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02. Urotelial Cancer (1375) > Bladder Tumors > Flashcards

Bladder Tumors Flashcards

Wieders Review

1
Q

What are the types of primary bladder tumors?

A
  1. Urothelial CA (TCC) (more than 90%)

Non-Urothelial:

  1. Squamous cell carcinoma (5%)
  2. Adenocarcinoma (1%)
  3. Small cell carcinoma
  4. Rhabdomyosarcoma (most commonly seen in children)
  5. Bladder pheochromocytoma
  6. Bladder lymphoma
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2
Q

Where do secondary (metastatic to bladder) bladder cancers come from in order of most common to least?

A

melanoma > colon > prostate > lung > breast

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3
Q

List 7 risk factors for bladder cancer?

A
  1. Smoking (carcinogenic ingredient is aromatic amines)
  2. Chronic cystitis (increased risk of SCC) ( causes = catheters, UTI’s, chronic bladder stones, schistosoma haematobium (bilharzial) infection.
  3. Chemical exposures (aromatic amines) - professions (hairdressers, dye workers, leather workers, painters, dry cleaners)
  4. Phenacitin
  5. Radiation to the bladder
  6. Pioglitazone (diabetic medication)
  7. Cyclophosphamide (chemotherapeutic)
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4
Q

What can cyclophosphamide cause and through what mechanism? How can you prevent this?

A

Hemorrhagic cystitis and increased risk of bladder cancer. Causes this via its metabolite - ACROLEIN.

MESNA should be given with cyclophosphamide as it will bind to ACROLEIN and facilitate its excretion.

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5
Q

What is a nephrogenic adenoma and what should you do about it?

A

A rare benign lesion in the bladder that is a metaplastic response to trauma or inflammation. Treat with transurethral resection and long term antibiotics (one year). They have a high recurrence rate.

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6
Q

What are the histological findings of a nephrogenic adenoma?

A

A single layer of cuboidal epithelium. Classic microscopic finding is HOBNAIL epithelial cells.

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7
Q

How does a nephrogenic adenoma present?

A

Dysuria, frequency and history of UTI

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8
Q

How do bladder tumors present?

A
  1. Most common is hematuria (microscopic or gross)
  2. Irritative LUTS (frequency, urgency, and dysuria) usually associated with high grade tumors or CIS
  3. Patients with advanced cancer may have bone pain (mets) or flank pain (ureteral obstruction, retroperitoneal mets)
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9
Q

How do you work up a bladder tumor?

A
  1. History and physical exam
  2. Cystoscopy
  3. CT urogram or KUB U/S
    4 Urinary cytology
  4. If there is high metastatic risk - order: LFT’s CT chest/abdomen/pelvis, bone scan if elevate ALP or bony pain
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10
Q

How do you diagnosis bladder cancer?

A

Transurethral resection of bladder tumor (TURBT)

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11
Q

What maneuver is important to perform in the clinical staging of bladder cancer?

A

Bimanual exam - clinical staging is based on bimanual exam AFTER turbt

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12
Q

What should be the goals of a successful TURBT?

A
  1. Remove enough tissue to determine depth of invasion
  2. Completely resect all visible tumor
  3. Do not perforate bladder
  4. Obtain good hemostasis following resection
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13
Q

When should you NOT resect all the tumor on TURBT?

A
  1. Extensive CIS is present - extensive resection or fulguration can lead to a contracted bladder
  2. The tumor appears unresectable via a transurethral approach
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14
Q

Who requires a repeat TURBT and why?

A

Anyone with TaHG or T1HG on initial resection - second TURBT finds residual disease in 25% of resections and upstages the pathology in 30% - ESPECIALLY if MUSCULARIS PROPRIA is absent.

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15
Q

How does fluorescence cystoscopy with hexaaminoleuvulinic acid (HALA) (heme precursor) work? How do you use it? Who should it be used in?

A
  1. HALA absorbed into urothelial cells where it is converted to protoporphyrin IX (PPIX). PPIX fluoresces under blue light and accumulates in malignant cells hence bladder cancer fluoresces
  2. Instillation intravesically
  3. May help improve detection of UC (especially CIS) but inflammation can generate high false positive rate.
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16
Q

What is an alternative enhanced visualization method to improve detection of bladder tumors that does NOT require any intravesical bladder instillation?

A

Narrow band imaging (NBI) - filters white light into blue and green regions. Blue and green absorbed by hemoglobin enhancing visualization of highly vascular tissues.

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17
Q

What is the obturator reflex?

A

Obturator reflex - obturator nerve runs near lateral walls of bladder. Resection in this area can stimulate nerve resulting in sudden leg adduction and resultant bladder perforation.

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18
Q

How can you avoid the obturator reflex?

A
  1. General anaesthesia with neuromuscular blockade (paralysis)
  2. Avoiding bladder over distension (may keep the nerves further away)
  3. Lowering the resection current
  4. Obturator nerve block with local anaesthesia
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19
Q

What are methods to reduce the risk of bladder perforation when performing a TURBT?

A
  1. Use caution when resecting tumors in a diverticulum (has no muscularis layer)
  2. Avoid the obturator reflex
  3. Avoid bladder overdistension
  4. Avoid deep resection of low grade tumors that seem low grade and superficial
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20
Q

What should you do about tumors at the ureteral orifice?

A
  1. Avoid extensive cauterization at the UO - can cause a distal ureteral stricture. If it is required use minimal low-current focal pinpoint cautery
  2. Cutting current over the UO is unlikely to cause postoperative UO obstruction secondary to stricture or edema. If patient has solitary kidney can consider placing a stent.
  3. Perform a renal scan, urogram, or U/S 3-6 weeks after resection over UO to ensure no obstruction.
  4. Resection of the UO can cause VUR. In patients with known VUR and UC there is 15-22x increased risk of UTUC hence upper tract surveillance should be initiated
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21
Q

Is it okay to perform a TURBT and TURP in the same operation?

A

Yes. Simultaneous TURP + TURBT for Ta or T1 bladder CA does not appear to increase the risk of subsequently developing UC in the prostatic urethra compared to TURBT alone.

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22
Q

What are the indications for a prostatic urethra biopsy?

A
  1. Multifocal UC of the bladder
  2. Tumor at bladder neck
  3. CIS of the bladder
  4. A visible abnormality suspicious for tumor in the prostatic urethra
  5. Unexplained positive urine tumor marker
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23
Q

If prostate invasion suspected how do you take the biopsies?

A

loop resection at 5 and 7 o’clock. If invasion not suspected cold cup biopsies can be taken.

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24
Q

What are the indications for random bladder biopsies?

A
  1. Planned partial cystectomy
  2. Abnormal urine tumor marker without tumor in the bladder
  3. Urine cytology shows high grade cells but biopsy shows low grade UC.
  4. After intravesical therapy for CIS to evaluate for complete response.
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25
Q

How do you grade bladder cancer?

A
  1. PUNLMP (papillary urothelial neoplasm of low malignant potential)
  2. Low grade (well differentiated)
  3. High grade (poorly differentiated)
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26
Q

What is the T-staging for bladder CA (AJCC 2010)?

