Robbins' Pathologic Basis of Disease, Volume 1Presenting the latest edition of this popular, comprehensive and practical text of pathology. Written with great clarity for easy readability, this reference offers detailed discussions of genetic disorders, cellular injury and death, neoplasia, the skeletal system and soft tissue tumors, and much more. Completely revised and updated, this edition is even more user-friendly with the use of text boxes for key topics in each chapter and a new full-color design. Features 1200 excellent 4-color illustrations! |
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Results 1-3 of 87
Page 77
... factor and thus it requires a progression factor for mitogenesis . Plasma , EGF , and insulin - like growth factors —can serve as progression factors in this process . PDGF has recently been shown to be active in vivo : when applied ...
... factor and thus it requires a progression factor for mitogenesis . Plasma , EGF , and insulin - like growth factors —can serve as progression factors in this process . PDGF has recently been shown to be active in vivo : when applied ...
Page 98
... factor VII , which in turn activates factor X. Then , on the platelet surface , factors Xa and Va interact with calcium and cata- lyze the conversion of prothrombin to thrombin . Thrombin converts fibrinogen to fibrin monomers and ...
... factor VII , which in turn activates factor X. Then , on the platelet surface , factors Xa and Va interact with calcium and cata- lyze the conversion of prothrombin to thrombin . Thrombin converts fibrinogen to fibrin monomers and ...
Page 696
... factors II , VII , IX , and X and protein C. Since the liver makes virtually all the clotting factors , severe parenchymal liver disease may be associated with a hemorrhagic diathesis . DIC ( p . 698 ) produces a deficiency of mul ...
... factors II , VII , IX , and X and protein C. Since the liver makes virtually all the clotting factors , severe parenchymal liver disease may be associated with a hemorrhagic diathesis . DIC ( p . 698 ) produces a deficiency of mul ...
Contents
Cellular Injury and Adaptation | 1 |
Inflammation and Repair | 39 |
Fluid and Hemodynamic Derangements | 87 |
Copyright | |
28 other sections not shown
Common terms and phrases
abnormal acid activity acute adult agents amyloid amyloidosis antibodies antigens arteries atherosclerosis bacterial blood bone cancer carcinogens carcinoma cardiac cause cellular changes chemical chromosome chronic clinical collagen complex damage death defects deficiency develop diagnosis disease disorders drugs edema effects endothelium Engl enzymes epithelial fatty fever fibroblasts fibrosis Figure fluid function gene genetic granulomas growth factor hemorrhage hepatic histologic host human immune immunologic increased induce infants infarction infection infiltration inflammation inflammatory injury interstitial intestinal intracellular involved lesions leukemia leukocytes levels lipid liver lung lymph nodes lymphocytes lysosomal macrophages malignant mechanisms mediators membrane metabolism monocytes mucosa muscle mutations necrosis necrotic neoplasms neutrophils normal occur oncogenes organs parasites pathogenesis patients phagocytic phagocytosis plasma platelet produce proliferation protein pulmonary reaction receptor renal respiratory response result risk serum skin specific syndrome synthesis tion tissue toxic tumor tumor cells ulcer usually vascular vessels viral virus viruses vitamin vitamin D