acute inflammation

Question 1

inflammation

Answer 1

repsonce of vasuclar living tissue to injury

• protective
• destroy, wall off or dilute injurious agent
• initiate repair

Question 2

features of acute inflammtion

Answer 2

1) red
2) hot
3) swollen
4) pain
5) loss of function

Question 3

actue vs chronic

Answer 3

• immediate onset
• short lived
• usually single episode
• neutrophils and other granulocytes
  eg dental abcess
• usually vascular responce
  Chronic
• gradual onset
• prolonged
• frustrated healing (repair and destruction occurring simultaneously)
• macrophages and lymphocytes
• usually cellular reponce

Question 4

causes of infection

Answer 4

bacteria
viruses
parasites
trauma
phsycial/chemcial agents
tissue necrosis
forign bodies
immune reactions

Question 5

examples of acute in the OC

Answer 5

abcess
acute pulpitis
lacterations
aute herpetic gingivostomatitis
parotitis
reactions to piercings

Question 6

steps of acute inflammation

Answer 6

vascualr

cellular

Question 7

events that occur acute vascular response

Answer 7

vasoconstriciton arterioes
arterioolar capillary and venule dilation
increased vascialr permeabilty
vascular stasis

Question 8

what casues vascular permeabiloty

Answer 8

histamine
C3a and C5a
leukotrines

Question 9

vasoilation

Answer 9

1) trauma and complement can cause mast cells to release histamine
2) causes vasodilation
3) platelet aggregation causes release of serotonin
4) factors from WBCs and Nitric oxide and prostaglandins can cause vasodilation

Question 10

increased vascualr permeability occurs by

Answer 10

retraction of endothelail cells
endothelial injuries
increased transport of fluid and proteins through endothelail cells (transcytosis)

Question 11

oedema

Answer 11

excess of fluid in tissues

Question 12

types od oedema

Answer 12

exudate

transudate

Question 13

exudate

Answer 13

• extravascular fluid with a high protein content
• seen in inflammation
• high protein content caused by plasma protein’s and WBC
• only get it when we have increased vascular permeability, to allow movement from vessels to the tissues

Question 14

transulate

Answer 14

• extravascular fluid with low protein content
• occurs in situations without increased permeability
• only fluid can move into tissues, not the protiens ect

Question 15

role of oedema

Answer 15

4) contains clotting cascade
- fibrin forms a barrier to spread of infection (fibrinogen converted to fibrin by thrombin
- coagulation may also promote inflammation
5) contains kininogens
- these are converted to kinins by proteases eg thrombin
- bradykinin – similar effect to histamine vascular dilation
6) dilutes bacterial and other toxins

Question 16

pathways to acitvate complement

Answer 16

classical
alternative
lectin

Question 17

classical pathway

Answer 17

• antibodies bound to antigen

- C1 detects this and triggers pathway

Question 18

alternative pathway

Answer 18

• C1 direct binding to pathogen via microbial surface molecules

Question 19

lectin pathwat

Answer 19

• plasma manose binding lectin? binds to microbes and directly activates c1

Question 20

degradation of C3

Answer 20

C3a can affect vascular permeability
C3b stays on the cell, along with previously generated fragments forms C5 convertase
splitting C5 into C5a and b
C5a affects VP
C5b remains attached, then attracts C6-9 and eventually forms membrane attack complex (drill hole in cell wall, allows fluids to come into cell and cause destruction of the cell)

Question 21

opsonisaiton is caused by

Answer 21

• C3b can also bind to pathogens and phagocytes have a C3b receptor with which to bind to this

Question 22

what does c3a c3b and c5a do

Answer 22

• dilation and increased vascular permeability C3a
• stimulate histamine release (C3a and C5a)
• promote formation of leukotrienes (attracts neutrophils) and prostaglandins (vasodilation)
• attracts phagocytes (C3a and C5a)

Question 23

membrane attack complex

Answer 23

C5-9 membrane attack complex (MAC)
- destroys microorganisms
MAC forms transmembrane channels
these disrupt the phospholipid bilayer = cell lysis and death

Question 24

cellular repsonce steps

Answer 24

1) Margination
- due to vascular stasis
- white blood cells drop to the edge of the blood vessel
2) Pavmentation
- neutrophils adhere using adhesion molecules on vessels walls known as selectins
- neutrophils then bind more strongly using integrins on their cell surface to ICAM on enodthemliall cells (promoted by IL-1, TNF alpha)
- ensure they only stop and stick to parts where there is inflammation
3) emigration
- movement of neutrophils between endothelial cells via chemotaxis via chemotactic gradient eg IL 8. C5a)
- move in between the endothelial cells
- neutrophils attracted by cytokines and parts of the complement system, aggregate around the area needed
4) Phagocytosis
- neutrophils and macrophages engulf and destroy microorganisms/necrotic tissue
- pseudopodia (projection) surrounds microorganism to form phagosome and destroyed by reactive oxygen species and hydrolytic enzymes (from lysosome)
- - lysosome binds with the phagosome within cytoplasm

Question 25

abscess

Answer 25

accumulation of pus at a non vital tooth by bacteria

Question 26

pus is made from

Answer 26

neutrophils with dead and dying bacteria

Question 27

what is a neutrophil

Answer 27

granulocyte

Question 28

pain is sude to

Answer 28

increased tissue pressure

inflammatory mediators stimulate pain fibres

Question 29

outcomes of acute

Answer 29

complete resoltuopn
healing by fibrsis (replaced by granultuon tissue fibroblasts collagen and endothelail cells)
progressin to chronic