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Papulosquamous/Desquamation Flashcards

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Dermatology Board Prep flashcards
1
Q

Most successful Rx for Psoriasis?

A

Immune-mediating medications

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2
Q

What is the etiology of Psoriasis?

Hint: influences and triggers

A

Psoriasis is influenced by genetic & immune-mediated components.

With or Without triggers, substantial leukocyte recruitment to dermis (activated T cells that induce keratinocyte proliferation)

Ramped-up,degregulated inflammatory process with large production of various cytokines

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3
Q

Psoriasis is assocated with increased production of what various cytokines?

A

Tumor necrosis factor-α [TNF-α]

Interferon-gamma

Interleukin-12

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4
Q

What particular cytokine production correlates with psoriasis flare ups?

A

TNF-α

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5
Q

Psoriasis Pathophysiology:

Explain what occurs and the characteristics of why that happens?

A

Vascular engorgement due to telangiectasis

Altered epidermal cell cycle (hyperplasia, turnover from 23 days to 3-5 days –improper cell maturation)

Parakeratosis (cells retain nuclei in stratum granulosum)

Cells fail to relesase adequate levels of lipids

Poor adherent stratum corneum –> flaking, scaling

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6
Q

Name the 4 skin layers?

A

From top to bottom:

Keratin surface (cornified cells)

Stratum granulosum

Stratum Spinosum

Stratum Basale)

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7
Q

What’s wrong with this picture?

A

Hyperkeratosis w parakeratosis

loss of granular layer

Acanthosis (diffused epidermal hyperplasia)

Enlongated rete regions (hyperproliferation)

Vascular dilation

Inflammation, T-lymphocytes in the dermis & epidermis

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8
Q

How will a pt present w Psoriasis?

A

Common (2-3% of world’s pop), Chronic

Erythematous, sharply demarcated papules & rounded plaques, covered by silvery micacous scale

Variably pruritic

Koebner’s phenomenon

Exacerbated by external factors (infections, stress, meds (lithium, beta blockers, anti-malarials))

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9
Q

What type of Psoriasis is pictured below?

A

Plaque-type (discoid)

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10
Q

How will a pt present w Plaque-type (discoid) psoriasis?

A

Most common form

Stable, slowly enlarging, indolent course

Unchanged for long periods

Usually symmetrical (elbows, knees, gluteal cleft & scalp)

Needs to be tx to resolve, will spontaneously remit

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11
Q

What type of skin lesion is pictured below?

A

Inverse psoriasis

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12
Q

How will a pt present w Inverse Psoriasis?

A

Shaply demarcated plaques

May be moist & w/o scales due to their location (intertriginous regions…axilla, groin, submammary region, navel, scalp, palms, soles

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13
Q

What type of Psoriasis follows infection w hemolytic Streptococci, withdrawl from steroids or anti-marlarial use?

A

Guttate Psoriasis (eruptive psoriasis)

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14
Q

Name the skin disorder pictured below.

A

Guttate psoriasis (eruptive psoriasis)

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15
Q

How will a pt present w Guttate Psoriasis?

Provide the DDx

A

Most common in children & young adults

Acute w no h/o psoriasis

small erythematous, scaling papules

DDx = Pityriasis rosea, 2nd syphilis

Acquire med hx and recent illnesses (typically follows infection w hemolytic Strept, withdrawl from steroids, antimalarial use)

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16
Q

Name this skin disorder.

A

Pustular psoriasis

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17
Q

Name this skin disorder

A

Erythrodermic psoriasis (i.e. severe pustular)

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18
Q

How will a pt present w Pustular Psoriasis?

A

Localized to palms/soles or generalized

Painful, erythematous w pustules (excudate: inflammatory or infected if cloudy)

Variable scale depending on location

Similar in size to eczema when limited to palms/soles

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19
Q

How will a pt present w Erythrodermic Psoriasis?

A

Generlized, often recurrent, w fever 102-104 for days

Sterile pustules

intense erythema (erythrodermic)

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20
Q

What is the eitology of Erythrodermic psoriasis?

A

Local irritants

Pregnancy

Medications

Infections

Systemic glucocorticoid withdrawl may precipiate

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21
Q

What is the tx for pt w Erythrodermic psoriasis?

