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patho chapter 2 voca

acute inflamation vocab

Inflammation beneficial host response to foreign invaders and cecrotic tissue. initiates repair prcocess can cause tissue damage and exacerbate the problem
Acute inflammation rapid response to cell injury or invading microbes and other foreign (non-self) substances that is designed to deliver leukocytes and plasma proteins to sites of injury
alterations in vessel caliber resulting in increased blood flow (vasodilation) and strucutal changes to permit plasma proteins to leave circulation (increased vascular permeability) Makes tissues red and swollen Vascular Changes
increased vascular permeability structural change that occurs in the vessel to permit plasma proteins to leave circulation during acute inflammation
Cellular events emigration of leukocytes (principally neutrophils) and accumulation at site of injury (celluar recruitment and activation)
neutrophils principle leukocyte to emigrate during ACUTE inflammation
cellular recruitment and activation the emigration of neutrophils (principally in acute) and accumulation at the site of injury
Vasodilation change in vascular caliber and flow vasodilation of the arterioles results in locally increase blood flow --> causes engorgement of down-stream micro-circulation (cappillaries and post capillary venules) -- erythema red/ warmth INCREASED volume of bloo
erythema redness/ warmth of tissue during an inflammatory response
transudate ultrafiltrate of blood plasma which moves form capillaries into tissues (increased vascular permeability
exudate protein rich fluid and cells move into interstitium
Edema refers to fluid accumulation in extravascular spaces which may be transudate or exudate
Endothelial cell contraction leads to intercellular gaps in capillaries and post capillary venules most comon and influential cause of increased vascular permeability REVERSIBLE process elicited by : 1. histamine 2. bradykinin 3. leukotrienes
Margination and Rolling step 1 of 4 of leukocyte recruitment weak and transient adhesions between leukocytes and endothelium mediated by selectins
selectins mediators of transient rolling
Firm Adhesion to Endothelium step 2 of 4 o leukocyte recruitment mediated by integrins expressed on leukocyte surfaces that bind to their ligands on Endothelial cells.Leukocytes interact w chemokines and activate leukocytes - change of integrins (molecular shift)lo->hi affinity
integrins firm adhesion mediator
Chemokines chemoattractant cytokines secreted by cells at sites of inflammation and displayed bound to proteoglycans on plasmalemma of Endothelial cells
Transmigration after firm adhesions on the endothelium leukocytes migrate through the vessels wall mostly in postcapillary venules. Driven by chemokines - PECAM-1 and CD31 expressed on leukocytes /endotheloial cells mediating binding necessary for diapedesis
diapedesis migration of leukocytes through the vessels wall
Chemotaxis migration tward sites of injury in extracellular tissues along a chemical gradient. Mediators include bacterial products/cytokines/chemokines/complement components/ leukotrienes
leukocyte activation activation of WBC at site of injury TLR and G protein receptors expressed on WBC recognize molecules that mediate activation binding to app ligands= functional outmocmes that change activity of WBC -> cause activation
toll like receptors TLR receptor on cell surface of leukocyte that recognizes products from microbes during leukocyte activation at site of injury
Phagocytosis (3 steps) enhanced function of leukocytes resulting from activation. Step 1: recognition and attatchment Step 2:engulfment with subsequent formation of phagocytic vacuole Step 3: killing and degradation of ingested material
leukocytes bind and ingest most microorganisms by surface receptors which either recognize cell componenets or recognize what?onins opsonins
Killing and degradation of phagocytosed microbes and dead tissues is done by what means reactive oxygen species, inducible nitric oxide synthetase and lysomsomal enzymes - all stimulated by activation
mediators that amplify inflammatory reaction produced after activation of WBC arachridonic acid metabolites (LEUKOTRIENES) and cytokines
lysosomal enzymes release after activation of WBC assist in killing and deradation of phagocytosed cicrobes and dead tissues // also released during inflammation causing leukocyte induced tissue injury
ROS reactive oxygen species released not only within the phagolysosome during leukocyte activation responsible for killing and degradation of phagocytosed microbes and dead tissues also into x-cellular space injuring neighboring cells - bystander effect -
RNS reactive nitrogen species released during leukocyte activation not only in phagocytosed microbes but also into x-cellular space, injuring neighboring cells also
macrophages activated leukocytes primarily responsible for secreting cytokines that stimulate further inflammation - macrophages are tissue fixed along lymphocytes as secrete cytokine as as inflammatory mediator and amplify reaction
cytokines (leukocyte recruitment) TNF and IL-1 also important in leukocyte recruitment activate Endothelial cells to increase expression of ligands for integrins ICAM - 1 and VCAM-1
