Urinary System 2 Tumours of the kidney, urinary tract and prostate Professor John Simpson.
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Transcript of Urinary System 2 Tumours of the kidney, urinary tract and prostate Professor John Simpson.
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Urinary System 2Tumours of the kidney, urinary
tract and prostate
Professor John Simpson
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Kidney, urinary tract and prostate - the important “tumours”
• Kidney– nephroblastoma (Wilms’ tumour) – children– renal cell carcinoma - adults
• Urinary tract– transitional cell (urothelial) tumour– squamous carcinoma of the bladder
• Prostate– (prostatic hyperplasia)– prostatic carcinoma
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Putting them into perspective -
• kidney and urinary tract tumours are generally less common in Africa, than in Europe, N America & Australasia– part of that difference is due to differences in
age expectations– the rest? - ? genetic ? environmental
• prostate hyperplasia and carcinoma common in races other than orientals
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Tumours of the kidney
• benign tumours clinically unimportant– almost always small, so just incidental
findings - e.g. cortical adenoma found in 20% autopsies
• metastatic tumours surprisingly uncommon, despite massive renal blood flow
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Malignant tumours of the kidney
The only important ones are -
• nephroblastoma (Wilms’ tumour)
• renal cell carcinoma
• transitional cell carcinoma of renal pelvis (essentially part of urinary tract)
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Where would malignant tumours of the kidney spread to?
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Nephroblastoma(Wilms’ tumour)
• one of commonest intra-abdominal tumours < 10 yrs age, but still not common
• occasionally bilateral
• mostly 1-5 years (can even be congenital)
• highly malignant tumour of mesoderm (renal blastema) – often already spread to lungs at time of diagnosis
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Nephroblastoma
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Nephroblastoma (Wilms’)
• usually quite big tumour– often presents as abdominal mass
• extension through renal capsule common• despite malignancy, excellent results if it
can be treated aggressively– combination of radiotherapy, nephrectomy
and chemotherapy
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Renal cell carcinoma(adenocarcinoma of the kidney)
• commonest (~90%) renal malignancy in adults, but < 3% all malignancies in countries where it is commonest (less common in Africa)
• ages 50s+ and male:female 2:1• usually large bulging tumour at renal pole (upper
> lower)• yellowish cut surface, often with cysts and
haemorrhage• often apparently sharp margins, due to
pseudocapsule
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Histology of renal cell CA
• derived from renal tubular cells
• 80 % are “clear cell” adenocarcinomas– abundant clear or granular cytoplasm -
contain glycogen and fat• (other histological types (“papillary” and
“chromophobe”) have better prognoses)• (classification of renal cell CA can now be based on
correlation of genetic and histological changes)
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Spread of renal cell carcinoma
• local, lymphatic and blood
• may invade perinephric fat
• can invade pelvi-calyceal system
• lymphatic – first to para-aortic nodes
• often invades renal vein………– blood spread most often to lungs (50%),
bones (33%), adrenals and brain
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Presentation of renal cell CAusually late – so often CA has already spread
• most often, haematuria • abdominal mass +/- loin pain
but, one of the great “mimickers”• metastasis (classically cannonball metastases in
lungs)• fever of unknown origin/night sweats• weight loss, malaise• paraneoplastic phenomena -
- secretion of erythropoietin, renin, parathormone, corticosteroids, eosinophilia, amyloidosis etc
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What could be the effects of secretion of erythropoietin, renin or parathormone?
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Prognosis of renal cell CA
5-yr survival rate overall ~ 50%• 70 % if no metastases• 15-20% if renal vein involved
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Risk factors for renal cell CA
• cigarette smoking is only definite association – e.g. 30-40% occur in smokers in UK, where <20% population smoke
• (rarely, genetic factors – e.g. in the very rare von Hippel-Lindau disease)
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URINARY TRACT TUMOURS
• the only common intrinsic tumours of the urinary tract are those of transitional epithelium (urothelium)
• variety of names - – transitional tumours– or transitional epithelial tumours– or transitional cell tumours– or urothelial tumours
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Transitional tumours
• common• spectrum of “benign” to malignant• behaviour can change with time, i.e. to become
more malignant• malignancy preceded by dysplasia/CA in situ• sometimes multiple
– suggesting field change in epithelium
• tract contents promote tumour development
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Does that remind you of tumours anywhere else?
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Transitional tumours
• age 50s - 70s: men > women• white > black >> oriental populations• arise anywhere in urinary tract, but bladder
(especially bladder base) >> pelvis/calyces > ureters > urethra
• often polypoidal & papillary/fronded, especially at first - if sessile (flat), more likely to be malignant (like colon)
• tumours may be preceded by dysplasia/CIS• “benign” = transitional papilloma: malign. =
transitional carcinoma
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Transitional tumours
• presentation- most often, haematuria- but also urinary infection and/or obstruction
• often prolonged natural history • carcinomas may present with metastases
– spread – local, lymphatic & blood – details depend on site of primary
• tumour cells exfoliate into urine, so cytological examination of urine can sometimes help in diagnosis
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Aetiological factors
chemical carcinogens• cigarette smoking• aniline dyes (dye, rubber, plastic, cable & gas
industries) – intermediate metabolites filtered by kidney, then carcinogenic substances released by β-glucuronidase (helped by acidity of urine)
• rarely, analgesic abuse (renal pelvis)chronic inflammation – not related, but
- schistosomiasis (bladder) and calculi (pelvis and bladder) both associated with squamous CA
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What tumours other than those of the urinary tract itself could cause urinary tract obstruction?
