Inflammation

Question 1

causes of inflammation

Answer 1

infection
tissue necrosis - release of contents
foreign bodies - themselves or something they release
immune reactions/hypersensitivity - normal response damagin own tissue

Question 2

steps of acute inflammation

Answer 2

fluidic phase
cellular phase
termination

Question 3

fluidic phase

Answer 3

vasodilation -
immune cells release cytokines –> vasodilation –> slows blood to give immune cell more time to work

increased vascular permeability -
allows cells to move where needed

Question 4

cellular phase

Answer 4

leukocyte recruitment

Question 5

termination

Answer 5

inciting agent gone

terminate due to -
short half life of neutrophils and chemical mediators
anti-inflammatory cytokines and arachidonic acid metabolites
anti inflammatory t cells
anti inflammatory macrophages

Question 6

pre formed chemical mediators

Answer 6

in granulocytes

histamines - mast cells - increase vasodilation, allergy
serotonin
lysosomal enzymes

Question 7

synthesised chemical mediators

Answer 7

produce at time of acute inflammation

cytokines - lymphocytes and macrophages
TNF and IL1 - main cytokines - t cells, mast cells and some epithelium - released when microbial products, immune complexes or foreign bodies
nitric oxide
prostaglandins - arachidonic acid - platelet aggregation

Question 8

liver factors

Answer 8

clotting factors - plasma proteins
complement

Question 9

dendritic cells

Answer 9

antigen presenting
incite innate immune system
mature to trigger active immune response
trigger innate to produce proinflammatory cytokine and active to produce t cells

Question 10

systemic effects of inflammation

Answer 10

caused by TNF, IL1, and IL6

trigger brain –> fever
trigger liver –> produce acute phase proteins (fibrinogen)
triggers bone marrow –> WBCs
slows heart –> lower CO
triggers thrombus formation

leads to coagulation through platelet activation and clotting factor release

Question 11

local effects of acute inflammation

Answer 11

pain
redness
heat
swelling

Question 12

coagulation —> inflammation

Answer 12

platelet activation and clotting factor release
linked through intrinsic clotting pathway

thrombin release –> cleaves fibrinogen to fibrin (proinflammatory) –> induces TNF/IL6/IL1 production, mediates leukocyte migration
fibrinogen - produced by hepatocytes and needed for hemostatic plug

Question 13

serous inflammation

Answer 13

cell poor
in space created by injury or into body cavity
not infected - low leukocytes

Question 14

catarrhal inflammation

Answer 14

thick, gelatinous
tissue with lots of goblet cells

Question 15

fibrinous inflammation

Answer 15

in membranes of body cavities
usually infectious microbes
sticky

Question 16

purulent/suppurative inflammation

Answer 16

pus
neutrophils and debris of necrotic cells
bacteria that cause liquefactive necrosis (Steph/strep)

Question 17

neutrophils

Answer 17

first immune cell response at area of inflammation
first 6-24 hours
rapid response to chemokines
short lived in tissue then undergo apoptosis
phagocytosis
recruit other cells
release antimicrobial agents

Question 18

chronic inflammation

Answer 18

occurring over a long time or fails to resolve

Question 19

causes of chronic inflammation

Answer 19

acute response fails to remove inciting stimulus
repeated episodes of acute inflammation
in response to specific pathogens

Question 20

biological mechanisms of chronic inflammation

Answer 20

resistance to phagocytosis -
fusobacterium necrophorum - produces metabolites that are toxic to neutrophils

persistence after phagocytosis -
mycobacteria - prevenet lysosomal fusion

isolation -
pyogenic bacteria (strep/staph) - neutrophils don’t swim well, also prevents antibiotic penetration

unresponsiveness -
foreign materials that can’t be phagocytosed

diseases of immunity -
autoimmunity and leukocyte defects

Question 21

process of phagocytosis

Answer 21

PAMP on bacteria or DAMP from damaged cells recognised by pattern recognition receptors

pathogen enclosed by cell - phagosome

combines with lysosome - phagolysosome

enzymes break down pathogen

waste products ejected

Question 22

cells involved in chronic inflammation

Answer 22

macrophages
lymphocytes
fibroblasts
dendritic cells

Question 23

macrophages

Answer 23

quickly sense acute inflammation
migrate in response to chemotaxin release
phagocytosis
present antigens to adaptive immune cells

also facilitate angiogenesis and remodel ECM

Question 24

abscess formation

Answer 24

neutrophils undergo necrosis –> liquefaction and pus
fibroblasts produce collagen and extracellular matrix proteins –> wall off area (fibrous capsule)

histo - neutrophils in lumen

Question 25

granulomatous inflammation

Answer 25

inciting agent not removed
medaited by macrophages

nodular - tuberculoid granulomas - mycobacterium bovis

diffuse - lepromatous - eosinophilic granuloma or mycobacterium leptae

histo - necrotic cell debris, activated macropahes, multinucleated giant cells (massive macrophages, lymphcytes

Question 26

mechanisms of healing

Answer 26

repair - parenchymal and connective tissue
healing - surface epithelia

regeneration - true healing -
no scar tissue
repair damaged components
proliferation of surviving cells
may involve steam cells

connective tissue deposition -
can’t resolve completely
scar tissue
fibrosis - collagen deposition

macrophages - clear offending agent and provide growth factor
angiogenesis - provides blood for nutrients and oxygen
formation of granulation tissue
remodelling of connective tissue - stable fibrous scar

Question 27

angiogenesis

Answer 27

formation of blood vessels

process -
proliferation of epithelium from site of injury
bone marrow endothelial precursor cells evolve

triggered by hypoxia