Dermatology I Flashcards

1
Q

List some Papulo-squamous diseases

A

(Papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis

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2
Q

1) List some examples of desquamation
2) List 2 examples of vesicular bullae
3) List 3 examples of acneiform lesions

A

1) Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis
2) Pemphigoid, pemphigus
3) Acne vulgaris, rosacea, folliculitis

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3
Q

List the 4 steps of skin formation

A

1) Cell division: Keratinocytes divide in the deepest (basal) layer
2) Cell differentiation: as cells move up in the dermis, they change shape and composition
3) Keratinization: cells secrete keratin proteins and lipids to form a matrix that protects the skin and gives it strength
4) Desquamation: the outer most layer of skin cells die and shed off from the skin

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4
Q

List 2 important things to do in a skin exam

A

1) Good lighting
2) Look for lesions that look different from other lesions on their body

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5
Q

List the 8 characteristics of skin lesions you need to memorize (hint: there’s a mnemonic)

A

CLAMPS TN
1) Color
2) Location/distribution (extent, pattern)
3) Arrangement (grouped vs disseminated & confluence (yes or no)
4) Margination (well- or ill-defined)
5) Palpation (consistency, temperature, mobility, tenderness, depth)
6) Shape
7) Type (ie, papule, macule, pustule)
8) Number: single vs multiple (# of lesions)

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6
Q

List and describe the 8 types of skin lesions

A

1) Crust
2) Cyst: firm (not hard and not squishy)
3) Macule: totally flat
4) Papule: raised bump
5) Pustule: pus-filled
6) Ulcer: lesion/ crevice
7) Vesicle: like a wheal, but not erythematous
8) Wheal: erythematous skin change, boggy, raised

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7
Q

Primary skin lesions:
1) Describe macules
2) Define patch

A

1) Non-palpable, < 1 cm diameter
Varied pigmentation from surrounding skin
No elevation or depression
2) Patch: macule > 1cm diameter

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8
Q

Primary skin lesions:
1) Describe papules
2) Describe pustules (type of papule)

A

1) Palpable, < 1 cm diameter, isolated or grouped
2) Small, circumscribed papule contains purulent material

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9
Q

Primary skin lesions:
1) What is a pustule?
2) What does it mean when they say it has exudate?

A

1) Circumscribed superficial cavity with purulent exudate
2) White, yellow, greenish-yellow, or hemorrhagic

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10
Q

Primary skin lesions:
1) What is a plaque? Give an example.
2) Define lichenification
3) What is a patch? Give an example.

A

1) Plateau-like elevation. Ex: psoriasis
2) Less defined large plaque that is thickened with rough skin
3) Patch: flat or barely elevated plaque
Ex: atopic dermatitis/ eczema

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11
Q

Primary skin lesions:
Nodule

A

Palpable, solid, fatty or cystic, round or ellipsoidal
Larger than papule (1-2 cm)
Think of it as a large papule
Tumor: nodule > 2 cm

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12
Q

Primary skin lesions:
1) Describe wheals (shape, elevation, color)
2) Are they stable? Explain
3) What is urticaria?

A

1) Irregularly-shaped, elevated, edematous
-Erythematous or paler than surrounding skin
2) Well-demarcated borders but not stable
Disappears within 24-48 hours
3) Multiple wheals/rash; “hives, whelps”

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13
Q

Primary skin lesions:
Vesicle/ bullas:
1) What are they both?
2) What is the difference?
3) Are they diffuse or well-defined? Thick or thin?
4) What are they filled with?

A

1) Blister
2) Vesicle <0.5 cm; Bulla >0.5 cm
3) Well-defined; roof is thin
4) Serum and blood

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14
Q

Secondary skin lesions:
1) Define crust
2) Define scales
3) Define erosion

A

1) Crust-dried serum, blood, or exudate
2) Scales-flakes
3) Erosion-epidermis defect (heals without scar) ex/scrape

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15
Q

Secondary skin lesions:
1) Define ulcer
2) Define scar
3) Define atrophy

A

Ulcer-defect in dermis or deeper (heals with scar) usually indented
Scar-fibrous tissue replacement
Atrophy-diminution of some or all layers of skin

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16
Q

True or false: you cannot cut off keloids, you can only inject them with steroids (which have the risk of atrophy)

A

True

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17
Q

What Hx do you need to take for derm concerns?

A

1) Demographics: age, race, sex, occupation, hobbies (chemical/toxin exposure?)
2) Constitutional symptoms (acute vs chronic)
3) History of skin lesions (OLD CARTS)
4) HPI
5) PMHx
6) FHx: skin cancer, skin disorders
7) SocHx
8) SexHx

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18
Q

For Hx of a skin lesion list the 8 Key Questions (OLD CARTS)

A

When did lesion appear (1st noticed)?
Where did lesion appear (site of onset)?
Does it come and go or is it constant?
Does it itch, hurt, or bleed?
How has it spread (pattern/evolution)?
How have individual lesions changed)?
What are provocative factors?
What are previous treatments? (topical, systemic)

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19
Q

Give examples of:
1) Desquamation (3)
2) Vesicular bullae (2)

A

1) Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis
2) Pemphigoid, pemphigus

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20
Q

1) Give 6 examples of papulo-squamous diseases (papules and plaques)
2) Give 2 examples of acneiform lesions

A

1) Dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis
2) Acne vulgaris, rosacea

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21
Q

Give 8 examples of eczema/ dermatitis

A

1) Dyshidrotic eczema
2) Lichen simplex chronicus
3) Nummular eczema
4) Contact dermatitis
5) Stasis dermatitis
6) Atopic dermatitis
7) Seborrheic dermatitis
8) Perioral dermatitis

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22
Q

Eczema/ dermatitis
1) Define it
2) What is its etiology?
3) Are the clinical findings always the same?

A

1) Inflammatory reaction of epidermis & dermis “the itch that rashes”
2) Multiple etiologies
3) Wide range of clinical findings

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23
Q

1) Define acute eczema
2) Define chronic eczema
3) What can both have?

A

1) Pruritis, erythema, vesiculation
2) Pruritis, xerosis, lichenification,
3) Hyperkeratosis, scaling, + fissuring

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24
Q

Describe dyshidrotic eczema:
1) Duration
2) Location
3) What it looks like
4) Painful or painless & what it may develop

A

1) Acute, chronic, & recurrent
2) Fingers, palms, & soles (lateral fingers & toes)
3) Sudden, deep-seated pruritic, clear “tapioca-like” vesicles
4) Painful when erosive. May develop bullae.

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25
Q

1) How can you treat dyshidrotic eczema? (2 ways)
2) What abt severe cases?

A

1) Strong steroids, IL steroids
2) PO prednisone

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26
Q

1) What is Lichen simplex chronicus?
2) What is the common age group? Sex?
3) What causes it?
4) Is it chronic or acute?

A

1) Localized lichenification in circumscribed plaques
2) Usually > 20 y/o, F>M
3) Caused by repetitive rubbing & scratching
-(i.e. pts with meth addictions, pts with anxiety/ psych issues, etc)
4) Chronic, usually relapsing

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27
Q

Lichen simplex chronicus:
1) What are some common sites?
2) What does it look like?
3) Tx?

A

1) Scalp, neck, extensor forearms, scrotum & lower legs
2) Thickened skin, excoriations
3) D/c scratching!, occlusive bandages, topical steroids, tar preps, IL steroids (small lesions), PO hydroxyzine

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28
Q

Nummular eczema:
1) Is it chronic or acute?
2) What does it look like?
3) Etiology?
4) Demographic?

A

1) Chronic, inflammatory
2) Coin-shaped plaques of grouped small papules & vesicles on erythematous base
3) Etiology unknown
4) Most > 50 y/o, M>F

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29
Q

Nummular eczema:
1) What is a key Sx?
2) Where on the body is it most common?
3) What are 3 potential treatments

A

1) Highly pruritic [coin shaped lesions]
2) Legs & upper extremities
3) Moisturizer, topical steroid, PUVA or UVB

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30
Q

Contact dermatitis:
1) Acute or chronic?
2) Sx?
3) Common causes?

A

1) Can be acute or chronic
2) Stinging, itching, burning, pain with fissures, weeps, crusting
3) Plastics, chemical residues on clothes, plants
Working in the yard? Plant exposure?

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31
Q

Contact dermatitis:
1) Presentation? [i.e. what does it look like?]
2) Tx?

A

1) Well-demarcated erythema and edema, non-umbilicated vesicles or papules
2) Remove etiologic agent, wet dressings/Burrow’s solution (OTC,) topical glucocorticoids, PO prednisone (if severe)

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32
Q

1) What is stasis dermatitis related to?
2) What are some common PE findings/ what does it look like?
3) Tx?
4) Is it cellulitis?

A

1) Related to venous insufficiency (pitting edema usually)
2) Inflammatory papules, hyperpigmentation, scaly and crusted erosions in lower legs and ankles
3) Avoid scratching, emollients throughout the day, topical corticosteroids, wrap legs/compression stockings (takes a while to Tx)
4) No

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33
Q

Atopic dermatitis:
1) Acute or chronic?
2) Demographic? What cycle does this perpetuate?
3) What other disorders does is it associated with?
4) What causes it?

A

1) Acute, subacute, chronic relapsing
2) Common in infancy, itch-scratch cycle
3) Frequent /w personal or FHx AD, allergic rhinitis, & asthma
4) Skin barrier dysfunction, IgE reactivity

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34
Q

Atopic dermatitis:
1) Eliciting/exacerbating factors
2) Does it itch? Dry or moist skin? Explain.
3) Are patches defined? What other types of lesions can it be associated with?

A

1) Eliciting/exacerbating factors: inhalants, microbials, aeroallergens, foods, season (winter,) and emotional stress
2) Dry skin, pruritis; “The itch that rashes”:
-Itch > scratch > rash > itch > scratch > rash
3) Poorly-defined erythematous patches, papules, & plaques with or without scaling

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35
Q

Atopic dermatitis:
1) What are the 3 types?
2) Tx?
3) When should you use PO steroids?

A

1) Infantile, child, & adult types
2) (acute/chronic): Avoid scratching
-Wet dressings
-Topical steroids
-Topical or PO antibiotics
-Hydration, emollients, or topical calcineurin inhibitors
-PO H1 antihistamines
3)Only for severe intractable cases

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36
Q

Seborrheic dermatitis:
1) Demographic?
2) Is it chronic or acute? Explain.
-When can it occur?
3) Who is it common in?
4) What is the distribution? Explain where it looks like in different places & where it’s often seen

A

1) Infancy, puberty, 20-50 years old, M>F
2) Chronic and relapsing.
-Worse in fall/winter (dry environment and stress). Summer: worse in some, better in others
3) Immunosuppressed (HIV, Parkinson’s, and nutritional deficiencies (zinc))
4) Scalp, face, trunk, genitalia and body folds.
-“Cradle Cap”: yellow greasy scales on scalp
-Often seen in hair bearing regions (eyebrows, central face, scalp): looks like dandruff

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37
Q

Seborrheic dermatitis:
1) Presentation
2) Tx options?

A

1) Pruritis, red plaques, greasy looking. Yellowish scales may be present on areas with a plethora of sebaceous glands.
2) Selenium sulfide (Selsen BLUE, Head and Shoulders,) topical antifungals, tar shampoo (Neutrogena T-gel,) mild topical steroids

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38
Q

Perioral dermatitis:
1) What does it look like?
2) What is a key element?
3) Who is it most common in?

A

1) Erythematous grouped papulopustules may become plaques with scales. Can have satellite lesions. May include perinasal and periorbital skin
2) Spares vermillion border
3) Most common in females 20-45

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39
Q

Perioral dermatitis:
1) Causes?
2) Tx?

A

1) Fluorinated toothpaste, topical corticosteroids
2) Eliminate steroids and irritants (cosmetics/skin care products) topical metronidazole, erythromycin or pimecrolimus

40
Q

Fixed drug eruption:
1) Define it
2) Is it solitary or multiple? Describe
3) Is it symptomatic?

A

1) Adverse cutaneous reaction to ingested drug
2) Solitary (or multiple) erythematous patch or plaque
3) Usually asymptomatic (may have pruritis, pain, burning)

41
Q

Fixed drug eruption:
1) Describe what the lesions look like and what type of lesion it is. Do they change?
2) Most common causes?

A

1) Sharply demarcated macule, round or oval
-Initially erythematous, then dusky red to violaceous
-May evolve to bulla, then erosion
2) TCN, sulfa, NSAIDs, barbiturates, OCPs, quinine, yellow food coloring

42
Q

Fixed drug eruption:
1) Does it resolve on its own?
2) What are the Txs (if any)?

A

1) Resolves in a few weeks after d/c offending agent
2) D/c drug topical steroids (non-eroded), antibiotic ointment (eroded), PO steroids for severe mucosal lesions

43
Q

Lichen planus:
1) What is it? Acute or chronic?
2) What are the 4 Ps?
3) Where is it found?

A

1) Acute or chronic inflammation involving skin or mucous membranes (In mouth/ vaginal mucousa appears white and lacy)
2) 4 Ps: Papule, purple, polygonal, pruritic (and flat topped)
3) Creases of arms and legs

44
Q

Lichen planus:
1) Demographic?
2) Etiology?
3) Tx?

A

1) 30-60 y/o, F>M
2) Idiopathic
3) Topical & PO steroids, cyclosporine

45
Q

List and describe the 2 types of contact dermatitis

A

1) Irritant: chemical (ex/hands)
-Soaps, detergents, solvents (Table 2-1, Fitzpatrick’s)
2) Allergic: Nickel/jewelry, plants (Table 2-2, Fitzpatrick’s)

46
Q

Pityriasis rosea:
1) Acute or chronic? When is it most common?
2) What is its first Sx?
3) When do the rest of the Sx occur? Describe what they look like

A

1) Acute rash, self-limited course, more common in fall
2) Initial single, primary (“herald”) patch usually on trunk (80% of patients)
3) Generalized secondary eruption 1-2 weeks later
-Fine scaling papules & patches in “Christmas tree”
pattern (lines of cleavage) on back

47
Q

Pityriasis rosea:
1) Does it resolve on its own?
2) What is its etiology?
3) What is its initial symptom? Describe what it looks like

A

1) Resolves spontaneously in 6-12 weeks
2) Probable: reactivation HSV-7 & HSV-6
3) Herald patch: oval, salmon-red plaque or patch 2-5 cm with fine collarette peripheral scale

48
Q

How do you treat pityriasis rosea?

A

1) PO or topical antihistamines
2) Topical steroids
3) UVB phototherapy or natural sunlight
4) PO steroids (usually just treating Sx)

49
Q

Psoriasis:
1) Who is it most common in?
2) What makes it worse?
3) What is it called when it has joint pain?

A

1) Usually a + FHx; All ages; M=F
2) Worse with stress, obesity
3) Psoriatic arthritis

50
Q

Psoriasis:
1) Describe what it looks like & where on the body it usually occurs
2) What else can it cause?

A

1) Pruritic well-demarcated, erythematous plaques with silver “scales” (when scraped off reveal pinpoint bleeding) -usually on knees, elbows, nails, palms, and soles of feet
2) Causes pitting in nails

51
Q

What are the 2 major types of psoriasis?

A

1) Eruptive: inflammatory, “raindrop” (guttate)
2) Chronic: stable (plaque) psoriasis

52
Q

Psoriasis:
1) What are some triggers?
2) What are the 2 ways to diagnose?
3) What are 2 DDxs?

A

1) Triggers: physical trauma, strep (guttate,) stress, drugs, alcohol
2) Clinical
-Biopsy for uncertain diagnosis
3) Eczema; Lichen simplex chronicus

53
Q

Guttate Psoriasis:
1) What does it look like?
2) What is it often preceded by?
3) Who is it most common in?
4) Is self-remitting? Explain

A

1) Drop-like scattered (scaly) red to pink lesions- diffuse (not necessarily on extensors)
2) Strep infection
3) Usually in children or young adults< 30; M=F
4) May self remit in several weeks to several months

54
Q

Guttate Psoriasis:
1) What may it progress to?
2) What are 2 DDxs?
3) What are 2 treatments?

A

1) Plaque psoriasis <30%
2) Pityriasis rosea, tinea corporis
3) Phototherapy, topical corticosteroids

55
Q

Plaque psoriasis: what are 4 treatments?

A

1) Topical Steroids and emollients – meds need to be able to penetrate skin
2) Kenalog intralesional injections - scalp
3) UVB light therapy
4) Biologic Agents- Humira, Remicade, Embrel, Methotrexate (“big guns”)}

56
Q

Describe follow-up for plaque psoriasis

A

Based on treatment; Biologic agent treatment needs annual labs and chest x-ray

57
Q

Erythema multiforme:
1) Who is it common in?
2) What is it? What is it most commonly due to?
3) What does it look like?

A

1) 50% patients <20 y/o, M>F
2) Cutaneous reaction (drugs, idiopathic), most commonly due to herpes simplex virus
3) Target lesions mucous involvement (oral/genital, + palms/soles, corneal ulcers, anterior uveitis), + pruritic or burning

58
Q

Erythema multiforme:
1) What does it typically look like?
2) List & describe the 2 categories

A

1) Typical target-like lesions & symmetry
2) Major: m/c 2/2 drug reaction, always mucosal involvement, fever, arthralgias,lesions in pharynx & larynx
-Minor: without mucous involvement or systemic symptoms, lesions on extremities & face-@ herpes outbreak

59
Q

Erythema multiforme:
1) Describe what it looks like over time
2) Where on the body?
3) What are the 2 ways to Dx?

A

1) Lesions develop over >10 days. Macule > papule >vesicles and bullae
2) Hands, feet, palms, soles, elbows, knees, mouth, torso, face, genitals
3) Clinical (biopsy may help confirm)

60
Q

List 5 treatments for erythema multiforme

A

1) Topical corticosteroids, PO steroids for disabling oral lesions
2) PO antihistamines
3) Wet dressings
4) Medicated (lidocaine, diphenhydramine) mouthwash for oral mucosal lesions
5) Ophthalmology referral for ocular lesions

61
Q

Describe the follow-up for erythema multiforme

A

Continuous antiviral therapy for recurrent HSV-associated EM

62
Q

Stevens-Johnson Syndrome (SJS) + Toxic Epidermal Necrolysis (TEN):
1) What are these conditions? What do they do to the skin?
2) What makes these 2 conditions different?

A

1) Acute, life-threatening mucocutaneous reaction
-Necrosis and detachment of epidermis
2) % of body surface involved

63
Q

Differentiate between SJS and TEN. Is there overlap?

A

1) SJS <10% epidermal detachment
2) TEN >30% epidermal detachment
(overlap 10-30%)

64
Q

SJS and TEN:
1) What is affected 90% of the time?
2) Where is it rarely found?
3) What can cause it? Give examples
4) Who is it more common in?

A

1) Mucous membranes (ocular, oral, and genital)
2) Rarely present on palms/soles
3) Idiopathic or drug-induced: anti-seizure meds, sulfa, allopurinol, NSAIDS
4) Higher incidence in HIV & active cancer. F>M.

65
Q

1) When do SJS/ TEN typically present? How do they start?
2) Describe what happens next & what it looks like
3) Describe the lesions
4) Where do the lesions typically start?

A

1) Usually 4 days to 4 weeks after drug exposure; Fever, malaise, and arthralgias (influenza like sx) for 1-3 days…THEN…
2) Skin is sloughing off and painful – burning, paresthesia, etc! Conjunctival burning/itching, and painful mouth lesions
3) Ill-defined, coalescing, erythematous macules with purpuric centers or diffuse erythema; pain out of proportion
4) On face and thorax and symmetric

66
Q

SJS/ TEN: How are they managed?

A

1) Admit to ICU or burn center, d/c offending agent/drug
2) IV fluids and electrolytes (treat as burn patient)
3) Narcotics for pain
4) Systemic glucocorticoids controversial (contraindicated late in disease course)
5) IVIG (if started early)
6) Surgical debridement not recommended
7) Lasts approximately 8-12 days

67
Q

1) What is Nikolski sign?
2) What is it pathognomonic for?

A

1) The ability to extend the area of superficial sloughing by applying gentle lateral pressure on the surface of the skin at an apparently uninvolved site.
2) Pemphigus, TEN

68
Q

Vesiculobullous disease: Bellous pemphigoid:
1) What is it? Who is it most common in and what does it look like?
2) What does it often start with? How is it different from pemphigus?

A

1) Autoimmune disease of elderly patients (60-80yrs) with pruritic, large, tense, bullae scattered but also in groups. 2) Urticarial eruption. Don’t rupture as easily as pemphigus.

69
Q

Vesiculobullous disease: Bellous pemphigoid:
1) Where on the body does it usually occur?
2) What are the Txs?

A

1) Axillae, medial thigh, groin, flexor UE, lower LE, can be in mouth
2) PO, topical steroids 50-100 mg QD or immunosuppressives

70
Q

Vesiculobullous disease: Pemphigus
1) Acute or chronic? What is it and what is the demographic?
2) Where does it tend to occur?
3) Where does it usually start? Is it symptomatic?

A

1) Chronic or acute, bullous autoimmune disease, adults 40-60
2) Scalp, face, chest, axillae, groin, umbilicus
3) Usually starts in mouth, no pruritis, but burning and painful

71
Q

Vesiculobullous disease: Pemphigus:
1) What does it look like on PE?
2) What is the Tx?

A

1) Vesicles and bullae, easily rupture, flaccid and weeping. + Nikolsky sign,
2) Dermatologist, high dose steroids and immunosuppression

72
Q

Acne vulgaris:
1) What is it?
2) What does it look like?
3) Who does it usually occur in? Where on the body?

A

1) Inflammation of pilosebaceous units
2) Seen with comedones (must have for diagnosis,) cysts, pustules and/or nodules
3) Occurs primarily in young people; on face, trunk, upper arms and sometimes buttocks

73
Q

Acne vulgaris:
1) What can it result in after it’s resolved?
2) Who is it more severe in?
3) Who is it less often found in?
4) Is it genetic?

A

1) Can result in pits, depressions, scars or hyperpigmentation
2) More severe in males than females
3) Less often in Asians and African Americans
4) Cystic acne can be familial

74
Q

Acne vulgaris:
1) What are 3 factors in pathogenesis?
2) What does follicular plugging result in? What does this do?

A

1) Follicular keratinization, androgens, Propionibacterium acnes
2) Comedone; traps sebum->androgens produce more sebum-> bacteria produce inflammatory response

75
Q

List some factors that can contribute to acne vulgaris

A

1) Meds: lithium, isoniazid, steroids, OCP,
2) Androgens; stress
3) Occlusion/pressure (hand on face)
4) Cosmetics
5) Pomade
6) Sweat

76
Q

Acne vulgaris:
1) When is it worse?
2) What type can be painful?
3) What are the two types of Comedones?
4) Does it always have comedones?

A

1) Worse in fall and winter
2) Nodulo-cystic type
3) Open= blackheads
Closed = white heads
4) Yes; required for acne diagnosis

77
Q

Acne vulgaris:
1) What labs?
2) What is the course?

A

1) None required
2) Often clears by early 20’s, flares in winter and with onset of menses

78
Q

1) What is the long term goal of acne vulgaris Tx?
2) How is this done?

A

1) Scar prevention
2) Remove plugging, treat bacteria

79
Q

1) How is mild acne vulgaris treated?
2) What medication treats it that can’t be used during pregnancy?
3) What works best?

A

1) Topical antibiotics (clindamycin and erythromycin 3%, 5% BID) and benzoyl peroxide gels 2%, 5%, 10%) this bleaches fabrics can get in combo
2) Topical retinoids gradual increase in strength from 0.01%, 0.025%, 0.05% cream, gel, liquid, or ointment (retinoic acid, adapalene (now OTC), tazarotene) can NOT use if pregnant
3) Combination therapy

80
Q

How is moderate acne vulgaris treated?

A

-Same regimen for minor plus PO antibiotics (Minocycline 50-100mg/d or doxycycline 50-100mg BID tapered to 5o mg/d as acne lessens.)
-Spironolactone 25-50mg QD.

81
Q

How is severe acne vulgaris treated?

A

Same as above with the addition of PO isotretinoin for cystic or refractory acne.

82
Q

PO isotretinoin:
1) How long does it take for complete remission?
2) How does it work?
3) What is a severe side effect?

A

1) Complete remission in most cases for months to years. 2) inhibiting sebaceous gland function and keratinization.
3) Is extremely teratogenic

83
Q

PO isotretinoin:
1) What does it cause in pregnancy?
2) What must a pt do before you Rx?
3) What can it cause when combined with tetracycline?

A

1) Teratomas
2) MUST have effective contraception and 2 neg pregnancy tests prior to initiating. C
3) Pseudotumor cerebri

84
Q

PO isotretinoin:
1) What must you check before you start?
2) What 2 things does it cause?
3) What else can it cause?

A

1) Lipids and transaminases prior to therapy as can cause elevated triglycerides and mild to moderate elevations of transaminases (normalize with dose reduction.)
2) Causes extremely dry skin and mucosa.
3) Can cause depression.

85
Q

Rosacea:
1) What is it?
2) Who is it most common in?
3) What does it look like?

A

1) Chronic inflammation of facial pilosebaceous units
2) 30-50 y/o, F>M
3) Episodic erythema, “flushing & blushing”

86
Q

Rosacea:
1) What are seen in stages 1-3? What is NOT seen?
2) What can trigger it?
3) What is the duration?

A

1) Stages I, II, & III: persistent erythema, telangiectasias, papules, tiny pustules, nodules
NO comedones
2) Hot liquids, spicy foods, alcohol/wine, aged cheese, exposure to sun & heat, stress
3) Days, weeks, months

87
Q

Define:
1) Phymas
2) Rhinophyma
3) Metophyma
4) Blepharophyma
5) Otophyma
6) Gnathophyma

A

1) Localized swelling of soft tissues of face due to variable combinations of fibrosis, sebaceous hyperplasia, + lymphoedema.
2) Nose
3) Forehead
4) Eyelids
5) Cauliflower ears
6) Chin

88
Q

Rosacea:
1) What is the late stage?
2) What is the distribution?
3) Are there recurrences? Explain

A

1) Rhinophyma, metophyma, blepharophyma, otophyma, gnatophyma
2) Symmetric on face. Rarely on neck, chest, back, & scalp.
3) Recurrences common; usually lifetime

89
Q

1-4) Rosacea Tx
5) What are Tx for severe cases?
6) When is surgery appropriate?

A

1) Reduce or eliminate alcohol & caffeine
2) Metronidazole gel or cream, ivermectin cream
3) Topical antibiotics
4) PO antibiotics better than topical (minocycline, doxycycline, TCN) in papulopustular rosacea
5) PO isotretinoin for severe disease
6) Surgery for rhinophyma; telangiectasia (lasers)

90
Q

Folliculitis:
1) What is it?
2) Describe what it looks like
3) Who is it more common in?

A

1) Inflammation or infection of superficial hair follicles
2) Perifollicular papules and/or pustules with surrounding erythema; hair bearing skin; often pruritic
3) More common in males

91
Q

Folliculitis:
1) Risk factors?
2) Etiology?

A

1) Prolonged antibiotic use, topical corticosteroids, hot tubs
2) Most common staph aureus; hot tub > pseudomonas aeruginosa

92
Q

1) How is folliculitis treated?
2) What if there’s no improvement after the first Tx?

A

1) Benzoyl peroxide wash (bleaches) topical mupirocin, clindamycin, erythromycin.
2) PO Cephalexin

93
Q

Hidradenitis suppurativa:
1) Is it acute or chronic?
2) What skin is it found on? Where?
3) Where is it typically found on women and men?

A

1) Chronic, suppurative
2) Apocrine gland skin; Axillae, inguinocrural, anogenital, inframammary, rarely scalp
3) F (axillae)>M (anogenital)

94
Q

Hidradenitis suppurativa:
1) What FHx is common?
2) Etiology?
3) Risk factors?

A

1) NC acne & HS
2) Unknown etiology
3) Obesity, smoking, genetic predisp. to acne

95
Q

Hidradenitis suppurativa:
1) What do the lesions look like?
2) What is the pathogenesis?

A

1) Tender open & double comedones, red nodules/abscesses (foul smelling), sinus tracts, “bridge” scars, hypertrophic & keloidal scars, contractures
2) Follicle plugging > dilated follicle & apocrine duct > inflammation > bacterial growth > extension of suppuration/tissue destruction > ulceration, fibrosis, sinus tracts > scarring

96
Q

Hidradenitis suppurativa:
1) Does it spontaneously remit? Explain
2) What are some treatments?

A

1) Usual spontaneous remission at >35 y/o
2) Intralesional steroids, then I&D abscess
-Prednisone for severe pain & inflammation
-Surgery (excision, skin grafting)
-PO antibiotics (chronic low-grade disease)
-Isotretinoin for early disease adalimumab (Humira)
-Psychological