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My VETS2007 > Wk3 Inflammation > Flashcards

Wk3 Inflammation Flashcards

1
Q

Compare features of acute and chronic inflammation

  • onset
  • cellular
  • tissue injury
  • local and systemic signs
A
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2
Q

What is inflammation?

A
  • Reaction of a vascularized living tissue to local injury → not dead tissue

the body reacting to something that is harmful - can be chemical factors or physiological factors etc.

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3
Q

What causes inflammation?

A

Basically everything:

  • infectious agents
  • endogenous causes (autoimmune reactions, new antigens released)
  • exogenous causes (infectious, traumatic, physical, chemical)
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4
Q

Why do we need inflammation?

A
  • Dilution/inactivation of biological and chemical toxins
  • killing microbes, necrotic tissue, neoplastic cells
  • degradation (foreign material)
  • providing healing factors → stimulating fibroblasts and scar/tissue repair**
    • Goal is to bring all of these cells to the site of damage/inflammation
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5
Q

What are some sentinel cells in tissues

A
  • macrophage
  • dendritic cells
  • mast cells
    • recruit monocytes/leukocytes etc. to cite
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6
Q

Why does excessive inflammation cause cancer?

A

inflammatory cells releasing growth factors and cytokines → cell proliferation which is a main factor of cancer cells

also by producing free radicals → destroy DNA

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7
Q

Signs of inflammation are: (5 clinical signs)

A
  • swelling
  • redness
  • feel warm/heat
  • pain
    • loss of function (Added bit later)
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8
Q

What causes redness in inflammation?

A

blood vessels dilation → e.g. scratching skin causes redness as blood vessel dilation occurs

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9
Q

What causes heat in inflammation

A

increased blood flow → increased temperature

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10
Q

what causes swelling in inflammation

A

extravascular accumulation of fluid → oedema → mediates swelling

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11
Q

why do we experience pain in inflammation

A

swelling and release of inflammatory mediators -→ stimulating pain

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12
Q

why do we have loss of function in inflammation

A

cell degeneration and necrosis

  • until tissue repair occurs, you will have some tissue that is lost
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13
Q

Features of acute inflammation**

A
  • Rapid onset
  • Short duration
  • exudation of fluid and plasma proteins
    • leukocytic emigration (neutrophils** → first cell on site (replaced after 3-7 days in chronic inflammation))
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14
Q

Features of chronic inflammation*** (duration, cell types, end result etc.)

A

Longer duration

lymphocytes and macrophages

proliferation of blood vessels

fibrosis

tissue necrosis

sequela to acute inflammation or can be directly chronic

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15
Q

Why are neutrophils first on site?

A
  • there are more in the blood and they respond quickly to chemokines → attach more firmly to the endothelium which is the first thing that occurs during inflammation
  • Remember: type of leukocyte depends on age of inflammatory response and type of stimulus…
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16
Q

What are the first cells to arrive in:

  • viral infections
  • allergies
    • parasitic infections
A
  • lymphocytes → viral
  • mast cells* → allergies
    • eosinophils → parasitic
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17
Q

2 triggers of inflammatory process are:

A
  • microbial or parasitic products within host tissue (PAMPs - pathogen associated molecular patterns)
    • cellular and tissue injury (DAMPS = damage associated molecular patterns)
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18
Q

what does activation of PAMPS and DAMPS do

A

activate macrophage, release cytokines, lipid mediators, chemokines → activation of inflammatory process*

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19
Q

Major components of acute inflammation

A

increased blood flow

neutrophil emigration

leakage of plasma proteins → oedema (fluid)

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20
Q

Why do we have vascular changes in acute inflammation?

A

have to have increase vascular change (larger vessels) so that inflammatory cells can get to the site of injury (leukocytes, neutrophils etc.)

