Allergy - Exam 4 Flashcards

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
Q

Examples of COMPLETE antigens that anesthetists use:

A

-large macromolecules (dextrans)
-polypeptides (protamine)

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26
Q

Most commonly used drugs are simple organic compounds of _ molecular wt (_ Da)

A

low
1000 Da

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27
Q

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

A

proteins
hapten-macromolecular complex

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28
Q

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

A

False. All is true except haptens by themself are NOT antigenic

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29
Q

A reactive drug metabolite such as _ derivative of penicillin is believed to bind with macromolecules to become _

A

penicilloyl
antigens

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30
Q

Agents given during anesthesia that act as antigens
-Haptens

A

-penicillin and its derivatives
-anesthetic drugs

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31
Q

Agents given during anesthesia that act as antigens
-Macromolecules

A

-Aprotinin
-Blood products
-Chymopapain
-Colloid Volume Expanders
-NMBD
-Protamine
-Latex

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32
Q

The _ of the fetus differentiates immature _ into -derives cells ( cells)

A

thymus
lymphocytes
thymus (T cells)

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33
Q

_ cells have receptors that are activated by binding with foreign antigens and secrete mediators that regulate the immune response

A

T cells

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34
Q

Subpopulations of T cells=

A

-helper
-suppressor
-cytotoxic
-killer

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35
Q

The 2 kinds of regulatory T cells are _ (OKT4) cells and _ cells (OKT8)

A

-helper (OKT4)
-suppressor (OKT8)

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36
Q

_ T cells are important for key _ cell responses whereas _ T cells inhibit immune function.

A

Helper
Efferent
suppressor

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37
Q

Infection of _ T cells by the retrovirus, HIV, produces a specific increase in the number of _ T cells

A

helper
suppressor

-fuck HIV dude :’(

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38
Q

_ T cells destroy mycobacteria, fungi, and viruses.

A

Cytotoxic

-NOT the killer T cells

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39
Q

_ T cells do not require a specific antigen to stimulate them to work

A

Killer

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40
Q

Both _ and _ T cells take part in the defense against tumor cells and in transplant rejection.

A

cytotoxic and killer

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41
Q

T cells produce _ that influence the response of other cell types involved in recognizing and destroying foreign substances.

A

mediators

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42
Q

_ 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.

A

B cell
antibodies
helper
T

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43
Q

B cells are also called _ -derived cells.

A

bursa

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44
Q

Antibodies are specific _ called _ that recognize and bind to a specific antigen.

A

proteins
immunoglobulins

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45
Q

Each antibody is composed of at least 2 _ chains and 2 _ chains that are bound together by _ bonds.

A

heavy
light
DISULFIDE

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46
Q

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)

A

Fab (light chain)
Fc (heavy chain)

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47
Q

_ function as specific receptor molecules for immune cells and proteins

A

antibodies

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48
Q

When antigens bind _ to the _ fragments, the antibody undergoes conformational changes to activate the _ receptor.

A

covalently
Fab
Fc

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49
Q

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.

A

histamine
mast cell
complement

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50
Q

Multiple therapeutic agents are based on _ fragments that bind IRREVERSIBLY to a specific molecular configuration or drug.

A

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)

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51
Q

What cleaves an immunoglobulin into 2 fab fragments and one Fc fragment?

A

Papain

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52
Q

Antigen binding occurs at that _ fragments and the _ fragment is responsible for membrane binding or complement activation.

A

Fab
Fc

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53
Q

5 major classes of antibodies:

A

IgG
IgA
IgM
IgE
IgD

GAMED

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54
Q

_, _ (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.

A

Monocytes
neutrophils
eosinophils
effector cells

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55
Q

The deposition of antibody or complement fragments on the surface of foreign cells is called _, which marks them to be killed by _ cells.

A

opsonization
effector

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56
Q

Complex acute inflammatory responses cause _ injuries.

A

host

-like with COVID-19

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57
Q

_ regulate immune responses by eating, processing, and presenting antigens to affect inflammatory, tumoricidal, and microbicidal functions.

A

Macrophages

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58
Q

Macrophages arise from circulating _ or can be confined to specific organs like the _

A

monocytes
lungs

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59
Q

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.

A
  1. microorganisms
  2. ingest, lymphocyte
  3. mediators, B and T lymphocyte
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60
Q

The first cells to appear in an acute inflammatory reaction are _ that contain _ hydrolases, _ proteases, and lysosomes.

