This document provides a dermatology revision guide for medical students at the University of Birmingham. It summarizes the dermatology curriculum to help students prepare for exams and their work as junior doctors. The guide covers topics like history taking, dermatology terminology, common inflammatory skin conditions like eczema and acne, benign and malignant skin tumors, skin infections, blistering diseases, and dermatological emergencies. It includes descriptions, diagrams, treatment options, and tips for exams. The overall purpose is to equip students with the essential dermatology knowledge needed for their studies and clinical practice.
Derm handbook for medical students and junior doctors 2010Derma202
This handbook provides dermatology education for medical students and junior doctors. It was created by Dr Nicole Yi Zhen Chiang and Professor Julian Verbov to address the essential learning outcomes outlined by the British Association of Dermatologists. The handbook covers key topics in dermatology including skin conditions, infections, cancers, clinical skills and management strategies in a concise and easy to understand format. It aims to equip readers with the necessary knowledge and skills to safely assess and treat patients presenting with skin disorders.
There are many different types of skin disorders that can be temporary or permanent. Temporary skin disorders include contact dermatitis and keratosis pilaris. Contact dermatitis causes itchy rashes from contact with irritants, while keratosis pilaris causes small bumps on the skin. Permanent skin disorders remain for life and include psoriasis, rosacea, and vitiligo. Skin disorders can be caused by genetic factors, illnesses, lifestyle, or environmental exposures. They are commonly treated with topical creams or prescription medications.
Dyschromatosis and Reticulate pigmentary disorderssanjay singh
This document summarizes several rare pigmentary disorders including reticulate pigmentary disorders, dyschromatosis, and related conditions. Key points include:
- Reticulate pigmentary disorders involve freckle-like macules joined at margins in a net-like pattern, while dyschromatosis involves interspersed hyperpigmented and hypopigmented macules.
- Several conditions are classified including acral, flexural, generalized types like reticulate acropigmentation of Kitamura and dyschromatosis symmetrica hereditaria.
- Genetic mutations in genes like ADAM10, DSRAD, KRT5 are associated with these conditions. Histopathology often
Rosacea: Inflammatory condition in DermatologyDrSaraHistology
Rosacea is a chronic skin condition that affects the face, characterized by flushing, persistent redness, small visible blood vessels, pimples or bumps, and thickened skin, especially on the nose, cheeks, chin, and forehead. It is classified into subtypes based on symptoms such as erythema, papules and pustules, and phymatous changes. Treatment aims to reduce inflammation and prevent worsening of symptoms. Left untreated, rosacea can progress and cause permanent changes to the facial structure over many years.
Skin diseases discussed in the document include alopecia, acne, amyloid disease, cellulitis, eczema, psoriasis, scabies, pityriasis alba, urticaria, basal cell carcinoma, seborrheic dermatitis and more. For each condition, causes, locations, symptoms and treatments are described in detail providing an overview of common dermatological conditions.
dermatology. disorders of sebaceous and sweat glands.(dr.faraydwn)student
1. The document discusses diseases of sebaceous glands and sweat glands, including sebaceous hyperplasia, adenoma sebaceum, sebaceous cysts, acne, and sebaceous gland carcinoma.
2. It provides details on the types and causes of acne, including hormonal factors, infections, diet, drugs, stress and lack of sleep. The pathogenesis of acne involves increased sebum production, pore blockage, and bacteria breaking down sebum into irritating fatty acids.
3. The clinical types of acne described include neonatal acne, juvenile acne, acne vulgaris, nodular cystic acne, acne
Scaly signs in dermatology. Article discussionhiloni5
Scaly signs in dermatology describes different types of scales that can be seen in various dermatological conditions. There are several key types of scales described including collarette, mica/wafer-like, furfuraceous, ichthyosiform, micaceous, oyster-like, greasy, trailing, double-edged, and cornflake scales. Certain signs can also be elicited from scaling lesions including the Auspitz sign seen in psoriasis, the carpet tack sign seen in discoid lupus erythematosus, and the scratch sign seen in pityriasis versicolor. Accurate diagnosis relies on observation of lesion morphology and patterns as well as identification of
This document discusses several common skin conditions and infections, including their causes, symptoms, and treatment. It covers folliculitis, furuncles, cellulitis, pediculosis, scabies, dermatitis, acne, impetigo, warts, dermatophytosis, and types of burns. The causes typically involve bacterial or fungal infections. Symptoms vary depending on the condition but often include inflammation, redness, itching, pustules, and pain. Treatments involve antibiotics, antifungals, anti-parasitic medications, and procedures like cryotherapy. Good hygiene and avoiding irritants are also recommended.
Derm handbook for medical students and junior doctors 2010Derma202
This handbook provides dermatology education for medical students and junior doctors. It was created by Dr Nicole Yi Zhen Chiang and Professor Julian Verbov to address the essential learning outcomes outlined by the British Association of Dermatologists. The handbook covers key topics in dermatology including skin conditions, infections, cancers, clinical skills and management strategies in a concise and easy to understand format. It aims to equip readers with the necessary knowledge and skills to safely assess and treat patients presenting with skin disorders.
There are many different types of skin disorders that can be temporary or permanent. Temporary skin disorders include contact dermatitis and keratosis pilaris. Contact dermatitis causes itchy rashes from contact with irritants, while keratosis pilaris causes small bumps on the skin. Permanent skin disorders remain for life and include psoriasis, rosacea, and vitiligo. Skin disorders can be caused by genetic factors, illnesses, lifestyle, or environmental exposures. They are commonly treated with topical creams or prescription medications.
Dyschromatosis and Reticulate pigmentary disorderssanjay singh
This document summarizes several rare pigmentary disorders including reticulate pigmentary disorders, dyschromatosis, and related conditions. Key points include:
- Reticulate pigmentary disorders involve freckle-like macules joined at margins in a net-like pattern, while dyschromatosis involves interspersed hyperpigmented and hypopigmented macules.
- Several conditions are classified including acral, flexural, generalized types like reticulate acropigmentation of Kitamura and dyschromatosis symmetrica hereditaria.
- Genetic mutations in genes like ADAM10, DSRAD, KRT5 are associated with these conditions. Histopathology often
Rosacea: Inflammatory condition in DermatologyDrSaraHistology
Rosacea is a chronic skin condition that affects the face, characterized by flushing, persistent redness, small visible blood vessels, pimples or bumps, and thickened skin, especially on the nose, cheeks, chin, and forehead. It is classified into subtypes based on symptoms such as erythema, papules and pustules, and phymatous changes. Treatment aims to reduce inflammation and prevent worsening of symptoms. Left untreated, rosacea can progress and cause permanent changes to the facial structure over many years.
Skin diseases discussed in the document include alopecia, acne, amyloid disease, cellulitis, eczema, psoriasis, scabies, pityriasis alba, urticaria, basal cell carcinoma, seborrheic dermatitis and more. For each condition, causes, locations, symptoms and treatments are described in detail providing an overview of common dermatological conditions.
dermatology. disorders of sebaceous and sweat glands.(dr.faraydwn)student
1. The document discusses diseases of sebaceous glands and sweat glands, including sebaceous hyperplasia, adenoma sebaceum, sebaceous cysts, acne, and sebaceous gland carcinoma.
2. It provides details on the types and causes of acne, including hormonal factors, infections, diet, drugs, stress and lack of sleep. The pathogenesis of acne involves increased sebum production, pore blockage, and bacteria breaking down sebum into irritating fatty acids.
3. The clinical types of acne described include neonatal acne, juvenile acne, acne vulgaris, nodular cystic acne, acne
Scaly signs in dermatology. Article discussionhiloni5
Scaly signs in dermatology describes different types of scales that can be seen in various dermatological conditions. There are several key types of scales described including collarette, mica/wafer-like, furfuraceous, ichthyosiform, micaceous, oyster-like, greasy, trailing, double-edged, and cornflake scales. Certain signs can also be elicited from scaling lesions including the Auspitz sign seen in psoriasis, the carpet tack sign seen in discoid lupus erythematosus, and the scratch sign seen in pityriasis versicolor. Accurate diagnosis relies on observation of lesion morphology and patterns as well as identification of
This document discusses several common skin conditions and infections, including their causes, symptoms, and treatment. It covers folliculitis, furuncles, cellulitis, pediculosis, scabies, dermatitis, acne, impetigo, warts, dermatophytosis, and types of burns. The causes typically involve bacterial or fungal infections. Symptoms vary depending on the condition but often include inflammation, redness, itching, pustules, and pain. Treatments involve antibiotics, antifungals, anti-parasitic medications, and procedures like cryotherapy. Good hygiene and avoiding irritants are also recommended.