  • increased movement of plasma proteins and leukocytes out of circulation
  • leaking membrane as well → so cells can move from intravascular to extravascular space to site of injury**
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21
Q

Reactions of blood vessels in acute inflammation***

A
  • injury
  • activation of inflammatory cells
  • proinflammatory chemical mediators → 2 pathways:
  • → vasodilation (by cytokines)
    • slowing of blood flow
    • leukocyte margination
  • OR to increased vascular permeability
    • fluid leakage to extracellular space*
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22
Q

***Events during inflammation: different mechanisms depending on biological/physical features of infectious agent are… (3 mechanisms)

A
  1. retraction of endothelial cells (histamine, other mediators)
  2. endothelial injury (caused by burns, microbial toxins, rapid)
  3. increased trancytosis → within endothelial cells, transport across cell layer and increased number of channels → more things going from blood into extravascular tissue
  • these can act together or alone
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23
Q

4 movements of the leukocyte recruitment to site of inflammation

A
  1. margination
  2. rolling
  3. diapedesis
  4. migration to agent
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24
Q

What is each stage of leukocyte recruitment mediated by?

A

mediated by adhesion molecules: cell surface proteins:

  • integrins is an example of one, glycoprotein
  • on leukocytes and endothelium
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25
Q

Explain rolling process of leukocyte immigration

A
  • temporarily bind to endothelium and then are released
  • weak interactions between selectins
    • selectins: E endothelium, P platelets, L leukocytes → these are mediating the rolling process
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26
Q

Explain stable adhesion process of leukocyte immigration

A
  • Stronger process
  • Binding of B2 integrin on leukocytes to ICAM1
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27
Q

What is leukocyte adhesion deficiency?

A

Cause: lack of B2 integrin expression

  • so leukocytes can undergo rolling but they never get into the tissue as they cannot form stable adhesion to endothelium
  • Causes ulcers, abscesses without puss, penumonia etc as not even neutrophils can get to the site of inflammation
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28
Q

Explain diapedesis in leukocyte immigration process

A

Adhesion molecules:

  • PECAM1
  • Junctional adhesion molecules (JAMs)
  • transport across the membrane into extracellular space and migrate to site of inflammation
29
Q

What is chemotaxis?

A

movement along a chemical gradient → movement of leukocytes towards the site of injury

  • change shape etc due to changing intracellular proteins
30
Q

What can chemoattractants be (exo and endo…)

A
  • exogenous: bacterial products
  • Endogenous: cytokines (IL8 attracting neutrophils, eotaxin attracting eosinophils, MCP macrophage protein)
31
Q

Functions of chemoattractants?

A
  • activation of inflammatory cells
  • antiviral activity
  • regulation of immune system
  • haematopoiesis, angiogenesis, cell growth
  • can also mediate cancer/tumour cells reproducing in other tissues → migrate to other tissue cites…
32
Q

What are the defensive functions of leukocytes once they are activated?

A
  1. phagocytosis
  2. liberation of substances that destroy extracellular microbes and dead tissues → substances within leukocytes granules** → released into extracellular space
  3. production of chemical mediators (cytokines) → amplify inflammatory response to fight infection quicker
33
Q

Chemical mediators: Histamine*

  • what are the producers of histamine?
A

mast cells** main ones

basophils

platelets

34
Q

What are the functions of histamine? (6 main ones)

A
  • vasodilation*
  • increased vascular permeability
  • pain and itchy
  • nerve reflexes
  • bronchial constriction → e.g. suffering from asthma, narrowing of respiratory tree as lots of histamine are being produced (contracts SM cells to narrow lumen)
  • eosinophilic chemotaxis → recruit eosinophils important in allergic reactions
35
Q

What is the main role of the complement system?

A
  • cascade of events with activation of plasma proteins after inflammation, injury, clotting etc.

to amplify the reaction from inflammatory cells → recruit and activate more leukocytes during infection etc.

