I.

LOWER URINARY TRACK:

URETERS:
CONGENITAL ANOMALIES:
1. DOUBLE AND BIFID URETER:
Distinct double renal pelvis or a single large pelvis is present.

Terminate into separate two ureters.

Combine before entering the bladder or at the ureteral orifice.

It occurs as a unilateral anomaly and has no clinical significance.

2. UPJ OBSTRUCTION:
Congenital obstruction of the ureter pelvic junction due to,

Increased collagen deposition between the muscle layers.

Causes constriction.

Obstruction.
It is fairly more common in females and a frequent cause of hydronephrosis.

3. DIVERTICULA:
Saccular outpouchings of the ureters.

Urine accumulation in these diverticula.

Increased bacterial growth.

Recurrent infections.

4. DIALATED URETER: (HYDROURETER)

5. TORTUROUS URETER:

TUMORS:
FIBROEPITHELIAL POLYPS:
It is a benign tumor of mesenchymal origin composed of epithelial tissues and a
fibrovascular core.
 It consists of a small mass projecting into the lumen called polyp. It is composed of a
vascular core and loose connective tissue covered by transitional epithelium.

UROTHELIAL CARCINOMA:
Malignant proliferation of urothelium of ureter produces a tumor that has a rare
incidence.

URETERAL OBSTRUCTION:

CAUSES:
Intrinsic:
Calculi.
Strictures.
Tumors.
Blood clots.
Neurogenic.
Extrinsic:
Pregnancy.
Enlargement of the fundus exerts pressure on the pelvic brim.

Obstruction of ureter.
Periureteral inflammation such as salpingitis, diverticulitis, sclerosing retro
peritoneal fibrosis& peritonitis etc.
Endometriosis.
Tumors of bladder, rectum, prostate & cervix etc.

SCLEROSING RETRO PERITONEAL FIBROSIS:

Fibrotic proliferative inflammatory process encasing the retro peritoneal structures
such as kidneys, aorta & renal track etc.

Cause obstruction of ureters.

Hydronephrosis.

Occurrence:
Middle age.
M> F.

Pathogenesis:
IgG 4 mediated inflammations also involving plasma cells produces fibrosis of
the retro peritoneal structures.
URINARY BLADDER:

CONGENITAL ANOMALIES:
1. VESICO-URETERAL FISTULA:
These are the abnormal connections b/w the bladder & vagina, rectum or uterus.
It is the most common congenital anomaly.

2. DIVERTICULUM:
Out-pouching in the wall of bladder is called diverticula. These may be;
Congenital:
Failure of development of muscularis mucosa.

Deficit area.

Dilated due to loss of muscle.

Diverticula.

Acquired:
Prostate enlargement or any other anomaly causing urine outflow obstruction.

Increased pressure in bladder.

Increased muscle thickening.

Interweaving regions have a deficit of muscle giving rise to a potentially weak area.

Diverticula formation.

3. EXSTROPHY OF BLADDER:
Developmental failure in the anterior abdominal wall of urinary bladder.

Bladder communicates to the outside through the defect in abdominal wall or lies as an opened
sac to the outside.

Increased risk of infections.

4. URACHAL ANOMALIES:
Urachus is the canal that connects bladder to the allantois during fetal stage. It is obliterated
after birth.
 If it persists;
Totally patent:
Forms fistulus urinary tract and connects bladder to the umbilicus.

Only central part persists:

Forms a cyst called urachal cyst. It may progress into malignant tumor e.g. carcinoma.

INFLAMMATION:
Inflammation of the urinary bladder due to microorganisms or toxins is called cystitis.

RISK FACTORS:
Prostate enlargement.
Congenital anomalies.
Bladder calculi.
Diabetes mellitus.
Tumors etc.

All these factors in one way or other way cause urinary obstruction that favors urine
stasis and growth of microorganisms.

CAUSES:
Bacteria:
E. coli.
Klebsiella.
Proteus.
Enterobacter.
Mycobacterium.

Fungi:
Candida albicans.
Cryptococcus.

Virus:
Adenovirus.
Mycoplasma.

Schistosomiasis.
Radiations etc.

SIGNS:
Fever.
Pain.
Chills.
 Nausea & vomiting.
Specific triad of symptoms of UTI includes.
Increased frequency of urination.
Lower abdominal pain or pain in the pelvic region.
Dysuria. Pain and burning sensation during urination.

Cystitis arises as a secondary disorder due to urinary stasis. Appropriate treatment is treatment
of the underlying cause of cystitis.

TYPES:
1. Interstitial cystitis.
2. Malakoplakia.
3. Polypoid cystitis.

INTERSTITIAL CYSTITIS:
It is the chronic inflammation of the bladder wall involving entire thickness of bladder
wall.

MORPHOLOGY:
Hunner ulcer:
It is a typical lesion of interstitial inflammation appearing as a red brown patch
on the mucosa.
It is surrounded by the radiating vessels.
The lesion might heal superficially thats why it is difficult to detect.

