Because BPH preferentially involves the inner portions of the prostate, the most common manifestations are related to lower urinary tract obstruction, often in the form of difficulty in starting the stream of urine (hesitancy)
Fig. 18.11 Nodularprostatichyperplasia.Well-definednodulescompresstheurethraintoaslitlikelumen.
http://ebooksmedicine.net
Fig. 18.12 Nodularhyperplasiaoftheprostate.(A)Low-powerphotomicrographdemonstratesawell-demarcatednoduleattherightofthefield,withaportionofurethraseentotheleft.Inothercasesofnodularhyperplasia,thenodularityiscausedpredominantlybystromal,ratherthanglandular,proliferation.(B)Higher-powerphotomicrographdemonstratesthemorphologyofthehyperplasticglands,whicharelargeandhavepapillaryinfoldings.
and intermittent interruption of the urinary stream while voiding. These symptoms frequently are accompanied by urinary urgency, frequency, and nocturia, all indicative of bladder irritation. Clinical manifestations of prostatic hyperplasia occur in only about 10% of men with pathologic evidence of BPH. The presence of residual urine in the bladder due to chronic obstruction increases the risk for urinary tract infections. In some affected men, BPH leads to complete urinary obstruction, with resultant painful distention of the bladder and, in the absence of appropriate treatment, hydronephrosis (Chapter 14). Initial treatment is pharmacologic, using targeted therapeutic agents that inhibit the formation of DHT from testosterone (such as 5-alpha reductase inhibitors) or that relax prostatic smooth muscle by blocking α1-adrenergic receptors. Various surgical techniques are reserved for severely symptomatic cases that are recalcitrant to medical therapy.
BPHischaracterizedbyproliferationofbenignstromalandglandularelements.DHT,anandrogenderivedfromtestosterone,isthemajorhormonalstimulusforproliferation.
BPHoriginatesintheperiurethraltransitionzone.Thehyper-plasticnodulesexhibitvariableproportionsofstromaandglands.Hyperplasticglandsarelinedbytwocelllayers,aninnercolumnarlayerandanouterlayercomposedofflattenedbasalcells.
Clinicalfindingsresultfromurinarytractobstructionandincludehesitancy,urgency,nocturia,andpoorurinarystream.Chronicobstructionpredisposestorecurrenturinarytractinfections.
Adenocarcinoma of the prostate and is the most common form of cancer in men, accounting for 27% of cancer cases in the United States in 2014. Its is uncommon before the age of 50 years. Over the past several decades, mortality from prostate cancer has decreased significantly, and it currently causes only 10% of cancer deaths in the United States.
The relatively low rate of mortality in men with prostate cancer is related in part to increased detection of the disease through screening (discussed later), but how effective screening is at saving lives is controversial. This seeming paradox is related to the wide variation in the natural history of prostate cancer, from aggressive and rapidly fatal to indolent disease of no clinical significance. Indeed, prostate carcinoma commonly is found incidentally at autopsy in men dying of other causes, and many more men die with prostate cancer than of prostate cancer. It is not currently possible to identify the tumors that will be “bad actors” with certainty; thus, while some men are no doubt saved by early detection and treatment of their prostate cancers, it is equally certain that others are being “cured” of clinically inconsequential tumors.
Clinical and experimental observations suggest that androgens, heredity, environmental factors, and acquired somatic mutations have roles in the pathogenesis and progression of prostate cancer.