Dermatology is the study of both normal and abnormal skin and associated structures such as hair, nails, and oral and genital mucous membranes. Skin diseases are very common, affecting up to a third of the population at any one time.
Skin diseases have serious impacts on life. They can cause physical damage, embarrassment, and social and occupational restrictions. Chronic skin diseases may cause financial constraints with repeated sick leave. Some skin conditions can be life-threatening.
There were several areas and topics of interest in dermatology including:
• Skin infections / infestations
• Atopic dermatitis/contact dermatitis
• Acne/rosacea, and warts
• Leg ulcers/wound care
• Skin cancer
Developing a differential diagnosis and a well-rounded approach to skin problems will help achieve the goal of early accurate diagnosis and treatment to reduce overall morbidity and mortality of skin disease.
The normal skin microflora and antimicrobial peptides protect the skin against infection. However, when there is skin damage, microorganisms can penetrate resulting in infection.
There are 3 main types of skin infections according to their sources: bacterial (e.g. staphylococcal and streptococcal), viral (e.g. human papilloma virus, herpes simplex and herpes zoster), and fungal (e.g. tinea, candida and yeasts). Infestations (e.g. scabies, cutaneous leishmaniasis) can also occur.
Staphylococcal scalded skin syndrome
It is commonly seen in infancy and early childhood, caused by the production of a circulating epidermolytic toxin from phage group II, benzylpenicillin-resistant (coagulase positive) staphylococci.
It develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins. A scald-like skin appearance is followed by large flaccid bulla. Perioral crusting is typical, while there is intraepidermal blistering in this condition. Lesions are very painful and sometimes the eruption is more localized. Recovery usually occurs within 5-7 days.
• Antibiotics (e.g. a systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin)
Superficial fungal infections
These are common and mild infections of the superficial layers of the skin, nails and hair, but can be severe in immunocompromised individuals. Three main groups of pathogens, namely dermatophytes (tinea/ringworm), yeasts (e.g. candidiasis, malassezia), moulds (e.g. aspergillus) are the cause of these infections.
The presentation varies with the site of infection
• Usually unilateral and itchy
• Tinea corporis (tinea infection of the trunk and limbs) – Itchy, circular or annular lesions with a clearly defined, raised and scaly edge is typical
• Tinea cruris (tinea infection of the groin and natal cleft) – very itchy, similar to tinea corporis
• Tinea pedis (athlete’s foot) – moist scaling and fissuring in toe webs, spreading to the sole and dorsal aspect of the foot
• Tinea manum (tinea infection of the hand) – scaling and dryness in the palmar creases
• Tinea capitis (scalp ringworm) – patches of broken hair, scaling and inflammation
• Tinea unguium (tinea infection of the nail) – yellow discoloration, thickened and crumbly nail
• Tinea incognito (inappropriate treatment of tinea infection with topical or systemic corticosteroids) – Ill-defined and less scaly lesions
• Candidiasis (candidal skin infection) – white plaques on mucosal areas, erythema with satellite lesions in flexures
• Pityriasis/Tinea versicolor (infection with Malassezia furfur) – scaly pale brown patches on upper trunk that fail to tan on sun exposure, usually asymptomatic
• Establish the correct diagnosis by skin scrapings, hair or nail clippings (for dermatophytes); skin swabs (for yeasts)
• General measures: treat known precipitating factors (e.g. underlying immunosuppressive condition, moist environment)
• Topical antifungal agents (e.g. terbinafine cream)
• Oral antifungal agents (e.g. itraconazole) for severe, widespread, or nail infections
• Avoid the use of topical steroids – can lead to tinea incognito
• Correct predisposing factors where possible (e.g. moist environment, underlying immunosuppression)
Eczema, acne and psoriasis are chronic inflammatory skin disorders that follow a relapsing and remitting course. There are many types of eczema but we shall just consider atopic eczema here. These skin disorders are not infectious.
Management is aimed at achieving control and not providing a cure, while complications are mainly due to the psychological and social effects.
Patient education is important in these chronic skin conditions and should concentrate on providing information about the nature of condition, aims of treatment and the available treatment options.
Eczema (or dermatitis) is characterized by papules and vesicles on an erythematous base. Atopic eczema is the most common type – usually develops by early childhood and resolves during teenage years (but may recur). The causes of atopic eczema are not fully understood, but a positive family history of atopy (i.e. eczema, asthma, allergic rhinitis) is often present. A primary genetic defect in skin barrier function appears to underlie atopic eczema, while exacerbating factors such as infections, allergens (e.g. chemicals, food, dust, pet fur), sweating, heat and severe stress may also trigger the disease.
