Clinical Dermatology PDF 4th Edition

# Clinical Dermatology ## 4th Edition ### Tailored for Medical Students, USMLE, PLAB, PA & Nursing ### Procedural Dermatology **Local Anaesthetic** - **Mechanism of Action:** - Use-Dependent blockade of Voltage-Gated Sodium Channels on Nerves - Prevents Action Potential Conduction along...

# Clinical Dermatology ## 4th Edition ### Tailored for Medical Students, USMLE, PLAB, PA & Nursing ### Procedural Dermatology **Local Anaesthetic** - **Mechanism of Action:** - Use-Dependent blockade of Voltage-Gated Sodium Channels on Nerves - Prevents Action Potential Conduction along Sensory Nerves - Very Quick Onset of Action - Also causes vasodilation -> Short Duration of Action (If without adrenaline) - **Lignocaine - Most Common:** - Rapid Onset (1-5mins) - Medium (30-120mins) - Max Dose: 4mg/kg - ≈ 50mL @ 1% Lignocaine - (Note: 1% Lignocaine = 1g/1000mL) - **+ Adrenaline:** - Improves Haemostasis - Bleeding - Systemic Absorption - Risk of systemic toxicity - Prolonged Effect - Max Dose: 7mg/kg (Higher Dose than without adrenaline) - Note: DO NOT USE IN DIGITS OR PENIS (or anywhere else with "End Arteries") - Note: DO NOT USE in LONG QT-Syndrome - **Naropin (Ropivicaine):** - Longer onset of action - Longer acting than lignocaine - Max Dose: 2-3mg/kg - **Topical Anaesthetic:** - Xylocaine Gel - Useful for Mucosal Surfaces (Eg: Oral Mucosa) - ELMA Cream - Useful for topical anaesthesia of skin - **Nerve Blocks:** - Digital Block (Ring Block) - Most Common - Blocks Digital Nerves - Use 2% Lignocaine (Because you want to inject as little as possible) - Wrist Blocks - Blocks Radial, Median, & Ulnar Nerves - Totally anaesthetizes the hand **Curettage & Electrocautery:** - **Indications:** - Warts - Keratoses - Molluscum contagiosum - Curettes can also be used for curette biopsy - **Wound Healing** - The curette wound can take some time to heal - If it is just a light curette such as tiny seborrheic keratoses with no cautery they can heal in a few days - A full curettage and electrodessication on the trunk might take 4 to 6 weeks to heal **Cryotherapy** - Cryotherapy is a very useful form of treatment for a number of benign skin lesions and few pre-malignant and malignant skin lesions - Liquid Nitrogen = The gold standard - **Indications:** - **Benign lesions:** - Molluscum contagiosum - Seborrheic keratosis - Skin tags - Warts - **Premalignant lesions:** - Actinic keratoses - Actinic Chelitis - **Malignant lesions:** - Superficial BCC - **Effects of Cryotherapy - 3 Main Groups:** 1. **Those responses we expect to happen:** - Pain on treatment and for a period afterwards - Oedema and swelling of the treated site and the surrounding tissue (Eg: periorbital swelling after treatment of lesions on the forehead) - Vesicle and bulla formation - Exudation weeping and crust formation 2. **Temporary Adverse Outcomes:** - Hypopigmentation - Hyperpigmentation - Secondary Infection 3. **Permanent Adverse Outcomes:** - Permanent Hypopigmentation - Scarring + Possible Retraction - Allopecia - Nail Dystrophy **Biopsy Techniques** - Many different Techniques - Technique depends on the Nature of the Lesion & Information Required - **Types:** - **Punch biopsy** - Leaves Minimal Scarring - Best for Cosmetically Sensitive Areas - (Eg: Face) - **Shave Biopsy** - Fast and easy to perform - Requires little equipment - A shave biopsy is excellent for nodular bulky lesions which are easy to shave off for histology - **Curette biopsy** - Fast and easy to perform - Requires little equipment - A shave biopsy is excellent for nodular bulky lesions which are easy to shave off for histology - **Incision Biopsy** - A biopsy set is required with scalpel, forceps, needle holders and fine scissors as well as a suture to perform a small incisional ellipse. Be sure to go through the dermis to get a full thickness specimen - Advantages: - Provides the best specimen for the pathologist to assess the tissue adequately - **Excision biopsy** - Similar to an incisional biopsy but the whole lesion is excised - Good pathology specimen **Wound Design** - Wounds should be designed so that scars sit in or parallel with the relaxed skin tension lines or the cosmetic junction lines - Excision margins are important to ensure complete removal of the lesion. For benign lesions the margins are usually 2mm to 5 mm. For malignant lesions the margins can vary from 3mm up to 2 cm depending on the nature of the pathology **Surgical Wound Repair** - **Suture Materials:** - **Synthetic Non-Absorbable:** - Nylon - Polypropylene - (Used on external surfaces where they are easily removed) - **Synthetic Absorbable:** - Monocryl - Vicryl (Polylactin) - (Broken down by the body via Hydrolysis &/or Proteolytic Enzymatic Degradation) - **Non-Synthetic Non-Absorbable:** - Silk - **Non-Synthetic Absorbable:** - Catgut (Being Phased out) - **Suture Sizes:** - Scale from 1-6 (1 = Thinnest (0.4mm); 2 = Thickest (0.8mm) - **Surgical Wound Repair:** - **Primary Repair:** - 6-8hrs - **Delayed Primary Repair** - In 72hrs - In surgical conditions - **Secondary Repair:** - After 72hrs - In surgical conditions - **Important Pre-Requisites:** - Wound needs to be CLEAN! - Eliminate Dead Tissue/Dead Space/Haematoma/Foreign Bodies - Finest Suture Material - Minimise Tension - Suture Removal @ Appropriate time for site of injury - 1-2 wks **Skin Grafts Vs Skin Flaps** - **Skin Grafts:** - Has been totally dethatched from its original location - Has NO intrinsic Blood Supply - Must be grafted onto Vascularised Tissue - It will initially survive via Simple Diffusion of Nutrients - Eventually, Neovascularisation -> New Blood Supply - **Types:** - **Full Thickness Graft (FTG)** - All of the Dermis & Epidermis - **Split Skin Graft (SSG)** - All of the Epidermis & some of the Superficial Dermis - **Skin Flaps:** - Has NOT been detached from its original location - Still Has Intrinsic Blood Supply - **Indications:** - Poor Vascularity of Location (Eg: Bare bone, Bare tendons) - Vital Structures (Eg: Exposed Vessels/joints) - Cosmetics (Eg: Face) - Usually gives a better result than a skin graft - **3 Basic Types:** - Rotation - Advancement - Transposition - **"Free" Flaps:** - Basically a Skin Graft, but the Blood Supply is Reconstituted using Microsurgery to reconnect the Artery and Vein ### Dermatitis (Eczema) #### Acute Dermatitis/Eczema: - **Types of Acute Eczema:** - Contact Dermatitis (Due to prolonged exposure to allergen) - Atopic Dermatitis - (Drug eczema) - (Photoeczema) - (Primary irritant dermatitis) - **Aetiology:** - Prolonged Contact with Allergen - Urine, Soaps, Antiseptics, Deodorants, Creams, Foreign Body, etc - Type IV Hypersensitivity (T-Cell Mediated) to Allergen - **Epidemiology:** - Family history - (in 70% of cases) - Most Common in Children - Genetics (50% of pts have a deficiency of the Epidermal Protein "Filaggrin") - Hypersensitivity - (Associated with other Atopies (Hay Fever [Allergic Rhinitis), and Asthma)) - **Pathogenesis:** - **Initial Exposure:** - Ag Processed by Langerhans Cells -> Presented to T-Cells in LN -> T-Cell Activation - **Re-Exposure:** - Type IV Hypersensitivity (T-Cell Mediated) reaction to Allergen - Epidermal Oedema + Small Blisters -> "Wet Eczema" - **Chronic Exposure:** - Hyperplasia, hyperkeratosis (lichenification) - "Dry Eczema" - **Morphology:** - **Gross:** - Erythema - Small Blisters - (Weeping & Crusting Blisters, Papules and Plaques) - Hyperkeratosis (If Chronic) - **Microscopic:** - Epidermal Blistering - Intra-Epidermal Oedema (Spongiosis) - Perivascular Inflammatory Infiltrate - **Clinical Features:** - Severe Itching - Patchy, Erythematous, Poorly Defined Rash - Usually in the Popliteal/Cubital Fossae & Face - Can be Generalised - **Dry Skin** - Excoriation (loss of the surface of the skin from