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Flashcards in Inflammation (Week 1) Deck (36):
0

Inflammation involves responses from what systems?

Vascular
Humoral
Neurologic
Cell

1

Inflammation designed to:

Break down and remove dead cells
Inactivate the injurious agent
Initiate healing of tissues

2

Humeral

Chemical components from cellular reactions carried in the blood by plasma and/or tissue fluid

3

Acute inflammation

Lasts hours to a few days
Rapid in onset
Stops when harmful stimulus is removed
Can become chronic if inflammatory stimulus is not removed

4

How can acute inflammation become chronic?

Poor rehab/tx can lead to alteration of joint structure and lead to more inflammation

5

Goal of acute inflammation

Deliver white blood cells and plasma proteins (antibodies) to the area of injury or infection

6

Why is chronic inflammation bad?

Inflammation can damage healthy tissue (leakage of hypochlorite & peroxynitrite)

8

How are WBCs delivered to injury/infection site

1. Vasodilation
2. Increased permeability of capillary walls
3. Chemotaxis

9

How does vasodilation help get WBCs to injury/infection site?

-Allows increased blood flow to area
-Reduces speed at which blood travels
-Sets up hemodynamic change that causes WBCs to collect along endothelium
-Gives WBCs more time to move thru capillary wall, resulting in more WBCs getting to site

9

Chemotaxis

Chemically mediated movement of WBCs
-along chemical gradient
-bacteria: produce peptides that are chemoattractants
-injured tissue: produces compounds (cytokines, IL-8, and leukotriene B4) that attach to WBCs and stimulate their migration

10

Inappropriate or poorly controlled inflammation is thought to contribute to:

Rheumatoid arthritis
Atherosclerosis
Type II diabetes
Some types of cancer
Lung fibrosis
Emphysema
Allergic reactions

11

What to white blood cells do?

Destroy foreign and dead tissues

12

What are Toll-like receptors and where are they found

Detect presence of infection
Found on surface of WBCs

13

What stimulates acute inflammation?

infection
tissue necrosis/injury
foreign bodies
immune reactions

14

What initiates vasodilation

histamine and nitric oxide acting upon vascular smooth muscle

15

How is vascular permeability increased?

histamine (primarily) causes endothelial cells contract, increasing the size of pores

16

how is edema drained from area

lymphatics; results in swelling of lymph nodes

17

what is an indication of infection

red streaks near a wound typically moving proximally; these red streaks will follow the course of lymph vessels

18

what do some WBCs that encounter microbes/dead tissue release?

tumor necrosis factor (TNF)
interleukin-1 (IL-1)
chemokines

19

what do TNF and IL-1 do?

enhance immune response to a microbea

20

what do chemokines do?

attract more WBCs to area

21

what are DMARDs

Disease Modifying Anti-Rheumatic Drugs (drug class)
-Slows, stops, and may reverse immunologic attack on healthy tissue
-2 Classes: biologic & classic

22

how do biologic DMARDs work?

inhibit TNF or some interleukins

23

How do WBCs recognize dead tissue?

receptors on WBCs recognize components released by injured/dead tissue: platelet activating factor, prostaglandins, leukotrienes

24

immune complex

antibody attached to something that does not belong

25

opsonization

signal for the WBCs that the item the antibody is attatched to should be phagocytosed

26

Process of WBC attaching to and phagocytosing object

1. immune complex formed (antibody attached to something that does not belong)
2. immune complex attaches to receptor on WBC
3. attachment activates WBC
4. Phagocytosis occurs
5. chemokines released to attract more WBCs
6. chemotaxis

27

what is the phagocytosed particle exposed to?

hydrogen peroxide + myeloperoxidase (enzyme) --> hypochlorite (active ingredient in bleach)
nitric acid--> peroxynitrite (highly corrosive)

28

2 types of mediators of inflammatory response

cell derived (humeral compounds)
plasma protein derived (from immune system & clotting cascade system)

29

cell derived mediators of inflammatory response

histamine
serotonin
phosphatidyl inositol
arachidonic acid
prostaglandins

30

histamine

released by mast cells when they undergo degranulation
cause vasodilation
cause increased capillary wall permeability

31

serotonin

released from platelets when they aggregate
cause vasodilation
cause increased capillary permeability

32

phosphatidyl inositol

part of every cell membrane
released into tissue fluid
acted upon by phospolipase --> arachidonic acid

33

arachidonic acid

can be converted into prostglandins, leukotrienes, and lipoxins

34

prostaglandins

converted from arachidonic acid by COX enzymes
COX1=good prostaglandins (necessary for normal tissue fxn)
COX2=bad prostaglandins (stimulation of pain, increased dilation and permeability of vessels)
COX3=not fully understood

35

how do steroids reduce inflammation?

inhibit phospholipase (converts phosphatidyl inositol --> arachidonic acid)