Robbins Pathologic Basis of DiseasePresenting 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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Page 103
... vessels ( angiogenesis ) and the proliferation of fibroblasts ( Fig . 4- 13 ) . These new vessels are leaky , allowing the passage of proteins and red cells into the extravascular space . Thus , new granulation tissue is often edematous ...
... vessels ( angiogenesis ) and the proliferation of fibroblasts ( Fig . 4- 13 ) . These new vessels are leaky , allowing the passage of proteins and red cells into the extravascular space . Thus , new granulation tissue is often edematous ...
Page 494
... vessels become smaller , but the ratio of wall thickness to lumen diameter becomes greater . Veins have a larger overall diameter , a larger lumen , and a thinner wall than corresponding arteries . Arteries are divided into three types ...
... vessels become smaller , but the ratio of wall thickness to lumen diameter becomes greater . Veins have a larger overall diameter , a larger lumen , and a thinner wall than corresponding arteries . Arteries are divided into three types ...
Page 517
... vessels associ- ated with asthma and blood eosinophilia Necrotizing vasculitis with few or no im- mune deposits affecting small vessels ( i.e. , capillaries , venules , or ... Vessel Vasculitis ( e.g. , giant Chapter 12 BLOOD VESSELS □ 517.
... vessels associ- ated with asthma and blood eosinophilia Necrotizing vasculitis with few or no im- mune deposits affecting small vessels ( i.e. , capillaries , venules , or ... Vessel Vasculitis ( e.g. , giant Chapter 12 BLOOD VESSELS □ 517.
Contents
GENERAL PATHOLOGY | 1 |
6 | 26 |
Acute and Chronic Inflammation | 50 |
Copyright | |
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abnormal acid activation acute adhesion amyloidosis angiogenesis antibodies antigens apoptosis associated bacteria bind blood cancer carcinogens carcinoma cause CD4+ cell cycle cell death cellular Chapter chemical chromosome chronic clinical collagen colon common cyclin cytokines damage deficiency develop disease disorders drugs edema effects endothelial cells endothelium enzymes epithelial cells extracellular matrix fever fibrosis Figure function gene genetic granulomas growth factor hepatitis host cells human immune increased induce infection infiltrate inflammation inflammatory integrins intracellular involved kinase lesions leukocytes liver lung lymph nodes lymphocytes lymphoma lysosomal macrophages malignant matrix mechanisms mediators membrane metabolism molecular molecules MORPHOLOGY muscle mutations necrosis neoplasms nervous system neutrophils normal occur oncogenes organisms oxidative parasites pathogenesis pathogens pathway patients peptide phagocytosis plasma platelet produce proliferation protein reactions receptor release renal respiratory response result signals skin surface syndrome synthesis T-cell tion tissue toxic toxin tumor tumor cells vascular viral virus viruses vitamin