This document provides information on describing basic skin lesions, including their morphology, types, shapes, configurations, arrangements, distributions, and primary and secondary lesions. It discusses features to note when describing a skin lesion such as size, type, shape, color, surface area, and distribution. It also defines different types of primary lesions like macules, patches, papules, plaques, nodules, vesicles, bullae, pustules, abscesses, wheals, and cysts as well as secondary lesions including scales, crusts, erosions, fissures, and scars. Finally, it covers some special skin lesions such as burrows, purpura, ulcers, and malar rashes.
This document discusses wounds, including their classification, stages of healing, types of healing, and factors that can affect the healing process. It also covers examining patients with wounds and potential complications. Wounds are breaks in the skin or mucous membranes and have signs like pain, bleeding, and an open defect. They can be classified based on their cause (surgical or accidental), type of injury (cut, puncture, etc.), and healing process (primary or secondary intention). The stages of wound healing are examination, inflammation, proliferation, and remodeling. Factors like nutrition, infection, ischemia, and medications can influence healing. Examining a wound includes assessing location, size, depth, underlying cause, and patient comorbidities
This document summarizes a case of melasma in a 25-year-old woman. Her skin darkening began during her first pregnancy and is exacerbated by sun exposure. Examination found hyperpigmented macules on her cheeks, nose, forehead and upper lip. The most likely diagnosis is melasma. Melasma is an acquired hyperpigmentation caused by sun exposure. Treatment includes azelaic acid cream applied twice daily and strict sun protection with broad spectrum sunscreen.
Here are some common causes of mouth ulcers to consider in the differential diagnosis:
- Herpes simplex virus infection
- Aphthous ulcers/canker sores
- Traumatic ulcers
- Ulcerative lesions of recurrent oral ulceration
- Behçet's disease
- Ulcerative lichen planus
- Syphilis
- Crohn's disease
- Deficiencies such as folate, iron, or vitamin B12
- Drug reactions
- Infections such as herpes zoster or tuberculosis
- Malignancies such as squamous cell carcinoma
A thorough history and examination is needed to help determine the underlying cause. Investigations may include
1) Facial melanoses refers to hyperpigmentation of the face caused by increased melanin production. Common types include melasma, lichen planus pigmentosus, pigmented contact dermatitis, and periorbital melanosis.
2) Melasma is the most common type of facial melanoses. It presents as symmetrical brown patches on sun-exposed areas of the face. Triggers include sun exposure, hormones, and genetic predisposition. Treatment focuses on preventing sun damage and using topical bleaching agents.
3) Lichen planus pigmentosus is a variant of lichen planus that causes slate gray macules on the face and neck. It is resistant
Primary skin lesions include macules, papules, plaques, nodules, tumors, and wheals. Secondary lesions develop from primary lesions and include scales, crusts, excoriations, fissures, erosions, ulcers, and scars. Special lesions occur under certain conditions and include erythema, telangiectasia, purpura, petechiae, ecchymoses, vibices, and hematomas. The document provides detailed definitions and descriptions of these various skin lesions.
Common skin diseases include:
- Scabies, caused by mites under the skin, which can be treated with sulfur or cleaning the infected environment.
- Ringworm, caused by a fungus and presenting as a red, itchy ring, which can be treated with antifungal creams.
- Eczema, whose cause is unknown but may be triggered by stress or irritants, presenting as inflamed, red, dry, and itchy skin, treated with corticosteroids or antihistamines.
- Psoriasis, cause unknown but involving too-rapid skin cell growth, appearing as thick red plaques covered in silvery scales, treated with steroid creams or phot
1. Juvenile dermatomyositis differs from adult DM in that it lacks calcinosis cutis, malignancy, and has less sex predominance and vasculitis. Adults can develop malignancy and positive anti-synthetase antibodies.
2. Two medications that can induce dermatomyositis are statins and hydroxyurea. Two features that differ DM lesions from LE are their violaceous hue and pruritus.
3. Indications for treatment of hemangiomas include obscuring vision, compromising airway, ulceration and pain, and being in a cosmetically sensitive area. The approach for starting propranolol includes testing for contraindications and slowly
Rosacea is a chronic (long-term) disease
that affects the skin and sometimes the eyes. The disorder is characterized by
redness, pimples, and, in advanced stages, thickened skin. Rosacea usually
affects the face. Skin on other parts of the upper body is only rarely
involved.
Psoriasis is a chronic, inflammatory skin condition that causes red scaly patches to appear on the skin. The most common form is plaque psoriasis, which accounts for 80-90% of cases, appearing as raised, red patches covered with silvery scales. Psoriasis occurs when skin cells multiply up to 10 times faster than normal. It is believed to be both a disorder of skin cell growth and an immune-mediated disease driven by T cells and cytokines. Psoriasis has no cure but can be managed with topical treatments and phototherapy. It affects the joints in 10-20% of cases (psoriatic arthritis).
Toxic epidermal necrolysis (TEN) is a rare, potentially fatal adverse drug reaction characterized by extensive skin detachment and mucous membrane involvement. It is caused by apoptosis of keratinocytes triggered by certain drugs in genetically susceptible individuals. TEN is diagnosed clinically based on >30% detachment of the epidermis. Management involves stopping the causative drug, supportive care, and investigational therapies to prevent apoptosis. Complications include infection, organ failure and death in around 30% of cases. Prognosis can be estimated using the SCORTEN severity-of-illness score.
Understanding Hyperpigmentation and Treating with Combined Strategies - NEW ...Jordana Lewis
The document discusses hyperpigmentation and melasma, outlining the causes and types of hyperpigmentation as well as protocols for treating it using a Yellow Peel chemical peel approach with combinations of retinol, salicylic acid, phytic acid, kojic acid, azelaic acid, and other ingredients over multiple treatments tailored to a patient's skin type and level of hyperpigmentation. The Yellow Peel protocols provide guidance on application times and endpoints based on a patient's phototype and hyperpigmentation severity to safely and effectively treat conditions like melasma, sun damage, and other causes of dark patches and spots on the skin
Acne vulgaris, or common acne, is a chronic inflammatory skin condition characterized by abnormalities in sebum production, follicular desquamation, bacterial proliferation and inflammation. It is the most common skin disorder, affecting over 17 million Americans. The main causes are P. acnes and S. epidermidis bacteria colonizing hair follicles and stimulating inflammation. Clinical manifestations range from non-inflammatory whiteheads and blackheads to inflammatory papules, pustules, cysts and nodules. Treatment focuses on reducing inflammation and preventing complications using topical and oral medications like benzoyl peroxide, antibiotics and retinoids. While acne usually resolves by the mid-20s, some patients
The document describes and classifies various skin lesions. It defines 26 different lesions including macules, papules, plaques, vesicles, bullae, pustules, cysts, nodules and wheals as primary skin lesions. Secondary skin lesions include scales, crusts, fissures, erosions, ulcers, lichenification and atrophy. Special skin lesions include telangiectasia, phlebectasia, burrows and comedones. Vasculopathies like petechiae, purpura and ecchymosis are also defined. Iris-like lesions are used to describe erythema multiforme. Each lesion is concisely defined and an example is provided.
Secondary lesions & Special lesions in dermatologySivaji Yadav
This document defines and describes various secondary skin lesions and special lesions. It discusses atrophy, erosion, excoriation, ulcer, scar, sclerosis, scale, crust, burrow, comedo, milium, telangiectasia, and target lesions. For each lesion, it provides details on clinical presentation, characteristics, and causes. Secondary lesions result from disruption of the skin surface, while special lesions have unique appearances or features.
Alopecia areata is an autoimmune disorder that causes unpredictable hair loss, usually in small patches on the scalp. There are three main types: alopecia areata, alopecia areata totalis (complete scalp hair loss), and alopecia areata universalis (full body hair loss). Current treatments include minoxidil, which can induce regrowth but loses effectiveness over time and has side effects like headaches and facial hair growth. Bakuchi seeds have properties that may help by improving circulation and stimulating new hair growth without side effects. Preparing a bakuchi seed extract and applying it topically could help treat alopecia areata and reduce reliance on minoxidil.
1. Cutaneous photosensitivity reactions require absorption of light energy by molecules, leading to damage and clinical disease.
2. Common photosensitivity disorders include polymorphic light eruption (PLE), chronic actinic dermatitis (CAD), and solar urticaria.
3. Clinical features, histopathology, and phototesting help differentiate types of photosensitivity dermatoses.
This document provides an overview of bacterial skin infections, including:
- Common non-specific bacterial infections caused by Staphylococcus aureus and Streptococcus such as impetigo, ecthyma, folliculitis, furunculosis, and cellulitis.
- Specific infections like leprosy caused by Mycobacterium leprae and cutaneous tuberculosis.
- Other infections discussed include erythrasma caused by Corynebacterium minutissimum and clinical features and treatments are provided for each condition.
The document examines both gram-positive bacterial infections of the skin as well as mycobacterial infections like leprosy and cutaneous tuberculosis. A range
The document provides information about examining the skin. It discusses the structure of skin including its three layers - epidermis, dermis and subcutaneous tissue. It describes epidermal appendages like hair, nails and glands. The functions of skin and appendages are explained. Guidelines are given for taking a skin history and conducting a physical examination including inspection, palpation and documentation of lesions. Common primary and secondary skin lesions are defined and examples are shown.
This document provides information on describing basic skin lesions, including their morphology, types, shapes, configurations, arrangements, distributions, and primary and secondary lesions. It discusses features to note when describing a skin lesion such as size, type, shape, color, surface area, and distribution. It also defines different types of primary lesions like macules, patches, papules, plaques, nodules, vesicles, bullae, pustules, abscesses, wheals, and cysts as well as secondary lesions including scales, crusts, erosions, fissures, and scars. Finally, it covers some special skin lesions such as burrows, purpura, ulcers, and malar rashes.
This document discusses wounds, including their classification, stages of healing, types of healing, and factors that can affect the healing process. It also covers examining patients with wounds and potential complications. Wounds are breaks in the skin or mucous membranes and have signs like pain, bleeding, and an open defect. They can be classified based on their cause (surgical or accidental), type of injury (cut, puncture, etc.), and healing process (primary or secondary intention). The stages of wound healing are examination, inflammation, proliferation, and remodeling. Factors like nutrition, infection, ischemia, and medications can influence healing. Examining a wound includes assessing location, size, depth, underlying cause, and patient comorbidities
This document summarizes a case of melasma in a 25-year-old woman. Her skin darkening began during her first pregnancy and is exacerbated by sun exposure. Examination found hyperpigmented macules on her cheeks, nose, forehead and upper lip. The most likely diagnosis is melasma. Melasma is an acquired hyperpigmentation caused by sun exposure. Treatment includes azelaic acid cream applied twice daily and strict sun protection with broad spectrum sunscreen.
Here are some common causes of mouth ulcers to consider in the differential diagnosis:
- Herpes simplex virus infection
- Aphthous ulcers/canker sores
- Traumatic ulcers
- Ulcerative lesions of recurrent oral ulceration
- Behçet's disease
- Ulcerative lichen planus
- Syphilis
- Crohn's disease
- Deficiencies such as folate, iron, or vitamin B12
- Drug reactions
- Infections such as herpes zoster or tuberculosis
- Malignancies such as squamous cell carcinoma
A thorough history and examination is needed to help determine the underlying cause. Investigations may include
1) Facial melanoses refers to hyperpigmentation of the face caused by increased melanin production. Common types include melasma, lichen planus pigmentosus, pigmented contact dermatitis, and periorbital melanosis.
2) Melasma is the most common type of facial melanoses. It presents as symmetrical brown patches on sun-exposed areas of the face. Triggers include sun exposure, hormones, and genetic predisposition. Treatment focuses on preventing sun damage and using topical bleaching agents.
3) Lichen planus pigmentosus is a variant of lichen planus that causes slate gray macules on the face and neck. It is resistant
Primary skin lesions include macules, papules, plaques, nodules, tumors, and wheals. Secondary lesions develop from primary lesions and include scales, crusts, excoriations, fissures, erosions, ulcers, and scars. Special lesions occur under certain conditions and include erythema, telangiectasia, purpura, petechiae, ecchymoses, vibices, and hematomas. The document provides detailed definitions and descriptions of these various skin lesions.
Common skin diseases include:
- Scabies, caused by mites under the skin, which can be treated with sulfur or cleaning the infected environment.
- Ringworm, caused by a fungus and presenting as a red, itchy ring, which can be treated with antifungal creams.
- Eczema, whose cause is unknown but may be triggered by stress or irritants, presenting as inflamed, red, dry, and itchy skin, treated with corticosteroids or antihistamines.
- Psoriasis, cause unknown but involving too-rapid skin cell growth, appearing as thick red plaques covered in silvery scales, treated with steroid creams or phot
1. Juvenile dermatomyositis differs from adult DM in that it lacks calcinosis cutis, malignancy, and has less sex predominance and vasculitis. Adults can develop malignancy and positive anti-synthetase antibodies.
2. Two medications that can induce dermatomyositis are statins and hydroxyurea. Two features that differ DM lesions from LE are their violaceous hue and pruritus.
3. Indications for treatment of hemangiomas include obscuring vision, compromising airway, ulceration and pain, and being in a cosmetically sensitive area. The approach for starting propranolol includes testing for contraindications and slowly
Rosacea is a chronic (long-term) disease
that affects the skin and sometimes the eyes. The disorder is characterized by
redness, pimples, and, in advanced stages, thickened skin. Rosacea usually
affects the face. Skin on other parts of the upper body is only rarely
involved.
Psoriasis is a chronic, inflammatory skin condition that causes red scaly patches to appear on the skin. The most common form is plaque psoriasis, which accounts for 80-90% of cases, appearing as raised, red patches covered with silvery scales. Psoriasis occurs when skin cells multiply up to 10 times faster than normal. It is believed to be both a disorder of skin cell growth and an immune-mediated disease driven by T cells and cytokines. Psoriasis has no cure but can be managed with topical treatments and phototherapy. It affects the joints in 10-20% of cases (psoriatic arthritis).
Toxic epidermal necrolysis (TEN) is a rare, potentially fatal adverse drug reaction characterized by extensive skin detachment and mucous membrane involvement. It is caused by apoptosis of keratinocytes triggered by certain drugs in genetically susceptible individuals. TEN is diagnosed clinically based on >30% detachment of the epidermis. Management involves stopping the causative drug, supportive care, and investigational therapies to prevent apoptosis. Complications include infection, organ failure and death in around 30% of cases. Prognosis can be estimated using the SCORTEN severity-of-illness score.
Understanding Hyperpigmentation and Treating with Combined Strategies - NEW ...Jordana Lewis
The document discusses hyperpigmentation and melasma, outlining the causes and types of hyperpigmentation as well as protocols for treating it using a Yellow Peel chemical peel approach with combinations of retinol, salicylic acid, phytic acid, kojic acid, azelaic acid, and other ingredients over multiple treatments tailored to a patient's skin type and level of hyperpigmentation. The Yellow Peel protocols provide guidance on application times and endpoints based on a patient's phototype and hyperpigmentation severity to safely and effectively treat conditions like melasma, sun damage, and other causes of dark patches and spots on the skin
Acne vulgaris, or common acne, is a chronic inflammatory skin condition characterized by abnormalities in sebum production, follicular desquamation, bacterial proliferation and inflammation. It is the most common skin disorder, affecting over 17 million Americans. The main causes are P. acnes and S. epidermidis bacteria colonizing hair follicles and stimulating inflammation. Clinical manifestations range from non-inflammatory whiteheads and blackheads to inflammatory papules, pustules, cysts and nodules. Treatment focuses on reducing inflammation and preventing complications using topical and oral medications like benzoyl peroxide, antibiotics and retinoids. While acne usually resolves by the mid-20s, some patients
The document describes and classifies various skin lesions. It defines 26 different lesions including macules, papules, plaques, vesicles, bullae, pustules, cysts, nodules and wheals as primary skin lesions. Secondary skin lesions include scales, crusts, fissures, erosions, ulcers, lichenification and atrophy. Special skin lesions include telangiectasia, phlebectasia, burrows and comedones. Vasculopathies like petechiae, purpura and ecchymosis are also defined. Iris-like lesions are used to describe erythema multiforme. Each lesion is concisely defined and an example is provided.
Secondary lesions & Special lesions in dermatologySivaji Yadav
This document defines and describes various secondary skin lesions and special lesions. It discusses atrophy, erosion, excoriation, ulcer, scar, sclerosis, scale, crust, burrow, comedo, milium, telangiectasia, and target lesions. For each lesion, it provides details on clinical presentation, characteristics, and causes. Secondary lesions result from disruption of the skin surface, while special lesions have unique appearances or features.
Alopecia areata is an autoimmune disorder that causes unpredictable hair loss, usually in small patches on the scalp. There are three main types: alopecia areata, alopecia areata totalis (complete scalp hair loss), and alopecia areata universalis (full body hair loss). Current treatments include minoxidil, which can induce regrowth but loses effectiveness over time and has side effects like headaches and facial hair growth. Bakuchi seeds have properties that may help by improving circulation and stimulating new hair growth without side effects. Preparing a bakuchi seed extract and applying it topically could help treat alopecia areata and reduce reliance on minoxidil.
1. Cutaneous photosensitivity reactions require absorption of light energy by molecules, leading to damage and clinical disease.
2. Common photosensitivity disorders include polymorphic light eruption (PLE), chronic actinic dermatitis (CAD), and solar urticaria.
3. Clinical features, histopathology, and phototesting help differentiate types of photosensitivity dermatoses.
This document provides an overview of bacterial skin infections, including:
- Common non-specific bacterial infections caused by Staphylococcus aureus and Streptococcus such as impetigo, ecthyma, folliculitis, furunculosis, and cellulitis.
- Specific infections like leprosy caused by Mycobacterium leprae and cutaneous tuberculosis.
- Other infections discussed include erythrasma caused by Corynebacterium minutissimum and clinical features and treatments are provided for each condition.
The document examines both gram-positive bacterial infections of the skin as well as mycobacterial infections like leprosy and cutaneous tuberculosis. A range
The document provides information about examining the skin. It discusses the structure of skin including its three layers - epidermis, dermis and subcutaneous tissue. It describes epidermal appendages like hair, nails and glands. The functions of skin and appendages are explained. Guidelines are given for taking a skin history and conducting a physical examination including inspection, palpation and documentation of lesions. Common primary and secondary skin lesions are defined and examples are shown.
This document provides guidance on examining patients presenting with skin diseases. It details the important aspects of history taking including primary and secondary lesions, subjective and objective symptoms, and pertinent questions regarding duration, site, evolution, and associated symptoms. Physical examination involves detailed description of lesions including morphology, distribution, and configuration. Key signs related to macules, papules, plaques, vesicles, pustules, and other eruption types are defined. The document emphasizes close examination of nails, hair, and mucosal surfaces to identify relevant findings.
This document provides guidance on evaluating and managing dermatological conditions. It discusses the functions of skin, taking a thorough history, conducting a full examination of the skin and appendages, selecting appropriate investigations like skin scrapings or biopsies, and developing a treatment plan. Topical therapies are often first-line and include creams, ointments, or gels applied correctly based on the skin condition and amount of surface area involved. Close monitoring of the patient's response to treatment is important.
This document provides information on examining the integumentary system. It discusses clinical examination of the skin, including distribution and morphology of lesions. Common terms used to describe skin lesions such as macules, papules, and plaques are defined. Hair disorders like alopecia areata and androgenetic alopecia are outlined. Finally, common nail changes and disorders are reviewed, including effects of trauma, nail changes in systemic disease like Beau's lines, and nail findings in conditions like iron deficiency and clubbing.
This document provides information on common skin infections in children. It discusses bacterial infections like impetigo, cellulitis, folliculitis, and staphylococcal scalded skin syndrome. It also covers fungal infections, viral infections, and parasitic infections. For accurate diagnosis, a thorough history and physical exam are important. Skin lesions should be classified based on characteristics like size, color, and morphology. Proper treatment depends on the specific infection and may involve topical antibiotics, oral antibiotics, or both.
This document provides information on malignant skin lesions and skin cancers. It discusses the anatomy and function of skin, pre-malignant lesions like actinic keratosis, Bowen's disease and conditions that increase risk of skin cancers like neurofibromatosis. It then describes the most common skin cancers - basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and malignant melanoma. For each cancer, it discusses epidemiology, etiology, clinical features, histopathology, prognosis and treatment options.
This document provides an overview of the integumentary system, including the structure and function of the skin and its layers. It discusses the epidermis and dermis in depth, describing the cells that make up each layer. The document also covers skin appendages like hair follicles, sebaceous glands, and nails. Additionally, it summarizes the functions of the skin and describes common skin conditions like psoriasis, outlining its causes, types, symptoms, and diagnostic evaluation.
This document provides information about examining the integumentary system, including the skin, hair, and nails. It discusses how to clinically examine the skin, such as observing the distribution, morphology, and involvement of specific areas. Common terms used to describe skin lesions like macules, papules, and plaques are defined. Hair disorders like alopecia areata and androgenetic alopecia are outlined. Finally, common nail changes and disorders from trauma, systemic diseases, and nutritional deficiencies are described.
The document discusses integumentary disorders and provides information on the anatomy and function of the skin. It describes the three layers of the skin - epidermis, dermis and subcutaneous tissue. It then discusses factors that influence skin integrity such as immobility, trauma, and malnutrition. Common dermatological terms and methods of describing skin lesions are also outlined. Finally, it provides an overview of common dermatological conditions like eczema, bacterial infections, fungal infections and viral infections.
This document provides an overview of a dermatopathology course, including learning objectives, session details, sample exam questions, and study tips. It discusses key histopathological terms, classifications of skin diseases, common and rare skin conditions, and outlines the curriculum to be covered, including acute and chronic inflammatory diseases, infections, blistering diseases, and neoplastic conditions.
This document defines and describes common paediatric skin lesions. It discusses primary lesions such as macules, papules, vesicles and pustules. It also covers secondary lesions including scaling, lichenification and crusting. The document provides details on the etiology, pathophysiology, clinical features, diagnosis and treatment of common paediatric skin conditions like acne, warts and scabies.
This document provides information about various skin diseases and disorders. It begins by defining different primary skin lesions such as macules, papules, nodules, etc. It then classifies skin disorders into five main categories: acute inflammatory dermatoses, chronic inflammatory dermatoses, infectious dermatoses, blistering disorders, and skin tumors. Examples of specific conditions are provided for each category. More detail is given about conditions like eczema, urticaria, pemphigus, and psoriasis - outlining their pathogenesis, clinical features, types, treatment and more. In summary, the document covers a wide range of skin diseases and lesions at both a high level and with more in-depth explanations of
This document provides an overview of common skin diseases in pediatrics. It begins with an introduction noting that skin complaints make up 1/3 of pediatric outpatient visits. It then covers the anatomy and functions of skin, differences between neonatal and adult skin, how to approach diagnosis, and classifications of pediatric skin disorders. Specific conditions discussed include toxic erythema of newborns, miliaria rubra, acropustulosis of infancy, transient neonatal pustular melanosis, neonatal acne, congenital syphilis, and milia. Intertrigo, diaper dermatitis, cutis marmorata are also summarized.
clinical dermatology Lange medical book 1st edition .
Wikipedia
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This document provides definitions and descriptions of terms related to normal skin anatomy and pathology. It begins with labeling diagrams of normal skin structures from the macroscopic to microscopic level. It then covers various skin conditions including pigmentation disorders, benign and malignant epidermal and dermal tumors, dermatoses, bullae, appendage disorders, panniculitis, and infections/infestations. For each condition, it lists key characteristics and histologic findings to aid in identification and diagnosis.
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
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The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
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Dermatology revision book
1. Dermatology 101
A dermatology revision guide for Birmingham medical students
Dr. Kalaprapa Asavisanu (FY1)
University of Birmingham
MBChB
Updated: February 2018
1
2. 2
Green boxes--‐ TIPS
Text in red/in red boxes --‐ common themes for OSCES
and MCQs
About this guideline
This booklet is aimed at 4th year medical students at the
university of Birmingham as a summary of the dermatology
curriculum.
The purpose is to prepare students for the MCQs, OSCEs and
work as junior doctors.
Disclaimer: This booklet does not represent the University of
Birmingham,any of the west midlands foundation trusts or the
British association of dermatologists. The views expressed in
these lectures are of the author only.
4. 4
History taking
Presenting complaint:
--‐ Site
--‐ Symptom
--‐ Duration
--‐ Associated symptoms e.g. pain, swelling, discharge, itch
--‐ Evolution of Sx – was it like this at the start?
Past medical history:
--‐ Past skin problems
--‐ Atopic triad: hay fever, eczema, asthma
Family history:
--‐ Skin cancer
Drug history:
--‐ Current meds
--‐ What have they tried
Social history
--‐ How isthis affecting their QoLe.g. confidence, clothes they wear,wherethey
go.
--‐ Sun bed, do they burn
--‐ Job – skin better whenaway?
Examination (Inspect, palpate, systematic
check)
Inspect
‘SSCAMM’
Site, Size, color, associated secondary features, morphology,
margins.
Palpate
‘Skin conditions must be touched tenderly’
Surface, consistency, mobility, tenderness, temperature
Systematic check: hair, nails, mucous membranes
If lesion pigmented:
ABCDE: Asymmetry, irregular border, ≥2 colors, diameters > 6 mm
Just describe
what you
see/feel!
And fill the gaps
with SSCAMM/Skin
conditions must be
touched tenderly--‐
Because sometimes
it takes longer to
remember the
pneumonic!
Dermatology
OSCE’s tend to
be history
taking stations.
Get a good
STORY.
And don’t forget
your ICE!
History and examination
5. 5
General terms
• Puritis– itchy (scabies, eczema, urticaria, lichen planus)
• Lesion – area of alteredskin
• Rash--‐ eruption (drug rash)
• Naevus – localized malformation of skin tissue
• Comedone – sebaceous follicle plug with sebum, bacteria + cellular debris.
(Can be open or closed = open: blackheads, closed: whiteheads)
Site
• Generalized--‐ all over body (scabies, chickenpox)
• Widespread--‐ extensive (drug eruption)
• Localized--‐ just one area of skin (burns)
• Flexural – body fold e.g. groin, popliteal, antecubital fossa (eczema)
• Extensor– knees, elbows, shins (psoriasis)
• Pressure areas – sacrum, buttocks, ankles, heels (pressure sores)
• Dermatome--‐ area supplied by a spinal nerve (shingles)
• Photosensitive--‐ sun--‐exposed areas e.g. face, neck (sunburn)
• Koebner--‐ linear eruption at site of trauma
(psoriasis)
Morphology
• Discrete--‐ separate lesions
• Confluent--‐ lesions merged
• Linear--‐ in line (scabies)
• Target--‐ dartboard rings (erythema multiforme)
• Annular--‐ circles (tinea)
• Discoid/nummular--‐ coin shaped (discoid eczema)
Color
• Erythema--‐ red – blanches on pressure – due to inflammation + vasodilation
(palmar erythema)
• Purpura--‐ red due to bleeding into skin/mucous membrane – DOES NOT
blanch on pressure (can be petechiae – small pinpoint macules or
ecchymoses--‐ larger bruise--‐like patch) –HSP, meningococcal septicaemia
• Hypopigmentation--‐ area of paler skin (pityriasis versicolor)
• De--‐pigmentation--‐ white skin due to no melanin (vitiligo)
• Hyper--‐ pigmentation – darker skin (post--‐ inflammatory changes in acne,
malaema )
Dermatology terminology
6. 6
Morphology
• Macule – small flat area < 5 mm (freckle)
• Patch – large flat area > 5 mm (port--‐wine stain)
• Papule--‐ small raised lesion < 5mm (xanthomata)
• Nodule – large raised round lesion > 5 mm (pyogenic granuloma)
• Plaque--‐ large raised area with flat top > 5 mm (psoriasis)
• Vesicle– small clear fluid filled lesion < 5 mm (chickenpox, pompholyx)
• Bulla – large fluid filled lesion > 5 mm (bullous pemphigoid, insect bites)
• Pustule– small pus filled bubble < 5 mm (acne)
• Abscess--‐ localized area of pus (paronychia)
• Wheal – raised area of dermal oedema
• Boil/furuncle – staph infection within a hair follicle
• Carbuncle--‐ multiple boils/furuncles
• Excoriation– loss of epidermis from trauma (scratching in eczema)
• Lichenification – well--‐defined toughened skin with accentuation of skin
markings
• Scales--‐ thick flakes of the top layer of the skin (psoriasis)
• Crust--‐ rough area of dried serum, blood, bacteria + cellular debris (impetigo)
• Scar--‐ new fibrous tissue can be: atrophic (thinning), hypertrophic
(hyperproliferation WITHIN wound boundary), keloid (hyperproliferation
BEYOND wound margin)
• Ulcer--‐ loss of epidermis and dermis, heals with scar (leg ulcers)
• Fissure – epidermal crack (eczema)
• Striae – linear areas which change from purple--‐ pink--‐ white (pregnancy,
growth spurts, steroid side effects)
Hair
• Alopecia--‐ hair loss (apolecia areata)
• Hirsutism – androgen--‐ dependent hair growth in a female (PCOS)
• Hypertrichosis--‐ non--‐androgen dependent pattern of excess hair
(hypertrichosis)
Nails
• Clubbing--‐ loss of angle between nail fold and nail plate (CF, bronchiectasis,
SBE, cyanotic heart diseases,IBD)
• Koilonychia – spoon--‐ shaped nail (iron def, congenital, idiopathic)
• Onycholysis--‐ nail separating from nail bed (trauma, psoriasis, fungal nail
infection, hyperthyroidism)
• Pitting--‐ depressions in nail plate (psoriasis, eczema, alopecia areata)
7. 7
Common MCQ
questions about side
effects/monitoring
of treatment
1) ECZEMA
1) Atopic eczema
Risk factor: family history (atopic triad: eczema,
asthma, hay fever).
Strong genetic cause. 90% +ve for family history.
Symptoms: itch, weep/crust/scaling lesion that is not well demarcated, sleep
disturbance/bleeding/ lichenification (prominent skinmarkingsduetochronic
scratching) on flexural areas.
Diagnosis: clinical
Treatment:
Eczema patient education:
1) Education: explain to patients that the natural
history is relapse--‐ remission. It will come and
goanditisnottheirfault.Complications:
infection + what to do (Abx). Prognosis: for
childhood eczema--‐ most people will grow out of it.
90% by teens.
2) Explain: that treatment is a control not a cure. Show
the two--‐tier approach.
3) Empathy: psychologicalsupport.
Avoid exacerbating agents.
Atopic eczema
Source: DermNet NZ
Liberalemollients. Soap substitutes,bathoils. –regular treatment whetherskinis
good/bad.
Topical therapies: topical steroids for flares, topical
immunomodulators (e.g. tacrolimus, pimecrolimus)--‐ steroid
sparing agents.
Oral therapy--‐ oral steroids, oral immunomodulators e.g.
ciclosporin (Monitor BP and renal function), azathioprine (Check TPMT and
LFT).
Other:antihistamine foritch, antibiotics e.g.flucloxacillin for secondarybacterial
infection,
Eczema: common OSCE
history taking station
which involves patient
counseling
Inflammatory skin conditions
8. 8
Emollients (Try to use as greasy as possible):
V greasy: epaderm
Greasy: hydrous ointment
Moderate: diprobase, double base.
Light: aveeno, E45.
Steroid (use for flares--‐ try to use as low potency as possible)
Mild: 1--‐2.5% hydrocortisone
Moderate:eumovate
potent: betnovate, elocon
v potent:dermovate.
Complication: infection (crusty/weeping lesions), eczema herpeticum (tx: aciclovir)
Oralsteroidss/e:HTN,growthsuppression, osteoporosis, GIulceration,mood
swings. Insomnia, acne, weight gain, DM, cushing’s syndrome.
Topical steroids s/e: skin thinning, infections, telangiectasia, straie, easy bruising
2) Discoid eczema--‐ a nummular dermatitis.
Discoid eczema
Source: DermNet NZ
3) Seborrheic eczema/dermatitis--‐ esp
young adults. M>F. diagnosis is based on
characteristicdistribution: sideof nose,forehead,
eyebrows,scalp, behind ears. (classic is red,flaky
lesions on side of nose)
Tx: anti--‐yeast e.g. ketoconazole
Seborrhiec dermatitis
Source: DermNet NZ
9. 4) Contact dermatitis – 2 types: 1) allergic 2)
irritant
I) Allergiccontact dermatitise.g.nickelisthe
most common causee.g. ear rings,watches.Ifthe
eczema is in a strangedistribution e.g. shape of a
belt,watch think allergic contact dermatitis.
Diagnosis: patchtesting.(type4hypersensitivity reaction).
NOT skin prick. Skin pricksarefor type1 hypersensitivity
reaction for things like food allergies.
II) Irritant contact dermatitis--‐ e.g. constantly
washing hands. No test,diagnosis basedon
history e.g. hair dressers,surgeons, chefs.
5) Venous eczema – usually elderly lower leg
due to venoushypertension.
Treatment: compression stockings.
6) Pompholyx eczema--‐ blisters in hands and
feet that is intensely itchy usually in summer +
winter months.
Allergic contact dermatitis
Source: DermNet NZ
Irritant contact dermatitis
Source: DermNet NZ
7) Asteatotic eczema--‐ in elderly people in lower legs, looks like a
cracked riverbed. Tx:moisturizer.
Treatment: moisturizer.
8) Photosensitive eczema--‐ sun induced
eczema.Only seein sunexposedareas.Sparing
under neck, under nose.
