Ch 317 Allergies anaphylaxis Flashcards by Cristina Yang

leukotriene biosynthetic pathway

arachidonic acid is metabolized by 5-lipoxygenase (5-LO) in the presence of an integral nuclear membrane protein, the 5-LO activating protein (FLAP)

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receptor has a preference for LTD4 and is blocked by the receptor antagonists in clinical use

CysLT1

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contains genes implicated in the control of IgE levels

region of chromosome 5 (5q23-31)

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Interleukin

control of IgE levels

IL-4

IL-13

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Interleukin

mucosal mast cell hyperplasia

IL-3

IL-9

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Interleukin

central to eosinophil development

IL-5 “EOSIN”

GM-CSF

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T cell response IL-4

TH2 subset

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T cell response interferon (IFN)

TH1

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T cell response

IL-6 and TGF

TH17

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(+) presence of specific IgE in patients with systemic anaphylaxis:
inject serum intradermally into a normal recipient, followed 24 h later by antigen challenge into the same site –> (+) wheal and flare

Prausnitz-Kaustner reaction

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implicate mast cell activation in a systemic reaction

Elevations of tryptase levels

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Dose epinephrine anaphylaxis

0.3 to 0.5 mL of 1:1000 (1 mg/mL) epinephrine SC or IM

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MOA epinephrine

a- and B-adrenergic effects, (vasoconstriction, bronchial smooth-muscle relaxation, and attenuation of enhanced venular permeability)

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involves only the superficial portion of the dermis, (well-circumscribed wheals with erythematous raised serpiginous borders and blanched centers that may coalesce to become giant wheals)

Urticaria

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well-demarcated localized edema involving the deeper layers of the skin, including the subcutaneous tissue

Angioedema

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Classification of Urticaria and/or Angioedema

Autoimmune

IgE-dependent

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Classification of Urticaria and/or Angioedema

dermographism, cold, solar

IgE-dependent

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Classification of Urticaria and/or Angioedema

Specific antigen sensitivity (pollens, foods, drugs, fungi, molds, Hymenoptera venom, helminths)

IgE-dependent

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Classification of Urticaria and/or Angioedema
Hereditary angioedema: C1 inhibitor deficiency: null (type 1) and dysfunctional (type 2)

Acquired angioedema: C1 inhibitor deficiency: anti-idiotype and anti-C1 inhibitor

Angiotensin-converting enzyme inhibitors

Bradykinin-mediated

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Classification of Urticaria and/or Angioedema

Necrotizing vasculitis

Complement-mediated

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Classification of Urticaria and/or Angioedema

Serum sickness

Complement-mediated

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Classification of Urticaria and/or Angioedema

Reactions to blood products

Complement-mediated

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Classification of Urticaria and/or Angioedema

Direct mast cell-releasing agents (opiates, antibiotics, curare, D-tubocurarine, radiocontrast media)

Nonimmunologic

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Classification of Urticaria and/or Angioedema

Agents that alter arachidonic acid metabolism (aspirin and NSAIDs, azo dyes, and benzoates)

Nonimmunologic

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appearance of a linear wheal at the site of a brisk stroke with a firm object or by any configuration

Dermographism

chronic idiopathic urticaria, presents in response to a sustained stimulus such as a shoulder strap or belt, running (feet), or manual labor (hands)

Pressure urticaria

pruritic wheals are of small size (1-2 mm) | precipitated by fever, a hot bath or shower, or exercise --attributed to a rise in core body temperature

Cholinergic urticaria

generation of bradykinin occurs with C1 inhibitor (C1INH) deficiency that may be inborn as an autosomal dominant characteristic or may be acquired through the appearance of an autoantibody

Angioedema without urticaria

40% patients with chronic urticaria have autoimmune cause as evidenced by findings of antibodies to ___

autoantibodies to the a chain of FcRI (35-45%) | AutoAb to IgE (5-10%)

activation markers on basophils

CD63 or CD203

autosomal dominant disease due to a deficiency of C1INH (type 1)

