Week 3: Derm Flashcards

Question

3 layers of the skin

Answer 1

Epidermis, dermis, hypodermis

Answer 2

Temperature regulation, protection, fluid retention, sensation, secretion.

Answer 3

-The superficial or outer layer of the skin, very thin (0.12mm) but can thicken and form corns or calluses with constant pressure or friction -includes rete pegs that extend into the papillary layer -Contains 5 sub-layers

Answer 4

Rete pegs (also known as rete processes or rete ridges) are the epithelial extensions that project into the underlying connective tissue in both skin and mucous membranes.

Answer 5

Stratum corneum (outermost) Stratum lucidum Stratum granulosum Stratum spinosum Stratum basale (germinativum)

Answer 6

Keratinocytes, melanocytes & merkel cells (keratinocytes are dead/empty by the time they reach the stratum lucidum & corneum)

Answer 7

-Basal layer where keratinocytes divide and move up to replace surface cells -Melanocytes synthesize melanin (pigment) -Merkel cells associated with sensory nerve endings

Answer 8

Layer of new keratinocytes. Polygonal shaped, has spinous processes projecting between adjacent keratinocytes

Answer 9

due to keratohyalin

Answer 10

Clear (dead) layer of cells containing eleidinà they become keratin as the cells move up to the corneum layer

Answer 11

Tough, superficial outer layer covering body (dead keratinocytes)

Answer 12

the “true skin” -irregular connective tissue layer with rich blood, lymphatic, and nerve supply -contains sensory receptors and sweat glands (apocrine, eccrine, sebaceous)

Answer 13

Papillary layer and reticular layer

Answer 14

Macrophages Mast cells Histocytes

Answer 15

-superficial fascia of varying thickness that connects to overlying dermis and underlying muscle -contains: macrophages, fibroblasts, fat cells, nerves, blood vessels, lymphatics, hair follicle roots

Answer 16

can synthesize and reorganize ECM Secrete collagen protein

Answer 17

hard, dead keratin

Answer 18

Nail fold includes skin surrounding the lateral and proximal aspects of the nail plate. The proximal nail fold overlies the matrix; its keratin layer extends onto the proximal nail plate to form the cuticle

Answer 19

The lunula (white half moon), which is visible through the nail plate, is the distal aspect of the nail matrix

Answer 20

The nail bed extends from the distal nail matrix to the hyponychium Hyponychium = short segment of skin lacking nail cover; begin at distal nail bed & terminates at the distal groove; skin rich in WBCs, prevents bacteria & debris from getting under nail

Answer 21

Growth: it takes about 5.5 months for fingernail to grow from matrix to free edge (toe nails take 12-18 months to be replaced)

Answer 22

'The nail matrix is the area where your fingernails and toenails start to grow. The matrix creates new skin cells, which pushes out the old, dead skin cells to make your nails. As a result, injuries to the nail bed or disorders that affect the matrix can affect your nail growth. The matrix synthesizes 90% of the nail plate

Answer 23

The nail bed extends from the distal nail matrix to the hyponychium (under the nail plate) Nail bed consists of parallel longitudinal ridges with small blood vessels at their base.

Answer 24

Transverse depressions or ridges of all the nails that appear @ lunula base after stressful event has temporarily interrupted nail formation Lines progress distally with normal nail growth, eventually disappear @ free edge Causes: high fever, scarlet fever, hand-foot-and-mouth disease, chemo

Answer 25

Separation of nail from nail bed starting at distal end and slowly progressing proximally S&S – nonadherent part of nail is white, yellow or green-tinged Causes include nail trauma, repeated wet work, vigorous repeated manicuring (digging under nails), false nails allergy and psoriasis Screen pts with unexplained onycholysis for hyperthyroidism, asymptomatic thyroid disease and iron deficiency

Answer 26

Treatment – cut separated portion of the nail. Promotes dryness and discourages infection. Yeast can grow in space between the nail and nail bed. Treat with topical agents (fungoid tincture that contains miconazole). Consider oral flucanazole for resistant cases – 150 mg daily for 5-7 days

Answer 27

What is it? Acute or chronic infection of the cuticle. Where is it? One or more fingers or toes may be involved Greatest risk factor? Individuals whose hands are frequently exposed to moisture Most common cause? Staphylococci and streptococci

Answer 28

Acute is rapid, painful inflammation of the cuticle. Abscess may develop, requiring incision and drainage. Pus can develop and expressed from the proximal nail fold. Nail plate is not typically affected, but can become discolored with ridges Chronic develops slowly, tender + swelling around proximal or lateral nail folds

Answer 29

Topical application of thymol. Oral antifungals NOT effective because they do not penetrate affected tissues. Prevention is key by keeping hands dry

Answer 30

Results from increased lateral pressure either by poorly fitting shoes, excessive trimmer of lateral nail plate or trauma S&S: pain and swelling Dermis is penetrated by the nail/lateral nail fold, and broken skin becomes purulent and edematous as granulation tissue grows with the penetrating nail Treatment: removal of the penetrating nail with scissors/curetting granulation tissue and using silver nitrate sticks to treat small areas of granulation Could lead to cellulitis which may require PO antibiotics

Answer 31

Focal collections of mucin (macromolecules in mucus) that don't have a cystic lining Dome-shaped, pink-white, typically occur on the dorsal surface of the distal phalanx in middle-aged and elderly people Cysts on the proximal nail fold could cause a longitudinal nail groove as it compresses the nail matrix cells When incised, exudate is clear, viscous, jelly-like

Answer 32

Typically benign, no intervention if pain free and does not compromise any function If treatment is needed: cryosurgery of the base: Remove cyst roof w/ scissors, expel gelatinous exudate Freeze the base Treated site will be edematous and exudative, and a bulla will usually develop Healing takes 4-6 weeks, and retreatment is frequently needed

Answer 33

*Lesions that present at the onset of disease Macules, papules, patch, plaque, wheal, nodule, tumor, vesicles, bulla, pustules, cyst, telangiectasia

Answer 34

Fine (0.5–1.0 mm), irregular red lines produced by capillary dilation; can be associated with acne rosacea (face), venous hypertension (spider veins in legs), systemic sclerosis, or developmental abnormalities (port-wine birthmarks)

Answer 35

*Changes to skin overtime due to disease progression Scales, lichenification, keloid, scar, excoriation, fissures, erosion, ulcer, atrophy

Answer 36

Linear crack or break from the epidermis to the dermis; may be moist or dry e.g athlete’s foot, cracks at the corner of the mouth

Answer 37

Loss of part of the epidermis; depressed, moist, glistening; follows rupture of a vesicle or bulla or chemical injury

Answer 38

Elevated, irregular-shaped area of cutaneous edema; solid, transient; variable diameter eg Insect bites, urticaria, allergic reaction Another description: migratory, well-circumscribed, erythematous, pruritic plaques on the skin. may be accompanied by angioedema, which results from mast cell and basophil activation in the deeper dermis and subcutaneous tissues and manifests as edema of the face and lips, extremities, or genitals.

Answer 39

Irregular-shaped, elevated, progressively enlarging scar; grows beyond boundaries of wound; caused by excessive collagen formation during healing

Answer 40

Rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation; often involves flexor surface of extremity eg chronic dermatitis, eczema

Answer 41

Secondary lesion Heaped-up, keratinized cells; flaky skin; irregular shape; thick or thin; dry or oily; variation in size eg. Flaky skin post medication reaction.

Answer 42

include cysts, lipomas, and fibromas

Answer 43

dried exudate on skin surface (composed of blood/serum/pus or combo)--> I.e. scab.

Answer 44

Small, flesh-colored/white/or dark bumps that give skin rough texture. Clogged hair follicle with keratin+oil. Typical of acne.

Answer 45

tiny white bumps that are clogged eccrine sweat glands, keratin filled little cysts just under epidermis. Found in babies; in adults, typically around eyes/nose/groin. Harder texture than comedone.

Answer 46

Petechia - <2-3mm, Nonblanchable punctate foci of hemorrhage. Causes: Platelet abnormalities (eg, thrombocytopenia, platelet dysfunction), vasculitis, and Infections (meningococcemia, Rocky Mountain spotted fever, other rickettsioses) Purpura - 3-10mm larger area of hemorrhage that may be palpable. Causes: leukocytoclastic vasculitis, coagulopathy. Large areas of purpura may be called ecchymoses (>1cm) or, colloquially, bruises.

Answer 47

A thread-like linear or serpiginous (wavy, serpent-like) tunnel in the epidermis typically made by a parasite (such as scabietic mites)

Answer 48

thick and clotted, in more severe or advanced inflammation. Ex: lungs in pt w/pneumonia

Answer 49

large number of leukocytes as in persistent bacterial infection.

Answer 50

Induced by endogenous pyrogens (meaning the person infected produces them), specifically cytokines (.e.g IL-1, released from neutrophils and macrophages). Pathogens can also produce exogenous pyrogens (meaning they come from outside the body, from a pathogen) Beneficial effect: most microorganisms are highly sensitive to small increases in body temperature Harmful effect: may enhance the host’s susceptibility to the effects of endotoxins associated with Gram-negative bacterial infections

Answer 51

Fever Leukocytosis Increase levels of circulating plasma proteins

Answer 52

more immature WBC’s are present than normal.

Answer 53

Increased Fibrinogen (one acute-phase reactant) -> increased adhesion among erythrocytes -> increased sedimentation rate, so testing for increased sedimentation rate can show you that the acute inflammatory response is underway.

Answer 54

Liver increases production of specific plasma proteins, called acute-phase reactants Acute-phase reactants reach max circulating levels 10-40 hrs after inflammation start IL-1 & IL-6 work together to make these proteins Increased Fibrinogen (one acute-phase reactant) -> increased adhesion among erythrocytes -> increased sedimentation rate, so testing for increased sedimentation rate can show you that the acute inflammatory response is underway. (Left Shift)

Answer 55

TO BE ANSWERED ONCE IN ILO ANSWERS

Answer 56

1) Inflammation & Coagulation: first 24h 2) Proliferation & New tissue formation: 3-14 d 3) Remodeling & Maturation: weeks to months

Answer 57

1) Inflammation & Coagulation: first 24h Fibrin acts as scaffold for cells for healing Platelets: clot, release growth factors that initiate proliferation of undamaged cells Neutrophils: clear wound of debris, bacteria Macrophages (come after neutrophils): Clear debris, release wound healing mediators and growth factors (GF), recruit fibroblasts, promote angiogenesis

Answer 58

2) Proliferation & New tissue formation: 3-14 d Wound sealed, fibrin clot replaced with normal or scar tissue Macrophage invasion of dissolving clot Recruitment and proliferation of fibroblasts-->collagen synthesis; epithelialization, contraction, differentiation Granulation tissue grows into wound from surrounding CT: has invasive cells, new lymph/capillaries Epithelial cells migrate under clot or scab; contact similar cells from all sides of wound to heal it Epithelialization of skin can be quickened if wound kept moist—> prevents fibrin clot from becoming scab

Answer 59

Continued cell differentiation, scar formation, remodeling Fibroblast action mainly: deposition collagen Tissue regeneration and contraction continue Scar is avascular

Answer 60

Bacteria = prokaryotes Lack nucleus Lack membrane-bound organelles (eg mitochondria, ER, golgi complex) CELL WALL - One of the most important structures of a bacterial cell Functions: - Protect bacteria from bursting - Help maintain their shape - Control molecules going in & out of the cell.

Answer 61

Thickness of cell wall (gram stain) Shape of bacteria

Answer 62

Use GRAM STAINING to determine the THICKNESS of the cell wall to identify and categorize different types of bacteria. Bacteria are stained with a dye called crystal violet. A thick cell wall retains the violet colour. A thin cell wall does not. Note: It is the peptidoglycans within the cell walls that retain the dye. Gram Positive bacteria = THICK cell walls. When dyed, they appear blue or purple. Gram Negative bacteria = THIN cell walls. When dyed, they appear pink or red.

Answer 63

Cocci = round/spherical shape Bacilli = rod shape Spirilla = spiral shape

Answer 64

Thrives/grows in oxygenated environment Soil, water, different surfaces Derive their energy from aerobic respiration (oxidative phosphorylation, Kreb’s cycle) → produces more energy Examples: Lactobacillus Tuberculosis

Answer 65

Grows in the absence of oxygen → cannot survive in the presence of O2 Lives in O2 depleted areas (eg digestive tract) Derive their energy from anaerobic respiration and by lactic acid or alcoholic fermentation → produces less energy Examples: E. coli Clostridium

Answer 66

Diseases caused by fungi Can be superficial (on or near the skin or mucous membranes), deep or opportunistic

Answer 67

Fungi that invade the skin, hair, or nails The disease they produce are called tineas (ringworms) Ie. Tinea capitis (scalp), tinea pedis (feet), tinea cruris (groin) The pathological fungi cause disease by adapting to the host environment. The fungi colonizes the skin and digest keratin. Phagocytes and T cells are important in controlling fungi

Answer 68

Staphylococcal (skin), Cholera (mucuous membranes), Streptococcal pneumonia (extracellular), TB (intracellular)

Answer 69

Tinea pedis (skin), Candidiasis eg. Thrush (Mucous Membranes), Sporotrichosis (extracellular), Histoplasmosis (intracellular).

Answer 70

Candida albicans --> causes cutaneous candidiasis

Answer 71

Tinea pedis Tinea cruris (jock itch) Tinea corporis (ringworm)

Answer 72

Common facial eruption characterized by redness, telangiectasia, flushing, blushing (vascular component), papules and pustules

Answer 73

Usually > 30 yrs old Can occur in children Cause unknown - genetic factors (Celtic & northern European), UV exposure, microorganisms, skin sensitivity, and food triggers (spicy foods or ETOH)

Answer 74

- Papules & pustules over forehead, cheeks, nose & around eyes (rarely elsewhere) -Erythema and telangiectasias present - In extreme cases, also have oily skin & edema (cheeks and nose) - CHronic deep inflammation of nose leads to irreversible skin thickening (rhinophyma)

Answer 75

Ocular symptoms: mild conjunctivitis - Conjunctival hyperemai, telangiectasias on lid, and others... (long complicated names I won't remember!) Just remember ocular symptoms possible :)

Answer 76

exacerbated by ingestion of hot foods & drinks, ETOH (esp redwine), heat, sunlight, & topical meds such as antiwrinkle creams and chemical peels

Answer 77

Chronic (years) with episodes of activity followed by quiescence - may result in permanent swellling of periocular tissues and firm facial edema

Answer 78

-develops in sebaceous follicles (primarily on face & upper chest/back) -lesions are noninflammatory or inflammatory (cystic) 4 principal causative factors: 1) Hyperkeratinization of the follicular epithelium 2) Excessive sebum production 3) Follicular proliferation of anaerobic Propionibacterium acnes (P.acnes) 4) Inflammation and rupture of a follicle from accumulated debris and bacteria

Answer 79

Increased androgen production during puberty causes increased size and productivity of sebaceous glands, which promotes P. acnes P. acnes produces extracellular enzymes that convert triglycerides into free fatty acids (FFAs) FFAs activate T-cells and th17 cells which cause inflammation and edema that results in pus formation and breakdown of the follicle wall

Answer 80

-Occurs primarily between ages 12-25 -tends to occur in families (if both parents have acne, 75% change that a child will develop it) -incidence same for all genders, although severe disease more often in males -associated with diets high in simple carbohydrates and dairy products

Answer 81

-flare-ups may be seen during periods of stress, before menstrual periods, with certain medications (corticosteroids, lithium, anticonvulsants, antituberculosis medications, iodides) -redness and pigmentation after resolution may take many months to fade -usually lasts 5 to 10 years after onset in adolescence -adult women can have chronic low-grade acne that can be challenging to manage

