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278 Chapter 6: Genitourinary system

Chronic cystitis, bladder stones and schistosomiasis be considered to be due to bladder cancer, until proven

through chronic inflammation and squamous meta- otherwise.
plasia predispose to squamous cell carcinoma.
Genetic: Macroscopy
Through polymorphisms of various cytochrome P450 Low-grade tumours have a papillary structure and look

enzymes, some individuals appear to oxidise ary- like seaweed. T2 is coral-like. Higher grade tumours
lamines more rapidly, which makes them more prone appear more solid, ulcerating lesions. TNM staging is
to malignancy, as this is the first step towards activa- used which requires cystoscopy and examination under
tion of these carcinogens. anaesthesia (EUA):
Acetylator status also affects predisposition. Slow Ta Papillae projecting into the bladder lumen.

acetylators de-activate carcinogens more slowly, in- Tis Transitional cell carcinoma in situ: intraepithelial
creasing the risk of cancer. tumour with a flat, red appearance.
Half of Caucasians inherit the complete lack of the T1 Started invading bladder wall: in mucosa or

Glutathione S transferase M1 allele. This enzyme submucosa (not palpable at EUA).
detoxifies carcinogens and these individuals have al- T2 Superficial muscle involved (rubbery thickening
most twice the risk of bladder cancer compared to on EUA).
those with one or two copies of the GSTM1 allele. T3 Deep muscle involved, through bladder wall
Radiotherapy, for example for pelvic tumours, pre- (mobile mass).
disposes to later development of bladder cancer. Cy- T4 Invading adjacent structures (fixed mass).
clophosphamideisanimportantcauseofbladdercancer.
It generally appears within a decade of treatment and is Microscopy
dose-related, but the risk is reduced by the concomitant Transitional cell carcinomas are graded from I to IV or
use of Mesna. G1 to G3, according to the cellular and nuclear pleomor-
phism and mitoses.
Pathophysiology G1 Well-differentiated.
It is thought that in most cases, the bladder and ureters G2 Moderately well differentiated.
become exposed to carcinogenic agents which are ex- G3 Poorly differentiated/anaplastic.
creted in high concentrations in the urine. This may ex-
plain why, in many cases, there is a ‘field change’ to the Complications
whole of the urothelium from renal pelvis to urethra, so Tumours of stage >T3 metastasise, but this is uncom-
that multiple and recurrent tumours occur. However, an mon.Thereisspreadtolymphnodesandvascularspread
individual’stumourshavealsobeenshowninmanycases to liver and bone.
to be monoclonal, so that local spread may also be partly
the cause. Adenocarcinoma arises from the urachal rem- Investigations
nants in the dome of the bladder. Cystoscopy is the main investigation, although all pa-
tients should also have a renal US or CT to exclude renal
Clinical features tumour or obstruction. IVU is useful at showing any
The most common presenting feature is painless frank filling defects in the ureters, as well as the bladder. If
haematuria. Other symptoms include pain and symp- IVU is not possible (e.g. due to renal impairment), then
tomssuchasincreasedurinaryfrequency,dysuriaand/or ureteroscopy and/or retrograde contrast studies should
urgency. Whilst all these symptoms are most commonly be performed from the bladder upwards.
caused by other conditions such as urinary tract infec-
tion, if they persist, bladder carcinoma should be sus- Management
pected. Pain may be felt in the loin when there is ob- Depends on stage:
struction, or suprapubically if there is invasion through i TisorTa, and T1 are initially treated by cysto-
the bladder wall. Haematuria over the age of 40 should scopic transurethral resection of the bladder tumour