Flashcards in Skin Path Deck (40):
Give a couple functions of skin? It is composed of what? Epidermis is comprised of ... and has what? List contents of the dermis
1. Barrier against environmental insults and fluid loss
2. Dermis and epidermis
3. Has keratinocytes and four layers: a. stratum basalis (regenerative, stem cell, layer) b. stratum spinosum (desmosomes between keratinocytes) c. stratum granulosum (granules in keratinocytes) d. stratum corneum (keratin in ANUCLEATE cells)
4. Dermis with CT, nerve endings, blood and lymphatic vessels, and adnexal structures (hair shafts, sweat glands, sebaceous glands)
Atopic (eczematous) dermatitis is what? Could be caused by what?
1. Pruritic, erythematous, oozing rash with vesicles and edema; often involves face and flexor surfaces!!
2. Type I hypersens reaction; associated with asthma and allergic rhinitis
Edgar Allen POE has been FLEXING HIS ELBOW to touch his FACE a lot recently, and he VEnts a lot now. Maybe he's befuddled by what the FIRST letter of the ALPHABET is!!!
Contact dermatitis: what's involved? how is it caused? treat?
1. Pruritic, erythematous, oozing rash with vesicles and edema
2. Arises upon allergen exposure (poison ivy and nickel jewelry, or type IV hypersens; irritant chemicals like detergents; drugs like penicillin)
3. Involves removal of offending agent and topical glucocorticoids, if needed
Edgar Allen POE continues to VEnt and now he's annoyed with poison ivy, his WATCH, and he's IRRITATED that his son uses DRUGS. I would say get rid of his WATCH and also give him some glucocorticoids.
1. Comedones (whiteheads and blackheads), pustules (pimples), and nodules; extremely common, especially adolescents
2. Chronic inflammation of hair follicles and associated sebaceous glands: hormone-associated increase in sebum production and excess kertain production block follicles, forming COMEDONES; propionibacterium acnes infection produces lipases that break down sebum, releasing proinflammatory FA's, resulting in pustule or nodule formation
3. Treat: benzoyl peroxide (antimicrobial) and vit A derivatives (isotretinoin) to reduce keratin production
Carlos Nancilla Pimps (comedones, nodules, pustules);
Sebum, keratin, follicle blockage = comedones;
P. acnes, lipases, FA's = nodules, pustules;
BP: for Bacteria (antimicrobial)
Vit A to reduce KERATIN
Psoriasis: involves, causes, labs, treatment
1. well-circumscribed, salmon-colored plaques with silvery scale, usually on EXTENSOR surfaces and the SCALP; maybe pitting of nails
2. excessive keratinocyte proliferation; possible autoimmune etiology (HLA-C assocation and lesions often in areas of TRAUMA!!)
3. Histo: acanthosis (epidermal hyperplasia), parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the stratum corneum), collection of neutrophils in stratum corneum (Munro microabscesses), thinning of epidermis above elongated dermal papillae and bleeding if scale picked off (Auspitz sign)
4. Treatment involves corticosteroids, UV light with PSORALEN, or immune-modulating therapy
I'm PLAGUED from trying to catch SILVER tuna and SALMON and now my ELBOW and HEAD hurt. Took a toll on my NAILS too.
Has LACey recovered from her punch and checked out Auspitz's AWESOME Munro Parakeet Collection? It's NEUTROPHILIC!! Corticosteroids, UV light, immune-modulating
Licen planus: involves, histo, causes
1. Pruritic, planar, purple papules, polygonal, often with reticular white lines on their surface (Wickham striae); usually involves wrists, elbows, and oral mucosa (this actually has Wickham striae);
2. inflammation of the dermal-epidermal junction with a "saw-tooth" appearance
3. Etiology is unknown: associated with CHRONIC HEP C VIRUS INFECTION
Wicki in Germany was telling me about the SIX P'S since he OWEd me information. As he was talking I saw his SAW-TOOTH. I hope he doesn't have chronic Hep C!!!
Pemphigus vulgaris: what's involved and the cause; presentation?
