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Allergic disorders Flashcards

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1
Q

Autoimmune disease

A

Reactions occur when self-antigens are recognized by the body’s normal defense mechanisms as foreign

    • B cells become hyperactive
    • increased amount of IgE
    • result = hypersensitivity or allergy response
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2
Q

What does hypersensitivity lead to?

A

Inflammation and destruction of healthy issue

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3
Q

What factors play a role in autoimmune disorders?

A

Genetric, hormonal and environmental

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4
Q

IgE-mediated allergic reactions: Atopic causes

A
  • Hereditary predisposition and production of local reaction to IgE antibodies
  • Allergic rhinitis
  • Asthma
  • Dermatitis/eczema
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5
Q

IgE-mediated allergic reactions: nonatopic causes

A

Lack of the genetic component and organ specific
Tetanus vaccine
Insect venom
Airborne allergens

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6
Q

Diagnostic testing for allergic disorders

A 
CBC
Eosinophil count
IgE levels 
Skin test
Radioallergosorbent testing 
Proactive testing
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7
Q

How can you obtain an eosinophil count?

A

nasal secretions/sputum

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8
Q

When would someones IgE levels be high?

A

with allergic diseases

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9
Q

Type 1 hypersensitivity

A

Anaphylactic

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10
Q

Type 1 (anaphylactic) s/s

A

Rapid onset
Edema in many tissues (larynx)
Hypotension, bronchospasm, cv collapse,
Local and systemic anaphylaxis

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11
Q

What is type II hypersensitivity?

A

Cytotoxic – system mistakenly identifies a normal constituent as foreign

Possible cell and tissue damage

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12
Q

Type 2 hypersensitivity (cytotoxic) – Myasthenia Gravis

A

mistakenly generates antibodies against normal nerve ending receptors

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13
Q

What is a type III hypersensitivity called?

A

Immune complex – formed when antigens bind to antibodies
– deposited in tissues or vascular endothelium

Result: increase in vascular permeability and tissue injury

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14
Q

What is type 4 hypersensitivity called?

A

Delayed-type – t-cell depended macrophage activation and inflammation cause tissue injury

example: TB test

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15
Q

What is anaphylaxis?

A

Severe allergic reaction - rapid onset - various systemic reactions

Type 1 hypersensitivity

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16
Q

When does an anaphylactic reaction occur?

A

Occurs when immune system produces IgE antibodies toward a substance that is normally nontoxic.

Antibodies are stored after initial exposure.

Re-exposure releases excess amounts of protein histamine.

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17
Q

what are s/s of histamine release?

A

Flushing, urticaria, angioedema, hypotension, bronchoconstriction

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18
Q

What are common foods that cause anaphylaxis?

A 
peanuts
tree nuts (walnuts, pecans, cashews, almonds)
shelfish (shrimp, lobster, crab)
fish
milk
soy
wheat
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19
Q

What are common medications that can cause anaphylactic reaction?

A

Antibiotics (especially penicillin and sulfa antibiotics) allopurinol
radiocontrast agents
anesthetic agents (lidocaine, procaine)
vaccines
hormones (insulin, vasopressin, adrenocorticotropic hormone [ACTH]
aspirin
nonsteroidal anti-inflammatory drugs [NSAIDs]).

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20
Q

What are other pharmaceuticals/biologic agents that can cause anaphylactic reaction?

A

Animal serums (tetanus antitoxin, snake venom antitoxin, rabies antitoxin), antigens used in skin testing

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21
Q

What insect stings can cause anaphylaxis?

A

Bees, wasps, hornets, yellow jackets, ants (including fire ants)

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22
Q

what is a common medical item that can cause an anaphylactic reaction?

A

Latex - medical and non-medical products

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23
Q

The severity of an anaphylactic reaction depends on what?

