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
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
3
Q
Describe the four phases of the inflammatory responee
A
- Initial insult
- Inflammation (inflammatory mediators)
- Demolition
- Repair
4
Q
What are the two types of inflammation?
A
- Acute
- Chronic
5
Q
Which type of inflammation make up the earlier/later response of inflammation>
A
Acute: Earlier
Chronic: Later
6
Q
Longevity of acute inflammation
A
Minutes-hours/days
7
Q
Longevity of chronic inflammation
A
Weeks+
8
Q
Major components of acute inflammation
A
- Neutrophils
- Fibrin
- Oedematous exudate
9
Q
Major cellular components of chronic inflammation (+end result)
A
- Macrophages
- Lymphocytes
- Plasma Cells
- Fibrosis/scarring
10
Q
Which of the two types of inflammation is possibly specific?
A
Chronic
11
Q
Can acute and chronic inflammation occur together?
A
Yes
12
Q
Causes of acute inflamation
A
- Infarction
- Trauma (e.g. UFC)
- Infections
13
Q
Aims of acute inflammation
A
- Deliver nutrients and defence cells
- Destroy any infective agents
- Remove debris
14
Q
List five clinical effects of acute inflammation. Think about why they occur
A
- Redness
- Heat
- Pain
- Swelling
- Loss of function
15
Q
Systemic effects of acute inflammation
A
- Malaise (feeling unwell)
- Myalgia (Muscle ache & pain)
- Arthralgia (joint pain)
- Decreased appetite
- Leukocytosis
- Fever
16
Q
Describe the mechanism of fever in inflammation
A
- Exogenous toxins
- Endogenous pyrogens
- Prostaglandins
- Neurotransmitters (inc. temp)
17
Q
What is exudation?
A
The process by which substances leave blood vessels, such as in the inflammatory response
18
Q
What is margination and emigration?
A
Margination: Neutropohils adhere to swollen endothelial cellls
Emigration: Neutrophils migrate through basement membrane
19
Q
What cells follow neutrophils out of the blood vessels later in the inflammatory response?
A
Macrophages and lymphocytes
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
21
Q
Which cells release cytokines to recruit neutrophils during the inflammatory response?
A
Macrophages and Neutrophils themselves
22
Q
Which is larger: macrophage or neutrophil
A
Macrophage (longer-lasting, but slower to get there)
23
Q
Name three inflammatory mediators responsible for prompting vasodilation
A
- Histamine
- Serotonin
- Prostaglandins
24
Q
Name two inflammatory mediators that are involved in increased vascular permeability
A
- Leukotrienes
- Platelet activating factor
25
What is exudate?
Protein rich fluid and cells that have escaped from blood vessels due to increased permeability
26
What is carried in the fluid of exudate? Where does it circulate though?
Carries:
- Nutrients
- Mediators
- Ig
Circulates through:
- Vessels
- Extracellular
- Lymph
27
What is the function of fibrin in exudate?
Prevents migration of micro-organisms and produces a scaffold that allows neutrophils and macrophages to migrate
28
How many neutrophils and macrophages are in exudate during acute inflammation?
Neutrophils: many
Macrophages: few
(obviously)
29
Describe the four kinds of acute inflammatory exudate
- 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
What are three results of acute inflammation?
- Resolution (little destruction)
- Repair (significant destruction)
- Insult persists (chronic inflammation)
31
How is exudate removed during resolution of acute inflammation?
Increased lymphatic drainage (e.g. blister heal)
32
Is scar tissue formed during REPAIR after acute inflammation (not resolution)?
Yes. House metaphor.
33
How is it that chronic inflammation can become a source of disease?
- 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
What are the causes of chronic inflammation?
- Unresolved acute inflammation
- Chronic exposure to irritant/toxin
- Immune-mediated
35
What type of chronic inflammation is caused by prolonged exposure to toxic agents
Granulomatous inflammation
36
What are the features of chronic inflammation?
- Immune cell infiltration
- Tissue destruction by offending agent/inflammatory cells
- Attempts at healing via fibrosis + angiogenesis
(Fighting, breaking, and rebuilding)
37
How are macrophages activated
Signals from T helper cells
38
What is the most dominant cell in chronic inflammation?
