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inflammation and wound healing > inflammation and wound healing > Flashcards

inflammation and wound healing Flashcards

1
Q

what is inflammation

A

local physiological response to tissue injury in vascularised connective tissue involving reaction of blood vessels which lead to accumulation of fluid and leucocytes in extravascular tissue

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2
Q

what type of response is inflammation

A

protective

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3
Q

what would happen without inflammation

A

Wounds and injured organs would never heal
Infections would go unchecked

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4
Q

in what cases can inflammation be harmful

A
  • Life-threatening hypersensitivity reactions
  • Chronic inflammatory diseases eg
    rheumatoid arthritis and Crohn’s disease
  • Repair by fibrosis may lead to problems such as
    disfiguring scars
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5
Q

what are the 2 types of inflammation

A

acute and chronic

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6
Q

what is acute inflammatioin

A

the initial rapid and often short lived series of tissue reactions to injury

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7
Q

what is chronic inflammation

A

the subsequent and often prolonged tissue reactions
following the initial response

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8
Q

what are the principle causes of acute inflammation

A
  1. infections e.g viruses, bacteria like ecoli
  2. hypersensitivity reactions e.g reactions to parasites
  3. Physical agents
    eg physical trauma, uv light, thermal injury (burns or frostbite)
  4. Irritant and Corrosive chemicals
    eg acids, alkalis, infecting agents releasing chemical irritants
  5. Foreign bodies
    eg splinters, dirt, sutures, restorative materials
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9
Q

physical characteristics of inflammation

A

redness (rubor) - acute inflamed tissue appears red due to dilation of small blood vessels

heat (calor) - increase temp of tissue due to increases blood flow thorugh region

swelling (tumor) - accumulation of fluid in extravascular space

pain (dolor) - due to stretching and distortion of tissues caused by increased fluid

loss of function - movement inhibited by pain

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10
Q

describe the processes of acute inflammation

A
  1. vascular phase
    - vasodilation (results in precapillary sphincter opening = increased blood flow therefor heat and redness)
  • increased permeability of blood vessels ( brought about by chemical mediators like histamine and bradykinin)
  1. Exudative and cellular phase
    - Fluid and cells escape from permeable venules
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11
Q

IDEK = Leakage of fluid is confined to POST CAPILLARY VENULES
Gaps in venules are largely intercellular
Endothelial cells contain contractile proteins, when stimulated by chemical
mediators they pull open transient pores
Endothelial cells are NOT damaged in this process

A
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12
Q

what is the net increase of extravascular fluid called

A

oedema

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13
Q

Explain the fluid exudate

A

during inflamation fluid containing immunoglobins (antibodies) and fibrinogen leaks out into surrounding tissue and is drained through the lymphatic system (oedema as blood vessels get wider to accomodate this fluid)

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14
Q

what is the diagnostic feature of acute inflammation

A

neutrophil accumulation in the extracellular space

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15
Q

functions of neutrophils

A

kill microorganisms
ingest offending agents
degrade necrotic tissue
produce chemical mediators
produce toxic oxygen radicals
produce tissue damaging enzymes

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16
Q

how does a neutrophil reach the site of an inflammatory stimulus

A

chemotaxis = locomotion orientated along a chemical gradient
by a combination of different processes that involving adhesion of circulating leucocytes to endothelial cells and subsequent migration through endothelium

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17
Q

what are the 3 stages in the neutrophils reaching the site of inflammatory stimulus

A
  1. Migration - occurs in venules, loss of intravascular fluid and increased plasma viscosity slows flow allowing neutrophils to flow in the plasmatic zone
  2. Adhesion - increased neutrophils adhesion results from interaction between adhesion molecules on its surface and the endothelial surfaces
  3. Transendothelial migration - once firm adhesion to the endothelium has been achieved, neutrophils insert pseudopodia into the junctions between endothelial cells. they then cross through the basement membrane and into the extravascular space
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18
Q

What substances attract neutrophils to the site of infection or inflammation?

A
  • bacterial products
  • complements components
  • cytokines
  • Products produced by neutrophils themselves
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19
Q

what is the definition of phagocytosis

A

complex process by which phagocytes such as neutrophils and macrophages engulf and ingest microorganisms or other cells and foreign particles

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20
Q

what are the 3 steps in phagocytosis

A
  1. recognitions and attachment
  2. engulfment -
  3. killing and degradation
21
Q

what is opsonization

A

process of coating a particle to target it for phagocytosis

22
Q

what is the role of Opsonins

A

they bind specifically to receptors on leucocytes and greatly enhance phagocytosis

23
Q

describe the process of phagocytosis

A
  1. recognitions and attachment - initiated by recognition of
    particles by leucocyte surface receptors
  2. engulfment - Attachment of a particle to a phagocyte receptor initiates the process of active phagocytosis. Engulfment involves cytoplasmic extensions to flow around the particle
    resulting in complete ‘engulfment’ of the particle within a phagosome
    made by the cell membrane
    This phagosome membrane then fuses with lysosomal membrane,
    resulting in discharge of the lysosome content into the phagolysosome
  3. killing and degradation = Killing of infectious agents occurs by 2 types of mechanism:
    i. Oxygen-dependent
    Phagocytosis results in products of oxygen reduction which cause
    intracellular killing of micro-organisms
    ii. Oxygen-independent
    Via the action of substances in leucocyte granules
    eg Lysozyme which attacks bacterial coat
    Defensins that are cytotoxic to microbes
    Acidic pH inside phagocytic vacuoles
    After killing, acid hydrolase from lysosomes degrade the
    microorganisms inside the phagolysosome
    During activation and phagocytosis, leucocyte products are released
    into the EXTRACELLULAR SPACE as well as into phagolysosome
24
Q

what are the effects of lysosomal product release

A

products may cause endothelial and tissue damage
1. Activates coagulation factor XII
2. Attracts other leucocytes into the area
3. Damages local tissues
4. Increases vascular permeability
5. Pyrogens producing systemic fever