A

The degree of allergy and the dose of allergen

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24
Q

Anaphylactic patterns: Uniphasic

A

Symptoms within 30 minutes of exposure

Resolve within 1-2 hours with or without treatment

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25
Q

Anaphylactic patterns: biphasic

A

Initial reaction – followed by subsequent symptoms up to 8 hours after first reaction
Need to be managed in ER

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26
Q

Anaphylactic patterns: protracted

A

Reaction that may last for 32 hours

Can include cardiogenic or septic shock and respiratory distress despite medical treatment

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27
Q

Anaphylaxis: mild s/s

A 
Peripheral tingling
Sensation of warmth
Sensation of fullness in the mouth and throat
Nasal Congestion
Periorbital swelling
Pruritus
Sneezing 
Tearing of the eyes
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28
Q

Anaphylaxis: moderate s/s

A 
Flushing
Warming
Anxiety
Itching
Includes all mild symptoms
Bronchospasm & edema of airway and larynx with dyspnea, cough and wheezing
Within 2 hours of exposure
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29
Q

Anaphylaxis: severe reaction

A 
Rapid Progression of symptoms
Bronchospasm
Laryngeal edema
Sever dyspnea
Cyanosis
Hypotension
Abrupt onset
Dysphagia
Abdominal Cramping
Vomiting/Diarrhea
Seizures
Cardiac Arrest
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30
Q

What is important to monitor when someone has an anaphylactic reaction?

A

Hemodynamic stability - HR, Rhythm, BP

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31
Q

Anaphylaxis reactions mngmnt

A 
Strict avoidance of potential allergens
Screening patients for allergies prior to medication
Wear a medical alert bracelet 
Desensitizing
Epinephrine
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32
Q

Epinephrine education considerations

A

No preparation
Carry it with you at all times
Education on how to administered
If used, must go to ER for monitoring for 12-14 hours

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33
Q

Anaphylaxis - medical management

A

Respiratory and cv - must be evaluated

High concentration of CO2 if cyanotic, dyspneic or wheezing

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34
Q

How to administer epi?

A

Upper extremity or thigh - SQ first

- IV if still needed

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35
Q

Adverse responses: epi

A

Mostly occur when given too much or given IV

High risk patients = elderly, HTN, arteriopathies, ischemic heart disease

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36
Q

When should you do if someone goes into cardiac arrest while treating them for anaphylactic reaction

A

Begin CRP then administer high concentration of o2

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37
Q

Anaphylaxis - antihistamines

onset use and types

A

Can take up to 80 minutes to only do 50% of the suppression
Used for urticaria and angioedema

H1: Diphenhydramine and Hydroxyzine
H2: Cetirizine and Loratadine and Fexofenadine

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38
Q

Anaphylaxis treatment: adrenergic agents do what?

A

Vasoconstriction of mucosal vessels

Limited use to avoid rebound congestion

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39
Q

What are sfx of adrenergic agents?

A

HTN, dysrhythmias, palpitations, CNS stimulant, irritability, tremors

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40
Q

What are examples of adrenergic agents for anaphylaxis treatment

A

Afrin - nasal

Alphagan P - eyes

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41
Q

Anaphylaxis - corticosteroid treatment

A

Used for urticaria & angioedema
Suppress major symptoms
Can take 2 weeks for full effect
Taper dosing

42
Q

Anaphylaxis treatment: IV fluids (NS), volume expanders, vasopressors

A

maintains BP and hemodynamics

43
Q

Anaphylaxis treatment: aminophyline

A

Used in conjunction with corticosteroids
Used on patients with Asthma or COPD
Improve airway patency and function

44
Q

What do we need to monitor while taking diphenhydramine?

A

anticholinergic effects – dry mouth, constipation, difficult urinating, loss of accommodation – acetachloline is your parasympathetic

45
Q

Anaphylaxis: nursing management

A

Initial action - access the patient for s/s of anaphylaxis

  • assess airway, breathing pattern and other vitals
  • increased edema and respiratory distress

Call 911 and initiation of emergent measures
Once recovered: explanation to avoid future exposure

In the event of an acute allergic reaction, the nurse recognizes that ET intubation may be difficult or impossible because it can result in increased laryngeal edema, bleeding, and further narrowing of the glottic opening. Fiberoptic ET intubation, needle cricothyrotomy (followed by transtracheal ventilation), or cricothyrotomy may be necessary

46
Q

what is allergic rhinitis

A

Hay Fever, seasonal allergic rhinitis – Most common form of chronic respiratory allergic disease

Caused by an allergen-specific IgE-mediated immunologic response

Often in conjunction with other conditions – conjunctivitis, sinusitis, and asthma

Severe symptoms can interfere with sleep, leisure and school/work activities

47
Q

Untreated allergic rhinitis can lead to what?

