By Roger S. Kirby MD FRCS(Urol) FEBU
This can be a condensed model of the author's winning Atlas of Prostatic Disease. The emphasis is on a succinct description of prostatic ailment in a principally illustrative layout. The publication covers the explanations, analysis and staging of prostate melanoma, benign prostatic hyperplasia and prostatitis. The sections on therapy were superior by way of the addition of algorithms to summarize the decision-making technique.
Men's overall healthiness is now a tremendous public wellbeing and fitness factor and prostatic illness may have an immense influence at the caliber of lifetime of many males. This ebook will supply a handy precis for urologists, fundamental care physicians and nurse practitioners
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Extra info for An illustrated pocketbook of prostatic diseases
ET1-induced angiogenesis further promotes osteoblastic metastases from the primary tumor. 26 AN ILLUSTRATED POCKETBOOK OF PROSTATIC DISEASES Figure 21 Local cell proliferation and metastatic capacity are different entities. Critical to the development of metastases is the loss of cell adhesion molecules such as E-cadherin. Absence of Ecadherin allows prostate cancer cells to ‘float off’ into the circulation and promotes the development of metastases. In the case of prostate cancer, these most frequently occur in bone or lymphatic tissues Figure 22 Angiogenesis describes the ability of a metastatic deposit to induce its own blood supply, which may be critical to its survival.
This mutant protein has no external component, with the result that the internal component continually signals the need for cell division, regardless of the presence or absence of EGF signal molecules15. 22 AN ILLUSTRATED POCKETBOOK OF PROSTATIC DISEASES Figure 18 Oncogenesis within the prostate is due to the conversion of proto-oncogenes to active oncogenes. In the case of the ras oncogene, this occurs as a result of a mutation, or ‘hit’, involving alteration of a single nucleotide base-pair Figure 19 The mutated ras oncogene p21 protein cannot be deactivated by guanosine triphosphate (GTP) cyclase and thus continues to signal inappropriately for cell growth and division Tumor suppressor genes As well as the influence of growth-promoting oncogenes, abnormal prostate cell growth may also be the result of loss of the growth-restraining influences of one or more tumor AN ILLUSTRATED POCKETBOOK OF PROSTATIC DISEASES 23 Figure 20 Tumor suppressor genes such as p53 are also important in the development of prostatic neoplasia.
Recent data confirm that men with larger prostates and higher PSA values suffer a faster rate of disease progression than those with smaller glands33. The explanation for these findings lies in the progressive expansion of the transitional zone by the adenoma (Figure 49). This process reduces the distensibility of the urethra during voiding and produces gradually increasing bladder outlet obstruction. This increase in prostate volume is associated with a progressive risk of lower urinary tract symptoms, and a negative impact on quality of life.
An illustrated pocketbook of prostatic diseases by Roger S. Kirby MD FRCS(Urol) FEBU