Acute Inflammation

Question 1

Toll Like Receptors (TLRs)

Answer 1

detect extracellular and ingested microbes

located on plasma membranes and endosomes

recognize PAMPs and in response produce and express cytokines, interferons, and lymphocyte activating membrane proteins/cytokines

Question 2

C5a

Answer 2

chemotaxis - especially of neutrophils

vasodilation

cell adherence

release of histamine from mast cells

release of lysosomal enzymes

Question 3

C5a

Answer 3

chemotaxis - especially of neutrophils

vasodilation

cell adherence

release of histamine from mast cells (degranulation)

release of lysosomal enzymes

Question 4

DAMPs

Answer 4

damage-associated molecular patterns present on all cells that are liberated or altered when cell damage occurs - induces production of IL-1 -> leukocytes -> inflammation

Question 5

exudation

Answer 5

process of blood vessel permeability changes moving fluid, plasma proteins, leukocytes into interstitial tissues or body cavities

Question 6

pus

Answer 6

purulent exudate - inflammatory exudate rich in leukocytes, debris of dead cells, and microbes

Question 7

exudate

Answer 7

extravascular fluid high in protein and cellular debris - indicates increased permeability of blood vessels due to inflammation

Question 8

transudate

Answer 8

fluid with low protein content, little or no cellular material, low specific gravity, produced as a result of osmotic or hydrostatis imbalance across vessels with normal permeability

Question 9

transudate

Answer 9

fluid with low protein content, little or no cellular material, low specific gravity

produced as a result of osmotic or hydrostatic imbalance across vessels with normal permeability

Question 10

vascular flow changes during inflammation - steps

Answer 10

vasodilation (via histamine) ->

increased blood flow at site of inflammation ->

premeability of microvasculature increases ->

outpouring of exudate ->

blood flow slowed, viscosity increased causes vascular congestion at site - localized redness ->

neutrophils accumulate on endothelium of vessels ->

neutrophils adhere to endothelium and migrate through to the interstitial tissue

Question 11

mechanisms for increased vascular permeability

Answer 11

retraction of endothelial cells elicited by histamine, bradykinin, leukotienes, and other chemical mediators

endothelial injury - resulting in endothelial necrosis and detachment

Question 12

leukocytes capable of phagocytosis

Answer 12

neutrophils and macrophages

Question 13

leukocytes capable of phagocytosis

Answer 13

neutrophils (respond quickly) and macrophages (slow response)

Question 14

molecules involved in leukocyte migration through endothelium of blood vessels

Answer 14

selectins - mediate initial weak binding, help it roll (via force of blood flow)

integrins - firm adhesion to endothelium

CD31 - mediates binding events needed for migration through the endothelium

C5a, leukotriene B, bacterial products - chemotaxis toward site of injury

C3b and antibodies - phagocytosis and killing of pathogens

Question 15

TNF and IL-1 in leukocyte movement through endothelium

Answer 15

cytokines that activate endothelial cells to increase their expression of ligands for integrins

Question 16

how do phagocytes kill microbes once they are engulfed and phagosome has fused with the lysosome?

Answer 16

reactive oxygen species:

phagocyte oxidase oxidizes NADPH and in the process reduces oxygen to superoxide anion (O2-), which is converted inti H2O2, then the enzyme myeloperoxidase (MPO) converts H2O2 and Cl- into OCl2 (bleach), a potent antimicrobial that destroys microbes via halogenation.

microbes also killed by reaction of NO and O2- creating free radical, and by granules released by neutrophils

Question 17

neutrophil exracellular traps (NETs)

Answer 17

extracellular fibrillar networks that concentrate antimicrobial substances at the sites of infection to prevent spread

Question 18

reasons leukocytes may damage tissue via releasing oxygen radicals and lysosomal content

Answer 18

normal tissue damage cuased by degranulation (release of granules containing enzymes/antimicrobial proteins)

asbestos and urate crystals lyse phagosomal membrane

large or oddly shapd materials are encountered and the leucocytes release granule enzymes in response to not being able to enguld them

Question 19

methods body uses to terminate acute inflammation

Answer 19

neutrophils have short half-lives, and are only produced while stimulus is present

production of inflammatory leukotrienes switches to anti-inflammatory lipoxins

anti-inflammatory cytokines are liberated: TGF-B and IL-10

Question 20

mechanism of inflammation

Answer 20

resident cells detect stimulus and release inflammatory mediators ->

venules dilate and become leaky ->

inflammatory cells marginate to vessel wall and migraint into tissue (neutrophils followed by monocytes and lymphocytes)

Question 21

histamine

Answer 21

vasoactive amine produced by mast cells and basophils

causes vasodilation and increased vascular permeability

Question 22

IL-1, IL-6, TNF

Answer 22

cytokines produced by macrophages, endothelial cells, and mast cells

cause endothelial expression of adhesion molecules (locally); fever, metabolic abnormalities, and hypotensive shock (systemically)

Question 23

lipoxins

Answer 23

produced from arachidonic acid via lipoxygenases, and binds to GCPRs.

inhibit inflammation by inhibiting recruitment of leukocytes

Question 24

leukotriene B4

Answer 24

produced in leukocytes and mast cells from arachidonic acid via lipoxygenases, and binds to GCPRs.

function: chemotaxis and leukocyte adhesion

Question 25

TNF, IL-1, IL-6

Answer 25

Cytokines produced by activated macrohages and dendritic cells. TNF also produced by T-lymphocytes and mast cells. role: endothelial activation, systemic response (fever, mebabolic changes - TNF induces cachexia, hypotension)

Question 26

substance P

Answer 26

neuropeptidesecreted by sensory nerves and leukocytes that have several functions: pain signal trnasmission, BP regulation, hormone secretion stimulation, increase vascular permeability.