Allergy - Exam 4 Flashcards

(288 cards)

1
Q

Nagelhout Anaphylaxis:
Assessment

A

Grade I: Cutaneous Signs- generalized erythema, urticaria, angioedema

Grade II: Cutaneous signs, HoTN, tachycardia, cough, difficult ventilation

Grade III: HoTN, tachycardia or bradycardia, arrhythmias, bronchospasm

Grade IV: Cardiac and/or respiratory arrest, PEA

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2
Q

Nagelhout Anaphylaxis:
Initial Treatment

A

Discontinue triggering agent

Trendelenburg position

Ventilation with 100%

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3
Q

Nagelhout Anaphylaxis:
Epinephrine doses

A

Grade I: n/a

Grade II: 10-20 mcg SC/IM

Grade III: 100-200 mcg SC/IM/IV q 1-2min; 1-4 mcg/min

Grade IV: 1 mg IV repeat as needed: 0.05-0.1 mcg/min

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4
Q

Nagelhout Anaphylaxis:
Fluids

A

Normal saline/lactated Ringer: 10-30 mL/kg or colloid: 10 mL/kg

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5
Q

Nagelhout Anaphylaxis:
Secondary Treatment.

A

Epi unresponsiveness: vasopressin: 2-10 units IV; norepinephrine: 0.05-0.1 mg/kg/min

Bronchospasm: albuterol or ipratropium inhalants, terbutaline 0.25 mg SC (may be repeated in 15-30min)

Preoperative B-blockade: glucagon 1-5 mg IV every 5 min; 5-15 mcg/min

Antihistamines: diphenhydramine or hydroxyzine: 0.5-1.0 mg/kg IV; ranitidine: 50 mg IV

Airway edema: hydrocortisone 250 mg IV

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6
Q

Nagelhout Anaphylaxis:
Post resuscitation steps

A

Serum tryptase < 120min

24-hr monitoring for reoccurrence

Patient/family notification of reaction

Referral to allergist

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7
Q

_ are inflammatory cell activators made to act as secondary messengers and activate endothelial and white cells

A

cytokines

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8
Q

Antibodies are specific proteins called _ that can recognize and bind specific antigens, usually _ and _ are implicated in allergic reactions

A

immunoglobulins
IgE
IgG

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9
Q

Immune competence during surgery can be affected by:

A

-direct effects of anesthetics
-hormonal effects of anesthetics
-immunologic effects of other drugs used
-type of surgery
-coincident infection
-blood products

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10
Q

Most of the allergic reactions evoked by IV drugs occur within _ mins

A

5min

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11
Q

In the anesthetized pt, the most common life-threatening manifestation of an allergic reaction is _ collapse, reflecting _ and decreased _ _

A

circulatory
vasodilation
decreased venous return

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12
Q

Some drugs given preoperatively, such as vanco, can release _ in a dose-dependent, _ fashion

A

histamine
nonimmunologic

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13
Q

People at increased risk for latex allergy would include:

A

-healthcare workers
-kids after mult procedures
-pts with specific food allergies

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14
Q

_ have several unique molecular features that make them potential triggers for anaphylaxis

A

NMBAs

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15
Q

Immunologic mechanisms:

A
  1. involve antigen interaction with antibodies or specific effector cells
  2. are reproducible
  3. are specific and adaptive
    -can distinguish foreign substances and amplify reactivity with inflammatory cells and proteins
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16
Q

T/F A hypersensitivity reaction is an appropriate immunologic response to antigens.

A

false
-INappropriate

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17
Q

Antigens are typically made of _ or _

A

proteins
carbohydrates

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18
Q

The immune response includes both _ _ and _ immunity.

A

cell-mediated
humoral

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19
Q

Which kind of immunity involves immune cells directed at eliminating or destroying pathogens or cells?

A

Cell-mediated

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20
Q

Which kind of immunity comprises antibodies and proteins (complement, cytokines, and signaling molecules) that can directly or in concert with cellular immunity orchestrate cell injury or destruction

A

humoral immunity

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21
Q

Cytokines/Chemokines are released as _ immune responses

A

humoral

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22
Q

Cytokine actions:

A

-help bring other immune cells to the site of injury
-cause additional inflammatory responses and fever
-increase capillary permeability
-hemostatic activation (pain, redness, edema locally and systemically)

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23
Q

Immune responses can be _ in onset and remember antigens for many years, especially following _

A

variable
immunizations

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24
Q

Molecules stimulating an immune response (antibody production or lymphocyte stimulation) are called _

A

antigens

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25
Examples of COMPLETE antigens that anesthetists use:
-large macromolecules (dextrans) -polypeptides (protamine)
26
Most commonly used drugs are simple organic compounds of _ molecular wt (_ Da)
low 1000 Da
27
For most drugs that are small molecules to become immunogenic, they must bind 2 circulating _ or tissues to result in an antigen, which is a _-macromolecular complex
proteins hapten-macromolecular complex
28
T/F Haptens are small molecular wt drugs or drug metabolites that bind to host proteins or cell membranes and sensitize pts and they are antigens
False. All is true except haptens by themself are NOT antigenic
29
A reactive drug metabolite such as _ derivative of penicillin is believed to bind with macromolecules to become _
penicilloyl antigens
30
Agents given during anesthesia that act as antigens -Haptens
-penicillin and its derivatives -anesthetic drugs
31
Agents given during anesthesia that act as antigens -Macromolecules
-Aprotinin -Blood products -Chymopapain -Colloid Volume Expanders -NMBD -Protamine -Latex
32
The _ of the fetus differentiates immature _ into _-derives cells (_ cells)
thymus lymphocytes thymus (T cells)
33
_ cells have receptors that are activated by binding with foreign antigens and secrete mediators that regulate the immune response
T cells
34
Subpopulations of T cells=
-helper -suppressor -cytotoxic -killer
35
The 2 kinds of regulatory T cells are _ (OKT4) cells and _ cells (OKT8)
-helper (OKT4) -suppressor (OKT8)
36
_ T cells are important for key _ cell responses whereas _ T cells inhibit immune function.
Helper Efferent suppressor
37
Infection of _ T cells by the retrovirus, HIV, produces a specific increase in the number of _ T cells
helper suppressor -fuck HIV dude :'(
38
_ T cells destroy mycobacteria, fungi, and viruses.
Cytotoxic -NOT the killer T cells
39
_ T cells do not require a specific antigen to stimulate them to work
Killer
40
Both _ and _ T cells take part in the defense against tumor cells and in transplant rejection.
cytotoxic and killer
41
T cells produce _ that influence the response of other cell types involved in recognizing and destroying foreign substances.
mediators
42
_ cells represent a specific lymphocyte cell line that can differentiate into specific plasma cells that synthesize _, which is a step controlled by both _ and suppressor _ cell lymphocytes.
B cell antibodies helper T
43
B cells are also called _ -derived cells.
bursa
44
Antibodies are specific _ called _ that recognize and bind to a specific antigen.
proteins immunoglobulins
45
Each antibody is composed of at least 2 _ chains and 2 _ chains that are bound together by _ bonds.
heavy light DISULFIDE
46
The _ fragment chain has the ability to bind antigen and the _ or crystallizable fragment chain is responsible for the unique properties of the different classes of immunoglobulins (cell binding and complement activation)
Fab (light chain) Fc (heavy chain)
47
_ function as specific receptor molecules for immune cells and proteins
antibodies
48
When antigens bind _ to the _ fragments, the antibody undergoes conformational changes to activate the _ receptor.
covalently Fab Fc
49
The results of antigen-antibody binding depend on the cell type, which causes a specific type of activation such as lymphocyte proliferation and differentiation into _-secreting cells, _ _ degranulation, and _ activation.
histamine mast cell complement
50
Multiple therapeutic agents are based on _ fragments that bind IRREVERSIBLY to a specific molecular configuration or drug.
Fab -examples of drugs would be Abciximab (platelet inhibitor that binds to IIb/IIIa receptors) and idarucizumab (binds to dabigatran and revers its anticoagulant effect)
51
What cleaves an immunoglobulin into 2 fab fragments and one Fc fragment?
Papain
52
Antigen binding occurs at that _ fragments and the _ fragment is responsible for membrane binding or complement activation.
Fab Fc
53
5 major classes of antibodies:
IgG IgA IgM IgE IgD GAMED
54
_, _ (polymorphonuclear leukocytes [PMNs]), and _ are important _ cells that move into areas of inflammation in response to specific chemotactic factors like lymphokines, cytokines, and complement-derived mediators.
Monocytes neutrophils eosinophils effector cells
55
The deposition of antibody or complement fragments on the surface of foreign cells is called _, which marks them to be killed by _ cells.
opsonization effector
56
Complex acute inflammatory responses cause _ injuries.
host -like with COVID-19
57
_ regulate immune responses by eating, processing, and presenting antigens to affect inflammatory, tumoricidal, and microbicidal functions.
Macrophages
58
Macrophages arise from circulating _ or can be confined to specific organs like the _
monocytes lungs
59
Steps of Macrophage action: 1. They are recruited and activated in response to _ or tissue injury 2.They _ antigens before they interact with receptors on the _ surface to regulate their action. 3. They then make _ to facilitate both _ and _ -lymphocyte responses.
1. microorganisms 2. ingest, lymphocyte 3. mediators, B and T lymphocyte
60
The first cells to appear in an acute inflammatory reaction are _ that contain _ hydrolases, _ proteases, and lysosomes.
neutrophils acid neutral
61
Once neutrophils are activated, they make hydroxyl _, _, and hydrogen _ which help kill microbes.
radicals, superoxide, peroxide
62
Although their function is unclear, inflammatory cells recruit _ to collect at sites of parasitic infections, tumors, and allergic reactions.
eosinophils
63
_ comprise 0.5-1% of circulating granulocytes in the blood and have _ receptors on their surface which work like those on mast cells.
Basophils IgE
64
_ cells are important for _ _ responses and have _ receptors on their surface which bind to specific antigents.
Mast immediate hypersensitivity IgE
65
Mast cells are fixed in _ and found in _ spaces of the _, _, and .
tissues perivascular skin, lung, and intestine
66
Mast cells are activated by a series of both _ and _ stimuli and once activated, they release physiologically active _ important to _ _ responses.
immune and nonimmune mediators immediate hypersensitivity
67
_ are inflammatory cell activators made by _ to act as second messengers and activate _ and _ cells.
Cytokines macrophages endothelial and white cells
68
Examples of cytokines:
-interleukins -tumor necrosis factor -interferon
69
Release of interleukin-1 and TNF cause:
-fever -neuropeptide release -endothelial cell activation -increased adhesion molecule expression -neutrophil priming -HoTN -myocardial suppression -catabolic state
70
_ help other lymphocytes communicate.
interleukins
71
Interleukins are _ _ made in response to cellular activation that control many aspects of immune and inflammatory responses by activating specific receptors on cells and vasculature.
regulatory proteins/polypeptides
72
T cell lymphocytes influence the activity of other immunologic and nonimmunologic cells by making an array of _ and secreting them.
interleukins
73
The PRIMARY humoral response to antigen and antibody binding is the activation of the _ system
complement
74
The complement system is an important _ system of inflammation, consisting of about _ different proteins that bind to activated antibodies, other complement proteins, and cell membranes.
effector 20
75
Complement activation can be activated by:
-IgG or IgM binding to an antigen -by plasmin thru the classic pathway -by endotoxin -by drugs thru alternate (properdin) paths
76
Specific fragments released during complement activation include:
-C3a -C4a -C5a -have important humoral and chemotactic properties
77
Main function of complement system is to recognize bacteria both directly and indirectly by attracting _ (chemotaxis) as well as increased adhesion of _ to antigens (opsonization), and cell _ by activation of complete cascade
phagocytes phagocytes lysis
78
C_ and C_ make fragments of the complement activation cascade, which are both are called _ and are potent vasoactive mediators
C3 and C5 anaphylactoxins (C3a, C5a)
79
Classic complement activation is started by _ esterase due to Ig_ or Ig_ antigens.
C1 IgG or IgM
80
An inhibitor of the complement cascade, the _ _ inhibitor ensures the system is turned off most of the time.
C1 esterase inhibitor
81
Alternative complement activation occurs via _ and _ interactions
endotoxin and drug
82
_ or _ angioedema is an example of a deficiency in an inhibitor of the C1esterase complement system.
Hereditary or acquired -C1 esterase deficiency
83
Hereditary angioedema is autosomal _
dominant
84
T/F Hereditary angioedema is associated with lymphoma, lymphosarcoma, chronic lymphatic leukemia, and macroglobinemia.
false, acquired angioedema
85
Hereditary/acquired _ is characterized by recurrent increased _ permeability of specific subcutaneous and serosal tissues, causing _ obstruction and respiratory/cardiovascular abnormality during surgery or without obvious precipitating cause.
angioedema vascular laryngeal
86
A significant pathophysiological manifestation of complement activation from PROTAMINE admin is _ _
pulmonary vasoconstriction
87
T/F Anesthesia and surgery depress specific host resistance mechanisms like lymphocyte activation and phagocytosis.
false NONspecific
88
Factors influencing immune competence during surgery:
-direct and hormonal effects of anesthetic drugs -hormonal responses to stress -immunologic effects of other drugs used -type of surgery -coincident infections -transfused blood products
89
4 kinds of hypersensitivity (allergic) reactions
type I-IV
90
Type _ reactions are anaphylactic or immediate-type hypersensitivity reactions.
type I
91
Type I hypersensitivity reactions include:
-anaphylaxis -extrinsic asthma -allergic rhinitis
92
Type I reactions cause physiologically active mediators to be released by _ cells and _ after antigen binding to Ig_ antibodies on membranes of these cells.
mast cells basophils IgE
93
Process of Type I immediate hypersensitivity reactions (anaphylaxis): 1. Involve Ig_ antibodies binding to mast cells or basophiles by way of their _ fragments. 2. On encountering immunospecific antigens, the Ig_ becomes cross-linked inducing _ , intercellular activation, and release of _.
1. IgE, Fc 2. IgE, degranulation, mediators -this reaction is independent of complement
94
T/F A type I reaction relies on the complement pathway.
false
95
Type _ reactions are AKA antibody-dependent cell-mediated cytotoxic reactions OR cytotoxic hypersensitivity
type II **think transfusion reactions (ABO incompatibility**, HIT, drug-induced hemolytic anemia) IgM or IgG
96
Type II reactions are mediated by either Ig_ or Ig_ antibodies directed against antigens on the surface of foreign cells.
IgG or IgM
97
Antigens involved in type II reactions can be either _ cell membrane components (A or B blood group antigens in ABO incompatibility reactions) or _ that absorb to cell surface, causing _ _ (autoimmune hemolytic anemia).
integral haptens anti-hapten antibodies
98
The cell damage in type II reactions is causes by:
-direct cell lysis after completement activation -increased phagocytosis by macrophages -killer T cell lymphocytes making antibody-dependent cell-mediated cytotoxic effects
99
Examples of type II reactions:
-ABO incompatibility transfusion reactions -drug-induced immune hemolytic anemia -heparin-induced thrombocytopenia (HIT)
100
Type _ reactions are caused by circulating soluble antigens and antibodies that bind to make insoluble complexes that settle in the microvasculature.
Type III
101
In type III reactions, the _ is activated and _ are localized to the site of _ deposition to cause tissue damage.
complement neutrophils complement
102
Examples of Type III reactions:
-classic serum sickness from snake bite antisera or antithymocyte globulin, SLE -immune complex injury
103
Type III reactions can occur thru mechanisms of _-mediated pulmonary vasoconstriction
protamine
104
Type III reactions are AKA _ _ reactions
immune complex
105
Type _ reactions occur from interactions of sensitized lymphocytes with specific antigens.
Type IV -think tissue rejection, graft v host, contact derm, TB skin test,poison ivy -involves lymphocyte reg, macrophage activation, and **mononuclear cell infiltration** **no immunoglobulin involved!!!!**
106
Type IV reactions are AKA _ _ reactions and require _ contact.
delayed hypersensitivity second
107
Type IV reactions are mainly _.
mononuclear
108
Type IV reaction timeline: -onset -peak -duration
onset: 18-24hr peak: 40-80hr duration: 72-96hr
109
Type IV reaction process: 1. Antigen-lymphocyte binding causes _ synthesis, _ proliferation, and generation of _ T cells. 2. The _ T cells attract _ and other inflammatory cells.
1. LYMPHOKINE, lymphocyte, cytotoxic 2. cytotoxic, macrophages
110
T/F Killer T cells are made specifically to kill target cells that bear antigens identical to those triggering the reaction.
False, cytotoxic, killer T cells are nonspecific
111
Type IV reactions are involved with reactions such as:
-tissue rejection -graft-vs-host reactions -contact dermatitis (poison ivy) -tuberculin immunity
112
complement plymorphonuclear
113
Risk of perioperative anaphylaxis is reported as between 1 in 3,500 and 1 in 20,000 with a mortality rate of _% with an additional _% surviving with severe brain damage.
4% 2%
114
More than 90% of allergic reactions evoked by IV drugs occur within _ min of administration.
5min
115
Most common life-threatening manifestations of allergic reactions in anesthetized pt include:
-circulatory collapse (vasodilation and decreased venous return)
116
The only manifestation of an allergic reaction may be refractory _ in anesthetized pts.
HoTN
117
When life-threatening allergic reactions mediated by antibodies occur, they are called _
anaphylactic AKA anaphylactoid
118
T/F Type IV reactions require complement activation
false TYPE II and III
119
Recognition of anaphylaxis in regional or GA -Respiratory s/s
-dyspnea -chest discomfort -coughing -wheezing -sneezing -laryngeal edema -decreased compliance -fulminant pulmonary edema -acute resp failure
120
Recognition of anaphylaxis in regional or GA -Cardiovascular s/s
-dizziness -malaise -retrosternal oppression -disorientation -sweating -loss of consciousness -HoTN -dysrhythmias -decreased SVR -arrest -pulm HTN
121
Recognition of anaphylaxis in regional or GA -cutaneous s/s
-itch -burning -tingling -urticaria(hives) -flushing -periorbital edema -perioral edema
122
Antigen binding to Ig_ antibodies cause anaphylaxis
IgE
123
T/F Anaphylaxis usually occurs on first contact of a substance
false -prior exposure is needed to produce sensitization
124
Anaphylactic reaction process 1. On exposure, the antigen binds and bridges 2 immunospecific IgE antibodies on the _ cells 2.Basophils then release stored mediators such as _, _, and chemotactic factors. 3. As this activates the cells, arachidonic acid metabolites (_ and _), kinins, and _ are created and released. 4.These mediators then cause a symptom complex of _ and upper airway _, vasodilation, and increased capillary _ and uritcaria.
1. mast 2. histamine, tryptase, 3. leukotrienes and prostaglandins, cytokines 4. bronchospasm, edema, permeability -this process is ENERGY and CALCIUM dependent
125
Histamine released during anaphylaxis stimulates which 3 receptors:
H1, H2, H3
126
H1 receptor functions once activated:
-releases endothelium-derived relaxing factor (nitric oxide) from vasc endothelium -increases cap permeability -contracts airway and vasc smooth muscle
127
H2 receptor activation causes:
-gastric secretion -inhibits mast cell activation -contributes to vasodilation
128
When injected into skin, histamine produces a classic _ and _ response
wheal and flare -increased cap permeability/ tissue edema and cutaneous vasodilation effect
129
Histamine undergoes a _ metabolism by enzymes histamine _-_ and _ _ found in _ cells.
rapid N-methyltransferase diamine oxidase endothelial
130
Factors are released from mast cells and basophils and cause _ migration (chemotaxis) and collect at the site of the inflammatory stimulus
granulocytes
131
_ chemotactic factor of anaphylaxis (ECF-A) is a small molecular wt peptide chemotactic for _ and release enzymes that inactivate _ and _.
Eosinophilic eosinophils histamine and leukotrienes
132
During anaphylaxis, a _ chemotactic factor is released that causes chemotaxis and activation of _ which may be responsible for recurrent manifestations of anaphylaxis.
neutrophilic neutriphils
133
_ and _ are made after mast cell activation from arachidonic acid metabolism of _ cell membranes thru either _ or _ pathways.
Leukotrienes and prostaglandins phospholipid lipoxygenase or cyclooxygenase
134
The classic slow reacting substance of anaphylaxis is a combo of leukotrienes _, _, and _.
C2, D4, and E4
135
Which produces a stronger bronchoconstriction effect, leukotrienes or histamine?
leukotrienes
136
Leukotrienes cause:
-bronchoconstriction (more than histamine) -increased cap permeability -vasodilation -CORONARY vasoconstriction -myocardial depression
137
_ _ is the major metabolite of mast cells and causes bronchospasm and vasodilation
Prostaglandin D2
138
Prostaglandins are potent mast cell mediators and cause:
-vasodilation -bronchospasm
139
Elevated serum levels of _ _ (metabolite of thromboxane A2), a _ made by mast cells as well as by PMSs, have been involved after Protamine reactions associated with pulm HTN.
thromboxane B2 prostaglandin
140
Small peptides called _ are made by mast cells and basophils.
kinins
141
Kinins cause:
-increased cap permeability -vasodilation -bronchoconstriction
142
Kinins stimulate _ endothelium to release _ factors, including _ and endothelium-derived relaxing factors like _ oxide.
vascular vasoactive prostacyclin nitric
143
_-_ _ is an UNSTORED lipid made in activated mast cells.
platelet-activating factor (PAF)
144
The more severe of an allergic reaction, the _ their PAF levels will be.
higher
145
Platelet-activating factor (PAF) aggregates and activates _ and _ to release inflammatory products.
platelets and leukocytes
146
The onset and severity of anaphylaxis is dependent on the _'s specific end-_ effects
mediator organ
147
Antigenic challenge in a sensitized pt usually causes immediate clinical manifestations of anaphylaxis but the onset ay be delayed by _ - _ min
2-20min
148
T/F All anaphylactic reactions run the same course in each individual
false -spectrum-like, varying manifestations
149
Biologic effects of anaphylaxis (Barash):
-histamine release -smooth musc contraction -increased vasc permeability -chemotaxis (movement of compounds thru body) -leukocyte and platelet aggregation -interleukin release
150
C3a mediated biologic processes of anaphylaxis:
-histamine release -smooth musc contraction -increased vasc permeability -chemotaxis (movement of compounds thru body) -leukocyte and platelet aggregation -interleukin release
151
C5a mediated biologic processes of anaphylaxis
-histamine release -smooth musc contraction -increased vasc permeability -interleukin release -NOT chemotaxis and leukocyte/platelet aggregation
152
Other immunologic and nonimune mechanisms release the same mediators independently from IgE, creating an _ like syndrome.
anaphylactoid
153
Complement activation follows both _ (antibody/classic) and _(alt) pathways to a series of multi-molecular self assembling proteins that release active fragments of _ and _
immune and nonimmune C3 and C5
154
C3a and C5a are called _ because they release _ from mast cells and basophils, contract _ muscle, increase cap permeability, and cause _ synthesis.
anaphylactoxins histamine smooth interleukin
155
C5a interacts with specific high affinity receptors on _ and _ causing _ chemotaxis, aggregation, and activation.
PMNs(neutrophils) and platelets leukocyte
156
Aggregated leukocytes from C5a embolize to various organs causing _ occlusion and liberation of inflammatory products like _ _ metabolites, _ free radicals, and _ enzymes.
microvasculature arachidonic acid metabolites O2 free radicals lysosomal
157
Antibodies of the Ig_ class directed against antigenic determinants or _ surfaces can also cause _ aggregation like C5a. These Ig_ antibodies are called _.
IgG granulocyte leukocyte IgG leukoagglutinins
158
Complement activation and PMN aggregation is involved in:
-transfusion reactions -pulm vasoconstriction from protamine reactions -ARDS -septic shock
159
Angioedema can occur from allergic reaction and also from _ deficiency states such as _ angioedema (HAE)
complement hereditary
160
HAE variants exist due to unopposed activation of multiple _ and mediators including _ and _, causing increased vascular permeability and edema
kinins bradykinin and kallikrein
161
HAE treatments include:
**C1 esterase inhibitors (C1-INH) ** -Cinryze and ViroPharma for prophylactic use every few days and Berinert for acute HAE attacks **Kinin pathway modulators** -ecallantide (Kalbitor, Dyax) **Bradykinin antagonists ** -Icatibant
162
T/F Nonimmune release of histamine involves basophils but not mast cells.
false, SPECIFIC mast cells, not basophils
163
_ mast cells are the only cells that release _ in response to both drugs and endogenous stimuli (neuropeptides)
Cutaneous histamine
164
T/F histamine release is dependent on the mu receptor
false -fentanyl and sufentanil do not release histamine
165
T/F Because the newer muscle relaxers are more potent on the NM junction, they also release histamine more than other NMBD.
False -regardless of potency on NM junction, all drugs that are mast cell degranulators are equally able to release histamine
166
Aminosteroidal agents like _ and _ at clinically recommended doses have a _ effect on histamine release.
rocuronium and pancuronium minor
167
Drugs capable of NONimmunogenic histamine release:
-Abx ( vanco and pentamidine) -basic compounds -hyperosmotic agents -MR (d-tubocurarine, metocurine, **atracurium**, mivacurium, doxacurium) -opioids (morphine, meperidine, codeine)
