Skin Based Disorders 1 PDF

Johnson & Wales University Physician Assistant Program Dermatology Module Skin Based Disorders I 2024 Mark Trott, MBA, MHP, PA-C Diplomate Fellow-SDPA [email protected] Agenda Session 1 Session 3 Intr...

Johnson & Wales University Physician Assistant Program Dermatology Module Skin Based Disorders I 2024 Mark Trott, MBA, MHP, PA-C Diplomate Fellow-SDPA [email protected] Agenda Session 1 Session 3 Intro to Dermatology Skin Based Disorders III Approach to the Dermatology Nevi and Skin Cancer Patient Skin Based Disorders IV Common Skin Lesions Session 4 Session 2 Hair and Nail Disorders Skin Based Disorders I Derm Diagnostic Procedures Topical Steroids Skills Lab Skin Based Disorders II Session 5 Derm Cases/Review Skin Based Disorders I Acne Adolescent Acne Chronic inflammatory disease of the pilosebaceous unit heavily influenced by androgens Epidemiology 12-25 Most common skin complaint in dermatology Associations Significant physical and psychosocial morbidity Acne Pathogenesis Follicular Hyperkeratinization Androgens stimulate keratinocyte proliferation in the follicular infundibulum Increased Sebum Production Androgens cause sebaceous glands to enlarge and produce more sebum Proliferation of Bacteria Bacteria proliferates in the sebum rich environment Cutibacterium acnes Inflammation Sebum + Bacteria = Inflammation Androgens Androgens Acne Lesions Microcomedo Plug formed by epithelial cells, sebum and bacteria in the follicular infundibulum Subclinical Acne Lesions Comedones As the microcomedo expands it forms a papule called a Comedone If the follicular ostium does not dilate the lesion formed is a Closed Comedone or “Whitehead” If the follicular ostium dilates the lesion formed is an Open Comedone or “Blackhead”  Acne Lesions Papules and Pustules Inflammation in and around the pilosebaceous unit results in erythematous papules and pustules Nodules and Cysts Extension of inflammation deeper in the dermis can result in painful nodules and cysts with significant scarring risk Acne Patterns T-Zone Forehead and central face Common with “early” acne “Hormonal” Lower face acne Along the mandibles and chin Truncal Shoulders, chest and back Acne Excoriee Traumatized acne from scratching or picking T-Zone Acne “Hormonal” Acne Truncal Acne Acne Excoriee  Acne Complications Pigment Alteration Postinflammatory Erythema Postinflammatory Hyperpigmentation Scars Atrophic Hypertrophic Keloidal Postinflammatory Pigment Alteration Post-inflammatory Erythema Post-inflammatory Hyperpigmentation Scarring Atrophic Scars Hypertrophic and Keloidal Scars Acne Lesion Summary Primary Lesions Secondary Lesions Open and Closed Comedones Pigment Alteration Inflammatory Papules + Pustules Erosions and Excoriations Nodules and Cysts Scars Atrophic Hypertrophic Keloidal Acne DX Clinical Consider contributing factors Hormonal PCOS Exogenous Androgens Acnegenic Medications Steroids Lithium Phenytoin Treatment Considerations Lesion Type Hormonal Factors Comedones Contraception Papules/Pustules Endogenous Androgens Nodules/Cysts Exogenous Androgens Post-inflammatory Pigment Skin Features Alteration Oily; Dry; Sensitive Excoriations Scarring Previous Treatments Adherence + Results Distribution T-zone; Truncal; Hormonal Psychosocial Impact What bothers the patient? Treatment Options- Topicals Topical Retinoids Comedolytic + Anti-comedogenic Mildly Anti-inflammatory Lightens PIH Helps other topicals penetrate Tretinoin- Retin A Adapalene- Differin Trifarotene- Aklief Tazarotene- Tazorac Treatment Options- Topicals Topical Antibiotics Anti-inflammatory Antibacterial Risk of bacterial resistance Clindamycin Erythromycin Sulfacetamide/Sulfur Treatment Options- Topicals Benzoyl Peroxide Antibacterial Reduces risk of bacterial resistance when used concurrently with antibiotics Mildly Comedolytic Vehicles- Cream/Gel/Lotion/Wash