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Flashcards in inflammation Deck (62):
1

what are the clinical signs and symptoms of inflammation?

-redness
-swelling
-heat
-pain

2

how does vascularity change during acute inflammation?

- vasodilation

- increased vascular permeability

3

what do the changes in vascularity (during ACUTE inflammation) cause?

promote:
fluid (edema) and inflammatory cell accumulation
in the tissue

4

vasodilation results in the relaxation of ________ arterioles

pre-capillary

5

what is vasodilation mediated by during acute inflammation/

Mediated by:
- NO
- PGs
- Histamine

6

what is transudate?

Low protein content, low specific gravity fluid

7

when is non-inflammatory transudate present? what about inflammatory transudate?

Non-inflammatory - intact endothelium

Inflammatory – early endothelial contraction

8

what is exudate?

High protein content, high specific gravity fluid

9

what are the types of exudate? (theres 3 types)

Fibrinous – high protein, few cells

Purulent – high protein, many cells

Sanguineous – high protein, blood

10

T/F: the occurrence of transudate fluid is a result of fluid and protein leakage

FALSE- thats exudate

transudate is just fluid leakage

11

___________ contractions lead to an immediate increase in permeability

endothelial contractions

12

____________ is a delayed response (develops 4-6 hours after injury) and causes further vascular permeability

endothelial retraction

13

what mediates endothelial contraction?

PAF, histamine, bradykinin, leukotrienes

14

what mediates endothelial cell retraction following DIRECT endothelial injury?

IL-1, TNF, IFN-gamma

15

_________ is mediated by the injurious agent, or by ROS/enzymes from NEUTROPHILS

direct endothelial injury

16

what substances are secreted by injured cells to increase the pain perception during inflammation?

Bradykinin

PGE2

17

the fever ("heat") associated with inflammation is associated with what cellular molecules?

IL-1

TNF

PGE2

18

what changes are seen in activated endothelial cells during inflammation? (4 changes)

1) Produce PGI2 and NO (vasodilation)

2) Contraction / retraction

3) Increase expression of adhesion molecules

4) Increase synthesis of mediators

19

what molecules facilitate leukocyte Adhesion?

- integrins

1) ICAM
2) VCAM

20

Emigration or transmigration of leukocytes is mediated by ___________

PECAM

21

__________ is the movement along a concentration gradient of chemotactic factors

chemotaxis

22

the _________ of leukocytes is driven by physical forces (stasis)

margination

23

list the chemotactic factors involved in PMN recruitment

1) PAF (potent)
2) LTB4 (potent)
3) Chemokines
4) Bacterial lipids and peptides
5) C5a
6) Fibrin degradation products

24

what molecules will mediate attachment during phagocytosis?

opsonins on target cells: IgG, C3b, collectins

these interact with Fc receptors on neutrophil

25

how does lysosomal degradation occur?

by fusion of engulfed target with the phagosome

26

what substances are released by the phagocyte during "oxygen bursts"

superoxide, hydrogen peroxide, hypochlorous radical

27

__________ is an enzyme active in the creation of HOCl (hypochlorous radical)

Myeloperoxidase

28

the presence of _________ defines acute inflammation

neutrophils

29

neutrophils begin to accumulate at the site of injury within ______ hours

6-24

30

neutrophils infiltrate tissue in response to tissue ________

necrosis

31

how do neutrophils react once they reach the site of injury? (hint: they can do 2 things)

- Undergo apoptosis after phagocytosis and digestion.

- Release reactive oxygen species and lysosomal enzymes

32

________ cells replace PMNs, usually beginning within 48 hours

Monocytes (macrophages and histiocytes)

33

T/F: the half-life of neutrophils is much longer than monocytes

FALSE

monocytes can last for months, while PMN's last only days

34

what are the functions of monocytes? (theres a shit-ton of them)

Phagocytosis
Antigen presentation
Cytokines
Enzymes
Plasma proteins
MPO - ROS
NO, Prostaglandins
Factors of healing and
repair

35

what are some "other" cell types (besides PMN's and monocytes) that are involved in injury/inflammation? what role do they play?

a) Lymphocytes, plasma cells

b) Eosinophils (allergic reactions, parasitic infections)

c) Mast cells – surface IgE (release histamine)

36

a ______ is characterized by diffuse, permeative infiltration of neutrophils with edema

cellulitis

37

a ______ is characterized by localized area of liquefactive necrosis

abscess

38

a ______ is characterized by an erosion of an epithelial surface exposing underlying connective tissue

ulcer

39

how does the length of time for chronic vs. acute inflammation differ?

acute inflammation: 10-14 days

vs.

chronic: months to years

40

_______ inflammation is innate whereas ______ inflammation relies upon specific, adaptive immune system

acute, chronic

41

T/F: although both acute and chronic inflammation can be reversible, only acute inflammation can be fatal

false- BOTH can be reversible and fatal

42

causes for chronic inflammation include:

1. Persistent infections
2. Prolonged exposure to a toxic agent
3. Immune-mediated inflammatory disease

43

______________ inflammation is often associated with tissue repair that induces fibrosis.

non-specific chronic inflammation

44

Granulomatous Inflammation is linked to what condition?

Linked to the delayed-type IV hypersensitivity immune reaction

45

what 4 cell types are associated with chronic inflammation?

1) lymphocytes
2) macrophages
3) plasma cells
4) eosinophils

46

Epithelioid (activated) histiocytes are often present in what form of inflammation?

Granulomatous Inflammation

47

during a granulomatous inflammatory event, ____________ coalesce to form multinucleated giant cells Langhans or foreign body type).

Epithelioid histiocytes

48

how does a site with granulomatous inflammation (a granuloma) heal?

by fibrosis

49

Older granulomas develop a rim of _________ and _______

fibroblasts and connective tissue

50

what bacterial infections are characterized by granuloma formation?

tuberculosis, cat-scratch fever

51

what types of fungal infections lead to granulomas?

coccidioidomycosis, histoplasmosis

52

sarcoidosis, Crohn’s disease are both characterized by ________ inflammation

Granulomatous

53

_________ is released by physical injury, or antigen binding to IgE, C3a and C5a, cytokines.

Histamine

54

cyclo-oxygenase and lipo-oxygenase are important enzymes in the formation of what mediators?

Prostaglandins (cyclo) and leukotrienes (lipo)

55

While prostaglandins generally cause vasodilation, ______________ causes vasoconstriction

thromboxane A2

56

thromboxane A2 promotes platelet aggregation, while ____________ inhibits platelet aggregation

prostacyclin

57

what cell types are "labile" (continuously dividing)?

hematopoietic cells, surface epithelium

58

parenchymal cells, smooth muscle cells, and fibroblasts are all considered ________ in respect to their proliferation rate

stable

59

what types of cells are "permanent", meaning they do not proliferate?

neurons, cardiac muscle

60

what is the primary cause of delayed healing?

infection

61

healing by ___________ is characterized by more inflammation and granuloma tissue formation

healing by secondary intention

62

what causes the wound contraction during healing by a secondary intention?

Wound contraction due to myofibroblasts