Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Spring '20/ L. BASICS- Immune, OR Hazards, OP > immune 1 > Flashcards

immune 1 Flashcards

1
Q

how does the immune system protect the body

A

by recognizing and removing foreign substances called ANTIGENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what substances make up antigens

A

proteins and carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do we call immune cells

A

cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the role of cell mediated immunity

A

immune cells directed at elimination or destruction of pathogen cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what substances make up humoral immunity

A

comprised of different antibodies and proteins such as “COMPLEMENT”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does humoral immunity work

what is the purpose of humoral immunity

A

the antibodies and proteins called COMPLEMENTS directly or in concert with cellular immunity cause cell injury and destruction

provide Host defense mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what process also uses protein mediators called cytokines and chemokine are released initially by inflammatory responses

A

humor immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

once cytokines and chemokine get release to the site of injury what is the response at the injury

A

brings other immune cells to the injury/ infection site causing further inflammatory responses, fever, and increase capillary permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the role of fever, increased capillary permeability, and the inflammatory response in the body

A

to allow other immune cells to migrate and translocate to the site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does the inflammatory response cause (4)

A

hemostatic activation

produces pain

erythema

local edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when the inflammatory response is activated producing pain, erythema, edema - are these effects only seen at that one area?

A

no depending on the injury it can be a systemic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how broad is the inflammatory effect of cytokines

A

they have an extensive spectrum of inflammatory effect

studied extensively in sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when is the onset of immune response

A

variable- from immediate (ANAPHYLAXIS) to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tell me about the “memory” of the immune response

A

it can remember antigens for many years, especially following IMMUNIZATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are antigens

A

molecules stimulating an immune response (antibody production or lymphocyte stimulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe most commonly used drugs compounds-

A

simple organic compounds of low molecular weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are complete antigens

A

polypeptides (protamine) and other large macromolecules (dextrans) are complete antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what do we call small molecular weight substances such as drugs or drug metabolites that bind to host proteins or cell membranes to sensitize patient

A

HAPTENS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

by themselves are haptens antigenic

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

for a small molecule to become immunogenic, it must form a stable bond with circulating proteins or tissue to result in an antigen - what is this called

A

hapten-macromolecular complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

molecular antigen structures in bacteria or fungi can they be immediately recognized as foreign

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is believe (although not proven) to happen to the active metabolite of PCN -penicilloyl-

A

(hapten) it is believe its binds with macromolecules to become antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how are the t cell receptors activated

A

their receptor binds with foreign antigens and secrete mediators that regulate the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the two types of regulatory T-cells

A

helper (OKT4)

suppressor (OKT8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does the suppressor cell do

A

inhibit the immune function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do the helpers cells do

A

stimulate cell responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does the thymus of the fetus do to immature lymphocytes

A

differentiates immature lymphocytes into thymus derived cells called T- cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

infection of helper T- cells with a retrovirus (HIV) - causes an increase in what

A

the number of suppressor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what do cytotoxic T cells do

A

destroy mycobacteria, fungi and viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

do natural killer cells need antigen stimulation to set up their role?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

name the two cells that take part in defense against tumor cells and in transplant rejection

A

cytotoxic t- cells and natural killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the role of t cells that produce mediators

A

they influence the response of other cell types involved in the recognition and destruction of foreign substances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

B- cells represent a specific lymphocyte cell line that can differentiate into specific plasma cells - what do they synthesize

A

antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

the process of b cells and their ability to differentiate into specific plasma cells that synthesize antibodies- how is this controlled?

A

by helper and suppressor t cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what else are B cells called

A

bursa- derived cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

why are b cells called bursa derived cells

A

BECAUSE IN BIRDS, THE BURSA OF FABRICIUS IS IMPORTANT IN PRODUCING CELLS RESPONSIBLE FOR ANTIBODY SYNTHESIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

name the 5 MAJOR CLASSES OF ANTIBODIES

A

IgG, IgA, IgM, IgD, AND IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

HAS AT LEAST 2 HEAVY CHAINS AND 2 LIGHT CHAINS THAT ARE BOUND TOGETHER BY DISULFIDE BONDS

A

each antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are antibodies

A

specific proteins called immunoglobuins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the antibody function

A

recognize and bind to specific antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DEPOSITION OF ANTIBODY OR COMPLEMENT FRAGMENTS ON THE SURFACE OF FOREIGN CELLS TO PROMOTE KILLING FOREIGN CELLS BY EFFECTOR CELLS. this process is known as

