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x 6102 Final > immunity/inflammation explosion > Flashcards

immunity/inflammation explosion Flashcards

1
Q

innate resistance/immunity

A 
natural epithelial barrier (first line of defense)
\+
inflammatory response (second line of defense)

confer innate resistance and protection to the body

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2
Q

specificity of response in innate immunity vs adaptive immunity

A

innate immunity responses are broadly specific

vs

adaptive immunity response is very specific towards a particular antigen

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3
Q

compare timing of defense between innate immunity and adaptive immunity

A

innate immunity:

  • first line (barriers): constant
  • second line (inflammatory): immediate response

adaptive immunity: delay between first exposure to antigen and max response, but upon subsequent exposure response is immediate

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4
Q

innate immunity: first line defense cells

A

epithelial

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5
Q

innate immunity: second line defense cells

A

Mast cells, granuloyctes, monocytes/macrophages, NK cells, platelets, endothelial cells

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6
Q

adaptive immunity: third line defense cells

A

T and B lymphocytes, macrophages, dendritic cells

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7
Q

innate immunity: first line defense peptides

A

Defensins, cathelicindins, collectins, lactoferrin, bacterial toxins

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8
Q

innate immunity: second line defense peptides

A

complement, clotting factors, kinins

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9
Q

adaptive immunity: third line defense peptides

A

antibodies, complement

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10
Q

innate immunity: first line defense protective mechanisms

A

anatomic barriers, cells and secretory molecules or cytokines and ciliary activity

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11
Q

innate immunity: second line defense protective mechanisms

A

vascular responses, cellular components, secretory molecules or cytokines, activation of plasma protein systems

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12
Q

adaptive immunity: third line defense protective mechanisms

A

activated T and B lymphocytes, cytokines and antibodies

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13
Q

inflammation

A

result of damage to the epithelial barrier in order to

  • limit extent of damage
  • protect against infection
  • initiate repair of the damaged tissue

non-specific, rapid initiation with no memory cells

can be activated s/t: infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation

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14
Q

plasma protein systems x3

A

complement system
clotting system
kinin system

function: via sequential activation of components (aka cascade) - help destroy/contain bacteria

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15
Q

complement system

A

may destroy pathogens directly and can activate/collaborate with every other component of the inflammatory response

3 pathways: classical, lectin, alternative

4 functions: anaphylatoxic activity, chemotaxis, opsonization, cell lyris

most important result: production of fragments during activation of C2, C3, C4, C5

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16
Q

where do the three pathways of the complement system converge?

A

activation of C3 → C3a + C3b

C3a: increased vascular permeability via stimulation of mast cells to release histamine

C3b: form thioester bonds - bind with pathogen surface → opsonization

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17
Q

effect of C3a upon activation

A

increased vascular permeability via stimulation of mast cells to release histamine

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18
Q

effect of C3b upon activation

A

form thioester bonds - bind with pathogen surface → opsonization

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19
Q

complement system: classical pathway

A

activated by adaptive immune system proteins (antibodies) bound to specific target (antigen)

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20
Q

complement system: lectin pathway

A

activated by mannose-containing bacterial CHO

- antibody independent!

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21
Q

complement system: alternative pathway

A

activated by gram negative bacterial and fungal cell wall polysaccharides

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22
Q

anaphylatoxic activity

A

rapid induction of mast cell degranulation

complement system function

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23
Q

chemotaxis

A

biochemical substance that attracts leukocytes to the site of inflammation

(complement system function)

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24
Q

opsonization

A

opsonins are molecules that tag microorganisms for destruction by cells of the inflammatory system

(complement system function)

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25
Q

clotting system end product

A

fibrin

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26
Q

clotting system pathways x3

A

intrinsic
extrinsic
common

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27
Q

clotting system functions x4

A
  • prevent spread of infection to adjacent tissues
  • trap microorganisms + foreign bodies at site of inflammation
  • forms clot to stop bleeding
  • provide framework for future repair/healing
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28
Q

kinin system function

A

augments inflammation with proteins that

  • promote vasodilation + increased capillary permeability
  • induce pain
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29
Q

how is the kinin system activated?

A

conversion of prekallikrein → kallikrein (identical to factor XIIa from the clotting system)

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30
Q

primary cells of inflammation x3

A

mast cell
endothelium
platelets

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31
Q

primary cell of inflammation: mast cell function

A

degranulation as immediate response to injury, bacterial/viral presence

release histamine →
- temporary/rapid large blood vessel constriction
- dilation of postcapillary venules
both increase blood flow into microcirculation

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32
Q

primary cell of inflammation: endothelium function

A
  1. produce NO & prostacyclin (PGI2) → synergistic
    - maintain blood flow/pressure
    - inhibit platelet activation
    - NO maintains vascular tone/continually relaxes vasculature
  2. express receptors to help leukocytes leave circulation
  3. retracts to allow fluid to pass into tissues
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33
Q

primary cell of inflammation: platelet function

A

stop bleeding

degranulation
- alpha granules: coagulation proteins, soluble adhesion molecules, growth factors, protease inhibitors, membrane adhesion molecules

  • dense granules: small molecules ie ADP, serotonin, Ca, Mg
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34
Q

damage to the endothelium promotes…?

A

clotting

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35
Q

mast cell

A

cellular bags of granules located in loose connective tissues close to blood vessels

found in large numbers in areas directly exposed to the environment
ex: skin, linings of GI & respiratory tracts

great number of stimuli causes activation → initiation of inflammatory response

(a primary cell of inflammation)

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36
Q

causes of mast cell degranulation x5

A
  • mechanical injuries
  • chemicals
  • pathogen activation of TLRs
  • allergens binding to IgE on mast cell surface
  • activated complement
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37
Q

toll-like receptor (TLR)

A

expressed on surface of many cells that have direct and early contact with potential pathogenic microorganism

recognize large variety of PAMPs

bridges between innate resistance and adaptive immune response via induction of cytokines that increase response of lymphocytes to foreign antigens on pathogens

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38
Q

pathogen-associated molecular pattern (PAMP)

A

molecular “patterns” on infectious agents or their products recognized by PRRs

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39
Q

pattern recognition receptors (PRR)

A

set of receptors that recognize a limited array of specific molecules (ex: PAMPs) on cells involved in innate resistance

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40
Q

mast cell degranulation effects x3

A

Histamine → vascular effects → dilation and increased permeability→ exudation

Neutrophil chemotactic factor → neutrophils attracted to site → phagocytosis

Eosinophil chemotactic factor of anaphylaxis → eosinophil attracted to site → phagocytosis and inhibition of vascular effects

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41
Q

effect of histamine binding to H1 receptor x2

A

H1 receptor is pro-inflammatory

bronchi smooth muscle cells → bronchoconstriction

neutrophils → augmentation of chemotaxis

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42
Q

effect of histamine binding to H2 receptor x2

A

H2 receptor is anti-inflammatory

parietal cells (stomach mucosa) → secretion of gastric acid

suppression of leukocyte function

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43
Q

leukotrienes

A

product of arachidonic acid from mast cell membranes

similar effects to histamine (smooth muscle contraction, increased vascular permeability)

more important in later stages of inflammation

L is for later!

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44
Q

Prostaglandins (PGE1 and PGE2)

A

effect similar to leukotrienes (increased vascular permeability)
+ cause neutrophil chemotaxis
+ induce pain via swelling (tissue distention/nociceptor activation)

P is for pain!

