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Pathophys II > Hyper & hypo immune disorders > Flashcards

Hyper & hypo immune disorders Flashcards

1
Q

Describe the difference between innate & adapative.

A

innate is a non-specific response that targets many common pathogens
adaptive must be developed individually

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2
Q

The innate system does not need a

A

prior exposure to elicit a response

it is passed on to each generation

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3
Q

The innate system is comprised of

A

epithelial & mucous membranes, complement factors, neutrophils, macrophages, & monocytes

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4
Q

The adaptive response has a

A

delayed response

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5
Q

The adaptive response develops

A

memory & specificity towards an antigen

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6
Q

The adaptive response is composed of

A

B & T lymphocytes

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7
Q

The principle cells of innate immunity include

A

myeloid cells

-macrophages, neutrophils, and dendritic cells

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8
Q

The principle cells of adaptive immunity are

A

T & B lymphocytes

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9
Q

The adaptive immune system is _____ as compared to the innate immune system

A

very powerful

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10
Q

Describe humoral immunity.

A

component of adaptive immunity

mediated by antibodies produced by B cells

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11
Q

Humoral immunity acts by

A

antibodies neutralize microbes, opsonize them for phagocytosis, and activate the complement system

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12
Q

Describe cell-mediated immunity

A

T cells activated by protein antigens from antigen presenting cells (APCs)

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13
Q

Cell mediated immunity requires repeat

A

antigen stimulation to perform their functions

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14
Q

The innate immune dysfunction includes

A

inadequate response, excessive response, & misdirected response

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15
Q

Excessive response is inclusive of

A

neutrophilia, monocytosis, asthma

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16
Q

Misdirected immune response includes

A

angioedema

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17
Q

Inadequate response includes

A

neutropenia, abnormal phagocytosis, deficient in the complement system, hyposplenism

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18
Q

Adaptive immune dysfunction include

A

defects in antibody production, defects in T lymphocytes, combined immune system defects, allergic reactions, anaphylaxis, & autoimmune disorders

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19
Q

Autoimmune means

A

reactions against self antigens

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20
Q

Hypersensitivity (definition)

A

excessive immunologic reactions to microbes or environmental agents dominated by inflammation

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21
Q

Atopy (definition)

A

propensity or genetic tendency to develop allergic reactions

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22
Q

Antibody is a

A

large Y shaped protein used by the immune system to identify and neutralize foreign objects such as pathogenic bacteria & viruses

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23
Q

Neutrophils are formed by

A

stem cells in the bone marrow

phagocytes that are found in the blood stream

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24
Q

Neutrophils make up

A

40-70% of all WBCs in humans

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25
Q

First responders to inflammation (especially bacterial) are

A

neutrophils

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26
Q

Neutropenia is defined as

A

a neutrophil count <1500/mm3

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27
Q

Types of neutropenia include

A

neonatal sepsis, Kostmann syndrome (autosomal recessive), acquired defects (chemotherapy, antivirals), autoimmune (lupus, RA), infection- the rate of consumption exceeds production

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28
Q

Treatments for neutropenia include

A

the cessation of medications that cause neutropenia, granulocyte colony-stimulating factor (filgastrim), and bone marrow transplants

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29
Q

For patients with neutropenia in the periop enviroment,

A

respecting asepsis is particularly important

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30
Q

The spleen is part of the

A

lymphatic system- like a large lymph node, primary blood filter

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31
Q

The primary creator of RBCs in fetal life & up to 5 months of age

A

is the spleen

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32
Q

The functions of the spleen include:

A

removes old RBCs, a blood reservoir, recycles iron, metabolized hemoglobin, stores 1/4 of circulating lymphocytes, stores & clears platelets
synthesizes antibodies in the white pulp
removes antibody-coated bacteria
the Globin portion of hemoglobin is degraded to amino acids, and the heme portion is metabolized to bilirubin

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33
Q

Hyposplenism is the

A

reduced spleen function

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34
Q

Asplenia refers to

A

the absence of normal spleen function
causes an increase of sepsis by 350 fold
a type of immuno-dysfunction

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35
Q

Sickle cell anemia & its’ relation to hyposplenism

A

can cause auto-infarction in the spleen resulting in vaso-occlusive disease

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36
Q

For patients with hyposplenism, they require

A

immunizations, travel restrictions, abx prophylaxis even with minor procedures, and alert warning bracelets

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37
Q

Leukocytosis is when the

A

WBC count is above normal range
a normal reaction often an inflammatory response but can also be from tumors, leukemias, stress, pregnancy, convulsions, and medications (corticosteroids, lithium, and beta agonists

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38
Q

Leukocytosis is different from

A

leukemia
acute leukemia- immature WBCs in the peripheral blood
chronic leukemia- mature, non-functioning WBCs in peripheral blood

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39
Q

Describe the difference between left upper shift & right shift

A

left upper shift- increase in the ratio of immature to mature neutrophils; bone marrow is trying to make more
right shift- decrease ratio of immature to mature neutrophils
shows bone marrow suppression (radiation sickness)

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40
Q

Eosinophilia is responsible for

A

allergic disorders

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41
Q

Describe eosinophilic esophagitis

A

chronic immune system disease in which a type of white blood cell (eosinophil) builds up in the lining of esophagus

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42
Q

The cause of eosinophilic esophagitis can be

A

a reaction to foods, allergens, or acid reflux, can inflame or injure the esophageal tissue

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43
Q

Damaged esophageal tissue from eosinophilic esophagitis can lead to

A

difficulty swallowing or cause food to get stuck when swallowing

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44
Q

Describe the difference between extrinsic and intrinsic asthma.

A

extrinsic- IgE production, allergens

intrinsic- triggers are unrelated to the immune system i.e. ETT placement, cold, exercise, stress, inhaled irritants

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45
Q

Neutrophilia occurs within

A

hours of an infection, granulocytes increase 2-3 fold

-mobilization of stored granulocytes and new from the bone marrow

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46
Q

Neutrophilia is defined as

A

neutrophils >7000/mm3

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47
Q

Neutrophilia may be a result of

A

pancreatitis, pyelonephritis, peritonitis & pna

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48
Q

Leukostasis is defined as & can lead to

A

> 100,000 mm/3

thick blood flow & WBC clumping, can lead to TIAs & strokes

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49
Q

Angioedema is can be

A

hereditary or acquired
results in subcutaneous & submucosal edema formation
often involves the face, extremities, & GI tract

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50
Q

Bradykinin mediated angioedema can be due to

A

autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
ACE-I
Acquired

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51
Q

Describe acquired bradykinin mediated angioedema.

A

lymphoproliferative disorders acquire C1 esterase inhibitor deficiency secondary to antibody production

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52
Q

Describe ACE-I angioedema.

A

drug-induced angioedema resulting from increased bradykinin availability to ACI-I mediated blockage of bradykinin catabolism

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53
Q

Describe autosomal dominant deficiency/dysfunction of C1 esterase inhibitor

A

the absence of C1 esterase inhibitor leads to release of vasoactive mediators that increase vascular permeability and produce edema by bradykinin
repeated bouts of facial and/or laryngeal edema lasting 24-72 hours

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54
Q

What should not be used for bradykinin-mediated angioedema?

A

catecholamines and histamines are not effective

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55
Q

What is the treatment for bradykinin-mediated angioedema?

