibodies. IgE plays no part in the aetiology of eczema but is important in asthma and hay
Drug history:
Cutaneous drug reactions are common.
Enquire about prescribed drugs and over the counter medication – do not forget the oral contraceptive pill!
Remember topical medication.
Note any known drug allergies.

Social and family history:
Intake of alcohol
Smoking – specify cigarettes, marijuana etc.
Living conditions
Family history of skin disease and/or atopy
Do any other family members or members of the household have a skin problem?


Occupational history:
Note occupation and hobbies – be specific.

EXAMINATION (2 main rules)
1. Good light
Best light is daylight
Next best is fluorescent light

2. Examine the skin in its entirety – includes scalp, oral mucous membranes, external ear, finger and
finger webs, external genitalia, toes and toe webs, nails.

Diagnosis is often made on the pattern of distribution. Therefore make a panoramic view first. Then look
for primary and predominant lesion and morphology of each.



Cornified layer Stratum corneum

Granular layer Stratum granulosum

Prickle cell layer Stratum spinosum

Basal layer Stratum basale

Malpighian layer = Prickle cell layer + Basal layer

Histologically, the epidermis consists of at least four cell types:
- keratinocytes
- melanocytes
- Merkel cells
- Langerhans cells

The basal layer is the germinative layer of the epidermis.
Keratinocytes are formed by division of cells in the basal layer.
Cells in the prickle cell layer are connected by the desmosome filament system.
In the granular layer, cells contain keratohyalin and membrane coating granules.
Further maturation leads to loss of nuclei and flattening of the cellular outline to form squames in the
stratum corneum.
The epidermal transit time or turnover time is approximately 28 days.

Melanocytes are dendritic cells derived from the neural crest.
They are found only along the basal layer of the epidermis.


The ratio of melanocytes to basal cells varies considerably from 1:4 in the cheek to 1:10 in the arm.
The melanin granules are transferred along the dendritic processes to adjacent keratinocytes where they are
actively phagocytosed.

The Merkel cell is a distinctive cell found in the epidermis of mammals.
It is present in the basal layer of the epidermis, particularly on acral non-hairy skin (palms and soles), and
also in association with hair follicles.
Merkel cells are also found within the dermis in association with Schwann cells of peripheral nerve
These cells are thought to function as slowly adapting sensory touch receptors.

Langerhans cells are dendritic cells present in the suprabasal layers of the epidermis.
They have also been found in the dermis.
It is now thought that the Langerhans cell is a bone-marrow-derived immunocompetent cell, which
provides a trap for contact antigens and presents them to T cells.

The dermis is the supporting layer of the skin and consists of a fibrous component (collagen and elastin)
together with the so-called ground substance.
Lying within it are the epidermal appendages and the neurovasculature, and a cellular component including
fibroblasts and various inflammatory cells.

Consists of the hair shaft surrounded by a downgrowth of epidermal cells into the dermis.
Supplied with blood vessels by an invagination of dermis known as the hair papilla.
Sebaceous glands open into the pilary (hair) canal, and some follicles in certain areas, notably in the axilla,
have, in addition, an apocrine gland.

Hair undergoes cyclical periods of growth divided into three phases:
Anagen, in which there is active hair growth – approximately 3 to 5 years
Catagen, the slowing down phase (phase of involution) – approximately 2 weeks
Telogen, the resting phase – 3 months

In children the hair covering the body is vellus hair.
The hair of the scalp, eyebrows and eyelashes is terminal hair, which has a medulla and is thicker and more
pigmented than vellus hair.
At puberty terminal hair develops in the axillae and pubic area of both sexes, and in the male, also in the
beard area and body.

There are 2 types of sweat glands:
1. Apocrine
- found in axillae and anogenital area
- function unknown but in animals responsible for scent production
2. Eccrine
- influenced by emotions and has thermoregulatory function




Main topical preparations used are:
- lotions
- creams
- ointments
- pastes
- gels

Almost pure water
Used in very wet lesions e.g. exuding lesions of eczema
Lotion commonly used is dilute potassium permanganate 1:10,000 soln, has antibacterial and drying effect
Calamine lotion also has a drying effect
Water and normal saline are examples of lotions

Semisolid emulsions containing both oil and water.
Oil in water (aqueous) creams are water miscible, cooling and soothing. They have a mild moisturizing and
emollient effect e.g. aqueous cream.
Water in oil (oily) creams are immiscible with water and therefore more difficult to wash off. They are
emollient, lubricant, moisturizing but less so than ointments.

Oil or grease based.
They are emollient and protective.
They restrict trans-epidermal water loss and are therefore hydrating and moisturizing.
Used on dry scaly lesions.

Powder in a greasy base.
Example is Dithranol in Lassar’s paste used in psoriasis.

Semisolid preparations with high molecular weight polymers e.g. methylcellulose and can be regarded as
semiplastic aqueous lotions.
They are non-greasy, water miscible, easy to apply and wash off.
Especially suitable for treating hairy parts of the body.

Special preparations
Emulsifying ointment – used as soap substitute and emollient

Hair pomade
- used for scaling of the scalp
- consists of 2% salicylic acid, 2% sulphur in an aqueous cream base

Divided into:

1% hydrocortisone cream .given under supervision for short periods of time (2 – 3 weeks) Side effects of topical steroids: 1.05% (Dermovate) . well-defined. which may be injected intralesionally. Clobetasol propionate 0. inflammatory disorder of the skin. 1/3 of patients recall a family history. Atrophy or thinning of the skin 2. American black.g.used in babies and children 2. non-infectious. Systemic absorption Triamcinolone is an injectable steroid.used on the face except in specific conditions . Hypopigmentation 3.05% (Eumovate) 3. 5 . 5 1. Strong association with human leucocyte antigens (HLA) B27 reported in pustular psoriasis and psoriatic arthropathy.g. erythematous (red) plaques covered by thick silvery scales. Clobetasone butyrate 0.most common in the Indian subcontinent . No race is exempt but: . Typical lesions: Symmetrical.least common in Afro-Caribbean. which may develop in sites of injury – KOEBNER PHENOMENON.g. Mild e. Very potent e. Aetiology: Affects both sexes equally. FURTHER READING Side effects of systemic steroids PSORIASIS Definition: A chronic. Telangiectasia 4. Potent e. Acne 5. Betamethasone valerate 0. The extent is variable and plaques may join to form irregular patterns.g. Japanese and North American population. Striae 6.1% (Betnovate) 4. Moderately potent e. Psoriasis is one of several disorders.

Onycholysis . FLEXURAL PSORIASIS (PSORIASIS INVERSUS) May occur in the major flexures as part of general cutaneous involvement but may specifically and predominantly affect flexures. The rete ridges in the basal layer become more prominent. Accumulation of neutrophils in the stratum corneum may lead to Munro micro-abscess formation.“Oil drop” discolouration .Beta-adrenergic blocking agents Common sites: Scalp Extensor surfaces of elbows and knees Lower back and sacrum Anterior chest Nails: Involvement of the nails occurs with or without psoriasis of the skin. Occurs more commonly in adolescents or young adults.Antimalarials . Increased vascularity leads to erythema. In some patients psoriasis never recurs. it is followed by the insidious onset of psoriasis vulgaris. Prognosis usually good. The turnover time is decreased resulting in abnormal maturation. bleeding points can be seen – AUSPITZ’S SIGN.Splinter haemorrhages GUTTATE PSORIASIS Guttate means raindrops. Nail changes include: . 6 Pathology: Cells in the basal layer divide uncontrollably. In most cases.Alcohol .Subungual hyperkeratosis . Sometimes nuclei are retained in the horny layer – this is called PARAKERATOSIS. In others. Precipitating factors: 1) Streptococcal infections in guttate psoriasis 2) Drugs may exacerbate the disease: . 6 . Commences 2 to 3 weeks after streptococcal throat infection. if the skin is scratched.Lithium . Acute in onset. resolves completely within 4 months.Thimble pitting .