A

neutrophils
acid
neutral

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61
Q

Once neutrophils are activated, they make hydroxyl _, _, and hydrogen _ which help kill microbes.

A

radicals, superoxide, peroxide

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62
Q

Although their function is unclear, inflammatory cells recruit _ to collect at sites of parasitic infections, tumors, and allergic reactions.

A

eosinophils

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63
Q

_ comprise 0.5-1% of circulating granulocytes in the blood and have _ receptors on their surface which work like those on mast cells.

A

Basophils
IgE

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64
Q

_ cells are important for _ _ responses and have _ receptors on their surface which bind to specific antigents.

A

Mast
immediate hypersensitivity
IgE

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65
Q

Mast cells are fixed in _ and found in _ spaces of the _, _, and .

A

tissues
perivascular
skin, lung, and intestine

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66
Q

Mast cells are activated by a series of both _ and _ stimuli and once activated, they release physiologically active _ important to _ _ responses.

A

immune and nonimmune
mediators
immediate hypersensitivity

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67
Q

_ are inflammatory cell activators made by _ to act as second messengers and activate _ and _ cells.

A

Cytokines
macrophages
endothelial and white cells

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68
Q

Examples of cytokines:

A

-interleukins
-tumor necrosis factor
-interferon

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69
Q

Release of interleukin-1 and TNF cause:

A

-fever
-neuropeptide release
-endothelial cell activation
-increased adhesion molecule expression
-neutrophil priming
-HoTN
-myocardial suppression
-catabolic state

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70
Q

_ help other lymphocytes communicate.

A

interleukins

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71
Q

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.

A

regulatory proteins/polypeptides

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72
Q

T cell lymphocytes influence the activity of other immunologic and nonimmunologic cells by making an array of _ and secreting them.

A

interleukins

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73
Q

The PRIMARY humoral response to antigen and antibody binding is the activation of the _ system

A

complement

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74
Q

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.

A

effector
20

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75
Q

Complement activation can be activated by:

A

-IgG or IgM binding to an antigen
-by plasmin thru the classic pathway
-by endotoxin
-by drugs thru alternate (properdin) paths

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76
Q

Specific fragments released during complement activation include:

A

-C3a
-C4a
-C5a

-have important humoral and chemotactic properties

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77
Q

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

A

phagocytes
phagocytes
lysis

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78
Q

C_ and C_ make fragments of the complement activation cascade, which are both are called _ and are potent vasoactive mediators

A

C3 and C5
anaphylactoxins (C3a, C5a)

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79
Q

Classic complement activation is started by _ esterase due to Ig_ or Ig_ antigens.

A

C1
IgG or IgM

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80
Q

An inhibitor of the complement cascade, the _ _ inhibitor ensures the system is turned off most of the time.

A

C1 esterase inhibitor

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81
Q

Alternative complement activation occurs via _ and _ interactions

A

endotoxin and drug

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82
Q

_ or _ angioedema is an example of a deficiency in an inhibitor of the C1esterase complement system.

A

Hereditary or acquired

-C1 esterase deficiency

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83
Q

Hereditary angioedema is autosomal _

A

dominant

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84
Q

T/F Hereditary angioedema is associated with lymphoma, lymphosarcoma, chronic lymphatic leukemia, and macroglobinemia.

A

false,
acquired angioedema

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85
Q

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.

A

angioedema
vascular
laryngeal

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86
Q

A significant pathophysiological manifestation of complement activation from PROTAMINE admin is _ _

A

pulmonary vasoconstriction

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87
Q

T/F Anesthesia and surgery depress specific host resistance mechanisms like lymphocyte activation and phagocytosis.

A

false
NONspecific

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88
Q

Factors influencing immune competence during surgery:

A

-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

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89
Q

4 kinds of hypersensitivity (allergic) reactions

A

type I-IV

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90
Q

Type _ reactions are anaphylactic or immediate-type hypersensitivity reactions.

A

type I

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91
Q

Type I hypersensitivity reactions include:

A

-anaphylaxis
-extrinsic asthma
-allergic rhinitis

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92
Q

Type I reactions cause physiologically active mediators to be released by _ cells and _ after antigen binding to Ig_ antibodies on membranes of these cells.

A

mast cells
basophils
IgE

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93
Q

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 _.

A
  1. IgE, Fc
  2. IgE, degranulation, mediators

-this reaction is independent of complement

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94
Q

T/F A type I reaction relies on the complement pathway.

