Acute Inflammatory Dermatoses Flashcards

1
Q

understand the hist-pathologic characteristics of acute inflammatory dermatoses

A

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2
Q

recognize and describe angioedema

A

Deep dermal and Subcutaneous swelling
Burning/Painful
Laryngeal Involvement = Emergency

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3
Q

differentiate Stevens Johnson Syndrome and Toxic Epidermal Necrolysis

A

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4
Q

recognize and describe fixed drug eruptions

A

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5
Q

recognize and describe panniculitis

A

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6
Q

erythema nodosum

A

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7
Q

erythema induratum

A

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8
Q

locations of:

Urticaria:                           
Erythema Multiforme:        
SJS/TEN: 				
Fixed Drug Eruption			 
Panniculitis:
A

Urticaria: Dermis
Erythema Multiforme: Epi/Dermis
SJS/TEN: Epi/Dermis
Fixed Drug Eruption Epidermis
Panniculitis: Subcut
Erythema Nodosum
Erythema Induratum

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9
Q

Urticaria

A

dermal edema, usually result of oral allergy
Transient Wheals
Persist for <24 hours (for any given wheal)
IgE and histamine mediated
Pruritic
Ask about new exposures/medications

Angioedema (severe form):
Deep dermal and Subcutaneous swelling
Burning/Painful
Laryngeal Involvement = Emergency

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10
Q

Urticaria and Angioedema Clues

A

Each patient needs a thorough history that details travel, recent infection, occupational exposure, meds (Rx and OTC), ingestion of foods, and any exposure to physical stimuli.
Careful family history documenting pre-existing allergies.
Comprehensive physical exam looking carefully at all skin surfaces, joints, conjunctiva and mucosal membranes.
Prevalence: 14-25% in US

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11
Q

urticaria vs angioedema

A
Urticaria:
Pruritic 
Transient raised wheals
Less than 24 hours
Pathology: dermal edema
\+/- eosinophils/lymphs/pmns 	
Angioedema
Intense swelling of the dermis and SQ
Painful>pruritic
Lip, eye, groin, palms/soles common
Laryngeal involvement = Emergency
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12
Q

Urticaria and AngioedemaCauses

A
I Immune
  A. Type I IgE Mediated
  B. Auto-immune
  C. Infectious
II Non-Immune
   A. Physical Urticarias
   B. Direct mast-cell degranulation
   C. Foods containing high levels of histamine
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13
Q

Urticaria and Angioedema:Causes: Immune

A

. Type 1 IgE mediated
Foods: shellfish, fish, peanuts, tree nuts, eggs, milk, soy, wheat. (* seen in adults) (seen in kids)
Latex
Stinging insects including hymenoptera (bees, wasps, hornets), fire ants, bedbugs, fleas, mites.
Medications: penicillin, cephalosporin, sulfa
Aeroallergens: dust mites, pollens, molds, animal dander

B. Autoimmune disease: Hashimoto’s immune thyroiditis (production of anti-thyroid antibodies), SLE, vasculitis.
(there may be thyroid anti-autobodies in the absence of thyroid dysfunction)

C. Infection: viral (cytomegalovirus, Epstein-Barr, HIV, hepatitis A, B & C); parasitic, fungal or bacterial.

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14
Q

Urticaria and Angioedema:Causes: Non-immune

A

Non-immune (no Ag-AB reaction; no prior sensitization needed; can happen with first exposure)
A. Physical urticaria
B. Direct mast cell de-granulation
C. Foods containing high levels of histamine

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15
Q

Physical Urticarias (Non-immune)

A
Solar (sun)
Cholinergic (sweating vs heat)
Cold urticaria
Dermographism (friction)
Aquagenic (water)
Vibratory angioedema
Pressure urticaria (burning hands, feet, butt)
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16
Q

Direct Mast Cell Degranulation (Non-Immune)

A
Narcotics (MS and codeine)
Aspirin
NSAIDs
Radiocontrast media
Dextran
ACE inhibitor angioedema
Vancomycin - “Red Man” syndromeSee flushing with hives after IV vancomycin
17
Q

Foods Containing High Levels of Histamine (Non-Immune)

A
Strawberries
Tomatoes
Shrimp
Lobster
Cheese
Spinach
Eggplant
18
Q

Urticaria and AngioedemaLaboratory Evaluation

A

Rule 1: don’t get carried away! Expensive lab evaluations usually have poor yields.

Basic evaluation includes CBC, ESR, TSH, and a basic chemistry panel

Consider throat culture, monospot if warranted by history

Check anti-thyroid antibody titer and FANA on female patients.

Punch biopsy to exclude vasculitis if lesion persists > 48 hrs or looks atypical

19
Q

Urticaria and AngioedemaTherapy

A

General measures: avoid allergen, avoid extremes of heat and cold, exercise, and alcohol (vasodilatation, flares, hives).

Acute urticarial hallmark of Rx is antihistamines, preferably non-sedating H1 blockers.

Chronic urticarial patients get frustrated! Cause of urticaria not found in 75-80%, but most improve slowly over 1-2 years.

20
Q

Erythema Multiforme

A

Reaction Pattern of blood vessels in the dermis
Secondary epidermal changes manifest clinically as erythematous iris-shaped papular and veisculobullous lesions
Involving extremities (especially palms and soles) and mucous membranes
Epidemiology: 50% are under 20 years and more frequent in males
Etiology: Cutaneous reaction to a variety of antigenic stimula (drugs vs infection vs idiopathic)
Drugs: Sulfonamides, phenytoin, barbiturates, phenylbutazone, penicillin, allopurinol
Infection: Herpes Simplex Virus, Mycoplasma
Idiopathic: more than 50%
Acute hypersensitivity reaction showing classic “target” lesions.
EM minor = mild form involving ≤ 1 mucosal site; major cause is post herpes simplex infections with onset of EM rash at day 10.
EM major = severe with extensive skin and mucous membrane involvement (Stevens-Johnson Syndrome). Usually due to drugs (sulfa, PCN, dilantin, tegretol) and after mycoplasma pneumoniae infection.

21
Q

Erythema MultiformeTherapy

A

Prevention: Control Herpes Simplex using Rx
Glucocorticoids: For severe ill-systemic prednisone
Supportive
Can differentiate EM from hives in that EM is fixed and usually does not itch

22
Q

Stevens Johnson Syndrome

A

Toxic Epidermal Necrolysis
Mucocutaneous Drug-Induced or Idiopathic Reaction Patterns
Skin Tenderness and Erythema of Skin and Mucosa
Followed by Extensive Cutaneous and Mucosa Epidermal Necrosis and Sloughing
Potentially Life Threatening

23
Q

Differentiation

A

Erythema Multiforme (1 mucosal membrane)

Stevens-Johnson Syndrome (SJS): Considered a Maximal Variant of EM Major (2+ mucosal membrane and < 10% epidermal detachment)

SJS/TEN overlap (10-30% epidermal detachment)

Toxic Epidermal Necrolysis (TEN): Maximal Variant of SJS (2+ mucosal membrane and 30% epidermal detachment)

24
Q

SJS/TEN Epidemiology

A

Age: any age, but most common >40 years
Equal sex incidence
Overall incidence: SJS: 1.2-6 per million population per year and TEN: 0.4-1.2 per million population per year
Risk Factors: Systemic Lupus Erythematosis, HLA-B12, HIV Disease

25
Q

SJS/TEN Etiology

A

Drugs are the leading causative factor
SJS: 50% associated with Rx often not clear
TEN: 80% strong association with Rx
Cytotoxic immune reaction aimed at destruction of keratinocytes expressing foreign (drug-related) antigens
Time from first drug exposure to symptoms is 1-3 weeks

26
Q

Toxic epidermal necrolysis (TEN)

A

it is unclear whether TEN is a severe form of erythema multiforme or a distinct disease

80% of cases have a strong association with a specific drug (list is similar to that for erythema multiforme)

TEN is a medical emergency, on the order of a total body burn

A severe hypersensitivity syndrome, life threatening
Begins within hours to days of exposure (up to 2 wks) with fever, malaise, arthralgias
Painful morbilliform rash develops during 1st wk, then becomes confluent, then bullous and exfoliative
Total detachment of epidermis (total body 2nd degree burn)

27
Q

SJS/TEN Therapy

A
Early Diagnosis and Withdrawal of Rx
ICU 
Management of IV Fluids/Electrolytes
Systemic Glucocorticoids Early?
High Dose Immunoglobulins for TEN
Debride only frankly necrotic skin
Treat complications
Mortality Rate for SJS 5% and for TEN 30%
Mortality related to sepsis, GI hemorrhage and fluid/electrolyte imbalance
28
Q

Fixed Drug Eruption

A

Definition: a localized, sharply demarcated erythematous patch that can itch, burn or be asymptomatic.
Predisposition for face and genitals.
Often heals as a hyperpigmented area.
Pseudoephedrine is non-pigmenting
Will recur in the same place if rechallenged
Unknown mechanism but felt to be immune.
Therapy: eliminate the offending drug.

29
Q

Panniculitis

A

Major focus of inflammation: subcutaneous tissue
Erythematous or violaceous nodule in the SQ fat
Described as lobular or septal depending on where disease process begins
Accurate diagnosis by skin biopsy

30
Q

Panniculitis Erythema Nodosum

A
Erythematous tender nodules
Septal panniculitis
Typically ANTERIOR shins
Young women most common
Triggers
         Infection (strep, TB, fungal)
   Meds (OCP, Sulfa, NSAIDS)
   Autoimmune (IBD, Sarcoid)
Treatment: rest, ice, pain control
31
Q

Panniculitis Erythema Induratum

A
Tender red nodules
Lobular panniculitis and vasculitis
Middle aged, usually female
Posterior legs>ant
Chronic, recurrent subcutaneous nodules and plaques with ulceration
Associated with TB