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4. Acute inflammation Flashcards

1
Q

What is inflammation

A

reaction of a vascularised living tissue to a local injury

  • eliminate the initial cause of cell injury and the necrotic cells and tissues arising from the injury
  • intimately associated with repair process
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2
Q

Objectives of inflammation

A
  • localise and eliminate the causative agent
  • limit tissue injury
  • begin the process of healing
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3
Q

Causes of inflammation

A
  • infectious agent
  • physical agent
  • chemical agent
  • immune reaction
  • necrotic tissue
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4
Q

Characteristics of acute inflammation

A
  • immediate and early response to injury
  • accumulation of fluid and protein
  • accumulation of polymorphonuclear cells (neutrophils)
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5
Q

Characteristrics of chronic inflammation

A
  • inflammation of prolonged duration

- accumulation of mononuclear cells (macrophages, lymphocytes, plasma cells)

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6
Q

Components of acute inflammation

A
  1. vasodilatation
  2. endothelial permeability
  3. extravasation of neutrophils
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7
Q

5 classic local signs of acute inflammation

A 
heat - vasodilatation
redness - vasodilatation
swelling - vascular permeability
pain - inflammatory mediator release
loss of function - pain/oedema
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8
Q

Two major events in acute inflammation

A
  1. vascular response
    - vasodilatation
    - increased vascular permeability
  2. cellular response
    - extravasation of neutrophils at site of infection
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9
Q

Vascular response in acute inflammation

A
  1. vasoconstriction - transient (few sec)
  2. vasodilatation
  3. increased vascular permeability -> exudation of protein rich fluid
  4. loss of fluid -> concentration of red cells and increased viscosity -> blood stasis
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10
Q

Increased vascular permeability is due to

A
  • increased hydrostatic pressure
  • decrease in intravascular osmotic pressure
  • changes in endothelial cells:
    a) endothelial cell contraction
    b) junctional retraction
    c) endothelial injury
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11
Q

Increased hydrostatic pressure

A

Vasodilatation -> increased blood flow -> increased hydrostatic pressure
-transudate

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12
Q

What is transudate

A
  • extravascular fluid with low protein concentration
  • specific gravity <1.012
  • hydrostatic imbalance
  • ultrafiltrate blood plasma
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13
Q

Decreased osmotic pressure

A

osmotic pressure of interstitial fluid increases

-exudate

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14
Q

What is exudate

A

-extravascular fluid with high protein concentration and cellular debris
-specific gravity >1.012
-alteration in vascular permeability
fluid emitted by an organism through pores or a wound

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15
Q

Cellular response to acute inflammation

A
  1. margination
  2. endothelial activation
  3. rolling
  4. adhesion/pavementing
  5. transmigration
  6. chemotaxis
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16
Q

What are the main effector cells in acute inflammation

A

Neutrophils

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17
Q

What is margination

A
  • leukocytes moving from the centre of the vessel towards the periphery
  • Normal flow - RBC and WBC flow in the centre of the vessel
  • a cell poor plasma is flowing adjacent to endothelium
  • as blood flow slows, WBC collect along the endothelium, -> margination
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18
Q

What is endothelial activation

A

the underlying stimulus cause release of mediators which activate the endothelium causing selectins and other mediators to be moved quickly to the surface

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19
Q

What is rolling

A

neutrophils bounce or roll along endothelial cells

  • transiently adhere to endothelial cells
  • mediated by selectins molecules
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20
Q

What is adhesion (pavementing)

A

leucocytes firmly adhere to endothelial cells

-mediated by integrins, ICAM-1 and VCAM-1

21
Q

What is transmigration

A
  • mediated by PECAM-1

- diapedesis - the passage of blood cells through the intact walls of capillaries

22
Q

What is chemotaxis

A

movement towards the site of injury

  • recognition of microbes and dead tissues
  • Toll-like receptors: recognise components of different type of microbes -> upregulation of NF-κB
23
Q

Leucocyte activation leads to

A

opsonisation - coating a bacterium or a particle to facilitate its phagocytosis

  • immunoglobulins
  • C3b (complement)
24
Q

Group of chemical mediators of inflammation

A
  1. Plasma-derived
    - circulating precursors
    - have to be activated
  2. Cell-derived
    - sequestered intracellularly
    - synthesized de novo
25
Q

Examples of chemical mediators of inflammation

A
  • vasoactive amine
  • plasma proteases
  • phospholipid-derived products
  • cytokines
  • nitric oxide
  • lysosomal enzymes
  • oxygen derived free radicals
26
Q

