L5 Seborrheic dermatitis, lichen planus, pityriasis, and psoriasis Flashcards

1
Q

What is seborrheic dermatitis?

A
  • think yellow, greasy looking scale
  • occurs in infants, then again as teenagers and adults
  • peak prevelance in 3rd and 4th decades
  • M>F
  • possibly a response to malessezia furfur (yeast) or its metabolites
  • > sebaceous glands create a favorable environment for M. furfur which is normally found on skin
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2
Q

What are the characteristics of seborrheic dermatitis?

A
  • COMMON, chronic, relapsing inflammatory dermatitis; can vary from MILD DANDRUFF to more extensive inflammatory dermatitis
  • worse with emotional stress and during cold/dry winter months
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3
Q

What is the clinical presentation for infants and adults?

A

Infants

  • CRADLE CAP yellow greasy adherent scales on the vertex of the scalp
  • can also be found in diaper area and axillary skin

Adults

  • erythematous coalescing macules, patches, or plaques with YELLOW GREASY-LOOKING SCALES
  • affects the scalp, face (eyebrows, eyelids, nasolabial folds), ears, pre-sternal skin and upper back
  • may be mre extensive and severe in patients with HIV/AIDS and Parkinsons’s disease
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4
Q

What is seborrheic blepharitis?

A
  • periocular presentation
  • eyelid edges pink or irritated
  • greasy-appearing flakes adherent to lashes

Treatment
-warm compresses and eyelid scrubs are the mainstay of treatment

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5
Q

What is the diagnosis and treatment or seborrheic dermatitis?

A

-clinical diagnosis based on appearance and location

Treatment

  • BLEPHARITIS and CRADLE CAP: olive oil, baby shampoo and warm water to loosen crusts
  • SCALP: antifungal agents and topical corticosteroids
  • ketoconazole shampoo or cream
  • selenium sulfide or anit-dandruff shampoo (selsun, sebulex, head and shoulders) that have anti fungal properties
  • FACE: low-potency topical corticosteroid cream, topical antifungal, or combination of the two
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6
Q

What are the characteristics of pityraisis rosea?

A
  • benign, VIRAL SKIN EXANTHEM of unknown etiology
  • HHV6/7
  • common in TEENS and YOUNG ADULTS; sping and fall
  • possible prodrome (H/A, malaise, pharyngitis)
  • primary lesion is a HERALD PATCH (usually on the trunk) followed bay a secondary rash 1-2 weeks later
  • largely asymptomatic, 50% have mild pruritis
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7
Q

What is the clinical presentation of pityraisis rosea?

A
  • HERALD PATCH- oval slightly raised lesion 2-5 cm, pink or salmon-colored with marginal collarette scale
  • Rash- fine scaled, pink, oval papules and plaques
  • CHRISTMAS TREE pattern
  • “cigarette paper” appearance of some plaques
  • SECONDARY SYPHILIS- do serologic test, rapid plasma reagin
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8
Q

What is the treatment for pityraisis rosea?

A
  • reassurance, rash is self-limiting but may persist 6-8 weeks
  • oral antihistimines prn pruritis
  • loratidine (claritin), cetirizine(zyrtec), diphenhydramine(benadryl)
  • medium strength topical corticosteroids
  • sun exposure helps
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9
Q

What is the clinical presentation of lichen planus?

A
  • referred to as the “FOUR P’s” pruritic, purple, polygonal, paules or plaques
  • papulosquaous eruption characterized by flat-topped violaceous paules
  • may affect the skin, genitalia, nails, scalp and oral cavity
  • most common places are the wrists, ankles, shins, back, penis, and MOUTH
  • Wickham’s striae- tiny white lines running throught the papules
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10
Q

What is lichen planus?

A
  • an immune-mediated response involving activated T cells.
  • affects about 1% of population; most frequently ADULTS 30-60y old
  • IDIOPATHIC- arises spontaneously
  • drugs that can cause it (gold salts, antihypertensives, antimalarials)
  • associating with hep C
  • KOEBNER phenomenon- development of lesions in sites of trauma (squamous cell also?)
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11
Q

How to diagnose and treat lichen planus?

A

-skin biopsy can confirm dx : punch or shave biopsy

Treatment
-self-limited disorder (resolves after 1-2 years), tx used to hasten resolution and manage pruritis
*1st line: Topical steroids or intralesional triamcinolone: high potency or super high potency on the trunk and extremities
2nd line: oral steroids, phototherapy, oral retinoids (acitretin) by dermatologist
-other options: cyclosporine (an immunosuppressant)

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12
Q

What is the incidence and etiology of psoriasis?

A
  • M=F women at younger age
  • can develop at any age; less common in children than adults
  • TWO PEAKS: 20-30 and then 50-60 years of age
  • 1/3 of patients have a first-degree relative with psoriasis aka hereditary component

Risk factors and triggers:
-hereditary
-infections (strep throat)
-medications (lithium, beta blockers, antimalarials)
-stress or skin injury (cut or bad sunburn)
-weather (cold/dry)
-tobacco and heavy alcohol use
Triggers can cause psoriasis to appear for the first time or to cause “flare-ups”

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13
Q

what is the pathophysiology of psoriasis?

A
  • overactive T-cells trigger immune response
  • increased blood flow/inflammation in the area causes body to make new skin cells more often
  • shortened cell cycle for keratinocytes: 36 hours vs 311 hours (normal)
  • decreased turn over time of the epidermis: 4 days from basal cell layer to stratum corneum vs. 27 days in normal skin

*skin cells pile up on the surface of the skin=PSORIASIS PLAQUE

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14
Q

What are the characteristics of psoriasis?

A
  • ERYTHMATOUS PLAQUES OFTEN COVERED WITH A SILVERY-WHITE SCALE
  • 70% of patients complain of PRURITIS, skin pain or burning
  • Various forms: localized or generalized; plaque, pustular, guttate, inverse or erythrodermmic

-can have associated nail psoriasis (nail pits, onycholysis) and psoriatic arthritis (PsA)

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15
Q

What is psoriasis vulgaris clinical presentation?

A

-most common form affects about 80% of patients
-erythematous plaques with sharply defined margins and thick silvery scale
-esions typically symmetrical
-smaller plaques join together to form larger plaques
Elbows, knees, scalp, umbilicus, intergluteal cleft, gentalia and nails are most commonly afected
*KOEBNER phenomenon and AUSPITZ (little droplets or seeds or blood)
-for auspitz sign: remove the plaque and reveal a smooth, red, glossy membrane with tiny punctate bleeding which are enlarged dermal capillaries

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16
Q

What often precedes onset of guttate psoriasis?

A

Streptococcal infection

Guttate=drops

17
Q

what are two life threatening forms of psoriasis?

A
  • pustular psoriasis: fever

- erythromdermic psoriasis

18
Q

What is a sign of psoriasis of fingernails?

A

-pitting, onycholysis(separation of nail from nail bed), and “oil spots” brown spots

19
Q

What are associated disorders of psoriasis?

A
  • Psoriatic arthritis (PsA): “usually seronegative” inflammatory arthritis (meaning usually rheumatoid factor negative)
  • most patients have skin involvement but arthritis precedes
  • inflammatory bowel disease, heart disease, metabolic syndrome, malignancy, and depression
  • ocular- blepharitis, conjunctivitis, xerosis, corneal lesions and uveitis
20
Q

How do you treat psoriasis?

A

*depends on the pattern and severity. no one regimen will work
General measures:
-sunshine (vitaminD, UVA, UVB)
-baths (moistens thick plaques)
-emollients to reduce pruritis and tenderness
-occlusive dressings
rest
DO NOT USE ORAL STEROIDS. PSORIASIS CAN WORSEN UPON DISCONTINUATION

Topical
-group 1 or 2 corticosteroids: clobetasol, betamethasone, diproprionate, fluocinonide, etc.
-steroid sparing agents: synthetic vitamin D- calcitriol and calcipotriene, coal tar, topical retinoids: tazarotene, topical calcineurin inhibitors: tacrolimus (protopic) and pimecrolimus (elidel)
-apply topical steroids after soaking
-ointment based for trunk/extremities
-lotion or cream on face
-lotion, solution, gel or foam on scalp
Taper group 1 steroids after 2-3 wks, to either a lower-potency or to pulse therapy
occlusive therapy, can wear gloves at night or can saran wrap around extremities

Phototherapy
-Broad band or narrow band UVB light, excimer laser, or PUVA (use of topical/oral psoralens (photosensitizers) plus UVA light
Systemic therapy: immunosuppressants: methotrexate, cyclosporin; oral retinoids (acitretin)
-biologic immunomodulators: etanercept(enbrel), infliximab(remicade), adalimumab(humira)
-phosphodiesterase-4 inhibitors: apremilast(otezla)

5-20% TBSA: vitamin D +/- UV therapy
>20% TBSA: systemic therapy +/- UV therapy
-if pt has PsA: biologic therapy($), refer to rheumatologist

21
Q

What is psoriatic arthritis?

A
  • inflammatory arthritis; affects up to 30% of pts with psoriasis, M=F
  • pain and stiffness in affected joints
  • stiffness in morning fades during the day
  • pain, joint line tenderness, and effusion present on exam often in ASYMMETRIC distribution
  • usually smaller joints: hands wrists and ankles
  • DIP joints an spine affected in half the cases

Elevated Sedimentation rate ESR and leukocytosis
(+) HLA-B27 association
Rheumatoid factor, ANA, anti-cyclic citrullinated peptide antibodies (anti-CCP) may be present (minority of patients)

-may also have tenosynovitis(achilles), enthesitis, dactylitis, nail lesions, and ocular involvement

22
Q

What is dactylitis?

A

known as “sausage digit” diffuse swelling of the digit

23
Q

How to diagnose psoriatic arthritis?

A
  • history and physical consistent with PsA
  • assess for: history of skin disease, involved joints, sxs of enthesitis, sausage digits, eye disease, inflammatory back pain, FH
  • lab testing to evaluate for systemic inflammation and other conditions
  • arthrocentesis and synovial fluid analysis
  • imaging - xrays of affected joints
24
Q

How do you treat psoriatic arthritis PsA?

A
  • should be coordinated between a rheumatologist, the primary care provider, and a dermatologist
  • NSAIDs
  • DMARDs (disease modifying antirheumatic drug)
  • Conventional (methotrexate) or a newer biologic (TNF inhibitor, adalimumab huira)
  • phosphodiesterase-4 enzyme inhibitor: apremilast (otezla)