scratching) due to itching and scratching - Lichenification (thickening of the skin with accentuated skin lines) - Crusting (scabbing) and weeping (loss of fluid through the surface of the skin) due to bacterial infection - (Contact dermatitis often has a regular shape (Eg: Square from Band-Aid)) - **Treatment:** - Modification of lifestyle to avoid exacerbating factors - Remove Allergen - Avoid Soaps - Use of moisturisers and bath additives - Treated with topical Corticosteroids (Symptomatic) - Antihistamines (For Itch) #### Atopic Dermatitis: Pathogenesis and clinical findings | Category | Description | |---|---| | Impaired Epidermal Barrier | (e.g. fillagrin and SPINK5 gene mutations)| | Increased trans-epidermal water loss | Exacerbation by long hot showers, sweating, stress | | Xerosis | Note: It is not yet fully understood if Atopic Dermatitis (AD) is initiated by skin barrier dysfunction ("outside-in" hypothesis), or immune dysregulation ("inside-out" hypothesis) | | Innate Immune System Defects | Defects in cell-mediated epidermal barrier repair process result in inflammation and leaky junctions between cells | | Impaired Epidermal Barrier | Disruption of stratum corneum allows penetration of irritants, microbes & antigens. Exacerbation by irritants and allergens: detergents, solvents, hard water, clothing, environmental aero-allergens (e.g. dust mites) | | Stimulation of cutaneous itch receptors | Pruritis | | Skin Infection | ↑ susceptibility to pathogenic cutaneous infections | | Adaptive Immune System Defects | Overexpression of Type 2 helper (Th2) cytokines and IgE in response to antigens. AD is commonly seen in people with a family history of atopic disease eg. allergic rhinitis, food allergy, asthma | | Altered Skin Microbiome | Skin colonization e.g. S. aureus may be an AD trigger (via toxin release) or a consequence | | Immune Dysregulation: Acute | Keratinocyte release of cytokine mediators - ↑Th2 & ↑ IgE | | Intracellular edema within epidermal layer, resulting in intraepidermal vesicles | Spongiosis | | ↑ IgE | | | Immune Dysregulation: Chronic | Chronic disease punctuated by acute flares with slow resolution. Hyperplasia of keratinocytes within stratum corneum (uppermost layer), resulting in excessive accumulation of fibrous protein keratin. | | Hyperkeratosis | Scale | | Acute: Inflammation of dermis | Acute AD | | Chronic: Hyperplasia of subcorneal epidermis (second layer) causes skin thickening and accentuated skin markings | Chronic AD | | Disruption of vesicles from scratching | Severe Pruritis | | Erythema | | | Lichenification | Plaques | | Spongiosis | | | Oozing | | | Crusting | | | Dry Scale | | | Dermal-Epidermal Junction | | | Dermal layer | | | Lichenification | Severe Pruritis | | Hyperkeratosis | | - **Distribution:** - Infants (<6 months): face, scalp, extensor surface of elbow. Primarily vesiculopapules. - Children (> 18 months - puberty): neck, extensor surface of elbows and knees. Primarily juicy papules. - Adults (beyond puberty): Forehead, neck, hands, feet. Primarily thick, dry, lichenified plaques. - **Legend:** - Pathophysiology - Mechanism - Sign/Symptom/Lab Finding - Complications **** ## Seborrheic Dermatitis - **Aetiology:** - Some heredity - Some association with commensal Malassezia yeast (fatty acid metabolites may cause inflammatory reaction) - **Risk Factors:** - Oily skin - Familial history of dermatitis/psoriasis - Immunosuppression - Parkinson's disease - Sleep deprivation/stress - **Epidemiology:** - Bimodal onset; Infancy (within the first months), or between 20-50yrs old - Most common in males - **Pathophysiology:** - Not completely known - **Clinical Features:** - Chronic/relapsing eczema (improves in summer; flares in winter) - Primarily affects sebaceous-rich regions (Scalp/face/trunk) - Ill-defined, localised scaly patches/scale - Blepharitis (scaly red eyelid margins) - Salmon-pink thin