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acute inflammation Flashcards

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1
Q

what is inflammation?

A
  • response of vascularised tissues

- provoked response to tissue injury

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2
Q

what is a provoked response to injury caused by?

A
  • chemical agents
  • cold, heat
  • trauma
  • ischemia
  • invasion of microbes ( infection)
  • foreign bodies
  • immune reactions ( hypersensitivity)
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3
Q

what does the process of inflammation serve to do ?

A
  • destroy, dilute or wall off the injurious agent ( build an extracellular matrix around whatever is there and stops its spreading)
  • protective response
  • induces repair
    . stops and neutralises things causing damage
  • can be potentially harmful if not controlled and lead to chronic inflammation
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4
Q

what is the nomenclature used to describe inflammation ?

A
  • the nomenclature used to describe inflammation in different tissues employs the tissue name and the suffix - itis
  • condition that ends in itis suggests that you have inflammation of that tissue
  • e.g.
    pancreatitis ( pancreas), meningitis ( meninges)
    arthritis
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5
Q

what is conjunctivitis ?

A

inflammation of the conjunctiva

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6
Q

what is uveatis?

A

inflammation of the uvea ( iris, ciliary body, choroid)

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7
Q

what is blepharitis?

A

inflammation of the blephara ( eyelids)

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8
Q

what is the process of illumination ?

A
  • inflammation is the process where your systemic immune system (white blood cells in the blood supply) are recruited into tissues to deal with injury
  • inflammation initially is acute inflammation which happens very rapidly
  • if body can’t handle acute inflammation than it would lead to chronic inflammation which is a much slower process
  • if chronic inflammation you will have to recruit other type of white blood cell from systemic circulation to help your neutrophils
  • you will recruit monocytes which will turn macrophages when they migrate into tissue
  • also recruit lymphocytes
  • chronic inflammation is more painful
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9
Q

what are the two types of inflammation?

A
  1. acute
    - onset
    - cellular infiltrate
    - tissue injury
    - local and systemic signs
    - fast
    - mainly neutrophils
    - usually mild and self-limited
    - prominent
  2. chronic
    - slow
    - monocytes/macrophages and lymphocytes
    - often severe and progressive
    - less prominent; may be subtle
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10
Q

what is the main difference between acute and chronic inflammation?

A

acute versus chronic inflammation are distinguished by the duration and the type of infiltrating inflammatory response

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11
Q

how can you get an acute inflammation?

A
  • via a splinter
  • you have foreign objects spiking into
  • you have microbes and bacteria coming in
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12
Q

what are cardinal signs of inflammation ?

A
  • rubor = redness
  • tumour = swelling
  • calor = heat
  • dolor = pain
  • functio laesa = loss of function
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13
Q

what is the point of inflammation ?

A
  • inflammation serves to rid you of both the initial cause of cell injury ( the microbe, toxin) and to clean up the area ( removal of necrotic cells )
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14
Q

what are the mediators of the inflammation response throughout the body ?

A
  • phagocytic leukocytes
  • plasma protein ( complement components and antibodies )
  • these circulate in your body and can be recruited to the site of injury in response to inflammation initiation
  • you also have resident cells ( sentinel cells ) in tissue that can respond to the initial cause of injury
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15
Q

what are the steps of acute inflammation?

A
  1. initial cause; agent ( located in extravascular tissue ) is recognised by host cells/molecules
  2. recruitment of leukocytes and plasma protein from circulation.
    attracted to site of agent
  3. leukocytes and proteins work in harmony to eliminate the causative agent
  4. the reaction is controlled and the agent is destroyed
  5. tissues can undergo repair
  • sentinel cells ( macrophages, dendritic cells and mast cells) recognise that something is there that shouldn’t
  • they then start to secrete mediators which are chemical signals , these migrate into your tissues and then they get a response from the endothelial cells in your vasculature and promote the cells that surround your blood vessels to start secreting into your blood stream which then tries to recruit your leukocytes from your circulation and signal that something is wrong

leukocytes help those cells to clear the site of injury

once reaction is controlled and agent is destroyed then they initiate tissue wound healing

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16
Q

what is tissue necrosis caused by ?