mycosis fungoides Usually areas of both erythema and scaling present. 3) Increased cutaneous blood flow leads to high output cardiac failure. 5) Increased loss of protein and iron through exfoliating scales leads to hypoproteinaemia and iron deficiency anaemia. 1) Patient often unwell with fever and leucocytosis.potent topical PUSTULAR PSORIASIS 2 forms of the disease: 1) Localised to the palms and/or soles 2) Generalised GENERALISED PUSTULAR PSORIASIS OF VON ZUMBUSCH Rare disorder but appreciable mortality. 4) There is increased loss of water because the epidermal barrier to water loss is impaired.g. has a fever and leucocytosis. 7 Causes of skin lesions in the groin: 1) Candidiasis 2) Eczema 3) Tinea cruris 4) Psoriasis 5) Erythrasma (Infection with Corynebacterium. which is erythematous and sore. Factors. tar 5) Corticosteroids . 2) Generalised vasodilatation leads to excessive loss of body heat and central hypothermia. Extensive sheets of small sterile yellow pustules cover skin. Systemic steroids or large quantities of very potent topical steroids may precipitate disease if reduced or withdrawn too quickly.systemic . which may precipitate erythrodermic psoriasis: 1) Infections 2) Hypocalcaemia 3) Antimalarial drugs 4) Irritants and topical application to skin e. SYSTEMIC STEROIDS SHOULD NEVER BE USED TO TREAT PSORIASIS. (Psoriasis is one of the most common causes but eczema. Complications of the disease include: 1) Septicaemia 2) Dehydration 3) Electrolyte imbalance 4) Hypocalcaemia 5) Hypoalbuminaemia Methotrexate and Acitretin are effective drugs for treating pustular psoriasis. 7 . The patient feels ill. turns coral pink on Woodlamp’s) ERYTHRODERMIC PSORIASIS The term “erythroderma” implies that greater than 90% of the cutaneous surface is involved.

Gastrointestinal haemorrhage (mucositis) 8 . 4) Salicylic acid may be added to other products or to an ointment base – keratolytic. aids removal of scales and improves penetration of keratolytics. SYSTEMIC If all have failed then systemic treatment should be used.Dithranol in Lassar’s paste 0. 8 methoxypsoralens given orally.Nausea and vomiting . Approximately 2 hours later.1 to 0. Topical psoralens either painted on to psoriasis or added to bath water followed by UVA may be used. 25% starch. 25% zinc oxide in soft paraffin Tar or Dithranol should not be used in the flexures.Liquid coal tar . 8 PSORIATIC ARTHROPATHY Predilection for distal interphalangeal joints and sacroiliac joint.5% (occasionally 1% prescribed) Lassar’s paste = 2% salicylic acid.2% sulphur in aqueous cream base.Tar shampoo 2) Emulsifying ointment as soap 3) Hair pomade: .Headache .2% salicylic acid . TREATMENT TOPICAL 1) Tar products: .Coal tar ointment . the skin is irradiated with UVA.Dithrocream 0.Used on delicate areas such as scalp. as they are irritant. face and flexures. 6) Topical corticosteroids . 7) Calcipotriol (Vitamin D analogue) PUVA = PSORALENS + ULTRAVIOLET A Psoralens are photosensitisers.Has a minor role . Methotrexate Indications for Methotrexate: 1) Severe incapacitating disease 2) No response to treatment 3) Erythrodermic psoriasis 4) Pustular psoriasis Common side effects: .1 to 2% . 5) Dithranol .

chronic active hepatitis and diabetes mellitus. PAS. Common side effects: . so-called Wickham’s striae.Fine white lines may be visible on the surface.Teratogenesis Cyclosporin A Main side effects . The disease is seen in association with various autoimmune disorders such as primary biliary cirrhosis.Increased liver enzymes .Anti-tuberculosis drugs e.g. . Hepatotoxicity Hydroxyurea Less effective than Methotrexate Acitretin (Vitamin A analogue) Effective in all forms of psoriasis. . inflammatory disorder of the skin.g.Thiazide diuretics . 9 .Sulphonylureas 9 .Increased serum triglyceride and cholesterol .Antimalarial drugs . streptomycin.Organic arsenicals . pruritic. isoniazid . Teratogenesis in early pregnancy (so all female patients should take contraceptive precautions) . Oligospermia . purple (violaceous) papules.Hypertension .Nephrotoxicity . Alopecia .Methyldopa . polygonal. . Typical lesions: .Flat-topped. myasthenia gravis.Dryness of skin and lips . Some drugs may induce lichenoid eruptions e.Lesions may appear at sites of trauma to the skin – Koebner Phenomenon Aetiology: Cause unknown.Diffuse interosseous calcification .Hypertrichosis LICHEN PLANUS Definition: A self-limiting.

Shins . Hypertrophic (commonly occurs on the legs) 7.lacy white patches on the buccal mucosa (pathognomonic) Nails may be affected causing longitudinal ridging or permanent destruction. 10 .widespread lesions with intense itching which interrupts normal activity . Actinic (occurring in sun-exposed areas) 6.P .hair involvement . Guttate Treatment: Mainly symptomatic. The scalp may be involved leading to scarring alopecia. Predominantly papular 2.Lumbosacral region .bullous L.oral ulcers . these then begin to subside leaving intense hyperpigmentation. which may remain for 2 –3 years.P. Clinical features: The eruption begins abruptly. Sites of predilection: . Annular (commonly occurs on the glans penis) 8. Bullous 4. Potent topical steroids Systemic steroids may be indicated in: .Wrists . Varieties of lichen planus: 1. Antihistamines for itching 2. 10 . Atrophic 3.atrophic L. Penicillamine A lichenoid eruption also occasionally occurs on the hands in those who come in contact with colour developer in photography. Linear 5. Usually very itchy.Genitalia The oral mucosa may be involved with: . New lesions continue to appear over 9 – 18 months. 1.nail involvement .Ankles .

Subacute 11 .chest . Second attacks are rare.e. Viral aetiology suspected. It is followed in 10 days to 2 weeks by an eruption of similar but smaller lesions 1 –3 cm.neck . ECZEMA All eczema is dermatitis but not all dermatitis is eczema.Acute .upper arms . Definition: A pattern of inflammation of the skin characterized clinically in the acute stage by ill-defined groups of erythematous vesicles and/or papules and in the chronic stage by scaling and lichenification. and then resolution occurs. In atypical varieties rule out secondary syphilis.back .upper thighs On the chest and back lesions tend to run along the skin lines giving a Christmas tree appearance. 11 PITYRIASIS ROSEA Definition: Acute self-limiting disorder of the skin. Mild topical steroids may be used. Clinical classification: . The distribution of lesions is essentially that of a T-shirt and shorts i.abdomen . FTA. Lichenification is defined as a thickening of the skin with an exaggeration of normal skin markings. do VDRL. Occurs most commonly between ages 10 to 35 years. Clinical features: Starts with an initial lesion called a herald patch which is a pink (rosea) oval patch 3 – 6 cm in diameter with a collarette of scale towards the periphery. Sometimes there is hyperpigmentation but not necessarily so. New lesions continue to appear for 2 –3 weeks. . Treatment: Purely symptomatic. The condition lasts 6 – 10 weeks. Antihistamines for itching.

