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Flashcards in Allergies Deck (111):
1

FOOD ALLERGY

2

Examples of IgE immunologic mediated responses.

IgE-Mediated

  • Oral allergy syndrome
  • Anaphylaxis
  • Urticaria

3

Examples of Non-IgE immunologic mediated responses to food?

Examples of Non-IgE mediated:

  • Protein-induced enterocolitis/enteropathy
  • Eosinophilic proctitis
  • Dermatitis herpetiformis

4

Examples of foods that cause a toxic, non-immunologic, response?

Toxic non-immunologic:

  • Scromboid fish poisoning
  • Bacterial food poisoning
  • Caffiene
  • Alcohol
  • Histamine

5

Examples of nontoxic (intolerance) non-immunologic reactions to food?

Non-toxic, non-immunlogic, reactions:

  • Lactose intolerance
  • Galactosemia
  • Pancreastic insufficiency
  • GB/Liver disease
  • Hiatal hernia
  • Anorexia

6

Top 3 Foods children are allergic to? Overal prevalence?

Children:

  • Milk (2.5%)
  • Egg (1.3%)
  • Peanuts (0.8%)

Overal - 6%

7

What food is most likely to cause allergy in adults?

Overall Allergy in Adults?

Adults

  • Shellfish (2%)
  • Peanuts (0.6%)

Overall: 3.7%

8

What is largest antigenic load the body processes?

Food

9

Antigen Absorption:

  • What decreases absorption?
  • What increases absorption?

Antigen Absorption?

  • Decreases: presence of other food and increase stomach acidity
  • Increases: presence of alcohol and decrease in stomach acidity

10

Type I IgE reactions vs. Type II vs. Type IV?

  • Type I IgE
    • Sensitization in mast cells of gut
    • Degranulation (mucous secretion, smooth muscle contraction, mucosal edema, and increased absorption of foreign antigens)
  • Type II reactions
    • Ab-dependent thrombocytopenia secondary to milk
  • Type IV
    • Supports role in atopic dermatitis, EGID

11

Clinical manifestations of IgE?

  • Skin
    • 84% of pts: urticaria, angioedema, atopic dermatitis
  • GI
    • 52%: edema, pruritis of lips/palate/pharynx, N/V
  • Respiratory
    • 32%: rhinitis, dyspnea, wheezing, cought

12

When should anaphylaxis be considered?

Most common reason cited for fatal reaction?

Anaphylaxis: 2+ organ systems involved

 

Fatal reaction: delay in administration of epinepherine

13

What are the highest risk foods resulting in anaphylaxis?

Anaphylaxis foods:

  • Peanuts
  • Tree nuts
  • Seafood

14

Fatal food anaphylaxis risks?

 

Often lack what symptoms?

Risks:

  • underlying asthma
  • symptom denial
  • previous severe reaction
  • delayed use of epinepherine

 

Often lack cutaneous symptoms

15

Oral allergy syndrome:

1. Usually due to?

2. What occurs?

3. Cause?

Oral allergy syndrome:

1. Fresh fruits and veggies

2. Oral pruritis, rapid onset, IgE-mediated

3. Cause - cross reactive proteins with pollen/food

16

Interpretation of Lab Tests?

Lab tests:

  • Positive prick/RAST
    • Presence of IgE ab NOT clinical reactivity (50% FP)
  • Negative prick/RAST
    • Excludes IgE ab (>95%)
  • ID skin test with food
    • Risk of systemic reaction and not predictive
  • Unproven (useless)
    • Neutralization, cytotoxic tests, applied kinesiology, hair analysis, IgG4

17

Absolute diagnosis?

Absolute diagnosis:

  • Elimination diets
    • Specific IgE ab negative - reintroduce food
    • Specific IgE ab positive - eliminate

18

Substitutes for infant formulas?

Formula substitution:

  • Soy
    • <15% soy allergy among IgE-cows milk allergy
  • Cow's milk protein hydrolysates
    • >90% tolerance in IgE-CMA
  • Partial hydrolysates
    • Not hypoallergenic
  • Elemental amino acid-based formulas
    • DOESNT CAUSE ALLERGY

19

Food allergy prevention is aimed at?

