Bakari Korchilava
Ureteral Anomalies
• Ureteral anomalies frequently occur with renal anomalies but may occur independently.
Complications include:
• Obstruction, vesicoureteral reflux, urinary tract infections, and urinary
calculus formation (due to urinary stasis)
• Urinary incontinence (due to abnormal termination of the ureter in the urethra,
perineum, or vagina)
• Diagnosis of ureteral anomalies may be suggested by abnormalities on routine prenatal
ultrasonography (eg, hydronephrosis) and occasionally by physical examination (eg,
finding an external ectopic ureteral orifice or a palpable mass). Ureteral anomalies
should be suspected in children with an episode of pyelonephritis or recurrent urinary
tract infections and in girls with persistent urinary incontinence. Testing typically
involves ultrasonography of the kidneys, ureters, and bladder before and after voiding,
and then fluoroscopic voiding cystourethrography.
• Ureteral anomaly treatments are surgical
URINARY BLADDER
• Several different types of congenital abnormalities of the bladder are recognized; these are
variously associated with increased risk of infection or neoplasia.
• Vesicoureteral reflux is the most common and serious congenital anomaly. vesicoureteral reflux
predisposes to ascending pyelonephritis and loss of renal function. Abnormal connections
between the bladder and the vagina, rectum, or uterus may create congenital vesico-uterine
fistulae.
• Diverticula are pouch-like invaginations of the bladder wall that vary from less than 1 cm to 10
cm in diameter and may be congenital or acquired. Congenital diverticula may be due to a focal
failure of development of the normal musculature or to a urinary tract obstruction during fetal
development. Acquired diverticula are most often associated with prostatic hyperplasia,
producing urinary outflow obstruction. The resulting increase in intravesical pressure causes
outpouching of the bladder wall and the formation of diverticula. Although most diverticula are
small and asymptomatic, they may come to clinical attention since they constitute sites of urinary
stasis and predispose to infection and the formation of bladder calculi.
• Exstrophy of the bladder is a developmental failure in the anterior wall of the abdomen and the
bladder. As a result, the bladder communicates directly with the abdominal surface .The exposed
bladder mucosa may undergo colonic glandular metaplasia and is subject to chronic infection
that often spreads to the upper urinary tract. Exstrophy is associated with an increased risk of
adenocarcinoma in the bladder remnant.
Neurogenic Bladder
Cystitis
Interstitial Cystitis
• Interstitial cystitis is noninfectious bladder inflammation that causes
pain (suprapubic, pelvic, and abdominal), urinary frequency, and
urgency with incontinence. Diagnosis is by history and exclusion of
other disorders clinically and by cystoscopy and biopsy. With
treatment, most patients improve, but cure is rare. Treatment varies
but includes dietary changes, bladder training, pentosan, analgesics,
and intravesical therapies.
Bladder Cancer
NON-UROTHELIAL BLADDER CANCERS
PATHOLOGY & CAUSES
• Bladder cancers that do not arise from the urothelium
• More invasive, poorer prognosis
• Squamous cell metaplasia: cells of urothelium → pancake-like appearance of squamous cells → differentiate
into squamous cell carcinoma
• Primary adenocarcinomas ▫ Frequently metastasize ▫ Derive from glandular tissue → produce a lot of mucin
• Adenocarcinomas of urachus
RISK FACTORS
• Chronic urinary tract infections (UTIs)
SIGNS & SYMPTOMS
• Bladder irritation
• Pain (location determined by tumor size/extent—flank, suprapubic, perineal, abdominal, etc.)