Hereditary angioedema | in 85%

Hereditary angioedema type II

autosomal dominant disease due to a dysfunctional protein

mech acquired form of C1INH deficiency:

1) excessive consumption (due to autoAb) | 2) autoantibody directed to C1INH

role of C1INH

blocks the catalytic function of activated factor XII (Hageman factor) and of kallikrein, as well as the C1r/C1s components of C1

Blood picture of clinical attacks of angioedema in C1INH-deficient patients

elevated bradykinin | decreased prekallikrein and high-molecular-weight kininogen (from which bradykinin is cleaved)

how ACEI causes angioedema

use of blockers results in impaired bradykinin degradation and explains the angioedema that occurs idiosyncratically in hypertensive patients with a normal C1INH

dibenzoxepin tricyclic compound with both H1 and H2 receptor antagonist activity, is yet another alternative

Doxepin

proven effective when H1 antihistamines fail

Cyproheptadine 8-32 | hydroxyzine

Rx urticaria

1) antihistamines

CysLT1 receptor antagonist

montelukast

therapy of inborn C1INH deficiency

attenuated androgens correct the biochemical defect and afford prophylactic protection; -->production functional C1INH sufficient to control the spontaneous activation of C1

used for preoperative prophylaxis

antifibrinolytic agent -aminocaproic acid

a kallikrein inhibitor

ecallantide

clonal expansion of mast cells that in most instances is indolent and nonneoplastic

Systemic mastocytosis

reddish-brown macules or papules that respond to trauma with urtication and erythema

Darier's sign | cutaneous lesions of urticaria pigmentosa

Acute urticaria duration

less than 6 weeks

Diagnostic criteria for systemic macrocytosis | MAJOR

Multifocal dense infiltrates of mast cells in bone marrow or other tissue or (+) tryptase or metachromasia

1% of patients with ISM have skin lesions that appear as tan-brown macules with striking patchy erythema and associated telangiectasia

telangiectasia macularis eruptiva perstans

Diagnostic criteria for systemic macrocytosis | MINOR

- Abnormal mast cell morphology : spindle shape and/or multilobed or eccentric nucleus - Aberrant mast cell surface phenotype with expression of CD25 (IL-2 receptor) and CD2 in addition to C117 (c-kit) - Detection of codon 816 mutation in peripheral blood cells, bone marrow cells, or lesional tissue - Total serum tryptase (mostly alpha) greater than 20 ng/mL

repeated subcutaneous injections of gradually increasing concentrations of the allergen(s) considered to be specifically responsible for the symptom complex

Immunotherapy, often termed hyposensitization

Triad of aspirin intolerance

Nasal polyps rhinosinusitis Asthma

Risk factors for nasal polyps

Aspirin intolerance | Chronic staphylococcal colonization

___% of individuals with asthma manifest rhinitis

70%

condition of enhanced reactivity of the nasopharynx in which a symptom complex resembling perennial AR occurs with nonspecific stimuli

vasomotor rhinitis | perennial nonallergic rhinits

Due to prolonged topical use of a adrenergic agents

rhinitis medicamentosa

Critical to etiologic diagnosis of AR

immunologic specificity for IgE

the most potent drugs available for the relief of established rhinitis

Intranasal high potenscy glucocorticoids

AE of azelastine, which may benefit patients with nonallergic vasomotor rhinitis

dysgeusia

Approved for treatment of both seasonal and perennial rhinitis which reduces both nasal and ocular symptoms

Montelukast

This nasal spray for AR has no side effects and is used prophylactically and on a continuous basis

Cromolyn sodium

Duration of immunotherapy

3-5 years

Contraindications of immunotherapy

significant CV disease | unstable asthma

Duration of urticarial eruptions

12-36 hours duration | except cholinergic/dermatographism lasting 2h

Most common sites of urticaria

extremities and face

Pathology of urticaria

edema of superficial dermis (urticaria) | subcutaneous tissue and deep dermis (angioedema)

Rx urticaria

Antihistamines Cyprohepatdine Montelukast No value: topical GC

Hallmark of anaphylactic reaction

onset of manifestation seconds to mines after the introduction of the allergen