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45
Q

platelet-activating factor

A

effect similar to leukotrienes (increased endothelial retraction → increased vascular permeability)
+ leukocyte adhesion to endothelial cells
+ activate platelets (DUH)

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46
Q

neutrophils

A

predominate in early inflammatory response - first responders!

phagocytes! ingest bacteria, dead cells, cellular debris

short lived, can’t divide, become part of pus

primary role: debris removal in sterile lesions, phagocytosis of bacteria in non-sterile

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47
Q

monocytes + macrophages

A
  • survive/divide in the inflammatory site
  • involved in activating adaptive immune system
  • primary cells that infiltrate tissue in wounds
  • remove cells/cellular debris
  • produce cytokines: suppress further inflammation and initiate healing

activation results in increased: phagocytic activity, size, plasma membrane area, glucose metabolism, number of lysosomes (predominate in late inflammation)

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48
Q

eosinophils

A

capable of phagocytosis

  • provide defense against parasites
  • regulate vascular mediators released from mast cells
  • help control vascular effects of inflammation
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49
Q

cytokine examples x4

A

lymphokines, interferon, interleukins, tumor necrosis factor-alpha (TNF-α)

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50
Q

interleukins

A

CYTOKINE!

  • alteration of adhesion molecule expression on many cell types
  • induce: leukocyte chemotaxis
  • induce: proliferation/ maturation of leukocytes in bone marrow
  • enhance adaptive immune response against pathogenic microorganisms + foreign substances

IL-1 and IL-6 = pro-inflammatory
IL-10 = anti-inflammatory

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51
Q

pro-inflammatory interleukins

A

IL-1 and IL-6

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52
Q

anti-inflammatory interleukins

A

IL-10

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53
Q

interferons

A

CYTOKINE!

  • primarily: protect against viral infections & modulate inflammatory response
  • produced/released by virally infected host cells in response to viral double-stranded RNA
  • does not directly kill viruses but prevents them from infecting additional healthy cells
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54
Q

TNF-α

A

CYTOKINE!

  • secreted by macrophages in response to PAMP recognition by TLR
  • local and systemic effects
  • endogenous pyrogen
  • increases liver synthesis of pro-inflammatory proteins
  • causes muscle wasting (cachexia) + intravascular thrombosis as consequence of prolonged production d/t severe infection or cancer
  • probably responsible for fatalities from shock caused by gram-negative bacterial infections
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55
Q

lymphokines

A

CYTOKINE!

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56
Q

most likely cause of fatalities from shock d/t gram neg bacteria

A

TNF-α

57
Q

local signs of acute inflammation x4

A

heat, redness - r/t vasodilation/increased blood flow

swelling - exudate accumulation

pain - pressure exerted by exudate; also d/t bradykinin + prostaglandins

58
Q

biochemical mediators that cause pain during acute inflammation

A

bradykinin

prostaglandin

59
Q

systemic signs of acute inflammation x3

A

fever
leukocytosis
plasma protein synthesis

60
Q

systemic sign of acute inflammation: fever

A
  • partially induced by specific cytokines released from neutrophils/macrophages = endogenous pyrogens (act directly on the hypothalamus)
  • kills microorganisms highly sensitive to temperature changes
  • harmful: increases susceptibility to gram neg endotoxins
61
Q

systemic sign of acute inflammation: leukocytosis

A

particularly an increase in neutrophils (especially immature, left shift)

62
Q

systemic sign of acute inflammation: plasma protein synthesis

A

acute phase reactants

pro- or anti-inflammatory - i.e. fibrinogen, CRP, haptoglobin, amyloid A, α-1 antitrypsin and ceruloplasmin

increase in fibrinogen = increased ESR

63
Q

fever can be harmful - why?

A

increases susceptibility to gram neg endotoxins

64
Q

pediatric self-defense mechanisms

A

neonates: transiently depressed inflammatory function & deficiencies in complement/collectins
- increased susceptibility to bacterial infections

65
Q

self-defense mechanism considerations for aging

A
  • at risk for impaired wound healing s/t underlying illness, comorbidities
  • slower rate of cell proliferation = increased healing time and areas of hypoxia s/t atrophy of underlying capillaries
  • diminished natural ability to ward off infection
66
Q

immunogen

A

most but not all antigens - induce immune response resulting in production of antibodies or functional T cells