Will bleach everything in the house! Treatment Options- Topicals Azelaic Acid Antibacterial Mildly Comedolytic Anti-inflammatory Tyrosinase Inhibitor Improves post-inflammatory hyperpigmentation Finacea Foam Azeleic Acid Gel Treatment Options- Topicals Dapsone- “Aczone” Anti-inflammatory Bacteriostatic For moderate to severe acne Caution: stains skin yellow if used with benzoyl peroxide Clascoterone- “Winlevi” Androgen receptor blocker Indicated for >12 Must use twice a day Treatment Options- Systemic Oral Antibiotics Anti-inflammatory Anti-bacterial Risk of bacterial resistance! Doxycycline Minocycline Erythromycin Azithromycin Subantimicrobial Dosing of Doxycycline Doxycycline 20mg po bid or Modified release 40mg po qd (ORACEA) Significant improvement in moderate acne, well tolerated, no detectable antimicrobial effect on skin flora, and no increase in number or severity of resistant organisms Arch Dermatol. 2003 Comparable efficacy and superior safety to doxycycline 100mg in moderate to severe inflammatory acne J Drugs Dermatol. 2015 Used effectively for Rosacea treatment since 2006! Treatment Options- Systemic Hormonal Combination OCP Estrogen decreases sebaceous activity and androgen production Progesterone is androgenic Drospironone is a progestin with both androgenic and anti- androgenic effects FDA approved OCP’s Ortho Tri-cyclen Estrostep Yaz Beyaz Treatment Options- Systemic Hormonal Spironolactone Androgen Receptor Blocker Inhibits Androgen Biosynthesis Decreases Testosterone and DHT Dosing Average effective dose is 100mg/day Maximum dose is 200mg/day NOT FDA approved for acne! But successfully used in clinical practice for > 30 years Spironolactone and Cancer? Spironolactone was not associated with any meaningful increase in the risk of breast cancer or other solid organ cancers in a systematic review and meta-analysis covering seven observational studies and a total population of over 4.5 million people JAMA Dermatol. 2022;158(3):275-282 Treatment Options- Systemic Oral Retinoids Isotretinoin- “Accutane” For moderate to severe recalcitrant nodulocystic acne Dosing 0.5-1mg/kg/day Target 120-150mg/kg total dose Clinical Effects Normalizes keratinocyte turnover Decreases sebum production Decreases bacterial colonization Isotretinoin Requirements Prescriber must be Registered with iPledge Patient must enroll in the iPledge program Common Side Effects Dryness; Chapped Lips; Nosebleeds Myalgias; Arthralgias Rare Side Effects Pseudotumor Cerebri Neutropenia Hepatotoxicity Hyperlipidemia Serious Side Effects Teratogenicity Depression and Suicide Isotretinoin….Risk vs Benefit? What about Steroids and Acne? Topical steroids In general-contraindicated for acneiform eruptions Oral steroids Sometimes used for severe flares Intralesional steroids For emergency relief Risk of atrophy + dyspigmentation Dosing: Kenalog 1 to 2.5mg/ml Acne Treatment Options- Summary Hormones Comedones Spironolactone Retinoids Clascoterone Mildly comedolytic Combination OCP’s Azelaic Acid Bacteria Benzoyl Peroxide Antibiotics Inflammation Benzoyl Peroxide Antibiotics Azelaic Acid Dapsone Dyspigmentation Mildly anti-inflammatory Retinoids Retinoids Azelaic Acid Azelaic Acid Severe acne Isotretinoin Acne is not always acne Rosacea Rosacea Chronic inflammatory disorder affecting the face Epidemiology Typical onset- 30-50 Familial in 10-20% of cases Rosacea Pathogenesis Some combination of Vascular Dysfunction Ultraviolet Light Exposure Genetic Factors Inappropriate immune response to cutaneous microorganisms Demodex mites Other? Bacillus oleronius Staphylococcus epidermidis Rosacea “Triggers” Sun exposure Alcohol Spicy foods Hot liquids Emotional stress Extremes of temperature Physical exertion Rosacea Clinical Presentation History of flushing and blushing Any or all of the following Erythema and Telangiectasia Papules and