Derm I-III & Clinical Derm Flashcards

Question

Acanthosis Nigricans-General

Answer 1

* may look similar to a seborrheic keratosis but lacks acanthosis and horn cyst. * Seen in **all ages,** can be associated with insulin resistance and malignancy. * Clinically presents as a **velvety plaque** most common on the **back of the neck or axilla.**

Answer 2

* gross: **Velvety**, papillomatous, hyperpigmented plaques, commonly found in the creases of the **axilla and neck** * Histo: \*\***papillomatosis**, hyperkeratosis, basal layer hyper-pigmentation (can also have that with SK from the melanin)

Answer 3

* SK: * middle age and up * roundish, flat or coin-like waxy plaques with velvety surface * acanthotic hyperkeratosis, horn cysts, *increased melanin* * Leser-Trelat sign=parananoplastic syndrome * sudden onset of SK, may have malignancy * ANig: * **benign** type=childhood * obesity/endocrine * hereditary * **malignant** type=middle age and up * can have other internal malignancies and secondarily get these velvety patches * epidermal papillomatosis, *increased melanin*

Answer 4

* benign polypoid growths most common at *sites of rubbing/friction*. * composed of an outgrowth of fibroblasts and collagen with vessels covered with normal or acanthotic epidermis

Answer 5

* Histo: more adipose tissue and vessels creating polyp-loose stroma * papillomatosis (skin surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae)-may or may not

Answer 6

* Not epidermal neoplasms at all but categorized here because of the misnomer in their name. * Actually are follicular cysts composed of the **infundibular portion of the hair follicle** (similar to nml epidermis with the exception of a loss of rete pegs). * Makes keratin (like epidermis) and thus appears as a keratin filled cystic structure lined by epidermis. * Most do not communicate with the epidermis and are therefore dermal based nodules.

Answer 7

1. Actinic keratosis (AK)-pre 2. Squamous cell carcinoma (SCC)-mal 3. basal cell carcinoma (BCC)-mal

Answer 8

* earliest identifiable lesion that can *eventually develop into an invasive squamous cell carcinoma (SCC)*. * lesions diagnosed in 14% of all visits to dermatologists, following only acne and dermatitis in frequency. * increasingly common with age * typically produced by UV radiation, but ionizing radiation, arsenic, or polycyclic hydrocarbon exposure may also cause them. * PE: the typical AK is a poorly-demarcated, **scaly slightly erythematous patch** found on **sun-exposed/damaged skin areas**: * face, balding scalp, posterior neck, and dorsal upper extremity. * feel rough or "gritty", may be difficult to see.

Answer 9

* tx with **cryotherapy or topical chemotherapeutic** to prevent progression to SCC

Answer 10

* T-cell lymphocytes ae the inflamm cells of the skin, look very blue * acute condition-lots of T-lymphocytes * can get neutrophils with ulcerations or cuts * Gross: ill-define scaly erythematous macules * Histo: some blebbing * **\*\*solar elastosis\*\***--due to sun damage * **basal layer atypia** with overlying **parakeratosis alternating with orthoparakeratosis** (=Hyperkeratosis of anuclear keratinocytes within the stratum corneum); (flag=another soft sign) * melanin sits in basal layer and acts as sunshade, protects lower levels from sun damage

Answer 11

* **2nd most common cutaneous skin tumor** * SCC are generally erythematous, scaly papules or plaques with ill-defined borders, may be confused with large, hypertrophic AKs (differentiate with biopsy) * Microscopically, SCC: proliferation of pleomorphic keratinocytes confined to the epidermis (SCC in-situ) --or-- extending into the dermis (invasive SCC).

Answer 12

* **sun-exposed sites, older indivs; M\>F** * **\<5% metastasixe** * AK=precursor lesion of SCC. BUT, some SCCs develop de novo and do not form from a previous AK. * Keratinocytes with one **\*\*TP53\*\* mutation after UV radiation** may undergo apoptosis. * often seen at pyrimidine dimers (Xeroderma pigmentosum) * if keratinocytes with mutated p53 suffer a 2nd hit or mutation, become resistant to further apoptosis, undergo clonal expansion=AKs * Uncontrolled proliferation of these abnml keratinocytes leads to the development of **invasive SCC**. * Other causes: * activating mutations in HRAS * los of fxn mutations in Notch receptors * *immunosuppression*, specifically *HPV5 and 8* * *other: industrial, chronic wounds, burn scars, arsenic, ionizing radiation*

Answer 13

* SCCs usually present as firm, skin-colored to pink, papules or plaques, commonly found on head/neck region of elderly indivs. * Other locations: trunk, arms, dorsal hands and legs. * Hyperkeratosis, ulceration or crusting may be found on its surface. * sometimes verrucous papules and nodules * Symptoms: itching, pain and bleeding may be associated with the lesion.

Answer 14

* proliferation of (islands) atypical keratinocytes (squamous pinkish cells) that **extend from the epidermis invading into the dermis** with an **uneven base** * proliferation of cells can be seen as slender, long strands or as bulky masses. * Indiv cells have a glassy eosinophilic cytoplasm, with large nuclei. * Mitotic figures and **keratin pearls** (with retained nuclei) are also seen. * Various degrees of differentiation may be seen and is usually described as well-, moderately-, or poorly differentiated. * Increasing degrees of malignancy show: * less demarcation between the tumor masses and the stroma, * greater atypia, less keratinization, and loss of intercellular bridges. * Other histologic variants: acantholytic, adenosquamous, spindle-cell, verrucous, and desmoplastic SCC.

Answer 15

* Excision for low risk SCCs (\<2 cm diameter, well differentiated) * Mohs micrographic surgery * Radiation therapy (used in combo with other modalities for aggressive, recurrent, or large inoperable tumors) * Cryotherapy (for small, superficial, or low-risk lesions)

Answer 16

* **\*\*Full thickness atypia, basal layer sparing** (“eyeliner sign”), may show skip areas but involves follicles (in contrast to AKs) * **no invasion into the dermis** (in contrast to SCC). * Bowen’s Disease: ***atypia at all levels of the epidermis***. * Clinically a plaque-like lesion * needs to be excised! * BoweNOID Papulosis: similar histo as Bowen’s Disease. * *\*\*HPV-induced, located on the genitals* * *may spontaneously regress/progress* * Frequently multiple papules

Answer 17

* most common non-melanoma skin cancer (80%) * **most common invasive cancer in humans** * more common in men (2:1) * RF: * older indivs * UV sun exposure * fair skin * immunosuppressed * FHx of skin cancer, radiation therapy * genetic (DNA mismatch) syndromes * nevoid BCC syndrome, **xeroderma pigmentosa**

Answer 18

* Sun-exposed areas=most frequent location of BCCs * but it can be found in anywhere in the skin. * subtypes: nodular BCC and superficial BCC * **Gorlin syndrome (i.e. Nevoid Basal Cell Carcinoma syndrome)** is characterized by: * *multiple BCCs during childhood* (before 20yo) * odontogenic keratocysts (of the jaw and skeletal defects) * Tumors associated with this dz: medulloblastoma, ovarian fibromas

Answer 19

pearly, pink papule with overlying telangiectasia

Answer 20

* blue cells, with picket-peripheral palisading * retraction artifact-secondary to processing, seperate from surrounding dermis * nodular type: islands of basaloid cells in the dermis

Answer 21

* UVB damages the DNA, produces C-T transition mutations. * **p53 and \*\*\*PTCH (patch) genes** are the major targets of UVB for the development of BCC. * p53=tumor-suppressor gene * regulates cell cycle and apoptosis * mutated in 56% of human BCC. * **PTCH gene (chrom 9q22) regulates Hedgehog signal transduction pathway** * "2 hit" hypothesis * mutated in 30-40% of **sporadic *Nevoid BCC i.e Gorlin syndrome.*** * In 50% of BCCs isolated from xeroderma pigmentosa both p53 and PTCH genes are mutated. * UV radiation induces a state of relative immunosuppression (by altering antigen-presenting mechanisms and producing immunosuppressive cytokines) that ultimately compromises tumor rejection.

Answer 22

Answer: Age, gender, exposure to UVB rays, chronic cutaneous wound

Answer 23

Answer: Familial mutation in either PATCH (\*BCC) or TP53 (secondary mutation) genes

Answer 24

Answer: SCC is *directly associated* with **sun exposure**. Tx: **local excision**. **\<5% metastasize.**

Answer 25

1. Freckle (ephelis) 2. Lentigo 3. Melanocytic Nevi 4. Melanoma

Answer 26

* **Small, tan-red to light brown macules (flat lesions) on sun-exposed areas.** * **Most common lesion of childhood.** * Increased melanin pigment within basal keratinocytes * Melanocytes may be *enlarged* (hyperplasia) but *nml density*

Answer 27

* **small, oval tan-brown** * **mucous membranes in any age** * melanocytic hyperplasia along the basal layer

Answer 28

* **Nevi=NESTS of melanocytes** * **Tan to brown macules and papules.** * **Common type**: Junctional, compound and intradermal: nests of melanocytes * **"Dysplastic"** Nevi – single and cytologically atypical melanocytes, in addition to nests with architectural atypia. * dysplastic is controversial term because it implies gradation to malignancy * papules/macules tend to arise in adolescence; start in epidermis as junctional then melanocytes move down into the dermis * becomes more compound and intradermal with age

Answer 29

* **Most \>10 mm, changes in color, size, shape of previous lesion. Variations in color. ABCDEs.** * Nests and single malignant (tumor)melanocytes cells

Answer 30

* cant see on nml skin * clearish cells in basal layer with dark angulated nuclei; ratio 1:10 (melanocytes to basal layer keratinocytes) * melanocyte hyperplasia-lots of sun exposure will increase ratio * darker skin does NOT mean more melanocytes, means the ones you have are more ACTIVE, make more melanin * melanosome in the melanocyte passes the pigment to keratinocyte * pigment hats over nuclei in keratinocytes protect genetic material by blocking out UV radiation * Melanocytes are derived from neuroectoderm * fxn: produce melanin pigment with tyrosinase.

Answer 31

nests of melanocytes are confined to the dermis

Answer 32

* **will always have activity at the epidermis** * will have fiberplasia lines in pink stuff aroun melanocytes * enlarged melanocytes at the (basal layer of epidermis) dermal-epidermal junction (DEJ) **increased in numbers and bridging of melanocytes** * disordered histological architecture, typified by less circumscription of the nevus cell nests and extension of the junctional nests beyond the intradermal component. * nests that vary in size, shape, and spacing. * upper dermis usually shows fibrosis and contains a host response of lymphocytes.

Answer 33

* ***\*\*looks like melanoma but its not!*** * **1978 by Clark: usually greater than 5 mm, flat to slightly raised macules, sun-exposed and protected areas.** * **\*\*Architecturally atypical:** melanocytic nests may be larger and fused = **bridging** (ODD!), and junctional component extends past dermal components = shouldering. * Single melanocytes along DEJ * Cytologic atypia – enlarged, angulated nuclear contours, hyperchromasia * Vast majority of lesions are **clinically stable** thus best considered as a risk factor for melanoma. * **\*\*\*Dysplastic Nevus Syndrome** – (\<10% of pts) **tendency to develop multiple dysplastic nevi and melanoma.** * **50% have melanoma by 60yo** * ****(b/c melanomas come from melanocytes, so high density of the latter=anyone of them can turn on and go bad) * AD, **\*\*\*CDKN2A\*\*\*** gene on chromosome **9p21** (and CDK4 on chromosome 12q14)

Answer 34

* deadly skin cancer. * Early recognition and surgical excision is critical. * ABCDE * **A=Asymmetrical** * **B=Border**-irregular, notched, blurred, uneven * **C=Color**, uneven-shades of brown, tan, blk, red, white, blue * areas of **regression** may be noted * **D=Diameter**: melanomas **grow in dimater** and usually are larger in diameter than the size of a pencil eraser **(6mm) in 95% of cases** * **E=Evolving:** changes in size, shape, color, levation, or new symptoms: bleeding, pruritus, pain * **Prognostic factors:** * **\*\*\*\*depth (Breslow)\*\*\*\*** * ****measured by an ocular micrometer, from the top of the granular layer of the epidermis to the base of the neoplasm * **# of mitotic figures (thin melanomas)** * **ulceration.** * Sentinel lymph node biopsy: positive is poor **prognostic indicator**. * usually done at 0.8mm depth

Answer 35

* Radial (epidermis highly involved) growth phase: Lentigo maligna, superficial spreading, acral/ mucosa lentigenous * **Vertical growth phase**: Nodular or progression (entirely dermal, small epidermal) of radial growth phase melanoma implies **metastatic potential.** * **\*\*\*Depth of invasion: in mm\*\*\*** * Mitotic Counts: per mm2 * \*\* All types of melanoma can transition to a vertical growth phase over time (sans tx) hence early diagnosis and tx is key to increase disease free survival.

Answer 36

* **Malignant melanocytes** are invading into the dermis as a nodule of spindle cells. * Melanin pigment can be seen. * overlying epidermis has nests (full thickness) and single cells of melanocytes demonstrated upward spread (melanoma in situ) * pagitoid spread when going up through epidermis

Answer 37

Atypical (with no space between them) appearing melanocytes arranged in nests with many **mitotic figures** and dark red nucleoli.

Answer 38

* Predominate melanoma in situ in which malignant melanocytes are filling the epidermis and demonstrating upward “pagetoid” growth pattern. * \*upward spread of melanocytes * melanophages are NOT pigment cells

Answer 39

often produce pigments

Answer 40

* **2 most important predisposing factors: inherited genes (familial) and sun exposure** * Relationship to sun not straight forward * 10-15% of melanomas are familial * 40% CDKN2A mutations leads to loss of p16/INK4a * Sporadic forms (de novo) * Also p16, increases in RAS and PI-3K/AKT signaling, \*\*\***BRAF**\*\*\* **mutations (60%)**, CKIT (non-sun exposed) * \***\*\*BRAF V600E mutations tested for** * **tx with vemurfenib (ZELBORAF)[anti-BRAF]\*\*.**

Answer 41

* **Stage 0: MIS** (melanoma in situ) * **Stage I/II: Confined to skin with any depth** * 5 year survival 79% and 34% respectively * **Stage III: nodal involvement** * 5 year survival 30-70% * **Stage IV: Distant skin or visceral metastasis** * 5 year survival 9-19%

Answer 42

compound dysplastic nevus

Answer 43

2-for-1 special

Answer 44

* epithelium lined with granular layer * keratin debris

Answer 45

* cutaneous, on face * Multiple flesh colored papules * **\*\*\*PTEN Mutations = Cowden’s Syndrome, AD** * **Increase risk for breast**, endometrial, thyroid ca * follicular based from epidermis to the dermis

Answer 46

* Pink – brown papule or nodule most common on lower extremities * DF “dimple sign:” Compressing the skin around the DF causes the nodule to “dimple” inward * secondary to bug bite or trauma in the area

Answer 47

* Scattered boomer-rang shaped cells of varying degree of cellularity with infiltration of the surrounding collagen at the border "trapping" * Hyperpigmented basal layer that “tables” (flattened rete ridges)

Answer 48

* Scattered boomer-rang shaped cells of varying degree of cellularity with infiltration of the surrounding collagen at the border "trapping" * **Hyperpigmented (increased melanocytes) basal layer** that “tables” (elongated but flattened rete ridges)

Answer 49

* Scattered **boomer-rang shaped cells** of varying degree of cellularity with infiltration of the surrounding **collagen at the border "trapping"** * Hyperpigmented basal layer that “tables” (flattened rete ridges)

Answer 50

* most commonly seen on youngish patients on the trunk. * CP: papules or nodules (often muti-nodular) ; **large nodule with multiple rotuberance** * DFSP is an uncommon cutaneous soft tissue neoplasm characterized by a slow, infiltrative growth pattern. * considerable morbidity because of its aggressive local invasiveness. * goes deep into adipose tissue, need major sx/grafting * Histopathological features: * Monomorphic spindle cells arranged in a “storiform”(irregularly whorled pattern) or “cartwheel” pattern. * **dense proliferation** of spindle cells in dermis * **\*\*\*CD 34 positive**

Answer 51

* rxn (like dermatofibroma) to trauma, often ears * *large fat collagen bundles* * (Nodular fibroblastic proliferation and the presence of hypocellular, glassy, eosinophilic, hyalinized and disordered collagen fibers in dermis.)

Answer 52

* often benign, but can be malignant * Trichelemomma-follicular neoplasm * cylindroma-eccrine/apocrine neoplasm * sebaceous adenoma-sebaceous neoplasm

Answer 53

* adnexal tumor, from glands of skin (apocrine) * "turbin tumor" around head/forehead * basoloid islands in puzzle pieces * compare and ocntrast to BCC: * no retraction artifact * different clefting * pink cylinders here!!

