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Me > (Ch20) EM and SJS/TEN > Flashcards

(Ch20) EM and SJS/TEN Flashcards

1
Q

Rashes that increase in Spring and fall

A

EM & PR

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2
Q

Most common cause of EM?

A

infections 90%
MC HSV1>HS2
followed by mycoplasma pneumonia

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3
Q

what percentage of EM preceded by herpes labials?

A

50%

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4
Q

other name of EM minor caused by HSV?

A

Von Hebra’s

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5
Q

most common cause of EM major

A

Mycoplasma pneumonia

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6
Q

Mycoplasma pneumonia EM clinical features?

A

Severe Mucocutanous involvement with atypical papular targets

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7
Q

genetic associations with EM

A

HLA-DQw3
HLA-DRw53
HLA-Aw33

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8
Q

causes/triggers of EM?

A
  1. Infections 90%
    viruses:
    - HSV 1,2
    - Parapox virus(orf)
    -VZV, EBV

Bacteria:
-Mycoplasma pneumonia
-Chylamydia
- TB

fungal:
-Histoplasma capsulatum

  1. Drugs <10%
  2. physical triggers (trauma, UV and Clod ) kobener must be prior rash not after
  3. poison Ivy and vaccines
    5.lupus & Bechet
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9
Q

which trigger or infection As/w Erythema nodosum

A

Histoplasma capsulatum

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10
Q

Drugs that can trigger EM?

A

SPAAN
Sulfa
Penicillin
Allopurinol
Anticonvulsants
NSAIDs

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11
Q

Pathogenesis of mycoplasma EM

A

molecular mimicry

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12
Q

which cell mediate HSV triggered EM

A

virus DNA transmitted by CD34+ to Th1 which releases IFN gamma

patients have normal immunity but may have difficulty clearing virus infected cells

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13
Q

Classic Primary lesion of EM

A

Typical targets
(3 zones)
1. center: dusky , vesicular or necrotic
2. pale oedematous rim
3. erythematous macule

Favours Face and distal extremities

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14
Q

Clinical lesions or features of EM

A

Typical targets
Atypical Papular targets (2 Zones)
+/- Mucosal involvement

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15
Q

what type of atypical targets present in EM vs SJS/TEN

A

Atypical Papular targets –> EM

Atypical Macular Targets–> SJS/TEN

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16
Q

Most common Location for EM rash

A

Dorsal hands and forearms

(UL>LL)
(distal > proximal)
face is a common location as well

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17
Q

Can EM progress to SJS?

A

No

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18
Q

clinical criteria to differentiate EM vs SJS/TEN

A

1.Type of lesions (typical and papular atypical targets)

  1. (Topography) Acrofacial distribution in EM

3.Abscence/presence of overt Mucosal involvement

  1. Path: ↓Eosin, ↓ epidermal necrosis
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19
Q

what are the systemic sx of EM

A

Fever and Arthralgia

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20
Q

EM Minor vs Major

A

both have targets (typical and papular atypical) and same distribution

Minor: no or mild mucosal involvement and no systemic sx

Major: Severe mucosal + systemic sx

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21
Q

oral variant of EM

A

MC in mid aged F
limited to oral cavity

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22
Q

MC mucosal location of EM

A

lips and buccal mucosa >ocular and genital

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23
Q

Earliest path sign of EM

A

Apoptosis of keratinocytes

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24
Q

Path of EM

A

basal Vacuolar interfacce dermatitis with apoptosis, spongosis and dermal inflammation and

absent or rare Eosin

normal SC. +/- vesicle

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25
Q

Path EM vs SJS/EM

A

EM: ↓Eosin, ↓ epidermal necrosis, ↑↑dermal inflammation

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26
Q

percentage of EM patient with HSV +ve PCR?

A

80%

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27
Q

Which part of the lesion to swab for HSV?

A

early papule or outer rim

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28
Q

how long does it take for EM to completely developed

A

72h

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29
Q

prognosis of EM?

A

Spontaneously resolves within 2 weeks without sequela

Severe mucosal may persist up to 6 weeks

ocular complications if not treated eye

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30
Q

Clinical course of EM?

A

abrupt onset 24h
fully developed 72h
resolves 2 weeks

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31
Q

Time limit to use antiviral ?

A

prior to sx
after sx ineffective

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32
Q

prophylactic Rx for EM?

A

Valtrex 1g/d for at least 6 months

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33
Q

Rx for EM

A

Mild Sx tx
Severe SCS/CsA/MMF/AZA

consider oral antihistamine for pruritus

antiseptic cream for rash

wound care
eye care
oral rinses/anethetics /antiseptics

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34
Q

EM vs Urticaria

A

EM:
1 -lesion’s centre damaged skin
2 -Fixed lesions
3 -fully developed 72h
4- no angiodema

Urticaria:
1 -centre normal skin
2 - transient lesions
3 - daily new lesions
4- +/-Angiodema

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35
Q

HSV recurrent EM frequency ?

A

2/year

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36
Q

RIME clinical features?

A

Clinical RIME:
1- Mucosal:
Severe mucositis
≥2 mucosal sites

2-cutanous:
-Vesiculobullous or atypical targets
- +/- sub corneal pustules
- <10% BSA

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37
Q

RIME prognosis ?

A

<5% ICU
10% ocular complications

38
Q

labs for RIME?

A

Mycoplasma:
- IgM: repeat multiple times
-IgG: 4 folds increase

39
Q

Ddx for EM

A

Urticaria
Serum sickness/like reaction
Fixed drug eruption

40
Q

Target lesion ddx

A

FREE Vanilla Sweet at target:
-Fixed Drug eruption
-Rowell syndrome /SLE
- EAC &EM
- Eruption light
-Vasculitis/Kawasaki
- Sweet syndrome & Sjs

41
Q

epidemiology of SJS/TEN

A

MC F elderly
SJS 1-6/mil
TEN 1/mil
annul incidence

42
Q

Risk factors of SJS/TEN

A
  1. Slow Acetylators
  2. Immunodeficent (AIDS,Lymphoma)
  3. combo RadioTx+ Aromatic Anticonvulsants
  4. HLA genes
43
Q

Which HLAs As/w Carbamazepine

A

HLA-B1502- Asians
HLA-B 3101- Europeans

44
Q

HLA associated with Abacavir

A

HLA-B 5701

45
Q

HLA As/w Allopurinol in Han Chinese

A

HLAB- 5801 han Chinese

46
Q

Which HLA As/w ocular complications in white?

47
Q

Main mediator of Apoptosis in SJS/TEN

A

Granulysin

48
Q

Factors involved in pathogenesis of SJS/TEN

A
  1. Drugs
  2. Granulysin
  3. FasL (induce caspases)
  4. Granzyme B and Perforins (holes and induce caspases)
  5. Annexin 1
49
Q

Drugs inducing SJS/TEN

A

1-3 weeks (earlier with re-exposure)

SPAAAN
Slufonamides
Penecillin
Anticonvulsant
Allopurinol
Anti-retovirals
NSAIDs

Sulfonimides abx don’t cross react with non abx sulfonmides (HCTZ)

50
Q

causes of SJS/TEN

A

almost always drugs but can be caused infections (same EM) and contrast

The Longer half life of the drug the higher risk of SJS/TEN

51
Q

time interval for SJS/TEN after drug

52
Q

Which meds can have delayed SJS/TEN up to 2 months after initiation?

A

Anticonvulsants

53
Q

Which anticonvulsant that does not cross react with aromatic anticonvulsant

A

Lamotrigine

54
Q

Which anticonvulsant that does not cross react with other anticonvulsant

A

Valoproic Acid

55
Q

SJS vs TEN

A

BSA
SJS<10%
Overlap 10-30%
TEN>30%

55
Q

Which meds has priority to DC other than culprit drug ?

A

Long hlaf life meds

56
Q

How to calculate BSA in SJS/TEN

A

Calculate detachable skin only (+ve Nikolsky)

57
Q

What type of targets in SJS/TEN

A

Atypical Macular targets

58
Q

What part of the body spared in SJS/TEN?

A

Distal extremities (except palms & soles)

59
Q

what type of blisters in SJS/TEN?

A

Flaccid that detach easily

60
Q

Clinical Signs of detachable skin?

A

Niklosky: detachable with Tangential pressure

Asboe-Hansen: detachable with vertical pressure

61
Q

What percentage of Respiratory involvement?

62
Q

Relative contraindications for IVIg?

A

Hypercoagulable state
IgA deficiency
Renal disease

63
Q

Three different concepts of neoantigenic drug–tissue complex is formation?

A
  1. Hapten/pro-hapten concept (covalent)
  2. p-i concept (non covalent)
  3. Altered peptide concept
64
Q

Earliest path sign of SJS/TEN

A

Apoptosis of individual keratinocytes

65
Q

Early and late path signs of SJS/TEN

A

Early: Apoptosis of individual keratinocytes

Late: full epidermal necrosis

both has eosin and sparse dermal lymph

66
Q

Scores to evaluate SJS/TEN severity ?

A
  1. SCORTEN (superior)
  2. ABCD-10 (has x3 points for dialysis)
67
Q

SCORTEN

A

TAMEBUG
each 1 point

  • Tachycardia >120
  • Age >40
  • Malignancy
  • Epidermal loss >10%
  • Bicarbonate <20
    -Urea >27
  • Glucose >250
68
Q

Mortality rate for scores

A

0-1-> 3%
2 -> 12%
3 ->35%
4 -> 58%
5 -> >90%

69
Q

Most important single risk factor for mortality ?

A

Bicarbonate <20

70
Q

Which factor correlate with prognosis ?

A

rapidity of drug DC

71
Q

impact of early drug DC?

A

30%/day reduction. in mortality

72
Q

Systemic meds for SJS/TEN?

A
  • high dose IVIG (block fas receptor)
  • TNFi Etanerecept
  • Cyclosporine
  • Dexamethasone
73
Q

Most common complication ?

A

Ocular (80%)
-Dry Eye syndrome (MC)
-Entropion
-Blindness
- persistent erosions

74
Q

other Complications of SJS/TEN

A

Ocular
Resp
Genital
Psych
electrolytes imbalance
insulin abnormality
hair loss
nail loss
eruptive nevi
Death

75
Q

Most common cause of Death?

A

infection
(Staph and Pseudomonas)

76
Q

Prognosis of SJS/TEN

A

Mortality rate
- SJS 5%
- TEN 30%

77
Q

When to measure SCORTEN

A

Day 1 and 3 of hospitalization

78
Q

Serologic test to differentiate SJS/TEN from morbiliform eruption

A

Granulysin and HMGB1

79
Q

Benzodiazepine As/w SJS/TEN

80
Q

Infection that increase risk of SJS?

81
Q

type of bed sheet in SJS/TEN

A

Aluminium bed sheet

82
Q

Why no need to graft the skin for SJS/TEN?

A

Complete Re-epitheliazation within 3 weeks

83
Q

Ddx for SJS/TEN

A

EM
gen bollous drug eruption
linear IgA bollous
TEC
SSSS
DRESS

84
Q

Wound care for SJS

A

Vaseline gauze/silicon non adherent dressing over detached skin and pressure areas

face with NS and mupirocin nostrils

incase of maceration use silver nitrate

85
Q

frist location for SJS/TEN rash

A

Trunk mostly and then face and other body

86
Q

Mention five infectious ethologies other than viral that can precipitate Erythema Multiforme?

A

Mycobacterial infection
Mycoplasma pneumoniae
Histoplasmosis
Dermatophytes
Salmonella

87
Q

Mention five contributing factors to increase mortality in Toxic Epidermal Necrolysis?

A
  1. Infection and sepsis
  2. Transepidermal fluid loss and electrolytes imbalance
  3. Insulin resistance and decrease insulin secretion
  4. Hypercatabolic state
  5. Multi organ failure and Acute respiratory distress syndrome
88
Q

What is the most important step in managing Toxic Epidermal Necrolysis?

A

Removal of the culprit drug is mainstay of treatment.

89
Q

What cytokines correlates with severity and mortality in Toxic Epidermal Necrolysis?

A

IL-15 level correlate with severity and mortality in Toxic Epidermal Necrolysis.

90
Q

19- What is the earliest Clinical sign of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis?

A

Fever, stinging eyes, and painful swallowing are the earliest sign of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis. They precede cutaneous manifestations by 1-3 days

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