A 
androgens- prophylactic therapy
antifibrinolytic therapy-inhibiting plasmin activation
C1 inhibitor concentrate
synthetic bradykinin receptor antagonist
recombinant plasma kallikrein inhibitor 
FFP- replaces the deficient enzyme
56
Q

Defects of T lymphocytes is known as

A

DiGeorge syndrome

57
Q

Defects of combined immune system defects is known as

A

severe combined immunodeficiency syndromes

58
Q

DiGeorge syndrome is a

A

thymic, thyroid, and parathyroid hypoplasia

due to a gene deletion–> decreased T cells (B cells are normal)

59
Q

S/S of DiGeorge syndrome include

A

cardiac malformations, facial dysmorphisms, truncus arteriosus, TOF, and cleft palate

60
Q

With DiGeorge syndrome, the degree of immunocompromise correlates with

A

the amount of thymus tissue present

61
Q

A complete absence of the thymus results in

A

severe combined immunodeficiency syndrome

62
Q

Treatment of DiGeorge syndrome is

A

thymus transplant or infusion of T cells

63
Q

Anesthetic considerations for DiGeorge syndrome include

A

SBE prophylaxis if required, calcium supplementation in hypoparathyroidism, strict asepsis due to risk for infection

64
Q

Severe combined immunodeficiency syndromes are

A

genetic mutations that affect T, B, & NK cell function/maturation
lack of receptor–> lack of interleukin signaling–> lack of NK, B, & T cell differentiation/maturation

65
Q

Babies with SCID appear

A

healthy at birth but are highly susceptible to severe infections

66
Q

The only treatment for SCID is

A

bone marrow or stem cell transplant, gene therapy or enzyme replacement

67
Q

Excessive adaptive immunity is inclusive of

A

allergic reactions, anaphylaxis, drug allergy

68
Q

Allergic reactions are

A

immune-mediated

“overreactions” of the immune system

69
Q

The four types of allergic reactions include

A

Type I- IgE
type II- IgG/IgM
Type III- immune complex
Type IV- T lymphocytes

70
Q

Type I immune mediated allergic reactions are different than other immune mediated reactions because

A

they are immediate

71
Q

Anaphylaxis is a

A

life-threating response involving
cardiovascular collapse (tachycardia, hypovolemia)
interstitial edema, urticaria
bronchospasm, laryngeal edema

72
Q

Anaphylaxis is caused by

A

immune mediated-IgE
previous exposure to antigens in drugs evokes production of antigen-specific IgE antibodies
subsequent exposure results in marked mast and basophil degranulation

73
Q

Nonimmune mediation or anaphylactoid is

A

via IgG or IgM
less common
direct release of histamine from mast or basophils

74
Q

Mediators include

A

vasoactive amines- histamines
lipid mediators- prostaglandins & leukotrienes
cytokines- tumor necrosis factor & chemokines

75
Q

Describe the role of vasoactive amines.

A

stored in mast cells
release upon mast cell degranulation
causes rapid vasodilation, increases vascular permeability, and smooth muscle contraction

76
Q

Describe the role of lipid mediators- prostaglandins & leukotrienes.

A

Prostaglandin is the most abundant mediator generated by the cyclooxygenase pathway in mast cells–> causes intense bronchospasm
the leukotrienes are the most potent vasoactive and spasmogenic agents known

77
Q

Describe the role of cytokines.

A

recruit, activate leukocytes and amplify

78
Q

Risk factors for anaphylaxis in anesthesia includes

A

asthma, atopy, multiple past exposure to latex, hereditary conditions (angioedema)

79
Q

Clinical manifestations of anaphylaxis include

A

tachycardia, bronchospasm, laryngeal edema, & cutaneous rash

80
Q

Plasma histamine concentrations return to

A

baseline 30-60 minutes after a reaction

81
Q

Diagnosis of anaphylaxis is through

A

clinical manifestations, plasma tryptase concentration, plasma histamine concentrations, and skin testing

82
Q

Describe plasma tryptase concentration.

A

tryptase is stored in mast cells and is released during immune-mediated reactions
indicates mast cell activation

83
Q

Management of perioperative anaphylaxis includes

A

remove the agent if possible, reverse hypotension & hypoxemia, replace intravascular fluid, inhibit further degranulation, inhibit release of vasoactive mediators, treat inflammation, relieve bronchospasm

84
Q

Describe the role of antihistamines in anaphylaxis treatment.