Macrophage
39
List some roles of macrophages in chronic inflammation
- Produce chemical mediators
- Bacterial and cell killing
- Phagocytosing debris, fibrin etc.
- Play a role in granulomatous inflammation
40
Monocyte vs macrophage lifespan
Monocyte: 1 day
Macrophage: months/years
41
Positives of macrophages in chronic inflammation
- Increased lysozymal enzymes
- Increased production of growth factors, cytokines and other mediators (increased angiogenesis and fibroblast proliferation)
42
Negatives of macrophages in chronic inflammation
Products of activated macrophages (NO, metabolites, proteases) are responsible for tissue damage and dissolution of extracellular materials/other cells
43
Describe granulomatous inflammation
- 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
Categories of giant cells
- 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
What do lymphocytes do when activated by antigens?
- Release macrophages-activcating cytokines
46
What cells are involved in chronic inflammation?
- Macrophages
- Lymphocytes
- Plasma cells
- Fibroblasts
- Eosinophils
- Endothelial cells
47
Aims of wound healing
- Remove damaged tissue
- Restore tissue function (regenerative healing)
- Restore structural continuity
48
Name and describe the two types of healing
Regenerative: Tissue replaced with parenchyman (functional) tissue
Non-Regenerative: Healing occurs via replacement of tissue with connective tissue (scar)
49
Give some examples of labile cells
Epidermis, GI tract, bone marrow, lymphoid organs
50
Give some examples of stable cells
- Liver
- Endocrine glands
51
Give some examples of permanent cells
- Cardiac cells
- Neurons
52
What notable condition is necessary for labile and stable cells to regenerate?
Intact connective tissue framework for them to follow
53
What are the three Rs of the phases of wound healing?
- Reactive phase (Haemostasis & inflammation)
- Reparative Phase (Granulation tissue)
- Remodelling Phase (Collagen Accumulation)
54
What occurs during haemostasis?
- Vascular spams
- Platelet aggregation
- Clot formation
55
During what stage of healing does epithelialisation occur? What does it entail?
- Occurs during reparative phase
- Epithelial layer grows under clot, separating it from underlying tissue
- Creates bridge between wound edges
56
What kinds of granulation tissue are at the site of an insult during reparative healing?
- Fibroblasts (wizards)
- Macrophages
- Collagen fibres
- Capillaries & lymph vessels
57
What is the role of myofibroblasts in reparative healing? What property allows them to do this?
- Myofibroblasts are contractile in nature
- This enables them to draw the edges of a wound closer together
58
What is involved in phase three of healing (what is this called?)
- Called remodelling
- Macrophages phagoyctose any remaining debris
- Scar formation: collagen and EC matrix
- Realignment of tissue
59
Compare the inflammatory responses of primary and secondary intention healing. Why is this the case?
- Secondary is more intense than primary
- Carry away large amounts of necrotic debris and exudate
60
Where does healing begin in the case of secondary intention healing? How much granulation tissue is formed relative to primary intention healing?
- From the bottom upwards
- Much large amounts of granulation tissue (e.g. fibroblasts, myofibroblasts, macrophages) formed
61
How long does primary intention healing take? What level of function usually remains after this type of healing?
- Takes approximately a week
- In most cases, complete function is returned with minimal scarring
62
Why is more scar tissue formed during secondary intention healing?
- 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
Are keratinocytes a type of granulation? Why does this make sense?
- Yes, they are a type of granulation
-They can re-epithelialise the epidermis
64
What is the function of granulation tissue?
- Protects wound surface from microbial invasion
- Fills the wound with new tissue and vasculature
- Necrotic -> Granulation -> Scar
65
Draw a map of sequential changes in granulation tissue over time
10.6.docx
66
Draw a map of regenerative bone healing (incl. fracture healing phases)
Check slides
67
Give one example of a local factor that influences wound healing
Mechanical factors (e.g. movement of new tissue)
68
Give one example of a systemic factor that influences wound healing
Age-reduced wizard (i.e. fibroblast) synthesis, and decreased collagen synthesis leading to impaired wound contraction
