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Animal Disease 1 > Inflammation and Healing > Flashcards

Inflammation and Healing Flashcards

1
Q

Why is apoptosis usually associated with little to no inflammation?

A

Fragments of cells in apoptosis remain encased in cell membrane as little buds, meaning DAMPs are not released, cytokines are not release by cells of the innate immune system and there is no acute inflammatory response.

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2
Q

What are the 5 clinical signs of inflammation?

A

Redness
Heat
Pain
Swelling
Loss of function

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3
Q

What is acute inflammation?

A

Innate immune response to a harmful stimulus, initiated by various biomolecules and their receptors. Part of the second line of defence.

Acute inflammation is a cascade of vascular and cellular events that aims to dilute, isolate, eliminate harmful stimulus, prepare for healing.

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4
Q

What triggers acute inflammation?

A

Endogenous – molecules form dead/damaged cells, such as damage associated molecular patterns.

Exogenous – molecules from microbes (LPS) – pathogen associated molecular patterns.

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5
Q

Describe the process of cell death by apoptosis.

A
  1. When a noxious stimulus affects a cell, the cell and the organelles begin to swell, in the initial stages of hydrophilic degeneration.
  2. Continues until the cell ruptures in a necrotic process.
  3. Low there is low levels of noxious stimulus or occasionally or a physiological response to stimulus, such as hormones, cell will start to die via a choregraphed process:
  4. It will form little cytoplasmic buds, which are subsequently released and engulfed by phagocytic cells, such as macrophages and neutrophils, in apoptosis.
  5. So fragments of cell remain enclosed by cell membrane.
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6
Q

What are DAMPs?

A

DAMPs are host biomolecules that can initiate and perpetuate an inflammatory response.

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7
Q

How are DAMPs generated?

A
  • Cell affected by harmful or noxious stimulus.
  • Cell swells and ruptures.
  • DAMPs are released, they are endogenous molecules released by the damaged cell.
  • These will then be taken up and recognised by pattern recognition receptors on various cells of the innate immune system, which are initiated to release cytokines (chemical messengers).
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8
Q

What are PAMPs?

A

PAMPs are small molecular motifs produced by microbes, such as lipopolysaccharide (LPS).

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9
Q

How are PAMPs recognised?

A
  • These are picked up by pattern recognition receptors specific to the PAMPs on cells of the innate immune system.
  • Stimulated to release cytokines.
  • Cytokines trigger acute inflammatory response.
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10
Q

What underlies each clinical sign of inflammation?

A

Redness – capillary dilatation (vascular)

Heat – capillary dilatation (vascular, exudative)

Pain – exudation, cellular degranulation, effects of mediators (vascular, exudative, cellular)

Swelling – exudative, capillary dilatation, congregation of cells (vascular, exudative, cellular)

Loss of function – pain, exudative

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11
Q

Name the 3 phases of acute inflammation?

A

Fluidic/vascular
Cellular/exudative
Reparative/cellular

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12
Q

How does vessel calibre get altered?

A
  • Mast cell produce vasoactive amines – histamine, serotonin
  • Endothelial cell produce bradykinin
  • Other mediators
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13
Q

Why does vessel caibre get altered?

A

Increase in vessel diameter slows blood flow, more time for next phases

Facilities cellular margination

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14
Q

What are 3 reasons that gaps between endothelial cells occur?

A
  • Junctional complexes opened, caused by vasoactive compounds, in venules, transient.
  • Direct damage to endothelium, inciting cause.
  • Leukocyte (NL) activity in capillaries and venules.
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15
Q

How do gaps in endothelial cells cause increased permeability?

A
  • Outflow of fluid, possibly proteins and RBCs
  • Changes from transudate to exudate = protein rich and cell-rich (SG = more than 1.02)
  • Classification, such as serous ,fibrinous, suppurative
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16
Q

Describe the cellular phase of acute inflammation.

A
  • Involves phagocytic cells, or those which release enzymes or mediators.
  • For example, neutrophils are first responders.
  • Leave capillaries and venules via leukocyte adhesion cascade.
  • Interactions of glycoprotein on leukocytes and receptors, such as selectins, integrins, PECAM1, on endothelium.
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17
Q

Describe leukocyte action.

