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Ul9 Urology Toronto Notes 2023

Approach to Renal Stones

Holical CT

Abtlomon/Polvis Although hypercalciuria is a risk factor

for stone formation,decreasing dietary

calcium is NOT recommended to prevent

stone formation.Low dietary calcium

leads to increased Gl oxalate absorption

and higher urine levels of calcium

oxalate

[ CT shows stone ] CT shows no stone -

Consider alternate causes i

[

KUB x-ray ]

y I

[Non-urgent pathway )

Stones and Infection

If septic,urgent decompression

via ureteric stent or percutaneous

nephrostomy is indicated. Definitive

treatment of the stone should be

delayed until the sepsis has cleared

Urgent Intervention required if:

1. Solitary kidney

2. Bilateral stones

3.Intractable pain or vomiting

4. Acute renal failure

i

Likelihood of

stone passage

Low High

I I

J [Non-uric acid stone] c ) c Uric acid stone Intervention Observation Indications for PCNL

Site >2 cm

• Staghorn

• UPJ obstruction with correction of

obstruction

• Calyceal diverticulum

• Large cystine stones (poorly

fragmented with SWL)

• Anatomical abnormalities preventing

retrograde access

• Failure of less invasive modalities

I

[Dissolution therapy ]

SWL

Ureteroscopy

PCNL

Stent/Nephrostomy

Figure 10. Approach to renal stones

Investigations

Table 12. Investigations for Renal Stones

CBC. U/A.Urine KUB x-ray Uric Acid PTH,24 h urine x 2 for

volume, Cr. Ca2\ Na •,

PO

*

1-, Mg 2’, oxalate,

citrate,± cystine

CT Scan (non-contrast) Abdominal

Ultrasound

Cystoscopy

C A S

Who gets it? iThose concerning Stone not seen

lor bladder stone on KUB

Recurrent Capstone

formers

paediatric cases

fveryone First episode renal colic Paediatric cases.

pregnant patients,

recurrent stone

formers,unsure

of Dx

90% ol stones arc Able losce adjaccnl organs. Identify and follow

exact location of stone(s).

plan for surgery,etc.

Helps rule out uric acid Can assess density olstone Visualize

stones (not visible on Gold standard diagnostic lest hydronephrosis

x-ray)

Most

Visualize bladder Suspected uric acid

Can provide access stone (urine PH

to ureter for stent <5.5 might suggest

placement if uric acid stone)

needed

Why isit done? Need lo rule out metabolic

cause lor stones

May show signs

ol infection,!

sensitivities

up stone without

radiation exposure

radiopaque

Good for follow-up

Cautions Presence of Not all stones visible Radiation (especially if

female of child bearing age)

Must be a non-contrast scan

leukocytes NOT on x-ray

always indicative of Do not mistake

infection phleboliths lor stonesl

Treatment

KIDNEY STONE Acute Treatment

1'

MEDICAL -<3

I

G

unolgusiciantiamutic

NSAIDs (lower mtru uroUjr.il pressure)

«blockers (increase rate of spontaneous passage in distal ureteral stones)

± antibiotics for bacteriuria

IV fluids if vomiting (do NOT promote stone pussegel 24 h urine collections must be done

AFTER discontinuing stone preventing/

promoting medications

J

INDICATIONS for

HOSPITAL TREATMENT

JTi r1

L J

intractable pain

intractable vomiting

fever (suggests infection)

compromised renal function (single kidney,bilateral obstructing stone)

pregnoncy

YES

Detailed metabolic studies are NOT

recommended unless complex patient

(recurrent stone formers,pregnancy,

paediatric patients,strong FMHx.

underlying kidney or systemic disease,

rare stone types,etc.)

A Intarventi k

1st lino: urotoric stent

ivm cystoscopy)

2nd lina:percutaneous

nephrostomy

+

1 V

Figure 11. Acute treatment of kidney stone

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U20 Ufology Toronto Notes 2023

KIDNEY STONE KIDNEY

Elective Treatment a Slockcrs as Medical Eipalsivc Ihcrapr lor

Ureteral Stones

C othrane OB Syst Rev 2018:4

^

D008509

Purpose loassesseffects of o-blockerscompared

with standard therapy for ureteral storesIcm or

smaller in adult patients presenting with symptomsof

uieteial stone disease.

Methods: mete analysis of(1RCIs for ureteral stone

passage in 10509 adidt patients.

Results:treatment with an o-blocker resulted in

-creased stone clearance (RR 1.45. 95% £1:1.36-1.55,

low qualitye«idence|. Subgroup analyses suggest

that o-blockers may be less effective for smaller

stones (s5 mm).

Conclusions a blockers likely increase stone

clearance,but also slightly mcrease the risk of mayor

adverse events.

>2 cm PCNL

1-2 cm SWL,URS,or PCNL

<1 cm URS or PCNL

MEDICAL

URETER.>10 mm Stones <5 mm likely to pass

spontaneously

Likely conservative if ureteral stone

<10 mm or kidney stone <5mm and

no complications/symptoms well

controlled

PO fluids and -Alockers

Treatment guided by stone type

(see Table 13)

Periodic imaging to monitor stone

position and assess for hydronephrosis

r

1st line:SWL or URS

2nd line:PCNL in rare cases

3rd line: laparoscopic/open stone

removal (rare!

INTERVENTIONAL

(if symptoms worsen

or fail to improve)

BLADDER

Cyslolitholapaxy ± TURP if BPH

Remove obstruction

(TURP, stricture dilation) Main Elective Treatment Options

1. Conservative medical management

2.Extracorporeal shockwave lithotripsy

(SWL):less invasive (sedation only,

no internal instrumentation),less

successful

3.Ureteroscopic (URS) laser lithotripsy:

slightly more invasive (usually GA

or spinal,instrumentation required,

usually outpatient),more successful

4.Percutaneous n.phrolithotomy (PCNL):

more invasive (requires GA.involves

puncture of kidney,often needs

admission),most successful for larger

stones

S Laparoscopic or open surgery:rare in

modern era unless performing other

concomitant procedure (e.g.UPJ

obstruction correction)

©Amy Cao 2019

Figure 12. Elective treatment of kidney stone

Prevention

•dietary modification

increase fluid (>2 L/d), citrate intake (lemon juice, orange juice)

reduce animal protein, oxalate, Na+,sucrose, and fructose intake

avoid high-dose vitamin C supplements

•medications

• thiazide diuretics for hypercalciuria

• allopurinol for hyperuricosuria

potassium citrate for hypocitraturia, hyperuricosuria

Tuberous Sclerosis

•Syndrome characterized by mental retardation, epilepsy, and adenoma sebaceum

•45-80% of patients also present with angiomyolipomas, which are often multiple and bilateral

Table 13.Stone Classification

Type of Stone Calcium (75-85%) Uric Acid (5-10%) Struvite (5-10%) Cystine (1%)

Etiology Hypercalciuria

Hyperuricosuria (25% of patients

with Capstones)

Hyperoxaluria (<S% of patrents)

Hypocitraturia (12% of patients)

Other causes:

Hypomagnesemia - associated with

hyperoxaluria and hypocitraturia

High dietary Ha

Decreased urinary proteins

High urinary pH,low urine volume (c.g.

Gl water loss)

Hyperparathyroidism,obesity,gout.DM

Radiopaque on KUB x-ray

Reducing dietary Ca J'isKOI an effective

method of prevention/treatment

Uric acid precipitates in low volume

acidic urine with a high uric acid

concentration:

Hyperuricosuria alone

Drugs (ASA,thiazides)

Diet (purine-rich red meats)

Hyperuricosuria with hyperuricemia (magnesium ammonium phosphate)

Infection withurea-splitting

organisms [Proteus.Pseudomonas, mucosal absorption and renal tubular

absorption o( dibasic aminoacids results in

Hycoplosmo.Scnalio. S. orirons ) "COLA"in urine (cystine, ornithine,lysine,

results in alkalineurinary pH arginine)

and precipitation of struvite

Autosomal recessive delect in small bowel

Providenoa.Klebsiella.

Gout

High rate of cell turnover or cell

death (leukemia,cytotoxic drugs)

Key features Perpetuates U1Ibecause the stone Aggressive stone disease seen in children

itself harbours organism

Acidic urine.pH <5.5 (NOT necessarily Stone and all foreign bodies must be Recurrent stone formation,

cleared to avoid recurrence

Associated with staghorn calculi

Positive urine dip and cultures

Hote:[. coli infection does not

cause struvite stones

M:F-3:1,UII more common in

female

Complete stone clearance

ABxlor 6 wk

Regular follow-up urine cultures

Radiolucenton KUB x -ray

Radiopaque onCl and young adults

elevated urinary uric acid) FMHx

Often staghorn calculi

Faintly radiopaque on KUB x-ray

Positive urine sodium nitroprusside lest,

urine chromatography lor cystine

Fluids to increase urine volume to >2 L/d

For calcium stones:Increase citrate in

diet,reduce salt,moderate oxalate-rich

foods,weight loss

Procedural/Surgical treatment Calcium oxalate:thiazides.

potassium citrate,t allopurinol

Mixedcalcium and struvite:ASx (stone

must be removed to treat infection)

Increased fluidintake

Alkalinization ol mine to pH 6.5

to1(potassium citrate,sodium

bicarbonate)

t allopurinol

Be carelul not be make urine too

alkaline(pH >7).can result in calcium

phosphate stones

Increased fluid intake (3- 4 L of urire/d)

Alkalinizc urine (bicarbonate,

potassium citrate),penicillamine/omercaptopropionylglycine or Captopril

(form complex with cystine)

SWL not efleclive

Treatment

MedicalIIstone <5 inm and no

complications

if stone >5 mm or presence of

complications +

Can observe selected,

asymptomatic renal stones

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U21 Urology TorontoNotes 2023

Urological Neoplasms

Approach to Renal Mass

[ Ultrasound ]

there is controversy over optimal

management of smallrenal masses T I

( Cystic ] Solid )

r

Percutaneous needle biopsies of cystic

renal masses may lead to peritoneal

seeding

Dense

Calcified

Septated

Hypoechoic CT

No calcification

Thin wall

(exclude

angiomyolipomal

1 f 1f T I

[ Stop ]

Small mass

(<4 cm)

Large mass

(>4 cm)

CT with contrast

’

Possible

aspiration or biopsy

Tuberous Sclerosis

• Syndrome characterized by mental

retardation,epilepsy,and adenoma

sebaceum

• 45-80%of patients aIso present with

angiomyolipomas.which are often

multiple and bilateral

I

T

Surgery ) ( Surveillance | Surgery J Possible

surveillance

Figure 13. Workup of a renal mass

'Imaging modality may bedifferent in cases of contrast allergy or elevated creatinine

APPROACH TO SMALL SOLID RENAL MASSES

• Initial workup:kidney function (creatinine, eGl;

R), chest x-ray, contrast CT or MR1, ± renal biopsy

• Limited life expectancy:watchful waiting

• <2 cm: active surveillance with imaging q3-6 months, proceed to intervention if growth >2 cm, or

growth >0.5 cm/vear, or patient preference

• 2-4 cm:active surveillance or definitive therapy (biopsy + thermal ablation or partial nephrectomy, if

feasible)

Benign Renal Neoplasms

CYSTIC KIDNEY DISEASE

• simple cysts: usually solitary or unilateral

• very common: up to 50% at age 50

• usually incidental finding on abdominal imaging

• Bosniak Classification is used to stratify for risk of malignancy based on cyst featuresfrom

contrast CT

• polycystic kidney disease

• autosomal recessive:multiple bilateral cysts, often leading to early renal failure in infants

• autosomal dominant: progressive bilateral disease leading to H'

I

'N and renal failure, adult-onset

• medullary sponge kidney:cystic dilatation of the collecting ducts

usually benign course, but patients are predisposed to stone disease

• von Hippel-Lindau syndrome: multiple bilateral cysts and/or renal cell carcinomas (50% incidence of

RCC)

renal cysts, cerebellar,spinal and retinal hemangioblastomas, pancreatic and epididymal cysts,

pheoch romocytomas

Table 14. Bosniak Classification of Renal Cysts

Class Features Risk of Malignancy Management Plan

I(simple cyst) Round,no septa/calcificationsf Near zero No follow- up

enhancement,homogeneous,

<20 HU

Thin seplnm (<1mm),fine

calcification,no enhancement.<3

cm.>20 HU

II(simple cyst) Minimal No follow-up

r T

IIF (minimally complex cyst) Multiple thin septa,calcifications. 5-20%

no enhancement.>3 cm,>20 HU

Irregular,thickened,calcified

septa with enhancement

Follow-up,imaging qG-12 mo.

surgical resection if lesion evolves

Surgical resection

" growing literature suggesting

surveillance might be safe

Surgicalresection

L J

III(complex cyst) >50%

'growing literature suggesting

might be lower +

Irregular,thickened,calcified >90%

septa with enhancement,

enhancing soft

- tissue components

IV (likelymalignant)

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U22 Urology Toronto Notes 2023

Gerota'

Table 15 sfascia . Benign Renal Masses

Angiomyolipoma (Renal Hamartoma) Renal Oncocytoma

-r

Epidemiology <10“

= of adultrenal tumours 3-7% ofrenal tumours T4 Adrenal

1 gland F>H H>F

Oncocytomas also found in adrenal,thyroid,and

parathyroid glands

Clonal neoplasm consisting of blood vessels (angio ).smooth Spherical,capsulated with possible central scar

muscle ( myo-).and fat ( lipoma)

Hay extend into regional lymphatics and other organs and

become symptomatic

Incidental finding on CT

Negative attenuation(- 20 HU) on CT is pathognomonic

Rare presentation of hematuria,flank pain,and palpable

mass (same as RCC)

Hay considersurgical excision or emboliration if

symptomatic (pain,bleeding) or higher risk of bleeding (e.g. Partialradical nephrectomy for large masses

pregnancy)

Potential role for mechanistic target of rapamycin (mTOR)

inhibitors in unresectable/metastatic disease

Follow with serial U/S

20 = associated with tuberous sclerosis (especially if

multiple,recurrent)

'

£

Characteristics Vein

Histologically organized aggregatesof eosinophilic cells

originating from intercalated cells ol collecting duct

Artery

Incidental finding on CT

Difficult to distinguish from RCC on imaging -treated as

RCCuntil proven otherwise

Biopsy may be performed torule out malignancy

Diagnosis

> 1 Ireter r CT

Renal

capsule

Renal cortex /

Renal medulla

Management Sunrei lance for most

SCarfy Vanderlee

^

Figure 14.RCC staging

Malignant Renal Neoplasms

RENAL CELL CARCINOMA

Etiology

• cause unknown

• originatesfrom proximal convoluted tubule epithelial cells in clear cell subtype (most common)

• hereditary formsseen with von Hippel-Lindau syndrome and hereditary papillary renal carcinoma

Epidemiology

• 85% of primary malignant tumours in kidney, ~3% of all malignancies

M:l =1.5:l

• peak incidence at ages 50-60

Pathology

• histological subtypes:clear cell (75-85%), papillary (10-15%), chromophobe (5-10%),collecting duct

(<1%),other (<1%)

• sarcomatoid elements in any subtype is a marker of poor prognosis

Risk Factors

• top 3 risk factors:smoking, HTN, obesity

• end-stage renal disease (acquired renal cystic disease)

• role of environmental exposures (aromatic hydrocarbons, etc.) remains an unproven risk factor for

development of RCC

Role of environmental exposures

(aromatic hydrocarbons, etc.) remains

an unproven risk factor for development

of RCC

RCC Systemic Effects:Paraneoplastic

Syndromes (10-40= of Patients)

• Hematopoietic disturbances:anemia,

polycythemia,raised Erythrocyte

Sedimentation Rate (ESR)

• Endocrinopathies:hypercalcemia

(increased vitamin 0 hydroxylation),

erythrocytosrs(increased

erythropoietin).HTN (increased

renin), production of other hormones

(prolactin,gonadotropins.TSH,

insulin, and cortisol)

• Hepatic cell dysfunction or Stauffer

syndrome:abnormal LFTs.decreased

W8C count,fever, areas of hepatic

necrosis:no evidence of metastases;

reversible following removal of

primary tumour

• Hemodynamic alterations:systolic

HTN (due to arteriovenousshunting),

peripheral edema (due to caval

obstruction)

Clinical Features

• usually asymptomatic:frequently diagnosed incidentally by U /SorCl'

(>50%)

• indicatorsfor poor prognosis: weight loss, weakness,anemia,bone pain

• classic “too late triad’found in 10-15%

gross hematuria 50%

flank pain <50%

• palpable mass <30%

• metastases:seen in a 1/3of new cases; additional 20-40% will go on to develop metastases (mostly in

late presentations orlarge tumours)

most common sites: bone, brain, lung, and liver

may invade renal veins and inferior vena cava (1VC) lumen

• this may result in ascites, hepatic dysfunction,right atrial tumour, varicocele, and pulmonary emboli

Investigations

• routine labs for paraneoplastic syndromes (CBC, ESR, LFTs, extended electrolytes)

. U/A

• renal U/S:solid vs. cystic lesion

• contrast-enhanced CT:higher sensitivity than U/S for detection of renal masses and for staging

purposes

• MR1:useful for evaluation of complex cystic lesions indeterminate on CT;good way to assess 1VC

thrombus

• renal biopsy:to confirm diagnosis, if considering observation or other non-surgical ablative therapy

• genetic testing:consider if l-

'

Hx of von Hippel-Lindau syndrome, non-clear cell carcinoma, bilateral/

multifocal tumour,onset <45 yr, FHx of renal tumour, or any renal tumour with Hx of pneumothorax,

dermatologic findings, associated tumours, lymphangiomyomatosis, or childhood seizure disorder

r -\

i

_ j

+

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U23 Urology Toronto Notes 2023

Staging

• involves abdo/pehrisCT,CX R, liver enzymes and Ll-

'

Ts, bone/head imaging (if symptoms dictate)

Table 16.2018 TNM Classification of Renal Cell Carcinoma (AJCC 8th edition)

T N M

IX:primary turnour cannot be assessed NX:regional lymph nodes cannot be assessed cMO no evidence of distant metastasis

T1:tumour <7cm.confined torenal

parenchyma

T1a:'

4cm

T1b:4-7 cm

NO: no regional lymph node metastasis cH1:presence of distant metastasis

N1:metastasis in regional lymph nodes pM1:presence of distant metastasis,

microscopicallyconfirmed

N Suffix

|sn):regional lymph node metastasis

identified by SLN biopsy only

(f):regional lymph node metastasis identified

by FNAor core needle biopsy only

T2:tumour >7 cm.confined torenal

parenchyroa

T2ia:>7 cm but<10 cm

T2b:>10 cm

T3:tumour extends into majorveins or

inephric tissues,but NOT into ipsilateral

enal or beyond 6erota"s fascia

T3a:into renal vein or sinus fat

T3b:into infradiaphragmatic IVC

T3c:into supradiaphragmatic IVC

per

adr

T4:tumour extends beyondGerota'

s fascia

including extension into ipsilateraladrenal

ISuffix

(m):if synchronous primary tumours are found

in single organ

Treatment

• surgical (open,

laparoscopic,robotic)

radical nephrectomy: en bloc removal of kidney, tumour, ipsilateral adrenal gland (in upper pole

tumours) and intact Gerota’

s capsule

• partial nephrectomy (parenchyma-sparing):small tumour (roughly <4 cm) orsolitary kidney/

bilateral tumours

surgical removal ofsolitary metastasis may be considered

• ablative techniques (percutaneous or lap-assisted)

radiofrequency ablation (RFA)

cryoablation

palliative radiation to painful bony lesions

• therapy for advanced stage

• nesv immunologic inhibitors (e.g. pembrolizumab, ipilimumab, nivolumab)

tyrosine kinase inhibitorsfor metastatic disease (e.g.sunitinib,sorafenib)

• IFNa:monotherapy has been largely replaced by molecularly targeted agentslisted above

Prognosis

• stage at diagnosis most important prognostic factor

• Tl:90-100% Syrsurvival

T2-T3:60% 5 yr survival

• metastatic disease:<5% 10 yr survival

• predictors of relapse: tumour grade, local extent of the primary tumour, presence of local metastases,

histological subtype

Carcinoma of the Renal Pelvis and Ureter

Etiology

• risk factors include:

smoking

dietary/chemical exposures (aristolochic acid, industrial dyes and solvents:aniline dyes)

analgesic misuse (acetaminophen, ASA, and phenacetin)

• Balkan nephropathy

prior exposure to cyclophosphamide

Epidemiology

• rare:accountsfor 5% of all UC

• frequently multifocal, 2-5% are bilateral

• M:F=3:1

• relative incidence: bladder:renal:ureter=100:10:1

• consider Lynch syndrome if PMHx for other malignancies (e.g. colorectal,stomach, prostate,

endometrial,etc.) +

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U2IUrology Toronto Notes 2023

Pathology

• 85% are papillary UC; others include SCC and adenocarcinoma

• UC of ureter and renal pelvis are histologically similar to bladder UC

Clinical Features

• gross/microscopic hematuria

• flank pain

• storage or voiding symptoms (dysuria only if lower urinary tract involved)

• flank mass ± hydronephrosis(10-20%)

Investigations

• Cl'

urogram

• cystoscopy and retrograde pyelogram

Treatment

• radical nephroureterectomy with excision of ipsilateral bladder cuff

• distal ureterectomy for distal ureteral tumours with concomitant ureteral reimplant

• segmental resection with uretero-ureterostomy forsome mid-ureteral tumoursis also done

• adjuvant chemotherapy (gemcitabine-platinum)

• enter

healt

Jretei

—Segment

of intestine

Stoma

Ileal conduit

j<ing role for endoscopic laser ablation in patients with low grade disease, poor baseline renal

Bladder Carcinoma

Etiology

• unknown, but environmental risk factors include:

smoking (main factor-implicated in 60% of new cases)

• aromatic amines: naphthylamines, benzidine, tryptophan, phenacetin metabolites

cyclophosphamide

• prior Hx of radiation treatment to the pelvis

• Schistosoma hematobium infection (associated with SCC)

• chronic irritation: cystitis, chronic catheterization, bladder stones (associated with SCC)

• aristolochic acid:associated with Balkan nephropathy (renal failure, upper tract UC) and Chinese

herbal nephropathy

Epidemiology

• 2nd most common urological malignancy

• M:F=3:1, more common among whites than blacks

• mean age at diagnosisis 65 vr

Segment

of colon

Ileocecal

valve

Stoma

Indiana pouch £

1

-

Pathology

• classification

• UC >90%

• SCC 5-7%

• adenocarcinoma 1%

others <1%

• stages and prognoses of UC at diagnosis

non-muscle invasive (75%) -> >80% overall survival

15% of these will progressto invasive UC

majority of these patients will have recurrence

invasive (25%) -» 50-60% 5yrsurvival

85% have no prior history ofsuperficial UC (i.e.de novo)

50% have occult metastases at diagnosis, and most of these will develop

evidence of metastases within 1 yr -lymph nodes, lung, peritoneum, liver

• carcinoma in situ -> flat, non-papillary erythematous lesion characterized by dysplasia confined to

urothclium

more aggressive, worse prognosis, higher recurrence rates following radical cystectomy,

associated with radioresistance

usually multifocal

» may progress to invasive UC

Clinical Features

• asymptomatic (20%)

• hematuria (key symptom:85-90% at the time of diagnosis)

• pain (50%) -> location determined by size/extent of tumour (e.g. flank,suprapubic, perineal,

abdominal, etc.)

• clot retention (17%)

• storage urinary symptoms -> consider carcinoma in situ

• palpable mass on bimanual exam > likely muscle invasion

• obstruction of ureters -> hydronephrosis and uremia (N/V and diarrhea); bad prognostic factor

Ureter

.Segment

intestine

-Urethra

ol

Ileal neobladder

Figure15.Ileal conduit,Indiana

pouch,ilealneobladder

overt clinical

Differential Diagnosis of Filling Defect

in Urinary Tract

• Urothelial carcinoma (differentiate

via cytology and CT scan)

. Uric acid stone (differentiate via

cytology and CT scan)

• Blood clot

. Pyelitis cystica

. Papillary necrosis

• Fungus ball

• Gas bubble from gas producing

organisms

n

L J

+

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U25Urology Toronto Xotcs 2023

Investigations

• U/A, urine C&S, urine cytology

• U/S

• CT scan with contrast > look for filling defects in upper tracts

• cystoscopy with biopsy (if small lesion)

• TURBT (gold standard, diagnostic, and often therapeutic) -> establish diagnosis and determine depth

of penetration

involvement of muscularis propria confirms muscle invasion (T2)

• specific bladder tumour markers (e.g. NM P-22, B

'

l

'A, Immunocyt, I DF); utility in clinical practice

debatable

The “field defect" theory helps to

explain why UC has multiple lesions and

has a high recurrence rate.The entire

urothelium (pelvis to bladder) is bathed

in carcinogens

The ENTIRE urinary tract must be

evaluated in patients with hematuria

unless there is clear evidence of

glomerular bleeding (eg.red cell casts,

dysmorphic RBCs. etc.)

Grading

• low grade: 210% invasive,60%! recur locally

• high grade: 50-80% are invasive or are expected to progress to invasive over time

Staging

• for invasive disease: examination under anesthesia following TURBT, CT, or MRI of abdomen and

pelvis,CT or MR urography,CT chest or CXR, hone scan in setting of bony pain/ hypercalcemia/

elevated ALF (metastatic workup)

Cystoscopy is the initial procedure of

choice for the diagnosis and staging of

urothelial malignancy

Table 17. 2018 TNM Classification of Bladder Carcinoma (AJCC 8th edition)

T N M

TX: primary tumour cannot be assessed NX:lymph nodes cannot be assessed cMO: no distant metastasis

Unexplained hematuria in any individual

>40 y/o must be investigated to rule out

a malignancy

TO: no evidence ol primary tumour

Ta: noninvasive papillary carcinoma

Tis: carcinoma inutti: "flat tumour"

NO: no lymph node metastasis cM1: distant metastasis

cM1n: distant metastasis limited to lymph

N1: single regional lymph node metastasis in nodes beyond the common iliacs

the true pelvis(hypogastric, obturator, external cM1b: non - lymph- node distant metastasis

T1: tumour invadessubepithclial connective iliac.or prcsacral lymph node)

tissue pM1: distant metastasis, microscopically

N 2: multiple regional lymph node metastasis In confirmed

the true pelvis(hypogastric, obturator, external pM1a:distant metastasis limited to

Iliac, or prcsacral lymph node metastasis) lymph nodes beyond the common Iliacs.

microscopically confirmed

pM1b: non -lymph node distant metastasis

microscopically confirmed

Tumour grade is the single most

important prognostic factor for

progression

T 2: tumour invades muscularis propria

pT2a: tumour invades superficial muscularis

propria linnet half )

pT2b: tumour invades deep muscularis

propria (outer hall)

N 3: lymph node metastasis to the common iliac

lymph nodes

See landmark Urology tneb table for more

information on neoadtuvant chemotherapy plus

cystectomy compared with cystectomy alone for

improved outcomesin patients with locally advanced

bladder cancer.

T3: tumour invades perivesical tissue

pT 3a: microscopically

pT 3b: macroscopically (extravesical mass)

N Suffix

|sn|: regional lymph node metastasis identified

by SIN biopsy only

(f ): regional lymph node metastasisidentified

T4:tumour invades anyof the following: by ENA or core needle biopsy only

prostatic stroma,seminal vesicles, uterus,

vagina, pelvic wall, abdominal wall

T4a: tumour invades prostalic stroma,

uterus.vagina

T4b: tumour invades pelvic wall,abdominal HMIBC and BCG

JUDO Publication 2015:15 EHCOIlEf <153

Summary:BCG isthe only intravesical therapy

associated with decreased risk of bladder cancer

progression: however,it is also associated with a hgh

rate of adverse events.More research is needed to

define optimal doselregimen.

Methods: BeviewofOvid Med me.Cochrane Central

Register of Controlled Trials.Cochrane Database

of SB.Health Technology Assessment. National

Health Sciences Economic Evaluation,databaseof

Jtbstractof Review of Effectsfor studies on HMIBC

interventions, including intravesical therapy.

Results: 3CG issuperior in prevention of bladder

cancer recurrence compared to no intravesical

therapy.BCG issupenor to doxorubicin,eprubieix.

and mitomycinin prevention of bladder cancer

recurrence.

wall

T Suffix

(m):synchronous primary tumours are found

in single organ

Deep Muscle Perivesical Fat

Superficial Muscle

Pelvic Wall or

Abdominal Wall >

5 Submucosa See landmark Urology Inals table for more

information on10-yr outcomesfor patients with

localized prostate cancer after monitoring,surgery,

or radiotherapy.

.1

Prostate 1 r-i

Mucosa 5 L J

Figure 16. UC of bladder

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U26 Urology Toronto Notes 2023

Treatment

Non-muscle invasive Muscle invasive Advanced/Metastatic

Low risk (Ta low-giade) T2.T3 T4,N+.M+

Chemo » radiation •

cystectomy

TURBT + intravesical chenio

Follow up with cystoscopy and cytology

Radical cystectomy + PLND

T urinary diversion (see

Figure 15)

-Radical cystectomy (male):

Removal ot bladder and

prostate en bloc

- Radical cystectomy (female):

Removal ol bladder, uterus,

ovaries and anterior vagina

(reproductive organs may be

spared with anterior tumours)

Radical local treatment

Maximal TURBT +

chemoradiation

Intermediate risk (Multifocal,recurrent Ta)

TURBT intravesical chento

BCG (lyr)

High risk (T1,Tis, Ta high-grade)

TURBTiintravesical chento

Repeat TURBT (2-6 wk)

BCG <3 yr)

'Amy Cao 2019

Figure 17. Treatment for bladder carcinoma

’Radical cystectomy (male):removal of bladder and prostate enblock,(female):removal of bladder,uterus,ovaries,and anterior vagina (reproductive

organs maybe spared with anterior tumours)

Prognosis

• depends on stage, grade,size, number of lesions, recurrence, and presence of CIS

IT:90% Syrsurvival

T2:55% 5 yr survival

• T3:30% 5 yr survival

T4/N+/M+:<5% 5 yr survival

Prostate Cancer

Etiology

• not known

• risk factors

• age >50 yr, risk increases 1% per yr after 65 yr

increased incidence in persons of African descent

high dietary fat (2x)

FMHx

1st degree relative (2x)

1st and 2nd degree relatives (9x)

positive BRCA (BReast CAncer gene) mutation

Epidemiology

• most prevalent cancer in males

• 3rd leading cause of male cancer deaths (following lung and colon)

• up to 50% risk of CaP at age 50

• lifetime risk of death from CaP is 3%

• 75% diagnosed between ages 60 and 85:mean age at diagnosis is 65

Pathology

• adenocarcinoma

>95%, often multifocal

• urothelial carcinoma of the prostate (4.5%)

associated with UC of bladder; does NOT follow TNM staging below; not hormone-responsive

• endometrial (rare)

carcinoma of the utricle

Anatomy

• 60-70% of nodules arise in the peripheral zone

• 10-20% arise in the transition zone

• 5- 10% arise in the central zone

L J

Clinical Features

• usually asymptomatic

• most commonly detected by DRh, elevated PSA, or as an incidental finding on TURP

• DRh: hard irregular nodule or diffuse dense induration involving one or both lobes

PSA:see PSA Screening, U28

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U27 Urology Toronto Notes 2023

•locally advanced disease

storage and voiding symptoms, ED (all uncommon without spread)

•metastatic disease

bony metastases to axial skeleton common

visceral metastases are less common (liver,lung, and adrenal gland most common sites)

leg pain and edema with nodal metastases obstructing lymphatic and venous drainage

tarty Detectioa of Prostate Caster Jtwricas

Urological Assocwticv GuideHues

JIW 2013:W:419.

t FproecegedSStoGSri

^

oaeMcsdr-gPSA

soteosg.itisstmegty recssuededs jesceed

fiesed9s raisesedp-efsteeces felowagstared

deosou-atag.

2 JostsePysoeectjr -trSe

^

ieeoagesfOS)

54yt at aierage sWIretccresded.

3. fait ae PS

*

surer-jroses age 70*yr orasy

sasmSlessttes a 10 to 6yrNeoettssty is

•

OlrttocsseaJed.

Methods of Spread

•local invasion

•lymphatic spread to regional nodes

obturator > iliac > presacral/para-aortic

• hematogenous dissemination occurs early

Investigations

. DRE

• PSA elevated in the majority of patients with CaP

•IRUS-guided needle biopsy

•bone scan (only if bone pain, high-risk disease, Gleason score >7,or PSA >20 ng/mL)

•CT scanning to assess metastases

•MR1:being investigated for possible role in detection,staging,MRI-guided biopsy, and active

surveillance

Table 18. 2018 TNM Classification of Prostate Carcinoma (AJCC 8th edition)

T N M

IX:primary tumour cannot be assessed NX:regional lymph nodes werenot assessed M0:no distant metastasis

10:no evidence of primary tumour NO:no regional lymph node metastasis cM1:distant metastasis

cM1a:nonregional lymph nodes

cMlb:bonefs)

cM1c other site|s) withor without bone

disease

11:clinicallyundetectable tumour,normal N1:spread to regional lymph nodes

OREandTRUS

T1a:tumour incidental histologic finding in N Suffix

<5% of tissue resected

T1b:tumour incidental histologic finding in

>5% of tissue resected

T1c:tumour identifiedby needle biopsy|due by fNA or cote needle biopsy only

to elevated PSA level)

(sn):regional lymph node metastasis

identified by SLN biopsy only

(f):regional lymph node metastasis identified confirmed

pM1:distant metastasis,microscopically

pM1a:nonregional lymph nodes,

microscopically confirmed

pM1b:bone(s) microscopically confirmed

pM1c:other sitefs) withor withoutbone

disease,microscopically confirmed

T2:palpable,confined to prostate

T2a:tumour involving < one half of one lobe

T2b:tumour involving > one half of one lobe,

but not both lobes

T2c:tumour involving both lobes

13:tumour extends through prostate capsule

T3a:extracapsular extension (unilateral or

bilateral)

T3b:tumour invading seminal veside(s)

T4: tumour invades adjacent structures

(besides seminal vesicles)

T Prefix

(c):clinicalI

(p):pathologicalI.There is no pathological T1

T Suffix

(m): synchronous primary tumours are found

in single organ

Table 19. Prostate Cancer Mortality Risk

Low-Risk (if any of

following)

Intermediate-Risk (if any of High-Risk (if any of

following) following)

PSA <10 10 20 >20

<7 (Gleason Group1)

pT1-2a

7 (Gleason Group 2 and 3)

pI2bI

- 2c

Gleason Score 8-10 (Gleason Group 4 and 5)

Stage pI34

Treatment

• T1/T2 (localized, low-risk)

if adequate life expectancy or no other significant comorbidities, consider active surveillance vs.

definitive local treatment (RP, brachytherapy, or EBRT)

• active surveillance for low-risk,small volume Gleason score <7 prostate cancer shown to be safe

for most

minimal differences in cure or recurrence rates between definitive treatment modalities

• in older population: watchful waiting and palliative treatment for symptomatic progression

alternative treatment options include: H1FU, cryoablation, focal laser ablation

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