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Musculoskeletal dysfunction > Inflammation and repair (2) > Flashcards

Inflammation and repair (2) Flashcards

1
Q

Describe the sequence of events in WBC activiation

A
  1. margination
  2. pavementing
  3. emigration
  4. chemotaxis
  5. phagocytosis & synthesis of biochemical mediators (cytokines)
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2
Q

Describe margination and pavementing

A

Haemodynamic changes - venule congestion → wbcs move to endothelium

Adhesion molecules on the endothelium i.e. selectins, ICAMs attach to adhesion molecules on wbcs i.e. β-integrins

Length of time of adhesion depends on strength of inflammatory response

Layer of wbcs stick to endothelium (pavementing)

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3
Q

Describe emigration

A

Wbcs squeeze through inter-endothelial cell junctions in venules → perivascular spaces

Circulating neutrophils diam approx. 10υm can reduce width to 1 υm

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4
Q

Describe chemotaxis

A

Directional migration of wbcs along a chemical gradient

Chemo-attractants i.e.

Complement fragments

Fibrinogen degradation products

Chemokines – small protein molecules produced at the inflammatory site by damaged resident cells i.e. IL-8, MIP (macrophage inflammatory protein), NAP-2 (neutrophil activating peptide) many more

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5
Q

Describe phagocytosis

A

Engulfing of large (i.e. bacteria / damaged cells) particles and destruction intracellularly

Surface attachment & engulfment

Formation of phagocytic vacuole & fusion to form phagolysosome

Digestion in phagolysosome

Debris extrusion

Process enhanced by opsonisation i.e. antibodies, complement fragments

Also by elevated body temperature – fever

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6
Q

Describe phagocytosis (particle destruction)

A

O2-dependent killing

“Respiratory burst” of phagocytosis

Increased O2 & energy utlisation by cell → creation of reactive O2 species (H2O2, O2-, HOCl∙)

Oxidant damage & peroxidation of membrane lipids

Normally occurs inside phagolysosome

Molecular scavengers of oxyradicals – SODs occur in circulation - ↓ effect extracellularly

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7
Q

Name chemical mediators

A

Histamine (& Seratonin)

Kinins

Neuropeptides

Arachidonic acid metabolites

Lipoxygenase (LO) pathway

Nitrous oxide

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8
Q

Describe the effects of histamine and seratonin

A

contraction of smooth muscle and ↑ bv permeability (Mast Cells)

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9
Q

Describe the effects of Kinins

A

i.e. bradykinin, leukokinin (precursors present in plasma)

Vasodilation, ↑ bv permeability

Stimulate release of histamine from Mast cells

Activate arachidonic acid cascade (for PG and leukotriene production)

Believed to be major mediator of pain in acute inflammation; effects on afferent nerve fibres

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10
Q

Describe the effects of neuropeptides

A

i.e. substance P, neurokinin from sensory nerves → pain, vasodilation & increased bv permeability

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11
Q

Describe the effects of arachdonic acid metabolites

A

Vasodilation, ↑ bv permeability, pain

Arachidonic acid cascade

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12
Q

Describe the effects of lipoxygenase (LO) pathway

A

lipoxins & leukotrienes

Enhance chemotaxis

Cause lysosomal enzyme release

Generate O2-

↑ wbc adhesiveness

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13
Q

Describe the complement system

A

Multicomponent system – “compliments” action of antibodies in killing pathogens

“Classical” and “alternate” pathways

Classical Ab related / alternate not Ab related

By-products of cascade i.e. C5a, C3a have direct inflammatory roles

↑ bv permeability

chemotactic

degranulation

↑ phagocytosis (opsonisation)

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14
Q

Describe the effects of nitrous oxide

A

Inflammatory stimulated endothelial cells generate NO (Ca++ dependent)

Cause net vasodilation

Also NO production from stimulated macrophages & monocytes

NO inhibitory and destructive to many pathogens

As well as previously mentioned cytokines and chemokines

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15
Q

What is the difference between repair and regeneration?

A

Difference between the two?

Healing by parenchymal tissue regeneration

Healing by CT replacement (scarring)

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16
Q

What does regeneration capability depend on?

A

Capability of the cells (labile or stable not permanent)

Maintenance of CT framework

17
Q

What tissues have ‘very good’ regeneration capabilities?

A

connective tissue, blood vessels, lymph vessels, bone marrow, fat, ovarian tissue, liver

18
Q

Which tissues have ‘good’ regeneration capabilities?

A

intestinal and gastric epithelium, bone (remodellng and periosteal growth)

19
Q

What tissues have ‘limited’ regeneration capabilities?

A

cartilage, ligament, tendon, kidney, pancreas

20
Q

What tissues have no regeneration capabilities?

A

seminiferous tubulus, neurones, cardiac muscle, eye

21
Q

Describe neuronal regeneration

A

Following peripheral nerve injury

If neurone body affected → whole neurone necrosis

If axonal →

Axon below damaged area degenerates

Above damaged area degenerates to proximal node of Ranvier (Wallerian degeneration)

As long as axonal tube / membrane intact axon will regenerate approx. 5mm/day

nb. Traumatic neuroma following limb amputation

22
Q

What are the different categories of tissue and wound repair?

A

Bleeding

Inflammation

Proliferative stage

Reorganisation / remodelling – MMPs very important in remodelling

23
Q

Describe repair

A

nitiated by the proliferation of fibroblasts and endothelial cells (2 - 3 days following tissue damage)

Fibroblasts develop from resident fibrocytes, becoming hyperplastic.

very large, active nuclei with little cytoplasm

They then start to lay down a matrix consisting of collagen fibres and mucopolysaccharide.

24
Q

Define primary intention

A

Following surgery and proper wound apposition healing

25
Q

Define secondary intention

A

If there is a deficit in the wound then healing is by secondary intention and granulation tissue will fill in this gap

26
Q

Describe CT repair

A

Fibroblastic response → collagen-rich scar tissue

Initially “granulation tissue” – fibro-vascular CT

Consists of fibroblasts, endothelial sprouts & capillaries, phagocytic cells (neutrophils & macrophages)

Re-epithelialisation from wound edges (if on surface) & islands of squamous epithelium

27
Q

Describe fibroblasts

A

Most widespread of mesenchymal tissues

“stable cells retaining proliferative capability”

In repair fast multiplication and synthesis of ECM components i.e. collagen

Activation by activated macrophages (MDGFs)

Produce growth factors at site of repair

Specialised fibroblast → myofibroblast

28
Q

Describe endothelial cells and macrophages

A

endothelial cells and the capillaries formed in repair tissue→ very permeable “leaky”

Easily leak exudate high in protein content (plasma protein) and wbcs into repair site

Wet appearance & scab on surface wounds

Also produce growth factor – PDGF (platelet derived growth factor)

Macrophages very important in healing

Phagocytic function

Also secrete growth factors

29
Q

Describe remodelling

A

Refinement of collagen and ECM

Chemical mediated but also affected by physical stress

Active process

may take months → year for final healing

30
Q

State the extracellular matrix components (and describe)

A

Collagen

Primarily Type I & Type III in fibrovascular CT (fibrillar types)

Type III finer random fibrils; eventually replaced by Type I

Higher tensile strength than other collagen fibres

Increase in strength takes time – not only related to amount of collagen at site but eventual remodelling

Can take weeks → months

31
Q

In relation to growth factors, what can protein stimulate?

A

cell proliferation & differentiation

synthesis of ECM

Some are chemotactic

Musculoskeletal dysfunction (12 decks)

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