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Fundamentals of Pathology > W12 Acute inflammation > Flashcards

W12 Acute inflammation Flashcards

1
Q

What is acute inflammation?

A

Initial rapid response to tissue injury
minutes/hours to develop
short duration (hours, days)

Acute inflammation is an innate immune response

Relatively non-specific: several types of injury

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2
Q

Triggers of acute inflammation - infections

A

bacteria, viruses, parasites, fungi, toxins

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3
Q

Triggers of acute inflammation - Tissue damage due to:

A

Physical agents
frost bites, burns, radiation (ionising, UV)

Chemical agents
chemical burns, irritants

Mechanical injury & ischemia
trauma, tissue crush, reduced blood flow

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4
Q

Triggers of acute inflammation - foreign bodies

A

splinters; sutures; dirt; swallowed bones; dentures

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5
Q

Acute inflammation - purpose

A

Alert the body
Limit spread (of infection and/or injury)
Protect injured site from becoming infected
Eliminate dead cells/tissue
Create the conditions required for healing
Acute inflammation is a beneficial response

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6
Q

If acute inflammation didn’t exist

A

No control of infections
Impaired wound healing
Injured tissues would not be repaired

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7
Q

Acute inflammation – the 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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8
Q

Signs of acute inflammation - redness

A

Redness (rubor)

increased blood flow (hyperaemia) to injured area

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9
Q

Signs of acute inflammation - swelling

A

Swelling (tumor)

fluid accumulation <= permeability of vessels

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10
Q

Signs of acute inflammation - heat

A

Heat (calor)

increased blood flow and metabolic activity

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11
Q

Signs of acute inflammation - pain

A

Pain (dolor)

release of pain mediators; pressure on nerve ends

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12
Q

Signs of acute inflammation - loss of function

A

Loss of function (functio laesa)

excessive swelling and pain

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13
Q

Acute inflammation – systemic changes

A

Acute inflammation = local response
symptoms and reactions take place in affected tissue
Can have some systemic manifestations

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14
Q

Fever

A

<= endogenous pyrogens (IL-1, TNF-alpha); <= exogenous pyrogens (microbial components)

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15
Q

Neutrophilia

A

<= G-CSF stimulation of bone marrow

replenish dead neutrophils
release of immature neutrophils

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16
Q

Acute phase reactants

A

C-reactive protein (CRP), fibrinogen, complement, serum amyloid A protein (SAP)
produced in the liver
induced by IL-6, IL-1, TNF-alpha
↑ fibrinogen => stacking of RBCs (rouleaux) => faster sedimentation rate (↑ESR)

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17
Q

Rare cases (systemic changes)

A

systemic inflammatory reaction => sepsis

widespread, severe manifestations

form of Systemic Inflammatory Response Syndrome (SIRS)

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18
Q

Vasodilatation (small vessels)

A

histamine, serotonin; released by injured cells, macrophages, mast cells

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19
Q

Increased blood flow to injured area

A

results in influx of white blood cells, fluid, oxygen, nutrients

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20
Q
  1. Increased vessel permeability (microvessels)
A

due to contraction of endothelial cells (histamine, serotonin, other)

results in leakage of fluid and cells in injured tissue

endothelial cell activation: increased adhesion molecules

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21
Q

What is the overall effect of the vascular events

A

Overall effect: leucocytes and plasma proteins exit vessels and enter inflammation site to deal with infection/damage

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22
Q

Inflammation summary

A

endothelial cell contraction
(histamine, serotonin, other)

leakage of fluid and cells in injured tissue

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23
Q

Inflammatory exudate

A

Inflammatory exudate (due to increased vessel permeability)

water, salts, small plasma proteins (fibrinogen)

=> get out of vessels and enter tissues or serous cavities

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24
Q

Transudate

A

fluid leaks due to altered osmotic/hydrostatic pressure; vessel permeability normal

