dermatology study guide

Question 1

scabies differential diagnosis

Answer 1

contact dermatitis, asteatotic dermatitis, insect bites, animal scabies, seborrheic dermatitis, psoriasis

Question 2

scabies clinical presentation

Answer 2

variable. Itching which is worse at night
Classic burrow present less than 20% of the time: essential lesion is a small, erythematous, nondescript papule, often excoriated and tipped with hemorrhagic crusts. Burrows are often absent or obscured by excoriation or secondary infection. Miniature wheals, vesicles, pustules, and rarely bullae may also be present.

Question 3

scabies risk factors

Answer 3

transmitted person to person by direct contact, in young adults, mode of transmission is often sexual contact. Transmission through clothes uncommon, more likely with higher parasite burdens as seen in crusted (Norwegian) scabies. Animals can get scabies but those mites are different and rarely reproduce on human skin. cross infection is unlikely unless the animal is untreated

Question 4

Scabies diagnostics

Answer 4

” scabies prep” : a drop of mineral oil is placed on a burrow, and the lesion is scraped with a no.15 blade. the sample is viewed under a microscope and examined for mites, eggs or feces. There are usually only a few scabies mites on a infected patient, the majority found on hands and wrists

Question 5

Scabies TX

Answer 5

topical application of 5% permethrin cream is tx of choice. Cream should be applied from the neck down, giving attention to the interdigtial webs, axillae, umbilicus, gluteal cleft, genitals, areas under the nails, and soles of feet.
in older adults, scabies can infest hairline - cream massaged head to toe.
medication left on 8 - 12 hours and then washed off. Repeat tx in 1 week.
Lubrication and topical corticosteroids are sued to treat any resulting inflammation and pruritus. Antibiotics should be given for infections secondary to scratching.

Question 6

Actinic Keratosis differential diagnosis

Answer 6

actinic keratoses, basal cell carcinoma, squamous cell carcinoma, malignant melanoma, dysplastic nevi

Question 7

Actinic Keratosis risk factors

Answer 7

advanced age ( older than 50)
median age of 40 yrs for malignant melanoma
exposure to UV light
fair complexion ( blond or red hair, blue, green or gray eyes)
smokers
skin damaged by burns and/or chronic inflammation
hx of blistering sunburns before 18 years of age increases risk

Question 8

Actinic Keratosis clinical presentation

Answer 8

persistent or recurrent reddened and roughened area that scales or crusts

Question 9

Actinic Keratosis diagnostics

Answer 9

biopsy suspicious lesions

shave or punch biopsy

Question 10

Actinic Keratosis treatment

Answer 10

Liquid nitrogen by a freeze - thaw technique to obtain a 1 to 3 mm rim of freeze, which allows appropriately slow thawing during 20 to 40 sec.

Question 11

Seborrheic dermatitis differential diagnosis

Answer 11

Psoriasis(main condition in the differential diagnosis of seborrheic dermatiti), atopic dermatitis, rosacea, tinea versicolor, pityriasis rosea, tinea corporis, secondary syphilis, systemic lupus erythematosus (SLE), and pemphigus foliaceous

Question 12

Seborrheic dermatitis risk factors

Answer 12

possible familial trend, possible link between infantile and adult forms, high association with HIV- infected individuals

Question 13

Seborrheic dermatitis clinical presentation

Answer 13

Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and in adults. oily, flaky skin on erythemic base around ears, nose, eyebrows and eyelids. red cracking skin in body folds - distribution area in adults: scalp, eyebrows, paranasal area, nasolabial fold, chin, behind ears, chest and groin

Question 14

Seborrheic dermatitis diagnostics

Answer 14

no diagnostic test, may consider possible skin biopsy to rule out other conditions if suspicious

Question 15

Seborrheic dermatitis tx

Answer 15

shampoo is the foundation of tx: baby shampoo or medicated shampoo such as salicylic acid shampoo, coal tar, ketoconazole 2%. If shampoo alone fails, topical steroid lotion in combo with shampoo for 2 -3 weeks of tx. For face/groin: low potency agents such as hydrocortisone 1% cream

Question 16

Impetigo differential diagnosis

Answer 16

contact dermatitis, tinea infection, eczema, varicella, bullous insect bites, mycobaterial fungal infections,

Question 17

Impetigo risk factors

Answer 17

can develop if bacteria get into healthy skin or into minor cuts, scrapes, or any other small openings (such as those caused by bug bites). The infection usually occurs in warm, humid conditions and is easily spread among people in close contact

The best way to keep from spreading or catching impetigo is to wash your hands often with soap and water. When washing is not possible, use alcohol-based hand rubs. It’s also a good idea to clean the surfaces in your home with a household cleaner.

