Pathoma: inflammation, inflammatory disorders, wound healing Flashcards Preview

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Flashcards in Pathoma: inflammation, inflammatory disorders, wound healing Deck (109)
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1

acute inflammation is characterized by

edema and neutrophils and tissue
arises in response to infection (to elim. pathogen) or tissue necrosis (to clear necrotic debris)
immediate response with limited specificity (innate immunity)

2

Toll-like receptors

present on cells of the innate immune system
activated by PAMPs (pathogen-associated molecular patterns)
activation results in up rgulation of NF-kB -> nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators
also present on cells of adaptive immunity and are involved in mediating chronic inflammation

3

CD14

co-receptor for TLR4 on macrophages recognizes lipopolysaccharide on the outer membrane of G- bacteria

4

Arachidonic acid metabolites

released from phospholipidcell membrane by phospholipase A2 and then acted upon by COX or 5-lipoxygenase

5

COX produces

prostaglandins

PGI2, PGD2, and PGE2 - mediate vasodilation and increase vascular permeability

PGE2 also mediates pain and fever

6

5-lipoxygenase produces

leukotrienes

LTB4 attracts and activates neutrophils

LTC4, LTD4, LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, bronchospasm, and increased vascular permeability

7

Mast Cells

throughout connective tissue
activated by - tissue trauma
- complement proteins C3a and C5a
- cross-linking of cell-surface IgE by antigen

8

Immediate response of Mast Cells

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

9

Delay response of Mast Cells

production of arachidonic acid metabolites - particularly leukotrienes

10

Complement

proinflammatory serum proteins that complement inflammation

11

Activation of complement occurs via 3 pathways

classical
alternative
mannose-binding lectin pathway

12

Classical Complement Pathway

C1 bind IgG or IgM that is bound to antigen

13

Alternative Complement Pathway

microbial products directly activate complement

14

mannose-binding lectin Complement Pathway

MBL binds to mannose on microorganisms and activates complement

15

All complement pathways result in production of

C3 convertase (C3 -> C3a and C3b) -> activates C5 convertase (C5 -> C5a and C5b)
C5b complexes with C6-C9 to form the membrane attack complex

16

C3a and C5a

Anaphalytoxins
trigger mast cell degranulation -> histamine-mediated vasodilation and increased vascular permeability

17

C5a

chemotactic for neutrophils

18

MAC

lyses microbes by creating a hole in the cell membrane

19

Hageman Factor
(Factor XII)

inactive proinflammatory protein produced in the liver
activated upon exposure to subendothelial or tissue collagen

20

Activated Hageman Factor activates

coagulation and fibrinolytic systems
complement
kinin system - kinin cleaves high molecular weight kininogen(HMWK) to bradykinin, which mediates vasodilation and increase vascular permeability as well as pain

21

Cardinal Signs of Inflammation

Redness - rubor
warmth - calor
swelling - tumor
pain - dolor
fever

22

redness - rubor
warmth - calor

due to vasodilation - increased blood flow
occurs via relaxation of arteriolar smooth muscle, key mediator are histamine, prostaglandins, and bradykinin

23

swelling - tumor

leakage of luid from postcapillary venules into the interstitial space (exudate)
key mediators are histamine (causes endothelial cell contraction) and tissue damage (endothelial cell disruption)

24

pain - dolor

bradykinin and PGE2 sensitize sensory nerve endings

25

Fever

pyrogens (LPS from bacteria) cause macrophages to release IL-1 and TNF which increase cyclooxygenase activity in perivascular cells of the hypothalamus

increased PGE2 raises temperature set point

26

Neutrophil Arrival and Function

1) margination
2) rolling
3) adhesion
4) transmigration and chemotaxis
5) phagocytosis
6) destruction of phagocytosed material
7) resolution

27

margination

vasodilation slows blood flow in postcapillary venules
cells marginate from center of flow to the periphery

28

rolling

selectin is upregulated on endothelial cells
P-selectin release from Veibel-Palade bodies mediated by histamine
E-selectin - induced by TNF and IL-1
selectins bind sialyl Lewis X on leukocytes
interaction results in rolling of leukocytes along vessel wall

29

adhesion

ICAM and VCAM are upregulated on endothelium by TNF and IL1
integrins upregulated on leukocytes by C5a and LTB4
interaction creates firm adhesion of leukocytes to vessel wall

30

transmigration and chemotaxis

leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants
neutrophils are attracted by bacterial products, IL8, C5a, and LTB4