A

false

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95
Q

Type _ reactions are AKA antibody-dependent cell-mediated cytotoxic reactions OR cytotoxic hypersensitivity

A

type II

think transfusion reactions (ABO incompatibility, HIT, drug-induced hemolytic anemia)
IgM or IgG

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96
Q

Type II reactions are mediated by either Ig_ or Ig_ antibodies directed against antigens on the surface of foreign cells.

A

IgG or IgM

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97
Q

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).

A

integral
haptens
anti-hapten antibodies

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98
Q

The cell damage in type II reactions is causes by:

A

-direct cell lysis after completement activation
-increased phagocytosis by macrophages
-killer T cell lymphocytes making antibody-dependent cell-mediated cytotoxic effects

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99
Q

Examples of type II reactions:

A

-ABO incompatibility transfusion reactions
-drug-induced immune hemolytic anemia
-heparin-induced thrombocytopenia (HIT)

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100
Q

Type _ reactions are caused by circulating soluble antigens and antibodies that bind to make insoluble complexes that settle in the microvasculature.

A

Type III

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101
Q

In type III reactions, the _ is activated and _ are localized to the site of _ deposition to cause tissue damage.

A

complement
neutrophils
complement

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102
Q

Examples of Type III reactions:

A

-classic serum sickness from snake bite antisera or antithymocyte globulin, SLE
-immune complex injury

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103
Q

Type III reactions can occur thru mechanisms of _-mediated pulmonary vasoconstriction

A

protamine

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104
Q

Type III reactions are AKA _ _ reactions

A

immune complex

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105
Q

Type _ reactions occur from interactions of sensitized lymphocytes with specific antigens.

A

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!!!!

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106
Q

Type IV reactions are AKA _ _ reactions and require _ contact.

A

delayed hypersensitivity
second

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107
Q

Type IV reactions are mainly _.

A

mononuclear

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108
Q

Type IV reaction timeline:
-onset
-peak
-duration

A

onset: 18-24hr
peak: 40-80hr
duration: 72-96hr

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109
Q

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.

A
  1. LYMPHOKINE, lymphocyte, cytotoxic
  2. cytotoxic, macrophages
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110
Q

T/F Killer T cells are made specifically to kill target cells that bear antigens identical to those triggering the reaction.

A

False,
cytotoxic, killer T cells are nonspecific

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111
Q

Type IV reactions are involved with reactions such as:

A

-tissue rejection
-graft-vs-host reactions
-contact dermatitis (poison ivy)
-tuberculin immunity

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112
Q
A

complement
plymorphonuclear

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113
Q

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.

A

4%
2%

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114
Q

More than 90% of allergic reactions evoked by IV drugs occur within _ min of administration.

A

5min

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115
Q

Most common life-threatening manifestations of allergic reactions in anesthetized pt include:

A

-circulatory collapse (vasodilation and decreased venous return)

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116
Q

The only manifestation of an allergic reaction may be refractory _ in anesthetized pts.

A

HoTN

117
Q

When life-threatening allergic reactions mediated by antibodies occur, they are called _

A

anaphylactic AKA anaphylactoid

118
Q

T/F Type IV reactions require complement activation

A

false
TYPE II and III

119
Q

Recognition of anaphylaxis in regional or GA
-Respiratory s/s

A

-dyspnea
-chest discomfort
-coughing
-wheezing
-sneezing
-laryngeal edema
-decreased compliance
-fulminant pulmonary edema
-acute resp failure

120
Q

Recognition of anaphylaxis in regional or GA
-Cardiovascular s/s

A

-dizziness
-malaise
-retrosternal oppression
-disorientation
-sweating
-loss of consciousness
-HoTN
-dysrhythmias
-decreased SVR
-arrest
-pulm HTN

121
Q

Recognition of anaphylaxis in regional or GA
-cutaneous s/s

A

-itch
-burning
-tingling
-urticaria(hives)
-flushing
-periorbital edema
-perioral edema

122
Q

Antigen binding to Ig_ antibodies cause anaphylaxis

A

IgE

123
Q

T/F Anaphylaxis usually occurs on first contact of a substance

A

false
-prior exposure is needed to produce sensitization

124
Q

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.