  • and make macrophages kill microbes in more efficient way
36
Q

Arachidonic acid* metabolites: what happens during injury to cell membrane?*

  • slide 51
A

Fatty acid inside of the membrane, injury to membrane by inflammation causes release of arachidonic acid

  • two enzymes: lipoxygenase pathway and cycloxygenase pathway
  • why does this matter? because important when taking steroids or aspirin etc.
    • they act on this cascade
37
Q

Relationship between steroids and NSAIDs and arachidonic acid (AA)

A

steroids and NSAIDs inhibit the arachidonic acid pathway

  • steroids are stronger as they inhibit higher up the pathway (the phospholipases stage before the arachidonic acid pathway is even started*
    • whereas NSAIDs inhibits COX-1 and 2 stage further down*
38
Q

Serous inflammation

A
  • acute inflammation
  • fluid with low plasma and no/low leukocytes
  • slight increased vascular permeability
39
Q

catarrhal inflammation: what occurs in this

A
  • uterus, trachea, stomach etc have goblet cells and mucous producing cells
  • inflammatory process is stimulating excessive amount of mucous.. occurs only in some organs, only with mucous producing or goblet cells
    • e.g. snotty nose is excessive mucous production
40
Q

Fibrinous inflammation (slide 55)

What is this?

A
  • Fibrin produced → means leakage of endothelial wall is quite massive → big increase in vascular change causes fibrinous inflammation (fibrin on the outside**)
41
Q

Systemic effects of acute inflammation:

A

Function: conserve energy and mobilise resources

  1. loss of appetite
  2. lethargy
  3. muscular wasting
  4. haemodynamic changing

Acute inflammation effects:

  1. fever
  2. leukocytosis
  3. alterations to acute phase proteins
42
Q

3 systematic effects of acute inflammation?

A
  1. fever
    * increase production of neurotransmitters
  2. leukocytosis
    * increased release of cells (young and not mature) → if infection is really bad you will have release of less mature neutrophils (as had to be released very quickly)
  3. acute phase proteins
  • increase during inflammation (serum amyloid, fibrinogen)
  • involved in fighting agent and tissue repair
43
Q

Outcomes of acute inflammation?

A
  1. resolution (best outcome)
  2. scarring (after substaintial tissue destruction)
  3. progression into chronic inflammation (Worst)
  • no resolution, infection is persisting..
44
Q

Key features of chronic inflammation

A
  • fibroplasia and angiogenesis (granulation tissue)
  • initiation of wound healing
  • lymphocytes, plasma cells, macrophages, MGCs
  • Necrosis: more than acute inflammation
  • no vascular changes like acute inflammation
45
Q

Why does inflammatory response become chronic or arise as chronic?

A
  • failed elimination of the inciting stimulus by the acute inflammation
  • unique features of the inciting stimulus
46
Q

Biological mechanisms resulting in chronic inflammation (slide 70)

A
  • persistence/resistance
  • isolation in encapsulated material: antibiotics not working
  • unresponsiveness (indestructible material)
  • autoimmunity and leukocyte defects
47
Q

Main cells of chronic inflammation: Difference between monocyte and macrophages

A

monocyte is in the blood

macrophages are in the tissue levels

  • can recognise macrophage as activates when you can see many vacuoles*
48
Q

**what are the 2 different activation pathways of macrophages in chronic inflammation?

A
  1. classical activation (M1 macrophages)
    * most important when have microbes causing chronic inflammation*
  2. alternative activation (M2 macrophages)
    * less microbicidal (M1 are already doing this*); involved in tissue repair (fibroblast activation, increased collagen, increased angiogenesis (formation of new blood cells)
49
Q

Other cells involved in chronic inflammation

A

lymphocytes

neutrophils: occur in persistent inflammation (chronic active inflammation) where reaction with features of both acute (necrosis, neutrophils) and chronic (macrophages and fibrosis)

50
Q

Difference between different distributions of lesions

focal

multifocal

diffuse

A

focal = 1 area being affected

multifocal = different focal spots e.g. 3

diffuse = cant see lesion as such because entire tissue is effect (many inflammatory cells)

51
Q

What is definition of repair after chronic inflammation

A

restoration of tissue architecture and function after an injury

52
Q

2 types of reactions after tissue damage/injury and what are the differneces between the two?

