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AGPCNP > derm > Flashcards

derm Flashcards

1
Q

what is the structure and function of the skin?

A 
Barrier against fluid loss
Protection from ultraviolet radiation
Thermoregulation
Cushioning
Immunologic protection
Appearance
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2
Q

Define macule

A

flat (nonpalpable), < 1cm in size

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3
Q

What is a patch?

A

flat (nonpalpable), > 1cm in size

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4
Q

What is a papule?

A

raised, < 1cm in size

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5
Q

What is a plaque?

A

raised (a broad papule), > 1cm in size

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6
Q

What is a nodule?

A

similar to a papule but > 1cm and located in the dermis or subcutaneous fat

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7
Q

What is a vesicle?

A

fluid filled, < 1cm in size

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8
Q

What is a bullae

A

fluid filled, > 1cm in size

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9
Q

What is a wheal?

A

(hive) – edematous papule or plaque that usually lasts < 24 hours

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10
Q

What is a scale?

A

dry or greasy laminated masses of keratin

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11
Q

What is crust?

A

dried serum, pus, or blood

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12
Q

What is a fissure?

A

a linear cleft through the epidermis or into the dermis

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13
Q

What is erosion?

A

loss of all or portions of the epidermis alone, heals without scarring

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14
Q

What is an ulcer?

A

complete loss of the epidermis and some portion of the dermis, heals with scarring

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15
Q

What is nummular dermatitis (etiology, age peaks)

A

“coin-shaped”
Etiology: unknown - classified as a form of atopic derm
2 peaks of age distribution - most common 6th to 7th decade of life M>F peak in 2nd to 3rd decade of life F>M

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16
Q

What is nummular dermatitis (presentation)?

A

round-to-oval crusted or scaly erythematous plaques
Most common arms and legs
Start as papules which coalesce into plaques with scale
Early lesions may be studded with vesicles containing serous exudate
Usually very pruritic
Often recurs in the same locations as old lesions
Lesions often symmetrically distributed
Waxes and wanes with winter

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17
Q

What is nummular dermatitis (ddx and treatment)?

A

DDx: contact derm, psoriasis, CTCL, pityriasis rosea, tinea corporis
Treatment: topical steroids, moisturization

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18
Q

Discuss topical steroids, use, risks, and recommendations

A

may alternate high potency with mid potency to reduce risk or use on weekends only
Risks of overuse of topical steroids include: atrophy, striae, telangiectasias, hypopigmentation (temporary), can have systemic absorption if using long-term on a large body surface area
Should recommend <14/28 days , 2-3 x week, Sat/ Sun use
classes (7) based on vasoconstrictive properties (ointment stronger than cream)

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19
Q

What are topical calcineurin inhibitors, when are they used, and where?

A

Topical calcineurin inhibitors (steroid sparing agents)
Tacrolimus (Protopic) ointment
Pimecrolimus (Elidel) cream

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20
Q

Discuss class 1 steroids and examples

A

superpotent
Clobetasol propionate
Betamethasone dipropionate
for scalp, palms, soles

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21
Q

Discuss class 3 and 4 steroids and examples

A 
mid-strength
Fluocinonide 
Betamethasone valerate
Triamcinolone
trunk and extremities
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22
Q

Discuss class 6 and 7 steroids and examples

A 
Class 6 and 7= low potency
Fluocinolone
Desonide
Hydrocortisone
face, genitals, intertriginous areas
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23
Q

Discuss allergic contact derm, common culprits, and etiology

A

Etiology: delayed type of induced sensitivity - cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity
~25 chemicals are responsible for as many as one half of all cases
Common culprits: Poison ivy, topical antibiotics (e.g., Neosporin, neomycin, bacitracin), nickel, rubber gloves, hair dye, textiles, preservatives, fragrances, benzocaine

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24
Q

Discuss allergic contact derm presentation and DDx

A

Presentation: pruritic papules and vesicles on an erythematous base
Acute onset
Geometric morphology (circles, lines, etc)
Lichenified pruritic plaques may indicate chronic ACD
Initial site of dermatitis often provides best clue regarding the potential cause
DDx: drug rash, nummular dermatitis, seb derm, tinea, urticaria

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25
Q

Discuss allergic contact derm treatment

A

Treatment: avoid offending agent, topical steroids or calcineurin inhibitors, antihistamines, cool soaks, emollients, oral prednisone in severe cases, need to treat 14-21 days. can refer for patch testing to help determine allergen

