Inflammation

Question 1

What is inflammation?

Answer 1

a host defense response to infection and tissue damage intended to eliminate the offending agents

Question 2

What are 4 main causes of inflammation?

Answer 2

infections (bacterial, viral, fungal, parasitic), tissue necrosis (ischemia, trauma, injury), foreign bodies (exogenous or endogenous), immune reactions (hypersensitivity)

Question 3

What is the onset and duration of acute inflammation?

Answer 3

develops within minutes to hours, short duration

Question 4

What are local features of acute inflammation?

Answer 4

redness, heat, swelling/edema

Question 5

What cells are involved in acute inflammation?

Answer 5

neutrophils and other phagocytes (innate immunity cells)

Question 6

What are the 3 possible outcomes of acute inflammation?

Answer 6

resolution, resolution w fibrosis, or progression to chronic inflammation

Question 7

What is the onset and duration of chronic inflammation?

Answer 7

develops over days to months, long duration

Question 8

What cells are involved with chronic inflammation?

Answer 8

lymphocytes, plasma cells, monocytes, macrophages, fibroblasts (adaptive immunity cells)

Question 9

What is the outcome of chronic inflammation?

Answer 9

progressive and sometimes severe tissue damage with fibrosis

Question 10

What effect does fibrosis have on tissue?

Answer 10

limits function

Question 11

What blood vessel changes occur in acute inflammation?

Answer 11

increased flow due to vasodilation, increased permeability

Question 12

What is the difference between endothelial cell retraction vs. injury?

Answer 12

retraction is induced by mediators and is rapid, short lived, and reversible
injury is caused by burns or toxins and can be rapid but long lived (resulting in edema)

Question 13

What two forces balance vessel pressure?

Answer 13

colloid osmotic pressure (water in) and hydrostatic pressure (water out)

Question 14

What are the two types of fluid leakage?

Answer 14

exudate and transudate

Question 15

Describe an exudate vessel.

Answer 15

fluid and protein leakage, vasodilation and increased permeability, characteristic feature of inflammation

Question 16

Describe a transudate vessel.

Answer 16

fluid but no protein leakage, not a feature of inflammation, usually associated with CHF and edema

Question 17

What is margination?

Answer 17

leukocyte movement to peripheral region of blood flow

Question 18

What receptors mediate margination?

Answer 18

selectins

Question 19

What receptors mediate leukocyte adhesion to endothelial cells?

Answer 19

integrin ligands

Question 20

What is diapedesis?

Answer 20

leukocytes traversing the endothelium

Question 21

Which process follows diapedesis?

Answer 21

chemotaxis

Question 22

What is chemotaxis?

Answer 22

migration along chemical gradient due to chemoattractants

Question 23

What are the two classes of chemoattractants?

Answer 23

exogenous (bacterial products) and endogenous (chemical mediators)

Question 24

What is the primary component of cellular infiltrate 6-24 hours after inflammation begins?

Answer 24

neutrophils

Question 25

What is the primary component of cellular infiltrate 24-48 hours after inflammation begins?

Answer 25

monocytes (macrophages)

Question 26

What are the steps in the process of phagocytosis?

Answer 26

1. recognition and attachment 2. engulfment of microbe and creation of phagosome 3. fusion of phagosome with lysosome to form phagolysosome 4. killing and degradation

Question 27

What are 3 pathways for microbial killing?

Answer 27

ROS, NO, lysosomal enzymes/proteins

Question 28

What is the killing agent formed in the ROS pathway?

Answer 28

hypochlorite OCl2-

Question 29

What is the killing agent formed in the NO pathway?

Answer 29

peroxynitrite ONOO-

Question 30

What are the 2 steps in the ROS pathway?

Answer 30

NADPH oxidase generates superoxide anion | superoxide anion generated H2O2 which works with myeloperoxidase and Cl to generate hypochlorite

Question 31

What are the 2 steps in the NO pathway?

Answer 31

inducible nitric oxide synthase (iNOS) generates NO | works with superoxide anion to generate peroxynitrate ONOO-

Question 32

What 4 lysosomal enzymes are responsible for microbial killing?

Answer 32

lysozyme, collagenase, elastase, acid hydrolase

Question 33

What are 3 protective mechanisms against unwanted tissue damage by killing pathways?

Answer 33

location, antioxidants, antiproteases

Question 34

What is the function of an antioxidant?

Answer 34

get rid of excess ROS in body

Question 35

What to antiproteases act against?