A 
Tx - cannot be assessed
T0 - no evidence of cancer
Ta - superficial bladder cancer
Tis - carcinoma in situ
T1 - invasive into lamina propria 
T2 - invasive into muscularis propria
        T2a - invasive into inner half 
        T2b - invasive into outer half 
T3 - invasive into perivesical fat
       T3a - microscopic invasion
       T3b - macroscopic invasion
T4 - Tumor invades into an adjacent structure (prostatic stroma, seminal vesicle, uterus, vagina, pelvic wall, abdominal wall.
        T4a - Tumor invades into prostatic stroma, uterus, 
                  vagina
        T4b - Tumor invades into pelvic wall or abdominal 
                  wall
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27
Q

What is the N-Staging and M-Staging for bladder CA (AJCC 2010)?

A

Nx - Regional lymph nodes cannot be assessed
N0 - No regional lymph node metastases
N1 - Single regional lymph node metastases in the true pelvis (hypogastric, obturator, external iliac, or presacral)
N2 - Multiple regional lymph node metastases in the true pelvis (hypogastric, obturator, external iliac, presacral)
N3 - Lymph node metastases to the common iliac

M0 - No distant mets
M1 - Distant mets

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28
Q

Why is SCC of the bladder more common in Egypt?

A

Schistosoma infection - bilharzial infections associated with SCC

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29
Q

Is the prognosis of SCC better or worse than UC?

A

Worse (except bilharzial SCC - well differentiated and low incidence of metastases)

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30
Q

How do you treat SCC of the bladder?

A

Less responsive to chemotherapy and radiation in comparison to UC. Treat localised bladder SCC with radical cystectomy, PLND, +/- urethrectomy

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31
Q

How do you classify bladder adenocarcinoma?

A
  1. Primary - arising from the bladder itself
  2. Urachal - arises from urachus
  3. Metastatic - from elsewhere
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32
Q

How do you work-up someone with adenocarcinoma found in the bladder?

A 
Need to ensure not metastatic disease:
(Possible sites of origin include: colon, stomach, lung, prostate, breast, endometrium and ovary)
Investigations:
1. CT abdo/pelvis with contrast
2. Chest imaging
3. Upper and lower GI endoscopy
4. In males PSA and DRE
5. In females: pelvic exam, CA-125, and mammogram
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33
Q

What is the prognosis of adenocarcinoma of the bladder in comparison to UC of the bladder?

A

Worse. Responds poorly to chemo or rads. No intravesical treatment options

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34
Q

How do you treat adenocarcinoma of the bladder?

A

Radical cystectomy with en bloc removal of the urachus, pelvic lymphadenectomy +/- urethrectomy. Treat metastatic adenocarcinoma based on primary.

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35
Q

What is specifically noted in the urine in urachal adenocarcinoma? What serum test may be abnormal?

A

Mucin (15-35% of the time), CEA

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36
Q

Where is localised urachal adenocarcinoma usually found in the bladder and how do you treat it?

A

Bladder dome (can be found on anterior wall as well) - treat with partial or radical cystectomy with en bloc resection of the urachus and umbilicus + PLND

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37
Q

What is the mean 5 year cancer free survival in urachal adenocarcinoma? What percentage of patients have local recurrence after excision?

A

55%, 20-50%

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38
Q

What is the confirmatory histological stain for small cell carcinoma of the bladder?

A

Stain positive for chromogranin A and synaptophysin (all other bladder cancers stain negative for this)

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39
Q

Small cell carcinoma is the most aggressive bladder cancer - what percentage of patients present metastatic?

A

50% - all patients with small cell carcinoma of the bladder should have a metastatic workup (CT abdominal/pelvis, chest imaging, Bone scan (if bony pain or elevated ALP), LFT’s)
OS < 50% @ 5 years

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40
Q

How do you treat small cell carcinoma of the bladder?

A

SYSTEMIC CHEMOTHERAPY
M0: systemic etoposide and cisplatin. If patients respond consolidate therapy with radical cystectomy and or pelvic radiation
M1: systemic chemo

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41
Q

What are the sites of bladder cancer metastases from most common to least?

A

Pelvic lymph nodes > liver > lung > bone

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42
Q

In what percentage of patients with CIS is urinary cytology positive?

A

95%

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43
Q

What kind of voiding symptoms does CIS produce?

A

Irritative LUTS

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44
Q

What is the likelihood of CIS recurring and progressing following BCG?

A

Recurrence - 30% after BCG

Progression - 20% after complete response to BCG

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45
Q

What are the characteristics of CIS with respect to its shape, grade and level of invasiveness?

A

Flat, high grade, and non-invasive

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46
Q

What is the first line treatment for CIS?

A

BCG induction (6 cycles) 3-4 weeks after TURBT

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47
Q

How and when do you check if CIS responded to BCG induction? If it is eradicated what should you do? if remains what should you do?

A
  1. Six weeks after completion of BCG - bladder biopsy and urine cytology at time of biopsy for persistence
  2. If eradicated after 1-2 induction courses of BCG maintenance BCG recommended
  3. If persistent CIS options include cystectomy or repeat BCG - if repeat induction BCG fails should consider subsequent cystectomy
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48
Q

What is the surveillance schedule for eradicated CIS?

A

Cystoscopy every 3-6 months for 2 years than less often if negative. Cytology is optional. Obtain CT urogram every 1-2 years (or IVU, retrograde pyelogram)

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49
Q

What are the rates for progression and recurrence for Ta lesions?

A

Progression - 5% progress to muscle invasion within 1 year of TURBT

Recurrence - 50% recur within 1 year of TURBT

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50
Q

What are the EORTC criteria used for their algorithm to predict recurrence and progression in Ta and T1 lesions ?

A
  1. Number of tumors: 1, 2-7, more than 8
  2. Tumor size: less than 3cm, greater than 3cm
  3. Primary recurrence rate: less than one year, more than
    one year
  4. T category: Ta or T1
  5. CIS: Y, N
  6. Grade: high or low
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51
Q

For first time TaHG lesions what should be the next step in management?

A

Re-resection TURBT - ensure correct stage and complete resection.

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52
Q

When is surveillance +/- fulguration of a Ta lesion an appropriate management strategy?

A

Low Risk TaLG lesions - TaLG tumor, benign urinary cytology, and current tumor appears small, low grade and Ta.

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53
Q

What are risk factors for recurrence of Ta lesions?

A
  1. Size greater than 2cm
  2. Recurrence less than 1 year from TURBT
  3. Incomplete resection
  4. Multiple tumors
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54
Q

If TaLG lesion is has a high risk of recurrence how should it be managed?

A

6 weeks of intravesical chemotherapy (mitomycin, thiotepa, epirubicin) administered 3-4 weeks after TURBT. If fails (recurrence) consider BCG

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55
Q

How should a TaHG lesion be managed?

A

6 weeks of BCG induction 3-4 weeks after TURBT

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56
Q

How should you follow up a TaLG lesion that has been treated adequately?

A

cystoscopy at 3 months and 9 months after TURBT than yearly. If any untreated tumors than cytology should be obtained

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57
Q

How should you follow up on a TaHG lesion that has been treated adequately?

A

Cystoscopy and urinary cytology every 3-6 months for two years and then less often.

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58
Q

In managing Ta bladder CA when do you consider upper tract imaging with CT urogram, IVU, or retrograde pyelogram?

A
  1. Every 1-2 years if tumor is high grade

2. When there are frequent recurrences

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59
Q

What are the recurrence and progression rates of T1 lesions?

A

Recurrence - 50-70% recur after treatment

Progression - 30-40% progress to muscle invasive disease after TURBT

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60
Q

What is the next step in management for a first presentation of a T1 lesion?

