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56 Cards in this Set

  • Front
  • Back
the reaction of vascularized living tissue to local injury is known as________?
why is inflammation considered a protective process?
inflammation: neutralizes the cause of injury rids the body of necrotic tissue
acute inflammation is characterized by ______________ and lasts how long?
neutrophils, lasts minutes to a few days
chronic inflammation is characterized by which cell types and lasts how long?
characterized by macrophages and lymphocytes, lasts days to years
in inflammation what does the following effect have:
1. vasodilation
2. structural changes in microvasculature
1. increased blood flow

2. allows plasma cells and leukocytes to leave the capillary.
Why is there slowing and stasis in the microvasculature during inflammation?
because of the increased vascular permeability
1. what is exudate?

2. what does it commonly cause?
1. protein rich fluid that leaks out of vascular system during inflammation

2. swelling is often due to exudate
1. what is transudate?

2. what are the normal components of transudate?
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
1. define edema

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

2. exudate rich in neutrophils
what forms the gaps in the microvasculature?
CONTRACTION or RETRACTION of endothelial cells
where do these gaps in microvasculature most commonly occur? (which type of vessel)
1. describe leukocyte dependent injury of the vasculature.

2. what is the timeframe for this injury in regards to inflammation?
1. leukocytes have a toxic effect when they adhere to the vascular wall, this damages the vessel.

2. it is a late inflammatory response
what are the three main cytokines that leak via gaps in the vasculature?


which cell type can intervene in allergic reactions and can kill parasites?
what are the two main functions of macrophages?
1. phagocytosis

2. synthesis of chemical mediators
what is chemotaxis?
migration along a chemical gradient
Name 3 endogenous chemotactic agents
IgG Fc, C3b and collectins are all examples of?
what most commonly mediates oxygen dependant degradation?
What are some mechanisms of oxygen independent microbial killing?
- lysozomes hydrolyzing the coating of bacteria
- lactoferrin
- Bacterial perm increasing protein
- defensins
where is MBP found and what does it do?
MBP is found in eosinophils

O2 independent mechanism of killing

it is cytotoxic to parasites
what would be observed in a defect of leukocyte adhesion? (2)
1. recurrent bacterial infections 2. impaired wound healing
Chediak-Higashi syndrome is a defect in which leukocyte function?
defect in phagocytosis (degranulation and killing)
chronic granulomous disease (CGD) is a result of a defect in which leukocyte function?
defect in microbiocidal activity
1. what is "frustrated" or "surface" phagocytosis?

2. why is this important?
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.
give an example of chronic inflammation caused by:

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

2. silica, asbestos

3. SLE, RA
what are the three types of mononuclear cells?
1. macrophages

2. lymphocytes

3. plasma cells
what is characteristically seen in chronic inflammation that is attempting to heal?
damaged tissue (from acute inflammation) is replaced by connective tissue
chronic granulomatous inflammation is caused by a granuloma. What is a granuloma and what surrounds it?
a granuloma is a nodular collection of epitheliod cells (specialized macrophages). These epithelial cells are surrounded by lymphocytes.
what are the two major causes of chronic granulomatous inflammation (general)
1. T-cell mediated immunity (TB-a delayed hypersensitivity rxn)

2. poorly digestible irritants, foreign body rxn (sutures, sliver)
There are six morphologic patterns of inflammation. Describe serous inflammation
effusion, an outpouring of thin fluid derived from serum
There are six morphologic patterns of inflammation. Describe fibrinous inflammation
exudate rich in fibrin organization is seen
There are six morphologic patterns of inflammation. Describe Suppurative (purulent) inflammation
mainly neutrophils present lots of necrotic cells edema
There are six morphologic patterns of inflammation. Describe an ulcer and what produces it.
a local defect or excavation of the surface of an organ, produced by sloughing of inflammatory necrotic tissue
There are six morphologic patterns of inflammation. Describe an abscess
a localized collection of neutrophils with liquified necrotic tissue in the center
There are six morphologic patterns of inflammation. Describe membranous inflammation
exudate seen on the surface
describe non-oxygen dependent bacterial killing by defensins
defensins are released by PMNs and some lysozomes - they kill tons of things (gram + and - bacteria, fungi, some enveloped viruses)
describe non-oxygen dependent bacterial killing by lactoferrin
lactoferrin competes with bacteria for iron (lactoferrin is an iron chelator)
what is responsible for the Rubor seen in inflammation?
Rubor=redness: caused by dilation of blood vessels
what is responsible for the Calor seen in inflammation?
Calor=heat: caused by increased blood flow to area of injury
what is responsible for the Dolor seen in inflammation?
Dolor=pain: caused by:

1. increased pressure (accumulated interstitial fluid)
2. mediators such as bradykinin
what is responsible for the Tumor seen in inflammation?
Tumor=swelling: caused by an extravascular accumulation of fluid
What are the most important effecter cells of chronic inflammation?
mononuclear phagocytes and lymphocytes
how are monocytes/macrophages activated and recruited?
1) monocytopoeisis, trigered by CSFs

2) vascular transmigration and chemotaxis

3) activation, via gamma interferon, LPS, polynucleotides
what are cytokines?

Who releases them?
= major molecular mediators of chronic inflammation released by

1) mononuclear phagocytes
2) lymphocytes
3) non leukocytes like endothelial cells, fibroblasts
what is the MAC
c5b - c9 lyses cell started by c5b
what do activated macrophages release?
1) lytic enzymes
2) phlogogenic lipid metabolites
3) toxic oxygen metabolites 4) plasma mediators or their activators (complement proteins, etc)
Describe granulomatous inflammation
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"
What are the 2 ways AA can be metabolized?
Cyclooxygenase path-->PG and thromboxanes

Lipoxygenase path-->leukotrienes
what is granulation tissue
tissue characterized by small new blood vessels with plump endothelium and active fibroblasts laying down collagen.
are b lymphocytes involved in chronic inflammation mediation?
What are the platelet derived mediators?
1) serotonin (-->inc vasc perm)

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

3) cationic proteins ( inc. vasc perm up)

4) histamine
are multinucleated giant cells found in granulomas
sometimes, not always
What are mast cell and basophil derived mediators?
leukotrienes (sm contract, vasc perm up)
In addition to sarcoidosis, what can cause granulomatous inflammation?
fungal infection
which cytokines are most important in directly causeing the systemic signs of chronic inflammatory disease?
IL-1 and TNF