Pathology Chapter 2

Front 1

Acute inflammation

Back 1

Edema,neutrophils in tissue.

Eliminate pathogen ,clear necrotic debris.

Innate immunity.

Front 2

Mediators of acute inflammation

Back 2

Toll like receptors, Arachnid acid metabolites, Mast cells, Complement, Hageman factor

Front 3

TLRs present on

Back 3

Cells of innate immunity ie macrophages,denritic cells....

Front 4

TLRs activated by

Back 4

PAMPs: pathogen associated molecular patterns

CD14( Co receptor of TLR4) on macrophage recognizes lipopolysaccharide (PAMP) on outer membrane of gram negative bacteria

Front 5

TLR activation leads to upregulation of

Back 5

NF-ķB (nuclear transcription factor that leads to activates immune response genes leading to production of many immune mediators)

Front 6

AA metabolites source

Back 6

Released from phospholipid cell membrane by phospholipaseA2 acted upon by Cyclooxygenase or 5-lipoxygenase

Front 7

Prostaglandins produced by

Back 7

Cyclooxygenase pathway

Front 8

Leukotrienes produced by

Back 8

5-lipoxygenase pathway

Front 9

Vasodilation and vascular permeability mediators

Back 9

PGI2 , PGD2 ,PGE2, Histamine, Bradykinin

Front 10

Pain and fever mediator

Back 10

PGE2

Front 11

LTC4 ,LTD4, LTE4

Back 11

Vasoconstriction, bronchospasm, increased vascular permeability ( slow reacting substances of anaphylaxis (

Front 12

LTB4

Back 12

Attracts and activates neutrophils

Front 13

Mast cell activation

Back 13

Tissue trauma, C3a or C5a , IgE

Front 14

Mast cell activation responses

Back 14

Immediate response~ release of histamines

Delayed response~ AA metabolites mainly leukotriens

Front 15

Complement activation pathways

Back 15

1. Classical pathway: C1 binds IgG or IgM that is bound to antigen.

2.Alternative pathway: microbial products directly activates complement.

3.Mannose-binding lectin pathway (MBL): MBL binds to mannose on microbes and activate complement

All pathways result in formation of C3 convertase

Front 16

C3 convertase

Back 16

It converts C3 to C3a and C3b which produces C5 convertase,,C5 convertase: C5 into C5a and C5b,,C5b complexes with C6-9 and form MAC

Front 17

MAC

Back 17

Membrane Attack Complex (C5bC6-9)

Lyses microbes by creating a hole in the cell membrane

Front 18

Anaphylotoxins C5a and C3a

Back 18

Mast cell degranulation= release of histamines= vasodilation, increased vascular permeability

Front 19

C5a

Back 19

Chemotactic for neutrophils

Front 20

C3b

Back 20

Opsonin for phagocytosis

Front 21

Hageman factor(Factor 12) activated by ____________ and it activates ___________

Back 21

Activated by exposure to sub endothelial or tissue collagen.

It activates: 1. Coagulation and fibrinolytic systems

2.complement

3.kinin system

Front 22

Bradykinin

Back 22

Vasodilation, increased vascular permeability, pain

Front 23

Cardinal signs of inflammation

Back 23

Redness(rubor) ,heat(calor) ,swelling (tumor) , pain (dolor) , fever

Front 24

Redness and heat

Back 24

Due to vasodilation =increased blood flow by relaxation of arteriole smooth muscle ~~Histamine prostaglandin and bradykinin

Front 25

Swelling

Back 25

Due to leakage of fluid from post capillary venues into interstitial space (exudate) ~~ Histamine (endothelial cell contraction and tissue damage = endothelial cell disruption)

Front 26

Pain

Back 26

Bradykinin, PGE2 ( sensitive sensory nerve endings)

Front 27

Fever

Back 27

IL-1 , TNF ( produced by macrophages in response to pyrogens like LPS from bacteria) , Increased PGE2 (raise temperature set point)