Best way to prevent?

Prevention is aimed at "high risk" newborn with FMHx:

Delay introduction of solid foods >6 months:

  • Milk/dairy: 6-12 months
  • Egg: 12-24 months
  • Peanut/tree nut/ seafood: >24-48 months

20

What is Eosinophilic GI Disorders (EGID)?

Primary eosinophilic GI disorders taht affect the GIT with eosinophil rich inflammation in the absence of known causes for eosinophilia (eg. drug reactions, parasites, malignancy)

21

Different types of EGID?

EGID: Eosionophilic....

  • Esophagitis
  • Gastritis
  • Gastroenteritis
  • Enteritis
  • Colitis

22

EGID signs and symptoms?

EGID S/S:

  • Failure to thrive
  • Ab pain
  • Irritability
  • Gastric dysmotility
  • N/V/D
  • Dysphagia
  • Reflux

23

EGID:

1. How can severity be reversed?

2. Most common foods?

3. What is found in tissues?

EGID:

1. Reverse severity with allergen free diet

2. Most common foods: milk, egg, wheat, soy, nuts, and seafood

3. Mast cell degranulation found in tissue specimens

24

EGID is a cross of what mediated disorders?

What is histologically characteristic?

EGID is a cross of Type I IgE and CMI disorders

 

Histologically characteristic: >24 eiosinophils/high power field

25

ALLERGIC RHINITIS

26

What is allergic rhinitis?

Risk factors?

IgE mediated inflammation of nasal mucous membranes

Risk factors:

  • +Family history
  • Ethnicity other than white
  • Birth in a pollen season
  • + inhalant skin tests
  • Early introduction of foods/formula
  • Sedentary lifestyle

27

3 most common complications/comorbidities of Allergic rhinitis?

Complications/Comorbidities of AR:

  • Chronic sinusitis (40-80%)
  • Asthma (38%)
  • Serous otitis media (21% in kids)

28

Signs and symptoms of AR?

 

Most common symptom of chronic allergic rhinitis

AR S/S:

  • nasal pruritis and sneezing
  • clear rhinorrhea with post nasal drip
  • Watery, itchy eyes
  • Fatigue, irritability, HA
  • Disrupted sleep and declines in cognitive processing

Chronic allergic rhinitis: Nasal obstruction

29

Pathophysiology:

How does sensitization occur?

Sensitization:

  • Macrophages present Ag to T/B cells
  • B cells mature into a plasma cell that produces an Ag specific strain of IgE
  • Plasma cells secrete this IgE and it binds to mast cell Fc receptors --> NOW SENSITIZED

30

What is the acute (early) phase response?

Acute phase response:

  • Re-exposure to Ag results in cross bridging to two IgE molecules and trigger degranulation
  • Vascular leakage, mucous secretion, and vasodilation
  • LTs/Acute Phase Proteins: function as chemotactic factors for immune cells 

31

What is the Late Phase Response (LPR)?

LPR:

  • Activation of leukocytes 2-12 hrs after acute phase
  • Hallmark is the activated eosinophil

32

Review:

1. APCs present by what class to T cell receptor?

2. What type of T cells are activated?

Review:

1. APCs present by MHC II

2. Activation of specific CD4+ helper T cells of Th2 phenotype and secretion of cytokines

33

Diagnoses:

What establishes a pattern?

Examples of seasonal allergies?

Diagnosis:

History establishes a pattern

Seasonal allergens:

  • Ragweed (August and Sept)
  • Tree (March-May)
  • Grass (May and June)
  • Molds (Spring-Fall)

34

Perennial allergens (long lasting) examples?

Perennial allergens:

  • Dust mites
  • Insects
  • Animal dander
  • Indoor molds

35

Phyical diagnosis of allergic rhinitis?

Physical diagnosis:

  • Pale/boggy/enlarged turbinades
    • Clear secretions
  • Dark puffy lower eyelids
    • Allergic shiners
  • Mouth breathing
    • Allergic Gape

36

Allergy testing?