A

Untreated – asthma, chronic nasal obstruction, chronic otitis media with hearing loss, anosmia

48
Q

Because allergic rhinitis is induced by airborne pollens or molds, it is activated by the following seasonal occurrences:

A

Early spring: Tree pollen (oak, elm, poplar), mold spores

Early summer: Rose pollen (rose fever), grass pollen (timothy, red-top)

Early fall: Weed pollen (ragweed), mold spores

49
Q

Allergic rhinitis clinical manifestations

A 
Sneezing, nasal congestion
Clear, watery, nasal discharge
Itchy eyes and nose, lacrimation
postnasal drip
headache
pain over paranasal sinuses
Epistaxis 
Nasal congestion or rhinorrhea
Enlarge anterior cervical lymph nodes 
Sinus tenderness on palpations
50
Q

Allergic rhinitis: diagnostics

A 
Nasal smear
Peripheral blood counts
Serum IgE
Epicutaneous and intradermal testing 
Radioallergosorbent test (RAST)
Food elimination and challenge
Nasal provocation test
51
Q

Allergic Rhinitis: avoidance therapy

A

Remove allergens

If acquires URI – take dep breaths and cough frequently to ensure gas exchange

Seek medical attention if get URI

52
Q

Allergic Rhinitis tx: antihistamines

A

used for mild allergic disorders

Seasonal basis – not continuous

53
Q

Allergic Rhinitis tx: adrenergic agents

A

Help relieve severity of symptoms of narrowing blood vessels in the nasal passageways

54
Q

Allergic Rhinitis tx: mast cell stabilizers

A

Reducing the release of histamine and other mediators of the allergic response

Benefits may take 1-2 weeks

55
Q

Allergic Rhinitis tx: corticosteroids

A

Anti-inflammatory actins – effective in preventing or suppressing the major symptoms of allergic rhinitis

56
Q

Allergic Rhinitis tx: immunotherapy

A

Allergy shots

57
Q

Allergic Rhinitis tx: homeopathic modalities

A

? look up ?

58
Q

Allergic Rhinitis: avoidance

A
  1. air cleaners/purifiers, humidifiers dehumiditers, keeping windows closed during high pollen counts and windy conditions
  2. Remove dust-catching furnishings. PETS – remove
59
Q

What is something to incorporate to reduce allergic rhinitis?

A

Using air-conditioning as much as possible

60
Q

How can allergic rhinitis affect QOL?

A

producing fatigue, loss of sleep, poor concentration, and interference with physical activities.

61
Q

What is contact dermatitis

A

Acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens

62
Q

What type of hypersensitivity is contact dermatitis

A

type 4

63
Q

What are the types of contact dermatitis

A

Allergic
Irritant
Phototoxic
Photoallergic

64
Q

Allergic contact dermatitis: etiology

A

Results from contact of skin and allergenic substance. Has a sensitization period of 10–14 days.

65
Q

Allergic contact dermatitis: clinical presentation

A

Vasodilation and perivascular infiltrates on the dermis
Intracellular edema
Usually seen on dorsal aspects of hand

66
Q

Allergic contact dermatitis: diagnostic testing

A

Patch testing (contraindicated in acute, widespread dermatitis)

67
Q

Allergic contact dermatitis: treatment

A

Avoidance of offending material

Burow solution (aluminum acetate in water) is a drying agent for weeping skin lesions or cool water compress

Systemic corticosteroids (prednisone) for 7–10 days

Topical corticosteroids for mild cases

Oral antihistamines to relieve pruritus

68
Q

Irritant contact dermatitis: etiology

A

Results from contact with a substance that chemically or physically damages the skin on a nonimmunologic basis. Occurs after first exposure to irritant or repeated exposures to milder irritants over an extended time.

69
Q

Irritant contact dermatitis: clinical presentation

A

Dryness lasting days to months
Vesiculation, fissures, cracks
Most common on hands and lower arms

70
Q

Irritant contact dermatitis: diagnostic testing

A

Clinical picture

Appropriate negative patch tests

71
Q

irritant contact dermatitis: treatment

A

Identification and removal of source of irritation

Application of hydrophilic cream or petrolatum to soothe and protect

Topical corticosteroids and compresses for weeping lesions

Antibiotics for infection, and oral antihistamines for pruritus

72
Q

Phototoxic contact dermatitis: etiology

A

Resembles the irritant type but requires sun and a chemical in combination to damage the epidermis.