• Hematuria
• Adenocarcinomas secrete mucin →mucusuria
TRANSITIONAL CELL CARCINOMA
PATHOLOGY & CAUSES
• Most common form of lower urinary tract cancer (bladder, urethra)
• AKA urothelial cell carcinoma
• Can also affect upper urinary tract (e.g. renal pelvis, ureter)
SIGNS & SYMPTOMS
• Hematuria
• Pain (location determined by size/extent of tumor: flank, suprapubic, perineal)
• Constitutional symptoms (severe disease)
• Dysuria; frequent/urgent urination
TREATMENT
Chemotherapy
• Non-aggressive: localised via catheter
• Aggressive: systemic
• SURGERY
• Non-aggressive: transurethral resection via cystoscopy (localized, non-invasive tumors)
• Aggressive: complete removal of prostate, bladder (cystoprostatectomy)
HYPOSPADIAS & EPISPADIAS
PATHOLOGY & CAUSES
• Congenital malformations characterized by abnormal urethral opening found ventrally (hypospadias),
dorsally (epispadias)
• Hypospadias more common
• Hyposadias -Urethral folds along penile urethra do not close properly → abnormal opening along penile
shaft’s ventral surface
• Epispadias-Genital tubercle grows in posterior direction instead of cranial direction.
RISK FACTORS
• Family history of hypospadias/epispadias
• Genetic factors causing hormonal disturbances ↓ androgens
• Maternal age > 35 years old
COMPLICATIONS
• Constriction of abnormal opening → urinary tract obstruction
• High risk of ascending urinary tract infections
SIGNS & SYMPTOMS
• Depends on location of abnormal urethral opening
• Difficulty urinating/incontinence
DIAGNOSIS
• Excretory urogram ▪ Series of X-rays used to visualize
substances passing through kidneys, bladder, urethra.
TREATMENT
• Hormone therapy for additional problems (e.g. low androgen
levels → micropenis)
• SURGERY ▪ Reconstruction of urethra within first two years of
life
ORCHITIS
CRYPTORCHIDISM
PATHOLOGY & CAUSES
• Common congenital condition characterized by incomplete/partial descent of testis into scrotal sac
• AKA undescended testes
• Usually unilateral; bilateral in ¼ of cases
RISK FACTORS
• Prematurity
• ↓ birth weight
• Twining
• 1st trimester maternal exposure to estrogens
• Family history of undescended testes
• Genetic syndromes associated with cryptorchidism (e.g. Down syndrome, Klinefelter syndrome)
COMPLICATIONS
Testicular atrophy, dysfunction → infertility
When malpositioned in inguinal canal →prone to trauma, testicular torsion
Left untreated/treatment delayed → germ-cell tumors,
EPIDIDYMITIS
TESTICULAR TORSION
VARICOCELE
PATHOLOGY & CAUSES
• Common testicular disorder of young adults characterized by dilatation of pampiniform venous plexus,
internal spermatic vein
• Most common cause of scrotal enlargement in young adults
• Impaired venous drainage → ↑ venous pressure → vein dilatation
• Usually left-sided (> 80%) due to ↑flow resistance from left testicular vein drainage into left renal vein.
TYPES
• Large ▪ Easily identified by inspection as distention
• Moderate ▪ Identified by palpation as “bag of worms”
• Small▪ Identified only by bearing down → ↑abdominal pressure → impeding drainage→ ↑ varicocele size
COMPLICATIONS
• Significant impairments in sperm production, quality due to ↑ heat, ↑pressure, ↓ oxygen, release of toxins
▫↓ sperm concentration ▫↓ motility ▫Abnormal morphology of spermatozoa
• Testicular damage, atrophy, poor sperm production, quality → infertility
• Contralateral testicle can also be affected
SIGNS & SYMPTOMS
• Usually asymptomatic
• Symptomatic ▫ Scrotal heaviness or scrotal pain
DIAGNOSIS
• Doppler ultrasound▪ Characteristic reverse blood flow
• Ultrasound/ CT scan ▪May be useful in right-sided varicocele →reveals retroperitoneal pathology
TREATMENT
• SURGERY ▪ Indicated if varicocele associated with discomfort/pain, testicular atrophy, infertility
• Surgical ligation/embolization
PENILE CANCER
Testicular Cancer
PROSTATITIS
BENIGN PROSTATIC HYPERPLASIA
PROSTATE CANCER