Testing:

  • Immunoassays - RAST/ELISA
    • Detects presence of Ag-specific IgE
    • Useful in those that cant be skin tested
  • Non-specific tests
    • Nasal smear for eosinophils
    • Serum total IgE
    • Peripheral blood eosinophils

37

HYMENOPTERA ALLERGY

38

3 classes of Hymenoptera and insects included?

  • Apids
    • Honey/Bumble/Sweat Bee
  • Vespids
    • Yellow Jacket, hornets, wasps
  • Formicids
    • Fire ants and hervester ants

39

What do most venoms contain?

Venoms:

  • Vasoactive amines
    • Histamine, dopamine, and NE
  • ACh
  • Kinins
  • Hyaluronidase

40

Major allergen in the honeybee?

 

Major allergen in vespids?

Honeybee: phospholipase A

 

Vespids: Antigen - 5

41

3 types of common venom induced reactions and symptoms?

  • Normal
    • Local pain/erythema/mild swelling
  • Large local
    • Extended swelling/erythema
  • Anaphylaxis: onset 15-20 min
    • Cutaneous: urticaria/flushing/angioedema
    • Respiratory: dyspnea
    • CV: hypotension/dizziness/loss of consciousness

42

Large local reaction:

1. Most represent what phase? Devolpment time?

2. How long to subside?

Large local reaction:

1. LATE phase IgE; Develops over 12-24 hrs

2. 5-10 days to subside

43

What type of reactions can occur to a large number of stings?

 

What specific reaction may happen with a large amount of fire ant stings?

Many stings:

  • Acute RF
  • Rhabdomyolysis
  • Hemolysis
  • ARDS
  • DIC

Fire ants: seizures

44

Name some reactions of unknown mechanisms?

Reactions of unkown mechanisms:

  • Serum sickness
  • Encephalitis
  • Peripheral/cranial neuropathy
  • Glomerulonephritis
  • Myocarditis
  • Guillan-Barre syndrome

45

Primary evidence of allergic reactivity?

History is the primary evidence of allergic reactivity

46

Skin testing for hymenoptera:

1. When?

2. Cross reactivity?

 

Skin testing:

1. Performed 4-6 weeks after a sting

2. Very high cross reactivity among vespids

 

47

Skin testing:

1. Reactivity correlation with severity of sting reaction?

2. Largest reactions in what patients?

Skin testing:

1. Degree of skin test reactivity does not correlate with severity of the sting reaction

2. Largest reactions are often in patients with large local reactions

48

What can large local reactions be mistaken for?

Large local reactions can be mistaken for cellulitis (unlikely if reaction appears 24-48 hrs after a sting)

49

ANAPHYLAXIS

50

Anaphylaxis definition?

A life-threatening, multiorgan, IgE mediated disorder characterized by signs and symptoms of histamine release and other mediators released from mast cells and basophils

51

Risk factors for anaphylaxis?

Risk factors:

  • Atopy
  • Gender/Age
  • Route/constancy of administration
  • Time since last reactions
  • Economic status

52

What things are NOT risk factors?

NOT risk factors:

  • Race
  • Geography
  • Chronobiology
  • Occupation

53

Gender differences?

Females>Males for:

  • Latex
  • Muscle relaxants
  • Aspirin (ASA)
  • Idiopathic and OVERALL

54

Risk factors in the role of Atopy in anaphylaxis?

Atopic Risk Factors:

  • Latex
  • Oral administration
  • Exercise
  • Radiocontrast media (RCM)

55

Non-Risk factors in the role of Atopy in anaphylaxis?

Non-risk factors of Atopy:

  • Parenteral administration
  • Penicillin/Insulin
  • Hymenoptera
  • Muscle relaxants

56

4 Mechanisms of anaphylaxis?

  • Immunologic
    • IgE-dependent
  • Non-IgE immunologic
    • C3a, C5a, and bradykinin
  • Nonimmunologic
    • Degranulation from physical factors (cold/exercise)
    • Degranulation from certain medications
  • Idiopathic

57

IgE- Mediated Haptens?

 

(hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein)

IgE Mediated Haptens:

  • ABX
    • Penicillin/Cephalosporins/Sulfa
  • Other theraputic agents
    • Folic acid
    • General anesthetics

58

IgE Mediated complete antigens?

