Robbins and Cotran Pathologic Basis of Disease (9th Edition) (Professional Edition)

Robbins and Cotran Pathologic Basis of Disease (9th Edition) (Professional Edition)

Abul K. Abbas, Vinay Kumar, Nelson Fausto, Jon C. Aster

Language: English

Pages: 3692


Format: PDF / Kindle (mobi) / ePub

Dependable, current, and complete, Robbins and Cotran Pathologic Basis of Disease, 9th Edition is the perennially best-selling text that you'll use long after your medical student days are behind you. A world-class author team headed by Drs. Vinay Kumar, Abul Abbas, and Jon Aster, delivers the latest, most essential pathology knowledge in a readable, interesting manner, ensuring optimal understanding of the latest basic science and clinical content.

High-quality photographs and full-color illustrations highlight new information in molecular biology, disease classifications, new drugs and drug therapies, and much more.
Rely on uniquely authoritative and readable coverage, ideal for USMLE or specialty board preparation, as well as for course work.
Simplify your study with an outstanding full-color, highly user-friendly design.
Stay up to date with the latest information in molecular and genetic testing and mechanisms of disease.• Consult new Targeted Therapy boxes online that discuss drug therapy for specific diseases.
Gain a new perspective in key areas thanks to contributions from new authors at the top of their fields.
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modifications of ribosomal RNAs. Loss of SNORP functions is believed to contribute to Prader-Willi syndrome. Molecular diagnosis of these syndromes is based on assessment of methylation status of marker genes and FISH. The importance of imprinting is not restricted to rare chromosomal disorders. Parent-of-origin effects have been identified in a variety of inherited diseases, such as Huntington disease and myotonic dystrophy and in tumorigenesis. Key Concepts Genomic Imprinting ▪

Nailfold capillary loops are distorted early in the course of disease, and later they disappear. Telltale signs of endothelial activation and injury (e.g., increased levels of von Willebrand factor) and increased platelet activation (increased percentage of circulating platelet aggregates) have also been noted. However, what causes the vascular injury is not known; it could be the initiating event or the result of chronic inflammation, with mediators released by inflammatory cells inflicting

immu­notherapy, with or without plasmapheresis may be necessary. Figure 12-39 Complications of heart transplantation. A, Cardiac allograft rejection typified by lymphocytic infiltrate associated with cardiac myocyte damage. B, Allograft arteriopathy, with severe diffuse concentric intimal thickening producing critical stenosis. The internal elastic lamina (arrow) and media are intact (Movat pentachrome stain, elastin black). (B, Reproduced with permission from Salomon RN, et al: Human coronary

platelets Vasodilation, increased vascular permeability, endothelial activation Prostaglandins Mast cells, leukocytes Vasodilation, pain, fever Leukotrienes Mast cells, leukocytes Increased vascular permeability, chemotaxis, leukocyte adhesion, and activation Cytokines (TNF, IL-1, IL-6) Macrophages, endothelial cells, mast cells Local: endothelial activation (expression of adhesion molecules). Systemic: fever, metabolic abnormalities, hypotension (shock) Chemokines Leukocytes, activated

signaling pathways that ultimately induce the production of proteins that are involved in driving cells through the cell cycle and other proteins that release blocks on the cell cycle (checkpoints) (Chapter 1). In addition to responding to growth factors, cells use integrins to bind to ECM proteins, and signals from the integrins can also stimulate cell proliferation. In the process of regeneration, proliferation of residual cells is supplemented by development of mature cells from stem cells.

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