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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
Q

Exudate

A

High protein content, and may contain some white and red cells

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26
Q

Migration and accumulation of cells

A

first step – neutrophils

involves a complex process of exit from blood vessels

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27
Q

Removal of pathogens/injured/dead cells

A

neutrophils phagocytose pathogens and dead tissue

neutrophils live briefly => dead neutrophils = pus

28
Q
  1. Migration and accumulation of monocytes
A

monocytes differentiate into macrophages

phagocytosis => clearance of injured site

release factors that promote tissue repair (TGF-beta)

29
Q

Acute inflammation - Neutrophil recruitment

A

Multistep process
Adherence to luminal surface of endothelium
Migration through vessel wall

30
Q

Neutrophil recruitment

A
  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
Q

Molecules involved in neutrophil recruitment (adhesion molecules)

A
  1. Selectins
  2. Integrins
  3. Immunoglubulin superfamily cell adhesion molecules
    (CAMs)
32
Q

E-selectin

A

induced by IL-1 and TNF-alpha (cytokines produced by macrophages, mast cells, endothelial cells at site of inflammation)

33
Q

L-selectin

A

Leucocytes (neutrophils, monocytes, lymphocytes) express L-selectin; ligands on endothelium

34
Q

Endotelial selectins

A

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
Q

Endotelial selectins

A

Endotelial selectins bind to ligands on neutrophils

Ligands – carbohydrates (PSGL-1, sialyl-Lewis^x)

36
Q

Selectins mediate rolling

A

Low affinity interaction => disrupted by flowing blood => repetitive binding and detaching => rolling; slow down

37
Q

Integrin activation by chemokines

A

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
Q

Integrins bind to ligands on endothelium

A

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
Q

ICAM-1

A

intercellular adhesion molecule-1

40
Q

VCAM-1

A

vascular cell adhesion molecule-1

41
Q

Neutrophil transmigration

A

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
Q

Neutrophil chemotaxis

A

Movement of cells through tissue towards inflamed sites

43
Q

Neutrophil chemotaxis - chemoattractants

A

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
Q

Cells at inflammation site change over time

A

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
Q

Other types of inflammatory responses:

A

eosinophils (allergies, parasite infections)

lymphocytes (viral infections)

46
Q

Pathogen destruction

A

Once at sites of inflammation immune cells (neutrophils, monocytes/macrophages) destroy & clear pathogens and dead cells

47
Q

Neutrophils - pathogen destruction mechanisms

A

Recognition of microbes/dead cells to oxygen-independent and oxygen-dependent killing

48
Q

Mechanisms involved: (pathogen destruction)

A

Release of granule content

Phagocytosis

Generation of reactive oxygen/nitrogen species

Formation of Neutrophil Extracellular Traps (NETs) (netosis)

49
Q

Neutrophil Extracellular Traps - NETs

A

Mesh of nuclear content (chromatin)

Mesh traps microbes

Contains anti-microbial molecules

50
Q

Specific granules (small)

A

lysozyme, collagenase, gelatinase, lactoferrin, alkaline phosphatase

51
Q

Azurophil granules (large)

A

myeloperoxidase, lysozyme, defensins, acid hydrolases, proteases (elastase, cathepsin G, collagenases, proteinase 3)

52
Q

Granule content can cause

A

Granule content can cause tissue damage

53
Q

Corticosteroid drugs

A

inhibit transcription of many inflammatory genes

54
Q

Acute inflammation - termination

A

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
Q

Outcomes of acute inflammation

A

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
Q

Outcomes of acute inflammation - summary

A
  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
Q

Outcomes of acute inflammation - summary

A
  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
Q

Acute inflammation – resolution/tissue repair - complete resolution

A

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
Q

Acute inflammation – resolution/tissue repair - Repair by replacement (fibrosis)

A

injured tissue replaced with connective tissue

scarring => can alter tissue function

TGF-beta released by macrophages promotes fibrosis

60
Q

Abscess

A

mass of necrotic (dead) tissue

caused by pyogenic (pus-forming) bacteria

can become chronic if not reabsorbed/drained

61
Q

High regeneration ability

A

(labile tissues; divide continuously)
epithelial cells (e.g. skin, airways, gut; blood cells)
sometimes perfect regeneration, no scarring

62
Q

Intermediate regeneration ability

A

(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
Q

No/little regeneration ability

A

(permanent tissues)
neurons, myocardium, skeletal muscle
heal with fibrosis, scarring, loss of function

64
Q

Factors that favour tissue resolution

A
  • 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
Q

Factors that prevent tissue healing

A

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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