NA 1 > Allergic response > Flashcards

Allergic response Flashcards

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1
Q

What is allergic response:

A

one part of the pathologic response the immune system has developed to recognize foreign substances

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2
Q

What are foreign substances?

A

ANTIGENS (Proteins/carbs)

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3
Q

Immune system fx:

A

Protects body against antigens

WIll recognize and REMOVE the antigens

Can respond inappropriately to cause hypersensitive allergic reactions

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4
Q

The body will tolerate which molecules?

A

That are like the host

Self tolerance (Not allergic to self)

Problems - dysfunction immune system –> autoimmune disorders (RA/Lupus)

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5
Q

Immune system categories:

A

innate (natural/nonspecific)

Adaptive (Acquired/specific)
- humoral
- cell mediated

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6
Q

Adaptive: cell mediated immunity:

A

Targets INTRACELLULAR pathogens

Immune cells directed at eliminating or destroying pathogens or cells

Regulates immune response

T cells

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7
Q

Adaptive: humoral immunity:

A

Targets EXTRAcellular pathogens

Antibodies and proteins can work directly or in combo with cellular immunity (t cells) to create cell injury and destruction to extracellular pathogens

B cells

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8
Q

B cells fx:

A

Recognize specific antigens (foreign substance) with surface receptors

Antibodies (immunoglobulin) bind to pathogens neutralizing or marking for destruction (neutralization, opsonization, complement activation)

Differentiate into plasma cells and memory B cells

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9
Q

What is the first line of defence?

A

Non-specific (Innate)

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10
Q

What is an antigen?

A

Any toxin or foreign substances that causes an immune response in the body

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11
Q

Complete antigens:

A

Capable of inducing a full immune response

Independently stimulates immune response

Anesthesia examples:
-blood products
-protamine
-dextran/volume expanders
-latex
-NMR

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12
Q

Incomplete antigens:

A

Needs something else (like a carrier protein) to cause a response

CANNOT independtly trigger immune response

Haptens - small molecules, incomplete antigens

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13
Q

Anesthesia examples of incomplete antigens:

A

PCN

Low molecular weights anesthetic drugs (1,000 Da)

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14
Q

Protamine:

A

Positively charged

Binds w negatively charged heparin to neutralize

Can act as antigen and bind to IgE antibodies –> cellular degranulation and histamine release

Some insulin preparations have protamine - may be more susceptible to proatmine repsonse if taking

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15
Q

Dextran:

A

Large macromolecules

Colloid volume expanders

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16
Q

Antibodies are called ____

A

Immunoglobulins

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17
Q

What are antibodies and the classes?

A

PROTEIN molecules

IgA, IgD, IgG, IgE, IgM

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18
Q

Structure of an antibody:

A

2 HEAVY chains and 2 light chains (BOUND by disulfide bonds)
- heavy chain determines structure and fx of each molecule

Fab fragment (Binds antigen)

Fc fragment (unique biologic properties of immunoglobulin)

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19
Q

T cells:

A

Lymphocyte
Thymus derived

Receptors activated by binding foreign antigens

Secrete mediators that regulat the immune response

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20
Q

Types of t cells:

A

Helper
suppressor
Cytotoxic
Killer

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21
Q
A
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22
Q

T cell army:

A

Cell mediated immune response - directed ata specific pathogen

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

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23
Q

B cells:

A

Lymphocyte
Part of antibody immune response
Devleoped in bone marrow

Main jon = secrete IgG, IgA, IgM, IgE, IgD

Differentiate into plasma and memory B cells

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24
Q

Plasma B cells:

A

Produce antibodies, neutralize pathogens, OPSOMIZE them for phagocytosis or active complement

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25
Memory B cells:
Provide rapid antibody production upon re-exposure (Body remembers what you were exposed to) - Antigen presenting cell (APC)
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Monocytes and macrophages are:
PHagocytes (Engluf and destroy pathogens)
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Monocytes do what in blood?
Circulate and differentiate into macrophages or dendritic cells
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Macrophages fx:
Aruse from monocytes; presents antigens to helper T cells
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Neutrophils (Polmorphonuclear leukocytes) are what? fx?
Phagocytes (Produce hydroxyl radicals, superoxide, hydrogen peroxide) Most abudnant WBC First response to infection
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Eosinophil fx:
Phagocytes/eosinophil Role in parasitic infections, tumors, allergic reactions
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Dendritic cells fx:
Phagocytes Antigen presenting cell Link innate and adaptive immunity by presenting antigens to T cells
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NK cells fx:
Recognize and destroy virus infected and cancer cells
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Basophils fx:
Granulocytes Circulate in blood and release histamine during allergic reaction IgE receptors on surface
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Mast cells fx:
Granulocyte Importnat in immediate hypersensitivity reaction Reside in tissues (Skin, lung intestine) IgE receptor on surface
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Cytokines:
Small proteins secreted by immune cells Inflammatory cell activators Synthesized by macrophages Secondary messengers that activate endothelial and white cells Examples TNF, Interleukin, growth factor, inerferon
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Interleukins:
Group of cytokines produced by leukoctes Play role in regulating immne response Antibodies
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Complement fx:
Primary humoral response to antigen and antibody binding is activation of complement system COllection of proteins (20) in blood and tissues that enhance immune responses
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Fx of complement:
Recognize bacteria directly and indirectly, opsoniztion (tagging), inflammation, cell lysis
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What does complement activate:
IgG or IgM binding to antigen, plasmin, endotoxin, drugs
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Dysfunction of complement leads to:
increased susceptibility to infections, autoimmune diseases, uncontrolled inflammation
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Hypersensitivity responses
Normally, the immune system works as a protective system, but it may react inappropriately and produce a hypersensitive (or allergic) response ----> require a pre sensitized state of the host ----> Four types of hypersensitivity responses Type I-IV
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Hypersensitivity responses Type I-IV:
I - anaphylaxis II: cytotoxic reactions III: immune complex reactions IV: delayed hypersensitivity reactions
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Type I hypersensitivity: type:
Anaphylaxis or immediate type hypersensitivty (happens in minutes) Involves IgE antibodies Type I reactions - anaphylaxis, drug allergy, asthma, allergic rhinitis/hay fever Antigen binds to preformed antibodies on mast cells and basophils
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Type I hypersensitivity leads to :
Release of histamine, leukotrienes, platelet activating factor
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What happens when mast cells explode?
HISTAMINE RELEASED -- attaches to HI receptor --> bronchoconstriction in lungs --> difficulty breathing. Vascular system --> vasodilation and increased permeability --> edema and hives PLATELET activating factor is released = Coronary artery construction --> Ischemia -Decreased coronary perfusion --> ischemia -Decreased contractility --> cV collapse
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Type II reactions:
Cytotoxic reactions ANTIBODY dependent cel mediated OR cytotoxic hypersensitivy Mediated by IgG or IgM Cell damage- direct cell lysis, opsonization, increased phagocytosis
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Examples of cytotoxic reactions:
ABO INCOMPATIBLE transfusion reactions acute transfusion rejection Myasthenia gravis Drug induced hemolytic anemia HIT
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Type III reactions:
Immune complex reactions IgG or IgM Snake bite, immune complex vascular injury (SLE or RA), protamine mediated pulmonary vasoconstriction Antibodies and antigens bind and make insoluble complexes that lead to vasculitis COMPLEMENT is activated - neutrophils produce tissue damage
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Type IV reactions:
Delayed hypersensitivity reactions CD4 T cells; CD8 CLT's TB skin test, poison Ivy Sensitized lymphocytes with antigens Manifests in 18024 hours, peak 40-80, disappear in 72-96 hours
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Types of Type IV reactions:
Tissue rejection Graft vs host Contact dermatitis TB skin test
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IgE mediated pathophysiology results in :
Bronchospasm Upper airway edema Vasodilation Inc. cap, permeability
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IgE mediated pathophysiology
Mast cells continue to spill out contents even if antigen is no longer present as triggering agent --> will continuie to potentiate ongoing symptoms Ongoing mediators of inflammation can lead to a return rebound of symptoms 6-8 hours following initial repsonse REASON why patients should be kept and monitored cloesely following control of s/s