Answer 35

elastases and collagenases

Question 36

What are 4 primary antioxidants?

Answer 36

superoxide dismutase, catalase, glutathione peroxidase, ceruplasmin/transferrin

Question 37

What are the 2 primary antiproteases?

Answer 37

alpha-1-antitrypsin and alpha-2-macroglobulin

Question 38

What are the 4 classes of mediators of acute inflammation?

Answer 38

vasoactive amines arachidonic acid metabolites cytokines/chemokines complement system

Question 39

What are the vasoactive amines?

Answer 39

histamine and serotonin

Question 40

What are AA metabolites derived from?

Answer 40

cell membrane phospholipids

Question 41

Which two enzymes create different AA metabolite pathways?

Answer 41

cyclooxygenase or lipoxygenase

Question 42

What inhibits the formation of AA?

Answer 42

steroids

Question 43

What inhibits the function of cyclooxygenase?

Answer 43

COX-1 and COX-2 inhibitors, aspirin, indomethacin

Question 44

Which 4 AA metabolites are derived from the cyclooxygenase pathway?

Answer 44

prostacyclin (PGI2), thromboxane A2 (TXA2), PGD2, and PGE2

Question 45

Which 7 AA metabolites are derived from the lipoxygenase pathway?

Answer 45

HETE, Leukotriene (LTB4, C4, D4, E4), Lipoxin (LXA4, B4)

Question 46

PGI2

Answer 46

causes vasodilation, inhibits platelet aggregation

Question 47

TXA2

Answer 47

causes vasoconstriction, promotes platelet aggregation

Question 48

PDG2, PGE2

Answer 48

causes vasodilation, increased vascular permeability

Question 49

HETE, LTB4

Answer 49

chemotaxis

Question 50

LTC4, D4, E4

Answer 50

bronchospasm, increased vascular permeability

Question 51

LXA4,B4

Answer 51

inhibition of inflammation

Question 52

What are the primary cytokines in acute inflammation?

Answer 52

TNF, IL-1, IL-6, chemokines, IL-17

Question 53

How do cytokines affect the endothelium?

Answer 53

increase permeability and expression of adhesion molecules

Question 54

How do cytokines affect the brain?

Answer 54

fever (TNF,IL-1,IL-6)

Question 55

How do cytokines affect the liver?

Answer 55

acute phase protein production increase (IL-1, IL-6)

Question 56

How do cytokines affect bone marrow?

Answer 56

Stimulate leukocyte production (TNF, IL-1, IL-6)

Question 57

How does TNF affect the heart?

Answer 57

low output

Question 58

How does TNF affect thrombosis?

Answer 58

increases risk

Question 59

How do cytokines affect muscles?

Answer 59

insulin resistance (TNF, IL-1)

Question 60

What are chemokines?

Answer 60

small chemoattractant proteins

Question 61

Where do chemokines bind?

Answer 61

bind to 7 transmembrane G-protein coupled receptors

Question 62

Which mediator is at the central part of the complement system?

Answer 62

C3

Question 63

What cleaves C3 and into what parts?

Answer 63

C3 convertase, C3a and C3b

Question 64

What is a MAC?

Answer 64

membrane attack complex

Question 65

What makes up a MAC?

Answer 65

C5b, C6-C9

Question 66

Which complement system mediators are involved in recruitment and activation of leukocytes?

Answer 66

C5a and C3a

Question 67

Which complement system mediator is involved in phagocytosis?

Answer 67

C3b

Question 68

What is pus?

Answer 68

collection of dead cells and cellular debris (both regular tissue and microbes)

Question 69

What are 3 causes of chronic inflammation?

Answer 69

persistent infections, hypersensitivity diseases, prolong exposure to toxins

Question 70

What are 3 morphologic feature of chronic inflammation?

Answer 70

mononuclear cell infiltration, tissue destruction, attempts at healing

Question 71

What are cellular features of granulomatous inflammation?

Answer 71

macrophages with abundant cytoplasm, giant cells, T lymphocytes, and variable necrosis

Question 72

What are some causes of granulomatous inflammation?

Answer 72

foreign material, mycobacterial or fungal infection, and certain immune reactions

Question 73

How do acute phase protein levels change during inflammation?

Answer 73

increase

Question 74

How do white blood cell levels change during inflammation?

Answer 74

increase (leukocytosis)

Question 75

What are the acute phase proteins?

Answer 75

C-reactive protein, fibrinogen, serum amyloid A, hepcidin