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Main causes of prostatic enlargement
• benign nodular hyperplasia
• carcinoma
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Benign nodular hyperplasia (BNH)
• affects most men, usually starting around age 50• (after age 40 or so, prostate gradually gets bigger)• incidence/severity increase with age (75% by 70s)• hyperplasia of connective tissue and glands – usually 60-
100 g (normal = ~30G)• involves more “central” parts, espec lateral or “median”
lobes, which are most sensitive to oestrogen• probably due to age changes in sex hormone levels (?
androgen:oestrogen levels) – orchidectomy protective
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Effects of BNH
• urinary infection and/or obstruction
• prostatic infection & infarction
• but not premalignant
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BNH of prostate
effects/complications• mainly due to abnormal bladder sphincter, so
disturbed micturition (“prostatism”)• partly mechanical effects of the enlarged
gland• but also smooth muscle-mediated contraction
of the prostate– prostatic smooth muscle tension mediated by α1-
adrenoreceptor localized in stroma– hence use of α-adrenergic receptor antagonists for
relief of urinary obstruction
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Prostatism
• frequency• nocturia• difficulty in starting and stopping• overflow dribbling• dysuria (painful micturition)
• in many cases, sudden, acute urinary retention
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Effects of BNH
• inability to empty bladder completely– ? due to raised level of urethral floor causing
residual urine
• static fluid vulnerable to infection
• catheterization or surgery can introduce organisms
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BNH of prostate
• secondary changes occur in bladder– hypertrophy, trabeculation and diverticulum
formation
• acute retention
• dilatation of urinary tract
• secondary urinary tract infection
• renal damage, even failure
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Carcinoma of the prostate
• in Europe, N America (blacks>whites) and Australasia, commonest male CA
• commoner than any female cancer• incidence increasing everywhere, but especially
in Africa - ? higher than elsewhere?• family history raises risk ~ x 2 or 3 • uncommon in orientals (but incidence increases
if they move to regions with higher incidence)• age of incidence later than any other CA
– old age (60s -80s)– younger in patients with family history
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Carcinoma of the prostate
• adenocarcinoma– probably arises from PIN (prostatic
intraepithelial neoplasia)
• affects peripheral parts of glands (especially posteriorly) – more androgen dependent
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Effects of CA prostate• local = same as those of BNH (prostatism,
obstruction, infection etc), but very often no local effects
• distant, due to metastases - local, lymph and blood – often presents with metastasis – “occult
carcinoma”
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Spread of CA prostate
• local – especially seminal vesicles and base of bladder
• blood - chiefly to bones, particularly axial skeleton (lumbar spine, proximal femur, pelvis, thoracic spine) and ribs– bony metastases typically osteoblastic/osteosclerotic
(in men, highly suggestive of CA prostate)– massive visceral dissemination unusual
• lymphatic spread – common, often before blood spread– initially to the obturator nodes followed by pelvic,
presacral, and para-aortic nodes
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Aetiology
• suspected risk factors are age, race, family history, hormone levels and environmental factors
• no proven environmental factors- e.g. increased consumption of fats or lack of protective factors in diet
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Aetiology
• like BNH, androgens believed to play role in pathogenesis– orchidectomy protective– oestrogens sometimes used in treatment
• genetic factors 1. increased incidence if family history 2. prostate cells with short repeats of CAG are highly
sensitive to androgens• shortest CAG repeats are in African-Americans, while longest are
in orientals• African-Americans have highest incidence of prostate cancer and
orientals the lowest
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PIN (prostatic intraepithelial neoplasia)
• likely precursor of CA• focal dysplasia/CIS of the glandular epithelium• may occur beside CA or on its own• low grade changes common, even in middle age
– not an indication for concern, but ? can evolve• if high grade PIN, say in a biopsy, surveillance
for CA mandatory• (anti-androgenic therapy can let it regress)
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Prognosis
• as with most tumours, variable according to grade and stage of tumour
• Gleason grading = histological grading of prostatic CA
• “latent” CA prostate– discovered as incidental finding in prostates
removed for BNH or at autopsy– very common in autopsies in very old men
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Markers of use in CA prostate
• prostate specific antigen
• prostatic acid phosphatase
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Prostate specific antigen (PSA)
• produced by prostatic epithelium– serine protease which liquefies semen coagulum
which forms after ejaculation
• normally tiny amounts in serum• elevated levels can occur in localised or
metastatic prostate CA• but levels can increase in other conditions of the
prostate and in ~ 20% CA cases PSA may be normal, so no value as screening test
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Prostatic acid phosphatase
• prostatic acid phosphatase– produced by prostate and seminal vesicle– present in semen
• serum levels may be raised in prostate disease, especially if CA metastasised
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Relationship between BNH and CA prostate
CA not 2ndry to BNH, because -• repeated TURs (transurethral resections) for
BNH don’t affect frequency of CA• lesions affect different parts of gland• geographic differences in incidence, e.g.
– BNH UK > Scandinavia– CA Scandinavia > UK
![Page 74: Urinary System 2 Tumours of the kidney, urinary tract and prostate Professor John Simpson.](https://reader035.fdocuments.in/reader035/viewer/2022062308/56649d985503460f94a82b14/html5/thumbnails/74.jpg)
Kidney, urinary tract and prostate - the important “tumours”
• Kidney– nephroblastoma (Wilms’ tumour) – children– renal cell carcinoma - adults
• Urinary tract– transitional cell (urothelial) tumour– squamous carcinoma of the bladder
• Prostate– (prostatic hyperplasia)– prostatic carcinoma