Resolution the outcome of the inflammation. When the injury is limited or short lived with no or minimal damage and tissue is capable of replacing any irreversibly injured cells
Progression to chronic inflammation non resolution of agent --> chronic inflammation / effector cells - molecular mediators drive inflam cascade TUBERCULOSIS # of organism low/ lesions big due to persistence of T cell macrophages to mediate granulomas
Scarring or fibrosis results after substanial tissue damage or when inflammation occurs in tissue that do not regenerate deep wounds - damage to epidermis and B Membrane also seen in liver and lung lobes exceeds capacity of tissue to regenerate
Abscesses Fibrinous inflammation extenisive neutrophilic infiltrates or due to certain bacteria/fungal infections STAPH STREP (pyogenic organisms) foci of granulocytes walled of by Fib CT tissue forming capsule usual outcome scarring
pyogenic (pus forming) organism
Serous inflammation produced characterised by outpouring of watery, protein POOR fluid that derives either from serum or from mesothelial cells lining pertoneal, pleural, or pericardial cavity BLISTER example
Fibrinous inflammation more severe injury/greater vascular permeability /lar molecules pass endothelial barrier/ appears eosinophilic/restoration may occur but failure to remove fibrin results in ingrowth of fibrin and Bl vessels - leading to scar. Fibrinous pericarditis image
Suppurative inflammation aka Purulent inflammation Abscess is an example of this presence of large amts of pus (Neutrophils,necrotic cells, edema fluid) large central necrotic region rimmed by layer of preserved Neutrophils with surrounding zone of dilated vessels and fibroblastic proliferation
Ulcer local defect or excavation of the surface or an organ or tissue that is produced by necrosis of cells and sloughing of necrotic inflammatory tissue - seen commonly on : Tongue,GI tract,skin
Histamine mast cells adj to vessels /basophils /platelets 1. physical injury 2. immune reaction binding of IgE Ab to Fc receptors on mast cells 3.C3a/C5a fragments of complement 4.leukocyte derived histamine releasing proteins 5.neuropeptides 6.cytokines IL-1 IL-8
Serotonin found primarily in platelet dense body granules released during platelet aggregation effects similar to those of histamine
eicosanoids Arachidonic Acid (AA) metabolites Prostaglandins/leukotrienes/lipoxins involved in vascular reactions (CHEMOTAXIS) synthesis increase at site of inflam act locally then quickly degrade major sources are leukocyte/mast cells/ endothelial cells/ platele
Cytokines ( (cell derived mediators) aka Interleukins (IL-1, IL-2, etc mediate leukocyte recruitment and migration Major cytokines in acute inflammation TNF and IL_1 and chemokines. TNF/IL1 -principally function in endothelial activation and systemic effect induce systemic acutephase reaction
systemic acutephase reaction reaction often associated with infection and inflammatory diseases. Fever, lethargy, hepatic synthesis of various acute phase proteins, metabolic wasting, neutrophil release into circulation, release of adrenocorticotropic hormone
chemoattractants chemokines
Complement system: The plasma proteins-complement system play important role in immunity and inflammation leads to generation of multiple breakdown products which are responsible for leukocyte chemotaxis,opsonization/ phagocytosis of microbes/other particles cell killing
Coagulation proteins: plasma protein mediator activated factor XII triggers clotting, kinin and complement cascades, and activates fibrinolytic systems
Kinin: Produced by proteolytic cleavage of precursors; mediate vascular reaction, PAIN
What are main components of inflammation 1. vascular reaction and 2. cellular response
What activates inflammatory response activated by mediators derived from plasma proteins and cells
WHAT ARE THE 5 R'S OF INFLAMMATORY RESPONSE 1. Recognition of injurious agent 2. Recruitment of leukocytes 3. Removal of agent 4. Regulation (control) of response 5. Resolution (repair)
immune reaction aka hypersensitivity reaction allergies or autoimmune reactions tend to be persistent --> chronic immune-mediated inflammatory disease
increased vascular permeability engorgement of capillaries leading to increased capillary intravascular hydrostatic pressure (transudate/exudate -edema)
TNF , IL-1 cytokines which are key molecules in mediating responses slower prolonged retraction of Endothelial cells results form the rearrangement of cytoskeletion in response to these cytokines
important process during inflammatory response is the deliver of leukocytes to hte site of injury and only the site of injury and activation of those leukocytes leukocyte recruitment
PECAM-1 (CD31) expressed on leukocytes and endothelial cells during transmigration ediates the binding events necessary for diapedesis.
collagenases what leukocytes degrade basement membranes with during transmigration (diapedesis)
G - protein - coupled receptors seven transmembrane receptors recognize bacterial peptides and mediators produced in response to peptides
Chemical Mediators of inflammation may be produced locally or may be circulating in blood induce effects by binding to specific receptors on target cells most are tightly regulated - decay quickly,inactivated by enzymes,are eliminated, are inhibited by other mediators or proteins.
