Skin

Question 1

4 layers of the epidermis and associated cell type

Answer 1

Stratum Basalis - regenerative/stem cell layer. Lies on basement membrane
Stratum spinosum - Desmosomes between keratinocytes gives histological “spines” connecting cells
Stratum Granulosum - granules in keratinocytes
Stratum corneum - Keratin in anucleate cell

Question 2

Atopic (Eczematous) Dermatitis

Answer 2

Pruritic, erthematous, oozing rash with vessicles and edema. Usually affects face and flexor surfaces. Is a type I hypersensitivity reaction associated with asthma and allergic rhinitis.

Question 3

Contact Dermatitis

Answer 3

Pruritic, erthematous, oozing rash with vessicles and edema arises with exposure to allergens. Type IV hypersensitivity. Remove agent and give topical glucorticoids. Examples include poison ivy, detergents, drugs like penicilin, or nickel (aka person has new watch or bracelet)

Question 4

Acne Vulgaris

Answer 4

Comedones (white/black heads), pustules (pimples), and nodules (scarred pimples). Results from chronic inflmation of hair follicles and their associated sebaceous glands. At puberty have increase in hormones and sebaceous glands produce excess sebum and get increased keratin. Keratin blocks duct and get build of sebum. Propionibacterium acnes infects follicles and produces lipases that break down sebum and release proinflammatory fatty acids and get pustule. Treat with antimicrobial (benzoyl peroxide) and vitamin a derivatives that will reduce keratin

Question 5

Psoriasis Clinical and History

Answer 5

Well circumscribed, salmon colored plaqueswith silvery scales usually on extensor surfaces and scalp. Pitting of nails also present. Due to excess keratinocyte proliferation.
Auspitz Sign = pinpoint bleeding when remove silver scale due to thinning of the dermis above elongate papillae.
Possibly autoimmune etiology (HLA-C) or trauma.
Treat with PUVA = Psoralem with UV light type A. Also use corticosteroids/immunemodulating therapy

Question 6

Psoriasis Histology

Answer 6

Acanthosis (epidermal hyperplasia)
Parakeratosis (hyperkeratosis with retention of keratinocyte nuclei in the stratum corneum)
Collections of neutrophils in the stratum corneum (munro microabscesses)
Thinning of epidermis above elongated dermal papillae.

Question 7

Lichen Planus

Answer 7

Pruritic, Planar, polgygonal, purple papulesoften with reticular white lines on their surface (Wickham Striae). Usually involves wrists, elbows, and oral mucosa. Saw tooth appearance of dermal-epidermal junction. Unknown etiology but associated with chronic hep C infection.

Question 8

Wickham Striae

Answer 8

reticular white lines on the surface of papule. Often sign of lichen planus

Question 9

Auspitz sign

Answer 9

pinpoint bleeding when remove silver scale due to thinning of the dermis above elongate papillae. Sign of psoriasis`

Question 10

Pemphigus vulgaris

Answer 10

Autoimmune destruction of desmosomes between keritinocytes due to IgG antibody against desmoglein (type II hypersensitivity).
Presents as skin and ORAL mucosa bullae. Acantholysis (separation) of stratum spinosum keratinocytes results in suprabasal blisters with thin walls that rupture easily (nokolsky sign).
Get tombstone appearance since basal cells stick to basement membrane.
Immunoflourescence highlights IgG surrounding keratinocytes in fish net pattern.

Question 11

Nikolsky sign

Answer 11

Thin walled bullae that rupture easily leading to shallow crusted erosions. Indicative of pemphigus vulgaris (IgG HSII attacks desmosomes)

Question 12

Bullous Pemphigod

Answer 12

Autoimmune (IgG antibody) destruction of hemidesmosomes (BP180 component) between basal cells and underlying basement membrane. Get subepidermal blisters of the skin. Bullae are tense and do not rupture easily. Immunoflourescence highlight IgG along basement (linear pattern).
DOES NOT INCLUDE ORAL MUCOSA

Question 13

Dermatitis Herpetiforms

Answer 13

autoimmune deposition of IgA at tips of dermal papillae presents as pruritic vessicles and bullae grouped (hepres like lesion). Strong association with celiac disease since IgA attacks gluten, so resolves with gluten free diet.

Question 14

Erythema Multiforme

Answer 14

Hypersensitivity reaction characterized by targetoid rash and bullae.
Seen most commonly with HSV infection but also mycoplasma infection, drugs (penicilin and sulfonamides), autoimmune (SLE) and malignancy.
If it includes oral mucosa and fever termed Stevens Johnson Syndrome.

Question 15

Stevens Johnson Syndrome

Answer 15

Erythema Multiforme (EM) with oral/lip involvement and fever. Toxic epidermal necrolysis is severe form with diffuse skin sloughing, resembling large burn (usually due to adverse drug reaction)

Question 16

Toxic Epidermal Necrolysis

Answer 16

severe form of Stevens Johnson Syndrome (erythema multiforme w/ lip/oral) with diffuse skin sloughing, resembling large burn (usually due to adverse drug reaction)

Question 17

Seborrheic Keratosis

Answer 17

Benign squamous proliferation seen in elderly. Raised, discolored, waxy, “stuck on” plaque.
Keratin Pseudocytes on histology
Sudden onset of many suggests carcinoma of GI tract and is called Lesser Trelat sign

Question 18

Lesser Trelat Sign

Answer 18

Sudden onset of multiple seborrheic keratosis. Suggests underlying GI carcinoma

Question 19

Acanthosis Nigrans

Answer 19

Epidermal Hyperplase with darkening of the skin. Often involves the axilla or groin. Assoicated with insulin resistance or gastric carcinoma

Question 20

Basal Cell Carcinoma

Answer 20

Upper Lip!!!!
malignant proliferation of basal cells of epidermis. Risk factors include UVBinduced dna damage (increased pyrimidine dimers), albinism, and xeroderma pigmentosum.
Presents as elevated nodule with central ulcerated crater surrounded by telangiectatic vessels.
“Pink pearl like”
Histology shows nodules of basal cells with peripgeral palisading.
Rarely mets. Surgical removal

Question 21

Squamous cell carcinoma

Answer 21

Lower Lip!!!!
Malignant proliferation of squamous cells with keratin pearls.
Risk factors include UVBinduced dna damage (increased pyrimidine dimers), albinism, and xeroderma pigmentosum. Additional risk factors include immunosupressive therapy, arsenic exposure, and chronic inflammation.
Presents as ulcerated, nodular mass
Rarely mets and do surgical removal
Actinic keratosis is a precursor lession (hyperkeratotic, scaly plaque)

Question 22

Actinic Keratosis

Answer 22

precursor lesion of squamous cell carcinoma. Hyperkeratotic, scaly plaque.

Question 23

Keratoacanthoma

Answer 23

Well differentiated squamous cell carcinoma that develops rapidly and regresses spontaneously. Cup shaped tumor filled with keratin debris

Question 24

Melanocytes

Answer 24

Derived from neural crest cells. Synthesize melanin in melanosomes using tyrosine as a precursor and are responsible for pigment.

Question 25

Vitiligo

Answer 25

Autimmune destruction of melanocytes leads to localized loss of skin pigmentation (easy in colored people but notice when light skinned people tan)

Question 26

Albinism

Answer 26

Congenital enxyme defect (tyrosinase) impairs melanin prduction. Increased risk for squamous cell carcinoma, basal cell carcinoma, and melanoma. Can be just eyes or eyes and skin

Question 27

Freckle (ephelis)

Answer 27

Small brown macule that darkens with sun due to increased melanosomes (not increased melanocytes)

Question 28

Melasma

Answer 28

Mask like hyperpigmentation of cheeks seen in pregnancy or oral contraceptives

Question 29

Nevus (mole)

Answer 29

Bengin neoplasm of melanocytes. Often assoicated with hair. If it becomes dysplastic then it is a precursor lesion to melanoma

Question 30

Melanoma and its 4 variants

Answer 30

Melignant neoplasm of melanocytes that is very deadly.
Risk factors include UVAb, albinism, xeroderma pigmentosum, dysplastic nevus syndrome (autosomal dominant disorder with formation of dysplastic nevi that progress to melanoma)
Asymetry, Borders are irregular, Color is not uniform, Diamter>6mm.
Characterized by two growth phases. Radial and Vertical. Degree of vertical growth is most important prognostic factor
1) Superficial Spreading = dominant radial growth early. good prognosis
2)Lentigo Maligna Melanoma = radial growth. good prognosis
3) Nodular = early vertical growth. poor prognosis
4) Acral Lentiguous = arises on palms or soles. Often in dark skinned and not related to UV light exposure

Question 31

dysplastic nevus syndrome

Answer 31

autosomal dominant disorder with formation of dysplastic nevi that progress to melanoma

Question 32

Impetigo

Answer 32

Superficial bacterial skin infection (Staph aureus or pyogenes). Erythematous macules that progress to pustules.
Get dry, crusted, honey colored serum

Question 33

Cellulitis

Answer 33

Dermal and subcutaneous infection usually due to staph aureus or pyogenes. Red, tender, swollen, rash with fever.
Risk factors include trauma, surgery, or insect bite

Question 34

Necrotizing Fasciitis

Answer 34

Necrosis of subcutaneous tissue due to infection with anaerobic “flesh eating” bacteria. Production of CO2 causes crepitis and is a surgical emergency

Question 35

Staphylococcal Scalded Skin Syndrome

Answer 35

Sloughing of skin with erythematous rash and fever due to Stap aureus infection. Exfoliative A and B toxins result in epidermolysis of stratum granulosum (as compared to toxic epidermal necrolysis that occurs at dermal-epidermal junction)

Question 36

Verruca (wart)

Answer 36

Flesh colored papules with rough surface. Caused by HPV infection of keratinocytes. Get koilocytic change.

Question 37

Molluscum Contagiosum

Answer 37

Firm, pink, umbilicated papules due to poxvirus. Affected Keratinocytes show cytoplasmic inclusions.
Most common in children, sexually active adults, and immunocompromised.