Derm wk 4 Flashcards

1
Q

Most skin drug reactions are

A

Inflammatory
Generalized
Symmetric

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2
Q

Immediate drug reactions

A

occur within 1 hour!

Urticaria (hives), Angioedema, Anaphylaxis

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3
Q

Delayed drug reactions

A

Often occur after 6 hours, sometimes even weeks- months after starting med

Exanthematous, Fixed drug eruption, Systemic (DIHS, SJS/TEN), Vasculitis

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4
Q

Most of the time, allergy testing is useless for med reactions, BESIDES with

A

PCN

PCN skin testing is preferred when evaluating possible type I, IgE mediated PCN allergy

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5
Q

Test for PCN allergy

A

PCN skin testing

look for IgE mediated PCN allergy

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6
Q

Risk factors for drug rxns

A
Female
Prior drug rxn
Recurrent drug exposure
HLA gene
Certain dz states- Mono or HIV positive
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7
Q

HIV positive often have dermatologic rxns to

A

Sulfa

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8
Q

Drug timeline

A

Onset of rash as day 0, then work backwards and forwards

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9
Q

Widespread, symmetric

Confluent erythematous macules and papules on trunk and extremities, AKA

A

“Morbilliform” measles-like eruption

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10
Q

macule

A

circumscribed, FLAT, discoloration that is <10 mm

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11
Q

Most common skin drug eruption

A

Exanthematous Drug Eruption

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12
Q

Details on Exanthematous Drug Eruption

A

Limited to Skin

Red macules and papules starting on the TRUNK and spread centrifugally to the arms/legs in symmetric fashion

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13
Q

What might be present along with the Exanthematous Drug Eruption classic mac-pap rash?

A

Mild fever
Itchiness

Rash starts 7-10 days after drug if 1st time, and 1-2 days after drug if recurrent

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14
Q

Papules

A

small also, <10 mm

but RAISED

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15
Q

Can you keep taking the drug if you get an Exanth Drug Eruption rash?

A

Yes but only if eruption is not severe and med can’t be subbed

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16
Q

How soon does Exanth Drug Erup last after stopping the med?

A

Clears up in a few days- week after med is stopped

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17
Q

Tx for Exanth Drug Eruption rash

A

Topical steroids
Oral antihistamine
Reassurance

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18
Q

Oral erythematous plaque with central bulla

A

Fixed drug eruption

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19
Q

FDE- Fixed drug eruption

A

Formation of one or more round or oval patches or plaques that recur at same site with re-exposure to the drug

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20
Q

Common culprits of FDE- fixed drug eruption

A
Laxatives
Tetracyclines
Metro
Sulfa
Barbs
NSAIDs
Salicyates (ASA)
Food coloring
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21
Q

Where do FDE often occur?

A

Mouth, genitalia, face, fingers, toes

but can occur anywhere

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22
Q

How quickly do FDE show up?

A

In prev sensitized ppl, as soon as 30 min- 8 hours after taking drug

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23
Q

Early lesions of FDE are sharply demarcated red macules (flat) —->

A

become raised, forming plaques, which may –> bullae then erosions

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24
Q

In the healing phase, lesions from FDE

A

violet hue followed by post inflammatory hyperpigmentation

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25
Q

Tx for FDE

A

Non-eroded: Potent topical steroid ointment

Eroded: Protective or antimicrobial ointment + dressing

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26
Q

Pt presents with combo of:

Rash + Facial edema

A

suspect drug rxn with Eosinophilia and Systemic sx

DRESS

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27
Q

If you suspect DRESS, what next

A

Order CBC- look for Eisinophilia, and LFT and Renal(kidney) fx test to evaluate for end organ damage

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28
Q

Normal platelet count

A

150-450

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29
Q

Normal Hematocrit

A

36-48%

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30
Q

Drug Induced Hypersensitivity Syndrome (DIHS) is AKA

A

DRESS- Drug Rxn w Eisinophilia and Systemic Sx

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31
Q

Skin eruption with systemic sx and internal organ involvement (Liver, Kidney, Heart)

A

DRESS
or
DIHS

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32
Q

Typical signs of DRESS or DIHS

A

Rash, red centrofacial swelling, fever, malaise, lymphadenopathy, involvement of other organs

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33
Q

Most pts experiencing DRESS/DIHS have what on labs

A

Eosinophilia

> 70% have this

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34
Q

How long does it take for DIHS/DRESS sx to occur?

