BMS175: Topic 1: Integumentary system

The components of the integumentary system

• Skin - Heaviest and Largest organ

• Hair

• Nail

• Glands

Skin

• Packed with tough protein called Keratin (make the skin surface hard to break)

• Biggest sensing organ, that react to heat, cold, touch, texture, pressure, vibration, and tissue injury

• Complex skeletal muscles pull on the skin to create subtle and varied facial expressions

• Thermoregulation (retain heat by expanding vessels of dermis and release heat by vasoconstriction)

• Prevents water entering and body losing water

• Barrier to UV rays not that good though

• Epidermis: outside of skin, made up of 5 different kinds of cells (Keratinocyte, Melanocytes, Tactile cells (touch receptors) (Superficial thin layer)

• Dermis: connective tissue, has cells (fibroblasts, adipocytes, macrophages), has matrix (collagen, elastin, reticular fibres), other structures (smooth muscles, blood cells, hair follicles)

• Hypodermis (Mostly fat) (not officially part of the skin) (connective tissue) has cells (fibroblasts, adipocytes, macrophages), has matrix (collagen, elastin) 8% thicker in women (decreases in age)

Subcutaneous Injections

• Into the fatty tissues just beneath skin (the Hypodermis)

Skin Wound Healing

• The level of the wound effects the healing process

• Dermal Wound (has inflammatory phase, Proliferation and migratory phase, maturation and remodeling phase)

• Hemostasis Phase: This is the initial phase where bleeding is stopped. Blood vessels constrict to reduce blood flow, and platelets aggregate to form a clot, effectively sealing the wound. Fibrin, a protein, acts like "blood glue" to hold the clot in place, forming a scab.

• The Inflammatory Phase: Following hemostasis, the inflammatory phase begins, characterized by redness, swelling, and warmth at the wound site. White blood cells, like neutrophils and macrophages, migrate to the area to clean debris, fight infection, and release growth factors. This phase prepares the wound bed for tissue repair. 

• Proliferation and Migratory Phase: In this stage, new tissue is formed to fill the wound. Granulation tissue, composed of new blood vessels and connective tissue, grows into the wound. Epithelial cells migrate across the wound surface to cover and protect the new tissue. Collagen, a protein that provides strength to the skin, is also produced during this phase. 

• Maturation and Remodeling Phase: The final stage involves remodeling the newly formed tissue and strengthening the scar. Collagen fibers are reorganized, and the scar gradually fades and flattens out. The scar may take months or even years to fully mature and reach its final strength. 

Hair

• First hair we grow is called Lanugo (very fine, downy, contains no pigment)

• Bulb at the bottom of hair follicle is called derma papilla

• Has 3 layers (Medulla, cortex

• Has a tube it sits in, has two layers

• Has it’s own receptor and its own bundle of smooth muscle cells

Nails

• Full of dead keratinocytes (skin cells)

• Lunule: moon shaped white area near the root

• The Matrix is where new nail cells grow

Glands

• Makes one or more substances, such as hormones

• Need sweat glands (widely distributed, two types: eccrine and apocrine)

• Apocrine is brought on by puberty

• Pheromones (that is your charm)

• Sweat is acidic (Ph from 4-6) which inhibits the growth of bacteria on the skin

• Sebum is oil prevents hair from becoming brittle, from sebaceous gland

• Mammary Glands (in female breast) produces milk

Integumentary System Health Challenges

Skin (hair and nails) is the interface between the external environment and the body. The largest organ with a very large surface area.

Exposed to many causes of cellular injury such as:

• Physical agents - radiation, including ultraviolet radiation;

• Physical agents - trauma, both pressure/blunt force and penetrating;

• Chemical agents - acids, industrial agents, plant toxins; and

• Changes in environment - heat, cold, dryness and wetness.

• Pathophysiology in the integumentary system can be categorised in four groups: – Neoplasia and cancers; – Inflammatory conditions; – Traumatic conditions; and – Vascular disorders.