67
Q

Haptens

A

small molecular weight antigens

cannot trigger immune response alone; do when bound to carrier protein

68
Q

epitope

A

aka antigenic determinant

precise portion of antigen configured for recognition/binding

69
Q

antigen-presenting cells (APCs)

A

during clonal selection, antigen is processed and presented to immune cells by APCs

T-helper cells interact with APCs & immunocompetent B or T cells → differentiation
B cells: active antibody-producing cells (plasma cells)
T cells: effector cells (i.e. T-cytotoxic cells)

70
Q

clonal diversity

A

all necessary receptor specificities are produced

generation takes place in primary (central) lymphoid organs: thymus, bone marrow

results: immature/immunocompetent T & B cells with receptors that can recognize virtually any antigenic molecule

these migrate to secondary (peripheral) lymphoid organs and await antigen

71
Q

primary (central) lymphoid organs

A

thymus, bone marrow

72
Q

secondary (peripheral) lymphoid organs

A

spleen, lymph nodes, adenoids, tonsils, Peyer patches

73
Q

clonal selection

A

antigen selects lymphocytes with compatible receptors, expands their population, causes differentiation into antibody-secreting plasma cells or mature T cells

results in mature, specific immune response against antigen

74
Q

APC + T helper interaction

A

During clonal selection, antigen processed/presented to immune cells by antigen-presenting cells (APCs)

T-helper cells interact with APCs + immunocompetent B or T cells → differentiation
B cells: active antibody-producing cells (plasma cells)
T cells: effector cells (i.e. T-cytotoxic cells)

75
Q

Humoral immunity

A

primary cells: B cells & circulating antibodies

Causes direct inactivation of microorganism or
activation of inflammatory mediators that destroy pathogen

Primarily protects against bacteria & viruses

76
Q

Humoral immunity primarily protects against

A

bacteria + viruses

77
Q

Cell-mediated immunity

A

Differentiates T cells

Kills targets directly, or stimulates the activity of other leukocytes

Primarily protects against viruses & cancer

78
Q

Cell-mediated immunity primarily protects against

A

viruses + cancer

79
Q

criteria that influence an antigen’s degree of immunogenicity

A

Degree of FOREIGNESS to a host – most important

Being appropriate SIZE – large molecules are most immunogenic

Having an adequate chemical COMPLEXITY – greater diversity = more immunogenicity

Being present in sufficient QUANTITY – high or low extremes can cause tolerance

80
Q

MHC class 1 - genes + function

A

MHC class 1 genes – HLA: A, B and C

present antigens to cytotoxic T cells
found on almost all cells except erythrocytes

81
Q

MHC class 2 - genes + function

A

MHC class 2 genes – HLA: DR, DP and DQ

present antigens to helper T cells
usually found on B cells and APCs

82
Q

Major Histocompatibility Complex aka

A

Human Leukocyte Antigen

Encoded from different genetic loci on short arm of chromosome 6

83
Q

stages of pathologic infection x4

A

colonization
invasion
multiplication
spread

84
Q

factors that influence infection by a pathogen x7

A 
Mechanism of action
Infectivity 
Pathogenicity 
Virulence
Immunogenicity 
Toxigenicity 
Portal of entry
85
Q

Infectivity

A

ability of the pathogen to invade and multiply in the host

86
Q

Pathogenicity

A

ability of an agent to produce disease - success depends on communicability, infectivity, extent of tissue damage and virulence

87
Q

virulence

A

capacity of pathogen to cause severe disease; potency

88
Q

immunogenicity

A

ability of a pathogen to produce an immune response

89
Q

toxigenicity

A

ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence

90
Q

portal of entry

A

route by which pathogenic microorganism infects the host - direct contact, inhalation, ingestion or bites of animals/insects

91
Q

factors that influence pathogenicity x4

A

communicability, infectivity, extent of tissue damage, virulence

92
Q

how do cytokines raise the thermoregulatory set point?

