Urology Lectures

Undergraduate students

Associate professor of urology Dr. Elsayed Salih Al-Azhar university

elsayedsalih@gmail.com
 Urology Lectures

Index Diagnosis of urinary tract diseases 1

Congenital Anomalies of UT 6
Congenital Polycystic kidney 8
Pelviureteric junction obstruction (PUJO): 11
Vesicoureteral reflux (VUR) 12
Bladder Exstrophy (Ectopic Vesica) 13
Hypospadias 14
Posterior Urethral Value (PUV) 16
Urinary tract injuries 17
Injuries of the kidney 17
Ureteric injury 20
Bladder injury 21
Urethral injuries 22
Urinary tract inflammation 24
Non-specific Urinary tract infection 24
Urinary tract infection: general treatment guidelines 26
Acute Pyelonephritis 27
Perinephric Abscess 28
Pyonephrosis 28
Interstitial Cystitis 29
Epididymitis and Orchitis 30
Urethritis 31
Prostatitis / Prostatodynia 31
Specific infections 33
UT Bilharziasis 33
Genito-urinary tuberculosis 35
Stone Disease 37
Management of urolithiasis 41
Extra-corporeal Shock Wave Lithotripsy (ESWL) 43
Percutaneous nephrolithotomy (PCNL) 44
Open renal stone surgery 44
Management of ureteric stones 45
Management of bladder stones 46
Prevention of stone formation 47
Obstructive uropathy 48
Hydronephrosis 50
Benign Prostatic Hyperplasia (BPH) 52
Urethral stricture 58
Anuria 59
Retention of urine 61
Hematuria 63
Urological neoplasms 66
Renal neoplasms 66
Renal Cell Carcinoma 68
Nephroblastoma 71
Neuroblastoma 73
Carcinoma of the Renal Pelvis and Ureter 73
Bladder cancer 74
Urinary Diversion 78
Prostate Cancer 79
Renal Transplantation 84
Voiding Dysfunction 86
Male infertility 88
Penile Complaints 91
Peyronie's Disease 91
Priapism 91
Erectile Dysfunction (ED) 93
Premature Ejaculation (PE) 95
Diseases of Testis and scrotum 95
Imperfect descend of the testis 96
Testicular Torsion 98
Varicocele 100
Testicular Tumors 102

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Diagnosis of urinary tract diseases

Symptomatology
1) Pain
▪ Analysis of pain includes:
1. Site.
2. Severity
3. Character.
4. Reference (Radiation)
5. What increase
6. what decrease.
7. Associated symptoms
▪ Site of pain:
A. Renal pain:
All types of pain can occur in kidney but the commonest are:
- Colicky pain (most common) or Dull aching pain.
1- Dull aching pain: due to distension of renal capsule. as in
• Acute inflammation of the kidney.
• Bleeding in a cyst.
• Peripheral renal tumor.
• Renal abscess.
• Acute hydronephrosis.
2- Renal colic:
▪ Most common cause is stone.
▪ Definition of colic:
spasmodic pain which occur in hollow viscous or tubular structure lined by smooth muscle due to
contraction of these muscles in an attempt to get rid of an obstructing agent.
▪ Character:
1. colicky pain in renal angle.
2. may radiate to epigastrium.
3. not related to posture
4. may be relieved by NSAlDs.
5. may be associated with nausea, vomiting & diaphoresis.
B. Ureteric pain:
1. Upper third: (T11 – L1 symp.) colicky pain similar to that of renal colic.
2. Middle third: should be differentiated from appendicitis on Rt side & diverticulitis on Lt side.
3. Lower third: (T12 - L2 symp.) (S2,3,4 parasymp.) most common causes are stones and
stricture.
Criteria: As renal colic +
✓ Referred to scrotal skin in male & labia major in female.

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✓ may be referred to tip of penis.

✓ pain usually associated with irritative voiding symptoms (frequency, urgency)
C. Urinary bladder Pain:
Common causes
1. full bladder (most important)
2. cystitis.
3. stones
4. Malignancy
Criteria:
▪ Character: dull aching or discomfort.
▪ Site: supra-pubic region.
▪ Referred to: tip of penis.
▪ Relieved by: evacuation of bladder in full bladder.
D. Prostatic Pain:
may be acute or chronic.
a) Acute pain:
• severe pain in the perineum.
• associated with: dyschasia (rectal dysentery), high grade fever and urine retention.
• e.g. acute prostatitis , prostatic abscess.
b) Chronic pain:
• pain in perineum, lower abdomen, around anus, tip of penis.
• due to chronic prostatitis.
E. Urethral Pain: Causes: stone or inflammation. Character: burning pain in urethra.
F. Testicular Pain
G. Epididymal Pain
2) Symptoms related to act of micturation
A. Obstructive voiding symptoms:
▪ Causes: - infra-vesical obstruction. - the commonest cause in elderly male is BPH.
▪ Criteria:
1) weak urinary stream.
2) difficulty
- to initiate (Hesitancy)
- to maintain (Intermittency)
- to terminate (Post-micturition dribbling)
3) sense of incomplete voiding.
4) retention of urine (acute or chronic) (see later)
B. Irritative voiding symptoms:
▪ due to bladder and urethral irritation (Malignancy, cystitis, stone)
▪ Criteria:

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1. frequency: by day (Diurnal) and by night (nocturia).

2. burning micturition.
3. urgency: strong desire to micturate which can't be postponed, can't hold urine whenever
desire develops.
4. urge incontinence: strong desire to micturate which can't be postponed and if postponed,
involuntary escape of urine drops will occur.
(C) Day and Night Incontinence:
- stress incontinence.
- urge incontinence (neurogenic, stone, cystitis, malignancy)
- Total incontinence as in → VVF (vesico-vaginal fistula)
- Paradoxical incontinence (false): retention with overflow as in BPH & urethral stricture.
3) Change in physical character of urine
A. Volume:
1. Normally — 0.5 - 1 ml / kg / h (800 - 1600 ml / day)
2. Decrease in volume
• < 400 cc / 24 h → oliguria (least volume to excrete toxic metabolite from the body)
• No urine / 12 h (with empty bladder) → anuria (see later)
3. Polyuria: Definition: urine output > 3L / day.
Causes:
a- Renal causes:
1. Nephrogenic diabetes insipidus (amyloidosis, hypokalemia, hypercalcemia)
2. Polyuric phase of ATN
3. Diuretics.
4. CRF.
b-Endocrinal causes:
1- DM.
2- Cranial diabetes insipidus.
3- Cushing disease (hypokalemia, glycosuria).
4- Conn's disease (hypokalemia).
5- Hyperparathyroidism (hypercalcemia).
Others: 1- Psychogenic (compulsive water intake).
2- Drugs as high doses of vitamin D
B. Color:
• Normally → golden or amber yellow.
• Red urine → hematuria (see later)
C. Aspect:
• Normally → clear.
• Turbid urine → pyuria, crystalluria, proteinuria, chyluria
• chyluria: The urine looks milky due to presence of lymph. The color clears on addition of ether.
• Pneumaturia (air in urine) → UTI by gas forming organism or vesico- colonic

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4) C.R.F symptoms:
• Anemia (pallor)
• Asthenia (weakness).
• Anorexia.
• Headache.
5) GIT symptoms; as
• renal colic with nausea & vomiting.
• pyelitis in newborn with gastroenteritis.
• due to: - reno-intestinal reflex. - peritoneal irritation. - organ relationship.
6) Metastasis symptoms: -Brain -Bone. -liver -lung. - others
7) Masses:
• renal mass.
• bladder mass
• scrotal mass
8) Infertility (see later)
9) Sexual dysfunction: (see later)
libido, erection, ejaculation, orgasm.
10) Other symptoms:
as urethral discharge and gynaecomastia.
Examination for Urinary tract diseases:
1) General examination:
2) Abdominal examination
3) Genital examination
4) Digital rectal examination
Investigations:
A. Laboratory investigations:
1) Biochemical blood tests for renal function
• serum urea
• serum creatinine.
• serum electrolytes.
• arterial blood gas
2) Urinalysis:
• for abnormal substances such as protein or signs of infection.
• dipstick urinalysis, involves the dipping of a biochemically active test strip into the urine
specimen to determine levels of tell-tale chemicals in the urine.
• Urinalysis can also microscopy, culture and sensitivity
3) tumor markers: as PSA and acid phosphatase

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B. Imaging
1) Ultrasound:
- Principle: It hits structure of the body then the reflected different intensities (according to
H2O content) are recorded. The same introducer receives the reflection.
- Can detect:
a) Solid from cystic mass.
b) post voided residual in the bladder
c) All types of stones, Radiolucent or Radio-opaque.
d) Trans rectal U/S (TRUS): For prostatic lesions, especially if PSA is high or abnormal
prostatic outline on DRE. can provide access for biopsies.
2) Radiology:
a) KUB
• is plain radiography of the urinary system the greatest utility of the abdominal radiograph
in urology is to evaluate for calculi (Fig. 1),
• check the presence and position of catheters and stents, and obtain a preliminary view
before performing other examinations.
• Bony abnormalities as spina bifida and sacral agenesis, fractures of the spine or pelvis,
osteoblastic metastases (typical of prostate carcinoma), osteolytic metastases (the
majority of solid tumors), or manifestations of hematologic disorders (sickle cell anemia,
myeloma) or Paget's disease
• Abnormal gas collections as Gas in the renal parenchyma or collecting system as a
result of recent instrumentation or emphysematous pyelonephritis
b) Intravenous pyelogram:
• Procedure: contrast (Urografin) is given lV kidney uptake concentration excretion.
• Value: diagnosis of:
1) Anatomical description of the urinary system
2) Stones, tumors (filling defect), diagnose renal artery stenosis
3) Differential kidney function.
4) Vesico-ureteric reflux, Congenital absence of kidney
5) Shattered kidney and Renal pedicle injury.
• Side effects
1. Anaphylactic shock.
2. Acute renal failure (contrast nephropathy).
• contraindications:
1) Renal impairment (blood urea > 50 mg %).
2) acute obstruction
• IVU infusion method: to decrease the incidence of contrast nephropathy of the dye.
• urografin (2 ml/kg) + saline infusion over 15 minutes.

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Figure 1: KUB with staghorn stone IVP IVP with stone Lt kidney
4) CT scans and MRI can also be useful in localizing urinary tract pathology.
5) voiding cystourethrogram is a functional study where contrast "dye" is injected through a
catheter into the bladder and urethra. diagnosis of VUR, stricture, PUV, Urethral injuries.
6) Renal arteriography:
• Mainly indicated to diagnose renal artery stenosis & A-V malformations.
• To differentiate between benign and malignant cysts:
a) If malignant abnormal vascularity.
b) lf benign avascular.
7) Radionuclide Imaging.
8) Surgical procedures
• Cystoscopy
• Biopsy
9) Urodynamic tests
evaluate the storage of urine in the bladder and the flow of urine from the bladder through the
urethra. It may be performed in cases of incontinence or neurological problems affecting the
urinary tract.

Congenital Anomalies of UT
A. Congenital anomalies of the kidney
1) Anomalies of Number
- unilateral renal aplasia. (renal agenesis)
- bilateral renal aplasia. (incompatible with life)
- super-numery kidney.
2) Anomalies of shape:
- Lobulated kidney (persistent fetal lobulation):
3) Anomalies due to abnormal fusion:
- S-shaped kidney
- L-shaped kidney.
- Discoid shaped kidney.
- Horse-shoe kidney (commonest)

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4) Anomalies due to failure of communication:

- solitary renal cyst.
- polycystic kidney.
5) Anomalies due to failure of migration:
- ectopic kidney
6) Anomalies in size:
- hypo-plastic kidney.
- hypertrophied kidney.
7) Anomalies of the renal pelvis:
- bifid pelvis.
- double pelvis.
- PUJO
8) Anomalies of renal vessels:
- renal artery stenosis → renal HTN
- aberrant renal artery → hydronephrosis.
B. (II) Congenital anomalies of ureter:
1) double ureter (common)
2) retro-caval ureter.
3) congenital mega-ureter.
4) ureterocele
5) vesicoureteric reflux.
C. (III) Congenital anomalies of urinary bladder:
1) Ectopia vesica (exstrophy)
2) Congenital anomalies of urachus:
- urachal diverticulum.
- urachal cyst.
- urachal sinus.
- patent urachus (fistula)
3) Congenital contracture of bladder neck (Marrion's disease).
4) Congenital diverticulum.
5) Septate, Bipartite urinary bladder.
D. Congenital anomalies of urethra:
- Phimosis.
- Paraphimosis.
- Meatal stenosis.
- Urethral values.
- Congenital urethral diverticulum
- Hypospadias.
- Epispadias

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Simple renal cyst:

Etiology:
Not clear whether the lesion is congenital or acquired. its
origin may be similar to polycystic kidney
Pathology:
• Thin-walled cortical cysts, measuring up to 10 cm, which
are filled with clear yellow fluid
• lined by single layer of cuboidal, flattened or atrophic
epithelium.

Clinical picture:
1. Usually asymptomatic. Figure 2: Simple renal cyst

2. Dull aching pain in the loin due to stretch of renal capsule.

3. Renal mass if large.
4. Acute symptoms if complications occurred as hemorrhage infection or rupture.
Investigations:
1. Ultrasound and CT scanning most helpful to differentiate it from complicated cyst of renal tumors
2. IVU: space occupying lesion
3. Renal angiography.
Treatment:
1. No treatment in most of cases but follow up is required.
2. Aspiration of the fluid in the cyst and sclerosing by 95 % alcohol.
3. Marsupialization or excision open or laparoscopic.
Congenital Polycystic kidney
Definition: Congenital bilateral cystic changes of the kidney.
Etiology:
• It's due to lack of communication between the ureteric bud and the metanephric mass resulting
in fluid accumulation & cyst formation.
• It's a hereditary disease.
Types:
1. Autosomal dominant (adult) polycystic kidney disease.
2. Autosomal recessive (infantile) polycystic kidney disease.
Autosomal dominant (adult) polycystic kidney disease:
Pathophysiology
• due to mutations in genes coding for polycystin 1 (PKD1, chromosome 16p, most common)
and polycystin 2 (PDK2, chromosome 4q)
• Also, associated with TSC2 / PKD1 contiguous gene syndrome
• Cysts form in all regions of the nephron, enlarging and expanding throughout life
• Normal renal function is maintained until mid-adulthood in most patients.

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Gross Description: Markedly enlarged kidneys with bosselated surface composed of subcapsular
cysts. Cysts contain clear to brown fluid
Micro Description:
• Cysts are lined by cuboidal or flattened epithelium.
• Functional nephrons exist between cysts with areas of global sclerosis, tubular atrophy,
interstitial fibrosis and chronic inflammation
Clinical Features
1. Third most common cause of end-stage renal disease
2. Patients present with hematuria, abdominal pain, hypertension, urinary tract infection or
urolithiasis
3. Associated with von Meyenburg complexes in liver (97%); hepatic cysts (50%); berry
aneurysms (10-30%); mitral valve prolapse (20%); cysts in pancreas, lung, spleen, pineal gland
and seminal vesicles; aortic aneurysms; hepatic fibrosis.
4. 25% die from infection, 40% from hypertension and heart disease and 15% from berry
aneurysms or stroke.
Complications:
1. Hematuria → due to rupture of cyst.
2. Polyuria → failure of kidney to concentrate the urine.
3. Renal HTN → renal ischemia → renin.
4. Renal failure.
5. Stone formation due to stasis & recurrent infection.
6. Malignant transformation.
DD: → from other renal swellings.
1. Hydronephrosis. (Bilateral or unilateral)
2. Renal tumor. (Wilm's tumor) (Bilateral)
3. Multi-cystic kidney (Unilateral)
Investigations: Figure 3: ADPCKD
1. KFT (for renal failure).
2. Urine analysis hematuria or pyuria.
3. U/S or CT scan: most accurate detect multiple cysts in both kidneys.
4. IVP: bilateral smooth spider leg appearance with elongated renal shadow.
Treatment
A. Conservative:
1. Control of HTN by salt restriction & antihypertensive.
2. Urinary antiseptics to guard against infection.
3. Correction of anemia.
4. Dialysis → if renal failure occurs.
B. Surgical:
• Rovsing operation: By puncture of superficial cysts to minimize pressure atrophy.
• Laparoscopic nephrectomy and Renal transplantation.

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Horse-shoe kidney:

Pathology:
• Fusion occurs early in embryonic life when the kidneys lie
low in the pelvis.
• Ascent of the kidney is arrested by the isthmus being
blocked by the inferior mesenteric artery.
• The renal pelvis lies on the anterior surface of the kidney.
• The ureters thus ride over the isthmus which connects the
lower poles.
Clinical picture:
1. one third of the patients remain asymptomatic.
2. The rest develop symptoms of complications as pain
hematuria and fever.
3. A hydronephrotic horseshoe kidney may be palpable Figure 4: Horse-shoe kidney
below the umbilicus.
investigations:
• IVU: the kidneys are in lower position; the lower poles are nearer to the midline and the lower
pole calyces point medially and lie medial to the ureter (Flower vase appearance).
Treatment:
• only for complications as stones or PUJO
• division of isthmus at the level of inferior mesenteric artery rarely needed.
Ectopic kidney

Site: usually near the pelvic brim and usually left sided.
etiology: failure of renal ascend & rotation.
Diagnosis
• Gives mass in iliac fossa.
• Renal ectopia may present diagnostic problems when
acute disease develops in the kidney. Surgeon may
remove it by mistake as an unexplained pelvic mass.
• IVU: ureter is short & straight.
• DD: abnormal mobile kidney (ptosed - floating)
Figure 5 :Ectopic kidney

Aberrant and Accessory renal arteries:

• single renal artery present in 80% of population
• aberrant arteries originate from artery other than aorta or main renal artery it is very rare.
• Accessory arteries originate from aorta or main renal artery.
• these vessels may compress PUJ  PUJO
• division of these arteries may cause ischemia and infarction of the corresponding portion of
renal parenchyma (end arteries).

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Renal Agenesis
• complete absence of one kidney.
• failed development or arrested ureteric bud.
• Usually unilateral and associated with pulmonary hypoplasia.
• Diagnosis: - Routine pre-natal U/S.
• Renal angiography (the only diagnostic method).
Renal Hypoplasia
• small sized one kidney while the other is normal.
• unequal division of the metanephric mass.
• The only presentation is Hypertension.
• TTT: Nephrectomy.
Renal Dysplasia
• Multi-cystic changes of the kidney
• lt is the most common congenital disorder of the kidney.
• Normal sized kidney but with impaired function.
• Failed communication of the renal tubules.
Pelviureteric junction obstruction (PUJO):
• lt is the most common cause of obstructive uropathy and hydronephrosis in children.
• More common in males.
• More common on left side, but bilateral in 10 - 20%.
Pathology: (figure 6)
• Narrowing (stenosis) of pelvi-ureteric junction and failure of relaxation.
• High insertion of the ureter.
• Extrinsic obstruction by aberrant renal vessels.
Presentation:
1. Antenatal diagnosed; by ultrasound (enlarged kidney).
2. infants: loin mass is the most common finding Figure 6: PUJ obstruction
3. Children: intermittent loin pain (especially after water intake).
4. adolescence: recurrent loin pain and UTl.
Investigations
1. IVU: pelvi-calyceal system dilatation with arrest of contrast at the PUJ.
2. Diuretic renography to assess:
• ability of the pelvis to empty after frusemide injection (obstruction).
• split renal function
3. Ultrasonography: important if poor renal function for hydronephrosis.
4. MRU and CT (figure 7)
Treatment: figure 7: MRU left PUJ
obstruction
1. Pyeloplasty: open or laparoscopicaly.

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• To correct the obstruction surgically.

• Anderson-Hynes pyeloplasty is the most common operation performed.
2. endoscopic endopyelotomy.
3. Nephrectomy in case of hopeless kidney function.
Vesicoureteral reflux (VUR)
common condition wherein urine passes retrograde from the bladder through the UVJ into the ureter
incidence
• ranges from 1-18.5% in normal children
• prevalence of VUR is higher among children with UTIs (15-70%, depending on age).
• 85% of VUR occurs in females
• common cause of antenatal hydronephrosis
• present in 50% of patients with PUV.
• 30% of children with reflux will have renal scarring
causes:
• primary reflux trigonal weakness, lateral insertion of the ureters, short submucosal
• secondary reflux: infravesical obstruction, posterior urethral valves or a neurogenic bladder
iatrogenic, secondary to ureteric abnormalities (e.g. ureterocele, ectopic ureter. or
duplication), and secondary to cystitis
Presentation
1. UTI, urosepsis
2. pyelonephritis
3. pain on voiding
4. symptoms of renal failure (uremia, hypertension)
Investigation:
1) Urine analysis
2) US
3) Ascending voiding cyst urethrogram (AVCUG) for diagnosis and staging (figure 8)
4) Radionucleotide study

Figure 8: grades of VUR reflux

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• Grade I - Reflux into nondilated ureter

• Grade II - Reflux into renal pelvis and calyces without dilation
• Grade III - Reflux with mild-to-moderate dilation and minimal blunting of fornices
• Grade IV - Reflux with moderate ureteral tortuosity and dilation of pelvis and calyces
• Grade V - Reflux with gross dilation of ureter, pelvis, and calyces, loss of papillary
impressions, and ureteral tortuosity
Complications
• Pyelonephritis
• hydroureter/hydronephrosis
Treatment:
▪ many children •outgrow" reflux (60% of primary reflux) annual renal U/S and VCUG/RNC to
monitor; renal scan if suspect new renal scar (episode of pyelonephritis)
▪ treatment Is dependent on the grade:
A. medical (grade I-III) - goal is to keep urine free of infection to prevent renal damage while
waiting for child to ·outgrow" their reflux
B. long term antibiotic prophylaxis at half the treatment dose for half the treatment time (TMP/
SMX, amoxicillin, or nitrofurantoin).
C. surgical:
1) (ureteroneocystostomy± ureteroplasty)
2) sub ureteral injection of Deflux or Macroplastique
indications:
a) failure of medical management
b) new renal scars
c) breakthrough infections
d) high grade reflux (grade IV or V - not an absolute indication)
▪ prognosis depends on degree of damage at the time of diagnosis
Bladder Exstrophy (Ectopic Vesica):

Incidence: 1 : 50000 of births more common in males

Embryologic mechanism: thought to be in part due to
failed reinforcement of the cloacal membrane by
underlying mesoderm.
Presentation: The classic manifestations are:
1. A defect in the abdominal wall occupied by both the
exstrophied bladder as well as a portion of
the urethra
2. small sized penis
3. A flattened puborectal sling
4. Separation of the pubic symphysis
5. Shortening of the pubic ramii
6. External rotation of the pelvis. Figure 9; Bladder Exstrophy

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7. Females frequently have a displaced and narrowed vaginal orifice, a bifid clitoris, and
divergent labia
Complications:
1. Vesicoureteral reflux
2. Bladder spasm
3. Bladder calculus
4. Urinary tract infections
5. Malignant transformation.
Treatment:
- Management at birth:
1. the exposed bladder is irrigated and a non-adherent film is placed to prevent as much contact
with the external environment as possible.
2. Primary (immediate) closure is indicated only in those patients with a bladder of appropriate
size, elasticity, and contractility.
- Modern therapy: is aimed at surgical reconstruction of the bladder and genitalia.
[1] Modern Staged Repair of Exstrophy (MSRE):
− the initial step is closure of the abdominal wall, often requiring a pelvic osteotomy.
− 2–3 years of age the patient then undergoes repair of the epispadias.
− bladder neck repair usually occurs around the age of 4–5 years.
[2] Complete Primary Repair of Exstrophy (CPRE)
- the bladder closure is combined with an epispadias repair
Hypospadias
Definition: It's a common congenital anomaly
in which the urethra open on the ventral
aspect of the penis or perineum instead of
the tip of penis
Incidence: 1/300 ♂ children
Etiology:
− Glandular: due to failure of canalization of
the glans.
− Penile: due to failure of fusion of two urethral
folds.
− Perineal type: occurs due to failure of
development of whole penile urethra.
Pathology;
− Types:
1. Glandular. EUM opens on under surface of
the glans.
2. Coronal: Meatus is at the coronal sulcus
Figure 10: Types of Hypospadias.

