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56 Cards in this Set
- Front
- Back
the reaction of vascularized living tissue to local injury is known as________?
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inflammation
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why is inflammation considered a protective process?
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inflammation: neutralizes the cause of injury rids the body of necrotic tissue
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acute inflammation is characterized by ______________ and lasts how long?
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neutrophils, lasts minutes to a few days
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chronic inflammation is characterized by which cell types and lasts how long?
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characterized by macrophages and lymphocytes, lasts days to years
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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. |
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Why is there slowing and stasis in the microvasculature during inflammation?
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because of the increased vascular permeability
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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 |
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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 |
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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 |
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what forms the gaps in the microvasculature?
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CONTRACTION or RETRACTION of endothelial cells
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where do these gaps in microvasculature most commonly occur? (which type of vessel)
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venules
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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 |
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what are the three main cytokines that leak via gaps in the vasculature?
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IL-1
TNF IFN-gamma |
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which cell type can intervene in allergic reactions and can kill parasites?
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eosinophils
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what are the two main functions of macrophages?
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1. phagocytosis
2. synthesis of chemical mediators |
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what is chemotaxis?
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migration along a chemical gradient
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Name 3 endogenous chemotactic agents
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C5a
LTB4 cytokines |
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IgG Fc, C3b and collectins are all examples of?
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opsonins
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what most commonly mediates oxygen dependant degradation?
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ROS (HOCl)
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What are some mechanisms of oxygen independent microbial killing?
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- lysozomes hydrolyzing the coating of bacteria
- lactoferrin - Bacterial perm increasing protein - defensins |
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where is MBP found and what does it do?
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MBP is found in eosinophils
O2 independent mechanism of killing it is cytotoxic to parasites |
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what would be observed in a defect of leukocyte adhesion? (2)
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1. recurrent bacterial infections 2. impaired wound healing
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Chediak-Higashi syndrome is a defect in which leukocyte function?
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defect in phagocytosis (degranulation and killing)
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chronic granulomous disease (CGD) is a result of a defect in which leukocyte function?
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defect in microbiocidal activity
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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. |
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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 |
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what are the three types of mononuclear cells?
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1. macrophages
2. lymphocytes 3. plasma cells |
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what is characteristically seen in chronic inflammation that is attempting to heal?
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damaged tissue (from acute inflammation) is replaced by connective tissue
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chronic granulomatous inflammation is caused by a granuloma. What is a granuloma and what surrounds it?
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a granuloma is a nodular collection of epitheliod cells (specialized macrophages). These epithelial cells are surrounded by lymphocytes.
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what are the two major causes of chronic granulomatous inflammation (general)
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1. T-cell mediated immunity (TB-a delayed hypersensitivity rxn)
2. poorly digestible irritants, foreign body rxn (sutures, sliver) |
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There are six morphologic patterns of inflammation. Describe serous inflammation
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effusion, an outpouring of thin fluid derived from serum
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There are six morphologic patterns of inflammation. Describe fibrinous inflammation
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exudate rich in fibrin organization is seen
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There are six morphologic patterns of inflammation. Describe Suppurative (purulent) inflammation
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mainly neutrophils present lots of necrotic cells edema
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There are six morphologic patterns of inflammation. Describe an ulcer and what produces it.
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a local defect or excavation of the surface of an organ, produced by sloughing of inflammatory necrotic tissue
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There are six morphologic patterns of inflammation. Describe an abscess
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a localized collection of neutrophils with liquified necrotic tissue in the center
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There are six morphologic patterns of inflammation. Describe membranous inflammation
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exudate seen on the surface
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describe non-oxygen dependent bacterial killing by defensins
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defensins are released by PMNs and some lysozomes - they kill tons of things (gram + and - bacteria, fungi, some enveloped viruses)
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describe non-oxygen dependent bacterial killing by lactoferrin
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lactoferrin competes with bacteria for iron (lactoferrin is an iron chelator)
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what is responsible for the Rubor seen in inflammation?
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Rubor=redness: caused by dilation of blood vessels
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what is responsible for the Calor seen in inflammation?
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Calor=heat: caused by increased blood flow to area of injury
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what is responsible for the Dolor seen in inflammation?
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Dolor=pain: caused by:
1. increased pressure (accumulated interstitial fluid) 2. mediators such as bradykinin |
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what is responsible for the Tumor seen in inflammation?
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Tumor=swelling: caused by an extravascular accumulation of fluid
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What are the most important effecter cells of chronic inflammation?
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mononuclear phagocytes and lymphocytes
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how are monocytes/macrophages activated and recruited?
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1) monocytopoeisis, trigered by CSFs
2) vascular transmigration and chemotaxis 3) activation, via gamma interferon, LPS, polynucleotides |
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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 |
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what is the MAC
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c5b - c9 lyses cell started by c5b
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what do activated macrophages release?
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1) lytic enzymes
2) phlogogenic lipid metabolites 3) toxic oxygen metabolites 4) plasma mediators or their activators (complement proteins, etc) |
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Describe granulomatous inflammation
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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"
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What are the 2 ways AA can be metabolized?
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Cyclooxygenase path-->PG and thromboxanes
Lipoxygenase path-->leukotrienes |
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what is granulation tissue
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tissue characterized by small new blood vessels with plump endothelium and active fibroblasts laying down collagen.
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are b lymphocytes involved in chronic inflammation mediation?
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no
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What are the platelet derived mediators?
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1) serotonin (-->inc vasc perm)
2) TxA2 (AA-->cyclooxygenasepath-->SM constriction 3) cationic proteins ( inc. vasc perm up) 4) histamine |
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are multinucleated giant cells found in granulomas
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sometimes, not always
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What are mast cell and basophil derived mediators?
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histamine
leukotrienes (sm contract, vasc perm up) PAF cytokines |
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In addition to sarcoidosis, what can cause granulomatous inflammation?
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fungal infection
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which cytokines are most important in directly causeing the systemic signs of chronic inflammatory disease?
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IL-1 and TNF
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