Answer 54

* also an adnexal! * overgrowth of sebaceous gland * Clinical: papule or small nodule. Yellowish. May be part of Lynch Syndrome / Muir Torre syndrome (MLH1, MSH2, MSH6) especially if multiple or cystic lesions * most common-face; anywhere else-do Lynch workup

Answer 55

* individual lobules where \>50% of the lobule contains mature sebaceous cells. * On the rim there will be increase in thickness of the basal cells of the sebaceous glands

Answer 56

* looks like granulation tissue (hence the granuloma) * dermal proliferation of vessels * epidermal cuff surrounds dermal proliferation of vessels * lobular capillary proliferation * mixed inflammatory infiltrate * often ulcerated and crusted

Answer 57

* smooth muscle cells known for having **bubbles**, some **cigar cells**, if in a different plane * small **fascicles of bland**, eosinophilic spindle cells in mid dermis (resembles arrector pili - smooth muscle of hair erection)

Answer 58

* **Panniculitis** * Erythema Induratum / Polyarteritus nodosum * Eyrthema nodosum * Tumors * Lipoma * Leimyoma

Answer 59

* Rare, inflammatory dz (vasculitis) of small and medium sized muscular arteries * **Multiple organs**; also **cutaneous** only variant involving small-med art. of subcutis * Presents as **palpable purpura** in the skin +/- ulceration often **lower limbs** * Histopathology: **Inflammation of arteries** in the subcutis with fibrin deposition. * there is eventual spilling out of the inflamm

Answer 60

* more macules (not purpuric like PAN) * most common on front of legs * may be associated with **drugs (sulfa or NSAID or OCPs)** or **infections (TB)** or be idiopathic * septal fibrosis and inflammation-inflamm is in septa mostly, spills over a bit into lobules * also: Giant cells and histiocytes

Answer 61

* **Lichenoid dermatitis** * Lichen planus * Lupus erythematosis * Lichen sclerosis * Erythema multiforme * SJS/TENS spectrum * **Psoriasiform Dermatitis** * Psoriasis * Lichen Simplex Chronicus * **Spongiotic Dermatitis** * Acute eczematous dermatitis * **Neutrophilic / Vascular dermatitis** * Leukocytoclastic vasculitis * **Granulomatous Dermatitis** * Sarcoidosis * **Bullous Dermatitis** * Pemphigus Vulgaris and Foliaceus * Bullous Pemphigoid * Dermatitis Herpetiformis

Answer 62

* band-like infiltrative lymphocytes focally kissy epidermis * can cause basal vascular change-some edema in basal keratinocytes * WHO??..... * **Lichen Planus\*\*** * Erythema Multiforme * SJS/TENS * Lupus erythematosus * Acute lupus erythematosus * Subacute cutaneous lupus erythematosus * Discoid lupus erythematosus * Lichen Sclerosis et Atrophicus * Dermatomyositis

Answer 63

* commonly located on the forearms * **6 Ps = Pruritic, purple, polygonal, papules / plaques** * **Wickham striate** * **Oral involvement common** * Histopathology: lichenoid lymphocytic infiltrate with epidermal hyperplasia, wedge-shaped HYPERgranulosis, sawtoothing

Answer 64

* High power of lichenoid dermatitis showing **\*\*\*colloid bodies (CB)\*\*\*** and lymphocytic infiltrate surrounding rete ridges. * CB-died, leave apoptotic looking material * basal-vascular changes, keratinocytes surrounded by edema

Answer 65

* **Lichenoid dermatitis with necrotic keratinocytes (\*\*civatte bodies\*\*) prominent or confluent (full thickness)** * EM: self resolving caused by infections most common HSV * **SJS /TENs spectrum: drug induced, defined by mucosal involvement and \*\*\*body surface involvement\*\*\*** (percentage can change) with TEN designated at \>30%. * tx like they have severe burns * Histo: EM and early SJS/TENS spectrum the lichenoid infiltrate is usually more sparse than LP (lichen planus) and the **necrotic keratiocytes are plentiful and high in the epidermis**.

Answer 66

* EM=anular targeted rash * resolved spontaneously * associated with viruses * subepidermal blister, with necrotic keratinocytes at all levels of the epidermis. * Clinically is a targetoid lesion with a pale/dusky center

Answer 67

widespread sloughing and oral mucosal involvement

Answer 68

* Necrotic keratinocytes at all levels of epidermis = full thickness necrosis * can also see the dermal splits

Answer 69

* predominant cutaneous, pts dont necessarily have the serologic markers * 10% DLE will have crossover with SLE thus have usual serologic or theyll develop it later * Discoid LE (DLE): epidermal atrophy w/interface, superficial and deep perivascular & periadnexal infiltrate of lymphocytes with plasma cells * **Dermal mucin (highlight with Alcian blue or colloidal Fe), BM thickening** * Subacute cutaneous LE (SCLE) and systemic LE (SLE): similar to DLE, but milder infiltrate, more vacuolar change; apoptotic cells more prominent in SCLE * DIF: positive “lupus band test”, deposition of IgG, IgA, IgM, ± C3 along basement membrane * lesions can be localized or general

Answer 70

use PAS stain to look at thickened membrane

Answer 71

* Histologic findings similar to LE, but often milder with epidermal atrophy and less inflam infiltrates, no deep or periadnexal infiltrates, less mucin * clearing of cells on basal layer, few deep * CP: (doc in PCM) * **proximal symmetrical muscle weakness** * periorbital edema with heliotrope discoloration * Gottron’s papules/Gottron’s sign on the distal fingertips * periungal telangiectasia * **cuticular dystrophy**. * **Violaceous erythema in shawl** or photodistribution hyperkeratosis/scale over palms and soles * **psoriasiform scalp dermatitis**. * diagnose clinically with: * elevated muscle enzymes * muscle biopsy with evidence of inflammation or perifascicular atrophy * thorough H&P

Answer 72

* Atrophy and papillary dermal edema with collagen sclerosis, follicular plugging * CP: whitish macule described "cigarette paper lesion" most common on the genitalia. * Histo: first presents as a lichenoid dermatitis. The lichenoid infiltrate gets "pushed down" leaving pink hyalized collagen material behind in its place * more cncern in older pts

Answer 73

* epidermal acanthosis, thickened throughout * inflammatory disorder of the skin-activated T-lymphocytes release cytokines, leading to proliferation of keratinocytes * **1-2% of people in United States affected (onset: 30s)** * **Associated with arthritis, myopathy, enteropathy, spondylitic joint disease, acquired immunodeficiency** * **Genetic and environmental factors**: * 2/3 affected have **\*\*HLA-C\*\*** ; but only 10% of HLA-C people have psoriasis * **\*\*\*CD4+ and CD8+ sensitized cells accumulate in epidermis,** antigen still unknown. * **\*\*\*Well demarcated plaques with adherent silvery white scales\*\*\*** * Elbows, knees, scalp, lumbosacral, intergluteal cleft and glans penis. * **30% have nail changes** * Yellow-brown discoloration with pitting * Onycholysis

Answer 74

* Psoriasiform hyperplasia with **parakeratotic “wafer-like” scale containing neutrophils.** * Munroe microabscesses = stratum corneum * Spongiform pustules = intraepidermal * **Thinning of the suprapapillary plates with dilated papillary blood vessels**. * **\*\*\*Auspitz sign\*\*\*-little pinpoints of bleeding upon scale removal** * **Frequent loss of the granular layer** and increased epidermal mitotic figures * eccythosis vulgaris also has this loss of granular layer-AD, acquired form

Answer 75

* general category of dermatitis including allergic contact and atopic dermatitis (eczema) * Histo for all: edema between keratinocytes, creating vesicle formation or space out keratinocytes * some superficial inflammation infiltrates as well as eosinophils

Answer 76

* Inflammatory disorder initiated by contact with an allergen to which a person has been *previously sensitized* * Gross: Erythematous papules, small vesicles, or weeping plaques, which are usually pruritic * **\*glove-like** (or shoe-like) distribution * Usually occurs 12-48 hrs after exposure to allergen (delayed, cell-mediated, Type IV hypersensitivity reaction) * Many plants are causes of allergic contact dermatitis: poison ivy!

Answer 77

* Vesicles or bullae at **any level of epidermis** * Diagnosis depends on assessment of three features: * Anatomic level of Split * could be subcorneal, intraepidermal, or subepidermal * Underlying mechanism responsible for split * Nature of inflammatory infiltrate * **Direct immunofluorescence (DIF)** * Demonstrates presence of autoantibodies in the epidermis of patient skin biopsy * IgG, IgA, IgM, C3 most commonly used

Answer 78

* Older indivs have **tense bullae** * location: Inner aspects of thighs, flexor surfaces of forearms, axillae, groin, and lower abdomen * **\*\*Subepidermal blister/seperation with eosinophils.\*\* (middle pic)** * ****presents in a linear fashion * IgG **Ab to hemidesmonsomes** where bullous pemphigoid antigen resides. The two Ag: * BPAG1: 230-kD * (pathogenic Ag) BPAG2: 180-kD = collagen XVIII

Answer 79

* Most common type of pemphigus * CP: Superficial vesicles and thin-walled **bullae that rupture easily**, leaving shallow, crusted erosions * Histopath: (suprabasilar) acantholysis results in **suprabasalar clefting = tombstoning**. * Dissolution due to IgG antibodies against desmogleins * Net-like IgG and C3 on direct immunofluorescence. * due to the positioning of desmosomes between keratinocytes

Answer 80

* most commonly found on forearm, very itchy * Pruritic papules / vesicles on erythematous base * **Assoc w/ celiac disease** * Ab to gliadin * ****both the vesicular dermatitis and the enteropathy respond to a **gluten-free diet** * **Granular IgA deposits in dermal papillae on direct immunofluorescence**.

Answer 81

* prototype=sarcoidosis (affects lungs); presence of chronic granulomatous inflamm within the skin

Answer 82

* **naked, non-caseating granulomas** (sparse lymphocytic infiltrate) located through the dermis. * diagnosis of exclusion and must rule out infectious causes.

Answer 83

* action around the vessels * Histo: acute vasculitis-neutrophils in the wall of the vessels * also see extravasation of fibrin on H&E

Answer 84

* purpura-red papules, mixed infiltrate surrounds and damages vessel which will leave fibrin band behind and RBC will come out (extravasated from vessels)

Answer 85

* CP: non-blanchable macules * Accompanied by arthritis, abdominal pain, and/or hematuria * Preceded by URI, ingestion of certain foods/drugs * Anticardiolipin Ab and neutrophil cytoplasmic Ab of IgA class * **IgA deposition in vessel wall using DIF studies**

Answer 86

* neoplasm of helper T-cells (CD4+) that originate in the skin * most common: **Mycosis Fungoides (see gross)** * truncal plaques or nodules * psoriasis is on the differential

Answer 87

* Mild epidermal hyperplasia * Papillary dermis has a band-like mononuclear cell infiltrate composed of hyperchromatic cerebriform cells with hyperchromatic **cerebriform nuclei** (known as mycosis cells) * **Pautrier’s microabscesses** may be seen in the epidermis, which are just aggregations of atypical lymphocytes * Dense infiltrate of atypical lymphocytes that “line up” along DEJ=soldiers! * epidermatropism-when lymphocyte wants to be by epidermis * Pic: * Left=atypical lymphocyte soldiers along DEJ * middle=Pautrier's microabscess * right=cerebriform nuclei

