CH2 - Inflammation, Inflammatory Disorders, and Wound Healing Flashcards Preview

Pathoma > CH2 - Inflammation, Inflammatory Disorders, and Wound Healing > Flashcards

Flashcards in CH2 - Inflammation, Inflammatory Disorders, and Wound Healing Deck (213)
Loading flashcards...
1

What does inflammation allow?

Allows inflammatory cells, plasma proteins (e.g., complement), and fluid to exit blood vessels and enter the interstitial space

2

Inflammation is divided into what?

Divided into acute and chronic inflammation

3

What is inflammation characterized by?

the presence of edema and neutrophils in tissue

4

Inflammation arises in response to what?

infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris)

5

innate immunity

Immediate response with limited specificity

6

What are the mediators of acute inflammation?

Toll-like receptors, Arachidonic acid (AA) metabolites, Mast cells, Complement, Hageman Factor

7

Toll-like receptors

Present on cells of the innate immune system (e.g., macrophages and dendritic cells)

8

How are TLRs attivated?

pathogen-associated molecular patterns (PAMPs) that are commonly shared by microbes, CD14 (a TLR) on macrophages recognizes lipopolysaccharide (a PAMP) on the outer membrane of gram-negative bacteria

9

TLR activation results in what?

upregulation of NF-kB, a nuclear transcription factor

10

What does NF-kB do?

activates immune response genes leading to production of multiple immune mediators

11

TLRs and chronic inflammation?

They are also present on cells of adaptive immunity (e.g., lymphocytes) and play an important role in mediating chronic inflammation.

12

Arachidonic acid (AA) metabolites

1. AA is released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase.

13

Cyclooxygenase

produces prostaglandins (PG) a. PGI2, PGD2 and PGE2 mediate vasodilation and increased vascular permeability. PGE2 also mediates pain.

14

5-lipoxygenase

produces leukotrienes (LT) a. LTB4 attracts and activates neutrophils. b. LTC4, LTD4 and LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, broncho spasm, and increased vascular permeability.

15

Where are Mast cells located?

1. Widely distributed throughout connective tissue

16

How are Mast cells activated?

(1) tissue trauma (2) complement proteins C3a and C5a (3) cross-linking of cell-surface IgE by antigen

17

Mast cells immediate response is?

involves the release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability

18

Mast cells delayed response is?

involves production of arachidonic acid metabolites, particularly leukotrienes.

19

Complement

proinflammatory serum proteins that complement inflammation

20

Where is complement located?

Circulate as inactive precursors;

21

Activation of complement occurs via what?

Classical pathway, Alternative pathway, MBL pathway

22

Classical pathway

C1 binds IgG or IgM that is bound to antigen

23

Alternative pathway

Microbial products directly activate complement.

24

Mannose binding lectin pathway

mannose binding lectin (MBL) pathway MBL binds to mannose on microorganisms and activates complement

25

All pathways of complement result in?

production of C3 convertase (mediates C3?>C3a and C3b, producing C5 convertase (mediates C5?>C5a and C5b)

26

What forms the MAC?

C5b complexes with C6-C9 to form the membrane attack complex (MAC)

27

C3a and C5a

(anaphylatoxins)?trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability

28

C5a

chemotactic for neutrophils

29

C5b

opsonin for phagocytosis

30

MAC

Lyses microbes by creating a hole in the cell membrane