A

Oral retinoids for non-pregnant pts

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22
Q

Name the disorder pictured along w characteristics

A

Nail psoriasis

Characteristics include:

Punctated pitting

onycholysis

nail thickening or subungual hyperkeratosis

Helpful in non-classic presentation

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23
Q

Name this disorder

A

Psoriatic arthritis

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24
Q

How dose Psoriatic arthritis present?

A

10-30% pt w skin sx

Hands & feet, sometimes large joints

Stiffness, pain & progressive joint damage

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25
Q

Name this disorder and characteristics.

A

Oral psoriasis

white lesions on oral mucosa, change severity daily

Can be severe cheilosis w extension crossing vermillion border

Geographic tongue may be a form

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26
Q

Name this skin lesion.

A

Lichen Planus

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27
Q

Name this skin lesion.

A

Lichen Planus

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28
Q

What is the distribution of Lichen Planus?

A

Predilection for wrists, shins, lower back, & genitalia

May affect skin, scalp, nails, & mucous membranes.

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29
Q

Name the 4 P’s and what disorder they describe.

A

Purple (violaceous)

Polygonal

Pruritic

Papule (flat-topped)

Papulosquamous disorder = Lichen Planus

30
Q

What is Wickham’s striae and what disorder does it belong to?

A

Superficial network of gray lines indicating Lichen Planus (can be seen in oral lichen planus too)

31
Q

Describe how Lichen Planus will present in areas other than skin.

A

Scalp - lichen planopilaris, may lead to scarring alopecia

Nail - may lead to permanent deformity or loss of fingernails/toenails

Mucous Membrane - most common buccal, mild, white reticulate eruption of mucosa to severe erosive stomatitis. May last years = increased risk for oral squamous cell carcinoma

32
Q

What is the DDx including Lichen Planus?

A

similar cutaneous eruptions occur

w numerous drugs: thiazide, diurectics, gold, antimalarials, penicillamine, & phenothiazines

w chronic graft-vs-host diease

Psoriasis (more red lesions and chronic)

associated w Hep C infection

33
Q

What is the duration & tx for Lichen Planus?

A

variable duration, most have spontaneous remission 6 mo to 2 yrs

Tx w topical glucocorticoids

34
Q

How will a pt typically present w Pityriasis Rosea?

A

Occurs more commonly in Spring & Fall

Initially Herald patch (2-6 cm annular lesion)

Followed by (days to weeks) smaller annular, oval, papular, scaling lesions on the trunk

Red to brown

Occurs as crops last up to 3-8 wks

DDx 2nd syphilis but its more common on palms/soles –rare in PR

Post-inflammatory hyper/hypopigmentation

Pregnancy = risk of miscarriage

PCR may show (Human Herpes Virus) HHV-7/HHV-6 in DNA tissues & secretions

35
Q

What is this lesion and what skin disorder does it suggest?

A

Herald patch = 2-6 cm annular lesion

First lesion to appear for Pityriasis Rosea

36
Q

Name the lesion below.

A

Christmas Tree shape lesion

Pityriasis rosea

37
Q

What are the tx of Pityriasis rosea?

A

Primary goal = relief of pruritus

mid-potency topical corticosteroids (systemic not recommended, no pruritic reflief, may prolong disease)

oral antihistamines

UV-B (may not help pruritis, result in post-inflammatory pigmentation changes

High dose Acyclovir (800 mg qid or 400 mg 5x) may help shorten disease if given early

38
Q

What is the pathophysiology for Erythema multiforme?

A

Not totally understood

Most likely immunologically mediated (keratinocyte is ultimate target of immune response)

Keratinocyte necrosis = 1st patho finding

Hypersensitivity rxn triggered by:

Bacterial

Viral (HSV)

Fungal

Chemical products (drugs (50% prevalence): slow acetylators w alt pathway oxida. by P450 ex sulfa, also anticonvulsants, barbituates).

Contact exposure: metals, flavoring & preservatives, tattooing, cold, foods, malignancy, hormonal

50% idiopathic

39
Q

Describe the 2 types of cell-mediated immune rxns.

A

Primary cell-mediated immune rxn = 9-14 days after the start of offending drug

2nd cell-mediated immune response = rxn hours to 1 or 2 days after recurrent exposure.

Associate w EM

40
Q

List predisposing conditions for EM.

A

2:1 males to females

Rare <3 yo or >50 yo

HIV infection

Corticosteroid exposure

Bone marrow transplant

SLE (systemic lupus erythematosus)

GVHD (graft-vs-host disease)

IBD (inflammatory bowl disease)

pts undergoing radiation, chemotherapy, neurosurgery for brain tumors

41
Q

What is the prognosis of EM Minor?

