Term
| what is the main component in the KININ SYSTEM? affects? |
|
Definition
| bradykinin --> increased vascular permeability and pain |
|
|
Term
| what do C5A (complement 5A) and LTB4 (leukotriene B4) have in common? |
|
Definition
| most potent CHEMOTACTIC FACTORS |
|
|
Term
| what is CHRONIC INFLAMMATION? |
|
Definition
| Inflammation which persists for prolonged periods of time and lasts for weeks, months or years and has LITTLE FLUID COMPONENT |
|
|
Term
| how does inflammation evolve form ACCUTE to CHRONIC? |
|
Definition
-persistence of the inflammatory stimulus e.g. microbes or non-degradeable substances
-interference with healing.
-repeated bouts of acute inflammation.
-Autoimmune diseases |
|
|
Term
| why do you see MAST CELLS and EOSINOPHILS in chronic inflammation? |
|
Definition
mast cells contain HISTAMINE
eosinophils contain ANTI HISTAMINE
*counteract each other |
|
|
Term
| how are PLASMA CELLS identified on a slide? |
|
Definition
| eccentric nucleus, perinuclear halo (white-golgi apparatus) |
|
|
Term
| how are LYMPHOCYTES identified on a slide? |
|
Definition
| almost all nucleus, very little cytoplasm |
|
|
Term
| what is the purpose of GRANULATION TISSUE? collagen is converted from what to what? |
|
Definition
| provides a scaffold for wound healing, type I to type III |
|
|
Term
| why does GRANULATION TISSUE contract? |
|
Definition
| it contains MYOFIBROBLASTS which allow for contraction, causes wound to "shrink" |
|
|
Term
| how are FIBROBLASTS identified on a slide? |
|
Definition
|
|
Term
| what do EOSINOPHILS FIGHT? mediated by what? granules contain what? |
|
Definition
|
|
Term
| when GRANULOMATOUS INFLAMMATION is present, what should always be the primary differential diagnosis? |
|
Definition
|
|
Term
| what CYTOKINES are secreted by LYMPHOCYTES which are responsible for ongoing macrophage activation? |
|
Definition
|
|
Term
| what types of cells are found in the CASEOUS GRANULOMA WALL? |
|
Definition
| EPITHELIOID CELLS (abundant cytoplasm), FIBROBLASTS (form a fibrous cap) |
|
|
Term
| what causes NON CASEOUS GRANULOMAS? |
|
Definition
|
|
Term
| what is present in high numbers in NON CASEOUS vs CASEOUS GRANULOMAS? |
|
Definition
|
|
Term
| what is a LANGHAN'S GIANT CELL? |
|
Definition
|
|
Term
| what differentiates GRANULATION TISSUE vs GRANULOMAS? |
|
Definition
GRANULATION TISSUE- neovascularization,...
GRANULOMAS- epithelioid cells, giant cells, caseous or non caseous granulomas |
|
|
Term
| what is the difference between an ABSCESS and CELLULITIS? |
|
Definition
ABSCESS is a LOCALIZED collection of PUS
CELLULITIS is a DIFFUSE collection of PUS |
|
|
Term
|
Definition
| inflammation of lymphatic channels |
|
|
Term
|
Definition
| inflammation of draining lymph nodes, painful |
|
|
Term
|
Definition
| microbes gain access to blood |
|
|
Term
| activated of macrophages produce what CYTOKINES which cause large scale systemic inflammation? |
|
Definition
|
|
Term
| what are the main cells of an ACUTE INFLAMMATORY RESPONSE? CHRONIC? |
|
Definition
acute-neutrophils
chronic- macrophages, lymphocytes, plasma cells, eosinophils |
|
|
Term
| recruited WBCs have what functions? |
|
Definition
-clean up necrotic debris
-drive synthesis of new extracellular matrix (ECM) |
|
|
Term
| what are the two types of repair? |
|
Definition
| resolution (regeneration) or scarring (replacement with different cells) |
|
|
Term
| restoration of liver mass after resection results from what process? |
|
Definition
| compensatory growth or compensatory hyperplasia |
|
|
Term
| who is the DIRECTOR of wound healing? |
|
Definition
|
|
Term
| what are the ROLES of the ECM? |
|
Definition
1) Mechanical support for cell anchorage
2) Determination of cell orientation (polarity)
3) Control of cell growth (cell adhesion-->growth and differentiation)
4) Maintenance of cell differentiation
5) Scaffolding for tissue renewal
6) Establishment of tissue microenvironments
(can provide boundary, filtration in kidney, track in cell motility)
7) Storage and presentation of regulatory molecules
(fibroblast growth factor (FGF) in BM) |
|
|
Term
| what are the three basic COMPONENTS of ECM? |
|
Definition
1) Fibrous structural proteins e.g. collagen and elastin
2) Water-hydrated gels e.g. proteoglycans and hyaluronan
3) Adhesive glycoproteins
*also FIBRONECTIN, LAMININ, and INTEGRINS |
|
|
Term
| what is the function of LYMPH NODES in inflammation? |
|
Definition
| filtration, phagocytosis, cellular immunity, antibody production |
|
|
Term
| what are the CARDINAL SIGNS of inflammation? |
|
Definition
| redness, swelling, heat, pain, loss of function |
|
|
Term
|
Definition
| response to cell/tissue injury by VASCULARIZED TISSUE, elicited to protect the host by eliminating the cause and necrotic debris |
|
|
Term
| how can inflammation damage the body? |
|
Definition
| anaphylaxis-->whole body reaction |
|
|
Term
| characteristics of ACCUTE INFLAMMATION? |
|
Definition
-Initial event in most inflammatory processes
-Abrupt onset
-Short duration
-Exudation of protein rich fluids
*Neutrophils |
|
|
Term
| characteristics of CHRONIC INFLAMMATION? |
|
Definition
-Longer duration
*Mononuclear inflammatory cells eosinophils
-Little to no fluid
- fibrosis |
|
|
Term
|
Definition
| the escape of fluids, proteins and cells from the vascular system implying increased vascular permeability |
|
|
Term
|
Definition
| inflammatory extravascular fluid with high protein concentrations, much cellular debris |
|
|
Term
| what are some types of EXUDATES? |
|
Definition
Serous – few cells,resembles serum
Purulent – numerous neutrophils, bacteria
Suppurative – numerous neutrophils, bacteria, cellular debris e.g. abscess
Hemorrhagic - many red blood cells; indicate severe capillary damage
Fibrinous - polymerized fibrin |
|
|
Term
| what VASCULAR FLOW CHANGES are associated with inflammation? |
|
Definition
CHANGES IN VASCULAR FLOW:
- vasoconstriction
- vasodilation
- slowing of circulation
- stasis (increased RBC and viscosity-->WBC margination) |
|
|
Term
| how is VASCULAR PERMEABILITY changed in inflammation? |
|
Definition
INCREASED PERMEABILITY
-Endothelial contraction
-Direct injury
-Leukocyte dependent injury
-Increased transcytosis
-Neovascularization |
|
|
Term
| what is the sequence of events from lumen to interstitium for LEUKOCYTES? |
|
Definition
| Lumen Margination Rolling Adhesion Transmigration Migration into interstitial tissues toward a chemotactic stimulus |
|
|
Term
| what are the ADHESION MOLECULES involved in MARGINATION? |
|
Definition
Integrins
Selectins
Immunoglobulin super family |
|
|
Term
|
Definition
| the lining up of PMNs along the vascular epithelium |
|
|
Term
| what are the three parts stages of PHAGOCYTOSIS? |
|
Definition
1-recognition and attachment
2-engulfment
3-killing and degradation |
|
|
Term
| examples of INHERITED KILLING DEFECTS in phagocytic cells? |
|
Definition
| myeloperoxidase deficiency, NADPH oxidase deficiency, chronic granulomatous disease |
|
|
Term
| ***what are the three outcomes of ACCUTE INFLAMMATION?*** |
|
Definition
-resolution-->return to normal
-scarring/fibrosis (abscess always results in scar)
-progression to chronic inflammation--> can scar or repair depending on tissue and severity of inflammation |
|
|
Term
| what are the MEDIATORS of IMMEDIATE VASCULAR events during inflammation? DELAYED? PROLONGED? |
|
Definition
IMMEDIATE-histamine, leukotrienes
DELAYED-complement, kinins
PROLONGED-direct endothelial injuries e.g. burns |
|
|
Term
| what are the major ADHESION MOLECULES involved in LEUKOCYTE vascular motility? |
|
Definition
-P and E SELECTIN
-ICAM I and VCAM I
-PECAM I/CD99 *transmigration of leukocytes |
|
|
Term
| what are WEIBLE-PALADE BODIES? where are they found? what induces them? |
|
Definition
| bodies containing P SELECTIN, found in endothelial cells, stimulated by HISTAMINE and THROMBIN to release P SELECTIN to go to the surface of cells |
|
|
Term
| what increases AVIDITY of INTEGRINS? |
|
Definition
| chemokines, IL8, PAF (platelet aggregating factor) |
|
|
Term
| what ADHESION MOLECULES are induced by CYTOKINES? |
|
Definition
|
|
Term
| what SIGNALING PATHWAY do inflammatory stimuli use? |
|
Definition
| G Protein signal transduction |
|
|
Term
| what product does NADPH OXIDASE make? SUPEROXIDE DISMUTASE? MYELOPEROXIDASE? |
|
Definition
| O2-, H2O2, hypochlorous acid *ultimate killer-adds halide |
|
|
Term
| what chronic metabolic disease has affects on adhesion, chemotaxis, and phagocytosis? |
|
Definition
|
|
Term
| why are new vessels LEAKY? |
|
Definition
| incompletely formed interendothelial junctions and increased transcytosis --> edema of surrounding tissue |
