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sbo2- patho

sbo2- patho

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Published by Kate Mendoza
SBO: PATHOLOGY ~~ INFLAMMATION AND REPAIR INFLAMMATION *** 1. ENUMERATE THE 4 CARDINAL SIGNS OF INFLAMMATION AND GIVE THE PATHOPHYSIOLOGIC MECHANISMS INVOLVED IN EACH (mnemonic: PRISH = Pain, Redness, Immobility- loss of fxn, Swelling, Heat) a. Dolor (Pain)- results in part from the distortion of tissues caused by edema, and it also is induced by certain chemical mediators of inflammation, such as bradykinin, serotonin, and the prostaglandins. b. Calor (Heat)- results from increased blood flow t
SBO: PATHOLOGY ~~ INFLAMMATION AND REPAIR INFLAMMATION *** 1. ENUMERATE THE 4 CARDINAL SIGNS OF INFLAMMATION AND GIVE THE PATHOPHYSIOLOGIC MECHANISMS INVOLVED IN EACH (mnemonic: PRISH = Pain, Redness, Immobility- loss of fxn, Swelling, Heat) a. Dolor (Pain)- results in part from the distortion of tissues caused by edema, and it also is induced by certain chemical mediators of inflammation, such as bradykinin, serotonin, and the prostaglandins. b. Calor (Heat)- results from increased blood flow t

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Published by: Kate Mendoza on Jun 18, 2011
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SBO: PATHOLOGY ~~ INFLAMMATION AND REPAIRINFLAMMATION***
1.
ENUMERATE THE 4 CARDINAL SIGNS OF INFLAMMATION AND GIVE THEPATHOPHYSIOLOGIC MECHANISMS INVOLVED IN EACH
(mnemonic: PRISH = Pain, Redness,Immobility- loss of fxn, Swelling, Heat)
a.
Dolor (Pain)-results in part from the distortion of tissues caused by edema, and it also isinduced by certain chemical mediators of inflammation, such as bradykinin, serotonin, andthe prostaglandins.
b.
Calor (Heat)-results from increased blood flow through the area and is experienced only inperipheral parts of the body such as the skin.
c.
Rubor (Redness)-caused by the dilation of small blood vessels in the area of injury.
d.
 Tumor (Swelling)-caused primarily by the accumulation of fluid outside the blood vessels.
e.
Functio laesa (Loss of fxn)-may result from pain that inhibits mobility or from severeswelling that prevents movement in the area.
2.ENUMERATE THE 3 MAJOR COMPONENTS OF THE ACUTE INFLAMMATORY RESPONSE ANDDESCRIBE THE IMPORTANT EVENTS IN EACH
a.Alterations in vascular caliber that lead to an increase in blood flow
 Transient arteriolar VASOCONSTRICTION
VASODILATION ( --> hyperemia --> increase hydrostatic pressure --> edema and wheal)
Slowing of circulation (increased permeability of venules and capillaries causes escape of proteins extravascularly --> increased vascularity of blood)
Margination of leukocytes (slowing circulation allows leukocytes to move towardsendothelium, roll over the endothelium, and then migrate through). The process of theleukocytes moving through the endothelium is known as TRANSMIGRATIONb.Structural changes in the microvasculature that permit plasma proteins and leukocytes toleave the circulation
 Thecomplement system, when activated, results in the increased removal of pathogens viaopsonisationandphagocytosis.
 Thekinin systemgenerates proteins capable of sustaining vasodilation and otherphysical inflammatory effects.
 Thecoagulation systemor clotting cascade which forms a protective protein mesh over sites of injury.
 Thefibrinolysis system, which acts in opposition to the coagulation system, tocounterbalance clotting and generate several other inflammatory mediators.
c.
Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent
Leukocyte localisation and recruitment to the endothelium local to the site of inflammation – involving margination and adhesion to the endothelial cells: Recruitmentof leukocytes isreceptor-mediated.
Migration across the endothelium, known as transmigration,via the process of diapedesis: Chemokine gradients stimulate the adhered leukocytes to move betweenendothelial cells and pass the basement membrane into the tissues.
Movement of leukocytes within the tissue viachemotaxis : Leukocytes reaching the tissue interstitium bind toextracellular matrixproteins via expressed integrinsandCD44to prevent their loss from the site.Chemoattractantscause the leukocytes to move along a chemotactic gradient towards the source of inflammation.
3.DEFINE CHRONIC INFLAMMATION AND GIVE THE CAUSES
Chronic inflammation- is inflammation of prolonged duration (weeks or months) in whichinflammation, tissue injury, and attempts at repair coexist, in varying combinations.Causes:
Persistent infections
Immune-mediated inflammatory diseases
Prolonged exposure to potentially toxic agents, either exogenous or endogenous
 
a.DIFFERENTIATE BETWEEN ACUTE AND CHRONIC INFLAMMATION CLINICALLY ANDPATHOLOGICALLY ACUTECHRONIC
Causative agent 
Pathogens, injured tissuesPersistent acute inflammation dueto non-degradable pathogens,persistent foreign bodies, orautoimmune reactions
Major cellsinvolved 
Neutrophils, mononuclear cells(monocytes, macrophages)Mononuclear cells (monocytes,macrophages, lymphocytes,plasma cells), fibroblasts
Primary mediators
Vasoactive amines, eicosanoidsIFN-γ and other cytokines, growthfactors, reactive oxygen species,hydrolytic enzymes
Onset 
ImmediateDelayed
Duration
Few daysUp to many months, or years
Outcomes
Resolution, abscess formation,chronic inflammation Tissue destruction, fibrosis,necrosis
4.
ENUMERATE THE DIFFERENT TYPES OF INFLAMMATORY EXUDATE AND GIVE THEPROTOTYPE EXAMPLES OF EACH
a.
Purulent or suppurative exudates- consists of plasma withboth active anddeadneutrophils,fibrinogen, andnecrotic parenchymal cells. This kind of exudate isconsistent with more severeinfections, and is commonlyreferred to as pus.
b.
Fibrinous exudates - iscomposed mainlyof fibrinogenandfibrin. It is characteristic of rheumaticcarditis, but is seen in allsevere injuries such asstrep throatandbacterialpneumonia.Fibrinousinflammation is often difficultto resolve due to the fact thatblood vessels grow into theexudate and fill the space thatwas occupied by fibrin. Often,large amounts of antibioticsare necessary for resolution.
 
c.
Catarrhalexudates - is seen inthe nose and throat and ischaracterized by a highcontent of mucus.
d.
Serous exudate (sometimesclassified asserous transudate) - is usuallyseen in mild inflammation, withlittle protein content. Itsconsistency resembles that of serum, and can usually beseen in certain disease statesliketuberculosis.
e.
Malignant (or cancerous) -pleural effusion is effusionwherecancer cellsarepresent. It is usually classifiedas exudate.
**1.DEFINE INFLAMMATION
Inflammation- (Latin,inflammare, to set on fire) is part of the complex biological responseof vasculartissues to harmful stimuli, such aspathogens, damaged cells, or irritants. Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healingprocess.
2.ENUMERATE THE MOST LIKELY MEDIATORS OF THE INFLAMMATORY EVENTS AND GIVETHE ROLE THAT EACH PLAY IN THE DIFFERENT INFLAMMATORY EVENTSMEDIATORPRINCIPAL SOURCESACTIONSCELL-DERIVED
HistamineMast cells, basophils, plateletsVasodilation, increased vascularpermeability, endothelialactivationSerotoninPlateletsVasodilation, increased vascularpermeabilityProstaglandinsMast cells, leukocytesVasodilation, pain, feverLeukotrienesMast cells, leukocytesIncreased vascular permeability,chemotaxis, leukocyte adhesionand activationPlatelet-activating factorLeukocytes, mast cellsVasodilation, increased vascularpermeability, leukocyte adhesion,chemotaxis, degranulation,oxidative burstReactive oxygen speciesLeukocytesKilling of microbes, tissue damageNitric oxideEndothelium, macrophagesVascular smooth musclerelaxation, killing of microbesCytokines (TNF, IL-1)Macrophages, endothelial cells,mast cellsLocal endothelial activation(expression of adhesionmolecules),

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