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25
Exudate
High protein content, and may contain some white and red cells
26
Migration and accumulation of cells
first step – neutrophils | involves a complex process of exit from blood vessels
27
Removal of pathogens/injured/dead cells
neutrophils phagocytose pathogens and dead tissue neutrophils live briefly => dead neutrophils = pus
28
3. Migration and accumulation of monocytes
monocytes differentiate into macrophages phagocytosis => clearance of injured site release factors that promote tissue repair (TGF-beta)
29
Acute inflammation - Neutrophil recruitment
Multistep process Adherence to luminal surface of endothelium Migration through vessel wall
30
Neutrophil recruitment
1. Margination & rolling 2. Integrin activation by chemokines 3. Firm adhesion to endothelium 4. Transmigration through endothelium into tissue 5. Chemotaxis to inflamed site
31
Molecules involved in neutrophil recruitment (adhesion molecules)
1. Selectins 2. Integrins 3. Immunoglubulin superfamily cell adhesion molecules (CAMs)
32
E-selectin
induced by IL-1 and TNF-alpha (cytokines produced by macrophages, mast cells, endothelial cells at site of inflammation)
33
L-selectin
Leucocytes (neutrophils, monocytes, lymphocytes) express L-selectin; ligands on endothelium
34
Endotelial selectins
Endotelial selectins bind to ligands on neutrophils Ligands – carbohydrates (PSGL-1, sialyl-Lewis^x) Low affinity interaction => disrupted by flowing blood => repetitive binding and detaching => rolling; slow down
35
Endotelial selectins
Endotelial selectins bind to ligands on neutrophils Ligands – carbohydrates (PSGL-1, sialyl-Lewis^x)
36
Selectins mediate rolling
Low affinity interaction => disrupted by flowing blood => repetitive binding and detaching => rolling; slow down
37
Integrin activation by chemokines
Neutrophils rolling slows them down => endothelial contact Neutrophils express integrins (LFA-1) Integrins in low affinity configuration; no binding to ligands Activated endothelial cells produce/bind chemokines Chemokines bind to receptors on neutrophils => integrin activation => high affinity configuration
38
Integrins bind to ligands on endothelium
integrin ligands: ICAM-1, VCAM-1integrin ligands induced by IL-1 and TNF-alpha (cytokines produced by macrophages, mast cells, endothelial cells at site of inflammation) => Firm adhesion of neutrophils to endothelium
39
ICAM-1
intercellular adhesion molecule-1
40
VCAM-1
vascular cell adhesion molecule-1
41
Neutrophil transmigration
Neutrophils migrate through interendothelial spaces Neutrophils pass through vessel wall and enter tissue Migrate (chemotaxis) through tissue towards inflamed site Gradient of chemoattractants guides migration in tissues
42
Neutrophil chemotaxis
Movement of cells through tissue towards inflamed sites
43
Neutrophil chemotaxis - chemoattractants
Guided by chemoattractants: produced at site of infection/damage diffuse into adjacent tissue and form a gradient bacterial components (peptides containing N-formyl-methionine-leucine-phenylalanine; lipids) chemokines (IL-8) complement components (C5a) leukotriene B4 (LTB4)
44
Cells at inflammation site change over time
neutrophils (6-24h); short lived; die in tissues (24/48h) monocytes (24-48h); survive longer, proliferate monocytes use similar mechanisms to leave blood vessels and enter sites of inflammation monocytes differentiate into macrophages in tissues
45
Other types of inflammatory responses:
eosinophils (allergies, parasite infections) lymphocytes (viral infections)
46
Pathogen destruction
Once at sites of inflammation immune cells (neutrophils, monocytes/macrophages) destroy & clear pathogens and dead cells
47
Neutrophils - pathogen destruction mechanisms
Recognition of microbes/dead cells to oxygen-independent and oxygen-dependent killing
48
Mechanisms involved: (pathogen destruction)
Release of granule content Phagocytosis Generation of reactive oxygen/nitrogen species Formation of Neutrophil Extracellular Traps (NETs) (netosis)
49
Neutrophil Extracellular Traps - NETs
Mesh of nuclear content (chromatin) Mesh traps microbes Contains anti-microbial molecules
50
Specific granules (small)
lysozyme, collagenase, gelatinase, lactoferrin, alkaline phosphatase
51
Azurophil granules (large)
myeloperoxidase, lysozyme, defensins, acid hydrolases, proteases (elastase, cathepsin G, collagenases, proteinase 3)
52
Granule content can cause
Granule content can cause tissue damage
53
Corticosteroid drugs
inhibit transcription of many inflammatory genes
54
Acute inflammation - termination
Anti-microbial mechanisms Inflammatory mediators not specific to microbes/dead tissues normal tissues can get damaged during inflammation Termination of acute inflammatory reaction – IMPORTANT !
55
Outcomes of acute inflammation
Inflammatory trigger eliminated => inflammation resolves recruited cells die (neutrophils – short life span in tissue) inflammatory mediators degraded (most short-lived) activation of regulatory mechanisms (anti-inflammatory) activation of tissue repair mechanisms Lost tissue replaced: cell regeneration / connective tissue
56
Outcomes of acute inflammation - summary
1. Complete resolution affected tissue restored to normal state 2. Repair lost tissue replaced by connective tissue (scarring, fibrosis) 3. Chronic inflammation acute inflammation cannot be resolved => chronic
57
Outcomes of acute inflammation - summary
1. Complete resolution affected tissue restored to normal state 2. Repair lost tissue replaced by connective tissue (scarring, fibrosis) 3. Chronic inflammation acute inflammation cannot be resolved => chronic
58
Acute inflammation – resolution/tissue repair - complete resolution
damaging agent removed injured tissue replaced by cells of the same type no change in tissue structure/function Restoration of normal tissue structure only if residual tissue is structurally intact Extensive tissue damage (infection/inflammation) => structure affected => incomplete regeneration & scarring
59
Acute inflammation – resolution/tissue repair - Repair by replacement (fibrosis)
injured tissue replaced with connective tissue scarring => can alter tissue function TGF-beta released by macrophages promotes fibrosis
60
Abscess
mass of necrotic (dead) tissue caused by pyogenic (pus-forming) bacteria can become chronic if not reabsorbed/drained
61
High regeneration ability
(labile tissues; divide continuously) epithelial cells (e.g. skin, airways, gut; blood cells) sometimes perfect regeneration, no scarring
62
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
63
No/little regeneration ability
(permanent tissues) neurons, myocardium, skeletal muscle heal with fibrosis, scarring, loss of function
64
Factors that favour tissue resolution
- Minimal destruction - Minimal cell death - Good regeneration ability of injured tissue - Fast clearance of infection - Quick removal of dead tissue (debris) - Removal of foreign material (sutures, bone fragments) - Immobilisation of wound edges (sutures)
65
Factors that prevent tissue healing
Infection Diabetes Poor general health/nutrition (protein/vitamin C deficiency) Old age Drugs: corticosteroids Extensive injury Poor vascular supply Extensive haemorrhage Foreign bodies (steel, glass, bone fragments) Pressure/torsion/movement on wound edges => dehiscence

Fundamentals of Pathology (23 decks)

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