Pathology Ch 2 - Inflammation

Front 1

contain and isolate injury, destroy invading microorg. and inactivate toxins in prep for healing

Back 1

What is the purpose of inflammation?

Front 2

vascular wall response and inflam cell response

Back 2

What are the 2 main components of inflammation?

Front 3

early onset, short duration, fluid exudation and PMN emigration

Back 3

What are some characteristics of acute inflammation?

Front 4

later onset, longer duration, involves lymphocytes and macrophages and induces BV prolif and scarring

Back 4

What are some characteristics of chronic inflammation

Front 5

heat, redness, edema and pain plus loss of function

Back 5

What are the 4 classic signs of inflammation plus the 1 newly added one?

Front 6

edema

Back 6

excess fluid in interstitial tissue or body cavities

Front 7

exudate

Back 7

inflammatory extravascular fluid that has high protein concentration and cellular debris

Front 8

exudation

Back 8

extravasation of fluid, proteins, blood cells from vessels into intersitial tissue or body cavities

Front 9

pus

Back 9

purulent inflammatory exudate rich in neutrophils and cell debris

Front 10

transudate

Back 10

extravascular fluid with low protein content

Front 11

hydrostatic pressure

Back 11

causes fluid to move out of the circulation

Front 12

plasma colloid osmotic pressure

Back 12

causes fluid to move into capillaries

Front 13

decreases

Back 13

exudation of protein-rich fluid into intersitial space due to increased vascular permeability ____ osmotic pressure

Front 14

stasis

Back 14

occurs when fluid loss causes concentration of RBC and increased blood viscosity

Front 15

margination

Back 15

accumulation of WBC along the endothelium

Front 16

formation of venule intercellular endothelial gaps

Back 16

most common cause of increased vascular permeability

Front 17

chemical mediators

Back 17

What causes endothelial cells in venules to contract?

Front 18

release of ROS and proteolytic enzymes

Back 18

How do leukocytes increase vascular permeability?

Front 19

margination/rolling/adhesion, transmigration and migration

Back 19

What are the 3 steps in extravasation?

Front 20

selectins; sialylated Lewis X

Back 20

these bind via lectin domains on cell surface glycoproteins; give an example

Front 21

immunoglobulin family: ICAM and VCAM

Back 21

these bind integrins on leukocytes

Front 22

sialyl-Lewis X

Back 22

name the leukocytes receptor that interacts with P-selectin:

Front 23

sialyl-Lewis X and PSGL-1

Back 23

name the leukocytes receptors that interacts with E-selectin:

Front 24

beta integrins: Mac and IFA

Back 24

name the leukocytes receptor that interacts with ICAM:

Front 25

integrins

Back 25

name the leukocytes receptor that interacts with VCAM:

Front 26

integrins

Back 26

bind to members of the immunoglobulin family and to extracellular matrix:

Front 27

modulate the surface expression or avidity of adhesion molecules

Back 27

How do chemokines affect adhesion and transmigration?

Front 28

P-selectin

Back 28

Which receptor is rapidly translocated to the endothelial cell surface after histamine exposure?

Front 29

IL1 and TNF

Back 29

What mediators activate endothelial cells by inducing E-selectin, ICAM and VCAM expression?

Front 30

high-affinity binding form of LFA and Mac (integrins)

Back 30

What occur with activation of the leukocyte to allow firm adhesion?

Front 31

PECAM on both endothelial cells and leukocytes

Back 31

What receptor/molecule is responsible for diapedesis?

Front 32

neutrophils

Back 32

What leukocytes predominates during the first 6-24 hours of inflam response?

Front 33

monocytes

Back 33

What leukocytes predominates after 24-48 hours of an inflam response?

Front 34

leukocyte surface G-protein-coupled receptor

Back 34

To what do chemotactic agents bind to initiate chemotaxis?

Front 35

PLAc and kinase activation; increased cytosolic Ca and GTPase activity; polymerization of actin causing cell movement

Back 35

What happens when a G-protein-coupled receptor on a leukocyte becomes activated?

Front 36

by extending pseudopods that bind the ECM and pull the cell forward

Back 36

How do leukocytes move?

Front 37

TLRs

Back 37

these surface molecules mediate innate leukocyte responses to different classes of microbes

Front 38

recognition and binding, engulfment, killing and degradation

Back 38

What are the 3 steps of phagocytosis?

Front 39

opsonins

Back 39

These enhance phagocytosis by binding to the leukocyte receptors:

Front 40

Fc fragment and C3b

Back 40

What are the major opsonins?

