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HOW TO USE THIS SECTION

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This section contains useful nomograms and reference material. Material is presented in alphabetical order by subject.

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ACID-BASE NOMOGRAM

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Figure 10-1.

ACID-BASE NOMOGRAM: Shown are the 95% confidence limits of the normal respiratory and metabolic compensations for primary acid-base disturbances. (Reproduced with permission from Brenner BM, Rector FC [editors]. Brenner & Rector’s the Kidney, 8th ed. Saunders/Elsevier, 2008.)

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COAGULATION CASCADE

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Figure 10–2.

COAGULATION CASCADE: Schematic representation of the coagulation pathways. The central precipitating event is considered to involve tissue factor (TF), which, under physiologic conditions, is not exposed to the blood. With vascular or endothelial cell injury, TF acts together with Factor VIIa and phospholipids (PL) to convert Factor IX to IXa and Factor X to Xa. The “intrinsic pathway” includes “contact” activation of Factor XI by XIIa-activated high molecular-weight kininogen complex (XIIa-HKa). Factor XIa converts Factor IX to IXa, which, in turn, converts Factor X to Xa, in concert with Factor VIIIa and PL. Factor Xa is the active ingredient of the “prothrombinase” complex, which includes Factor Va and PL, and converts prothrombin to thrombin (TH). TH cleaves fibrinopeptides from fibrinogen, allowing the resultant fibrin monomers to polymerize, and converts Factor XIII to XIIIa, which cross-links the fibrin clot. TH also accelerates and augments the process (in dashed lines) by activating Factor V and VIII, but continued proteolytic action also dampens the process by activating protein C, which degrades Factor Va and VIIIa. TH activation of Factor XI to XIa is a proposed pathway. There are natural plasma inhibitors of the cascade: tissue factor pathway inhibitor (TFPI) blocks VIIa/TF and thus inactivates the “extrinsic pathway” after the clotting process is initiated; antithrombin (AT) blocks IXa, and Xa, and thrombin. Arrows = active enzymes; dashed lines with arrows = positive feedback reactions, which are considered important to maintain the process after the “extrinsic pathway” is shut down by TFPI; dashed lines with solid dots = inhibitory effects; PK = prekallikrein. Note that the contact system (PK, HK, and XII) actually contributes to fibrinolysis and bradykinin formation in vivo, and its role in initiation of the intrinsic pathway in vivo is questionable.

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COMPLEMENT SYSTEM

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Figure 10-3.

COMPLEMENT SYSTEM: The classic (antigen-antibody complexes), alternative (microbial surfaces) and lectin (microbial surfaces) pathways of activation of the complement system. Each wavy line with arrow Image not available. indicates that there has been proteolytic cleavage of the molecule at the tip of the arrow; a complex with a line over it indicates that it is now enzymatically active. Note that, following cleavage, all smaller fragments are labeled with an “a,” and all larger fragments are labeled with a “b.” Hence, the C3 convertase is depicted as C4b,2b with a line ...

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