Question 18

Impetigo clinical presentation

Answer 18

Non-bullous impetigo is the most common form of impetigo. Lesions begin as papules that progress to vesicles surrounded by erythema. Subsequently they become pustules that enlarge and rapidly break down to form thick, adherent crusts with a characteristic golden appearance; this evolution usually occurs over about one week. Lesions usually involve the face and extremities. Multiple lesions may develop but tend to remain well localized. Regional lymphadenitis may occur, although systemic symptoms are usually absent.

Bullous impetigo is a form of impetigo seen primarily in young children in which the vesicles enlarge to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust – in an adult should prompt investigation about HIV

Ecthyma is an ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis. They consist of “punched-out” ulcers covered with yellow crust surrounded by raised violaceous margins

Question 19

Impetigo diagnostics

Answer 19

The diagnosis of impetigo often can be made on the basis of clinical manifestations. The key clinical findings of non-bullous impetigo, bullous impetigo, and ecthyma include:

●Non-bullous impetigo – Papules, vesicles, and pustules that rapidly break down to form golden adherent crusts; often located on the face or extremities

●Bullous impetigo – Flaccid, fluid-filled bullae that rupture and leave a thin brown crust; often located on the trunk

●Ecthyma – “Punched-out” ulcers with overlying crusts and raised violaceous borders

Question 20

Impetigo treatment

Answer 20

Bullous and non-bullous impetigo can be treated with either topical or oral therapy. Topical therapy is used for patients with limited skin involvement, whereas oral therapy is recommended for patients with numerous lesions

Mupirocin and retapamulin are probably equally effective topical therapies. Mupirocin is applied three times daily and retapamulin is applied twice daily. The recommended length of treatment is five days

Oral therapy should be administered to patients with numerous impetigo lesions or ecthyma. Dicloxacillin and cephalexin are appropriate treatments because S. aureus isolates from impetigo and ecthyma are usually susceptible to methicillin. A seven day course of antibiotics is recommended.

Question 21

Stevens - Johnson syndrome

Answer 21

a severe, life -threatening systemic reaction with fever, malaise, cough, sore throat, chest pain, vomiting, diarrhea, myalgia, arthralgia and sever skin manifestations with painful bullous lesions on mucous membrances

Question 22

Dermatophytoses: tinea capitus; tinea coporis; tinea pedis

Answer 22

dermatophytes are the most common fungi that invade the skin and nails, proliferate within the nonviable keratinized tissues.

capitus: head/scalp
coporis: body
cruris: jock itch
pedis: athletes foot
manus: hand
unguium: nail

Question 23

Dermatophytoses differential diagnosis

Answer 23

atopic dermatitis; figurate erythemas; granulomatous dermatoses; papulosquamous eruptions; psoriasis; skin cancer; uticaria; alopecia areata; impetigo; pediulosis; erythema multiforme; cutaneous lupus erythematous; secondary syphilis; contact dermatitis; dyshidrosis

Question 24

Dermatophytoses risk factors

Answer 24

usually acquired through inhalation of endemic fungi in the environment, also transmitted through close contact with infected people or animals. tinea corpis is the second most common infection passed from dogs and cats to humans.

Question 25

Dermatophytoses clinical presentation

Answer 25

characterized and named by thier location. start out as patchy, scaly areas, erythemtous plaques and papules(ringworm of the body in circular formation), intergitial scaling, maceration and fissuring. depending on the oranism, the lesions may become inflamed, boggy and pustular

Question 26

Dermatophytoses diagnostics

Answer 26

KOH microscopy preparation is valuable and cost effective: provides rapid confirmation of many types of fungal infections. An adequate specimen is obtained by scraping the active, leading border of the infection. Under the microscope, look for the diagnostic branching appearance typically seen with these organisms, a positive result. other lab tests include: skin culture on sabourauds medium woods lamp examination skin or nail biopsy

Question 27

Dermatophytoses TX

Answer 27

Most dermatophyte infections can be managed with topical treatments. For patients with limited tinea pedis, tinea corporis, or tinea cruris,treat with a topical antifungal drug with anti-dermatophyte activity rather than systemic therapy. Examples of effective topical antifungal agents are azoles, allylamines, ciclopirox, butenafine, and tolnaftate. Oral antifungal therapy is used for extensive infections or infections refractory to topical therapy. eg; griseofulvin for 2 to 4 months Nystatin is not effective for dermatophyte infections

Question 28

Tinea versicolor differential diagnosis

Answer 28

pityriasis alba; pityriasis rosea; vitiligo; seborrheic dermatitis; secondary syphilis; viral exanthem

Question 29

Tinea versicolor risk factors

Answer 29

high heat and humidity - condition is more prevalent during the summer and in hot, humid regions. Tinea versicolor is not related to poor hygiene. hyperhidrosis, and the use of topical skin oils

Question 30

Tinea versicolor clinical presentation

Answer 30

macules, patches, and thin plaques of tinea versicolor can be hypopigmented, hyperpigmented, or mildly erythematous A fine scale is often present on affected skin In adolescents and adults, tinea versicolor is most commonly found on the upper trunk and proximal upper extremities, and less often on the face and intertriginous areas. In contrast, when tinea versicolor occurs in children, it is likely to involve the face mild pruritis

Question 31

Tinea versicolor diagnostics

Answer 31

KOH preparation | skin cluture if indicated

Question 32

Tinea versicolor TX

Answer 32

common antifungal creams such as imidazoles. oral antifungal agents can also be used.

Question 33

Psoriasis differential diagnosis

Answer 33

lichen planus; lichen simplex chronicus; flat warts; pityriasis rosea; rheumatoid Arthritis; reactive arthritis; seborrheic dermatitis; atopic dermatitis; ; fungal infections; gout; pseudogout; syphilis; nummular eczema; SCC

Question 34

Psoriasis risk factors

Answer 34

genetic factors; smoking; obesity; drugs (eg; beta blockers, lithium, etc..); infections; alcohol; vit D defeciency the peak times for disease onset are ages 30 to 39 and ages 50 to 69 years The scalp, extensor elbows, knees, and back are common locations for plaque psoriasis.

Question 35

Psoriasis clinical presentation

Answer 35

thick, red plaques with sharply defined border and adherent silvery scale Psoriasis occurs in a variety of clinical forms. The major clinical categories include: ``` ●Chronic plaque psoriasis ●Guttate psoriasis ●Pustular psoriasis ●Erythrodermic psoriasis ●Inverse psoriasis ●Nail psoriasis ```

Question 36

Psoriasis diagnostics

Answer 36

diagnosis usually based on presentation of silvery scales on red, erythematous plaques biopsy useful in pustular disease nail cultures useful to differentiate for fungal dx

Question 37

Psoriasis TX

Answer 37

not curable to treat symptoms a combination of therapies centered on topical tx can manage the disease: moderate to high potency topical glucocorticosteroids applied two or three times per day over 2 to 3 weeks. UV light oral medications such as oral retinoids and methotrexate biologic agents such as TNF antagonists coal tar preparations

Question 38

Onychomychosis differential diagnosis

Answer 38

psoriasis; eczema; trauma; lichen planus; onychogryposis; herpetic whilow; subungual malignant melanoma; PVD; pityriasis; medications; trophic changes; black nail paronychia; darier's disease; endocrine disorders

Question 39

Onychomychosis risk factors

Answer 39

risk factors include advanced age, swimming, tinea pedis, psoriasis, diabetes, immunodeficiency, genetic predisposition, and living with family members who have onychomycosis

Question 40

Onychomychosis clinical manifestations

Answer 40

onychomycosis is any infection of the nails caused by a fungus. Tinea unguium is a dermatophyte infection of the nail plate, although the terms are often used interchangeably

Question 41

Onychomychosis clinical manifestations

Answer 41

onychomycosis is any infection of the nails caused by a fungus. Tinea unguium is a dermatophyte infection of the nail plate, although the terms are often used interchangeably Onychomycosis is marked by nail thickening, yellowish nail discoloration, onycholysis, and subungual debris. If left untreated, nail infections can lead to total nail dystrophy. Paronychia (erythema and swelling surrounding the nail plate) may be an associated finding.

Question 42

Onychomychosis diagnostics

Answer 42

KOH smear and culture CBC and differential LFTs

Question 43

Onychomychosis TX

Answer 43

Treatment of onychomycosis is not mandatory in all patients. We suggest treating onychomycosis in: ●Patients with a history of cellulitis of the lower extremity, especially if repeated, who have ipsilateral toenail onychomycosis ●Patients with diabetes and toenail onychomycosis who have additional risk factors for cellulitis (ie, prior cellulitis, venous insufficiency, edema) ●Patients who are experiencing discomfort or pain associated with infected nails ●Immunosuppressed patients ●Patients who desire treatment for cosmetic reasons Although 50% of nail dystrophies are due to onychomycosis, a patient should never be treated with systemic antifungal agents without confirmed infection based on direct microscopy, fungal culture, or histopathology. Systemic antifungal agents are costly and can have rare, undesirable side effects and toxicities. Treatment options for onychomycosis include topical and systemic antifungal drugs, laser treatment, photodynamic therapy (PDT), and surgery. In addition, patients with symptomatic onychomycosis may benefit from measures to reduce discomfort regardless of whether they proceed with curative treatments. The most effective therapy for onychomycosis is terbinafine 250 mg p.o. daily for a duration of 12 weeks for toenail infections and 6 weeks for fingernail infections. As a less expensive alternative regimen, pulse dosing of terbinafine can be used with only a slight decrease in efficacy (250 mg p.o. for 7 days, for 1 week per month for 3 months). Topical urea is a keratolytic agent useful for removing hyperkeratotic nail debris in patients who forgo antifungal treatment (symptom relief)

Question 44

Warts differential diagnosis

Answer 44

seborrheic keratosis; callus; lichen planus; SCC; molloscum contagiosum; amelanotic melanoma; foreign body

Question 45

Warts risk factors

Answer 45

infection occurs when the virus comes in contact with skin that is broken or has been traumatized. The virus enters the hosts epidermal epithelial cells and uses the hosts resources to replicate. warts can occur singly or in groups and can coalesce to form plaques called mosaic warts. auto inoculation can come from cutaneous trauma, such as from shaving or scratching. transmission is usually through direct skin contact. Genital infection is usually acquired through sexual contact. individuals with decreased cellular immunity are at risk for more recalcitrant HPV infection. more common in kids and young adults more common among certain occupations such as handlers of meat, poultry, and fish

Question 46

Warts clinical manifestations

Answer 46

benign epidermal neoplasms caused by various forms of HPV virus

Question 47

Warts diagnostics

Answer 47

The diagnosis of cutaneous warts is based upon clinical appearance. If there is doubt, a no. 15 blade can be used to scrape off any hyperkeratotic debris and reveal thrombosed capillaries, manifesting as black dots. If dermatoscopic examination is performed, these may appear as homogenous black to red dots and globules The wart also will obscure normal skin markings, also known as dermatoglyphics (lines palms and bottom of feet). Rarely, a shave biopsy is indicated to confirm the diagnosis.

Question 48

Warts TX

Answer 48

Topical salicylic acid and cryotherapy with liquid nitrogen are the most common treatments for common and plantar warts and have the strongest evidence for efficacy Intralesional immunotherapy with skin test antigens (ie, mumps, Candida, or Trichophyton antigens) may lead to the resolution both of the injected wart and additional untreated warts

Question 49

Pediculosis differential diagnosis

Answer 49

lice; scabies; hair casts; seborrheic dermatitis; tinea capitus; peidra

Question 50

Pediculosis risk factors

Answer 50

exposure to crowded public areas such as schools; inability to clean and launder clothing, bed linens sexual contact with infected people poor hygiene

Question 51

Pediculosis diagnostics

Answer 51

Demonstration of lice or nits on hair visually or under microscope. Wood's lamp demonstrates fluorescent nits.