73
Q

Phototoxic contact dermatitis: clinical presentation

A

Similar to irritant dermatitis

74
Q

Phototoxic contact dermatitis: diagnostic testing

A

Photopatch test

75
Q

Phototoxic contact dermatitis: treatment

A

Same as for allergic and irritant dermatitis

76
Q

Photoallergic contact dermatitis: etiology

A

Resembles allergic dermatitis but requires light exposure in addition to allergen contact to produce immunologic reactivity.

77
Q

Photoallergic contact dermatitis: clinical presentation

A

Similar to allergic dermatitis

78
Q

Photoallergic contact dermatitis: diagnostic testing

A

photopatch test

79
Q

Photoallergic contact dermatitis: treatment

A

Same as for allergic and irritant dermatitis

80
Q

What is Atopic Dermatitis

A

Type I immediate hypersensitivity disorder characterized by inflammation and hyperreactivity of the skin, often causing pruritus

Significant elevation of serum IgE and peripheral eosinophilia

81
Q

s/s - atopic dermatitis

A

pruritus and hyperirritability of the skin

    • Excessive dryness
    • Immediate redness appears and followed in 15-30 second by pallor – persisting for 1-3 minutes
82
Q

Atopic dermatitis - management

A

Stop the itching and scratching

Cope with the disorder

83
Q

What kind of hypersensitivity is dermatitis Medicamentosa

A

Type 1

84
Q

Dermatitis Medicamentosa: causes and s/s

A

Drug reactions

s/s:
Appear suddenly
Vivid color
Intense characteristics – similar of infectious origin
Disappear rapidly after the medication is withdrawn
Rash can be generalized or systemic

85
Q

Dermatitis Medicamentosa management

A

Find the cause
Stabilize patient
Frequent assessments
Carry a card identifying their allergy to this medication

86
Q

Urticaria is what type of hypersensitivity

A

Type 1 hypersensitivity allergic reaction

87
Q

Urticaria s/s

A

Pinkish, edematous elevation
Vary in size and shape
Itch
Local discomfort

88
Q

Angioneurotic Edema s/s

A

Deeper layers of the skin – diffuse swelling
Involves lips, eyelids, cheeks, hands, feet, genitalia and tongue
Suddenly – 2 hours – lasting 24-36 hours

89
Q

s/s food allergy

A

urticaria, dermatitis, wheezing, cough, laryngeal edema, angioedema

GI – swelling of lips, tongue, abdominal pain, nausea, cramps, vomiting/diarrhea

90
Q

Food allergy - management

A

Family to help recognize symptoms
Children – food allergies disappear over time
Education – read labels, contamination

91
Q

What type of hypersensitivity of serum sickness

A

Type 3

92
Q

What is happening with serum sickness?

A

Hypersensitivity complexes get deposited in tissues or vascular endothelium – increase vascular permeability and tissue injury – vasculitis

Often from prevention of infectious diseases – tetanus, PNA, rabies, diphtheria, botulism

Begins 6-10 days after administration – inflammatory reaction at the site of injection of the medication – followed by regional and generalized lymphadenopathy and fever

93
Q

Serum sickness - s/s

A

Skin rash, joints are tender and swollen
Vasculitis – any organ, common in the kidney
Cardiac involvement

94
Q

Serum sickness: management

A

treat the clinical syndrome symptomatically

95
Q

Latex allergy is an implication with what other conditions?

A

Implicated in rhinitis, conjunctivitis, contact dermatitis, urticaria, asthma, and anaphylaxis

96
Q

What food sensitivities are related to latex allegies?

A

kiwi, bananas, pineapples, mangoes, passion fruit, avocados, and chestnuts

97
Q

What happens if latex allergy is a type 1 response?

A

rapid onset – urticaria, wheezing, dyspnea, laryngeal edema, bronchospasm, angioedema, hypotension, and cardiac arrest

98
Q

Latex allergies: risk factors

A

healthcare workers, atopic allergies, multiple surgeries, factory workers

99
Q

Latex allergy: prevention

A

Avoid latex if at all possible

Ask about Allergy prior to any procedure

100
Q

A latex allergy can cause what?

A

Irritant contact dermatitis

Allergic contact dermatitis

NURSING 3 (16 decks)

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