A

histamine 1 antagonist- diphenhydramine- competes with histamine for membrane receptor sites
histamine 2 antagonist- ranitidine
helps to decrease pruritus and bronchospasm
not as effective in treating anaphylaxis once vasoactive mediators have been released

85
Q

The dose of epinephrine for anaphylaxis is

A

1-10 mcg/kg IV bolus, repeat every 1-2 minutes as needed

86
Q

Epinephrine works by

A

increasing intracellular cAMP, restoring membrane permeability and decreasing the release of vasoactive mediators
beta agonists effect- relaxes bronchial smooth muscle

87
Q

If a patient is unresponsive to epi–>

A

vasopressin, glucagon, or norepinephrine

88
Q

The role of corticosteroids in anaphylaxis is

A

has no known effect on degranulation of mast cells or antigen-antibody interactions
-takes several hours for effect
may enhance the beta agonist effects of other drugs or inhibition of the release of arachidonic acid responsible for production of leukotrienes and prostaglandins

89
Q

Beta 2 agonists can be useful

A

when delivered by MDI or nebulizer for treatment of bronchospasm in anaphylaxis

90
Q

Patients with _____ are at increased risk for anaphylaxis

A

allergies (asthma, fruits, or medications)

91
Q

Previous uneventful exposure does

A

not eliminate the possibility of anaphylaxis on second exposure

92
Q

Anaphylaxis can occur

A

on first exposure due to cross-reactivity with other gents

93
Q

Anaphylaxis is NOT

A

intolerance, idiosyncratic reactions, or toxicity

94
Q

Intolerance is the

A

inability to tolerate the adverse effects of a medication

-example is muscle pain & statins

95
Q

Idiosyncratic reactions are

A

drug-reactions that are not related to the known pharmacological properties of a drug
-examples are antiepileptic drugs & dyskinesias

96
Q

Toxicity is a result of

A

having too much drug in a person’s system at one time

97
Q

Any medication administered during anesthesia can produce

A

an allergic reaction
most reactions manifest within 5-10 minutes
latex is typically delayed >30 minutes because it must be absorbed through the skin

98
Q

Common drugs associated with perioperative anaphylaxis are

A

muscle relaxants, antibiotics, and latex

99
Q

The most common muscle relaxants to cause anaphylaxis are

A

rocuronium and succinylcholine

100
Q

With muscle relaxants and anaphylaxis, there is

A

cross-sensitivity within classes

101
Q

Some over the counter cosmetics contain ammonium ions and are capable of

A

sensitizing patients to developing IgE antibodies to quaternary & tertiary ammonium ions
morphine & neostigmine also contain ammonium ions

102
Q

The histamine release from atracurium administration is

A

nonimmune mediated

103
Q

The most common anaphylaxis reaction among the antibiotics is

A

penicillin

- clinical illness misattributed to PCN in some cases (viral rash vs. PCN rash)

104
Q

IgE antibodies can

A

wane over time- may have a reaction as a child but able to take it as an adult

105
Q

Penicillin contains two allergenic components also present in other antibiotics:

A

B-lactam ring (found in cephalosporins)

R-group side chain (found in cephalosporins)

106
Q

The second most common antibiotic allergic reaction is

A

sulfonamides

most common cause of Stevens-Johnson syndrome

107
Q

Vancomycin may also cause

A

allergic reactions although most are non IgE but rather direct release related to the rate of the drug infusion

108
Q

A feature that distinguishes latex-induced allergic reactions from other drug-induced allergic reactions is its

A

delayed onset, typically longer than 30 minutes after exposure
antigen from rubber gloves absorbed across mucous membranes into systemic circulation
can also be inhaled

109
Q

At risk individuals for latex include

A

spina bifida, multiple previous operations, history of fruit allergy, and healthcare workers

