Path: Inflammation

Front 1

the reaction of vascularized living tissue to local injury is known as________?

Back 1

inflammation

Front 2

why is inflammation considered a protective process?

Back 2

inflammation: neutralizes the cause of injury rids the body of necrotic tissue

Front 3

acute inflammation is characterized by ______________ and lasts how long?

Back 3

neutrophils, lasts minutes to a few days

Front 4

chronic inflammation is characterized by which cell types and lasts how long?

Back 4

characterized by macrophages and lymphocytes, lasts days to years

Front 5

in inflammation what does the following effect have:
1. vasodilation
2. structural changes in microvasculature

Back 5

1. increased blood flow

2. allows plasma cells and leukocytes to leave the capillary.

Front 6

Why is there slowing and stasis in the microvasculature during inflammation?

Back 6

because of the increased vascular permeability

Front 7

1. what is exudate?


2. what does it commonly cause?

Back 7

1. protein rich fluid that leaks out of vascular system during inflammation

2. swelling is often due to exudate

Front 8

1. what is transudate?


2. what are the normal components of transudate?

Back 8

1. fluid with low protein content (this fluid leaks out of vascular system on a regular basis). it is non-inflammatory.


2. transudate consists of mainly H2O and albumin

Front 9

1. define edema


2. define pus

Back 9

1. excess fluid in interstitial tissue or serous cavity (can be transudate or exudate)

2. exudate rich in neutrophils

Front 10

what forms the gaps in the microvasculature?

Back 10

CONTRACTION or RETRACTION of endothelial cells

Front 11

where do these gaps in microvasculature most commonly occur? (which type of vessel)

Back 11

venules

Front 12

1. describe leukocyte dependent injury of the vasculature.


2. what is the timeframe for this injury in regards to inflammation?

Back 12

1. leukocytes have a toxic effect when they adhere to the vascular wall, this damages the vessel.

2. it is a late inflammatory response

Front 13

what are the three main cytokines that leak via gaps in the vasculature?

Back 13

IL-1

TNF

IFN-gamma

Front 14

which cell type can intervene in allergic reactions and can kill parasites?

Back 14

eosinophils

Front 15

what are the two main functions of macrophages?

Back 15

1. phagocytosis

2. synthesis of chemical mediators

Front 16

what is chemotaxis?

Back 16

migration along a chemical gradient

Front 17

Name 3 endogenous chemotactic agents

Back 17

C5a
LTB4
cytokines

Front 18

IgG Fc, C3b and collectins are all examples of?

Back 18

opsonins

Front 19

what most commonly mediates oxygen dependant degradation?

Back 19

ROS (HOCl)

Front 20

What are some mechanisms of oxygen independent microbial killing?

Back 20

- lysozomes hydrolyzing the coating of bacteria
- lactoferrin
- Bacterial perm increasing protein
- defensins

Front 21

where is MBP found and what does it do?

Back 21

MBP is found in eosinophils

O2 independent mechanism of killing

it is cytotoxic to parasites

Front 22

what would be observed in a defect of leukocyte adhesion? (2)

Back 22

1. recurrent bacterial infections 2. impaired wound healing

Front 23

Chediak-Higashi syndrome is a defect in which leukocyte function?

Back 23

defect in phagocytosis (degranulation and killing)

Front 24

chronic granulomous disease (CGD) is a result of a defect in which leukocyte function?

Back 24

defect in microbiocidal activity

Front 25

1. what is "frustrated" or "surface" phagocytosis?



2. why is this important?

Back 25

1. when a leukocyte cannot phagocytose a microbe (most often due to its large size).


2. This can cause additional damage because lysozyme is released into the tissue.

Front 26

give an example of chronic inflammation caused by:

1. organisms producing delayed hypersensitivity
2. prolonged exposure to toxic agents
3. autoimmunity

Back 26

1. TB

2. silica, asbestos

3. SLE, RA

Front 27

what are the three types of mononuclear cells?

Back 27

1. macrophages

2. lymphocytes

3. plasma cells

Front 28

what is characteristically seen in chronic inflammation that is attempting to heal?

Back 28

damaged tissue (from acute inflammation) is replaced by connective tissue

Front 29

chronic granulomatous inflammation is caused by a granuloma. What is a granuloma and what surrounds it?

Back 29

a granuloma is a nodular collection of epitheliod cells (specialized macrophages). These epithelial cells are surrounded by lymphocytes.

