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Mechanisms of Disease > Lecture 2.1: Acute Inflammation > Flashcards

Lecture 2.1: Acute Inflammation Flashcards

1
Q

What is Acute Inflammation?

A

Protective rapid response of living tissue to injury

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2
Q

Characteristics of Acute Inflammation

A

• Immediate
• Short duration
• Innate
• Stereotyped
• Initiated to limit tissue damage

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3
Q

Causes of Acute Inflammation

A

• Microbial Infections
• Hypersensitivity Reactions (acute phase)
• Physical Agents
• Chemicals
• Tissue Necrosis
• Anything which can injure tissue!

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4
Q

Key Features of Acute Inflammation (3)

A
  1. Vascular and cellular reactions (accumulation of fluid & neutrophils in tissues)
  2. Controlled by a variety of chemical mediators derived from plasma or cells
  3. Protective, but can lead to local complications and systemic effects
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5
Q

Clinical Presentations of Acute Inflammation

A
  1. Rubor (redness)
  2. Tumour (swelling)
  3. Calor (heat)
  4. Dolor (pain)
  5. Functio Laesa (loss of function)
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6
Q

Changes in Tissue during Acute Inflammation

A
  1. Changes in blood flow - ↑ blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells

1 & 2 are Vascular Phases
3 is the Cellular Phase

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7
Q

What Structures are involved in Blood Flow?

A

• Larger arteries
• Smaller arteries
• Arterioles
• Capillaries
• Venules
• Veins
• Capillaries

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8
Q

Vascular Phase: Changes in Blood Flow

A
  1. Transient vasoconstriction of arterioles
  2. Followed by vasodilatation of arterioles and then capillaries -> ↑ blood flow
  3. ↑ vascular permeability -> exudation of protein-rich fluid into tissues
  4. Slowing of circulation
  5. Vascular Stasis
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9
Q

Why does Vascular Stasis occur?

A

Because blood more viscous due to increased concentration of red cells in vessels from leaked fluid

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10
Q

Vascular Phase: Increased Vascular Permeability (3)

A
  1. Hydrostatic Pressure
    • Arteriolar dilatation: hydrostatic pressure ↑
    capillaries relative to pressure interstitial fluid
  2. Osmotic Pressure
    • Increased venular permeability: osmotic
    pressure ↓ capillaries relative to the interstitial
    fluid

1 + 2 = Net flow of protein rich fluid (exudate) into tissue spaces = Oedema

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11
Q

What is Starling’s Law?

A

Movement of fluid across vessel wall governed by balance of forces of hydrostatic and colloid osmotic pressure between intravascular and extravascular space

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12
Q

What is included in Plasma Proteins?

A

• Immunoglobulins to help destroy
microorganisms
• Coagulation factors such as fibrinogen which
deposits a fibrin

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13
Q

Vascular Phase: Mechanisms of Vascular Leakage (4)

A

1) Endothelial Cell Contraction
• Chemical mediators e.g. histamine, C5a, NO

2) Endothelial Cell Injury
• Direct e.g. trauma, chemicals, microbial toxins
• Indirect e.g. toxic oxygen species and proteolytic enzymes from neutrophils

3) Structural re-organisation of cytoskeleton
• Cytokine mediated e.g. interleukin-1, TNF

4) Transcytosis
• VEGF induces ↑ channels in endothelial cells

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14
Q

What is Transudate Fluid? Where is it found?

A

Low Protein Content
Fluid in extravascular space or serous cavity

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15
Q

What is Exudate Fluid? Where is it found?

A

High Protein Content
Fluid in extravascular space or serous cavity

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16
Q

Types of Exudate

A

• Purulent e.g. meningitis
• Haemorrhagic/Serosanguinous eg malignancies
• Serous eg: blister
• Fibrinous: eg: fibrinous pericarditis

17
Q

Neutrophil Extravasation

A

1) Vascular stasis causes neutrophils to line up
along endothelium=Margination
2) Roll along endothelium = Rolling
3) Stick avidly to endothelium = Adhesion
4) Emigrate through the endothelium= Migration /
Diapedesis

18
Q

Neutrophil Extravasation: Rolling

A

Selectins expressed by endothelial cells bind to carbohydrate ligands (sLex) on neutrophils

Increased by several cytokines secreted by macrophages, mast cells and endothelial cells

Examples: IL-1 and TNF

19
Q

Neutrophil Extravasation: Adhesion

A

Integrins expressed by neutrophils bind to integrin ligands on the endothelium

C5a, leukotriene B4, IL-1 and TNF increase expression

20
Q

Neutrophil Extravasation: Diapedesis

A

Chemotaxins stimulate neutrophils to migrate through the inter-endothelial cell junctions

Receptor ligand binding – selectins, integrins

Rearrangement of cytoskeleton

Examples of Chemotaxins: C5a, leukotriene B4, bacterial peptides

21
Q

How do neutrophils escape from vessels?

A

• Relaxation of interendothelial cell junctions
• Digestion of vascular basement membrane
• Movement

22
Q

Opsonisation

A

Opsonins are extracellular proteins that, when bound to substances or cells, induce phagocytes to phagocytose the substances or cells with the opsonins

23
Q

Oxygen-Dependent Killing Mechanisms

A

• Oxygen derived free radicals are released into the phagosome
• Toxic oxygen species (Superoxide) is converted to hydrogen peroxide •
• Oxygen or respiratory burst

24
Q

How is Superoxide converted to H2O2?

A

By myeloperoxidase from neutrophil granules

H2O2-myeloperoxidase-halide system –> hypochlorite

25
Q

Oxygen-Independent Killing Mechanisms

A

Enzymes e.g. lysozyme, protease, nuclease, phospholipase from neutrophil granules can form holes in microbial membranes

26
Q

Summary of role of Neutrophils in Acute Inflammation (5)

A
  1. Neutrophils migrate to site of injury by
    chemotaxis
  2. Phagocytose and kill microorganisms
  3. Eliminate foreign material and necrotic tissue
  4. Produce growth factors for repair
  5. Activated neutrophils may release toxic
    metabolites and enzymes causing damage to
    normal host tissue
27
Q

What is the role of Chemical Mediators?

A

To modulate the inflammatory response

28
Q

Chemical Mediator Groups

A

• ENDOGENOUS (Cell-derived)
• Vasoactive amines, e.g. histamine, serotonin
• Vasoactive peptides, e.g. bradykinin
• Chemokines
• Arachidonic acid metabolites from plasma
membrane phospholipids
• Nitric oxide

Mechanisms of Disease (11 decks)

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