GenitoUrinary Cancer

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Genito-Urinary Tumors Surgery 3 Prostate Cancer Hormone control o The prostate starts to develop at puberty, under the contol

l of the androgenic sex hormones testosterone and DHEA. Their secretion is regulated by pituitary hormones: LH stimulates testosterone secretion by the testicles, while ACTH stimulates DHEA secretion by the adrenal glands. These two hormones, testosterone and DHEA, control prostate function. The prostate secretes seminal fluid, which serves manly as a liquid medium for sperm Hypothalamus. This gland exerts central control on pituitary hormone release Pituitary Adrenal Prostate Testicle Cancer of the prostate o Adenocarcinoma of the prostate usually occurs at the periphery of the gland (contrary to prostate adenoma), and this explains why urinary symptoms are absent in the initial stages Known risk factors o Family history: at least two close relative (father, brother, grandfather) with prostate cancer o Carribean or African origin Potential (controversial) risk factors o Environmental factors such as pesticides and cigarette smoke o Certain treatments such as testosterone Frequency o Prostate cancer is rare before the age of 50 years (0.3%). Its clinical incidence then increases rapidly. Nearly half of all cases of prostate cancer are diagnosed after 75 years of age Stages o Stage 1 chance of discovery of a non palpable tumor. An isolated rise in the PSA level can lead to diagnosis

Stage 2 tumor limited to the prostate 2a involvement of one prostate lobe 2b ivolvement of both lobes o Stage 3 tumor extension beyond the prostatic capsule 3a extracapsular extension 3b extension to the seminal vesicles o Stage 4 extension to adjacent organs (here, the bladder) N+ regional LN involvement M distant metastases Who qualifies? o A1 all men aged from 50 to 75 years (life expectancy at least 10 years): routine yearly screening. If the first PSA value is less than 1 ng/ml, the next screening test may be done two years later o A2 screening for prostate cancer must start earlier (45 years) in teo categories of men at risk: Family history: at least two close relatives (father, brother, grandfather) with prostate cancer Carribean or African origin How? o B1 rectal digital examination o B2 measurement of PSA (prostatespecific antigen) Serum total PSA assay is the first test o PSA cut-points: generally 4 ng/ml. values can vary from one laboratory to another and from one test method to another. Consecutive tests should be done in the same laboratory to ensure that the same test is used o PSA > 4 ng/ml: urologist opinion; possible need for prostatic biopsies o PSA < 4 ng/ml: repeat the assay each year o PSA < 1 ng/ml: possible to repeat the assay every two years (discuss) Rule out recent urogenital infection (urinalysis) What is PSA? o PSA is a biological marker secreted by the prostate. Some PSA circulates in free form, while the rest is bound to other o

proteins. The proportion of the bound form rises in prostate cancer Endorectal sonography o Used to study the structure of prostatic tissuye, measure abnormalities, and guide prostatic biopsies Prostatic biopsies o BI before the examination A few days before Blood tests (clotting) and urinalysis (infection). Two hours bedore the examination Antibiotic prophylaxis Lavage No need to fast o B2 the examination No need for hospitalization (usually) Not painful (local anesthesia in some cases) Time: about 15 minutes Endorectal sonographic guidance Abdominopelvic CT scan o To determine node extension Endorectal MRI o To assess periprostatic extension before treatment Criteria of choice o Life expectancy The age limit for curative (surgery, irradiation) is usually 75 years (or life expectancy 10 years or less) Tumor stage PSA level, biopsy findings, gleason score General state Available treatments o Locoregional treatments Surgery Radiotherapy Brachytherapy o Systemic treatments Hormone therapy Chemotherapy Principles o Prostate cancer is hormone-dependent. Castration (medical or surgical) and

estrogen are both effective, especially in locally advanced or metastatic forms. The aim is to suppress androgen secretion and to obtain a minimal blood testosterone level of <3 ng/ml (level of castration). Androgen secretion is only properly suppressed if treatment is strictly adhered to Medical castration with LHRH analogs (central action) Androgen antagonists: competitive blockade of androgen binding to receptors on malignant prostatic cells Overview o Indications Initially used in early-stage disease, chemotherapy is now reserved for hormone-resistant disease, i.e. after failure of hormone therapy Principles Cells are targeted during division. The main target is the DNA contained in the nucleus, and the spindles that guide DNA division. The aim is to kill malignant cells Surgery o Locoregional: if urethral compression (transurethral resection) or ureteral compression o Bone surgery: for osteolytic lesions (consolidation) or spinal compression due to vertebral metastasis Other treatments o To relieve symptoms, prevent complications, or slow disease progression

RENAL CANCER Overview o Renal cell cancer 2% of all cancers, majority of renal malignancies o Incidence is rising better imaging o Surgery the only evidence-based curative therapy for patient with localized disease. Where indicatedPartial Nephrectomy should be considered

