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Dermatology Board Prep > DERM (19) Urticaria, Erythema, and Purpura > Urticaria and angioedema > Flashcards

Urticaria and angioedema Flashcards

1
Q

Key clinical components of urticaria?

A

Wheals lasts <24 hrs. They are pale to pink-red, edematous papules and plaques w/ central clearing that tend to be pruritic

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2
Q

What is the overlap b/w angioedema and wheals and urticaria?

A

Urticaria can have wheals, angioedema, or both

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3
Q

Clinical presentation of angioedema

A

ill-defined, deeper dermal and subQ +/- submucosal swelling. There is minimal to no overlying erythema. Lesions tend to be painful and pruritic and extracutaneous involvement can include the respiratory or GI systems

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4
Q

What is the pathogenesis of urticaria?

A

Pathogenesis mediated by the release of preformed and newly formed granules from mast cells -Preformed: histamine, heparin, chymase (tryptase) -Newly formed: PG, LT, PAF

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5
Q

What are some common mast-cell degranulating stimuli?

A

Immune-mediated: IgE against allergen (type I hypersensitivity) - Anti-IgE receptor and anti-FcεRI (chronic autoimmune urticaria) -Nonimmune-mediated: codeine, substance P, KIT ligand, C5a (anaphylatoxin) -Nettle stings -Medications: NSAIDs, ACEi

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6
Q

Definition of chronic urticaria?

A

Urticaria occurring for > 6 weeks

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7
Q

Describe acute urticaria?

A

M/c in children -Presents as large annular or polycyclic erythematous plaques (urticaria multiforme from dusky purple appearance) -Most common cause is idiopathic followed by URI

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8
Q

Describe chronic urticaria?

A

-M/c in adults (4th decade, W>M) -includes autoimmune form - a/w thyroid dz and celiac dz -Most common cause is idiopathic followed by inducible factors

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9
Q

Name and describe the 4 types of physical urticaria?

A

(i) mechanical stimuli: dermographism (affect 10% general population); delayed-pressure (wheals>24h; a/w arthralgias and malaise; sustained pressure to skin) (ii) temperature changes: cold (transition from cold->hot) >> heat-induced - use ice cube test (wheal on rewarming); idiopathic cause - <5% a/w cryoglobulins or cryofibrinogen (iii) physical exercise/sweating: cholinergic (body temp dependent)>adrenergic (blanched halo); exercise-induced anaphylaxis (not from increased body temp) (iv) solar (5-10 min exposure → UVA +/- visible light > UVB) and aquagenic (temp-independent)

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10
Q

Describe urticaria vasculitis?

A

The lesions tend to burn +/- painful, lasts >24h, purpura on resolution *commonly has extracutaneous sxs (arthralgias, abd pain, pulmonary dz, nephritis, uveitis)

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11
Q

Describe Schnitzler’s syndrome?

A

Associated with monoclonal gammopathy (IgM>>IgG) -Presents with fever, arthralgia, elevated ESR, LAN, leukocytosis

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12
Q

Describe Still’s disease?

A

Presents with fever (cyclic), pharyngitis, arthralgias, LAN, elevated ferritin

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13
Q

Serum-like sickness rxn?

A

Systemic drug reaction presents with fever, LAN, arthralgias, acral edema

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14
Q

Urticaria managment?

A

Do not get aggressive labs like allergy testing, other blood tests -eliminate modifiable causes -avoid NSAID’s, codeine products -trial of 2nd gen H1 antihistamines (cetirizine) can use up to 4x the standard dosing -Can consider using doxepin @ night, anticholinergic, do not use in glaucoma pts and those on MAOI -Can add H2 blocker -Omalizumab (anti-IgE mAb) for chronic autoimmune form

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15
Q

Desribe angioedema with no wheals?

A

*Pathogenesis - edema mediated by bradykinin NOT histamine (urticaria-angioedema) *Acquired vs hereditary* -Acquired: present later in life - a/w lymphoproliferative d/o (MGUS, lymphoma) - check C1q levels to differentiate from hereditary type I: a/w lymphoproliferative d/o type II: a/w autoimmune phenomenon → autoantibodies against C1-inh

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16
Q

Two types of angioedema w/ no wheals?

A

Type I: a/w lymphoproliferative d/o
Type II: a/w autoimmune phenomenon → autoantibodies against C1-inh

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17
Q

What are the 3 types of hereditary angioedema?

A

Type I: deficient C1 esterase inh (C1-inh), low C4 Type II: dysfunctional C1-inh, low C4 Type I and II both favor acral surfaces, GI system (acute abd), and larynx (laryngeal edema → airway compromise) *Type III: normal C4 levels; later-onset - affect face m/c and favor W>M

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18
Q

What medications are not effective in non urticarial angioedema?

A

Antihistamines, epinephrine, and steroids

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19
Q

What managment should be done for the non-urticarial angioedemas?