Answer 82

Development of lesions in sebaceous follicles (primarily on face and upper chest/back) Noninflammatory: comedones are open (blackheads) or closed (whiteheads) with accumulated material that causes distension of the follicle and thinning of follicular canal walls Inflammatory: in closed comedones when the follicular wall ruptures and expels sebum into the surrounding dermis and initiates inflammation -pustules form when the inflammation is close to the surface -red papules & cystic nodules develop when inflammation is deeper, causing mild to severe scarring

Answer 83

Type IV, T-cell–mediated, delayed-type hypersensitivity reaction to an environmental allergen that has 2 phases:

Answer 84

Sensitization to an antigen: allergens (through complex pathway) causes T cells to differentiates into memory/effector T cells. - asymptomatic, may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids). During differentiation, sensitized T cells become able to express cutaneous homing antigens (eg, cutaneous lymphocyte antigens) that enable them to migrate from cutaneous capillaries to the epidermis. Allergic response after reexposure: When antigen-presenting cells present the antigen to the sensitized T cells, the T cells can expand and trigger an inflammatory reaction at that location (elicitation phase of ACD), resulting in the characteristic symptoms and signs of ACD.

Answer 85

- sensitization phase may be brief (6 to 10 days for strong sensitizers such as poison ivy) or prolonged (years for weak sensitizers such as sunscreens, fragrances, and glucocorticoids). - Typically takes ≥ 1 day after exposure to become noticeable and takes 2 to 3 days to become further aggravated (crescendo reaction)

Answer 86

- more pruritic than painful - Skin changes range from erythema, scaling, and edema, through vesiculation to severe swelling with bullae - pattern usually suggests a specific exposure, such as linear streaking on an arm or leg (eg, due to brushing against poison ivy) or circumferential erythema (under a wristwatch or waistband). The site of contact is where the allergen contacted the skin, very often the hands, because they touch so many substances. Although the palms and the palmar sides of the fingers are most exposed, ACD often starts in the web spaces between fingers because the thick stratum corneum prevents or delays allergen penetration on the palms and palmar sides of the fingers (also on the soles). - With airborne exposure (eg, perfume aerosols), areas not covered by clothing are predominantly affected. Although ACD is typically limited to the site of contact, it may later spread because of scratching.

Answer 87

ICD is a nonspecific inflammatory reaction to toxic substances contacting the skin. Numerous substances can irritate the skin, including Chemicals (eg, acids, alkalis, solvents, metal salts) Soaps (eg, abrasives, detergents) Plants (eg, poinsettias, peppers) Chronic moisture (eg, from body fluids, urine, and saliva) Properties of the irritant (eg, extreme pH, solubility in the lipid film on skin), environment (eg, low humidity, high temperature, high friction), and patient (eg, very young or old) influence the likelihood of developing ICD.

Answer 88

Acute ICD: Potent irritants, such as caustic chemicals, can damage the skin immediately, typically manifesting with acute burning or stinging pain. Chronic or cumulative ICD: Less potent irritants require longer (chronic) or repeated (cumulative) periods of skin contact to cause ICD; these forms typically manifest with pruritus.

Answer 89

Occupational ICD is ICD caused by one or more of the many possible work-related skin irritants. It can be acute, chronic, or cumulative. Atopic disorders increase risk of ICD because of impaired skin barrier function and lower threshold for skin irritation.

Answer 90

Phototoxic dermatitis is a variant in which a topical (eg, perfumes, coal tar) or ingested (eg, psoralens) agent becomes a skin toxin only after exposure to ultraviolet light, most typically long-wave ultraviolet light (UVA). Phototoxic dermatitis, therefore, occurs only in UV-exposed skin, typically with a sharp demarcation.

Answer 91

- Can be immediate depending on the irritant and potency, or chronic and need repeated exposure before causing a reaction. - Resolution may take up to 3 weeks after discontinuation of exposure. Reactivity is usually lifelong, so identified allergens must be avoided lifelong. Patients with phototoxic dermatitis can have flare-ups for years when exposed to sun (persistent light reaction); however, this is very rare. ICD typically decreases in intensity [decrescendo reaction] after 1 or 2 days.

Answer 92

- more painful than pruritic (pruritis more common if chronic/cumulative) - Signs range from erythema, scaling, and edema to erosions, crusting, and blistering.

Answer 93

"Results from a viscious cycle of dermatitis associated with elevated T-cell activation, hyperstimulatory Langerhans cells, defective cell-mediated immunity & overproduction of immunoglobulin by B cells. - Stratum corneum barrier dysfx and ceramide (epidermal lipid) deficiencies - Genetic factors: familial predisposition - Environmental factors: triggered by excessive bathing, harsh soaps, Staph aureus colonization, sweating, rough fabrics & wool

Answer 94

Epidermal barrier dysfunction: cutaneous inflm is T-cell mediated delayed-type hypersensitivity reaction --> hypersensitivity downregulates antimicrobial peptides --> more susceptible to skin infection!

Answer 95

- Primarily affects children in urban or developed countries - Most people with the disorder develop it before age 5, many of them before age 1; however, atopic dermatitis may even begin during late adulthood. - Childhood atopic dermatitis frequently resolves or lessens significantly by adulthood. - Many patients or their family members who have atopic dermatitis also have allergic asthma and/or immediate-type hypersensitivities that manifest, for example, as allergic seasonal or perennial rhinoconjunctivitis. The triad of atopic dermatitis, allergic rhinoconjunctivitis, and asthma is called atopy or atopic diathesis.

Answer 96

Atopic dermatitis in children often abates by age 5 years, although exacerbations are common throughout adolescence and into adulthood. - Girls and patients with severe disease, early age of onset, family history, and associated allergic rhinitis or asthma are more likely to have prolonged disease. Even in these patients, atopic dermatitis frequently resolves or lessens significantly by adulthood.

Answer 97

Acute phase - lesions are intensely pruritic, red, thickened, scaly patches or plaques that may become eroded due to scratching. Chronic phase - scratching and rubbing create skin lesions that appear dry and lichenified. Intense pruritus is a key feature. Itch often precedes lesions and worsens with dry air, sweating, local irritation, wool garments, and emotional stress.

Answer 98

Distribution of lesions is age specific. In infants, lesions characteristically occur on the face, scalp, neck, eyelids, and extensor surfaces of the extremities. In older children and adults, lesions occur on flexural surfaces such as the neck and the antecubital and popliteal fossae. Erythroderma (Erythema that covers more than 70% of the body surface area) is rare but can result when atopic dermatitis is severe.

Answer 99

Secondary bacterial infections (superinfections), especially staphylococcal and streptococcal infections (eg, impetigo, cellulitis) are common.

Answer 100

-A type of squamous cell carcinoma -Referred to as 'squamous cell carcinoma in situ' (SCC in situ) -In situ meaning: surface form (non-invasive)

Answer 101

Dysplastic lesion, usually confined to epidermis (intraepidermal), but may extend in to the dermis -Causes of cellular dysplasia is multi-factorial, but most common = UV light, radiation, chemicals (arsenic), and HPV

Answer 102

Most frequently diagnosed in Caucasian individuals -Usually >60 and rarely <30

Answer 103

Insidious onset. Lesions = slow-growing and evolve over months to years. If untreated, can extend laterally (over many years) and become invasive.

Answer 104

Location: may be found in both sun-exposed and sun-protected areas Lesion: solitary, barely raised, red or pink patches or plaques (often mistaken for psoriasis or eczema) -may have focal areas of pigmentation (mimicking superficial basal cell carcinoma or nevi) -are minimally symptomatic and mimic other benign processes -> Pt may delay care/dx as a result

Answer 105

Lyme disease

Answer 106

Pseudomonas

Answer 107

Warts (condylomata acuminata if genital)

Answer 108

Molluscum Contagiosum

Answer 109

Seborrheic keratosis

Answer 110

Internal malignancy

Answer 111

Those closest to lymph & highly vascularized areas

Answer 112

HIGHLY teratogenic. Requires negative preg test to prescribe & the client should also be on birth control

Answer 113

Has white layer on top & when you attempt to scrape it away, should see little specks of blood

Answer 114

It crusts over (yum)

Answer 115

If several hair follicles become infected and abscesses form in each hair follicle, it can happen that these infections cluster together, leading to the appearance of what is known as a carbuncle.

Answer 116

- opportunistic infection caused by the yeastlike fungus Candida albicans. - C. albicans is found throughout the body but likes mostly moist, warm environments. It’s usually harmless, however it can proliferate when the immune system is weakened. Candida typically lives on the skin or mucous membranes. - Candida overgrowth can damage nearby tissues the most common being damage of the skin or mucous membrane. Destroyed cells and keratin protein accumulate to form a white lesion - pseudomembranous. - Overgrowth can also occur when there is less microbial competition. Normal microflora inhibits candida growth. However when conditions such as antibiotics usage reduce bacteria, candida can proliferate leading to inceased blood flow to affected tissues causing red painful lesions - erythematous. In most cases you see a mix of both pseudomembranous and erthyematous components.

Answer 117

immunodeficiency, antibiotics usage, diabetes, pregnancy, cushing’s, infants 6 months and younger,It neoplastic blood disorders.

Answer 118

Candidiasis is more prevalent in old age and infants 6months or younger. It is also common in pregnant women and kids using inhaled steroids. Oral candidiasis or thrush is the most common infection. It is a global infection but more prevalent in poorly nourished population.

Answer 119

*It is an infection of the dermis and subcutaneous tissues characterized by fever, erythema, inflammation, and pain *Commonly caused by S.Aureus, CA-MRSA, or group B streptococci Can occur near surgical wounds or trauma site

Answer 120

Diabetes, cirrhosis, poor lymphatic circulation, renal failure, poor nutrition, HIV, ETOH, cancer, chemotherapy, pre-existing skin issues and substance abuse are predisposing factors. *Trauma and surgery are risk factors

Answer 121

sepsis & chronic edema

Answer 122

*Localized pain and tenderness occur for a few days before presentation *Time for healing after treatment is initiated is 12 days *Most cases improve when pt is on oral antibiotic therapy for 5 days.

Answer 123

Expanding redness, warmth, and pain of the skin. Pus can accumulate under the skin and cause blisters (Power-Kean, p.1050). Vesicles, blisters, hemorrhage, necrosis or abscesses can occur. Skin Is slightly raised and border is indistinct Pain on palpation.

Answer 124

*Very common on lower extremities or pinna (ear) or in local anatomic abnormalities that affect circulation.

Answer 125

Genital warts . HPV Types 6 & 11 most often.

Answer 126

Multiple sexual partners & high risk partners Unprotected sex Immunocompromised Smoking Not vaccinated (The HPV9 vaccine [Gardasil] protects against types 6 and 11)

Answer 127

No but co-infection with other types of HPV (which may be higher risk) is very common

Answer 128

Sexual transmission (but just needs skin to skin contact, not necessary mixing of bodily fluids...)

Answer 129

No, can be chronic and latent for months to years.

Answer 130

No, not curative. Warts may recur due to subclinical infection, re-infection, or immunosuppression May resolve on own within a few months, but may also maintain or progress if not treated

Answer 131

Not often but can occur

Answer 132

Located on genitalia, groin, perineum, anal skin, perianal skin, and/or suprapubic skin Urethral, cervical, or anal involvement possible If extensive, may interfere with defection or urination, or urethral bleeding

Answer 133

Infections more extensive and difficult to treat in immunocompromised (such as HIV, diabetes)

Answer 134

Diagnosis usually based solely on clinical presentation and physical assessment Limited to anogenital region and surrounding areas Biopsy possible for definitive diagnosis, and to rule out malignancy Assess for signs of other STIs: ulcerations, vesicles, or discharge & test accordingly *HPV testing not routine for warts

Answer 135

Fungal infection of the skin Ringworm (the tineas): tinea unguium (nail) tinea pedis (foot) tinea cruris (groin/thigh/buttock) or “jock itch” tinea corporis (body) tinea capitis (scalp)

Answer 136

-Dermatophytes originate from animals (zoophilic) and from soil (geophilic) -Transmission occurs with direct contact of infected animals or humans, or indirectly by contact with contaminated fomites (on shower floors). -Predisposing factors include moist, macerated skin, exposure to animals (e.g., cows, kittens, dogs), affected family members (especially tinea capitis and onychomycosis), topical corticosteroid use, immunosuppressed states (diabetes, chemo), and athletics (wrestlers).

Answer 137

Microsporum Trichophyton Epidermophyton. - The organisms metabolize keratin and cause a range of pathologic clinical presentations

Answer 138

-Classically, dermatophyte infections elicit papules and plaques with a rounded edge and white scale (ringworm lesion) -Dermatophytes infect hair follicles, causing pink to red papules and nodules. -Pustules are caused by more intense inflammation. -Tinea Pedis (foot) patterns: Interdigital—extend onto plantar and dorsal foot Scaly-thickened skin or moccasin type Vesicular-may be pustular-allergic response to fungus -Tinea Cruris (groin/thigh/buttock) Half-moon red plagues with advancing scale and pink-red papules and pustules in the groin Scrotum rarely involved -Tinea Corporis (body) patterns: Annular plagues (classic) Deep inflammatory-red nodules and pustules Majocchi’s granuloma-deep hair follicle infection -Tinea Capitis (scalp) patterns: Seborrheic dermatitis-most common Inflammatory-boggy scalp-may be confused with cellulitis Black dot-large areas of alopecia Pustular minimal scaling. Posterior cervical adenopathy present.

Answer 139

An acute, immune-mediated condition affecting skin + mucous membranes (including genital) Produced by a cytotoxic immune response directed against keratinocytes expressing foreign viral or drug antigens - Infections are the cause for ~90% of cases. Commonly in herpes simplex type 1 & 2. Other common cases are Mycoplasma pneumoniae, and upper respiratory tract infections.

Answer 140

Most common in young adults (20-40) but can happen in children

Answer 141

Usually self-limiting and resolves in 1 month without scarring

Answer 142

- Characterized by numerous target-shaped skin lesions with many types of lesion morphologies (hence name multiforme): target lesions, erythematous macules and papules, urticarial-like lesions, vesicles, and bullae. - Target lesions begin as dusky-red, round macules and papules that may burn and itch. - Early lesions appear suddenly in a symmetric or crop pattern on the palms, soles, backs of the hands and feet & forearms and legs. Bullae and erosions may be present in the oral cavity (NOT to be confused with SJS) - Dx not made until early lesions evolve into target lesions during a period of 24 to 48 hours. - Target lesions have an “iris” because of centrifugal spread à circumference of 1-3cm - The center of the iris can appear dark red, purpuric, or vesicular. - This central area is surrounded by a pale area of edematous skin, which is in turn surrounded by a sharp discrete ring of erythema.

Answer 143

Inflammation of hair follicle. Develops from proliferation of microorganisms or trauma around the opening of the hair follicle. Inflammation is a result of the release of chemoactive factors/enzymes. - Often S. Aureus - Can result from tinea infection in beard - Prolonged skin moisture, skin trauma, occlusive clothing, topical agents, and poor hygiene are contributing factors.

Answer 144

Eruption is abrupt. Can spread to other parts of body by shaving. Symptoms last for a few days. should improve once mechanical irritant is removed or topical/oral antibiotics are initiated. Can have recurrent bacterial infections if patient has nasal carriage of S. aureus- treat with oral abx.

Answer 145

Lesions appear as dome shaped pustules with surrounding area of erythematous halos around follicle. Can be tender. Most prominent on scalp, arms leg, axilla, and trunk. Rarely cause systemic symptoms.

Answer 146

Furuncle (boil) – an inflammation of hair follicles. They are walled-off, deep and painful, firm or fluctuant mass enclosing a collection of puss. It often evolves from a superficial folliculitis Carbuncle – an extremely painful, deep, interconnected aggregate of infected, abscessed hair follicles The main difference is that a furuncle is one boil on the skin, whereas a carbuncle is a cluster or collection of boils.

Answer 147

Any hair-bearing site can be affected. Sites of high friction and sweating are most typically affected (like under the belt, the anterior thighs, the buttocks, the groin, the axillae, and the waste Furuncle – *deep dermal or subcutaneous, firm, red, swollen, and painful mass. * 1 – 5 cm in diameter *No systemic symptoms Carbuncle – *deep, tender, firm subcutaneous erythematous papules enlarge to deep-seated nodules that can be stable or fluctuate *Favoured sites are back of the neck, upper back, and lateral thighs. *Malaise, chills, and fever may precede or occur during the height of infection.

Answer 148

Several Days: they can rupture or be reabsorbed * Apply warm, moist compresses to encourage spontaneous drainage If not resolving and becoming systemic, can make an incision and drain, and treat with systemic antibiotics

Answer 149

Oral - type 1 Genital - type 2

Answer 150

80-90 % of people with symptomatic (Type2) infection will have recurrence within one year

Answer 151

via resp. droplets, direct contact with an active lesion or Salva or cervical secretions containing virus HSV enters nerve endings in the skin directly or travels down peripheral nerves to dorsal root ganglia (DRG) where it stays inactive

Answer 152

Occurs after symptomatic or asymptomatic primary infection Local skin trauma, systemic changes reactivate virus Virus then travels via peripheral nerves down to initial infection site

Answer 153

Mostly asymptomatic Early signs = Tenderness, pain, mild paresthesia Later: lesions, grouped vesicles (more numerous and spaced out than secondary infection) Localized pain, tender lymphadenopathy, headache, fever, generalized aches Lesions on mucous membrane accumulate exudate, lesions on skin form crust Gingivostomatitis + pharyngitis most frequent (Type1) Vulvovaginitis/painful vaginal + cervical erosions in women w genital infection May have proctitis, anorectal pain, discharge, constipation or tenesmus in men or women Recurrent Infection: Early signs (same as primary) lesion formation with rapid formation of papules and then vesicles dome-shaped, tense vesicles rapidly umbilicate systemic symptoms rare

Answer 154

Inflm of the rectum

Answer 155

Primary Infection: Early signs occur before onset of lesions 3-7 days after contact Lesions last 2-6 weeks and heal without scaring Recurrent Infection: Early signs last 2-24 hrs Lesions appear within 12 hrs after 2 - 4 days vesicles rupture and form erosions or crust crust sheds in ~8 days recurrent disease

Answer 156

Herpes simplex type 1 has been detected in up to 78% of cases, and herpes zoster has been detected in 30% of cases - Etiology still not fully known

Answer 157

Shingles& chicken box (Shingles is known as Herpes Zoster)

Answer 158

in trigeminal and dorsal root ganglia.

Answer 159

- initial symptoms of pain and paresthesia localized to the affected dermatome (the cutaneous area innervated by a single spinal nerve, followed by vesicular eruptions that follow a facial, cervical, or thoracic lumbar dermatome. Approximately 15 to 20% of individuals experience postherpetic neuralgia (pain) with reactivation of the virus. Local symptoms are alleviated with compresses, calamine lotion, or baking soda.

Answer 160

Common, highly contagious bacterial superficial skin infection Caused by Streptococcus pyogene and/or Staphylococcus aureus (80%). May occur after a minor skin injury, ex. Insect bite, or within lesions of atopic or another dermatitis. Often develops on normal skin.

Answer 161

Highest rate of infection in children in close physical contact with each other Most common bacterial skin infection of children More likely in warm, moist, humid climates Poor hygiene pre-disposes

Answer 162

Self-limited but can spread and last weeks-months if untreated Chronic untreated impetigo can lead to ecthyma (deeper, dermal infected lesions), Bullous formation

Answer 163

True, generally asymptomatic and painless

Answer 164

Lesions may be localized or widespread Common on face Uncommon on trunk Lesions generally asymptomatic and painless Two clinical forms: Bullous Impetigo - Thin-roofed bullae turn from clear to cloudy. Bullae quickly collapse, leaving an inner-tube shaped rim with a central thin, flat, honey-colored, stuck on crust - Lesions enlarge and coalesce, minimal surrounding erythema, thick crust accumulates in longer lasting lesions - Mild adenopathy Nonbullous Impetigo (Crusted) - Vesicles/pustules rupture, exposing red, moist base - Tinea-like scaling border forms as lesions enlarge - Firmly adherent crust, ranging in color from honey-yellow to white-brown - Little surrounding erythema, satellite lesions appear beyond the periphery

Answer 165

Mostly occurs in 30-60 year old range, rare in children and elderly, 10% have family hx of same, can be linked to certain medications and Hep C

Answer 166

Lesions are self-limiting, average duration 6-18 months

Answer 167

Benign autoimmune inflammatory disorder of skin and mucous membranes. Cause unknown, but may involve T cells, adhesion molecules, cytokines, perforin and antigen presenting cells

Answer 168

Pruritic purple/pink papules and plaques on scalp, extremities, nails, and mucous membranes (five P’s of Lichen Planus: pruritic, planar (flat topped), polygonal, purple, papules)

Answer 169

Corticosteroids (topical or systemic), Antihistamines, glucocorticoids, systemic or topical retinoids

Answer 170

Most common in children under 10 and older adults Risk factors: Sexual activity Contact sports immunocompromised (previously late marker in HIV) Warm moist environments like steam rooms, saunas, and pools Atopic dermatitis – mixed evidence

Answer 171

Caused by molluscum contagiosum virus infection in the skin Belongs to poxvirus family MCV1 and MCV2 as the most common genotypes of virus Genetics similar to variola and vaccinia viruses, also replicates in cytoplasm of cell Virus DNA codes for proteins that inhibit host immune response

Answer 172

Spread by direct skin-to-skin contact, fomites (such as towels) and sexual contact Can also spread on a person’s body via autoinoculation Remains contagious until the bumps are gone

Answer 173

Considered chronic, localized infection 2-6 week average incubation period Lesions often resolve on their own within 2-12 months, minority of cases take up to 3-5 years

Answer 174

No it's not protective - you can get reinfected

Answer 175

Not painful. May or may not be pruritic

Answer 176

Presents as small 2-5mm flesh-coloured dome-shaped papules that often have dimple in center (“umbilicated”) Lesions may be alone or grouped Firm lesions May have larger, more extensive lesions if immunocompromised (such as HIV) May have inflammation, erythema and scaling around lesions Can occur anywhere on the skin but most often trunk, axillae, face, genital regions Does not occur on palms or soles

Answer 177

Considered STI when spread to genitals of adult If seen in genitalia of children, likely due to autoinoculation (do not presume STI or sign of child abuse)

Answer 178

common, eczematous patches or plaques surrounding lesions

Answer 179

Diagnosis usually based solely on clinical presentation and physical assessment Distinguishing feature is umbilication (central indent) in papules Can be mistaken for many other skin conditions – skin biopsy can help differentiate Those with genital lesions should be tested for STIs

Answer 180

Tinea of the nails

Answer 181

-prevalence increases with age -affects 15-20% of 40-60 year olds -trauma (i.e., from tight fitting shoes) and immunosuppression increase risk for infection

Answer 182

-starts in 1-2 nails and spreads -most patients develop lifelong infection (unless treated)

Answer 183

-yellow/ white nail plate -elevated due to accumulation of hyperkeratotic debris within the plate -brittle, thick nails -may disrupt surrounding skin and predispose to bacterial infection of surrounding area (paronychia)

Answer 184

Lice infection

Answer 185

children affected most frequently -typically diagnosed by teacher, school nurse, camp nurse -girls> boys -rare in African American patients

Answer 186

-life span of louse is about 1 month, lays 7-10 eggs per day. These take 8 days to hatch and another 8 days to mature -adult lice can survive 55 hours without host

Answer 187

Head louse (pediculus capitis) Body louse (pediculus corporis) Crab/ pubic louse (phthirus pubis) (most contagious sexually transmitted infection!)