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26
Q

Discuss drug eruptions common culprits and etiology

A

A drug-induced reaction should be considered in any patient who is taking medications and suddenly develops a symmetric cutaneous eruption (usually occurs w/in the first 2 wks of tx)
Common culprits: antimicrobial agents, NSAIDs, cytokines, chemotherapeutic agents, anticonvulsants, psychotropic agents

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27
Q

Discuss drug eruptions presentation and ddx

A

Presentation: Lesions usually appear proximally and generalize within 1-2 days
DDx: contact dermatitis, erythroderma, leukocytoclastic vasculitis, measles, pityriasis rosea, lichen planus, psoriasis (pustular), urticaria, syphilis

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28
Q

Discuss drug eruptions treatment

A

Treatment: discontinue offending agent
Can treat symptoms with antihistamines and topical steroids
Most drug eruptions are mild, self-limited, and usually resolve within 2 weeks of stopping the offending agent;
Note: some reactions can be life-threatening (SJS/TEN)

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29
Q

Discuss morbilliform drug reaction

A 
most common form of drug reaction
Primary Lesion
Macules, papules
Secondary Changes
none
Configuration
coalescing
Distribution
Generalized
Color
Red
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30
Q

Discuss urticaria etiology and age range

A

Etiology: release of histamine & other vasoactive substances from mast cells & basophils
15-20% of the general population is affected at some point during their lifetime
May be acute (lasting < 6 wk) or chronic (lasting > 6 wk)
Can occur at any age, but chronic urticaria is more common in the 40s and 50s

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31
Q

Discuss acute urticaria

A

cause unknown in > 60% of cases; known causes include: infections (ask about recent illness and travel); caterpillars/moths; foods (e.g. shellfish, nuts); drugs (e.g. PCN, sulfonamides, salicylates, NSAIDs); environmental factors (e.g. pollens, chemicals, plants, danders, dust, mold); latex; exposure to undue skin pressure, cold, or heat; emotional stress; exercise

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32
Q

Discuss chronic urticaria

A

cause unknown in 80-90% of patients; known causes include all of the above as well as: autoimmune disorders; chronic medical illness; cold urticaria, cryoglobulinemia, or syphilis; mastocytosis; inherited autoinflammatory syndromes

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33
Q

Discuss urticaria presentation

A

Presentation: blanching, raised, palpable wheals
Occur on any skin area and are usually transient (last < 24 hrs) and migratory
Dermatographism may occur (urticaria resulting from light scratching)

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34
Q

What are s/s included with urticaria that should send someone to the ED?

A

Physical exam should focus on conditions that might precipitate urticaria or could be potentially life threatening – refer or send to ED if:
Angioedema of the lips, tongue, or larynx
Urticarial lesions that are painful, long lasting (> 36-48 hrs), ecchymotic, or leave residual hyperpigmentation upon resolution (suggests urticarial vasculitis)
Systemic signs or symptoms - arthralgias, arthritis, weight changes, lymphadenopathy, bone pain
Scleral icterus, hepatic enlargement, or tenderness that suggests hepatitis or cholestatic liver disease
Evidence on the skin of bacterial or fungal infection
Listen to the lungs for signs of asthma or pneumonia

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35
Q

Urticaria DDx and treatment

A

Treatment: H1 antihistamines (ie Benadryl, hydroxyzine, Zyrtec)
May add H2 antihistamines (ie ranitidine) for severe or persistent urticaria
Glucocorticosteroids for refractory cases
Zyrtec should be dosed bid; Doxepin, tricyclic antidepressants with potent antihistamine properties, or Xolair may be useful in chronic urticaria

36
Q

Discuss seb derm etiology

A

Etiology: related to a pathologic overproduction of sebum; may involve an inflammatory reaction to the yeast Malassezia

37
Q

Discuss Seb derm presentation and ddx

A

Presentation:
Erythema with greasy yellowish scale on the “T-zone” of the face, scalp, behind the ears, central chest , intertigo
Dandruff
Can affect intertriginous areas
Usual onset occurs with puberty
Worsens with changes in seasons, trauma, stress, Parkinson disease, AIDS, certain medications
DDx: Atopic or contact dermatitis, rosacea, perioral dermatitis, tinea, impetigo

38
Q

Treatment for Seb Derm

A

Shampoo at least every other day (shampoos that contain salicylic acid, tar, selenium, sulfur, or zinc are especially helpful) – leave on for 5 minutes before washing off
Clobetasol 0.05% solution or Derma-Smoothe/FS (mineral/peanut oil + fluocinolone 0.1%) for severe flaking on the scalp
Ketoconazole 2% cream twice a day (for face, ears chest)
Hydrocortisone 2.5% cream – short-term use during flares
Tacrolimus ointment or pimecrolimus cream as steroid sparing agents