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Histamine and anaphylaxis:
H1 and H2 are involved Histamine stored in mast cells and basophils
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H1 function:
Activates endothelium derived relaxing factor (NO) leading to increased vascular permeability, vasodilation, smooth muscle contraction (Not blood vessels)
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H2 function:
Cardiac stimulation Gastric acid secretion Inhibits mast cells Vasodilation
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Peptides fx
Eosinophilic chemotactic factor - thought to release enzymes that inactivate histamine and leukotrienes
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Arachidonic acid fx:
Leukotrienes - bronchoconstriction, increased cap perm/vasodilation, coronary vasoconstriction, myocardial depression
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Prostaglandins fx:
Mast cell mediators Vasodilation/increased cap perm, bronchospasm, pulmoonary hypertension Prostaglandin D2= bronchospasm and vasodilation Thromboxane A2 = protamine reactions and pulm HTN
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Kinins fx:
Released from mast and basophils Vasodilation, increased cap perm, bronchoconstriction Stim. vascular endothelium to release vasoactive factors (Prostacyclin and NO)
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Platelet activating factor fx:
Released from mast cells Aggregates and activates platelets to release inflammatory products
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Anaphylaxis NON IgE mediated:
Complement activation Immunologic (Antibodyy mediated) - direct classic type I hypersensitivity reaction Nonimmunologic (alternative)/Lectin pathways
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Nonimmunologic (alternative)/lectin pathways for non IgE mediated anaphylaxis:
No need to antibody antigen interactions Anaphylactoid --> C3a and C5a produced Histmaine released - smooth muscle contraction -- increased cap perm - interleukin synthesis (Cytokines) C5a > PMNs/neutrophils & platelets > aggregated and activated > embolize > microvascular occlusions/inflammation > leukoagglutinins attack > result is pulmonary leukostasis > leading to endothelial damage, increased permeability and pulmonary HTN
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Non-IgE mediated reactions Hereditary angioedema (HAE)
Complement deficiency state Presents with life threatening episodes of airway edema and GI edema/diarrhea Due to deficiency or dysfunction in C1 esterase inhibitor (regulatory protein in complement, fibrinolytic and kinin pathways) > uncontrolled activation of complement system, kallikrein-kinin system, bradykinin production (increased vascular permeability > edema)
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Management of HAE:
Historical - anabolic steroids and antifibrinolytics Current = CI esterase inhibitor concentrates, kinin pathway modulator, bradykinin antagonist
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Non igE mediated histamine release is:
Dose dependent, non immunologic histamine release due to mast cell activation and NOT basophils
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Non IgE mediated Histmaine release medication causes:
Antibiotics (Vanco) Basic compounds (Morphine, vanco, succ, protamine, radiocontrast Hyperosmotic agents Muscle relaxants (atracurium, mivacurium) Opioids (Morphine, meperidine, codeine)
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Anaphylactoid reactions are ____ antibody mediated but are rather:
NOT Result of a direct action of a drug Common
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In true anaphylactic allergic reactions, anaphylactic reactions are _____ antibody mediated
IgE Type I hypersensitivity reactions
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Most common drug responsible for allergic reaction and what percent?
Succ 62-81% Structure: contains flexible molecule that can cross link two mast cell IgE receptors causing immediate release from mast cells and basophils without hapenating to larger carrier molecules More common with Benzylisoquinolium compounds than aminosteroid Cross sensitivity between NMBA and DMR
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Latex allergy:
From milkywhite sap of Hevea brasiliensis (rubber tree plant) IgE dependent IMMEDIATE hypersensitivity reaction to latex products
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People at risk for latex allergy:
Health care workers Children with spina bifida Food allergies - bananas, kiwis, avocados
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Prevention of latex allergy
Avoid latex Antihistamines - not proven to work
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Cross sensitivity food with latex:
Bananas Kiwi Apple Avocado Chestnut Carrot/celery Papaya Potato Tomato Melons
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Common remaining sources of latex include:
Rubber stoppers from medicine vials Drug is in carpujet - know if there is latex in the plunger of syringe Med vials/containers not covered by rules that state med devices must be labeled accordingly if they contain latex Currently in US - NOT required that medications are labeled for presence of latex
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Latex free substances:
Polyvinyl Neoprene Silicone
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If a medical product contains latex the manufacturer is ____ to label it as such, what about meds?
REQUIRED NOT True for meds
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Patient care with latex allergy:
Prophylactic tx H1 and H2 blockers Steroids Prophylaxis has NOT been shown to decrease the occurrence of an anaphylactic response
