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Dermatology 101 images to ruin your afternoon :) Tutorial by Devangi Vyas (with credit to Haider Nazerali + Marianne Gazet) dv122@ic.ac.ukTILOS COVERED I. Summarise: normal human anatomy and physiology (at all stages of life) and the pathology, pathophysiology and population health burden of key diseases and disorders II. Skin disorders: Skin disorders: Describe how extracutaneous diseases, multisystemic disorders and drug hypersensitivities manifest in the skinLECTURE TIMELINE 1. General Derm 2. Skin InSystemic 3. Infections + 4. SkinCancer + Terminology Disease InfestationsOf Skin ManagementLECTURE TIMELINE 1. General Derm 2. Skin InSystemic 3. Infections + 4. SkinCancer + Terminology Disease InfestationsOf Skin ManagementEtymology Prefixes Suffixes Aden/o- Necr/o- -blastic -phasia Angi/o- Neur/o- -cytic -plastic Cardi/o- Nephr/o- -dynia -trophy Cephal/o- Ophthalm/o- -ectasis -centesis Col/o- Ren/o- -emia -ectomy Crani/o- Phleb/o- -iasis -graphy Facii/o- Pleur/o- -ism -opsy Haem/o- Pneum/o- -itis -ostomy Hepat/o- Rhin/o- -lysis -otomy Ile/o- Thromb/o- -malacia -osis Litho- Uro- -megaly -plasty -oma -scopy Mening/o- Sclero- My/o- -pathy -penia Myel/o-How to describe a lesion? Flat, doesn't involve any change in the thickness or texture of the skin Fluid-filled sac or lesion, fluid trapped under a thin layer of skin Solid elevation of skin with no visible fluid Flat but raised Nodule but filled with pusExamples: Pustule Macule Patch Plaque Papule Nodule WhealDescribing Rashes What is a rash? A widespread eruption of lesions What is a maculopapular rash? Flat discoloured skin lesions + small raised bumpsPurpura Petechiae Macular Purpura Ecchymoses PapularLECTURE TIMELINE 1. General Derm 2. Skin InSystemic 3. Infections + 4. SkinCancer + Terminology Disease InfestationsOf Skin ManagementSkin in Systemic Diseases Rest of body Skin Skin targeted by multisystemic disorders Skin conditions suggestive of underlying condition Skin signs of systemic disorders Systemic disease secondary to skin disorderSkin in Systemic Diseases Rest of body Skin Skin targeted by multisystemic disorders Skin conditions suggestive of underlying condition Skin signs of systemic disorders Systemic disease secondary to skin disorderPunch Biopsy • Biopsy of skin done under local anaesthetic. • Cells taken + examined for inflammatory patterns/cell abnormalities to look for neoplasia. • Can also look for autoAB via immunofluorescence + can be sent for tissue culture.Skin Targeted by Multisystem Disorders Lupus Erythematosus Dermatomyositis Vasculitis Sarcoidosis Graft vs Host Disease DRESS Pruritus Carcinoid Syndrome ErythrodermaLUPUS ERYTHEMATOSUS 2 main groups: Systemic Lupus Erythematosus (SLE) + Cutaneous MAIN Investigations : (discoid) Lupus Erythematosus. • ANA anti nuclear antibodies • Anti-dsDNA SLE: • Anti-Sm - Autoimmune disease • Antiphospholipid - Body's immune system mistakely attacks healthy tissue • Complement level (low!) - Affects skin, joints, kidneys, brain + other organs • Direct Coomb’s test 3 types of Diagnostic Criteria: - Mucocutaneous: alopecia, oral ulcers, cutaneous lupus - Haematological: haemolytic anaemia, thrombocytopenia, leukopenia - ImmunologicalLUPUS ERYTHEMATOSUS Systemic Lupus Erythematosus Livedo Cutaneous (Discoid) Lupus Erythematosus reticularis Neonatal Lupus Chilblains Subacute cutaneous lupus Palpable purpura Discoid lupus Photodistributed (sun- erythematous rash Neonatal lupusDERMATOMYOSITIS Long term autoimmune inflammatory disorder which affects skin + muscles. Symptoms: skin rash + worsening muscle weakness over time - 'photo-distributed pink-violet rash favouring scalp, periocular regional + extensor surfaces' - 'proximal extensor inflammatory myopathy'. • ANA – screen