Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Foundational toolkit III - wk1 > inflammation and healing > Flashcards

inflammation and healing Flashcards

(50 cards)

Start Studying
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

Study These Flashcards
A

greater than 48 hrs and beyond

22
Q

what are the main histologic and pathologic features of acute inflammation

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

what are outcomes of acute inflammation

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

progression of chronic inflammation occurs when:

Study These Flashcards
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
there is a shift of cellular elements from neutrophils to: ____, ____, ____, etc. when acute inflammation progresses to chronic inflammation
lymphocytes, monocytes, plasma cells
26
a hallmark for chronic inflammation
**tissue destruction**
27
lymphocytes | in chronic inflammation
antibody- and cell-mediated immune reactions
28
plasma cells | in chronic inflammation
develop from activated B lymphocytes, produce antibody against antigens or altered tissue components
29
macrophages | in chronic inflammation
* 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
what are the 3 special types of chronic inflammation
* granulomatous inflammation * pyogranulomatous inflammation * abcess formation
31
what is granulomatous inflammation
* **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
what is pyogranulomatous inflammation
* **epitheliod macrophages** forming **granulomas** with admixed **neutrophils and necrosis** * implies certain etiologic agents
33
what is abcess formation
* 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
main points of acute inflammation
* **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
main points of chronic inflammation
* **long time frame** (days, weeks, years) * **lymphocytes, plasma cells, and macrophages** * **fibrous connective tissue** deposition * tissue **necrosis**
36
what are the 4 phases of wound repair
1. hemostasis 2. acute inflammation 3. proliferation 4. remodeling
37
what is complete resolution of acute inflammation
* typical outcome to **limited injury** (mosquito bite) * mediators decay quickly * vascular permeability returns to normal * leukocytes die, edema and proteins removed by macrophages
38
tissue regeneration is ____% normal when resolved
100
39
what is regeneration
* **replacement** by cells of the same type * requires intact framework * occurs by **compensatory growth** -> organ becomes functional due to cell **hyperplasia** and **hypertrophy**
40
what determines whether a tissue will undergo regeneration or healing
* type of tissue damaged * damage to the extracellular matrix * extent of the wound * blood supply, nutrition
41
# regeneration continuously dividing (labile) tissues=
cells proliferate throughout life (gut epithelium)
42
# regeneration quiescent (stable) tissues=
low level of replication; may undergo division in response to stimuli (e.g. parenchymal cells of liver, kidneys, and pancreas)
43
# regeneration post-mitotic(permanent/terminally differentiated) tissues=
cannot undergo mitotic division in postnatal life (neurons, cardiac muscle cells) | cannot undergo renegeration
44
what is healing
* restoration of integrity to injured tissue * typically involves **collagen deposition and scar formation**
45
# wound healing what is the inflammation phase
* 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
# wound healing what is the proliferation phase
* 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
# wound healing remodeling/maturation phase
* 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
does tissue return to 100% normal structure and function with wound healing
no
49
what are disruptors of wound repair
* bacterial infections * poor nutriton * glucocorticoid therapy * mechanical factors * poor apposition/dehiscence * poor perfusion * amount of tissue injured * tissue type
50
abnormalities in tissue repair
* 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.
© 2025 Bold Learning Solutions. Terms and Conditions