A
  1. mast
  2. histamine, tryptase,
  3. leukotrienes and prostaglandins, cytokines
  4. bronchospasm, edema, permeability

-this process is ENERGY and CALCIUM dependent

125
Q

Histamine released during anaphylaxis stimulates which 3 receptors:

A

H1, H2, H3

126
Q

H1 receptor functions once activated:

A

-releases endothelium-derived relaxing factor (nitric oxide) from vasc endothelium
-increases cap permeability
-contracts airway and vasc smooth muscle

127
Q

H2 receptor activation causes:

A

-gastric secretion
-inhibits mast cell activation
-contributes to vasodilation

128
Q

When injected into skin, histamine produces a classic _ and _ response

A

wheal and flare

-increased cap permeability/ tissue edema and cutaneous vasodilation effect

129
Q

Histamine undergoes a _ metabolism by enzymes histamine - and _ _ found in _ cells.

A

rapid
N-methyltransferase
diamine oxidase
endothelial

130
Q

Factors are released from mast cells and basophils and cause _ migration (chemotaxis) and collect at the site of the inflammatory stimulus

A

granulocytes

131
Q

_ chemotactic factor of anaphylaxis (ECF-A) is a small molecular wt peptide chemotactic for _ and release enzymes that inactivate _ and _.

A

Eosinophilic
eosinophils
histamine and leukotrienes

132
Q

During anaphylaxis, a _ chemotactic factor is released that causes chemotaxis and activation of _ which may be responsible for recurrent manifestations of anaphylaxis.

A

neutrophilic
neutriphils

133
Q

_ and _ are made after mast cell activation from arachidonic acid metabolism of _ cell membranes thru either _ or _ pathways.

A

Leukotrienes and prostaglandins
phospholipid
lipoxygenase or cyclooxygenase

134
Q

The classic slow reacting substance of anaphylaxis is a combo of leukotrienes _, _, and _.

A

C2, D4, and E4

135
Q

Which produces a stronger bronchoconstriction effect, leukotrienes or histamine?

A

leukotrienes

136
Q

Leukotrienes cause:

A

-bronchoconstriction (more than histamine)
-increased cap permeability
-vasodilation
-CORONARY vasoconstriction
-myocardial depression

137
Q

_ _ is the major metabolite of mast cells and causes bronchospasm and vasodilation

A

Prostaglandin D2

138
Q

Prostaglandins are potent mast cell mediators and cause:

A

-vasodilation
-bronchospasm

139
Q

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.

A

thromboxane B2
prostaglandin

140
Q

Small peptides called _ are made by mast cells and basophils.

A

kinins

141
Q

Kinins cause:

A

-increased cap permeability
-vasodilation
-bronchoconstriction

142
Q

Kinins stimulate _ endothelium to release _ factors, including _ and endothelium-derived relaxing factors like _ oxide.

A

vascular
vasoactive
prostacyclin
nitric

143
Q

- _ is an UNSTORED lipid made in activated mast cells.

A

platelet-activating factor (PAF)

144
Q

The more severe of an allergic reaction, the _ their PAF levels will be.

A

higher

145
Q

Platelet-activating factor (PAF) aggregates and activates _ and _ to release inflammatory products.

A

platelets and leukocytes

146
Q

The onset and severity of anaphylaxis is dependent on the ’s specific end- effects

A

mediator
organ

147
Q

Antigenic challenge in a sensitized pt usually causes immediate clinical manifestations of anaphylaxis but the onset ay be delayed by _ - _ min

A

2-20min

148
Q

T/F All anaphylactic reactions run the same course in each individual

A

false
-spectrum-like, varying manifestations

149
Q

Biologic effects of anaphylaxis (Barash):

A

-histamine release
-smooth musc contraction
-increased vasc permeability
-chemotaxis (movement of compounds thru body)
-leukocyte and platelet aggregation
-interleukin release

150
Q

C3a mediated biologic processes of anaphylaxis:

A

-histamine release
-smooth musc contraction
-increased vasc permeability
-chemotaxis (movement of compounds thru body)
-leukocyte and platelet aggregation
-interleukin release

151
Q

C5a mediated biologic processes of anaphylaxis

A

-histamine release
-smooth musc contraction
-increased vasc permeability
-interleukin release

-NOT chemotaxis and leukocyte/platelet aggregation

152
Q

Other immunologic and nonimune mechanisms release the same mediators independently from IgE, creating an _ like syndrome.

A

anaphylactoid

153
Q

Complement activation follows both _ (antibody/classic) and _(alt) pathways to a series of multi-molecular self assembling proteins that release active fragments of _ and _

A

immune and nonimmune
C3 and C5

154
Q

C3a and C5a are called _ because they release _ from mast cells and basophils, contract _ muscle, increase cap permeability, and cause _ synthesis.

A

anaphylactoxins
histamine
smooth
interleukin

155
Q

C5a interacts with specific high affinity receptors on _ and _ causing _ chemotaxis, aggregation, and activation.

A

PMNs(neutrophils) and platelets
leukocyte

156
Q

Aggregated leukocytes from C5a embolize to various organs causing _ occlusion and liberation of inflammatory products like _ _ metabolites, _ free radicals, and _ enzymes.

A

microvasculature
arachidonic acid metabolites
O2 free radicals
lysosomal

157
Q

Antibodies of the Ig_ class directed against antigenic determinants or _ surfaces can also cause _ aggregation like C5a. These Ig_ antibodies are called _.

A

IgG
granulocyte
leukocyte
IgG
leukoagglutinins

158
Q

Complement activation and PMN aggregation is involved in:

A

-transfusion reactions
-pulm vasoconstriction from protamine reactions
-ARDS
-septic shock

159
Q

Angioedema can occur from allergic reaction and also from _ deficiency states such as _ angioedema (HAE)

A

complement
hereditary

160
Q

HAE variants exist due to unopposed activation of multiple _ and mediators including _ and _, causing increased vascular permeability and edema

A

kinins
bradykinin and kallikrein

161
Q

HAE treatments include:

A

**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
Q

T/F Nonimmune release of histamine involves basophils but not mast cells.

A

false,
SPECIFIC mast cells, not basophils

163
Q

_ mast cells are the only cells that release _ in response to both drugs and endogenous stimuli (neuropeptides)

A

Cutaneous
histamine

164
Q

T/F histamine release is dependent on the mu receptor

A

false
-fentanyl and sufentanil do not release histamine

165
Q

T/F Because the newer muscle relaxers are more potent on the NM junction, they also release histamine more than other NMBD.

A

False
-regardless of potency on NM junction, all drugs that are mast cell degranulators are equally able to release histamine

166
Q

Aminosteroidal agents like _ and _ at clinically recommended doses have a _ effect on histamine release.

A

rocuronium and pancuronium
minor

167
Q

Drugs capable of NONimmunogenic histamine release:

A

-Abx ( vanco and pentamidine)
-basic compounds
-hyperosmotic agents
-MR (d-tubocurarine, metocurine, atracurium, mivacurium, doxacurium)
-opioids (morphine, meperidine, codeine)

168
Q

T/F Pretreating with antihistamines before giving drugs known to release it helps inhibit its release.

A

false
-they just compete with histamine at the receptor site and can attenuate decreases in SVR

169
Q

Treatment of anaphylaxis must be titrated to _ stability with monitoring.

A

cardiopulmonary

170
Q

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.

A

5-32
24

171
Q

Barash Anaphylaxis mgmt during anesthesia
-Initial tx:

A

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
Q

Barash Anaphylaxis mgmt during anesthesia
-Secondary tx

A

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
Q

T/F During an anaphylactic reaction under anesthesia, the use of the anesthetic agent as a bronchodilator is acceptable

A

false, not strong enough, esp if pt is hypotensive, more likely for cardiac collapse

174
Q

Hypovolemia during anaphylactic reactions can cause up to _% loss of intravascular fluid into the interstitial space.

A

40%

175
Q

If giving 2-4L or LR or NS doesn’t help during anaphylaxis and pt is still hypotensive, can give an extra _-_mL/kg.

A

25-50mL/kg

176
Q

What would cause the CRNA to seek out additional hemodynamic monitoring during anaphylaxis?

A

refractory HoTN
-get a TEE if poss

177
Q

_ _ pulmonary edema with loss of intravascular volume can occur after anaphylaxis

A

Fulminant noncardiogenic
-requires intravascular repletion with careful hemodynamic monitoring until capillary defect improves

178
Q

DOC for anaphylactic shock

A

epi

179
Q

How does Epi help in anaphylaxis?

A

-alpha-adrenergic effects vasoconstrict to reverse HoTN

-beta 2 stimulation bronchodilates and inhibits mediator release by increasing cAMP in mast cells and basophils

180
Q

Why would a pt under spinal anesthesia need more catecholamines during anaphylaxis?

A

they may be partially sympathectomized

181
Q

How to set up 5-10mcg boluses of Epi for anaphylaxis:

A

-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
Q

What is the ideal method of Epi admin during anaphylaxis?

A

infusion
-not always practical tho

183
Q

Y/N Your pt is experiencing anaphylaxis but their BP is 102/75 and no laryngeal edema noted, give IV Epi still?

A

No

184
Q

Y/N Your pt is experiencing anaphylaxis but their BP is 102/75 but they have mild laryngeal edema, give IV Epi still?

A

NO, GIVE SUBCUTANEOUSLY

185
Q

T/F H2 agonists are to be given in all forms of anaphylaxis.

A

FALSE
H1 ANTagonists, not H2 agonists

186
Q

Which kind of antihistamine should be given in all forms of anaphylaxis?

A

H1 antagonists

187
Q

Why give H1 antagonists via IV slowly during anaphylaxis?

A

they also have antidopaminergic effects and can cause precipitous HoTN in hypovolemic pts

188
Q

Epi infusions may be needed in pts with persistent _ or _ after initial initial resusc.

A

HoTN and bronchospams

189
Q

T/F Epi infusions are ideal for refractory HoTN from decreased SVR during anaphylaxis

A

False
Norepi

190
Q

Which bronchodilator may be particularly useful during anaphylaxis if the pt takes beta blockers?

A

Ipratropium

191
Q

High dose corticosteroids should be given early during anaphylaxis despite not being truly beneficial until _-_hr later.

A

4-6

192
Q

If a pt’s face is edematous after anaphylaxis, their _ probably is too.

A

airway
-keep intubated until edema subsides and check an air leak test to see if safe to extubate and DL to be sure

193
Q

Vasodilatory shock is characterized by HoTN with _ CO

A

HIGH
not low!
-inability of alpha-adrenergic mechs to compensate

194
Q

Starting dose for vasopressin:

A

0.01unit/min

195
Q

Predictable adverse drug rxns account for _% of adverse drug effects

A

80%

196
Q

Most serious predictable drug reactions are toxic and directly related to _ or an unintended route of admin.

A

overdose

197
Q

The most common type of adverse drug reaction are _ _ and they happen at normal doses.

A

side effects

-drug interactions as well

198
Q

Net effects of morphine on BP depend on:

A

-blood volume
-sympathetic tone
-ventricular function

199
Q

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.

A

False
immune response (allergy), not non-immune

200
Q

In absence of prior drug exposure, allergic symptoms rarely appear less than_ wks of continuous treatment.

A

1wk

201
Q

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

A

false

202
Q

The most vital information in determining which drugs are responsible for an allergic reaction is:

A

time between exposure and symptoms

203
Q

T/F Any one antigen can produce diffuse spectrum of allergic responses in pts

A

true
-PCN can cause type I- type IV reactions or all 4 depending on pt and other factors

204
Q

T/F Most anesthetic agents have been reported to produce anaphylactic reactions

A

TRUE

205
Q

_ are the most common drugs responsible for evoking INTRAOPERATIVE allergic reactions

A

MRs

206
Q

T/F There is no cross sensitivity between Succinylcholine and NDMR

A

false

207
Q

Unexplained intraoperative cardiovascular collapse has been attributed to anaphylaxis triggered by _

A

latex

208
Q

T/F If a pt has a history of allergies, they should be assumed to be allergic to anesthetic drugs and be given pretreatment

A

false

-history of allergies alone is a poor predictor

209
Q

Anesthetic agents implicated in Allergic Reactions During Anesthesia

A

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
Q

Other agents implicated in allergic reactions during anesthesia

A

-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
Q

The most important factor in diagnosis of allergies is the awareness of the physician that the event may be related to _ the pt received

A

drugs

212
Q

The only way to PROVE an allergic reaction is _ _ but this is not safe

A

direct challenge

213
Q

T/F Anesthesia-given test doses are the same in test doses given for allergy testing

A

false

214
Q

The demonstration of -specific Ig antibodies is accepted as evidence that the pt is at risk for anaphylaxis if the drug is given.

A

drug-specific
IgE

215
Q

Leukocyte Histamine release allergy tests are associated with false-_ and are therefore not used really.

A

positives

216
Q

T/F The enzyme-linked immunosorbent assay (ELISA) measures drug-specific antibodies.

A

false, antigen-specific, not drug

217
Q

ELISA evaluates immunospecific Ig_ directed against the suspected antigen, and has been used to prove Ig_ antibodies in proteins such as _.

A

IgE
IgE
Protamine

218
Q

T/F ELISA testing that proves antibodies will always illicit a symptomatic reaction

A

false
could be asymptomatic

219
Q

_ testing is a method most often used AFTER anaphylactic reactions to anesthetic drugs.

A

Skin

220
Q

Skin allergy testing causes a _ and _ representing cutaneous vasodilation and local edema respectively within minutes of exposure.

A

flare and wheal

221
Q

T/F Intradermal testing is so accurate, it can detect even colloid and contrast allergies.

A

false

222
Q

T/F Skin allergy testing can be used to determine cross-sensitivities of similar drugs

A

true

223
Q

The most common drugs to cause anaphylaxis during the perioperative period include:

A

-abx
-blood products
-chlorhexidine
-NMBD
-polypeptides (aprotinin, latex, protamine)
-intravascular volume expanders

224
Q

Most cases of anaphylaxis involve Ig_

A

E

225
Q

In the periop setting, which drug has a higher chance of causing anaphylaxis, NMBD or abx?

A

Abx!!!
not NMBD

226
Q

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.

A

true

-pt should get allergy test before receiving another one

227
Q

2 main prophylactic abx for surgery:

A

-vanco
-cephalosporins

228
Q

T/F You can have an allergy to cephalosporins without an allergy to penicillin

A

true

229
Q

What abx can a pt with a penicillin allergy have prophylactically?

A

Vanco

230
Q

Your pt with a penicillin allergy receives vanco and after admin experiences severe HoTN and flushing, why could this be happening?

A

-vanco releases histamine and if given too quickly can cause these effects (REDMAN syndrome, just slow gtt down)

231
Q

There is a high cross sensitivity between penicillins and _ generation cephalosporins.

A

1st gen

232
Q

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

A

beta lactam

-give them a skin test to see if they still have IgE antibodies, if they do, avoid cephs

233
Q

Latex allergy is an immediate Ig_ hypersensitivity reaction to latex proteins

A

IgE

234
Q

Populations at risk for latex allergy:

A

-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
Q

T/F Latex allergy pts should wear a Medic Alert bracelet

A

true

236
Q

2 types of LA skin tests

A

-direct challenge or provocative dose testing

-helps determine if pt can have amides or esters

237
Q

_ LA skin tests are uncommon and the LA skin tests have an excellent _ predictive value

A

Positive
Negative

238
Q

T/F LA allergies are true allergies

A

false, pseudo allergies or NONimmune responses

239
Q

Who experiences NMBA allergies more, men or women?

A

women

240
Q

Steroidal-derived NMBAs and other similar molecules can produce false _ skin tests

A

positive
-this is bc most NMBA have cutaneous vascular effects even in small doses

241
Q

Cell-mediated immunity involves:

A

-T cells
-phagocytes
-cytokines

immune cells directed at eliminating or destroying pathogens/cells

242
Q

Humoral immunity involves:

A

-antibodies and proteins (complement cascade)
-B cells
-fluids of body and liquid noncellular components like plasma/lymph

243
Q

B and T cells are part of _ immunity and are specific

A

acquired
-not innate!
-directed at microbes(specific)

244
Q

Complete antigens can cause full responses whereas incomplete antigens require assistance such as _ _.

A

carrier proteins

245
Q

Haptens are considered _ antigens

A

incomplete
-not an antigen by itself

246
Q

Examples of complete antigens:

A

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
Q

_ T cells inhibit immune function

A

suppressor

248
Q

_ T cells destroy MEMBRANES but not the actual cell, other cells do this

A

killer

249
Q

_ T cells are complements to killer T cells

A

Cytotoxic

250
Q

T/F T cells secrete antibodies

A

false
B cells do this

251
Q

Which B cells perform opsonization, memory or effector cells?

A

effector

252
Q

T cells are made in the thymus and B cells are made in the _

A

bone

253
Q

T/F Anaphylactoid (non-immune) reactions do not require a previous exposure

A

true

-think IV contrast
-directly starts complement or releases histamine

254
Q

T/F Mast cells and basophils are involved in anaphylactoid (nonimmune) reactions

A

false
-JUST mast cells

255
Q

When mast cells are degranulated and basophils release inflammatory mediators, which substances are released?

A

main ones she cares about:
Tryptase
Prostaglandin D2
Leukotriene LTC4
TNF

256
Q

What does tryptase do?

A

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
Q

What does prostaglandin D2 do?

A

released by basophils when mast cells degranulate

causes:
bronchoconstriction
pulm and cardiac vasoconstriction
periph vasodilation
vasc permeability
HoTN
flushing
urticaria

258
Q

What does LEukotriene LTC4 do?

