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NA 1 > Anaphylaxis > Flashcards

Anaphylaxis Flashcards

1
Q

immune system categories

A
  • innate (natural) –> born with
  • adaptive (acquired) –> vaccines
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2
Q

2 type of immune system response

A
  • cell-mediated immunity
  • humoral immunity
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3
Q

cell-mediated immunity

A
  • immune cells directed at eliminating or destroying pathogens or cells
  • T cells, phagocytes, cytokines
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4
Q

Humoral immunity

A
  • different antibodies and proteins (exp. complement)
  • can work directly or in combo with cellular immunity to create cell injury and destruction
  • B cells
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5
Q

specific (acquired) immunity has

A

B cells & T cells

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6
Q

Non-specific (innate) immunity has

A
  • Barriers (skin & stomach acid)
  • Inflammatory response (vasodilation & phagocytes)
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7
Q

complete antigen

A

capable of inducing a full immune response

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8
Q

antigen

A

is any toxin or foreign substance that causes an immune response in the body

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9
Q

incomplete antigen

A
  • needs something else (like a carrier protein) to cause a response
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10
Q

Haptens

A

small molecules, incomplete antigens

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11
Q

complete antigen 2 examples

A

protamine & dextran

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12
Q

Dextran

A
  • large macromolecules
  • colloid volume expanders
  • sometimes used in vascular surgery
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13
Q

Protamine

A
  • positively charged
  • binds with neg charged heparin to neutralize
  • Can act as an antigen and bind to IgE antibodies –> cellular degranulation and histamine release
  • some insulin preparations have protamine: may be more susceptible to protamine response if taking it
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14
Q

2 types of immune response

A
  • antibody-mediated
  • cell-mediated
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15
Q

antibody mediated

A

humoral = fluids of the body
B-lymphocytes

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16
Q

cell-mediated

A

phagocytes
T-cells
cytokines

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17
Q

antibodies also called

A

immunoglobulins

they are protein molecules

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18
Q

5 major classes of antibodies

A

IgA
IgD
IgG
IgE
IgM

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19
Q

structure of antibody

A
  • 2 heavy chains and 2 light chains: heavy chain determines the structure and function of each molecule
  • Fab fragment (antigen binding sites)
  • Fc fragment
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20
Q

B-cells and T-cells

A

specialized immune system lymphocytes

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21
Q

where are T-cells derived?

A

thymus

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22
Q

how are T-cells activated?

A

receptors are activated by binding foreign antigens

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23
Q

T-cells secrete __ that regulate the immune response

A

mediators

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24
Q

Types of T-cells

A
  • helper (regulatory)
  • Suppressor (regulatory)(inhibit immune functions)
  • cytotoxic
  • killer (not directly, release cytokines, an things to destroy membrane and have more thinks come in to destroy)
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25
Q

function of T-helper

A
  • support cells, assist other cells in the immune process
  • help B-cells mature into plasma cells and memory cells
  • activate cytotoxic t-cells and macrophages
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26
Q

function of suppressor t-cells

A

main function = shut down T-cell immunity

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27
Q

function of cytotoxic t-cells

A

kill virus-infected cells and tumor cells

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28
Q

T-cell “army”

A

cell-mediated immune response directed at a specific pathogen

T-cells main job = release mediators that tell other cells what to do

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28
Q

killer cells

A
  • dont directly attack a pathogen
  • kills things without a reason (antigen)
  • transplant rejection
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29
Q

B-cells are part of __ the immune response system

A

antibody

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30
Q

where are B-cells made?

A

bone marrow

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31
Q

two type of B-cells

A

memory & effector

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32
Q

effector cells

A

actually do something (opsonization)

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32
Q

memory cells

A

body remembers what you were exposed to

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33
Q

B-cells have receptors (antibodies) on the surface that allow them to attach to a

A

specific antigen

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34
Q

each B-cell has a different

A

antibody

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35
Q

how do B-cells do their job?