A
  • Initial removal of dead tissues and bacteria
  • Phagocytosis or degranulation
  • Produce inflammatory mediators
  • Produced from bone marrow, increased by colony stimulating factors
  • Short lived
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18
Q

Outline the leukocyte adhesion cascade.

A
  1. Blood flows left to right in this dilated, leaky capillary.
  2. Neutrophil present which moves to the end in margination.
  3. Moves towards the end of the capillary and forms loose bonds with the endothelium via the interaction of glycoproteins with receptors celled selectins on the endothelium, causing it to roll along the endothelium.
  4. Switch in cytokines so that more strongly bonded receptors appear on the endothelium so that firmer adhesion occurs by integrins.
  5. Neutrophil bound firmly to the endothelium.
  6. Neutrophil transmigrates through gaps in endothelium.
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19
Q

Where do neutrophils congregate and how?

A
  • Neutrophils congregate in inflammatory exudate
  • Follow gradients of chemotactic molecules and mediators to site of initiation/of noxious stimulus
  • Aided by proteases, cell adhesion, shape change
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20
Q

How are mediators derived?

A

Mediators are broadly cell or liver derived.

  • The ones produced by cells are either secreted from granules and then pre-made, so they can be released very quickly or they are actually produced by cells and are newly synthesised, so will take slightly longer.
  • Liver derived mediators are often produced by the liver and they are produced as precursor proteins, which are then subsequently activated.
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21
Q

Describe histamine action.

A
  • Performed and stored in mast cell granules
  • Various factors stimulate degranulation, such as cytokines and allergens
  • Actions: vasodilation, increased permeability, itching and pain
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22
Q

What are the 2 main pathways cleave arachidonic acid from the cell membrane?

A

Lipoxygenase – produces the intermediate leukotrienes.

Cyclooxygenase – produces the mediators prostaglandins, thromboxanes and lipoxin

All involved in inflammation but may all have different functions: leukotrienes, prostaglandins and thromboxanes are pro-inflammatory and lipoxin is anti-inflammatory.

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23
Q

What are the properties of free radicals?

A
  • Superoxide anion has no derivates – neutrophils and macrophages
  • Pro-inflammatory actions
  • Antioxidants – superoxide dismutase
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24
Q

List the pro-inflammatory actions of free radicals.

A
  • Active endothelial cells – increases adhesion molecules
  • Injure endothelial cells, causing increased permeability
  • Enhance cytokine production
  • Chemotactic factors inactive antiproteases (membrane damage)
  • Nitrogen oxide – smooth muscle relaxation in diodilation
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25
Q

What are cytokines?

A
  • Protein group produced by many cells
  • Modulate function of other cell types
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26
Q

What are the 5 families of cytokines?

A

Haematoproteins – growth factors for cell colonies

Interferons – antiviral, cell growth, immune activation

Chemokines – chemo-attractants

Tumour necrosis factors – activate signalling pathways for cell survival, death and differentiation

Interleukins – promote leukocyte development and differentiation

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27
Q

How is acute inflammation resolved?

A
  • Stimulus removed
  • Degradation of pro-inflammatory mediators
  • Down-regulation of receptors
  • Dephosphorylation of signalling molecules
  • Anti-inflammatory mediators, such as cytokines and lipoxins
  • Death of inflammatory cells
  • May progress to chronic inflammation, leading to tissue repair
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28
Q

What are the mechanisms that normally stop the acute inflammatory response persisting?

A
  • Loss of initiating stimulus
  • Degradation of pro-inflammatory mediators
  • Down-regulation of receptors
  • Dephosphorylation of signalling molecules
  • Anti-inflammatory mediators e.g. regulatory cytokines, lipoxins
  • Apoptosis / phagocytosis of inflammatory cells
  • May proceed to chronic inflammation, tissue repair
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29
Q

What are the outcomes of acute inflammation?