Describe skin lesions

• Pathological or traumatic breach of normal skin

• Skin has abnormal appearance compared to the skin around it

• Primary skin lesions are those which develop as a direct result of disease, and appear as original lesions

• Secondary lesions are those that evolve from primary lesions or develop as a consequence of the persons activities, and have an appearance that has been changed by normal progress over time

• Morphology is the form, structure and physical appearance of the lesion

• The morphology is an indicator of the pathophysiology of the lesion

• Specific terms are used to describe the morphology of skin lesions

Primary Lesion Morphology

• Macule - A flat, circumscribed area that is a change in the colour of the skin; is less than 1cm in diameter

• Papule - An elevated circumscribed area that is less than 1cm in diameter

• Patch - A flat, non palpable, irregular-shaped macule more than 1cm in diameter

• Plaque - Elevated, firm and rough lesion with a flat surface top greater than 1cm in diameter

• Wheal - Elevated, irregular-shaped area of cutaneous oedema (the accumulation of excess fluid in the skin); solid, transient; variable in diameter

• Nodule - Elevated, firm, circumscribed lesion; deeper in dermis than papule; 1-2cm in diameter

• Tumour - Elevated, solid lesion; may be clearly demarcated; deeper in dermis; greater than 2cm in diameter

• Vesicle - Elevate, circumscribed, superficial does not extend into the dermis; filled with serous fluid; less than 1cm in diameter

• Bulla - Vesicle greater than 1cm in diameter

• Pustule - Elevate, superficial lesion; similar to a vesicle but filled with purulent fluid

• Cyst - Elevated, circumscribed, encapsulated lesion; in dermis or subcutaneous layer; filled with liquid or semisolid material

• Telangiectasia - Fine, irregular red lines produced by capillary dilation

Second Lesion Morphology

• Scale - Heaped up, keratinised cells; flaky skin; irregular shape; thick or thin; dry or oily; variation in size

• Lichenification - Rough, thickened epidermis secondary to persistent rubbing, itching or skin irritation; often involves flexor surface to extremity

• Keloid - Irregularly shaped, elevated, progressively enlarging scar; grows beyond the boundaries of the wounds; caused by excessive collagen formation during healing

• Scar - Thin to thick fibrous tissue that replaces normal skin following injury or laceration to the dermis

• Excoriation - Loss of the epidermis; linear, hollowed-out, crusted are

• Fissure - Linear crack or break from the epidermis to the dermis; may be moist or dry

• Erosion - Loss of part of the epidermis; depressed, moist, glistening; follows rupture of a vesicle or bulla

• Ulcer - Loss of epidermis and dermis; concave; varies in size

• Atrophy - Thinning of the skin surface and loss of skin markings

Skin Cancers

• Australia has the highest rates of skin cancers globally, and skin cancers are our most common cancers.

• Highest prevalence are basal cell carcinoma, squamous cell carcinoma and melanoma.

• Cancer is uncontrolled and rapid proliferation of cells, specifically malignant tumours or neoplasms.

• Neoplasia and neoplasm means ‘new formation’ and refers to an abnormal growth

• Malignant tumours grow rapidly, lack differentiation (anaplasia) and organisation, are not encapsulated, invade local structures and tissues and spread to distant sites through lymphatic and blood vessels (metastasis).

• This contrasts with benign tumours which are slow growing, encapsulated, maintain cell differentiation and do not invade or metastasise.

Cancer Fundamentals

• Uncontrolled growth in cancer is due to mutations, particularly in the genes that normally regulate the cell cycle.

• Proto-oncogenes encode proteins that regulate when cells progress through the cell cycle to mitosis.

  • A mutated proto-oncogene is an oncogene, protein becomes too active and accelerates cell division.

• Tumour suppressor genes encode proteins that stop the cell cycle and check for mistakes, correcting them if possible or starting apoptosis.

  • A mutated tumour suppressor gene can’t stop the cycle and it will progress without checking.

• Other mutations may occur in genes encoding growth factors and hormones, and the receptors for these.

Describe the Pathophysiology of Basal Cell Carcinoma

• Most common form of skin cancer in Australia and New Zealand, estimated to be at least two-thirds of non-melanoma skin cancers.

• Arises from the dividing cells in the basal layer of the epidermis. • Repeated exposure to solar UV radiation, especially ultraviolet B (UVB, 280–320 nm).

• Exposure during childhood and adolescence significantly increases risk.

• Both UVA and UVB damage DNA.

  • UVB is absorbed directly by DNA, causing changes in a number of genes.

  • UVA causes DNA damage by generating oxygen, breaks in the DNA molecule.

  • Alterations in particular tumour suppressor genes related to basal cell carcinoma.

  • Decrease repair of UV-induced DNA damage and induce cell cycle proliferation.

• Slow-growing tumours, rarely metastasise.

• Most frequent on body areas that are exposed to the sun - face, head, neck, shoulders and back.

• Three common growth patterns each with different clinical features:

• Superficial - common, particularly in young. Lesions are flat, erythematous, scaling macules with colour change. If untreated, they will enlarge, reaching 5–10 cm in diameter.

• Nodular - more common in the elderly. Begin as small pink nodule, enlarges and becomes ulcer surrounded by a raised, rolled pearly border.

• Morphoeic - sclerosing (to harden) growth pattern, pale scar that feels hard on palpation and rarely ulcerates. Tend to be longstanding and highly invasive.

Basal Cell Carcinoma Treatment

• Complete surgical excision with 4–5 mm margin

• Highly aggressive - Mohs surgery, margins examined

• Non-aggressive, well-defined lesions - cryotherapy (liquid N2)

• Superficial - Imiquimod 5% cream 5x week for 6 weeks to the tumour and a 5-mm margin of normal skin surrounding it. Stimulates an immune response.

• Superficial on the trunk and limbs - curettage (surgical scraping) and diathermy electrodesiccation (local heat)

• Superficial and thin nodular basal cell carcinomas - photodynamic therapy. Light activates a photosensitizers localised in tumour tissue to form cytotoxic reactive oxygen species.

• Radiation therapy only for carcinomas not suited to surgery or as adjuvant to surgery for persistent or advanced carcinomas.

• Follow-up monitoring is important.

Describe the pathophysiology for Squamous Cell Carcinoma

• Second most common of the non-melanoma skin cancers • Arising from keratinocytes in the outer layers of the epidermis.

• May arise from skin or other sites lined by squamous epithelium e.g. oesophagus, mouth and vagina.

• Precursor lesions, invasive and may metastasise.

• Aetiology - cumulative sun exposure. Risk factors age (> 50 years), male, fair skin (that burns easily without tanning), blue/green eyes, blond/red hair, chemical pollution, x-rays, immune suppression, smoking, pre-existing ulcers or scars and genetic syndromes.

• In addition, a number of precancerous conditions including solar (acitinic) keratosis and squamous cell carcinoma in situ (Bowen's disease) can develop into squamous cell carcinoma. Those with > 15 solar (acitinic) keratosis are 10–15 times more at risk of developing squamous cell carcinoma than those with none.

• Treatment options for squamous cell carcinoma are similar to those for basal cell carcinoma.

• Majority arise from pre-cancerous conditions:

• Solar (acitinic) keratoses - lesions with atypical nuclei in the epidermal basal layer and hyperkeratosis (thickening of skin) associated with chronic exposure to UV radiation.

• Appear as irregular plaques with a rough, hard, hyperkeratotic surface with a sandpaper-like texture if palpated.

• Associated with middle age and found commonly on face, ears and back of hands.

• Usually the same colour as the surrounding skin although they can be pink, red or brown.