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3. Penile: EUM opens on the under surface of the shaft of the penis may be distal, midpenile
and proximal.
4. Peno-scrotal.
5. Perineal: The scrotum is split. The urethra opens between its 2 halves
- The distal part of urethra (corpus spongiosum distal to the urethral opening) is replaced by
fibrous band (chordee).
- The ectopic meatus lies on the ventral aspect of the penis .
- The prepuce is not complete on the ventral aspect like a hood over glans (hooded prepuce)
- hypospadias is anterior (50%), middle (30%) and posterior (20%) (Figure 10).
Diagnosis:
1. Abnormal prepuce present dorsally only (hooded prepuce).
2. Urethral opening more proximal than usual.
3. abnormal stream of urine.
4. 10% of patients have inguinal hernia or undescended testis.
5. 8% of patients have upper urinary tract anomalies.
6. After puberty: Bowing of penis downwards during erection due to presence of fibrous
chordee.
Complications:
1. stenosed meatus.
2. ventral curving of the penis.
3. Infertility.
4. psychological problem.
Treatment:
• age of repair: most suitable time for repair is 6 m - 2 y
• Types of operations:
1. Glandular hypospadius: MAGPI → Meatal Advancement & Glanuloplasty Incorporated.
2. Other types: Snodgrass. - Mathieu repair
• Elements of Repair:
1. Orthoplasty (straightening) of significant curvature of penis.
2. Meatoplasty & glanuloplasty.
3. Urethroplasty.
• Complications of Repair:
1. Bleeding. 2. Haematoma.
3. Fistula (commonest) 4. Stenosis.
5. Infection. 6. Glanular breakdown.
7. Meatal retraction.

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Epispadias:
Definition:
• abnormal opening of urethra on the dorsum of the penis.
• It occurs in around 1 in 120,000 male and 1 in 500,000 female births
Types:
a) lncomplete type:
− Subdivided into: glanular, mid-penile or peno-pubic.
− The patient is continent.
b) Complete type:
− The condition is associated with ectopia vesica
(exstrophy-epispadias complex).
− The patient is incontinent.
Treatment: during the first 7 years of life, reconstruction
of the urethra, Figure 11: Epispadius
. closure of the penile shaft and mobilization of the corpora
Posterior Urethral Value (PUV):
• An obstructing membrane in the posterior male urethra as a result of abnormal in
utero development.
• It is the most common cause of bladder outlet obstruction in male newborns.
Pathology:
1. Hydronephrosis.
2. Vesico-ureteric reflux.
3. Bladder dysfunction.
4. Deterioration of renal function
Clinical picture:
− Antenatal diagnosis: bilateral hydronephrosis.
− Neonatal period: poor stream, acidosis, and raised blood urea. Urinary tract infection in the
dilated system resulting in septicemia.
− Older children: poor urinary stream, hematuria, or retention of urine
− lt shows a distended bladder and palpable kidneys.
Investigation
− Kidney function test: for complication
− Abdominal ultrasound: bilateral hydronephrosis, a thickened bladder wall with
thickened smooth muscle trabeculations, and bladder diverticula.
− Voiding cystourethrogram (VCUG) is more specific for the diagnosis. Vesicoureteral
reflux is also seen in over 50% of cases.
− Renogram
Treatment:
− Primary management by endoscopic valve ablation.
− Vesicostomy or ureterostomy followed by valve ablation in selected cases.

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Urinary tract injuries

I. Injuries of the kidney:
Incidence: injuries of the kidney are relatively rare due to:
▪ The kidneys are well protected by the rib cage and by the heavy muscles of the back.
▪ The kidneys are mobile in their adipose fat & thus flee away from the force of trauma.
▪ The fibrous capsule does protect the parenchyma from splitting.
▪ Renal injuries are potentially serious and may be complicated by injuries of other organs.
Etiology:
1. Predisposing factors:
a. Enlarged kidney (hydronephrosis)
b. Fracture ribs / vertebrae.
c. Ptosed kidney.
2. Precipitating factors:
a. Blunt trauma: (commonest 85%) e.g. Motor vehicle accident, falling from height.
b. Penetrating renal trauma: e.g. Gunshot, stab wound.
c. Iatrogenic injuries during surgery.
d. Spontaneous rupture due to minor unnoticed trauma.
Grading of renal injury: (table 1 and figure 12).
Table 1: the American Association for the Surgery of Trauma (AAST) renal injury grade system
Grade Type of injury Description
I Contusion Microscopic or gross hematuria, urologic studies normal
Hematoma Subcapsular, non-expanding without parenchymal laceration
II Hematoma Non-expanding perirenal hematomas confined to the retroperitoneum
Laceration Superficial parenchymal lacerations less than 1 cm in depth without
urinary extravasation
III Laceration Parenchymal lacerations greater than 1 cm in depth without urinary
extravasation
IV Laceration Parenchymal lacerations extending through the renal cortex, medulla,
and collecting system
Vascular injury Injuries involving the main renal artery or vein with contained
hemorrhage
V Vascular injury Completely shattered kidney
Complete avulsion of renal hilum which devascularized kidney
Clinical picture:
▪ Symptoms:
1. History of Trauma.
2. Pain in the flanks. lt may be obscured by injury to other organs.
3. Hematuria: (degree is not proportionate to severity).
✓ lt may appear some hours after injury.
✓ lt can occur between third day and third week after the accident.
✓ May be absent in:

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a) Superficial tear.
b) Avulsed pedicle or ureter.
c) Traumatic anuria.
d) Severe hypotension.

4. Nausea vomiting and abdominal distension,

due to retroperitoneal hematoma involving
splanchnic nerves (resembling paralytic ileus).
5. Oliguria due to hypovolemia and hypotension.
6. Retention of urine due to clots in the bladder.
▪ Signs:
General Examination:
1. Shock (hemorrhagic or neurogenic)
2. Hematuria (95%)
3. Anuria. (in severe cases)
4. Associated injuries as fracture rib with or
without pneumothorax. Figure 12: grading of renal injury
Local Exam:
1. Marked tenderness & rigidity in the hypochondrium & lion
2. Swelling in the lion due to pseudo haemato-hydronephrosis
3. Shifting dullness in cases of internal hemorrhage.
Picture of complications.
Complications:
I- General: 1-shock. 2- injury to other organ.
II-Local:
✓ Pseudo haemato-hydronephrosis. The degree of hematuria
✓ Secondary hemorrhage. does not correlate with the
✓ Infection and peri-nephric abscess. degree of injury; in fact, renal
✓ Renal failure pedicle avulsion or acute
thrombosis of segmental renal
✓ Hypertension.
arteries can occur in the
✓ Renal atrophy
absence of hematuria while
✓ Renal artery stenosis. renal contusions can present
✓ Renal calculi with gross hematuria.
Investigations:
1) urine analysis.
2) Plain X-ray: show →
a. Fracture lower ribs or spine, and Foreign body.
b. Blurring of psoas shadow by the perinephric haematoma
3) U/S: It can detect injury, its type & extent.
4) I.V.P: to visualize the upper urinary tract as soon as the shock is controlled. lt may show:
✓ Normal function & configuration of kidney if the injury is minimal.
✓ Deformed renal pelvis or calyces if there is laceration or blood clots.

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✓ Extravasation of contrast within the renal shadow or into perirenal space.

✓ Non-visualization of kidney due to total pedicle avulsion, arterial thrombosis or severe
contusion causing vascular spasm.
✓ Confirms the presence of a functioning kidney on the opposite side, as nephrectomy of
the injured kidney may be needed.
5) C.T scanning: (the best), show:
✓ Parenchymal lesion.
✓ Urine extravasation,
✓ Lack of contrast uptake suggests renal artery injury.
✓ Associated injury of other organs.
6) Arteriography: can detect any renal vessel injury & localize the arterial bleeding which can
be controlled by embolization.
7) Renal isotope scanning in selected cases.
Treatment:
1. Renal trauma is an acute emergency.
2. Most renal injuries will be cured by conservative management, as most injuries (85%) are minor.
3. The principles of trauma victims care should be followed.
I. Conservative management:
1) Hospitalization with bed rest until hematuria has stopped & local signs of injury have subsided.
2) Analgesics for pain.
3) Large fluid intake to guard against clot retention & for hypovolemia.
4) Broad spectrum antibiotics to guard against secondary infection.
5) Follow up parameters:
a. Pulse, blood pressure and size of any peri-renal mass.
b. Repeated samples of urine are examined and compared grossly for red color.
c. Hemoglobin & hematocrit estimations.
d. Repeated urine analysis for RBCs.
II. surgical management:
❖ Indications:
1) Persistent progressive hematuria or failure to stabilize vital signs.
2) Presence of a progressively enlarging peri-renal mass.
3) Evidence of peri-renal infection.
4) Penetrating injuries.
5) Renal pedicle injury (5% of all injuries).
6) Presence of an associated intraperitoneal injury.
7) indications for delayed surgery:
• lf hydronephrosis develops; it is treated by relief of obstruction.
• lf hypertension develops; vascular repair or nephrectomy is performed.
❖ Technique;
1) Trans peritoneal approach.

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2) traumatized devascularized renal tissue is debrided.

3) Small defects of cortical tissue are sutured. Large defects are filled by omental or perirenal
fat to obliterate dead space.
4) Water-tight closure of the pelvi-calyceal system.
5) Partial nephrectomy is done if one pole of the kidney is avulsed.
6) Nephrectomy is done if the kidney is shattered or with complete avulsion of vascular pedicle,
if the other kidney is functioning well.

II. Ureteric injury:

Etiology:
1) External penetrating trauma. (Rare)
2) Surgical (operative) trauma (iatrogenic) "Commonest" as in hysterectomy, CS, colorectal injury.
3) Instrumental injury → Endoscopic stone extraction.
4) Radiation injury.
Clinical picture:
✓ Anuria if bilateral.
✓ Urinary leakage and fistula
✓ Renal mass (hydronephrosis)
✓ History of trauma.
✓ Renal pain and fever.
✓ Hematuria.
Investigations:
1) U/S.
2) Excretion urography or ascending retrograde urography may reveal obstruction or
extravasation.
3) CT scan with contrast showing extravasation of the dye.
Management
A. lf immediate diagnosis:
✓ Fair patient condition: uretero-vesical continuity should be restored by 1ry anastomosis.
✓ Poor patient condition: deliberate ligation of the proximal end of the ureter and nephrostomy
for drainage of urine then delayed repair.
B. If delayed diagnosis: Temporary nephrostomy, then delayed repair.
C. Types of repair:
1) lf no loss of length: primary end-to-end anastomosis over a double pigtail catheter.
2) If there is little loss of length
✓ Psoas hitch of bladder: re-implantation of the ureter into the bladder.
✓ Boari's operation: a flap of bladder wall is fashioned into a tube to replace the lower ureter.
3) lf there is marked loss of length:
✓ Uretero-ureterostomy: end-to-side implantation of the ureter into the contralateral ureter.
✓ Replacement of the damaged ureter by a segment of ileum or mobilized appendix.
✓ Nephrectomy in selected cases when the outcome is poor and the other kidney is normal.

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III. Bladder injury

Etiology:
1. Blunt trauma:
a. Direct: blow or kicks in the suprapubic region.
b. Indirect: fracture pelvis, (most common in extra-peritoneal type)
2. Penetrating trauma: stab, gun shots and instrumentation as cystoscopy or during TURP or
TURT.
3. Spontaneous rupture of diseased U.B.
Pathology:
There are 3 types of rupture ( figure 13):
1. Extra-peritoneal rupture (65%) → urine leakage to inferior & lateral side to UB
2. Intra-peritoneal rupture (25%) → urine leakage above bladder.
3. Combined. (10%)
Clinical picture: table 2
Extra-peritoneal type Intra-peritoneal type

Figure 13
1) History of • blunt (MVC, falls, and crush injury) vs. penetrating trauma to lower
trauma. abdomen, pelvis, or perineum
• blunt trauma is associated with pelvic fracture in 97% of cases
2) Shock. Marked. Mild.
3) Pain and Pain and tenderness is suprapubic Suprapubic pain &tenderness
tenderness which remain localized for long time which soon become generalized in
then spreads up to the abd. wall. the abdomen (peritonitis)
4) Desire of There's intense desire for No desire for micturition
micturition. micturition but the patient can't void
urine.
5) PR Soft swelling around the prostate Feel extra-vasated urine as fullness
and bladder. in the recto-vesical pouch.
6) Catheterization Show small amount of urine and Show small amount of urine and
blood. blood.

Complications-
1) Shock and Hemorrhage.
2) Peritonitis in the intra-peritoneal type.
3) Pelvic abscess in extra-peritoneal type.
4) Associated injuries e.g. rupture urethra.

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investigations:
1. Plain X-ray show fracture pelvis.
2. Abdominal U/S.
3. IVU → show leakage of dye from the bladder.
4. ascending cystourethrography.
5. C.T cystography.
Management:
I) Emergency: correct hemorrhage & shock.
II) Extra-peritoneal rupture:
(1) Urethral catheter drainage →Tear will close within 10 - 14 days.
(2) Open surgery & Injury repair:
Indications:
1- failed conservative treatment (no healing > 10 days)
2- Bone fragment projecting in the bladder.
3- Extension of tear to bladder neck (Incontinence)
4- Rectal perforation.
Technique: Trans-vesical approach.
III) Intra-peritoneal & combined injury:
- No conservative treatment because the urine in peritoneal cavity can lead to peritonitis
- line of ttt → Exploration & Repair.
IV) Fracture pelvis: External fixation.
V) Post-injury management:
1- Prophylactic antibiotic. 2- Follow up by cystography.

IV. Urethral injuries:

1. Posterior Urethral injury
Etiology:
• common site of injury is junction of membranous and prostatic urethra due to blunt trauma,
MVCs, pelvic fracture shearing force on fixed membranous and mobile prostatic urethra
• other causes: iatrogenic (instrumentation)
Types:
a) Contusion.
b) Laceration that does not involve the whole circumference.
c) Laceration that involves the whole circumference.
d) Complete circumferential laceration with torn of puboprostatic ligament.
Clinical Features
▪ Blood at urethral meatus
▪ High riding prostate on digital exam
▪ Sensation of voiding without urine output
▪ Swelling and butterfly perineal hematoma
▪ Distended bladder

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complications:
▪ Blood loss and hemorrhagic shock are common.
▪ Deep extravasation of urine to extraperitoneal space
▪ Injury of external sphincter (sphincter urethrae).
▪ Urethral stricture.
▪ Impotence may result due to injury of the nerves to the corpora cavernosa that pass adjacent
to the membranous urethra.
2. Anterior urethral injury
Etiology:
• straddle injury can crush bulbar urethra against pubic rami
• other causes: iatrogenic (instrumentation, prosthesis insertion), penile fracture,
masturbation with urethral manipulation
Types:
a) Contusion.
b) Laceration that does not involve the whole circumference.
c) Laceration that involves the whole circumference.
Clinical picture
• History of trauma
• Blood at meatus
• Perineal hematoma
Complications:
▪ Urinary extravasation: if the patient try to void urine extravasates to superficial perineal pouch.
▪ Urethral fistula.
▪ Infection and sloughing of the perineal skin in neglected cases.
▪ Peri urethral abscess.
▪ Stricture of urethra.
Investigations of urethral injury:
▪ Ascending urethrogram: Shows site of extravasation and type of injury.
▪ Urgent IVU to detect associated urinary.
Treatment of urethral injury:
a) Simple contusions - no treatment
b) Partial urethral disruption: Figure 14: Ascending
• Very gentle attempt at catheterization by urology staff urethrogram with posterior
urethral injury
• With no resistance to catheterization- foley x 2-3 weeks
• With resistance to catheterization - suprapubic cystostomy or urethral catheter alignment in or
periodic flow rates/urethrograms to evaluate for stricture formation
c) Complete disruption:
• Immediate repair if patient stable,
• Delayed repair if unstable (suprapubic tube in interim) Do not catheterize if
suspect urethral injury.

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Urinary tract inflammation

Non-specific Urinary tract infection
Definitions:
▪ UTI is a broad term used to describe microbial colonization of the urine. It includes infection
of the structures of the urinary tract from the kidney down to the urethral meatus. Infection
of organs such as the prostate and epididymis are also included in the definition.
▪ Bacteriuria denotes the presence of bacteria in the urine, which is usually free of bacteria.
It can be symptomatic or asymptomatic.
▪ Pyuria is the presence of white blood cells (WBCs) in the urine and is generally accepted
as an indication of infection and as an inflammatory response of the urothelium to the
bacteria.
▪ Bacteriuria without pyuria is an indication of bacterial colonization without infection.
▪ Sterile pyuria occurs with tuberculosis, stone disease or cancer.
Types:
1. Uncomplicated UTI is a term describing infection in healthy patients who have a structurally
and functionally normal urinary tract.
2. Complicated UTI is usually associated with elements which increase the chances of
acquiring bacteria and decreasing treatment efficacy. Incidence increases if alterations to
host defensive mechanisms. These include obstruction, prostate enlargement in men,
urethral stenosis in women, vesicoureteric reflux, diabetes mellitus, human
immunodeficiency virus and spinal cord injuries with high-pressure bladders.
UTIs may be isolated, recurrent, or unresolved:
• Isolated UTI: an interval of at least 6 months between infections.
• Recurrent UTI: >2 infections in 6 months or 3 within 12 months. Recurrent UTI may be
due to re-infection (i.e. infection by different bacteria) or bacterial persistence (infection by
the same organism originating from a focus within the urinary tract). Bacterial persistence
is caused by the presence of bacteria within calculi (e.g. struvite stone,) within a
chronically infected prostate (chronic bacterial prostatitis,) within an obstructed or atrophic
infected kidney, or occurs because of a bladder fistula (with bowel or vagina) or UD.
• Unresolved infection: implies inadequate therapy and is caused by natural or acquired
bacterial resistance to treatment, infection by different organisms, or rapid re-infection.
Pathogenesis
Causative organism:
▪ Gram-negative bacteria: Escherichia coli (the most common), Proteus, and Klebsiella.
▪ Gram-positive bacteria include E. faecalis and S. saprophyticus.
▪ Chlamydia trachomatis
▪ Mycoplasma (Ureaplasma urealyticum)
▪ fungi (Candida)
Predisposing factor
1. Bacterial virulence factors.
2. Bacterial adherence to vaginal and urothelial epithelial cells.

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3. Anatomical and functional urinary tract abnormalities,

4. Pregnancy
5. Stones
6. Old age
7. Diabetes
8. Immunosuppression
9. Urinary tract instrumentation
10. Indwelling catheters.
11. UTI in women is common and the incidence increases with age. Sexually active women are
at the highest. It has been noted that some women have recurrent UTI/cystitis at regular
intervals possibly linked to oestrogen levels.
Rout of spread:
▪ Ascending infection → the commonest.
▪ Hematogenous spread.
▪ Lymphatic spread from colon.
Diagnosis: Depends upon
1. Site of UTI
2. Acute or chronic
3. Complicated or un complicated UTI
4. Predisposing factor present
5. Age of the patient
Clinical Features
▪ Storage symptoms (frequency, urgency, dysuria)
▪ Voiding symptoms (hesitancy, post-void dribbling, dysuria)
▪ Hematuria
▪ Pyelonephritis: more severe symptoms (including constitutional symptoms, CVA
tenderness)
General investigation of UTI
Midstream urine (MSU) examination C&S:
▪ Dipstick: leukocytes ± nitrites ± hematuria
▪ Microscopy: >5 WBC/HPF in un-spun urine or >10 WBC/HPF in spun urine, bacteria, ±
WBC casts
▪ Gram stain: GN bacilli, GP cocci,> 1 bacterium/oil immersion field
▪ Culture and sensitivity: midstream, catheterized or suprapubic aspirate
Further investigation:
required if:
• Acute pyelonephritis, a pyonephrosis or perinephric abscess is suspected.
• Recurrent UTIs develop.
• The patient is pregnant.
• Unusual infecting organism (e.g. Proteus), suggesting the possibility of an infection stone.