cell derived Mediators effects are vasodilation/increased vascular permeability. Products of tissue macrophages mast cells/endothelial cells/recruited WBC and platelets. Either(1)preformed and sequestered in intracell granules(2) synthesized in light of cellular activation
Vasoactive amines cell derived mediators of inflammation include histamine and serotonin
eicosanoids metabolic pathways Arachidonic Acid (AA) metabolites act along 1 of 2 pathways 1. cyclooxygenase pathway 2. Lipoxygenase pathway
cyclooxygenase pathway metabolic pathway of eicosanoids (1 of 2) in which synthesis of prostaglandins and thromboxanes occurs
lipoxygenase pathway Arachidonice Acid (AA) metabolite pathway (1 of 2) in which synthesis of leukotrienes and lipoxins occurs
chemokines (cell derived mediators) sm proteins principally act as chemoattractants for diff subgroups of leukocytes. 2 major groups CXC CC chemokines based on amino acid arrangement bound to proteoglycans on endothelial cells bind to specific chemokine receotpros (CXCR4 and CCR5 on WBC)
ROS - Reactive oxygen species (cell derived mediator) ROS synthesized via NADPH oxidase pathway and released from activated neurtophils and macrophages/phagolysosomes destroy microbes necrotic released in lo level increase chemokine/cytokine/adhesion molecule expression. release hi level cell injury or death
Reactive Nitric Oxide synthesized in light of nitric oxide synthetase in neurons, macrophages, and Endothelial cells inducible NOS in macrophages and Endothelial cells induced by IL-1, TNF, IFN gamma, and endotoxin in inflammatory reactions
CXC CXC chemokines - one amino acid separating cysteines and act primarily on neutrophils Ll-8 produced mainly in response to microbial products and other cytokines IL-1 & TNF
CC CC chemokines - have adjacent cysteine residues and include monocyte chemoattractant protein 1 MCP-1 and macropphage inflammatory protein MIP1alpha, RANTES, and eotaxin
NO (nitric oxide) roles in inflammation include 1.relax of vascular sm muscle 2.antagonism of all stages of platelet activation(adhesion,aggregation,degranulation)3.reduction leukocyte recruitment at inflam sites 4.action as microbicidal (cytotoxic)agent w/wo superoxide radicals in activated macropha
Lysosomal Enzymes of leukocytes mediate acute inflammation/released after cell death/leakage during formation phagocytic vacuole/attempt to phagocytose large indigestable surfaces. ACID PROTEASES/NEUTRAL PROTEASES kept in check by ANTIPROTEASES role in microbial killing, tissue inju
C3a & C5a (ANAPHYLATOXINS)1 vascular effects: complement system of plasma protein derived mediators increase vascular permeability /cause vasodilation by inducing mast cells release histamine/action mimic mast cells main cellular effectors of allergic reaction C5a activates lipoxyy pathway of AA metabolism in neutro/macro-release more inflam mediators
C3a & C5a (ANAPHYLATOXINS)2 Leukocyte Activation, adhesion and chemotaxis complement system of plasma protein derived mediators C5a activates leukocytes, incrasing their adhesion to endothelium and is a potent chemotactic agent for neurtophils monocytes eosinophils and basophils
C3a & C5a (ANAPHYLATOXINS)3 phagocytosis: complement system of plasma protein derived mediators when fixed to a microbial surface C3b and its inactive proteolytic product iC3b act as opsonins, augmenting phagocytosis by neutrophils and macrophages, which express receptors for these complement products
what is the activation of the complement system of plasma protein derived mediators controlled by? controlled by the cell associated and circulating regulatory proteins. Presence of these inhibitors in host cell membranes protects normal cells from inappropriate damage during protective reactions against microbes
What 4 systems involved in the inflammatory response is initiated by factor XII of the intrinsic coagulation cascade? 1. the kinin system -vasoactive kinins 2. clotting system- inducing activation of thrombin, fibrinopeptides and factor X 3. the fibrinolytic system - producing plasmin and inactivating thrombin 4. complement system producing anaphylatoxins C3a and C5a.
FACTOR XII of the intrinsic coagulation cascade protein synth by the liver that circulates inactive form until encounters collagen/B. Membrane/activated platelets at site Endothelial injury. -->conformational change XIIa expose serine center-cleaves protein substrates of the kinin/coagulation systems
clotting system factor XIIa driven cascade activates thrombin which cleaves circulating soluble fibrinogen to generate an insoluble fibrin clot. Factor Xa an intermediate in the clotting cascade causes increased vascular permeability and WBC emigration
Thrombin participate in inflam by binding to protease-activated receptors expressed on platelets endothelial cells/other cells types.Binding thrombin to receptors on endothelial cells --> activation and enhanced leukocyte adhesion; also generates fibrinopeptides
Fibrinolytic system activated when factor XII inducing clotting mechanism exist to limit clotting by cleaving fibrin , solubilizing the fibrin clot
plasminogen activator and kallikrein cleave plasminogen (plasma protein bound up in evolving fibrin clot resulting in plasmin
Plasmin multifunctional protease that claves fibrin adn is importaing in lysing clots. Also while cleaving C3 -> C3a - vasodilation and vascular permeability increase also can activate FACTOR XII amplifying the entire set of responses
Kinin system (BRADYKININ) leads to ultimately formation of bradykinin. Like histamine bradykinin increases vascular permeability, arteriolar dilation, bronchial smooth muscle contractions. Causes pain when injected in skin. actions short lived rapidly degraded by kininases.
Kalikrein (intermediate of kinin system) intermediate within the kinin cascade with chemotactic activity, also potent activator of FACTOR XII
Created by: duncanreeves