A

Re-resection TURBT to confirm stage and complete resection

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61
Q

What is first line treatment for a T1 tumor?

A

Induction (6 cycles) of BCG; 3-4 weeks after TURBT

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62
Q

When would you consider an upfront partial or radical cystectomy for T1 lesions?

A

High grade, associated CIS, multifocal T1 tumor, LVI, or tumor cannot be completely excised

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63
Q

What are your options if 6 weeks following BCG induction administration there is noted biopsy confirmed T1 tumor?

A
  1. Repeat induction BCG

2. Cystectomy

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64
Q

How should you manage a patient that is tumor free following induction BCG?

A

Maintenance BCG

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65
Q

How should you surveil a patient with T1 lesions that are treated with BCG?

A

Cystoscopy and urine cytology q3-6 months x 2 years than less frequently. CT urogram (or IVU/ Retrograde pyelogram q1-2 years)

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66
Q

For patients with T2-T4 N0M0 disease what are their treatment options?

A
  1. NACT followed by radical cystectomy, urinary diversion, and pelvic lymphadenectomy (Gold standard)
  2. Radical cystectomy, PLND, and urinary diversion (if cannot tolerate NACT)
  3. Bladder preservation therapies
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67
Q

How do you treat bladder cancer patients that present with T4b N1-3, M1 disease?

A

Systemic chemotherapy +/- EBRT for local control

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68
Q

Is systemic chemotherapy for UC curative?

A

No

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69
Q

What are first line chemotherapeutic regimens for treatment of UC?

A
  1. Gemcitibine and Cisplatin (GC)
  2. Dose dense methotrexate, vinblastine, adriamycin, cisplatin (DDMVAC)
    * similar survival between two regimens but GC less toxic*
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70
Q

What is the most effective chemotherapeutic agent against UC?

A

Cisplatin

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71
Q

What are types of urothelial CA with variant histologies?

A

UC can mutate into variant histology giving hybrid urothelial CA (glandular differentiation, squamous differentiation). Still treated as UC. Worst variant histology = micropapillary or nested.

72
Q

What are the principles of managing urothelial CA in a diverticulum?

A
  1. Minimise elevated risk of perforation with resection
  2. CIS can be treated with fulguration and BCG
  3. Low grade papillary can be treated with TURBT +/- intraveical therapy
  4. Recurrent or high grade tumors should be treated with a diverticulectomy or partial or radical cystectomy
73
Q

What are the principles of managing urothelial CA in the prostatic urethra?

A
  1. Non-invasive TCC can be treated with TURBT +/- TURP + BCG
  2. If tumor recurs in prostate (especially high grade or invasive) consider radical cystectomy and urethrectomy
  3. If UC invading into prostatic stroma - treatment is radical cystectomy and urethrectomy.
74
Q

What are the two types of intravesical chemotherapy?

A
  1. Chemotherapy (mitomycin, thiotepa, epirubicin)

2. Immunotherapy (BCG, interferon)

75
Q

What are the three main indications for intravesical therapy?

A
  1. Eradication of CIS with or without an associated papillary tumor
  2. Eradication of residual papillary tumor after incomplete resection.
  3. To reduce the recurrence and progression of completely resected tumors
76
Q

What is the MAJOR difference in terms of prognosis (recurrence and progression) between BCG and intravesical chemotherapy?

A

BCG decreases recurrence AND progression whereas intravesical chemotherapy only decreases recurrence.

77
Q

BCG is superior to intravesical chemotherapy for what kind of bladder lesions?

A
  1. CIS
  2. High grade tumors
  3. T1 tumors
78
Q

How long must you wait after a TURBT before giving BCG?

A

2 weeks minimum

79
Q

When can intravesical chemotherapy first be given?

A

Single dose within 24h after TURBT (ideally within 6 hours) - recommended for Ta tumors (mitomycin or epirubicin in the ABSENCE of bladder perforation because it decreases recurrence by 13%)

80
Q

What bladder tumors can be treated with intravesical chemotherapy and with what regimens?

A

Ta lesions with risk factors for recurrence.

  1. Induction: 6-9 doses once weekly 3-4 weeks after TURBT
  2. Maintenance: started right after induction 1 cycle every 1-3 months for up to one year.
81
Q

What are contraindications to giving intravesical chemotherapy?

A
  1. Gross hematuria
  2. Urinary infection
  3. Bladder perforation
  4. Traumatic catheterization
82
Q

How do you optimize the effects of intravesical mitomycin?

A

Alkalanize urine to pH>6 (mitomycin more effective at this pH)

83
Q

What is the technique for instilling intravesical chemotherapy within 6 hours after TURBT?

A
  1. CANNOT do if there is a bladder perforation
  2. Empty bladder, place catheter and install chemo into bladder and then clamp catheter.
  3. Hold in bladder for 2 hours or until patient becomes uncomfortable
  4. Can remove catheter after draining
84
Q

What investigations need to be performed before instilling intravesical chemotherapy?

A

U/A - check for gross hematuria and UTI

85
Q

What are principles of instillation of intravesical chemotherapy?

A
  1. Empty bladder prior to instillation
  2. Instillation through catheter.
  3. Attempt to hold in bladder for 2 hours.
86
Q

How does mitomycin C work?

A

Alkylating agent (inhibits DNA synthesis)

87
Q

What is the usual dose of mitomycin C?

A

40mg in 20cc sterile water administered intravesically

88
Q

What are the side effects of intravesical mitomycin C?

A
  1. Contact dermatitis

2. Irritative LUTS

89
Q

Why is systemic absorption of mitomycin rare? What can happen if it is absorbed?

A

It has a high molecular weight. Can cause myelosuppression

90
Q

What are the indications for intravesical thiotepa? (only FDA approved intravesical chemotherapeutic agent)

A

Ta, T1 and CIS bladder cancer

91
Q

How does thiotepa work?

A

alkylating agent (inhibits DNA synthesis)

92
Q

What is the dose of thiotepa?

A

60mg in 30-60cc of NS instilled weekly for 6 weeks than monthly for up to one year

93
Q

What are the possible side effects of thiotepa?

A

irritative LUTS, myelosuppression (higher than mitomycin as thiotepa has lower molecular weight) need to check complete blood count prior to every instillation.

94
Q

How does Epirubicin work?

A

Anthracycline - intercalating agent that inhibits DNA synthesis

95
Q

What is the dose of epirubicin?

A

40-100mg in 40-100cc of NS

96
Q

What are the side effects of epirubicin?

A

Irritative voiding symptoms. If absorbed systemically (low chance high molecular weight) can cause myelsuppression

97
Q

The average age of patients with bladder cancer in the United States is:
a. 65.
b. 69.
c. 73.
d. 76.
e. 78.

A

c. 73. In the United States, the mean age of diagnosis is 73.

98
Q

Inverted papillomas are:
a. a benign tumor of the bladder.
b. a precursor to low-grade papillary cancer. c. chemotherapy resistant.
d. an invasive tumor.
e. best treated with antibiotics.

A

a. A benign tumor of the bladder. When diagnosed according to strictly defined criteria (e.g., lack of cytologic atypia), inverted papillomas behave in a benign fashion with only a 1% incidence of tumor recurrence (Sung etal., 2006; Kilciler etal., 2008). Occasionally, inverted papillomas are present with coexistent urothelial cancer elsewhere in the urinary system, occurring more commonly in the upper tract than the bladder (Asano etal., 2003). The use of fluorescence in situ hybridization to evaluate chromosomal changes can distinguish between an inverted papilloma and a urothelial cancer with an inverted growth pattern (Jones etal., 2007).