Front 30

what are the two major causes of chronic granulomatous inflammation (general)

Back 30

1. T-cell mediated immunity (TB-a delayed hypersensitivity rxn)

2. poorly digestible irritants, foreign body rxn (sutures, sliver)

Front 31

There are six morphologic patterns of inflammation. Describe serous inflammation

Back 31

effusion, an outpouring of thin fluid derived from serum

Front 32

There are six morphologic patterns of inflammation. Describe fibrinous inflammation

Back 32

exudate rich in fibrin organization is seen

Front 33

There are six morphologic patterns of inflammation. Describe Suppurative (purulent) inflammation

Back 33

mainly neutrophils present lots of necrotic cells edema

Front 34

There are six morphologic patterns of inflammation. Describe an ulcer and what produces it.

Back 34

a local defect or excavation of the surface of an organ, produced by sloughing of inflammatory necrotic tissue

Front 35

There are six morphologic patterns of inflammation. Describe an abscess

Back 35

a localized collection of neutrophils with liquified necrotic tissue in the center

Front 36

There are six morphologic patterns of inflammation. Describe membranous inflammation

Back 36

exudate seen on the surface

Front 37

describe non-oxygen dependent bacterial killing by defensins

Back 37

defensins are released by PMNs and some lysozomes - they kill tons of things (gram + and - bacteria, fungi, some enveloped viruses)

Front 38

describe non-oxygen dependent bacterial killing by lactoferrin

Back 38

lactoferrin competes with bacteria for iron (lactoferrin is an iron chelator)

Front 39

what is responsible for the Rubor seen in inflammation?

Back 39

Rubor=redness: caused by dilation of blood vessels

Front 40

what is responsible for the Calor seen in inflammation?

Back 40

Calor=heat: caused by increased blood flow to area of injury

Front 41

what is responsible for the Dolor seen in inflammation?

Back 41

Dolor=pain: caused by:

1. increased pressure (accumulated interstitial fluid)
2. mediators such as bradykinin

Front 42

what is responsible for the Tumor seen in inflammation?

Back 42

Tumor=swelling: caused by an extravascular accumulation of fluid

Front 43

What are the most important effecter cells of chronic inflammation?

Back 43

mononuclear phagocytes and lymphocytes

Front 44

how are monocytes/macrophages activated and recruited?

Back 44

1) monocytopoeisis, trigered by CSFs

2) vascular transmigration and chemotaxis

3) activation, via gamma interferon, LPS, polynucleotides

Front 45

what are cytokines?

Who releases them?

Back 45

= major molecular mediators of chronic inflammation released by

1) mononuclear phagocytes
2) lymphocytes
3) non leukocytes like endothelial cells, fibroblasts

Front 46

what is the MAC

Back 46

c5b - c9 lyses cell started by c5b

Front 47

what do activated macrophages release?

Back 47

1) lytic enzymes
2) phlogogenic lipid metabolites
3) toxic oxygen metabolites 4) plasma mediators or their activators (complement proteins, etc)

Front 48

Describe granulomatous inflammation

Back 48

A special form of chronic inflammation characterized by granulloma formation. Granuloma is a dense accumulation of predominantly mononuclear phogocytes, typically with many showing difenrentiation into "epithelioid cells"

Front 49

What are the 2 ways AA can be metabolized?

Back 49

Cyclooxygenase path-->PG and thromboxanes

Lipoxygenase path-->leukotrienes

Front 50

what is granulation tissue

Back 50

tissue characterized by small new blood vessels with plump endothelium and active fibroblasts laying down collagen.

Front 51

are b lymphocytes involved in chronic inflammation mediation?

Back 51

no

Front 52

What are the platelet derived mediators?

Back 52

1) serotonin (-->inc vasc perm)

2) TxA2 (AA-->cyclooxygenasepath-->SM constriction

3) cationic proteins ( inc. vasc perm up)

4) histamine

Front 53

are multinucleated giant cells found in granulomas

Back 53

sometimes, not always

Front 54

What are mast cell and basophil derived mediators?

Back 54

histamine
leukotrienes (sm contract, vasc perm up)
PAF
cytokines

Front 55

In addition to sarcoidosis, what can cause granulomatous inflammation?

Back 55

fungal infection

Front 56

which cytokines are most important in directly causeing the systemic signs of chronic inflammatory disease?

Back 56

IL-1 and TNF