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Flashcards in Acute Inflammation Deck (21)
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1
Q

Define acute inflammation

A

immediate/early response to injury (minutes/days)

2
Q

What are the common causes of acute inflammation?

A
  • infection
  • physical agents e.g. burns
  • chemical agents
  • immune responses
  • tissue death from any cause
3
Q

What are the consequences of acute inflammation?

A
  • 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
4
Q

What are the main components of acute inflammation?

  1. Vascular response
  2. Inflammatory cell infiltration
A
  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
5
Q

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

A
  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
6
Q

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

A
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
7
Q

Describe the control of leukocyte migration

A
  • interaction between receptors on leukocytes and ligands on endothelial cells
  • regulation of receptor linage expression by cytokines and chemokines
8
Q

What causes pain in acute appendicitis?

A
  • neutrophils in serosa

- aggravatie nerve fibres on surface

9
Q

What are the 4 bowel layers called?

A

mucosa
submucosa
muscularis
serosa

10
Q

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

A
Chemotaxis = migration along chemical gradients 
Chemotactic substances
- bacterial products 
- complement components 
- leukotrienes 
- chemotactic cytokines 
Other effects (facilitate migration)
- leukocyte activation 
- endothelial cell activation
11
Q

Describe the steps of phagocytosis

A
  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
12
Q

see chemical mediators table

A

see table

13
Q

Define suppurative inflammation

A

also known as purulent inflammation

  • formation of pus
  • requires infection with pyogenic bacteria
14
Q

What is pus?

A
  • material composed of neutrophils, necrotic cells and bacteria
  • complication of infection with pyogenic bacteria
15
Q

What is an abcess?

A
  • a localised collection of pus
16
Q

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

A

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)

17
Q

What are the 3 possible options for after acute inflammation?

A
  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
18
Q

What are the classical clinical features of acute inflammation?

A

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

19
Q

How can you clinically differentiate viral and bacterial meningitis?

A

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

20
Q

What is the clinical application of defects in leukocyte function?

A
  • hereditary (uncommon) e.g. chronic granulomatous disease
  • acquired e.g. leukaemia
  • -> predispose to bacterial infections, which may be life-threatening
21
Q

Give examples of broad spectrum and targeted anti-inflammatory therapy

A

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)