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20 Cards in this Set

  • Front
  • Back

Pemphigus
- A serious autoimmune mucocutaneous blistering disorder caused by what?
- What does it cause?
- What is the course?
- Treatment?

- IgG autoantibodies against desmogleins
- Acantholysis and intraepidermal bullae
- Fatal without glucocorticoid therapy
- systemic glucocorticoids, immunosuppressive agents, manage fluids and infections

Pemphigus Vulgaris
- Skin findings?
- what persists before skin involvement?


- Where are the extracutaneous sites?
- What is a positive Nikolsky sign?

- Flaccid bullae which rupture leaving shallow crusted erosins
- Oral ulcers
- Nasopharynx, larynx, esophagus, ear, eye, urethra, anal and colonic mucosa
- Dislodged epidermis by lateral pressure near lesions

Bullous pemphigoid
- A bullous autoimmune disease usually found in whom?


- Pathogenesis?


- What are the two forms of antigen recognized?
- What will find on IF?
- What will you find on the skin?
- When will oral lesions appear?
- What is the course?


- Treatment?

- Elderly patients
- Auto-antibodies react with basal cell-basement membrane hemi-desmosomes
- BPAG1 and BPAG2


- Linear deposition of IgG and complement in the basement membrane zone
- Tense bullae and a negative nikolsky sign
- After skin lesions
- Permanent remission after therapy, some even w/o therapy
- Systemic prednisone alone or combined with azathioprine

Dermatitis Herpetiformis
- A rare, chronic , intensely burning, pruritic papulovesicular eruption associated with?
- Relatives to this kind of patient will have increased risk for what disease?
- Pathogenesis?
- What do you see on IF?


- Treatment?

- Gluten-sensitive enteropathy and IgA deposits in upper dermis


- Celiac disease
- IgA antibodies react to gluten in diet, these antibodies cross react with reticulin which is a component of fibrils that anchor the epidermal basement membrane to the dermis.
- Deposits of IgA localized to the tips of dermal papillae
- Sulfones; gluten free diet

Acne Vulgaris
- Pathogenesis?
- What stimulates sebaceous glands to make more sebum?
- What produces pro inflammatory mediators which causes a sterile inflammatory response to the pilo-sebaceous unit?
- What spills the contents in the dermis provoking an inflammatory response that leads to scarring?
Types
- Small papules with central black keratin plug
- Follicular papules without a central plug


- erythematous papules, nodules and pustules
- What is the goal of therapy?

- Keratinous material in the pilosebaceous unit becomes dense blocking secretion of sebum; plugs are called comedones
- Androgens


- Bacterial lipase
- Distended follicle walls rupturing
- Non-inflammatory open comedones
- Non-inflammatory closed comedones
- Inflammatory
- Remove the plugging of the pilar drainage, reduce sebum production and treat bacterial colonization

Rosacea
- Disorder characterized by what? (4)
- It has four stages


- Pathogenesis
- Course
- Treatment

- Persistent flushing, erythema, papules and telangectasia
- Flushing episodes, persistent erythema, pustules and papules and then rhinophyma which is permanent thickening of the nasal skin by confluent erythematous papules and follicular prominence
- Repeated exposures to triggers of flushing
- Recurrences are common, may resolve spontaneously but it is usually life long.
- Topical antimicrobials, oral antibiotics, retinoids, rhynophyma is treated surgically

Panniculitis - inflammation of the subcutaneous fat
- What are the two patterns ?

- Septal and lobular

Erythema nodosum
- Acute onset of symmetric, tender, erythematous, warm nodules and plaques located where?
- more common in whom?
- Associations?
- Etiology?


- Treatment?

- Anterior lower legs
- Women
- Infections, drugs, sarcoidosis, inflammatory bowel disease, malignant neoplasms
- Suspected hypersensitivity reaction
- Treat associated disorder, systemic corticosteroids are rarely indicated

Pityriasis rosea (Common acute papulosquamous eruption)
- Etiology?
- What is hallmark lesion and pattern?
- Contagious?
- Course?

- Unknown
- Herald patch and Christmas tree pattern


- Doesn't appear to be contagious
- Clears up in about 6-12 weeks

Verruca Vulgaris - Common Wart
- What kind of virus infection is this associated with?
- What's the course?


- Treatment?

- Human papillomavirus (HPV) infection
- Persist for months up to years and often regress spontaneously
- Topical salicylic acid preparations or liquid nitrogen and very light electrocautery for initial therapy

Mulluscum contagiosum
- Viral skin infection, what's the virus called?


- Transmission?


- Course?
- Treatment?

- Mulluscum contagiosa virus
- Direct skin contact
- May persist for months or occasionally years and remit
- No treatment for children, topical imiquimod cream, curettage, cryotherapy

Herpes Simplex Virus
- What are the two subtypes?
- Involvement of a finger or hand in dentists
- Tzank smear
- Course?


- Treatment?

- HSV-1 and HSV-2 (genital kind)
- Herpetic whitlow
- Unroof a vesicle and scrape the base onto a slide. Viral cytopathy present in cells
- Primary episode resolves completely in around 15 days, however the virus persists and becomes latent within the ganglia of the corresponding sensory nerve


- Acyclovir topical and oral

Varicella Zoster/Chickenpox virus infection
- Where does remain where it can be reactivated as shingles?


- Mode of spread?
- How does it manifest when it reactivates?


- Post-herpetic neuralgia
- Treatment?

- Anterior horn cells
- Highly contagious
- Painful outbreak of papules and vesicle in a dermatome distribution (pain is called prodrome)
- Pain may persist for months or year


- Acyclovir; prevention through vaccination

- Acute, deep-seated, red hot, tender nodule or abscess, evolves from a staphylococcal folliculitis
- Deeper infection composed of interconnecting abscesses usually arising in several contiguous hair follicles. Staph aureus in most cases
- Treatment?

- Furuncle
- Carbuncle


- Incision and drainage plus systemic antimicrobial therapy

Impetigo
- Superficial skin infection, which bacteria?
- How does it spread?
- What is the bullous version caused by?
- Skin findings
- Treatment

- Staph Aureus
- Close contact through primary breaks in skin or secondary involvement of rash or preexisting lesion
- Epidermolytic toxin
- Golden yellow honey crusts
- Topical or systemic antibiotics

Cellulitis
- Bacterial infection of skin and subcutis, which bacteria?
- This is a bacteria that involves the lymphatics, so what happens as a result?
- Treatment?

- Strep. Pyogenes 2/3 and S. Aureus 1/3
- Lymphangitis
- Abx

Scarlet fever
- Group A streptococcus pharyngitis with what?
- Clinical findings?


- Skin findings?


- Treatment?

- Erythrogenic toxin
- Strawberry tongue
- Sand paper rash
- Systemic Antibiotic

Dermatophyte infections
- Fungal infection of what?
- What are the three species?


- Histological findings?
- How do you test for fungal hyphae?
- Treatment

- Keratin of the stratum corneum, hair or nail
- Microsporum, trichophyton and epidermophyton
- Fungal hyphae in the stratum corneum on PAS fungal stain
- KOH prep
- Topical anti-fungals

Pityriasis Versicolor
- Superficial fungal infection by which fungus?
- Histological findings will reveal what?
- Treatment?

- Malassezia furfur
- Short septate hyphae that look like spaghetti and meatballs
- Topical anti-fungals

Candida infection
- Persistent/recurrent infections where?


- What forms do the fungal organisms take?
- Pre disposing factors
- What are examples of mucosal candidasis?
- Treatment?

- Skin, nails and oropharynx
- Yeast and pseudohyphal forms
- Immunosupression, diabetes, cushings disease, pregnancy, malnutrition
- Oral thrush, angular cheilitis, vulvovaginal thrush
- Topical nystatin or chlortrimazol; oral fluconizol