• Commonly present as itchy, erythematous dry scaly patches
• More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults
• Acute lesions are erythematous, vesicular and weepy (exudative)
• Chronic scratching/rubbing can lead to excoriations and lichenification
• May show nail pitting and ridging of the nails
• General measures – avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute
• Topical therapies – topical steroids for flare-ups; topical immunomodulators (e.g. tacrolimus, pimecrolimus) can be used as steroid-sparing agents
• Oral therapies – antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. acyclovir) for secondary herpes infection
• Phototherapy and immunosuppressants (e.g. oral prednisolone, azathioprine, ciclosporin) for severe non- responsive cases
Acne vulgaris is an inflammatory disease of the pilosebaceous follicle triggered by hormonal (androgen) imbalance. Contributing factors include increased sebum production, abnormal follicular keratinization, bacterial colonization (Propionibacterium acnes) and inflammation.
• Non-inflammatory lesions (mild acne) – open and closed comedones (blackheads and whiteheads)
• Inflammatory lesions (moderate and severe acne) – papules, pustules, nodules, and cysts
• Commonly affects the face, chest and upper back
• General measures – no specific food has been identified to cause acne, treatment needs to be continued for at least 6 weeks to produce effect
• Topical therapies (for mild acne) – benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties)
• Oral therapies (for moderate to severe acne) – oral antibiotics, and anti-androgens (in females)
• Oral retinoids (for severe acne)
Psoriasis is a chronic inflammatory skin disease due to hyperproliferation of keratinocytes and inflammatory cell infiltration. Chronic plaque psoriasis is the most common type. It is triggered by a complex interaction between genetic, immunological and
environmental factors, while precipitating factors including trauma (which may produce a
Koebner phenomenon), infection (e.g. tonsillitis), drugs, stress, and alcohol, may also trigger the disease.
• Well-demarcated erythematous scaly plaques
• Lesions can sometimes be itchy, burning or painful
• Common on the extensor surfaces of the body and over scalp
• Auspitz sign (scratch and gentle removal of scales cause capillary bleeding)
• 50% have associated nail changes (e.g. pitting, onycholysis)
• 5-8% suffer from associated psoriatic arthropathy – symmetrical polyarthritis, asymmetrical oligomonoarthritis, lone distal interphalangeal disease, psoriatic spondylosis, and arthritis mutilans (flexion deformity of distal interphalangeal joints)
• General measures – avoid known precipitating factors, emollients to reduce scales
• Topical therapies (for localised and mild psoriasis) – vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations
• Phototherapy (for extensive disease) – phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA
• Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement) – methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters, and biological agents (e.g. infliximab, etanercept, efalizumab)
Wound healing is a complex biological process that consists of hemostasis, inflammation, proliferation, and remodeling. Large numbers of cell types—including neutrophils, macrophages, lymphocytes, keratinocytes, fibroblasts, and endothelial cells— are involved in this process. Multiple factors can cause impaired wound healing by affecting one or more phases of the process and are categorized into local and systemic factors. The influences of these factors are not mutually exclusive. Single or multiple factors may play a role in any one or more individual phases, contributing to the overall outcome of the healing process.
Stages of wound healing
● Vasoconstriction and platelet aggregation
● Clot formation
● Migration of neutrophils and macrophages
● Phagocytosis of cellular debris and invading bacteria
● Granulation tissue formation (synthesized by
fibroblasts) and angiogenesis
● Re-epithelialization (epidermal cell proliferation and migration)
● Collagen fibre reorganization
● Scar maturation
The proper oxygen level is crucial for optimum wound healing. Hypoxia stimulates wound healing such as the release of growth factors and angiogenesis, while oxygen is needed to sustain the healing process.
Many medications, such as those which interfere with clot formation or platelet function, or inflammatory responses and cell proliferation have the capacity to affect wound healing.
Medications that have a significant impact on healing, include glucocorticoid steroids, non-steroidal anti-inflammatory drugs, and chemotherapeutic drugs.
These are rapidly progressive skin conditions and some are potentially life-threatening. Early recognition is important to implement prompt supportive care and therapy. When related to drug reactions, the offending drug should be withdrawn.
