Inflammation: Presentations, Players, Process Flashcards Preview

IMSK Exam 2 > Inflammation: Presentations, Players, Process > Flashcards

Flashcards in Inflammation: Presentations, Players, Process Deck (37):
1

What are the goals of inflammation?

Respond to injurious insult
Remove problem or injured cells
Restore/repair injured tissues

2

What are the six initiators or stimulators of inflammation?

Infections
Trauma
Physical or chemical agents
Tissue necrosis
Foreign bodies
Hypersensitivity immune reactions

3

Which inflammation stimulators release inflammasomes?

Trauma
Physical or chemical agents
Tissue necrosis
Foreign bodies

4

What are the five signs of inflammation?

Heat
Redness
Swelling
Pain
Loss of function (chronic)

5

What is the sequence of events in inflammation?

Recognition
Chemical mediator release
Vascular permeability
Migration and activation of cells
Termination/resolution

6

What does vasodilation cause?

Heat and redness

7

What vascular changes occur in altered hemodynamics?

Brief constriction then vasodilation from histamine

8

What happens to vascular structure in inflammation?

Endothelial cells contract increasing the space between them

9

What causes redness at the site of inflammation?

Hemoconcentration due to loss of blood plasma leaving RBCs in circulation

10

What is exudate?

Fluid leaked contains protein and cells (inflammation)

11

What is transudate?

Not a lot of protein or cells are in the fluid leaked (non inflammatory)

12

Is exudate or transudate due to inflammation?

Exudate

13

What is effusion?

Excess fluid in cavities

14

What does serous mean?

Yellow, straw-like color, few cells

15

What does serosanguinous mean?

RBCs present, red tinge

16

What does fibrinous mean?

Large amounts of fibrin present due to activation of coagulation cascade

17

What does purulent mean?

Large number of polymorphonucleocytes (neutrophils) present

18

What are endogenous chemicals?

Chemicals that activate and amplify the inflammation process

19

What are the three types of endogenous chemicals?

Plasma-derived
Cell-derived
Extracellular matrix

20

What are the three functions of the complement system?

Phagocytosis/Destruction
Vascular inflammatory effects
Cellular inflammatory effects

21

What are cell derived chemical mediators of inflammation?

Vasoactive amines
Arachidonic acid metabolites
Platelet activating factor
Lysosomal molecules
Cytokines
Chemokines
Nitric oxide
Interferon
ROS
Neuropeptides

22

What do lipoxins do?

Suppress inflammation by inhibiting WBC recruitment

23

What does alpha-1-antitrypsin do?

Inhibits neutrophil elastase

24

What happens if alpha-1-antitrypsin isn't present?

Neutrophil elastase destroys the elastin leading to emphysema

25

What are the steps in WBC extravasation?

Margination (hemodynamics; slowing of blood movement)
Rolling (selectins)
Adhesion to endothelium (integrins)
WBC migration

26

What cells play a major role in acute inflammation?

Neutrophils

27

What cells play a major role in chronic inflammation?

Lymphocytes
Macrophages
Plasma cells
Fibroblasts (prominent fibrosis)

28

What are the outcomes of inflammation?

Resolution
Healing by fibrosis
Ongoing chronic inflammation

29

What are the causes of chronic inflammation?

Persistent infection or injurious stimulus
Prolonged exposure to injurious stimulus
Autoimmunity

30

What are histiocytes?

Longstanding resident macrophages in tissue (typical cause chronic inflammation)

31

What occurs in granulomatous inflammation?

Macrophages form a syncytium multinucleated giant cell

32

When do caseating granulomas form?

In necrosis

33

What occurs in TB?

Caseating granulomatous inflammation

34

What occurs in sarcoidosis?

Noncaseating granulomas

35

What are the systemic effects of inflammation?

Fever
Elevated plasma acute phase reactants
Complete blood count: Elevated WBCs, increased PMN (granulocytosis bacterial), increased lymphs (lymphocytosis viral)

36

What is ESR?

Erythrocyte sedimentation rate

37

What is the basis for the Rouleaux test?

Increased plasma proteins causes a decrease of charge on RBC membranes causing RBCs to stack higher and faster