• Recommended therapy - cryotherapy, topical medications including 5% 5-fluorouracil cream (antimetabolite), imiquimod 5% cream, 3% diclofenac gel (apoptotic, inhibits cell proliferation and suppresses angiogenesis) or photodynamic therapy.

• Squamous cell carcinoma in situ (Bowen's disease) – abnormal keratinocytes confined to the epidermis.

• Lesions are full thickness of the epidermis, well-demarcated, erythematous scaly patches up to several centimetres in diameter. Most common ears, face, hands and lower legs.

• More likely to progress to invasive disease. Development of lump or bleeding may indicate lesion progressed to invasive squamous cell carcinoma.

• Treatment - cryotherapy, lesion excision and cauterisation to the base, 5-fluorouracil cream, imiquimod cream and photodynamic therapy.

• About 5% of squamous cell carcinomas metastasise - aggressive, potential for recurrence. Treatment is usually surgical excision.

Describe the pathophysiology for Melanoma

• Highest incidence of melanoma in Australia, 11x higher than global average. Fourth most common malignant cancer in Australia and the most common cancer for 15 to 44 years.

• Arises from melanocytes, pigment cells producing melanin.

• Rapid progression with high rate of metastasis. • Cause involves both environmental and genetic factors.

  • Intermittent exposure to UV radiation in sunlight. Individuals who have had sunburn (with blistering) 2x more likely to develop melanoma. Highest risk if sunburn occurs in childhood.

  • Fair skin and blond/red hair increased risk, possible associated with melanocortin receptor gene variation.

  • Other risk factors - previous history of skin cancer, presence of multiple melanocytic naevi or atypical naevi, family history, (p16 gene mutation).

• Melanoma Clinical Manifestations

• Variable size, shape and colour, with irregular borders.

• During horizontal growth phase – flat, vertical growth phase - become raised. May itch or bleed.

• Four main types of melanomas:

• Superficial spreading - most common (~70%), on sun-exposed areas e.g. the back and legs. May arise from an existing naevus that shows change in size, shape or colour. The mean age for superficial spreading melanomas is 40 years old.

• Nodular melanomas - ~15%, commonly in fifth or sixth decade of life. Raised dome-shaped lesions often with a uniform blue-black colour and tend to bleed.

• Lentigo - ~10–15% of melanomas, more common in the elderly. Slow-growing, pigmented macule that is undergoing change. They can invade the dermis and become a lentigo malignant melanoma.

• Acral lentiginous - 1–3% of melanomas in Australia. Flat light-coloured or pink lesion on the palms of hands or soles of feet. Equally common in fair-skinned and dark-skinned people and is thought to have no relationship with UV exposure.

• Diagnosis on biopsy results.

• Early diagnosis and treatment essential, highly invasive

• Standard treatment for primary melanoma is wide local surgical excision of skin and subcutaneous tissue.

• Invasion into deeper tissue risks spread to the regional lymph nodes.

• Risk of metastasis linked to thickness of the primary melanoma

• Greater than 1 mm in thickness - sentinel lymph node biopsy. If biopsy is positive, lymph node dissection and chemotherapy, radiotherapy or targeted biological therapies.

Pressure Injuries\

Pressure injuries. The force (body weight) exerted on a unit of area (skin contact area). Pressure over a bony prominence compresses tissues lying between the skin and underlying skeleton, occluding blood vessels. Prolonged occlusion from pressure above 32mmHg leads to ischaemia, necrosis and ulceration. Shear is mechanical force acting in parallel to a plane, which distorts capillaries and soft tissue causing ischaemia. Friction opposes the movement of one surface against another and may lead to superficial skin erosions that initiate pressure injury. Moisture increases the risk of pressure injury.

• Skin tears are wounds caused by shearing, friction or blunt trauma to the skin.

• Both pressure injuries and skin tears are categorised according to increased severity.

Main extrinsic factors contributing to pressure injuries:

• Pressure

• Shear

• Friction

• Moisture

Stage 2 Pressure Injury

• Partial thickness loss with exposed dermis

• The wound bed is pink or red and moist

• May appear as an intact or ruptured blister

Stage 3 Pressure Injury

• Full thickness loss

• Subcutaneous fat, muscle or tendons are visible

• No bone visible

Unstageable Pressure Injury

• Where the full thickness skin and tissue loss has occurred and where the extent of the tissue loss cannot be confirmed

Dermatitis

• Dermatitis or eczema - most common inflammatory condition of the skin. • Both exogenous and endogenous aetiology.

• Exogenous - irritant contact dermatitis and allergic contact dermatitis.

• Endogenous - atopic dermatitis and seborrhoeic dermatitis.

• Acute dermatitis is associated with pruritus, erythema, vesicles and scales.

• Chronic dermatitis manifestations include pruritus, dryness of the skin, skin thickening, hyperpigmentation and sometimes fissures.

• Seborrhoeic dermatitis - Malassezia yeasts, affects areas rich in sebaceous glands e.g. scalp (cradle cap, dandruff), eyebrows, nasolabial folds, behind the ears, axillae, chest. Scaly, white or yellow plaques, treated with shampoos containing sulphur, salicylic acid, zinc pyrithione or tar.

Irritant Contact Dermatitis

• Most common occupational skin disorder, usually affecting hands, frequent in nurses.

• Non-allergic inflammatory response to chemical or physical agents, from either one or many exposures.

• Common trigger substances - water, soap, detergents, oils, acids, alkalis and rubber.

• Environmental factors such as heat, low humidity (↑ ceramide production) and UV radiation.

• Mechanical factors such as friction, occlusion and pressure

• Exposure to the irritant triggers a cascade of skin barrier disruptions, cellular damage and release of chemical mediators resulting in an inflammatory response.

• Irritants damage the skin by direct cytotoxicity, lipidbarrier removal, cell membrane damage and the breakdown of proteins.

• Once irritant penetrates damaged stratum corneum, keratinocytes release cytokines and stimulate MHC antigens which promote inflammation.

• Tumour necrosis factor-alpha (TNF-α) is the major mediator of inflammation.

Allergic contact dermatitis

• Type IV delayed T-cell mediated hypersensitivity reaction.

• Allergens - metals, chemicals, microorganisms, drugs and latex.

• Allergen penetrates the epidermis - friction, heat exposure, humidity, frequent handwashing.

• Allergen binds to a protein, Langerhans' cells (skin macrophages) transport antigen to lymph nodes and present it to T lymphocytes, activates immune response – Sensitisation phase.

• When the chemical allergen is encountered again a rapid, more aggressive immune response occurs – Inflammatory phase.

• Inflammatory response causes rash with pruritus, erythema, oedema and vesicular lesions. The lesions may weep, increasing the risk of secondary infections.

• Diagnosis via patch testing.

• Management - removal of the irritant and topical corticosteroids. Oral corticosteroids may be required in severe cases.

Atopic Dermatitis

• Atopy - tendency to produce exaggerated IgE immune response to environmental substances.

• Chronic inherited inflammatory skin disorder.

• Aetiology – multifactorial, environmental triggers and genetic factors including altered innate and adaptive I

• Pathogenesis - Epidermal barrier dysfunction likely has a primary role. Genetic alterations in epidermal barrier components include mutations in the filaggrin gene (protein for formation and hydration of the skin barrier). Changed lipid composition, decrease in ceramides, a major water-retaining molecule.

• Increased transdermal water loss, entrance of antigens, pathogens and nonspecific irritants that activate inflammatory response.

Acne Vulgaris

• Inflammatory disorder of the pilosebaceous follicle, common in adolescents, may persist during adult life. Most intense and severe clinical cases occur in males.

• Polymorph cutaneous lesions including comedones, papules, cysts, pustules and abscesses that may scar.

• Overactive pilosebaceous ducts, blockage of the ducts, excessive sebum production and proliferation of Propionibacterium acnes.

• Androgens stimulate the sebaceous glands → increased sebaceous secretion → retention of sebum due to hyperkeratosis → formation of comedones. Bacteria proliferate → release free fatty acids → papules (deep) & pustules (surface) forms. Rupture initiates inflammation, may scar.

Acne Rosacea

• Chronic, adults, characterised by central facial erythema, telangiectasia, lesions, oedema and flushing with periods of exacerbation and remission.

• Genetic and environmental factors - sunlight, heat, cold, alcohol and emotional stress are triggers.

• Degradation of dermal collagen and elastic tissue by reactive oxygen species and increased enzymes degrade the dermal layer. Superficial cutaneous vasculature damage. Inflammation.

• Bullous hyperplasia of the nose (rhinophymain) in prolonged cases.

Cutaneous lupus erythematosus

• Inflammatory autoimmune disease, limited to skin or with multi-organ involvement (systemic lupus erythematosus (SLE)) with chronic, subacute and acute forms.

• Pathophysiology - Genetic and environmental factors. Predisposition to the different subsets may relate to different genes. Major environmental factor is UV light. Medications, hormones, stress, viruses and skin trauma triggers. Initiation of autoimmune response by UV-induced keratinocyte apoptosis, autoantibodies, T cells, B cells and vascular changes induce lesions.

• Acute - erythematous rash on both cheeks and across the nose in a butterfly pattern.

• Subacute - maculopapular rash that may occur on any part of the body.

• Chronic - lesions usually on areas exposed to light, erythematous, raised with scaling. Progression to central hypopigmented and border hyperpigmented. Lesions spread and may merge → scarring.

Papulosquamous disorders

• Skin disorders that present with scaly papules and plaques and include psoriasis, lichen planus and pityriasis rosea.

• Psoriasis - chronic immune-mediated inflammatory disorder characterised by hyperproliferation of keratinocytes, infiltration by T lymphocytes and vascular changes in the dermal layer. Hyperplasia of epidermal spinosum layer and incomplete differentiation of granular and cornified layers.

• Aetiology - genetic (>10 genes) and environmental including stress, alcohol, trauma, infections and some medications e.g. ACE inhibitors and β-adrenergic receptor blockers.

• Inflammation - Antigens are presented to T lymphocyte → activated T lymphocytes migrate into the skin and when they encounter the initiating antigen they release cytokines → keratinocyte activation, hyperproliferation and abnormal growth of dermal blood vessels.

• Increased epidermal cell turnover → epidermis thickens and plaque forms. • Blood vessels in dermal papillae become tortuous and dilated → increased permeability → erythema.

Bacterial infections

• Primary or secondary e.g. associated with psoriasis and dermatitis, often opportunistic.

• Folliculitis - inflammation of the hair follicle. Staphylococcus aureus invade follicle and trigger inflammation. Superficial lesions are small pustules with a surrounding area of erythema. The pustules develop in clusters and form crusts.

• Furuncles (boils) spread of bacterial infection through the follicular wall into the surrounding dermis, also Staphylococcus aureus. Lesions are small, painful red nodules that become pustular and develop central necrosis, may scar.

• Carbuncles are collections of infected hair follicles, extending into the lower dermis and subcutaneous tissue and forms an erythematous, painful swollen nodule that drains pus through multiple openings of the skin. Fever and malaise due to inflammatory response.

• Cellulitis - spreading infection of the dermis and subcutaneous tissues, Streptococcus pyogenes, Staphylococcus aureus. Often on lower limbs, in the elderly. Periorbital form in children. Infected area is red, hot, swollen and painful due to inflammatory response, also produces systemic effects of fever, malaise and vomiting. Lesion that allowed bacterial entry often present.

• Staphylococcal scalded skin syndrome is due to Staphylococcus aureus toxins that reduce keratinocyte adhesion and destroy the epidermis, resulting in separation below the granular layer. Redness, blistering and desquamation of the skin resembles a scald or burn. Mainly children <5 years prior to anti-staphylococcal toxin antibodies or in immunosuppressed adults. Fever, irritability and with spreading erythematous and painful large fragile bullae. Rupture causes large areas of epidermis to slough off and resemble burns.

• Impetigo (‘school sores’) - contagious superficial infection mainly in children. Staphylococcus aureus , Streptococcus pyogenes and group A beta-haemolytic streptococci. Entry via damaged skin, transmission through direct contact. Small blisters with yellow/honey-coloured fluid which burst within 1–2 days leaving a yellow crust. The skin underneath is red and inflamed. Untreated lesions can develop into skin ulcers that penetrate the dermis, called ecthyma. These lesions are painful and can leave scars

• Paronychia - infection of the nail fold. Staphylococci or streptococci. Damaged nail fold allows bacterial entry, causing a painful inflammation. Pus accumulation forms abscess that may need to be incised and drained. Chronic paronychia from Candida albicans following damage to the cuticle allowing warm, moist environment for growth of the microorganism.

Viral Infections

• Herpes simplex virus (HSV): type 1 and type 2. HSV enters mucous membranes or abraded skin, into epithelial cells and replicates within them. Moves along sensory nerve pathways to the dorsal root ganglia where latent infection is established. Primary infection may be relatively severe with systemic manifestations such as fever and malaise. Antibodies reduce severity of recurrent activations.

• HSV-1 generally oral and respiratory mucosa, transmitted by respiratory droplets or direct contact with infected saliva. Lesions are small, inflamed painful vesicles that ulcerate and crust (‘cold sores’), commonly on the lips, in the mouth and around the nose, preceded by burning, tingling or stinging. UV exposure, stress, fatigue or skin irritation may trigger reactivation of the virus.

• HSV-2 typically genitalia, spread by sexual contact. Treatment is symptomatic and the lesions usually resolve within 2 weeks.

Varicella-zoster Virus

• Varicella (chickenpox) infection remains dormant in trigeminal and dorsal root ganglia and can reactivate many years later to cause herpes zoster (shingles).

• Highly contagious, transmitted by direct contact with fluid from the vesicles or airborne respiratory droplets. Pre-rash systemic manifestations such as fever, headache, sore throat and malaise. Maculopapular lesions that become vesicles, progress to pustules that crust and are very itchy. Lesions are most numerous on the trunk and less so on the face, scalp and limbs.

• Herpes zoster results from reactivation of dormant varicella virus, more prevalent in older and immunosuppressed people. Triggers include stress and illness. Rash usually occurs on the skin of a single or adjacent dermatome(s), commonly thoracic, cervical and lumbosacral possible. If the ophthalmic branch of the trigeminal nerve is infected, severe and permanent eye damage can occur.

• Tingling, itching or pain in the area of the affected nerve precedes rash of vesicles with an erythematous base, following the line of the affected nerve.

Human papillomavirus

• Warts (verrucae) are benign epidermal lesions caused by the human papillomavirus, transmitted by direct contact. Common warts (verruca vulgaris) are raised lesions with rough surfaces, flat warts (verruca plana) are flat smooth lesions and plantar warts occur on the soles of the feet

• Genital warts (condylomata acuminata) are a common STI. >40 papillomaviruses can infect the anogenital tract of men and women. The warts are soft, raised lesions that may appear in clusters with a cauliflower-like appearance. Affect external genitalia including the penis, scrotum, vulva, perineum and perianal area. They may also appear in the vagina, on the cervix or in the anus.

• Human papillomavirus vaccine (Gardasil) prevents cervical cancer, precancerous lesions and genital warts due to the human papillomavirus.

Fungal Infections

• Dermatophytes (‘skin plant’) are fungi that invade keratin. Most common species: Epidermophyton, Microsporum and Trchophyton genera.

• Superficial infections of the skin are termed tinea or dermaphytosis.

• Dermatophytes produce enzymes that digest the keratin causing scaling and hair breakage and produce an immune response.

• Tinea is classified according to the body region infected: Tinea corporis (ringworm of the body); Tinea capitis (scalp); Tinea pedis (‘athlete's foot’); Tinea manus (hand); Tinea cruris (groin and pubic area); Tinea unguium (onchomycosis) is a fungal infection of the nails.

Candida albicans

• Opportunistic infection causing candidiasis.

• Skin candidiasis occluded moist areas of skin rub together and soften, commonly under the breasts, the axillae, groin and webs of fingers and toes. The rash appears red, inflamed and pustular sometimes with white exudate. The area is painful.

• Oral candidiasis most common, appears as white patches on the tongue and oral mucosa. Under the white plaque the tongue is red, swollen and painful. Ulceration may occur in severe cases.

• Vaginal candidiasis appears as red, swollen vaginal and labial membranes with whitish discharge and may be associated with burning, itching and pain as well as dysuria or dyspareunia at times. In more severe cases the rash can extend to the perianal and groin areas.

• Candidal balanitis causes red, tender papules and pustules on the glans and shaft of the penis.

Parasitic infestations

• Scabies - Sarcoptes scabiei mite transmitted by direct skin-to-skin contact or indirectly from contaminated items. The female mite burrows into the stratum corneum and lays eggs which hatch 10 days later into larvae and travel back up to the surface of the skin to mature. Intense pruritus (itching) is the result of a hypersensitive reaction to components of saliva, eggs and faecal material of the mites. The scabies rash consists of papules, vesicles and erythema

• Pediculosis - blood-sucking lice. The female louse lays eggs (nits) which hatch in 7–10 days giving rise to nymphs that become adults in 10 days. Capitis (head lice), corporis/humanus (body lice) and pubis (pubic lice).

• Ticks are bloodsucking parasites and vectors of bacterial, rickettsial, protozoal and viral diseases. Ticks penetrate the skin, breaking through dermal blood vessels. Tick saliva contains anticoagulants and immunosuppressant prostaglandins. Lesions are itchy, painful, erythematous macules, papules or nodules. Granuloma, lichenification and secondary infections may occur. Allergic reactions are the most serious condition associated with ticks. Tick paralysis is rare, most likely in children, caused by neurotoxins.

Traumatic conditions of the integumentary system

• Burns can be caused by thermal, electrical, chemical or radiation sources.

• Pathogenesis involves both local and systemic responses.

• Local (zoned) responses are coagulative necrosis closest to the burn source, blood stasis and fluid leakage in surrounding tissue and hyperaemia in neighbouring tissue.

• Systemic effects depend on extent and depth of burns, include loss of vascular integrity and inflammation both causing plasma leakage, burn shock, electrolyte imbalance and organ damage. Severe infection risk and intense pain.

• Classified by the total body surface area depth of the burns. In Australia burn depth is most frequently described as: – epidermal – superficial dermal partial thickness – mid-dermal partial thickness – deep dermal partial thickness – full-thickness

Vascular disorders

• Cutaneous vasculitis - inflammation of the skin blood vessels and lymphatics. Inflammation may arise through direct injury to the vessel wall by bacteria or viruses or drug toxicity, indirect injury by activation of antibodies generating inflammation, indirect injury through activation of the complement system.

• Scleroderma - rare, chronic autoimmune disease of connective tissue characterised by fibrosis in the skin (localised) and organs (systemic). Large collagen deposits, inflammation and vascular narrowing. Skin becomes hard, shiny, taut and tightly connected to the underlying tissue, ulcers on the fingers, and hard calcium nodules. Environmental and genetic factors. Serious complications of systemic scleroderma arise from damage to major organs.

• Port-wine stain (naevus flammeus) - congenital capillary malformation composed of dilated vessels in the papillary dermis. It presents as pink, red or purplish macules.