Urticaria, Angioedema and Anaphylaxis
Urticaria, angioedema and anaphylaxis are triggered by idiopathic causes, food (e.g. nuts, sesame seeds, shellfish, dairy products), drugs (e.g. penicillin, contrast media, non-steroidal anti-inflammatory drugs (NSAIDs), morphine, angiotensin-converting enzyme inhibitors (ACE-I)), insect bites, contact (e.g. latex), viral or parasitic infections, autoimmune, and hereditary (in some cases of angioedema).
Urticaria is due to a local increase in permeability of capillaries and small venules. A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic factors) play a role but histamine derived from skin mast cells appears to be the major mediator. Local mediator release from mast cells can be induced by immunological or non-immunological mechanisms.
• Urticaria (swelling involving the superficial dermis, raising the epidermis): itchy wheals
• Angioedema (deeper swelling involving the dermis and subcutaneous tissues): swelling of tongue and lips
• Anaphylaxis (also known as anaphylactic shock): bronchospasm, facial and laryngeal oedema, hypotension; can present initially with urticaria and angioedema
• Antihistamines for urticaria
• Corticosteroids for severe acute urticaria and angioedema
• Adrenaline, corticosteroids and antihistamines for anaphylaxis
Eczema herpeticum (Kaposi’s varicelliform eruption)
It is a widespread eruption and represents a serious complication of atopic eczema caused by Herpes simplex virus.
• Extensive crusted papules, blisters and erosions
• Systemically unwell with fever and malaise
• Antivirals (e.g. aciclovir)
• Antibiotics for bacterial secondary infection
Necrotising fasciitis is a rapidly spreading infection of the deep fascia with secondary tissue necrosis caused by Group A haemolytic streptococcus, or a mixture of anaerobic and aerobic bacteria. It carries a mortality rate of up to 76%.
• Severe pain
• Erythematous, blistering, and necrotic skin
• Systemically unwell with fever and tachycardia
• Presence of crepitus (subcutaneous emphysema)
• X-ray may show soft tissue gas (absence should not exclude the diagnosis)
• Urgent referral for extensive surgical debridement
• Intravenous antibiotics
Skin cancer is one of the most common cancers. In general, skin cancer can be divided into: non-melanoma (basal cell carcinoma and squamous cell carcinoma) and melanoma (malignant melanoma). Malignant melanoma is the most life-threatening type of skin cancer and is one of the few cancers affecting the younger population. Sun exposure is the single most preventable risk factor for skin cancer.
Squamous cell carcinoma
It represents a locally invasive malignant tumor of the epidermal keratinocytes or its appendages, which has the potential to metastasize. Squamous cell carcinoma risk factors include excessive UV exposure, pre-malignant skin conditions (e.g. actinic keratoses), chronic inflammation (e.g. leg ulcers, wound scars), immunosuppression and genetic predisposition. Its prognosis depends on tumor size, site, histological pattern, depth of invasion, perineural involvement, and immunosuppression.
• Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
• Surgical excision – treatment of choice
• Mohs micrographic surgery – may be necessary for ill-defined, large, recurrent tumors
• Radiotherapy – for large, non-resectable tumors
Malignant melanoma is an invasive malignant tumor of the epidermal melanocytes, which has the potential to metastasize. The risk factors include excessive UV exposure, skin type I (always burns, never tans), history of multiple moles or atypical moles, and family history or previous history of melanoma. Main symptoms are more common on the legs in women and trunk in men (e.g. bleeding, itching).
The ‘ABCDE Symptoms’ rule (*major suspicious features):
Diameter > 6mm
Evolution of lesion (e.g. change in size and/or shape)*
• Surgical excision – definitive treatment
• Radiotherapy may sometimes be useful
• Chemotherapy for metastatic disease
• Recurrence of melanoma based on Breslow thickness (thickness of tumor): <0.76mm thick – low risk, 0.76mm-1.5mm thick – medium risk, >1.5mm thick – high risk
• 5-year survival rates based on the TNM classification (primary Tumor, regional Nodes, Metastases): stage 1 (T <2mm thick, N0, M0) – 90%, stage 2 (T>2mm thick, N0, M0) – 80%, stage 3 (N≥1, M0) – 40- 50%, and stage 4 (M ≥ 1) – 20-30%
- British Association of Dermatologists. Dermatology: Handbook for medical students & junior doctors.
- Jenny E. Murase. Understanding the importance of dermatology training in undergraduate medical education. Dermatol Pract Concept 2015;5(2):18
- Guo and L.A. DiPietro. Factors Affecting Wound Healing. J Dent Res 89(3):219-229, 2010