168
T/F Pretreating with antihistamines before giving drugs known to release it helps inhibit its release.
false -they just compete with histamine at the receptor site and can attenuate decreases in SVR
169
Treatment of anaphylaxis must be titrated to _ stability with monitoring.
cardiopulmonary
170
Despite aggressive treatment, severe anaphylactic reaction can persist from _ - _ hrs and pts will need to go to the ICU for _ hr of monitoring at least.
5-32 24
171
Barash Anaphylaxis mgmt during anesthesia -Initial tx:
Stop giving antigen if poss Airway and 100% O2 DC ALL anesthetic agents IV volume expansion -2-4L crystalloid/colloid for HoTN Give Epi -5-10mcg IV bolus for HoTN, titrate PRN -0.1-1mg IV for cardiovascular collapse
172
Barash Anaphylaxis mgmt during anesthesia -Secondary tx
Antihistamines -0.5-1mg/kg diphenhydramine Catecholamine infusion, titrated to desired effect -Epi 4-8mcg/min (HoTN and bspasm) -Norepi 4-8mcg/min (refractory shock) Bronchodilators -inhaled albuterol, terbutaline, and/or anticholinergic agents for persistant bronchospasm Corticosteroids -0.25-1g hydrocortisone (IgE rxns especially) OR -1-2g methylprednisolone (**DOC if thought to be complement-mediated or for Protamine rxns**) Airway check before extubation Refractory shock: vasopressin and additional monitoring/echo
173
T/F During an anaphylactic reaction under anesthesia, the use of the anesthetic agent as a bronchodilator is acceptable
false, not strong enough, esp if pt is hypotensive, more likely for cardiac collapse
174
Hypovolemia during anaphylactic reactions can cause up to _% loss of intravascular fluid into the interstitial space.
40%
175
If giving 2-4L or LR or NS doesn't help during anaphylaxis and pt is still hypotensive, can give an extra _-_mL/kg.
25-50mL/kg
176
What would cause the CRNA to seek out additional hemodynamic monitoring during anaphylaxis?
refractory HoTN -get a TEE if poss
177
_ _ pulmonary edema with loss of intravascular volume can occur after anaphylaxis
Fulminant noncardiogenic -requires intravascular repletion with careful hemodynamic monitoring until capillary defect improves
178
DOC for anaphylactic shock
epi
179
How does Epi help in anaphylaxis?
-alpha-adrenergic effects vasoconstrict to reverse HoTN -beta 2 stimulation bronchodilates and inhibits mediator release by increasing cAMP in mast cells and basophils
180
Why would a pt under spinal anesthesia need more catecholamines during anaphylaxis?
they may be partially sympathectomized
181
How to set up 5-10mcg boluses of Epi for anaphylaxis:
-get 0.5 or 1mL of epi from a 1:10,000 solution (100mcg/mL) OR -mix 2mg epi into 250mL bag to get 8mcg/mL
182
What is the ideal method of Epi admin during anaphylaxis?
infusion -not always practical tho
183
Y/N Your pt is experiencing anaphylaxis but their BP is 102/75 and no laryngeal edema noted, give IV Epi still?
No
184
Y/N Your pt is experiencing anaphylaxis but their BP is 102/75 but they have mild laryngeal edema, give IV Epi still?
NO, GIVE SUBCUTANEOUSLY
185
T/F H2 agonists are to be given in all forms of anaphylaxis.
FALSE H1 ANTagonists, not H2 agonists
186
Which kind of antihistamine should be given in all forms of anaphylaxis?
H1 antagonists
187
Why give H1 antagonists via IV slowly during anaphylaxis?
they also have antidopaminergic effects and can cause precipitous HoTN in hypovolemic pts
188
Epi infusions may be needed in pts with persistent _ or _ after initial initial resusc.
HoTN and bronchospams
189
T/F Epi infusions are ideal for refractory HoTN from decreased SVR during anaphylaxis
False Norepi
190
Which bronchodilator may be particularly useful during anaphylaxis if the pt takes beta blockers?
Ipratropium
191
High dose corticosteroids should be given early during anaphylaxis despite not being truly beneficial until _-_hr later.
4-6
192
If a pt's face is edematous after anaphylaxis, their _ probably is too.
airway -keep intubated until edema subsides and check an air leak test to see if safe to extubate and DL to be sure
193
Vasodilatory shock is characterized by HoTN with _ CO
HIGH not low! -inability of alpha-adrenergic mechs to compensate
194
Starting dose for vasopressin:
0.01unit/min
195
Predictable adverse drug rxns account for _% of adverse drug effects
80%
196
Most serious predictable drug reactions are toxic and directly related to _ or an unintended route of admin.
overdose
197
The most common type of adverse drug reaction are _ _ and they happen at normal doses.
side effects -drug interactions as well
198
Net effects of morphine on BP depend on:
-blood volume -sympathetic tone -ventricular function
199
T/F Unpredictable adverse reactions to drugs are usually dose-dependent and not related to the drugs pharmacologic actions but often related to non-immune response of the individual.
False immune response (allergy), not non-immune
200
In absence of prior drug exposure, allergic symptoms rarely appear less than_ wks of continuous treatment.
1wk
201
T/F Even if a new drug for the pt has been administered with no issue for several months, it is still likely the cause of an allergic reaction
false
202
The most vital information in determining which drugs are responsible for an allergic reaction is:
time between exposure and symptoms
203
T/F Any one antigen can produce diffuse spectrum of allergic responses in pts
true -PCN can cause type I- type IV reactions or all 4 depending on pt and other factors
204
