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Harrison's Principles of Internal Medicine, Twenty-First Edition
Brand new, in original packaging. 2-volume Harrison's Internal Medicine 21st edition.
4384 pages, Hardcover
Published March 28, 2022
131 people are currently reading
134 people want to read
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Displaying 1 - 5 of 5 reviews
November 26, 2024
No lo recomiendo. Causa traumas.
Want to read
February 24, 2024diabetes mellitus definition, is presented
April 19, 2024
Best book for post graduate students
Read
December 6, 2024I haven't read the whole book (obviously). But it was a fundamental thing during my years in med school, and I didn't hate this particular book. Sweat or bitter, this is what it was.
March 11, 2025
The most important detail mentioned in this book about diabetes :
“ In the early stages of the disorder, glucose tolerance remains near-normal, despite insulin resistance, because the pancreatic beta cells compensate by increasing
insulin output (Fig. 403-7). A number of pathophysiologic mechanisms contribute to type 2 DM and their relative importance varies from individual to individual. As insulin resistance and compensatory hyperinsulinemia progress, the pancreatic islets in certain individuals are unable
to sustain the hyperinsulinemic state, manifesting as IGT, defined as elevations in postprandial glucose. A decline in insulin “
“ The precise molecular mechanism leading to insulin resistance in type 2 DM has not been elucidated.
Insulin receptor levels and tyrosine kinase activity in skeletal muscle are reduced, but these alterations are most likely secondary to hyperinsulinemia and are not a primary defect. Therefore, "postreceptor" defects in insulin-regulated phosphorylation/dephosphorylation appear to play the predominant role in insulin resistance. Abnormalities include the accumulation of lipid intermediates within skeletal myocytes, which “
“ In the early stages of the disorder, glucose tolerance remains near-normal, despite insulin resistance, because the pancreatic beta cells compensate by increasing
insulin output (Fig. 403-7). A number of pathophysiologic mechanisms contribute to type 2 DM and their relative importance varies from individual to individual. As insulin resistance and compensatory hyperinsulinemia progress, the pancreatic islets in certain individuals are unable
to sustain the hyperinsulinemic state, manifesting as IGT, defined as elevations in postprandial glucose. A decline in insulin “
“ The precise molecular mechanism leading to insulin resistance in type 2 DM has not been elucidated.
Insulin receptor levels and tyrosine kinase activity in skeletal muscle are reduced, but these alterations are most likely secondary to hyperinsulinemia and are not a primary defect. Therefore, "postreceptor" defects in insulin-regulated phosphorylation/dephosphorylation appear to play the predominant role in insulin resistance. Abnormalities include the accumulation of lipid intermediates within skeletal myocytes, which “
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Displaying 1 - 5 of 5 reviews