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I3 Exam 1 > Acute Inflammation and Healing - Latham > Flashcards

Acute Inflammation and Healing - Latham Flashcards

1
Q

What are the four steps of the vascular response?

A
  1. smooth muscle relaxation in arteries and arterioles to allow blood to rush in
  2. vascular dilation = hyperemia (blood moving fast)
  3. endothelial cells contract creating intracellular gaps
  4. increased vascular permeability = first water and salt leak out including fibrinogen and immunoglobulins
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2
Q

What is transudate?

A

extravascular fluid that is low in protein at first when the intracellular gaps are small

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3
Q

What is exudate?

A

when large mols like fibrinogen and immunoglobulins leak out
= inflammatory edema

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4
Q

What is phase I of acute inflammation?

A

vascular response

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5
Q

What is phase II of acute inflammation?

A
  1. marginate and roll
  2. adhere to EC
  3. transmigrate through EC gaps
  4. move to site of injury along chemoattract gradient
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6
Q

neutrophils

A

PMNs - major effector cells of acute inflammation

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7
Q

What does congestion lead to?

A

decreased blood flow and stasis as edema increases which leads to a loss of laminar flow

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8
Q

What do chemoattractants and integrins allow for?

A

allows neutrophils to squeeze out through endothelial gaps

- can break through the basement membrane and move into the extravascular matrix

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9
Q

selectins

A

platelets, leukocytes, and endothelial cells express selectins

  • bind to glycoprotein receptor
  • rolling
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10
Q

integrins

A

adherence, migration

  • tighter binding
  • can bind to PECAM (platelet endothelial cell adhesion molecule)
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11
Q

What is the first responder cell

A

neutrophil

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12
Q

What is the second responder cell

A

monocytes - move into the tissues by same mechanism as neutrophil

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13
Q

What attracts monocytes

A
  • cells bind to fibrin matrix and move toward an increasing chemotaxis concentration
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14
Q

What are exogenous signals?

A

bacterial products - LPS

- PAMPs

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15
Q

DAMPs

A

endogenous signals

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16
Q

Endogenous signals

A

necrotic cells and fibrinopeptides

  • complement - produces byproducts along the way
  • leukotriene
  • chemoattractant factors
  • tells responding cells where to go
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17
Q

Complement 5a

A

a very good chemoattractant

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18
Q

LTB4

A

a product of the AA breakdown

- chemoattractant

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19
Q

IL-8

A

chemokine for neutrophils

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20
Q

MCP-1

A

monocyte chemoattractant

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21
Q

Where are mast cells found

A

connective tissue all over the body

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22
Q

Which two cell types contain preformed histamine

A

mast cells and platelets

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23
Q

What do trauma and burns stimulate?

A

mast cells and platelets to have immediately release of preformed histamine

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24
Q

What is the major player in the acute inflammatory response in the first 20-30 minutes?

A

histamine

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25
Q

what is the maintenance of vascular tone dependent on

A

nitric oxide

- released from stimulated endothelial cells to affect smooth muscle relaxation

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26
Q

What macrophages use NO for?

A

to produce antimicrobial free radicals

  • cells contain inducible NO
  • which can metabolize arginine
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27
Q

prostaglandins

A

vasoactive properties

- systemic signs of infection = fever pain

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28
Q

What produces LTB4

A

leukotrienes produce LTB4 as a chemoattractant to neutrophils

29
Q

Which cytokines activate macrophages and induce selections?

A

TNF alpha, IL-1

30
Q

Which cytokine is responsible for fever?

A

IL-1

31
Q

Which cytokine acts as a chemotaxis for PMNs

A

IL-8

32
Q

bradykinin

A
  • production of pain
33
Q

C5a

A

chemotaxin

- vasoactive

34
Q

c3b

A

oxidant

35
Q

why do we ice

A

constrict the vessels and decrease blood flow and alleviate some pain

36
Q

neutrophil phagocytosis

A
  • rich in myeloperoxidase
  • antibody coats particle and binds to receptor for antibodies on the neutrophil (Fc receptor) to help the neutrophil to engage
  • factor C3 coats particulate matter
37
Q

opsonin

A

coat the particulate matter to engulf by phagocytosis to enhance phagocytosis
- antibody or C3

38
Q

Do neutrophils require oxygen?

A

no, but it can do an even better job with oxygen
- with oxygen it can take NADPH and oxidize it will allow it to reduce oxygen to create free radicals to kill whatever is ingested

39
Q

Myeloperoxidase

A

neutrophil has these in abundance

- myloperoxidase can produce OCl- free radical

40
Q

What does neutrophil tissue infiltration tell us

A

acute inflammation

- first responders to injury

41
Q

What do macrophages tell us

A

what monocytes become as they move into the issues

- increase after 24-28 and become predominant cell type

42
Q

What is inflammatory edema

A

fluid exudate, protein rich

43
Q

purulent suppurative

A

pus = cell rich

44
Q

fibrinous exudate

A

exudate that is rich in fibrin

45
Q

mucinous exudate

A

exudate that is rich inmucin

46
Q

sanginous exudate

A

hemorrhagic, common with necrosis

47
Q

What would meningitis in the brain show

A

suppurative exudate

- pus between the gyri

48
Q

abscess

A

liquefactive necrosis of tissue surrounded by normal tissue

  • suppurative exudate
  • rich in neutrophils
49
Q

ulcer

A

liquifactive necrosis at tissue surface

  • suppurative exudate
  • on the surface of the mucosa
50
Q

leukocytosis

A

increased release of neutrophils from marrow

- systemic sign of acute inflammation

51
Q

What does a release of IL-1 cause

A

leukocytosis

- increased release of neutrophils from marrow

52
Q

What is released into systemic circulation during a fever?

A

prostaglandin and IL-1

- affect thermoregulation on hypothalamus and pulse rate

53
Q

What do IL-6 and IL-1 stimulate the liver to produce?

A

acute phase proteins = CRP

- bind to dead cells and pathogens and activates complement cascade

54
Q

What do elevated levels of CRP indicate?

A

active levels of inflammation

- could be sign of heart attack

55
Q

erythrocyte sedimentation rate

A

ESR

- IL-6 and IL-1 increase liver synthesis of fibrinogen which leads to increased RBC aggregation –> sediment

56
Q

What are DAMPs chemoattractants to?

A

neutrophils

57
Q

Which cell is the key effect cell for healing

A

macrophage

  • produce EGG, VGF, GFG, TGFalpha (promote cell growth)
  • fibrogenesis
  • metallaproteinases (wound remodeling)
58
Q

what are the 4 steps for healing and repair?

A
  1. removal of edema and debris
  2. regeneration of native tissues - need activate macrophages to make all the growth factors
  3. organization - proliferation of 3 major cell types
  4. fibrosis - scar
59
Q

What reabsorb edema during healing?

A

lymphatics

60
Q

Which cells remove cell and tissue debris during healing?

A

macrophages

61
Q

granulation tissue

A

the term that is used for wound healing, provisional tissue that is laid down

  • contains macrophages that release growth factors
  • endothelial cells - angiogenesis
  • fibroblasts to make collagen
62
Q

fibrosis/scar formation

A

macrophages recognize fibrovascular granulation tissue

  • fibroblasts contract to close the wound and synthesize collage to create strength within the scar
  • mature scar has few cells and little vascular support
63
Q

During mid-late wound organization which factors are important?

A

TGFbeta, FGF, PDGF

- stimulate fibroblast proliferation/motility, collagen, fibronectin synthesis

64
Q

healing by first intention

A
  • stitching to bring the wound close together
  • decrease the amount of time for healing
  • decrease the provisional tissues that are necessary
  • pretty good union by two weeks
65
Q

healing by second intention

A
  • although you can bring in new epidermal cells but the tissue underneath may not be so good at replication
  • left with scar that can be seen or may be present under the skin
66
Q

keloid

A
  • production of excess collagen for wound healing
  • excessive scar production
  • keloid overlaps with normal skin
67
Q

What are the key cells in chronic inflammation

A

macrophages and lymphocytes are the key cells

68
Q

When does CT proliferation occur in acute inflammation

A

as inflammation subsides

69
Q

When does CT proliferation occur in chronic inflammation

A

with ongoing inflammation

I3 Exam 1 (12 decks)

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