Question 52

Pediculosis TX

Answer 52

Topical pediculicides are the most common initial treatments. ( permethrine) Manual removal of lice (wet combing) is sometimes used as an alternative to topical pediculicide therapy. Oral therapy is occasionally required for refractory infestations. Regardless of the treatment selected, the presence of living lice should be confirmed prior to treatment

Question 53

Pediculosis clinical manifestations

Answer 53

severe itching and scratching of whatever area the infestations is in - head, neck, groin, body excoriated skin from scratching visible lice and nits in hair, body or clothing papules with an erythemic base may develop on the genital area, axilla, chest, beard or eyelashes

Question 54

Candidiasis differential diagnosis

Answer 54

aphthous ulcers; leukplakia; miliaria; bacterial infection; erythrasma; seborrheic dermatitis; atopic dermatitis; tinea cruris; inverse psoriasis; mycosis fungoides; scabies; bacterial vanginosis; trichomoniasis; allergic contact dermitits; pediculosis pubis;

Question 55

Candidiasis risk factors

Answer 55

immunosuppression: candida albicans, a yeast, can be normally found on mucous membranes, GI tract, in the vagina and on the skin. it is opportunistic and behaves like a pathogen in the presence of immunosuppression. predisposing factors: obesity, medications such as abx or corticosteroids, malnutrition, diabetes and other endocrine diseases, HIV/AIDS. a local environment that is warm, moist, macerated or occluded favors the growth of this organism

Question 56

Candidiasis clinical manifestations

Answer 56

fungal infection of the mucus membranes and/or skin, occurs frequently in women, children and the elderly

Question 57

Candidiasis diagnostics

Answer 57

KOH preparation; skin cluture/biopsy if indicated

Question 58

Candidiasis TX

Answer 58

Oral: nystatin oral suspension/ gentian violet aqueous solution topical: nystatin cream/ mycolog II vaginal: clotrimazole/ miconazole/ terconazole

Question 59

Folliculitis: furuncle (boils) and carbuncle differential diagnosis

Answer 59

folliculitis; acne vulgaris; ingrown hair follicle; | keratosis pilaris; contact dermatitis

Question 60

Folliculitis: furuncle (boils) and carbuncle risk factors

Answer 60

break in the skin tissue; use of razors on skin; poor hygiene; diabetes

Question 61

Folliculitis: furuncle (boils) and carbuncle clinical manifestations

Answer 61

outbreak of pustules on the face, scalp or extremities that do not resolve despite proper hygiene and care; tenderness and itching at site furuncle (boil/abscess): a deep pustule, tender, firm or fluctuant, found in groin, axilla, waistline, buttocks carbuncle: a group of follicles coalescing into one larger, painful, infected area; may see fever and chills excoriated folliculitis: chronic thickened, excoriated papules or nodules

Question 62

Folliculitis: furuncle (boils) and carbuncle diagnostics

Answer 62

culture and sensitivity to verify appropriate abx coverage gram stain KOH/wet prep fungal culture hair if fungi suspected

Question 63

Folliculitis: furuncle (boils) and carbuncle TX

Answer 63

For small furuncles, warm compresses to promote drainage are usually sufficient treatment. Larger furuncles, carbuncles, and abscesses require incision and drainage, and material should be sent for culture and susceptibility testing The role of antimicrobial therapy for treatment of skin abscesses, furuncles, and carbuncles depends on individual clinical circumstances. In general, antibiotic therapy (in addition to incision and drainage) is warranted for patients in any of the following categories: ●Multiple lesions or single abscess ≥2 cm ●Extensive surrounding cellulitis ●Associated comorbidities or immunosuppression ●Signs of systemic infection ●Inadequate clinical response to incision and drainage alone ●Presence of an indwelling medical device (such as prosthetic joint, vascular graft, or pacemaker) ●High risk for transmission of S. aureus to others (such as in athletes, military personnel) Management with incision and drainage alone (in the absence of antimicrobial therapy) is generally sufficient for otherwise healthy patients with skin abscess

Question 64

Cellulitis differential diagnosis

Answer 64

cellulitis; abscess; dermatitis; erysipelas( a superficial skin infection that commonly occurs on the face, ears and /or lower legs. more commonly seen in older adults. presents with erythema of the skin with a distinct, demarcated border commonly caused by group A strep.)