A
  • ischemia
  • trauma
  • foreign body - can cause tissue necrosis or infection
  • hypersensitivity ( immune reaction)
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17
Q

how do the cells recognise the offending agent/foreign body ?

A

1- cellular receptors

  • integral protein in plasma membrane
  • toll like receptors ( TLRs)
  • expressed on cell that will contact foreign microbe
  • epithelial cells, dendritic cells, macrophages, leukocytes
  1. sensors of cell damage
    - necrotic cells that know they will die release ATP or DNA in cytoplasm which leads to IL 1 release
    IL 1 recruits leukocytes
  2. antibodies and complement proteins
    - proteins in systemic circulation which act to put flags to something that shouldn’t be there
    - they bind to the outside of microbes and stick up signal( opsonisation)
  3. circulating proteins
    - complement system
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18
Q

how do macrophages respond to initiate an inflammatory response ?

A
  • phagocytose cellular debris or microbes
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19
Q

how do mast cells and dendritic cells respond to initiate an inflammatory response ?

A
  • secrete contents of granules into extracellular space
  • they respond to that agent by sending mediators ( IL1 or TNF alpha ), those mediators diffuse through your tissue and keep diffusing until they hit your blood vessels
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20
Q

how do phagocytes and sentinel cells that recognise the injurious agent respond ?

A

they release signals to prompt immune system into action

  • the signals can be
  • cytokines
  • lipid messengers
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21
Q

what happens once mediators come in contact with the endothelial cells of vasculature or other smooth muscle muscle cells ?

A
  • they induce a vascular response
22
Q

what is the vascular involvement during acute inflammation?

A

1- alteration of vascular caliber

  • following very brief vasoconstriction ( seconds), then you get vasodilation which means you have a slight slowing of the flow, and because you got a larger surface area for blood to be you have blood pooling creating redness and warmth
    ( rubor and calor )

2-changes of microvasculature

  • endothelial cells that lines blood vessels start to have gaps between themselves which cause
  • increased permeability for plasma proteins and allowing plasma and plasma protein out of blood into localised tissues and cells creating swelling ( tumour)
  • fluid loss leads to increase in concentration of red blood cells and slowed white blood cell flow which will be forced outside blood vessels

( stasis )- when white blood cells forced to the endothelial cells and they slow down their flow rate

3- emigration of leukocytes from microcirculation

  • white blood cells stop binding to endothelial cells
  • due to stasis and activation of leukocytes , this leads to migration into extravascular space towards offending agent
23
Q

what is tumor caused by ?

A
  • tumor ( swelling ) is a result of oedema
24
Q

what is oedema a result of ?

A

oedema is a result of inflammation chronic or acute

- vascular changes and fluid leakage during acute inflammation lead to oedema in a process called exudation

25
Q

what are the two process that can cause oedema in the body ?

A

1- transudate
. result of hydrostatic imbalance- this force water outside of circulation into the tissue around- this is known as ultrafiltrate of plasma which has a low protein content

. or osmotic imbalance-

2- exudate-
. result of inflammation
. vascular permeability- water and plasma protein can come out of plasma
. high protein content

26
Q

why do we make leaky blood vessels ?

A
  • we want the vascular permeability to open up gaps between endothelial cells so that leukocytes can get out of blood stream
  • this goes through a process of leukocyte extravasation
27
Q

what is leukocyte extravasation ?

A

process where leukocytes go from in your blood stream out into tissues

  • extravasation of leukocytes happens in a series of coordinated events:
margination
rolling
adhesion
transmigration ( diapedesis )
migration
28
Q

what is a critical function of the vascular inflammatory response ( stasis and vascular permeability) ?

A
  • deliver leukocytes to the site of injury in order to clear microbes and debris
29
Q

what are the first inflammatory cells recruited to a site of inflammation?

A
  • neutrophils ( first 6-24 hours )
30
Q

what does inflammatory response consist of?

A

inflammatory response consists of a vascular and a cellular reaction

31
Q

what happens when an inflammatory response is triggered ?

