A&p Lec20 Acute Inflammation: Mediators And Morphologic Features

Front 1

What are some chemical mediators of inflammation?

Back 1

vasoactive amines, plasma proteases, arachidonic acid metabolites, platelet activating factor, cytokines and chemokines, nitric oxide, lysosomal contents, oxygen derived free radicals, neuropeptides.

Front 2

What are 2 vasoactive amines?

Back 2

-histamine

-serotonin

Front 3

What causes the release of vasoactive amines?

Back 3

-physical injury

-immune reaction

-anaphylatoxins C3a and C5a

-etc

Front 4

What are the sources of vasoactive amines?

Back 4

-mast cells - histamines

-platelets - histamine and serotonin

Front 5

What effects do vasoactive amines have in an inflammatory response?

Back 5

-vasodilation

-increased vascular permeability

-endothelial activation (histamine)

Front 6

Where are mast cells located?

Back 6

in loose connective tissue near blood vessels in the skin, in the lining of the GI tract and airways

Front 7

What are 4 groups of plasma proteases (cascade system)?

Back 7

-complement system - activated by plasmin

-Kinin system - bradykinin - associated w/ pain
---activated by Hageman factor

-clotting system - activated by Hageman factor

-Fibrinolytic system

Front 8

What does the plasma protease Complement system comprise of?

Back 8

C3a & C5a recruit leukocytes to destroy microbe

MAC (membrane attack complex) - lysis of microbe

C3b - bacteria has receptor for C3b and it allows it to be phagocyzed.

Front 9

What does the plasma protease Clotting system comprise of?

Back 9

-Activated by Hageman factor (Factor XII) which is activated by collagen and basement membrane

-Fibrin released (can leak into tissue w/ inflammation)

Front 10

What does the plasma protease Fibrinolytic system comprise of?

Back 10

Fibrin degradation products

Front 11

What are the pathways of the plasma protease cascade?

Back 11

Factor XII (Hagemen's) activates Factor XIIa which activates both the clotting and kinin cascades. Following the clotting cascade acivates Fibrin. Following the Kinin cascade activates Bradykinin and moves into the Fibrinolytic System. The Fibrinolytic system activates Plasmin which degrades Fibrin and also activates the complement cascade - C3a

Front 12

What is an Arachidonic acid?

Back 12

20 carbon fatty acid w/ double bonds at C5, 8, 11, 14 (eicosatetraenoic acid)

Front 13

What are the 2 main pathways of Arachidonic acid in inflammation?

Back 13

-Cyclooxygenase produces prostaglandins

-5 lipoxygenases produces leukotrienes

Front 14

What drugs block which pathays of Arachidonic acid?

Back 14

Corticosteroids block AA acid release from membranes - blocks both pathways (cyclooxygenase and lipoxygenase)

ASA and NSAIDs inhibit just cyclooygenase

Front 15

In Arachidonic acid metabolites, what does cyclooxygenase eventually do by producing portaglandins?

Back 15

-PGE2 - vasodilation, potentiate edema

-PGI2 - vasodilation, inhibits platelet aggregation

-TXA2 - vasoconstriction, promotes platelet aggregation

Front 16

In Arachidonic acid metabolites, what does lipoxygenase eventually do by producing leukotrienes?

Back 16

- 5-HETE & LTB4 - chemotaxis

-LTC4, LTD4, & LTE4 - vasoconstriction, bronchospasm, increased permeability

-LXA4 & LXB4 - vasodilation, inhibit neutrophil chemotaxis, stimulate monocyte adhesion

Front 17

What are the 3 isoforms of nitric oxide sythase and where are they located?

Back 17

-eNOS - endothelial cells - this one reduces platelet adhesion

-nNOS - neural tissue

-iNOS - (inducible) in macrophages

Front 18

What are some characteristics of Nitrous Oxide?

