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PATH2220 > 7 - Inflammation (early events) > Flashcards

7 - Inflammation (early events) Flashcards

1
Q

Goal of inflammatory reaction

A

To bring leukocytes and plasma proteins normally circulating in blood to the site of infection of tissue damage, eliminate the causative agent an initiate healing

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2
Q

Types of inflammation

A

Acute or chronic

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3
Q

onset of acute and chronic inflammation

A
  • Acute: Fast (minutes or hours)
  • Chronic: Slow (days, months or years)
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4
Q

Cells involved in acute and chronic inflammation

A
  • Acute: Mainly neutrophils
  • Chronic: Monocytes/macrophages, lymphocytes
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5
Q

Tissue injury, fibrosis of acute and chronic inflammation

A
  • Acute: Mildm self limited
  • Chronic: Often severe, progressive
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6
Q

Local and systemic signs of acute and chronic inflammation

A
  • Acute: Prominent
  • Chronic: less prominent
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7
Q

Cardinal signs of inflammation

A
  • Redness (increased blood flow)
  • Heat (increased blood flow)
  • Swelling (leakage of cells and fluid into tissues)
  • Pain (increased nerve sensitivity due to chemical mediators)
  • Loss of function
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8
Q

Causes of inflammation

A
  • Infective agents
  • Foreign bodies (dirt, splinters, implants)
  • Immune reactions (hypersensitivity & autoimmune)
  • Tissue necrosis (death)
  • Physical agents (trauma, heat, cold)
  • Chemical agents (drugs, toxin)
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9
Q

Inflammatory process

A
  • Offending agent is recognised by Macrophages, dendritic cells and mast calls which then produce chemical mediators (cytokines)
  • Leukocytes (neutrophil and monocytes) are recruited from the circulation to the site where the offending agent is located
  • Leukocytes and proteins are activated to destroy and eliminate the offending substance
  • The reaction is controlled and terminated
  • The damaged tissue is repaired
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10
Q

Two components of inflammatory responses

A

Vascular changes and cellular events

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11
Q

Vascular changes

A

Maximise movement of proteins and leukocytes from circulation to site of infection/injury.

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12
Q

Examples of vascular changes

A

Vasodilation, increased bloodflow and permeability

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13
Q

Vasodialtion

A
  • Action of mediators (histamine) on vascular smooth muscle
  • Initial constriction (transient)
  • Arterioles dilate followed by capillary bed expansion
  • Increased blood flow → redness & heat
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14
Q

Increased permeability

A
  • Outpouring of protein rich fluid into extravascular tissues (exudate)
  • causes swelling
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15
Q

Two ways permeability is changed

A
  1. Retraction of endothelial cells (gaps appear between endothelial cells)
  2. Endothelial injury (Direct damage)
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16
Q

End result of change permeability

A
  • Fluid and proteins escape
  • small molecules first, fibrinogen last
  • ↑ osmotic pressure of tissue
  • swelling
17
Q

Cellular events

A
  • Leukocytes that are recruited to sites of inflammation eliminate the offending agents following their activation
  • Most important leukocytes in typical inflammatory reactions are the ones
    capable of phagocytosis
  • Neutrophils and macrophages (slower responders)
18
Q

Which cells produce growth factors that aid in repair

A

Macrophages, stay longer than other cells

19
Q

Role of cytokines in leukocyte emigration

A

TNF and IL-1 act on the endothelium of venules near the site of infection to initiate leukocyte emigration into tissues

20
Q

Role of chemokines in leukocyte emigration

A

Provide signals to leukocytes to help them traffic to the site of infection once they have migrated into
tissues (chemotaxis)

21
Q

TNF and IL-1 actions

A

Endothelial activation (pain, fever, metabolic abnormalities)

22
Q

Loose attachment and rolling of leukocytes

A
  • In response to cytokines, endothelial cells upregulate expression of adhesion molecules called selectins
  • selectins bind to surface carbohydrates on leukocytes
  • repetitive process of leukocytes becoming tethered to the endothelium, flowing blood disrupting binding and bonds reforming downstream
23
Q

Firm adhesion

A
  • in response to chemokines, integrins expressed on leukocytes assume a highaffinity state
  • endothelial cells upregulate expression of adhesion molecules ICAM-1 and
    VCAM-1 that bind to integrins expressed by leukocytes
  • firm binding of integrins to their ligands arrests the rolling, cytoskeleton of
    leukocytes is reorganised such that they spread out on the endothelial surface
24
Q

Leukocyte migration

A
  • chemokines stimulate the motility of leukocytes, as do bacterial products and products of complement activation
  • leukocytes begin to migrate between endothelial cells, through the vessel wall
    and along the concentration gradient of these chemoattractants
25
Q

Chemotaxis

A

Movement of leukocytes after emigration towards an
increasing concentration of a chemotactic agent (usually a protein or polypeptide)

26
Q

Chemoattractants

A

Both exogenous and endogenous substances can
act as chemoattractants (e.g. bacterial products, chemokines, complement components)

27
Q

Leukocyte activation

A
  • Leukocytes require activation in order to perform functions
  • Neutrophils and macrophages can become activated
  • Induced by a variety of chemical mediators
  • Functions following activation include phagocytosis, lysis/killing of injurious particles and release of further chemical mediators
28
Q

Phagocytosis

A

The process by which neutrophils and macrophages ingest debris / foreign particles

29
Q

3 phases of phagocytosis

A
  1. Recognition and attachment by receptors on
    surface of macrophages
  2. Engulfment
  3. Killing and degradation
30
Q

Phagocytosis engulfment

A
  • Pseudopods form around organism
  • Foreign material incorporated within cell vacuole (phagosome)
  • Fusion with lysosomes and release of lysosomal contents
31
Q

phagocytosis killing and degradation

A

Reactive oxygen species, nitric oxide, lysosomal enzymes

32
Q

Resolution

A

Restoration of tissue to a completely normal state after acute inflammation or other tissue damage or death

33
Q

When is resolution most likely to occur

A
  • when cell death and tissue damage is minimal
  • when damaged cells are capable of regeneration
  • when causative organism is rapidly eliminated
  • where local conditions favour removal of exudate
34
Q

Process of resolution

A
  1. Return to normal permeability
  2. Drainage of fluid & proteins into lymph
  3. Pinocytosis into macrophages
  4. Phagocytosis of apoptotic neutrophils
  5. Phagocytosis of necrotic debris
  6. Disposal of macrophages
35
Q

Serous inflammation

A
  • Characterised by presence of thin, watery fluid in exudate
  • Commonly seen in blisters from burns or viral infections
36
Q

Purulent inflammation

A
  • Large amounts of pus (dead leukocytes & bacteria), neutrophils, necrotic cells, edema fluid
  • Caused by pyogenic bacteria (staph spp.)
  • Central region of necrotic cells with infiltration of neutrophils
37
Q

Fibrinous inflammation

A
  • Characterised by entry of fibrinogen (clotting factor) into tissues
  • Fibrinogen is cleaved to form fibrin and when not
    removed it can lead to scarring
  • Inflexible sheets of fibrin
38
Q

Ulcerative inflammation

A
  • Excavation in tissue surface produced by shedding of necrotic inflammatory tissue
  • Commonly seen in mucosa of mouth, stomach and
    intestines

PATH2220 (33 decks)

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