Lecture 20 – Acute inflammation Flashcards

1
Q

Acute Inflammation (3)

A
  • Initial rapid response to tissue injury. Takes minutes/hours to develop and lasts for a short duration (hours, days).
  • Acute inflammation is an innate immune response.
  • Relatively non-specific: several types of injury.
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2
Q

Trigger of acute inflammation (6)

A

1) Infections
• Bacteria, viruses, parasites, fungi, toxins
2) Tissue damage due to:
• Physical agents
Frost bites, burns, radiation (ionising, UV)
• Chemical agents
Chemical burns, irritants
• Mechanical injury & ischemia
Trauma, tissue crush, reduced blood flow
3) Foreign bodies
• splinters; sutures; dirt; swallowed bones; dentures

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3
Q

Purpose of acute inflammation (3)

A
  • Alert the body.
  • Limit spread (of infection and/or injury).
  • Protect injured site from being infected.
  • Eliminate dead cells/tissue.
  • Create the conditions required for healing.
  • It is a beneficial response.
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4
Q

5 Rs

A
RECOGNITION of injury.
RECRUITMENT of leucocytes.
REMOVAL of injurious agent.
REGULATION (closure of inflammatory response).
RESOLUTION/REPAIR of affected tissue.
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5
Q

Signs of acute inflammation

A

Signs of acute inflammation:
• Redness (rubor)
• Increased blood flow (hyperaemia) to injured area
• Swelling (tumour)
• Fluid accumulation = Permeability of vessels
• Heat (calor)
• Increased blood flow and metabolic activity
• Pain (dolor)
• Release of pain mediators; pressure on nerve ends
• Loss of function (function laesa)
• Excessive swelling and pain

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6
Q

Acute inflammation – systemic changes (6)

A

Acute inflammation – systemic changes:
• Acute inflammation = local response
• Fever
• Neutrophilia
• Acute phase reactants
o  fibrinogen  stacking of RBCs (rouleaux)  faster sedimentation rate (ESR).
• Rare cases: systemic inflammatory reaction  sepsis. Widespread, severe manifestations. Form of Systemic Inflammatory Response Syndrome (SIRS).

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7
Q

Acute inflammation – VASCULAR events (4)

A

Vasodilation - histamines released by injured cells.
Increased blood flow to area - influx of WBCs.
Increased vessel permeability - leakage of fluid and cells into injured area.
Overall effect: leucocytes and plasma proteins exit vessels and enter inflammation site to deal with infection/damage.

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8
Q

Acute inflammation - CELLULAR events (3)

A

1) Migration and accumulation of cells
o First step – neutrophils.
o Involves a complex process of exit from blood vessels.
2) Removal of pathogens/injured/dead cells
o Neutrophils phagocytose pathogens and dead tissue.
o Neutrophils live briefly  dead neutrophils = pus.
3) Migration and accumulation of monocytes
o Monocytes differentiate into macrophages.
o Phagocytosis  clearance of injured site.
o Release factors that promote tissue repair (TGF-).

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9
Q

Acute inflammation - Neutrophil recruitment (8)

A
•	Multistep process.
•	Adherence to luminal surface of endothelium.
•	Migration through vessel wall.
1)	Margination & rolling
2)	Integrin activation by chemokines
3)	Firm adhesion to endothelium
4)	Transmigration through endothelium into tissue
5)	Chemotaxis to inflamed site
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10
Q

Acute inflammation - Neutrophil recruitment - Adhesion (5)

A

Selectins - Mediate rolling of neutrophils. Low affinity interactions –> disrupt flow of blood –> rolling slows down.

Intergrins - Activates chemokines –> Neutrophil rolling slows them down
Low affinity = No binding to ligands.

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11
Q

Neutrophil transmigration (3)

A

Through interendothelial spaces.
Migrate (chemotaxis) through tissue to inflammed site.
Gradient of chemoattractants guides migration in tissues.

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12
Q

Neutrophil chemotaxis (3,4)

A

Migrate (chemotaxis) through tissue to inflammed site.
Gradient of chemoattractants guides migration in tissues.
Produced at site of infection.
Diffuse into adjacent tissue and form gradient.

Bacterial components
Chemokines (IL-8)
Complements (C5a)
Leukotrienes LTB4

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13
Q

Pathogen destruction (4)

A

Neutrophils -> O2 in(dependent) methods.
Release granule content.
Phagocytosis.
Formation of NETS (neutrophil extracellular traps) -> Mesh of nuclear content (chromatin), traps microbes and has anti microbial molecules.

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14
Q

Granules (6)

A

Small/Specific - Alkaline phosphorylases/lysozyme/gelatinase.
Large/Azurophil - Acid hydrolases/Proteases/lysozyme.

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15
Q

Tissue repair – regeneration ability (3,2,2,2)

A
  • HIGH REGENERATION ABILITY (labile tissues; divide continuously).
  • Epithelial cells (e.g. skin, airways, gut; blood cells).
  • Sometimes perfect regeneration, no scarring.
  • INTERMEDIATE REGENERATION ABILITY (stable tissues)
  • Normal state: quiescent cells (G0/G1); injury  division.
  • May regenerate when injured.
  • e.g. liver, kidney, pancreas; endothelial cells, fibroblasts.
  • If extensive injury  scarring.
  • NO/LITTLE REGENERATION ABILITY (permanent tissues).
  • Neurons, myocardium, skeletal muscle.
  • Heal with fibrosis, scarring, loss of function.
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16
Q

Factors that favour tissue resolution

A

Factors that favour tissue resolution:
• Minimal destruction.
• Minimal cell death.
• Good regeneration ability of injured tissues.
• Fats clearance of infection.
• Quick removal of dead tissue (debris).
• Removal of foreign material (sutures, bone fragments).
• Immobilisation of wound edges (sutures).

17
Q

Factors that prevent tissue healing

A

Factors that prevent tissue healing:
• Infection.
• Poor general health/nutrition (protein/Vitamin C deficiency/diabetes).
• Old age.
• Drugs: corticosteroids.
• Extensive injury.
• Poor vascular supply.
• Extensive haemorrhage.
• Foreign bodies (steel, glass, bone fragments).
• Pressure/torsion/movement on wound edges  dehiscence.