Adolescent and adult phase: (early teens to early twenties) Lesions primarily dry. woolly clothing. vaccinia. Acanthosis is hyperplasia and thickening of the prickle-cell layer. acanthosis is the dominant feature. face. scalp. wrists. . In the chronic stage. lichenified. neck and extensor extremities with erythematous papulovesicles and oozing. .g. Increased susceptibility to viral infections.Abnormal tendency to vasoconstriction. and knees. possibly foods and anxiety. The atopic state. hay fever and urticaria are commonly associated with atopic dermatitis.More susceptible to wart. . Exogenous ENDOGENOUS ATOPIC DERMATITIS . Stimuli. dry skin. Endogenous – constitutional in origin 2. 12 . heat. hyperpigmented plaques in flexor areas and around the eyes.Common.Asthma.Usually starts for 1st time at age 2 – 6 months – INFANTILE ECZEMA. occurring in all races and affecting over one percent of children . often localized in flexor folds of neck. Infantile phase: (age 2 months to 2 years) Involvement primarily of chest. either in the patient or the immediate family 2. 3. Persistent hand dermatitis may be the only remnant of an atopic diathesis. herpes simplex and molluscum contagiosum viruses.Pressure on skin leads to blanching. which do not cause itching normally affects them e. In the subacute stage. elbows. spongiosis diminishes and acanthosis increases. .Often starts on the face and spreads to the trunk and limbs. Childhood phase: (age 4 to 10 years) Lesions less acute and exudative.E. White dermographism. Associated abnormalities: 1. . itches more than other eczemas because atopic patients have a lower threshold for itching. . Classification based on aetiology: 1. Chronic Histology: Histological hallmark = spongiosis Spongiosis means intercellular epidermal oedema – this is most prominent in the acute stage.A. 12 .

g. 4. Increase lubrication of the skin. Patient education. Bacterial sepsis 2. Cataracts 7. 3. Bath additives Most based on liquid paraffin. aqueous cream Should be used liberally. Often impressive how the cream form of a steroid may be totally ineffective. creams in general are not satisfactory vehicles because they tend to have a drying effect. yet a switch to the ointment form of the same steroid transforms the response.000 solution (pale pink) applied for 10 – 15 mins. For the treatment of eczema. Kaposi’s varicelliform eruption If acute and vesicular. Management of infection: 1. Infection with herpes simplex may lead to generalized herpes and ECZEMA HERPETICUM . Conjunctival irritation 8. Management of the dryness: 1. 2 – 3 times per day for 2 – 3 days. Xerosis or dry skin 5. Diet 3. Molluscum contagiosum and warts 3. Hospitalization 4.g. Potassium permanganate has both drying effect and antibacterial effect. Antihistamines for itching 2. Vehicles A vehicle is an inert carrier of the active ingredient. Keratoconus or conical cornea Management: General: Confirm diagnosis if necessary with skin biopsy. 13 . potassium permanganate 1:10. emulsifying ointment 2. General purpose emollients e. Soap substitutes e. Other aspects of management: 1. Psychological aspects Specific Management of the dermatitis: 1. Eczema herpeticum and eczema vaccinatum have similar eruptions known collectively as KAPOSI’S VARICELLIFORM ERUPTIONS 4. Ointments are far better. Topical steroids The choice of steroids depends on the site and stage of the dermatitis. Alopecia areata 6. Keratoconjunctivitis 9. 13 .

May benefit from occlusion. axillae and napkin area. affecting primarily the scalp.Emulsifying ointment and aqueous cream. . Sometimes condition starts in napkin area rather than face Secondary infection with bacteria or Candida may occur.0 is needed.Combined preparations with steroids.Responds to mild topical steroids. Tar: Before the advent of hydrocortisone in 1952. For body and limbs hydrocortisone often too weak except in children and more powerful steroids required.5% is usually ineffective. . Management: 1. Treatment of the cradle cap Arachis oil useful. in axillae and in some cases on the body.Bandages impregnated with tar. Clinical features: Eruption usually begins with yellow coarse scales in scalp so-called “cradle cap”. 14 . Topical steroids . Reassurance Condition improves over ensuing few weeks. 0. Emollients . The stage: Chronic lichenified dermatitis will usually require a potent steroid. 2. SEBORRHOEIC DERMATITIS Infantile seborrhoeic dermatitis: Common self-limiting inflammatory condition occurring within the first few weeks of life.Coal tar ointment. either a moderately potent or a potent one. Infant otherwise perfectly healthy. Occurs under neck. tar was mainstay of treatment. 14 Site: Hydrocortisone is usually the steroid used on the face. Various ways of prescribing tar . Aetiology: Cause unknown. Separate entity from adult seborrhoeic dermatitis and does not lead to adult form. Very potent steroids rarely required in atopic dermatitis. face. Spreads onto face with yellow crusts particularly around eyebrows and ears. so in practice 1.

Hydrocortisone may be mixed with sulphur or imidazole antifungal e. 15 Adult seborrhoeic dermatitis An eczematous process of varying degrees of severity with a propensity for the scalp. which contain tar. face. eyebrows. Scalp involvement either as dandruff sometimes coupled with erythema. Stasis can be demonstrated by pitting oedema. Presternum and upper back: Potent steroids although tends to relapse very quickly.g. Aetiology Cause unknown. flexures and upper trunk. 2% sulphur. Reasonable to use creams because more cosmetically acceptable than ointments on face.g. STASIS DERMATITIS (Gravitational. Face and scalp: Glabella. Responds well to frequent washing (often daily) with shampoos. ears. Tends to become complicated by topically applied medication. Clinical features: Ill-defined roughness. Flexural SE Management: Scalp: Mild seborrhoeic dermatitis of scalp commonly called dandruff. eyelids and ale of the nose. post-thrombotic. Often does not itch. Presternum and upper back: 3. 15 . stasis should be treated with bandaging. varicose veins. If erythema present. moustache area. topical steroids indicated. miconazole in Daktacort. 2.g. In addition to treatment of the eczema with topical steroids. sideburns. 2% sal acid in aqueous cream base. redness and scaling of the skin. usually potent. Face: Hydrocortisone as 1%. However role of Pityrosporum ovale suspected since last century. In severe cases may use salicylic acid products e. Varicose) Associated with venous stasis e. Distribution: 1. Lesions start around the ankle and gradually spread up the leg. selenium sulphide or ketaconazole.

Allergic Irritant contact dermatitis: Defn: Dermatitis.metal .rubber .perfumes .medicaments The most common industrial allergens . provided that the irritant agent is sufficiently concentrated and the exposure to it is long enough. Reaction does not occur with the first exposure for the immune system requires priming. Aetiology: An irritant dermatitis can occur in any individual.1% hydrocortisone cream  anti-Candida agent may be used in napkin dermatitis. lip licking. Certain individuals more prone to it particularly atopic subjects. Occupation change ? Allergic contact dermatitis: Delayed hypersensitivity reaction. The most common non-industrial allergens: .chromates in cement 16 . Emollients should be used liberally. the potential to react persists indefinitely and the dermatitis will recur if patient re-exposed to allergen. Results from repeated insults to the skin. which results in dermatitis. Management: The irritant substance should be removed from the skin and avoided. . disinfectants.nail varnish .dyes .Potent steroids are usually necessary for irritant hand dermatitis. Once a predisposed individual has become sensitized.some plants . Topical glucocorticosteroids: .Dribbling. Oral antihistamines for itching. .Irritant .Napkin dermatitis . bleach. which results from overexposure of the skin to an irritant substance. There are many contact allergens so referral to a dermatologist is almost always necessary because patch tests required.cosmetics . which accumulate and eventually result in dermatitis. 16 EXOGENOUS CONTACT DERMATITIS . Examples: . Skin must be kept out of water as much as possible. thumb sucking in children.Irritant dermatitis of the hands: detergents.