1. Autoimmune destruction of desmosomes between keratinocytes
2. IgG antibody against desmoglein (type II hypersens)
3. Skin and oral mucosa BULLAE: acantholysis (separation) of stratum spinosum keratinocytes results in suprabasal blisters, basal layer cells remain attached to BM via hemidesmosomes, a "tombstone" appearance, thin-walled bullae rupture easily (Nikolsky sign), leading to shallow erosions with dried crust, immunofluorescence highlights IgG surrounding keratinocytes in a "fish net" pattern
It's VULGAR when someone breaks one's BASE from beneath them. Maybe I'm just TOO SENSITIVE, but they get up and their SKIN and MOUTH are bloodied thanks to that BULLY. Now you might as well make a TOMBSTONE for those kids, thanks to fucking NIKOLSKY. Oh well, I'm Going to Go FISHING.
Bullous pemphigoid: involves, caused by, presentation, lab
1. Autoimmune destruction of hemidesmosomes b/w basal cells and underlying BM
2. IgG antibody against hemidesmosome components (BP180) of BM
3. Blisters of the skin, usually in elderly, but ORAL MUCOSA spared: basal cell layer detached from BM, and tense bullae do not rupture easily (clinically milder than pemphigus vulgaris)
4. Immunofluorescence highlights IgG along BM (linear pattern)
On the SUBWAY, I saw this guy hit an OLD MAN with ONE LEG AND ONE ARM. He got up and SEEMED to be MILD. His mouth wasn't even bleeding, and he was able to still walk in a STRAIGHT LINE.
Dermatitis herpetiformis: involves, presentation, association
1. Autoimmune deposition of IgA at tips of dermal papillae
2. Presents as pruritic vesicles and bullae that are grouped
3. Association with CELIAC; resolves with GLUTEN-FREE diet
That guy was ITCHING for some sex, so he BULLIED her into licking his Ass and sticking his FINGER TIPS into her mouth. Hope she doesn't also have Celiac!!!
Erythema multiforme: involves, associations, special form
1. Hypersens reaction with targetoid rash and bullae (targetoid appearance due to central EPIDERMAL NECROSIS surrounded by erythema)
2. Associated most commonly with HSV infection, also Mycoplasma infection, drugs (penicillin and sulfonamides), autoimmune disease, and malignancy
3. EM with oral mucosa/lip involvement and fever is termed Stevens-Johnson syndrome: toxic epidermal necrolysis is a severe form of SJS with diffuse sloughing of skin, resembling a large burn; most often due to ADVERSE DRUG REACTION
In the ME, they get HYPERSENS to women cheating so they BULLY them and TARGET them for stoning. The woman could end up with HERPES, while the men might get really MMAD.
Stevens Johnson is in the Front Office for Eastern Michigan. He wants to move to the big TEN, and it BURNS him inside right now that he can't do it, so he'll start SNORTING COCAINE.
Seborrheic keratosis: what is it, presentation, other signs?
1. benign squamous prolif: common tumor in ELDERLY
2. presents as RAISED, DISCOLORED plaques on extremities or face, with a coin-like, waxy, 'STUCK-ON' appearance (keratin pseudocysts on histo)
3. Leser-Trelat sign is sudden onset of MULTIPLE SEBORRHEIC KERATOSES and suggests underlying carcinoma of the GI tract
Dino at the pool is PLAGUED with issues in his ARM, LEGS, FACE. He will never spare COINS, but as long as nothing comes up, won't have to worry about LT tackling them and hurting their GUT.
Acanthosis Nigricans: what is it, associated with what?
1. epidermal hyperplasia with darkening of skin (velvet-like skin), often involves AXILLA OR GROIN
2. associated with insulin resistance or malignancy (GASTRIC CARCINOMA)
These BLACKS get DARKER and they have that PUBIC HAIR. They need to stop eating WATERMELON and try not eating too much CHICKEN.
