Acute And Chronic Inflammation

Front 1

inflammation which is not immunotspecific and involves Neutrophils primarily

Back 1

acute inflammation -

characterized by exudate - pus

Front 2

what three cells are involved extensively in chronic inflammation which is immunotspecific

Back 2

lymphocytes, plasma cells, macrophges

Front 3

3 major evenst occuring in acute inflammation

Back 3

Hemodynamic change
increased vascular permiabiilty
extravasation fo leukocytes

Front 4

vessel changes in acute inflammation

Back 4

increased blood flow to area of injury (redness)
vascular permeability (swelling)

Front 5

"mopping up" in acute inflammation is primarily done by

Back 5

PMNs, some macrophages

Front 6

hemoconcentration

Back 6

slowed flow near injury - so more conc of cells in vascular space which increases the chances that they will interact with EC

Front 7

5 mechanisms of edema formation

Back 7

1. increased hydrostatic
2. decreased blood oncotic
3. endothelial damage
4. dcreased lymphatic damage
5. Na+ retention by the kidnes

Front 8

what is the differene between transudate and exudate

Back 8

exudate is turbid and viscous (like pus)- it has many cells in it

Transudate is watery with few cells

NOTE: they both have the same spec. Grav, and protein content

Front 9

4 families of adhesion moleculees

Back 9

1. selectins
2. Immunoglobulin Superfamily (ICAM, VCAM)
3. Integrins
4. Glycoprotiens (bind selectins)

Front 10

P Selectins bind

Back 10

platelets and endothelium
(PSGL-1)

Front 11

E selectins bind

Back 11

Endothelium (ESL-1 glycoprotein)

Front 12

L selectins

Back 12

bind Leukocytes

(CD34, glycam1)

Front 13

selectins bind

Back 13

glycoproteisn

Front 14

Ig superfamily bind

Back 14

integrins

ICAM-1 binds LFA-1, MAC-1

VCAM-1 binds a4B1 and 7

Front 15

in the immunoglobulin gene superfamily and important for self aggregation and diapedesis

Back 15

PECAM-1 binds CD31 on endthelial cells

Front 16

exogenous chemoattractants

Back 16

target derived

e.g bacterial lipids

Front 17

endogenous chemoattractants

Back 17

(host derived)

e.g chemokines (e.g C5a, LTB4, IL-8)

Front 18

collectins are opsonins that bind what kind of leukocyte receptor

Back 18

C1q

Front 19

the C3b opsonin binds what on leukocyte

Back 19

CR!, CR2, CR3 (Mac-1)

Front 20

a bulla is what kind of inflammation

Back 20

serous inflammation

Front 21

pericarditis is what kind of inflammation

Back 21

fibrinous

Front 22

an abscess is what kind of inflammation

Back 22

suppurative

Front 23

Hashimotos Thyroiditis and multiple sclerosis results in what kind of inflammation

Back 23

chronic

Front 24

three cells seen in Granuloma (dont count giant cells which are often, but not always present)

Back 24

T cells, plasma cells, epitheloid histiocytes

Front 25

four outcomes of inflammation

Back 25

1. resolution
2. abscess formation
3. fibrosis (scar)
4. chronic inflammation

Front 26

the two meanings of "chronic" - we use them both!

Back 26

1. histpathological: lymphocytes, plasma cells, macrophages,
2. temporal: stays around for a long time

NOTE: any process of acute inflammation (w/PMNs) can become "temporally chornic" if it fails to resolve but this does not necessarily mean that it is histopathologically chronic (e.g staph aureus in AIDs patient) - slide 40

Front 27

fistula

Back 27

an abnormal connection or passageway between organs or vessels that normally do not connect.