110
Q

Propofol was formerly advised

A

that it should be used in caution in patients with a history of egg, soy, or peanut allergy
it contains preservatives which are what people are typically allergic to

111
Q

Propofol allergy is thought to be

A

IgE mediated with the 2-isopropyl-group or the preservative

112
Q

The combination of these conditions preclude individuals who are taking NSAIDs to rhinorrhea, bronchospasm, and angioedema:

A

asthma, hyperplastic sinusitis, & nasal polyps

113
Q

Allergies to NSAIDs are not

A

IgE mediated but rather due to inhibition of cyclooxygenase 1 that promotes synthesis of leukotrienes and subsequent release of mediators from basophils and mast cells

114
Q

With NSAIDs, allergic reactions do not typically

A

occur with Cox-2 specific inhibitors

115
Q

Allergic reactions to radiocontrast media are more common with

A

ionic, high-osmolar contrast agents

-the higher the iodine, the greater the risk of adverse reaction

116
Q

Allergic reactions to radiocontrast media are often

A

non-immune mediated & can be treated with corticosteroids and histamine antagonists

117
Q

Allergic reactions to local anesthetics are more likely for

A

ester type> amide type

most reports are the adverse events of intravascular injections or systemic absorption of additives

118
Q

Dyes may lead to

A

(are found in cosmetics & soap) and may lead to prior sensitization

119
Q

Other sources of allergic reactions include

A

halothane (induced hepatitis)
chlorhexidine
synthetic volume expanders
blood products

120
Q

Autoimmune disorders include

A

SLE, RA, autoimmune hepatitis

121
Q

Anesthetic considerations for misdirected adaptive immunity include

A

specific vulnerable organs, consequences of therapy, acceleration of other disease process (i.e. CV disease)

122
Q

Autoimmunity is a

A

type of hypersensitivity to self-antigens. Antibodies inappropriately mark self-components as foreign

123
Q

Autoimmune disease can be divided into

A

organ-specific or system

124
Q

Systemic disease is

A

immune complexes & autoantibodies

  • principally affect the connective tissues and blood vessels of involved organs
  • even though the immunologic reactions are not specifically directed against constituents of connective tissue or blood vessels
125
Q

Since the graft donor and recipient host are genetically different,

A

some of these differences are recognized by the immune system and are responsible for immune destruction of the graft, called rejection

126
Q

Grafts exchanged between nonidentical individuals of the same species are called

A

allografts

127
Q

Histocompatibility determines if the

A

tissue graft (histo=tissue) will be accepted (compatible) by the receiving individual

128
Q

The major histocompatibility complex in humans are

A

polymorphic genes that differ among individuals

-they function to recognize T cells

129
Q

If the graft donor expresses MHC molecules that differ from those in the recipient, the graft is recognized as

A

foreign by the recipient’s T cells leading to rejection

130
Q

To prolong graft survival the following is needed:

A

immunosuppression via corticosteroids, anti-T cell antibodies, drugs that inhibit T- cell function

131
Q

Immunosuppression carries the risk of

A

opportunistic fungal and viral infections

-reactivation of latent viruses (cytomegalovirus) as well as an increased risk of cancers

132
Q

Graft vs. host disease is a

A

syndrome commonly associated with bone marrow and stem cell transplants
The donor’s WBCs which remain with the donated tissue (graft) recognize the recipient (host) as foreing

133
Q

Graft vs. host disease is not

A

the same as a transplant rejection

the donor’s immune system reject the recipient

134
Q

The treatment for graft vs. host disease is

A

to suppress T-cells via steroids & calcineurin inhibitors

-suppress the synthesis of pro-inflammatory cytokines

135
Q

Tumor lysis syndrome is a

A

rare, potentially lethal disease of massive lysis of tumor cells resulting in release of intracellular substances into the blood stream
-potassium, phosphate & uric acid

136
Q

Causes of tumor lysis syndrome include

A 
steroids
after treatments (chemoembolization, radiofrequency ablation)

Pathophys II (43 decks)

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