Question 65

Cellulitis risk factors

Answer 65

age ( older than 45); immunocompromised; | chronic medical condition (diabetes); hx of IV drug abuse; alcoholism; PVD; hx of previous cellulitis occurrence

Question 66

Cellulitis clinical manifestations

Answer 66

erythema, pain, swelling and warmth, fever, malaise, chills, lymphadenopathy of adjacent lymph nodes to site of infection, trauma to tissue, drainage /discharge at site, erythemic streaks progressing away from the site, systemic s/s of infection

Question 67

Cellulitis diagnostics

Answer 67

blood cultures; gram stain; culture from abscess; CBC with diff; CRP creatinine; bicarb; creatine phosphokinase ultrasound for asses for abscess xray if suspicious for osteomyelitis CT or MRI may be considered when assessing for nec fasc.

Question 68

Cellulitis TX

Answer 68

Management of cellulitis and erysipelas should include elevation of the affected area and treatment of underlying conditions. Elevation facilitates gravity drainage of edema and inflammatory substances. The skin should be sufficiently hydrated to avoid dryness and cracking without interdigital maceration. Many patients with cellulitis have underlying conditions that predispose them to developing recurrent cellulitis (these include tinea pedis, lymphedema, and chronic venous insufficiency). In such patients, treatment should be directed at both the cellulitis and the predisposing condition. Patients with edema may benefit from treatment with compressive stockings and diuretic therapy Patients with mild cellulitis may be treated with oral antibioticsTreatment with parenteral antibiotics is warranted for patients with signs of systemic toxicity, rapid progression of erythema, immunocompromise, and/or proximity to an indwelling device (such as a prosthetic joint or a vascular graft; cellulitis should be considered a manifestation of device infection if it originates on the skin directly overlying the prosthesis site). Parenteral therapy is also appropriate for patients with persistence or progression of symptoms despite 48 to 72 hours of appropriate oral therapy.The approach to antibiotic selection for treatment of cellulitis depends on whether the clinical presentation consists of purulent or nonpurulent cellulitis see algorithm for oral abx treatment for cellulitis in uptodate

Question 69

WHEAL (hive):

Answer 69

Fleeting skin elevation that is irragularly shaped because of edema ( eg; mosquito bit)

Question 70

VESICLE (blister):

Answer 70

Elevated, sharply defined lesion containing serous fluid. Usually less than 1 cm( eg; chicken pox)

Question 71

BULLA (plural, bullae):

Answer 71

Large, elevated, fluid filled lesion greater than 1 cm (eg: partial thickness burn)

Question 72

CYST:

Answer 72

Elevated, thick walled lesion containing fluid or semisolid matter

Question 73

PUSTULE:

Answer 73

Elevated lesion less than 1 cm containing purulent material. Lesions larger than 1 cm are described as boils, abscesses or furuncles ( acne or impetigo)

Question 74

LICHENIFICATION

Answer 74

Epidermal thickening resulting in elevated plaque with accentuated skin markings. usually results from repeated injury through rubbing or scratching ( eg; chronic atopic drematitis)

Question 75

EXCORIATION

Answer 75

Superficial, linear abrasion of epidermis. Visible sign of itching caused by rubbing or scratching ( atopic dermatitis)

Question 76

FISSURE

Answer 76

Deep linear split through epidermis into dermis ( tinea pedis)

Question 77

KELOID

Answer 77

Irregularly shaped, elevated, progressively enlarging scare; extends beyond the boundaries of the wound; caused by excessive collagen formation during post- surgical healing