99
Q

The incidence rate of urothelial cancer:
a. has been decreasing recently because of less smoking.
b. is higher in women than in men.
c. is highest in developed countries.
d. peaks in the fifth decade of life.
e. is higher in Asia than Europe.

A

c. Is highest in developed countries. Sixty-three percent of all bladder cancer cases occur in developed countries, with 55% occurring in North America and Europe. There is a geographic difference in bladder cancer incidence rates across the world, with the highest rates in Southern and Eastern Europe, parts of Africa, Middle East, and North America, and the lowest in Asia and underdeveloped areas in Africa (Ferlay etal., 2007). The incidence of urothelial cancer peaks in the seventh decade of life.

100
Q

The mortality rate of urothelial cancer:
a. is primarily related to lack of health care access.
b. has been decreasing since 1990.
c. is highest in underdeveloped countries.
d. is proportionally higher in women than in men.
e. is proportionally higher in white men than in African American men.

A

b. Has been decreasing since 1990. The mortality rate of urothelial cancer has decreased by 5% since 1990, primarily because of smoking cessation, changes in environmental carcinogens, and healthier lifestyles (Jemal etal., 2008).

101
Q

What is the risk of a white male developing urothelial cancer in his lifetime?
a. Less than 5%
b. 20%
c. 40%
d. 60%
e. 80%

A

a. Less than 5%. A white male has a 3.7% chance of developing urothelial cancer in his lifetime, which is roughly 3 times the probability in white females or African American males and more than 4.5 times the probability of an African American female (Hayat etal., 2007; Jemal etal, 2008).

102
Q

The most common histologic bladder cancer cell type is:
a. squamous.
b. adeno.
c. urothelial.
d. small cell.
e. leiomyosarcoma.

A

c. Urothelial.Histologically, 90% of bladder cancers are of urothelial origin, 5% squamous cell, and less than 2% adenocarcinoma or other variants (Lopez-Beltran, 2008). Urothelial carcinoma is the most common malignancy of the urinary tract and is the second most common cause of death among genitourinary tumors.

103
Q

The mortality rate from bladder cancer is highest in:
a. the United States.
b. England.
c. South America.
d. China.
e. Egypt.

A

e. Egypt. The mortality rate from bladder cancer in Egypt is three times higher than in Europe and eight times higher than in North America because squamous cell carcinoma is highly prevalent in Egypt (Parekh etal., 2002).

104
Q

Recent evidence suggests that physician practice may be related to bladder cancer deaths in the elderly. What percentage of deaths could be avoided?
a. Less than 5%
b. 30%
c. 50%
d. 70%
e. 90%

A

b. 30%. Mortality from bladder cancer is highest in elderly persons, particularly those past the age of 80, accounting for the third most common cause of cancer deaths in men over the age of 80 (Jemal etal., 2008). Whether this increase in mortality rate is related to tumor biology or changes in physician practice with the elderly is unclear. Recent evidence suggests that physician practice may be related to bladder cancer deaths in the elderly (Morris etal., 2009). These authors estimated that 31% of all bladder cancer deaths were avoidable, more commonly in noninvasive than invasive disease.

105
Q

Which gene is most commonly mutated in high-grade muscle invasive urothelial cancer?
a. Cyclin A
b. TP53
c. FGFR-3
d. HRAS
e. PTEN

A
  1. b. TP53. High-malignant potential, non–muscle-invasive bladder cancer is more likely associated with deletions of tumor suppressor genes such as TP53 and RB (Chatterjee etal., 2004a; George etal, 2007; Sanchez-Carbayo etal, 2007).
106
Q
  1. Which gene is most commonly mutated in carcinoma in situ (CIS)?
    a. PI3K
    b. RB
    c. FGFR-3
    d. HRAS
    e. CD-44
A

b. RB. All CIS is high grade by definition. The genetic abnormalities associated with CIS include alterations to the RB, TP53, and PTEN genes (Cordon-Cardo etal., 2000; Lopez-Beltran etal, 2002; Cordon-Cardo, 2008).

107
Q

Which gene is most commonly mutated low-grade papillary urothelial carcinoma (LgTa)?
a. PTEN
b. RB
c. FGFR-3
d. HRAS
e. CD-44

A

c. FGFR-3. Low-grade urothelial carcinoma is typically papillary in nature with a fibrovascular stalk and frequent papillary branching with increased cellular size, some nuclear atypia, and occasional mitotic figures. These tumors almost universally display alterations of genes in chromosome 9 and frequent mutations in FGFR3, PI3K or, alternatively, Ras genes.

108
Q
  1. The chemotherapy proven to cause urothelial cancer is: a. doxorubicin. b. bleomycin. c. ifosfamide. d. etoposide. e. cyclophosphamide.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 518). Elsevier Health Sciences. Kindle Edition.

A
  1. e. Cyclophosphamide.The only chemotherapeutic agent that has been proven to cause bladder cancer is cyclophosphamide (Travis etal., 1995; Nilsson and Ullen, 2008). The risk of bladder cancer formation is linearly related to the duration and intensity of cyclophosphamide treatment, supporting a causative role. Phosphoramide mustard is the primary mutagenic metabolite that causes bladder cancer in patients exposed to cyclophosphamide.
109
Q

The increased risk of developing bladder cancer for a man who has a sister with bladder cancer is:
a. twofold.
b. 10-fold.
c. 20-fold.
d. 40-fold.
e. 60-fold.

A

a. Twofold.First-degree relatives of patients with bladder cancer have a twofold increased risk of developing urothelial cancer themselves, but high-risk urothelial cancer families are relatively rare (Aben etal., 2002; Murta-Nascimento etal., 2007; Kiemeney, 2008).

110
Q

The risk of a family member developing bladder cancer if a first-degree relative has the disease is:
a. related to secondhand smoke.
b. higher in men.
c. higher in smokers.
d. related to inheritance of low-penetrance genes.
e. most common in high-grade cancer.

A

d. Related to inheritance of low-penetrance genes. The hereditary risk seems to be higher for women and nonsmokers, but it is not related to secondhand exposure to smoking in families. Most likely, there are a variety of low-penetrance genes that can be inherited to make a person more susceptible to carcinogenic exposure, thus increasing the risk of bladder cancer formation.

111
Q

The percent of patients presenting with non–muscle-invasive disease is:
a. less than 5%.
b. 20%.
c. 40%.
d. 60%.
e. 80%.

A

e. 80%.At initial presentation, 80% of urothelial tumors are non–muscle-invasive. There are multiple growth patterns of urothelial cancer, including flat carcinoma in situ (CIS), papillary tumors that can be low or high grade, and sessile tumors with a solid growth pattern. Non–muscle-invasive cancers can be very large because of lack of the genetic alterations required for invasion.

112
Q

A 30-year-old man has gross hematuria, and cystoscopy reveals a papillary tumor. Transurethral resection of the tumor reveals a noninvasive 2-cm papillary low-malignant-potential urothelial tumor. Muscle is present in the resected specimen. All of the tumor is resected. The best treatment is:
a. intravesical bacille Calmette-Guérin (BCG). b. repeat cystoscopy with random bladder biopsies.
c. radical cystectomy because of the patient’s young age.
d. immediate mitomycin C intravesical therapy.
e. observation.

A

d. Immediate mitomycin C intravesical therapy.PUNLMP is a papillary growth with minimal cytological atypia that is more than seven cells thick and is generally solitary and located on the trigone (Holmang etal., 2001; Sauter etal., 2004). PUNLMP is composed of thin papillary stalks where the polarity of the cells is maintained and the nuclei are minimally enlarged. PUNLMP has a low proliferation rate and is not associated

113
Q

The external agent most implicated in causing urothelial cancer is:
a. β-naphthylamine.
b. 4-aminobiphenyl.
c. perchloroethylene.
d. trichloroethylene.
e. 4,4′-methylene bis(2-methylaniline).

A

a. β-naphthylamine. One of the first and most common chemical agents implicated in the formation of bladder cancer in dye and rubber workers is β-naphthylamine (Case and Hosker, 1954). Activation of aromatic amines allows DNA binding by enzymes that are selectively expressed in the population, making some subjects more susceptible to cancer formation, as described earlier related to the NAT-2 and the GSTM1 polymorphisms.

114
Q

If a woman stops smoking for 10 years after 30 pack-years of smoking, her risk of developing bladder cancer:
a. is the same as if she still smoked.
b. is the same as if she never smoked.
c. is unrelated to the intensity of smoking.
d. is very low because of her gender.
e. gradually decreases with time.

A

e. Gradually decreases with time.Smoking cessation does make a difference in urothelial cancer formation. Smokers who have stopped for 1 to 3 years have a 2.6 relative risk, and those who have stopped for more than 15 years have a 1.1 relative risk of bladder cancer formation (Wynder and Goldsmith, 1977; Smoke IAfRoCT, 2004).

115
Q

A man exposed to high doses of radiation (more than 500 mSv):
a. has the same risk of urothelial cancer formation as a nuclear plant worker.
b. will likely develop urothelial cancer within 5 years.
c. is more likely to develop urothelial cancer if he is younger than 20 years.
d. is two times more likely to develop urothelial cancer.
e. should be quarantined for 3 months.

A

d. Is two times more likely to develop urothelial cancer. There is a significant increased risk of dying from any cancer if a person is exposed to greater than 50 mSv. The relative risk of urothelial cancer formation is 1.63 in men and 1.74 in women. Interestingly, urothelial cancer formation after radiation is not age related, but the latency period is 15 to 30 years. However, there is no association with low-dose or industrial exposure of radiation therapy and bladder cancer formation. Importantly, urologic technicians and nuclear radiation workers do not have an increased risk of urothelial cancer formation.

116
Q

One of the main changes between the AJCC 7th edition and AJCC 8th edition for bladder cancer is:
a. there should be two grades of non-muscle-invasive bladder cancer. b. multiple positive pelvic lymph nodes is considered stage 3 disease.
c. perivesical fat involvement by tumors is stage T3.
d. CIS can be low or high grade.
e. Ta grade 1 tumors should be considered cancerous.

A

b. Multiple positive pelvic lymph nodes is considered stage 3 disease. Broadly speaking, non–muscle-invasive bladder cancer is composed of stage 0 (noninvasive) and stage 1 (invasion into subepithelial connective tissue), muscle-invasive organ-confined bladder cancer is of stage 2, muscle-invasive locally advanced bladder cancer is stage 3, and metastatic disease is stage 4. Whereas prior AJCC editions viewed positive lymph nodes as stage 4 regardless of the quantity or location, the 2017 AJCC staging update now views nodal disease in the absence of systemic metastases as stage 3.

117
Q

Genetic abnormalities associated with low-malignant potential Ta tumors include:
a. fibroblast growth factor receptor-3 (FGFR-3).
b. TP53.
c. retinoblastoma (RB) gene.
d. PTEN.
e. loss of chromosome 17.

A

a. Fibroblast growth factor receptor-3 (FGFR-3).Genetic abnormalities associated with low-grade cancer include deletion of 9q and alterations of FGFR-3, HRAS, and PI3K (Holmang etal, 2001; Cordon-Cardo, 2008). Low-grade carcinomas are immunoreactive for cytokeratin-20 and CD-44. The TP53, retinoblastoma (RB), and PTEN genes and loss of chromosome 17 are all associated with high-grade cancer.

118
Q

A 40-year-old man has a T1 high-grade urothelial cancer on initial presentation. Muscle was present in the biopsy specimen. The next treatment is:
a. BCG.
b. repeat transurethral resection of a bladder tumor (TURBT).
c. radical cystectomy.
d. immediate mitomycin C instillation. e. neoadjuvant chemotherapy followed by radical cystectomy.

A

b. Repeat transurethral resection of a bladder tumor (TURBT).Because of this understaging, the American Urological Association (AUA) guidelines call for a repeat transurethral resection in patients with T1 tumors to assess for muscle-invasive disease even if muscle was present in the specimen (Hall etal, 2007).

119
Q

A 73-year-old man with a history of Ta bladder cancer is found to have a 0.5-cm papillary lesion in the prostatic urethra and undergoes extensive transurethral resection of the prostate, revealing high-grade noninvasive disease of the prostatic urethra without ductal or stromal involvement. The next best step is:
a. perioperative mitomycin C.
b. surveillance cystoscopy every 3 months.
c. mitomycin C therapy. d. induction of and maintenance with BCG therapy.
e. radical cystectomy.

A

d. Induction of and maintenance with BCG therapy. For patients with noninvasive prostatic urethral cancer, transurethral resection of the prostate with BCG therapy is appropriate (Palou etal, 2007). For patients with prostatic ductal disease, a complete TURP is warranted, plus BCG therapy. Although a radical cystectomy could be performed, a more conservative organ-sparing treatment is recommended.

120
Q

A 62-year-old man undergoes a transurethral biopsy of a bladder tumor at the dome. Final pathology reveals muscle-invasive urothelial and small cell carcinoma. Metastatic workup is negative. The next step is:
a. intravesical gemcitabine therapy.
b. partial cystectomy.
c. radical cystoprostatectomy.
d. external beam radiotherapy.
e. chemoradiation therapy.

A

e. Chemoradiation therapy. Small cell carcinoma of the bladder should be considered and treated as metastatic disease, even if there is no radiologic evidence of disease outside the bladder. Small cell carcinoma of the bladder accounts for much less than 1% of all primary bladder tumors. In general, small cell carcinoma of the bladder is very chemosensitive, and the primary mode of therapy is chemoradiation therapy or chemotherapy followed by cystectomy.

121
Q

When cisplatin-based chemotherapy is used, which of the following genetic mutations is associated with the worst prognosis?

a. FGFR-3 mutations
b. PTEN
c. TP53
d. RB
e. PTEN, TP53, and RB

A

e. PTEN, TP53, and RB. Overall genetic instability is the hallmark of invasive urothelial cancer, but, specifically, alterations of TP53, RB, and PTEN carry a very poor prognosis (Chatterjee etal, 2004a). FGFR-3 mutations are associated with noninvasive bladder cancer.

122
Q

When cisplatin-based neoadjuvant chemotherapy is used, which of the following genetic mutations is associated with an improved response?
a. FGFR-3 mutations
b. ERCC2
c. TP53
d. RB
e. ERCC2, FANCC, and ATM

A

e. ERCC2, FANCC, and ATM . The recent application of genomics to large cohorts of MIBCs has produced major breakthroughs in disease heterogeneity with obvious implications for clinical management. Whole transcriptome studies identified basal and luminal molecular subtypes (Choi etal., 2014; TCGAR, 2014; Damrauer et al., 2014), and patients with basal tumors appeared to derive the most benefit from neoadjuvant chemotherapy (NAC) (Seiler etal 2017; McConkey etal., 2018). In parallel, two other groups demonstrated that inactivating mutations in DNA damage repair genes (including ERCC2, FANCC, ATM) were associated with response to NAC (Van Allen etal., 2014; Serebriiskii et al., 2015). These findings are now being prospectively examined within the context of the Southwest Oncology Group’s (SWOG’s) completed S1314 trial. In addition, two groups have designed prospective clinical trials to test whether DDR mutations can be used to guide bladder preservation in patients treated with NAC, and several groups are considering clinical trials to select MIBC patients for NAC based on basal molecular subtype membership.

123
Q

Tumor suppressor genes are activated by: a. gene amplification.
b. translocation.
c. point mutations.
d. DNA methylation.
e. microsatellite instability.

A

c. Point mutations. Tumor suppressor genes are mainly activated by allelic deletion of one allele followed by point mutations of the remaining allele. Tumor suppressor genes are recessive or have a negative effect, resulting in unregulated cellular growth. Proto-oncogenes are generally activated by point mutations in the genetic code, gene amplification, and gene translocation. The activated proto-oncogenes become oncogenes that can cause cancer, and this is considered a positive or dominant growth effect (Lengauer etal, 1998; Wolff etal, 2005; Cordon-Cardo, 2008).

124
Q

The risk of urologic malignancy in a man with recurrent gross hematuria, but who had a previous negative evaluation, is:
a. less than 5%.
b. 20%.
c. 40%.
d. 60%.
e. 80%.

A

a. Less than 5%.Gross, painless hematuria is the primary symptom in 85% of patients with a newly diagnosed bladder tumor (Khadra etal, 2000; Alishahi etal, 2002; Edwards etal, 2006). The gross hematuria is usually intermittent and can be related to Valsalva maneuvers; therefore any episode of gross hematuria should be evaluated even if subsequent urinalysis is negative. Fifty percent of patients with gross hematuria will have a demonstrable cause, 20% will have a urological malignancy, and 12% will have a bladder tumor (Khadra etal, 2000). The risk of malignancy in patients with recurrent gross or microscopic hematuria that had a full, negative evaluation is near zero within the first 6 years (Khadra etal, 2000).

125
Q

Which of the following is not a high-risk factor in urothelial cancer formation in patients with microscopic hematuria?
a. Age younger than 40 years
b. Smoking
c. History of pelvic radiation
d. Urinary tract infections
e. Previous urologic surgery

A

a. Age younger than 40 years. The guidelines recommend consideration for reevaluation of low-risk individuals with microscopic hematuria, but repeat evaluation every 6 months with a urinalysis, cytology, and blood pressure (to detect renal disease) is recommended for high-risk patients. Age younger than 40 years is the only factor that is not associated with an increased risk of malignancy.

126
Q

Commercially available fluorescence in situ hybridization kits test for abnormalities in which of the following chromosomes?
a. 3, 7, 9, 17
b. 2, 5, 8
c. 4, 6, 9
d. 1, 10, 12
e. 13, 14, 16

A
  1. a. 3, 7, 9, 17. Fluorescence in situ hybridization (FISH) identifies fluorescently labeled DNA probes that bind to intranuclear chromosomes. The current commercially available probes evaluate aneuploidy for chromosomes 3, 7, 17, and homozygous loss of 9p 21 (Zwarthoff, 2008). The median sensitivity and specificity of FISH analysis is 79% and 70%, respectively (van Rhijn etal, 2005).
127
Q

Microsatellite analysis: a. detects telomeric repeats.
b. amplifies DNA repeats in the genome. c. evaluates abnormalities on chromosome 9.
d. detects DNA methylation.
e. identifies hereditary urothelial cancer.

A

b. Amplifies DNA repeats in the genome. There are multiple markers available to identify short DNA repeats present throughout the chromosomes that are lost in some tumor cells. Microsatellite analysis amplifies these repeats in the genome that are highly polymorphic, and PCR amplification can detect tumor-associated loss of heterozygosity by comparing the peak ratio of the two alleles in tumor DNA in a urine sample with that ratio in a blood sample from the same individual (Steiner etal, 1997; Wang etal, 1997). The sensitivity and specificity of microsatellite analysis for the detection of urothelial carcinoma range from 72% to 97% and 80% to 100%, respectively (Steiner etal, 1997; Wang etal, 1997). Microsatellite analysis evaluates abnormalities on all chromosomes.

128
Q

Smoking is responsible for what percent of bladder cancer in males?
a. 5%
b. 20%
c. 40%
d. 60%
e. 80%

A

c. 40%. Smoking is responsible for 30% to 50% of all bladder cancers in males, and smokers have a twofold to sixfold greater risk for bladder cancer (Brennan etal, 2000; Boffetta, 2008). Smoking cessation will decrease the risk of eventual urothelial cancer formation in a linear fashion. After 15 years of not smoking, the risk of cancer formation is the same as for a person who never smoked (Smoke IAfRoCT, 2004). The strong influence of smoking in bladder cancer formation prevents accurate determination of other, less significant dietary, micronutrient, or lifestyle changes that may alter bladder cancer formation.

129
Q
  1. Which of the following is not sensitive to cisplatin chemotherapy? a. High-grade urothelial cancer b. Micropapillary cancer c. Squamous cell cancer d. Adenocarcinoma e. Small cell cancer

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 520). Elsevier Health Sciences. Kindle Edition.

A
130
Q

Nested variant of urothelial cancer can be confused with:
a. cystitis cystica.
b. micropapillary cancer.
c. squamous cell cancer.
d. small cell cancer.
e. high-grade urothelial cancer.

A

a. Cystitis cystica. The nested variant of urothelial cancer is a rare but aggressive cancer that has a male-to-female ratio of 6:1 and can be confused with benign lesions, such as Von Brunn nests that are in the lamina propria, cystitis cystica, and inverted papillomas (Holmang and Johansson, 2001). There is little nuclear atypia in nested variant urothelial carcinoma, but the tumor cells will often contain areas with large nuclei and mitotic figures. The mortality rate from nested variant urothelial carcinoma, despite aggressive therapy, is significant, with 70% dying of their disease within 3 years (Paik and Park, 1996).

131
Q

The most common sarcoma involving the bladder is:
a. angiosarcoma.
b. chondrosarcoma.
c. leiomyosarcoma.
d. rhabdomyosarcoma. e. osteosarcoma.

A

c. Leiomyosarcoma.Leiomyosarcoma is the most common histologic subtype, followed by rhabdomyosarcoma and then, rarely, angiosarcomas, osteosarcomas, and carcinosarcomas. The male-to-female ratio is 2:1, and the average age at presentation is in the sixth decade of life. There are no clear agents that cause bladder sarcomas, although there is an association with pelvic radiation and systemic chemotherapy for other malignancies (Spiess etal, 2007). Importantly, bladder sarcomas are not smoking related.

132
Q

Signet ring cell cancers: a. have a good prognosis.
b. are sensitive to doxorubicin chemotherapy.
c. usually present in advanced stage.
d. are responsive to radiation therapy.
e. are low-grade at initial presentation.

A

c. Usually present in advanced stage. Primary signet ring cell carcinoma of the bladder is extremely rare, making up less than 1% of all epithelial bladder neoplasms (Morelli etal, 2006). Signet ring cell carcinoma can be of urachal origin and directly extend into the bladder. These tumors generally present as high-grade, high-stage tumors and have a uniformly poor prognosis. The primary treatment is radical cystectomy; however, in the majority of cases there are regional or distant metastases at the time of presentation, and the mean survival time is less than 20 months (Torenbeek etal, 1996). There are reports of elevated carcinoembryonic antigen (CEA) in patients with signet ring cell carcinoma. The prognostic significance of this elevated serum marker is unclear (Morelli etal, 2006). Understaging is very common in signet ring cell carcinoma, with peritoneal studding common at the time of surgical exploration.

133
Q

The risk of bladder cancer formation in a spinal cord–injured patient is:
a. less than 5%.
b. 20%.
c. 40%.
d. 60%.
e. 80%.

A

a. Less than 5%. Spinal cord–injured patients are at risk for developing squamous cell carcinoma, most likely due to chronic catheter irritation and infection. Older studies have suggested a 2.5% to 10% incidence of squamous cell carcinoma in the spinal cord–injured population, with a mean delay of 17 years after the spinal cord injury (Kaufman etal., 1977). More recent analysis of the association of spinal cord injury and bladder cancer formation has shown a remarkably lower risk of bladder cancer formation of 0.38%, most likely because of better catheter care (Bickel etal., 1991). This supports the concept that chronic infection and foreign bodies can lead to bladder cancer formation.

134
Q

For patients undergoing radical cystectomy for urothelial cancer, the risk of identifying prostatic urethral disease is:
a. less than 5%.
b. 20%.
c. 40%.
d. 60%.
e. 80%.

A

c. 40%. Prostatic urethral cancer is associated with urothelial cancer of the bladder in 90% of cases, primarily CIS, and most will have multifocal bladder tumors. However, the incidence of prostatic urethral disease in patients with primary urothelial cancer is only 3% (Rikken etal., 1987; Millan-Rodriguez etal., 2000). Secondary prostatic urethral involvement in patients with a history of urothelial cancer is approximately 15% at 5 years and 30% at 15 years, almost uniformly associated with extensive intravesical therapy (Herr and Donat, 1999). For patients undergoing radical cystectomy for urothelial cancer, the risk of identifying prostatic urethral disease is 40%.

135
Q

Which of the following is NOT a risk factor for prostatic urethral cancer?
a. Previous intravesical therapy
b. CIS of the trigone
c. CIS of the distal ureters
d. Low-grade urothelial cancer
e. Recurrent bladder tumors

A

d. Low-grade urothelial cancer.Risk factors for prostatic urethral involvement are CIS of the trigone, bladder neck, distal ureters, recurrent bladder tumors, and a history of intravesical chemotherapy (Wood etal., 1989b). Low-grade tumors rarely involve the prostatic urethra.

136
Q

A 70-year-old man has microscopic hematuria. Cytology and computed tomography (CT) scan are negative. Cystoscopy reveals a raised 3-mm lesion on the trigone. The lesion is biopsied and is depicted in Fig. 135.1A and B, and is reported as adenocarcinoma. The next step in management is:
a. review the pathology slides with the pathologist.
b. cystectomy.
c. intravesical chemotherapy.
d. bone scan.
e. ask for special stains from pathology.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 520). Elsevier Health Sciences. Kindle Edition.

A

a. Review the pathology slides with the pathologist. This is a classic inverted papilloma, and the inexperienced pathologist might mistake it for an adenocarcinoma. The location of the lesion would be unusual for adenocarcinoma, particularly in a patient with no risk factors, and should alert the clinician to review the slides with the pathologist.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 524). Elsevier Health Sciences. Kindle Edition.

137
Q

A 65-year-old man has gross hematuria. He has a history of tuberculosis. Cytology is suspicious, CT scan is normal, and cystoscopy reveals a papillary lesion cephalad to the trigone. The lesion is visually completely resected (Fig. 135.2) and is reported as high-grade invasive urothelial carcinoma. The next step in management is:
a. intravesical BCG.
b. immediate intravesical mitomycin c. repeat transurethral resection of bladder at the previous biopsied site.
d. a cystectomy.
e. ask the pathologist if there is muscularis propria in the specimen.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 520). Elsevier Health Sciences. Kindle Edition.

A
  1. e. Ask the pathologist if there is muscularis propria in the specimen. There are clear bundles of muscularis propria in the micrograph making the tumor at least a T2.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 524). Elsevier Health Sciences. Kindle Edition.

138
Q

See Fig. 135.3. The depicted findings have an association with:

a. bladder carcinoma.
b. previous trauma.
c. recurrent urinary tract infections.
d. urolithiasis.
e. ureteral spasm.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 520). Elsevier Health Sciences. Kindle Edition.

A
  1. a. Bladder carcinoma. Pseudodiverticulosis of the ureter is associated with bladder carcinoma in 30% of cases. This association has led many to recommend that patients with this diagnosis undergo surveillance of their bladder for the development of urothelial neoplasms. The etiology is unknown.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 524). Elsevier Health Sciences. Kindle Edition.

139
Q

Fig. 135.4A is a delayed contrast-enhanced image through the pelvic ureters, and Fig. 135.4B is an early contrast-enhanced image through the bladder. The next step in management is:

a. shockwave lithotripsy.

b. percutaneous nephrostolithotomy.

c. cystoscopy.

d. cystoscopy with ureteroscopy.

e. follow-up with imaging in 6 months.

A
  1. d. Cystoscopy with ureteroscopy. There are multiple enhancing masses in the fluid-filled urinary bladder on the early image. On the delayed image, the ureters are opacified with contrast, and there is a filling defect seen in the mildly dilated right ureter, suspicious for a synchronous ureteral lesion.

Wein, Alan J.; Kolon, Thomas F.. Campbell-Walsh-Wein Urology Twelfth Edition Review E-Book (CampbellWalsh) (p. 524). Elsevier Health Sciences. Kindle Edition.

140
Q

What are inverted papillomas associated with?

A

Chronic inflammation

141
Q

What is cystitis grandularis?

A

Cystitis glandularis is a rare benign disorder of the urinary bladder characterized by the formation of cysts in the bladder’s submucosa. The cysts are lined by glandular epithelium and can be filled with clear, straw-colored fluid. Symptoms include recurrent urinary tract infections, frequency, urgency and dysuria. The condition is typically diagnosed using cystoscopy and biopsy, and treatment options include observation, medical therapy, or surgery.

142
Q

What is pelvic lipomatosis?

A

Pelvic lipomatosis is a rare condition characterized by the abnormal growth of fat within the pelvic region. The condition is benign and usually asymptomatic but it can cause symptoms such as urinary obstruction, constipation, and abdominal pain. Pelvic lipomatosis can be diagnosed by a combination of imaging studies such as CT or MRI and physical examination. Treatment is typically surgical, with the goal of removing the excess fat and relieving any symptoms caused by the condition. In most cases, the condition is benign and non cancerous, but a biopsy is performed to confirm it.

143
Q

Bladder cancers in adolescents and young adults are generally what?

A

Well differentiated and noninvasive

144
Q

The intensity and duration of smoking is linearly related to what?

A

The risk of developing bladder cancer with no plateau. Cessation reduces the risk.

145
Q

The is a clear association between decreased risk of urothelial cancer and?