New generation of targeted medical therapies increased the survival of patients with metastatic disease o Transitional cell carcinoma of the renal pelvis and ureter is rare o Renal cancer 85% are adenocarcinoma or renal cell carcinoma o Arising from the tubular cell in the renal parenchyma o TCC 10%, arising from the urothelium of the renal pelvis and the ureter Epidemiology o RCC 2% of all cancer diagnosed worldwide o Incidence 60-70 y/o o Male to female ratio: 1.5:1 o 50% of patients will die of their condition and 25% will have metastasis at presentation Etiology o 98% are sporadic o 2% occur in individuals with inherited genetic redisposition o Environmental factors Smoking Obesity Low socio-economic status Nutrition plays important role o Anatomical factors Congenital and acquired abnormalities of the anatomy Horseshoe kidney and acquired cystic kidney o Medical factors Hypertension Dialysis o Genetic factors Von-Hippel-Lindau (VHL) Hereditary papillary RCC Familial clear cell RC Clinical features o Rarely with classic triad of flank pain, hematuria and flank mass o 50% of RCC are detected incidentally o Full medical history, fatigue, weight loss, pyrexia o Paraneoplastic syndrome Hypertension Hypercalcemia o

Anemia Polycythemia Stauffers syndrome Investigations o CBC, blood chem. o UTZ cystic, solid and complex renal lesions o Contrast enhanced CT of the chest and abdomen gold standard in staging Treatment o Surgery is the gold standard in the treatment of renal cancer o Radical nephrectomy (open or lap) o Partial nephrectomy absolute in solitary functioning kidney; relative in bilateral, multifocal or CRI. Elective in less than 7 cm with normal contralateral kidney o For metastatic disease: poor prognosis o Immunotherapy First line treatment (interleukin, interferon); TKI (Sunitinib and Sorafenib) Prolongs progressions free survival o Radiotherapy limited role mainly for palliation of painful bone mets o RCC are not sensitive to traditional chemotherapeutic agents

Transitional Cell Ca of the Ureter and renal Pelvis & the Ureter Presents with painless visible hematuria Clot colic Dx is made by CT urogram or IVU Ureteric cytology, retrograde pyelography and uteroscopic biopsy Treatment o Lap or open radical nephroureterectomy o Percutaneous or ureteroscopic tumor ablation Bladder Tumor Introduction/Epidemiology o Most common tumor the the urinary system o Male to female ratio 5:2 o 80% of new cases diagnosed in patients over 65 years old o Biggest risk factor smoking

Occupational exposure to traumatic amines, printing, hairdressing, iron and aluminum processing, industrial paintings, gas and tar manufacturing Presentation o 80% painless visible hematuria o Other symptoms: dysuria, bladder pain, urgency o Painful hematuria, irritative symptoms indicates muscle invasive disease or CIS o Flank pain maybe a sign of ureteric obstruction Investigation o Urinalysis o Cytology only good for more advance tumor o Imaging o UTZ o IVU o CT urogram o Cystoscopy Procedure performed by urologist allows visual access to the urethra, prostate, bladder Treatment o Superficial bladder cancer 70-80% of newly diagnosed bladder cancer Risk of progression is slow Managed w/ TURBT and intravesical chemo Low risk tumor grade 1 or 2 Aim of treatment is to remove all visible tumor TURBT High risk tumor grade 3 or CIS Significant risk of recurrence and upstaging of their disease BCG or primary cystectomy o Muscle invasive bladder cancer 15-20% at time of presentation initial management TURBT, CT of the chest and abdomen for staging Treatment option Cystectomy o

External radiotherapy Selective presentation Neo-adjuvant (cisplatin)

bean bladder chemo

Penile Cancer Uncommon malignancy less than 1% of all male cancer Early recognition provides the best chance of cure High index of suspicion for any rapidly changing lesion or one which has failed to respond to initial treatment Risk factors o Common in men 50-70 o Presence of foreskin, phimosis, poor hygiene o HPV infection, chronic inflammation, smoking, chewing tobacco Investigation o All patients with suspected penile cancer should have a bx o 95% are SCC o 5% are melanomas, sarcomas, or basal cell carcinoma o CT SCAN chest, pelvis, and abdomen to assess metastasis o Surgical staging lymph nodes Treatment o Partial or total penectomy w/ adequate margin o Durgical lymph node staging for palpable and non palpable nodes o Role of chemo and radiotherapy Neo-adjuvant therapy to render inoperable cases operable Adjuvant treatment for high risk disease w/ evidence of nodal spread Palliative treatment for aggressive, metastatic disease in patients with good performance status

Testicular Tumors

95% are germ cell tumors: 60% are seminomas, 40% are non seminomas Non germ cell tumors uncommon (Leydig cell tumors, sertoli cell tumors and lymphomas) Testicular germ cell tumors most common neoplasm in male for age 15-44 although averall they are rare (6/100,000) Lymphatic spread is most common cause of matastasis via spermatic cord lymphatics to the retroperitoneal lymph node Hematogenous invasion lung, liver, bone, brain Clinical assessment o 90% presents w/ a lump, 31% have pain o Serum tumor markers (AFP and HCG) o UTZ 100% sensitivity to confirm testicular tumor o CT Scan of chest, abdomen, pelvis done for staging purposes after radical orchidectomy o Bone scan can also be done patients w/ increased alkaline phosphatase o CT or MRI of the brain for signs of brain mets Management o For seminoma: surveillance, radiotherapy, chemo o For non seminoma: surveillance, chemo (BEP), RPLND

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