Bladder Tumors Flashcards

Question

How do you grade bladder cancer?

Answer 1

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

Answer 2

``` 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 ```

Answer 3

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

Answer 4

Schistosoma infection - bilharzial infections associated with SCC

Answer 5

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

Answer 6

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

Answer 7

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

Answer 8

``` 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 ```

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

55%, 20-50%

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

Pelvic lymph nodes > liver > lung > bone

Answer 18

Irritative LUTS

Answer 19

Recurrence - 30% after BCG | Progression - 20% after complete response to BCG

Answer 20

Flat, high grade, and non-invasive

Answer 21

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

Answer 22

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

Answer 23

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)

Answer 24

Progression - 5% progress to muscle invasion within 1 year of TURBT Recurrence - 50% recur within 1 year of TURBT

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

6 weeks of BCG induction 3-4 weeks after TURBT

Answer 31

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

Answer 32

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

Answer 33

1. Every 1-2 years if tumor is high grade | 2. When there are frequent recurrences

Answer 34

Recurrence - 50-70% recur after treatment | Progression - 30-40% progress to muscle invasive disease after TURBT

Answer 35

Re-resection TURBT to confirm stage and complete resection

Answer 36

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

Answer 37

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

Answer 38

1. Repeat induction BCG | 2. Cystectomy

Answer 39

Maintenance BCG

Answer 40

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

Answer 41

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

Answer 42

Systemic chemotherapy +/- EBRT for local control

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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.

Answer 47

1. Chemotherapy (mitomycin, thiotepa, epirubicin) | 2. Immunotherapy (BCG, interferon)

Answer 48

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

Answer 49

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

Answer 50

1. CIS 2. High grade tumors 3. T1 tumors

Answer 51

2 weeks minimum

Answer 52

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%)

Answer 53

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.

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

U/A - check for gross hematuria and UTI

Answer 58

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

Answer 59

Alkylating agent (inhibits DNA synthesis)

Answer 60

40mg in 20cc sterile water administered intravesically

Answer 61

1. Contact dermatitis | 2. Irritative LUTS

Answer 62

It has a high molecular weight. Can cause myelosuppression

Answer 63

Ta, T1 and CIS bladder cancer

Answer 64

alkylating agent (inhibits DNA synthesis)

Answer 65

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

Answer 66

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

Answer 67

Anthracycline - intercalating agent that inhibits DNA synthesis

Answer 68

40-100mg in 40-100cc of NS

Answer 69

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

Answer 70

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

Answer 71

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 et al., 2006; Kilciler et al., 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 et al., 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 et al., 2007).

Answer 72

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 et al., 2007). The incidence of urothelial cancer peaks in the seventh decade of life.

Answer 73

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 et al., 2008).

Answer 74

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 et al., 2007; Jemal et al, 2008).

Answer 75

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.

Answer 76

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 et al., 2002).

Answer 77

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 et al., 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 et al., 2009). These authors estimated that 31% of all bladder cancer deaths were avoidable, more commonly in noninvasive than invasive disease.

Answer 78

9. 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 et al., 2004a; George et al, 2007; Sanchez-Carbayo et al, 2007).

Answer 79

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 et al., 2000; Lopez-Beltran et al, 2002; Cordon-Cardo, 2008).

Answer 80

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.

Answer 81

12. e. Cyclophosphamide. The only chemotherapeutic agent that has been proven to cause bladder cancer is cyclophosphamide (Travis et al., 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.

Answer 82

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 et al., 2002; Murta-Nascimento et al., 2007; Kiemeney, 2008).

Answer 83

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.

Answer 84

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.

Answer 85

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 et al., 2001; Sauter et al., 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

Answer 86

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.

Answer 87

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).

Answer 88

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.

Answer 89

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.

Answer 90

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 et al, 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.

Answer 91

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 et al, 2007).

Answer 92

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 et al, 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.

Answer 93

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.

Answer 94

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 et al, 2004a). FGFR-3 mutations are associated with noninvasive bladder cancer.

Answer 95

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 et al., 2014; TCGAR, 2014; Damrauer et al., 2014), and patients with basal tumors appeared to derive the most benefit from neoadjuvant chemotherapy (NAC) (Seiler et al 2017; McConkey et al., 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 et al., 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.

Answer 96

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 et al, 1998; Wolff et al, 2005; Cordon-Cardo, 2008).

Answer 97

a. Less than 5%. Gross, painless hematuria is the primary symptom in 85% of patients with a newly diagnosed bladder tumor (Khadra et al, 2000; Alishahi et al, 2002; Edwards et al, 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 et al, 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 et al, 2000).

Answer 98

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.

Answer 99

30. 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 et al, 2005).

Answer 100

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 et al, 1997; Wang et al, 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 et al, 1997; Wang et al, 1997). Microsatellite analysis evaluates abnormalities on all chromosomes.

Answer 101

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 et al, 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.

Answer 102

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).

Answer 103

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 et al, 2007). Importantly, bladder sarcomas are not smoking related.

Answer 104

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 et al, 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 et al, 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 et al, 2006). Understaging is very common in signet ring cell carcinoma, with peritoneal studding common at the time of surgical exploration.

Answer 105

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 et al., 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 et al., 1991). This supports the concept that chronic infection and foreign bodies can lead to bladder cancer formation.

Answer 106

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 et al., 1987; Millan-Rodriguez et al., 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%.

Answer 107

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 et al., 1989b). Low-grade tumors rarely involve the prostatic urethra.

Answer 108

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.

Answer 109

2. 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.

Answer 110

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.

Answer 111

2. 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.

Answer 112

Chronic inflammation

Answer 113

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.

Answer 114

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.

Answer 115

Well differentiated and noninvasive

Answer 116

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

Answer 117

Healthy diet

Answer 118

Chronic irritation, bacterial infection, and radiation

Answer 119

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

Answer 120

Loss of chromosome 9

Answer 121

Old system of grade 2 and 3

Answer 122

Good; less good; poor

Answer 123

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

Answer 124

TP53, RB, PTEN

Answer 125

FGFR-3 and deletions in chromosome 9

Answer 126

Porphyrin-induced fluorescent cystoscopy and narrow-band imaging

Answer 127

Leiomyosarcoma, rhabdomyosarcoma, angiosarcoma, osteosarcoma, carcinosarcoma

Answer 128

Schistosoma haematobium

Answer 129

Micropapillary and nested patterns

Answer 130

A reduced risk of recurrent transitional cell carcinoma

Answer 131

90%; 5%; <2%

Answer 132

High grade; RB, TP53, PTEN

Answer 133

Cyclophosphamide

Answer 134

15-20 years; not age related

Answer 135

Chemosensitive

Answer 136

Zero within the first 6 years

Answer 137

Micropapillary

Answer 138

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.

Answer 139

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.

Answer 140

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.

Answer 141

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.

Answer 142

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.

Answer 143

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.

Answer 144

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.

Answer 145

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.

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