Acute Inflammation Flashcards

1
Q

Definition of acute inflammation

A

Immediate/early response to injury

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2
Q

Common causes of acute inflammation

A
Infection - bacterial, viral, other 
Physical agents - burns 
Chemical agents 
Immune responses 
Tissue death from any cause
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3
Q

Consequences of acute inflammation

A

May be beneficial- bacterial killing, removal of dead tissue
Potentially harmful effects - lung damage in pneumonia, kidney damage in acute pyelonephritis
May precede to chronic inflammation, healing and repair

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4
Q

2 main components of acute inflammation

A

Vascular response

Inflammatory cell infiltrate

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5
Q

Components of the vascular response in acute inflammation

A
  • vasodilation –> inc blood flow (redness and warmth)

- increased permeability –> oedema (swelling

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6
Q

Inflammatory cell infiltrate of acute inflammation

A

Mainly neutrophils
Macrophages (during later stages)
Lymphocytes may also be involved

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7
Q

Vascular changes in acute inflammation

A

Vasodilation (arterioles)
- increased blood flow through the capillary bed)
Increased permeability (cap bed, venules)
- protein-rich fluid escapes into extravascular space
- inc concentration of erythrocytes (congestion)
- inc blood viscosity
- reduced blood flow (stasis)
Leukocyte margination
- loss of axial streaming
- first stage in process of leukocyte emigration

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8
Q

4 phases of leukocyte migration

A

Margination
Rolling
Adhesion
Transmigration

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9
Q

What occurs in the 4 phases of leukocyte migration

A

Margination- movement to the periphery of blood vessel
Rolling - transient weak binding to endothelium
Adhesion - firm adhesion to endothelium
Transmigration - movement into the extravascular space

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10
Q

What are the adhesion molecules involved in leukocyte migration

A

Margination - mainly linked to stasis - loss o axial streaming
Rolling - selectins - selectin receptor is on the endothelium and the ligand is on the cell
Adhesion - integrins - receptor ICAM is in the endothelium and the integrin is on the cell
Transmigration - platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31)

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11
Q

What is chemotaxis

A

Migration along chemical gradients

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12
Q

What are chemotactic substances

A

Bacterial products
Complement e.g. C5a
Leukotrienes
Chemokines

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13
Q

Other effects of chemotactic molecules

A

Leukocyte activation

Endothelial cell activation

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14
Q

What is phagocytosis?

A

Ingestion and destruction of foreign particles

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15
Q

Steps of phagocytosis

A

1) recognition and attachment of particle to leukocyte
- opsonins - IgG, C3b
2) engulfment
- pseudopods surrounds the particle
- form a phagocytic vacuole
3) killing and degradation
- production of reactive oxygen metabolites
- release of lysosomal enzymes

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16
Q

General aspects of chemical mediators in acute inflammation

A

May be locally produced or systemic
Most act on specific receptors expressed on target cells
Mediator function is tightly regulated
Others act in a non specific way

17
Q

What are vasoactive amines

A

E.g. Histamine, serotonin

Effects arteriolar dilatation and inc permeability

18
Q

What do kinins do

A

Arteriolar dilation
Inc permeability
E.g. Bradykinin

19
Q

Action of kinins

A
Vasodilation 
Inc permeability 
Leukocyte adhesion 
Chemotaxis 
Opsonins for phagocytosis
20
Q

Action of the clotting cascade

A

Leukocyte adhesion
Chemotaxis
E.g. Thrombin

21
Q

Action of Arachidonic acid metabolites

A

Prostaglandins
Leukotrienes
Lipotoxins

Vasodilation
Inc permeability
Leukocyte response

22
Q

Action of cytokines

A

TNF
IL-1

Endothelial activation, induction of systemic acute phage response

23
Q

Action of oxygen derived radicals

A

Vasodilation
Bacterial killing

Nitric oxide

24
Q

Action of chemokines

A

Migration and activation of inflammatory cells

IL8

25
Q

What is suppurative (purulent) inflammation

A

Pus
- material composed neutrophils, necrotic cells and bacteria
- complication of infection with pus forming (pyogemic) bacteria
Abscess
- a localised collection of pus

26
Q

Examples of suppurative infection

A

Bacterial meningitis - pus on meninges

Brain abscess - in temporal lobe - direct parsed from middle ear infection

27
Q

Diseases with lymphocytes rather than neutrophils

A

Viral infection

  • acute viral hep- A, B, C
  • viral meningitis - mumps, coxsackievirus
  • viral myocarditis - coxsackievirus, echovirus

Immune mediated hep - usually has a chronic cause

28
Q

Sequelae of acute inflammation

A
Resolution 
- limited/short lived injury 
-return of tissue to normal state 
Scarring/fibrosis 
- more extensive tissue damage  
-tissues with little capacity for regeneration
- abscess formation 
Progression to chronic inflammation
29
Q

Clinical aspects of acute inflammation

A

1) classical features: Heat, redness, swelling, pain
2)raised white cell count in blood - mainly Neutrophils
- particularly high in pyogenic bacteria
- also present in non-infective causes - MI
- neutrophils rich leukocytosis in other bodily fluids
E.g. CSF fluid in bacterial meningitis

30
Q

Defects in leukocyte function

A
  • hereditary (uncommon) chronic granulatomous disease
  • acquired e.g. Leukaemia

Predispose to bacterial infection , which may be lif threatening

31
Q

Anti-inflammatory therapy

A

Broad spectrum
- NSAIDs inhibit cyclo-oxygenate enzymes involved with arachidonic acid metabolism to produce prostaglandins
Targeted treatment
- therapies blocking specific chemical mediators or receptor ligand interaction e.g. Anti-TNF antibodies, anti ICAM-1