Path: Inflammation

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the reaction of vascularized living tissue to local injury is known as________?: inflammation
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): venules
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?: IL-1

TNF

IFN-gamma
which cell type can intervene in allergic reactions and can kill parasites?: eosinophils
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: C5a
LTB4
cytokines
IgG Fc, C3b and collectins are all examples of?: opsonins
what most commonly mediates oxygen dependant degradation?: ROS (HOCl)
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?: no
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?: histamine
leukotrienes (sm contract, vasc perm up)
PAF
cytokines
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

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