39
Q

Etiology psoriasis

A

Etiology: Multifactorial disease that appears to be influenced by genetic and immune-mediated components

40
Q

Psoriasis presentation and triggers

A

Presentation: Characterized by red papules and plaques with adherent silvery scale
Triggers: Physical trauma, stress, infection (Strep, HIV), pregnancy, medications

41
Q

Drugs that can trigger psoriasis

A 
NSAIDs
Antibiotics
Steroids
Antimalarials
Lithium
ACE inhibitors
Beta-blockers
Calcium channel blockers
Interferon
Tetanus
Antihistamines
42
Q

What do do at each clinic visit for psoriasis?

A 
Ask about joint pain
10% of patients have Psoriatic Arthritis (PsA) (Refer to Derm or Rheum)
Estimate body surface area (BSA)
An average palm = 1%
Disease Severity: 
Mild <5% BSA
Moderate = 5-10% BSA (Refer to Derm)
Severe >=10% BSA (Refer to Derm)
Note – psoriasis is associated with cardiovascular disease, smoking, alcohol, metabolic syndrome, lymphoma, depression, suicide
43
Q

Describe psoriasis vulgaris and distribution

A 
Chronic and stationary - lesions can persist for years
Distribution:
Elbows
Knees
Scalp
Lumbosacral
Umbilicus
nail pitting and other nail changes are common
44
Q

Describe Koebner’s phenomenon

A

Occurs in 20% of patients

Non-specific trauma can lead to formation of psoriasis in the area of irritation

45
Q

Describe inverse psoriasis

A

Involvement limited to skin fold regions
Usually associated with minimal scaling
Distribution: axilla, inframammary region, genitocrural region, neck
Often confused with intertrigo

46
Q

Describe topical treatment for psoriasis

A

Topical steroids
Hydrocortisone 2.5% ointment (low strength) – good for short term use on face, penis, and intertriginous areas
Triamcinolone 0.1% ointment (medium strength)
Clobetasol 0.05% ointment (high strength)
Synthetic Vitamin D
Dovonex (calcipotriene) cream – helps reduce scale
Topical calcineurin inhibitors – steroid sparing agents (good for face, penis, intertriginous areas
Protopic ointment
Elidel cream
Common treatment regimen
calcipotriene bid Mon-Fri and clobetasol oint bid Sat-Sun for lesions on trunk and extremities; hydrocortisone or calcineurin inhibitor for face, penis, and intertriginous areas

47
Q

Describe etiology and prevalence of tidea pedis

A

Etiology: dermatophyte infection of the soles of the feet and interdigital spaces, commonly caused by Trichophyton rubrum
Prevalence increases with age; M > F

48
Q

Describe tinea pedis presentation and ddx

A

Presentation: pruritic, scaling in a moccasin distribution, often with painful fissures between the toes
Can sometimes confirm diagnosis with KOH prep
DDx: contact dermatitis, dyshidrotic eczema, psoriasis

49
Q

Describe treatment for tinea pedis

A 
topical Azoles (ketoconazole)
topical Allylamines (terbinafine)
Castellani’s paint (especially good for the interdigital webspaces)
Apply to bottoms, sides, and interdigital areas of the feet once or twice/day for at least 2 weeks, depending on which agent is used
50
Q

Describe ochomycosis etiology, presentation, DDX

A

Etiology: a fungal infection of the toenails or fingernails
Presentation: asymptomatic subungual hyperkeratosis and onycholysis, usually yellow-white in color
Should confirm diagnosis before treating - clip nail to send for PAS or put in dermatophyte medium
DDx: Lichen planus, psoriasis, trauma

51
Q

Describe onchomycosis treatment

A

Oral Terbinafine, itraconazole (6 weeks for fingernails; 12 weeks for toenails - check baseline Cr, LFTs, CBC and recheck if tx >6 weeks
If orals contraindicated (liver disease) may try ciclopirox lacquer or urea 40% with topical terbinafine but this is often not effective; Jublia is a new topical solution on the market (but treatment is 48 wks!)
Inform patients that it can take a year for the entire nail to grow out and appear normal; recurrence is common even after systemic treatment; clean shoes and use topicals as maintenance

52
Q

Describe intertrigo etiology

A

Etiology: an inflammatory condition of skin folds resulting from heat, moisture, and friction
Often colonized by infection - usually candida but can also be bacterial, fungal, or viral
A common complication of obesity and diabetes