T/F Most anesthetic agents have been reported to produce anaphylactic reactions
TRUE
205
_ are the most common drugs responsible for evoking INTRAOPERATIVE allergic reactions
MRs
206
T/F There is no cross sensitivity between Succinylcholine and NDMR
false
207
Unexplained intraoperative cardiovascular collapse has been attributed to anaphylaxis triggered by _
latex
208
T/F If a pt has a history of allergies, they should be assumed to be allergic to anesthetic drugs and be given pretreatment
false -history of allergies alone is a poor predictor
209
Anesthetic agents implicated in Allergic Reactions During Anesthesia
Induction agents -cremophor-solubilizing drugs -barbiturates -etomidate -propofol LA -para-aminobenzoic ester agents MR -sux -pancuronium -d-tubocurarine -metocurine -atracurium -vecuronium -mivacurium Opioids -meperidine -morphine -fentanyl
210
Other agents implicated in allergic reactions during anesthesia
-Abx (PCN, quinolones, sulfonamides, vanco, cephalosporins) -Aprotinin -Blood products -bone cement -chlorhexidine -steroids -heparin -lasix -cyclosporine -chymopapain -mannitol -**protamine** -contrast -latex -sugammadex -colloids -vasc graft material
211
The most important factor in diagnosis of allergies is the awareness of the physician that the event may be related to _ the pt received
drugs
212
The only way to PROVE an allergic reaction is _ _ but this is not safe
direct challenge
213
T/F Anesthesia-given test doses are the same in test doses given for allergy testing
false
214
The demonstration of _-specific Ig_ antibodies is accepted as evidence that the pt is at risk for anaphylaxis if the drug is given.
drug-specific IgE
215
Leukocyte Histamine release allergy tests are associated with false-_ and are therefore not used really.
positives
216
T/F The enzyme-linked immunosorbent assay (ELISA) measures drug-specific antibodies.
false, antigen-specific, not drug
217
ELISA evaluates immunospecific Ig_ directed against the suspected antigen, and has been used to prove Ig_ antibodies in proteins such as _.
IgE IgE Protamine
218
T/F ELISA testing that proves antibodies will always illicit a symptomatic reaction
false could be asymptomatic
219
_ testing is a method most often used AFTER anaphylactic reactions to anesthetic drugs.
Skin
220
Skin allergy testing causes a _ and _ representing cutaneous vasodilation and local edema respectively within minutes of exposure.
flare and wheal
221
T/F Intradermal testing is so accurate, it can detect even colloid and contrast allergies.
false
222
T/F Skin allergy testing can be used to determine cross-sensitivities of similar drugs
true
223
The most common drugs to cause anaphylaxis during the perioperative period include:
-abx -blood products -chlorhexidine -NMBD -polypeptides (aprotinin, latex, protamine) -intravascular volume expanders
224
Most cases of anaphylaxis involve Ig_
E
225
In the periop setting, which drug has a higher chance of causing anaphylaxis, NMBD or abx?
Abx!!! not NMBD
226
T/F If a pt has an allergy to a NMBD there is a good chance they have cross sensitivity to another type of MR.
true -pt should get allergy test before receiving another one
227
2 main prophylactic abx for surgery:
-vanco -cephalosporins
228
T/F You can have an allergy to cephalosporins without an allergy to penicillin
true
229
What abx can a pt with a penicillin allergy have prophylactically?
Vanco
230
Your pt with a penicillin allergy receives vanco and after admin experiences severe HoTN and flushing, why could this be happening?
-vanco releases histamine and if given too quickly can cause these effects (REDMAN syndrome, just slow gtt down)
231
There is a high cross sensitivity between penicillins and _ generation cephalosporins.
1st gen
232
Even tho most pts will be ok if they have a penicillin allergy and receive cephalosporin, they shouldn't indiscriminately get them, especially if the pt has had reactions to _ _ abx
beta lactam -give them a skin test to see if they still have IgE antibodies, if they do, avoid cephs
233
Latex allergy is an immediate Ig_ hypersensitivity reaction to latex proteins
IgE
234
Populations at risk for latex allergy:
-HC workers -kids with spina bifida or urogenital abnormalities -certain food allergies (bananas, avocado, kiwi-cross sensitivity with **latex**) -atopy (genetic condition where you get allergies easily, esp **latex**)
235
T/F Latex allergy pts should wear a Medic Alert bracelet
true
236
2 types of LA skin tests
-direct challenge or provocative dose testing -helps determine if pt can have amides or esters
237
_ LA skin tests are uncommon and the LA skin tests have an excellent _ predictive value
Positive Negative
238
T/F LA allergies are true allergies
false, pseudo allergies or NONimmune responses
239
Who experiences NMBA allergies more, men or women?
women
240
Steroidal-derived NMBAs and other similar molecules can produce false _ skin tests
positive -this is bc most NMBA have cutaneous vascular effects even in small doses
241
Cell-mediated immunity involves:
-T cells -phagocytes -cytokines immune cells directed at eliminating or destroying pathogens/cells
242
Humoral immunity involves:
-antibodies and proteins (complement cascade) -B cells -fluids of body and liquid noncellular components like plasma/lymph
243
B and T cells are part of _ immunity and are specific
acquired -not innate! -directed at microbes(specific)
244
Complete antigens can cause full responses whereas incomplete antigens require assistance such as _ _.
carrier proteins
