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WEEK 10: 10.6 Inflammation Flashcards

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1
Q

What are different ways the body can be injured?

A

oxygen deprivation
immunological reactions
nutritional imbalance
infectious agents
chemical agents
physical agents (burns)

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2
Q

How does the body protect itself after injury has occured?

A

inflammation

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3
Q

What is inflammation?

A

a protective response designed to rid the organism of cause and consequence of injury, closely linked with healing/repair

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4
Q

What are the different stages of inflammation?

A

Initial insult –> inflammation —> inflammatory mediators (vasodilation, recruit cells) —> demolition (tissues and damaged cells cleared) -> repair (new tissue layered down)

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5
Q

What are the key components of inflammation?

A

Blood components: cells, proteins
Blood vessels & endothelium
Chemical mediators
Cellular & extracellular components of connective tissue

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6
Q

What are the 2 types of inflammation

A

acute & chronic

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7
Q

Differentiate the timing of occurrence, longevity, major components and specificity of acute and chronic inflammation

A

Acute:
earliest response
minutes –> hours-days
neutrophils, fibrin, oedematous exudate
non-specific
Chronic:
later response
weeks –> months-years
macrophages, lymphocytes, plasma cells, fibrosis/scarring
specific/non-specific

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8
Q

Define acute inflammation

A

inflammation that occurs directly following insult/injury to the body, and tends to last minutes/hours/days. it involves immediate vasodilation of focal blood vessels & increased permeability of vessels

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9
Q

What are the causes of acute inflammation?

A
  • certain infections (eg. bacterial)
  • physical trauma
  • infarction
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10
Q

What are the aims of acute inflammation?

A
  • deliver nutrients and defence cells
  • destroy any infective agents
  • remove debris
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11
Q

What are the clinical effects of acute inflammation?

A

redness - vessel dilation/increased blood flow
heat - hyperaemia
pain - pressure effects on nerve endings & chemical factors
swelling - accumulation of exudate
loss of function - direct local damage

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12
Q

What are systemic effects of acute inflammation?

A

malaise, myalgia (muscle aches), arthralgia (joint pain) & decreased appetite
leukocytosis (increased WBC)
fever

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13
Q

describe the vascular & cellular response in acute inflammation

A
  1. initial dilation of focal blood vessels increasing blood flow, then blood flow slows
  2. vessels become leaky and permeable, permitting passage of water, salts & small proteins from the plasma into the damaged area
  3. circulating neutrophils are attracted to damaged area and adhere to swollen endothelial cells & migrate through basement membrane into damaged area
  4. later macrophages and lymphocytes migrate to damaged area
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14
Q

How/where are neutrophils produced?

A

They are produced by maturation of precursor cells in bone marrow

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15
Q

Further describe neutrophils

A

They are the most numerous white cells in blood
they have a short life span
they are motile and move easily from vessels into tissues

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16
Q

What role do neutrophils play in acute inflammation

A

chemical mediators attract them to the site of damage
they actively phagocytose and destroy bacteria
they release free radicals and lysosomal enzymes to break down extracellular matrix when they die

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17
Q

What is neutrophilia?

A

it is the raised neutrophil count in the blood. cytokines cause neutrophilia to occur

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18
Q

What role do monocytes/macrophages play in inflammation?

A

monocytes travel in blood to all tissues of the body, migrate out of capillaries and transform into macrophages
monocytes leave circulation at sites of inflammation, phagocytose tissue debris and pathogens and initiate an immune response

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19
Q

What is exudate?

A

protein rich fluid & cells that have escaped from blood vessels due to an increase in vascular permeability eg. in inflammation

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20
Q

What is the composition of exudate?

A

fluid - carries nutrients, mediators and immunoglobulins
fibrin - network of fibrin prevents migration of micro-organisms and produces a scaffold that assists in the migration of neutrophils and macrophages through the damaged area
many neutrophils ingest and kill offending agents
few macrophages phagocytose and kill bacteria or assist in repair

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21
Q

describe the function of acute inflammatory exudate

A

it carries proteins, fluid and cells from local blood vessels into the damaged area to mediate local defenses. it also breaks down and removes damaged tissues.

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22
Q

what are 4 types of acute inflammatory exudate?

A

serous:
- absence of prominent cellular response
- outpouring of thin fluid devoid of cells
- eg. blister/burn injury
fibrinous:
- large amounts of fibrin
- common in membrane lined cavities, such as the pleura, pericardium and peritoneum
- eg. pericarditis
purulent/suppurative
- large quantities of pus (neutrophils, necrotic cells & oedema)
hemorrhagic
- contains many RBCs released from damaged and ruptured blood vessels

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23
Q

What are the 3 outcomes of acute inflammation

A

Resolution - return of damaged tissue to normal, tissue damage minimal, dead cells replaceable, phagocytes clear debris and exudate is removed by increased lymphatic drainage
Repair - damaged tissue must undergo organisation and repair, scar tissue forms, healed tissue differs from original tissue
Chronic inflammation - damaged tissue unable to repair itself because the injurious stimulus persists, inflammation becomes chronic

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24
Q

After acute inflammation, if insult persists and progresses, what occurs?

A

chronic inflammation

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25
What is chronic inflammation?
Inflammation of prolonged duration in which active inflammation, tissue destruction and attempts at healing/repair all occur simultaneously
26
Can chronically affected tissue undergo resolution?
No, it will instead heal via organisation and repair
27
What do causes of chronic inflammation include?
unresolved acute inflammation prolonged exposure to potentially toxic endogenous/exogenous agents immune-mediated (inappropriate activation of immune system)
28
Explain osteomyelitis in regards to it being unresolved acute inflammation
It is a persistent infection in the bone and marrow. involves chronic inflammatory cells and their cytokines stimulating bone resorption and deposition of reactive bone tissue. Treatment is with antibiotics and surgical debridement
29
Explain prolonged exposure to potentially toxic agents as a cause of chronic inflammation
An example of this can be wear particles in prosthetic implants. degradation over time can release toxic exogenous agents (wear particles) which causes granulomatous inflammation
30
Explain immune-mediated causes of chronic inflammation
An example is rheumatoid arthritis, which is a chronic systemic inflammatory disorder caused by inappropriate activation of the immune system, as it identifies its own cells as being foreign and initiates an immune response, which can result in the destruction of articular cartilage, loss of joint space, active bone resorption and influx of immune cells.
31
What are common systemic effects of chronic inflammation?
arthralgia (aches in joint) + myalgia (muscle aches/pain) fever leukopenia (decrease in circulating WBC) chronic fatigue and insomnia depression/anxiety/mood disorders GI complications like constipation, diarrhea, acid reflux weight gain/weight loss frequent infections
32
What are features of chronic inflammation?
- mononuclear cell infiltration (macrophages, lymphocytes, plasma cells) - tissue destruction induced by persistent offending agent or by the inflammatory cells - attempts at healing by replacing damaged tissue with connective tissue via fibrosis + angiogenesis
33
Explain how macrophages are involved in chronic inflammation
they are the most dominant cell in chronic inflammation when activated, they produce chemical mediators, participate in bacterial/cell killing, remove extracellular debris, fibrin and foreign materials and they play a role in granulomatous inflammation (multi-nucleated giant cell)
34
What are macrophages activated by?
signals from helper T cells (lymphocytes)
35
what is the lifespan of a tissue macrophage?
it can live for several months or years
36
What is the maturation of a bone marrow stem cell to a tissue macrophage mediated by?
growth factors, cytokines, adhesion molecules and cellular interactions
37
What are the positives of activated macrophages ?
they stimulate angiogenesis (formation of new blood vessels) they stimulate fibroblast proliferation they encourage the production of cytokines, growth factors and other mediators they increase lysosomal enzymes and reactive oxygen species (ROS)
38
What are the negatives of activated macrophages?
- the products of activated macrophages are responsible for a lot of tissue injury in chronic inflammation, and dissolution of extracellular material
39
What is granulomatous inflammation?
a special type of chronic inflammation characterised by focal collections of macrophages, epithelioid cells and multinucleated giant cells that amass to form a granuloma
40
What kind of response is granuloma formation?
a protective response to chronic infection, which can lead to tissue necrosis due to secretory products of the cells involved
41
What are multinucleated giant cells categorized as?
langhans giant cell: nuclei arranged peripherally foreign body giant cell
42
Describe how an injury can cause granulomatous inflammation
injury involving bacteria, fungus or a foreign particle ------> inability to digest inciting agent ----> failure of acute inflammatory response ----> persistence of injurious agent -----> recruitment of macrophages with epithelioid/giant-cell formation ----> cell-mediated immune response/sequestration within macrophages ---> granuloma formation
43
What is a lymphocyte
a cell that proliferates in bone marrow and tissues, is long-lived and participates in chronic inflammation
44
How do lymphocytes participate in chronic inflammation?
When an antigen is activated, lymphocytes release macrophage-activating cytokines and persist in a positive feedback loop until inflammatory stimulus is removed
45
What are the different types of lymphocytes that can be present in chronic inflammation ?
B cell, helper T cell, cytotoxic T cell, regulatory T cell, natural killer cell
46
What are plasma cells role in chronic inflammation?
- They play a part in the humoral immune response - They are terminally differentiated B-cells (mediated by T helper cells) - Each plasma cell can only produce one kind of antibody - Each cell is specific to a particular antigen
47
What are the other cells involved in chronic inflammation?
fibroblasts: cells of the connective tissue produce/secrete all components of extracellular matrix involved in the immune response & in would healing endothelial cells form new blood vessels (angiogenesis) eosinophils abundant in IgE-mediated immune reactions (allergic/parasitic) granules contain toxic proteins
48
Describe the organisation & repair outcome of chronic inflammation