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These further investigations will include

1. KUB X-ray.
2. IVU (looking for infection stones in the kidney; avoid in pregnant women).
3. renal USS.
4. CT scanning.
5. cystoscopy.
Urinary tract infection: general treatment guidelines
1. Antimicrobial drug therapy:
Empirical treatment involves the administration of antibiotics (table 3) according to the
clinical presentation and most likely causative organism before culture sensitivities are
available.
Table 3: Antibiotics
Drug indication Duration Limitation of use
TMP/SMX Simple uncomplicated cystitis 3 days Stevens Johnson
Recurrent cystitis Long term as syndrome
prophylaxis ? Safety in last 2 weeks of
14 days pregnancy
Pyelonephritis
4-6 weeks Resistance = 20% in the
Prostatitis
community
Epididymitis/orchitis (Gram 2 weeks
negative organism)
nitrofurantoin Simple uncomplicated cystitis 7 days Contraindicated in renal
Recurrent cystitis failure
Pulmonary toxicity/fibrosis
ciprofloxacin Cystitis 3 days ? Safety in pregnancy
Pyelonephritis 7-14 days Achilles tendon rupture
gentamicin Severely ill patients with Nephrotoxic
pyelonephritis, prostatitis Ototoxic

2. Definitive treatment:
✓ Once urine or blood culture results are available, antimicrobial therapy should be adjusted
according to bacterial sensitivities.
✓ Underlying abnormality should be corrected if feasible (i.e. extraction of infected calculus;
removal of catheter; nephrostomy drainage of an infected, obstructed kidney).
3. General preventative advice
▪ Encourage a good fluid intake, cranberry juice, double voiding, avoid constipation.
▪ In women: voiding before and after intercourse; wiping perineum from ‘front to back’ after
voiding.

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Acute Pyelonephritis
Definition: infection of the renal parenchyma with local and systemic manifestations
Etiology
1. ascending (usually GN bacilli) or hematogenous route (usually GP cocci)
2. causative microorganisms: E. coli (most common), Klebsiella, Proteus, Pseudomonas,
Enterococcus jaecalis, Enterobacter, S. Aureus, S. saphrophyticus
3. common underlying causes of pyelonephritis: stones, strictures, prostatic obstruction,
vesicoureteric reflux, neurogenic bladder, catheters, DM, sickle-cell disease, PCKD,
immunosuppression, post-renal transplant, instrumentation, pregnancy
Clinical Features
1. rapid onset (hours - day)
2. LUTS including frequency, urgency, hematuria
3. fever, chills, nausea, vomiting, myalgia, malaise
4. CVA tenderness or exquisite flank pain
5. dysuria is not a symptom of pyelonephritis without concurrent cystitis
Complications
1. Septicemia and septic shock.
2. Pyonephrosis.
3. Perinephric abscess.
4. Chronic pyelonephritis & renal hypertension.
5. Chronic renal failure if the disease affects both kidneys.
D.D:
1. Acute cholecystitis. Ultrasound can differentiate.
2. Acute appendicitis.
3. Perinephric abscess.
4. Basal pneumonia and pleurisy.
Investigations
1. urine examination, C&S
2. blood: CBC with differential: leukocytosis, left shift
3. imaging - indicated if suspect complicated pyelonephritis or symptoms do not improve with
72 hours of treatment
• IVP
• Abdo/pelvic U/S
• CT
4. Cystoscopy
Treatment
• may treat as outpatient if hemodynamically stable, ciprofloxacin PO for 7-14 days or
cotrimoxazole (TMP/SMX) PO for 14 days
• severe or non-resolving: admit, hydrate and treat with ampicillin IV and gentamycin IV
• emphysematous pyelonephritis: emergency nephrectomy
• stone obstruction: admit and emergency stenting or percutaneous nephrostomy tube

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Perinephric Abscess
Routs of infection:
1. Hematogenous: From distant focus (tonsils, osteomyelitis).
2. Extension from neighboring suppurative focus:
3. Such as pyelonephritis, appendicitis, cholecystitis.
4. Infection of a peri-nephric hematoma.
Clinical picture:
1. Hectic fever, anorexia, headache and rigors.
2. Acute onset with pain in the loin associated with nausea and vomiting.
3. The loin is tender and rigid and, as the infection progresses, swelling can be detected.
4. valuable sign is flattening of the normal concavity of loin
D.D: (As acute pyelonephritis).

investigations:
1. High leukocytosis.
2. Ultrasonography or CT scan: most diagnostic
3. Plain X-Ray: Raised indented copula of the
diaphragm, obliteration of psoas shadow and
scoliosis.
4. IVP a "Mathe's sign". X-Ray in erect and lying
posture: Loss of normal mobility of the kidney.
Figure 15: Ct of perinephric
Treatment: abscess
Under antibiotic cover, immediate drainage is done through:
• Lumbar incision in large abscess.
• Percutaneous drainage in selected cases.

Pyonephrosis
Retention of infected urine and pus in the kidney due to obstructing agent.
Etiology:
• Primary, when infection and obstruction occurs simultaneously
• Secondary, when infection occurs on top of previously hydronephrotic kidney
Clinical picture: (Pain -Fever -Swelling -Pyuria)
1. Closed type (complete obstruction)
(No pus comes out with urine due to the obstructing agent, toxemia is severe)
• General: hectic fever, rigors, anorexia, headache, malaise...etc.
• Local:
a. Loin pain (throbbing) and tenderness (pus under tension).
b. Renal swelling: usually small (large in secondary type).
2. Open type (partial obstruction)

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(The pus comes out in large amount so toxemia is less severe).

• Presents with triad of anemia, fever & renal swelling (large).
• With or without secondary cystitis (pyuria, frequency, burning micturition).
Complications:
1. Septicemia and septic shock.
2. Pyemia.
3. Permanent renal scarring.
4. Peri-nephric abscess.
Investigations:
1. Urine analysis
2. High leukocytosis.
3. Ultrasonography or CT scan:
4. Plain X-Ray and IVP: stone and delayed execration
D.D: as acute pyelonephritis.
Treatment:
1. Drainage by ureteral stent placement or nephrostomy tube with antibiotics.
2. Management of the cause as stones and stricture.
3. Nephrectomy in nonfunctioning kidney
Acute cystitis: see previously in general principals
Recurrent/Chronic Cystitis
▪ predisposing factors as described above
▪ possible relation to intercourse (postcoital antibiotics), perineal colonization
▪ investigations may include cystoscopy, ultrasound, CT
▪ antibiotic prophylaxis if >3 or 4 episodes per year in females
Etiology: unknown but theories:
a. increased epithelial permeability, autoimmune, neurogenic
b. associations: severe allergies, irritable bowel syndrome (IBS), fibromyalgia
Treatment
1. low-dose prophylaxis (nitrofurantoin, TMP/SMX)
2. lifestyle changes (limit caffeine intake, increase fluid/water intake, smoking cessation)
3. post-menopausal women: consider topical or systemic estrogen therapy
4. no treatment for asymptomatic UTI except in pregnant women or patients undergoing urinary
tract instrumentation
Interstitial Cystitis (Painful Bladder Syndrome)
Definition
Chronic urgency, frequency ± pain without other reasonable causation
Etiology: unknown but theories
a. increased epithelial permeability, autoimmune, neurogenic, defective glycosaminoglycan
(GAG) layer overlying mucosa

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b. associations: severe allergies, irritable bowel syndrome (IBS), fibromyalgia

Classification
a. non-ulcerative (more common) -younger to middle-aged
b. ulcerative - middle-aged to older
Diagnosis: required criteria:
1. glomerulations (submucosal petechiae) or Hunner's ulcers on cystoscopy.
2. pain associated with the bladder or urinary urgency
3. negative urinalysis, C&S
Differential Diagnosis
1. UTI, vaginitis, bladder tumor
2. Radiation/ chemical cystitis
3. Eosinophilic and tb cystitis
4. Bladder calculi
Treatment
1. Patient empowerment (diet, lifestyle)
2. Pentosan polysulfate (elmiron)
3. Low dose amitriptyline
4. Bladder hydrodistention (also diagnostic) under general anesthesia
5. Intravesical dimethylsulfoxide (dmso) or cystistat
6. Surgery (augmentation cystoplasty and urinary diversion ± cystectomy)

Epididymitis and Orchitis

Etiology
1. infection: gonorrhea or Chlamydia trachomatis
2. mumps infection may involve orchitis after parotiditis
If unsure between
3. rare causes: diagnosis of epididymitis and
• TB torsion: go to OR.
Remember: torsion  6 has poor
• syphilis prognosis.
• granulomatous (autoimmune) in elderly men
• amiodarone (non-infectious cause, involves only head of epididymis)
 note: epididymitis is much more common than orchitis
Risk Factors
1. UTI
2. instrumentation/ catheter
3. reflux
4. increased pressure in prostatic urethra (straining. voiding. heavy lifting) may cause reflux of
urine along vas deferens → sterile epididymitis
Clinical picture:
1. Sudden onset scrotal pain and swelling ± radiation along cord to flank

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2. Scrotal erythema and tenderness

3. Fever
4. Storage symptoms, purulent discharge
5. Reactive hydrocele
Investigations Prehn sign: pain may be
1. Urinalysis (pyuria), urine C&S relieved with elevation of testis in
epididymitis but not in testicular
2. Urethral discharge: Gram stain/culture
torsion. Poor sensitivity
3. Colour-flow Doppler ultrasound specially in children.
4. Nuclear medicine scan
Treatment
1. Rule out torsion
2. Antibiotics:
• N. gonorrhea or C. trachomatis - cefixime 400 mg PO once followed by azithromycin 1 g
single dose or doxycycline 100 mg bid x 10 days
• Coliforms- broad spectrum antibiotics (quinolone) x 14 days
3. Scrotal support, ice, analgesia
Complications
• Testicular atrophy
• Infertility problems

Urethritis
Common causes: infectious, inflammatory (e.g. reactive arthritis)
Table 4: infectious Urethritis: Gonococcal vs. Non-Gonococcal

Prostatitis / Prostatodynia
▪ Most common urologic diagnosis in men <50 years
▪ Incidence 10-30%
▪ Acute bacterial, chronic bacterial, abacterial subtypes

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Table 5: Comparison of three Types of Prostatitis

Type 1: Acute bacterial Prostatitis Type II: Chronic Type Ill: Chronic Pelvic
bacterial Prostatitis Pain Syndrome
(Abacterial)
Etiology • coli most common (see previously) • Recurrent • Divided into
• Ascending urethral infection and exacerbations of inflammatory and non-
reflux into prostatic Ducts acute prostatitis inflammatory subtypes
signs and • lntraprostatic reflux of
• Often associated with outlet
symptoms urine ± urethral
obstruction (BPH) recent
cystoscopy, prostatic biopsy • Recurrent UTI with hypertonia
same organism • Multifactorial
• Most infections occur in the
peripheral zone (immunological
neuropathic,
neuroendocrine,
psychosocial)
Clinical • Acute onset fever, chills, malaise • Frequently • Pelvic pain, storage
picture • Rectal, lower back and perineal pain asymptomatic with LUTS, ejaculatory pain,
Storage and voiding LUTS normal prostate on postejaculatory pain
DRE
• Hematuria
Investigations • Rectal exam • Urine C&S: 4 • DRE variable
• Enlarged, tender, warm prostate specimens • Urine C&S negative on
• Urine C&S: 4 specimens Colony counts in serial specimens
EPS and VB3 should • Prostate biopsy shows
✓ VB1 (voided bladder urine): initial
exceed those of initial histological inflammation
(urethra)
and midstream by 10
✓ VB2: midstream (bladder) times (suggests
✓ EPS (expressed prostatic prostate as bacterial
secretion (prostate). source)
✓ VB3: post-massage DRE
(prostate)
• Urine R&M
• Blood CBC, C&S
Treatment • Supportive measures (antipyretics, • Extended course of • Trial of antibiotic therapy
analgesics, stool softeners) antibiotics (3-4 fluoroquinolone or
• PO antibiotics for 4 weeks to prevent months) doxycycline if Chlamydia
complications. • fluoroquinolones, trachomatis is suspected
TMP/SMX or ɑ-blocker to relieve
• Admission criteria: sepsis, urinary
doxycycline; sphincter spasms,
retention, immunodeficiency
addition of an ɑ- NSAIDs and supportive
• IV antibiotics {ampicillin and measures for
blocker may reduce
gentamicin) if severe symptomatic relief
symptoms
• Mid-stream urine C&S at 1 and 3
months post antibiotic therapy
• Avoid catheterization due to risk of
bacteremia and systemic infection
• Small drainage catheter may be
inserted if obstruction suspected

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Specific infections
UT Bilharziasis:
Etiology: It is due to Schistosoma haematobium mainly in 94% and by S. mansoni in 4%.
Life cycle of Schistosoma in figure 16

Figure16: Life cycle of Schistosoma haematobium.

Pathological changes in the bladder:

A. Gross appearance;
1. Redness of mucosa due to granulation tissue.
2. Granularity of mucosa.
3. Bilharzial nodule.
4. B. tubercle
5. B. Polyp (projection above surface):
▪ The polyp may be single or multiple but few.
▪ The size varies but does not exceed 2 cm in diameter,
▪ Small polyps are sessile but as they increase in size they acquire a pedicle and take a
mulberry shape.
4. Ulcers: Minute ulcers produced by the extrusion of the ova may fuse and form a large
saucer shaped or excavating ulcer. Phosphatic encrustation of the floor of the ulcer may
occur.
5. Sandy patches: Due to atrophied mucosa overlying calcified ova in the submucosa which
appear like sand under water.
6. Bilharzial fibrosis
7. Leukoplakia due to squamous metaplasia.
8. Carcinoma

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B. Microscopic picture
1. Hyperplasia.
2. Brunn nests: Are buds of hyperplastic epithelium which are later separated from the surface
to form subepithelial nests.
3. Cystitis cystica: Results from degeneration and vacuolization of the central cells of Brunn
nests.
4. Cystitis Glandularis: The Brunn nests undergo metaplasia into columnar epithelium.
5. Squamous metaplasia.
Clinical picture:
1. Terminal hematuria is the symptom of early infestation.
2. Frequent and painful micturition.
3. Clinical picture of complications.
Complications:
1) secondary infection.
2) Stone formation.
3) Bladder neck obstruction (BNO).
4) Stricture ureter.
5) Squamous cell carcinoma of the bladder.
6) Hypochromic microcytic anemia and weakness.
7) Contracted bladder.
8) Vesico-ureteric reflux.
9) Hydronephrosis.
Investigations:
▪ Urine analysis.
▪ Immunological tests: ELISA & CFT.
▪ Plain X-Ray: Calcification or stones.
▪ IVU; stricture ureter and contractrde bladder
▪ Cystoscopy: pathological lesion as cystitis, polyp or ulcer.
Treatment:
▪ Anti - Bilharzial drugs as Praziquantel
▪ Treatment of associated lesions:
1. Secondary infection: Antibiotics.
2. Ulcers Small superficial. Anti-Bilharzial drugs + Antibiotics.
3. Chronic deep ulcer: Surgical excision or diathermy coagulation.
4. Polyps: Cystoscopic fulguration.
5. Ureteric stricture endoscopic dilatation
6. BNO: endoscopic incision or Wedge excision.
7. Contracted bladder: augmentation cystoplasty.
8. Malignancy by radical cystectomy

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Genito-urinary tuberculosis
Etiology:
▪ Causative organism: Mycobacterium T.B human type (75%)
▪ Route of infection:
o Hematogenous (mainly): from T.B focus (mediastinal or mesenteric)
o Ascending infection (sometimes): from T.B prostatitis, seminal vesiculitis or
cystitis
▪ Precipitating factor: low resistance of the patient
Pathology:
A. The kidneys:
▪ Tuberculous bacilluria may occur without naked eye lesions in the kidneys.
▪ The initial naked eye lesion is a minute cortical focus.
▪ The microscopic foci may heal or progress to chronic T.B. lesion.
▪ Infection spreads through the tubules and lymphatics to reach the papillae of the
pyramids.
▪ Tuberculous follicles in a papilla coalesce and later on burst into the related calyx.
▪ Tuberculous material enters the renal pelvis which becomes involved, Ulceocavernous
type.
▪ The lesion in the cortex coalesces and caseates to form cavities in the renal substance,
caseocavernous type.
B. The Ureter:
▪ Becomes involved, the wall becomes thickened, fibrotic and later shortened
▪ the golf hole appearance of the ureteric orifice as seen on cystscopy.
▪ Stricture lower third.
C. the bladder:
Affection of the bladder results in a thickened fibrosed and contracted bladder with decreased
capacity.
✓ The other kidney & Genital organs (seminal vesicles, prostate & epididymis) become
affected by ascending infection from the bladder or Haematogenous.
Clinical picture:
1. Frequency the earliest & main symptoms due to:
• irritation by tuberculous debris.
• Polyuria of the failing kidney.
• Tuberculous cystitis,
• Contracted bladder at which stage the frequency becomes very severe.
2. Pyuria, haematuria & painful micturation.
3. T.B toxaemia.
4. It is unusual for a T.B kidney to be palpable.
5. The prostate, seminal vesicles, vas, and epididymis should be examined by P/R for
nodules

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Complications:
1- Kidney:
• T.B pyonephrosis
• T.B hydronephrosis
• Stones
• T.B perinephric abscess
• Military T.B
• Renal failure
2- Ureter: stricture ureter
3- Urinary bladder: Hematuria and Contracted bladder
4- Genital organs: - infertility
Investigations:
1. Bacteriological examination of the urine:
✓ Ziehl Neelsen method and examined for the acid-fast bacilli.
✓ Culture on Lowenstein medium (98% accuracy).
2. Plain X-Ray may reveal calcified areas.
3. IVP:
✓ Hydronephrosis
✓ Moth eaten appearance
✓ Small contracted bladder
✓ Stricture ureter
4. Cystoscopy:
✓ TB lesions as tubercle or ulcer
✓ Thimble bladder
✓ Golf hole ureteric orifice.
5. Retrograde uretropyelography.
6. Chest X-ray, Tuberculin test & PCR.
Treatment:
▪ Medical treatment:
1. Sanatorium admission
2. Diet: good diet, vitamins & minerals
3. (anti tubercular drugs)
✓ Rifampicin (600 mg daily) orally together with
✓ INH (300 mg daily) orally.
✓ Ethambutol and pyrazinamide
▪ Open surgical treatment: Under cover with anti- T.B. therapy:
1. Nephro-ureterectomy: Indicated in unilateral nonfunctioning kidney.
2. augmentation cystoplasty: contracted bladder.

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Stone Disease
Incidence
▪ Prevalence of 2-3%
▪ Male: female = 3:1, peak incidence 30-50 years of age
▪ Recurrence rate: 10% at one year, 50% at 5 years, 60-80% life time
Stone Pathogenesis
Mechanism of formation: Unknown but theories:
1) Saturation of urine by salts:
• It depends on:
1. type of solute (concentration).
2. PH of urine.
3. Temperature.
• It's important to decrease recurrence of stone by control of PH and solute.
2) Super-saturation:
• Above saturation level.
• due to absence of:
a) Inhibitors → inhibit stone formation (organic nephrocalcin, inorganic → Mg citrate)
b) Complexing agents e.g. ca citrate
c) Without nucleus formation.
3) Nucleation: e.g. epithelial cells, urinary crystals, RBCs, WBCs, ….
4) Crystal formation:
5) Crystal aggregation.
6) Crystal retention: factor that increase retention.
a) Pelvi-ureteric junction obstruction (PUJO)
b) Medullary sponge kidney
c) UT obstruction.
d) Crystals & epithelial adhesion.
Etiology: (Predisposing factors)
(I) Pre-renal Causes:
1) Hypercalcemia due to:
A. Idiopathic hypercalciuria (60%):
1. Excess absorption of Ca from GIT (commonest)
2. Excess excretion of Ca in urine
B. Hypercalciuric state (40%) e.g.
1. Hyper-parathyroidism
2. Hyperthyroidism (↑ bone catabolism)
3. Cushing syndrome
4. Paraneoplastic syndrome (PTH like) (Bronchogenic carcinoma, Renal cell carcinoma)
5. Multiple Myeloma → ↑Adrenalin (pheochromocytoma)

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6. Vit. D toxicity.
2) Hyper-oxaluria: due to:
a) 1ry hyper-oxaluria (oxalosis): due to enzyme deficiency in liver → ↑ oxalate formation.
b) 2ry hyper-oxaluria (dietary): - ↑ intake ↑ absorption (in short bowel syndrome)
3) Hyperphosphaturia: - ↑ intake of proteins.
4) Hyper-uricosuria: in
a) Gout & during ttt of leukemia.
b) ↑ purine intake → Red meat liver (adenine & guanine → xanthine oxidase → uric acid)
c) lead to uric acid nucleus upon which oxalate will ppt.
5) Cystinuria: due to ↑ absorption.
6) Low citrate level: acidosis → ↓ serum citrate → hypocitraturia as citrate → precipitation of
calcium as ca oxalate.
(II) Renal Causes:
due to renal tubular necrosis → kidney fails to excrete H+ ions → alkalosis of urine (ppt of Ca
phosphate) & acidosis of blood.
(III) Post-renal Causes:
a) Infection.
b) Stasis of urine.
Classifications of urinary stones: according to
1. Stone size
2. Stone location: Stones can be classified according to anatomical position: upper, middle or
lower calyx; renal pelvis; upper, middle or distal ureter; and urinary bladder.
3. X-ray characteristics
Types of Stones
• Character of stone in hyper-parathyroidism:
(1) Ca Oxalate stone (60 %): 1-Radio-opaque. 2-Multiple. 3-Bilateral.
• Commonest type • E-coli is the commonest organism of UTI but
not form stone.
• Oxalate stone is hereditary. • Most common stone is Ca oxalate.
(2) Ca Phosphate stone (10%): • Most opaque stone is Ca phosphate (as
composition of bone)
• Usually in association with Ca oxalate. (10%)
• Pure phosphate stone are rare (5%)→ due to renal tubular acidosis.
(3) Struvite stone (5-10%)
• Triple phosphate stone = Ammonium, Mg, Phosphate, Carbonate "CO3"
• Infection stone (Mg, PO4, NH4 + CO3)
• Formed by urea splitting organism: Proteus Mirabilis, Pseudomonas, Klebsiella.
• Mechanism: Urea → organism by urease enzyme in bacteria → ammonium (NH4) + H2O →
alkaline urine → ppt of Mg, NH4 & PO4.
(4) Uric acid stone. (5-10%) Metabolic stone
(5) Cystine stone. (1%) Metabolic stone
(6) Xanthine stone → Radiolucent
(7) Matrix stone → soft gelatinous material in urine

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Pathology of stones:
Table 6: Composition of stone:
calcium Calcium Uric acid stone Cystine
oxalate phosphate stone
1-No.: - Single - Single or Multiple. - Multiple - Multiple
2- Size: - Moderate - large - Small - small
3- Shape: - Irregular - Oval or - Oval facetted -Oval
stagehorn
4- Surface: - Spiky - Smooth -Smooth - Smooth
5- - Ca oxalate - Ca phosphate - Pure uric acid - Cystine
Composition: -Triple PO4→ PO4, - Ca++ urate (sulphur
Mg, NH4, HCO3 containing)
6- Colour: - White - Dirty white - Yellow -Yellow
7- - Hard - Chaky friable -Hard -Hard
consistency:
8- Cross - Amorphous - Laminated - Amorphous -Amorphous
section:
9- X-ray - Radio- - Radioopaque. - Pure → radio-lucent. -Radio
opaque - Ca urate → opaque due
to sulphur
Radio-opaque.

Clinical Features
1. Urinary obstruction ± upstream distention ± pain
▪ Flank pain from renal capsular distention (non-colicky).
▪ Severe waxing and waning pain radiating from flank to groin, testis, or tip of penis due to
stretching of collecting system or ureter (ureteral colic)
2. Writhing, never comfortable, nausea, vomiting, hematuria (90% microscopic), diaphoresis,
tachycardia, tachypnea
3. Occasionally symptoms of trigonal irritation (frequency, urgency).
4. Bladder stones result in: storage and voiding luts, terminal hematuria, suprapubic pain.
5. If fever, rule out concurrent pyelonephritis or obstruction.
Differential Diagnosis of Renal Colic
1. Acute ureteral obstruction (other causes):
a) UPJ obstruction
b) sloughed papillae
c) clot colic from gross hematuria
2. acute abdominal crisis: biliary, bowel, pancreas, abdominal aortic aneurysm.
3. Gynecological: ectopic pregnancy, torsion/rupture of ovarian cyst, pelvic inflammatory disease
(PID)
4. pyelonephritis (fever, chills, pyuria)
5. radiculitis (L1): herpes zoster, nerve root compression

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Location of Stones
A. Kidney
▪ Calyx
- May cause flank discomfort, recurrent infection or persistent hematuria
- May remain asymptomatic for years and not require treatment
▪ Pelvis
- Tend to cause obstruction at ureteropelvic junction (upj)
- Staghorn calculi (renal pelvis and one or more calyces)
- Often associated with infection that will not resolve until stone is cleared
▪ Ureter: <5 mm diameter will pass spontaneously in 75% of patients
C. Bladder
D. Urethra
Complications:
1- Haematuria: due to injury to mucosa.
2- Infection: pyonephrosis, pyelonephritis, pyelitis, cystitis.
3- Migration, repeated attack of colic.
4- Obstruction: hydronephrosis, retention or anuria.
5- Malignancy: due to chronic irritation.
6- Renal Failure.
Investigations
2. screening labs
i. CBC  elevated WBC in presence of fever suggests infection
ii. Electrolytes, Cr, BUN ± to assess renal function
iii. Urinalysis: R&M (WBCs, RBCs, crystals), C&S

2. imaging
i. (KUB) kidneys, ureters, bladders x-ray
• to differentiate opaque from non-opaque stones
(e.g. uric acid, indinavir)
• 90% of stones are radiopaque (figure 17).
ii. CT scan: accurate method of diagnosing renal and
i. ureteric stones (except) indinavir stones. Allows
Radiopaque Radiolucent
ii. accurate determination of stone size and location and
KUB Calcium Uric Acid
good definition of pelvicalyceal anatomy (figure 18). Struvite indinavir
Cysteine
iii. abdominal ultrasound CT Calcium indinavir
Struvite
• May demonstrate stone (difficult in ureter) Cysteine
Uric Acid
• May demonstrate hydronephrosis
iv. IVP:
• Anatomy of urine collecting system, degree of obstruction, extravasation
3. cystoscopy for suspected bladder stone

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4. stone analysis
5. metabolic studies: if recurrent stone formers:
✓ serum electrolytes, Ca, PO4, uric acid, creatinine and urea
✓ PTH if hypercalcemic
✓ 24 hour urine: for creatinine, Ca, PO4 , uric acid, Mg, oxalate, citrate

Figure 17: Radiograph of the right Figure 18: Non- contrast CT scanning with Large
kidney showing a complete (11 mm) stone in the left ureter at the L5 level. left
staghorn calculus. hydroureteronephrosis with reduced parenchyma.

Management of urolithiasis:
Acute
1. medical
▪ analgesic (NSAID and morphine) ± antiemetic
▪ alpha-blockers: increase rate of spontaneous passage in distal ureteral stones
▪ antibiotics for UTI
▪ IV fluids if vomiting (note: IV fluids do NOT promote stone passage)
2. interventional: if obstruction endangers patient
(i.e. sepsis, renal failure)
▪ ureteric stent (via cystoscopy)
▪ percutaneous nephrostomy (image-guided or US guided)
Elective managment
▪ Medical (conservative)
indication hospitalization:
▪ ESWL. 1. intractable pain
▪ Endoscopy. 2. intractable vomiting
3. Fever ( infection)
▪ Open Surgery. 4. Compromised renal function
5. Single kidney with ureteral
obstruction
6. bilateral obstructing stones

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Management of Renal stones

1) Medical.
2) Extra-corporeal Shock Wave Lithotripsy (ESWL)
3) Percutaneous nephrolithotomy (PCNL)
4) Combined PCNL and ESWL
5) Open renal stone surgery
a) Pyelolithotomy.
b) Extended pyelolithotomy
c) Nephrolithotomy.
d) Pyelonephrolithotomy
e) Partial nephrectomy.
f) Simple nephrectomy.
6) Laparoscopic stone extraction.
Medical (conservative):
Aim: Indication of interference:
1. Pain
• Spontaneous passage. 2. Obstruction.
• ↓ metabolic activity →↓stone recurrence. 3. Infection.
4. Functional loss.
Indications:
• Small stone < 5 mm
• No infection
• No distal obstruction
Include:
1) Antispasmodic: e.g. buscopan.
2) Analgesic: up to morphia.
3) Antiseptic: to guard against infection.
4) ↑fluid intake: esp. water (3-4 litre / day)
5) Diet:
• Ca containing stone → ↓use of milk & milk products.
• Oxalate stone → ↓ Tomato, Spanish, Mango, Strawberry, Coffee
• Uric acid →↓ Red meat, Liver, Coffee, Tea, Coca, Soup.
6) Drugs:
• Ca oxalate stone → Vit. B6 (pyridoxine)
• Phosphate stone → Aceto hydroxamic acid (urease inhibitor)
• Uric acid stone → Xanthine oxidase inhibitors (Allopurinol)
• Cystine stone → D-penicillamine, Mercapto-propionyl glycine (Best), Acetyl cystein.
7) PH of urine:
• Dilution of urine: slight alkalinization of urine.
• Alkalinization of urine: in uric acid & cystein stone by potassium citrate
• Acidification of urine: in Ca & PO4 stone by vit.C.

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8) Chemolysis of stone:
i. Irrigation of the cavity for repeated time by drugs:
1. Uric acid stone → - alkalinization of Urine. - Allopurinol.
2. Cystine stone → - alkalinization. - MPG.
3. Sturvite stone → -acidification, -antibiotic, -urease inhibitor (acetohydroxamic acid)
ii. Only used to ↓ size & so spontaneous passage.
iii. Not used in Ca oxalate.

Orange & Lemon (Citric acid) → produce alkalanization and not

acidification as citric acid enters Kreb's cycle → HCO3

Extra-corporeal Shock Wave Lithotripsy (ESWL)

Objective
• To treat renal calculi, proximal calculi, and mid ureteral calculi which cannot pass through the
urinary tract naturally
• Shockwaves are generated and focused onto stone  fragmentation, allowing stone
fragments to pass spontaneously and less painfully (figure 19)
Methods:
A. Ultrasonic lithotripsy:
▪ Explosion of the stone using ultrasonic waves.
▪ The micro-fragments will pass spontaneously in the urine.
B. Electro-hydraulic lithotripsy:
▪ Explosion of the stone by shock waves, directly at the calculus.
▪ Micro-fragments will pass spontaneously in the urine.
Indication: potential first-line therapy for renal and ureteral calculi less than 2 cm in size

Contraindication:
1) Acute urinary tract infection or urosepsis
2) Bleeding disorder or coagulopathy
3) Pregnancy
4) Obstruction distal to stone
5) Impaired renal function.
Complications
1) bacteriuria and bacteremia
2) post-procedure hematuria
3) ureteric obstruction (by stone fragments)
4) peri-nephric hematoma Figure 19: stone fragmentation by ESWL. The stone is
centered in the machine following which the stone is
broken up with soundwaves.

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PCNL
Indications:
1. Stone > 2 cm (especially hard
2. Urinary obstruction.
3. Cystine stones
4. ESWL failure.
Method;
1. Establish a track for percutaneous
endoscopy,
2. A nephroscope is introduced at
the location of the stone.
3. Small stone extracted with
forceps.
4. Large stone fragmented by
lithotripsy (either laser ultrasonic
or pneumatic)
5. lnsertion of a nephrostomy tube
for 48 hours for drainage. Figure 20: PCNL
Advantages:
1. small incision
2. Short hospital stay.
3. minimal operative and postoperative complications.
Complications
1. Hemorrhage.
2. Extravasations of irrigation used fluid.
3. Residual stones.
4. injury of Renal or other organs injury e.g. colon, pleura.

Open renal stone surgery

It becomes 3rd choice method for renal stone management.
Indications:
▪ Failure of previous lines of treatment.
▪ Complex renal stones
▪ Presence of congenital anomalies as horse shoe kidney
Incision: flank incision (mainly)
Technique:( figure 21)
Pyelolithotomy.
▪ Always tried first especially with extra-renal pelvis.
▪ lt can to be done in intra-renal pelvis using Gil Vernet retractor.
▪ incision in the posterior aspect of the renal pelvis then the stone is removed.

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Advantages:
a) Minimal bleeding.
b) No damage for renal parenchyma.
c) Rapid healing
Nephrolithotomy.
Indicated when pyelolithotomy cannot be done:
▪ Stone in a calyx with narrow neck.
▪ lntra-renal pelvis.
▪ Dense adhesions around the pelvis.
Disadvantages: The reverse of advantages of pyelolithotomy. Figure 21: Open renal stone surgery
▪ The incision is in the substance of the kidney may be through by
ln Brodel's line (in the posterior aspect of the kidney ▪ Nephrolithotomy
▪ Pyelolithotomy
between lateral 1/3 and medial 2/3).
▪ Radial incision directly on the stone.
Partial nephrectomy. if multiple stones impacted in nonfunction part of the kidney.
Simple nephrectomy. lf the kidney is non-functioning provided that the other kidney is normal.

Management of ureteric stones

Conservative management: see previous
Active management: the ureteric stone
Indications: management depend on site, size
and effect of the stone
1. Stone large than 5mm
2. Distal obstruction
3. Persistent pain
4. Failure of medical treatment
5. Evidence of infection
Type of management: depend on site size and effect of
the stone
1. ESWL
2. Push bang technique: pushed to kidney then
PCNL
3. Ureteroscopy (URS):
Aim: Stone extraction or fragmentation.
Technique;
▪ Cystoscope and insertion of guide wire to ureteric
orifice
▪ dilatation of distal ureter and introduction of URS
▪ visualization of stone then extraction by forceps or
Dormia basket.
Figure 22: Ureteroscopy
▪ Fragmentation may be needed

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Types of lithotripsy
c. U/S waves.
d. Electro-hydrolytic.
a. Laser.
b. Pneumatic, (lithoclast)
Complications
▪ Infection
▪ Perforation
▪ Avulsion
▪ Stricture ureter
▪ Migration of stone
▪ Difficulty to introduce guide wire
1. Open ureterolithotomy
Incision :
▪ Stone upper 1/3 → flank incision (stone is best extracted by pyelolithotomy)
▪ Stone middle 1/3 → abernathy incision 2 inches above the asis and passes
downwards and medially to mid-inguinal point (muscle cutting).
▪ Stone lower 1/3 → midline supra-pubic incision.
2. Laparoscopic ureterolithotomy

Management of bladder stones

Instrumental: lf < 2 cm
▪ Cystolitholapaxy (Trans-urethral): mechanical compression of the stone using lithotrate then
removal of the fragments by Ellik's evacuator.
▪ Cystolithotripsy: fragmentation by lithotripsy U/S waves, Electro-hydrolytic, Laser or
Pneumatic (lithoclast)
Surgical: suprapubic cystotolithotomy,
Indications
a. Larger and harder stones
b. Cases where open prostatectomy or bladder diverticulectomy is indicated.
c. Failure of stone fragmentation
d. In children

Management of urethral stones:

▪ Posterior urethra: Supra-pubic cystolithotomy for stone firmly impacted supported by
urethral dilator & removed trans-vesical.
▪ Penile urethra: trial of removal by forceps if failed, External urethrotomy will be done
▪ Glandular urethra: External meatotomy.

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Prevention of stone formation

1. dietary modification:
▪ Increase fluid (>2 L/day), potassium intake
▪ Reduce animal protein, oxalate, sodium, sucrose, and fructose intake
▪ Avoid high-dose vitamin C supplements
2. The stone should be chemically analyzed.
3. Treating infection and other causes of stone formation.
4. Follow up of stone formers to detect early recurrence.
5. Metabolic work-up to know etiology of the stone.
▪ Serum Ca and phosphorus to exclude hyperparathyroidism.
▪ 24-hour urine collection for the following whose normal values are:
a. Ca <300 mg.
b. Uric acid <800 mg.
c. Oxalates <40 mg.
d. Citrates 300-900 mg.
6. medications:
i. Thiazide diuretics for hypercalciuria
ii. Allopurinol for hyperuricosuria
iii. Potassium citrate for hypocitraturia

Although hypercalciuria is a risk factor

for stone formation. decreasing dietary calcium
is NOT recommended to prevent stone ✓ Calcium oxalate stones:
formation. Low dietary calcium lead to 1. Avoid diet rich in oxalates.
increased oxalate absorption and higher 2. Hydrochlorothiazide 50 mg/d aids in the
urinary levels of calcium oxalate. dissolution of Ca oxalate stones.
3. Citrates 5 mg bid inhibits crystallization of
oxalates.
✓ Uric acid stones
1. Avoid diet rich in purines.
2. Rule out myeloproliferative or neoplastic
- Ca oxalate stone is ppt in neutral PH. diseases.
- Ca phosphate & Struvite stones are ppt in 3. Urine should be kept alkaline, e.g. by NaHCO3 1
alkaline PH. gm tds.
- Cystine & Uric acid stones are ppt in acidic 4. Allopurinol 30 mg/day is indicated in patients with
PH. hyperuricemia.
- Citrate inhibit ppt of Ca. ✓ Struvite stones
- Mg inhibit ppt of oxalate. 1. Aluminum hydroxide orally restricts phosphate
- Pyrophosphate inhibit ppt of phosphate. absorption.
- Hyper-oxaluria is an inborn error of 2. Long term antibiotics to eradicate UTl.
metabolism of glycine. 3. Avoid indwelling catheters.
- Hard stones: 4. Increase urine acidity by vitamin c
▪ Ca oxalate monohydrate stone.
▪ Cystine stone.
▪ Some types of uric acid stone.

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Obstructive uropathy
Obstruction anywhere in the urinary tract associated with changes in the urinary system proximal
to the obstruction.
Classifications
1. Acute or chronic obstruction.
2. Partial or complete obstruction.
3. Unilateral or bilateral obstruction.
4. Congenital or acquired obstruction.
5. Extrinsic or intrinsic obstruction.
Etiology
I. Unilateral
A. Kidney and pelvis:
• Congenital:
1. Horse-shoe kidney.
2. Aberrant renal vessels crossing the pelvis.
3. PUJ obstruction.
• Acquired
1. Stones.
2. Tumors of the kidney or pelvis.
3. Renal TB.
B. Ureteric obstruction:
• From outside:
1. Pressure from adjacent structures e.g.
▪ Gartner duct cyst, pregnancy,
▪ Tubo-ovarian abscess
▪ Diverticular abscess, cancer cervix, rectum...etc.
2. Aberrant blood vessels and Aneurysm
3. Idiopathic retro-peritoneal fibrosis.
4. Retro-caval ureter.
5. Retroperitoneum:
▪ Fibrosis, Hematoma,Lymphocele,Lymphoma
▪ Metastatic tumor (eg, breast, prostate, testicular).
▪ Pelvic lipomatosis,Sarcoidosis,TB
• ln the wall
1. Congenital stenosis.
2. Ureterocele.
3. inflammatory stricture after repair of damaged ureter, calculus or ureteric TB.
4. Neoplasm of ureter or bladder cancer involving the ureteric orifice.
• ln the lumen:
1. Stone (commonest).

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2. Blood clot
3. Fungus ball
4. Urothelial carcinoma
5. Sloughed renal papillae
II. Bilateral (lower urinary tract obstruction)
A. Congenital:
1. Posterior urethral valve (PUV).
2. Phimosis.
B. Acquired
1. prostatic hyperplasia (BPH) (commonest). most common
2. Cancer prostate. causes differ by age:
• Children: Anatomic
3. Post-operative bladder neck scarring. abnormalities as PUJO and PUV
4. Urethral stricture (e.g. post-traumatic). • Young adults: Calculi
Sequalae of obstructive uropathy • Older adults: BPH or prostate
cancer,
1. Hydronephrosis.
2. Retention of urine.
3. Calcular anuria.
Pathology:
1. Urethra  dilatation
2. Bladder:
✓ Early: muscle hypertrophy and trabeculation and diverticula
✓ Late: Bladder dilatation and atony chronic retention
3. Ureter: muscle hypertrophy then atony and dilatation  hydroureter.
4. Kidney:
a) Morphological:
✓ Pelvic hypertrophy  pelvic atony and dilatation
✓ Parenchymal thinning and atrophy.
b) Functional: increased intra-pelvic pressure  urine excretion stops  decrease GFR
✓ Unilateral: contralateral hypertrophy
✓ Bilateral: renal impairment
Diagnosis:
Clinical picture:
1. Pain is common, usually along T11 to T12.
2. Absolute anuria occurs with complete obstruction at the level of the bladder or urethra
or bilateral obstruction.
3. Infection complicating obstruction may cause: dysuria, pyuria, urgency and frequency,
pyelonephritis, and occasionally septicemia.
4. palpable flank mass, particularly in massive hydronephrosis of infancy and childhood.
Investigations
A. Urinalysis and serum electrolytes, BUN, and creatinine.

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B. Imaging: for suspected ureteral or more proximal

obstruction:
1. Abdominal ultrasonography is the initial imaging test
of choice in most patients without urethral
abnormalities.
2. Voiding cystourethrography and cystourethroscopy
for suspected urethral obstruction.
3. IVU (figure 23)
4. Pelvi-abdominal CT.
5. Antegrade or retrograde pyelography is preferred to
studies that involve vascular administration of
contrast agents in the azotemic patient.
6. Radionuclide scans.
7. MRU (Magnetic resonance of urine).
Treatment: consists of eliminating the cause of
obstruction
a) Temporarily by: JJ stent or nephrostomy tubes.
Figure 23: IVP with
b) Permanently by:
hydroureteronephrosis
Surgery as pyeloplasty, ureteroplasy and urethroplasty
Instrumentation (eg, endoscopy, lithotripsy)

Hydronephrosis
Definition:
• Dilation of the renal pelvis and calyces, usually caused by obstruction of the free flow of urine
from the kidney. Untreated, it leads to progressive atrophy of the kidney.
• One or both kidneys may be affected.
• In hydroureteronephrosis, there is distention of both the ureter and the renal pelvis and calices.
• The obstruction is acute or chronic, partial or complete, unilateral or bilateral.
Etiology: see obstructive uropathy
Diagnosis:
 Presentations of hydronephrosis
1) Mild pain or dull achinq pain in the loin:
a) lncreases by excessive fluid intake.
b) Often associated with dragging heaviness.
c) The kidney may be palpable.
2) Attacks of acute renal colic: may occur with no palpable swelling.
3) lntermittent hvdronephrosis (with Dietl's crisis)
• Acute renal pain + renal swelling→some hours later → no pain or swelling but large volume
of urine is passed.
 C/P of the cause
• Stone: colic, painful hematuria.

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• BPH: prostatism (LUTs).

• TB: constitutional symptoms, frequency.
 C/P of the complications
e.g. Hypertension, fever (in infections) and in late cases ) renal failure.
Complications:
1) Renal hypertension.
2) Renal failure (if bilateral hydronephrosis or unilateral in the only functioning kidney).
3) Infection  pyonephrosis (2ry).
4) Pressure atrophy.
5) Others: calcification - rarely hemorrhage or rupture (more liable to trauma).
D.D: polycystic kidney, hypernephroma, liver swellings and splenomegaly.
Investigations:
For diagnosis
1) U/S: detects the size of the kidney and the thickness of the renal cortex.
2) lVU:
▪ Dilatation of renal pelvis.
▪ Flattening of calyces.
▪ Clubbing.
▪ Ballooning of the calyces, widening of the waist.
▪ Later, faint nephrogram around dilated calyces (soap-bubble appearance).
3) Ascending (retrograde) pyelography indicated if IVU is contraindicated due to renal failure.
4) Renal isotope scanning detects the remaining functioning parenchyma.
5) Plan X-Ray: Abnormal psoas shadow. Stone, calcifications.
For complications
▪ KFTs: for renal failure.
▪ Urine analysis: polyuria of low specific gravity.
▪ CBC & ESR: to exclude infection.
For the cause
▪ Trans-rectal U/S for BPH.
▪ Cystoscopy  bladder lesions (bilharziasis or tumor).
Management of the cause: As
1) Stones → Pyelolithotomy, Ureterolithotomy
2) Stricture → excision and end to end anastomosis
3) Aberrant Vessel → Transection of the ureter and anastomosis in front of the vessel
4) Benign Prostatic Hyperplasia → Transurthral resection of Prostate (TURP)
5) Carcinoma of Prostate → TURP+ Hormonal Therapy
6) Urethral Stricture → Urethroplasty
7) Meatal Stenosis → Meatoplasty
8) Phimosis → Circumcision

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Benign Prostatic Hyperplasia (BPH)

Definition: Benign condition associated with symptom complex (syndrome) of what's called LUTS
(lower urinary tract symptoms)
hyperplasia of stroma and epithelium in periurethral area of prostate (transition zone)
zonal anatomy of prostate:

Figure 24: Zonal anatomy of the prostate

Epidemiology
• age-related. Extremely common (50% of 50 year olds, 80% of 80 year olds)
• 25% of men will require treatment
Etiology: Unknown but theories:
1) Hormonal dependent theory: (Role of Androgen)
a) Testosterone → 5 α-reductase enzyme → dihydrotestosteront (DHT)→ ↑ growth factors
→ enlargement.
b) Role of estrogen: (Hormonal imbalance) there's associated ↑ of serum estrogen. (↑ E / T
Ratio)
a) Secretion of intermediate peptide growth factors may play role in development of BPH.
2) Programmed cell death regulation (Apoptosis): impaired apoptosis (↑ cell growth )
3) Neoplastic theory: BPH is considered as Benign tumor.
4) Inflammatory theory: (not accepted): based on appearance of chronic infl. cells e.g.
lymphocytes in stroma.
Pathology: figure 25

Site.
Most commonly arises from
submucous group of glands in
▪ Transitional zone (peri-urethral)
 lateral lobes.
▪ lf arising from CZ sub-cervical
glands  middle lobe.
Figure 25: of BPH

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Macroscopic
Changes ln the prostate:
1. No gritty sensation during cutting it.
2. Fibrous trabeculae divide the adenoma into lobules.
3. Yellowish in color.
Changes ln the urethra:
1. Urethral narrowing as it is stretched and compressed from side to side.
2. This narrowing interferes with bladder emptying.
3. Exaggeration of the normal posterior curve of the urethra.
The urinary bladder, ureters and kidney show changes as in obstructive uropathy.
Microscopic
a) Hyperplasia of acini (fibro-myo-adenoma),
b) Dried prostatic secretion  corpora amylacia.
Clinical picture:
symptoms
1) voiding symptoms:  AUA prostatic
symptom score (IPSS)
a) Hesitancy, (FUNWISE)
b) Straining. 1. Frequency
2. Urgency
c) Weak/interrupted stream 3. Nocturia
d) incomplete bladder emptying 4. Weak Stream
5. Intermittency
▪ Decreased flow rates may be seen on uroflowmetry 6. Straining
▪ Due to outflow obstruction and/or impaired detrusor contractility 7. Emptying, feeling of
incomplete
2) storage symptoms:  Each symptom take score
a) urgency, of 5:
✓ 1-7 = MILD symptom
b) frequency, ✓ 8-19 = MODERATE
c) nocturia, symptom
✓ 20-35 = SEVERE symptom
d) urgency incontinence
 Dysuria not included in the
▪ thought to be due to score
1. Detrusor over activity
2. Deceased compliance
3. Congestion of the bladder mucosa.
4. Increased residual urine.
5. Complications: cystitis, stones & trigonal irritation.
3) Sexual symptoms: increased libido at the start, later impotence occur.
4) Symptoms of complications.
Signs
▪ General:
a) Exclude complications (uremia, fever).
b) Exclude DD (cystitis, cancer prostate with metastasis, neurological examination for DM and
Parkinsonism).

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▪ Local:
a) Mass or tenderness in the renal angle (hydronephrosis).
b) Supra-pubic palpable bladder (retention).
c) DRE: prostate is
✓ Smooth,
✓ Rubbery
✓ Symmetrically enlarged prostate size doesn't
correlate with either symptom
✓ Median sulcus preserved.
or mode of management
✓ Notch between it & seminal vesicle is preserved.
✓ Mucosa of rectum mobile over prostate
Complications:
1. Retention of urine:
a) Acute retention of urine is sometimes the 1st presentation of BPH. Retention is precipitated
by excess fluid intake, alcohol, wintry weather, cystitis, diuresis, constipation, unrelieved
sexual excitement. Acute retention is very painful and needs urgent intervention.
b) Chronic retention with overflow incontinence. The condition is painless and the actual
complaint of the patient is incontinence.
2. Overflow incontinence
3. Hydronephrosis and renal compromise
4. Infection
5. Hematuria
6. Bladder stones
 Assess LUTS and effect on quality of life, may include self-administered questionnaires (AUA
symptom and impact score)
D.D :
1. Cancer prostate.
2. Chronic prostatitis
3. Bladder tumors.
4. Bladder calculi.
5. Detrusor muscle weakness or instability.
Investigations:
Laboratory:
1. Urine analysis.
2. liver & kidney function.
3. Urine culture.
4. PSA (prostate specific Ag) (see later)
Uroflowmetry
▪ Q max (peak) = normal > 15 ml / sec.
▪ Less than 10 ml / sec means
obstruction to bladder outflow (figure 26). Figure 26: uroflowmetry of man with BPH Qmax
is 7 ml/sec.

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Imaging:
▪ Abdominopelvic US:
a) visualize kidney changes,
b) measure amount of post-voiding residual urine in the bladder
c) diagnose any bladder pathology.
▪ TRUS. (Trans-rectal ultrasound)
a) asses size of prostate,
b) exclude presence of focal lesion
c) U/S guided biopsy can be taken.
▪ IVU: to show (figure 27)
a) back pressure on the kidney.
b) the bladder floor can be elevated
c) distal ureters lifted medially
(J-shaped ureters or fishhook ureters).
Figure 27: IVU of BPH
d) Chronic bladder outlet obstruction can lead to detrusor
hypertrophy, trabeculation and formation of bladder diverticula.
Urodynamic study in selected cases

Treatment:
I. Conservative for those with mild symptoms:
• watchful waiting - of patients improve spontaneously
• includes life style changes (e.g. evening fluid restriction, planned voiding)
• avoid ppt factor e.g. Excess work, worry, weather (cold), wine, women, withholding urine in
bladder, spices, constipation.
II. Medical therapy:
1. α-blockers: reduce stromal smooth muscle tone e.g. terazosin (Hytrin) doxazosin
(Cardura), tamsulosin, alfuzosin (Xatral), silodosin
2. 5α-reductase inhibitors: blocks conversion of testosterone to DHT; acts on the epithelial
component of the prostate reduces prostate size e.g. finasteride (Proscar), dutasteride
(Avodart)
3. combination shown to be synergistic
4. Phytotherapy.
III. Minimal Invasive therapy:
1- Intra-prostatic stent.
2- Trans-urethral needle ablation.
3- Balloon dilatation.
4- Thermotherapy. Microwave heat therapy.
5- Endoscopic transurethral cryo-ablation of the prostate.
IV. Surgical
A. Endoscopic

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1. TURP (Trans-Urethral Resection of Prostate)

Objective
 To partially resect the periurethral area of the prostate (transition zone) to decrease
symptoms of urinary tract obstruction (figure 28)
 Accomplished via a cystoscopic approach using an electrocautery loop, irrigation (glycine},
and illumination
Indications
1) Obstructive uropathy (large bladder
diverticula, renal insufficiency)
2) Refractory urinary retention
3) Recurrent UTIs
4) Recurrent gross hematuria
5) Bladder stones
6) Intolerance/failure of medical therapy

Complications
Figure 28: TURP
• Acute:
1) Intra- or extraperitoneal rupture of the bladder
2) Rectal perforation
3) Incontinence
4) Incision of the ureteral orifice (with subsequent reflux or ureteral stricture)
5) Hemorrhage
6) Epididymitis
7) Sepsis
8) Transurethral resection syndrome (also called "post-TURP syndrome·)
✓ Caused by absorption of a large volume of the hypotonic irrigation solution used, usually
through perforated venous sinusoids, leading to a hypervolemic hyponatremic state
✓ Characterized by dilutional hyponatremia, confusion, nausea, vomiting, hypertension,
bradycardia, visual disturbances, CHF. and pulmonary edema
✓ Treat with diuresis and (if severe) hypertonic saline administration
• Chronic:
1) Retrograde ejaculation (>75%}
2) Erectile dysfunction (5-1 0% risk increases with increasing use of cautery)
3) Incontinence (<1%)
4) Urethral stricture
5) Bladder neck contracture
2. Trans-urethral vaporization.
3. Trans-urethral Incision.
4. Laser:
▪ Lasers use concentrated light to generate precise and intense heat.

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▪ There are several different types of prostate laser surgery, including:

a) Photo selective vaporization of the prostate (PVP).
b) Holmium laser ablation of the prostate (HoLAP).
c) Holmium laser enucleation of the prostate (HoLEP).
B. Open prostatectomy
Indications
1. Very large prostate.
2. Bladder diverticula
3. Bladder stones.
4. TURP is not possible for another reason.
Types
 Trans vesical prostatectomy
 Retropubic (Millin's) prostatectomy
Bladder diverticulum
Definition A diverticulum is an outpouching in the bladder. It can be either congenital or acquired.
Types:
a) Congenital diverticula are usually diagnosed in childhood or on prenatal ultrasound.
b) Acquired bladder diverticula are often due to bladder outlet obstruction from
• BPH
• Urethral stricture
• Neurologic disease.
Acquired diverticula are most typically seen in
elderly men and often associated with BPH.
Clinically
1) Bladder diverticula are often asymptomatic
2) urinary retention
3) urinary tract infection,
4) blood in the urine.
5) Stone bladder
6) Tumor Figure 29: bladder diverticulum
Diagnosis
1. imaging studies
• CT scan
• Ultrasound incidentally.
• Cystogram
2. Cystoscopy
treatment:
▪ Treatment of the cause.
▪ Congenital or acquired diverticula do not always require treatment
▪ Open and laparoscopic diverticulectomy. If there is complication

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Urethral stricture
Definition
• decrease in urethral caliber due to scar formation in urethra (may involve corpus spongiosum)
• M>F
Etiology
1) Congenital: failure of normal canalization may cause bilateral hydronephrosis
2) Trauma:
a) Instrumentation (most common)
b) External trauma (e.g. Burns, straddle injury)
c) Other: foreign body, removal of inflated Foley catheter, etc.
3) inflammation:
a) Long-term indwelling catheter
b) Balanitis xerotica obliterans (lichen sclerosis or chronic progressive sclerosing
dermatosis of the male genitalia) causes meatal stenosis
4) Neoplastic;
a) Urethral polyps
b) Venereal warts
c) Carcinoma of the urethra.
Clinical Features:
1) voiding symptoms (obstructive symptoms)
2) urinary retention
3) related infections: recurrent UTI, secondary prostatitis/epididymitis
Complications
1. Retention of urine.
2. Urethral diverticulum.
3. Extravasation of urine with peri-urethral fistula.
4. Stone formation.
5. Infertility.
6. Infection e.g. urethritis, cystitis...etc.
7. Squamous cell carcinoma.
8. Renal insufficiency.
9. Straining  precipitating hernia, hemorrhoids...etc.
Investigations
1) laboratory findings
• Flow rates <10 ml/s (normal-20 ml/s) on uroflowmetry
• Urine culture usually negative, but may show pyuria
2) radiologic findings
• Voiding cystourethrogram (VCUG): will demonstrate location (figure 30)
• Urethral ultrasonography.

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3) Uroflowmetry: reveals obstructed flow

4) Urethroscopy.

Treatment
1) Urethral dilatation:
• Temporarily increases lumen size by breaking
up scar tissue
• Healing will often reform scar tissue and recreate
stricture
2) Visual internal urethrotomy (viu):
• Through the urethroscope and under direct Figure 30: AVCUG
vision, the stricture is incised with sharp knife
blade usually at the 12 O'clock position.
3) Open surgical reconstruction:

• Complete stricture excision ± anastomosis, ± urethroplasty depending on location and size

of stricture
• Types of urethroplasty
a) Anastomotic,
b) Buccal mucosal onlay graft,
c) Scrotal or penile island flap.
d) Johansen's urethroplasty

Anuria
Definition.: No urine excretion for 12 h.
OR excretion of < 400 cc / 24 h (with empty bladder) = oliguria.
Types: (Etiology)
(1) Pre-renal causes:
▪ Shock (hypovolemic, septicemic, cardiogenic, neurogenic)
▪ Heart failure.
▪ Hemorrhage
(2) renal causes: - due to bilateral renal disease.
a. Diseases:
1. Acute glomerulonephritis.
2. Systemic Lupus Erythematosus.
3. polycystic kidney
b. Toxic:
1. endogenous, (bile)
2. exogenous: NSAIDs, aminoglycosides (streptomycin), anti. TB (INH)

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(3) Post-renal causes:

▪ obstruction → bilateral (calcular anuria)
→ unilateral with solitary kidney.
▪ infiltration of both ureter by tumor. e.g cancer Cervix.
▪ accidental ligation of both ureter e.g. during hysterectomy.
▪ stricture.
Diagnosis:
▪ History: of urinary stone. SLE, drugs.
▪ Symptoms:
a) renal colic.
b) anuria.
c) uremic symptoms: headache, drowsiness, lassitude, nausea, hiccough, constipation.
d) lastly, subnormal temperature, irregular breathing, muscle twitches → coma and
death.
▪ Examination;
a) 1st exclude retention by percussion of bladder and catheter.
b) uremia (earthy look with acidotic breathing)
c) palpation of kidney: ↑size of kidney. tender → obstruction.
d) P.V or PR to find tumor: Which is common cause of post-renal anuria.
Investigations:
A. Laboratory:
− Increased S. Urea and creatinine (1st)
− K & Na.
− ABG → PH, O2 saturation & HCO3
B. Radiology:
− U/S → most important.
− Plain X-ray → stones.
− C.T (±)
Treatment:
1. Pre-renal:
A) Treatment of the cause. B) replacement therapy.
2. Renal: treatment of the cause.
3. Post-renal:
i. Cystoscopic catheterization of both ureters.
ii. PCN (Percutaneous Nephrostomy) if obstruction.
iii. Treatment of the cause.
4. Indications of hemodialysis:
i. HCO3 < 12mEq/L.
ii. Pulmonary oedema.
iii. K > 7 mEq / L.
iv. ECG changes.

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Retention of urine
Definition
Failure of bladder evacuation with functioning kidneys.
Types
1- Acute retention: Sudden complete failure to pass urine, Painful.
2- Chronic retention: The patient can pass urine but some urine always remains in the
bladder (residual urine increases), Painless.
3- Retention with overflow (false incontinence): Micturition is replaced by a continuous
dribbling of urine from an over-distended bladder on top of neglected chronic retention,
Painless.
Etiology
A. Outflow obstruction:
1- bladder neck or urethra:
a) calculus,
b) clot,
c) foreign body,
d) neoplasm
2- prostate:
a) BPH,
b) prostate cancer,
c) prostatitis
3- urethra:
a) stricture.
b) phimosis,
c) traumatic disruption
B. Bladder innervation:
1- spinal cord: injury, disc herniation, multiple sclerosis
2- stroke
3- DM
4- post-pelvic surgery
C. Pharmacologic:
1- anticholinergics
2- narcotics
3- antihypertensives (ganglionic blockers, methyldopa)
4- over-the-counter cold medications containing ephedrine or pseudoephedrine
5- antihistamines
6- psychosomatic substances
Clinical Features
1. palpable and/or percussible bladder (suprapubic)

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2. Possible purulent/bloody meatal discharge

3. DRE - size of prostate, anal sphincter tone
4. Neurological- presence of abnormal deep tendon reflexes, saddle sensation, etc.
Investigations
• CBC, electrolytes, Cr, BUN, urine R&M, C&S,
• ultrasound, post void residual (PVR) scan
• cystoscopy,
• urodynamic studies,
Treatment
A. Guiding principles are to treat underlying cause of retention and use least invasive treatment
possible
B. Catheterization:
• Contraindicated in trauma patient unless urethral disruption has been ruled out
• Acute retention: immediate catheterization to relieve retention, leave foley in to drain
bladder, follow up to determine cause
• Chronic retention: intermittent catheterization by patient is commonly used; definitive
treatment depends on etiology
C. Suprapubic cystotomy
D. For post-operative patients with retention:
• Encourage ambulation
• Alpha-blockers to relax bladder neck
• May need catheterization
E. Definitive treatment will depend on etiology as
1. Urethral stone:
a. Prostatic urethra! Stone:
b. Push to bladder to be crushed by litholapaxy and evacuate fragments.
c. If failed  supra-pubic cysto-lithotomy.
d. Penile urethral stone:
e. Local anesthetic gel & try forceps extraction
2. Urethral stricture: VIU and put urethral catheter.
3. Bladder stone:
▪ lf <2 cm: cystoscopic litholapaxy.
▪ lf >2 cm: cysto-lithotomy.
4. BPH:
- Medical treatment may be used if it's the 1st attack of retention: 5-alpha reductase inhibitor
and ɑ-blockers.
- Surgical:
a) Trans-Urethral Resection of Prostate (TURP).
b) Open surgery (trans-vesical or retro-pubic prostatectomy).

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Hematuria
Definition: presence of > 3-5 RBCs / H.P.F in concentrated urine.
Types:
1- According to the severity:
a. gross hematuria.
b. microscopic hematuria (< 5 / H.P.F)
2- According to the relation to the urinary system:
i. initial → urethra.
ii. terminal → bladder & post. urethra (Bilharz.)
iii. total → kidney, ureter or bladder.
3- According to the associated pain:
i. painful (e.g. stones)
ii. painless (e.g. renal & UB tumors)
4- True or false.
5- Factitious hematuria.
6- According to the origin.
i. urologic: from peripheral calyces to external meatus.
ii. nephrological: glomerular in origin.
Etiology:
1- Urologic:
a. trauma.
b. stones.
c. infection. neoplasm.
d. BPH
e. iatrogenic.
2- Nephrological:
a. poststreptococcal glomerulonephritis (PSGN).
b. Systemic Lupus erythematosus.
c. Exercise hematuria.
3- General cause:
a. Liver impairment
b. hemophilia.
c. Thrombocytopenia.
d. DIC
e. sickle cell anemia.
f. Von Willebrand disease.
4- Exercise hematuria: e.g. long distance runner.
5- Factitious: vaginal bleeding.
6- Idiopathic: 20%

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Diagnosis:
A) History:
1- Age:
a) Child
− Most common nephrological cause → PSGN
− Most common urologic cause —> UTI
b) Adult → most common causes → stones & tumors.
c) Old age male → B.P.H. & cancer bladder
2- Sex: female → ask about menstruation. most common in female → cystitis.
3- Analysis of hematuria:
a) Color of hematuria: smoky urine (coca cola color) → PSGN
b) Time of hematuria:
• Initial → urethral causes.
• Terminal → bladder causes.
• Total → kidney, ureter or bladder causes,
c) Shape of blood clots:
• Discoid → vesical causes.
• Worm like → supra-vesical cause,
d) Other symptoms:
• frequency
− Diurnal → stone bladder.
− Nocturnal → BPH.
− Diurnal & nocturnal → cystitis.
• Pain
− Colicky → stone.
− Dull aching → inflammation.
e) History of: - trauma. - drugs e.g. rifampicin - passage of stone
II) Examination:
A. General:
1- Vital parameters: - Temp → infection.
2- Hypertension → lower limb edema.
3- Nephrotic syndrome.
4- Purpuric rash: ITP.
B. Abdominal:
1- renal masses: renal causes or hydronephrosis due to lower causes
2- full bladder: BPH.
3- cirrhotic liver: bleeding tendency.
C. PR or PV:
- Bladder mass.

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- BPH.
- Cancer prostate.
Investigations:
• Laboratory:
1- urine:
− Urine analysis.
− Urine culture.
− Urine cytology.
− Zeihl Neelsen.
2- Blood: - CBC. - ASO titer.
3- Hematologic tests (Bleeding & clotting times)
• Imaging:
1. KUB X-ray
2. Abdominal U/S.
3. IVU
4. Ascending cystography.
5. Angiography.
6. CT
• Endoscopy: cystourethroscopy.
• Renal biopsy.
DD:
▪ Causes of red urine:
i. Hemoglobinuria.
ii. Myoglobinuria.
iii. Food e.g. Beet root
iv. Drugs e.g.
− Rifampicin,
− Adriamycin,
− Metronidazole.
− Cyclophosphamide → hemorrhagic cystitis → hematuria.
• Causes of urethral bleeding.
Treatment
• General measures:
for shocked patient: IV fluids, blood transfusion, continues blood rrigation….
• Definitive treatment of the cause.

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UROLOGICAL NEOPLASMS
Renal neoplasms
Approach to Renal Mass (figure 31)

Figure 31: Workup of a Renal Mass

(A) primary tumors:
1 - Benign tumors:
Adenoma (most common benign tumor), papilloma, fibroma, lipoma, hemangioma, oncocytoma.
2- Malignant tumors:
a) Parenchymal: (90%)
1. Renal cell carcinoma (hypernephroma, clear cell carcinoma, renal adenocarcinoma (75%)
2. Wilm's tumor (nephroblstoma) (10%)
3. Leiomyosarcoma, hemangiosarcoma (5%)
b) Urothelial: (10%)
1. Transitional cell carcinoma. (TCC)
2. Sq. cell carcinoma. (SCC)
(B) secondary tumors:
1. Lung cancer 2. Breast cancer 3. Stomach cancer
4. Leukemia. 5. Lymphoma.
Benign Renal Neoplasms
Renal cysts
1. Simple cysts
▪ Very common - up to 50% at age 50
▪ Usually incidental finding on abdominal imaging
2. Classification of cysts (i.e. simple and complex)
Bosniak classification is used to stratify for risk of malignancy based on cyst features (Table 7)
3. polycystic kidney disease (see previously)
4. medullary sponge kidney

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▪ Dilatations of the collecting ducts

▪ Usually benign course, but predispose to calcium phosphate stones
5. Von hippel-lindau syndrome
▪ Renal cysts, cerebellar and retinal hemangioblastomas, pancreatic and epididymal cysts
▪ 30-40% incidence of renal cell carcinoma
6. Peripelvic and parapelvic cysts
Table 7 : Bosniak Classification of Renal Cysts.

Bengin renal mass (table 8)

Table 8: Benign Renal Masses

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Renal adenocarcinoma [Renal Cell Carcinoma (RCC)]

Etiology cause unknown
• Originates from proximal convoluted tubule epithelial cells
• Risk factors: smoking (results in 2x increased relative risk), cadmium exposure, employment
in leather industry
• Familial incidence seen with von Hippel-Lindau syndrome
Epidemiology
• Eighth most common malignancy (accounts for 3% of all newly diagnosed cancers)
• 85% of primary malignant tumors in kidney
• Male : female = 3:1
• Peak incidence at 50-60 years of age
Pathology
• Adenocarcinoma
• Cell origin: PCT
• Gross appearance:
- Arise from one pole of the kidney usually upper pole.
- Bilateral (2 - 3%)
- Variable in size & yellow in color (high fat content)
- Pseudo capsule (compressed surrounding tissue)
- Area of hemorrhage and necrosis (mosaic app.)
• infiltrate renal pelvis early
• microscopic appearance: histological subtypes:
a) Clear cell type,
b) Granular type,
c) Spindle cell type,
d) Papillary type,
e) Chromophobe cell type
Mode Spread:
• Direct:
a) Intrinsic renal pelvis (early) → hematuria.
b) Extrinsic → capsule → perinephric fat → surrounding tissue.
• Lymphatic: Hilar L.N → para-aortic L.N. → thoracic duct → virchow L.N.
• Blood: (main route)
a) Embolization: lung, bone, liver, brain (LBLB)
b) Permeation: renal vein → IVC → R.A
Clinical Features
 Usually asymptomatic- frequently diagnosed incidentally by U/S or CT
 Poor prognostic indicators: weight loss, weakness, anemia, bone pain

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 Local effects: classic "too late triad" found in 10-15%:

1. Gross hematuria 50%
2. Flank pain <50%
3. Palpable mass <30%
 Was called the "internist's tumor" because of paraneoplastic symptomatology, now
called the radiologist's tumor· because of incidental diagnosis imaging
 Systemic effects: paraneoplastic syndromes (10-40% of patients)
1. Hematopoietic disturbances:
• Anemia, polycythemia, raised esr.
2. Endocrinopathies:
• Hypercalcemia (increased vitamin d hydroxylation),
• Erythrocytosis (increased erythropoietin),
• Hypertension (increased renin),
• Production of other hormones (prolactin, gonadotropins, tsh, insulin and cortisol)
3. Hepatic cell dysfunction - "stauffer's syndrome":
• Abnormal liver function tests, decreased wbc count,
• Fever,
• Areas of hepatic necrosis;
• No evidence of metastases;
• Reversible following removal of primary tumour
4. Hemodynamic alterations:
• Systolic hypertension (due to av shunting),
• Peripheral edema (due to caval obstruction)
 Metastases: seen in 15% of new cases to bone, brain, lung and liver most common sites
Investigations
1. Routine labs fur paraneoplastic syndromes (cbc, esr, lfts)
2. Urinalysis (60-75% have hematuria)
3. Renal ultrasound (solid vs. Cystic lesion)
4. CT scan (to distinguish solid vs. cystic lesion and to determine extent and operability)
5. IVP (mass lesion): no longer routinely done
6. MRI
7. Angiography: no longer routinely done
8. Renal biopsy needed in selected cases
9. For staging: Involves creatinine, chest x-ray, liver enzymes and functions, bone scan
Staging:
I. ROBSON
• Stage I: confined to renal parenchyma.
• Stage II: extend to perinephric fat but with intact fascia
• Stage III:

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✓ a → Renal vein & / or IVC.

✓ b → Regional L.N.
✓ c → a+b
• stage IV:
✓ a → surrounding tissue.
✓ b → distant metastases.
II. TNM classification
T - Primary tumour
▪ T1 Tumour < 7 cm in greatest dimension, limited to the kidney
a) T1a Tumour < 4 cm in greatest dimension, limited to the kidney
b) T1b Tumour > 4 cm but < 7 cm in greatest dimension, but not more than 7 cm
▪ T2 Tumour > 7 cm in greatest dimension, limited to the kidney
▪ T3 Tumour extends into major veins or directly invades adrenal gland or perinephric tissues
but not beyond Gerota’s fascia
a) T3a Tumour directly invades adrenal gland or perinephric tissues but not beyond Gerota’s
fascia
b) T3b Tumour grossly extends into renal vein(s) or its segmental branches, or the vena cava
below the diaphragm
c) T3c Tumour grossly extends into vena cava or its wall above diaphragm
▪ T4 Tumour directly invades beyond Gerota’s fascia
N - Regional lymph nodes
N0 No regional lymph node metastasis
N1 Metastasis in a single regional lymph node
N2 Metastasis in more than 1 regional lymph node
M - Distant metastasis
M0 No distant metastasis
M1 Distant metastasis
TNM stage grouping (Figure 32)
• Stage I T1 N0 M0
• Stage II T2 N0 M0
• Stage III
o T3 N0 M0
o T1, T2, T3 N1 M0
• Stage IV
o T4 N0,N1 M0
o Any T N2 M0
o Any T Any N M1 Figure 32: TNM stage grouping

Treatment
I. surgical
• Radical nephrectomy: en bloc removal of kidney, tumor ipsilateral adrenal gland (in upper
pole tumors) and intact Gerota's capsule md paraaortic lymphadenectomy

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• partial nephrectomy: <4 cm tumor or solitary kidney/bilateral tumors

• surgical removal of solitary metastasis may be considered
II. New modalities:
a) Cryoablation.
b) High intensity focused U/S.
c) Radio-frequency ablation.
III. radiation for palliation - painful bony lesion
IV. chemotherapy: NOT effective
V. advanced stage:
• anti-angiogenesis
• (anti-VEGF)
• anti-tyrosine kinase: sunitinib
• anti-IL 2: daclizumab
Nephroblastoma (Wilm's Tumor)
• arises from abnormal proliferation of metanephric blastoma
• 5% of all childhood cancers, 5% bilateral
• average age of incidence is 3 years
• 1/3 hereditary (autosomal dominant) and 2/3 sporadic
• familial form associated with other congenital abnormalities and gene defects
Pathology
• site: arise from one pole of the kidney usually upper pole. bilateral (5%)
• Gross appearance:
1. Huge, pinkish or grayish white in color.
2. pseudo capsule
3. area of hemorrhage and necrosis (Mosaic apperance )
4. infiltrate Renal pelvis late
• Microscopic appearance: two types of tissue:
1. epithelial elements: abortive tubule and glomeruli.
2. C.T elements: muscle fibers cartilage and even bone.
• Histological types:
a. favorable (90%): multilocular cysts, congenital mesoblastic nephroma, rhabdomyosarcoma.
b. unfavorable (10%): anaplasia, rhabdoid tr. of kidney (RTK), clear cell sarcoma.
Staging: It's post-nephrectomy staging
• Stage I: Tumor is confined to the kidney & was completely excised
• Stage II: Tumor extend beyond the kidney but capsule intact, completely excised without residue.
• Stage III: Tumor. resectable but with residue &/or L.N &/or biopsied Tumor & /or rupture.
• Stage IV: Distant hematogenous spread.
• Stage V: Bilateral renal involvement.

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Clinical Features
1. Abdominal mass: large, firm, unilateral (most common presentation in 80%)
2. Hypertension (60%)
3. Flank tenderness
4. Microscopic hematuria
5. Nausea/vomiting
Associated Anomalies with Wilm's tumor:
1) WAGR syndrome:
• Wilm's tumor (50%). 2-Aniridia. 3-Mental Retardation
• Genito-urinary anomalies (hypospadias, cryptorchidism, duplication of collected system). 5-
Deletion of chromosome 11 P13
2) Beckwith-Weidemann syndrome:
microcephaly, macroglossia, macrosomia, hemihypertrophy, Wilm's Tt. (4 – 10%)
3) Drash syndrome: Wilm's Tr., nephropathy, Gut anomalies
4) Isolated aniridia (30%)
5) Isolated hemihypertrophy,
6) Isolated Gut anomalies.
DD:
1. Neuroblastoma
2. Hepatoblastoma.
Investigations
• For diagnosis
3. U/S (pelvi-abdominal) ± percutaneous needle biopsy.
4. CT scan (spiral): asses tumor response to chemo and radiotherapy.
5. Plain urinary tract (PUT): soft tissue shadow with crescentic calcification.
6. IVU: displaced pelvi-calyceal system (rarely invaded).
7. Ascending pyelogram to diagnose early changes in the pelvis.
8. Renal angiography to differentiate cysts from solid swelling (now replaced by CT).
9. Urine analysis: hematuria.
10. Catecholamines are within normal.
• For staging
a. CXR.
b. Bone scan.
c. Pelvi-abdominal U/S.
Treatment
• always investigate contralateral kidney
• treatment of choice is radical nephrectomy ± radiation ± chemotherapy
Prognosis
• generally good; overall 5-year survival about 80%
• metastatic disease may respond well

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Neuroblastoma
Malignant tumor of the neural crest (supra-renal gland, sympathetic chain)
incidence: < 2 years.
Clinical picture:
1. It is the most common abdominal tumor in children
2. Abdominal mass:
3. irregular
4. may cross the midline.
Investigations:
Laboratory:
• Urine analysis.
• VMA (Venyl Mandelic Acid) HVA (Homo-Valinic Acid).
b- Imaging:
• U/S.
• C.T
• MRI.
• X-ray → diffuse calcification.
c- Metastatic:
• Bone marrow aspiration.
• Bone Survey.
• Chest X-ray.
• Brain Scan.
Treatment: Multi-modal → Surgery + Chemotherapy + Radiotherapy

Carcinoma of the Renal Pelvis and Ureter

Epidemiology
▪ rare. account for 496 of all urothelial cancers
▪ frequently multifocal, 2-596 are bilateral
▪ M:F=3:1
▪ relative incidence- bladder : renal :ureter = 100:10:1
Pathology
▪ papillary urothelial cell carcinoma (UCC); 85% (othen include squamous cell. adenocarcinoma)
▪ UCC of kidney md ureter are histologically similar to bladder UCC
Risk Factors
▪ smoking
▪ chemical exposure (industrial dyes and solvents)
▪ analgesic abuse (acetaminophen, ASA, and phenacetin)
▪ Balkan nephropathy (chronic interstitial nephropathy in countries such as Serbia, Montenegro.
Romania. Bulgaria)

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Clinical Features
a. gross hematuria (70-90% of patients)
b. microscopic hematuria
c. flank pain
d. dysuria
e. flank mass caused by tumor or associated hydronephrosis
Investigations
Cytology: detection of Mg. cells in urine sample aspirate from ureter or pelvis of the affected side.
Imaging:
1- IVU(Intraluminal filling defect) 2- U/S, CT & MRI
3- Retrograde uretero-pyelography. 4- Ureteroscopy.
Treatment
(1) Nephro-ureterectomy with excision of bladder cuff: - It's the standard ttt.
(2) Segmental ureterectomy & uretero-vesical re-implant: for distal ureter tumor.
(3) Renal sparing procedure:
• Indication: 1- Solitary kidney. 2- Bilateral disease. 3- low grade, non invasive tr. 4- CRI
• Types: 1 - Tumor resection. 2-Fulguration. 3-Laser ablation.
• Then local chemotherapy (mitomycin) or BCG.
• Long term follow up with images & ureteroscope is mandatory.
(4) treatment of metastatic tumors: chemotherapy → platin-based regimens.

Bladder cancer
Incidence:
• Bladder cancer is the second most common genitourinary neoplasm
• The peak incidence is in persons from 50 to 70 years old
• male-to-female predominance of 3:1.
Etiology:
1. Industrial toxins (orthoaminophenols). Continuous contact with aniline dyes, a-
naphthylamine, 4-aminobiphenyl, and benzidine used in the rubber,leather, textile, and dye
industries.
2. Cigarette smoking
3. Other risk factors include cyclophosphamide, alkylating agents such as thiotepa, and
phenacetin-containing analgesics. Radiotherapy of the pelvis is also a risk factor for bladder
cancer.
Pathology
• Tumor classification
1. Transitional cell carcinoma accounts for more than 90% of all cases of bladder cancer.
a) Papillary transitional cell carcinoma appears as an exophytic frondular lesion. The size
and number of lesions vary. This is the most common form of transitional cell carcinoma in
the bladder. Most of these tumors are small and noninvasive.

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b) Sessile transitional cell carcinoma appears as a less frondular, more solid lesion with a
broad base. These tumors have a greater tendency to be invasive.
c) Carcinoma in situ appears as flat, nonpapillary, somewhat erythematous epithelium; it may
occur in association with an exophytic lesion or separately from it. The presence of
carcinoma in situ is an indicator of increased biologic aggressiveness. Papillary or sessile
tumors are more likely to recur or invade when associated with carcinoma in situ.
2. Squamous cell carcinoma accounts for 8% of cases of bladder cancer and is usually associated
with chronic irritation of the urothelium (e.g., schistosomiasis, bladder calculi, foreign bodies).
3. Adenocarcinoma accounts for 1% of cases and is associated with chronic infection, bladder
exstrophy, or urachal remnants in the dome of the bladder. It tends to be mucus-secreting tumors.
4. Others: several types of small-cell carcinoma, sarcoma, melanoma, and carcinoid tumors.
• Staging: TNM staging of bladder carcinoma (figure 33)
Tx Primary tumor cannot be assessed
T0 No evidence of primary tumor
Ta Non-invasive papillary carcinoma
Tis Carcinoma in situ (flat disease)
T1 Tumor invades sub epithelial connective tissue
T2 Tumor invades muscularis propria (detrusor):
T2a = inner half
T2b = outer half
T3 Tumor invades beyond muscularis propria into perivesical fat:
T3a = microscopic
T3b = macroscopic
T4a Tumor invades any of: prostate, uterus, vagina, bowel
T4b Tumor invades pelvic or abdominal wall
Nx Regional (iliac and para-aortic) lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single lymph node below the common iliac bifurcation
N2 Metastasis in a group of lymph nodes below the common iliac bifurcation
N3 Metastasis in a common iliac node
Mx Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis present

Figure 33: The T staging of bladder cancer.

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• Grading:
GI → highly differentiated (good prognosis)
GII → moderately differentiated
GIII → poorly differentiated (anaplastic)
• Spread:
1. Direct spread:
• Intrinsic → to the wall of U.B.
• Extrinsic → to rectum, vagina, uterus, prostate, pelvic wall
2. Blood spread: Liver, Lung, Bone and Brain.
3. Lymphatic spread:
→ obturator L.N → internal iliac L.N → common iliac L.N → presacral L.N → para-aortic L.N.
Diagnosis
Clinical Features
Symptoms
1. hematuria (key symptom: 85-90% at the time of diagnosis)
2. pain (50%)
3. clot retention
4. asymptomatic
5. storage urinary symptoms - consider carcinoma in situ
6. palpable mass on bimanual exam -+ likely muscle invasion
7. obstruction of ureters ± hydronephrosis and uremia (nausea, vomiting and diarrhea)
8. metastases:
• hepatomegaly, lymphadenopathy, bone lesions
• lower extremity lymphedema if local advancement or lymphatic spread
Signs:
• General: search for distant metastasis.
• Local: - Bimanual exam.: (P.V or P.R + abd. hand) → for ant. bladder mass.
DRE (P.R): for staging.
EUA → Examination under anaesthesia.
Investigations
A. Laboratory:
1. Urine analysis: microscopic hematuria
2. Urinary cytology.
3. Flow cytometry is the computerized analysis of DNA content in exfoliated cells.
4. Other urine tests. Bladder tumor antigen (BTA, Bard) and NMP22 (Matritech)
B. Radiologic examinations.
1. KUB (Plain X-ray) show:Soft shadow (mass( and Calcification in B.
2. Pelvic U.S: bladder mass
3. The IVU demonstrates a filling defect in the bladder

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4. Spiral CT with contrast.

5. MRI
C. Cystoscopy. the entire bladder mucosa must be carefully inspected. Biopsy of the primary
lesion should be accompanied by biopsies of adjacent, normal-appearing areas to rule out
multicentric involvement.
D. Metastatic work Up: Chest X-ray , bone scan, determination of alkaline phosphatase, and
liver function tests

Staging procedures
1. Cystoscopy: documents the location, size, and appearance of any bladder tumor
2. Transurethral resection of bladder tumor (TURBT), endoscopic resection of tumor performed under
anesthesia, to remove as much tumor as possible and assess the degree of muscle invasion.
3. Bimanual examination is performed under anesthesia before and after TURBT; it allows assessment of
tumor size and any fixation to surrounding pelvic organs or the pelvic side wall.
4. Pelvic US may help determine the extent of local invasion. The transurethral and transrectal probes may
provide better staging.
5. CT of the pelvis may detect nodal metastases greater than 2 cm in size and provide gross assessment
of the extent of local disease.
6. MRI better staging procedure for muscle-invasive disease.
7. Metastatic work up

Treatment
A. Superficial (non muscle invasive) disease: Tis, Ta, T1
1. TURBT (Endoscopic Resection) → "Ta" Trans-urethral resection of bladder tumor.
2. Adjuvant intravesical Chemotherapy & immunotherapy → "Tis and T1
• Chemotherapy → Adriamycin, Mitomycin, Thiopeta.
• Immunotherapy → BCG
follow up: By regular cystoscopy + urine cytology. For early detection of Recurrence.
NB :
• 75% of TCC are superficial. May needed cystectomy in select patients
• S.C.C / adenocarcinoma are considered as invasive.
B. Invasive disease: T2a, T2b, T3
A. Radical cystectomy with urinary diversion
We remove:
1. Bladder & its peritoneal cover.
2. Distal ureter.
3. In ♂ → distal vas deferens, seminal vesicle, whole prostate & prostatic urethra. In ♀ →
tubes, uterus, upper 1/3 of vagina)
4. Regional L.N (Ext. & Int. iliac L.N)
5. Urethra if involved.
B. irradiation in selected cases
C. advanced/metastatic disease: T4a, T4b, N+, M+
initial combination systemic chemotherapy ± Irradiation ± surgery

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Urinary Diversion
Indications:
1. Congenital: ectopia vesica with failed repair.
2. Traumatic: vesico-uretero-vaginal fistula.
3. Infection: Bilharzia, TB.
4. Malignancy: muscles invasive cancer bladder.
5. Functional: neurogenic bladder.
Methods:
A. Non continent: as Ileal loop conduit:
✓ Ileal segment connected to lower ends of ureter & then to skin by stoma.
✓ Urine collecting bag attached to skin to collect / evacuate bladder.
B. Continent:
1. Rectal diversion: (e.g. ureterosigmoidostomy)
✓ Urine collects in colon & controlled by anal sphincter.
✓ Very high incidence for complication (esp. hyperchloremic acidosis)
2. Ileocaecal bladder (continent cutaneous diversion)
✓ Caecum & terminal ileum are isolated.
✓ Caecum is closed & the 2 ureters are impacted into it.
✓ The terminal ileum is opened to the skin.
✓ Controlled by ileocaecal valve which open only when patient pass a catheter.
3. orthotopic or neobladder diversion.
✓ Ileal segment is implanted in the same site of removed UB & depend on the external urethral
sphincter.
✓ It's better as it simulates normal bladder.
Complications:
A. General (Metabolic):
1. ↑ loss of K.
2. Hyperchloremic metabolic acidosis →due to digestion of urea by bacteria into NH4 → (↑
H+ → metabolic acidosis), CL → absorbed (hyperchloremic)
B. GIT complications:
1. Ileum resection → nutritional deficiency esp. vit B12.
2. Multi Vit. deficiency.
3. Activation of pro-carcinogens → active carcinogen → cancer intestine
(adenocarcinoma)
e.g. Nitrite / Nitrate → colonic bacteria → Nitrosamine (active carcinogen)
C. UT complications:
1. Incontinence of continent diversion.
2. Obstruction → hydronephrosis.
3. Infection (pyelonephritis)
4. Stone formation.
5. Renal failure (if bilateral).

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Prostate Cancer
Incidence:
▪ PC is the second most common malignancy in male adults as well as the second most
common cause of cancer-related deaths.
▪ At the age of 50, about 15% of prostates contain islands of cancer; by the age of 80, the figure
is nearly 100%.
▪ PC is 50% greater in blacks than in whites and relatively uncommon in Asians.
Etiology:
1. Genetic Influences. The risk for development of prostate cancer is increased two to three
times if a father or brother has had the disease.
2. Hormonal factors. Virtually all prostate cancer cells exhibit some degree of androgen
dependence.
3. Chemical factors. Workers in the rubber, fertilizer, and textile industries have increased rates
of prostate cancer, as do men continuously exposed to cadmium.
4. A diet high in saturated fat and cigarette smoking have also been suggested to have an
association with prostate cancer.
Pathology:
▪ Histological types
1. Glandular:
▪ Adenocarcinoma (95%)
▪ Squamous cell carcinoma and transitional cell carcinoma rarely.
2. Stromal: Rhabdomyosarcoma, Leiomyosarcoma, Fibrosarcoma.
▪ Site: (of adenocarcinoma)
a) Peripheral zone (70 %) More than 95% of PC are adenocarcinomas arising
b) Transitional zone (20 %) from prostatic acinar cells at the periphery of the gland.
This contrasts with BPH, which develops from inner peri
c) Central zone (10%) urethral tissues.
▪ Grading:
✓ Prostate cancer exhibits a wide variety of histologic appearances.
✓ The Gleason system is the most widely used today because it has the best clinical correlation.
✓ Gleason established five grades of glandular morphology (Figure 34). The two most prominent
glandular patterns are graded from 1 to 5. The sum of these two grades will range from 2 to
10, with 2 representing the most differentiated and 10 representing the most anaplastic tumors.
✓ There is a rough correlation between the Gleason grade and the biologic behavior of the tumor.