The patient will recover if antigen permanently removed. but relapses if antibiotics are withdrawn. which constitute a battery. Iatrogenic contact dermatitis can be avoided if doctors refrained from prescribing topical anaesthetics. eyelid margins. neck. SECONDARY DERMATITIS Usually secondary to an infestation or infestation. then skin inspected for dermatitis corresponding to application site of allergen. The skin manifestations usually become less severe with age perhaps with maturation of the immune system. rubber . Other HTLV 1 associated disorders: Adult T cell leukaemia/lymphoma HTLV 1 associated myelopathy / Tropical spastic paraparesis (HAM/TSP) Uveitis  optic atrophy Patients are more prone to developing: Crusted scabies Corneal opacities Lymphocytic intersitial pneumonitis Chronic bronchiectasis 17 . The disease responds to antibiotics. glues Management: The diagnosis of a suspected contact dermatitis should always be confirmed by patch testing. Staphylococcus aureus and /or -haemolytic streptococci are commonly cultured from the anterior nares and skin. dyes . Sometimes seen in children with otitis externa or nasal discharge – it is suspected that these children develop an allergy to a component of the bacteria. resins in the plastic industry . axillae. Some reactions delayed so skin inspected after further 48hrs. paranasal skin. May be associated with scabies therefore patient should be examined carefully. If scabies is treated with topical steroids it may lead to crusted scabies. to which other relevant potential allergens are added. The chemicals are put into aluminium wells fitted into an adhesive tape and then stuck on to patient’s back. topical antihistamines. The average age of disease onset is 2 years and 60% of patients are female. There is also a chronic watery nasal discharge sometimes associated with crusting. and groin as well as a generalized fine papular rash. The pathogenesis is as yet undefined. 17 . Removed after 48 hrs. external ear and retroauricular areas. There are 20 common allergens. HTLV 1 ASSOCIATED INFECTIVE DERMATITIS Characterized by a severe exudative dermatitis of the scalp.

Vesicular type (Acute tinea pedis) 3. Tinea manum: (dermatophyte infection of the hand) Tinea unguium: (dermatophyte infection of the nails) Features include: .thickening .brittle nails with crumbling . Epidermophyton 3. Microsporum Further divided into: Zoophilic – originates in animals Anthropophilic – originates in man Geophilic – originates in the soil Zoophilic and geophilic dermatophytes are extraneous fungi and therefore lead to increased inflammation and atypical presentations Tinea pedis: (dermatophyte infection of the foot) 1.onycholysis Tinea cruris: (dermatophyte infection of the groin) 18 .Sometimes referred to as moccasin-type Ide reaction: Eczematous reaction on hands in response to dermatophyte infection of the feet. Pityriasis versicolor DERMATOPHYTES 3 main classes 1.Discolouration . 18 FUNGAL DISEASES OF THE SKIN 2 main groups: 1.subungual hyperkeratosis . Hyperkeratotic type (Chronic tinea pedis) . Deep Superficial fungal infections: 1. Dermatophytes: characterized by well-formed hyphae. Interdigital type (Athlete’s foot) 2. Candida albicans and other species of Candida 3. Superficial 2. Trichophyton 2. heels and sides of feet . which mat together to form mycelia 2.Affects soles.

Terbinafine (Lamisil) – in topical preparation (cream).Scalp and hair infection Tinea capitis must be treated with a systemic drug for at least 4 weeks.Tolnaftate (Tinactin) cream and powder 2.mounted in potassium hydroxide solution and viewed under the microscope for hyphae . Nystatin and Amphotericin are not effective against dermatophytes. scaly and sometimes vesicular. . Treatment Topical: Small areas can be treated topically. . 1.Infection affecting large areas of the body . Keratolytic drugs . Candida and Pityriasis versicolor.Most common organisms are: Microsporum audouini Microsporum canis .Naftifine (Exoderil) 4. scaling of scalp with short broken hairs.Active advancing edge which is raised. 19 Tinea corporis: (dermatophyte infection of the body) .Presents as round patch of alopecia. The polyenes. Same can be done for nail and hair clippings.Can form circinate irregular patterns.Whitfield’s ointment: benzoic acid + salicylic acid . Griseofulvin: 19 . Alkylamines: .Acute infections . Imidazoles: Eg miconazole (Daktarin) clotrimazole (Canesten) 3.Nail infection . effective against dermatophytes.Common in children.sent to Microbiology for culture. . uncommon in adults. Tinea capitis: (dermatophyte infection of the scalp and hair) . Ciclopirox olamine (Batrafen) Systemic: Indications for systemic treatment are: . .Fluoresces green under Wood’s light if caused by the above organisms Identification Scrapings can be taken from skin lesions: . 1.

. 2.or hyperpigmented.Typically affects adolescents and young adults. Naftifine (Exoderil) 7. Ciclopirox olamine Systemic: 1. irregular patches (sometimes slightly raised).g. which is normally a commensal but becomes pathogenic in warm humid conditions. 2. the organism is sometimes known as Malassezia furfur. 3. Alkylamines: Terbinafine (Lamisil) – may be used systemically in dermatophyte infections. 250mg daily for 6 weeks for fingernails. Ketaconazole 200mg daily for 5 days or 400mg stat. Imidazoles e. . Selenium sulphide 2. Candida and Pityriasis versicolor. 250mg daily for 3 months for toenails.Well-defined. They become pathogenic by budding and producing filaments known as pseudohyphae – in this state.Mainly occurs on the upper part of the body. 20 . miconazole (Daktarin). ketaconazole shampoo or cream (Nizoral) 4. toenails – 3 courses 4. In nail infections. Particular individuals seem susceptible and it tends to be recurrent in these persons. . 20 In tinea capitis give Griseofulvin for 4 – 6 weeks + topical treatment (selenium sulphide or Ketaconazole shampoo to reduce infectivity).Hypo.May have mild itching. Terbinafine cream (Lamisil) 6. Sodium thiosulphate 3. PITYRIASIS VERSICOLOR Caused by yeast. Half strength Whitfield’s ointment – irritation is a common side effect. .Mildly scaly. Treatment: Topical: 1. Caused by the unicellular yeast Pityrosporum orbiculare and Pityrosporum ovale. Imidazoles: Ketaconazole – effective against dermatophytes. subsequent course repeated after 21 days. . Triazoles: Itraconazole – effective against dermatophytes. clotrimazole (Canesten).used in dermatophyte and Candida infections In nail infections Itraconazole can be given: 200mg daily for 3 months OR 200mg bd for 7days. Fluconazole . Candida and Pityriasis versicolor.5% shampoo (Selsun) 5. Clinical features: . fingernails – 2 courses.

Chronic paronychia: .Maceration .Iatrogenic factors e.Bolstering of the nailfold . Eighty percent of normal individuals harbour the yeast as a commensal in the oropharynx. Candida intertrigo: (Intertrigo is a dermatological term that indicates an eruption. steroids. 21 2.Dark pigmentation of the nails Oral candidosis (thrush): . Factors that favour candidosis: . imidazoles. which occurs between two apposing skin surfaces) .Neutropenia .Satellite lesions Treatment: Topical: Nystatin.Loss of cuticle . Systemic: Imidazoles e.Damage to the stratum corneum .Immunosuppression . which on removing shows an erythematous base. genitalia. Itraconazole 100mg daily for 5 days. immunosuppressed. Amphotericin. Intravenous Amphotericin B used in resistant cases of systemic candidiasis but toxic.Inflammation of the nailfolds . Fluconazole (Diflucan).Erythema .Common in diabetes . menstruation and pregnancy .g.White patches on the mucous membranes.Uraemia and malignant disease .g. Cushing’s disease . healthy individuals who are edentulous and neglect oral and dental hygiene.g.Susceptible individuals include: neonates.Extremes of age. . DEEP FUNGAL INFECTIONS 21 . Itraconazole (Sporanox).Occlusion .Occurs in persons whose hands are much exposed to water . Ketaconazole Triazoles e. oral contraceptives. antibiotics.Endocrinopathies eg. diabetes mellitus. flexures and nails usually caused by Candida albicans.White exudate . CANDIDA Candidosis (Candidiasis) is a common infection of the mouth. gastrointestinal tract or vagina.