Pustules Phymatous changes Skin hypertrophy and sebaceous gland enlargement Ocular involvement Conjunctivitis, blepharitis, styes, or chalazions Rosacea Sub-types Erythemato-Telangiectatic Rosacea Rosacea Sub-types Papulo-Pustular Rosacea Rosacea Sub-types Phymatous Rosacea Rosacea Sub-types Ocular Rosacea- up to 50% Rosacea DX Clinical Rosacea RX Photoprotection Modify Triggers Camouflage Telangiectasia Green Tinted Makeup Laser or IPL Tinted Sunscreen Phymatous Rosacea Topicals Surgical Paring/Sculpting Metronidazole Ivermectin Ocular Rosacea Azelaic Acid Doxycycline Sodium Sulfacetamide/5% Sulfur Ophthalmology Oral antibiotics Doxycycline Erythromycin Periorificial Dermatitis (POD) Perioral Dermatitis Chronic localized inflammatory disorder of unknown etiology that favors periorificial skin of the face Epidemiology 90% Women- 20-45 10% Men and Children Periorificial Dermatitis History Frustrated Patient Longstanding waxing and waning “acne that never goes away” Repeatedly Treated Medications “don’t help” or “make it worse” Topical Steroids Often Tried They help but the condition worsens on withdrawal Periorificial Dermatitis Clinical Presentation Pinpoint papules and pustules on a background of erythema located around facial orifices Often accompanied by scaling, itching or burning Periorificial Dermatitis DDX Acne Rosacea Eczema DX Clinical Periorificial Dermatitis RX Eliminate Steroids and Irritants Topicals Erythromycin Clindamycin Metronidazole Azeleic Acid Calcineurin Inhibitors Tacrolimus; Pimecrolimus Oral Antibiotics Tetracyclines Doxycycline Minocycline Erythromycin Folliculitis Superficial Folliculitis Inflammation of the upper portion of the hair follicle Etiology Non-infectious Mechanical injury to the hair follicle Infectious Bacterial Staph; Pseudomonas Fungal Pityrosporum Non-infectious Folliculitis Etiology Trauma, Friction or Occlusion Shaving Tight clothing Scratching or rubbing Clinical Presentation Folliculocentric papules and pustules Non-infectious Folliculitis DX Clinical Culture to r/o bacterial folliculitis RX Modify habits Topical Benzoyl Peroxide Clindamycin Erythromycin Bacterial Folliculitis Staph aureus Most common pathogen Staph likes to colonize the nares, umbilicus, perineum and hair follicles MRSA Bacterial Folliculitis Clinical Presentation Painful or itchy erythematous folliculocentric papules and pustules DX Clinical Culture Bacterial Folliculitis RX Topical Clindamycin Benzoyl Peroxide Oral Antibiotics Dicloxacillin Cephalexin MRSA Doxycycline Clindamycin Trimethoprim/Sulfamethoxasole Bacterial Folliculitis Pseudomonas “Hot Tub Folliculitis” Pseudomonas infection of the hair follicle Etiology Pseudomonas exposure from contaminated water sources Hot Tubs Pools Water Parks Pseudomonas Folliculitis Clinical Presentation Pruritic red folliculocentric papules and pustules occurring within days of exposure Most lesions on “covered” skin Bathing suit distribution Intertriginous areas Pseudomonas Folliculitis DX Clinical History of some exposure to potentially contaminated water Bacterial Culture Pseudomonas Folliculitis RX Most cases are self limited 7-14 days if no re-exposure Topical Steroids for Pruritus Topical Regimens Gentamycin 1% acetic acid soaks- dilute vinegar Systemic Antibiotics Severe or resistant cases or immunosuppression Ciprofloxacin Fungal Folliculitis Pityrosporum Folliculitis Proliferation of Malassezia furfur in the hair follicles A commensal lipophilic yeast Risk Factors Young age Heat and Humidity Sweating Occlusive Clothing Immunosuppression Pityrosporum Folliculitis Clinical Presentation Acute onset of pruritic monomorphic erythematous papules and pustules Sebaceous Distribution Forehead Upper Trunk Shoulders and Proximal Arms Pityrosporum Folliculitis DDX Acne Keratosis Pilaris Miliaria Rubra Pityrosporum Folliculitis DX Clinical KOH Prep Short broad