scaly and ill-defined plaques in skin folds - **Infantile Seborrheic Dermatitis:** - Numerous Dermatoses in the 1st 3 Months of Life - Erythematous but Non-Itchy Rash involving the face, scalp, neck, axillae and nappy area. The lesions are well defined and covered in greasy scale - **Adult Seborrheic Dermatitis:** - Erythema and fine, greasy scale on the cheeks, nose and nasolabial folds - Scale and itching of the scalp and eyebrows - Well defined but non-scaly erythema of the axillae, groin, scrotum and perianal skin - **Management:** - Keratolytics (Eg: Salicylic Acid) - Topical antifungals (Eg: Ketoconazole) - Mild topical steroids - (Isotretinoin for moderate/severe seborrheic dermatitis) **** ## Stasis Dermatitis (Venous Eczema) - **Aetiology:** - Venous insufficiency + Gravity - **Epidemiology:** - Middle-older-aged patients - 20% of over 70yr olds - **Risk factors:** - History of DVT in affected limb - Varicose veins - Venous leg ulcers - **Pathophysiology:** - Venous insufficiency → Failure of calf pump mechanism - → blood pools in leg veins → increased venous hydrostatic pressure → oedema - Fluid collecting in tissues → Activation of innate immune response - **Clinical Features:** - May form discrete patches or become confluent/circumferential - Itchy red, blistered & crusted plaques - On one or both lower legs - Orange-brown macular pigmentation due to Haemosiderin deposition - Champagne bottle shape of lower leg - **Management:** - **Reduce Dependent Oedema:** - Elevate feet when sitting - Walk regularly - Elevate feet above bed level overnight - Graduated compressing stockings long-term - **Treat Eczema:** - Dry up oozing patches with potassium permanganate or dilute vinegar on gauze compress - Oral antibiotics to avoid secondary infection - Topical steroid - Moisturising cream - Avoid injury to skin - **Treat Varicose Veins:** - Consult vascular surgeon - Sclerotherapy/laser **** ## Lichen Simplex Chronicus - **Aetiology:** - Repetitive scratching and rubbing, which arises because of chronic localised itch. The primary itch can be due to: - Atopic Eczema - Contact eczema - Venous eczema - Psoriasis - Lichen planus - Fungal infection - **Epidemiology:** - Males and females - Unusual in children - Association with anxiety/OCD - **Pathophysiology:** - Repetitive scratching/rubbing -> hyperkeratosis & inflammation - **Clinical Features:** - Chronic, lichenified eczema/dermatitis - May be single or multiple plaques - Dry/scaly surface - Leathery induration - Scratch marks - **Management:** - Potent topical steroids 4-6wks until plaque is resolved - Coal tar preparations - Moisturisers - Antihistamines for itch - Antidepressant for psychosomatic aetiologies **** ## Erythema Multiforme: - **Aetiology:** - Hypersensitivity reaction - Some genetic tissue-type associations (HLA-B15, -B35, A33, -DR53, -DQB1*0301) - **Pathogenesis:** - Hypersensitivity Response to: - Infections (Herpes simplex, Mycoplasma) * Most common - Drugs (Sulphonamides, penicillin, barbiturates) - Malignancy (Carcinoma, lymphoma) - Auto-Immune (Eg: Lupus, SS, Dermatomyositis) - **Morphology:** - **Gross:** - Variable Lesions: Papules/Plaques/Nodules/Blisters/Ulcers - Characteristic "Targetoid" Lesions - Central Grey Necrosis - Erythematous raised border - **Microscopic:** - Dyskeratosis - Necrotic Keratinocytes - Spongiosis (Epidermal Oedema) - Epidermal Lymphocytes - Destruction of Basal Epidermal Layer - **Clinical Features:** - Acute & Self-limiting - Commonly affects young adults (20-40yrs) The document includes a detailed description of various types of dermatitis (eczema), along with their etiologies, pathogenesis, clinical features, and management strategies. Additionally, it provides information about skin grafts, flaps, and related procedures. The text is complemented by illustrative images depicting the different conditions, facilitating comprehension of the content.