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Flashcards in Inflammation Deck (53):
1

5 cardinal signs of inflammation

dolor (pain), tumor (swelling), rubor (erythema), calor (heat), functio laesa (loss of function)

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stages of acute inflammatory response

irritation, sensation, activation of vascular/cellular responses, leukocyte migration, invasion, evacuation, systemic rejection

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transudate

not due to increased vascular permeability, no increase in protein concentration, occurs with osmotic or hydrostatic imbalance (i.e. nephrotic syndromes)

4

exudate

acute inflammatory fluids due to increased vascular permeability, protein & cellular debris present

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4 possible types of acute inflammation

serous, fibrinous, suppurative, ulcerative inflammation

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pus

a purulent exudate composed of many neutrophils and necrotic cell debris with/without microbes

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abscess

part of suppurative inflammatory response

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ulcer

focal erosion of a superficial tissue plane (usually skin or mucosal surface) with active acute inflammation. margins become more defined with chronicity

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morphology of chronic inflammation

presence of lymphocytes, macrophages, eosinophils, neutrophils. alteration of tissue architecture

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morphology of granuloma

aggregates of epithelioid histocytes/activated macrophages with multinucleated giant cells. if necrotizing, caseous necrosis is present.

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mechanism of granulomatous inflammation

foreign antigen activates CD4 T cell, which produces cytokines (TNF, IL17) that recruit monocytes to activate (INF gamma) tissue macrophages=fusion to giant cells and granuloma.

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general causes of inflammation

microbial infections, necrotic tissue, physical agents, foreign bodies, immune rxns, trauma, chemical agents

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ultimate goal of inflammatory process

phagocytosis and restoration of tissue integrity and function

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characteristics of acute inflammation

rapid onset, short duration, increased tissue fluid, accumulation of neutrophils

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characteristics of chronic inflammation

longer duration, infiltration of macrophages/monocytes/lymphocytes, alteration of tissue histoarchitecture including fibrosis

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pathophysiology of rubor/calor

vascular dilation, increased blood flow during acute inflammatory response

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pathophysiology of tumor

increased vascular permeability leading to tissue edema and accumulation of neutrophils

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pathophysiology of dolor

chemical mediators such as bradykinin

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pathophysiology of function laesa

tissue damage, pain, swelling

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components of acute inflammation

vascular and cellular response

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three major processes of acute inflammation

1. alterations in vascular caliber that lead to an increase in blood flow
2. structural changes in the microvasculature that permit plasma proteins and leukocytes to leave circulation
3. emigration, accumulation, activation of leukocytes to eliminate offending agent

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components of acute inflammatory vascular rxn

vasodilation (histamine, NO), increased permeability (endothelial gaps due to histamine, bradykinin, leukotrienes), stasis, leukocyte accumulation

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components of acute inflammatory cellular rxn

leukocyte extravasation (cell surface molecules), leukocyte activation (arachidonic acid metabolites/cytokines), phagocytosis, termination of inflammatory response

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increased permeability via gaps due to endothelial contraction

histamine, bradykinin, leukotrienes

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mechanisms for increased vascular permeability

endothelial gaps, direct injury, leukocyte mediated injury, increased transcytosis pathways, new vessel formation (inherently leaky)

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edema

increased fluid in interstitial tissues or serous cavities

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effusions

pathologic accumulation of fluid in a body cavity

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ascites

specific term for an effusion of the abdominal or peritoneal cavities

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adhesion molecules in acute inflammation

selectins, immunoglobulin family adhesion proteins, integrins

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selectins

(E,P,L-selectins) expressed on leukocytes and endothelial cells that facilitate the rolling of neutrophils. but don't bind to each other

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Ig family adhesion proteins

(ICAM, PECAM) expressed on endothelial cells and bind to integrins on the surface of leukocytes to facilitate leukocyte adhesion and transmigration

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integrins

expressed on leukocytes and participate in rolling and extravasation

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chemotactic factors for neutrophils

bacterial products, complement components especially C5, arachidonic acid metabolites (leukotrienes), and kallikrein

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histamine

early mediator of vascular rxn including vasodilation and increased permeability. preformed in mast cells, act mainly on endothelial receptors

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serotonin

vasodilation, increased permeability. preformed in platelets (released upon aggregation) and neuroendocrine cells.

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arachidonic acid

fatty acid residing in cell membrane phospholipids. can be converted into prostaglandins, leukotrienes, lipoxins, TxA2, chemotactic molecules, etc.

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cytokines involved in inflammation

TNF alpha & IL1 (from inflammasome) =both local and systemic effects. fever, fatigue, endothelial effects, fibroblast effects, increased cytokine production

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nitric oxide

produced by endothelial cells and macrophages, relaxes vascular smooth muscle resulting in dilation. inhibits platelet aggregation

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platelet activating factor (PAF)

triggers release of histamine, activates platelets, enhance neutrophil adhesion

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importance of factor 12 in inflammation

links kinin (kallikrein=chemotaxis), coagulation (intrinsic pathway), and complement systems.

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leukocytosis

elevated white blood count (left shift, bandemia)

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erythrocyte sedimentation rate (ESR)

nonspecific test for systemic inflammatory response. increased fibrinogen leads to rouleaux formation and increased density=faster sedimentation

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how does increased fibrinogen cause rouleaux formation?

it reduces the surface negative charge on cells so that RBCs don't repel each other and actually clump together

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when is ESR increased?

inflammation, malignancy, pregnancy

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when is ESR decreased?

polycythemia, sickle cell anemia, congestive heart failure, hypofibrinogemia, microcytosis

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serous inflammation

fluid collection (vascular>cellular). blisters

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fibrinous inflammation

vascular permeability increases sufficiently to allow increasingly large molecules such as fibrinogen to lead to sticky coagulum (common on body linings)

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suppurative inflammation

inflammatory exudate composed of bacteria, sloughed/necrotic cells, and neutrophils

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4 possible outcomes of acute inflammation

complete resolution, abscess formation, chronic inflammation, scar formation

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complete resolution of acute inflammation

most often occurs when injurious agent is eliminated and process is short lived.

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abscess

cavitated lesion of acute inflammation with central accumulation of neutrophils plus cell and tissue debris. over time a fibrous ring separates the cavity from the surrounding tissue

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chronic infection initiator cells

macrophages via INF-gamma

53

causes of granulomatous inflammation

TB!!!!, mycobacteria, leprosy, syphilis, foreign bodies, autoimmune mediated, etc