Surgery part 2 pdf - د.أحمد

Lec:6

Surgery

Hematuria

DEFINITION

More than three red blood cells are found in

centrifuged urine per high-power field microscopy

( > 3 RBC/HP).

Normal urine:

no red blood cell or less than three red blood cell

According to the amount of RBC in the urine, hematuria can be classified as:

microscopic hematuria: normal colour with eyes

gross hematuria: tea-colored, cola-colored, pink or even red

ETIOLOGY

#Diseases of the urinary system—the most common cause

a. Vascular



arteriovenous malformation



arterial emboli or thrombosis



arteriovenous fistular



nutcracker syndrome



renal vein thrombosis



loin-pain hematuria syndrom



cogulation abnormality



excessive anticogulation

b. Glomerular



IgA nehropathy



thin basement membrane disease (incl.Alport syndrome)



other causes of primary and secondary glomerulonephritis

c. Interstitial



allergic interstitial nephritis



analgesic nephropathy



renal cystic diseases



acute pyelonephritis



tuberculosis



renal allograft rejection

d. Uroepithelium



malignancy



vigorous excise



trauma



papillary necrosis



cystitis/urethritis/prostatitis(usually caused by infection)



parasitic diseases (e.g. schistosomiasis)



nephrolithiasis or bladder calculi

e. Multiple sites or source unknown



hypercalciuria



hyperuricosuria

#System disorders

a. Hematological disorders



aplastic anemia leukemia



allergic purpura hemophilia



ITP (idiopathy thrombocytopenic purpura)

b. Infection



infective endocarditis



septicemia



epidemic hemorrhagic fever (Hantaan virus)



scarlet fever (



-hemolytic streptococcus)



leptospirosis (leptospire)



filariasis (Wuchereria bancrofti, Brugia malayi)

c. Connective tissue diseases



systemic lupus erythematosus (SLE)



polyarteritis nodosa

d. Cariovascular diseases



hypertensive nephropathy



chronic heart failure



renal artery sclerosis

e. Endocrine and metabolism diseases



gout



diabetes mellitus

#Diseases of adjacent organs to urinary tract



appendicitis salpingitis



carcinoma of the rectum



carcinoma of the colon



uterocervical cancer

#Drug and chemical agents



sulfanilamides anticogulation



cyclophosphamide mannitol

#miscellaneous



exercise “idopathic” hematuria

CLINICAL FEATURE



Color 

depends on the amount of red blood cell in the urine and the pH (see slide 4)

normal: light yellow, pH 6.5



pH  acidic: more darker (brown or black) // alkaline: red

DIFFERENTIAL DIAGNOSIS



Polluted urine: menstruation



Drug and food: phenosulfonphtha lein (PSP),uric acid, vegetable



Porphyrism: porphyrin in urine (+)



Hemoglobinuria
hemolysis
soy-like, very few RBC under the microscopy
occult blood test (+)

HEMOGLOBINURIA

RBC abnormality



Defects of RBC membrane structure and function (hereditary spherocytosis)



Deficiency of enzymes (favism)



Hemoglobinopathy (thalassemia)



PNH

Mechanical factor (artificial heart valve), infection

or mismatched blood transfusion

LABORATORY TESTS

#Three-glass test

Method: collecting the three stages of urine of a patient during micturition

Result:



the initial specimen containing RBC—the urethra



the last specimen containing RBC—the bladder neck and trianglar area,
posturethra



all the specimens containing RBC—upper urinary tract, bladder

#Phase-contrast microscopy

To distinguish glomerular from post glomerular bleeding



post glomerular bleeding: normal size and shape of RBC



glomerular bleeding: dysmorphic RBC (acanthocyte)

ACCOMPANIED SYMPTOMS



Hematuria with renal colic

o renal stone, ureter stone
o if with dysuria, miction pause or staining to void: bladder or urethra stone



Hematuria with urinary frequency,urgency and dysuria

o bladder or lower urinary tract (tuberculosis or tumor)
o if accompanied by high spiking fever, chill and loin pain: pyelonephritis



Hematuria with edema and hypertension

o glomerulonephritis
o hypertensive nephropathy



Hematuria with mass in the kidney

o neoplasm
o hereditary polycystic kidney



Hematuria with hemorrhage in skin and mucosa

o hematological disorders
o infectious diseases



Hematuria with chyluria

o filariasis

Lec:7

Surgery

Trauma in Urology

#Renal injuries

RI account for 1-5% of all traumas



BLUNT – car, sport accidents –majority!



PENETRATING –gunshots, stab wounds

AAST classification

(American Associaton for the Surgery of Trauma)

1. Contusion, non-expanding subcapsular haematoma, no laceration
2. Non-expanding perirenal haematoma, cortical laceration < 1 cm deep, no urinary

extravasation

3. cortical laceration > 1cm, no u.extravasation
4. Laceration: through corticomedullary junction into collecting system OR vascular:

segm. renal artery or vein injury with contained haematoma

5. Shattered kidney OR major vascular injury (renal pedicle injury or avulsion)

1,2 = minor injuries – 85-95% 3,4,5 = major injuries

Diagnosis



Trauma history, past renal injury, surgery or renal abnormalities



examination (haematuria, flank pain, flank abrasions, rib fractures, abd.tenderness)



Urinalysis, blood count, creatinine



Primary imaging -> USG!!



Enhanced abdominal CT !



Intraoperative one/shot IVP



Second/line imaging – MRI,Scinti,Angiography

Treatment



WW – grade I-III in stable patients



Surgery (all penetrating injuries, in blunt injuries if: major blood loss, unstable
patient, urinary extravasation, nonviable kidney, pedicle avulsion,...)

Complications

1. Early: Haemorrhage, retroperitoneal urinoma, haematoma, abscess
2. Late: Hypertension, AV fistula, calculi, PNF, late bleeding

#Ureteral injuries

1.  Pelvic surgery (uro, gyn, gen.s.)
2.  Pelvic/abdomninal masses
3.  PID
4.  post RT
5.  Penetrating injury

Clinical findings



Flank pain, tenderness



Sepsis



Hydronephrosis



Paralytic ileus



VV / UV fistula / watery discharge via vagina



Labs /CRP,Leu,urinalysis,creatinine

Imaging

1.  USG
2.  IVU  / enhanced CT !
3.  APG
4.  Radionuclide scanning

Treatment

1. First-line urinary diversion !!! (nephrostomy, ureteral stenting)
2. Reconstructive surgery /reanast., reimpl., substitutions, crossed diversion,

autoTPL…/

#Bladder injuries

1.  direct external force, road accidents
2.  iatrogenic / gyn-obs, uro, sur/
3.  intraperitoneal disruption
4.  extraperitoneal disruption

Clinical finding



Haematuria



Pelvic , abd. pain (pelvic fracture presented in 90% of bladder inj.)



Haemorrhage, Shock



Acute abdomen !!! (intraperit)

Imaging

1.  Pelvic & Abdominal USG
2.  Cystography (300ml) !
3.  CT cystography

Treatment

1. Extraperit. – bladder drainage (epi, catheter)
2. Intraperit. – open surgery required!

#Urethral injuries

1.  Posterior/ Anterior urethra
2.  Laceration, transection, contusion
3.  External forces (falls astride an object, perineal blow, …)
4.  Iatrogenic (catheter, uro )

Posterior urethra

assoc. w/ pelvic fractures - > prostate avulsion from the membranous u. -> apical
displacement of the prostate - > Pelvic urinoma, haematoma

Diagnostic radiology (DR Exam.) :

1.  blood at the urethral meatus
2.  X- Ray  (pelvic fracture)
3.  Urethrography

Treatment

1. drainage (suprapubic cystostomy)
2. immediate surgery (suspected bladder lacerations, disruptions, massive pelvic

bleeding, etc.)

3. delayed surgery (>3 months after the injury)

Complications after delayed surg.repair

1.  ED                     30-35%
2.  Incontinence       5%
3.  Stricture              5%

Anterior urethra

1.  straddle injury
2.  iatrogenic instrumentations
3.  self-instrumentations

Clinical findings



perineal, penile, scrotal haematoma



urethral bleeding



normal DRE

Diagnosis:

Urethrography

Treatment

1.  suprapubic cystostomy
2.  surgical repair (in case of urethral laceration, bleeding w/o extravasation)
3.  follow-up (stricture!)

#Penile & Scrotal injuries

1. Penile fracture (sex. intercourse -> disruption of the tunica albuginea -> haematoma,

CAVE: urethral injury)

2.  Penile constriction – rings
3.  Penile amputation
4.  Scrotal  injury  (hematocele,  testicular  disruption,  torsion,  skin  avulsion,  traumatic

amputations)

Lec:8

Surgery

Neurogenic bladder

NEUROGENIC BLADDER

Description of NB

Dysfunction of the urinary bladder due to disease of the central nervous system or
peripheral nerves involved in the control of micturition.

Epidemiology

Prevalence of voiding dysfunction (VD) is reported for specific conditions:

1.  Cerebrovascular accident: 20-50%
2.  Parkinson disease: 35-70%
3.  Multiple sclerosis: 50-90%
4.  Diabetes mellitus: 5-60%

Risk factors

1.  Neurologic disease, injury, or congenital malformation
2.  DM
3.  Radical pelvic surgery

Genetics

Genetic diseases that may be associated with NB include:

1.  Muscular dystophy
2.  Hereditary spastic paraplegia
3.  Neurofibromatosis
4.  Familial dysautonomia

Classification of Neurogenic Bladder

Most often done using urodynamic classification scheme:

1. Neurogenic DO (hyperreflexia): uncontrolled reflex bladder contraction

o Loss of inhibitory impulses from cortical centers; primitive reflex pathways

2. Detrusor underactivity (areflexia):

o Interruption of sacral reflex arc; no detrusor contraction
o Typically low-pressure storage of high volume up to 500 ml

3. DSD: abnormal reflexive sphincter contraction during involuntary detrusor

contraction

o Functional BOO, elevated intravesical pressure
o Secvondary damage: pressure, infection, urolithiasis