MALAKOPLAKIA:
It is characterized by the formation of soft patches on the surface of mucous membrane
of bladder or ureter. It arises from chronic bacterial infections e.g. E. Coli &protease. It
mostly occurs in immunosuppressed people such as transplant recipients.

MORPHOLOGY:
Yellowish soft and raised mucous plaque filled with macrophages having
defective phagocytic function.
Ca salts are deposited in the lysosomes of macrophages causing increase in size
of lysosomes. They are called as Michalis Gutman bodies.
Macrophages have large size, abundant cytoplasm and are also filled with
phagocytosed bacterial products and dead cells.

POLYPOID CYSTITIS:
It is the inflammation of bladder and ureter mucosa due to catheterization. The
urothelium takes form of a polypoid projection due to sub mucosal edema.
BLADDER OBSTRUCTION:
Occurs predominantly in males.

CAUSES:
Males:
Prostatic hyperplasia.
Females:
Cystocele of bladder which is hernial protrusion of bladder in vaginal wall.
Congenital strictures in urethra.
Inflammatory strictures in urethra.
Bladder tumors.
Mechanical obstruction by calculus.
Neurogenic obstruction due to damage to the controlling nerves.

METAPLASTIC LESIONS:
1. CYSTIC GLANDULARIS & CYSTIC CYSTICA:
Nests of the urothelium in the bladder wall called as Brunn nests.

Grow deeper into the lamina propria.

Central epithelial cell of the nest may undergo metaplasia;

Cuboidal/columnar epithelium. Inner cells retract & form cystic spaces.

Cystic glandularis. Cystic cystica.

Coexist as cystitis cystica et glandularis.

2. SQUAMOUS CELL METAPLASIA:

Chronic cystitis or recurrent injury to the bladder wall.

Transitional epithelium transforms into;

Non keratinizing squamous epithelium.

More durable lining.

It has a tendency to transform into squamous cell carcinoma.
 3. NEPHROGENIC ADENOMA:
When renal tubular epithelium is shredded.

Implanted at the injured sites in urothelium layer.

Urothelium is replaced by cuboidal epithelium.

Takes papillary growth pattern of growth.

Increased chances of carcinoma.

The implanted cells may infiltrate lamina propria and detrusor muscle mimicking TCC.

URINARY BLADDER TUMORS:

These tumors may be;
Benign.
Malignant.
Malignant tumors may be of epithelial origin (95%) or mesenchymal origin (5%).

UROTHELIAL CELLTUMORS:
Malignant neoplastic proliferation of Urothelial cells is called UCC or TCC.

RISK FACTORS:
Smoking.
Schistosomiasis.
Naphthylamine.
Azo dyes.
Cyclophosphamide high doses.
Alcohol.
Phenacetin.

OCCURRENCE:
Older adults (50 -80 years)
Males > Females.

SIGNS:
Painless hematuria. (Classic sign)
Dysuria,
Increased frequency.
Pyelonephritis.
PATHOGENESIS:
Non invasive carcinoma:

Mutations.

FGFR 3 gene. Ch#9 deletions. HRAS gene.

Tyrosine kinase receptor PTCH & TSC-1 genes. Proto-oncogene.

Protein. Inhibit growth of cells normally.

Gain of function loss of function mutation. Gain of function mutation.

Mutation.

Increased growth. Uncontrolled cell growth. Increased growth.

Non invasive carcinoma.

Loss of tumor suppression by mutation in Tp53 & RB gene.

Uncontrolled & increased cell growth.

Invasive carcinoma.

MORPHOLOGY:
1. Urothelial papilloma.
Benign.
Younger individuals.
Less than 1% bladder tumors.

Gross:
o Single small structure.
o Attached to mucosa by means of a stalk.
 Histology:
o No mitotic bodies.
o No necrotic areas.
o Cells resemble the normal urothelial cells.
o Papillary growths have both;
Fibro vascular cores.
Neoplastic cell coverings.
o May progress into invasive carcinoma.
o Inverted papillomas are completely benign.

2. Papillary urothelial neoplasms of low malignant potential:

Thicker urothelium.
Tumor is Larger in size.

3. Low grade urothelial papillary carcinoma:

No mitotic bodies towards the base.
Necrotic areas are absent.
Tumor cells are evenly spaced, coherent &maintain polarity.
Cells exhibit mild cytologic atypia, have hyper chromatic nuclei.
May or may not recur or invade.

4. High grade urothelial papillary carcinoma:

Atypical cells which have lost polarity and are dyscohesive.
Tumor cells have hyperchromatic nuclei.
Highly invasive and metastatic.
Mitotic bodies are found frequently.
Focal Necrotic areas are seen.

5. Carcinoma in situ: (flat urothelial carcinoma)

Malignant cells present in the flat urothelium may follow either of the two patterns.
Form full thickness.
Scattered tumor cells in normal urothelium. (Pagetoidspread)

Non cohesive cells which are shredded in urine.

Mitotic bodies are present.
Focal necrotic areas are present.
If untreated, may transform into invasive carcinoma.

6. Invasive urothelial carcinoma:

Papillary growth pattern.
High grade tumor.
If it involves muscularis mucosa, it has bad prognosis.