A

B-cells exposed to antigen
- become activated
- start replicating

Turn into different cells
- memory cells
- effector cells

Effector cells produce antibodies
- antibodies attach to virus and “tag” them
- opsonization

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35
Q

B-cells make antibodies how

A
  1. binding to antigen
  2. chemical signal (helper t-cell) comes
  3. becomes plasma cell
  4. releases antibodies
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36
Q

how do T-cells do their job?

A
  • T-cells are mobilized when they encounter a cell such as a dendritic cell or B-cell that has digested an antigen and is displaying antigen fragments bound to its MHC molecules
  • cytokines help the T-cell mature
  • the MHC-antigen complex activates the T-cell receptor and the T-cell secretes cytokines
  • some cytokines spur the growth of more T-cells
  • some t-cells become helper cells and secrete cytokines that attract fresh macrophages, neutrophils, other lymphocytes, and other cytokines to direct the recruits once they arrive on the scene
  • some t-cells become cytotoxic cells and track down cells infected with viruses
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37
Q

innate immunity

A

epithelial barriers
mast cells
phagocytes
dendritic cells
complement
NK cells and ILCs

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38
Q

adaptive immunity

A

B lymphocytes –> plasma cells –> antibodies
T lymphocytes –> effector T cells

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39
Q

hypersensitivity responses

A
  • normally, the immune system works as a protective system, but it may react inappropriately and produce a hypersensitive (or allergic) response
  • require a pre-sensitized state of the host
  • four types of hypersensitivity responses
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40
Q

Hypersensitivity reactions names

A

Type 1: anaphylaxis
Type 2: cytotoxic reactions
Type 3: immune complex reactions
Type 4: delayed hypersensitivity reaction

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40
Q

Type I reactions

A
  • extrinsic asthma
  • allergic rhinitis
  • anaphylaxis

antigen binds to preformed antibodies on mast cells and basophils. leads to –> release of histamine, leukotrienes, platelet-activating factor

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41
Q

Type I involves what antibodies?

A

IgE antibodies

cross-linking of 2 IgE antibodies is the key, starts degranulation and release of mediators

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41
Q

Type I reaction also called

A

immediate-type hypersensitivity (happens in minutes)

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42
Q

what happens when the mast cell explodes?

A
  • histamine is released
  • platelet-activating factor is released
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43
Q

when histamine is released..

A

attaches to H1 receptor
- lungs: broncho-constriction –> difficulty breathing
- vascular system: vasodilation and increased permeability –> edema and hives

H2 increased gastric secretion and further exhibits vasofilation

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43
Q

when platelet-activating factor is released…

A
  • coronary artery constriction –> ischemia
  • decreased coronary perfusion –> ischemia
  • decreased contractility –> cardiovascular collapse
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44
Q

anaphylactoid (non-immunogenic)

A
  • No IgE involvement
  • less severe
  • mast cell activation only
  • happens when a drug directly releases histamine or starts complement system
  • no previous exposure to antigen required
  • think IV contrast reaction
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44
Q

anaphylactic (immunogenic)

A
  • IgE mediated
  • severe reactions
  • mast cells & basophils
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45
Q

non-immunologic release of histamine, have histamine release with no

A

anaphylaxis

still release histamine but hopefully Benadryl can compete to knock it off

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46
Q

arachidonic acid metabolites

A

leukotrienes & prostaglandins: bronchoconstriction and vasodilation

47
Q

Histmaine

A

H1 receptor:
- vasodilation
- increased vascular permeability
- smooth muscle contraction (not vascular)

H2 receptor:
- cardiac stimulation (tachy)
- gastric acid secretion

48
Q

another name for type II reactions

A

cytotoxic reactions

aka antibody-dependent cell-mediated or cytotoxic hypersensitivity

49
Q

type II reaction is mediated by what antibodies?

A

IgG or IgM

50
Q

think of what when you see type II reaction.

