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Foundations Of Medicine > 10.6 Inflammation > Flashcards

10.6 Inflammation Flashcards

1
Q

What is inflammation?

A

A protective response designed to rid an organism of both the cause and consequences of injury

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2
Q

Is the end product tissue after inflammation the same as the original structure?

A

No; can be different, but tries to resemble the original structure

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3
Q

Describe the four phases of the inflammatory responee

A
  1. Initial insult
  2. Inflammation (inflammatory mediators)
  3. Demolition
  4. Repair
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4
Q

What are the two types of inflammation?

A
  • Acute
  • Chronic
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5
Q

Which type of inflammation make up the earlier/later response of inflammation>

A

Acute: Earlier
Chronic: Later

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6
Q

Longevity of acute inflammation

A

Minutes-hours/days

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7
Q

Longevity of chronic inflammation

A

Weeks+

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8
Q

Major components of acute inflammation

A
  • Neutrophils
  • Fibrin
  • Oedematous exudate
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9
Q

Major cellular components of chronic inflammation (+end result)

A
  • Macrophages
  • Lymphocytes
  • Plasma Cells
  • Fibrosis/scarring
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10
Q

Which of the two types of inflammation is possibly specific?

A

Chronic

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11
Q

Can acute and chronic inflammation occur together?

A

Yes

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12
Q

Causes of acute inflamation

A
  • Infarction
  • Trauma (e.g. UFC)
  • Infections
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13
Q

Aims of acute inflammation

A
  • Deliver nutrients and defence cells
  • Destroy any infective agents
  • Remove debris
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14
Q

List five clinical effects of acute inflammation. Think about why they occur

A
  • Redness
  • Heat
  • Pain
  • Swelling
  • Loss of function
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15
Q

Systemic effects of acute inflammation

A
  • Malaise (feeling unwell)
  • Myalgia (Muscle ache & pain)
  • Arthralgia (joint pain)
  • Decreased appetite
  • Leukocytosis
  • Fever
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16
Q

Describe the mechanism of fever in inflammation

A
  • Exogenous toxins
  • Endogenous pyrogens
  • Prostaglandins
  • Neurotransmitters (inc. temp)
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17
Q

What is exudation?

A

The process by which substances leave blood vessels, such as in the inflammatory response

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18
Q

What is margination and emigration?

A

Margination: Neutropohils adhere to swollen endothelial cellls
Emigration: Neutrophils migrate through basement membrane

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19
Q

What cells follow neutrophils out of the blood vessels later in the inflammatory response?

A

Macrophages and lymphocytes

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20
Q

What is the most common type of leukocyte? What do they release to perform their function?

A
  • Neutrophils
  • Release free radicals, lysosomal enzymes to break down extracellular matrix when they die
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21
Q

Which cells release cytokines to recruit neutrophils during the inflammatory response?

A

Macrophages and Neutrophils themselves

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22
Q

Which is larger: macrophage or neutrophil

A

Macrophage (longer-lasting, but slower to get there)

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23
Q

Name three inflammatory mediators responsible for prompting vasodilation

A
  • Histamine
  • Serotonin
  • Prostaglandins
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24
Q

Name two inflammatory mediators that are involved in increased vascular permeability

A
  • Leukotrienes
  • Platelet activating factor
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25
Q

What is exudate?

A

Protein rich fluid and cells that have escaped from blood vessels due to increased permeability

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26
Q

What is carried in the fluid of exudate? Where does it circulate though?

A

Carries:
- Nutrients
- Mediators
- Ig
Circulates through:
- Vessels
- Extracellular
- Lymph

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27
Q

What is the function of fibrin in exudate?

A

Prevents migration of micro-organisms and produces a scaffold that allows neutrophils and macrophages to migrate

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28
Q

How many neutrophils and macrophages are in exudate during acute inflammation?

A

Neutrophils: many
Macrophages: few
(obviously)

29
Q

Describe the four kinds of acute inflammatory exudate

A
  • Serous (thin/watery; blister-like)
  • Firbinous (large amounts of fibrous (e.g. pericarditis))
  • Purulent/suppurative (pus made of neutrophils, necrotic cells & oedema)
  • Haemorrhagic (RBCs from damaged blood cells)
30
Q

What are three results of acute inflammation?

A
  • Resolution (little destruction)
  • Repair (significant destruction)
  • Insult persists (chronic inflammation)
31
Q

How is exudate removed during resolution of acute inflammation?

A

Increased lymphatic drainage (e.g. blister heal)

32
Q

Is scar tissue formed during REPAIR after acute inflammation (not resolution)?

A

Yes. House metaphor.

33
Q

How is it that chronic inflammation can become a source of disease?

A
  • Chronic inflammation persists until the source of insult subsides
  • Some insults (e.g. stress) can be chronic
  • Therefore, inflammation can last for so long that it becomes the source of damage
34
Q

What are the causes of chronic inflammation?

A
  • Unresolved acute inflammation
  • Chronic exposure to irritant/toxin
  • Immune-mediated
35
Q

What type of chronic inflammation is caused by prolonged exposure to toxic agents

A

Granulomatous inflammation

36
Q

What are the features of chronic inflammation?

A
  • Immune cell infiltration
  • Tissue destruction by offending agent/inflammatory cells
  • Attempts at healing via fibrosis + angiogenesis

(Fighting, breaking, and rebuilding)

37
Q

How are macrophages activated

A

Signals from T helper cells

38
Q

What is the most dominant cell in chronic inflammation?

A

Macrophage

39
Q

List some roles of macrophages in chronic inflammation

A
  • Produce chemical mediators
  • Bacterial and cell killing
  • Phagocytosing debris, fibrin etc.
  • Play a role in granulomatous inflammation
40
Q

Monocyte vs macrophage lifespan

A

Monocyte: 1 day
Macrophage: months/years

41
Q

Positives of macrophages in chronic inflammation

A
  • Increased lysozymal enzymes
  • Increased production of growth factors, cytokines and other mediators (increased angiogenesis and fibroblast proliferation)
42
Q

Negatives of macrophages in chronic inflammation

A

Products of activated macrophages (NO, metabolites, proteases) are responsible for tissue damage and dissolution of extracellular materials/other cells

43
Q

Describe granulomatous inflammation

A
  • Macrophages, mutlinucleated giant cells and epitheliod cells amass a substance they cannot digest and form a granuloma
  • Granuloma formation is a protective mechanism against chronic infection, but can lead to tissue necrosis due to released products
44
Q

Categories of giant cells

A
  • Langhans giant cell: Nuclei arranged peripherally (not associated with disease)
  • Foreign body giant cell: Indigestible material idenfitied within cytoplasm of giant cell (associated with disease)
45
Q

What do lymphocytes do when activated by antigens?

A
  • Release macrophages-activcating cytokines
46
Q

What cells are involved in chronic inflammation?

A
  • Macrophages
  • Lymphocytes
  • Plasma cells
  • Fibroblasts
  • Eosinophils
  • Endothelial cells
47
Q

Aims of wound healing

A
  • Remove damaged tissue
  • Restore tissue function (regenerative healing)
  • Restore structural continuity
48
Q

Name and describe the two types of healing

A

Regenerative: Tissue replaced with parenchyman (functional) tissue
Non-Regenerative: Healing occurs via replacement of tissue with connective tissue (scar)

49
Q

Give some examples of labile cells

A

Epidermis, GI tract, bone marrow, lymphoid organs

50
Q

Give some examples of stable cells

A
  • Liver
  • Endocrine glands
51
Q

Give some examples of permanent cells

A
  • Cardiac cells
  • Neurons
52
Q

What notable condition is necessary for labile and stable cells to regenerate?

A

Intact connective tissue framework for them to follow

53
Q

What are the three Rs of the phases of wound healing?

A
  • Reactive phase (Haemostasis & inflammation)
  • Reparative Phase (Granulation tissue)
  • Remodelling Phase (Collagen Accumulation)
54
Q

What occurs during haemostasis?

A
  • Vascular spams
  • Platelet aggregation
  • Clot formation
55
Q

During what stage of healing does epithelialisation occur? What does it entail?

A
  • Occurs during reparative phase
  • Epithelial layer grows under clot, separating it from underlying tissue
  • Creates bridge between wound edges
56
Q

What kinds of granulation tissue are at the site of an insult during reparative healing?

A
  • Fibroblasts (wizards)
  • Macrophages
  • Collagen fibres
  • Capillaries & lymph vessels
57
Q

What is the role of myofibroblasts in reparative healing? What property allows them to do this?

A
  • Myofibroblasts are contractile in nature
  • This enables them to draw the edges of a wound closer together
58
Q

What is involved in phase three of healing (what is this called?)

A
  • Called remodelling
  • Macrophages phagoyctose any remaining debris
  • Scar formation: collagen and EC matrix
  • Realignment of tissue
59
Q

Compare the inflammatory responses of primary and secondary intention healing. Why is this the case?

A
  • Secondary is more intense than primary
  • Carry away large amounts of necrotic debris and exudate
60
Q

Where does healing begin in the case of secondary intention healing? How much granulation tissue is formed relative to primary intention healing?

A
  • From the bottom upwards
  • Much large amounts of granulation tissue (e.g. fibroblasts, myofibroblasts, macrophages) formed
61
Q

How long does primary intention healing take? What level of function usually remains after this type of healing?

A
  • Takes approximately a week
  • In most cases, complete function is returned with minimal scarring
62
Q

Why is more scar tissue formed during secondary intention healing?

A
  • Epithelia can only proliferate and regenerate once granulation fills the wound to the level of the original epithelium
  • Greater amount of collagen synthesis
  • Wound contraction is more frequent
63
Q

Are keratinocytes a type of granulation? Why does this make sense?

A
  • Yes, they are a type of granulation
    -They can re-epithelialise the epidermis
64
Q

What is the function of granulation tissue?

A
  • Protects wound surface from microbial invasion
  • Fills the wound with new tissue and vasculature
  • Necrotic -> Granulation -> Scar
65
Q

Draw a map of sequential changes in granulation tissue over time

A

10.6.docx

66
Q

Draw a map of regenerative bone healing (incl. fracture healing phases)

A

Check slides

67
Q

Give one example of a local factor that influences wound healing

A

Mechanical factors (e.g. movement of new tissue)

68
Q

Give one example of a systemic factor that influences wound healing

A

Age-reduced wizard (i.e. fibroblast) synthesis, and decreased collagen synthesis leading to impaired wound contraction

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