A

OPSONIZATION:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the role of macrophages

A

regulate immune responses by processing and presenting antigens to effect inflammatory, tumoricidal, and microbicidal functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

where do macrophages come from

A

circulating monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

where are macrophages confined to

A

specific organs- such as the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

_____ ingest antigens before they interact with receptors on the lymphocyte surface to regulate their action

A

MACROPHAGES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

macrophages synthesize mediators to facilitate what two responses

A

b lymphocyte and t lyphocyte responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the first cell to appear in acute inflammatory reaction

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

once neutrophils are activated what do they produce

A

hydroxyl radicals

superoxide

hydrogen peroxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

once neutrophils produce hydroxyl radicals, superoxide, hydrogen peroxide what happens next

A

microbial killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what do neutrophils contain

A

acid hydrolases

neutral proteases

lysosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the function of eosinophils

A

unclear

52
Q

where are eosinophils formed

A

exclusively in the bone marrow

53
Q

how long do eospinphils travel to reach their final destination

A

8-12 hours

54
Q

inflammatory cells recruit eosinophils to collect at what 3 sites

A

parasitic infections

tumors

allergic reactions

55
Q

esoniphils are seen in allergic diseases, name 3

A

asthma

auto immune disease

hay fever

56
Q

name the acute/chronic allergic diseases basophils are seen in

A

anaphylaxis, asthma, dermatitis

57
Q

basophils comprise what percent of circulating granulocytes in the blood.

how common are they?

A

0.5-1%

least common

58
Q

basophils contribute to resistance to what two things

A

internal parasites and ectoparasites (such as ticks)

59
Q

basophils IgE RECEPTORS ARE ON THE SURFACE WHICH FUNCTION SIMILARLY TO THOSE ON …

A

MAST CELLS.

60
Q

what are mast cells important for

A

immediate hypersensitivity responses

61
Q

mast cells are tissue fixed and located where

A

perivascular spaces of skin lung and intestine

62
Q

what lies on the surface on mast cells and bind to specific antigens

A

ige receptors

63
Q

once mast and Kinin cells are activated what do they release

A

physiologically active mediators important to immediate hypersensitivity responses

64
Q

where are kinins synthesized

A

in mast cells and basophils

65
Q

kinins produce what physiologic response

A

vasodilation

increased capillary permeability

bronchoconstriction

66
Q

kinins stimulate vascular endothelium to release what

A

vasoactive factors, including prostacyclin and endothelial-derived relaxing factors such as NO

67
Q

TYPE I REACTION:

what type

what is released and what does it bind to?

A

anaphylactic or immediate type hypersensitivity reaction.

PHYSIOLOGICALLY ACTIVE MEDIATORS ARE RELEASED FROM MAST CELLS AND BASOPHILS AFTER ANTIGEN BINDING TO IgE ANTIBODIES ON THE MEMBRANES OF THESE CELLS. THIS INCLUDES ANAPHYLAXIS, EXTRINSIC ASTHMA, ALLERGIC RHINITIS

68
Q

TYPE II REACTION:

Mediated by what antibodies?

A

ANTIBODY-DEPENDENT CELL-MEDIATED CYTOTOXIC HYPERSENSITIVITY OR CYTOTOXIC REACTIONS.

MEDIATED BY EITHER IgG OR IgM ANTIBODIES DIRECTED AGAINST ANTIGENS ON THE SURFACE OF FOREIGN CELLS

69
Q

what are the antigens in type 2 reactions

A

THESE ANTIGENS MAY BE EITHER INTEGRAL CELL MEMBRANE COMPONENTS OR HAPTENS

70
Q

allergy type 2 reaction integral cell membrane components

A

A OR B BLOOD GROUP ANTIGENS IN ABO INCOMPATIBILITY REACTIONS

71
Q

what is the role of haptens in type 2 reaction

A

absorb to the surface of a cell, stimulating the production of antihapten antibodies (autoimmune hemolytic anemia)

72
Q

cell damage examples type 2 reaction

A

drug induced immune hemolytic anemia

heparin induced thrombocytopenia

incompatibility transfusion reactions

73
Q

type 2 cell damage produced by

A

direct cell lysis after complete complement cascade activation

increased phagocytosis by macrophages

killer t cell lymphocytes producing antibody dependent cell mediated cytotoxic effects

74
Q

type 3 allergy reaction results from

A

circulating soluble antigens and antibodies that bind to form insoluble complexes that deposit in the microvasculature

75
Q

type 3 reaction role of neutrophils

A

localized to the site of complement deposition to produce tissue damage

76
Q

what is “activated” in type three allergy reaction

A

complement

77
Q

type 3 allergy reactions examples

A

serum sickness after snake antisera

antithymocyte globulin

immune complex vascular injury

occur through mechanisms of protamine mediated pulmonary vasoconstriction

78
Q

how fast is type IV reaction
manifest within?
peak?
disappear?