A

Injury counteracted with repair and healing = return to normal structure and function

Sustained damage = chronic inflammation, possibly fibrosis. or central necrosis and abscess formation

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30
Q

When does chronic inflammation occur?

A
  • Stimulus is not removed
  • Repeated acute inflammation
  • Unique characteristics of stimulus/host
  • In healing/tissue repair
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31
Q

What cells are involved in chronic inflammation?

A

Involves mononuclear cells, natural killer T cells, macrophages (+variants), stromal cells (fibroblasts and endothelial cells).

Aims to overcome the stimulus and heal/or isolate it.

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32
Q

What are the characteristics of chronic inflammation?

A
  • No fluid exudation
  • Mononuclear cells and macrophages
  • Persistence of necrosis
  • Various facets of tissue repair
  • All may be present together, usually 1 cellular pattern predominates
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33
Q

What are some examples of persistence/resistance of inflammatory stimulus?

A
  • Stimulus ‘hides’ from immune response
  • Stimulus is resistant to destruction
  • Genetic dysfunction in host
  • Some agents provoke chronic inflammation at outset
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34
Q

How are monocytes recruited?

A
  • Rolling (selectins), adhesion, transmigration (adhesion molecules and other mediators)
  • In the tissue, monocytes transform to macrophages under the influence of T-regulatory lymphocytes and mediators
35
Q

What are the functions of macrophages in chronic inflammation?

A

classical, wound healing, regulatory, epithelial/MGCs

  • Debridement – removal of injured tissue and debris
  • Antimicrobial activity
  • Chemotaxis and proliferation of fibroblasts and keratinocytes
  • Angiogenesis
  • Deposition and remodelling of extracellular matrix
36
Q

What immune processes does chronic inflammation involve?

A

Chronic inflammation involves phagocytosis and regulation of other inflammatory cells, or tissue repair. Also triggers adaptive immune system: process and present antigen and regulation of T lymphocytes.

37
Q

What is the structure of granulomas?

A
  • Macrophages, neutrophils or central acellular area
  • Macrophages, epithelial macrophages and multi-nucleated giant cells.
  • Lymphocytes, plasma cells, macrophages, fibrous capsule
38
Q

What are caseative granulomas?

A
  • Macrophages engulf organisms
  • Organisms resits digestion due to waxy out layer and multiplies in macrophages
  • Macrophages die and are engulfed by other macrophages. This continues in waves.
  • Central caseous necrosis (accumulated dead cell) may mineralise.
39
Q

What are eosinophilic granulomas?

A
  • Eosinophils dominate with macrophages, lymphocytes and plasma cells
  • Eosinophils are significant in responses to parasites and hypersensitivity reactions
  • But eosinophilic granuloma are thought to involve TH2 directed response to unknown antigen.
40
Q

Describe abscess formation.

A
  • Acute inflammation leaves pus. Pus is comprised of enzymes, liquefied cells, and live/dead organisms if bacteria is involved.
  • Serous(watery), purulent (thick) or caseous (dry and crumbly)
  • Macrophages direct fibroblasts to produce collagen and extracellular matrix proteins.
  • Results in formation of slender connective tissue wall that matures into thick fibrous capsule over a number of weeks.
41
Q

Define regeneration and healing.

A

Regeneration – growth of parenchymal cells to replace lost structures

Healing = repair – tissue response to a wound. Involves regeneration and fibrous tissue formation, to varying extents

42
Q

What does regeneration and healing depend on?

A
  • Retention of tissue scaffold, which is important for support, also many cytokines and growth factors
  • Properties of cells, such as their ability to regenerate
  • Hypoxia, blood supply and other factors
43
Q

Describe the different types of cell proliferation.

A
  • Liable proliferation – continuously divide, for example epithelia and bone marrow cells. These are stem calls have a prolonged capacity to regenerate in asymmetric replication.
  • Quiescent/stable populations – normally low level of division but can increase in response to stimuli, such as in liver, kidney, endothelial and mesenchymal cells.
  • Permanent cells have little or no ability divide, such as cells in the myocardium and CNS.
44
Q

What can chronic inflammation lead to?

A

Fibrosis

45
Q

What is the role of macrophages in chronic inflammation?

A
  • Secretion of cytokines and growth factors
  • Orchestration of multiplication of endothelial cells, sprouting of new blood vessels in angiogenesis and division of stromal cells.
  • Recruitment of other cells, such as immune cells and MCs
  • Thus the beginning of tissue repair
46
Q

What are the roles of endothelial cells in chronic inflammation?

A
  • Endothelial cells damaged, leading to platelet adherence to exposed ECM facilitated
  • Lead to platelets being activated and attraction of more platelets
  • Endothelial cells trigger fibrin polymerisation and entrap RBCs.
  • Angiogenesis – endothelial cells involved in new vessel formation.
47
Q

How do mast cells and fibroblasts contribute to extracellular matrix?

A

Mast cells – proteolytic enzymes (chymase and tryptase) may help to remodelling of the extracellular matrix.

Fibroblasts – produce collagen and extracellular matrix.

48
Q

Why is mature scar tissue white?

A

Mature scar tissue (fibrosis) contains relative few capillaries.

49
Q

What 4 primary phases are involved in wound healing?

A

Haemostasis
Inflammation
Proliferation
Remodelling

50
Q

Describe haemostasis phase.

A
  • Starts immediately
  • Initial reactionary vasoconstriction
  • Platelets (thrombocytes) adhere to damaged endothelium and plugs the wound
  • Fibrin mesh is formed and stabilises platelet and red blood cells, causing a clot
  • Blood vessels subsequently dilate
51
Q

Describe the inflammatory phase.

A
  • ‘Defensive’ / ‘demolition’ phase – removal of debris and bacteria
  • Associated with cardinal signs
  • 24-48 hrs after initial injury, NLs reach peak population at site
  • Neutrophils numbers decrease after ~3 days
  • Macrophages increase and continue debris removal
52
Q

Describe proliferation phase.

A
  • 4-24 days
  • Initiates filing and covering wound site
  • Filling the defect via granulation tissue formation – immature connective tissue and new blood vessels )nothing to do with granulomatous inflammation)
  • Re-epithelisation – when epithelial cells migrate from wound bed and margins to cover surface
  • Extent according to size of wound and defect to be healed
53
Q

What are the steps of angiogenesis and neovasculature?

A
  1. Degradation of extracellular matrix
  2. Migration of endothelial cells via chemotaxis
  3. Multiplication and lumen formation
54
Q

What induces angiogenesis and how are new vessels stabilised?

A

Hypoxia, cytokines and growth factors induce vascular endothelial growth factor expression and stimulates process.

New vessels are stabilised and support cells, basement membranes and extracellular matrix.

55
Q

How do vascular endothelial growth factor produce collagen?

A
  1. VEGF causes increased permeability
  2. Exudation of plasma protein, such as fibrinogen
  3. Fibrin = provisional stroma for fibroblast growth
  4. Growth factors and cytokines recruit and stimulate fibroblasts
  5. Fibroblasts deposit collagen (fibrillar protein)
  6. Granulation tissue replaced by fibroblasts, collagen and other components and decreased vascular components
56
Q

How is connective tissue remodelled?

A
  • Depends on balance between synthesis vs degradation of extracellular matrix components
  • Matrix metalloproteinases are important and are produced by fibroblasts, macrophages and neutrophils
  • Stimulation of matrix metalloproteinases activity – some of the same growth factors and cytokines that stimulate collagen production, phagocytosis and physical stress
  • Inhibition – steroids, TGF-beta and tissue inhibitors
57
Q

Describe remodelling/maturation phase.

A
  • Collagen fibres reorganise, remodel and mature
  • Wound bed progressively increases in tensile strength and flexibility
  • Fibroblasts lead to myofibroblasts, characteristics of smooth muscle
  • Wound margin contracts and edges of the wound start to come together, collagen maturing also fibroblast contraction
  • Remodelling phase varies considerably in length to completion/stability
58
Q

In what ways does growth factor VEGF contribute to the proliferative phase of wound healing?

A

Stimulates angiogenesis

59
Q

What is meant by the term Tertiary Intention Wound Healing? What effect (quantitatively) does this form of healing have on scar tissue formation?

A

Healing, which is delayed, perhaps because it is required to be slowed down e,g, when a drain is used to allow excessive fluid to drain, or when a prosthetic device is used for support. Scar tissue (i.e. fibrosis) will be increased.

60
Q

What is primary/first intention/union?

A

Wound edges in close apposition with minimal tissue defect. Such as clean surgical incision closed by stitches or staples

61
Q

What is secondary/second intention/union?

A
  • Greater tissue defect and/or edges can’t be apposed
  • Longer repair and healing time
  • More likely to involve scar tissue formation
  • More likely to become contaminated/infected
62
Q

What is tertiary/third intention/union?

A

Involves the need to keep a wound open, in order for a drain to be inserted, for example.

63
Q

Describe the progression of wound strength.

A
  1. Haemostasis
  2. Inflammation
  3. Granulation tissue formation
  4. Collagen accumulation (synthesis, remodelling, maturation)
  5. Modification of collagen fibres, ceasing synthesis. cross links and increased fibre size.
64
Q

What are 3 complications of wound repair?

A

Deficient repair – inadequate nutrition; age; mechanical stress (tension, movement); inadequate vascularisation; ongoing inflammation (prostheses, contamination, infection); health; endocrinological causes – may cause dehiscence (wound breakdown)

Excessive formation of repair components - Granulation tissue. Collagen > fibrosis.

Contractures, adhesions. May affect organ / tissue function

65
Q

What are the factors favouring fibrosis/scarring?

A
  • Prolonged / repetitive tissue damage
  • Large area of damage – larger defect that needs to fill the granulation tissue and the granulation tissue becomes gradually replaced by collagen fibrous tissue.
  • Tissue cells not able to renew – specifically pertinent in myocardium
  • Inadequate blood supply / hypoxia – hypoxia is a stimulus of granulation tissue
  • Wound contamination – infection, foreign material
  • General state of health / nutrition – may be a co-morbidity or an issue with nutrition can promote fibrosis
  • Movement / instability – frequent or repetitive tissue damage and frequent stretching or moving of the area is more likely to result in fibrosis.
66
Q

Outline the process of developing fibrosis in chronic inflammation.

A
  1. Persistent stimulus of chronic inflammation activates macrophages and lymphocytes
  2. Prolonged production of growth factors and cytokines.

Cytokines – increased collagen synthesis
Growth factors – increased fibroblast proliferation
TIMPs – decreased matrix metalloproteinase activity

  1. Deposition of collagen enhanced by decreased activity of MMPs
  2. Therefore there is increased regulation of collagen production
  3. Increased fibroblast activity and so leads to fibrosis
67
Q

Outline the process of developing fibrosis in chronic inflammation.

A
  1. Growth factors - proliferation of fibroblasts and endothelial cells (angiogenesis)
  2. Cytokines - deposition of collagen
  3. Reduced matrix metalloproteinase - reduced collagen degradation

> > > Fibrosis

68
Q

What damage can a liver lobule sustain without any abnormality?

A

If something caused scattered random hepatic damage, hepatic parenchymal cells can regenerate themselves. So bottom left could be healed without any abnormality to the healed liver.

69
Q

What damage would liver lobules have to sustain for permanent abnormality and how would this happen?

A

If there were something more marked that caused structural change within the support tissues, which are important in allowing normal regeneration of the hepatocytes, there is acute inflammation.

  1. This will become chronically inflamed, will granulate and will be replaced by collagen and fibrosis.
  2. Fibrosis will contract.
  3. Liver overall function will decrease where cells have been damaged and remaining hepatic parenchymal cells will start to become hyperplastic to restore liver function to normal.
  4. These are deformed, there is connective tissue and contracted fibrous material deforms the residual viable hepatic lobules.
70
Q

Give the order of events of acute inflammatory response.

