Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Foundational toolkit III - wk1 > inflammation and healing > Flashcards

inflammation and healing Flashcards

1
Q

what is inflammation

A
  • complex response of vascularized tissues to cell damage in order to eliminate offening agents
  • protective mechanism to remove injurious stimuli and to initiate the healing process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

inflammation develops through a series of steps:

5 R’s

A
  • recognition
  • recruitment
  • removal
  • regulation
  • repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does inflammation look like

A
  • rubor (redness)
  • calor (warmth)
  • tumor (swelling)
  • dolor (pain)
  • functio laesa (loss of function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is acute inflammation

A
  • takes several hours to several days
  • many endogenous and exogenous triggers
  • if acute inflammation fails to clear the stimulus -> chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the 3 sequential phases of acute inflammation

A
  • fluidic
  • cellular
  • reparative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

fluid phase of acute inflammation

vasodilation

A
  • hisamine, nitric oxide (NO)
  • hyperemia -> increased blood flow (calor, rubor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

fluid phase of acute inflammation

endothelial cell activation

A
  • increased vascular permeability -> fluid, protein, fibrinogen exudation -> edema (tumor)
  • fibrinogen = important plasma protein normally floating around in blood -> fibrin in tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

fluid phase of acute inflammation

increased blood viscosity

A

slower blood flow -> allows leukocytes to accumulate along endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 4 stages of the cellular phase in acute inflammation

A
  • margination
  • rolling
  • stable adhesion
  • transendothelial cell migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

step 1

margination

A
  • bridge between fluidic and cellular phases
  • vasodilation (reduced blood flow, increased blood viscosity, leukocytes line up along endothelial surface)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

step 2

rolling

A
  • transient, WEAK binding between endothelial cell and leukocyte
  • selectins (some on endothelial cells, some on leukocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

step 3

stable adhesion

A
  • leukocytes STRONGLY adhere to endothelium
  • requires leukocyte and endothelial cell activation (cytokines - IL-1, IL-6, IL-8, TNF; complement factors)
  • integrins (beta-integrains on leukocyte surface)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

step 4

transendothelial cell migration

A
  • leukocytes move across endothelial cell layer into tissue
  • PECAM-1 (CD31)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are 4 variations of acute inflammation

A
  1. serous inflammation
  2. catarrhal inflammation
  3. fibrinous inflammation
  4. suppurative inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is serous inflammation

A
  • low plasma protein, little or no leukocytes
  • thermal injury to skin (burns) -> blister
  • acute allergic responses -> watery eyes and runny nose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is catarrhal inflammation

A
  • thick gelatenous fluid containing abundant mucus
  • chronic inflammation of airways of the respiratory system -> chronic asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is fibrinous inflammation

A
  • due to endothelial cell activation/injury -> leakage of fibrinogen -> formation of fibrin
  • body cavities
  • synovial membranes of joints
  • meninges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is suppurative inflammation

A
  • inflammation with high plasma protein and high numbers of leukocytes, predominantly neutrophils -> pus
  • due to pyogenic bacteria (pyometra ex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

kinetics of neutrophils in inflammation

A

6-24 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

kinetics of monocytes (macrophages) in inflammation

A

24 hrs and beyond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

kinetics of lymphocytes and plasma cells in inflammation

A

greater than 48 hrs and beyond

22
Q

what are the main histologic and pathologic features of acute inflammation

A
  • neutrophils first, then macrophages
  • plasma/fluid leakage -> edema +/- fibrin
23
Q

what are outcomes of acute inflammation

A
  • progression to chronic inflammation
  • complete resolution
  • healing by fibrosis
24
Q

progression of chronic inflammation occurs when:

A
  • acute response is unresolved/inciting cause is not cleared
  • repeated episodes of acute inflammation w/ extensive injury and necrosis
  • establishment of an autoimmune reaction
25
Q

there is a shift of cellular elements from neutrophils to: ____, ____, ____, etc. when acute inflammation progresses to chronic inflammation

A

lymphocytes, monocytes, plasma cells

26
Q

a hallmark for chronic inflammation

A

tissue destruction

27
Q

lymphocytes

in chronic inflammation

A

antibody- and cell-mediated immune reactions

28
Q

plasma cells

in chronic inflammation

A

develop from activated B lymphocytes, produce antibody against antigens or altered tissue components