Pathophysiology

Voiding center include:



Higher centers (suprapontine):

o Function: inhibit sacral micturition center
o Predicted type of VD with suprapontine lesion would be detrusor overactivity (DO)

due to loss of inhibition on sacral micturition center



Pontine micturition center (PMC):

o Function: coordinates sphincter relaxation during bladder contraction
o Predicted type of VD with lesion between pontine and sacral micturition center is DO

and detrusor-sphinecter dyssynergia (DSD)



Sacral micturition center (SMC):

o Function: mediates reflex and voluntary bladder contraction
o Predicted type of VD with lesion of SMC is detrusor underactivity or areflexia

Peripheral lesions: VD is variable including:

1.  Detrusor underactivity
2.  Impaired bladder sensation
3.  Impaired sphincteric function

o Upper motor neuron lesion: spastic, uninhibited: injury above spinal cord micturition

center

o Lower motor neuron lesion: flaccid, atonic, areflexic: injury in the pelvic nerves or

spinal micturition center

o Spinal shock: Immediately after injury, regardless of the level, there is a stage of

flaccid paralysis with numbness below the level of the injury that lead to bladder
overfilling to the point of overflow incontinence & rectal impaction. It lasts few
weeks up to 6 months .

o Autonomic dysreflexia (AD): A potentially life threatening condition that can cause

rapid, extreme BP elevation, headache, diaphoresis, bradycardia, sweating, nausea
and piloerection in patients with spinal cord lesions at and above the 6th thoracic

vertebral level (T6). Causes: noxious stimulus below the level of injury such as:
bladder distention, bowel distention, or pain activate sympathetic neurons causing
unopposed reflex sympathetic activity

Commonly associated conditions

A. CNS diseases:

1.  CVA
2.  SCI
3.  TM
4.  MS
5.  PD
6.  Normal-pressure hydrocephalus

B. PNS disease:

1.  Radical pelvic surgery:
2.  AP resection
3.  radical hysterectomy
4.  DM
5.  IDP
6.  Spinal stenosis
7.  GB syndrome

C. Neural tube defects (NTD)

D. Static disorders of development: as CP

Diagnosis

History:

1. Voiding symptoms:

o  Irritative or obstructive
o  UI: urge, stress
o  Spastic Neuropathic Bladder:

 The severity of symptoms depends on the site and extent of the lesion as well as

the length of time from injury.

 OAB syndrome: urinary urgency with or without UUI, usually associated with

frequency and nocturia

o Flaccid (Atonic) Bladder:

 principal urinary symptom is urine retention with overflow incontinence. Male

patients lose their erections.

 Extremity reflexes are hypoactive or absent. Sensation is diminished or absent

2. History of any risk factor:

  neurologic disease: onset, duration
  DM
  Congenital disorders: NTD , CP .

3. Method of urinary management:

  Volitional or reflex voiding
  Condom catheter urinary collection
  CISC
  Indwelling urethral or suprapubic catheter
  Crede, Valsalva voiding

4. UTI:

 Severity of infection: febrile, hospitalization, IV antibiotics required
 Frequency of recurrence

5. Urolithiasis :

  episodes
  surgical intervention
  calculus composition

6. AD: SCD above T6

Physical Examination

1.  HTN: renal dysfunction, AD
2.  Generalized edema: severe renal insufficiency
3.  Palpable flank mass: HN
4.  Flank tenderness: ureteral obstruction, pyelonephritis
5.  Abdominal mass: distended bladder, urinary retention
6.  UI: stress maneuvers, Marshall test
7.  Testicular mass: epididymitis/epididymo-orchitis, secondary abscess
8.  prostate: size: BPH may coexist with NB dysfunction
9.  Sacral abnormalities: sacral dimple or tuft of hair, sacral agenesis

10. Neurologic: sacral root, perianal sensation, sensory level, anal tone, sphincter

control, bulbocavernosal, knee, ankle, and toe reflexes.

Diagnostic tests

A. Blood studies:

1. Serum chemistry: RFT
2. CBC: elevated WBC, secondary anaemia due to ↓ renal function or chronic infection

B. Urinalysis:

1.   Proteinuria: renal dysfunction
2.  pyuria, nitrite, leukocyte esterase: acute or chronic infection
3.  Hematuria: infection or lithiasis

Imaging

Imaging is most important in pts with risk factors for upper tract compromise:

A. DSD: particularly males who void reflexively

B. Impaired bladder compliance

1. Renal US: to screen for calculus, HN, or mass

2. KUB: radio-opaque calculi

3. Excretory urography:

 Delayed excretion of contrast with high urinary-storage pressures
 HUN: marked elevation of intravesical pressure (ie, NDO/DSD) or calculi

4. VCUG: for VUR, urethral abnormaity

5. Nuclear medicine renal scan: Sequential studies detect deterioration of renal function

6. MRI: bladder neck and posterior urethra

Diagnostic procedures

1) Cystourethroscopy: degree of trabeculation, diverticuli, bladder capacity, stone, ureteral

orifice competency, integrety of BN and external sphincter, Cx of chronic catheterization
and infection

2) Urodynamics: Technique used to obtain graphic recording of activity in UB, urethral

sphincters , & pelvic musculature .

Components include:

1.  Uroflowmetry.
2.  Cystometry.
3.  Urethral pressure profile.
4.  EMG.

Necessary to determine effective urologic management for all pts with neurogenic lower
urinary tract dysfunction

Differential Diagnosis

1.  Cystitis.
2.  Chronic urethritis.
3.  Vesical irritation secondary to stone.
4.  Interstitial cystitis.
5.  Cystocele.
6.  Infravesical obstruction (LUTS).

Treatment

1. UDS are essential to detrmine lower urinary tract function or dysfunction and to plan

urologic Mx

2. Control intravesical pressure and empty the bladder effectively: in order to protects

upper tracts, preserve renal function, continence, & control infection



Spontaneous voiding with continence is possible with NDO controlled medically



Voiding by trigger technique: tapping the abdomen suprapubically, tugging on the
pubic hair, squeezing the penis, or scratching the skin of the lower abdomen,
genitalia, or thighs.



Urinary darinage: SCIC or external collection appliance (condom)



SCIC: most effective Rx; requires low storage pressure



Indwelling cath: avoid due to Cx (UTI, erosion, calcui, etc)

Treatment of spinal shock

1. Bladder drainage: must be instituted immediately and maintained: by clean self

intermittent catheterisation(CSIC), indwelling catheter or suprapubic cystostomy

2. Increase fluid intake to 2 – 3 L/day

3. Prophylaxis for calculus formation by reducing calcium & oxalate intake & decrease vit

D from diet

Spastic neuropathic bladder

Medication:

First line:

1-- Anticholinergics: to improve urinary storage
pressure/↓ involuntary contraction:

a. Oxybutynin

b. Hypscyamine

c. Tolterodine

2-- 1-adrenergic blockers:↓internal sphincter
resistance, lower voiding pressure; ineffective for
DSD, may control symptoms of AD:

a. Doxazosin

b. Terazosin

c. tamsulosin

Second line:

1-- Botulinum toxin:

a. Injection into external sphincter

for DSD: short-lived , requires
repeated inj.

b. Inj. Into detrusor muscle for DO:

Duration of action is 3-9 mon
requires repeated inj.

2-- Vanilloid agents instillation:
capsaicin and resiniferatoxin:

Suppress uninhibited involuntary
detrusor contraction

Surgery

1. Endoscopic sphincter ablation or stenting



Only males with DSD



Requires condom catheter

2. Augmentation cystoplasty: using intestinal segment to enlarge the badder: Intermittent

cath for urine drainage

3. Cystectomy with continent urinary reservoir and catheterizable stoma:



For pts with limited dexterity specially in females



Ileal or colon pouch



Continent cathetrizable stoma (appendix or terminal ileum)

4.  Ileovesicostomy (bladder chimney): for those unable to perform CSIC (quadriplegia)
5.  Cystectomy with ileal conduit
6.  Sacral rhizotomy at S3-4: Conversion of the spastic bladder to a flaccid bladder
7.  Sacral neuromodulation (bladder pacemaker): of the sacral nerve roots to accomplish

bladder evacuation in selected cases

Flaccid neuropathic bladder

1.  Crede maneuver (manual suprapubic pressure) accompanied by straining
2.  Bladder training & care , voiding every 2hr
3.  CSIC every 3-6 hr
4.  Parasympathomimetic drugs like bethanecol chloride ( Urecholine), 5 – 50 mg every 6-

8hr

5. Surgery:

o TURP in hypertrophied bladder neck or BPH
o Implanting an artificial sphincter.

Complications

1.  Recurrent UTI: cystitis, periurethritis, prostatitis, epididymoorchitis, pyelonephritis
2.  Calculus formation
3.  Urinary retention
4.  HUN
5.  Renal impairment and amyloidosis
6.  Neoplastic transformation: associated with chronic catheter
7.  Urethral erosion
8.  Sexual dysfunction
9.  AD

Mx of AD

1. Acute management: removal of triggering stimulus by bladder drainage or rectal

decompression

2. Chronic treatment:



blockers



calcium channel blocker



Botulinum toxin injection

3. Prophylaxis before cystoscopy: Oral nifedipine (20mg), 30 min before cystoscopy as

prophylaxis

Prognosis:

Proper urologic Mx greatly improves QoL in pts with NB dysfunction

Follow up

Annual evaluation in high risk pts may include:

1. UDS
2. imaging: typically renal US

Serum creatinine

Lec:9

Surgery

Renal Parenchyma Neoplasm

Adenocarcinoma

(Renal cell carcinoma) :



Adenocarcinoma of kidney represent about 3% of adult cancer



Male-female ratio 2-1



equal in whites and blacks

Etiology



The cause is unknown.



There are various theories:

o  Environmental and occupational factors
o  Cigarette smoking
o  Chromosomal aberration and tumor suppressor genes(chromosome 3 and 8)

Aquired cystic disease

Pathology



The tumor occur in equal frequency in either kidney , originates in the cortex , grow
out in the perinephric tissue



it is characteristically yellow to orange because of high lipid content

Pathogenesis



RCC is a vascular tumor , tend to spread by Direct invasion , Vascular invasion is
through renal vein



About 1\3 of patients have metastasis at presentation



The most common site of distant metastasis is lung oppposite kidney Followed by
liver, bone

Tumer staging



Stage 1: tumor is confined within kidney parenchyma



Stage II : tumor involve perinephric fat but is confined within Gerota,s fascia



Stage IIIa : tumor involve the main renal vein or inferior vena Cava



Stage IIIb :tumor involve regional lymph node



Stage IIIc : tumor involve both local vessels and regional lymph node



Stage IVa : tumor involves adjacent organs (colon,pancreas,….)



Stage IVb :distant metastasis

TNM Classification

Clinical picture

  It has a wide variety of presentation
  Classic triade :
1.  gross haematuria
2.  Flank pain
3.  Palpable mass
  Occur in about 10-15% of patients, frequently in advanced disease.
  Abd  pain , abd mass,
  (30%) Symptoms of metastasis disease: Dyspnea ,cough ,headache ,bone pain

Paraneoplastic syndrome



Erythrocytosis



Hypercalcemia



Hypertention



Nonmetastatic hepatic dysfunction

  3-10% of RCC present by paraneoplastic syndrome
  RCC is the most common cause of paraneoplastic erythrocytosis
  Hypercalcemia occur in about 20% of patients with RCC
  Hypertention  in  40%

Laboratory findings:



CBC anemia (30%)



High ESR



Haematuria (60%)

Imaging:



IVP 75% accurate



U\S



CT scan it is the leader for diagnosis and staging And detect distant metastasis



Renal angiography



MRI



Fine needle aspiration idicated in :

1. metastatic disease , planned for nonsurgical management

establishing diagnosis in patients who are not surgical Candidate

Differential diagnosis:

1.  Carcinoma of renal pelvis
2.  Renal lymphoma
3.  Adrenal cancer
4.  Benign renal tumor
5.  Renal cysts
6.  Renal abscess

Treatment:



Localised disease : Stage (I, II , IIIa ) –

< Radical nephrectomy



Disseminated disease:

o  30% of RCC are metastatic
o  The role of radical nephrectomy is limited
o  It is a palliative therapy
o  Radiotherapy (RCC is a radioresistant)
o  Chemotherapy  (is also chemotherapy  resistant )

Prognosis is according to stage:



T1 disease 5 years survival 88-100%



T2 T3a 5 years survival 60 %



T3a 5 years survival rate 15-20 %

Benign tumer



Renal adenoma is the most common benign tumor



Renal oncocytoma occur in variant organ ( adrenal, salivary gland, thyroid,…)
represent about 3% of kidney tumor



Angiomyolipoma: is very rare

Bladder carcinoma



Male- female ratio 3-1



Common in wights than in blacks



Is the second most common cancer of genitourinary tract



Average age is 65 years



85% are Localised , 15 % have distant sites

Pathogenesis and Etiology

o Cigarette smoking account for 50 % of men and 30% of women the causative agent

are to be alpha and beta naphthylamine wich are secreates in urine of smokers

o  Occupational exposure to certain chemicals(rubber ,petroleum, printing industries)
o  Cyclophosphamide
o  Artificial sweeeners
o  Calculi and infection
o  Genetic predisposition

Staging

Hystopathology



Papiloma

: is uncommon

o Represent about <2 % of all transiotional cell
o Tumor , has a very good prognosis

 Transitional cell carcinoma:

o  Accounts for 90% of all bladder cancer
o  Appears as papillary exophytic lesion
o  May be sessile or ulcerated

 Non Transitonal cell carcinoma

1- Adenocarcinoma :



Accounts for <2% of bladder cancer



Mucous secreting tumor



Arise along the floor of bladder



Muscle invasion is usually present



5 years survival <40%

2- Squamous cell carcinoma :



Accounts for 5-10% of bladder tumor



Often associated with H\O bilharsial infectionVesical caculi , chr ctheterisation



In Egypt represent about 60% of bladder cancer

3- Undifferentiated carcinoma :



Is rare , represent < 2% of bladder carcinoma



4 mixed carcinoma



Constitute 4-6% of all bladder carcinoma



Composed of transitional , squamous, or Undifferentiated carcinoma

Clinical picture

A – Symptoms :



Haematuria is the presenting symptom in 85-90%

o May be gross or micriscopic
o Intermittent rather than constant



Symptoms of vesical irritability



Symptoms of advanced disease

B - Signs :



The majority of patients have no pertinent physical signs.



patients with advanced disease may have a Palpable mass, Hepatomegaly and
supraclavicular lymph node Indicates advanced disease.

Laboratory findings:



The most common is hematuria



Azootemia in case of ureteral occlusion



Anemia may be a presenting symptom due to chr blood loss and replacement of
bone marrow by metastatic cells.



Urine cytology .