Back 18

-short half-life ensures local action

-NO is a potent vasodilator and helps kills microorganisms

-NO stored and can act quickly unlike prosteglandins and leukatrins which are made on demand

Front 19

What are Tachykinins?

Back 19

rapidly acting neuropeptides
-substance P
-Neurokinin A

Front 20

What are the sources of Tachykinins (neuropeptides)?

Back 20

nerve fibers esp in GI tract and lungs

Front 21

What are the actions of Tachykinins (neuropeptides)?

Back 21

-Vasodilation

-Increased vascular permeability

-Pain - rapidly induce gut tissue contraction

(You get an amplified effect when all these actions act together)

Front 22

What 3 pathways can lead to opsinization with C3b, release of C3a, and formation of MAC?

Back 22

-Alternative pathway (by C3b binding to microbe)

-Lectin pathway (via C3b binding to mannose-binding lectin on microbe)

-Classical pathway (via C3b binding to antibody on microbe)

Front 23

What are the mophologic patterns of edema in inflammation?

Back 23

-may be transient

-may have secondary waves

-protein concentration can vary
---if the protein [ ] is low, it will not stain well on H&E. Cells appear separated and more spread out than in usual sections

Front 24

What is serous inflammation?

Back 24

out pouring of thin fluid into tissue or bady cavity

-low protein concentration-transudate

Front 25

What is an example of serous inflammation and the causes and manifestation?

Back 25

Blister in skin

-fluid accumulates w/in epidermis or between epidermis and dermis

-Causes - mechanical trauma, burn, viral infection

-when Viral infection is cause, the fluid filled space is called a VESSICLE

Front 26

What is fibrinous inflammation?

Back 26

Fibrin is deposited - appears as an eosinophilic meshwork

-due to greater vascular permeability than that producing serous inflammation
---larger molecules including fibrinogen leak from vessel

Front 27

What is the precoagulant stimulus in fibrinous inflammation?

Back 27

Tissue factor, collogen, etc. - start clotting cascade

-Fibrinogen is cleaved by thrombin to form Fibrin

Front 28

Where is Fibrinous inflammation seen and what is the end result?

Back 28

Seen in body cavaties - pleural, peritoneal, and pericardial sac

Fibinolysis - resolves

Scar - organizes

Front 29

What is suppurative inflammation?

Back 29

Suppurative = purulent
-production of pus (purulent exudate)

Front 30

What causes suppurative inflammation and what does the pus consist of?

Back 30

Pyogenic bacteria are most common - staphs and strepts

-neutrophils, edema fluid (exudate), necrotic cells
---acute appendicitis

Front 31

What is an abcess?

Back 31

a focal collection of purulent inflammatory tissue.

Front 32

What are the characteristics of an abcess?

Back 32

-confined space

-central region contains necrotic tissue, exudates, and leukocytes

-surrounded by a zone of neutrophils

-outermost zone of vascular dilation and fibroblastic proliferation

Front 33

What is an ulcer?

Back 33

a local defect or excavation of the surface of an organ or tissue (epithelium)

Front 34

What causes an ulcer?

Back 34

due to sloughing of inflammatory necrotic tissue:

-Mucosa (mouth, stomach, urinary tract)

-Skin (pressure or circulatory disturbance)

-Intense neutrophilic infiltrate

(Can become chronic)

Front 35

What is cellulitis?

Back 35

a diffuse acute inflammation that spreads along fascial planes

Front 36

What is lymphangitis?

Back 36

inflamed lymphatics

-lymphatics are endothelial lined, thin walled channels that help return tissue fluid to the systemic circulation

Front 37

What is lymphadenitis?

Back 37

inflamed lymph node

Front 38

What is bacteremia?

Back 38

bacteria circulating in the blood

Front 39

What is Hematogenous infectction?

Back 39

occurs when circulating bacteria (bacteremia) seeds other organs

Front 40

What is Septicemia?

Back 40

systemic disease associated w/ the presence and persistence of pathogenic microorganisms or their toxins in the blood

Front 41

Back 41