29
Q

macrophages

in chronic inflammation

A
  • responsible for much of the tissue injury in chronic inflammation (ROS, ECM proteases)
  • important role in healing -> induce fibroblast activation and proliferation -> collagen deposition, and antiogenesis
30
Q

what are the 3 special types of chronic inflammation

A
  • granulomatous inflammation
  • pyogranulomatous inflammation
  • abcess formation
31
Q

what is granulomatous inflammation

A
  • epithelioid macrophages, multinucleated giant cells, variable # of lymphocytes and plasma cells, surrounding an indigestible organism, particle, or central necrotic area
  • surrounded by fibrosis
  • implies certain etiologic agents
  • granuloma = one of more isolated foci of granulomatous inflammation
32
Q

what is pyogranulomatous inflammation

A
  • epitheliod macrophages forming granulomas with admixed neutrophils and necrosis
  • implies certain etiologic agents
33
Q

what is abcess formation

A
  • occurs when the acute inflammatory response fails to rapidly eliminate inciting stimulus
  • enzymes and inflammatory mediators from neutrophils -> liquefy tissue to form pus
  • a collection of pus circumscribed by a fibrous capsule that is visible grossly
34
Q

main points of acute inflammation

A
  • rapid onset (seconds to minutes), short duration (minutes to days)
  • fluid and plasma proteins leak into tissues (edema)
  • fibrinogen -> fibrin
  • leukocytes (neutrophils) migrate into tissues
  • if unresolved, leads to chronic inflammation
35
Q

main points of chronic inflammation

A
  • long time frame (days, weeks, years)
  • lymphocytes, plasma cells, and macrophages
  • fibrous connective tissue deposition
  • tissue necrosis
36
Q

what are the 4 phases of wound repair

A
  1. hemostasis
  2. acute inflammation
  3. proliferation
  4. remodeling
37
Q

what is complete resolution of acute inflammation

A
  • typical outcome to limited injury (mosquito bite)
  • mediators decay quickly
  • vascular permeability returns to normal
  • leukocytes die, edema and proteins removed by macrophages
38
Q

tissue regeneration is ____% normal when resolved

A

100

39
Q

what is regeneration

A
  • replacement by cells of the same type
  • requires intact framework
  • occurs by compensatory growth -> organ becomes functional due to cell hyperplasia and hypertrophy
40
Q

what determines whether a tissue will undergo regeneration or healing

A
  • type of tissue damaged
  • damage to the extracellular matrix
  • extent of the wound
  • blood supply, nutrition
41
Q

regeneration

continuously dividing (labile) tissues=

A

cells proliferate throughout life (gut epithelium)

42
Q

regeneration

quiescent (stable) tissues=

A

low level of replication; may undergo division in response to stimuli (e.g. parenchymal cells of liver, kidneys, and pancreas)

43
Q

regeneration

post-mitotic(permanent/terminally differentiated) tissues=

A

cannot undergo mitotic division in postnatal life (neurons, cardiac muscle cells)

cannot undergo renegeration

44
Q

what is healing

A
  • restoration of integrity to injured tissue
  • typically involves collagen deposition and scar formation
45
Q

wound healing

what is the inflammation phase

A
  • 24hrs after injury; lasts up to 96 hrs
  • macrophages = necessary for tissue repair (remove cell debris, degrade ECM, release growth factors necessary for proliferation phase)
  • fibrin = loose gel-like matrix to serve as the scaffold for granulation tissue
46
Q

wound healing

what is the proliferation phase

A
  • lasts up to 3-4 weeks
  • granulation tissue = proliferation of new blood vessels, fibroblasts, and deposition of early collagen (necessary for re-epithelialization, sometimes called the “wound bed”
47
Q

wound healing

remodeling/maturation phase

A
  • begins ~3-4 weeks after injury, but only after the other phases are successfully completed (can last years)
  • granulation tissue (blood vessels and immature CT) converted to mature CT (fibrosis)
  • mediated by TGF-B -> pro-fibrosis, anti-inflammatory
  • extracellular collagen formation -> ECM reestablished
  • contraction of tissue
  • fibroblasts, myofibroblasts
48
Q

does tissue return to 100% normal structure and function with wound healing

A

no

49
Q

what are disruptors of wound repair

A
  • bacterial infections
  • poor nutriton
  • glucocorticoid therapy
  • mechanical factors
  • poor apposition/dehiscence
  • poor perfusion
  • amount of tissue injured
  • tissue type
50
Q

abnormalities in tissue repair

A
  • inadequate granulation tissue formation
  • ecessive formation
  • aberrations of cell growth and ECM production
  • contraction

Foundational toolkit III - wk1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions