Acute inflammation

Question 1

Bad outcomes of acute inflammation

Answer 1

Allergy
Lupus
Rheumatoid arthritis
Analphyaxis

Question 2

Positive effects of acute inflammation

Answer 2

Protective
Destroy, wall off or dilute injurious agent
Initiate repair
Inflammation is response of vascular living tissue to injury

Question 3

Acute vs chronic

Answer 3

Onset immediate vs gradual
Short lived vs prolonged
Usually single episode vs frustrated healing
Neutrophils and other granulocytes vs macrophages and lymphocytes

Question 4

Granulatomous inflammation

Answer 4

Specific types of chronic inflammation
Collection of macrophages (granuloma)
Lymphocytes
Giant cells
Wall off substances
Chrohn's, Sarcoidosis, TB

Question 5

Features of acute inflammation

Answer 5

Celsus (AD 35)
-rubor (red)
-calor (hot)
-tumor (swollen)
-dolor (pain)
Virchow (added loss of function)

Question 6

Examples in oral cavity

Answer 6

Abscess
Acute pupitis 
Lacerations
Acute herpetic gingivostomatis
Parotitis
Reactions to piercings

Question 7

Causes: infection due to

Answer 7

Bacteria (exotoxins and endotoxins, enzymes)
Viruses (intraceluular replication causing cell damage)
Parasites

Question 8

Causes

Answer 8

Infection due to bacteria, viruses, parasites
Trauma
Physical and chemical agents
Tissue necrosis (death of part of tissue) - would happen after heart attack
Foreign bodies e.g. splinters, dirt, sutures
Immune reactions

Question 9

Causes: tissue necrosis

Answer 9

Death of part of tissue

Usually occurs due to lack of blood supply e.g. heart attack

Question 10

Vascular events

Answer 10

Vasoconstriction of arterioles
-affected area becomes white (local axon reflex)
Arteriolar, capillary and venule dilation
-affected area red and warm
-histamine, serotonin, nitric oxide, prostaglandins
> Vascular permeability
-swelling due to oedema
-histamine, C3a and C5a, leukotrienes
Vascular stasis
-loss of fluid slows blood flow

Question 11

Normal vs inflamed capillary bed

Answer 11

Normal: nearer heart plasma proteins forced into tissues, osmotic pressure further away from heart allows plasma proteins to reenter blood supply
Inflammation: > vascular permeability (so gaps between endothelial cells) causing oedema (no osmotic pressure as chemicals induce many plasma proteins to move into tissues as exudate)

Question 12

Role of oedema

Answer 12

Contains complement
Opsonization (may contain antibodies which act as an 'opsonin' and aid phagocytosis
Contains clotting cascade
Contains kininogens
Dilutes bacterial and other toxins

Question 13

Once complement for oedema activated –>

Answer 13

C3a, C3b and C5a produced
Dilation & > vascular permeability (C3a)
Stimulate histamine release (C3a and C5a)
Promote formation of leukotrienes (attracts neutrophils) and prostaglandins (vasodilation)
Attract phagocytes (C3a and C5a)

Question 14

Opsonization

Answer 14

Aids phagocytosis
Antibody binds to pathogen allowing Fc receptor on phagocyte to bind Fc region on antibody
C3b can also bind to pathogens and phagocytes have a C3b receptor with which to bind to this
C5-9: membrane attack complex (MAC) destroys micro-organisms
MAC forms transmembrane channels
-these disrupt phosoplipid bilayer = cell lysis and death

Question 15

Membrane Attack Complex function

Answer 15

C5-9: membrane attack complex (MAC) destroys micro-organisms
MAC forms transmembrane channels
-these disrupt phosoplipid bilayer = cell lysis and death

Question 16

Complement

Answer 16

• innate immunity (not adaptable)
• C1-C9 (found inactivated in plasma)
• classical pathway (anitbodies bound to antigen)
• alternative pathway (direct binding to pathogen)

Question 17

Clotting cascade

Answer 17

Fibrin forms barrier to spread of infection (fibrinogen converted to fibrin by thrombin)
Thrombin and Hageman factor promote the inflammatory response

Question 18

Kininogens

Answer 18

Converted to kinins by proteases (e.g. thrombin)

Bradykinin - similar effect to histamine

Question 19

Vascular reponse takes hour long

Answer 19

Minutes

Question 20

Vascular response followed by

Answer 20

Cellular response

• hours
• neutrophils followed by macrophages
• 5 main stages described

Question 21

Cellular response stages

Answer 21

Margination
Pavementation
Emigration
Aggregation
Phagocytosis

Question 22

Margination

Answer 22

Due to vascular stasis

Question 23

Pavementation

Answer 23

Neutrophils adhere using adhesion molecules on vessel wall known as selectins
Neutrophils then bind more strongly using integrins on their cell surface to ICAM on endothial cells (promoted by IL-1, TNF alpha)

Question 24

Emigration

Answer 24

Movement of neutrophils between endothelial cells via chemotaxis via chemotactic gradient (e.g. IL-8, C5a)

Question 25

Phagocytosis

Answer 25

Neutrophils and macrophages engulf and destroy microorganisms/ necrotic tissue
Pseudopodia (projection) surrounds microorganism to form phagosome, and destroyed by oxygen species and hydrolytic enzymes
Degranulation (defensins, lyzozyme, lactoferrin)
NETS (Neutrophil extracellular traps)

Question 26

Abscess

Answer 26

Suppuration

Question 27

Neutrophil

Answer 27

Granulocyte (basophil, eosinophil)
50-75% of WBCs
3 methods to destroy pathogens

Question 28

NETS

Answer 28

Neutrophils Extracellular Traps
NETS released as neutrophils die
DNA acts as meshwork containing proteases
Increases con^n of antimicrobials
Limits diffusion/ surrounding tissue damage

Question 29

Pain

Answer 29

> in tissue pressure due to oedema

Inflammatory mediators stimulate pain fibres e.g. bradykinin and prostaglandins

Question 30

Outcomes of acute inflammation

Answer 30

Complete resolution: common response to trauma
Healing by fibrosis: common on skin and in specialised tissue e.g. heart and brain
-granulation tissue (fibroblasts and endothelial cells - matures into scar tissue)
Progression to chronic inflammation
-acute inflammatory response fails to get rid of injurious agent e.g. foreign body
-interference with normal process of healing e.g. neutropenia, radiotherapy

Question 31

What releases histamine, serotonin, nitric oxide

Answer 31

Trauma, complement, cytokines etc. –> mast cells –> histamine
Endothelial cells and phagocytes –> nitric oxide
Platelet aggregation –> serotonin

Question 32

Examples of plasma proteins

Answer 32

Albumin, proteins from complement cascade