OBSTRUCTIVE UROPATHY 2 (PROSTATE)

OBSTRUCTIVE UROPATHY 2
(PROSTATE)
LEARNING OBJECTIVES
Students should be able to :
• Describe the gross anatomy.
• Evaluate the causes of Prostitis
• Understand the pathogenesis of Prostitis
• Explain the management of Prostitis.
• Evaluate the clinical course of
Prostitis.
PROSTATE GLAND
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Retroperitoneal Organ
20 gms in adults
Encircles neck of urinary bladder & urethra
No true capsule
4 biologically and anatomically distinct lobes identified
Central
Peripheral
Transitional
Ant. Firomuscular tissue
PATHOLOGY OF PROSTATE
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Inflammations
Hyperplasia
Tumors
INFLAMMATION
PROSTATITIS IS DIVIDED INTO 4 TYPES
1- Acute Bacterial Prostatitis:
Ac diffuse / focal inflamm
Causative organism
E coli
Enterococci
Staphylococci
C/F:
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Chills, fever, dysuria
Tenderness, bogginess
of gland on rectal examination
Routes:
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Urinary reflux
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Lymph-hematogenous spread
Surgical implantation
Catheterization
Urethral dilation
Resection procedures
Cystoscopy
Diagnosis:
Urine culture
2- Chronic Bacterial Prostatitis:
C/O :
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low back pain
Dysuria
Suprapubic Pain
Perineal Discomfort
Recurrent UTI
or Asymptomatic
Diagnosis:
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WBCs in expressed secretions
Urine culture
Causative Organisms
E coli
Gram –ve cocci
Enterococci
Staphylococci
CHRONIC PROSTATITIS
3- Chronic Abacterial Prostatitis:
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Most common type
Clinically undistinguished from chronic bacterial prostatitis
No H/O Recurrent UTI
>10 WBC s /HPF
Culture Negative
C/O:
C trachomatis
Uroplasma urealaticum
Mycoplasma homis
4- GRANULOMATOUS
PROSTATITIS
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Tuberculous Prostatitis:
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Mycotic/ Fungal granulomatous prostatits:
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Post biopsy granuloma:
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Allergic granulomatous prostatits:
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Calculi & amyloidosis:
BENIGN ENLARGEMENT
NODULAR HYPERPLASIA
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Nodules in periurethral
Hyperplasia of stromal and epithelial cells
Patient is 50 +
Incidence
20% ♂ 40 years of age
70% ♂ 60 years of age
90% ♂ 70 years of age
No direct correlation between histological change and clinical
symptoms
NODULAR HYPERPLASIA
PATHOGENESIS:
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Cell proliferation
Impaired cell death (Main component )
Androgen (Dihydro testosterone) dependant prostatic growth
- 2 5 α reductase coverts testosterone into DHT in
STROMAL cells
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transcription of growth factors
– DHT has more affinity for AR & stronger bonds than
testosterone
NODULAR HYPERPLASIA
Clinical Presentations
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Urinary difficulty
Retention
Dribbling
Frequency
Urgency
Nocturia
Inability to empty bladder- Infections
Difficulty in stopping urine stream
Dysuria
NODULAR HYPERPLASIA
Morphology
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60-100 gms
Transition zone
Predominantly stromal initially, epithelial later
C/S: No true capsule
– STROMAL: pale –grey, tough, no fluid
– EPITH.: yellow-pink, soft, milky white fluid
M/S: NODULARITY
Varibly sized, dilated glands
Glands lined by double layered epith
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Fibromuscular stroma
NODULAR HYPERPLASIA
NODULAR HYPERPLASIA
NODULAR HYPERPLASIA
NODULAR HYPERPLASIA
Complications:
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Hypertrophy
Trabeculation
Diverticulation
Hydronephrosis
UTI
Acute retention
NODULAR HYPERPLASIA
Management
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Lifestyle  decrease fluid intake, moderate alcohol
and caffeine- consumption .
2. Medications
Alpha blockers ( α1-adrenergic receptor antagonists) the most common choice for initial therapy
- relax smooth muscle
5α-reductase inhibitor
3. Surgery
- TURP
CARCINOMA PROSTATE
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Most common type of Ca in men
29% of cancers in USA
9% of cancer deaths
Incidentally diagnosed to aggressive
A disease of men >50 years of age
Uncommon in Asians
High incidence in blacks70 % arise from peripheral zone
Prostate Intraepith Neeoplasia (PIN)
CARCINOMA PROSTATE
ETIOLOGY:
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Environmental factors- fats, lycopenes
Androgens
Genetic 
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Inherited polymorphisms ; relatives, BRCA, 8q24
Epigenetic alterations ;GSTP1
Somatic mutations
CARCINOMA PROSTATE
Microscopy:
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Well differentiated gland pattern (ADENOCARCINOMA)
Small crowded glands with straight luminal borders
Single uniform layer of cuboidal or low coloumnar cells
Outer basal layer absent
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N/C ratio disturbed
Back to back arrangement, little intervening stroma
Less differentiated variant show cell to grow in sheets, nests
and cords.
CARCINOMA PROSTATE
Grading
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It is important as there is good correlation b/w prognosis and
degree of differentiation
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Gleason grading 5 grades on the basis of :
Based on:
1- Glandular pattern
2- Degree of differentiation
GLEASON GRADING
STAGING OF CARCINOMA PROSTATE
CARCINOMA PROSTATE
CLINICAL COURSE:
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Asymptomatic, Incidental finding on Rectal exam or PSA
Urinary symptoms---- advanced cancer
Back pain----- advanced cancer, usually fatal
Digital rectal exam
Trans rectal U/S
Trans rectal Needle biopsy– for Diagnosis
CARCINOMA PROSTATE
Clinical Course:
Prostate Specific Antigen (PSA):
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Most important test for Diagnosis and Management
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Serine protease normally secreted in semen
Minute amounts in serum , normally
Generally 4ng/ml is cutoff for prostate cancer
Serum PSA levels used as cancer detection test; False + &- ve
Refinements in estimation and interpretations, using
– PSA density
– PSA velocity
– Ratio of free and bound PSA
– Age specific references
THANK YOU
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