A

released by basophils when mast cells degranulate

causes:
bronchoconstriction
airway remodeling
angioedema
nitric oxide induction
vasc permeability
HoTN

259
Q

What does TNF do?

A

released by basophils when mast cells degranulate

causes:
neutrophil activation
chemokines
cytokines
effector cell recruitment

260
Q

What kind of reaction would a TB skin test be?

A

type 4

261
Q

What kind of reaction would hemolytic reaction be?

A

type 2

262
Q

What kind of reaction does NOT use immunoglobulin?

A

Type IV
-it is T CELL mediated

263
Q

Why would you miss a lot of s/s of anaphylaxis in anesthetized pts?

A

-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
Q

Which immunoglobulin is the most abundant?

A

IgG

265
Q

What are some signs on the vent that will show if pt is having anaphylaxis?

A

Bronchospasm
-low or no EtCO2
-low SaO2
-high PIP
-mucus plugging from laryng edema

266
Q

Order of most common drugs causing anaphylaxis perioperatively:
>Latex>

A

MR>latex> Abx

267
Q

Which MR is most likely to cause anaphylaxis?

A

Sux
-molecule is flexible an can easily cross link with IgE bc it is DIVALENT

268
Q

Which MR classes are more common to cause anaphylaxis, benzylisoquinolinium or amino-steroid complexes?

A

Benzylisoquinolinium

269
Q

T/F Pt is allergic to Roc, is Vec ok?

A

no

270
Q

Why could someone having Roc for the first time have an anaphylactic reaction?

A

The metabasulfites that cause the reaction are in a lot of household products

271
Q

1 agent that causes anaphylaxis in kids?

A

latex

272
Q

T/F Both medical devices and med vials must be labeled to say whether there is latex in them or not

A

False
med vials dont for some reason

273
Q

T/F Ok to pretreat for latex allergies?

A

true!
-won’t prevent attack, but can attenuate some s/s

274
Q

Why would a 1st gen cephalosporin and PCN both possible cause reaction?

A

they both have a beta lactam ring
-cant really swap pcn for ancef (but we still do sometimes)

-best bet go with vanco

275
Q

In the GENERAL PUBLIC, which causes anaphylaxis more, abx or MR?

A

Abx

276
Q

Y/N Can a pt with a shellfish allergy have Protamine? What about a fish allergy?

A

Shellfish = yes
Fish= no
protamine comes from salmon sperm

277
Q

Pts at higher risk of Protamine allergy:

A

-vasectomy (salmon sperm factors compete somehow?)
-salmon/fish allergy
-insulin use (NPH-P stands for protamine)

278
Q

Pt has environmental allergies and takes various medications for them, what could they be taking and what effects could it have?

A

pseudophedrine - high BP
antihistamine - increased duration/effect of drugs
nasal inhaled corticosteroids - BG, HTN

279
Q

How to get 10mcg of Epi to give in boluses from 1mg/mL Epi?:

A

-Draw 1mL (100mcg) then dilute with 9ml SW = 10mcg/mL
-give MORE epi in spinal pts bc response will be blunted

280
Q

Why is Epi the gold standard for anaphylaxis?

A

-prevents degranulation of mast cells
-CV support
-Dilates airway

281
Q

How to give 1 unit of vaso in 20unit.mL vial?

A

get 20mL syringe, draw 1mL, the n19mL of saline = 1unit/mL

282
Q

What can be given if anaphylactic pt is on b blocker and HoTN despite everything?

A

Glucagon! -antidote for beta blockers!
1-5mg IVP or 20-30mcg/kg

283
Q

T/F Use methylene blue for refractory HoTN if other methods are exhausted

A

true
-stops nitric oxide synthetase
1-2mg/kg bolus, then 0.5mg/kg/hr infusion

284
Q

T/F Sulfa allergies carry cross sensitivity

A

false

285
Q

Which blue dye is known to CAUSE hypersensitivity reactions?

A

Isosulfan blue
-not methylene blue- used for refractory HotN

286
Q

If pt has allergic reaction to roc, which MR can they theoretically have?

A

cisatracurium

287
Q

Under anesthesia, Type I allergic reactions will present with which 4 s/s?

A

-HoTN
-Bronchospasm
-Increased PIP
-Urticaria

288
Q

Y/N Ok to use H1 blockers if pt is having CV collapse?

A

no