Download Robbins & Cotran Pathologic Basis of Disease: With STUDENT by Vinay Kumar PDF

By Vinay Kumar

One of many best-selling scientific textbooks of all time, Robbins and Cotran Pathologic foundation of sickness is the only e-book that just about all clinical scholars buy, and is additionally time-honored through physicians around the globe. A "who's who" of pathology specialists can provide the main liable, present, and entire insurance of brand new crucial pathology wisdom. whilst, masterful enhancing and a realistic association make studying each idea remarkably effortless. on-line entry through scholar seek advice comprises self-assessment and evaluate questions, interactive case stories, downloadable photographs, video clips, and a digital microscope that permits you to view slides at various magnifications. the outcome is still the precise resource for an optimum realizing of pathology.

  • Offers the main authoritative and accomplished, but readable insurance on hand in any pathology textbook, making it excellent for USMLE or forte board coaching in addition to for direction work.
  • Includes entry to the entire contents on-line through pupil seek advice, in addition to self-assessment and evaluate questions, over a hundred interactive medical case reviews, downloadable photographs, movies, and a digital microscope that shall we clients view slides at diverse magnifications.
  • Delivers a cutting-edge knowing of the pathologic foundation of disorder via thoroughly up-to-date assurance, together with the newest mobile and molecular biology.
  • Demonstrates each suggestion visually with over 1,600 full-color photomicrographs and conceptual diagrams - many revised for even greater quality.
  • Facilitates studying with a good full-color, hugely elementary design.

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Extra resources for Robbins & Cotran Pathologic Basis of Disease: With STUDENT CONSULT Online Access, 8e

Sample text

Most toxic chemicals are not biologically active in their native form but must be converted to reactive toxic metab- CHAPTER 1 Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death olites, which then act on target molecules. This modification is usually accomplished by the cytochrome P-450 mixed-function oxidases in the smooth ER of the liver and other organs. The toxic metabolites cause membrane damage and cell injury mainly by formation of free radicals and subsequent lipid peroxidation; direct covalent binding to membrane proteins and lipids may also contribute.

On histologic examination the necrosis takes the form of foci of shadowy outlines of necrotic fat cells, with basophilic calcium deposits, surrounded by an inflammatory reaction. Fibrinoid necrosis is a special form of necrosis usually seen in immune reactions involving blood vessels. This pattern of necrosis typically occurs FIGURE 1–12 Liquefactive necrosis. An infarct in the brain, showing dissolution of the tissue. FIGURE 1–13 Caseous necrosis. Tuberculosis of the lung, with a large area of caseous necrosis containing yellow-white and cheesy debris.

The functional consequences may be severe at this stage. For instance, heart muscle ceases to contract within 60 seconds of coronary occlusion. Note, however, that loss of contractility does not mean cell death. If hypoxia continues, worsening ATP depletion causes further deterioration. The cytoskeleton disperses, resulting in the loss of ultrastructural features such as microvilli and the formation of “blebs” at the cell surface (see Figs. 1–9 and 1–10). “Myelin figures,” derived from degenerating cellular membranes, may be seen within the cytoplasm (in autophagic vacuoles) or extracellularly.

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