BCC: what is it, risk factors, presentation, histo, treatment
1. Malignant prolif of basal cells of epidermis (MOST COMMON CUTANEOUS MALIGNANCY)
2. UVB-induced DNA damage and prolonged exposure to sunlight, albinism, xeroderma pigmentosum
3. elevated nodule with central ulcerated crater surrounded by dilated (telangiectatic) vessels: 'pink, pearl-like papule'; look at the UPPER LIP
4. Nodules of basal cells with peripheral palisading
5. Surgical excision (metastasis RARE)
PPP; Also the PP, or peripheral palisades
Squamous Cell Carcinoma: what is it, risk factors, presentation, treatment, precurosr, developed version
1. malignant prolif of squamous cells with formation of KERATIN PEARLS
2. risk factors: UVB-induced DNA damage and prolonged exposure to sunlight, albinism, and xeroderma pigmentosum, along with immunosuppressive therapy, aresenic exposure, chronic inflammation (scar from burn)
3. ulcerated nodular mass, usually on FACE (lower lip)
4. excision (metastasis uncommon)
5. actinic keratosis a precursor of SCC: hyperkeratotic, scaly plaque, often on the face, back, or neck
6. Keratoacanthoma: well-differentiated SCC that develops rapidly and regresses spontaneously (cup-shaped tumor filled with keratin debris)
Forensic Files: in Texas a lady who was getting poisoned was IMMUNE to CHRONIC ARSENIC. She had some mass on her lower lip. AK-47's are given to kids, who join the Shooting Company Core, to make them Killers who drink their dead enemies blood out of CUPS.
What are melanocytes? Where do you get them from, and what are some other things about them?
Responsible for skin pigmentation and present in BASAL layer of epidermis;
derived from NEURAL CREST;
synthesize MELANIN in melanosomes using tyrosine as a precursor molecule;
pass MELANOSOMES to keratinocytes
localized loss of skin pigmentation due to AUTOIMMUNE destruction of MELANOCYTES
Albinism is what? What's it due to? What can it involve and what are you at risk for?
1. congenital lack of pigmentation
2. enzyme defect (usually tyrosinase) that impairs MELANIN production
3. Could involve eyes (ocular) or both eyes and skin (oculocutaneous)
4. Increased risk of squamous cell carcinoma, basal cell carcinoma, and melanoma due to reduced protection against UVB
An albino kid has those red eyes and they can be really pale!!! No melanin, mo problems (BCC, SCC, melanoma)
Freckle (Ephelis) is
a small, tan to brown macule that darkens when exposed to sunlight (increased number of melanosomes!!);
Jews = Melanosomes increase
a mask-like hyperpigmentation of the cheeks associated with PREGNANCY and ORAL CONTRACEPTIVES
Melissa has such colorful, rosy CHEEKS. Must be the BABY, but I thought she was on OC's?
Nevus is what? What's present at birth? What comes later? How is it characterized? What can arise?
1. Benign neoplasm of melanocytes
2. Congenital nevus present at birth (often associated with hair)
3. Acquired nevus comes later in life (have nests of melanocytes at dermal-epidermal junction, a junctional nevus, the MOST COMMON MOLE IN CHILDREN; grows by extension into dermis, a compound nevus; junctional component is eventually lost resulting in an intradermal nevus, most common mole in ADULTS;
4. flat macule or raised papule with symmetry, sharp borders, evenly distributed color, small diameter
5. dysplasia may arise (dysplastic nevus), a precursor to melanoma
My friend with the HAIRY mole owns a junkyard. Indeed, Junk Can Interest Delinquents (Dysplasia)
Melanoma: what is it, risk factors, ABCD, ____ growth phases, variants?
1. malignant neoplasm of melanocytes (most common cause of death from skin cancer)
2. UVB-induced DNA damage; additional risk factor is dysplastic nevus syndrome (autosomal dominant: dysplastic nevi formation that may progress to melanoma)
3. Asymmetry, Borders are irregular, Color is not uniform, Diameter > 6 mm
4. radial growth (horizontally along epidermis and superficial dermis, low risk of metastasis), THEN vertical growth into deep dermis (DEPTH OF EXTENSION, or Breslow thickness, is most important prognostic factor predicting metastases
5. Variants: superficial spreading (most common subtype; dominant early radial growth results in good prognosis), lentigo maligna melanoma (lentiginous proliferation or radial growth; good prognosis), nodular (early vertical growth, poor prognosis), acral lentiginous (on PALMS or SOLES, often in dark-skinned individuals, NOT UV light exposure related!!)
SAX, but also a DNS (AD); football: if you get too FAT, can still play football; if you get too TALL, you're in trouble for playing
Impetigo: what is it, who does it affect, presentation?
1. superficial bacterial skin infection (most often due to S aureus or S pyogenes)
2. commonly children
3. erythematous macules that progress to pustules, usually on FACE; rupture of pustules results in erosions and dry, crusted, honey-colored serum!!
Cellulitis: what is it, presentation, risk factors, and course of disease?
1. deeper (dermal and subcutaneous) infection, usually due to S aureus or S pyogenes
2. presents as red, tender, swollen rash with FEVER
3. recent surgery, trauma, insect bite
4. could progress to necrotizing fasccitis with necrosis of subcutaneous tissue due to anaerobic 'flesh-eating' bacteria infection (SURGICAL EMERGENCY and production of CO2 leads to crepitus)
Staph scalded skin syndrome: what is it and what's it due to? Histology?
1. sloughing of skin with erythematous rash and fever; leads to significant skin loss
2. S aureus infection (exfoliative A and B toxins result in epidermolysis of the stratum granulosum
3. Distinguish from toxic epidermal necrolysis by level of skin separation; separation in TEN occurs at the dermal-epidermal junction
Verruca: what is it, what's it due to, presentation?
1. flesh-colored papules with a rough surface
2. HPV infection of keratinocytes, characterized by koilocytic change
3. Hands and feet common
Molluscum contagiosum: what are they and when do they emerge?
1. Firm, pink, umbilicated papules due to poxvirus; affected keratinocytes show CYTOPLASMIC INCLUSIONS (molluscum bodies)
2. most often arise in children (can occur in sexually active adults and immunocompromised individuals)
What contributes to development of dysplastic nevi?
RAS, BRAF activation, maybe increased CDK4 activity (not inhibited by p16/INK4a
Seborrheic Keratoses have activating mutation in
Fibroepi polyp buzz words?
Flesh-colored, bag-like tumors; fibrovascular cores covered by benign squamous epithelium; think obesity, diabetes, intestinal polyposis
Actinic keratosis: buzzwords
cutaneous horn; sandpaper-like consistency; actinic cheilitis; elastosis (thickened, blue-gray elastic fibers); parakeratosis)
In NBCCS (basal cell carcinoma) there loss of ____ function leads to SMO and GLI1 constitutive activation
PTCH (regulates the SHH pathway)
Most common form of fibrous histiocytoma is ____ with what appearance? Characterized by what?
firm, tan to brown papules; dematofibroma;
overlying epidermal hyperplasia, characterized by downward elongation of hyperpigmented rete ridges (pseudoepitheliomatous hyperplasia)
Dermatofibrosarcoma protuberans: hallmark is what and what's the appearance?
Translocation with genes encoding collagen 1A1 (COL1A1) and PDGFbeta; fibroblasts radially arranged (storiform) and a honeycomb pattern (dermis into subcutaneous fat)
Mastocytosis: encompasses a spectrum of rare disorders characterized by
increased numbers of mast cells in the skin (urticaria pigmentosa); look for effects of histamine, heparin, and other substances released when mast cells degranulate;
urticaria pigmentosa (oval, red-brown, nonscaling papules and small plaques)
Ichthyosis: key feature
variations in thickness of epidermis and the stratum granulosom!!!
Urticaria usually released as a result of...
exposure to pollens, foods, drugs (mast cell, IgE) and is type I; opiates, curare, antibiotics (mast cell, not IgE); not mast cell, not IgE (e.g. hereditary angioneutoric edema)
Acute eczematous dermatitis synonymous with
Epidermolysis bullosa is a
proclivity to form blisters at sites of pressure, rubbing, or trauma, at or soon after birth; have simplex type (mutations in keratin 14 or 5), junctional type (defects in subunits of laminin or maybe BPAG2), scarring dystrophic types (type VII collagen mutation)
Erythema Nodosum presents as; what can cause it; what is seen histologically?
erythematous plaques and nodules on the lower legs that is an inflammatory reaction, maybe type IV hypersens; think infections like beta-hemo strep, TB, drugs like sulfa or OCs, or IBD and neoplasms; shows edema, fibrin exudate, neutrophilic infiltration, then lymphocytes, histiocytes, giant cells, eosinophils