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Dermatology Board Prep > DERM (19) Urticaria, Erythema, and Purpura > EM, SJS, TEN > Flashcards

EM, SJS, TEN Flashcards

1
Q

Most common cause of EM?

A

HSV (HSV1 more common)

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2
Q

What seperates EM minor and major?

A

In EM minor the target lesions are associated with minimal mucosal involvement and NO systemic symptoms

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3
Q

What is the most common cause of erythema multiforme (EM) major?

A

Mycoplasma Pneumoniae

It often has severe mucous membrane involvement (simulates SJS).

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4
Q

What is the major driver of prognosis in SJS and TEN

A

Speed at which culprit drug is identified and withdrawn.

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5
Q

What is the major mediator of apoptosis in SJS and TEN

A

Granulysin –> secreted in cytotoxic granules of CD8+ T-cells/NK-cells, directly damages keratinocytes.

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6
Q

What is the difference in distribution between EM and TEN/SJS?

A

Distal extremities are relatively spared in SJS/TEN and lesions tend to be more proximal. This is reversed in EM

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7
Q

What is the SCORTEN system?

A

For gauging prognosis in SJS/TEN: has to be done on day 1 and day 3 Tachycardia (>120bpm) Age (>40) Malignancy Epidermal loss >10% Bicarbonate Urea (>17) Glucose (>120)

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8
Q

What is the most important indicator of mortality within the SCORTEN scoring?

A

Serum bicarbonate (<20mmol/L)

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9
Q

Does bactrim and furosemide cross-react for SJS TEN?

A

NO! sulfa abx do not cross-react with other sulfa medications like furosimide

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10
Q

Epidemiology for EM?

A

Young adults; slight male predominance, 90% of cases d/t infection (HSV 1>2), drugs (<10%, NSAIDS, abx, sulfa, antiepileptics, TNF-a inhibitors), systemic dz, physical triggers.

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11
Q

What Infections can cause EM?

A

HSV, Mycoplasma pneuoniae (mucosal involvement), histoplasma capsulatum, parapoxvirus (orf)

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12
Q

Describe classic target lesions in EM?

A

<3mm, regular round shape, well-defined border, 3 distinct zones: 2 concentric rings of color change surrounding central circular zone that has evidence of damage to the epidermis (vesicles, blister, dusky appearance)

Usually palpable!

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13
Q

Describe atypical target lesions?

A

Round, edematous, macular, only 2 zones or poorly defined border

Macules are key, classic lesions tend to be palpable

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14
Q

Difference between SJS/TEN and EM lesions?

A

In SJS the lesions tend to be macular, non-palpable, non-elevated atypical targets. They also tend to be more centrally distributed with more involvement of the mucous membranes

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15
Q

Most common locations for EM?

A

Distal extremities (UE>LE), palms, neck, face and trunk are commonly involved as well.

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16
Q

Definition of EM minor?

A

Target lesions w/ minimal mucosal involvement and NO systemic sx’s.

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17
Q

Definition of EM major?

A

Mycoplasma pneumonia is most common, target lesions w/ severe mucosal involvement and systemic sx. Mucosal sx’s are severe and rapidly develop into painful erosions that involve buccal mucosa and lips. -Systemic sx’s are usually fever, asthenia, arthralgias, joint swelling, pulmonary

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18
Q

What cause of EM also tends to have concomitant EN?

A

Histoplasma capsulatum

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19
Q

Timeline of EM?

A

Almost all lesions appear within 24 hours, full development by 72 hours, pruritus and burning, individual lesions remain fixed at the same site for 7 days or longer.

Episode lasts 2 weeks and heals without sequelae in post pts.

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20
Q

What is the earliest histologic sign of EM?

A

Apoptosis of individual keratinocytes

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21
Q

Differential diagnosis for EM?

A

Giant urticaria, fixed frug eruptions (neuts, pigment incontinence), subcutaneous LE, Kawasaki disease, erythema annulare centrifugum, vasculitis

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22
Q

Difference between urticaria and EM?

A

For urticaria: central zone is clear, lesions are transient, new lesions appear daily, associated w/ swelling of face hands or feet.

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23
Q

Treatment for EM minor compared to major?

A

Minor: oral antihistamines for 3-4 days, topical therapy Major: pred 0.5-1mg/kg/day or pulsed methylprednisolone (20mg/kg/day for 3 days). May be a/w ocular complications.

24
Q

Etiology of SJS/TEN?

A

Nearly always drug-related

25
Q

Histology of SJS/TEN?

A

Extensive keratinocyte cell death tends to be more pauci-immune at the DEJ

26
Q

Sx’s of SJS/TEN?

A

High fever, moderate to severe skin pain, anxiety,e and asthenia

27
Q

What defines prognosis in SJS/TEN?

A

Speed at which culprit drug is identified and withdrawn

28
Q

What are the % body surface areas that define SJS vs overlap vs TEN?

A

Up to 10% = SJS 10-30% = overlap >30= TEN

29
Q

What is the major mediator of apoptosis in SJS/TEN?

A

Granulysin –> secreted in cytotoxic granules of CD8+ t-cells/ NK-cells

30
Q

What are the causes of cell death in SJS/TEN?

A

Granulysin (major mediator of apoptosis), FasL(CD95L) activation of caspases, apoptosis; Granzyme B and perforin: Poke holes in the target cell, activate caspases

31
Q

Causes besides drugs of SJS/TEN?