Imaging

Used To:

1-  Evaluate the upper urinary tract
2-  Assess the depth of muscle infiltration
3-  Presence of regional or distant metastasis



IVU: the most common imaging test for evaluation of hematuria



CTscan



Cystourthroscopy

Treatment:



TUR or laser vaporization : For patients with single low grade, noninvasive tumor



Partial cystectomy : For solitary infiltrating tumor (t1-t3) cancer of bladder diverticula



Radical cystectomy : In locally advanced disease

Ureteral and Renal pelvis



Carcinoma of renal pelvis and ureter are rare , Represent about 4% of all utothelial
cancer



Ratio: bladder renal pelvis ureter

51 3 1



Age group > 65 years



Patients with single upper tract carcinoma are at risk of Developing bladder
carcinoma (30-50%) and contralateral Upper tract (2-4%).

Etiology and pathology

As urinary bladder carcinoma

Clinical picture :



Haematuria 70-90%



Flank pain 50%



Irritative symptoms



Weight loss



Flank mass

Laboratory fingings :



Hematuria is identified in majority of cases



Anemia



Elevated liver function

Imaging :



IVU



Retrograde pyelography is more accurate



CTscan identify soft tissue abnormality of renal pelvis



Ureteropyeloscopy allow direct visualization of upper urinary tract

Treatment :



Based on: grade, stage, position and multiplicity



The standard therapy is nephroureterectomy .

Tumor of distal ureter

distal ureterectomy and ureter reimplantation

Lec:10

Surgery

Benign diseases of male genitalia

MALE GENITAL SYSTEM



PENIS



SCROTUM, TESTIS, & EPIDIDYMIS



PROSTATE

PENIS



MALFORMATIONS



INFLAMMATORY LESIONS



NEOPLASMS

MALFORMATIONS OF THE PENIS

ABNORMAL LOCATION OF URETHRAL ORIFICE ALONG PENILE SHAFT

1. HYPOSPADIAS (VENTRAL ASPECT) MOST COMMON (1/250 LIVE MALE BIRTHS)

2. EPISPADIAS (DORSAL ASPECT)

Both MAY BE ASSOCIATED WITH OTHER GENITAL ABNORMALITIES



INGUINAL HERNIAS



UNDESCENDED TESTES

CLINICAL CONSEQUENCES

1.  CONSTRICTION OF ORIFICE
2.  URINARY TRACT OBSTRUCTION
3.  URINARY TRACT INFECTION
4.  IMPAIRED REPRODUCTIVE FUNCTION

INFLAMMATORY LESIONS OF THE PENIS

1-) SEXUALLY TRANSMITTED DISEASES

2-) BALANITIS (BALANOPOSTHITIS)

INFLAMMATION OF THE GLANS (PLUS PREPUCE) ASSOCIATED WITH POOR LOCAL HYGIENE
IN UNCIRCUMCISED MEN



SMEGMA

DISTAL PENIS IS RED, SWOLLEN, TENDER



+/- PURULENT DISCHARGE

3-) PHIMOSIS



PREPUCE CANNOT BE EASILY RETRACTED OVER GLANS



MAY BE CONGENITAL



USUALLY ASSOCIATED WITH BALANOPOSTHITIS AND SCARRING



PARAPHIMOSIS (TRAPPED GLANS)



URETHRAL CONSTRICTION

4-) FUNGAL INFECTIONS : CANDIDIASIS



ESPECIALLY IN DIABETICS



EROSIVE, PAINFUL, PRURITIC



CAN INVOLVE ENTIRE MALE EXTERNAL GENITALIA

NEOPLASMS OF THE PENIS

SQUAMOUS CELL CARCINOMA (SCC)

EPIDEMIOLOGY

1. UNCOMMON – LESS THAN 1 % OF CA IN US MEN
2. UNCIRCUMCISED MEN BETWEEN 40 AND 70

PATHOGENESIS

1.  POOR HYGIENE, SMEGMA, SMOKING
2.  HUMAN PAPILLOMA VIRUS (16 AND 18)
3.  CIS FIRST, THEN PROGRESSION TO INVASIVE SQUAMOUS CELL CARCINOMA

CLINICAL COURSE



USUALLY INDOLENT



LOCALLY INVASIVE



HAS SPREAD TO INGUINAL LYMPH NODES IN 25% OF CASES AT PRESENTATION



DISTANT METS RARE



5 YR SURVIVAL



70% WITHOUT LN METS



27% WITH LN METS

LESIONS INVOLVING THE SCROTUM

1- ) INFLAMMATION : TINEA CRURIS (JOCK ITCH)



SUPERFICIAL DERMATOPHYTE INFECTION



SCALY, RED, ANNULAR PLAQUES, PRURITIC



INGUINAL CREASE TO UPPER THIGH

2- ) SQUAMOUS CELL CARCINOMA



HISTORICAL SIGNIFICANCE



SIR PERCIVAL POTT, 18TH CENTURY ENGLISH PHYSICIAN



CHIMNEY SWEEPS

3- ) SCROTAL ENLARGEMENT

1. HYDROCELE - MOST COMMON CAUSE



ACCUMULATION OF SEROUS FLUID WITHIN TUNICA VAGINALIS



INFECTIONS, TUMOR, IDIOPATHIC

2. HEMATOCELE

3. CHYLOCELE : FILIARIASIS - ELEPHANTIASIS

4. TESTICULAR DISEASE

LESIONS OF THE TESTES



CONGENITAL



INFLAMMATORY



NEOPLASTIC

CRYPTORCHIDISM AND TESTICULAR ATROPHY



FAILURE OF TESTICULAR DESCENT

EPIDEMIOLOGY :



ABOUT 1% OF MALES (AT 1 YR)



RIGHT < LEFT, 10% BILATERAL

PATHOGENESIS

1. HORMONAL ABNORMALITIES

2. TESTICULAR ABNORMALITIES
3. MECHANICAL PROBLEMS

CLINICAL COURSE

1.  WHEN UNILATERAL, MAY SEE ATROPHY IN CONTRALATERAL TESTIS
2.  STERILITY
3.  INCREASED RISK OF MALIGNANCY (3-5X)
4.  ORCHIOPEXY



MAY HELP PREVENT ATROPHY



MAY NOT ELIMINATE RISK OF MALIGNANCY

OTHER CAUSES OF TESTICULAR ATROPHY

1.  CHRONIC ISCHEMIA
2.  INFLAMMATION OR TRAUMA
3.  HYPOPITUITARISM
4.  EXCESS FEMALE SEX HORMONES

THERAPEUTIC ADMINISTRATION

ii.

CIRRHOSIS

5.  MALNUTRITION
6.  IRRADIATION
7.  CHEMOTHERAPY

INFLAMMATORY LESIONS OF THE TESTIS

1.  USUALLY INVOLVE THE EPIDIDYMIS FIRST
2.  SEXUALLY TRANSMITTED DISEASES
3.  NONSPECIFIC EPIDIDYMITIS AND ORCHITIS



SECONDARY TO UTI BACTERIAL AND NON-BACTERIAL



SWELLING, TENDERNESS



ACUTE INFLAMMATORY INFILTRATE

4. MUMPS



20% OF ADULT MALES WITH MUMPS



EDEMA AND CONGESTION



CHRONIC INFLAMMATORY INFILTRATE



MAY CAUSE ATROPHY AND STERILITY

5. TUBERCULOSIS



GRANULOMATOUS INFLAMMATION



CASEOUS NECROSIS

6. AUTOIMMUNE GRANULOMATOUS ORCHITIS



RARE FINDING IN MIDDLE AGED MEN

TESTICULAR NEOPLASMS

EPIDEMIOLOGY



MOST IMPORTANT CAUSE OF PAINLESS ENLARGEMENT OF TESTIS



5/100,000 MALES, WHITES < BLACKS (US)



INCREASED FREQUENCY IN SIBLINGS



PEAK INCIDENCE 20-34 YRS



MOST ARE MALIGNANT



ASSOCIATED WITH GERM CELL MALDEVELOPMENT



CRYPTORCHIDISM (10%)



TESTICULAR DYSGENESIS(XXY)

PATHOGENESIS

1. 95% ARISE FROM GERM CELLS



ISOCHROMOSOME 12, i(12p), IS A COMMON FINDING



INTRATUBULAR GERM CELL NEOPLASMS

2. RARELY ARISE FROM SERTOLI CELLS OR LEYDIG CELLS ; THESE ARE OFTEN BENIGN
3. Lymphoma ; men < 60 yo

WHO CLASSIFICATION OF TESTICULAR TUMORS

ONE HISTOLOGIC PATTERN (60%)
1.  SEMINOMAS (50%)
2.  EMBRYONAL CARCINOMA
3.  YOLK SAC TUMOR
4.  CHORIOCARCINOMA
5.  TERATOMA

MULTIPLE HISTOLOGIC PATTERNS (40%)
1.  EMBRYONAL CA + TERATOMA
2.  CHORIOCARCINOMA + OTHER
3.  OTHER COMBINATIONS

CLINICAL COURSE OF TESTICULAR TUMORS



USUALLY PRESENT WITH PAINLESS ENLARGEMENT OF TESTIS



MAY PRESENT WITH METASTASES

a. NONSEMINOMAS (MORE COMMON) : LYMPH NODES, LIVER AND LUNGS
b. SEMINOMAS : USUALLY JUST REGIONAL LYMPH NODES



TUMOR MARKERS (hCG AND AFP)