Front 41

NADPH oxidase

Back 41

O2 dependent mechanisms of phagocytosis occur via activation of this oxidase:

Front 42

NADPH oxidase

Back 42

This converts O2 to superoxide anion and eventually produces hydrogen peroxide (during phagocytosis):

Front 43

myeloperoxidase (MPO)

Back 43

this converts hydrogen peroxide and Cl- to hydrochlorite and is the most effective means of killing bacteria

Front 44

frustrated phagocytosis (large undigestable material), premature fusion of lysosome, lysosome damage by ingested material (urate)

Back 44

lysosomal enzymes can be released into the extracellular space by:

Front 45

leukocyte adhesion deficiency type II

Back 45

defect in fucose metabolism causing loss of sialyl Lewis X

Front 46

leukocyte adhesion deficiency type I

Back 46

defective synthesis of beta2 integrins (LFA and Mac)

Front 47

Chediak-Higashi syndrome

Back 47

defect in phagolysosome formation

Front 48

chronic granulomatous disease

Back 48

defect in microbicidal activity of leukocyte (NADPH defect)

Front 49

histamine and serotonin

Back 49

these mediators cause vasodilation and increased cell permeability:

Front 50

C3a and C5a (anaphylatoxins)

Back 50

these complement fragments cause mast cell release of granules:

Front 51

contact with collagen, thrombin, ADP, Ag-Ab complexes and PAF

Back 51

these 5 things all cause platelet release of granules:

Front 52

complement, kinin and clotting systems

Back 52

these 3 plasma-derived mediators play key roles in inflammation:

Front 53

activation of C3

Back 53

this is the most important step in the complement cascade for its biologic functioning:

Front 54

binding of Ab-Ag complex to C1

Back 54

this is how the classical pathway of the complement system begins:

Front 55

binding of a microbe product (endotoxin) to C1

Back 55

this is how the alternative pathway of the complement system begins:

Front 56

plasma mannose-binding lectin binds to microbe carb and activates C1

Back 56

this is how the lectin pathway of the complement system begins:

Front 57

C3a: released; C3b: covalently attached to cell/molecule where complement is being activated

Back 57

What is the function of the 2 products of the cleavage of C3?

Front 58

C3b and other complement fragments

Back 58

These combine to cleave C5

Front 59

binds the late components (C5-9) to form the membrane attack complex (MAC)

Back 59

What does C5b do after the cleavage of C5?

Front 60

C3a and C5a (anaphylatoxins)

Back 60

these stimulate histamine release from mast cells and increase vascular permeability and vasodilation

Front 61

C5a

Back 61

This complement pathway product is a powerful leukocyte chemoattractant:

Front 62

C3b

Back 62

This complement pathway product is an opsonin:

Front 63

DAF (cell associated) and C1 inhibitor (circulating)

Back 63

regulates complement activation (2)

Front 64

paroxysmal nocturnal hemoglobinuria

Back 64

caused by a defect in DAF, characterized by recurrent complement-mediated red cell lysis and anemia

Front 65

hereditary angioneurotic edema

Back 65

caused by C1 inhibitor deficiency, characterized by episodic potentially life-threatening edema

Front 66

kininogens; to form bradykinin

Back 66

these plasma proteins are cleaves by kallikreins to form _____

Front 67

bradykinin

Back 67

causes BV dilation, increased vascular permeability and pain

Front 68

12

Back 68

Hageman factor

Front 69

12 (Hageman factor)

Back 69

this clotting factor converts prekallikrein to kallikrein

Front 70

12 (Hagemena factor)

Back 70

this clotting factor can also activate the fibrinolytic system

Front 71

eicosanoids

Back 71

these are derived from cell membrane-derived arachidonic acid and are signaling molecules

Front 72

cyclooxygenases and lipoxygenases

Back 72

2 major enzyme classes of eicosanoids

Front 73

prostaglandins and throboxanes

Back 73

2 enzymes in the cyclooxygenase class

Front 74

cyclooxygenase

Back 74

Aspirin inhibits what enzyme?

Front 75

leukotrienes and lipoxins

Back 75

2 enzymes in the lipoxygenase class

Front 76

prostaglandin I2 and E2

Back 76

these cyclooxygenases cause vasodilation

Front 77

prostaglandin E2

Back 77

this cyclooxygenase increases sensitivity to painful stimuli and mediates fever

Front 78

thromboxane A2

Back 78

this cyclooxygenase causes vasoconstriction

Front 79

leukotriene C4, D4 and E4

Back 79

these lipoxygenases causes vascular permeability

Front 80

leukotriene B4

Back 80

this lipoxygenase is a chemotactic agent

Front 81

lipoxins

Back 81

these lipoxygenases may be engogenous negative regulators of leukotriene action

Front 82

PAF

Back 82

phospholipid derived mediator produced by mast cells and other leukocytes

Front 83

PAF

Back 83

causes platelet aggregation, vasodilation, increased vascular permeability and increased leukocyte adhesion and chemotaxis

Front 84

cytokines

Back 84

these are produced mostly by activated lymphocytes and macrophages

Front 85

IL and TNF

Back 85

these are the major cytokines mediating inflammation

Front 86

activated macrophages

Back 86

TNF and IL are produced mainly by what cell?

Front 87

activate endothelial cells; induce acute-phase response; regulate body mass (TNF) by suppressing appetite

Back 87

these are the functions of TNF and IL:

Front 88

cachexia; TNF

Back 88

pathologic state characterized by weight loss and anorexia accompanying some infections and neoplasias; is caused by sustained production of ______

Front 89

CXC

Back 89

class of chemokine that acts to recruit neutrophils

Front 90

CC

Back 90

class of chemokine that recruit monocytes, eosinophils, basophils and lymphocytes

Front 91

C

Back 91

class of chemokine that are relatively specific for lymphocytes

Front 92

CX3C

Back 92

class of chemokine that promotes firm adhesion of lymphocytes and monocytes (cell surface form) and is a chemoattractant (soluble form)

Front 93

through G-protein-linked receptors

Back 93

How do chemokines mediate their activites?

Front 94

endothelium-derived relaxation factor

Back 94

What is an alternate name for NO?

Front 95

inhibits platelet aggregation and adhesion; kills certain microbes and tumor cells

Back 95

Actions other than vasodilation of NO include:

Front 96

eNOS

Back 96

Which type of NOS is responsible for maintaining vascular tone?

Front 97

iNOS

Back 97

What type of NOS is responsible for reducing leukocyte recruitment?

Front 98

specific (secondary) and azurophil (primary)

Back 98

What are the 2 granules types of the neutrophil?

Front 99

specific (secondary)

Back 99

What type of neutrophil granule contains lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator and histaminase

Front 100

azurophil (primary

Back 100

What type of neutrophil granule containsmyeloperoxidase, lysozyme, defensins, acid hydrolase, neutral protease

Front 101

Substance P

Back 101

neuropeptide that is a mediator of vascular permeability, transmits pain signals, regulates BP and stimulates immune and endocrine cell secretion

Front 102

prostaglandins, NO, histamine

Back 102

these mediators are important to vasodilation:

Front 103

vasoactive amines, C3a and C5a (liberate amines), bradykinin, leukotrienes, PAF, substance P

Back 103

these mediators are important to increased vascular permeability:

Front 104

C5a, leukotriene, chemokines, IL, TNF, bacterial products

Back 104

these mediators are important to chemotaxis:

Front 105

IL, TNF, prostaglandins

Back 105

these mediators are important to fever

Front 106

prostaglandins, bradykinin

Back 106

these mediators are important to pain:

Front 107

neutrophil and macrophage, lysosomal enyzmes, oxygen metabolites, NO

Back 107

these mediators are important to tissue damage:

Front 108

resolution, fibrosis, progression to chronic inflammation

Back 108

3 outcomes of acute inflammation:

Front 109

serous inflammation

Back 109

type of acute inflammation involving tissue fluid accumulation, indicates modest increase in vascular permeability

Front 110

fibrous inflammation

Back 110

type of acute inflammation involving marked increases in vascular permeability, exudates with fibrinogen

Front 111

suppurative or purulent inflammation

Back 111

type of acute inflammation involving production of purulent exudates consisting of leukocytes and necrotic cells

Front 112

infiltration with macrocytes, lymphocytes and plasma cells, tissue destruction, angiogenesis and fibrosis

Back 112

these are characteristics of chronic inflammation:

Front 113

cytokines produced by T cells (interferon gamma) and nonimmune factors (endotoxins)

Back 113

these 2 types of mediators activate macrophages:

Front 114

interferon gamma

Back 114

This is the most important activating factor for macrophages

Front 115

eosinophils

Back 115

this cell type is characteristic of immune reactions mediated by IgE and parasitic infections

Front 116

eotaxin (a CC chemokine)

Back 116

eosinophil recruitment is dependent on this chemokine:

Front 117

major basic protein (MBP)

Back 117

eosinophil granules contain this:

Front 118

granulomatous inflammation

Back 118

this distinctive form of chronic inflammation is characterized by focal accumulation of activated macrophages

Front 119

enlarged and flattened; epitheliod macrophages

Back 119

this is what macrophages look like and are called upon activation:

Front 120

TB

Back 120

a granuloma that is called a tubercle is caused by this:

Front 121

lymphoid follicle and sinusoidal phagocyte hyperplasia

Back 121

nodal enlargement during lymphadenitis is caused by:

Front 122

acute phase responses; severe cases are systemic inflammatory response syndrome (SIRS)

Back 122

systemic changes associated with inflammation are collectively known as:

Front 123

fever, production of acute phase proteins, leukocytosis, increased BP and HR, decreased sweating, anorexia

Back 123

what are some clinical and pathological acute phase responses?