Question 78

Herpes Simplex 1 & 2 (HSV 1 &2) differential diagnosis

Answer 78

Erythema multiforme; Varicella; Impetigo; Stomatitis; Herpes Zoster; SJS; Herpangina

Question 79

Herpes Simplex 1 & 2 (HSV 1&2) risk factors

Answer 79

Immunocompromised patients; Prior HSV infections; Exposure to virus

Question 80

Herpes Simplex 1 &2 (HSV 1 & 2) clinical presentation

Answer 80

HSV 1 : primarily oral lesions, but can infect genitals HSV 2: primarily genital lesions, but can infect oral site three distinct phases: primary, latent and recurrent infection groups of vesicles on a red base

Question 81

Herpes Simplex 1 &2(HSV 1 &2) diagnostics

Answer 81

Viral cultures

Question 82

Herpes Simplex 1 &2(HSV 1& 2) TX

Answer 82

symptomatic tx for initial HSV 1 infections ( tylenol for pain, etc) For recurrent HSV 1 and initial/recurrent HSV 2 ( for genital herpes treat all pts regardless of severity, presentation, timing, etc): Acyclovir or Famciclovir orrally

Question 83

Acne Vulgaris differential diagnosis

Answer 83

Acne/steroid rosacea; folliculitis; perioral acne; drug induced acne; keratosis pilaris; sebaceous hyperlasia; flat warts; nevus comedonicus

Question 84

Acne Vulgaris risk factors

Answer 84

age (adolescence); external irritants to skin; hormones; medications; hot, humid weather

Question 85

Acne Vulgaris clinical presentation

Answer 85

pimples on face, chest, back and shoulders that do not resolve with over the counter tx; possible acne rosecea - telangiectasia, flushing and rhinophyma Open comedones (blackheads) and closed comedones (whiteheads), and erythematous papules and pustules. Nodules and cysts can result in pitted or hypertrophic scars. severe: nodules, cysts, scars

Question 86

Acne Vulgaris diagnostics

Answer 86

diagnosed by physical examination; blood tests necessary if adrenal or gonadal dysfunction is a possible cause.

Question 87

Acne Vulgaris TX

Answer 87

advise proper cleansing and life style changes; topical benzoyl or tretinoin cream advancing to oral tetracycline/erythromycin if topicals not affective; Accutane( isotrentinoin) restricted to tx of recalcitrant nodulocystic acne that has been unresponsive to standard therapies.

Question 88

Rosacea differential diagnosis

Answer 88

sun damage; seborrheic dermatitis; Acute cutaneous lupus erythematosus; Dermatomyositis; Acne vulgaris;

Question 89

Rosacea risk factors

Answer 89

family hx; triggers that stimulate flushing - sun, exercise, spicy foods, etc.

Question 90

Rosacea clinical manifestations

Answer 90

rosacea is characterized by centrofacial erythema and telangiectasias; Affected patients also often exhibit flushing and sensitivity of facial skin;

Question 91

Rosacea diagnostics

Answer 91

The patient history and physical findings are usually sufficient for the diagnosis of this disorder.

Question 92

Rosacea TX

Answer 92

start with neutral soaps and avoidance of irritants; metronidazole 1% gel, cream or lotion twice daily; oral abx can be tried if topical ineffective - tetracycline 250 to 500 mg twice daily. Telangiectasis, often the result of constant flushing, may respond to laser tx

Question 93

Atopic dermatitis differential diagnosis

Answer 93

contact dermatitis; seborrheic dermatitis; ichthyosis vulgaris; bacterial/fungal infections; neoplastic disease; immunologic and metabolic disorders

Question 94

Atopic dermatitis risk factors

Answer 94

immune dysfunction leading to IgE dysfunction; family hx of atopic triad( asthma, allergic rhinitis, dermatitis); exposure to allergen/topical medication/skin irritants; stress

Question 95

Atopic dermatitis clinical manifestations

Answer 95

pruritic, erythmematous, dry patches of skin, often with scale. Linear excoriations may be seen as a secondary change. Borders initially not well defined, crusting and oozing common. Itching, impossible to relieve; dryness.

