SBO: PATHOLOGY ~~ INFLAMMATION AND REPAIRINFLAMMATION***
ENUMERATE THE 4 CARDINAL SIGNS OF INFLAMMATION AND GIVE THEPATHOPHYSIOLOGIC MECHANISMS INVOLVED IN EACH
(mnemonic: PRISH = Pain, Redness,Immobility- loss of fxn, Swelling, Heat)
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.
Calor (Heat)-results from increased blood flow through the area and is experienced only inperipheral parts of the body such as the skin.
Rubor (Redness)-caused by the dilation of small blood vessels in the area of injury.
Tumor (Swelling)-caused primarily by the accumulation of fluid outside the blood vessels.
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
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.
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:
Immune-mediated inflammatory diseases
Prolonged exposure to potentially toxic agents, either exogenous or endogenous