A

in the 3rd week (but range 1-12 weeks) after starting the medication

Sx can persist and recur for many weeks after stopping drug

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35
Q

What is fatality rate for DRESS/DIHS?

A

up to 10%

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36
Q

Common meds causing DIHS/DRESS

A
Allopurinol
Abx- Sulfa, PCN, Mino, Metro
AntiTB- Isoniazid
Anticonvulsant- Phenytoin, Carbamazepine, Lamotrigine
NSAIDs
Anti-HIV- Abacavir
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37
Q

Approach to pt with suspected DIHS

A

Stop (or sub) all culprit meds and discontinue non-essential meds

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38
Q

Tx for DIHS

A

mild: topical steroids + systemic antihistamines
severe: systemic steroids (prednisone) and taper gradually weeks- months

severely ill: ICU

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39
Q

“Sloughing rash”

On Sulfa and Bactrim for UTI

A

SJS/TEN!!

Widespread erosions on face, upper trunk, and arms

Begin as painful flaccid blisters

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40
Q

How do SJS and TEN differ?

A

BSA- % body surface area that is involved

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41
Q

Mortality rate of SJS

A

5-12 %

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42
Q

Mortality rate of TEN

A

> 20%

worse!

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43
Q

SATANN is a mnemonic to help remember common meds that can cause SJS/TEN!

A
Sulfa
Allopurinol
Tetra, thiacetazone
Anticonvulsant
NSAIDs
Nevirapine
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44
Q

What precedes the rash of SJS/TEN?

A

Fever
HA
Runny nose
Myalgias by 1-3 days

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45
Q

How soon after taking med does SJS/TEN start?

A

within 8 wks after drug initiation

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46
Q

Red, irregularly shaped, dusky red to purple macules,

that progressively coalesce

A

SJS/TEN rash description

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47
Q

Dark center of atypical target lesion may blister

A

SJS/TEN

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48
Q

Classifying SJS/TEN

A

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

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49
Q

Mucous membrane involvement associated with SJS/TEN

A

Red –> painful erosions of the buccal, ocular, and genital mucosa

Mouth, Eyes, Genitals

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50
Q

Whats the worst part of Eye involvement with SJS/TEN

A

Many will suffer permanent Eye sequelae, even blindness

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51
Q

SJS/ TEN complications

A
Eye damage
Oral cavity sicca synd and pain
GU damage
Pulmonary- bronchitis, bronchiectasis
Fluid/electrolyte disturbance
Nutrition requirements
Secondary INFECTION
52
Q

SJS/TEN Tx

consult Dermatology and Ophthalmology

Burn unit

A

IV steroids, IVIG, Cyclosporine, or Etanercept are given variable at diff centers

53
Q

Prevention of SJS/TEN

FDA recommends

A

Test for HLA-B 1502 for all pts SOUTHEAST ASAIN starting Carbamaz

Test for HLA-B 5701 for ALL PTS starting Abacavir

54
Q

Another gene association

A

HLA-B 5801 genetic screening for some Southeast Asain, Japanese, European patients starting Allopurinol

55
Q

Genes and associations

A

HLA 1502: Carbamazepine
HLA 5701: Abacavir
HLA 5801: Allopurinol

56
Q

1502

A

Carbamazepine

57
Q

5701

A

Abacavir

58
Q

5801

A

Allopurinol

59
Q

Cardinal sx of Urticaria

A

Pruritis

60
Q

Urticaria is caused by

A

swelling of the upper dermis

61
Q

Angioedema

A

Same mechanism as hives, but in the DEEP DERMIS and SUBQ

swelling is the major manifestation

62
Q

Angioedema and/or Urticaria can be the ________ of Anaphylaxis

A

Skin portion

assessment of the Respiratory and Cardiovascular sx are vital!

