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DMD 5243 Cellular/Histological Change > Inflammation and Repair (Bikman) > Flashcards

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?

A

constant

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
Q

If the hydrostatic pressure is greater than the oncotic pressure, fluid will ___ the capillaries.

A

leave the capillaries.

Hydrostatic pressure pushes h2o out of capillaries.

26
Q

If the onctoic pressure is greater than the hydrostatic pressure fluid will ____ the capillaries.

A

enter the capillaries

Oncotic pressure pulls h2o into the capillaries towards plasma proteins in capillaries

27
Q

____ is the accumulation of fluids in interstitial spaces

A

Edema

28
Q

Edema can be caused by what four things changes?

A

increase in hydrostatic P
decrease in plasma proteins
increase in capillary permeability
lymph obstruction

29
Q

What are the two ways to describe edema based on the composition of fluid?

A

Transudate vs Exudate

30
Q

With Transudate edema, what does it look like?

What cause transudate edema?

A

very clear, high water content, low proteins/cells

caused by increased hydrostatic pressure

31
Q

with Exudate edema, what does it look like?

What causes exudate edema?

A

cloudy/opaque , high proteins/cells

caused by increased capillary permeability

32
Q

In regards to acute inflammation, the cellular response type would cause what cells to migrate to injury site?

A

Leukocytes, which can kills pathogens but can also damage other tissue..

33
Q

What are the four steps of Leukocytes going to injury site?

aka leukocytes adhesion cascada

A
  1. margination and rolling
  2. adhesion (selections)
  3. transmigration (integrins)
  4. chemotaxis
34
Q

what cells help with the adhesion of leukocytes ?

A

selections, theses are cellular adhesion molecules near infection site.

35
Q

what cells help with the transmigration of leukocytes?

A

integrins

36
Q

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?

A

1st. neutrophils, then monocytes, which become macrophages.

37
Q

what are oposonins?

A

anitbody that marks a pathogen for an immune response, helps leukocytes correctly ID and engulf pathogens

38
Q

What are the three mediators of inflammation?

A

phospholipase A2
cyclooxygenase
lipoxygenase

anti-inflammatory steroid would inhibits these

39
Q

Chronic inflammation would be signaled by what cells?

A

monocytes and macrophages.

40
Q

what is a granuloma?

A

pattern of inflammation of aggregates of activated macrophages and lymphoocytes

41
Q

what do omega 3 fatty acids do to inflammation?

what do saturated fatty acids do to inflammation?

A

decrease inflammation

increase inflammation

42
Q

what are the two steps of repair? which is 1st intention and which is second intention?

A

1st intention- regeneration

2nd = scar forming

43
Q

____ tissues are always proliferating, and are best able to regenerate.

A

Labial

examples include skin, GI epithelium, bone marrow, oral muscosa

44
Q

Which tissue type has no proliferation, and will always scar?

A

Permanent tissue

in neurons and cardiac MM

45
Q

Scar formation involved what three steps?

A
  1. angiogenesis (new blood vessels forming)
  2. migration and proliferation of fibroblasts
  3. remodeling of tissue

DMD 5243 Cellular/Histological Change (5 decks)

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