Figure 34 : The Gleason system.

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▪ Route of spread.
a) Direct:
− Intrinsic: involve the rest of prostate.
− Extrensic: upward→ UB, ureter.
− downward→ urethra.
− laterally→ sciatic nerve & iliac blood vessels.
− forward→ pubic bone.
− backward → rectum "but very late & rare due to presence of Denonvilliers' fascia between
prostate and rectum..
b) lymphatic: to the external iliac (obturator group), internal iliac, and presacral nodes.
Occasionally, the supraclavicular nodes are involved via the thoracic duct.
c) Hematogenous: spread to bone, lung, liver, and kidneys occurs late in the disease.
▪ Staging (TNM classification)
T (primary tumor)
TX - Primary tumor cannot be assessed
T0 - No evidence of primary tumor
T1a - Tumor incidental histologic finding in less than or equal to 5% of tissue resected
T1b - Tumor incidental histologic finding in greater than 5% of tissue resected
T1c - Tumor identified by needle biopsy T2 - Tumor confined within prostate
T2a - Tumor involving less than or equal to half of a lobe
T2b - Tumor involving more than half of a lobe but not more than 1 lobe
T2c - Tumor involving both lobes
T3 - Tumor extending through the prostatic capsule; either no invasion into the prostatic apex
or invasion into, but not beyond, the prostatic capsule
T4 - Tumor fixed to or invading adjacent structures other than seminal vesicles (eg, bladder
neck, external sphincter, rectum, levator muscles, pelvic wall)
N (nodes)
NX - Regional lymph nodes cannot be assessed
N0 - No regional lymph node metastasis
N1 - Metastasis in regional lymph node or nodes
M (metastasis)
MX - Distant metastasis cannot be assessed bone is the commonest site of
M0 - No distant metastasis metastasis in cancer prostate
1- lumbar vertebra. 2- pelvic bone. 3- head
M1 - Distant metastasis
of femur. 4- thoracic spine, sternum, skull &
✓ M1a - Nonregional lymph node(s) head of humerous.
5- Ribs.
✓ M1b - Bone(s)
Tumours which prefer bone metastasis are:
M1c - Other site(s) - Cancer thyroid → skull.
- Cancer breast → lumbar vertebrae.
- Cancer prostate → above 5 bony sites

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Diagnosis
Symptoms of local disease
• with PSA screening, most prostate cancers are diagnosed at an asymptomatic stage.
• When symptoms do occur, diseases other than prostate cancer may be the cause. For
example, urinary frequency, urinary urgency, and decreased urine stream often result from
BPH.
Symptoms of advanced disease
• Weight loss and loss of appetite
• Anemia
• Bone pain, with or without pathologic fracture
• Neurologic deficits from spinal cord compression
• Lower extremity pain and edema due to obstruction of venous and lymphatic tributaries by
nodal metastasis
• Uremic symptoms can occur from ureteral obstruction caused by local prostate growth or
retroperitoneal adenopathy secondary to nodal metastasis.
Physical Examination
• Cancer cachexia
• Bony tenderness
• Lower-extremity lymphedema or deep venous thrombosis
• Adenopathy
• Overdistended bladder due to outlet obstruction
• Neurologic examination, including determination of external anal sphincter tone, should be
performed to help detect possible spinal cord compression. Findings such as paresthesias
or wasting are uncommon, however.
Digital rectal examination
A nodule, asymmetry, difference in texture, and bogginess are important clues and should be
considered in conjunction with the PSA level
DD:
▪ BPH
▪ Other causes of nodular prostate:
- T.B prostatitis. - Cancer prostate.
- B prostatitis. - Calcification.
▪ From other causes of retention & haematuria.
Investigations
Laboratory:
A. Prostate-specific antigen (PSA)
▪ a glycoprotein produced only by prostate cells. Thus, it is specific to the prostate but not to
prostate cancer.
▪ normal level less than 4 ng/ml elevated level suggesting prostate cancer
▪ measured total serum PSA is a combination of free (unbound) PSA (15%) and compl.exed
PSA (85%)

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▪ PSA levels have been measured in many ways: PSA density, PSA velocity, age-specific
PSA, free PSA.
▪ Advantages of PSA measurement:
1. screening asymptomatic men (in conjunction with digital rectal examination);
2. staging prostate cancer,
3. therapeutic decision making: patients with serum PSA levels <10.0 ng/mL are most likely to
respond to local therapy
4. disease monitoring, follow response to radical prostatectomy and radiotherapy.
5. outcome prediction
B. Prostatic acid phosphatase: useful in detecting metastatic disease and in monitoring
therapy.
Imaging
1. Transrectal ultrasonography (TRUS) valuable in assessing the presence and extent of
prostate cancer and guide biopsy procedures.
2. Plain X ray: of chest, pelvic and spine to detect metastasis
3. Bone scanning:
• detecting metastatic disease
• 80% are osteoblastic lesions and 5% osteolytic; the rest are mixed
• Phosphate labeled with technetium 99m is rapidly taken up by bone.
• Bone scans are more sensitive than skeletal radiography.
• increased uptake occurs in arthritis, fractures, Paget's disease, and
hyperparathyroidism and after recent trauma.
4. CT can assess gross local extension and nodal metastases larger than 2 cm.
5. Molecular staging. Polymerase chain reaction amplification can detect circulating PSA
messenger ribonucleic acid (mRNA) in the blood or bone marrow of patients with known
metastatic disease.
6. Endorectal coil MRI
Pelvic lymphadenectomy for staging.
Prostate biopsy. under guidance of TRUS. indicated in:
✓ A palpably suspicious DRE regardless of PSA level
✓ PSA >4.0 ng/mL
✓ PSA greater than the patient’s age-specific range
✓ Increased PSA velocity particularly in the setting of a strong family history of prostate
cancer.
Treatment.
1. Watchful waiting: used for older men with small well differentiated tumor who do not
have signs or symptoms or have other medical conditions and for men with life expectancy
more than 10 years .
2. Radical prostatectomy: A surgical procedure to remove the prostate, surrounding
tissue, seminal vesicles and lymph nodes. in fit patients with localized cancer. complications
include: urinary incontinence, impotence.

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two types of radical prostatectomy:

o Retropubic prostatectomy : open or Laparoscopic
o Perineal prostatectomy.
3. Radiation therapy:
• used in locally advanced cancer and in unfit patients. two types:
a) External radiation therapy
b) Internal radiation therapy: a radioactive substance sealed in needles, seeds, wires,
or catheters that are placed directly into or near the cancer.
• Radiation therapy can cause impotence and urinary problems.
• radiation may be used in bone metastasis to relief pain.
4. Cryosurgery: a treatment that uses an instrument to freeze and destroy prostate cancer cells.
5. Hormone therapy:
used for patients with advanced cancer or localized cancer and patient unfit for surgery or radiation.
the cancer prostate is an androgen sensitive tumor. Hormone therapy for prostate cancer may
include the following:
A. Orchiectomy: a surgical procedure to remove both testicles, the main source testosterone. it
may cause impotence and decreased libido.
B. Luteinizing hormone-releasing hormone agonists can stop the testicles from making
testosterone. Examples are leuprolide, goserelin, and buserelin.
C. Antiandrogens block the action of testosterone. Examples are flutamide, bicalutamide.
D. Drugs that can prevent the adrenal glands from making androgens include
ketoconazole and aminoglutethimide.
E. Estrogens: can prevent the testicles from making testosterone. However, estrogens are
seldom used today in the treatment of prostate cancer because of the risk of serious side
effects including DVT.
7. Chemotherapy
8. Bisphosphonate therapy as zoledronate, reduce bone disease when cancer has spread to
the bone.
9. Treatments for bone pain include the following:
• Pain medicine.
• External radiation therapy.
• Strontium-89 (a radioisotope).
• Bisphosphonate therapy.
• Corticosteroids.
10. Transurethral resection of the prostate (TURP): to relieve symptoms caused by a tumor in
patients cannot have a radical prostatectomy.

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Renal Transplantation
Options of treatment of end stage renal failure:
(1) Renal transplantation.
(2) Dialysis: - Hemodialysis (through A-V fistula)
- Peritoneal dialysis (by Tencoffs catheter)
→ Renal transplantation is better with the following advantage over dialysis:
1) Belter quality of life: - ↓ time. -↑ work. -↑ sexual performance
2) more economic.
Causes of end stage renal failure:
Adult:
1. chronic glomerulonephritis (commonest)
2. HTN.
3. Diabetic nephropathy.
4. Adult Polycystic kidney.
Child:
1) Nephropathy.
2) Obstructive uropathy (with progressive hydronephrosis, with gradual loss of function):
Post. urethral valve. - BNO. - Neurogenic bladder.
Types of donor
1) Cadaveric (heart beating)
2) Cadaveric (non-heart beating)
3) Living-related.
4) Live unrelated
Contraindications of Renal transplantation:
Absolute:
1) Active systemic renal disease, i.e. SLE.
2) HIV or other active infection.
3) Active malignancy.
4) History of metastatic cancer or cancer with a higher recurrence risk (i.e. lymphoma).
5) Significant cardiac disease (previous MI, coronary artery bypass graft (CABG), angina).
6) pregnancy
Relative:
1) Age: usually transplantation is done when there's life expectancy ≥ 10 y.
2) viral hepatitis: dialysis is used till the ptn either cured or converted to sero –ve
Immunosuppressive drugs: Any drug may be used in:
- Induction.
- Maintenance.
- Treatment of rejection (usually high dose steroid in acute rejection)
Drugs include:

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(1) Azathioprine (Imuran)

- Mech. of action: - B.M depression → pancytopenia → ↓ Th cells.
- S.E.: - ↓ leucocytic count. - anemia.
- ↓ platelets. - used in maintenance therapy.
(2) Corticosteroids:
- Mechanism: suppression (specific, non-specific) of immune response.
- used in all types (maintenance, induction, rejection)
(3) ALG / ATG. (Anti-leucocytic / Anti-thymocyte globulin)
- Polyclonal Ab.
- used in: - Induction.
- Rejection (steroid resistant > 5 days)
(4) OKT3 (mono-colonal Ab)
(5) Cyclosporine
- Mech: -Act on IL2 (important for Tc activation)
- so it prevent only Tc & preserve Ts/humoral /nonspecific response
- SE: Nephrotoxic (↑ S. creatinine)
(6) Rapamycine (Rapamune)
- Mech: as cyclosporine
- Advantage: not nephrotoxic
Complications of renal transplantation
Graft dysfunction can occur early or late and may be due to medical or surgical causes.
Rejection
This manifests as renal function deterioration (oliguria, rising creatinine, hypertension, and
proteinuria). Patients may be asymptomatic, have systemic symptoms (fever), or local symptoms,
including graft tenderness or swelling. Investigate with percutaneous renal biopsy.
1) Hyperacute rejection (intraoperatively or within days): due to preformed antibodies to
allograft MHC. Treatment is graft removal. Accelerated rejection (within fi rst week): due to
cellular presensitization. Treatment is intensive antirejection treatment, with temporary
dialysis support.
2) Acute allograft rejection (occurs in the first 3 months): affects around 20–30% (90% respond
to steroids). Classified as acute cellular rejection (ACR) which is T-cell-mediated or acute
humoral rejection (AHR) which is antibody-mediated. ACR: treat with a steroid bolus. If this
fails, employ intensified immunosuppression, conversion to tacrolimus, and T-cell-depleting
agents. AHR: steroid bolus, conversion to tacrolimus, and IV immunoglobulin treatment.
3) Chronic allograft rejection (months to years): is multifactorial and affects around 30%.
Treatment options include conversion from CNI to mTOR inhibitor, or CNI reduction with
MPA 9 steroid cover.
Other
1) Post-transplant malignancy. Most affect the skin (40%) or lymphatic system (11%).
2) Graft loss due to recurrence of original renal disease.

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3) Urinary tract: urinary leak, ureteric stricture/obstruction, fistula, stones, perinephric

collections (lymphocele, haematoma, urinoma, abscess).
4) Vascular complications: renal artery stenosis or thrombosis, renal vein thrombosis,
pseudoaneurysm, A–V fistula, atheromatous vascular disease.
5) Drug toxicity.
6) Infection.
7) Diabetes (thought to be due to the use of corticosteroids and tacrolimus).
8) Hypertension.
Results of renal transplantation
*Patient survival after 1 y → 90%
*Graft survival: 1y → 90%; 5ys → 60%; 10ys → 40%
→ due to chronic rejection

Voiding Dysfunction
• two phases of lower urinary tract function:
1. Storage phase - bladder filling and urine storage
• accommodation and compliance
• no involuntary contraction
2. Voiding phase - bladder emptying
• coordinated detrusor contraction
• synchronous relaxation of outlet sphincters
• no anatomic obstruction
 voiding dysfunction can therefore be classified as:
• failure to store - due to bladder or outlet
• failure to void - due to bladder or outlet
• three types of symptoms: storage (formerly known as irritative), voiding (formerly known as
obstructive), post-void
Failure to Store: Urinary Incontinence
Definition: involuntary leakage of urine
Etiology
1) Urgency incontinence:
a. Detrusor over activity:
• CNS lesion, inflammation/infection (cystitis, stone, tumor), bladder neck obstruction (tumor,
stone), BPH
b. Decreased compliance of bladder wall:
• CNS lesion, fibrosis
• Sphincter/urethral problem
2) Stress urinary incontinence (SUI):
a. Urethral hypermobility

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1. Weakened pelvic floor allows bladder neck and urethra to descend with increased intra-
abdominal pressure
2. Urethra is pulled open by greater motion of posterior wall of outlet relative to anterior wall
3. Associated with childbirth, pelvic surgery, aging, levator muscle weakness
b. Intrinsic sphincter deficiency (ISD)
• Pelvic surgery, neurologic problem, aging and hypoestrogen state
c. Intrinsic sphincter deficiency and urethral hypemobility can co-exist
Epidemiology
• variable prevalence in women: 25-45%
• F:M=2:1
• more frequent in the elderly, affecting 5-15% of those living in the community and 50% of
nursing home residents
Table 9: Urinary Incontinence: Types and Treatments

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Male infertility
▪ Infertility affects up to 15 per cent of couples.
▪ A male factor is solely responsible in about 20 per cent of infertile couples and contributory in
30–40 per cent of cases.
▪ Azoospermia is found in 15–20 per cent of the infertile male population, and in 10 per cent the
sperm density is below 1 million/ml.
Causes of male infertility can be classified into three major groups:
 non-obstructive infertility (60 %): inadequate sperm production by the testes:
1- Hormonal abnormalities
- Idiopathic isolated gonadotropin deficiency
- Kallmann syndrome
- thyroid abnormalities
- hyperprolactinemia
- Brain tumors
- head injuries
- radiotherapy
2- Genetic causes
- Y chromosome microdeletions,
- aneuploidy and chromosomal translocations.
- Klinefelter’s syndrome (47 XXY),
3- Varicocele
4- Undescended testes
5- Exposure to gonadotoxins
6- Iatrogenic causes
7- Orchitis
8- Testicular torsion
9- Testicular trauma
10- Testicular tumors
11- Autoimmune infertility
12- idiopathic
 obstructive infertility (38 %):
normal sperm production, but there is a blockage in the genital tract
1- Congenital absence of the vas deferens
2- Vasectomy
3- Vasal obstruction
4- Epididymal obstruction
5- Ejaculatory duct obstruction
6- Kartagener syndrome
 Coital infertility (2 %): normal sperm production and patent genital tract; however, infertility
is secondary to sexual dysfunction, which impairs intromission or ejaculation.
1- Erectile dysfunction
2- Premature ejaculation
3- Penile deformities
4- Anejaculation
5- Retrograde ejaculation

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History
1. medical history (past illness, diabetes, trauma, CF, genetic syndromes)
2. surgical history (orchidopexy, cryptorchidism, prostate)
3. fertility history (pubertal onset, previous pregnancies, duration of infertility, treatments)
4. sexual history (erection/ejaculation, timing, frequency, STDs)
5. family history
6. medications (e.g. nitrofurantoin, cimetidine, sulfasalazine, spironolactone, alpha-
blockers)
7. social history (alcohol, tobacco, cocaine, anabolic steroids)
8. occupational exposures
Examination
▪ general examination: to evaluate the secondary sexual characters, such as body hair, fat
distribution and the presence of gynecomastia.
▪ local examination of the genitalia to assess
- testicular size, consistency and the presence or absence of testicular lesion.
- the epididymis is examined to detect swellings that indicate obstruction
- the vasa are palpated to confirm their presence
- exclude the presence of a varicocele.
Investigations
1- Semen analysis At least two tests are
performed, three weeks apart. This is the WHO guidelines for normal semen
baseline investigation for male infertility. The Volume 1.5-5 ml
results of semen analysis provide a guide to pH >7.2
whether or not other investigations are Viscosity < 3 (scale 0-4)
Sperm concentration >20 million/ml
needed. Total sperm number >40million/ejaculate
2- Semen culture Semen culture is indicated in Percent motility > 50%
the presence of chronic infections of the Forward progression >2 (scale 0-4)
Normal morphology >50%, >30%, >14%
genital tract. This is indicated by genital pain,
Round cells < 5 million/ml
painful ejaculation or the presence of white Sperm agglutination <2 (scale 0-3)
blood cells in semen (>5 per high-power field).

3- Male reproductive genetic profile: includes

- karyotype,
- Y chromosome microdeletions
- cystic fibrosis gene mutations.
4- Hormonal profiles:
- The basic hormones that are tested are FSH, LH, prolactin and testosterone.
- Other hormones may be tested if there is a clinical indication.
5- Imaging
a) Scrotal ultrasound and colour Doppler is done to assess the testes and epididymi to
detect their dimensions and exclude the presence of tumors or varicocele.

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b) A transrectal ultrasound: if there is a suspicion of distal genital tract blockage or

abnormality.
c) MRI of the pelvis may help in diagnosing obstructions and abnormalities in the distal
genital tract. also help in locating the testes in cases of undescended testes.
d) Vasography (assess patency of vas deferens)
6- Immunologic studies (antisperm antibodies in ejaculate and blood)
7- Testicular biopsy
Treatment
• lifestyle
i. regular exercise, healthy diet
ii. eliminate lifestyle habits described above
• medical
i. endocrine therapy
ii. treat retrograde ejaculation discontinue anti-sympathomimetic agents, may start a-
adrenergic stimulation (phenylpropanolamine, pseudoephedrine, or ephedrine)
iii. treat underlying infections
• surgical
1- varicocelectomy (if indicated) Terminology
(A)spermia - complete lack of semen
2- vasovasostomy (vasectomy reversal)
(Asthenozoo)spermia - reduced sperm motility
3- epididymovasostomy
(Azoo)spermia - absence of sperm cells in semen
4- transurethral resection of blocked ejaculatory (Hyper)spermia - large semen volume
ducts (Hypo)spermia - small semen volume
5- assisted reproductive technologies (ART) (Oligozoo)spermia - few spermatozoa in semen
a- sperm washing + intrauterine insemination (Necrozoo)spermia - dead or immobile sperms
(IUI) (Teratozoo)spermia - sperm with abnormal morphology
b- in vitro fertilization (IVF)
c- intracytoplasmic sperm injection (ICSI)

Figure 35. Infertility Workup

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Penile Complaints
Peyronie's Disease
Definition
• Benign curvature of penile shaft secondary to fibrous thickening of tunica albuginea
• Commonly on dorsal surface resulting in upward curvature of erect penis - may occur at any site
Etiology
a. Exact etiology unknown
b. Trauma/repeated microtrauma  inflammation  fibrosis
c. Familial predisposition
d. Related to diabetes mellitus, vascular disease, autoimmunity, dupuytren's contracture
e. Role of vitamin e deficiency. beta-blockade, elevated serotonin
Clinical Features
• Penile curvature and pain with erection
• Penile shortening and poor erection distal to plaque
Treatment
1. Depends on pain and interference with intercourse
2. Watchful waiting (spontaneous resolution in up to 50%)
3. Vitamin e, potassium paraaminabenzoate (potaba) -limited efficacy
4. Intra lesion verapamil
5. Surgery if stable disease, significant deformity and failed medical. therapy
• excision of plaque ± prosthesis
Priapism
Urological emergency
Definition
• Prolonged unwanted erection lasting >4 hours
• Tumescence (swelling) of corpora cavernosa (often painful) with flaccid glans penis (no corpora
spongiosum involvement)
Classification
1) Low-flow (most common): reduced / absent cavenosal blood flow  hypoxia, acidosis
 ischemia
2) High-how: unregulated arterial flow with normal tissue oxygenation
Etiology
• Primary - 60% idiopathic
• Secondary:
1. Thromboembolic: including
a) Sickle cell,
b) Thalassemia,
c) Total parenteral nutrition,
d) Dialysis,

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e) Leukemia,
f) Solid tumors
2. Neurogenic-
a) Spinal cord injury
b) Autonomic neuropathy
3. Traumatic
a) Cavenosal artery laceration
b) Arterio-venous fistula
4. Medication
a) Intracavernosal drug injection
b) Alpha-blockers,
c) Anticoagulants.
d) Antidepressant,
e) Antipsychotics
f) Anxiolytic,
g) Cocaine, marijuana. Alcohol
Treatment
• Treat reversible causes (e.g.leukophorms if leukemia, treat sickle cell crisis)
• High flow often self-limited - observation vs. Arterial embolization
• low flow:
1. Urgent need decompression via needle aspiration of blood
2. Phenylephrine injection into the corpora cavernosa.
3. Shunt creation between cavenosum and spongiosum if no response within 1hour
Complications: erectile dysfunction due to corporal fibrosis if treatment delayed (50%)
Phimosis
Definition
• Inability to retract foreskin over glans penis
• May be caused by balanitis (infection of glans), often due to poor hygiene or congenital
• Normal congenital adhesions separate naturally by 1-2 years of age
Treatment: circumcision, dorsal slit, proper hygiene (trial of topical corticosteroids in children)
Complications; balanoposthitis (inflammation of prepuce), paraphimosis, penile cancer
Para-phimosis
Urological emergency
Definition: foreskin caught behind glans leading to edema -+ unable to reduce foreskin
Treatment:
• Squeeze edema out of the glans with manual pressure (analgesia required)
• Pull on foreskin with fingers while pushing on glans with thumbs
• If fails, perform dorsal slit or circumcision
• Elective circumcision for definitive treatment (paraphimosis tends to recur)
Complications: infection, glans ischemia, gangrene

