Renal System- Urinary Bladder By Leonard

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Renal System- Urinary Bladder by Leonard

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Renal System- Urinary Bladder by Leonard

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Define Obstructive Uropathy

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Urinary tract obstruction anywhere from renal calyces down to distal urethral meatus

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Common causes

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Congenital anomalies: urethral valves, strictures/stenosis;
-VRR (vescico-ureto reflux); UPJ (uretero pelvic junction) narrowing are the 2 most common congenital anomolies
-Calculi
-BPH
-Tumors
Inflammation, fibrosis
-Cellular/tissue
-Pregnancy- enlarged uterus puts pressure on urinary bladder
-Uterine prolapse and cystocele
-Functional (neurogenic)

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Common sequelae

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-Stagnation of urine with
-Increased risk of infection (E coli and its fimbriae)
-Increases risk of calculi

-Loss of renal function from hydronephrosis with associated cortical atrophy

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Obstructive Uropathy – Clinical Considerations

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Presentation: depends upon underlying cause
General
-Pain (e.g., renal colic from ureteral stone)
-Altered U/O – stream, amount, etc. (E.g., BPH)
Unilateral obstruction may be asymptomatic
-Preservation of normal function of one kidney
Bilateral partial obstruction
-Chronic tubulointerstitial nephritis; HTN
-Polyuria, nocturia: inability to concentrate urine
Bilateral complete obstruction
-Oliguria, anuria
-Urine output must be restored for survival

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Clinical Presentation of urolithiasis

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-5-10% of US population; M>F; peak age 20-30s
-Familial/hereditary tendencies (e.g., inform error in metabolism)
-Smaller stones: pass into ureter → renal colic and obstruction; hematuria
-Larger stones: remain in kidney → hematuria, or asx
-both: Calculi produce inflammation and predispose to infection

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Most common type of stones are made of

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Calcium (oxalate and/or phosphate) - ~ 70%
-radiopaque
-Hypercalcemic states
-Hyperparathyroidism, diffuse bone disease, *sarcoidosis
-Hypercalciuria w/o hypercalcemia

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What are "triple stones" made of?

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Struvite (“triple stones”):
magnesium, ammonium, phosphate
-Bacterial infections (Proteus, certain Staph. spp.)
-Urea → ammonia (increase urine pH)
Large stones (staghorn calculi)

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Uric acid stones of an xray

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-radiolucent
-Hyperuricemia (gout, rapid cell turnover)
-Tendency to excrete urine with pH < 5.5

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Cystine stones. how do you get them?

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-Genetic defects in renal reabsorption of amino acids
-Stones form at low urine pH

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Congenital/Developmental Anomalies:
Diverticula
-true, acquired, congenital

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True diverticula: out-pouchings of visceral organ consisting of all layers of the wall of the organ

Acquired: increased intraluminal pressure (secondary to obstruction “downstream”)

Congenital: defect in bladder wall muscle development &/or fetal urine outflow obstruction

*Infection and/or stone formation from stagnant urine

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What is Bladder Exstrophy?

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Exstrophy
~ 33 per 1,000,000 live births
-Anterior bladder wall and abdominal wall are absent
-Exposes bladder mucosa to external environment
-Increased risk of cystitis and carcinoma (adenocarcinoma)

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Urachal Cyst presentation, features, and neoplastic association

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Urachal cysts:
-Most common urachal anomaly
-Suprapubic palpable mass (lower part of urachus)
-Columnar lining

Prone to neoplastic transformation → adenocarcinoma*
-Account for less than 0.5% of all bladder cancers, but ~ 1/3 of adenocarcinomas

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Wait, what is the urachus, and what can happen if it's patent?

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Urachus: vestigial remnant of the connection of bladder apex to the allantois (located at umbilicus)
-Very rare

Patent urachus: communicating duct between umbilicus and urinary bladder → infection

May close spontaneously; typically requires surgical closure

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General causes of cystitis, acute and chronic

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-Systemic signs (fever, malaise) uncommon in uncomplicated (localized) cystitis
-Infectious
-Bacterial: E. coli, Proteus, Klebsiella, Enterobacter (normal flora)
-Fungal: Candida – typically in immunocompromised patients or long-term antibiotic use
-Schistosomiasis (Schistosoma haematobium)
-Middle East, northern Africa (Egypt)
-Viruses, Chlamydia, Mycoplasma (Adenovirus: hemorrhagic cystitis)
-Chemical or physical agents
-Drugs and other chemicals
-Cytotoxic chemotherapy (e.g., cyclophosphamide): hemorrhagic cystitis
-Radiation -Calculi (mechanical trauma)

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Cystitis – “Special” Forms
Interstitial cystitis:
clinical presentation, possible outcomes

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“Chronic pelvic pain syndrome”
-Etiology uncertain; F >> M
-Recurrent, severe, intermittent suprapubic pain, hematuria, urinary urgency
-No evidence of bacterial infection
-May result in transmural fibrosis with dysfunctional bladder
-May mimic in situ urothelial carcinoma

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Cystitis – “Special” Forms
Malacoplakia:
histology and relation to pathology

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Macroscopic: soft, tan/yellow slightly elevated mucosal plaques

Micro: large, foamy macrophages mixed with multinucleated giant cells and lymphocytes
-***Michaelis-Gutmann bodies within lysosomes of macrophages
-? Defect in phagocytic process

Chronic bacterial infections
-E. coli
-Immunosuppressed transplant patients

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Metaplastic Changes in the Urinary Bladder. What is it? Example, and why.

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Metaplasia: alteration of the epithelium from its typical mature form to a different type of epithelium (usually mature as well)
-E.g., transitional epithelium to columnar or squamous epithelium

Metaplastic epithelium offers a beneficial protective feature in an injurious or potentially pathologic environment
-Columnar, mucus cells (glandular): protection against chemical environment
-Squamous: protection against physical (and possible chemical) environmental stressors
-Effects of smoking, recurrent infections, mechanical trauma (e.g., stones)

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Most common neoplasm...compare papillary and flat

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Vast majority (~ 95%) are epithelial; Urothelial (transitional cell)
Benign: urothelial papilloma
Premalignant (precancerous)
-Papillary: papillary urothelial neoplasm of low malignant potential (PUNLMP)
-Flat: urothelial carcinoma in situ (CIS)
-Tends to be multifocal and greater tendency to progress to more aggressive malignant neoplasm
-Multifocal – pagetoid spread of tumor cells

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Transitional Epithelium CANCERS:

-compare recurrence of papillary urothelial carcinoma vs. Flat

-importance of grading and staging in diagnosis of TCC

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Papillary urothelial carcinoma – tend to recur and may be multifocal
-Not all are invasive (into muscularis propria)
-Histologic grade
-Low grade <10% invade; <10% progress to higher grade tumors
-High grade ~ 80% invade
-Invasive or noninvasive
-Key staging criterion – depth of invasion

“Flat” – associated with CIS – tend to be multifocal and may recur
-Invasive, by definition
-Tend to be high-grade tumors

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Ta
T1
Tis
T2

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Ta - noninvasive, papillary

Tis- carcinoma in situ (noninvasive, flat)

T1- Lamina propria invasion

T2- muscularis propria invasion (decide to surgically remove the bladder or not)

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Squamous cell carcinoma: where do you see it most?

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-~ 3-7% of bladder cancers in USA

-More common in countries where urinary **schistosomiasis is endemic

-Associated with chronic irritation or infection of the urinary bladder

-Most common type of bladder cancer associated with schistosomiasis (70%)
-middle eastern countries and north africa

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Bladder cancer epi/pathogenesis... who gets it more...significant modifiable risk factors

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Incidence:
-3M > F; 50-80 yo
-More common in developed countries; urban > rural
-Generally no familial association

Significant modifiable risk factors
-Tobacco: cigarette smoking (most important)***
-Arylamine chemicals (2-naphthylamine)***
Schistosoma haematobium infection
Long-term analgesic use
Long-term exposure to high doses of cyclophosphamide
Radiation exposure

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Classic presention of urinary bladder cancer?

Risk of recurrence and progression related to?

Prognosis?

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-Classic presentation: painless hematuria

-Tendency to recur, often with higher grade cancers
-Risk of recurrence and progression related to
-Tumor size
-Stage
-Grade
-Multifocality
-Presence of CIS in surrounding mucosa

-Prognosis
-Histologic grade and stage at diagnosis
-Importance of early detection and resection

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Treatment of urinary bladder cancers depends on grade, stage, and flat vs. papillary. go.

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Small, localized papillary tumors
-Transurethral resection of bladder tumor (TURBT)
-Close follow-up surveillance : urine cytology, cystoscopy

CIS, high-grade papillary TCC, multifocal disease, history of rapid recurrence
-Topical immunotherapy/chemotherapy
-Intravesical installation of bacillus Calmette-Guerin (BCG)
-Local inflammatory reaction destroys tumor

Tumor invading muscularis propria; tumor refractory to BCG; metastatic tumor
-Cystectomy
-Possibly systemic chemotherapy