Answer 88

* Verruca Vulgaris * Molluscum Contagiosum * HSV * Impetigo * Superficial Fungal (Dermatophytosis) * Scabies * Common Deep fungal infections (Blasto, crypto, histo)

Answer 89

* **HPV** driven, transmitted by contact, breaches skin barrier * **Verruca Vulgaris (warts)** – common type * hyperkeratotic dome shaped papules or nodules located most commonly on the hands * Verruca plana – face and dorsal hands * Verruca plantaris / palmaris * Condyloma acuminatum (genital and peri-anal) – HPV 6,11 * Histo: * hyperkeratosis * hypergranulosis * papillomatosis * koilocytes: vacuolated keratinocytes with raisin-like nuclei * Rete ridges often slope inward at borders of lesion (arborization)

Answer 90

* causes: poxvirus * location: breast and genitalia * RF: immunocompromised pts * Histo: Molluscum bodies (Henderson-Patterson bodies): keratinocytes contain very large intracytoplasmic inclusions that compress the nucleus and aside * crater-produced by epidermal hyperplasia

Answer 91

* **Herpes simplex virus (HSV) 1&2 and varicella zoster virus (VZV)** * Both part of **human herpes virus family**. * Both **dbl stranded DNA virus** with similar mechanisms for infection and ability to cause both primary and reactivated (latent) infection * Both cause a **vesicular viral exanthem** * Positive Tzanck or **direct fluorescence antibody (DFA)** (rapid) of the blister contents and positive by viral culture * Histo: * **3M’s** = molding, multinucleated, marginated chromatin seen in tissue or *Tzanck Smear*

Answer 92

* HSV1/ HSV 2: * First infection often asymptomatic * *Primary or latent infection* can present as *vesicle or erosions*. * Oral = more commonly HSV 1 * Genital = more commonly HSV 2 * **Primary VZV infection = chicken pox** * Vesicles on red base/papules/crusted erosions (**all stages present)** * Transmitted by respiratory secretions and cutaneous lesions (four days prior until all lesions crusted). Vaccination available * **Reactivation of infection = shingles** * Focal unilateral/**dermatomal** distribution unless disseminated. * Painful/pruritic vesicle most common on trunk * Increased in pts **\>50 or immunocompromised.**

Answer 93

* HZV involvement of the nose alerts the physician to the possibility of ocular involvement * can result in vision impairment if not treated promptly.

Answer 94

* Most common cause is **Staph aureus** but **group A beta hemolytic Streptococcus** is also common * Specifically exfoliative *toxins A and B* from Phage II Group 71 staphylococci attack epidermis resulting in subcorneal splitting. * Most common in **children** presents as **flaccid blisters that collapse** easy resulting in **honey colored crust** * Topical treatment * *Mupirocin* * Histo: Subcorneal blister with neutrophils and bacteria present * Microbio Correlation: Gram stain of the blister contents shows **gram positive cocci in clusters**.

Answer 95

* dermatophytes (fungus that live on keratin) * tinea versicolor * tinea nigra * candidiasis: intertrigo, thrush, paronychia

Answer 96

* superficial fungal infections caused by a dermatophyte-a species of fungi belonging to genera: *Microsporum, Trichophyton, and Epidermophyton=TINEA* * **dermatophytes digest and invade keratin and may infect skin, nails, hair, and general body surfaces * Seen as hyphae on KOH prep and in corneal layer using PAS stain of tissue. * Classified according to location of infection * tinea *pedis* * tinea *cruris*-genital region * tinea *corpora*-anular scaly plaque on skin * tinea *capitis*-head; cause of allopecia

Answer 97

* onychomycosis: dermatophyte infection of the **nail plate** * breakdown keratin and some of the squames * Left: **PAS stain**, Right: **KOH preparation**-if positive will demonstrate branching septate hyphae

Answer 98

* **Tinea versicolor** presents as macules and patches of *hypo/hyperpigmentation* on trunk. * **Hyphae and yeast** forms can be seen on H&E

Answer 99

* Location: hands or between digits * *Sarcoptes scabiei mite*; female 0.4 mm * leave scabetic poop behind, very contagious * RF: Overcrowding/poor hygiene/sexual contact * Papulovesicular, persistent nodules, and Norwegian (crusted) forms

Answer 100

* endemic in Chicago * Epidermal acanthosis, dermal necrosis and histiocytes. Broad based budding yeast forms present in tissue. * mixed inflammation with neutrophils, giant cells

Answer 101

* single, larger form filled with tiny yeast forms

Answer 102

* Large, intracellular or free yeast-like organisms, **mucin stains thick capsule** * stain with Mucicarmine-smaller than blasto

Answer 103

* Small intracytoplasmic organisms with surrounding clear halo, giant cells, PAS & GMS+ * mucicarmine negative (vs. crypto which is positive)

Answer 104

* Cutaneous and Skeletal Muscle Pathology * Cutaneous histology almost identical to acute lupus except frequently **more epidermal atrophy** * Myositis: perivascular mononuclear cell infiltrate , tubuloreticular inclusion in endothelial cells with myofiber damage in a paraseptal or perifascicular pattern. * Some pts have auto-Ab * against Mi-2 (nuclear helicase) most specific but low sensitivity * aminoacyl tRNA synthetase (ARS) assoc with lung dz-poor prognosis * *p155/p140 (assoc with increased risk of malignancy)*; paraneoplastic presentation * Elevated creatine kinase (CK)-muscle dz * 15-30% have pulm dz (most common besides muscle dz) * Adult and juvenile forms * **\*\*\*Adult form may be associated with _underlying cancer_**