22 . Treatment: Oral potassium iodide – 10 drops. Aetiological agents of mycetoma: Eumycetoma Actinomycetoma Madurella mycetoma Actinomyces species Nocardia species Streptomyces species Found on limbs and exposed areas. MYCETOMA Caused by a number of organisms. Limbs affected. PARASITIC INFESTATIONS SCABIES Causative mite – Sarcoptes scabiei. Eumycetoma may respond to itraconazole. Site of predilection – limbs. Transmitted by prolonged physical and usually intimate contact. Amphotericin B given intravenously. 5 fluorocytosine may be used alone or in combination with Ketaconazole or Itraconazole. Treatment: Surgical excision is the treatment of choice for early lesions. Usually acquired from trauma in agricultural work. sulphonamides or tetracyclines. 3 times daily after meals. 22 SPOROTRICHOSIS Caused by Sporothrix Schenkii. Discrete fungating lesions. Amphotericin B sometimes used intralesionally. CHROMOBLASTOMYCOSIS Caused by several fungi including Cladosporium and Phialophora species. Alternatively. a saprophyte of vegetation. which may be fungi (eumycetoma) or bacteria (actinomycetoma). Produces discrete fungating lesions. Treatment: Excise small lesions Actinomycetoma may respond partially to penicillin. which run along the lymphatics. Has chronic discharging sinuses with granules.

burrows (pathognomonic) . gamma benzene hexachloride. (Application should be renewed after the first 12 hours. Patients are usually immunosuppressed. commonly irritates the skin. are: .Around the nipples . 23 The newly fertilized female burrows into the epidermis and lays her eggs. Permethrin should be used for 12-14 hours in infants and children up to 2 years.pustules . neck. Identify burrow. Lesions. Apply lotion or cream and keep this on for 24 hours without bathing.Axillary folds . Bathe and wash all bed linen. Crusts are hyperinfested with mites. 23 . avoid in children.papules .Sides of fingers and finger webs .) A further treatment for 24 hrs may be required for benzyl benzoate.Peri-umbilical area . Itching may persist for weeks after treatment completed.Natal cleft .Infragluteal fold . Clinical features: Itching is the most obvious and manifestation of scabies and in some cases may be the only one. 3. Permethrin does not usually require a second treatment.Penis and scrotum in men . ears. which may be seen. face. Treatment: 1. Gamma benzene hexachloride (Rid) – avoid in infants 3. View under microscope. Place on slide with few drops of potassium hydroxide soln. 2.secondary eczema Sites of predilection: . application should be extended to scalp. 4.Wrists . All contacts must be treated. Scrape off debris and mite.Elbows . Benzyl benzoate (Ascabiol) – do not use in infants.Ankles and feet in children Diagnosis: 1. Permethrin (Nix) – treatment of choice for infants. In infants and children up to 2 years. 2. Crusted scabies: Presents clinically with numerous crusts over the body especially on prominent areas such as knees and elbows as well as the usual areas of predilection for scabies.

malaise  Then crops of macules. which become vesicles surrounded by erythema  The contents of the vesicles become turbid and crusted  Individual lesions are at different stages of development  The distribution is centripetal which means that the trunk is most extensively affected.  Complications include: varicella pneumonia and encephalitis. Herpes Zoster (shingles)  Caused by the same virus that transmits varicella (chickenpox)  The virus lies dormant in the dorsal root or cranial nerve ganglion after a patient recovers from chickenpox  There may be a latent period of several decades before the virus is reactivated and commences to spread along the cutaneous nerve Clinical Features  The first symptom is the abrupt onset of pain or discomfort  Examination reveals an eruption which corresponds to a dermatome  Each individual lesion begins as a red macule which rapidly becomes a papule and then a vesicle surrounded by erythema  The vesicles may become confluent and evolve to become pustular haemorrhagic and finally scabbed Complications  Involvement of certain dermatomes e. VIRAL INFECTIONS OF THE SKIN Varicella (chickenpox) Clinical Features  Caused by varicella zoster. followed by the upper arms and thighs  The disorder is quite pruritic  Lesions are found in the mouth Management  Uncomplicated varicella only requires symptomatic treatment. a double-stranded DNA virus belonging to the herpes group  Incubation period 9 – 23 days  Mild prodrome of fever. acyclovir may be given orally or intravenously.g. the ophthalmic branch of the trigeminal nerve  Disseminated herpes zoster 24 . then the face and scalp. 24 Treatment: Same as above but several applications may be required.  In complicated cases or immunosuppressed individuals.

25  Postherpetic neuralgia Management  Acyclovir  Analgesia and bed rest  Topical antibiotics may help to prevent bacterial infection  REMEMBER live chickenpox virus is present in the lesions until the scabs have formed so someone who has never had chickenpox can catch it from a patient with shingles Molluscum Contagiosum  Caused by a pox virus  Common in children and young adults  Close contact in children and sexual transmission in adults are well recognized as means of spread Clinical Features  Typical lesion is an asymptomatic flesh-coloured or dome-shaped papule with a central depression  This ‘umbilication’ is the most important diagnostic sign  An individual lesion lasts about 2 months  The outbreak resolves spontaneously within a year Management  Some dermatologists leave them alone  Cryotherapy with liquid nitrogen can be done  The lesions can be pierced with a cocktail stick dipped in iodine  Imiquimod (Aldara) – an immune modulator Viral Warts  Due to an infection of skin or mucous membranes by the human papilloma virus  Warts are contagious and spread more easily if there is local trauma to the skin  Commonly contracted from institutions where there are communal bathing and changing facilities Clinical Types  Common warts (verrucae vulgaris)  Plane warts  Palmar and plantar warts  Mosaic warts  Anogenital warts (condylomata acuminata) Management  Salicylic acid preparations with or without lactic acid  Podophyllin  Glutaraldehyde or formaldehyde  Imiquimod  Liquid nitrogen  Cautery 25 .

amoxycillin + clavulinic acid. between 10 days and 3 months after infection  The chancre is a painless ulcer with an indurated edge  Spirochaetes may be demonstrated by dark-ground microscopy  Local lymph nodes are enlarged but quite painless  The chancre heals spontaneously within 1 – 3 months Secondary Syphilis  This occurs 6 – 8 weeks after the chancre  The patient usually presents with a fever and rash  The eruption is widespread  It does not itch 26 . latent or tertiary  The former two stages are infectious Primary Syphilis  The primary lesion or chancre occurs at the site of inoculation. 26 BACTERIAL INFECTIONS OF THE SKIN Carbuncle  A carbuncle is an acute abscess of contiguous hair follicles caused by Staphylococcus aureus  Staphylococcus aureus is usually also present in the nose axillae and perineum  It is most common in adolescents and young adults  The patient is usually healthy Management  Incise and drain pus  A swab should be taken for culture and sensitivity  Cloxacillin. contagious and superficial infection of the skin caused by either Staphylococcus aureus or β haemolytic streptococcus or both  Starts as large or small blisters with yellow pus  The blisters rupture and purulent exudate dries to form honey-coloured crusts  Occasionally nephritis may occur three weeks after infection with the nephritogenic strain of streptococcus Syphilis  An infection with the spirochaete Treponema pallidum  Syphilis is usually sexually transmitted but may be acquired from maternal disease in utero or from infected blood products or instruments  The disease is divided into stages known as primary. secondary. erythromycin are usually effective Impetigo  An acute.

cysts. pustules. comedones. . 90% of teenagers have acne . Commoner in females than in males. Lesions are papules. Thought to be physiological . . borderline and lepromatous based on the immunological status of the patient  Designated TT – BT – BB – BL – LL  Neurological involvement occurs Management  Dapsone  Rifampicin  Clofazimine ACNE VULGARIS Definition: A chronic inflammatory disorder affecting the pilosebaceous unit which is characterized by the formation of comedones. erythematous papules and pustules. 27  There is a generalized lymphadenopathy  Initially the rash is macular and pink (roseola)  It becomes papular and more widespread  Annular configurations may occur  In the intertriginous areas the papules may become eroded – condylomata lata  ‘Snail-track’ ulcers appear in the mouth  Moth-eaten alopecia is common Tertiary Syphilis  The gumma is the hallmark of tertiary syphilis  Dermal gummata are firm brownish-red papules or nodules which are usually arranged in an annular manner  Mucosal gummata may occur and the tongue may be diffusely infiltrated Management  Intramuscular long-acting penicillin – treatment of choice  Tetracycline  Erythromycin Leprosy(Hansen’s Disease)  A chronic infection principally of the skin and nervous system caused by Mycobacterium leprae  The disease is transmitted by inhalation or ingestion of infected nasal droplets  The degree of involvement depends largely on the immunological status of the patient and the bacteriological load  Leprosy is classified into tuberculoid. 27 .

