Dermatologic diseases: Urticaria, Contact dermatitis Flashcards

1
Q

What is the definition of chronic urticaria?

A

Presence of urticaria for at least six weeks

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2
Q

What is the pathogenesis of CU?

A

Mast cell degranulation can occur via IgE independent pathways.

Basophils/mast cells are triggered by the following mechanism:

  • IgE binds to the α-subunit of its high-affinity receptor, FcɛRI, on mast cells and basophils and, if present at high concentrations, can activate these cells regardless of the specific antigen. We used to look for specific auto antigens like anti TPO but this has not made any clinical difference yet in phenotyping.
  • In addition, the cross-linking of IgE by their respective allergens, autoallergens and IgG anti-IgE antibodies can lead to mast cell and basophil activation and mediator release in allergic, autoallergic and autoimmune urticaria, respectively.
  • IgG autoantibodies to IgE and FcɛRI were the first autoantibodies described in the context of autoimmune CSU. Most studies report that 20–50% of patients with CSU have these autoantibodies This is type IIb in CSU.
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3
Q

Management of CU?

A

Second generation H1 antagonists are the first line treatment.

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4
Q

Allergic contact dermatitis: What is the most common form? What is the reaction caused by?

A

Toxicodendron dermatitis, formerly known as Rhus dermatitis, also known as poison ivy, poison oak, and poison sumac, is the most common form of allergic contact dermatitis seen in pediatric and adult patients in US.

Reaction is caused by urushiol, oleoresin oil found in the sap that oozes easily from any crushed part of the plant.

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5
Q

What foods are cross reactive with oleoresin oil?

A

Mango, as well as cashew nut shells and Ginkgo tree fruit pulp can cause similar reactions to that of Toxicodendron dermatitis because of cross reactivity of the oleoresin oil.

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6
Q

Allergic contact dermatitis to plants causes

A
  • Anacardiaceae family of plants causes the most cases of plant dermatitis= Toxicodendron dermatitis, formerly known as Rhus dermatitis, also known as poison ivy, poison oak, and poison sumac.
  • Plants from Rutaceae family including orange, grapefruit, lemon and lime are common sensitizers and are seen quite often in food preparers and barworkers.
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7
Q

What is hypocomplementemic urticarial vasculitis syndrome (HUVS)

A
  • Chronic urticarial rash which may bruise or become purpuric and hypocomplementemia
  • Biopsy leukocytoclastic vasculitis
  • Arthralgia and/or arthritis; uveitis, episcleritis, and /or conjunctivitis
  • Proteinuria, hematuria, renal insufficiency, and/or glomerulonephritis
  • Abdominal pain, nausea, vomiting, and/or diarrhea
  • Positive anti-C1q antibodies.
  • Lung involvement in HUVS includes coughing, hemoptysis, shortness of breath, pleural effusions, and COPD
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8
Q

History for allergic contact dermatits

A
  • Delayed-type eczematous dermatitis
  • Wear jewelry, apply nail polish, or dye her hair?
  • Skin cream or wash (scented or unscented)?
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9
Q

Most frequent causes of allergic contact dermatitis with a periocular/periorbital distribution

A
  • Metal (nickel, gold)- nickel products in jewelry and cosmetics
  • Fragrances
  • Preservatives
  • Antibiotics
  • Paraphenylenediamine (hair dyes or in hairstylists)
  • Thimerosal
  • Acrylates- distribution of rash especially along hand and nail bed, along with eyelid dermatitis may suggest involvement of nail polish/acrylic nails

(Products label “unscented” can contain fragrances along with masking scents or odor-neutralizing chemical and is not synonymous with products labeled “fragrance-free.”)

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10
Q

Management of allergic contact dermatitis

A
  • Patch testing may be helpful in deciphering the potential sensitizer
  • Avoidance of sensitizing agents
  • Use of fragrance-free (not unscented) products such as petrolatum
  • Low-potency topical steroid ointment or topical calcineurin inhibitor
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11
Q

If indicated by history or physicial exam in chronic urticaria, what are some limited laboratory testing that can be included?

A

CBC with differential
ESR and/or CRP
Liver enzyme
TSH
H. pylori infection
Mastocytosis
Malignancy
Skin biopsy (refractory CU, vasculitis suspected, other nonurticarial immunologic skin diseases are a consideration)

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12
Q

What is contact urticaria (clinical features and testing)

A

Clinical presentation
- Contact urticaria appears w/in 30min of exposure (vs. allergic contact dermatitis)
- Systemic symptoms can be seen (GI and nasopharyngeal) ?on ingestion
- Plant- and animal-derived proteins most common causes in workplace
- Bakers and agricultural workers highest risk
- Cooks, butchers, restaurant personnel, veterinarians, hairdressers, florists, and forestry workers also affected
- Foods implicated: meats, fish, eggs, fruits, vegetables, and flour and associated enzymes (α-amylase)

Investigations
- Percutaneous testing
- Open testing: Apply small amt of presumed offending agent to normal skin on volar aspect of forearm, observe for 20-60 minutes for wheal-and-flare
- Consider serum specific IgE but many protein allergens not identified yet
- Oral challenge can differentiate from IgE-mediated food allergy (esp if systemic symptoms)

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13
Q

Contact dermatitis from methylisothiazolinone

A

A chemical preservative found in many water-based products such as sunscreen, cosmetics, hair products, liquid soap, laundry products, premoistened facial wipes and baby wipes

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14
Q

Contact dermatitis from sporting goods such as tennis rackets, building construction, and vehicle parts; distribution of rash is on hands

A

Bisphenol A is often found in sporting goods such as tennis rackets, building construction, and vehicle parts; therefore, favoring the distribution of the rash is on the hands

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15
Q

Contact dermatitis from shoes and leather with rash distribution on dorsum of feet

A

Potassium dichromate is found in shoes and leather so the rash distribution is usually on the dorsum of the feet.