test • CK high Bloods • LFTS – ALT often high Subtypes w clinical features can be • Skin biopsy predicted by Specific• EMG - electrmyography autoantibody profile : Tests • Anti-p155 • Screen for internal malignancy • Anti-MDA5 OtherDERMATOMYOSITIS Photo-distributed; pink-violet rash; extensor surfaces + periocular Ragged cuticles Digital ulcers Photosensitive erythema Gottron’s papules Heliotrope rash Shawl sign V-signVASCULITIS • Inflammation of the blood vessels (small, medium or large) -> tissue damage. • Cause unknown??? • Minor (only affects skin) vs Major (heart/kidneys affected) x IgA vasculitis (Henoch-Schönlein purpura): • Can get biopsy for direct immunofluorescence to detect IgA • PALP – Purpura, Arthritis/arthralgia, Lethargy+/- GI symptoms and Proteinuria • May later develop glomerulonephritis so keep checking urine!!VASCULITIS Subcutaneous nodules Digital necrosis along blood vessels Henoch-Schönlein purpura Purpura Retiform purpura Ulcers SARCOIDOSIS Rare condition that causes small patches of red + swollen tissue (granulomas) to develop in organs. • "Systemic Granulomatous disorder of unknown origin" • Usually affects LUNGS and SKIN (symptoms depend on organ) • Diagnosis of exclusion + evaluate for internal organ involvement Cutaneous manifestations (33%) 'The great mimicker' - very variable Granuloma: organised aggregation of activated macrophages that forms Histology: non caseating epithelioid granulomas in response to chronic inflammation.SARCOIDOSIS SCAR SARCOID ERYTHEMA NODOSUM LUPUS PERNIO GRAFT VS HOST DISEASE • Multi-organ disease • Affects 10-80% of allogenic haematopoietic stem cell transplants (HSCT) • Pathogenesis: donor T cells attack antigens in recipient (who's immunocompromised) How can you if a rash is caused • Mainly affects: skin, liver, GI tract by a drug or GvHD? • 2 major forms = acute + chronic Face or acral involvement Diall indicate GvHD more likelyEmergency Reactions Presenting with Skin Signs Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) Stevens-Johnson Syndrome/ T oxic Epidermal Necrolysis ErythrodermaDRESS Drug Reaction w Eosinophilia + Systemic Symptoms • Widespread serious systemic reaction with cutaneous, haematological Treatment: and solid‐organ disturbances. Withdrawal of culprit medication Corticosteroids are first line - may • Underlying mechanism not known. Mortality 5-10% require months of treatment !! • Starts 2-6 weeks after drug exposure Features: • Skin manifestations: • Fever ≥ 38.5°C • Rash • Face, upper trunk and extremities are initial sites of involvement • Characteristic rash e.g. facial oedema • Lymphadenopathy • Widespread rash >50% BSA • Peripheral eosinophilia >0.7 × 109 Internal Organ Involvement: Triggers: DRUGS (duh its in the name) !!!! • Liver= hepatitis, most frequent cause of death • Ibuprofen • Kidneys (interstitial nephritis) • Sulphonamides • Heart (myocarditis) • Anti-epileptics (carbamazepine, phenytoin, • Brain lamotrigine) • Thyroid (thyroiditis) • ABx (vancomycin, amoxicillin, minocycline, • Lungs (interstitial pneumonitis) piperacillin-tazobactam)SJS/TEN Derm Emergency (rare) !!! Overall mortality 30% :( Drugs cause >805 of cases + can be started up to 3w prior to rash onset. Symptoms: • Prodromal: flu-like symp • Abrupt onset of lesions on trunk > face/limbs • Macules, blisters, erythema – atypical targetoid • Blisters merge – sheets of skin detachment • Extensive full thickness mucocutaneous necrosis <2-3 days Complications eroded GI tract, interstitial pneumonitis, neutropenia, liver and heart failureSTEVENS-JOHNSON SYNDROME/ TOXIC EPIDERMAL NECROLYSIS ERYTHRODERMA Generalised erythema affected >90% BSA • Impaired in skin function + consequences: – Peripheral edema – Tachycardia – Loss of fluid and proteins – Disturbances in thermoregulation – Risk of sepsis Management: – Underlying cause – Hospitalisation if systemically unwell – ABC: restore fluid/electrolyte balance, circulatory status + manage body temperature – Emollients to support skin barrier – +/- topical steroids +/- antibioticsEmergency Reactions Presenting with Skin Signs •Drug Reaction with Eosinophilia and Cutaneous, haematological and solid‐organ Systemic Symptoms (DRESS) disturbances: fever rash (>50% BSA) lymph nodes facial oedema SJS is <10% TEN >30% BSA: full •Stevens-Johnson Syndrome / T oxic Epidermal Necrolysis thickness skin detachment (skin falls of like wall paper) Generalised erythema (red skin) >90% •Erythroderma Mixed cause: eczema psoriasis drug reaction idiopathic PRURITIS • Uraemia Itching without rash suggestive of internal cause. • Cancer INVESTIGATIONS: • Pruritus of old age • Iron deficiency/overload • FBC, LDH • Renal profile • LFTs • Ferritin • X-RAY CHEST • HIV and Hepatitis A/B/CCARCINOID SYNDROME intermittent facial flushing, watery diarrhoea, and a sensation of wheezing after meals. He says the flushing • Signifies metastases of a episodes come on suddenly, last for several minutes, and are not related to emotions or temperature. He has also malignant carcinoid tumour. lost 4kg unintentionally. On examination: • Facial flushing over cheeks and nose • 5-HT secretion + flushing in • Mild right upper quadrant tenderness 25% cases. • No rash or lymphadenopathy • Other symptoms: diarrhoea, bronchospasm + hypotensionSkin Conditions Suggestive of Underlying Condition • IBD: Pyoderma gangrenosum GI conditions • IBD: Erythema nodosum Many cause • Coeliac: Dermatitis herpetiformis dermatitis !!! Nutritional Deficiencies • Anaemia Chronic Kidney Disease • Calciphylaxis • Pruritis • Palmar Erythema Chronic Liver Disease • Jaundice • Pruritus • Opportunistic Infections Immunodeficiency • Acanthosis Nigricans Diabetes Mellitus Other Endocrinology • Xanthoma (hyperlipidaemia) • Pretibial myxodoema (Grave’s) DisordersLECTURE TIMELINE 1. General Derm 2. Skin InSystemic 3. Infections + 4. SkinCancer + Terminology Disease InfestationsOf Skin ManagementSkin Infections and Infestations Common Bacterial Infections Viral Infections Fungal Infections Parasitic InfectionsBacterial Infections: Quick Fire QuizBACTERIAL INFECTIONS Staphylococcus aureus: Streptococcus pyogenes: Impetigo Impetigo Folliculitis: Furunculosis, Carbuncles Cellulitis Cellulitis Ecthyma Ecthyma Erysipelas Staphylococcal scalded skin syndrome Scarlet fever (SSSS) Necrotizing fasciitis Superinfects other dermatoses (e.g. Superinfects other dermatoses (e.g. leg atopic eczema, HSV , leg ulcers) ulcers) Expresses virulence factors that confer B-haemolytic attaches to epithelial surfaces. It pathogenic properties to cause havoc. has M protein + hyaluronic acid capsule.Panton Valentine Leukocidin Beta-pore forming toxin • Increased morbidity, mortality, transmissibility • Painful, multi-site, recurrent, present in contacts Extracutaneous: Necrotising fasciitis, Necrotising pneumonia + Purpura fulminans Skin: recurrent + painful abscesses, folliculitis + cellulitis 5 Cs - Close contact, contaminated items, crowding, cleanliness, cuts Tx=> Abx, nasal ointment, chlorhexidine body wash, treat contactsFOLLICULITIS • Follicular erythema; sometimes pustular. • May be infectious or non-infectious (in HIV) • Recurrent cases may arise from nasal carriage of S.aureus esp if they express PVL • Treatment: •Antibiotics (usually flucloxacillin or erythromycin) •Incision and drainage is required for furunculosis.PSUEDOMONAL FOLLICULITIS • Hot tub folliculitis, swimming pool, depilatories, wet suits • 1-3 days post exposure • Mostly self-limiting – no treatment req !! • Rarely can cause abscess, lymphangitis, fever • Severe or recurrent cases => oral