Answer 188

Acquired by personal contact or indirectly (sharing brushes, towels, contact with clothes, toys, furniture, carpet, bedding infested by lice)

Answer 189

-Parasites infest hair of scalp, body, pubic region; survive by sucking blood: mouthparts attach to host, pierce skin, secreting a toxic saliva. This mechanical trauma and toxin produce pruritic dermatitis. Primary lesion is pinpoint red macule, papule, or wheal with hemorrhagic puncture site Usually can’t see this due to excoriation, wheals, crusts

Answer 190

pruritus, crawling sensation -sometimes have posterior cervical adenopathy -can occur on eyelashes in children (can cause blepharitis (inflammation of eyelid), purulent discharge -visible nits/ ova (oval, yellow) on hair shaft- usually about 6.5 mm to 1 cm from surface -diagnosis confirmed by visualization of live lice- systematically comb hair with fine tooth nit comb

Answer 191

= a vesiculobullous disease Pemphigus is a group of rare skin disorders that cause blisters and sores on the skin or mucous membranes, such as in the mouth or on the genitals. Can be life threatening (mostly due to cutaneous infection)

Answer 192

-rare -most prevalent between 40-50 years, but can occur in all ages -genetic component -environmental (viral infections, medication-induced, dietary intake, radiation, surgery) and endogenous (emotional or hormonal) influences

Answer 193

-oral erosions precede onset of skin blisters by weeks or months -erosions last for weeks before healing with brown hyperpigmentation -weeks to years- may go into remission

Answer 194

BASICALLY IMMUNE RESPONSE DESTRUCTS CELL TO CELL ADHESION --> fluid accumulation --> blister formation -caused by circulating antibodies targeting the cell surface adhesion molecule “desmoglein” (cell to cell adhesion in epithelium) at the desmosomal cell junction in the suprabasal layer of the epidermis (layer above the basal layer) -IgG antibodies and complement (C3) bind to the desmoglein adhesion molecules, resulting in destruction of cell-to-cell adhesion (acantholysis) in the basal layer of the epidermis, fluid accumulation, and blister formation

Answer 195

-bullae from 1-3cm or larger (localized moving to generalized if untreated) Rupture easily Traction on skin increases formation -painful, superficial erosions (loss of part of epidermis following rupture of vesicle or bulla- appears depressed, moist, glistening) -minimal itching (more tender, irritated)

Answer 196

Pemphigus vulgaris - Most common, mean onset 60 years - Oral lesions precede onset of skin blistering - Most face, scalp, axilla - Blister ruptures easily (thin fragile epidermis) **Are many more types that I'm not going to go into - see ILO

Answer 197

-young adults (typically 10-35 years) -possibly has higher prevalence in winter -unsure if infectious transmission- there has been temporal case clustering- i.e., outbreaks in frat houses or military barracks

Answer 198

-rash appears over 2-3 weeks and self resolves in 1-3 months

Answer 199

-self limiting inflammatory disorder -may be triggered by virus- herpeslike virus (HHV6 or HHV7) is most likely cause

Answer 200

-itching -characteristic rash: starts with HERALD PATCH on trunk, then develops numerous pink papules and plaques following langer lines, sloughing of scales leaves collarette pattern -occasionally preceded by headache, fatigue, sore throat development of lesions

Answer 201

-diagnosis follows clinical appearance of lesion -differentials include secondary syphilis (consider serologic test for syphilis if lesions on palms or soles), psoriasis, medication eruption, nummular eczema, seborrheic dermatitis -skin biopsy only if atypical or recurrent

Answer 202

Chronic, relapsing, proliferative inflammatory disorder involving skin, scalp, and nails. Caused in large part by abnormal T-lymphocyte function. Inflammatory cascade of immune cells and inflammatory mediators

Answer 203

Flares triggered by local factors (skin injury, scratching); systemic factors (Strep and HIV), stress, meds (Lithium, beta blockers, interferons, antimalarials)

Answer 204

Can be all ages Onset: usually presents by 40 years old; onset usually 20-30 years and 50-60 years. If onset later in life, associated with comorbidities of obesity, HTN, smoking, DM Marked by remissions and exacerbations; can be mild/moderate/severe Commonly family history (90% of cases)

Answer 205

Thick dermis and epidermis due to cellular hyperproliferation, altered keratinocyte differentiation, and expanded dermal vasculature Increased turnover time for shedding epidermis (from 3-4d to 14-20d). More germinative cells, increased transit time through dermis. Bypass cell maturation and keratinization Epidermis thickens, forms plaques that are silvery due to loosely cohesive keratin Capillary dilation and increased vasculature to accommodate increased cell metabolism—> erythema

Answer 206

Pink to red papules and plaques with thick white scale.

Answer 207

Plaque (psoriasis vulgaris): most common, 80-90% of cases Lesions: well-demarcated, thick, silvery, scaly, erythematous plaque surrounded by normal skin. Small erythematous papules enlarge and coalesce into larger lesions. Typically on face, scalp, elbows, knees and sites of trauma. Inverse (intertriginous) psoriasis: rare, involves red, moist, fissured lesions that develop in skin folds (axillae, groin, intergluteal cleft). Guttate psoriasis: more common in young adults and children. Small round oval red papules all over trunk/extremities post streptococcal respiratory tract infection. Can resolve in 6-12 months. Pustular psoriasis: intense inflammation resulting in blisters of noninfectious pus (collections of neutrophils) Erythrodermic psoriasis: severe form; onset can be acute if drug-induced or steroid withdrawal, or chronic if from poorly controlled psoriasis; pruritus or pain with widespread, scaling lesions that cover large area of body. Can also have fever, weight loss, protein loss, and lymphadenopathy.

Answer 208

Joint Disease: 30% develop psoriatic arthritis of hands, feet, knees and ankle joints Psoriatic nail disease: pits, nail whitening, friable nails, yellow spots, splinter hemorrhage, thickened nail beds, separation of distal end of nail plate from nail bed (onycholysis)

Answer 209

Est. worldwide prevalence is 200 million people. Can affect all ages and socioeconomic status groups but is common in resource-limited regions Transmitted by close personal contact with lesions or affected clothing or bedding Common in tropical settings (The Pacific and Latin America) Crusted scabies more common in epidemic situations such as among institutionalized (long term care, prisons) or immunocompromised patients

Answer 210

Caused by parasitic infestation of the epidermis with Sarcoptes scabiei var. hominis Mite feces causes and allergic response which causes itching

Answer 211

Key word = BURROWS Intensely pruritic, inability to stop scratching, worse at night Typically other family members will also be experiencing the symptoms Lesions: linear, curved, or S-shaped burrow, slightly elevated vesicle or papule, 1-2mm wide May develop into scattered inflamed pustules, linear vesicles, papules or even larger nodules Due to itching, lesions may be excoriated, hemorrhagic, or crusted Found in intertriginous areas (skin folds) including finger webs, wrists, sides of hands and feet, lateral fingers and toes, genitalia including glans penis, buttocks, scrotum In infants, the palms, soles, and scalp may be more commonly affected Pruritis may persist after treatment completed for weeks to months

Answer 212

Identification of mites, eggs, feces with microscopy Scabies preparation: mineral oil over burrow then scraped with #15 blade and applied to glass slide Potassium hydroxide and heat make it easier to identify mites, but destroys mite feces

Answer 213

Subtype “crusted (Norwegian) scabies” Common among patients with dementia, Down syndrome, immunosuppression Thick crusting and eczematous dermatitis on hands and feet

Answer 214

Occurs in all ages In 5% of adults Affects men more than women More severe in patients with neurologic disorders (Parkinson’s, stroke, head trauma) and pts infected with HIV

Answer 215

Unknown. Proposed theories include genetic predisposition, phospholipases from Malassezia yeasts, immunosuppression and epidermal hyperproliferation

Answer 216

Cradle cap - usually resolves by 1 year old

Answer 217

Chronic inflammation of the skin pink to yellow papules and plaques with greasy scale involve scalp, central face, ears and presternal areas. Common adult locations eyebrows, base of eyelashes, nasolabial folds and paranasal skin, and external ear canals. May effect flexural skin – postauricular (behind ear), inguinal and inframammary folds (underneath breasts) as well as anogenital area Common peds locations – scalp (cradle cap), diaper area and axillary skin

Answer 218

Circumscribed area of raised erythema and edema of the superficial dermis. Angioedemia (welts or swelling deeper within the skin or mucous membranes, most seen in eyes and mouth) associated with both chronic and acute urticaria.

Answer 219

Most associated with type I hypersensitivity reactions to medications (penicillin, Aspirin), certain foods (strawberries, shellfish, food dyes), environmental exposure (pollen, animal dander, insect bites), systemic diseases (intestinal parasites, lupus erythematosus), or physical agents (heat or cold)

Answer 220

Histamine release --> blood vessels in skin contract --> fluid leakage appears as wheals, welts, hives

Answer 221

Can occur almost instantly depending on the exposure. Most lesions resolve spontaneously within 24 hours, but new lesions may appear. All possible causes of the reaction should be removed.

Answer 222

S&S: Circumscribed area of raised erythema and edema of the superficial dermis Epidemiology? Either idiopathic or autoimmune in origin Pathophysiology? Involves inappropriate activation of mast cells Time course? Recurrent wheals for more than 6 weeks Treatment? Avoiding triggers, non-drowsy antihistamines, treating underlying causes if autoimmune. (Page 2034 of patho book)

Answer 223

= the common wart!

Answer 224

Occur most commonly in children and young adults More common among certain occupations, I.e. handlers of meat, poultry, and fish. Predisposing conditions for extensive or recalcitrant involvement include atopic dermatitis conditions associated w/decreased cell-mediated immunity (e.g. AIDS, organ transplants)

Answer 225

HPV Types 2, 4, 7

Answer 226

Infection occurs by direct skin contact, w/maceration or sites of trauma predisposing patients to inoculation Reservoir for HPV = individuals with clinical or subclinical infection Transmission via inanimate objects has been proposed but has not been proven

Answer 227

Incubation time approx 2-6 months Course is highly variable; spontaneous resolution w/time and development of cell-mediated immune response is the rule In children approx 2/3’s of all warts spontaneously regress w/in 2 yrs Warts in immunocompromised pt can be widespread, intractable, and chronic

Answer 228

Can develop anywhere on skin around the nail and frequently appear on the cuticle, and sometimes the area beneath the nail. Warts involving the cuticle can affect nail growth and cause nail deformity.

Answer 229

Acquired disorder characterized by a loss of functional melanocytes resulting in depigmentation of skin

Answer 230

Unknown etiology, commonly attributed by triggering events including physical injury, illness, sunburn, emotional stress or pregnancy, but no definite cause May be associated with autoimmune diseases such as thyroiditis, pernicious anemia, Addison's disease, systemic lupus erythematous, rheumatoid arthritis or diabetes, or genetic syndromes such as Vogt-Koyanagi-Harada syndrome Theories for melanocyte destruction include genetic, autoimmune, neural, biochemical, oxidative stress, viral infection and melanocyte detachment mechanisms

Answer 231

Most frequent cause of skin depigmentation Prevalence rates 0.1 - 2 % in adults and children Affects males and females equally, no racial, ethnic or socio-economic differences May appear at any age from early childhood to late adulthood but 1/2 of patients experience onset before age 20 Peak incidences between 20-30 year old's, 70-80% of adults develop vitiligo prior to age thirty, and 1/3 of those with vitiligo are children

Answer 232

Variable course, may be localized or rapidly spread to generalized depigmentation

Answer 233

White macules coalesce into patches, pigmentation may remain around hair follicles 2 types: segmental and nonsegmental Segmental vitiligo do not cross the midline Nonsegmental vitiligo may be distributed or localized to the acral sites (distal extremities, face, gluteal area)

Answer 234

Physical exam, skin biopsy usually unnecessary Lab tests for lupus, RA, thyroid disease, CBC may be helpful to exclude causes Differential diagnosis: lupus erythematosus, pityriasis alba, piebaldism

Answer 235

A slow growing cancer of the skin that looks like a dome Benign, squamous cell differentiation arising from hair follicles Rapidly growing, “volcano craters” nodule with a distinctive clinical appearance = low grade squamous cell carcinoma The epidermis is expanded with atypical keratinocytes The keratin core is composed of eosinophilic, glassy appearing, atypical, prematurely keratinized cells

Answer 236

50-70 years. Rare <40yrs of age White people with fair complexions are more often affected Highest among smokers and males Chemical exposure and human papillomavirus have been implicated as causes in animal models, although in humans is controversial.

Answer 237

Left undisturbed, keratoacanthomas may resolve spontaneously or progress into invasive squamous cell carcinoma Historically described as a regressing or absorptive lesion – however now are being treated like squamous cell carcinoma 3 Growth phases: 1) Proliferative phase, a solitary papule appears suddenly, then rapidly grows to its max size over 2-4wks. 2) Mature phase, the lesion is stable in size and appearance for wks – months; may appear crateriform if the core has been partially removed 3)Resolving phase, the base becomes indurated, the central core is expelled, and the base resorbs, leaving a pitted scar. Resolution may take several months.

Answer 238

Solitary flesh-coloured to dull red, volcano like, crater shaped, 0.5cm-2cm. Rarely will attain a size from 1cm to 10cm and are locally destructive. Central keratotic plug or depression conceals a deep keratinous cavity – gives volcano shape Sun-exposed extremities, forearm, neck, legs, face, dorsal hand Does not appear on palms or soles Nodule is firm, tender to palpation/pressure, grows rapidly Subungual (under toenail or fingernail) can occur, painful and locally destructive

Answer 239

Presume diagnosis of squamous cell carcinoma pending biopsy result and clinical follow-up An excisional biopsy or shave biopsy shld be preformed Excise deep enough to evaluate the dermis for possible invasion Radiation therapy is considered for tumors in area, where excisional surgery might result in deformity

Answer 240

Basal cell carcinoma

Answer 241

History of intense intermittent ultraviolet exposure More common with increasing age More common for those with white or fair skin, less common for Hispanic, Asian skin, very rare in African American individuals

Answer 242

Initial tumours are small and hard to detect Lesions grow slowly over months to years Metastasis is rare because tumors do not invade blood or lymph vessels

Answer 243

Mostly occurs on sun exposed areas of the body Pink, violaceous, pearly-white; may have speckled brown, black, blue Papules or nodules Smooth surface, telangiectasias Enlarges slowly, flattens centrally, or may develop raised rolled border Often bleed, erode, become crusted, ulcerate at the centre

Answer 244

Based on clinical assessment, history of sun exposure, progression of lesion Biopsy

Answer 245

Nodular (most common, head and neck) Pigmented (similar to nodular but with speckled melanin) Morpheaform and Sclerosing (most recurring, subtle, aggressive, difficult to visualize and excise entire lesion) Superficial (least aggressive, trunk and extremities, flat lesion) Micronodular (microscopically extends beyond visible border thus difficult to fully excise and will likely recur) Advanced BCC (large, untreated, have invaded deeper tissues and may impair function or visibly deform surrounding structures)

Answer 246

Squamous cell carcinoma (SCC)

Answer 247

Actinic keratosis

Answer 248

Less common but with a higher mortality rate in dark-skinned people, often diagnosed at an advanced stage Increased risk with cumulative sun exposure over time. Occupational exposures: coal, tar, pitch, creosote, arsenic, radium Immunosuppression, chronic infections Men>women Increasing age. Scar tissue. SCC here = 30% chance of mets. A Marjolin ulcer is a deep aggressive SCC that develops over a thermal injury scar. Chronic ulcers and chronic inflammatory diseases ie. lupus, hidradenitis suppurativa, lichen planus/sclerosis, osteomyelitis Some strains of HPV Genetic disorders that affect the skin. Actinic keratosis (AK) may become SCC.