A

Mycoplasma pneumoniae, contrast media, dengue virus, CMV

32
Q

Clincal presentaton of SJS/TEN?

A

Skin sx preceded by prodrome (1-3 days before skin) Fever, stinging eyes, dysphagia, anorexia, rhinorrhea Atypical (2 rings) poorly demarcated targetoid macular (non-palpable) lesions w/ mucocutaneous erythema & skin pain -dusky plaques w/ full-thickness sloughing (grey-hue) -Flaccid blisters -Macules variable size and shape -can become confluent Atypical & macular*** differentiate from EM (papules, palpable) 1st on trunk –> neck, face and proximal upper extremities Unlike EM, distal extremities relatively spared Flaccid blisters have positive Nikolsky/Asboe-Hansen

33
Q

Systemic sx’s seen in SJS/TEN

A

Fever, lymphadenopathy, hepatitis & cytopenias

34
Q

Factors associated w/ worse survival in SJS/ TEN?

A

Increasing age, extent of epidermal detachment, number of medications, elvation of serum urea, creatine and glucose, neutropenia, lymphopenia, and thrombocytopenia, late wihtodrawal of causative drug

35
Q

Components of the SCORTEN system?

A

Tachycardia (>120bpm), Age (>40), Malignancy, Epidermal loss >10%, bicarbonate, Urea (BUN> 27), Glucose (>250)

36
Q

Most common cause of death in SJS/TEN?

A

Infection

37
Q

Sequelae of SJS/TEN?

A

Symblepharon, entropion, cutaneous scarring, blindness, persistent erosions in eys, eruptive melanocytic nevi, persistent erosion of mucosal membranes, phimosis, vaginal synechiae, nail dystrophy, and diffuse hair loss.

38
Q

SJS/TEN treatment?

A

Controlled pressure, thermoregulated bed and aluminum survival sheet, careful care of detached areas, especially back and pressure sites should be covered w/ vaseline gauze until re-epithelialization has occurred. -Mupirocin/antibiotic ointment should be applied around ears, nose, mouth, and silicone dressing can be used to cover erosive denuded areas of skin.

39
Q

What is good about silicone dressings in the setting of SJS/TEN ?

A

Does not need to be changed and can be left in place until re-epithelialization occurs but the surface should be cleansed daily w/ isotonic sterile sodium chloride solution

40
Q

Consults needed for SJS/TEN?

A

Optho and OB/GYN/Urology

41
Q

Eye care in SJS/TEN?

A

Eyelids should be gently cleased daily wiht isotonic sterile NaCl solution + opthoalmic anitbiotic ointment applie to eyelids -antibiotic eye drops 3x daily to cornea to reduce bacterial olonization which can lead to scarring

42
Q

Nostril care in SJS/TEN

A

Cleansed daily with a sterile cotton swab, moistened with isotonic sterile NaCl solution + antibiotic ointment (mupirocin)

43
Q

Mouth care in SJS/TEN?

A

Should be rinsed several times a day using syringe with isotonic sterile NaCl solution then aspirated if pt unconscious

44
Q

Anogenital/Interdigital care in SJS/TEN

A

Daily short applications of silver nitrate solution (0.5%) in case of maceration or simply sterile NaCl solution if no maceration

45
Q

Pharmacologic tx for SJS/TEN?

A

IV/oral steroids are mainstay early in the disease course (3 days pulse) -Can also consider IVIG, Cyclosporine, and Etanercept

46
Q

What serologic tests can be helpful in distinguishing morbilliform drug rash from SJS/TEN?

A

Granulysin (80% sensitivity), 95% specificity High mobility group protein B1 (HMGB1)

47
Q

What infectious disease increases the risk of SJS/TEN?

A

AIDS = 1000 fold increase in risk

48
Q

What important genetic groups have increased risk of SJS/TEN?

A

HLA-B*1502 (Asians and East Indians exposed to carbamazepine = 220-fold increase in risk)

HLA-B*3101 (Europeans exposed to carbamazepine)

HLA-B*5701 (Abacavir)

HLA-B*5801 (Han Chinese exposed to allopurinol)

HLA-DQB1*0601 (white patients wiht SJS + ocular complications

49
Q

What is the relationship between the half-life of a drug and outcomes in SJS/TEN?

A

Drugs with longer half-lives tend to portend to worse outcomes

50
Q

What are the most common medications associated with SJS/TEN?

A

Allopurinol, anticonvulsants (lamotrigine, carbamazepine, phenytoin, and phenobarbital)

  • Valproic acid does not cross-react with these
  • Lamgotrigine does not cross-react with the aromatic anticonvulsants
51
Q

When is the risk for SJS/TEN highest for starting medications that can cause it?

A

Risk highest within the first 2 months

52
Q

What screening genetic tests should be routinely performed to prevent SJS/TEN?

A

HLA-B*1502 in East Asian patients prior to giving carbamazepine and HLA-B*5701 prior to starting abacavir

53
Q

What is the most common sequelae after SJS/TEN?

A

Ocular sequelae (80%) can include dry eye syndrome (most common), entropion, symblepharon, blindness, scarring, and persistent erosions

54
Q

What is the most common cause of death in SJS/TEN?

A

Infection (S. Aureus and Pseudomonas)

55
Q

Why is there an increased risk of SJS/TEN in patients with HIV?

A

Loss of skin-protective CD4+/CD25+ regulatory T-cells

DERM (19) Urticaria, Erythema, and Purpura (7 decks)

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