Increased sebum production: Sebaceous glands directly under androgen hormonal control . papules and pustules result. of which P. If deeper.P.Cheeks .causing inflammation .bacteria c) Pityrosporum ovale – yeast.bacteria b) Staphylococcus epidermidis .Free fatty acids produced in the follicle by action of enzymes associated with P. Presence of skin micro-organisms: Pilosebaceous duct and skin surface colonized by important micro-organisms: a) Propionibacterium acnes .May be target organ over-activity (increased conversion of testosterone by enzyme 5a reductase at androgen receptor of sebaceous glands.Caused by failure of the epidermis lining the duct to keratinize properly so keratin not shed correctly .It has been shown in some women that sex-hormone binding globulin is reduced leading to elevated levels of serum unbound testosterone . acnes elaborates small molecular weight peptide which attracts polymorphonuclear leukocytes to microcomedones and initiates inflammation 28 .Upper chest .Back .e. acnes act as a primary irritant .Forehead . The production of inflammation 1. nodules.attracting white blood cells.The comedone represents blockage of the pilosebaceous duct by a keratin plug . Blockage of pilosebaceous canal: . .Shoulders Pathogenesis: 4 major aetiological factors: 1. 4. The production of inflammation: . Skin bacteria contribute to the pathogenesis by: . acnes is dominant.Chin . comedones. Increased production of sebum 2.Nose .Less commonly. 2. cysts and scarring may occur 3. high overall androgen production. Excessive keratinisation at follicle mouth causing blockage of the pilosebaceous canal 3. Presence of skin micro-organisms 4.disrupting the follicle wall .If blockage superficial. it can be a feature of a virilizing disease i. 28 (Comedones = whiteheads + blackheads) Common sites: .

Tight fitting clothes. norethindrone and norethindrone acetate 2.Some oral contraceptives may cause acne to flare especially those which contain the androgenic and antioestrogenic progestogens norgestrel. friction. Activation of complement releases neutrophil hydrolytic enzymes which rupture the follicular wall . Medicaments . 29 . Aggravating factors: 1. Iodide in seaweeds if eaten in large amounts. Chlorides Halothane .Antiepileptic drugs: Phenobarbitone and derivatives Phenytoin and hydantoin derivatives .Hormones: Topical and systemic corticosteroids ACTH Androgens Danazol . Climatic conditions . 5.Pressure.There may be premenstrual exacerbation . in radiological materials and in drugs used in the treatment of thyroid disease. Other exo-enzymes produced by P.Lubricating oil 29 . Drugs .Often becomes worse in hot humid climate 3.Halogens: Iodides in cough mixtures. rubbing and squeezing from clothing or behavioural habits 6. Mechanical trauma .Heavy oils.Oily or greasy cosmetics 4. P. Occlusive circumstances .Halogonated hydrocarbons .Anti-tuberculosis drugs Isoniazid Rifampicin 7.Tar . Bromides (rarely given nowadays). Endocrine factors . greases . acnes is also a potent activator of complement via the classical pathway . acnes may also contribute to rupture. Industrial: .

Topical antibiotics Clindamycin . . Mild acne – topical treatment Moderate and severe acne – topical and oral treatment TOPICAL TREATMENT Topical preparations largely a) antibacterial b) keratolytic (exfoliating) i. 10% concentrations as cream or gel. 4. discos. Irritates the skin. 5. Avoid aggravating factors. Also available in 5% and 10% soaps and washes. thus inhibiting the formation of comedones while helping existing comedones to become loosened and expelled.Increases basal cell mitosis (epidermal cell turnover) and decreases the cohesiveness of horny cells. 4. 3.e.Available as solution.Less effective.5. Sometimes combined with other antibacterials.025%. reducing the faulty keratinization at the pilosebaceous duct. Isotretinoin (Isotrex) gel 30 . .Available in 0. Benzoyl peroxide .Keratolytic . gel or lotion Erythromycin . ointment or gel sometimes in combination with other anti-acne agents Tetracycline .May produce temporary yellow discolouration that may be washed off after 1 hr with no decrease in drug effectiveness .exfoliating Available in 2.Available in 1% concentration in alcoholic solution.antibacterial .1% concentrations. Stieva-A) cream or gel .Causes erythema.Will fluoresce under long wave ultraviolet light eg. Increase to twice daily to the point of mild dryness and erythema but not discomfort.050% and 0. 1. . 0. peeling and increased sensitivity to sunlight. Chemical exfoliating agents 1-2% ppt sulphur 1-2% salicylic acid 1-2% resorcinol 2. Retinoids (vitamin A analogues) Tretinoin (Retin A. 30 MANAGEMENT: Determine effect of disorder on patient’s morale. therefore start with weakest strength nightly.

Adapalene (Differin) gel .Not yet available in Jamaica ORAL TREATMENT: ANTIBIOTICS: 1.Least expensive. . .Must be taken on an empty stomach. Oral tetracycline .Absorption not decreased by milk. .Drug interaction with metallic irons Al.Overall most effective antibiotic to treat acne.Used in a similar way to tetracycline but more expensive and may cause abdominal cramps HORMONAL THERAPY Diane .Teratogenic: females must be on adequate contraception . ALTERNATIVE MEDICATION Spironolactone 31 . . Similar to Tretinoin but less irritating.Given for a course of 4 months . then decrease to maintenance dosage 250 – 500mg per day. RETINOIDS Isotretinoin (Roaccutane) . Oral erythromycin .Candida vaginitis . ethinyloestradiol 35 micrograms.Similar to Tretinoin but less irritating. increased plasma lipids and liver enzymes . cyproterone acetate 2 mg and oestrogen. Tazarotene (Tazorac) gel . . . Mg. .Less expensive than minocycline but more expensive than tetracycline.Special oral contraceptive pill with an anti-androgen. few side effects.Minor gastrointestinal tract irritation . Doxycycline .Can be taken with food drink and with milk. 3. Ca present in antacids and milk.More expensive. .Initiate therapy at 250mg qds or 500mg bd (half hour before meals or 2 hours after) until clear improvement.Has to be given for a minimum of 6 months. 31 .Side effects include dryness of skin and lips.35 . 2. Minocycline . 4.Should not be given to children under the age of 12 nor administered during pregnancy.Indicated in severe nodulo-cystic acne.

May cause hypo. 32 . infection.No treatment except protection from the sun Acquired 1.Ethers of hydroquinone: Component of many creams Bleaches skin unevenly leading to confetti-like depigmentation Pigmentation returns after discontinuing use .No cure or treatment except camouflage with cosmetic cover creams 2.Clinical features: Total lack of body pigment Nystagmus Photophobia Poor visual acuity Prone to developing skin cancer at an early age . piebaldism is associated with deafness . psoriasis. Vitiligo . Post inflammatory .Thought to be auto-immune in origin 32 . etc. burns. Oculocutaneous albinism .Prime effect is by reducing sebum excretion In female patients over the age of 30 years oral spironolactone for 6 months is of considerable benefit.Occur following eczema. Phenol may cause hypopigmentation 3.Has anti-androgenic properties .Characterised by patch of white hair in front (forelock) associated with patches of depigmented skin usually on the forehead .In Waardenburg’s syndrome. 2.Skin usually depigmented .Inherited as an autosomal dominant gene . Piebaldism (partial albinism) .E.Heterogenous group of at least four distinct autosomal recessive disorders .Electron microscopy studies confirm the absence of melanocytes in affected areas .or depigmentation . discoid L. DISORDERS OF PIGMENTATION HYPOPIGMENTATION Congenital 1.The two most common varieties are the tyrosinase-negative and tyrosinase-positive types . Exposure to chemicals .

g. are allowed.g.May occur on extensor surfaces such as elbows. Naevus of Ito – shoulders Naevus of Ota – around eyes 4. alopecia areata . which result from scratching. Scratch marks and prurigo papules. nose. Blue naevi . front of the shins. myasthenia gravis.Lesions are frequently periorificial in that it occurs around mouth. Addison’s disease.Melanocytes found in the lower dermis . Café au lait spots of neurofibromatosis .Lesions slightly elevated .Disappearance of lesion related to gradual reduction of melanogenesis 2. Skin disorders 2. Causes: 1. pernicious anaemia. knees.Associated with axillary freckling GENERALIZED PRURITUS Pruritus means itching for which there is no obvious cause in the skin.Pigmented melanocytes present in the deeper layers of the reticular dermis .Persist into adult life 3.Failure of melanocytes migrating from the neural crest to arrive at the dermo-epidermal junction .No universally successful treatment . nipples.May be intertriginous e. thyroid disease.Greater than 5 spots abnormal . backs of the hands and feet. eyes. on the flexor surfaces of the wrists and in the oral mucosa as well .Lesion eventually disappears .Represent a migratory arrest of melanocytes from the neural crest .Management consists of: Photoprotection: Sunscreens which block UVB and UVA to prevent burning of affected skin Topical glucocorticosteroids: Potent or very potent topical steroids may be effective in producing repigmentation of areas of vitiligo PUVA: Requires anywhere between 100 and 300 treatments Camouflage: using cosmetic cover creams Bleaching of normal skin: in those with extensive vitiligo HYPERPIGMENTATION Congenital 1. in groin and axillae . umbilicus and anus . 33 May be associated with other auto-immune conditions e.10 –20% show spontaneous repigmentation . Mongolian blue spot . Systemic disorders Skin disorders: 33 .

Aquagenic pruritus .Distinct from aquagenic urticaria. Xeroderma (dry skin) Systemic disorders: 1. 2. .If the condition is not recognized. 4. 34 1. 4.Pediculosis corporis. Pruritus is thought to be due to deposition of bile salts in the skin. ii) Hypothyroidism and hyperthyroidism iii) Diabetes mellitus iv) Diabetes insipidus v) Hypoparathyroidism 3.In scabies generalized itching may precede skin lesions. Dermatitis herpetiformis . Drug reaction from oral or parenteral drugs Two mechanisms: i) Allergic e. Urticaria and dermographism . 3. 2.g. codeine. Haematological disorders i) Iron deficiency anaemia 34 .Itching may precede skin lesions 7. aspirin. Hepatic disease Pruritus in liver disease is a symptom of biliary obstruction (cholestasis). penicillin ii) Non-specific liberation of histamine e. morphine. Parasitic infestations . itching may precede jaundice.g. In primary biliary cirrhosis. Drug reaction to topically administered drugs 5. Chronic renal disease Exact mechanism unknown. Bullous pemphigoid .Prurigo of pregnancy In the last trimester of pregnancy may get generalised itching due to hormonal changes in pregnancy. sufferers are liable to be labelled neurotic. Recurs with each pregnancy and severity increases.Itching may be present but no lesions. Endocrine i) Pregnancy .Itching may precede skin lesions 6. . 5.

ova and cysts. Sulphonamides. 7.Antihistamines . 1. Onchocerciasis. urea & electrolytes. 35 . treat the cause.Baths . 35 ii) Leukaemias and lymphomas especially Hodgkin’s lymphoma iii) Polycythaemia rubra vera 6.Cool clothing . if first time 9 to 10 days .If previously sensitised starts within 2 to 4 days.Sedatives . liver function tests.May start after drug discontinued .Cholestyramine in cases where cholestasis is a cause If underlying cause found. filiariasis. Management: Thorough history. lasts 1 to 2 weeks if drug discontinued . Treatment: Symptomatic treatment includes: . Examine skin thoroughly as well as full systemic examination. abdomino-pelvic ultrasound may be indicated in particular cases depending on history and examination findings.CBC.May simulate scarlet fever or measles .g. . Further investigation e. thyroid function tests. Exanthematous (Toxic Erythema) . glucose.Stools examination for parasites.Commonest of all cutaneous reactions . chest x-ray.Usually short-lived. ESR. DRUG ERUPTIONS Commonest side effects of drugs. round worm. If no cause found do: .Commonest causes: Ampicillin. Malignant tumours Carcinomatosis occasionally causes pruritus. Gold salts. Gentamicin. Tropical and intestinal parasites Infestation with hookworm.

Drug-induced alopecia . Drug-induced lupus erythematosus-like syndrome .Aspirin may cause urticaria by an allergic or a pharmacological mechanism . Procainamide. Eczematous 36 . Beta blockers.Commonest causes: Penicillins. Toxic epidermal necrosis .May form blisters if severe .Area becomes erythematous and oedematous within 24 hrs . Penicillin. Dexamethasone .Pemphigus and pemphigoid may be drug induced 10. Dapsone.Anagen alopecia may be caused by cytotoxic drugs .g. and nitrazepam .Commonest causes: Methyldopa. Phenothiazines. Methyldopa. Sulphonamides (and related drugs). Salicylates. Urticaria . 11. Dapsone. Drug-induced acne .Clinical features include dusky erythema. morphine. Animal sera. Bullous eruptions .Bullae often at pressure areas may be seen in-patients comatose after overdosage with barbiturates. Griseofulvin. Fixed drug eruptions . Thiazides. Photosensitivity .Commonest causes: Hydrallazine. 6. Isoniazid.Common causes: Sulphonamides. Cephalosporins.Telogen hair loss has been caused by thiouracils and heparin 8. 3. 4.Commonest causes: Amiodarone. Quinine (found in tonic water). .Abnormal lab findings are usual but anti-DNA antibodies are absent .Commonest cause is systemic steroids e. Phenolphthalein. Thiazides.Commonest causes: Phenolphthalein (found in laxatives). Drug-induced lichenoid eruptions . methadone. Barbiturates.Heals with slate blue colour .Caused by (a) direct histamine liberators e. Prednisone. Phenytoin. 36 2. 5. Nalidixic acid.See Acne Lecture notes 7. codeine (b) Allergic reaction . Tetracycline.Eczematous rash in light exposed areas .g. Tetracycline. blistering and peeling of necrotic skin .Starts with prodrome of itching and burning . Sulphonamides.Erythema multiforme (see notes) . Antimalarials.More pigmented and pruritic than idiopathic L. 9. P.

37 . Mepacrine. Any type of opportunistic infection is more likely in patients with AIDS and will generally be more severe. and may occur: 1. infections are frequent and severe and opportunistic infections occur. Lymphadenopathy may occur without other signs of the disease. The main features are that the common inflammatory skin diseases are more florid. Minocycline. At this time HIV antibody testing may still give negative results. Sometimes there is an effect on the central nervous system. headache. and resistant to treatment in patients with late HIV infection.Phenothiazines: bluish black pigmentation SKIN MANIFESTATIONS OF HIV INFECTION Skin lesions are often the first manifestation of HIV infection. Sulphonamides. It is more extensive and inflamed than usual.Common causes: Ampicillin. Systemic drugs 12.Lead: grey discolouration . The role of Pityrosporum organisms is indicated by the response to imidazole antifungal drugs. Erythroderma / Exfoliative dermatitis . Kaposi’s sarcoma occurs in 34% of homosexual men and in 5% of other cases. As a consequence of immunosuppression (late stage HIV infection and AIDS). lymphadenopathy and gastrointestinal upset occur. 37 . 14. Seborrhoeic eczema is common and may be the only evidence of HIV infection initially. Psoriasis is more widespread.Mepacrine: yellow discolouration . Odd pigmentation . 13. In addition. Thinning and straightening of the hair occurs at low CD4 counts. Topical applications .Common causes: Tetracycline. Skin manifestations of AIDS and late stage HIV disease are many and variable. Gentamycin.Silver: grey discolouration . For this reason it may be important to retest suspected cases 6 – 8 weeks later. severe. As a manifestation of the primary HIV infection 2. Chloroquine. Fever. Acute HIV infection (seroconversion illness) is associated with clinical changes in about a half of cases. Gold. Hyperpigmentation . although an antigenaemia soon develops. malaise. Acquired ichthyosis and xerosis occur commonly in late stage HIV disease and AIDS. A transient maculopapular eruption occurs with erythema and erosion of the palate in some patients.