A

delayed hypersensitivity reaction
manifest in 18-24hrs
peak 40-80 hours
disappear 72-96hrs

79
Q

what does a type IV reaction result form

A

the interactions of sensitized lymphocytes with specific antigens

80
Q

type 4 allergy cytotoxic t cells are produced to do what

A

kill target cells that bear antigens identical with those that triggered the reaction

81
Q

type IV reaction 4 examples

A

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

82
Q

intraoperative allergic reaction risk of periop anaphylaxis is reported how often

A

1:3,500 AND 1:20,000

83
Q

intraoperative allergic reaction mortality %?

surviving % with severe brain damage

A

4%

2% surviving with brain damage

84
Q

> 90% of the allergic reactions evoked by IV drugs occurs with in how many minutes of administration

A

5 minutes

85
Q

what is the most common life threatening manifestation of an allergic reaction

A

circulatory collapse

86
Q

circulating collapse is reflecting what hemodynamics

A

vasodilation with resulting decrease venous return

87
Q

how is anaphylaxis initiated

A

an antigen binding to IgE antibodies

88
Q

how is sensitization produced

A

prior exposure to the antigen is needed

89
Q

can a patient have an allergic history and not know it

A

yes

90
Q

Arachidonic acid metabolites: name the 4 that are released. why are they released

A

Arachidonic acid metabolites: (leukotrienes and prostaglandins), kinins, and cytokines are subsequently synthesized and released in response to cellular activation in anaphylactic reaction

91
Q

On re-exposure, binding of the antigen to bridge two immuno-specific IgE found on the surfaces of mast cells and basophils release

A

Histamine

Tryptase

Chemotactic factors

arachidonic acid metabolites (leukotrienes and prostaglandins)

kinins

cytokinins

92
Q

The released mediators (from arachidonic acid metabolites) and histamine, tryptase, and chemotactic factors, kinins and cytokinins produce a symptom complex of:

A 
Bronchospasm
Upper airway edema in respiratory system
Vasodilation
Increased capillary permeability in the CV system
Urticaria
93
Q

when activated what do mast cells and basophils produce

A

different mediators

94
Q

when activated releases endothelium derived relaxing factor (nitric oxide) from vascular endothelium, increases capillary permeability, and contracts airway and vascular smooth muscles

A

H1:

95
Q

Activation causes gastric secretion, inhibits mast cell activation and contributes to vasodilation. When injected into the skin, histamine produces the classic wheal and flare…(Wheal: increased capillary permeability producing tissue edema: Flare: cutaneous vasodilation)

A

H2:

96
Q

how does histamine undergo rapid metabolism

A

by histamine N methyltransferase and diamine oxidase which is found in the endothelial cells

97
Q

drug of choice for anaphylactic reaction

A

EPI

98
Q

Hypotension EPI dose

A

5-10mcg bolus titrate to effect

99
Q

dose of epi for CV collapse full IV cardiopulmonary resuscitative

A

0.1-1mg of EPI should be given until hemodynamically stable

100
Q

patents with laryngeal edema without hypotension should receive EPI what route

A

sub Q because IV should not be given in normotensive patients

101
Q

what do we know about anesthetized patients and their sympathoadrenergic responses to acute anaphylactic shock/ spinal or epidural

A

may need larger doses of catecholamines

102
Q

what are the epi effects we need to treat anaphylactic reaction

A

vasoconstriction to reverse hypotension. beta 2 receptor stimulation bronchodilator and inhibits mediator release by camp in mast cells ad basophils

103
Q

what do we do to anesthetic volatiles in an anaphylactic reaction

A

turn off anesthetic drugs (not the bronchodilator you want especially if hypotension is involved)

they also interfere with the body compensatory response to CV collapse

104
Q

what is the risk of halothane to the myocardium during an anaphylatic response

A

halothane sensitizes the myocardium to EPI

105
Q

why do we give fluids during an anaphylactic response-

A

40% loss of intravascular fluid into the interstitial space causing rapid hypovolemia

106
Q

how much fluid do we give initially

A

2-4liters of LR or NS or colloid

107
Q

how much additional fluid do they need after the 2-4l bolus

A

25-50ml/kg given if hypotension persists.