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16
Q

Most frequent cause of allergic contact dermatitis

A

The most common chemical classes to cause allergic dermatitis include fragrances, preservatives, excipients, nickel, and sun screening agents.

topical antibiotics?

17
Q

Contact dermatitis from dental implants, artificial joints, and engines

A

Cobalt dichloride is found in dental implants, artificial joints, and engines. Cobalt allergy affects about 2% of the general population. Affected areas are those where direct contact occurs.

18
Q

delayed-type IV hypersensitivity reaction to component of hair dye

A

Para-phenylenediamine (PPD)

relevant to both people that color their hair as well as hairdressers

PPD is also found in black henna tattoos, which can lead to sensitization and subsequent dermatitis with re-exposure

The most common allergens implicated in causing contact dermatitis to hair care products include:
* Cocamidopropyl betaine
* Para-phenylenediamine (PPD)
* Fragrances
* Preservatives
* Glycerol thioglycolate

19
Q

The 15 most frequently positive allergens of the NACDG (North American Contact Dermatitis Group) 2009-2010 patch test include:

A
20
Q

What is the Urticaria Activity Score 7 (UAS7)?

A

Interpretation:

A cutoff of 11 points for UAS7 showed sensitivity and specificity of 74% and 86%, respectively (Hawro 2018).

21
Q

A 25-year-old woman has CSU well controlled on cetirizine, 20 mg twice daily x6m.

Has history of NSAID exacerbated cutaneous disease with acute urticaria and angioedema, reproduced on three occasions within one hour of taking ibuprofen 200 mg.

How do you counsel her about NSAID use for her chronic HAs?

A

Answer:
Reintroduce therapeutic dose NSAIDs under direct observation while on antihistamines

  • CSU often exacerbated by NSAID use. NSAID-exacerbated cutaneous disease (NECD) has been reported in more than a quarter of patients with CSU
  • Guideline-based recommendations advise the avoidance of NSAIDs in CSU patients with NECD. Difficult for patients with comorbid conditions that require NSAIDs
  • Several recent studies have reported that CSU control with antihistamines often leads to temporary tolerance of NSAIDs
  • However, due to the residual risk of breakthrough reactions, the NSAID challenge should be performed under direct observation
22
Q

Percentage of patients with CSU that have associated angioedema

A

40%
typically affects the face, extremities, and genitals

23
Q

Treatment of CSU

A
24
Q

Dose of omalizumab

A

150 or 300mg
q4weeks

300mg has faster and better response rates

25
Q

Biomarkers associated with poor response to omalizumab

A

Associated with refractory disease and a poor response to omalizumab
- Low baseline total serum IgE

Associated with poor response to omalizumab:
- eosinopenia (<50 cells/µL)
- basopenia (<10 cells/µL)
- high CRP (>3 mg/mL).

26
Q

Exercises can trigger two different types of urticaria/anaphylaxis, and how to diagnose them

A

1) Exercise- induced urticaria/anaphylaxis (EIU/EIA)
2) Cholinergic inducible urticaria (rarely anaphylaxis) (ChoIU)

Diagnosis of EIA
- Provocation test of implicated food or drug intake, followed by exercise challenge (often treadmill for 30 min or point of sweating)

Diagnosis of ChoIU
- Exercise challenge and if positive, then
- At least 24 hours later, followed by passive warming test to raise the core body temperature 1.0 degree Celsius from baseline (often via hot water bath challenge)

27
Q

Histaminergic urticaria and angioedema. Percent presenting with angioedema alone?

A
28
Q

History for urticaria and angioedema

A
  • is there pruritus? this can differentiate from bradykinin mediated
29
Q

Pathophysiology of CSU

A
30
Q

Side effects of 1st generation antihistamines

A

1st generation agents associated with risk for sedation and anti-cholinergic effects

31
Q

Bradykinin vs histamine medaited angioedema

A

2-5 days of swelling in bradykinin vs. 24h in histamine

Bradykinin: No urticaria (but can have Erythema marginatum) and Edema is not warm, usually nonpruritic and nonpitting

32
Q

What type of allergen is a third patch test (7-10 days) reading recommended?

A

Allergens that can present with positive results beyond 5 days include metals (gold, potassium dichromate, nickel and cobalt), antibiotics (neomycin, bacitracin), corticosteroids, dyes (p-pheneylenediamine, disperse blue) and acrylates.

33
Q

Common triggers of allergic contact dermatitis

A

mitzl- MethylIsoThiaZoLinone

34
Q

Auto-Immune Driven Bullous Skin Disease

A
35
Q

Leukocytoclastic vasculitis

A

LCV is a histopathologic term that defines vasculitis of the small vessels in which the inflammatory infiltrate is composed of neutrophils. After degranulation, neutrophils undergo death and break down, a process named leukocytoclasia, releasing nuclear debris, also described as nuclear dust.

Histologic findings in leukocytoclastic vasculitis (LCV), which are observed in urticarial vasculitis (UV) as well as other disorders, include the following:

●Injury and swelling of endothelial cells, usually of the postcapillary venules

●Extravasation of red blood cells

●Fragmentation of leukocytes with nuclear debris (leukocytoclasis)

●Fibrin deposition in and around the vessels

●Perivascular infiltrate composed mostly of neutrophils