A

stimulation of prostaglandin synthesis and turnover in thermoregulatory (brain) and non-thermoregulatory (peripheral) tissue

93
Q

exogenous pyrogens

A

derived from outside the host, in general arise from external sources involving invading microorganisms

Little evidence they cause fever directly

94
Q

endogenous pyrogens

A

ex: IL-1, IL-6, TNF
- in general tend to arise from colonizing flora
- induce central fever
- cytokines raise the thermoregulatory set point

95
Q

5 steps required for development of successful vaccination

A
  • characterize desired protective immune RESPONSE
  • identify appropriate ANTIGEN to induce response
  • determine most effective ROUTE
  • optimized NUMBER/TIMING of doses to induce protective immunity in large proportion of at-risk population
  • most effective yet safe FORM in which to administer vaccine
96
Q

recombinant vaccination

A

vaccine produced through recombinant DNA technology. This involves inserting the DNA encoding an antigen (such as a bacterial surface protein) that stimulates an immune response into bacterial or mammalian cells, expressing the antigen in these cells and then purifying it from them.

ex: Hep B, HPV

97
Q

viral vaccine types x3

A

attenuated
inactivated
recombinant

98
Q

bacterial vaccine types x3

A
  • conjugated (to carrier proteins)
  • toxoids
  • extracted capsular polysaccharides
99
Q

percentage of population needed to achieve herd immunity

A

~85%

100
Q

attenuated vaccine examples x4

A

MMR
varicella
polio (PO)
rotavirus

101
Q

inactivated vaccine examples x3

A

hepatitis A
polio (IM)
influenza

102
Q

recombinant vaccine examples x2

A

Hep B, HPV

103
Q

conjugated vaccine examples x1

A

HiB

104
Q

toxoid vaccine example

A

DTaP, DT

105
Q

extracted capsular polysaccharide vaccine examples

A

meningococcal

pneumococcal

106
Q

most susceptible cells to HIV and why that’s important

A

Activated T cells more efficiently support HIV replication (HIV = chronic activation of uninfected T cells with HIV-specific TCR)

Does not bode well for vaccine development if the induced and supposedly protective CD4+ cells are also the most susceptible targets for HIV

107
Q

factors leading to bacterial resistance x4

A

capacity to INACTIVATE ANTIBIOTICS

MODIFICATION of target molecule (ex: modified abx sensitive binding site on ribosome → resistance to abx that interfere with protein synthesis)

ALTERATION of METABOLIC PATHWAYS that may be sensitive to abx to alternative more abx resistant pathways

mediated by MULTI-DRUG TRANSPORTERS in microorganism membrane (prevent entrance or increase efflux of abx)

108
Q

how T helpers interact with B and T cells

A

APC “activates” T-helper cell

helper T goes to immunocompetent B or T cells → differentiation

B cells: active antibody-producing cells (plasma cells)

T cells: effector cells (i.e. T-cytotoxic cells)

109
Q

what do T cytotoxic cells destroy?

A

cancer cells or cells infected with virus

110
Q

what do natural killer cells destroy?

A

abnormal cells that don’t express MHC I

NK are cytotoxic cells that are not antigen specific

111
Q

what do T reg cells do?

A

regulate immune response to avoid attacking self & avoid overactivation of immune response

112
Q

antibodies protect against invaders how? x4

A
  1. Agglutination - insoluble particles clump together
  2. Precipitation - soluble antigens become insoluble precipitate
  3. Neutralization - antibodies cover the toxic parts of the antigen
  4. Lysis - cause rupture of the cellular membrane on the offending agent

these are just beginning steps, complement system needs to come in next

113
Q

what three molecules needed for opsonization?

