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Pathology  ` PATHOLOGY—CeLLuLAr InjurY                   Pathology  ` PATHOLOGY—InfLAMMATIOn          SECtIoN II       213




                   `  PATHOLOGY—InfLAMMATIOn

                  Inflammation           Response to eliminate initial cause of cell injury, to remove necrotic cells resulting from the
                                          original insult, and to initiate tissue repair. Divided into acute and chronic. The inflammatory
                                          response itself can be harmful to the host if the reaction is excessive (eg, septic shock), prolonged
                                          (eg, persistent infections such as TB), or inappropriate (eg, autoimmune diseases such as SLE).
                   Cardinal signs
                   SIGn                  MeCHAnISM                                MeDIATOrS
                   Rubor (redness), calor   Vasodilation (relaxation of arteriolar smooth   Histamine, prostaglandins, bradykinin, NO
                    (warmth)              muscle) Ž  blood flow
                   Tumor (swelling)      Endothelial contraction/disruption (eg, from   Endothelial contraction: leukotrienes (C 4 , D 4 ,
                                          tissue damage) Ž  vascular permeability   E 4 ), histamine, serotonin
                                          Ž leakage of protein-rich fluid from
                                          postcapillary venules into interstitial space
                                          (exudate) Ž  interstitial oncotic pressure
                   Dolor (pain)          Sensitization of sensory nerve endings   Bradykinin, PGE 2 , histamine
                   Functio laesa (loss of   Cardinal signs above impair function (eg,
                    function)             inability to make fist with hand that has
                                          cellulitis)
                   Systemic manifestations (acute-phase reaction)
                   Fever                 Pyrogens (eg, LPS) induce macrophages to
                                          release IL-1 and TNF Ž  COX activity in
                                          perivascular cells of hypothalamus Ž  PGE 2
                                          Ž  temperature set point
                   Leukocytosis          Elevation of WBC count; type of cell that
                                          is predominantly elevated depends on
                                          the inciting agent or injury (eg, bacteria
                                          Ž  neutrophils)
                    plasma acute-phase   Factors whose serum concentrations change   Notably induced by IL-6
                    proteins              significantly in response to inflammation
                                         Produced by the liver in both acute and chronic
                                          inflammatory states



                  Acute phase reactants  More FFiSH in the C (sea).
                   POSITIVe (uPreGuLATeD)
                   Ferritin              Binds and sequesters iron to inhibit microbial iron scavenging.
                   Fibrinogen            Coagulation factor; promotes endothelial repair; correlates with ESR.
                   Serum amyloid A       Prolonged elevation can lead to amyloidosis.
                   Hepcidin               iron absorption (by degrading ferroportin) and  iron release (from macrophages) Ž anemia of
                                          chronic disease.
                   C-reactive protein    Opsonin; fixes complement and facilitates phagocytosis.
                                         Measured clinically as a nonspecific sign of ongoing inflammation.
                   neGATIVe (DOWnreGuLATeD)
                   Albumin               Reduction conserves amino acids for positive reactants.
                   Transferrin           Internalized by macrophages to sequester iron.










          FAS1_2019_04-Pathol.indd   213                                                                                11/7/19   4:02 PM
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