Answer 249

Originates in dermis Can extend into epidermis UVR absorbed by the DNA of cutaneous keratinocyte cells, cause mutation of the progenitor cells. Affects pathways = decreasing cell apoptosis, increasing cell growth/proliferation.

Answer 250

More likely than BCC to metastasize, through lymphatic system or parotid glands. If untreated, can mets to bone, salivary glands, muscle or even distantly to brain, liver or lungs <2mm tumour depth = rarely metastasizes >5 mm tumour depth = 20% rate of mets

Answer 251

Can take months or years to invade surrounding tissue. Presentation is constant or can recur after excision. Can form slowly from a present AK or can form/progress suddenly and aggressively. Of particular concern are lesions on the lip, ear and scalp – can mets to regional lymph nodes.

Answer 252

Patients’ first presentation to a healthcare provider is commonly with an enlarging non-healing lesion that sometimes bleeds. The next common presentation is pruritis.

Answer 253

Pink -> dull red Firm Dome-shaped nodule Yellow-white scale/crusting over central cavity Can become red, more raised, with necrotic tissue in centre. May smell foul. Multiple lesions may appear May be painful or pruritic Commonly found on lower lip

Answer 254

Bowen's Disease Full thickness SCC. Slow to advance. Appears as pink, scaly patch with clear borders. Usually only in the epidermis but may extend to dermis.

Answer 255

Melanoma = malignant tumour of the skin originating from melanocytes (cells that produce the pigment melanin).

Answer 256

Superficial spreading melanoma (SSM) – the most common; Lentigo malignant melanoma (LMM) → frequently found in older adults and confused with age spots; Primary nodular melanoma (PNM) → aggressive tumour; Acral lentiginous melanoma (ALM) → rare and aggressive and occurs on non-hair-bearing surfaces (i.e., palms of the hands and soles of the feet) and mucous membranes in people with darker skin.

Answer 257

30% of melanomas develop within a pre-existing nevus… whereas the remaining 70% develop “de novo”

Answer 258

Colour change, size change, irregular notched margin, itching, bleeding or oozing, nodularity, scab formations, ulcerations.

Answer 259

Pathogenesis of melanoma is complex… Familial melanomas → associated with CDK4 & CDKN2A genes. Both are highly penetrant susceptibility genes and result in melanoma. Melanomas have a high mutation rate stimulated by UV radiation Relationship between melanoma & nevi is important - Most nevi never become suspicious, however, suspicious pigmented nevi need to be evaluated & removed.

Answer 260

Personal or family hx (or both) UV radiation exposure (including sunbed use before age 30) Fair hair Fair skin with repeated sunburns Freckles Immunosuppression Being a younger female Being an older male Geographical location (high UV exposure) Past pesticide exposure 3+ clinically atypical (dysplastic) nevi/moles

Answer 261

white women 25-29 years old.

Answer 262

Note: Melanoma metastasizes quickly, so it has a lower 5-yr survival rate than nonmelanoma skin cancers. BUT it is still curable if caught & treated early. EARLY DETECTION IS CRITICAL TO DECREASE MORTALITY

Answer 263

Female patients Younger patients Thinner melanoma (better prognosis than thicker melanoma) Melanoma on extremity (vs on the head, trunk, neck)

Answer 264

Melanomas usually have dark brown or black pigmentation; They start as small mole-like growths that increase in size, change colour, become ulcerated, and bleed easily from slight injury. When it develops on a pre-existing nevus, there is usually a focal area of colour change. Note: Focal colour change is more specific for melanoma than the colour itself (that is, no colour is diagnostic)

Answer 265

A – Asymmetry (one half doesn’t look like the other half) B – Border irregularity C – Colour variations (varying hughes & colours) D – Diameter larger than 6mm E – Elevation or Evolving (raised appearance or rapid enlargement)

Answer 266

Not a disease, but a genetically predisposed response to androgens Males: premature hair loss of hair on central scalp Females: hereditary, central diffuse hair thinning

Answer 267

= "Male pattern baldness" Androgen-sensitive follicles are transformed into vellus-like follicles (short, thinned, light coloured hair) Androgen-sensitive hair follicles are on the top of the scalp, and androgen-insensitive follicles are on the sides and back of the scalp Over time, these vellus-like hair falls off, and the scalp becomes smooth and shiny

Answer 268

Common hereditary alopecia is poorly understood Affected scalp hairs have a shortened anagen cycle and progressive miniaturization of hair follicles Early and late onset of hair loss can happen with or without high androgen levels (androgen – primarily male sex hormones produced in the testes, which contributes to skeletal growth, pubic and axillary hair growth pg.772) Heavy menses can cause iron deficiency, and increase hair shedding Recent discontinuation of an estrogenic oral contraceptive may lead to hair loss Contraceptives containing androgenic progestins may cause or prolong androgenetic alopecia.

Answer 269

Unknown, but related to genetic and hormonal changes Prevalence increase with advancing age May affect 6-25% of premenopausal women

Answer 270

thyroid disease (TSH), iron deficiency (serum iron determination, total iron-binding capacity, ferritin level) connective tissue disease (checking anti-nuclear antibody level) should consider further testing if: irregular menses, hirsutism (excessive hair growth on face, chest, & back), virilization (development of male characteristics), acne, galactorrhea, or infertility.

Answer 271

Incease growth of secondary sexual hair (on the chest, axillae, and pubic and beard areas. First signs of balding: increased frontotemporal (type I) and midfrontal recession (type II – M shaped recession) The proceeds to hair loss in a round area on the vertex (the crown), then to the top of the scalp (Types III-VII). Type I – Triangular frontotemporal recession – normally in young men

Answer 272

Begin any time after puberty and fully expressed by the 40’s

Answer 273

Hereditary hair loss begins at an early age: 20’s -30’s, and fully expressed in 40’s Postmenopausal hair loss: begins in 50’s, 60’s, or 70’s

Answer 274

Women rarely become completely bald like men Hair loss is gradual, not abrupt Most experience gradual hair loss on the top of the scalp, with retention of normal hairline, and no frontotemporal recession. Increased spacing between hairs Hair on the central scalp are thin and short, while hairs on the frontal hairline are normal Type I – Triangular frontotemporal recession – usually in women after puberty

Answer 275

Non-scarring hair loss Thought to be immunological- T cell mediated Triggering cause is unknown- genetic susceptibility plays a role Hair follicle danger signals attract T cells to the hair follicles resulting in immunological damage. Stress is frequently cited as the cause but there is little evidence that it plays a role

Answer 276

Most common in children and young adults May be associated with thyroid disease, pernicious anemia, Addisons disease, vitilgo, lupus, Ulcerative colitis, diabeties, and down syndrome.

Answer 277

Regrowth begins in 1-3 months and may be followed by loss in other areas. Prognosis for total permanent regrowth in cases with limited involvement is good but is poorer for patients with more involvement.

Answer 278

Hair loss may be diffuse, patchy , or band like at the margins of the scalp Sudden occurrence of one or several areas of hair loss of 1-4 cm. Eyelashes, eyebrows, beard, and other parts of the body are rarely involved. Sharply defined hair loss usually round or oval Skin is typically very smooth or have short stubs of hair. Diffuse fine nail pitting occurs in up to 30% of cases Structural and functional abrnomalities of the thyroid may occur

Week 3: Derm Flashcards

(311 cards)