ciprofloxacinFURUNCLE VS CARBUNCLE • Furuncle = deep follicular abscess • Carbuncle = involvement with adjacent connected folliclesCELLULITIS • Infection of lower dermis + subcutaneous tissue • Tender swelling with ill-defined, blanching erythema or oedema • Most cases: Streptococcus pyogenes & Staphylococcus aureus • Oedema is a predisposing factor • Treatment: systemic antibioticsIMPETIGO • Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion. • Caused by • Streptococci (non-bullous) • Staphylococci (bullous) • Often affects face (perioral, ears, nares). • Treated with topical +/- systemic antibiotics. • Impetiginisation: occurs in atopic dermatitis -> superimposed infection -> gold crustingBORRELIOSIS (LYME DISEASE) • Annular erythema from Borrelia-infected tick bite • Borreliosis; 1-30 days from infection you get fever + headache. • Many secondary lesions develop but smaller to initial region. • Neuroborreliosis • Arthritis • Carditis SYPHILIS Primary • Painless chancre w firm Secondary: Tertiary (rare now): indurated border • Systemic spread of spirochetes (50d • Years later if untreated • Appears within 10-90d after chancre) • Gumma skin lesions – nodules • Systemic symptoms + plaques • Painless regional • Orogenital lesions like ulcers + • Gummatous lesions, neurological lymphadenopathy 1w after 1o condylomata lata in vulvular + anal area or cardiovascular complications chancre Lues Maligna: • Pleomorphic skin lesions w pustules, nodules + ulcers with necrotising vasculitis Treponema pallidum is the bacteria causing it. Diagnosis: Clinical findings, serology + strong index of suspicion for 2o. Treatment: IM benzylpeniciilin OR oral tetracyclin (if penicilin allergic)Viral Infections: Quick Fire QuizHERPES SIMPLEX VIRUS Conditions: • Oral lesions: cold sores • Genital lesions • Herpetic whitlow • Eczema herpeticum • Neonatal HSV Diagnosis: Swab for Polymerase chain reaction Treatment (DON'T DELAY): • Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection • Intravenous 10mg/kg TDS X 7-19 days if severe, systemic or at risk.ORAL + GENITAL HSV • Primary + recurrent vesicular eruptions • Favour orolabial + genital regions • Transmission can happen even during asymp periods of viral shedding • HSV-1 = direct contact w contaminated salive/other infectious secretions. • HSV-2 = sexual contact. Symptoms: • Within 3-7d of exposure • Post transmission: replicates at mucocutaneous site of • Lymphadenopathy, malaise, infection + travels by retrograde axonal flow to dorsal root anorexia first then vesicles on ganglia. erythematous base • Crusting + resolution within • Reactivation – spontaneous, UV, fever, local tissue damage 2-6w + stress.HERPETIC WHITLOW • HSV (1>2) infection of digits – pain, swelling and vesicles (vesicles may appear later) • Misdiagnosed as paronychia or dactylitis • Often in childrenECZEMA HERPECTICUM • On a background of eczema • It’s an emergency! • Monomorphic, punched out erosions (excoriated vesicles)FUNGAL INFECTIONS • What are fungi? • Eukaryotic organisms • Chitinous cell walls, plasma membranes containing ergosterol, 80S RNA • Yeasts – single celled, reproduce by budding • Candida • Cryptococcus • Histoplasma (dimorphic) • Moulds – multicellular hyphae, grow by branching and extension • Dermatophytes • Aspergillus • MucormycosesCANDIDIASIS • Candida Albicans • Predisposed by occlusion, moisture, warm temperature + diabetes mellitus • Most sites show erythema oedema, thin purulent discharge • Can become systemicPITYRIASIS VERSICOLOR • Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale • Fungus = Malassezia spp. • Begins during adolescence (when sebaceous glands become active) • Flares when temperatures and humidity are high – Immunosuppression • Treatment = topical antifungals (Topical azole) DERMATOPHYTES • Dermatophytes – fungi that live on keratin • Trichophyton rubrum -> most fungal infections • Trichophyton tonsurans -> most tinea capitis • Kerion – an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp: • Tender scalp + posterior cervical lymphadenopathy • Frequently secondarily infected with S.aureus Id Reaction – inflammatory reaction at sites distant from associated dermatophyte infection. • May include urticaria, hand dermatitis or erythema nodosum. • Secondary to strong hot immunological response against fungal antigens.OPPORTUNISTIC FUNGAL INFECTIONS • Mucormycosis • Oedema then pain then eschar • Fever, headache, proptosis, facial pain, orbital cellulitis +/- CN dysfunction • Treatment = aggressive debridement + antifungal therapy amphoteracinINFESTATIONS Scabies – Sarcoptes species • Female mates, burrows into epidermis, lays eggs and dies • Treatment = permethrin, oral ivermectin where 2 cycles of treatment are required Lice • Hair - lives in hair • Body - lives in clothes • Pubic - pubic hair, axilla, eyebrow and eyelash - lays eggs on hair shaft Bedbugs • Itchy wheals, dine alone at night, rapidly and painlessly • Live behind wallpaper, under furniture • Fumigation of homeLECTURE TIMELINE 1. General Derm 2. Skin InSystemic 3. Infections + 4. SkinCancer + Terminology Disease InfestationsOf Skin ManagementSkin Cancers Melanoma Basal Cell Carcinoma Squamous Cell Carcinoma Merkel Cell Carcinoma Cutaneous T-Cell LymphomaSkin Cancers BCC SCC MelanomasMELANOMA • Malignant tumour arising from melanocytes • Leads to >75% of skin cancer deaths • Can arise on mucosal surfaces (e.g oral, conjunctival, vaginal) + within uveal tract of eye • Risk factors o Genetic: Fhx (CNKN2A mutations), light skin, DNA repair defects o Environmental: sun exposure/sunbeds o Phenotypic: atypical melanocytic nevi or >100 on whole bodySkin Cancers – worrying signs Worrying signs Border irregularity Colour variegation Diameter greater than 5mm E evolving: change in colour, shape or size GARBE'S RULEMELANOMA SUBTYPES Superficial Spreading Nodular Lentigo maligna Acral lentiginous UnclassifiableSUPERFICIALLY SPREADING • 60-70% of all melanomas • Most common type in fair-skinned individuals • Most freq seen on trunk of men + legs of women • Can arise de novo or in pre-existing nevus •In up to 2/3 of tumours, regression (visible as grey, hypo-or depigmentation) occurs due to host immune system reacting to tumour. •After a slow horizontal (radial) growth phase, limited to epidermis, a more rapid vertically oriented growth phase: development of noduleNODULAR • 2d most common type of melanoma in fair skinned individuals • 15-30% of all melanomas • Most commonly trunk, head and neck, M>F • Usually dark nodule –but can be pink or red, may be ulcerated, bleeding • Develops rapidly • De novo vertical growth phase without the horizontal growth phase. Present more advanced stage, with poorer prognosis.LENTIGO MALIGNA + ACRAL LENTIGINOUS Lentigo Maligna Acral lentiginous Slow growing macule Uncommon: ~5% of all melanomas skinyo chronically sun damaged palms soles around the nail It is an in-situ melanoma Incidence similar across all racial and 5% progress to invasive melanoma ethnic groups (afro-carrib + asians)OTHER MELANOMA Nail melanoma Amelanotic melanomaINVESTIGATIONS • 'If in doubt, take it out' • Dermatoscopy o Can improve correct diagnosis of melanoma by nearly 50% o not in isolation but history + RF status important • Excision Biopsy for histological assessment o Measure Breslow thickness – prognosis worse if >1mm o Stratum granulosum -> bottom of tumourMANAGEMENT • Wide local Excision • Margin depends on Breslow thickness • Sentineal lymph node biopsy -> LN dissection • Imaging • TNM staging • Immunotherapy (unresectable/mets) • CTLA-4 inhibition (Ipilimumab) • PD-L1 (programmed cell death ligand) inhibitors (Nivolumab) • Mutated oncogene targeted therapy = combo of BRAF inhibitor (e.g encorafenib) + MEK inhibitor (e.g trametinib)DIFFERENTIAL DIAGNOSIS Basal cell Seborrhoeic carcinoma keratosis DermatofibromaKERATINOCYTE DYSPLASIA/CARCINOMA OVERVIEW • Predominantly pale skin types • Solar induced UV damage • Actinic keratoses ▪ Dysplastic keratinocytes • Bowen’s disease ▪ Squamous cell carcinoma in situ • Squamous cell carcinoma ▪ Invasive cancer ▪ Possible metastasise • Basal cell carcinoma ▪ Locally invasive ▪ Virtually never metastasisesAK/BD TREATMENT • 5-fluorouracil cream • Cryotherapy • Imiquimod cream • Photodynamic therapy • Curettage and cautery • ExcisionBCC vs SCC • Squamous cell carcinoma • Background of sun-damaged skin BCC Treatment: • Different appearances + radily growing + ill-defined margins • Standard Surgical Excision • Investigation – clinical sufficient, biopsy if unsure, US • Mohs MIcrographic Surgery – regional LN +/- FNA critical site/recurrent BCC/aggressive subtype • Topical, Radiotherapy, • Basal cell carcinoma Photodynamic, Curretage • BCC is the most common skin cancer • Median age at diagnosis is 68 SCC Treatment: • Investigation – clinical enough, biopsy if unsure • Skin + Lymph Node exam • Excision • BCC:SCC 4:1 • Both commoner in pale skin types • Radiotherapy • Cemipilimab (mets + 2o prev) • Both more common in men vs women (2-3:1)SCC Can have different appearances • Erythematous to skin coloured • Papule • Plaque-like • Exophytic • Hyperkeratotic • Ulceration Arises within background of sun-damaged skin. Rapidly growingBCC Main subtypes: Nodular- Superficial • Nodular: Most common subtype • Approximately 50% of all BCCs • Typically: shiny, pearly papule or nodule • Superficial: Well-circumscribed, erythematous, macule/patch or thin papule/plaque • Morphoeic: less common, slighly elevated/depressed area, light pink-white + more aggressive • Basquamous: histological feaures of both BCC + SCCKERATOCANTHOMA • Rapidly enlarging papule that evolves into sharply circumscribed, crateriform nodule with keratotic core • Difficult!!! Its sorta harmless but tries to trick us – is it a vriant of SCC? Or is it pseudo-malignancy? • Hard to distinguish clinically + historically from SCC • Resolves slowly over months + most occur on head/neck/sun exposed areasMERKEL CELL CARCINOMA • Origin cell NOT a Merkel cell • 80% are associated with polyomavirus • UV exposure also an aetiological factor (20%) • Head + neck region of older adults • Aggressive malignant behaviour • >40% develop advanced disease • Solitary, rapidly growing nodule – pink-red to violaceous with a firm, dome-shape. You can also get ulceration!MERKEL CELL CARCINOMA • Origin cell NOT a Merkel cell • 80% are associated with polyomavirus • UV exposure also an aetiological factor (20%) • Head + neck region of older adults • Aggressive malignant behaviour • >40% develop advanced disease • Solitary, rapidly growing nodule – pink-red to violaceous with a firm, dome-shape. You can also get ulceration!QUESTIONS • VSAQ 1: What investigation would you do if you find a melanoma which is deeper than 1mm? • VSAQ 2: What type of surgery would you do to treat basal cell carcinoma? • VSAQ 3: What carcinoma is significantly associated with polyomavirus?ANSWERS • VSAQ 1: What investigation would you do if you find a melanoma which is deeper than 1mm? Sentinel Lymphoma Node Biopsy • VSAQ 2: What type of surgery would you do to treat basal cell carcinoma? Mohs Micrographic Surgery • VSAQ 3: What carcinoma is significantly associated with polyomavirus? Merkel Cell CarcinomaQUESTIONS SBA-1ANSWERS SBA-1QUESTIONS SBA-2ANSWERS SBA-2QUESTIONS SBA-3ANSWERS SBA-3Thank you for listening :) Feel free to email me: dv122@ic.ac.uk