A

Lesions evolve over 1-2 wks & ultimately subside w/i 2-3 wks w/o scarring

Recurrences common (33% of cases assoc. w/ apparent or subclinical HSV infection)

42
Q

What is the prognosis of EM major?

A

Mortality rate < 5% - directly proportional to total BSA of sloughed epithelium

More protracted course; may require 3-6 weeks

Heal with hyper/hypopigmentation, scarring only if 2nd infection

43
Q

What skin disorder is pictured below?

A

Target or Iris lesion assoc. w EM

44
Q

Describe the target lesion assoc. w EM.

A

Reg round shape w 3 concentric zones:

  • dusky or darker red center
  • paler pink or edematous zone
  • peripheral red ring

Some have only 2 zones:

dusky or darker red center

pink or lighter red border

May not be apparent until several days after onset

45
Q

How will a pt present w EM Minor?

A

Prodromal sx are usually absent or mild flu-like illness

Abrupt onset of rash, occurs w/i 3 days, spread distal to central

Pruritis is gen absent

46
Q

How will EM Major present?

A

50% of pts have flu-like prodrome (1-14 pre rash)

Spread same as Minor (distal to central)

Promient mucosal involvment, oral mucosa erosions, conjunctival inflammation, genital lesions (paintful urination)

47
Q

What are the tx for EM?

A

1 tx symptoms

Most cases self limited (oral antihistamines, analgesics, local skin care, soothing mouthwash)

Severe cases - meticulous wound care, Burrow or Domeboro solution dressings

Hydration/monitor fluid status for extensive skin involvment (66-75% fluid resuscitation for similar size burn)

Drug suspected - withdraw drug (reduce risk by 30%/day) All med started in the preceding 2mo

D/C all unnecessary meds

Infections tx after tests & antiseptics to avoid superinfection

Topical lubricants for dry eyes, sweep conjunctival fornices, removal of fresh adhesions

HSV assoc EM - antiviral for prevention (started after eruption of EM has no effect)

48
Q

What is the general rule of tx for all Psoriasis presentations?

A

Avoid excess drying or irriation of skin

Maintain adequate cutaneous hydration

49
Q

What is the tx for localized, plaque-type psoriasis?

A

Mid-potency topical - long-term use complicated by tackyphylaxis ( loss of effect) & atrophy

Topical vit D analogue (Calcipotriene)

Retinoid (tazarotene)

Coal tar, salicylic acid, & anthralin replaced bu previous topical agents

50
Q

What are the tx for Mild/Moderate widespread Psoriasis?

A

UV light, natural or artificial, UV-B light, narrowband UV-B, & UV-A spectrum w either oral or topical psoralens (PUVA) extremely effective

Long-term use of UV light assoc w increased incidence of non-melanoma & melanoma skin cancer

UV-light therapy is contraindicated in pt receiving cyclosporine (should be used w great care in immunocompromised pts due to increased risk of developing skin cancers)

51
Q

What are the tx for severe, widespread Psoriasis?

A

Methotrexate (esp for pt w psoriatic arthritis)

Acitretin (esp when immunosuppression must be avoided, teratogenicity limits use

Cyclosporin

No oral glucocorticoids (risk of Pustular Psoriasis when d/c)

52
Q

What is the class, route, freq, and possible AEs for Methotrexate?

A

C:Anti-metabolite

R: Oral

F: Weekly

AEs: Hepatotoxicity, pulmonary toxicity, pancytopenia, potential for increased malignancies, ulcerative stomatitis, nausea, diarrhea, teratogenicity

53
Q

What is the class, route, freq, and possible AEs for Acitretin?

A

C: Retinoid

R: Oral

F: Daily

AEs: Teratogenicity, osteophyte formation, hyperlipidemia, IBD flare up, hepatoxicity, depression

54
Q

What is the class, route, freq, and possible AEs for Cyclosporine?

A

C: Calcineurin inhibitor

R: Oral

F: BID

AEs: Renal dysfunc, hypertension, hyperkalemia, hyperuricemia, hypomagnesemia, hyperlipidemia, increased risk of malignancies

55
Q

What does tx w Cyclosporine or Biologics target?