|
|
Term
| Most important factors that induce angiogenesis |
|
Definition
1) basic fibroblast growth factor (bFGF)
2) vascular endothelial growth factor (VEGF) |
|
|
Term
| two PROCESSES by which blood vessels are formed- |
|
Definition
1) VASCULOGENESIS--> from ANGIOBLASTS in embryogenesis
2) ANGIOGENESIS or NEOVASCULARIZATION-preexisting vessels send out capillary sprouts -->initially have no lumen |
|
|
Term
| what are the two type of MEDIATORS of inflammation? |
|
Definition
PREFORMED-histamine, serotonin
NEWLY SYNTHESIZED- prostoglandins, leukotrienes, cytokines |
|
|
Term
| what are the PLASMA PROTEASES involved in inflammation? |
|
Definition
Complement System
Kinin System
Clotting System |
|
|
Term
| briefly describe the COMPLEMENT SYSTEM? |
|
Definition
-three pathways that all converge at C3
-C3a & C5a release histamine which increases vascular permeability
-form MAC complex which --> lysis of cells |
|
|
Term
| ***what are the most important MEDIATORS for VASODILATION?*** |
|
Definition
|
|
Term
| ***what are the most important MEDIATORS for VASCULAR PERMEABILITY?*** |
|
Definition
Vasoactive amines
C3a, C4a & C5a (Anaphylatoxins)-via HISTAMINE
Bradykinin
Leukotrienes C4, D4, E4
PAF
Substance P |
|
|
Term
| ***what are the most important MEDIATORS for FEVER?*** |
|
Definition
|
|
Term
| ***what are the most important MEDIATORS for PAIN?*** |
|
Definition
|
|
Term
| ***what are the most important MEDIATORS for TISSUE DAMAGE?*** |
|
Definition
-Neutrophil and Macrophage lysosomal enzymes
Cationic proteins, acid proteases, neutral proteases
-Oxygen metabolites
-Nitric oxide |
|
|
Term
| is TISSUE DAMAGE a big problem in inflammation? why of why not? |
|
Definition
| no, because checks and balances exist (e.g. antioxidants and oxygen radicals)--> can be damaging if inflammation is chronic |
|
|
Term
| is TISSUE DAMAGE a big problem in inflammation? why of why not? |
|
Definition
| no, because checks and balances exist (e.g. antioxidants and oxygen radicals)--> can be damaging if inflammation is chronic |
|
|
Term
| neutrophils are a hallmark of acute inflammation, what about CHRONIC? |
|
Definition
| mononuclear cells-->***MACROPHAGES***, lymphocytes, plasma cells, mast cells, eosinophils |
|
|
Term
| what is the MONONUCLEAR PHAGOCYTIC SYSTEM (MPS)? |
|
Definition
| variations of resident macrophages (kupffer cells, microglial cells, alveolar macrophages etc.) filter particulate matter and alert T and B cells in case of a problem |
|
|
Term
| CHARACTERISTICS of MACROPHAGES- |
|
Definition
-short lived as MONOCYTES ~1 day
-activation causes them to increase size and increase killing ability |
|
|
Term
| why are MACROPHAGES said to be capable of a broad range of BIOLOGICAL ACTIVITIES? |
|
Definition
1) Acid and neutral proteases
2) Other enzymes
-plasminogen activator
→↑↑↑ proinflammatory substances
3) Complement components & Coagulation factors |
|
|
Term
| in cases of CHRONIC INFLAMMATION how do macrophages maintain their numbers? |
|
Definition
|
|
Term
| how are MACROPHAGES able to merge to form a giant multinucleated cell? |
|
Definition
|
|
Term
| MAST CELLS are "armed" with what antibody isotype? what is their role in CHRONIC inflammation? |
|
Definition
IgE-->involved in acute ANAPHYLATIC SHOCK
CHRONIC-->elaborate cytokines e.g. TNF |
|
|
Term
| GRANULOMATOUS INFLAMMATION only results from certain pathogens, what are the most likely causes? |
|
Definition
***1) Mycobacterium tuberculosis -> TB***
2) Treponema pallidum -> Syphillis
3) Fungi
4)foreign bodies-splinters, metals, breast implants etc. |
|
|
Term
| GRANULOMATOUS INFLAMMATION doesn't always kill the foreign body, but provides another function by doing what? |
|
Definition
| walling off the pathogen to keep it from spreading |
|
|
Term
|
Definition
-Many activated macrophages with granular cytoplasm and indistinct boundaries
-surrounding collar of lymphocytes secreting cytokines (IL 2, IFN gamma) to activate macrophages
*well circumscribed-->focal or multi focal |
|
|
Term
| what do OLDER GRANULOMAS have which differs from younger ones? |
|
Definition
| ring of fibroblasts (scarring) which walls off infection and contains things |
|
|
Term
| what are the GIANT CELLS often present in GRANULOMAS? |
|
Definition
| fusion of 20+ macrophages |
|
|