A

regeneration → going back to normal

scar formation → patching up the injury and some changes in the structure/function of the original organ

53
Q

What is involved in regeneration in tissue repair process?

A

Limited process in mammals* only a few exceptions:

  • can only happen in organs with stem cell compartment or high cellular turnover**
    • SKIN → stem cells and high cell turnover in the epidermis
    • HAEMATOPOIETIC SYSTEM
    • GI TRACT
54
Q

When does scar formation occur in tissue repair?

A
  • damages tissue incapable of complete reformation
  • e.g burn on skin
  • high damage in skin (Wide and deep tissue damage)
55
Q

What is involved in cell and tissue regeneration?

A
  1. cell proliferation
  2. integrity of extracellular matrix
  3. development of mature cells from tissue stem cells (skin, intestine, cornea)
56
Q

Tissues of the body are divided into three categories…

A
  1. labile/ continuously dividing tissues
  2. stable tissues
  3. permanent tissues
57
Q

continuously dividing tissues: how do these tissues effect regeneration?

A

easy regeneration after damage

  • e.g. enterocytes: epidermis, GIT, transitional epithelium are continuously dividing
  • continuously lost and replaced: can regenerate
58
Q

stable tissues in regeneration:

A
  • Cells have proliferative activity
  • capable of dividing after injury**
    • e.g. the liver are stable tissues
  • Remarkable capacity to regenerate (after tumour etc. in liver after operation)
59
Q

permanent tissues in tissue repairation (slide 104)

A

any injury is irreversible and repair can occur ONLY by SCAR FORMATION

  • examples: BRAIN and HEART**
60
Q

When does repair by scar formation occur

A
  1. tissue injury is severe or chronic with extensive damage
  2. nondividing cells are injured
  • NO restitution of the original structure, but ‘patching’
61
Q

What factors influence the repair process:

A
  1. intensity and duration of the infection/stimulus
  2. conditions inhibiting repair (e.g. not cleaned properly, blood supply.)
  3. various diseases inhibiting repair (vitamin C deficiency effects collagen formation)
62
Q

Angiogenesis:

A

formation of new blood vessels from pre-existing vessels

63
Q

Why is angiogenesis important during wound healing?

A

Needs nutrients and oxygen supply for wounds to heal (just like normal tissues). Thus this comes from blood vessels, therefore we have more blood vessels during these stages.

  • oxygen supply
  • removal of waste products
  • drainage of excess fluid
  • vascular pathway for cells

Also seen in cancer…

64
Q

Second step of wound healing in scar formation: formation of granulation tissue

A

granulation tissue: pretty rough/granular

  • at this stage is not mature scar
  • many fibroblasts but not many collagen fibres → more dominated by blood vessels
65
Q

last stage of scar formation: maturation of the connective tissue

A
  • less cellular: but LOTS of connective tissue in this stage
  • patching: not original tissue anymore in scar formation
66
Q

Remodelling of the connective tissue (slide 111)

A
  • only the connective tissue necessary to repair the defect should be produced (balance in productive of connective tissue)
67
Q

First intention healing in skin wounds:

A
  • first intention: not much damage, mild scaring and regeneration on top is very effective
  • where scar is we have normal tensile strength of the skin but no hair follicles etc.
68
Q

second intention healing* in wound repair

A
  • intense inflammation
  • massive tissue loss
  • substantial scar formation
  • takes more time to heal
  • reduced tensile strength with increased risk of ulceration..
    • lots of tissue loss so lesion will be repaired but will be more prone to ulceration

My VETS2007 (8 decks)

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