Benign Prostatic Hyperplasia: Pathogenesis and Clinical ...

Benign Prostatic Hyperplasia: Pathogenesis and Clinical Findings

Hormonal alterations (result of aging process)

    -> Incr testosterone to DHT conversion via 5-alpha-reductase -> DHT binds to AR within prostate cells, especially in transitional zone

    -> Incr aromatization of androgens to estrogens via enzyme P450 aromatase -> Estrogen binds to ERs in the prostate -> altered gene expression

-> Initiation of ER and AR -dependent production & secretion of peptide growth factors (IGF-1, EGF, FGF-related proteins)

Inflammation & immune dysregulation -> Bacterial infection, diet, hormones, urine reflux, autoimmune response, or combination -> Incr proliferation of immunocompetent cells (lymphocytes, macrophages, granulocytes) -> Prostate Inflammation: Incr tissue injury and activation of inflammatory cytokines (IL-2, IL-15, IL-17) -> Chronic process of tissue remodeling activates hyper-proliferative programs via Incr growth factors and Decr apoptosis -> Stromal proliferation, transdifferentiation, and extracellular matrix production -> Bladder outlet obstruction due to mass effect (static component)

 - Postmicturition: Dribbling, incomplete emptying

 - Voiding Symptoms: Hesitancy, weak steam, intermittency, straining

 - Storage Symptoms: Urgency, nocturia, incontinence, frequency

Chronic retention of urine & inability to completely empty the bladder -> Hydronephrosis, Acute or chronic renal injury, Hematuria, Urinary retention, UTIs & bladder stones

#BPH #Benign #Prostatic #Hyperplasia #Prostate #Pathophysiology #Urology #Signs #Symptoms #Diagnosis
Contributed by

The Calgary Guide to Understanding Disease
Account created for The Calgary Guide to Understanding Disease - Linking pathophysiology to clinical presentation -

Related content