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Erectile Dysfunction (ED)

Definition
consistent (>3 months duration) or recurrent inability to obtain or maintain an adequate erection for
sexual performance
Physiology
▪ Erection involves the coordination of psychologic, neurologic, hemodynamic, mechanical and
endocrine components
▪ Nerves: sympathetic (t11-12), parasympathetic (s2-4), somatic [dorsal penile/pudendal nerves
(s2-4)]
▪ Erection ("point")
parasympathetics  release of nitric oxide (no)  increased cgmp levels within corpora
cavernosa leading to:
1. Arteriolar dilatation
2. Sinusoidal smooth muscle relaxation -+ increased arterial inflow and compression of penile
venous drainage (decreased venous outflow)
▪ Emission ("shoot")
1. Sensory afferents from glans
2. Secretions from prostate, seminal vesicles, and ejaculatory ducts enter prostatic urethra
(sympathetics)
▪ Ejaculation ("shoot")
1. Bladder neck closure (sympathetic)
2. Spasmodic contraction of bulbo-cavernosus and pelvic floor musculature (somatic)
▪ Detumescence
Sympathetic nerves, norepinephrine, endothelin-1 -+ arteriolar and sinusoidal constriction
 penile flaccidity
Classification
a) Psychogenic (10%)
b) Organic (90%)
Etiology (IMPOTENCE)
1. Iatrogenic: pelvic surgery/pelvic radiation
2. Mechanical: Peyronie's, post-priapism
3. Psychological: depression, stress, anxiety, PTSD, widower syndrome
4. Occlusive vascular: arterial (hypertension, diabetes, smoking, hyperlipidemia, peripheral
vascular disease, smoking), venous (impaired vena-occlusion)
5. Trauma: penile/pelvic.
6. Extra factors: renal failure, cirrhosis, COPD, sleep apnea, malnutrition
7. Neurogenic: CNS (e.g. Parkinson's, multiple sclerosis, spinal cord injury, Guillain-Barre
spina bifida, stroke), PNS (e.g. diabetes, peripheral neuropathy)
8. Chemical: antihypertensives, sedatives, antidepressants, antipsychotics, anxiolytics,
anti-androgens (including 5-alpha reductase inhibitors), statins, GnRH agonists, illicit
drugs

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9. Endocrine: diabetes, hypogonadism, hyperprolactinemia, hypo/hyperthyroid

Diagnosis
1. Complete history (sexual, medical, and psychosocial)
2. Self-administered questionnaires (international index of erectile function, sexual health
inventory for men questionnaire, ed intensity scale, ed impact scale)
3. Focused physical exam, including vascular and neurologic examinations
4. Lab investigations - based on clinical picture
a) Risk factor evaluation: fasting blood glucose or hbalc, cholesterol profile
b) Other: tsh, cbc, urinalysis
c) Hypothalamic-pituitary-gonadal axis evaluation: testosterone (free and total), prolactin,
lh, fsh
5. Specialized testing
▪ Non-invasive: nocturnal penile tumescence monitor
▪ Invasive:
a) Intracavernsous injection of papaverine or pge1 - rule out significant arterial or venous
impairment
b) Doppler studies pre- and post-papaverine injection - cavernosal anatomy and arterial flow
evaluation (penile-brachial index <0.6 suggestive of vascular cause}
c) Angiography of pudendal artery post papaverine injection -post-traumatic ED evaluation
only fur possible vascular reconstruction
d) Dynamic cavernosometry and cavernosography- to evaluate leakage from penile veins
Treatment
▪ Lifestyle changes (alcohol, smoking), psychological (sexual counseling and education)
change precipitating medications
Oral medication
1. Sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra): inhibits phosphodiesterase type 5
2. Yohimbine: a-blocker that is best fur psychogenic ED
3. Trazodone: serotonin antagonist and reuptake inhibitor
4. Androgen replacement therapy: if hypogonadism
▪ Vacuum devices: draw blood into penis via negative pressure, then put ring at base of
penis once erect
▪ MUSE: Male Urethral Suppository for Erection - vasoactive substance (PGE1) capsule
into urethra
Invasive:
1. Intracorporal vasodilator injection/self-injection
▪ Triple therapy (papaverine, phentolamine, PGE1) or PGE1 alone
▪ Complications include priapism, Peyronie's plaque and hematoma
2. Implants: malleable or inflatable
3. Vascular surgery: microvascular arterial bypass and venous ligation.

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Premature Ejaculation (PE)

Definition: occurrence of ejaculation prior to when one or both partners desire it
Types:
a) Primary PE: never experienced sexual activity without the presence of premature ejaculation
b) Secondary PE: the individual once had acceptable ejaculatory control, but now experiences
premature ejaculation.
Epidemiology
• 30-70% prevalence
• Most common sexual dysfunction reported in men 18-30 years old, associated with
secondary impotence in men 45-65 years old
Investigations
• Indicated by history and physical
• Testosterone levels if in conjunction with impotence
Treatment
• must rule out and treat any associated general medical conditions.
• referral to psychiatry, couples counseling or sex therapy
• SSRIs have been found to be effective in some cases
• Clomipramine.

Diseases of Testis and scrotum

Embryology:
• Seminiferous tubules → spermatogenesis. Sertoli cells → support.
• Interstitial cells of Leydig → testosterone
• Originate from the genital ridge.
• Descends from the retroperitoneal space to scrotum guided by the gubernaculum
through the inguinal canal & takes 3 sheaths from it
• Levels of descent of testis during intrauterine life:
→ int. inguinal ring → 7th month
→ inguinal canal → 8th month
→ scrotum → end of 8th month
blood supply:
• Arterial:
1. Testicular artery from aorta.
2. Cremastric artery from inf. Epigastric artery.
3. Artery of the vas (inf. Vesical from int. Iliac)
• Venous: Pampiniform plexus → testicular vein.
Rt → IVC
Lt → Lt renal vein

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Imperfect descend of the testis

Types:
A. Cryptoid:
true UDT → arrest of the descend of the testis at any station of its normal pathway of
descent.
• External inguinal ring, (most common)
• Inguinal canal.
• Abdominal
B. Ectopic:
presence of the testis at any site outside the normal pathway of descent.
Common in
✓ Superficial inguinal pouch (lat. To pubic tubercle)
✓ base of the penis.
✓ at other side of scrotum.
✓ behind the bladder in pelvis.
✓ in the thigh.
(C) Retractile:
- it changes its position in & out the scrotum.
- descend when the body is worm & ascend with stress or cold weather due to stimulation of
adrenaline & contraction of cremastric muscle.

Undescended testis (UDT)

Incidence:
- preterm → 30-38%
- full term → 3-4%
- at 1year & adult → 0.8% (so it's surgically corrected at 1 y)
- Familial → 4%
Risk factor:
- The mother has a family history of unexplained newborn deaths or abnormal genitalia.
- The fetus has Down syndrome.
- The mother is younger than 20 or older than 35.The mother has been exposed to pesticides
or other toxic chemicals.
- The mother is in poor health.
Causes of non-descent:
1. defective gubernaculum.
2. hormonal imbalance e.g. 1ry testicular dysfunction, gonadotrophic defect (usually bilateral
UDT)
3. short testicular artery.
4. Inadequacy of inguinal canal.

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The sites of arrest:

- lntra-abdominal.
- inguinal canal. (most common site of arrest).
- Superficial inguinal pouch (very rare): it must be differentiated from retractile testis which is
more common.
- At neck of scrotum
Complications:
1. Psychological
2. Liability to trauma & torsion which may occur intra-uterine leading to vanishing testis
(DD: strangulated hernia).
3. Epididymo-orchitis due to urinary tract anomalies
4. Sterility ln bilateral cases (cryptorchidism)
- Due to injury of the exocrine function of the testis due to destruction & hyalinization of the
seminiferous tubules.
- There is no effect on endocrine function (normal testosterone, normal 2ry sexual characters,
erection, ejaculation "prostatic fluid" & no impotence but Azoospermia)
- This becomes irreversible destruction by the age of 16 years.
5. Liability to malignancy (Seminoma) 30 times more than normal.
This is due to dysgenetic testis (& may affect the patient even after a successful orchiopexy) so
orchiopexy is done only for early detection of malignancy.
6. indirect inguinal hernia is present in about 90% of cases & might be complicated.
Diagnosis:
Clinical:
1. empty scrotum (unilateral or bilateral)
2. Poorly developed scrotum.
3. The median scrotal raphe is deviated towards the affected side.
4. The Testis:
- Usually present in the inguinal canal.
- lt is not well developed.
- Associated other anomalies (hvpospadius)
Investigations:
1. Radiological.
- U/S → diagnose it in inguinal canal.
→ can't diagnose intra-abdominal testis due to gases in the intestine which obscure it.
- CT& MRI
2. Laparoscopic.
3. Laboratory:
- FSH / LH
- to differentiate between 1ry testicular dysfunction & gonadotrophic effect especially if
bilateral UDT.

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Treatment:
(1) Hormonal:
→ pregnyl (gonadotrophin extracted from placenta) • acute abdomen with empty scrotum is
considered as testicular torsion until
→ good till 20% of cases esp. in bilateral UDT.
proved otherwise.
(2) Surgical: orchiopexy • abdominal mass with empty scrotum is
Open or laparoscopic considered as testicular tumor until
proved otherwise.
Aim: descend of the testis.
→ dissect the vas.
• If the testis is palpable: → one stage orchiopexy.
(± incision of post, wall of inguinal canal clipping the inf. epigastric artery)
• If the testis is non-palpable (abdomen):
→ one stage orchiopexy. OR → 2 stage orchiopexy.
If the age of the patient is more than 10 years: orchiectomy may nedded (to avoid cancer)

Testicular Torsion
(Surgical emergency)
Definition
lt is the most common pediatric urologic emergency, in which the testis there is rotation of the testis
& epididymis around the axis of the spermatic cord blocking the blood supply of the testis.
Etiology
Predisposing Factors
1. lnversion of the testis (the most common)
• Anterior lnversion (more common)
2. Polar inversion (epididymis on upper pole associated abnormal tunica vaginalis)
3. lmperfectly descended testis (incomplete or ectopic)
4. Long mesorchium.
5. High investment of the tunica vaginalis (Clapper in a bell effect).
6. Spirally attached cremasteric muscles.
7. Separation of epididymis from body of testis --- torsion around the pedicle between them.
Precipitating Factors: Straining or minor but spontaneous torsion may occur.
Pathology:
• The testis rotates from outside inwards.
• Gangrene occurs within 8-12 hours if the condition is not treated.
Symptoms
1. Pain: sudden severe agonizing pain in scrotum & lower abdomen.
2. Swelling: Testicular swelling.
3. Reflex symptoms; Nausea, vomiting & collapse.
Signs
General: pallor, sweating & tachycardia (up to shock).

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Local : (figure 36)

1. Torsion of imperfectly descended testis:
• The scrotum is empty in the corresponding side.
• The inguinal canal is swollen, tender.
2. Torsion of the complete descended testis:
a) The scrotum:
• Swollen, red & tender.
• Dimple in site of gubernaculum.
• Elevation of the scrotum increase the pain.
b) The cord: twist might be felt on the cord.
c) The testis is:
• High up in position.
• Tender & irreducible. Figure 36: Appearance of
torsion of the testicle.
• Small vaginal hydrocele.
• The crernasteric reflex is absent in the affected side.
DD. acute scrotum
1. Mumps orchitis, which never attacks boys before puberty;
2. Epididymitis, which is always secondary to obvious urinary infection;
3. Fat necrosis, which is occasionally seen in infants;
4. Cancer, which in older boys and men can present with inflammation.
5. Torsion of an appendix testis, which cannot be distinguished from torsion of the testis
without exploration.
6. Strangulated inguinal hernia: irreducible, no impulse on cough,
7. Idiopathic scrotal edema.
Investigations:
• It is important to untwist the testicle before it dies from ischemia, and no investigation should
be allowed to delay surgical exploration.
• A Doppler or radioisotope scan may show absence of arterial circulation in the testicle but
is justified only if it will not delay matters.
Treatment
• The testicle is explored through a transverse scrotal incision. The tunica vaginalis is opened,
and the testicle is untwisted.
• All too often it is necrotic and must be removed.
• Because torsion occurs in about 10% of cases on the other side, the other testicle should be
fixed
Torsion of the appendix testis:
Tiny cysts are usually present at the upper pole, one on the epididymis (Wolffian duct origin), the
other on the testis (Mullerian duct origin). Apart from being of interest to embryologists either can
twist on its stalk, exactly mimicking torsion of the testicle and equally requiring urgent exploration

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Varicocele
Definition:
A varicocele is an abnormal enlargement of the pampiniform venous plexus in the scrotum
Incidence
• Varicoceles develop slowly and may not have any symptoms.
• They are most frequently diagnosed when a patient is 13–30 years of age.
• They occur in 20% of all males
Causes:
A. Primary varicocele: unknown cause
• occurs when the valves within the veins along the spermatic cord do not work properly.
• This results in backflow of blood into the pampiniform venous plexus.
• Venous backflow increases vein diameter because of excessive pressure, and testosterone
pooling
• Pooled blood is toxic and may cause damage to the testicles and veins
 Why primary varicocele more common on left side than right?
1. Pelvic colon passes on the left testicular vein.
2. The left testicular vein is longer than the right
3. The left testicular vein opens at right angle in the left renal vein.
4. Left suprarenal gland secretes adrenaline near the mouth of the left testicular vein
5. The left common iliac vein is crossed by the right common iliac artery this causes higher
pressure in the veins of the vas & cremasteric vein
6. The left testicular artery arches over the left renal vein in 16% of cases.
8. Valves at the end of the left testicular vein are usually malformed while on the right side are
usually competent.
B. Secondary varicocele: is due to compression of the venous drainage of the testicle.
1. A pelvic or abdominal malignancy as renal cell carcinoma
2. Nutcracker syndrome: the superior mesenteric artery compresses the left renal vein.
3. retroperitoneal fibrosis or adhesions
Diagnosis:
Symptoms
1. Pain: increase by prolonged standing or hot weather
2. Dragging pain: due to relaxation of Dartos and cremasteric muscles.
3. Throbbing pain in case of thrombophlebitis.
4. Swelling: scrotal swelling.
Signs
• General: Patient is usually tall & thin & visceroptosis may be present.
• Local:
1. Left side of the scrotum hangs lower than the right side.
2. Scrotal skin may have dilated veins.

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3. Scrotal neck test fullness at the neck of the scrotum.

4. Varicosity is felt as a bag of worms.
5. Thrill on cough may be felt due to turbulence of blood flow.
6. Swelling which disappears when patient lies down scrotum is elevated.
7. Small secondary hydrocele can be detected by pinching test.
Complications
1. Subfertility (20 % of cases) due to decrease motility of sperms (asthenospermia) Why?
Thermal Theory:
a- The temperature difference between scrotum & rectum has to be 2.5oc.
b- lf less this might impair spermatogenesis.
c- Even if unilateral due to transmission of heat by contact with the other side.
2. Thrombosis and thrombophlebitis
3. Secondary hydrocele: Due to chronic congestion of the testis.
4. Testicular atrophy (very late)
• Chronic congestion→ venous pressure →  arterial blood supply→ testicular atrophy.
• The testis becomes softer in consistency and smaller in size.
5. Neurosis
DD: lnguino-scrotal swelling.
Grading:
• Subclinical (not palpable): detected by Doppler reflux on Valsalva maneuver
• Grade I: present only with Valsalva
• Grade II: present without Valsalva
• Grade III: visible through the skin
Investigations
a- Laboratory
Semen analysis (for medico-legal importance)) stress pattern. (asthenospermia and
oligospermia)
b- Radiological
1. Duplex scan: detects reversed blood flow & bilaterality.
2. Scrotal or Transrectal U/S:
• Best test to evaluate the seminal vesicles and ejaculatory ducts.
• Valuable in visualizing and grading varicocele.
3. Abdominal U/S → to exclude 2ry varicocele e.g. hypernephroma.
Management:
A. Conservative Treatment
• Reassurance of the patient as the condition is usually self limiting around the
• age of 40 years (Psychological support).
• Scrotal support (may cause subfertility due to high temperature).
• Sedatives.

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• Avoid constipation, pelvic congestion.

• Cold baths to the scrotum.
B. Operative Treatment: (Varicocelectomy)
Indications:
• Failure of medical treatment (Severe symptoms that can't be tolerated).
• Complications:
1. Subfertility.
2. Recurrent thrombophlebitis
3. Failure of medical commission.
4. Neurotic patient.
Approaches:
1. Inguinal approach
2. Sub inguinal approach
3. Scrotal approach
4. Retroperitoneal approach (Palomo)
5. Laparoscopic varicocelectomy
C. Percutaneous venous embolization

Testicular Tumors
Etiology; Unknown but there is predisposing factors:
3) Congenital: undescended testis.
4) Traumatic: horse riding trauma → so usually occur in high socioeconomic level.
5) Inflammatory: viral orchitis (mumps)
6) Hormonal: foetal exposure to maternal estrogen
7) Racial: white Caucasians > blacks (may be HLA association)
Classification:
A. Primary:
1. Germ cell tumors, (spermatogonia)
2. Non-germ cell tumors, (sertoli cell & interstitial cell of Leydig)
B. Secondary:
1. Leukemia.
2. Lymphoma.
3. Metastasis (prostate, GIT)
Germ cell Tumors
Incidence: 90-95%
Types:
A. Seminoma. 60 %
B. Non Seminoma 40 %

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A. Seminoma
Site: - arise from seminiferous tubules in the mediastinum of testis. - it is adenocarcinoma.
Characters:
- Highly radiosensitive & chemo sensitive.
- It may secrete hcg (b-hcg).
- Age: 30 - 40 y.
- Seminoma metastases → 15 - 20 %
Types:
1. Classic seminoma (85 %) '
2. Anaplastic seminoma (10 %)
3. Spermatocystic seminoma (5 %)
B. Non-Seminoma
Characters:
- Resistant to radiotherapy but sensitive to chemotherapy.
- Aggressive tumor.
- Secrete HCG & α-feto protein.
- Age: 10-30y.
- Non seminoma metastases → 70 - 75 %
Types:
1. Embryonal carcinoma (20 %)
2. Teratoma (5%): - arise from embryonic totipotent cell in rete testis.
adult type (malignant) - children (benign)
3. Choriocarcinoma (1%): secretes HCG.
aggressive. - hematological spread.
4. Yolk sac tumor (1%): secretes α-fetoprotein.
5. Mixed cell type (40 %): teratocarcinoma 25 %
Diagnosis:
Clinical picture:
a- symptoms:
1. Asymptomatic (10 %) (painless swelling)
2. Symptomatic → dull aching pain. → acute pain (hemorrhage)
3. Metastasis symptoms
• Headache & blurring of vision.
• Cough, hemoptysis.
• Spontaneous fracture of bone.
4. Gynecomastia.
b- Signs:
1. regular non tender swelling in scrotum.
2. Abdominal mass → retroperitoneal L.N.

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→ Tumor in undescended testis.

3. 2ry hydrocele.
Complications:
4. Fungating & ulceration.
5. Infection & hemorrhage.
6. 2ry hematocele.
1. Distant metastasis
2. Gynecomastia.
3. Cachexia.
DD:
from other causes of testicular & scrotal swelling (hydrocele, haematocele, varicocele,
hernia...... ect)
Investigations:
1) For Diagnosis:
a) Laboratory: Tumor markers
Def.: these are markers measured by radio-immune assay & are essential to monitor
response to treatment. e.g. α-fetoprotein, β-HCG, LDH.
b) Radiology:
• U/S
• X-ray
• CT
2) For Distant metastasis:
- Chest: plain X-ray. - Liver: abdominal U/S.
- Brain: brain scan. - Bone: bone survey.
3) Pre-operative investigations:
- CBC. - ECG. - Kidney function. - liver function.
(E) Spread:
1- Direct: - rare.
epididymis, spermatic cord & scrotum.
2- Blood: lung, bone, liver, brain
3- Lymphatic:
• retroperitoneal L.N. → para-aortic L.Ns. → cysterna chyli → thoracic duct Virchow's gland.
• if epididymis is involved → internal iliac L.N.
• if scrotum is involved → superficial inguinal L.N.
(F) Staging:
• Stage 1: Tumor is confined to testis.
• Stage II: retro-peritoneal L.N.
IIa → L.N mass < 5 cm in diameter.
IIb → L.N mass 5 - 10 cm in diameter.
IIc → L.N mass > 10 cm in diameter.
• Stage III:

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IIIa → L.N above diaphragm.

IIIb → distant metastasis.
Treatment:
Main operation is high inguinal orchiectomy.
(through inguinal incision → cord is ligated & divided at level of deep ring)
A) Seminoma: (Highly radio-sensitive)
- Stage I & IIa → orchiectomy + Radiotherapy (2500 - 3000 rads)
- Stage IIb & IIc → orchiectomy + Chemotherapy with 2 cycles of BEP
(Bleomycin, Etopside & cisplatine) or Radiotherapy.
- Stage III → orchiectomy + chemotherapy with 4 cycles of BEP.
OR Radiotherapy.
OR Retroperitoneal L.N dissection.
B) Non Seminoma: orchiectomy +
- Stage 1 → surveillance (follow up) OR retro-peritoneal L.N dissection.
- Stage II a & b → chemotherapy ( 2 cycles BEP)
- Stage IIc & III → chemotherapy (4 cycles BEP)
N.B: Follow up by Tumour markers & C.T
-Prognosis: 5 year survival rate is:
Seminoma Non Seminoma
Stage 1 & II 95% 90%
Stage III 80 % 60%

Table 10: Differentiating between Scrotal Masses

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