A

Short term: IV C-1 inhibitor Long-term: androgen (oral danazol)

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20
Q

What are the most common triggers of drug-induced immunologic urticaria?

A

Penicillins, cephalosporins, latex gloves or medical devices

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21
Q

What common medication can worsen chronic urticaria in up to 30% of patients?

A

Aspirin

22
Q

How is the timing of drug-induced acute urticaria different than other forms?

A

Can be more delayed (days after triggering event)

23
Q

What are the most common causes of chronic urticaria?

A

60% = idiopathic and autoimmune-autoantibodies against FcepsilonR1 or Fc portion of IgE, infection-related and pseudo-allergic

35% = Physical

Vasculitis = 5%

24
Q

How common is autoimmune urticaria?

A

Up to 50% of chronic urticaria

25
Q

What conditions are associated with chronic urticaria?

A

Thyroid disease, vitiligo, IDDM, RA

26
Q

How long does chronic urticaria usually last?

A

3-5 years

27
Q

What is the most common physical urticaria?

A

Dermatographism

28
Q

When does dermatographism-induced urticaria tend to be worst?

A

In the evening

29
Q

What is the timing of pressure urticaria?

A

Tends to be quite delayed (up to 12 hrs after pressure event)

30
Q

What is the clinical presentation of delayed pressure urticaria?

A

Occurs in areas of high friction or pressure (waistline after wearing tight clothes)

Painful, itchy and possibly long-lasting. Can even be associated with arthralgias, malaise, and flu-like symptoms

31
Q

What warning about swimming must be discussed with patients with cold-induced urticaria?

A

They must never swim alone

The cold of the water can lead to a massive release of histamine leading to hypotension

32
Q

What are some triggers of secondary cold urticaria?

A

Cryoglobulinemia, cryofibrinogenimia, hepatitis, lymphoproliferative dz, or mononucleosis

33
Q

What is the clinical presentation of cholinergic urticaria?

A

Distinct lesions (multiple 2-3mm slightly papular wheels w/ pronounced flare of erythema

  • Occur after sweating/increased body temp in young adults
  • Can have systemic sx’s of faintness, wheezing, etc
34
Q

In what disease is aquagenic urticaria more commonly seen in?

A

Cystic fibrosis

35
Q

What is the treatment of Schnitzler’s syndrome?

A

Anakinra first line

36
Q

What is the histology of urticaria?

A

Superficial dermal edema, vasodilation, scant perivascular and interstitial infiltrate that is predominantly made up of neutrophils (>eos and lymphs)

37
Q

What labs should be pursued in chronic/recalcitrant urticaria?

A

CBC, ESR/CRP, thyroid antibodies, thyroid function tests, anti-FcepisilonR1/anti-IgE antibodies, immunoassays, functional assays (HRA) and autoreactivity (ASST)

38
Q

What test must be performed/what must be ruled out in angioedema without urticaria?

A

C1 esterase inhibitor deficiency

39
Q

What is the screening test of choice for acquired and inherited angioedema?

A

C4 (or CH50) [C4 will be low]

40
Q

What is the inheritance pattern for all forms of inherited angioedema?

A

Autosomal dominant for all

41
Q

What is the difference between type I and type II heritable angioedema?

A

Type I = decreased levels of C1 esterase inhibitor and Type 2 = decreased function but normal to elevated levels

42
Q

What is the difference between type I and type II acquired angioedema?

A

Type I: Consumption of C1 esterase inhibitor

Type II: Antibodies against C1 esterase inhibitor

43
Q

What is the cause of hereditary angioedema type III?

A

Activating mutation in Hageman factor (FXII)

44
Q

What type of angioedema has low levels of C1q?

A

Only see in acquired angioedema

45
Q

What is the timing of ACEi induced angioedema?

A

Occurs within the first 3 weeks most commonly, all occur within the first year

46
Q

How do ACEi cause anigioedema?

A

Block kinase II –> Elevated bradykinin

47
Q

What are the clinical features of angioedema?

A

Unlike urticaria it tends to be painful, non-erythematous, non-pitting, non-pruritic (but can burn)

Commonly lasts 2-5 days (worst in the first 36 hrs)

48
Q

What are the most commonly affected areas in angioedema?

A

Face, lips, eyelids, throat, ears and nose

49
Q

What are a couple of differences in the presentation of hereditary angioedema type III vs the other types?

A

Type III tends to have a later age of onset (teens), and has more facial edema

50
Q

What labs should be checked if hereditary or acquired angioedema is suspected?

A

Check C4, C1 inhibitor (quantification and function) and C1q

51
Q

What is the treatment of hereditary angioedema?

A

Type 1 (C1 inh deficiency): Oral danazol is the treatment of choice for prophylaxis and C1 inh concentrate is the treatment of choice for acute attacks

Icatibant is a synthetic bradykinin B2 receptor antagonist

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

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