and necrotic lesions. HIV infection may thus present with a wide variety of skin conditions. Herpes zoster virus infection is common. The majority of patients with malignant acanthosis nigricans have an adenocarcinoma usually of the gastrointestinal tract. Skin changes occur on flexural and exposed areas. with florid lesions and systemic spread. In over 50% of patients. play a part. often found on the trunk. papular. The surface feels and looks velvety. particularly at the corners of the mouth. the mucous membrane of the tongue is thrown into folds and warty lesions occur on the oral mucosa. The cause is unknown. 3. varying from red and purple to brown. 38 Eosinophilic folliculitis (papular prurigo of HIV disease) an itchy folliculitis. Other features include warty lesions and skin tags. Oral hairy leukoplakia caused by Epstein-Barr virus. the skin becomes thrown into folds and hyperpigmented. but can be disseminated or produce lesions in the classical site – the ankle. occurs in many cases. May also be associated with lymphomas. less commonly in the genito-urinary system. Acanthosis nigricans In malignant acanthosis nigricans. may occur in 30-50% of patients with AIDS. Dermatomyositis Juvenile dermatomyositis is not associated with malignancies. often with associated bacterial infection infection is very common. 38 . Mycobacteria may cause both cutaneous and systemic lesions. Fungal infections may be widespread and with increased inflammation and hyperkeratosis. Herpes simplex virus produces widespread and sometimes persistent ulcerating lesions. SKIN DISORDERS ASSOCIATED WITH MALIGNANCY 1. Candidiasis. and in the pharynx Cryptococcus neoformans and Histoplasma capsulatum are occasional opportunistic pathogens and can produce inflammatory. Pruritus 2. on the palate. Perianal warts can proliferate and cervical intraepithelial neoplasia occurs. commonly with several present at the same time. Kaposi’s sarcoma presents with polychromic plaques and nodules. Any unusually florid skin condition that is resistant to treatment should raise the suspicion that HIV infection may be present. Often two dermatomes are affected. but it is possible that Demodex spp. They are common on the palate and nose.

Distinctive mauve erythema on dorsum of hands. Other conditions associated with malignancy .DR4  There is an association with various autoimmune diseases such as rheumatoid arthritis  The IgG antibodies are directed against the intercellular cement substance Clinical Features 39 . bronchus or ovary. .Scaling and mauve erythema (heliotrope discolouration . 4.Pigmentation .Ragged. Skin and skeletal muscles affected. 39 Adult dermatomyositis is associated with malignancies in ¼ of cases. . Breast and renal carcinoma.Photosensitive dermatitis. Associated malignancies include carcinoma of breast.Bullous pemphigoid . hypertrophic cuticles.Erythroderma . limb girdle (shoulder and pelvic girdle). . BLISTERING DISORDERS A blistering disorder is an autoimmune condition in which the primary lesion is a blister Pemphigus Vulgaris A serious autoimmune disorder of intraepidermal cell cohesion. . resulting in flaccid blisters and painful erosions of the skin and mucous membranes Aetiology  Rare autoimmune disorder  Most common in Jews  Strongly associated with HLA. Skin lesions: . Muscle involvement: .Erythematous papules over the knuckles (Gottron’s sign). Paget’s disease of the nipple Looks like unilateral eczema of the nipple. . . 5. 100% have underlying intraductal carcinoma.May spread to involve intercostal muscles and muscles used in swallowing.Acquired ichthyosis .Paraneoplastic pemphigus All the previously described conditions except Paget’s disease of the nipple are non-metastatic.e.pathognomonic) on the eyelids. Contains malignant cells.Proximal myopathy i. malignant melanoma and lymphoma may metastasize to the skin.Nailfold telangiectasia.

larynx. including the pharynx.  However. cervix and rectum.  In a small proportion of patients. face.  Oral lesions are unusual.  There is a distinctive endemic variety which occurs in rural South America and in particular Brazil. 40  In 50 percent of patients the disorder starts in the mouth with flaccid blisters which result in painful erosions  However.  Itching. epidemic or drug-induced forms Aetiology  Most cases are idiopathic. is present. scaling and crusting. oesophagus. eventually. Diagnosis  Skin biopsy for routine histology and immunofluorescence is indicated. Clinical Features  Recurrent superficial erosions occur. urethra.  IgG is deposited intercellularly in the granular layer  Circulating IgG autoantibodies.  The scalp. all stratified squamous epithelial mucosal surfaces may be involved. associated with burning. conjunctivae. penis. are also present in most patients Management 40 . suprabasal intraepidermal blisters occur  Linear deposits of IgG may be demonstrated between the epidermal cells in 100% of patients during active disease  The majority of patients manifest circulating antibodies against the intercellular cement Pemphigus Foliaceus A clinical variant of pemphigus with blistering just below the stratum corneum that occurs in idiopathic. which react with intercellular cement. the disorder is drug-induced.vulva.  All skin may be involved  Blisters are flaccid and may arise on normal or erythematous skin  They break easily to leave erosions which are painful  These erosions do not heal spontaneously Diagnosis  The diagnosis may be confirmed by a skin biopsy  There is oedema and disappearance of the intercellular bridges in the lower epidermis  This gives rise to acantholysis (separation of the cells in the prickle cell layer)  Subsequently. chest and back are involved in a distribution similar to seborrhoeic dermatitis. often severe.  The Nikolsky sign is a helpful positive physical sign. seen with erythema. the whole cutaneous surface may be affected.  The histology shows a subcorneal acantholytic blister.  Intact flaccid blisters are rarely observed.

cyclophosphamide. azathioprine and cyclosporin A permits the dose of glucocorticoid to be reduced.  However. characterized by itchy tense blisters and caused by an autoimmune process that affects the dermoepidermal junction Aetiology  Relatively common in the elderly  Affects both sexes equally and all races  Considered to be an autoimmune process and is often associated with other autoimmune disorders  Circulating IgG autoantibodies to the basement membrane zone of the dermoepidermal junction have been demonstrated in the sera. dapsone and plasmapheresis have been used. cyclosporin A and high dose intravenous pulse therapy with methylprednisolone 41 . the lesions are of amore urticarial nature  The mucous membranes are involved in a minority of patients Diagnosis  Skin biopsy is taken for histopathology and immunofluorescence  The pathology shows that the entire epidermis makes up the roof of the blister  Almost all patients show IgG and C3 at the epidermal basement membrane zone in a linear manner Management  The condition is more benign than pemphigus  Lower doses of corticosteroids e. malignant disease should be suspected in patients with oral ulceration and in seronegative patients Clinical Features  The condition is usually intensely itchy  The patient presents with blisters which are usually symmetrical in distribution  Blisters usually involve the limbs first and then the trunk  Blisters are tense and are usually but not always surrounded by erythema  The blisters eventually become haemorrhagic and break leaving denuded eroded skin  Occasionally in the early stages.  Other agents such as gold. per day are required  Azathioprine has a steroid-sparing effect  Other therapeutic regimens: sulphones.g. such as methotrexate. Bullous Pemphigoid A serious condition of spontaneous blistering. Prednisone 40 mg. 41  Prior to the introduction of systemic glucocorticosteroids. the disorder was fatal in the majority of cases  These drugs seem to act by decreasing autoantibody levels  Initially very high doses of systemic glucocorticosteroids are employed  The advent of other immunosuppressant agents.