inflammation

Question 1

inflammation

Answer 1

protective response to eliminate initial cause of cell injury as well as necrotic tissue resulting from initial insult

Question 2

acute inflammation

Answer 2

rapid, non-specific response to injury or pathogen that’s designed to deliver WBC and plasma proteins to sites of injury

rapid, short lived, non-specific

Question 3

cells involved in acute inflammation

Answer 3

neutrophils and macrophages

Question 4

cardinal signs of acute inflammation

Answer 4

pain, swelling, heat, redness, loss of function

Question 5

causative agents of acute inflammation

Answer 5

pathogens, immune response, tissue necrosis, chemical or physical injury

Question 6

components of acute inflammation

Answer 6

vascular and cellular changes

Question 7

vascular changes

Answer 7

1. increase in local blood flow increased blood vessel calibre (vasodilation)
2. structural changes in blood vessels (increased permeability) to permit plasma proteins and cells to leave circulation

Question 8

cellular changes

Answer 8

1. emigration of white blood cells from circulation into site of injury (leucocyte recruitment)
2. activation of white cells (leucocyte activation)
3. destruction of injurious agent by white cells (phagocutosis and degradation)

Question 9

vasodilation

Answer 9

caused by action of chemical mediators (histamine from mast cells) on arteriolar smooth muscle, followed by capillary bed expansion

increased blood flow leads to redness and heat

Question 10

increased permeability

Answer 10

leakage of plasma with plasma proteins into extravascular space leads to swelling

caused by contraction of endothelial cells in post-capillary venules (controlled by chemical mediators) and endothelial injury

Question 11

chemical mediators in vascular response

Answer 11

histamine, serotonin, prostaglandins, leukotrienes, platelet-activating factor kinins

Question 12

histamine

Answer 12

source - mast cells, platelets and basophils

action - vasodilation, increased permeability

Question 13

serotonin

Answer 13

source - platelets

action - vasodilation, increased permeability

Question 14

prostaglandins

Answer 14

source - mast cells, leucocytes

action - increase permeability of blood vessel, leucocyte adhesion, chemotaxis and degranulation

Question 15

leukotrienes

Answer 15

source - mast cells, leucocytes

action - increased permeability, leucocyte adhesion and activation, chemotaxis

Question 16

platelet-activating factor

Answer 16

source - leucocytes, mast cells

action - vasodilation, increased permeability

Question 17

kinins

Answer 17

source - plasma (produced liver)

action - vasodilation, increased permeability

Question 18

leucocyte recruitment

Answer 18

from vascular lumen into extravascular space towards site of injury

initiated by cytokines and chemokines release from macrophages in damaged tissue, which cause expression of selectins and integrins allowing adhesion of leucocytes to vascular walls

Question 19

chemotaxis

Answer 19

travel within tissue to site of injury

transport leucocytes to site of injury by chemical gradient - chemotactic molecules bind cell surface receptors on leucocytes and moves extending pseudopods containing contractile filaments

Question 20

leucocyte activation

Answer 20

activated by bacterial or viral products and inflammatory mediators secreted by macrophages and mast cells in tissue

Question 21

phagocytosis

Answer 21

1. recognition and attachment by receptors on leucocyte cell surface
2. engulfment
3. killing and degradation - fusion of phagosome with lysosome, killed by enzymes and degradation by lisosomal acid hydolases

Question 22

chemical mediators cell response

Answer 22

cytokines, chemokines, prostaglandins, leukotrienes, nitric oxide, reactive oxygen species, proteases, complement

Question 23

cytokines

Answer 23

source - macrophages, endothelial cells, mast cells

action - endothelial activation

Question 24

chemokines

Answer 24

source - leucocytes, macrophages

action - leucocyte activation, chemotaxis

Question 25

nitric oxide

Answer 25

source - endothelium, macrophages action - killing microbes

Question 26

reactive oxygen species

Answer 26

source - leucocytes action - killing microbes

Question 27

proteases

Answer 27

source - plasma (Liver) action - leucocyte chemotaxis and activation

Question 28

complement

Answer 28

source - plasma (liver) action - endothelial activation, WBC recruitment

Question 29

outcomes of acute inflammation

Answer 29

resolution - restoration to normal, only occur if stimulus eliminated and minimal damage healing with scarring - removal of stimulus but damage too severe to allow resolution progress to chronic if stimulus persists

Question 30

chronic inflammation

Answer 30

prolonged, delayed onset caused by ongoing inflammation, tissue injury and healing occurring simultaneously specific and characterised by mononuclear cell infiltrate cardinal sign is loss of function

Question 31

causes of chronic inflammation

Answer 31

1. persistent infection by microbes difficult to eradicate 2. immune-mediated inflammatory diseases (hypersensitivity) 3. prolonged exposure to toxic agents

Question 32

mononuclear cells or chronic inflammation

Answer 32

macrophages (activated to histiocytes) lymphocytes (B and T cells attracted to site of injury by chemokines, T cells secrete more cytokines to activate macrophages) plasma cells (produce antibodies)

Question 33

granulomatous inflammation

Answer 33

collections of epitheloid histiocytes, some fused, forms due to cytokine production (T cells) in response to persistent inflammation due to infection with organisms which are resistant to phagolysosomal degradation (Tb) or foreign bodies the immune system can't remove

Question 34

systemic effects of inflammation

Answer 34

fever, sepsis, leucocytosis, elevated plasma levels of acute-phase proteins

Question 35

fever

Answer 35

occurs in response to pyrogens - exogenous and endogenous substances, - prostaglandins (reset hypothalamic thermostat) help fight pathogens

Question 36

sepsis

Answer 36

hypotensive shock, disseminated intravascular coagulation

Question 37

leucocytosis

Answer 37

elevated numbers of WBC in blood

Question 38

elevated plasma levels of acute phase proteins

Answer 38

cause chronic disease

Question 39

repair

Answer 39

restoration of tissue architecture and function after an injury

Question 40

regeneration

Answer 40

replacement of damaged components and return to normal state labile and stable tissues

Question 41

healing with scarring

Answer 41

injured tissue incapable of complete restitution, repair occurs by laying down connective tissue permanent tissues, controlled by growth factors

Question 42

healing - repair by scarring

Answer 42

1. formation of new blood vessels 2. migration and proliferation of fibroblasts 3. deposition of extracellular matrix 4. maturation and organisation of fibrous tissue

Question 43

healing with scarring outcomes

Answer 43

acute and chronic inflammation, ischaemic necrosis, wounds and bone fractures

Question 44

growth factors

Answer 44

produced by macrophages and platelet in site of injury (TGF-B, VEGF, PDGF, EGF, FGF)

Question 45

actions of growth factors

Answer 45

chemotaxis, fibroblast migration and proliferation, angiogenesis, increase synthesis of extra-cellular matrix collagen, stimulate epithelial proliferation