IgE Mediated complete antigens:

  • Animal/Human proteins
    • Egg vaccines/stinging insects/animal dander
  • Hormones
    • Insulin/progesterone
  • Enzymes
  • Foods
  • Latex
  • Allergenic extracts
    • Skin testing/immunotherapy

59

Non-IgE Immunologic

Due to activation of?

Examples?

Non-IgE Immunologic:

Due to activation of compliment anaphylatoxins and bradykinin from the contact system

Examples:

  • RCM
  • Dextran
  • Oversulfated chondroitin sulfate

60

Examples of nonimmunologic agents that can cause anaphylaxis?

Non-immunologic Anaphylaxis

  • Drugs
    • Aspirin and NSAIDs
    • Opiates and Ethanol
  • Physical
    • Exercise
    • Cold/Hot (air/water)
    • UV radiation

61

Key to all forms of anaphylaxis/anaphylactoid reactions?

 

What is the rule of 2's?

Mast cell/basophil degranulation is the key

 

Rule of 2's: signs and symptoms occur within 2 minutes to 2 hours after exposure

62

Degranulation preformed mediators?

Degranulation newly generated mediators?

Preformed

  • Histamine
  • Tryptase and carboxypeptidase A
  • Proteoglycans (heparin)

Newly generated

  • PGD2 and LTD4
  • PAF
  • Kinins

63

Pathophysiology:

Mediators result in an abrupt increase in?

Increase in

  • Vascular permeability
  • Vasodilation
  • Bronchoconstriction
  • Mucous secretion

64

Most common organs involved?

Cutaneous (>90%)

Respiratory (55-60%)

Cardiovascular (30-35%)

Shock (30%)

65

Anaphylaxis gross pathology?

Gross pathology:

  • Pulmonary hyperinflation
  • Laryngeal edema
  • RT edema

66

Anaphylaxis histology?

Histology:

  • Increased bronchial secretions
  • Eosinophilic infiltration
    • Of RT, spleen, and liver sinusoids

67

Anaphylaxis serologic indications?

Serology:

  • Elevated:
    • Histamine (rises in 5 min; only lasts up to 1 hr)
    • Tryptase (Lasts up to 5 hrs)
    • Carboxypeptidase A3
      • May be the better marker
    • Urinary histamine metabolites may remain elevated for up to 24 hours

68

Anaphylaxis evaluation:

_____ is the key.

What supports the diagnosis?

Anaphylaxis eval:

History is the ky

Physical exam supports the diagnosis

69

I know it says we dont need to know treatment buttt....

 

What position should a patient be in for the treatment of anaphylaxis and why?

Patient should lie flat bc those sitting up may be subject to an "empty heart" and sudden death

70

ASTHMA

71

Asthma definition?

Inflammation is associated with?

Asthma - is a chronic inflammatory disorder of the airways (doesnt matter what severity)

 

Inflammation is associated with hyperresponsiveness and airflow limitations

72

What is the strongest predisposing factor for the development of asthma?

Atopy, the genetic predisposition for IgE mediated responses, is the strongest predisposing factor

73

Asthma complications/comorbidities?

Asthma complications/comorbidities:

  • 80% of allergic asthmatics also have AR
  • 40% of all patients with AR experience asthma at some point

74

Exercise induced bronchospasm:

General population versus patients with AR?

Asthmatics?

Exercise induced bronchospasm:

  • 10% of general population
  • 40% of individuals with AR
  • ALL Asthmatics
    • For some, this will be the only asthmatic manifestation

75

Cluster 1 phenotype?

Cluseter 1 (15%)

  • Younger with child hood onset
  • Mostly female
  • Minimal meds
  • Atopic with normal lung function

76

Cluster 2 phenotype?

Cluster 2 (44%)

  • Occurs in 30's with childhood onset/atopic
  • 2/3 female
  • 2/3 have normal lung function
  • 30% use >3 meds

77

Cluster 3 phenotype?

Cluster 3 (8%)

  • Obese older females
  • Late onset
  • NON atopic asthma
  • Moderate reduction in lung function
  • Frequent OCS for exacerbations

(OCS = oral corticosteroids)

78

Cluster 4/5 phenotypes?