53
Q

Describe intertrigo presentation, ddx

A

Presentation: Erythema, cracking, and maceration with burning and itching at sites in which skin surfaces are in close proximity (axillae, perineum, inframammary creases, abdominal folds, inguinal creases)
DDx: contact dermatitis, seborrheic dermatitis, cellulitis, inverse psoriasis, acanthuses nigricans

54
Q

Describe intertrigo treatment

A

Treatment: Barrier creams such as zinc oxide paste, compresses with Burow solution 1:40 or dilute vinegar, absorbent powders and moisture-wicking undergarments, exposing the skin folds to air, topical antifungal agents for secondary infections (e.g., clotrimazole, econazole, ciclopirox, miconazole, ketoconazole, nystatin)

55
Q

Describe scabies etiology, presentation, ddx

A

Etiology: Sarcoptes scabiei
In developed countries, scabies occur primarily in institutional settings and long-term care facilities; also common among children
Presentation: Extremely itchy, especially at night
Often involves armpits, groin, umbilicus, wrists, fingerwebs, nipples
Primary lesions typically include small papules, vesicles, & burrows
DDx: atopic dermatitis, bug bites, folliculitis, psoriasis

56
Q

Describe scabies treatment

A 
Treatment: topical antiscabietic agents (e.g., Permethrin 5%) are applied from the neck down with repeat application in 7 days, oral ivermectin is also effective
Pruritus may continue for up to 2 weeks after successful treatment
Antipruritic agents (e.g. sedating antihistamines) and/or  antimicrobial agents (for secondary infection) may be needed
All family members and close contacts must be evaluated and treated for scabies, even if they do not have symptoms
* Itchy papules on the penis are scabies until proven otherwise
57
Q

Describe zoster etiology

A

the reactivation of the varicella-zoster virus (VZV) in a dermatome
A person of any age with a prior varicella infection may develop zoster, but incidence increases with age due to declining immunity

58
Q

Describe zoster presentation and DDx

A

Pre-eruptive phase: characterized by unusual skin sensations or pain within the affected dermatome that heralds the onset of lesions by 48-72 hours
Active eruptive phase: marked by lesions that begin as erythematous macules and quickly develop into vesicles; new lesions form over 3-5 days
Lesions in the eruptive phase tend to resolve over 10-15 days
Can be very painful and cause chronic neuralgia
DDx: poison ivy, atopic dermatitis

59
Q

Describe zoster treatment

A

antivirals (e.g. acyclovir, valacyclovir, and famciclovir)
Patients are infectious until the lesions have dried
Zostavax for people ages 50 and older can help prevent zoster

60
Q

Discuss herpes zoster ophthalmicus

A

important not to miss – involves the trigeminal (fifth cranial) nerve; vesicles may appear on the tip or side of the nose (Hutchinson sign) and urgent referral to ophthalmology is required

61
Q

Discuss folliculitis etiology

A

primary inflammation of the hair follicle resulting from infections, follicular trauma or occlusion
Superficial folliculitis is common and often self-limited
Affects all races, ages, and men and women equally

62
Q

Discuss folliculitis presentation and ddx

A

acute onset of erythematous, folliculocentric papules and pustules associated with pruritus or mild discomfort
DDx: Acne, contact dermatitis, milia, miliaria, insect bites

63
Q

Discuss folliculitis treatment

A

uncomplicated superficial folliculitis can be treated with antibacterial soaps and good hand washing technique
refractory or deep lesions with a suspected infectious etiology may need empiric treatment with topical and/or oral antibiotics that cover gram-positive organisms (choose a drug that covers MRSA in areas of high prevalence or in predisposed patients)
mupirocin ointment in the nasal vestibule twice a day for 5 days may eliminate the S aureus carrier state in recurrent folliculitis

64
Q

Discuss CA-MRSA prevalence

A

Prevalence: Studies have shown ~ 25-30% of the population is colonized with MSSA (usually on skin or in nasal passages)
A study in a California ED found 51% of patients presenting for evaluation of a skin infection had +MRSA cultures

65
Q

Discuss CA-MRSA presentation and transmission

A

Presentation: infections usually manifest as folliculitis or a similar skin infection (patients often present with a “spider bite” or “infected pimple”)
Transmission of CA-MRSA is though an open wound or from contact with a CA-MRSA carrier

