Inflammation and Repair (Bikman) Flashcards

1
Q

Inflammation is a complex reaction resulting in ___, ____ and ____ leaving the circulation to enter site of injury/ infection.

A

fluid, plasma proteins, and leukocytes

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2
Q

5 R’s of Inflammation

A
recognition
recruitment 
removal 
regulation
resolution
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3
Q

sights of Inflammation (5)

A
Dolor
Calor
Rubor
Tumor
Functio Laesa
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4
Q

Dolor meaning?

A

pain

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5
Q

Calor?

A

heat

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6
Q

Rubor?

A

redness

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7
Q

Tumor?

A

swelling

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8
Q

functio laesa

A

loss of function

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9
Q

What cells infiltrate the injury site with acute inflammation?

A

neutrophils

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10
Q

What cells infiltrate the injury site with chronic inflammation? (2)

A

monocytes/macrophages and lymphocytes

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11
Q

What cells mediate inflammation?

What cell is the first to respond to injury?

A

monocyte, lymphocyte, neutrophil, eosinophil, and basophil cells

first to respond are neutrophil

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12
Q

What are the two types of acute inflammation?

A

Vascular and Cellular

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13
Q

In regards to acute inflammation, what does the vascular type do?

A

change in vessels, increases blood flow allowing plasma proteins to leave vessel

(increased vasodilation and increased vessel permeability )

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14
Q

What is the main mediator of vessel changes with acute inflammation?

What cells make that mediator?

A

Histamine, which increases vasodilation and increased vessel permeability

made by Mast cells

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15
Q

In regards to acute inflammation, what does the cellular type do?

A

emigration of leukocytes from blood circulation–> injury site

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16
Q

What two things help recognize injury of cell with acute inflammation?

A

Pattern Recognition receptors and infammasomes.

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17
Q

what do infammosomes do?

A

identify products of cellular damage and active caspases.

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18
Q

What are some results of increased vasodilation and increased vascular permeability?

A

redness and swelling
stasis (dilated vessels packed with RBCs)
margination (leukocytes at surface of injury)

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19
Q

with hydrostatic pressure, what causes it to change?

A

heart beating, h2o volume, gravity, and size of vessels, h20 is pushed out of vessel

20
Q

with oncotic pressure, what causes it to change?

A

plasma proteins , h2o is pulled towards plasma proteins into capillaries.

21
Q

Where is hydrostatic pressure the greatest? Arterial end or venous end?

A

Arterial end

22
Q

Does Oncotic pressure change or stay constant throughout capillaries?

23
Q

Which pressure type would be considered a pulling force?

A

oncotic pressure, pulls h20 into capillaries towards plasma proteins

24
Q

what pressure type would be considered a pushing force?

A

hydrostatic pressure, pushes h20 out of capillaries..

25
If the hydrostatic pressure is greater than the oncotic pressure, fluid will ___ the capillaries.
leave the capillaries. Hydrostatic pressure pushes h2o out of capillaries.
26
If the onctoic pressure is greater than the hydrostatic pressure fluid will ____ the capillaries.
enter the capillaries Oncotic pressure pulls h2o into the capillaries towards plasma proteins in capillaries
27
____ is the accumulation of fluids in interstitial spaces
Edema
28
Edema can be caused by what four things changes?
increase in hydrostatic P decrease in plasma proteins increase in capillary permeability lymph obstruction
29
What are the two ways to describe edema based on the composition of fluid?
Transudate vs Exudate
30
With Transudate edema, what does it look like? What cause transudate edema?
very clear, high water content, low proteins/cells caused by increased hydrostatic pressure
31
with Exudate edema, what does it look like? What causes exudate edema?
cloudy/opaque , high proteins/cells caused by increased capillary permeability
32
In regards to acute inflammation, the cellular response type would cause what cells to migrate to injury site?
Leukocytes, which can kills pathogens but can also damage other tissue..
33
What are the four steps of Leukocytes going to injury site? | aka leukocytes adhesion cascada
1. margination and rolling 2. adhesion (selections) 3. transmigration (integrins) 4. chemotaxis
34
what cells help with the adhesion of leukocytes ?
selections, theses are cellular adhesion molecules near infection site.
35
what cells help with the transmigration of leukocytes?
integrins
36
within the first 24 hours of injury what cells would you expect to see at injury site? during 24-48, what cells would you expect to see?
1st. neutrophils, then monocytes, which become macrophages.
37
what are oposonins?
anitbody that marks a pathogen for an immune response, helps leukocytes correctly ID and engulf pathogens
38
What are the three mediators of inflammation?
phospholipase A2 cyclooxygenase lipoxygenase anti-inflammatory steroid would inhibits these
39
Chronic inflammation would be signaled by what cells?
monocytes and macrophages.
40
what is a granuloma?
pattern of inflammation of aggregates of activated macrophages and lymphoocytes
41
what do omega 3 fatty acids do to inflammation? what do saturated fatty acids do to inflammation?
decrease inflammation increase inflammation
42
what are the two steps of repair? which is 1st intention and which is second intention?
1st intention- regeneration | 2nd = scar forming
43
____ tissues are always proliferating, and are best able to regenerate.
Labial examples include skin, GI epithelium, bone marrow, oral muscosa
44
Which tissue type has no proliferation, and will always scar?
Permanent tissue | in neurons and cardiac MM
45
Scar formation involved what three steps?
1. angiogenesis (new blood vessels forming) 2. migration and proliferation of fibroblasts 3. remodeling of tissue