Acute Inflammation

Question 1

Define acute inflammation

Answer 1

immediate/early response to injury (minutes/days)

Question 2

What are the common causes of acute inflammation?

Answer 2

• infection
• physical agents e.g. burns
• chemical agents
• immune responses
• tissue death from any cause

Question 3

What are the consequences of acute inflammation?

Answer 3

• may be beneficial (e.g. bacterial killing, removal of dead tissue)
• also potential harmful effects (e.g. lung damage in pneumonia, kidney damage in acute pyelonephritis)
• may precede chronic inflammation, healing and repair

Question 4

What are the main components of acute inflammation?

1. Vascular response
2. Inflammatory cell infiltration

Answer 4

1. Vascular response
   - vasodilation –> increased blood flow (redness, warmth)
   - increased permeability –> oedema (swelling)
2. Inflammatory cell infiltration
   - mainly neutrophils
   - macrophages (during later stages)
   - lymphocytes may also be involved

Question 5

What are the 3 components of vascular changes in acute inflammation?

Answer 5

1. vasodilation of arterioles
   - increased blood flow through capillary bed
2. increased permeability (capillary bed, venules)
   - protein-roch fluid escapes into intravascular space
   - increased concentration of erythrocytes (congestion)
   - increased blood viscosity
   - reduced blood flow (stasis)
3. Leukocyte margination
   - loss of axial streaming
   - first stage in process of leukocyte migration

Question 6

Describe the 4 stages of leukocyte migration and the adhesion molecules involved

Answer 6

Margination 
- movement to periphery of blood vessel
- mainly related to stasis, loss of axial streaming 
Rolling 
- transient weak binding to endothelium 
- selectins 
Adhesion 
 - firm adhesion to endothelium
- integrins 
Transmigration 
- movement into extravascular space 
- PECAM-1, CD31

Question 7

Describe the control of leukocyte migration

Answer 7

• interaction between receptors on leukocytes and ligands on endothelial cells
• regulation of receptor linage expression by cytokines and chemokines

Question 8

What causes pain in acute appendicitis?

Answer 8

• neutrophils in serosa

- aggravatie nerve fibres on surface

Question 9

What are the 4 bowel layers called?

Answer 9

mucosa
submucosa
muscularis
serosa

Question 10

Define chemotaxis
List some chemotactic substances
What are the other effects of chemotactic molecules?

Answer 10

Chemotaxis = migration along chemical gradients 
Chemotactic substances
- bacterial products 
- complement components 
- leukotrienes 
- chemotactic cytokines 
Other effects (facilitate migration)
- leukocyte activation 
- endothelial cell activation

Question 11

Describe the steps of phagocytosis

Answer 11

1. recognition and attachment of particle to leukocyte
   - opsonins (e.g. IgG, C3b)
2. engulfment
   - pseudopods surround particle
   - formation of phagocytic vacuole
3. killing and degradation
   - production of reactive oxygen metabolites
   - release of lysosomal enzymes

Question 12

see chemical mediators table

Answer 12

see table

Question 13

Define suppurative inflammation

Answer 13

also known as purulent inflammation

• formation of pus
• requires infection with pyogenic bacteria

Question 14

What is pus?

Answer 14

• material composed of neutrophils, necrotic cells and bacteria
• complication of infection with pyogenic bacteria

Question 15

What is an abcess?

Answer 15

• a localised collection of pus

Question 16

List the 3 viral and 1 immune mediated diseases with lymphocytes rather than neutrophils

Answer 16

Viral infections
- acute viral hepatitis - Hep A, B, C
- viral meningitis - coxsackievirus, mumps
- viral myocarditis - coxsakievirus. echovirus
Immune mediated diseases
- autoimmune hepatitis (usually has a chronic course)

Question 17

What are the 3 possible options for after acute inflammation?

Answer 17

1. resolution
   - limited/short-lived injury
   - return of tissue to normal state
2. scarring/fibrosis
   - more extensive tissue damage
   - tissues with little capacity for regeneration
   - abscess formation
3. progression to acute inflammation

Question 18

What are the classical clinical features of acute inflammation?

Answer 18

Classical clinical features
- heat (calor)
- redness (rubor)
- swelling (tumor)
- pain (dolor)
Raised white cell count (mainly neutrophils)
- particularly high in pyogenic bacterial infection
- also present in non-infective causes (e.g. MI)
- neutrophil-rich leukocytosis in other body fluids e.g. CSG in bacterial meningitis

Question 19

How can you clinically differentiate viral and bacterial meningitis?

Answer 19

lumber puncture
bacterial = neutrophils in CSF
viral = lymphocytes in CSF

Question 20

What is the clinical application of defects in leukocyte function?

Answer 20

• hereditary (uncommon) e.g. chronic granulomatous disease
• acquired e.g. leukaemia
• -> predispose to bacterial infections, which may be life-threatening

Question 21

Give examples of broad spectrum and targeted anti-inflammatory therapy

Answer 21

Broad spectrum
- NSAIDS inhibit cyclooxygenase enzymes (COX-1, COX-2) involved with arachidonic acid metabolism to produce prostaglandins
Targeted treatments
- therapies blocking specific chemical mediators or receptor-ligand interactions (e.g. anti-TNF antibodies, anti-ICAM-1)