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Allergology > Ch 317 Allergies anaphylaxis > Flashcards

Ch 317 Allergies anaphylaxis Flashcards

1
Q

leukotriene biosynthetic pathway

A

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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2
Q

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

A

CysLT1

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3
Q

contains genes implicated in the control of IgE levels

A

region of chromosome 5 (5q23-31)

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4
Q

Interleukin

control of IgE levels

A

IL-4

IL-13

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5
Q

Interleukin

mucosal mast cell hyperplasia

A

IL-3

IL-9

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6
Q

Interleukin

central to eosinophil development

A

IL-5 “EOSIN”

GM-CSF

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7
Q

T cell response IL-4

A

TH2 subset

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8
Q

T cell response interferon (IFN)

A

TH1

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9
Q

T cell response

IL-6 and TGF

A

TH17

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10
Q

(+) 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

A

Prausnitz-Kaustner reaction

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11
Q

implicate mast cell activation in a systemic reaction

A

Elevations of tryptase levels

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12
Q

Dose epinephrine anaphylaxis

A

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

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13
Q

MOA epinephrine

A

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

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14
Q

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)

A

Urticaria

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15
Q

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

A

Angioedema

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16
Q

Classification of Urticaria and/or Angioedema

Autoimmune

A

IgE-dependent

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17
Q

Classification of Urticaria and/or Angioedema

dermographism, cold, solar

A

IgE-dependent

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18
Q

Classification of Urticaria and/or Angioedema

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

A

IgE-dependent

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19
Q

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

A

Bradykinin-mediated

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20
Q

Classification of Urticaria and/or Angioedema

Necrotizing vasculitis

A

Complement-mediated

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21
Q

Classification of Urticaria and/or Angioedema

Serum sickness

A

Complement-mediated

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22
Q

Classification of Urticaria and/or Angioedema

Reactions to blood products

A

Complement-mediated

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23
Q

Classification of Urticaria and/or Angioedema

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

A

Nonimmunologic

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24
Q

Classification of Urticaria and/or Angioedema

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

A

Nonimmunologic

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25
Q

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

A

Dermographism

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26
Q

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

A

Pressure urticaria

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27
Q

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

A

Cholinergic urticaria

28
Q

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

A

Angioedema without urticaria

29
Q

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

A

autoantibodies to the a chain of FcRI (35-45%)

AutoAb to IgE (5-10%)

30
Q

activation markers on basophils

A

CD63 or CD203

31
Q

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

A

Hereditary angioedema

in 85%

32
Q

Hereditary angioedema type II

A

autosomal dominant disease due to a dysfunctional protein

33
Q

mech acquired form of C1INH deficiency:

A

1) excessive consumption (due to autoAb)

2) autoantibody directed to C1INH

34
Q

role of C1INH

A

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

35
Q

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

A

elevated bradykinin

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

36
Q

how ACEI causes angioedema

A

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

37
Q

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

A

Doxepin

38
Q

proven effective when H1 antihistamines fail

A

Cyproheptadine 8-32

hydroxyzine

39
Q

Rx urticaria

A

1) antihistamines

40
Q

CysLT1 receptor antagonist

A

montelukast

41
Q

therapy of inborn C1INH deficiency

A

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

42
Q

used for preoperative prophylaxis

A

antifibrinolytic agent -aminocaproic acid

43
Q

a kallikrein inhibitor

A

ecallantide

44
Q

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

A

Systemic mastocytosis

45
Q

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

A

Darier’s sign

cutaneous lesions of urticaria pigmentosa

46
Q

Acute urticaria duration

A

less than 6 weeks

47
Q

Diagnostic criteria for systemic macrocytosis

MAJOR

A

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

48
Q

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

A

telangiectasia macularis eruptiva perstans

49
Q

Diagnostic criteria for systemic macrocytosis

MINOR

A
  • 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
50
Q

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

A

Immunotherapy, often termed hyposensitization

51
Q

Triad of aspirin intolerance

A

Nasal polyps
rhinosinusitis
Asthma

52
Q

Risk factors for nasal polyps

A

Aspirin intolerance

Chronic staphylococcal colonization

53
Q

___% of individuals with asthma manifest rhinitis

A

70%

54
Q

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

A

vasomotor rhinitis

perennial nonallergic rhinits

55
Q

Due to prolonged topical use of a adrenergic agents

A

rhinitis medicamentosa

56
Q

Critical to etiologic diagnosis of AR

A

immunologic specificity for IgE

57
Q

the most potent drugs available for the relief of established rhinitis

A

Intranasal high potenscy glucocorticoids

58
Q

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

A

dysgeusia

59
Q

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

A

Montelukast

60
Q

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

A

Cromolyn sodium

61
Q

Duration of immunotherapy

A

3-5 years

62
Q

Contraindications of immunotherapy

A

significant CV disease

unstable asthma

63
Q

Duration of urticarial eruptions

A

12-36 hours duration

except cholinergic/dermatographism lasting 2h

64
Q

Most common sites of urticaria

A

extremities and face

65
Q

Pathology of urticaria

A

edema of superficial dermis (urticaria)

subcutaneous tissue and deep dermis (angioedema)

66
Q

Rx urticaria

A

Antihistamines
Cyprohepatdine
Montelukast

No value: topical GC

67
Q

Hallmark of anaphylactic reaction

A

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

Allergology (3 decks)

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