Front 124

pyrogens

Back 124

substance that stimulate prostaglandin synthesis in the hypothalamus

Front 125

C-reactive protein, fibrinogen and serum amyloid A protein

Back 125

3 of the best known acute phase proteins are:

Front 126

leukemoid reactions

Back 126

extraordinary high levels of leukocytes

Front 127

neutrophilia

Back 127

bacterial infections usually cause this type of leukocytosis

Front 128

lymphocytosis

Back 128

viral infections usually cause this type of leukocytosis

Front 129

eosinophilia

Back 129

parasitic infections usually cause this type of leukocytosis

Front 130

DIC, hypoglycemia and septic shock

Back 130

sepsis induced release of large amounts of cytokines can cause this clinical triad:

Front 131

Vasodilation, edema, and tissue damage respectively

Back 131

To what tissue processes do the cardinal signs of inflammation, redness, heat and swelling correspond?

Front 132

Blood flow and plasma volume

Back 132

In considering the forces that regulate fluid distribution, what are the two determinants of hydrostatic pressure?

Front 133

By exposure to negatively charged surfaces

Back 133

How is the the Hageman factor (clotting factor 12) activated?

Front 134

By stimulating tissue and inflammatory cells to secrete additional inflammatory mediators

Back 134

How do kinins amplify the inflammatory response?

Front 135

Cell lysis by the membrane attack complex

Back 135

What is the end point of compliment binding to cells?

Front 136

One moleclule of C1q , two molecules of C1r and two molecules of C1s

Back 136

What are the components of the C 1 complex?

Front 137

By the action of activatated of C1 on C4

Back 137

How is C3 convertase produced?

Front 138

C6, C7, and C8 bind the cell membrane in sequence and C7 forms a channel through the lipid bilayer

Back 138

How does the membrane attack complex (MAC) lyse cells?

Front 139

Factor 1 and serum carboxypeptidase

Back 139

What two plasma enzymes inactivate complement?

Front 140

Some viruses and mycobacteria use cell bound complement components to facilitate their entry into cells

Back 140

How might complement be exploited by infectious agents?

Front 141

Membrane Phospholipids

Back 141

From what cell components are arachidonic acid and platelet activating factor derived?

Front 142

By inhibiting cyclooxygenases 1 and 2 (COX-1 and COX-2)

Back 142

How do non-steroidal anti-inflammatory drugs exert the effects on prostaglandin synthesis?

Front 143

A mixture of leukotrienes

Back 143

What is slow reacting substance of anaphylaxis?

Front 144

Heat Shock Proteins

Back 144

What stress induced protein family helps protect from inflammatory injury?

Front 145

Nervous, immune, and endocrine systems

Back 145

What systems are linked by neurokinins?

Front 146

By injury to nerve terminals during inflammation

Back 146

How are neurokinins released?

Front 147

They are potent vasoconstrictors and vasopressors

Back 147

What are the effects of endothelins?

Front 148

Dendritic cells

Back 148

Which cell type is the most effective antigen presenting population?

Front 149

Immunoglobulin E

Back 149

Which immunoglobulin type is found on the surface of mast cells and basophils?

Front 150

Contact with filbrillar collagen of with thrombin

Back 150

What are the main stimuli for platelet aggregation?

Front 151

Azurophillic granules

Back 151

Which neutrophil granules are most important in killing bacterial invaders?

Front 152

Serine proteinases and Metalloproteinases are neutral and act in the extracellular fluid. Cysteine and aspartic proteinases are acidic and act in the acidic environment of phagocytic lysosomes

Back 152

Where do the four types of neutrophil proteinases act?

Front 153

They reduce production of a powerful pro-inflammatory cytokine tumor necrosis factor alpha (TNF-a)

Back 153

How do anti-inflammatory cytokines like IL 6 limit inflammation?

Front 154

Infectious agents, trauma, cancer, and immune reactions

Back 154

What are the four major causes of chronic inflammation?

Front 155

Matrix Metalloproteinases and cysteine proteases

Back 155

The activities of what enzymes are central to the tissue destruction of chronic inflammation?

Front 156

By granuloma formation

Back 156

How does the body protect itself from chronic infection from organisms that cannot be destroyed by neutrophils?

Front 157

Langhans giant cells

Back 157

What are the characteristic cells in multinucleated granulomas formed in response to foreign infectious agents such as tuberculosis?

Front 158

IL 13 and transforming growth factor beta

Back 158

Which cytokines are most important in the progression of granulomas to fibrotic nodules?

Front 159

Pain

Back 159

What is the result of the stimulation of nociceptors?