Pathology - Lecture 3

Front 1

Transudation

Back 1

escape of non-protein containing fluids from blood vessels

Front 2

Exudation

Back 2

escape of protein rich fluids (plasma) from blood vessels

Front 3

Stagnation

Back 3

slowing of blood flow in blood vessels due to local drop in blood pressure and transudation/exudation

Front 4

Formed elements

Back 4

blood cells; RBCs, WBCs, platelets

Front 5

Axial core

Back 5

central column of rapidly flowing blood in blood vessels

Front 6

Plasmic core

Back 6

cell free zone of plasma b/w the axial core and the endothelial lining of blood vessels

Front 7

opsonins

Back 7

substance such as Abs and antimicrobial binding proteins that enhance phagocytosis

Front 8

Cytokines

Back 8

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

Front 9

Leukocytosis

Back 9

increased numbers of circulation WBCs (> 10,000/mm cubed)

Front 10

Leukopenia

Back 10

decreased numbers of circulating WBCs (< 5,000/mm cubed)

Front 11

shift from L to R

Back 11

increased demand on bone marrow to produce more WBCs, especially neutrophils, results in release of more immature cells (band cells). Shift to L in developmental sequence. Appearance of fewer immature cells and more mature cells indicates recovery and is referred to as shift to R

Front 12

band cells (non-segmented neutrophils)

Back 12

name for immature neutrophils in which the nucuels is not segmented, but appears as a band. If observed in circulation, indicative of shift to L

Front 13

cardinal signs of inflammation

Back 13

1. dubor - redness
2. calor - heat
3. dolor - pain
4. tumor - swelling

Front 14

5th cardinal sign

Back 14

functio laesa - loss of function

Front 15

Local components of acute inflammatory response

Back 15

1. vascular response
2. cellular response
3. hemostatic response
4. acquired (adaptive, specific) immune response

Front 16

Local component - vascular response

Back 16

1. hemodynamic changes - inc. blood flow or hyperemia (redness & heat)
2. permeability changes - inc. vascular permeability occurring mainly in postcapillary venules (swelling & swelling associated pain)

Front 17

local component - cellular response

Back 17

1. cell types
2. adhesion & emigration of inflammatory cells
3. chemotaxis
4. phagocytosis of microorganisms
5. killing of microorganisms
6. digestion of dead microorganisms

Front 18

cell types of local inflammation

Back 18

1. ** PMNs
2. endothelial cells
3. platelets
4. monocytes - macrophages
5. eosinophils
6. mast cells
7. basophils
8. NK cells

Front 19

Adhesion and emigration of inflammatory cells in local component of acute inflamm.

Back 19

neutrophils are 1st WBCs to arrive at site of injury; monocytes and other cells arrive later and undergo similar delivery

Front 20

Delivery of neutrophils and other cells during adhesion and emigration of local component of acute inflamm.

Back 20

1. margination
2. tethering
3. adhesion
4. emigration (diapedesis)

Front 21

margination

Back 21

as rate of blood flow slows in post capillary venules, neutrophils leave axial flow and approach lining of endothelial cells

Front 22

tethering

Back 22

interaction b/w cell surface molecules on neutrophils and those on "Activate" endothelial cells result in partial sticking of cells together in rolling attachments

Front 23

adhesion

Back 23

more substantial attachment subsequently develops that results in a cobble stone pavement like lining of endothelial cells (pavementing)

Front 24

emigration (diapedesis)

Back 24

neutrophils leave venules by ameboid motion b/w endothelial cells to enter the tissue

Front 25

chemotaxis in local component of acute inflamm.

Back 25

once in the tissues WBCs are directed to their targets by chemoattractants that may come directly from target or by other chemotactic molecules produced by infected or damaged cells or by WBCs in the area

Front 26

phagocytosis of microorganisms in local component of acute inflamm.

Back 26

successful phagocytosis requres attachment of a phagocytic cell to its target. Opsonins are substances that provide attachment sites and enhance the process

Front 27

killing of microorganisms in local component of acute inflamm.

Back 27

1. phagocytic cell killing in endocytic vesicle:
a. O2 dependent killing
b. O2 independent killing
2. extracellular (nonphag cell killing)

Front 28

O2 dependent killing

Back 28

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

Front 29

O2 independent killing

Back 29

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

Front 30

Extracellular killing

Back 30

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

Front 31

hemostatic response in local component of acute inflamm.