Clusters 4/5 phenotypes (33%)

  • Severe airflow obstruction
  • Variability in age of onset
  • Atopic status
  • Use of OCS

79

Aspirin Sensitive Asthma:

Percent? Atopy?

Classic cases presentation?

Aspirin Sensitive Asthma:

  • 5-10% of asthmatics will worsen with Aspirin/NSAIDs
  • 2/3 of these are NOT atopic
  • Classic presentation
    • Nasal polyps with chronic sinusitis
    • Asthma with peripheral eiosinophilia
    • ASA/NSAID sensitivity

(often have high levels of LTs)

80

Diagnosis:

50% of asthmatics will have?

Diagnosis

50% of asthmatics will have NORMAL PFT (pulmonary functions?) at rest

81

IMMUNODEFICIENCY

82

Main categories of primary immunodeficiency?

  • Complement deficiency
  • Immunoglobulin (B cell) deficiency
  • Lymphocyte defects (T cell)
  • Phagocyte Defects

83

Acquired immunodeficiencies?

Acquired ID:

  • Malnutrition
  • AIDS
  • Chemotherapy
  • Organ transplant

84

What does Compliment normally regulate?

Complement regulates:

  • Mast cell degranulation
  • Smooth muscle contraction
  • Chemotaxis of leukocytes
  • Phagocytosis

85

Compliment deficiencies result:

Classic pathway?

C3 deficiency?

Late components?

Classic Pathway (C1/2/4)

  • Recurrent GP infections and high autoimmune incidence

C3 deficiency

  • Recurrent pyogenic infections with GP and GN

Late Components (C5-9)

  • Recurrent neisserial infections

86

Complement Deficiency - Hereditary Angioedema:

Signs and Symptoms?

Hereditary Angioedema S/S:

  • Nonpitting edema of skin, GI, and respiratory tract
    • Skin = asymmetric; no pruritis or hives
    • Bowel wall edema = cramping and diarrhea
    • Laryngeal edema = most common cause of death

87

Hereditary angioedema:

Deficiency? 

Genetics?

Mediator responsible for the angioedema?

Hereditary Angioedema:

  • Deficiency of C1 esterase inhibitor
  • Genetics: AD inheritance
  • Mediator: Bradykinin (degradation slowed in absence of the enzyme)

88

Hereditary angioedema:

Levels of C4?

Levels of C2?

Levels of C1 INH?

Hereditary angioedema:

  • C4: low or absent all the time
  • C2: drops during attacks only
  • C1 INH: low/absent OR nonfunctional

89

Symptoms of Antibody deficiency?

Ab Deficiency S/S:

  • Recurrent OM/Sinusitis/pneumonia
  • Cellulitis
  • osteomyelitis
  • meningitis
  • Enteric infections

90

X Linked Agammaglobulinemia:

Also known as?

What is abnormal? Linked to what part of X?

X Linked Agammaglobulinemia:

  • AKA Bruton's
  • Abnormal Tyrosine kinase
  • Linked to q22

91

X Linked Agammaglobulinemia:

What kind of infections?

Due to what bugs?

X Linked Agammaglobulinemia:

Recurrent Sinopulmonary pyogenic infections due to:

  • H. influenzae
  • Staph
  • Strep
  • Pneumococci
  • Meningococci

92

X Linked Agammaglobulinemia:

Other infections? What do they lead to?

X Linked Agammaglobulinemia:

  • Sinusitis, pneumonia, abscesses, meningitis, septiciemia

Infections lead to:

  • bronchiectasis
  • Pulmonary insufficiency

93

X Linked Agammaglobulinemia:

Resistance to fungi/viruses/GN -- intact or no? Why?

X Linked Agammaglobulinemia:

Resistance to fungi/viruses/GN:

  • Intact
    • Normal T cell number and function

94

X Linked Agammaglobulinemia:

Diagnosis:

Levels of Immunoglobulins and B lymphocytes?

 

X Linked Agammaglobulinemia:

Diagnosis:

Low to absent levels of all Ig, B lymphocytes, and circulating plasma cells

95

Common variable immunodeficiency:

Suceptible to same infections as? But also?

Increased incidence of what cancer?

Common variable immunodeficiency:

Suceptible to same infections as Brutons and also Giardia

Increased incidence of lymphomas

96

Common variable immunodeficiency:

Signs/Symptoms?

Common variable immunodeficiency S/S:

  • Lymphadenopathy
  • Splenomegaly
  • Lymphoid hyperplasia of the gut

97

Common variable immunodeficiency:

B cell and T cell levels and functions?

Common variable immunodeficiency:

  • B cell
    • Present but abnormal function
  • T cell
    • Levels usually normal
    • Function may not be normal

98

Most common primary immunodeficiency?

IgA deficiency

99

IgA deficiency:

What types of recurrent infections?

May have anti-IgA abs that can cause what?

IgA:

  • Recurrent sinopulmonary infections

 

  • Anti-IgA antibodies
    • Anaphylaxis when given blood products

100

T cell ID:

Often occur when? And how does it present?

What can occur with live viral vaccines?

T cell ID:

Often occur in infancy

Present as failure to thrive with diarrhea

Live viral vaccines can result in severe illness

101

T Cell ID:

What is Hyper-IgM syndrome linked to?

What occurs in DiGeorge?

T Cell ID:

  • Hyper IgM syndrome
    • CD40 ligand
  • DiGeorge
    • Thymic dysplasia/aplasia
    • Facial clefts, hypocalcemia, cardiac defect

102

T cell ID

What is reticular dysgenesis?

What is Ommen syndrome?

T Cell ID:

  • Reticular dysgenesis
    • Early defect in hematopoesis
  • Ommen syndrome
    • Hypereosinophila
    • High IgE
    • Hymphocytosis
    • Hepatomegaly
    • Rashes from birth

103

T Cell ID:

What occurs in Wiskott Aldrich syndrome?

Wiskott Aldrich Syndrome:

  • Small platelets
  • Petechiae
  • Eczema
  • Early sinopulmonary infections
  • Atopy

104

T Cell ID:

What is Ataxia Telangectasia?

What serum levels are increased?

T Cell ID:

  • Ataxia Telangectasia:
    • Loss of motor milestones in early childhood
    • Telangectasias appear later
    • Increased alpha fetal protein in serum

105

Phagocyte Defects:

Average number of neutrophils?

What is neutropenia?

Phagocyte Defects:

  • Neutrophils: 5000/mcl
  • Neutropenia: <1000/mcl

106

Phagocyte Defects:

Chronic granulomatous disease:

Presents?

Infections with what bugs?

Chronic Granulomatous disease:

Presents with lymphadenopathy

Infections with:

  • Staph aureus
  • Aspergillus
  • Nocardia

107

Phagocyte Defects:

Chronic granulomatous disease:

Defect is in?

Bacteria/fungi and what enzyme cause recurrent life threatening infections?

 

Chronic Granulomatous Disease:

Defect: Oxidative killing of ingested microorganisms

Bacteria/Fungi + catalase = life threatening

 

108

Phagocyte Defects:

Chronic granulomatous disease:

Organs affected?

Chronic granulomatous disease:

Organs:

  • Lungs
  • Liver
  • Lymph nodes
  • Skin
  • Bone

 

109

Phagocyte Defects:

Leukocyte adhesion deficiency:

What is this?

How is it clinically characterized?

Mutation in?

Leukocyte adhesion deficiency:

  • Neutrophils fail to mobilize and migrate
  • Characterized by:
    • Delayed separation of umbilical cord
    • Gingivitis
    • Severe scarring skin infections
  • Mutation in CD18

110

Phagocyte Defects:

Chediak-Higashi syndrome:

Inheritance?

Infections?

Signs/symptoms?

Chediak-Higashi syndrome:

  • Autosomal Recessive
  • Recurrent cutaneous and sinopulmonary pyogenic inf.
    • Dont respond well to abx
  • Signs:
    • Partial oculo-cutaneous albinism
    • mental retardation
    • neuropathy (late)
    • Weird hair sheen

111

In the lab what does the presence of isohemagglutinins indicate?

Isohemagglutinins:

Presence indicates IgM antibodies to blood groups