hyphae and yeast cells “Spaghetti and Meatballs” Pityrosporum Folliculitis RX Topical Antifungals Ketoconazole 2% shampoo Apply 5-10 minutes before shower then rinse off at least twice a week for 4 wks Antifungal Creams BID for 2-4 weeks Ketoconazole Econazole Clotrimazole Ciclopirox Systemic Antifungals Fluconazole 100-200mg po qd x 1-3 wks Itraconazole 200mg po qd x 1-2 weeks 2.0 cm Abscess Cutaneous Abscesses Localized inflammation and pus in the dermis or subcutaneous tissue Non-Infectious “Sterile” Abscess Normal skin flora Infectious Staph aureus Streptococci Abscess Clinical Presentation Localized painful or tender warm erythematous fluctuant mass Furuncles- “BOILS” Abscesses around hair follicles Abscess DX Clinical Bacterial Cultures Abscess RX Warm compresses Incision and drainage Intralesional steroids if inflamed Oral Antibiotics Dicloxacillin Cephalexin MRSA Doxycycline Clindamycin Trimethoprim/Sulfamethoxasole Impetigo Impetigo Contagious superficial bacterial infection of the skin Etiology Occasionally a primary infection More often a secondary infection “Impetiginized eczema” Epidemiology More common in children Impetigo Clinical Presentation 1 Non-Bullous Impetigo Erythematous vesicles or pustules that transition into erosions with a characteristic overlying golden or honey colored crust Pathogens Staph aureus; Strep pyogenes Impetigo Clinical Presentation 2 Bullous Impetigo Vesicles enlarge forming flaccid bullae that break leaving well demarcated superficial erosions with an overlying yellow-brown crust Pathogens Strains of staph that produce exfoliative toxins Impetigo Impetigo DX Clinical Look closely for yellow Bacterial Culture Impetigo RX Limited disease Gently bathe away the crusts Mupirocin ointment Extensive disease Cephalexin Dicloxacillin Erythromycin MRSA Doxycycline Clindamycin Trimethoprim/Sulfamethoxasole 1.2 cm Ecthyma Ecthyma Ulcerative bacterial infection Deeper than impetigo Extends through the epidermis into the dermis Etiology Group A beta-hemolytic strep Staph co-infection is common Ecthyma Clinical Presentation “Punched-out" ulcers with yellow or brown crust and elevated erythematous to violaceous border Ecthyma DDX Impetigo Abscess Spider bite DX Clinical Cultures Ecthyma RX Aggressive saline soaks to remove crusts Systemic antibiotics Cephalexin Dicloxacillin Erythromycin MRSA Doxycycline Clindamycin Trimethoprim/Sulfamethoxasole Erysipelas Erysipelas Bacterial infection of the upper dermis Most common on face and extremities Etiology Bacterial invasion of traumatized or diseased skin Most common pathogen GABHS: Strep pyogenes Erysipelas Risk Factors Extremes of age Debilitated patients Poor lymphatic drainage Erysipelas Clinical Presentation Unilateral painful red hot indurated plaque with sharply demarcated border May have overlying vesicles, bullae and purpura Lymphadenopathy is almost always present Erysipelas DX Clinical Labs CBC/Diff ASO Titer Erysipelas RX Empiric oral therapy Penicillin Clindamycin if PCN allergic Hospitalization and IV antibiotics Infants or the elderly Immunocompromised Fever >100.5 Rapid progression of erythema Can’t tolerate oral therapy Disease progression after 48 hours of empiric oral therapy This is raised, painful and hot to touch Cellulitis Cellulitis Bacterial infection of the deep dermis and subcutaneous tissue Most common on face or extremities Cellulitis Etiology Direct bacterial inoculation through compromised skin Pathogens Immunocompetent Staph aureus and Strep pyogenes Immunocompromised Consider Gram negative pathogens Cellulitis Risk Factors Minor skin trauma Body piercing Insect bite Animal bite Surgical procedures Peripheral vascular disease Lymphatic disorders IV Drug Use Immunosuppression Cellulitis Clinical Presentation Unilateral irregularly bordered plaque with warmth, tenderness and edema Color varies with skin tone Sometimes associated with Vesicles, Bullae, or Pustules Erosions; Necrosis Lymphangitis; Lymphadenopathy Cellulitis Lymphangitis Weeping Erosion Cellulitis DDX Venous Stasis Dermatitis Lymphedema Necrotizing Fasciitis Is this Cellulitis? Cellulitis DX Clinical Misdiagnosed 30% of the time! Culture any open wounds or debrided material Cellulitis RX Early or Limited Disease Empiric Oral Therapy Cover for MRSA Rest and elevation Mark the leading edge and do short interval monitoring Severe cases Hospitalization Broad Spectrum IV antibiotics Cellulitis and Erysipelas That can’t be good!! Necrotizing Fasciitis Necrotizing Fasciitis Deep bacterial infection that tracks along fascial planes causing progressive destruction of the fascia and overlying subcutaneous fat Most common on legs A life threatening medical and surgical emergency Necrotizing Fasciitis Risk Factors Breach of skin integrity Minor or major trauma Skin disease Recent surgery or procedure IV Drug use Immunosuppression Diabetes Malignancy Obesity Alcoholism Necrotizing Fasciitis Type 1- Polymicrobial Elderly, Immunocompromised or Diabetic Aerobic and anaerobic bacteria Type 2- Monomicrobial Healthy individuals without obvious risk factors Strep pyogenes or Staph aureus Necrotizing Fasciitis Clinical Course ~50% with fever and rapidly worsening severe localized or regional pain Typical Progression Erythema and Edema Bullae, Ecchymosis and Necrosis Rapid progression> Septic Shock> Death Necrotizing Fasciitis Fournier Gangrene Necrotizing Fasciitis involving the lower abdominal wall, perineum or genitals Most common in Diabetics s/p surgical debridement Necrotizing Fasciitis DDX Cellulitis Erysipelas Pyoderma Gangrenosum Pyoderma Gangrenosum Necrotizing Fasciitis DX Clinical A sick patient Fever, lethargy, hypotension, tachycardia Severe pain Worsening “Cellulitis” Bullae, ecchymosis, necrosis Labs CBC/Diff; Creatinine; CRP; CK; AST Obtain blood cultures prior to initiation of antibiotics Imaging Necrotizing Fasciitis RX Hospitalization Immediate Surgical Intervention IV antibiotics Initial empiric RX followed by culture directed antibiotic therapy Vancomycin or linezolid PLUS piperacillin-tazobactam If you think it might be necrotizing fasciitis… contact surgery immediately! 2.0 cm Dermatophyte Infections Dermatophyte Infections Infections caused by fungi that require keratin for survival 3 Genera of Dermatophytes that can infect skin, hair or nails Trichophyton Microsporum Epidermophyton Dermatophyte Infections Pathogenesis The fungus produces keratinases that break down keratin allowing invasion of skin, hair or nails Dermatophyte Infections Transmission Human to Human Animal to Human Soil to Human Fomite Transmission Dermatophyte Infections Skin Tinea Corporis-trunk/extremities Tinea Faciei- face Tinea Cruris- inguinal Tinea Manuum- hands Tinea Pedis- feet Hair Tinea Capitis- scalp Tinea Barbae- beard Nails Tinea Unguium- Onychomycosis Tinea Corporis Clinical Presentation Annular scaling patches or plaques with central clearing Extensive confluent or coalescing lesions can be seen with immunosuppression Tinea Corporis Tinea Corporis Tinea Faciei Tinea Corporis Tinea Cruris Tinea Manuum Tinea Pedis Tinea Pedis Most common dermatophyte infection Variants Interdigital- most common Moccasin Distribution Inflammatory Ulcerative Bullous Tinea Pedis Tinea Pedis Interdigitale Moccasin Distribution Tinea Pedis Inflammatory Tinea Pedis Ulcerative Tinea Pedis Tinea Pedis Bullous Tinea Pedis Dermatophyte Infections DX Clinical KOH Exam Dermatophyte Infections RX Local Skin Disease Topical Antifungals- 2-6 weeks Imidazoles- Clotrimazole ; Econazole Allylamines- Terbinafine, Naftifine Extensive or Resistant Disease Oral Antifungals 2-4 weeks Terbinafine Itraconazole Fluconazole Tinea Capitis Tinea Capitis Scalp dermatophyte infection Major causes Trichophyton