A

transfusion reactions

51
Q

example of type II reactions

A
  • ABO incompatible transfusion reactions
  • drug-induced hemolytic reactions
  • Heparin-induced thrombocytopenia (HIT)
51
Q

type II reactions

A

cell damage (cytotoxic)
- direct cell lysis
- increased phagocytosis

52
Q

complement activation

A
  • helps the immune system to do its job
  • part of the immune system that enhances (or complements) the ability of antibodies or phagocytic cells to:
  • recognize bacteria
  • “tag” bacteria
  • break bacteria apart
53
Q

complement activation has how many different proteins?

A

20

54
Q

complement activation starts how

A

with IgG or IGM and release vasoactive mediators (C3a, C4a, C5a)

55
Q

example of complement system gone bad?

A

acute pulmonary vasoconstriction after protamine

55
Q

Type III reactions name

A

immune complex reactions

56
Q

Type III reactions, think of

A

snake bite, SLE

56
Q

Type III reaction

A

antibodies and antigen bind and make insoluble complexes that lead to vasculitis

57
Q

Type III reactions involve what antibodies?

A

IgG or IgM

58
Q

T/F complement is activated in type III reactions

A

True

neutrophils produce tissue damage

59
Q

Type IV reaction AKA

A

delayed hypersensitivity reaction

60
Q

what should you think of with Type IV reactions

A

think TB test, poison ivy

61
Q

type IV reactions

A

sensitized lymphocytes + antigens

62
Q

type IV reactions manifest in

A

18-24 hrs

63
Q

Type IV reactions disappear in

A

72-96 hrs

64
Q

type of reactions with Type IV

A
  • tissue rejection
  • graft-host
  • contact dermiatits
  • TB skin test
65
Q

drugs capable of non-immunogenic histamine release

A
  • abx: Vance, pentamidine
  • hyperosmotic agents: contrast media, mannitol
  • neuromuscular blockers: atracurium, mivacurium
  • opioids: morphine, meperidine, codeine
  • dextrans
66
Q

drugs capable of producing complement activation

A
  • cardiopulmonary bypass
  • dextrans
  • protamine
  • radiocontrast agents
67
Q

extra bad things than happen with anaphylaxis

A
  • Mast cells can continue to spill out their content even if the antigen is no longer present as a triggering agent.. will continue to potentiate ongoing symptoms
  • ongoing mediators of inflammation can lead to a return rebound of symptoms 6 to 8 hours following the initial allergic response.. this is the reason that patients should be kept and monitored closely following control of initial symptoms
68
Q

which histamine receptors are involved in anaphylaxis?

A

H1 & H2

69
Q

where is histamine stored?

A

mast cells and basophils

70
Q

H1 does what?

A

vasodilation, increased vascular permeability, smooth muscle contraction ( but not blood vessels)

71
Q

H2 does what?

A

cardiac stimulation and gastric acid secretion

72
Q

H2 does what

A

presynaptic terminal is the NS

73
Q

H4 does what

A

in vasculature in lungs, spleen, gut –> inflammation

74
Q

what other things can cause anaphylaxis symptoms?

A
  • peptides
  • kinins
  • Arachidonic acid
  • platelet-activating form

not just histamine

75
Q

Arachidonic acid

A

leukotrienes:
- bronchoconstriction (more intense than histamine)
- increased capillary permeability
- coronary vasoconstriction
- myocardial depression

76
Q

peptides

A

Eosinophilic chemotactic factor (ECFA) –> thought to release enzymes that inactivate histamine

77
Q

kinins

A

released from mast cells and basophils
- vasodilation
- increased capillary permeability
- bronchoconstriction

78
Q

platelet-activating facor

A
  • released from mast cells
  • aggregates and activates platelets to release inflammatory products
79
Q

greater than 90% of perioperative anaphylaxis are evoked by

A

IV drugs and occur within 5 mins

80
Q

risk of perioperative anaphylaxis is

A

1: 3,500– 1: 20,000

mortality rate = 4%

81
Q

most common clinical features of anaphylaxis during A

A
  • cardiovascular symptoms (73.6%)
  • cutaneous symptoms (69.6%)
  • bronchospasm (44.2%)

sometimes your only symptom is refractory hypotension (dilute epi and give it)

82
Q

causative agents of anaphylaxis perioperativley

A
  • muscle relaxants (succ, roc, atr)
  • latex (gloves, foley, tourniquets)
  • abx (pnc & other beta lactams)
  • hypnotics (prop, thiopental)
  • colloids (dextran, gelatin)
  • opioids (morphine, meperidine)
  • other substances (protamine, bupivacaine)
83
Q

what percent of NMB drugs cause anaphylaxis reactions? and what’s the most common

why?

A

62-81%
succinylcholine

  • structure contains flexible molecules that can cross-link two mast cells IgE receptors, more common w/ benzylisoquinoline compounds than with amino-steroid complexes
  • cross-sensitivity between NMBA in most ppl
  • may cause direct mast cell degranulation
84
Q

latex comes from what?

A

milky white sap of Hevea brasiliensis

85
Q

latex reaction is __ mediated

A

IgE

86
Q

people at risk for latex reaction

A
  • healthcare workers
  • children with spina bifidia
  • food allergies: bananas, kiwis, avocado
87
Q

crodd sensitivtiy to latex

A

bananas, kiwis, apple, avocado, chestnut, carrot/celery, papaya, potato, tomato, melons

87
Q

prevention of latex

A
  • avoid latex
  • antihistamines – not proven to work
88
Q

one of the top three causative agents of anaphylaxis under A and #1 agent in children

A

latex

89
Q

what things still have latex in them that you have to be careful about in the medical environment

A
  • rubber stoppers from medicine vials,
90
Q

latex free substances

A

polyvinyl
neoprene
silicone

91
Q

usual presenting reaction of abx allergic reaction

A

cutaneous

91
Q

prophylactic treatment for latex allergies

A

H1 & H2 blockers
steroids

prophylaxis has not shown to decrease the occurrence of an anaphylactic response

92
Q

the most general cause of anaphylaxis in general population and may account for __ of all anaphylactic deaths in the US

A

75%

93
Q

most common abx that ppl are allergic too

A

penicillin

incidence of anaphylaxis is very low with vanco

94
Q
A
94
Q
A
95
Q
A
96
Q
A
96
Q
A
97
Q
A
98
Q
A
99
Q
A
100
Q
A
101
Q

vancomycin is a potent __ releaser

A

histamine

rare anaphylaxis
severe hypotension with rapid IV administration

102
Q

LA allergic reactions are

A

uncommon

103
Q

LA ester agents

A

para-aminobenzoic (PABA) metabolite

104
Q

Sugammadex

A

delayed approval several time for concern of hypersensitivity reachtions

105
Q

sugammadex reactions

A
  • most are mild
  • most occur within 5 mins
  • the risk of anaphylaxis but the mechanism is unclear: does not seem to increase with repeated exposure, risk of hypersensitivity seems to increase with higher doses
106
Q

what hypnotic is most likely to have an allergic reaction to?

A

thipental

107
Q

T/F methohexital causes anaphylaxis reactions

A

False

108
Q

prop allergic reaction usually involve __ __

A

egg white

made with egg lectin (yolk) current evidence says okay with egg allergies

108
Q

T/F allergic reactions with etomidate, ketamin, and benzos are often

A

false

super rare

109
Q

Aprotinin incidence of allergic reactions are __ to __ %

A

0.5; 2.8

110
Q

heparin involve what antibody in the allergic reaction?

A

IgE reaction very rare

HIT more common

111
Q

protamine 0.4-0.8% can form allergic reaction, __ if previously exposed

A

higher

fish allergy or men with vasectomies

112
Q

protamine made from

A

salmon sperm

113
Q

how does heparin work

A

binds with heparin and neutralizes it

114
Q

patient can have 3 types of “protamine reactions”

A
  • caused by histamine release
  • caused by protamine-heparin complex
  • anaphylaxis at higher risk with hx of: vasectomy, salmon allergy, insulin use (NPH)
115
Q

atopic patients

A

may easily develop antibody-mediated allergic responses to foods, environmental factors, and drugs

116
Q

expressed signs and symptoms in atopic patients

A

allergic rhinitis
asthma

NA 1 (15 decks)

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