Effects of vasoactive amines

A

vascular dilatation and leakage

a) Histamine
- found in mast cells, basophils and platelets
- released in response to stimuli
- promotes arteriolar dilation and venular endothelial contraction
- results in widening of interendothelial cell junctions with increased vascular permeability
b) Serotonin
- found in platelets
- released when platelets aggregate

27
Q

Effects of plasma proteases

A
  1. complement system
  2. kinin system
  3. clotting system
28
Q

How does the complement system works

A

a) classical pathway
- require antibodies to activate
- C1 binds to IgG or IgM that is bound to antigen
b) alternative pathway
- dose not require antibody to activate
- microbial surface

29
Q

Complement system role

A
  1. in immunity
    - C5-9 complex
    - membrane attack complex (MAC C5-9)
    - punches a hole in the membrane
  2. in inflammation
    - C3a and C5a
    - vascular effects: increase vascular permeability and vasodilation
    - cellular effects: leucocyte activation, adhesion and chemotaxis (C5a), phagocytosis (C3b)
30
Q

How does Kinin system works

A

leads to formation of bradykinin

31
Q

What does bradykinin cause

A
  • increased vascular permeability
  • arteriolar dilatation
  • smooth muscle contraction
  • pain
32
Q

How does the clotting system works

A

activation key is factor XII (F12)

  • Hageman factor
  • end result is fibrin
33
Q

What are the examples of phospholipid derived products

A
  • arachidonic acid derivatives

- platelet activating factor

34
Q

What is arachidonic acid

A

complement of cell membrane phospholipids

  • occur in 2 major pathway:
    a) lipoxygenase
  • produce leucotrienes
  • LTB4 - attract and activate neutrophils
  • LTC4, LTD4, LTE4
  • vasoconstriction, vasospasm, bronchospasm, and increased permeability
    b) cyclooxygenase
  • produce prostaglandins and prostacylins
  • prostaglandins: PGI2, PGD2, PGE2
  • vasodilation and permeability
  • PGE2 - fever
  • prostacylin vs TXA2 = vasodilatation vs vasoconstriction
  • platelet aggregation: inhibit vs promote
35
Q

What does Phospholipase A2 do and how is it blocked

A

cleave fatty acid in position two of phospholipids, hydrolyzing the bond between the second fatty acid “tail” and the glycerol molecule into arachidonic acid
-blocked by Steriods

36
Q

What does cyclooxygenase do and how is it blocked

A

converts arachidonic acid to prostaglandins

-blocked by aspirin and NSAIDS

37
Q

What does platelet activating factors do

A
  • induces aggregation of platelets
  • causes vasoconstriction and bronchoconstriction
  • enhance leucocyte adhesion, chemotaxis and degranulation
38
Q

Effects of nitric oxide

A
  • toxic to bacteria
  • vasodilation
  • tissue damage
39
Q

Effects of oxygen derived free radicals

A
  • elimination of bacteria
  • tissue damage:
    a) direct injury to endothelial cells
    b) injury to ECM
    c) injury to other cell types
40
Q

What causes vasodilatation

A
  • vasoactive amines
  • prostaglandins
  • bradykinin
  • complemet (C3a and C5a)
  • NO
41
Q

What causes vascular leakage

A
  • vasoactive amines
  • bradykinin
  • complement
  • tissue damage
  • leucotrienes
  • PAF
42
Q

What causes chemotaxis

A
  • complement (C5a)
  • leucotrienes
  • cytokines
  • bacterial products
43
Q

What causes pain

A
  • prostaglandins (PGE2)
  • bradykinin
  • oedema
44
Q

What causes tissue damage

A
  • lysosomal enzymes
  • oxygen metabolites
  • NO
45
Q

What causes fever

A
  • cytokines
  • prostaglandins
  • pyrogens cuse macrophages to release IL-1 and TNF
  • increase cyclooxygenase activity on perivascular cells of hypothalamus -> PGE2
46
Q

Beneficial effects of inflammation

A
  • dilution of toxins
  • arrival of antibodies on the site of inflammatiokn
  • drug transport
  • delivery of nutrients and oxygen
  • fibrinogen -> fibrin (delays bacterial spread)
  • destruction of microbial agents
  • removal of tissue debris
  • stimulation of immune response
47
Q

Harmful effecrts of inflammation

A
  • mechanical effects: e.g. epiglottitis
  • impaired blood flow: e.g. acute meningitis
  • impaired function
  • tissue destruction due to effect of inflammatory mediators and activation of clotting system that activates microthrombi
48
Q

Outcome of acute inflammation

A
  • resolution
  • abscess formation - walled off collection of pus
  • progression to chronic inflammation
  • healing and repair

FIP (24 decks)

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