Venous eczema +
lipodermatosclerosis
Source: DermNet NZ
Pompholyx eczema
Source: DermNet NZ
Asteatotic eczema
Source: DermNet NZ
9
11. 11
3) Psoriasis
Chronic inflammatory skin disease due to keratinocyte hyperproliferation.
1) Chronicplaquepsoriasis (mostcommon type)–
Symptoms: symmetrical red, well circumscribed, scaly plaques.
Treatment:
Topicaltherapy:vitamindanalogue (calcipotriol, calcitriol), topical corticosteroids,
coal tar, topical retinoids
Phototherapy (extensive disease)--‐ e.g. PUVA
Oral therapy (extensive, severe psoriasis)--‐ methotrexate, ciclosporin.
Biologics--‐ infliximab, etanercept
50% of patients have nail changes. 15% have arthritis.
Auspitz sign--‐ scratch--‐ get pinpoint bleed.
Extra--‐dermatological signs: nails: pitting, onycholysis, subungal hyperkeratosis, oil
drop sign,
S/E of treatment:
Methotrexate: hepatotoxicity, neutropenia
Ciclosporin; HTN, nephrotoxicity
PUVA: skin cancer, photoaging
Acitretin: hyperlipidaemia, dry skin, teratogenic
Scoring for severity of psoriasis: PASI
Other types of psoriasis:
2)Guttate psoriasis(raindrop lesions usually
on the back)
Salmon colored paint drop. 2 weeks post--‐
streptoccoccal throat infection. In children it is
usually self--‐limiting. 40% will go on to develop
chronic plaque psoriasis. Tx: can use UV light,.
Guttate psoriasis
Source: DermNet NZ
Common MCQ
questions about side
effects of treatment
12. 12
3)Erythrodermic psoriasis--‐ derm emergency--‐ skin extensively red. Get
high output cardiac failure +dehydration (moredetail see‘erythroderma’ section).
4) Palmoplantar pustular psoriasis--‐ yellow sterile
pustules on palmes and soles.
Tx: Bed rest. Bland emollients e.g. 50:50.
Other types:Seborrheic(usually onnasolabial fold, behind ears),flexural.
Psoriasis is associated with:
--‐ ocular inflammation: iritis/episcleritis
--‐ IBD
--‐ Psoriatic arthritis (classically DIP)
--‐ Nail psoriasis (40--‐50%)
--‐ Metabolic syndrome: DN, hyperlipidaemia, HTN, high BMI, MI.
--‐
Patient counseling: control not cure. Lesions are not contagious.
Chronic plaque psoriasis
Source: DermNet NZ
Chronic plaque psoriasis
Source: DermNet NZ
Chronic plaque psoriasis on the
elbow
Source: DermNet NZ
Palmoplantar pustulosis
Source: DermNet NZ
13. 13
Epidermis lesions
1) Seborrheic
keratosis--‐
--‐ often trunk. After 40 years. Often
multiple. Stuck on cornflake
appearance.
Treatment: leave it alone. Can
remove for cosmetic reasons but
not available on NHS.
Seborrhoiec keratosis
Source: DermNet NZ
Seborrhoiec keratosis
Source: DermNet NZ
Melanocyte lesions
2) Melanocytic naevi akamoles--‐ most common benign skin lesion.
Generally after puberty + early life.
3types:1)junctional (flat pigmented macule) 2)compound (warty pigmented
papule/nodule) 3) Intradermal: skin colored papule
Other types of nevi: blue naevi, halo naevi.
If any doubt about moles it should be excised for histology.
Junctional naevi--‐ flat mole
Source: DermNet NZ
Intradermal naevi--‐ skin
colored papule/nodule
Source: DermNet NZ
Compound naevi--‐ warty--‐
pigmented
papule/nodule
Source: DermNet NZ
Benign skin tumors
14. 14
Hair follicle lesions
3) Epidermoid cyst--‐ central punctum. Can be excised
under LA for cosmetic reasons.
Blood vessel lesions
4) Angioma--‐ aka campbell de morgan spots aka
cherry angioma–acquiredovergrowthofcapillaries.
No tx neededbut can belasered off or cauterized.
5) Pyogenic granuloma – lobular proliferation of
BV.Localized traumaoftenatrigger.Surgical removal
usually by curettage and cautery. Sample must be
submitted for histology as appearance can mimic a
melanocytic and non--‐pigmented melanoma.
6) Telangiectasia – dilated BV of central arteriole and
surrounding capillary network. Increase in pregnancy.
Treat: laser for cosmetic reasons.
7) Capillary hemangioma (strawberry
naevus) – most common benign tumor in infancy.
Nearly all resolve over severalyears.
Epidermoid cyst--‐ note the
characteristic central punctum
Source: DermNet NZ
Cherry angioma (can mimic
nodule melanoma)
Source: DermNet NZ
Pyogenic granuloma
Source: DermNet NZ Telangiectasia
Source: DermNet NZ
Capillary hemangioma
Source: DermNet NZ
15. 15
Fibroblast lesions:
8) Dermatofibroma--‐ firm nodule in dermis.
Most often occur after insect bite. Treatment:
none--‐ needed if diagnosis in doubt can do excision
biopsy. (theskin dimples on pinching thelesion)
9) Keloid--‐ fibrous tissue overgrowth BEYOND the
site of trauma. Treatment: occlusive dressing
with silicone, steroid cream/tape/injection. E.g.
triamcinolone.
10) Hypertrophic scar--‐ fibrous
overgrowth WITHIN the scar boundaries.
Dermatofibroma
Source: DermNet NZ
Pinching of a dermatofibroma causes
skin to dimple
Source: DermNet NZ
Hypertrophic scar--‐
hypertrophy stays within
wound margins
Source: DermNet NZ
Fat lesions
11) Lipomas--‐ v common, slowly growing,
doughy feeling subcutaneous nodules.
Commonly in: shoulder, neck, trunk, arms.
Can be surgically excised under LA.
Sebaceous gland lesions
12) Sebaceous adenoma – benign
overgrowth of sebaceous glands.
13) Sebaceous gland hyperplasia--‐
common in middle age/elderly people--‐ soft yellow,
domed papulesusually on theface.Treatment:none
needed but can be flattened with gentle cautery.
Keloid scar--‐ hypertrophy
extends beyond wound margins
Source: DermNet NZ
Sebaceous gland hyperplasia
Source: DermNet NZ
16. 16
1) BCC(most common type of skin cancer)
Most common skin cancer. Mets is v rare.
Risk factors: UV exposure, sunburn, family history,
immunosuppression.
Presentation/types
Nodular (most common)--‐ pearly nodule with telangiectasia.
On temple, nose.
Superficial (plaque--‐ like)--‐ esp on back + limbs e.g. radiotherapy to spine for
lymphoma can get lesions on back.
Cystic, morphoeic , keratotic, pigmented.
Classical presentation: pearly nodulewith telangiectasia. (but may benecroticor
ulcerated with a pearly rollededge).
Treatment
Surgical (mainstay)--‐ excision margin 4 mm (if tumor ≥2 cm then 6 mm margin)
MoHs – for high risk recurrent tumors.
Radiotherapy when surgery not appropriate e.g. frail, elderly.
Small, low risk lesions – cryotherapy, curettage, cautery, imiquimod cream.
Curettage + cautery/ topical therapy like imiquimod--‐ only in small + superficial
lesions.
High risk tumors: on eye, nose, lips, nasolabial fold, ear, ≥2 cm diameter, ill--‐defined,
immunosuppressed, infiltrative, recurrent/incompletely excised.
Follow up: low risk tumors don’t need to be followed--‐ up. Follow up tailored to
clinical picture.
Nodular BCC
Source: DermNet NZ
Nodular BCC
Source: DermNet NZ
Nodular BCC
Source: DermNet NZ
Skin cancers:
common OSCE
stations
Skin cancers
17. 17
Superficial BCC
Source: DermNet NZ Morphoeic BCC
Source: DermNet NZ
2) Solar keratosis/actinic keratosis (pre--‐cancerous
lesion) – 10% becomeSCC
Risk factors: fair skin, outdoor job, old age.
Presentation:scaly rough patches on aredbackground often on head,tip of
ear, back of hands. Feels like sandpaper.
Treatment: prevention: hats, sunscreen.
Cryotherapy, 5--‐ fluorouracil cream, imiquimod, curettage + cautery and
excision.