A
  1. Vasodilation reduces the rate of blood flow and leukocytes move towards the endothelial surface (margination).
  2. The leukocytes roll along the endothelial surface. This is facilitated by weak binding of receptors on leukocytes to selectins on endothelial cells (rolling).
  3. Various inflammatory mediators activate the leukocytes and cause them to express a new set of receptors – integrins. The integrins bind to adhesion molecules on the endothelial cells creating a firm connection between the leukocytes and endothelial cells (stable adhesion).
  4. The leukocytes emigrate between endothelial cells to cross from the vessels into the extravascular tissue and adhere to extracellular matrix proteins (transendothelial migration).
  5. In the perivascular tissues, the leukocytes migrate to sites of injury by following follow chemotactic gradients (chemotaxis).
71
Q

Distinguish the typical composition of transudate and exudate.

A

Transudate = Low protein concentration; low number of inflammatory cells

Exudate = High protein concentration; high number of inflammatory

72
Q

Inflammatory exudates can contain fibrinogen from the blood plasma. What happens to fibrinogen in the exudate?

A

It is polymerised to form insoluble fibrin

73
Q

Describe serous exudate.

A

The fluid within the site of inflammation is essentially a transudate with a low concentration of plasma proteins and no or few inflammatory cells. The fluid appears watery and clear or slightly yellow.

74
Q

Describe catarrhal exudate.

A

Secretion of mucus mixes with the inflammatory fluid making it appear thick and mucinous or gelatinous. It is typically seen at sites of normal mucus production such as the respiratory tract or gastrointestinal tract.

75
Q

Describe fibrinous exudate.

A

The fluid exudate typically contains a high concentration of plasma proteins and relatively low numbers of inflammatory cells. This is often associated with severe endothelial injury that allows leakage of large plasma proteins, such as fibrinogen. The fibrinogen then polymerises to form fibrin. It is most commonly seen at sites of serous membranes, such as the pericardium, pleura and peritoneum; and synovial membranes (joints); and in the lungs.

76
Q

Describe the suppurative/purulent exudate.

A

There is accumulation of fluid (pus) with high numbers of leukocytes – mainly neutrophils, and high concentration of plasma proteins.

77
Q

How does healing tendons compare with skin?

A

Tendons have a tendons heath and synovial fluid. Blood vessels form outside tendon/do not contains blood vessels, unlike skin tissues.

78
Q

Which 2 ways can tendons be healed?

A

Extrinsic – inflammatory cells and fibroblasts migrate form outside, such as paratenon, synovium and tendon sheath.

Intrinsic – cells (tenocytes) from epitenon and endotenon migrate and proliferate and produce collagen.

79
Q

What are the factors to consider with tendon healing?

A
  • Vasculature – limited inflammation, poor oxygen and nutrients supply for repair
  • Intrinsic or extrinsic healing? – depends if one predominates
  • Fore through tendon through healing – unable to prevent weight bearing during covalence
  • Time scales – longer: I = 14 days, P = 2-6 weeks, R = 6-10 weeks M = up to a year
  • Effects of the repair, such as scar tissue, on tendon – less elastic
80
Q

How can ligaments be healed?

A
  • Dense bundles of collagen with fibrocytes, little ground substance
  • Relatively poor vasculature, less than tendons
  • This means that there is limited inflammation and poor oxygen and nutrients supply for repair
  • Intrinsic healing will predominate
81
Q

How can mild injuries to ligaments be treated?

A

Rest and restricted exercise, NSAIDs. Prevent ligament getting more load than necessary. If animal is very active, some owners may be able to afford surgery.

82
Q

How can moderate ligament injury be treated?

A

Splint and restricted exercise with longer recovery time.

83
Q

How can severe ligament injury be treated?

A

Labradors are more prone to ligament tear. If it is a small enough dog, it may be able to be treated and left. Larger dogs will definitely need surgery:

  • Cheaper option: take out ligament and alter the angle of the femur in one operation.
  • Replace cruciate ligament by an external one, like some wire or suture material.
  • Tibial tuberosity advancement
  • Tibial plateau levelling osteotomy

Animal Disease 1 (25 decks)

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