Question 96

Atopic dermatitis diagnostics

Answer 96

culture skin lesions to determine viral, bacterial or fungal etiology KOH preparation blood work: serum IgE elevated with atopic dermatitis.

Question 97

Atopic dermatitis TX

Answer 97

``` eliminate allergens (food, environmental); potent topical corticosteroid Betamethasone valerate 0.1% two to three times daily; antihistamine of choice; for severe cases - oral steroid. if needed, abx for secondary infections ```

Question 98

Contact dermatitis differential diagnosis

Answer 98

irritant/allergic contact dermatitis; candidiasis; tinea pedis, corporis, cruris; drug reactions; pityriasis rosea; scabies

Question 99

Contact dermatitis clinical manifestations

Answer 99

In acute cases, lesions tend to be vesicular or bullous. Subacute cases are papular, erythematous, and scaly. Look for well-demarcated borders and geometric shapes with straight edges and right angles. Eyelid edema is frequently seen when the allergen is innocently transferred from finger to lid. Innocent transfer to other parts of the face and genital areas may also occur. Affected areas are typically severely pruritic. Contact dermatitis can be found at any body location. When the dermatitis is chronic, thickened plaques develop and secondary bacterial infection is possible.

Question 100

Contact dermatitis risk factors

Answer 100

skin reactivity to irritants is highest in infants and tends to decrease with age affects more women than men hobbies, occupation(hairdresser, nurse, etc) jewelry High temperatures, increased humidity and air flow appear to decrease the skin barrier function and increase the penetration of irritants

Question 101

Contact dermatitis diagnostics

Answer 101

none if source known, otherwise a wet mount (KOH, saline) can rule out fungal, culture/sensitivity of pustules, patch test to rule out allergic contact dermatitis.

Question 102

Contact dermatitis TX

Answer 102

removal of irritating agent; high potency topical corticosteroids - Hydrocortisone 2.5%ointment for mild forms, super high for severe/chronic cases. also have pt use emollients and moisturizers to reduce dryness and promote healing

Question 103

Basal cell carcinoma differential diagnosis

Answer 103

actinic keratoses; BCC/SCC; malignant melanoma; dysplastic nevi;

Question 104

Basal cell carcinoma risk factors

Answer 104

sun damage; immunosuppression; genetic factors; smoking;

Question 105

Basal cell carcinoma clinical manifestations

Answer 105

nodular tumor with pearly surface, telangiectasia on surface and depressed center or rolled edge. 70 percent of BCCs present on the face and head.

Question 106

Basal cell carcinoma diagnostics

Answer 106

skin biopsy (shave, punch or excisional)

Question 107

Basal cell carcinoma TX

Answer 107

electrodesiccation and curettage

Question 108

Squamous cell carcinoma differential diagnosis

Answer 108

BCC; actinic keratoses; malignant melanoma; dysplastic nevi

Question 109

Squamous cell carcinoma risk factors

Answer 109

sun; age; immunosuppression; family hx,

Question 110

Squamous cell carcinoma clinical manifestations

Answer 110

irregular papule with scaly, friable, bleeding surface; roughened, scaling area that doesn't heal and readily bleeds

Question 111

Squamous cell carcinoma diagnostics

Answer 111

skin biopsy ( shave, punch or excisional)

Question 112

Squamous cell carcinoma TX

Answer 112

total excision

Question 113

Malignant Melanoma differential diagnosis

Answer 113

actinic keratoses; BCC/SCC; solar lentigo; seborrheic keratosis; common nevus; leukoplakia

Question 114

Malignant Melanoma risk factors

Answer 114

age; sun exposure; fair complexion; smokers; skin damaged by burns/inflammation; hx of blistering sunburns before 18 y/o increases risk.

Question 115

Malignant Melanoma clinical manifestation

Answer 115

asymmetrical tumor of skin with irregular border, variation in color, greater than 6 mm in diameter, can metastasize to any organ

Question 116

Malignant Melanoma diagnostics

Answer 116

biopsy

Question 117

Malignant Melanoma TX

Answer 117

biopsy any suspicious lesion, excision of lesion with margins, referral to dermatologist for skin cancer screenings - every 3 months for 5 years, then every 6 months.