Back 31

if blood vessels have been disrupted as part of injury, the arrest of bleeding is accomplished by hemostatic response

Front 32

acquired immune response in local component of acute inflamm.

Back 32

contact w/ specific microorganisms either for the 1st time or for the umpteenth time results in an immune response usually directed specifically at those microorganisms

Front 33

Systemic components of acute phase response

Back 33

produce effects at a distance from area of tissue damage.

ex. severe bacterial infection - fever and elevated WBC count

Front 34

Initiation of systemic component of acute phase

Back 34

at site of injury, monocytes and macrophages are stimuated to produce & release several different types of molecules - cytokines, which enter circulation to bind & alter activity of target cells

Front 35

major cytokines acute phase reponse

Back 35

1. interleukin-1
2. interleukin-6
3. tumor necrosis factor (TNF)

Front 36

mechanisms of systemic component of acute phase

Back 36

1. hepatocytes stimulated to release acute phase proteins:
2. hypothalamus stimulated to upregulate the set point for body temperature
3. tissues, mainly muscle and adipose, are stimualted to increase metabolic activity providing heat for the production of fever
4. bone marrow stimulated to produce more WBCs. Normal circulating WBC count ranges from 5,000 - 10,000/mm cubed

Front 37

Acute phase proteins

Back 37

1. antimicrobial binding proteins
2. increased amounts of fibrinogen and other components of clotting system
3. ceruloplasm
4. transferrin
5. various components of complement system

Front 38

antimicrobial binding proteins

Back 38

ex. C-reactive protein (CRP)

Front 39

ceruloplasm

Back 39

scavenges O2 radicals generated by phagocytic cells

Front 40

transferrin

Back 40

binds iron thus reducing amt available to certain iron requiring bacteria

Front 41

exudate of acute inflammation

Back 41

consists of plasma, neutrophils, monocytes/macrophages, fibrin, and dead surrounding tissue but one component often dominates

Front 42

purulent (suppurative) exudate

Back 42

composed largely of neutrophils and dead tissue (pus)

Front 43

serous exudate

Back 43

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

Front 44

fibrinous exudate

Back 44

white membrane covering a lesion in an exudate composed largely of water

Front 45

chronic inflammation

Back 45

inflamm response of prolonged duration lasting for weeks, months, years. causes tissue damage and is accompanied by simultaneous attempts at healing and repair.
-- can be preceded by acute, or can be primary response

Front 46

causes of chronic inflamm. as primary response

Back 46

1. viral infxn
2. persistent microbial infxn (tuberculosis)
3. parasitic or fungal infxn
4. prolonged exposure to toxic substances
-- exogenous material - silicosis & other pneumoconioses
-- endogenous material - lipid components leading to atherosclerosis
5. foreign body
6. autoimmune diseases
7. idiopathic

Front 47

morphology of chronic inflamm.

Back 47

1. cellular inflitrate dominated by mononuclear WBCs (chronic inflammatory cell) consisting of:
-- lymphocytes
-- plasma cells
-- monocytes/macrophages
2. tissue destruction caused by both causative agent and inflammatory response itself
3. attempts at repair of damaged tissue occur simultaneously w/ inflamm response

Front 48

granulomatous inflammation

Back 48

a form of chronic inflamm characterized by presence of granulomas which are nodules formed by a core of epitheloid cells surrounded by a collar of lymphocytes

Front 49

epitheloid cells

Back 49

activated macrophages that become enlarged and flattened resembling epithelial cells

Front 50

Langhans cells

Back 50

giant cells with a horseshoe pattern of nuclei and are typical of tubercular granulomas. In foreign body giant cells that nuclei are scattered throughout the cell

Front 51

examples of granulomatous inflamm

Back 51

causes from infections and infestations
a. bacterial infxns
1. tuberculosis
2. leprosy
3. syphilitic gummas
4. cat scratch disease
b. fungal infxns
1. histoplasmosis
2. blastomycosis
3. etc.
c. parasitic infestations
1. schistosomiasis
2. etc.

Front 52

examples of non-infectious causes incude

Back 52

a. foreign bodies - suture material, talc, bone and tooth fragments, splinters, etc
b. sarcoidosis
c. Crohn's disease