63
Q

Course of hives

A

Appear within minutes, enlarge, and then disappear in hours

Rarely last longer than 12 hours

64
Q

Urticaria can be Acute or Chronic

A

Acute: <6 weeks
Chronic: recurrent more than 2 days per week longer than 6 weeks

65
Q

Common cause of Acute Urticaria

A
Idiopathic
Infection- URI, strep, worms
Food- shellfish, nuts, fruit 
Drug rxns
IV products- contrast or blood products
66
Q

Cholinergic Urticaria

A

triggered by heat and emotion

67
Q

Dermatographism

A

most common form of physical urticaria- sharply localized edema/wheal within seconds-min of skin being rubbed

68
Q

Urticaria Multiforme

A

Kiddos

Polycyclic or Annular lesions with dusky and ecchymotic centers along with acral edema (fingers and toes= acral)

69
Q

Urticaria Multiforme

A

improves w Antihistamines

70
Q

Immunologic urticaria

A

related to IgE

Antigen binds to IgE on the mast cell causing degranulation and release of Histamine

71
Q

Non-Immunologic urticaria

A

not dependent on the binding of IgE receptors

i.e. ASA induced hives

72
Q

Diffuse red papules coalescing into plaques

A

Wheals

73
Q

Is lab testing required for ACUTE Urticaria?

A

No

74
Q

Common causes of hives via the IgE mediated mechanism

A

PCN

Other Abx

75
Q

Common cause of NON-IgE mediated mechanism

A

ASA

76
Q

30% of Chronic Urticaria is MADE WORSE BY

A

ASA/NSAID use

77
Q

Evaluating chronic urticaria

A

Encourage pt to take picture to show you
Often, no external cause can be identified

If physical trigger suspected, a challenge test with the trigger may be performed

78
Q

IgE mediated food allergy more common with

A

Acute urticaria

79
Q

Average duration of Chronic Urticaria

A

2-5 years,

but can extend beyond this

80
Q

What can someone with Chronic Urticaria try

A

Avoid tight triggers
Stop Ibuprofen or other NSAID use

Start 1st gen Antihistamine i.e. Hydroxyzine

81
Q

Reassurance for chronic urticaria

A

About 1/2 patients undergo remission within 1 year

82
Q

1st line tx for Acute and Chronic Hives

A

Oral H1 Anthistamine

83
Q

What types of ppl may require Renal dosing when taking H1 Antihistamines

A

Children
Elderly
Pts w Kidney or Live impairment

84
Q

CAUTION in using H1 Antihistamines in

A

Glaucoma
Prostatic hyperplasia
Respiratory dz

85
Q

1st Gen Antihistamine

A

Diphenhydramine
Hydroxyzine
Chlorpheniramine

86
Q

2nd Gen Antihistamine

A

Cetirizine
Loratadine
Fexofenadine

87
Q

Refer to derm if Hives have 1 of the following:

A
  • last more than 48 hrs
  • painful and burning
  • systemic sx
  • no response to Antihis
  • leave pigment change upon resolution
88
Q

Tx for Anaphylaxis

A

Epi
IVF
Oxygen

89
Q

Adult dosage for Epi treating Anaphylaxis

A

0.3-0.5 mL in 1:1000 epi dilution IM

repeat every 10-20 min as necessary

90
Q

Child <30 kg dosage for Epi treating Anaphylaxis

A

0.01 mL/kG

91
Q

Most common cause of urticaria in kids is

A

Viral illness

92
Q

“itchy red rash” waxing and waning, involving her face

A

mother has hx of Asthma and Allergic Rhinitis

sounds like ATOPIC DERMATITIS (eczema) case

93
Q

Chronic, pruritic, inflammatory skin disease

A

Atopic Dermatitis

one of the most commin skin disorders in developed countries

94
Q

Onset of Atopic Derm

A

usually b/w 3-6 mo

90% diagnosed by age 5

95
Q

How often does Atopic Derm persist into adulthood?

A

30%

96
Q

“The itch that rashes” bc Atopic Derm is itchy and then pts scratch it which makes it

A

WORSE

97
Q

Distribution of Atopic Derm

A

Symmetric

98
Q

Lesions are red and scaly

May display vesiculation, oozing, and crusting

A

More chronic lesions can even become lichenified

99
Q

Lichenification

A

epidermal thickening with accentuated skin lines from chronic irritation

100
Q

Atopic Derm for INFANTS and TODDLERS affects what body parts

A

Scalp
forehead
cheeks
Extensor surfaces

(back of arms, back of legs)

101
Q

Atopic Derm for Older children affects what body parts

A

FLEXORAL areas

neck, elbows, knees, wrists, ankles

102
Q

Eczema is a nonspecific term encompassing

A

Itchy
Erythema
Scale

103
Q

Atopic Dermatitis is a more specific type of

A

Eczematous dermatitis

104
Q

Factors thought to contribute to Atopic Dermatitis

A

Genetic pre-D
Skin barrier dysfx
Immune dysregulation
Environment

105
Q

Best tx for a child’s face with Atopic Dermatitis

A

Hydrocortisone 2.5% ointment

106
Q

Super high potency steroid

A

Clobetasol

like a CLUB, super STRONG

107
Q

High potency steroid

A

Fluocinonide

108
Q

Medium potency steroid

A

Triamcinolone

109
Q

Low potency steroid

A

Desonide

Hydrocortisone

110
Q

Bathing rec for someone with Atopic Derm

A

Apply moisterizer after bathing
Limit use of soap/cleanser
Dilute bleach baths

111
Q

Refer pt with Atopic Derm to Dermatology when

A

Recurrent skin infection
Extensive/severe dz
Sx poorly controlled w topical therapy

112
Q

Systemic therapy for Atopic Derm

A
Light therapy w NbUVB
Immunosupp meds:
-Cyclosporine
-Mycophenolate mofetil
-MTX
-Azathioprine
113
Q

Biologic drug for Atopic Derm

A

Dupilumab

monoclonal antibody directed against IL-4 and IL-3

114
Q

If low dose steroid is not working to control flare

A

Increase dose, then taper off once sx are controlled

115
Q

How is food related to AD

A

Food allergy is a known trigger in 20-30% of pts w Mod-Sev AD

116
Q

Atopic march

A

Atopic derm –> Rhinitis –> Asthma

117
Q

Explaining Atopic Derm boy’s foot

A

Lichenified red plaques with overlying scale, fissuring, hemorrhagic and brown crust

118
Q

What do you need to consider in pts that have Weepy flares of AD?

i.e. when Pustules, Erosions, or Crusting are present- yellow, brown, hemorrhagic

A

Skin Bacterial Culture

bc secondary infection from Staph or Group A Strep is common

119
Q

Way to describe the boy

s face that had white spots

A

Poorly defined HYPOPIGMENTED patches w fine scale on the face

120
Q

Pityriasis Alba may present as

A

Poorly defined hypopigmented patches w fine scale on the face

121
Q

What is Pityriasis Alba?

A

Mild, often no sx, form of Atopic Derm of the face

122
Q

Poorly marginated, hypopigmented, slightly scaly patches on the CHEEKS

A

Pityriasis Alba

123
Q

Who is Pityriasis Alba usually found in?

A

Young children w darker skin

often in spring or summer when the unaffected skin tans, becomes more noticeable

124
Q

Tx for Pityriasis Alba

A

Moisterizer BID

Sun protection

125
Q

If no improvement of Pityriasis Alba after moisterizing and sun protection, consider

A
  • Low strength topical steroid

- Topical calcineurin inhibitor

126
Q

Long term tx for AD vs Acute care

A

Emollients and gentle care

Acute flare: topical steroids