A

Healthy diet

146
Q

What have been associated with the development of bladder cancer?

A

Chronic irritation, bacterial infection, and radiation

147
Q

There is no convincing evidence that what increases the risk of bladder cancer?

A

Alteration in fluid intake, alcohol consumption, ingestion of artificial sweeteners, or analgesic abuse

148
Q

80% of the time, low-grade, low-stage urothelial neoplasia (papillary urothelial neoplasia of low malignant potential) is associated with what genetic alteration?

A

Loss of chromosome 9

149
Q

Low-grade (stage 1), low-stage urothelial neoplasia is called papillary urothelial neoplasia of low malignant potential (PUNLMP), the terms low grade and high grade replace what?

A

Old system of grade 2 and 3

150
Q

Prostatic urethral involvement by transitional cell carcinoma without invasion carries what prognosis? When it invades prostatic stroma? When it invades the substance of the prostate from the bladder?

A

Good; less good; poor

151
Q

Low-grade papillary lesions have what recurrence rate?Progression to muscularis propria invasion? What about high-grade?

A

60%; 10%; 50% progression; 80% recurrence

152
Q

Angiolymphatic invasion is what type of prognostic sign?

A

Poor

153
Q

Alterations of what genes are poor prognostic indicators in muscularis propria invasive urothelial cancer?

A

TP53, RB, PTEN

154
Q

What genetic alterations are associated with low-grade non-muscularis propia invasive disease?

A

FGFR-3 and deletions in chromosome 9

155
Q

What have been used to increase the sensitivity of cystoscopy?

A

Porphyrin-induced fluorescent cystoscopy and narrow-band imaging

156
Q

List the sarcomas of bladder in decreasing order of frequency.

A

Leiomyosarcoma, rhabdomyosarcoma, angiosarcoma, osteosarcoma, carcinosarcoma

157
Q

What is the causative agent of squamous cell carcinoma in endemic regions?

A

Schistosoma haematobium

158
Q

Altered growth patterns such as what carry a poor prognosis?

A

Micropapillary and nested patterns

159
Q

Normal bladder urothelium is less than how many layers thick? Papillary lesions are greater than how many layers thick?

A

Seven

160
Q

The incidence of urothelial cancer peaks in which decade of life?

A

Seventh

161
Q

There is some evidence to indicate that BCG plus oral administration of vitamins A, B6, C, E, and zinc result in what?

A

A reduced risk of recurrent transitional cell carcinoma

162
Q

Histologically, what percentage of bladder cancers are of urothelial origin? Squamous cell? Adenocarcinoma or other variants?

A

90%; 5%; <2%

163
Q

All CiS is what grade by definition? The genetic abnormalities associated with CiS are alterations to what genes?

A

High grade; RB, TP53, PTEN

164
Q

What is the only chemotherapeutic agent proven to cause bladder cancer?

A

Cyclophosphamide

165
Q

First-degree relatives of patients with bladder cancer have a what fold increased risk of developing urothelial carcinoma themselves?

A

Twofold

166
Q

Urothelial cancer formation after radiation is age or not age related? What is the latency period?

A

15-20 years; not age related

167
Q

Small cell carcinoma of the bladder is very what?

A

Chemosensitive

168
Q

The risk of malignancy in patients with recurrent gross or microscopic hematuria who had a full, negative evaluation is near what percent?

A

Zero within the first 6 years

169
Q

Neoadjuvant chemotherapy is not effective in what urothelial carcinoma?

A

Micropapillary

170
Q

Question: What is low-grade papillary urothelial carcinoma with inverted growth pattern?

Answer choices:

A) A type of invasive urothelial carcinoma
B) A type of urothelial carcinoma with a high risk of recurrence
C) A type of urothelial carcinoma that lacks an invasive appearance and does not invade into the muscularis propria
D) A type of urothelial carcinoma that has irregular nests and shows variation in cell size

A

C) A type of urothelial carcinoma that lacks an invasive appearance and does not invade into the muscularis propria.

Explanation: Low-grade papillary urothelial carcinoma with inverted growth pattern is a variant of urothelial carcinoma that is characterized by a lack of invasive appearance and an absence of invasion into the muscularis propria. It has rounded nests that are fairly uniform in size and usually crowded. It is important to distinguish this variant from the large nested variant of urothelial carcinoma, which has a more aggressive clinical behavior.

171
Q

What syndrome and blood changes are associated with using the stomach for urinary diversion? Also, list the associated abnormalities, symptoms, and treatment.

A

The stomach is associated with severe metabolic alkalosis, with a decrease in K+ and Cl–, and an increase in pH. The associated abnormality is elevated aldosterone. Symptoms include lethargy, muscle weakness, respiratory insufficiency, seizures, and ventricular arrhythmia. Treatment involves H2 blockers, proton pump inhibitors, and if life-threatening, arginine hydrochloride infusion and/or removal of the segment.

172
Q

What happens to serum potassium levels during alkalosis, and what is the physiological explanation for this change?

A

During alkalosis, serum potassium levels decrease. The increase in blood pH leads to the movement of hydrogen ions out of the cells, and in exchange, potassium ions move into the cells, resulting in a decrease in extracellular potassium concentration.

173
Q

Explain the syndrome, blood changes, associated abnormalities, symptoms, and treatment when using the ileum/colon for urinary diversion.

A

The ileum/colon is associated with hyperchloremic metabolic acidosis, with a decrease in K+ and an increase in Cl–, along with a decrease in pH. Associated abnormalities are total-body potassium depletion and hypocalcemia. Symptoms include fatigue, anorexia, lethargy, and weakness. Treatment consists of potassium citrate, sodium citrate, citric acid, sodium bicarbonate, chlorpromazine, and nicotinic acid.

174
Q

Why does the use of the ileum/colon for urinary diversion lead to hypokalemia?

A

The use of the ileum/colon leads to hyperchloremic metabolic acidosis, causing initial potassium movement out of the cells. The kidneys respond by excreting H+ and K+ to correct the acidosis, and increased aldosterone secretion also promotes potassium excretion. Chronic urinary loss of potassium in this diversion further contributes to hypokalemia.

175
Q

Describe the electrolyte disturbances, associated abnormalities, symptoms, and treatment when the jejunum is used for urinary diversion.

A

The jejunum is associated with hyperkalemic, hypochloremic metabolic acidosis, characterized by a decrease in Na+ and Cl–, and an increase in K+, with a decrease in pH. Abnormalities include elevated renin and angiotensin. Symptoms are lethargy, nausea, vomiting, dehydration, and muscle weakness. Treatment is intravenous hydration, sodium bicarbonate, thiazide, and if life-threatening, removal of the segment.

176
Q

Why does the use of the jejunum for urinary diversion lead to hyperkalemia?

A

The jejunum’s use for urinary diversion leads to hyperkalemia through increased absorption of potassium, loss of sodium and chloride, and the complex response of the renin-angiotensin-aldosterone system, which may prioritize sodium retention over potassium excretion.

177
Q

How do the large intestine and small intestine differ in terms of hyperkalemia or hypokalemia when used for urinary diversion?

A

The small intestine (e.g., jejunum) may lead to hyperkalemia due to increased potassium absorption and altered sodium and chloride balance. The large intestine (e.g., ileum/colon) often results in hypokalemia due to hyperchloremic metabolic acidosis, increased aldosterone secretion, and chronic urinary loss of potassium.

02. Urotelial Cancer (1375) (11 decks)

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