If persistent stimuli is removed, damaged tissue must undergo repair (resolution not possible) fibrosis ---> scar formation Healed tissue will differ from original parenchymal tissue May see loss of function
49
Describe the outcome of chronic inflammation if the insult persists indefinitely (unresolved)
a poor prognosis can result in disease-specific morbidity & mortality like alzheimers, cancer, CVD, chronic kidney disease, COPD, diabetes, IBD, rheumatoid arthritis
50
What does the repair stage involve
Wound healing
51
What are the aims of wound healing?
to remove damaged tissue from wound site to fill a gap caused by tissue destruction to restore structural continuity of injured part to restore function to damaged tissue
52
Define regenerative healing
The tissue is replaced with parenchymal (functional) tissue, eg. fracture healing
53
Define non regenerative healing
healing occurs by replacement of tissue with connective tissue (scar), rather than parenchymal tissue eg. myocardial infarction
54
What are the cells that can undergo regenerative healing? briefly describe them
Labile cells - populate tissues that are in a constant state of renewal and can divide easily, and can undergo hyperplasia & therefore CAN regenerate Stable cells - populate tissues that are renewed slowly, can undergo hyperplasia and therefore CAN regenerate
55
Explain why permanent cells cannot undergo regenerative healing?
They are terminally differentiated (cannot enter cell cycle) Cannot undergo hyperplasia and therefore CANNOT regenerate (eg. neurons, cardiac cells, skeletal cells)
56
What are the 3 phases of wound healing?
1. reactive phase 2. reparative phase 3. remodeling phase
57
Explain the reactive phase of wound healing
involves haemostasis: - vascular spasm - platelet aggregation - clot formation inflammation: - eliminate pathogens and limit damage - inflammatory cell migration - vascular changes like vasodilation - signs of acute inflammation eg. heat, swelling, redness, pain
58
Explain the reparative phase of wound healing
involves epithelialisation: - epithelial layer begins to grow under the clot, seperating the clot from underlying tissue and creating a bridge between edges of the wound granulation tissue: - involves fibroblasts, myofibroblasts, macrophages, collagen fibres, capillaries and lymphatic vessels myofibroblasts: - derivatives of fibroblasts - contractile properties Wound contraction: - draws the edges of the wound closer to reduce the area
59
explain the remodeling phase of wound healing
involves macrophages scar formation involves collagen + extracellular matrix realignment of the tissue
60
What is primary intention healing?
It occurs in wounds with dermal edges that are close together, the proximity of the wound edges allows for ease of clot formation. It involves proliferation of fibroblasts and granulation tissue, and in most cases is a complete return to function with minimal scarring
61
What is secondary intention healing?
It occurs when the sides of the wound are further away, resulting in an extensive loss of cells and tissue in which the inflammatory reaction is more intensive, to carry away the large amounts of necrotic debris and exudate.
62
When can the epithelia proliferate/regenerate in secondary intention healing
once granulation tissue fills the wound to the level of the original epithelium, and greater amount of collagen synthesise to fill in the damaged area
63
What is the function of granulation tissue
it protects the wound surface from microbial invasion and further injury it fills the wound from its base with new tissue & vasculature it replaces necrotic tissue until replacement by scar tissue
64
What are the components of granulation tissue
new, thin walled blood vessels fibroblasts collagen keratinocytes endothelial cells
65
What are the 4 phases of fracture healing
1. formation of a haematoma & granulation tissue 2. formation of the soft callus 3. conversion to the hard callus 4. remodelling
66
explain the first phase
since a fracture severs blood vessels of the bone, haemostasis is activated and a blood clot forms. fibroblasts, macrophages, osteoclasts, osteoblasts invade the facture site and cellular invasion & activity converts the blood clot to a soft fibrous mass known as granulation tissue
67
explain the second phase
angiogenesis continues fibroblasts deposit collagen in the granulation tissue chondroblasts produce patches of fibrocartilage these factors make the granulation tissue stronger but still malleable forms soft callus
68
explain the third phase
osteoblasts enter soft callus and produce bone material forms a collar/ring around fracture hard callus semented to the dead bone around fracture and acts as temporary splint essential to ensure broken bone is immobilised
69
explain the fourth phase
hard callus persist for 3-4 months osteoclast dissolves small fragments of bone osteoblast deposit spongy bone to bridge the gap between broken ends spongy bone strength enhanced by compact bone conversion remodeling process can remove all signs of practice
70
what is an example of non regenerative healing
myocardial infarction
71
what are local and systemic factors that affect wound healing
local: infection, mechanical factors like movement, foreign bodies, vascular supply, size/location/type of wound systemic: poor nutrient supply, metabolic status, circulatory status, drug therapies, age-reduced collagen and fibroblast synthesis

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