25
what do neutrophils undergo after phagocytosis
apoptosis
26
what is the role of chemical mediators of acute inflammation
endogenous chemical mediators that drive the process of inflammation
27
what do chemical mediators cause
1. Vasodilatation 2. Emigration of neutrophils 3. Chemotaxis 4. Increased vascular permeability 5. Itching and pain
28
what chemical mediators of inflammation are released
1. Histamine 2. Lysosomal compounds 3. Serotonin 4. Chemokines 5. Leukotrienes 6. Prostaglandins
29
what factors does the plasma do in inflammation
it contains 4 enzymatic cascade systems which mediate various aspects of inflammation 1. Complement system 2. Coagulation system 3. Kinin system 4. Fibrinolytic system
30
what are the beneficial effects of acute inflammation
1. Dilution of toxins- can be carried away by lymphatics 2. Entry of antibodies- due to increased vascular permeability 3. Stimulation of the immune response- fluid exudate containing antigens reaches local lymph nodes 4. Fibrin Formation – impedes movement of micro-organisms 5. Delivery of nutrients and oxygen - aided by blood flow 6. Transport of drugs – eg antibiotics
31
what are the harmful effects of acute inflammation
* Digestion of normal tissues * Swelling – eg laryngeal oedema, brain swelling * Inappropriate inflammatory response – eg type I hypersensitivity
32
what are the systemic effects of acute inflammation
1. Fever 2. Constitutional Symptoms 3. Weight Loss 4. Reactive Hyperplasia of the Reticuloendothelial System 5. Haematological Changes
33
what factors favour progression from acute to chronic inflammation
1. Indigestible substances such as glass and suture material 2. Deep seated suppurative inflammation in which drainage is delayed or inadequate will result in a thick abscess wall composed of fibrous/granulation tissue 3. Recurrent episodes of acute inflammation and healing may eventually result in the clinicopathological entity of chronic inflammation
34
what are 6 examples of chronic inflammation
1. Resistance of infective agent to phagocytosis and intracellular killing eg Tuberculosis, leprosy, viral infections 2. Foreign body reactions to endogenous materials eg gout (may be acute or chronic) 3. Foreign body reactions to exogenous materials eg asbestos 4. Some autoimmune diseases eg. Rheumatoid arthritis 5. Specific diseases of unknown aetiology eg ulcerative colitis 6. Primary granulomatous diseases eg sarcoidosis
35
what are the cells that are most predominant in chronic inflammation
lymphocytes, plasma cells and macrophages A few eosinophils may be present but neutrophil polymorphs are scarce
36
what cells can be replaced if lost
ONLY labile and stable
37
what can cells be divided into
labile - (multiply continually throughout life) eg GI Tract, Bone Marrow stable - (only multiply when receive stimulus to do so) eg Hepatocytes, Endothelium permanent populations- Permanent (cannot multiply) eg Neurones, Skeletal Muscle
38
what is meant by the term restitution
complete restoration of the tissue to normal after an episode of acute inflammation
39
what factors favour restitution
* Minimal cell death and tissue damage * Occurrence in an organ or tissue with regenerative capacity eg liver * Rapid destruction of the causal agent * Rapid removal of fluid and debris by good local vascular drainage
40
describe repair by connective tissue fibrosis
Tissue destruction includes loss of parenchymal cells and the associated stromal framework Non-regenerated parenchymal cells replaced by connective tissue (granulation tissue) which in time produces fibrosis and scarring
41
what does repair by connective tissue fibrosis involve
1. Angiogenesis- formation of new blood vessels 2. Migration and proliferation of fibroblasts 3. Deposition of collagen 4. Maturation and organisation of fibrous tissue - remodelling
42
what is organisation of tissues
replacement by granulation tissue
43
what factors favour organisation
* Large amounts of fibrin formed * Substantial necrosis * Exudate and debris cannot be removed or discharged
44
describe repair with scarring and the contrast between first and second intention
First Intention - Surgical scar - Closely apposed edges Minimal granulation tissue Minimal fibrosis Second Intention - Ulcerated surface - Edges widely separated Prominent granulation tissue Prominent fibrosis
45
what are the local factors that influence wound healing
* Infection – single most important cause of delay in healing * Mechanical factors – ie early motion of wounds delays healing * Foreign bodies – ie sutures or glass * Size, location and type of wound – wounds heal better in richly vascularised areas
46
what are the systemic factors that influence wound healing
* Nutrition – wound healing profoundly influenced by ability to synthesise protein and collagen * Metabolic status – diabetes is associated with delayed healing * Circulatory status – an adequate vascular supply is essential for normal cellular function (hypoxia, reduced local nutrition) * Hormones – glucocorticoids are anti-inflammatory but impair collagen synthesis
47
what are the pathological aspects of wound repair
1. Deficient scar formation – wound dehiscence/ulceration 2. Excessive formation of repair components – keloid scar 3. Formation of contractures – exaggerated contraction results in deformity of the wound and surrounding tissues
48
In summary wound healing is a complex but orderly phenomenon involving a number of processes: * Induction of acute inflammatory response * Regeneration of parenchymal cells (if possible!) * Migration and proliferation of parenchymal and connective tissue cells * Synthesis of collagen * Remodelling/organisation of connective tissue and parenchymal components

inflammation and wound healing (1 decks)

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