tonsurans > 90% in US Epidemiology Children 3-7 years old In the US- most common in children of African heritage Tinea Capitis Contagion Direct contact with Infected individual or animal Contaminated object Comb, brush, or hat Tinea Capitis Clinical Presentation Scaly Patches or Plaques with Broken Hairs Alopecia Inflammation Posterior Cervical Adenopathy Tinea Capitis DX Consider tinea capitis in any child with scalp alopecia and scaling Endothrix LAB KOH exam of involved skin Microscopic exam of hair Trichoscopy Fungal cultures? Ectothrix Tinea Capitis Complication Kerion Acute inflammatory reaction to severe dermatophyte infections in hair bearing areas Scalp; Beard; Eyebrows; Vulva Clinical Presentation Boggy, inflamed crusted plaques studded with pustules 2ᴼ Bacterial infections are common Add bacterial cultures to the workup Scarring alopecia Tinea Capitis RX Oral antifungals Dosing based on body weight Terbinafine for 4-8 wks Griseofulvin for minimum of 8 wks Adjunctive measures Antifungal shampoos Follow up to ensure resolution For Kerion Treat as above Treat Secondary Infections Prednisone 0.5mg/kg/d tapered over 7-10 days for severe cases Onychomycosis Dermatophyte Infection of Nail Toenails > Fingernails Risk Factors Longstanding Tinea Pedis Trauma Immunosuppression  Onychomycosis Variants Distal-Lateral Onychomycosis Superficial White Onychomycosis Proximal Subungual Onychomycosis By far the most common Diabetes; HIV; Children Least common HIV/AIDS Onychomycosis Clinical Presentation Nail plate thickening, discoloration, onycholysis, and subungual debris Differential Diagnosis Only 50% of Nail Trauma Psoriasis Dystrophies are Fungal Lichen Planus Onychomycosis Onychomycosis Diagnosis Fungal Culture Send clippings to lab in saline 80% sensitive and quick PCR Testing Sensitive and Specific Limitations: availability and cost KOH Exam Fast and cost effective >90% sensitive with… Adequate specimen Clinician expertise Onychomycosis RX Oral Antifungals- most effective Terbinafine 250mg po qd 12 weeks for toenails 6 weeks for fingernails Itraconazole Fluconazole Side effects of Oral Antifungals Hepatotoxicity Pancytopenia Exfoliative Dermatitis- SJS/TEN Onychomycosis RX Topical Antifungals Need to be applied daily for 24 weeks for fingernails and 48 weeks for toenails Efinaconazole 10% solution Tavaborole 5% solution Ciclopirox 8% nail lacquer Other Mechanical Debridement Surgical or Chemical Nail Avulsion Laser Case: 1 yr old with “Rash on face” Itchy rash on face for 1 week and getting worse Which of the following therapeutic options is most appropriate for this condition? A. 1% Hydrocortisone Ointment B. Mupirocin Ointment C. Nystatin Ointment D. Oral Cephalexin Case: 16 yr old with “Acne and Discoloration” Which of the following therapeutic options, if used for 3 months, will be most helpful addressing her concerns? A. Benzoyl Peroxide + Salicylic Acid B. Tretinoin + Azeleic Acid C. Dapsone + Benzoyl Peroxide D. Spironolactone Case: 60 yr old with “ Painful rash on face” Rash on right cheek for 5 days and getting worse The patient reports fever, chills, pain, swelling, and the rash feels “hot” She has swollen lymph nodes Case: 60 yr old with “ Painful rash on face” This clinical presentation is most consistent with which of the following? A. Ecthyma B. Erysipelas C. Cellulitis D. Necrotizing Fasciitis Case: 60 yr old with “ Painful rash on face” What pathogen is most commonly associated with this condition? A. Staph aureus B. Strep pyogenes C. Pseudomonas D. Combination of aerobic and anaerobic bacteria Skin Based Disorders I: Summary Acne Erysipelas Rosacea Cellulitis Periorificial Dermatitis Necrotizing Fasciitis Folliculitis Staph/MRSA Dermatophyte Infections Pseudomonas Tinea Corporis, Faciei, Cruris, Manuum Pityrosporum Tinea Capitis Abscess Kerion Impetigo Tinea Pedis Ecthyma Onychomycosis