A

Opsonins + antibody + C3b

114
Q

Hypersensitivity

A

altered immunologic response to an antigen resuting in disease or damage to host

115
Q

Allergy

A

Exaggerated response against an environmental antigen (exogenous)

116
Q

Autoimmunity

A

disturbance in immunologic tolerance of self-antigens

autoimmune diseases

117
Q

Alloimmunity

A

aka isoimmunity

immune reaction to tissues of another individual

Directed against beneficial foreign tissues (i.e. transfusions, transplants)

118
Q

allergy vs immunity

A

allergy: deleterious response to exogenous
immunity: protective response

119
Q

desensitization

A

minute qtys of allergen injected in increasing doses over prolonged period; may reduce severity of the allergic reaction in treated pt

associated with risk of systemic anaphylaxis

120
Q

desensitization associated with increased risk of what

A

anaphylaxis

121
Q

immediate vs delayed hypersensitivity

A

Immediate - occur min - hours
ex: anaphylaxis

Delayed - may take several hours, max intensity days after exposure
ex: TB skin test

122
Q

type I hypersensiivity

A

pollens, molds and fungi, foods, animals, cigarette smoke, house dust

ALMOST ANYTHING IN THE ENVIRONMENT

123
Q

Type II, III, IV hypersensitivities

A

II & III: rare but may include abx and soluble antigens produced by infectious agents (hep B)

II: usually against allergic haptens that bind to surface of cells and elicit IgG or IgM

IV: plan resins, metals, acetylates, rubber, cosmetics, detergents, topical abx

124
Q

5 general mechanisms by which type II hypersensitivity can affect cells

A
  1. cell destroyed by IgG/IgM or complement-mediated lysis
  2. cell destroyed via phagocytosis (macrophages)
  3. neutrophils release granules
  4. ab-dependent cell mediated cytotoxicity: natural killer cells use Fc to recognize ab on target cell and release toxic substances that destroy target cell
  5. modulation/blocking normal function of recetors by anti-receptor an
125
Q

likely causes of autoimmune diseases x4

A
  1. sequestered antigen
  2. complication of ID
  3. development of neoantigen
  4. defective peripheral tolerance
126
Q

neoantigen

A

likely cause of autoimmune disease: produces allergic reaction that can lead to autoimmunity

  • many are haptens which become immunogenic once they bind to self-proteins
127
Q

likely causes of autoimmune diseases

1. sequestered antigen

A

self-antigen doesn’t always encounter immune system; barriers hiding them in a tissue are removed leading to antigenic sensitization against that tissue

128
Q

likely causes of autoimmune diseases

2. complication of ID

A

antigen from infectious agent resemble self-antigen so ab and T cell produced to protect against it also recognize self-antigen as foreign

129
Q

likely causes of autoimmune diseases

4. defective peripheral tolerance

A

defect in regulatory cells allowing expansion of clones of autoreactive cells and development of autoimmune disease

130
Q

ab against antigens of ABO systems are usually

A

IgM

131
Q

where is Rh expressed and what does + express

A

RBC

expresses D antigen on RhD protein

132
Q

Immune deficiency

A

impaired function of T cells, B cells, phagocytes and/or complement

133
Q

most severe immunodeficiency

A

severe combined immunodeficiency (T & B cell deficient)

SCID

134
Q

primary immune deficiency

A

(congenital) - most result of single gene defect

135
Q

vertical transmission of HIV

A

mom to baby

without tx, develop HIV within 6 mo + life expectancy less than 3 years

136
Q

how soon does HIV ab appear?

A

within 4-7 weeks of infection

sexual transmission can result in seronegative for 6-14 mo

137
Q

definition of AIDS

A

based on labs & clinical symptoms

  • seropositive
  • CD4 cells less than 200
  • atypical/opportunistic infection
138
Q

HIV pathophys

A

RNA retrovirus (info stored on RNA instead of dsDNA)

carries reverse transcriptase which translates RNA to DNA bits

carries integrase which adds to host cell DNA

results in:

  • major immunologic finding: significant decreased in CD4 T helper cells
  • decreased T cells, especially T-memory (seem more susceptible)
  • decreased thymic production of new T cells
  • damaged secondary lymphoid organs, especially lymph nodes
139
Q

HIV structure

A

Gp120 protein (binds CD4 on helper T)

co-receptors:
CXCR4 prefer T cell to form syncytium (fusion of multiple infected cells)

CCR5 prefer macrophages + no syncytium

x 6102 Final (3 decks)

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