A

Serves as Psoriasis tx, immunoregulation directed at T cell-mediated disorder

Immunosuppressive agents

Biologic agents - more selective immunosuppressive properties, better safety profiles

56
Q

What are some concerns of Biologic tx for Psoriasis?

A

TNF-inhibitors may worsen CHF, also assoc. w PML (progressive multifocal leukoencephalopathy)

Not be initiated if severe infection

Routine screening for TB required (reactivation risk)

Malignancies, risk of certain ones - may limit use

57
Q

Name the Biologics approved for Psoriasis or Psoriatic Arthritis?

A

Alefacept

Etanercept

Adalimumab

Infliximab

58
Q

Name this lesion.

A

EM Minor

(notice 2 zones, central red and outer lighter red/pink)

59
Q

What are the 4 etiologic categories of SJS, TEN & combo?

A

Infectious (HSV, AIDS, viral, bacterial, 50% report URI) seen most common in children

Drug-induced: antibiotics (PCN & sulfa), analgesics, cough/cold meds, NSAIDs, psychoepileptics, & antigout. Assoc w multiple HLA (human lymphocytic antigen) alleles w drug exposure

Malignancy-related

(above 2 common in adults)

Idiopathic (25-50% cases)

60
Q

How will SJS, TEN, combo present in pt?

A

Begins w nonspecific URI lasting 1-14 days

Mucocutaneous, non-pruritic lesions develop abruptly in cluster (2-4 wk). Can be urticarial but nonpruritic

Fever or localized worsening = superimposed infection

Oral mucositis - may limit ability to eat/drink..dysuria

Conjunctival or corneal inflammation (27-50%)

61
Q

How do you distinguish btw SJS, TEN, combo?

A

SJS (Stevens-Johnson Syndrome) = minor form of TEN w <10% BSA detachment

SJS/TEN combo = detachment of 10-30% BSA

TEN (Toxic Epidermal Necrolysis) = detachment of >30% BSA

62
Q

What are the general characteristics of SJS/TEN?

A

Immune-complex-mediated hypersensitivity complex involving skin & mucous membranes (oral, nasal, eye, vaginal, urethral, GI, LRT)

GI and respiratory involvement may progres to necrosis

Biopsy = only specific test applicable

DDx w EM (r/o due to acute disseminated epidermal necrosis)

63
Q

What are the 2 main forms for Bullous pemphigoid?

A

Generalized bullous form & vesicular form

64
Q

How will a pt present w generalized bullous form of Bullous pemphigiod?

A

Most common w tense bullae on any part of the skin surface.

Predilection for flexural areas

rare oral & minor ocular mucosa involvement

heal w/o scarring or milia formation

65
Q

How will a pt present w vesicular form of Bullous pemphigoid?

A

Less common

groups of small tense blisters

often on urticarial or erythematous base

66
Q

What are the tx for Bullous pemphigoid?

A

Anti-inflammatory agents (corticosteroids, tetracyclines, dapsone)

Immunosuppressants (azathioprine, methotrexate, mycophenolate, mofetil, cyclophosphamide)

Anti-CD20 antibody (rituximab, specific in targeting antibody-producing B cells)

67
Q

What is the general presentation of Bullous pemphigoid?

A

onset: acute or subacute

Blisters are large & tense, round or oval

chronic, autoimmune, subepidermal, blistering skin disease

Urticarial plaques/bullae

start as urticarial eruption, over wk to months - develop into bullae

Lesions usually pruritic

May be tender at site of erosion

Typically clear fluid, can be hemorrhagic

localized or generalized throughout body (10-25% mucous membranes)

Presence of IgG autoantibodies

68
Q

What is the prognosis for Bullous pemphigoid?

A

untreated = persist for months to yrs w spontaneous remissions & exacerbations

treated = remits w/i 1.5 to 5 yrs

increased morbidity & mortality:

aggressive or widespread disease

high dose corticosteroids/immunosuppressive agents required for control

underlying medical conditions - comorbiditis, avg age 65

69
Q

What history may be important relating to Bullous pemphigoid onset?

A

Recent UV irradiation, X-ray therapy, exposure to certain drugs (furosemide, NSAIDs, captopril, penicillamine, antibiotics)

Recent vaccinations (common in children)

urticarial lesions

70
Q

Identify this skin lesion.

A

Bullous pemphigoid

71
Q

What are the 2 important goals of tx for Bullous pemphigoid?

A

Reduce inflammatory response

Reduce autoantibody production

Derm (1 decks)

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