A
  • when an inflammatory response is triggered
  • sentinel cells notice that there is an infection and they start secreting mediators like IL1 or TNF alpha which are secreted into tissue
  • these mediators create a concentration gradient where its highest in concentration near where site of infection
  • comes in contact with endothelial cells of vasculature
  • endothelial cells respond to these chemical mediators by opening gaps between themselves but they shuttle proteins to surface called E and P selections
  • proteins are sticking out of surface
  • mediators also respond by secreting more chemical messengers into blood stream like cytokines and chemokines
  • due to the opening of gaps between endothelial cells we’re losing water and plasma out into extravascular tissues so stasis is going on
  • neutrophils are pushed into endothelial cells and they are also responding to chemical signals and starts to express on its own plasma membrane other proteins
  • you have L -selectins on neutrophil
  • stasis is pushing cells down towards the endothelial cells this is the process of margination
  • L- selectin on neutrophil starts to bind with glycoproteins sticking up on endothelial cells
  • this ensure that neutrophil doesn’t go back to circulation
  • leukocytes go through a process of rolling which rolls along the endothelial cells till it reaches a patch of endothelium which has highest concentration of chemical mediators
  • at this site you also have other proteins being expressed on your endothelial cells
    e. g. ICAM-1
  • at the same time other proteins are being expressed by your neutrophil called b- intergrins
  • then you have the process of ( transmigration ) - diapedesis - migration between endothelial cells from blood into tissues
  • cell can migrate across endothelial through one of those open gaps
  • that’s triggered by a protein called PECAM-1
  • leukocyte has come out of blood and its sitting in tissue
  • leukocyte must migrate to site and it does that by migrating through chemotactic gradient - gradient where you have a variable concentration of a chemical
32
Q

summary of extravasation of leukocytes?

A

1- margination : stasis ( slower flow ) allows more white blood cells to be re-distributed to the endothelial surface of the vascular lumen

2- rolling: leukocyte adhere transiently to endothelial surface
. mediated by selectins which bind to complimentary ligands expressed on opposing cells

P- selectin ( on platelets and endothelium)
E-selectin ( on endothelium)
L- selectin ( on leukocyte)
expression of these selectins in induced by TNF, IL1, histamine and chemokines secreted by sentinel cells

3- adhesion: mediated by integrins i.e.ICAM

4- transmigration ( diapedesis ) : leukocytes travel through inter- endothelial spaces mediated by PECAM

5-migration: leukocytes migrate along a chemotactic gradient to site of injury ( chemotaxis )

33
Q

what do neutrophils and monocytes do?

A
  • eliminate the infection or dead cells causing the inflammation
  • once a leukocyte has reached the point source of the inflammatory response they become activated- recognition by TLRs and other phagocytic receptors
  • this triggers phagocytosis
34
Q

what what is phagocytosis and what what are its outcomes ?

A
  • phagocytosis is the engulfment of something from outside of a cell into vesicle inside cell called the phagosome
  • its outcome involves three distinct steps

. recognition and
attachment through receptors
. engulfment and fusion of phagosome and lysosome

. killing and degradation of ingested material

35
Q

what are the 3 mechanism involved in the intracellular destruction of microbes and debris ?

A

free radical formation through production of

  1. reactive oxygen species
  2. reactive nitrogen species
  3. lysosomal enzymes
36
Q

how are microbes mostly killed ?

A

mostly killed though free radical species

  1. reactive oxygen species
  2. reactive nitrogen species
37
Q

how are debris cleared ?

A

debris cleared through all three mechanism

  1. reactive oxygen species
  2. reactive nitrogen species
  3. lysosomal enzymes
38
Q

what are reactive oxygen species ?

A
  • these produced by the rapid assembly of an enzyme called phagocyte oxidase
  • this oxidises NADPH this reaction reduces oxygen to superoxide anion
  • process is triggered by the respiratory burst
  • spontaneous dis mutation creates hydrogen peroxide from superoxide anions
  • azurophilic granules in neutrophils contain MPO enzyme
  • this enzyme in the
    presence of cl can convert hydrogen hydrogen peroxide to hypochlorite
  • an efficient and potent anti-microbial
  • hydrogen peroxide also dissociates to create hydroxyl radicals which are anti-microbial
  • this all happens in lysosomes and phagosomes - otherwise kill host cell
39
Q

what is nitric oxide ?

A
  • produce by nitric oxide synthase ( NOS)
    iNOS ( induced NOS) - specific enzyme that produce NO in macrophages and neutrophils
  • NO reacts with superoxide anions to generate peroxynitrite
  • this is a free radical ( like ROS ) which attacks lipids, protein and nucleic acids
40
Q

what are the two types of granules that leukocytes contain ?

A

leukocytes contain lysosomal granules

  1. specific - contain enzymes that break down specific protein
    contain lysosome , collagenase, gelatinase
    - good at clearing debris because debris has a specific enzyme
  2. azurophil:
    help in production of free radicals
    contain MPO, acid hydrolases, proteases
41
Q

when is inflammation neutralised

A
  • after you done phagocytosis - then as long as you cleared debris then inflammation stops
  • nothing is triggering white blood cells to come in
42
Q

what are mediators of acute inflammation?

A
  • molecules that not only initiate the inflammatory response , but that also regulate the following response until resolution
  • all mediators are involved different roles
43
Q

what are sentinel cells?

A
  • first line of defence

- they tend to be mast cells and macrophages

44
Q

what are mast cells function ?

A
  • mast cells tend to sit around blood vessels and are full of granules that contain things like histamine - so can trigger endothelial cells to start responding
  • they also have ability to up regulate the production of specific mediators inflammation such as protein or lipids
  • can send cytokines and chemokines
  • richest source of histamine
  • located in connective tissue/basement membranes
  • adjacent to blood vessel
  • release of PAF ( platelet activating factor) leads to serotonin and histamine release from activated platelets
  • mast cells are very important sentinel cell in hypersensitivity reactions
45
Q

what do histamine and serotonin do ?

A
  • histamine and serotonin induce vasodilation and increase vascular permeability
  • they are produce by mast cells
46
Q

what comes out when you have oedema or tumor ?

A
  • water and plasma proteins
  • plasma protein play role in mediating the inflammatory response
  • so you can factor XII ( involved coagulation) and complement system ( lots of inactive complement protein in the blood supply and when you have an inflammatory response they become activated and break up )
    e. g. C3a and C5a which are anaphylatoxins

C3b - opsonin - combines with microbe and acts as a flag
C5b-C9 MAC- form membrane attack complex

47
Q

what is kinin - bradykinin system ?

A
  • kinins are vasoactive peptides derived plasma proteins

- bradykinin increase vascular permeability, contraction of smooth muscles, vasodilation and pain

48
Q

how is coagulation system involved in inflammation ?

A
  • thrombin provides the main link between coagulation and inflammation by binding to protease activated receptors on platelets, endothelium and smooth muscle and leukocytes
PAR-signaling induces:
chemokines
endothelial adhesion molecules ( ICAM)
P-selectin
COX-2
PAF
NO
49
Q

what is complement system?

A
  • you have complement protein in your blood
  • they combine to microbes once they get into the extracellular space
  • activated to become proteolytic enzymes that degrade other complement proteins- complement cascade- leading to breakdown of C3
50
Q

what is arachidonic acid ?

A
  • type of mediator
  • arachidonic acid is derived from conversion of linoleic acid
    arachidonic acid can be then broken apart further to produce eicosanoids
  • eicosanoids are hormones called autocoids and can initiate immune response
51
Q

what are different morphological patterns of acute inflammation that can be found ?

A
  • serous - exudation of non viscous serous fluid from mesothelial cells
    sometimes contain plasma from vascular leakage
  • purulent - inflammation that results in pus information ( neutrophils , dead cells and fluid )
  • fibrinous - when increase permeability allows fibrin to pass into tissues and procoagulent is present then a fibrinous exudate is deposited
  • ulcerative - inflammation near an epithelium causing necrosis and exposure of underlying issues ( ulcer )
52
Q

what are outcome of acute inflammation ?

A
  • complete restitution
  • abscess formation ( encapsulation and pus )
  • chronic inflammation
  • wound healing with sear formation

Neural Biology 1 (58 decks)

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