Actinic keratosis
Source: DermNet NZ
Actinic keratosis
Source: DermNet NZ
18. 18
3) Bowen’s disease (SCC insitu)
Fixed, non--‐itchy erythematous patch of skin often slightly
scaly on the lower legs of elderly women. Can be
mistaken for patches of eczema/psoriasis.
Treatment: 5--‐ fluorouracil, cryotherapy,
imiquimod.
Actinic keratosis
Source: DermNet NZ
4)Keratoacanthoma
Variant of SCC.
Fleshy basewithkeratinplug. Treatedthesameway asSCCs.
(see below)
Actinic keratosis
Source: DermNet NZ
Common MCQ
question
19. 19
5) SCC(secondmost common typeof skin ca)
Risk factors: UV exposure, pre--‐malignant conditions (e.g. AKs),
immunosuppression, family history, chronic inflammation (e.g. leg ulcers).
Presentation: ill defined nodule, ulceration, keratotic.
Mets uncommon but highest in poorly differentiated tumors esp on high risk sites
e.g. lip, tongue, ear, or if it occurs in areas of chronic ulceration/scarring.
Important topalpate how deepthe lesion is becausemay extenddownwards.
Management
Surgery (mainstay)--‐ 4 mm margin (if tumor ≥2 cm then 6 mm margin)
MOHs--‐ for high risk lesions--‐ large, recurrent/ or where margins may be technically
difficult to achieve or are indistinct.
Radiotherapy--‐ for those not suitable for surgery e.g non--‐resectable tumors.
High risk:perineuralinvasion, >20mm,vertex,ears, backgroundofbowens.
SCC follow--‐up:
Low risk at 3months and discharge if no signs of recurrence.
High risk: follow up for 2 years at 3--‐month intervals
SCC
Source: DermNet NZ
High risk SCC
Source: DermNet NZ
SCC
Source: DermNet NZ
20. 2
0
6)Mycosis fungoides
T cell lymphoma of skin.
Presentation; scaly, erythematous, atrophic
skin +/--‐ depigmentation.
Prognosis: very good. The majority of
patients have normal life expectancy.
Stagedaccording todegreeofskin,LN+
haematological involvement.
Treatment: moisturizer, topical steroids,
phototherapy (lesions very sensitive to
light).
For more extensive disease may need radiotherapy or chemo.
Mycosis fungoides
7) Malignant melanoma Source: DermNet NZ
Riskfactors:UVexposure,peoplewhoeasily burn(skintypeIandII),multiple
moles, family history.Phenotype:think red/blonde hair/freckleswithfair skin.
Presentations: ABCDE (asymmetry, irregular borders, more than 2 colors,
diameters>6mm,quick growth/evolutionoflesion). NEW andCHANGINGarekey
features.
*old moles tend not to become melanomas.
Types
Superficial spreading melanoma--‐ usually lower limbs. [most common type)
Nodular melanoma--‐ usually in trunk. Round, asymmetrical, deeply pigmented,
irregular shape often with inflamed (red) edge.
Lentigo maligna melaenoma – usually face in the elderly.
Acral lentiginous melanoma--‐ nail, palms, soles, often in the elderly
Subungal melanoma: melanoma from nail matrix. Hutchinson’s sign (pigmentation
through nail fold--‐ important sign of subungal melanoma)
Treatment
Surgery(mainstaydefinitivetreatment)
Radiotherapy
Chemotherapy (for metastatic disease).
21. 21
Breslows thickness + ulceration are main prognostic factors. 20% of patients
will relapse. Main pattern of spread: lymphatics [so in follow up clinic feel the
lymph nodes).
Follow up: anything more than stageIais high risk follow up for 5 years.Lowrisk 1
year.
How does melanoma kill? Through spread via BV, lymphatics to vital organs.
Superficial spreading melanoma
Source: DermNet NZ
Acral melanoma
Source: DermNet NZ
Lentigo maligna melanoma
Source: DermNet NZ
Nodular melanoma
Source: DermNet NZ
22. 22
1) Erysipelas/cellulitis
Bacterial infection of the skin
Erysipelas--‐ superficial form of cellulitis (dermis and upper sc)
Cellulitis--‐ dermis and sc infection.
Symptoms:
Cellulitis--‐ often lower limbs, swelling erythema, warmth. Systemically
unwell: fever, malaise. Lymphangitis (seen as red streaky marks)
Erysipelas--‐ often on face well--‐defined, red border (cellulitis is less well
defined).
Treatment: Antibiotics e.g. flucloxacillin.
Skin infections
Cellulitis of the left
leg
Sou rce: Waikato district
health board, DermNet NZ
Erysipelas of the face
Sou rce: D@nderm
23. 23
2) Staphylococcalscaldedskinsyndrome
Blistering condition caused by exotoxins from certain strains of Staph Aureus. Often in
children.
Presentation: scald--‐like appearance, bullae, perioral crusting. V painful.
Treatment: Antibiotics (e.g. flucloxacillin), analgesia
Severe SSS
Source: DermNet NZ
3) Fungal skin infections
3 main groups: 1) Dermatophytes (tinea/ringworm), years (e.g. malassezia fur
fur, candidiasis), 3) moulds (e.g.aspergillosis)
Tinea: exactly what it is called depends on location of infection.
Tinea corporis (trunk/limbs)--‐ annular sessions, itchy, scaly edges.
Tinea cruris (groin/natal cleft) – similar to tinea corporis
Tinea pedis (feet aka atheletes foot)--‐ scaling and dryness of palms.
Tinea manuum (hand)--‐ scaling and dry palmar creases.
Tinea unguium (nail)--‐ yellow crumbly, thick nails
Tinea capitis (scalp)--‐ patches of baldness, scales.
Tinea incognito (when tinea infections are incorrectly treated with corticosteroids)--‐
ill defined (not as scaly as the above lesions).
Very severe SSS
Source: Dr. Raimo
Suhone n. DermNet NZ
25. 25
Candidiasis – white plaques on mucous membranes,
erythema with satellite lesions esp in nappy area.
Pityriasis versicolor – infection with malassezia
furfur--‐ pale brown patches usually on upper back that
fail to tan.
Diagnosis
Samplese.g.hair, skinscrapings, nail clippings for tinea
and swabs for yeasts likecandidiasis
Treatment
Ifsmallskinlesion: topical antifungal e.g.terbinafine
cream
Widespread lesions or nail infections e.g. oral
itraconazole., oral terbinafine
NO CORTICOSTEROIDS--‐ can cause tinea incognito.
4)Impetigo
Pityriasis versicolor
Source: DermNet NZ
Pityriasis versicolor
Source: DermNet NZ
Golden crust usually around mouth in children. Takeswabfor
culture.
Tx:localized:mupirocin topical therapy.Widespread:oral
flucloxacillin
5) Folliculitis--‐ pustule centered hair follicles usually beard,
groin, mustache.95%staph.aureus.Tx:oralflucloxacillin.
6) Viral warts--‐ HPV 6,11 – genital warts. HPV 16,18 – cervical
cancer.
Folliculitis
Source: DermNet NZ
Viral wart
Source: DermNet NZ
26. 26
7) Pityriasis rosea--‐ rash thought to be related to HHV 6/7. Starts as a herald
patch and then get red/pink patches all over body in a characteristic
‘Christmas tree; distribution). URTI symptoms preceded 70% of the time.
Treatment: none needed self--‐limiting.
Pityriasis rosea--‐ herald patch
Source: DermNet NZ
Pityriasis rosea
Source: DermNet NZ
27. 27
What causes blisters? Trauma, infection, drugs, autoantibodies + genetic diseases.
1) Bullous pemphigoid
Blistering condition caused by antibodies against type 17 collagen.
Presentation: tense blisters. Often lesions are itchy. Mucosal involvement less
common.
Treatment:
General:wounddressing, septicprecautions
localized disease: topical steroids
Widespread disease--‐ oral steroids, immunosuppressive agents e.g. azathioprine,
mycophenolate mofetil, methotrexate.
Bullous pemphigoid
Source: DermNet NZ
Bullous pemphigoid
Source: DermNet NZ
Blistering skin disorders
29. Always whatever the emergency:
1) A--‐E assessment
2) Withdrawal ofcause
3) Manage complications e.g. infection,
fluid loss, hypothermia
4) Consider any specifictreatments
1) Urticaria,angioedema,anaphylaxis
Uriticaria/Anphylaxis--‐ oedema from leaky capillaries in layers
of skin (urticarial) and mucosa (angioedema)
Anaphylaxis--‐ life threatening systemic hypersentivity reaction
Symptoms
Uritcaria--‐ itchy wheals
Angioedema--‐ swelling of lips, tongue, larynx (larynx swelling
manifests as stridor, hoarseness, respiratory distress)
Anaphylaxis--‐ bronchospasm, hypotension, stridor, facial
oedema.
Common causes: food e.g. nuts, shellfish, drugs e.g NSAIDs,
ACEi,, contrast, idiopathic, autoimmune, hereditary.
Treatment:
Urticaria: antihistamine
Angioedema: antihistamine, if severe e.g. noisy breathing,
difficulty talking, hypotension--‐ treat as anaphylaxis
Anaphylaxis:IMAdrenaline (0.5 mg,0.5mlof1:1000),oxygen,
steroids(200mgIVhydrocortisone),antihistamine e.g.10mg
IV chlorphenamine + admit for observation for 6--‐12 hrs.
Know the doses for
anaphylaxis--‐ 5th year
MCQ/OSCES
Angioedema2
o9
f the hands
Sou rce: DermNet NZ
Urticaria
Source: DermNet NZ
Angioedema of the lips
Sou rce: DermNet NZ
Angioedema of the face
Sou rce: DermNet NZ
Dermatological emergencies
30. 30
2) Erythema multiforme (EM), Stevens--‐Johnson
syndrome (SJS), Toxic epidermal necrolysis (TENS)
Hypersensitivity reactions causing death and detachment of epidermis
Symptoms
EM--‐ typically target lesions
Cause often unknown, HSV main known cause. Mucosal involvement absent/limited
to one mucosal surface.
SJS and TENS is a continuum of each other--‐ both involves mucocutanous necrosis.
The main difference is the TBSA involved.
SJS <10% TBSA
Maincauses:drugsandinfection.
10--‐30% TBSA –SJS/TENS overlap
TENS > 30% TBSA
Main causes: drugs e.g.
Sulfonamides: co--‐trimoxazole,
beta--‐lactam: penicillin, cephalosporins,
anticonvulsants: lamotrigine, carbamazepine, phenytoin, phenobarbitone,
allopurinol, paracetamol, nevirapine, NSAIDS
Treatment:
EM: most need no treatment--‐ self--‐limiting. Consider e.g. aciclovir for herpes labialis
SJS/TENS: Removecausee.g.stopdrug.Supportivetreatment e.g.skincarethe
sameasburns,fluidbalance, analgesia, treatment secondary infection,temperature
control. ITU for TENS.
Predictive mortality scale: SCORETEN
33. 33
4)Erythroderma
Exfoliative dermatitis involving > 90% of skin
Symptoms: whole skin, red, hot, flaky, patients are systemically unwell: malaise,
lymphadenopathy.
Causes: psoriasis, eczema, drug (penicillin, sulphonylurea, allopurinol),
malignancies (lymphoma)
Treatment: Removal of cause e.g. stop drug, supportive treatment; bed rest,
emollients (50/50),wetwraps,fluidresuscitation,temperature control,treatment
secondary infection.
Erythroderma
Source: D@nderm
Erythroderma
Source: D@nderm
Erythroderma
Source: D@nderm
34. 34
5)Eczema herpeticum
Infection of an eczematous area with HSV.
Symptoms: extensive crusted blisters, erosions.
Treatment:aciclovir andantibiotic cover e.g.flucloxacillin +withhold steroidsin
eczematous areas.
Less severe eczema herpeticum on the
flexural aspects of the wrists and hands
Source: D@nderm
Severe eczema herpeticum
on theface
Source: D@nderm
Severe eczema
herpeticum on the face
Source: D@nderm
Very severe eczema herpeticum on
the face
Source: D@nderm
Very severe eczema herpeticum on
the face
Source: D@nderm
35. 35
6) Necrotisingfasciitis
Surgical emergency! Infection of deep fascia usually polymicrobial in
diabetes/immunosuppressed patients but in healthy people usually Strep pyogenes
(Group A strep).
Symptoms:severepainoutofproportion ofclinical appearance,blisters,necrotic
skin, systemically unwell (tachycardia,fever).
Treatment: IV antibiotics, urgent surgical debridement
Necrotising fasciitis –
dusky, cyanotic and
gangrenous
Source: DermNet NZ
Necrotising fasciitis –
necrotic
Source: DermNet NZ
Necrotising fasciitis – a
rapidly destructive infection
Source: DermNet NZ
36. Diabetes mellitus:
Skin manifestation: candidiasis, granuloma annulare (self--‐
limiting, topical/oral steroid, steroid injections), necrobiosis
lipoidica (PUVA), diabetic shin spots and gangrene.
Drug photosensitivity--‐ severe erythema of sun exposed
area--‐ drug induced photosensitivity e.g. doxycycline,
amiodarone,
Hypercholesterolemia: xanthomata (cholesterol deposit
anywhere in the body)
Endocrine:
Addison’s disease--‐ generalized hyperpigmentation.
Haemochromatosis--‐ hyperpigmentation of skin. (bronze
skin)
Thyroid--‐ pre--‐tibial myxoedema.
Erythema nodosum: sarcoidosis, IBD, TB, pregnancy (self--‐
limiting, tx cause)
Systemic sclerosis: sclerodactyly, microstomia,
telangiectasia.
Sub--‐acute endocarditis: splinter
haemorrhage.
Heliotrope sign--‐ purple violaceous
erythema around eyes: dermatomyostiis.
(in dermatomysositis--‐ hunt for malignancy
in elderly people there is usually an
underlying malignancy--‐ esp breast, lung,
ovarian,gastriccancer)Tx:corticosteroids,
azathioprine, methotrexate
Necrobiosis Lipoidica
Source: DermNet NZ
Granuloma annulare
Source: DermNet NZ
Pyoderma gangrenosum
(IBD/rheumatoid arthritis). Acutely
inflamed +ulceratedskin,dusky,blue
edge to lesion. Despite looking
purulent it is sterile. Treatment:
topical/systemic steroids
Pyoderma gangrenosum
Source: DermNet NZ
Heliotrope rash
Source: DermNet NZ
Erythema nodosum
Source: DermNet NZ
36
Skin signs insystemic disease
37. 37
Too much hair: PCOS, idiopathic, ovarian tumor, adrenal
tumor, congenital adrenal hyperplasia, obesity
Too little hair:
1) Telogen effluvium--‐ scalp condition characterized
by early entry of hair in the telogen phase
(resting/shedding phase) e.g. eating disorder,
childbirth, chronic illness and major surgery.
2) Anagen effluvium--‐ scalp condition where you get
hair falling out in itsgrowthphase/pathologic loss
of anagen or growthphase hair e.g. radiotherapy,
chemotherapy.
3) Alopecia areata--‐ autoimmune condition where you
get discrete areas of scalp hair loss.
4) Alopecia universalis--‐ hair loss of all hair including
eyebrow,pubic hair, eyelashand scalp hair.
5) Alopecia with fungal infections e.g. tinea capitis--‐
can potentially cause scarring
Anagen effluvium
Source: DermNet NZ
Hair
38. 38
1) Delusionalparasitosis
Patient has fixeddelusions that thereareinsects,mites,bacteriain their skin
despite evidence to suggest otherwise.
‘Matchbox’ sign--‐ patients will bring things which they believe to be the parasite,
bacteria to doctors e.g. in matchboxes, on celotape, bring bits of hair, fluff, carpet.
Differentials ofdelusional parasitosis:organic disease (e.g.dementia,alcohol, drugs,
thyroid,trueinfestation), psychiatriccondition e.g.hypochondria, schizophrenia,
paranoia.
Examination, appropriate blood tests (e.g FBC,
U&E, LFT, TFT, B12, folate,), skin sample
(whatever the patient brings) and very rarely
skin biopsy.
Management: joint consultation with
dermatologist and psychiatrist.May usenew
atypical antipsychotic e.g. risperidone,
olanzapine, quetiapine.
Manage co--‐morbidities: e.g. depression with
SSRI
Manage skin e.g. emollients, antibiotics for
secondary infection.
2) Folie--‐a--‐deux
Excoriations due to delusional parasitosis
Source: DermNet NZ
--‐ when theindex casethinks they havetheparasite family membersthink they
have it too.
--‐ Treatment for index caseisantipsychotics but family just treat their skine.g.
moisturizers, abx for secondary infection.
Skinandthemind
39. 39
References:
Backgroundinfo
Dermatology: A handbook for medical students & junior doctors
Dr. Nicole Chiang
Professor Julian Verbov
Dermatology e--‐learning modules
University of Birmingham
Illustrations
DermNet NZ
https://www.dermnetnz.org/
D@nderm
http://www.danderm--‐ pdv.is.kkh.dk/atlas/index.htmll