Pathology Lecture 3: Overview Of Inflammation

Front 1

What are the main purposes of inflammation?

Back 1

kill, remove, or sequester agents of injury and to allow the host to adapt and ultimately restore normal function

Front 2

Transduation

Back 2

escape of non-protein containing fluids from blood vessels

Front 3

Exudation

Back 3

escape of protein rich fluids (plasma) from blood vessels

Front 4

Plasma zone

Back 4

cell free zone of plasma between the axial core and the endothelial lining of blood vessels

Front 5

Opsonins

Back 5

substances such as Abs and antimicrobial binding proteins that enhance phagocytosis

Front 6

Cytokines

Back 6

substances secreted by WBCs that influence events in inflammation and the immune response

Front 7

Leukocytosis

Back 7

increased numbers of circulating WBCs (greater than 10,000 mm3)

Front 8

Leukopenia

Back 8

decreased numbers of circulating WBCs (less than 5,000 mm3)

Front 9

Shift to the left in the developmental sequence

Back 9

increased demand on the bone marrow to produce more WBCs especially neutrophils results in the release of more immature cells (band cells)

Front 10

Shift to the right in the developmental sequence

Back 10

the appearance of fewer immature cells and more mature cells which indicates recovery

Front 11

What are the 4 cardinal signs of inflammation?

Back 11

1. Rubor
2. Calor
3. Dolor
4. Tumor

Front 12

5th sign that is sometimes added?

Back 12

Functio laesa --> loss of function

Front 13

What are the vascular responses of acute inflammatory response?

Back 13

1. Hemodynamic changes

2. Permeability changes (increased vascular permeability occuring mainly in the postcapillary venules)

Front 14

What are the cells involved in the acute inflammation process?

Back 14

-polymorphonuclear neutrophil (indicator cell)

-MNM BEEP:
monocytes, NK cells, mast cells, basophils, endo cells, eosinophils, platelets

Front 15

Margination

Back 15

as the rate of blood flow slows in the post cap venules, neutrophils leave the axial flow and approach the lining endo cells

Front 16

Tethering

Back 16

interaction btwn cell surface molecules on the neutrophils and those on "activated" endo cells resulting in a partial sticking of the cells, a rolling attachment

Front 17

Adhesion

Back 17

a more substantial attachment that subsequently develops

results in a cobble stone pavement like lining of the endo cells (pavementing)

Front 18

Emigration (diapedesis)

Back 18

neutrophils leave the venules by ameboid motion btwn the endo cells to enter the tissues

Front 19

Phagocytic cell killing in endocytic vessicle: Oxygen dependent killing

Back 19

a respiratory burst of activity results in the production of O2 derived toxic radicals that kill most bacteria and fungi

Front 20

Phagocytic cell killing in endocytic vessicle: Oxygen independent killing

Back 20

involves the release of the contents of granules that contain a number of antibacterial agents

Front 21

Extracellular (nonphagocytic cell killing)

Back 21

in response to certain PAMPs and cytokines, neutrophils release fibrous nets (NETS) that bind trap and kill microorganisms

Front 22

Initiation

Back 22

1. site of injury, monocytes and macros produce and release cytokines, enter circulation and bind to and alter the activity of target cells and tissues

Front 23

What are the major cytokines involved in the acute phase response?

Back 23

1. Interleukin-1 (IL-1)

2. Interleukin - 6 (IL-6)

3. TNF

Front 24

What are the acute phase proteins that hepatocytes synthesize and release?

Back 24

1. Antimicrobial binding proteins
2. Fribrogen and other components of the clotting system
3. Ceruloplasm
4. Transferrin
5. various components of C

Front 25

Ceruloplasm

Back 25

scavenges oxygen radicals generated by phagocytic cells

Front 26

Exudates of acute inflammation

Back 26

-substances appearing at site of injury

-basically consists of plasma, neutrophils, monocytes, macrophages, fibrin, and dead surrounding tissue

Front 27

Purulent (suppurative) exudate

Back 27

-an exudate composed largely of neutrophils and dead tissue (pus)

Front 28

Serous exudate

Back 28

watery exudate consisting largely of plasma accumulates in areas of injury such as burns and in blisters

Front 29

Fibrinous exudate

Back 29

white membrane covering a lesion is an exudate composed largely of fibrin

Front 30

What are causes of chronic inflammation as a primary response?

Back 30

1. Viral infx
2. persistent microbial infx
3. Parasitic or fungal infx
4. prolong exposure to toxic substances
5. foreign body
6. autoimmune diseases
7. idiopathic

Front 31

General features of chronic inflammation

Back 31

1. cellular infiltrate dominated by mononuclear WBCs
2. Tissue destruction
3. Attempts at repair of damaged tissue occur simultaneously w/ the inflammatory process

Front 32

What are the 3 mononuclear WBCs or chronic inflammatory cells in chronic inflammation?

Back 32

1. Lymphocytes
2. Plasma cells
3. Monocytes/macros

Front 33

Langhan cells

Back 33

giant cells w/ a horseshoe patern of nuclei and are typical of tubercular granulomas

Front 34

Foreign body giant cells

Back 34

the nuclei are scattered throughout the cell

Front 35

Examples of noninfectious causes of chronic inflammation

Back 35

1. Foreign bodies (sutures, bone/tooth fragments)
2. Sarcoidosis
3. Crohn's disease