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Abs presenting reaction and most common abx?
Cutaneous Most common BETA LACTAMS (penicillin) Vaco - incedence of anaphylaxis very low
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Cross reactions may occur withwhich antibioitic:
First gen cephalosporins Less likely with second or third generation cephalosporins
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Vancomycin is a:
Potent histmaine releasing agent Rare anaphylaxis Severe hypotension and flushing with rapid IV admin
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In the general public, the most common anaphylaxis trigger is:
Abx
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LA and allergic reactions:
uncommon Ester agents - PABA - Procaine, chloroprocaine, tetracaine, benzocaine True allergy --> amide often safe alternative
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Most adverse reactions with locals are due to:
Epi or toxicity
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Sugammadex reactions:
Most are mild reactions Most occur within 5 mins Risk of anaphylaxis but mechanism unclear Does not seem to increase with repeated exposure Risk of hypersensitivity seems to increase with higher doses
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Barbitures and allergies:
Mostly with thiopental methohexital - no anaphylaxis
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Propofol and allergy:
Egg white Made with egg lecithin (yolk) Current evidence says OK
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Etomidate, ketamine, and benzxos allergy:
Very rare
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Inhalation agents allergy:
No anaphylaxis
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Heparin allergy:
IgE very rare HIT more common
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Protamine reaction:
0.4-0.8% can form allergic reaction; higher if previously exposed Fish allergy or men with vasectomies
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Protamine molecule:
Made from salmon sperm Strong base
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Protamine fx:
Binds with heparin and neutralizes it making a complex that no longer offers anticoagulation
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3 types of proamine reaction:
Caused by histamine release side effects of protamine - NON IgE mediated Caused by protamine heparin complex Anaphylaxis at a higher risk with history of - Vasectomy - Salmon allergy - Insulin use (NPH)
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Atopic patients:
May easily develop antibody mediated allergic response to foods, enviornmental factors, and drugs
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EXPRESSED signs and symptoms of atopic patients:
Allergic rhinitis Asthma Dermatitis Be very suspicious for S/Sx of allergic reaction when caring for these patients
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Environmental allergies:
Manifest as allergic rhinitis Atopic dermatitis patients may be on antihistamines, pseudoephedrine, and nasal inhaled corticosteroids
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Anesthetic considerations with environmental allergies:
Importance to distinguish between allergies and viral URI - Related to cancelling vs. proceeding with case and choosing type of anesthesia Inhalaed nasal steroids do not cause adrenal suppression - patients will not require stress dose of steroids the day of sx Acute use of pseudoephedrine may be associated with increases in BP
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Factors that influence allergic response:
Prior exposure - certain dyes, foods, drugs, houshold chemicals (NMBA) Female gender at risk - apples AFTER puberty Atopic individuals young age Pregnancy
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Isofulfan blue:
Lymphazurin 1% Being used increasingly for lymph node mapping Patients may exhibit hypersensitivyt reaction without prior exposure due to use of triphenylmethane dyes in household items
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With isosulfan blue, what carries no cross sensitivity:
Sulfa Methyline Blue
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Who are treated with premedications with isosulfan blue?
Breast patients with antihistamines and corticosteroids
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SE of isosulfan blue:
Blue hives
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What does isosulfan blue bind to?
Serum albumin after admnistration and methylene blue does not
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Methylene blue use:
Late rescue tx in anaphylaxis refractory to cats
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Treatemnt of anaphylax steps 6:
1. Call for help 2. STOP administration of antigen 3. airway maintenance and 100% O2 4. discontinue ALL anesthetic drugs 5. provide volume expansion 6. EPINEPHRINE: 5-100mcg
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Epinephrine with anaphylaxis:
1. hypotension = 5-10 mcg IV 2. Cardiovascular collapse = 0.1-1mg 3. no epi if not hypotensive 4. SQ appropriate for laryngeal edema without hypotension
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Epi pen concentration:
0.3mg of 1:1000 epi
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Secondary tx for anaphylaxis during anesthesia:
Antihistamines - H1/H2 blockers Epi/Norepi Bronchodilators, corticosteroids, vasopressin for refractory hypotension, bicarb, glucagon, methylene blue
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Post resuscitation for anaphylaxis:
Serum tryptase - key diagnostic step to evaluate involvement of mast cells (Central in allergic and anphyalctic reaction) 24 hour ICU monitor Patient/family notification Referral to allergist
NA 1
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