TREATMENT SUCCESS DEPENDS ON HISTOLOGY AND STAGE



SEMINOMAS VERY SENSITIVE TO BOTH RADIO- AND CHEMOTHERAPY

DISEASES OF THE PROSTATE



PROSTATITIS



NODULAR HYPERPLASIA



CANCER

PROSTATITIS



ACUTE BACTERIAL PROSTATITIS



CHRONIC BACTERIAL PROSTATITIS



CHRONIC ABACTERIAL PROSTATITIS

ACUTE BACTERIAL PROSTATITIS

ETIOLOGY

SAME ORGANISMS THAT CAUSE UTI as : E coli, OTHER GNR

PATHOGENESIS



ORGANISMS ASCEND FROM URETHRA AND URINARY BLADDER



RARELY, HEMATOGENOUS SPREAD

MORPHOLOGY



ACUTE INFLAMMATION, ESPECIALLY IN THE GLANDS, WITH MICROABSESSES



CONGESTION, EDEMA

CLINICAL COURSE

1.  DYSURIA, FREQUENCY, LOW BACK PAIN, PELVIC PAIN
2.  ENLARGED, EXQUISITELY TENDER
3.  +/- FEVER OR LEUKOCYTOSIS
4.  USUALLY RESOLVES WITH WITH AB RX

CHRONIC PROSTATITIS

ETIOLOGY

1.  MAY FOLLOW ACUTE PROSTATITIS
2.  MAY DEVELOP INSIDIOUSLY
3.  CULTURE POSITIVE (BACTERIAL) : SAME ORGANISMS THAT CAUSE AP
4.  CULTURE NEGATIVE (ABACTERIAL)



MAY BE RELATED TO : CHLAMYDIA TRACHOMATIS , UREAPLASMA UREALYTICUM



MOST COMMON FORM OF CP

MORPHOLOGY



LYMPHOCYTIC INFILTRATE



NEUTROPHILS AND MACROPHAGES



SOME EVIDENCE OF TISSUE DESTRUCTION

CLINICAL COURSE



SIMILAR TO AP ; LESS ACUTE SYMPTOMS , MORE RESISTANT TO AB RX



CBP OFTEN ASSOCIATED WITH RECURRENT UTI

NODULAR HYPERPLASIA

OTHER TERMS USED



GLANDULAR AND STROMAL HYPERPLASIA



BENIGN PROSTATIC HYPERTROPHY (HYPERPLASIA)

EPIDEMIOLOGY



OCCURS IN 20% OF MEN OVER 40



OCCURS IN 90% OF MEN OVER 70

PATHOGENESIS OF NODULAR HYPERPLASIA



PROLIFERATION OF BOTH EPITHELIAL AND STROMAL ELEMENTS



BOTH ANDROGENS AND ESTROGENS MAY PLAY A ROLE



NOT SEEN IN MALES CASTRATED BEFORE PUBERTY



INHIBITORS OF TESTOSTERONE METABOLISM USEFUL IN TREATMENT



RELATIVE INCREASE IN ESTROGENS IN OLDER MEN MAY INCREASE DHT RECEPTORS
IN PROSTATE

CLINICAL COURSE OF NODULAR HYPERPLASIA



SYMPTOMS OCCUR IN ONLY 10% OF MEN WITH NODULAR HYPERPLASIA



HESITANCY



URINARY RETENTION



URGENCY, FREQUENCY, NOCTURIA, UTI



TREATMENT : MEDICAL or SURGICAL



COMMON CAUSE FOR ELEVATED PROSTATE SPECIFIC ANTIGEN (PSA)

CARCINOMA OF THE PROSTATE

EPIDEMIOLOGY



MOST COMMON VISCERAL CANCER

o  ABOUT 70/100,000 MEN IN US
o  200,000 NEW CASES/YR IN US
o  20% ARE LETHAL



SECOND MOST COMMON CAUSE OF CANCER DEATH IN MEN



PEAK INCIDENCE OF CLINICAL CANCER IS 65-75 YO



LATENT CA IS EVEN MORE PREVALENT : >50% IN MEN > 80 YO

PATHOGENESIS

1. HORMONAL FACTORS



DOES NOT OCCUR IN EUNUCHS



ORCHIECTOMY AND/OR ESTROGEN TREATMENT INHIBITS GROWTH

2. GENETIC FACTORS



INCREASED RISK IN FIRST ORDER RELATIVES



BLACKS > WHITES (SYMPTOMATIC CA)

3. ENVIRONMENTAL FACTORS



GEOGRAPHIC DIFFERENCES IN INCIDENCE OF CLINICAL CANCER (NOT OF LATENT CA)



CHANGE IN INCIDENCE WITH MIGRATION

CLINICAL COURSE



OFTEN CLINICALLY SILENT



DIGITAL RECTAL EXAM (DRE)



PROSTATE SPECIFIC ANTIGEN (PSA)

 4 ng/ml IN PERIPHERAL BLOOD

o FREE PSA < 25%



TRANSRECTAL ULTRASOUND



NEEDLE BIOPSY



PROSTATISM (LIKE BPH)



METASTASES ; OSTEOBLASTIC



TREATMENT- SURGERY, RADIATION, HORMONES, CHEMO

STAGING

A (T1) MICROSCOPIC ONLY

B(T2) MACROSCOPIC (PALPABLE)

C(T3 &T4) EXTRACAPSULAR

D(N1-3,M1) METASTATIC

PROGNOSIS DEPENDENT ON STAGE AND HISTOLOGIC GRADE

1. 90% 10 YR SURVIVAL FOR A AND B

2. 10-40% 10 YR SURVIVAL FOR C AND D