COLLOID NOT PROVEN MORE EFFECTIVE IN ANAPHYLATIC SHOCK

108
Q

what do we do for refractory hypotension

A

may require TEE for rapid assessment of intraventricular volume and ventricular function assessment

109
Q

if we think the patient will have an allergic reaction what do we give

A

Pretreatment of antihistamines before giving drugs known to release histamine does not inhibit histamine release, but rather compete with histamine at the receptor and may attenuate decreases in SVR.

110
Q

what do we know about the things given in the or causing a release of

A

histamine release in a dose dependent non immunologic fashion

111
Q

why is the or is there non immunlogic histamine release

A

mechanism is not clear

112
Q

non immunologic release of histamine is known to represent a select mast cell and not ____ activation

A

basophil

113
Q

what is the only cell population that releases histamine in response to both drugs and endogenous stimuli

A

human cutaneous mast cells

114
Q

what receptors is histamine release not dependent on? why is that?

A

mu receptors/c fentanyl and sufentanil do not release histamine in human skin

115
Q

antibodies of IgG class- if directed against antigenic determinants or granulocyte surfaces can also produce {what}

A

leukocyte aggregation

116
Q

antibodies of IgG class are called

A

leukoagglutinins

117
Q

investigators have associated complement activation and PMN aggregation in producing the clinical expression of what 4 things

A

transfusion reactions

pulmonary vasoconstriction after protamine reactions

ARDS

septic shock

118
Q

Interacts with specific high affinity receptors on polymorphonuclear leukocytes (PMNs) and platelets causing leukocyte chemotaxis, aggregation, and activation.

A

C5a: non IgE mediated reaction

119
Q

Aggregated leukocytes embolized to various organs, producing microvascular occlusion and liberation of inflammatory products such as arachidonic acid metabolites, oxygen free radicals and lysosomal enzymes.

A

C5a: non IgE mediated reaction

120
Q

They release histamine from mast cells and basophils, contract smooth muscles, increase capillary permeability, and cause interleukin synthesis.

A

C3a and C5a are the anaphylatoxins.

121
Q

Immunologic and non-immunologic mechanisms release many of the same mediators without IgE involvement and can present an identical clinical syndrome of

A

anaphylaxis

122
Q

Compliment activation follows both:
immunologic:
non-immunologic

A

Immunologic: antibody mediated or “the classic pathway”

Non-immunologic: alternative to the classic pathway

123
Q

These include a series of multimolecular, self-assembling, proteins that release biologically active complement fragments of ____

A

c3 c5

124
Q

Peptide Mediators of Anaphylaxis

A

Factors are released from mast cells and basophils that cause granulocyte migration (chemotaxis) and collect at the site of the inflammatory stimulus
Eosinophil (eosinophilic chemotactic factor) in acute allergic response is unclear
Eosinophils release enzymes that can inactivate histamine and leukotrienes
Neutrophilic chemotactic factor is release as well and may be responsible for the recurrent manifestations of anaphylaxis

125
Q

Arachidonic Acid Metabolites

A

Arachidonic Acid Metabolites
Leukotrienes and prostaglandins are both synthesized after mast cell activation from arachidonic acid metabolism of phospholipid cell membranes through either lipoxygenase or cyclooxygenase pathways
Classic slow reacting substances of anaphylaxis is a combination of leukotrienes C4, D4, E4.
Leukotrienes: produces bronchoconstriction, increased capillary permeability, vasodilation, coronary vasoconstriction, any myocardial depression
Prostaglandins : potent mast cell mediators. Produces vasodilation, bronchospasm, pulmonary hypertension, and increased capillary permeability
Prostaglandin D2: major metabolite of plasma levels of thromboxane B2 which is a metabolite of thromboxane A2

126
Q

recognition of anaphylaxis

what is onset?

what are the reactions expected?

A

Onset and severity of reaction r/t the mediator’s specific end-organ effect

An antigenic challenge in a sensitized patient usually produces immediate clinical manifestation of anaphylaxis BUT the onset may be delayed 2-20 minutes.

Reactions may range from minor clinical changes to full blown syndrome leading to death

Spring '20/ L. BASICS- Immune, OR Hazards, OP (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions