Inflammation

Question 1

stages of acute inflammation

Answer 1

fluidic
cellular

Question 2

causes of acute inflammation (4)

Answer 2

infection - response to pathogen or toxins its produces
tissue necrosis - release cell contents
foreign bodies - either direct irritant effect or due to traumatic tissue injury
immune reactions - hypersensitivity, normal immune response damages own tissues

Question 3

fluidic phase processes

Answer 3

immune cells mediator release (eg. cytokines) –>
vasodilation (slows blood, more time for immune cells to work) & increased vascular permeability (cells more able to move into the space where they are needed)

Question 4

Inflammation Appearance

Answer 4

Pain
Redness - increased blood flow in the area
Heat
Swelling

Question 5

Acute inflammation - chemical mediators

Answer 5

pre-formed - sit in granulocytes
- histamine - mast cells, vasodilation
- serotonin
- lysosomal enzymes

newly synthesized - produced at time of inflammation
- cytokines - lymphocytes and macrophages
- tumor necrosis factor and IL1 - main cytokines - t cells and mast cells
- nitric oxide
- prostaglandins - arachidonic acid

Liver factors
- factor XII - clotting factor
- complement

Question 6

Dendritic cell function

Answer 6

antigen presenting cells
incited by innate immune system
mature to activate active immune system
innate - produce local cytokines
active - activate T-cells

Question 7

systemic effects of acute inflammation

Answer 7

trigger brain to produce fever
trigger liver to produce acute phase proteins
trigger bone marrow to form WBCs
TNF slows heart - lowers output
thrombus formation
effects on skeletal muscle
platelet activation/aggregation
clotting factor release
thrombin - cleave fibrinogen to fibrin - pro inflammatory
fibrinogen - scaffolding for hemostatic plug (synthesised in liver)

Question 8

Exudate types (4)

Answer 8

serous - clear, cell-poor - in spaces created by cell injury or into body cavities, not infected
catarrhal/mucoid - gelatinous/thick - in tissues where lots of goblet cells
fibrinous - sticky - caused by infectious microbes, in membranes of body cavities
suppurative/purulent - pus - neutrophils, usually bacteria causing liquefactive necrosis

Question 9

neutrophil function in acute inflammation

Answer 9

first response cells - first 6-24 hours
rapid response to chemokines
short lived in tissue - undergo apoptosis
phagocytosis
recruit other cells
release antimicrobial agents

lobular nucleus and granular cytoplasm

Question 10

termination of acute inflammation

Answer 10

when inciting agent is gone
due to:
- short life of neutrohphils and chemical mediators
- anti-inflammatory cytokines and arachidonic acid metabolites
- anti-inflammatory t-cells
- anti-inflammatory macrophages

Question 11

chemotaxis

Answer 11

movement of an entity in response to a chemical stimulus

Question 12

DAMPs

Answer 12

damage associated molecular pattern

produced by damaged tissue, recognised by macrophages and dendritic cells and presented to trigger cytokine release

Question 13

PAMPs

Answer 13

pathogen associated molecular patterns

produced by microbes, recognised by macrophages and dendritic cells and presented to trigger cytokine release

Question 14

cellular phase process

Answer 14

PAMPs/DAMPs –> cytokines –> mast cells –> inflammatory mediators released

Question 15

chronic inflammation

Answer 15

occurs over a long time and/or fails to resolve

acute response fails to kill inciting agent
repeated episodes of acute inflammation
in response to specific pathogens

Question 16

chronic inflammation mechanisms

Answer 16

agents that resist phagocytosis - eg bacteria that produce toxins that kill leucocytes
persistence after phagocytosis - mycobacteria - prevent lysosomal function, can’t fuse
isolation - hide within pus or other liquid
unresponsiveness - can’t be broken down, eg. plant materials, suture materials
immune disease - autoimmunity, leukocyte deficits

Question 17

phagocytosis

Answer 17

leukocyte engulfs bacteria
forms phagocyte - pinched cell membrane containing pathogen
fuse with lysosome - phagolysosome

virulence factors of bacteria may block lysosome fusion

Question 18

key inflammation cells

Answer 18

macrophages - phagocytosis
lymphocytes
fibroblasts - wall off infection or rebuild scaffolding of tissue
dendritic cells - present antigens

Question 19

abscesses

Answer 19

form due to myeloperoxidase by neutrophils + cellular remnants of dead neutrophils –> pus
(rabbits, reptiles, birds, fish - no myeloperoxidase)
neutrophils in lumen

chronic - fibroblasts produce collagen and extracellular matrix proteins to wall off area

Question 20

granulomatous inflammation

Answer 20

inciting agent not removed
mediated by macrophages
nodular or diffuse

histo - necrotic cellular debris, activated macrophages, multinucleated giant cells, lymphocytes

Question 21

healing mechanisms (2)

Answer 21

regeneration - true healing and repair
- back to normal, no scar tissue
- repair damaged components
- proliferation of cells that have survived injury
- may involve tissue stem cells

connective (fibrous) tissue deposition
- when injured tissue can’t resolve completely or supporting tissue damaged
- scar tissue
- fibrosis - extensive deposition of collagen