Answer 105

* **Gottron’s Papules (left)** * Over knuckles * violaceous erythema +/- scale * **Heliotrope Rash (right)** * upper lid is common (sun protected site) * some puffiness and edema * violaceous (heliotrope is a **purple flower**) * more lavendar that typical rosatia

Answer 106

* holster sign * flagellate erythema * Gottron's papules on the knuckles * shawl sign * nailfold changes-thickening of cuticles

Answer 107

* **\*\*\*Malar “butterfly” rash\*\*\*** * Photosensitive—spares nasolabial folds * areas shielded from the sun * May be transient * will occur after sun exposure, last temporarily, then fade away with tx and time * \*\*\*Associated with systemic lupus (SLE) * positive serology (ANA, dsDNA, etc) * Lichenoid dermatitis marked by basal vaculolar change * Overlying parakeratosis/scale +/- follicular plugging * Increased dermal mucin

Answer 108

* sometimes more patchy * subacute * photosensitive * violaceous erythema

Answer 109

* \*\*Scarring depressed plaques (top left) * Head and neck, ears (**conchal bowls**\*) * Scarring alopecia * **Central hypopigmentation** * **Peripheral hyperpigmentation** * skin looks shiny-indicative of scarring * Perifollicular lichenoid dermatitis with vacuolar interface change * Mucin deposition (lots of involvement around hair follicles) * Thickened basement membrane. * Most pts do NOT have systemic lupus (serology negative)-esepcially if cutaneous, limited to head and neck * Positive direct immunofluorescence for IgG, IgM, C3

Answer 110

* Periungual erythema * Ragged cuticles * Capillary loop drop-out * \*\*\*Knuckles are classically spared (opposite of DM)-occurs between the joints

Answer 111

* Scleroderma * “Bound-down”-to deeper structures, cant pull it up * Sclerodactyly-distal to proximal (starts and hands and feet) * Decreased oral aperture-cant open mouth as wide * May affect other organ systems-mostly lung, heart, GI * **75% Female**

Answer 112

* **“CREST”** * **C**alcinosis cutis * **R**aynaud’s * **E**sophageal dysmotility * **S**clerodactyly * **T**elangiectasias (spot on ring finger) * **anti-centromere Ab** * More benign course than progressive systemic sclerosis

Answer 113

* hard, white-ish yellow-ish nodules-little rocks in the ermis, very difficult to tx

Answer 114

* **“Disease”stands alone** * 5-10% of healthy women * 90% idiopathic * 8:1 female:male * “**Phenomenon**” associated with **connective tissue disease** * ****\*\*extremely common in SLE pts; cardinal feature of scleroderma * Cold sensitivity * episodic **vasospasm** of small vessels with pain (due to ischemia) and **color change** * white, then becomes cyanotic/blue, then hyperemic/red * Tx with warming (especially core), avoid vasoconstrictors (worsened by beta-blockers)

Answer 115

* Often associated with localized scleroderma (morphea) * White atrophic plaques * bound-down plaques * hypopigmented * more proximal, rarely digits * Genital or extragenital * Sites of trauma * Ex: injury or radiation

Answer 116

* "great mimicker" * anular, pink-brown non-scaly, indurated plaque, expect nml epidermis * also: erythema nodosum, ill-defined nodules * Non-caseating granulomas * Often in scars/sites of trauma * Elevated ACE levels * May be systemic: * Pulmonary (90%) * Cardiac

Answer 117

* Associated with diabetes in 14-65% * **Pre-tibia most common** * **Atrophic yellow-pink plaques** with violaceous border * can see blood vessels underneath, very shiny

Answer 118

* auto-inflammatory (no infection) * extremely painful * Inflammatory ulcer with rolled, dusky violaceous border * Associated with: * inflammatory bowel disease (crohns, UC) * inflammatory arthritis * hematologic disorders (espeically on the hand) * \*\*\*Pathergy-minimal trauma (or local debriment) can induce or worsen dz

Answer 119

* Retiform “**stellate**” (jagged) purpura on fatty areas * stellate-affecting the vessels (medium-sized), see that pattern of its branching * Central black eschar * Path shows calcium in the vessels * Extremely painful due to ischemia * Patients with end stage renal disease and hemodialysis * *High mortality* * Tx: sodium thiosulfate

Answer 120

* **Vasculitis** * **Inflammatory** * Size of lesions gives a clue to size of involved vessels * Destruction of vessels

Answer 121

* extravasation of red cells into the skin * two types: * NON-blanching *palpable* purpura * macular *non-palpable* purpura

Answer 122

* Vasculopathy * Non-inflammatory * Size of lesions gives a clue to size of involved vessels * Thrombo-embolic * restiform/stellate form * (image is early calciphylaxis)

Answer 123

* very small vessels high up in the skin; palpable purpura * **Type III Hypersensitivity (immune complexes)** * Small purpuric papules * Predominantly lower legs * +/- pruritus * May ulcerate focally * 50% idiopathic * Triggers: * *Drugs*: * Antibiotics: esp beta-lactam * NSAIDS * Diurects * Any drug * *Infections* * URI, **esp strep** * Viral hepatitis * HIV * Bacterial endocarditis * *Foods*

Answer 124

* v. common; NOT an infection * nml white count, no fever * red brown plaques with edema swelling=shiny * hot, often non-tender

Answer 125

* skin stretched out, gets cracked, starts weeping * itching, not much pain

Answer 126

severe, chronic cases

Answer 127

* stellate white depressed papules, surrounding stasis dermatitis * common around ankles

Answer 128

* sequelae for untreated stasis * medial lower leg=most common spot * arterial ulcers are painful because of ischemia

Answer 129

* Vascular “birthmark” * Slow-flow * Grows in proportion to the child * May be associated with other syndromes

Answer 130

* Congenital vascular anomaly * 40% apparent at birth * Most common on the face * May flare in puberty * Diagnosis confirmed by ultrasound

Answer 131

* benign, dont scar, fade away * Erythematous blanching macules and papules coalescing * Most common in summer and fall

Answer 132

* Hand-foot-mouth disease * Vesicles on the palms and soles * football shaped, oval * Oral lesions * Buttocks may be involved * Fever and malaise prodrome (ahead of eruption) * Usually follows a benign course (approx 3 wks)

Answer 133

* \*\*Slapped cheeks * \*\*Followed by **reticulated eruption on extremities (erythema)** * Arthralgia in 10% (more common in adults than kids) * Winter and Spring * \*Fetal infection may cause anemia, fetal hydrops, or death * careful around pregnant women!! * May also cause acral purpura “gloves & socks”

Answer 134

* Erythema migrans * Annular erythema at site of tick bite * Occurs in 60-90% of patients with Lyme * Secondary lesions may occur * Borrelia burgdorferi * Tx: Doxycycline (adults) or Amoxicillin (kids)

Answer 135

* Pruritic edematous non-scaly plaques = “wheals” * Swelling due to plasma leakage * sometimes dermatographic-scratch the skin and it breaks into hives * Peau d’orange appearance * Transient (\<24h), often annular or round * Type 1 Hypersensitivity * Many causes: * Allergy * Autoimmunity * Drug * Infection * Dietary pseudoallergens * Idiopathic (50%) * Angioedema swelling is deeper in the dermis and subcutis or submucosal tissue * May affect mouth, bowel * Less red, more painful than itchy

Answer 136

* NOT the same thing are urticaria, path shows **MAST CELLS** * red-brown papules * lesions are NOT transient

Answer 137

* this is due to a drug allergy, it is NOT the zoster form * Look for “outside in” pattern * Common culprits: * Topical antibiotics * Topical cleansers-Chlorhexadine * Nickel * Plants (poison ivy)

Answer 138

* Numerous pink papules coalescing over torso and proximal extremities * DDx: “bug or drug” (looks like viral exanthem) * 3.6 per 1000 among hospitalized patients * Increased incidence associated with: * HIV * Connective tissue disease * Hepatitis * OK to tx through the eruption * Usually starts 7-10 days after initiation of the drug * May start even after discontinuation of the drug * Often starts in intertriginous and dependent areas * May become erythrodermic (entire skin is red) * No blisters * No mucous membrane involvement

Answer 139

* DRESS: * **D**rug * Common culprits: * Aromatic Anti-convulsants * Anticonvulsant Hypersensitivity Syndrome * Patients MUST avoid all aromatic anticonvulsants * Antibiotics (minocycline) * Sulfonamides (sulfasalazine) * Allopurinol * Antiretrovirals (abacavir) * **R**eaction (Rash) * **E**osinophilia * **S**ystemic * **S**ymptoms

Answer 140

* Fever * Rash: morbilliform, infiltrated, or exfoliative dermatitis * Facial swelling, lymphadenopathy * Hematologic abnormalities * eosinophilia * atypical lymphocytes * Visceral involvement * Liver, heart, kidney, lung * Delayed onset: Symptoms usually develop 2-6 weeks after initiation of the drug * Rare * Mortality may be as high as 10% (*liver failure*) * Must discontinue and avoid the offending drug

Answer 141

* Lesions appear 1-2 wks after exposure * With subsequent exposure, they appear within 24 hrs in the same “fixed” location * Dusky, may blister * Sulfa, NSAIDS, barbiturates, tetracyclines, carbamazepine * Superficial and deep perivascular inflammation with necrotic keratinocytes

Answer 142

* Targetoid lesions * **90% Infectious causes** (HSV, **mycoplasma**, etc) * **\<10% Drugs** (NSAIDS, sulfa, antiepileptics, antibiotics) * **Does not progress to TEN!** * *EM Minor*: targets, extremities, face, rare mucosal, no systemic sx. HSV and other infections * *EM Major*: targets + occasional bullae, extremities, face, severe mucosal invovlement, systemic sx. Mycoplasma, HSV, other infection, rarely drug

Answer 143

* Dusky macules +/- epidermal detachment * Macular atypical targets * \<10% detachment * Trunk, face * **Severe mucosal involvement (right)** * Systemic symptoms * May progress to TEN * **Drugs are usually causative**

Answer 144

* Epidermolytic lesions = Painful skin lesions * epidermis detached, underlying dusky erythema * Mucous membrane involvement * Blisters \<10% (SJS), 10-30% (overlap), \>30% (TEN) * Fever/malaise/systemic symptoms * Stinging eyes * Dysphagia * Usually \<8 weeks exposure to the drug * Average mortality 1-5% (SJS) to 25-35% (TEN)

Answer 145

* \>30% Epidermolytic lesions * Dusky erythema * Painful skin

Answer 146

* **\*\*Allopurinol (50%)** * Anti-convulsants * NSAIDS * Anti-retrovirals * Antibiotics * TMP-SMX (Bactrim) * Sulfonamides * Aminopenicillins * Cephalosporins * Quinolones * Chlormezanone

Answer 147

* **\*\*BROAD-SPECTRUM UVA/UVB** sunscreen * **physical** blockers: titanium dioxide, zinc oxide * **chemical** sunscreens: Parsol 1789, oxybenzone, Mexoryl, helioplex, antihelios * UV Radiation: UVA (tan) and UVB (burn) contribute to premature skin aging and skin cancer * necessary to block both!! * SPF: sunburn protection factor * measures only UVB protection * recommend SPF 30+ * 1 oz ("golf ball size") each application * apply every 1.5-2hr * water resistant=40 min * v. water resistant=80 min

Derm I-III & Clinical Derm Flashcards

(173 cards)