245
Haptens are considered _ antigens
incomplete -not an antigen by itself
246
Examples of complete antigens:
Protamine -positive charge, binds with negative heparin to neutralize it -acts as an antigen and binds with IgE, causing cell degranulation and histamine release (immune reaction) Dextran -large macromolecules, colloid volume expanders
247
_ T cells inhibit immune function
suppressor
248
_ T cells destroy MEMBRANES but not the actual cell, other cells do this
killer
249
_ T cells are complements to killer T cells
Cytotoxic
250
T/F T cells secrete antibodies
false B cells do this
251
Which B cells perform opsonization, memory or effector cells?
effector
252
T cells are made in the thymus and B cells are made in the _
bone
253
T/F Anaphylactoid (non-immune) reactions do not require a previous exposure
true -think IV contrast -directly starts complement or releases histamine
254
T/F Mast cells and basophils are involved in anaphylactoid (nonimmune) reactions
false -JUST mast cells
255
When mast cells are degranulated and basophils release inflammatory mediators, which substances are released?
main ones she cares about: Tryptase Prostaglandin D2 Leukotriene LTC4 TNF
256
What does tryptase do?
released by basophils when mast cells degranulate activates preKallikreain and complement, bradykinin and anaphylactoxins (C3a, C5a) **check this lab if pt is having or has had anaphylactic rxn to confirm**
257
What does prostaglandin D2 do?
released by basophils when mast cells degranulate causes: bronchoconstriction pulm and cardiac vasoconstriction periph vasodilation vasc permeability HoTN flushing urticaria
258
What does LEukotriene LTC4 do?
released by basophils when mast cells degranulate causes: bronchoconstriction airway remodeling angioedema nitric oxide induction vasc permeability HoTN
259
What does TNF do?
released by basophils when mast cells degranulate causes: neutrophil activation chemokines cytokines effector cell recruitment
260
What kind of reaction would a TB skin test be?
type 4
261
What kind of reaction would hemolytic reaction be?
type 2
262
What kind of reaction does NOT use immunoglobulin?
Type IV -it is T CELL mediated
263
Why would you miss a lot of s/s of anaphylaxis in anesthetized pts?
-pt cannot communicate -drugs can blunt effects/ pain -pt is already intubated so airway signs could be missed or hard to notice -drapes can get in way of seeing cutaneous changes -cutaneous s/s are sometimes transient
264
Which immunoglobulin is the most abundant?
IgG
265
What are some signs on the vent that will show if pt is having anaphylaxis?
Bronchospasm -low or no EtCO2 -low SaO2 -high PIP -mucus plugging from laryng edema
266
Order of most common drugs causing anaphylaxis perioperatively: _>Latex>_
MR>latex> Abx
267
Which MR is most likely to cause anaphylaxis?
Sux -molecule is flexible an can easily cross link with IgE bc it is **DIVALENT**
268
Which MR classes are more common to cause anaphylaxis, benzylisoquinolinium or amino-steroid complexes?
Benzylisoquinolinium
269
T/F Pt is allergic to Roc, is Vec ok?
no
270
Why could someone having Roc for the first time have an anaphylactic reaction?
The metabasulfites that cause the reaction are in a lot of household products
271
#1 agent that causes anaphylaxis in kids?
latex
272
T/F Both medical devices and med vials must be labeled to say whether there is latex in them or not
False med vials dont for some reason
273
T/F Ok to pretreat for latex allergies?
true! -won't prevent attack, but can attenuate some s/s
274
Why would a 1st gen cephalosporin and PCN both possible cause reaction?
they both have a beta lactam ring -cant really swap pcn for ancef (but we still do sometimes) -best bet go with vanco
275
In the GENERAL PUBLIC, which causes anaphylaxis more, abx or MR?
Abx
276
Y/N Can a pt with a shellfish allergy have Protamine? What about a fish allergy?
Shellfish = yes Fish= no protamine comes from salmon sperm
277
Pts at higher risk of Protamine allergy:
-vasectomy (salmon sperm factors compete somehow?) -salmon/fish allergy -insulin use (NPH-P stands for protamine)
278
Pt has environmental allergies and takes various medications for them, what could they be taking and what effects could it have?
pseudophedrine - high BP antihistamine - increased duration/effect of drugs nasal inhaled corticosteroids - BG, HTN
279
How to get 10mcg of Epi to give in boluses from 1mg/mL Epi?:
-Draw 1mL (100mcg) then dilute with 9ml SW = 10mcg/mL -give MORE epi in spinal pts bc response will be blunted
280
Why is Epi the gold standard for anaphylaxis?
-prevents degranulation of mast cells -CV support -Dilates airway
281
How to give 1 unit of vaso in 20unit.mL vial?
get 20mL syringe, draw 1mL, the n19mL of saline = 1unit/mL
282
What can be given if anaphylactic pt is on b blocker and HoTN despite everything?
Glucagon! -antidote for beta blockers! 1-5mg IVP or 20-30mcg/kg
283
T/F Use methylene blue for refractory HoTN if other methods are exhausted
true -stops nitric oxide synthetase 1-2mg/kg bolus, then 0.5mg/kg/hr infusion
284
T/F Sulfa allergies carry cross sensitivity
false
285
Which blue dye is known to CAUSE hypersensitivity reactions?
Isosulfan blue -not methylene blue- used for refractory HotN
286
If pt has allergic reaction to roc, which MR can they theoretically have?
cisatracurium
287
Under anesthesia, Type I allergic reactions will present with which 4 s/s?
-HoTN -Bronchospasm -Increased PIP -Urticaria
288
Y/N Ok to use H1 blockers if pt is having CV collapse?
no