66
Q

Discuss CA-MRSA treatment

A

I & D of the abscess and tx with appropriate antibiotics when indicated; wound exudates should be cultured to determine the causative organism and appropriate antibiotics
Oral antibiotics: Trimethoprim-sulfamethoxazole DS twice daily, w/ or w/o rifampin 600 mg/d; doxycycline 100 mg twice daily; clindamycin 450 mg 3 times a day (96% sensitive)

67
Q

Discuss rosacea including etiology and ddx

A

Chronic inflammatory disease of the central face with 4 types:
Erythematotelangiectatic
Papulopustular
Phymatous (Glandular Rosacea)
Ocular
Etiology: unknown but vasculature, climatic exposures, chemicals and ingested agents, pilosebaceous unit abnormalities, microbial organisms, increased neoangiogenesis, and several other factors may play a role
More common in fair-skinned persons of European and Celtic origin
DDx: lupus, seborrheic dermatitis, perioral dermatitis

68
Q

describe Erythematotelangiectatic Rosacea

A

History of flushing
Central facial erythema
Telangiectasias not essential

69
Q

Describe Papulopustular Rosacea

A

Central facial erythema
Papules or pustules
Edema

70
Q

Describe Phymatous Rosacea

A

Thickened edematous skin
Nose most commonly affected
Sebaceous hyperplasia

71
Q

Describe Ocular Rosacea

A

Ocular symptoms occur prior to cutaneous manifestations in ~20% of patients
Blepharitis and conjunctivitis
Staph infections common

72
Q

What are topical treatments for rosacea?

A 
Sunscreen!!!!!
A daily broad-spectrum sunscreen is recommended for all patients with rosacea
Metronidazole 
Azelaic acid
Sodium sulfacetamide/sulfur
Protopic
Erythromycin
Clindamycin
Tretinoin
Benzoyl peroxide
73
Q

Describe systemic treatments for rosacea

A 
Tetracyclines
DCN and MCN >> TCN
Azithromycin
Metronidazole
Isotretinoin
74
Q

What are key points when evaluating alopecia?

A

Detailed history, onset, stress, medications, diet , grooming , family history
Patchy or diffuse > 50% loss before noticeable
Scarring or non scarring
Loss of hair follicle openings
Scarring requires biopsy

75
Q

Describe telogen effluvium

A

-stress, + hair pull test, > 25% telogen hair , non scarring, diffuse- consider Thyroid ds, drugs, nutrition (cbc, Tsh, iron, ferratin)

76
Q

Describe androgenic alopecia

A

-family hx, non scarring, male pattern. Consider androgen excess in females

77
Q

Describe trichotillomania

A

-emotional, broken hairs, non scarring, patchy. Dif: areata, fungal

78
Q

Describe alopecia areata

A

-acute onset,smooth patches, autoimmune( DM, thyroid, vitiligo), exclamation point hairs, non scarring. Dif: tricho, fungal.
Topical steroids, ILK ,PUVA

79
Q

Describe alopecia d/t SLE

A

Scarring or non scarring, other signs

steroids , hydroxychloroquine

80
Q

Describe tinea capitis

A

Seborrea like, patchy , broken hair. Occipital lymph nodes.

Requires systemic, griseofulvin, terbinafine, itraconazole 1-3 months , follow LFTs

81
Q

describe lichen planopillaris

A

F>M. pustular ,erythema localized

scarring

82
Q

describe folliculitis decalvans

A

expanding patch with pustules to periphery

scarring

83
Q

describe acne keloidalis nuchae

A

expanding patch with pustules to periphery to nape of neck

scarring

84
Q

Describe bullous pemphigoid

A

Autoimmune blistering disease
Presence of circulating immunoglobulin G autoantibodies ( BP230, BP180)
Prodromal period : pruritus eczematous / urticarial lesions ( weeks to months)
Bullous phase abrupt onset widespread blister formation – tense, oval , round. Abdomen, flexor surfaces
Assess for ocular, mucosal involvement , genitalia, negative Nilolsky

85
Q

Describe triggers for bullous pemphigoid

A

Pharmocologic : Lasix, phenacetin, enalapril , nsaids, vaccines, ampicillin, pcn, cephalexin
Traumatic : burns, radiation,
Infections: Human herpesvirus, Epstein barr , CMV, Hepatitis b and c
Differential Dx: contact, urticaria , bites, dermatitis

86
Q

Describe treatment for bullous pemphigoid

A

Promote healing, reduce itching, prevent secondary infections
Topical steroids
Systemic oral steroids
Referral for biologic treatment :methotrexate, rituximab ,cellcept , azathioprine

AGPCNP (30 decks)

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