Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FTK III- Gen Path > Inflammation > Flashcards

Inflammation Flashcards

(45 cards)

Start Studying
1
Q

Cardinal signs of inflammation

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
2
Q

Acute Inflammation

A

several hours to several days
exogenous and endogenous triggers
3 phases: fluidic, cellular, reparative
failure to clear stimulus –> chronic inflammation

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

Acute inflamm.- fluidic phase

A

vasodilation- due to histamines and nitric oxide; causes hyperemia (increased blood flow–> calor and rubor)
endothelial cell activation (increased vascular permeability–> fluid, protein, fibrinogen exudation –> edema (tumor))
increased blood viscosity (slower blood flow allows leukocytes to accumulate along endothelium)
leukocyte adhesion cascade begins

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

fibrinogen

A

important plasma protein floating in blood
** in tissues= fibrin

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

acute inflamm.- cellular phase

A

margination
rolling
stable adhesion
transendothelial cell migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

margination

A

bridge between fluidic and cellular phases of acute inflammation
due to vasodilation (reduced flow and increased viscosity) WBCs line up along endothelial surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

rolling

A

transient, weak binding between endothelial cell and leukocyte
**Selectins on both endothelial cells and WBCs interact and facilitate rolling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

stable adhesion

A

WBCs strongly bind to endothelium
cytokines (**IL-1, IL-6, IL-8, TNF), complement factors, and other inflammatory mediators activate WBCs and endothelial cells
** Integrins on WBC surface facilitate stable adhesion

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

Transendothelial cell migration

A

WBCs move across endothelial cell layer into tissue
** Facilitated by PECAM-1 (CD31)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

variations of acute inflammation

A

serous inflammation
catarrhal inflammation
fibrinous inflammation
suppurative inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

serous inflammation

A

low plasma proteins, little or NO WBCs
thermal injury –> blister
acute allergic response–> watery eyes and runny nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

catarrhal inflammation

A

thick gelatinous fluid containing abundant mucus
ex. chronic inflammation of airways –> asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

fibrinous inflammation

A

due to endothelial cell activation/injury leading to leakage of fibrinogen
leads to formation of fibrin
occurs in body cavities, synovial membranes of joints, and meninges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

suppurative inflammation

A

inflammation with high plasma protein and high number of leukocytes (predominantly neutrophils)–> pus
due to pyogenic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how long do neutrophils take to respond in inflammation?

A

6-24 hours
predominate in acute inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how long do monocytes take to respond to inflammation?

A

24 hours and beyond
** become macrophages in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how long do lymphocytes and plasma cells take to respond to inflammation?

A

greater than 48 hours and beyond
part of adaptive immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

main histologic features of acute inflammation

A

neutrophils (first) then macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

main pathologic features of acute inflammation

Study These Flashcards
A

plasma/fluid leakage–> edema +/- fibrin

20
Q

when does progression to chronic inflammation occur?

Study These Flashcards
A

acute response is unresolved/inciting cause isn’t cleared
repeated episodes of acute inflammation with extensive injury and necrosis
establishment of an autoimmune response

21
Q

histologic changes in progression to chronic inflammation

Study These Flashcards
A

shift of cellular elements from neutrophils to lymphocytes, macrophages, and plasma cells
also eosinophils and mast cells

22
Q

pathologic changes in progression to chronic inflammation

Study These Flashcards
A

tissue destruction is one of the hallmarks of chronic inflammation

23
Q

lymphocytes role in chronic inflammation

Study These Flashcards
A

antibody and cell-mediated immune reactions

24
Q

plasma cells role in chronic inflammation

Study These Flashcards
A

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

25
macrophages role in chronic inflammation
responsible for much of the tissue injury in chronic inflammation (ROS, extracellular matrix proteases) important role in healing- induce fibroblast activation and formation which leads to collagen deposition and angiogenesis
26
types of chronic inflammation
granulomatous inflammation pyogranulomatous inflammation abscess formation
27
granulomatous inflammation
activated epithelioid macrophages, multinucleated giant cells mainly some lymphocytes and plasma cells surrounded by fibrosis (deposition of collagen)
28
granuloma
one or more isolated foci of granulomatous inflammation
29
pyogranulomatous inflammation
epitheliod macrophages forming granulomas with admixed neutrophils and necrosis typical with fungi
30
abscess formation
occurs when acute inflammatory response fails to rapidly eliminate inciting stimulus enzymes and inflammatory mediators from neutrophils liquefy tissue to form pus seen grossly as pus circumscribed by a fibrous capsule
31
acute vs chronic inflammation
acute: rapid onset, short duration, fluid and plasma proteins leak into tissues (edema), fibrinogen --> fibrin, neutrophils migrate into tissues, leads to chronic inflammation if unresolved chronic: long time frame (days to weeks to years), lymphocytes, plasma cells, and macrophages, fibrous connective tissue deposition, tissue necrosis
32
outcomes of acute inflammation
progression to chronic inflam. complete resolution leads to regeneration healing by fibrosis
33
complete resolution of acute injury
typical outcome to limited injury mediators decay quickly, vascular permeability returns to normal, leukocytes die, edema, proteins removed by macrophages tissue regeneration= 100% normal when resolved
34
regeneration
replacement of cells of the same type requires an intact framework occurs by compensatory growth--> organ becomes functional due to cell hyperplasia and hypertrophy
35
what determines whether or not a tissue will undergo regeneration or healing
type of tissue damaged damage to ECM extent of wound blood supply, nutrition
36
continuously dividing (labile) tissues
cells that proliferate throughout life ex: gut epithelium
37
quiscent (stable) tissues
low level of replication; may undergo division in response to stimuli ex; cells of liver, kidney, and pancreas
38
post-mitotic (permanent/terminally differentiated) tissues
cannot undergo mitotic division in postnatal life ex: neurons, cardiac muscle cells
39
healing by fibrosis
restoration of integrity to injured tissue; typically involves collagen deposition and scar formation
40
4 temporal phases of wound repair/healing
hemostasis (vascular phase) acute inflammation (cellular phase) proliferation (granulation tissue) remodeling (maturation phase, contraction)
41
inflammation phase of wound repair/healing
24 hour after injury macrophages are necessary for tissue repair- remove cell debris and degrade ECM and release GF and fibroblasts necessary for proliferation phase fibrin is a loose gel-like matrix to serve as scaffold for granulation tissue
42
proliferation phase of wound repair/healing
lasts up to 3-4 weeks (depends on size of wound) granulation tissue= proliferation of new blood vessels, fibroblasts, and deposition of early collagen (necessary for re-epithelialization and sometimes called "wound bed")
42
remodeling/maturation pahse of wound repair/healing
begins ~3-4 weeks after injury but only after previous phases are complete can last years granualtion tissue (BV and immature CT) is converted to mature CT (fibrosis) TGF-B mediates fibrosis (pro-fibrosis and anti-inflammatory) Extracellular Collagen formation (ECM restored) contraction of tissues by fibroblasts and myofibroblasts ** Tissues do not return to 100% normal structure and function
42
Disruptors of repair
bacterial infection poor nutrition glucocorticoid therapy (inhibits TGF-B) mechanical factors poor apposition/dehiscence poor perfusion amount of tissue injured tissue type
42
abnormalities in tissue repair
inadequate granulation tissue repair excessive formation aberrations of cell growth and ECM production (exuberant granulation tissue is common in distal limbs of horses) contraction

FTK III- Gen Path (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions