etiopathology, diagnosis, staging, management

1. CARCINOMA PROSTATE
Presenter:
Dr. Nisanth P
Junior Resident
Dept. of Surgery
1
Moderator:
Dr Farhanul Huda
Additional Professor
Dept. of Surgery

2. THE ENIGMA !
2

3. STORY OF ARJUN SINGH..
3
• Mr. Arjun Singh a 52 year old male patient presented to the OPD for an annual health check up.
• He is the 2nd male child in his family. His father had history of prostate cancer.
• It is his 4th visit to the urologist. His initial visit was at his 40th age.
• At his 1st visit he was made aware of the optional PSA testing and its importance as he has a family
history of prostate cancer.
• His subsequent visits at the age of 45 and 50, he was evaluated with PSA, PSA was less than 1.5ng/ml in
all 3 occasions.

4. • He is healthy, sexually active with no urinary complaints.
• No bone pain or tenderness. His bowel and bladder habits are normal.
• Not a diabetic or hypertensive.
4

5. On further evaluation, he has no pallor, icterus or Lymphadenopathy.
CVS, RS within normal Limits
P/A no organomegaly
• On Digital rectal examination , There is no prostatomegaly, or any palpable lesions in prostate.
• His biochemical parameters are normal except PSA .
• PSA was 4.5ng/ml.
• His PSA value was at previous visit 2 years back was 1.5ng/ml.
• PSA velocity 1ng/ml/year
5

6. OVERVIEW
◦ EPIDEMIOLOGY
◦ ETIOPATHOLOGY
◦ DIAGNOSIS INCLUDING SCREENING
◦ STAGING
◦ MANAGEMENT
◦ RECENT UPDATES
6

7. EPIDEMIOLOGY
◦ 3RD most common cancer world wide in both sexes, 2nd most common cause of death in males
(GLOBOCAN 2018)
◦ African Americans-60% higher incidence
◦ What is cull effect??
◦ Mortality rate is decreasing (SEER)
◦ Median age at diagnosis: 67 years & death: 77 years
7

8. INDIA: WHERE DO WE STAND?
Shalu Jain et.al
8

9. RISK FACTORS
1. Familial& genetic: BRCA, HOXB13
2. Chronic Inflammation& infection: PIA PIN
3. Estrogens
4. Vitamin D deficiency
5. Smoking
6. Diet: use of statin decreases the risk (Platz et al)
7. Sexual activity: more frequency of ejaculation is protective (Leitzmann et. Al)
8. Obesity (Masko et al)
9

10. Molecular Genetics of Ca Prostate
10

11. TUMOUR MARKERS
BLOOD
• PSA
• PSMA
• Human kallikrein 2
• endoglin
• CTCs
URINE
• Prostate Cancer Antigen 3
• TMPRSS2: ERG gene fusion
• Metabolomics (Sreekumar
A et al)
• Annexin A3
• Micro RNA
TISSSUE BASED
• α methyl CoA Racemase
• epigenetics
11

12. PSA
◦ Human kallikrein peptide 3 (hk3)
◦ Zymogen secreted by prostatic epithelium, found in prostatic & seminal fluids
12

13. ◦ 60-95% in complexed forms
◦ 106 times in prostatic fluid
◦ Elevated serum PSA levels = disruption of cellular architecture within the prostate gland (BPH,
prostatitis, prostate cancer and with prostate manipulation ; prostate massage, prostate biopsy) (Wang
et al,)
13

14. Q:Most common cause of mortality in patients with Ca Prostate?
A: Heart diseases..!
◦ There is no safe threshold for biopsy
◦ Consensus Threshold for biopsy= 2.6 ng/ml
◦ Biopsy in elevated PSA patients (4-10ng/ml) = 40% detected as cancer, with 20% false negative rate
14

15. PSA SCREENING: SHOULD WE GO FOR IT?
◦ PSA screening reduced mortality and increased incidence of ca prostate in US
◦ PLCO trial: no difference in mortality
◦ ERSPC trial: mortality reduced with screening
◦ USPSTF in 2012 recommended against PSA screening
◦ Potential for over diagnosis and overtreatment for whom treatment is of minimal benefit
◦ AUA: shared decision making for 55-69 years
15

16. 16

17. 17

18. ◦ PSAD(PSA Density):
◦ PSA divided by volume
◦ For recurrence assessment
◦ PSAV (PSA Velocity):
◦ Rate of change of PSA values
◦ >0.75ng/ml/year- s/o cancer
◦ %fPSA:
◦ More complexed PSA in cancer
◦ Cutoff: 25%
◦ hK2:
◦ Poorly differentiated cancer
18

19. ◦ PHI:
◦ tPSA, f PSA, [-2] proPSA
◦ high-grade disease compared to either tPSA or %fPSA (Catalona et al,)
◦ 4K Pannel:
◦ likelihood of clinically significant prostate cancer (Carlsson et al,)
◦ Includes t PSA, fPSA, iPSA, hK2
◦ PSMA
◦ Increased tissue expression- worse prognosis after surgery
◦ 68Ga-PSMA PET- biochemical recurrence after primary therapy
19

20. WORKUP
20

21. Clinical features
◦ Frequently absent at the time of diagnosis
◦ Most prostate cancers are detected at localized stage, hence asymptomatic
◦ Nonspecific urinary symptoms, hematuria, hematospermia
◦ 6% are metastatic, mainly to bones- c/o bone pain ; becoming unusual
◦ Weight loss, weakness, pain
◦ Anemia
◦ CKD
21

22. DIAGNOSIS
◦ DRE
◦ Below PSA 3 ng/ml- DRE has limited role
◦ PSA+ DRE= increased detection rate and PPV ( Catalona et al)
◦ Sim’s lateral position.
• Craniocaudal and transverse dimension
• Consistency / Mobility • Any firm/ elevated area and its size.
• Typical finding ca prostate- Hard, nodular, asymmetrical, may or may not be raised above the surface of
gland and is surrounded by compressible prostatic tissue. – Prostatic induration - BHP nodule/ calculi/
infection/ granulomatous prostatitis / infarction
◦ Specificity- 50% and Sensitivity- 70% – Only 25-50% of men with an abnormal DRE have cancer. – DRE +
PSA specificity 87%
22

23. RADIOLOGY
◦ CXR
◦ CECT PELVIS
◦ MRI PELVIS (mp MRI)
◦ MR SPECTROSCOPY
◦ BONE SCAN (PSA >20)
23

24. EAU UPDATES 2020
24

25. PROSTATE BIOPSY
25

26. 26
◦ Hypoechoic foci on TRUS: s/o carcinoma
◦ More common at PZ

27. INDICATIONS OF BIOPSY
◦ No safe PSA threshold level ( Prostate cancer prevention trial- Thompson et al)
◦ AUA: 55-69 year -shared decision making of PSA screening
1. Suspicious DRE
2. In patients with symptoms s/o ca prostate
3. Symptoms s/o metastasis
4. Ca Prostate detected on TURP FOR BENIGN PROCEDURES
5. Rising PSA values
6. Extensive PIN
7. Positive urinary PCA3
27

28. ◦ Left lateral decubitus position
◦ Oral antibiotic prophylaxis (AUA 2014)
◦ Sextant biopsy scheme: improved cancer detection over DRE/US guided lesion take ( Hodge et al )
◦ In PSA 4-10 ng/ml : initial detection- 22%
◦ Extended 12 core biopsy – (Bjurlin et al) - AUA white paper endorsed -CURRENT STD. OF CARE
◦ Q: What to do if biopsy negative, but persistently elevated PSA patients?
Ans: Saturation prostate biopsy- 18/21 core (Stewart et al)
28

29. PATHOLOGY
◦ PIN
◦ LGPIN: shouldn’t comment, no greater risk of Ca. (Epstein et al)
◦ HGPIN: mean risk of Ca. in biopsy after 1 year- 26.4%, not significantly higher
◦ Treatment: repeat biopsy after 3/ 1 year based on risk
29

30. ADENOCARCINOMA
◦ Grade- Gleason system (1974)
◦ 2-10
◦ Most prevalent and second most prevalent groups added
◦ If only one pattern: doubling of same pattern done
◦ Gleason 6 : 97% cured of disease ,5 years after radical prostatectomy (Johns Hopkins Study group –
Pierorazio et al)
30

31. 31

32. 32

33. USES
◦ Pathologic stage
◦ Side specific EPE
◦ EPE into neurovascular bundle
◦ Progression after radical prostatectomy
◦ Candidates of brachytherapy, active surveillance, focal therapy
◦ Prognosis following RT/ Cryotherapy/ HIFU
33

34. STAGING
34

35. 35

36. Management
◦ Only about 16% of men diagnosed with ca prostate ultimately die of it (biologic indolence)
◦ Treatment
◦ Depends on stage, patient's age and Gleason score
• EARLY
• LOCALLY ADVANCED
• METASTATIC
◦ 3 risk group
36
STAGE INITIAL PSA Gleason grade
LOW RISK T1 –T2a <10 ng/ml ≤ 6
INTERMEDIATE RISK T2b 10- 20 7
HIGH RISK ≥ T2c >20 8-10

37. Localized disease
• Conservative Management
• Radical radiotherapy
• Radical prostatectomy
• Cryoablation
37

38. Locally advanced disease
• Radical radiotherapy
• Hormonal therapy
38

39. Metastatic disease
• Palliative RT
• Hormonal therapy
39

40. Conservative management
◦ Watchful waiting
◦ Monitoring the patient until he develops metastases that require palliative treatment
◦ Active surveillance
40

41. Active Surveillance
◦ Active monitoring allows delayed primary treatment if there is evidence of cancer progression.
41

42. Watchful waiting
Low risk cases
• Life expectancy < 10 yrs
• Elderly patients
• Low volume disease (<2.5cc) with PSA <10 and GS 2-6
◦ Probability of progression of disease <2%/yr.
• Palliative, not curative
• As disease progresses palliative measures initiated
• If a man lives long enough he will die from prostate cancer
42

43. Active monitoring
◦ now being studied in younger patients with low volume,low- or intermediate-grade tumors to avoid or
to delay treatment that might not be immediately necessary.
• Those with curable disease destined to progress would be monitored- multiple extended biopsy
procedures and imaging studies.
• The patients who opt for active monitoring should be evaluated with DRE (annual) and PSA (6 monthly)
testing and consider having repeated prostate biopsy procedures yearly or biennially
43

44. Active Monitoring - Disadvantages
• Multiple extended biopsy procedures may complicate subsequent attempts at nerve-sparing surgery or
delay treatment until the window of opportunity for cure is closed.
• Treatment is more likely to be successful if it is given earlier while the tumor is smaller and the
prospects for potency-sparing surgery are greater.
• It can avoid or delay treatment for some patients, but there will inevitably be those who will miss their
opportunity for cure and, ultimately progress to metastases and death from prostate cancer
44

45. When to abandon surveillance?
◦ Gleason 4/5 present
◦ >2 biopsy cores involved
◦ >50% biopsy core involved
◦ Absence of cancer on repeated biopsies- low chance of progression ( Carter et al )
◦ Scandinavian prospective RCT: after 18 year follow-up cancer specific mortality is significantly higher in
W&W group compared to radical prostatectomy ( Bill et al 2014 )
◦ PIVOT trial: radical prostatectomy didn’t reduce mortality compared to W&W ( Wilt et al 2012 )
45

46. Surgical Management
•Radical Prostatectomy
◦ It has been performed for around 150 years ( Kuchler 1866 )
No treatment has supplanted radical prostatectomy, and it still remains the “gold standard”
46

47. RADICAL PROSTATECTOMY
Selection of patients
• <60 years
• Good General Condition.
• Life expectancy >10yrs
• Completely resectable tumor. T2 or less
• No life threatening ancillary disease.
• Usual upper age is 75 years.
47

48. Approaches
• Perineal.
• Retropubic.
• Laparoscopic.
• Robotic.
48

49. Perineal
◦ Advantage - less blood loss and a shorter operative time than the retropubic approach.
◦ Disadvantages
1. it does not provide access for a pelvic lymph node dissection
2. there is a higher rate of rectal injury
3. there is occasional postoperative fecal incontinence that does not occur commonly with other
approaches.
4. It is more difficult to spare the cavernous nerves through the perineal approach.
49

50. 50

51. Retropubic
Preferred by most urologists because of
◦ their familiar surgical anatomy
◦ the lower risk for rectal injury
◦ Lower risk of postoperative fecal incontinence
◦ the wide exposure and access for pelvic lymphadenectomy and prostate excision, with preservation of
the neurovascular bundles
◦ and the lower risk for positive surgical margins
51

52. Radical prostatectomy involves complete removal of the prostate gland and seminal vesicles and usually
includes a modified pelvic lymph node dissection as well.
• Surgical steps.
1. pelvic lymphadenectomy;
2. opening of the endopelvic fascia and limited incision of the puboprostatic ligaments;
3. suture ligation and transection of Santorini's dorsal venous complex;
4. Dissection of the urethra at the apex of the prostate and transection of the urethra (sometimes the
anastomotic sutures are placed at this point in the operation);
5. Dissection of the prostate from the neurovascular bundles;
52

53. 6. Securing and transection of the prostatic pedicles;
7. Transection and reconstruction of the bladder neck;
8. Dissection of the seminal vesicles and ampullary portions of the vasa deferentia; and
9. Performance of the vesicourethral anastomosis
53

54. Robotic/Lap. Assisted Radical Prostatectomy
54

55. 55

56. 56

57. 57

58. Developing space of Retzius
58

59. 59

60. Ligation of deep dorsal vein complex
60

61. Division of posterior bladder neck
61

62. Dissection of seminal vesicles and vas
deferentia
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63. Preservation of NVB
63

64. Prostatic pedicle ligation
64

65. Apical dissection and division of urethra
65

66. Vesicourethral anastomosis
66

67. 67

68. The Open Vs Robotic Debate
◦ RALP has become the dominant surgical approach in U.S
◦ Blood loss and transfusion rates lower with RALP
◦ Operative times longer with MIS
◦ Excellent urinary continence with RALP
◦ potency -Outcomes are comparable and in some cases superior outcomes with experienced hands for
RALP
◦ Oncologic safety-comparable
◦ Higher cost with RALP
68

69. Complications of RRP
Rate of complication is less than 10%
• Early Complications
1. • Hemorrhage
2. • Rectal, vascular, ureteral, or nerve injury; urinary leak or fistula.
3. • Thromboembolic and cardiovascular events; urinary tract infection;
4. • lymphocele
5. • wound problems Bleeding
6. DVT
69

70. Late complications
◦ Erectile dysfunction
• Urinary incontinence
• Inguinal hernia
• Urethral stricture.
70

71. RETURN OF FUNCTIONS
◦ The return of urinary continence is associated with the patient's age: more than 95% of men younger
than 50 years are continent after surgery; 85% of men older than 70 years regain continence
◦ The return of erectile function after radical retropubic prostatectomy correlates with the age of the
patient, preoperative potency status, and the extent of nerve-sparing surgery.
• In most patients, erections usually begin to return as partial erections 3 to 6 months after surgery and
may continue to improve for up to 3 years or more .
71

72. Prognosis after surgery
• STAGE LOCAL CONTROL at 5 yrs
• T1a- T2a > 95%
• T1b - 2b > 92%
• T3a > 82%
• Overall biochemical relapse rate 17%
• PSA relapse free survival rates 84% - 5 year, 74% -10 year and 66% for 15 years
• Factors predictive of high chances of local recurrence
72

73. Radiotherapy
• Radical
• Adjuvant
• Palliative
73

74. Forms of radiotherapy
• Conventional Radiotherapy
◦ Uses beams of gamma radiation (usually photons) directed at the prostate and surrounding tissues
through multiple fields
74

75. Conformational Radiotherapy
◦ The radiation beams conform to the shape of the treatment target
75

76. Intensity Modulated radiotherapy
◦ Intensity-modulated radiation therapy (IMRT),is a form of three dimensional conformal radiotherapy
(3D-CRT) and can provide localization of the radiation dose geometrically and minimize injury to
surrounding structures.
◦ Inverse treatment planning
76

77. ◦ IMRT- deliver higher doses of RT with lower GI toxicity
77

78. Side effects of RT
Acute – 60% in 3rd week of RT
• Rectal - discomfort, tenesmus, diarrhoea
• Urinary- frequency, urgency, nocturia
• Urinary incontinence
Late – 6 months/ later
• Chronic diarrhoea , proctitis, rectal-anal stricture
• Bleeding PR- 3.3%, bowel obstruction. perforation- 0.6%
• Erectile dysfunction (10–85%)
78

79. Brachytherapy
◦ With brachytherapy, radioactive sources (seeds or needles) are implanted directly into the prostate
gland, and sometimes into the surrounding tissues,
◦ to deliver a high dose of radiation to the tumor while sparing, to the extent possible, the bladder and
the rectum.
79

80. Why-
• Prostate has slow growth which remains localized for a long period
• Small t/t volume
• Potency well maintained with minimal complications
• Older patients>60 yr, less tolerace to high dose XRT
◦ Isotopes used
• IODINE 125
• PALLADIUM 103
• IRIDIUM 192
80

81. Relative contraindications of brachytherapy
• Large median lobe
• High GS
• H/o multiple pelvic surgeries
• DM with healing problems
• SVI, ECE
• Apical lesion
• Gland size > 60 cc or pubic arch interference
• Prior pelvic RT
81

82. What’s new?
◦ PROTON THERAPY?
◦ Hypofractionation reduces overall course (2Gy/day) – Withers et al
◦ Extreme fractionation- (6.7 to 10 Gy)-good biochemical control (Madsen et al)- need more phase III trial
◦ Non inferiority in both CHHiP study and PROFIT trial
◦ Stereotactic body RT (Cyberknife)
82

83. ◦ Targeted RNA based therapy- PSMA targeted siRNA chimeras-target prostate cancer cells and knock
down mRNAs and proteins- growth delay (McNamara et al)
◦ Immunotherapy- ipulimumab for CTLA 4 blockade ( Slovin et al)
◦ Cancer vaccines
◦ Sipuleucel-T
◦ ProstVac-VF
◦ Radio-Gene therapy
1. suicide gene therapy-prodrugs
2. oncolytics
83

84. FOCAL THERAPY- WHY?
84

85. 1. CRYOTHERAPY
2. HIFU
3. Photodynamic therapy
4. Photothermal therapy
5. Irreversible elctroporation
85

86. Hormonal Therapy
◦ Prostatic epithelium undergoes atrophy after Castration (Hunter 1840)
◦ Noticeable improvement in clinical status with castration (Huggins,1941)
◦ MECHANISM OF ANDROGEN AXIS BLOCKADE
1. Ablation of androgen sources
2. Antiandrogens
3. Inhibition of LHRH or LH
4. Inhibition of androgen synthesis
86

87. 87

88. ◦ Male sex hormones (testosterone, androgens) are critical to growth of prostate cancer.
• Primary androgen deprivation therapy may be appropriate for older men, those with significant medical
comorbidities precluding the use of curative therapy.
◦ Normalization of PSA < 4ng/ml - 60-70%
• Tumor masses will decrease by half or more in 30-50%
• Improvement in symptoms (bone pain, urinary obstruction)- 60%
88

89. ADT
ablation ANTIANDROGENS INHIBITION OF LH/LHRH INHIBITION OF
ANDROGEN SYNTHESIS
orchiectomy Cyproterone acetate DES Aminoglutethimide
Flutamide Leuprolide Ketoconazole
Bicalutamide Goserelin Abiraterone
Nilutamide Triptorelin
Enzalutamide Histrelin
Cetrorelix,
Abarelix
Degarelix
89

90. Bilateral orchiectomy - testosterone ↓ by 90% within 24 hrs of surgery
• One year survival rate of 73 % and a five-year survival rate of 35 % in Stage IV
90

91. ◦ There is no evidence that 3 months of neoadjuvant ADT prior to radical prostatectomy improves
biochemical outcomes (Soloway et al)
◦ ADT+EBRT=improved overall survival rate ( Crook et al )
◦ Combined Androgen Blockade ( CAB)
• Blocks androgen production from the testes (95%) and the adrenals (5%)
• GnRH agonists + antiandrogen (flutamide, bicalutamide, nilutamide)
• Have not been shown to be superior to GnRH therapy alone
• Higher cost and more side effects than GnRH therapy alone
91

92. Side-effects of hormonal therapy
92
Castration Oestrogens LHRH agonists
Loss of libido
• Erectile dysfunction
• Hot flashes (55–80% )
• Gynaecomastia and breast pain (49–
80% DES, 10–20% castration)
• Increase in body fat
• Decrease in bone mineral density
• Osteoporosis
• Muscle wasting
• Anaemia
• Cognitive decline
Cardiovascular toxic
effects (Acute MI, CHF,
CVA, DVT, pulmonary
embolism)
• Flare phenomenon
due to initial rise
of testosterone
• Might worsen
symptoms
• Costly

93. ADT response
◦ Patients with >80% drop in PSA following ADT within 1 month survived significantly longer ( Aria et al)
◦ In lymph node metastatic prostate cancer, ADT improves overall survival if the primary tumor is
removed but has no significant effect if the primary tumor is not removed.
93

94. Antiandrogens
• Steroidal
• Pharmacological S/E-loss of libido, erectile dysfunction, but rarely Gynaecomastia
• Non-steroidal
• Pharmacological S/E- gynaecomastia (49–66%), breast pain (40–72%), hot flushes (9–13%)
• Non-pharmacological S/E related to individual drugs
• Androgen deprivation is one of the most effective therapies against any solid tumor;
unfortunately, with time, almost all prostate cancers will become androgen refractory
94

95. CASTRATION-RESISTANT
PROSTATE
CANCER(CRPC)
95

96. 96

97. • Virtually all patients eventually develop clinical evidence of resistance to treatment.
• Progression-free and overall survival figures of patients with metastatic disease with various methods of
Androgen Deprivation Therapy have ranged from 12 to 20 months and 24 to 36 months
97

98. HOW ?
98

99. • Somatic alterations of the androgen receptor.
• a molecularly altered androgen receptor can still undergo ligand dependent activation by other
hormones such as estrogens and progestational agents and non–ligand-dependent activation by
growth factors and cytokines.
• Androgen ablation affects primarily the cell death rate by inducing apoptosis. As the tumor progresses,
the threshold of apoptosis progressively rises to a point that cell proliferation exceeds cell death.
• This results in the accumulation of endocrine-independent cells
99

100. 100

101. Treatment of CRPC
• Discontinuation of antiandrogens (both steroidal and nonsteroidal) an result in short-term clinical
responses.
• Second-line hormonal manipulation
1. • Aminoglutethimide
2. • ketoconazole
3. • corticosteroids
• cytotoxic chemotherapy
101

102. CHEMOTHERAPY
• Response rates vary from 20-60%
• Improvement is usually temporary
• Patients who progress after further hormonal manipulation may be candidates for chemotherapy
• FDA-approved agents
• Mitoxantrone
• DOCETAXEL
◦ CABAZITAXEL
• Main benefit is improvement in pain with limited objective responses and NO Survival benefit
102

103. PALLIATIVE MANAGEMENT
103

104. 104

105. BONE TARGETED THERAPY
• Bisphosphonates:
• Aledronate (Fosamax)
• Zoledronate (Zometa)
• Pamidronate (Aredia)
• Strong affinity for bone
• Directly inhibit osteoclast activity: prevent bone resorption induce osteoclast apoptosis
• Rationale
• Bone resorption increased in metastasis which contributes to skeletal morbidity
• ADT further increases bone resorption
105

106. 106

107. 107

108. 108

109. 109

110. 110

111. 111

112. 112

113. 113

114. NEUROENDOCRINE/ANAPLASTIC
PHENOTYPE
114

115. EAU 2020 UPDATES
115

116. 116

117. ◦ Counselling regarding individual treatment options is often biased by financial incentives and physician
biases (Bekelman et al. 2013)
117

118. 118
THANK YOU

119. TAKE HOME MESSAGE
◦ CA PROSTATE is a biologically indolent cancer
◦ A shared decision should be taken for PSA screening
◦ A guided 12 core biopsy should be sought in all clinically indicated cases and reported using Gleason
scoring
◦ Management decision is taken after proper risk stratification among surveillance, surgery,RT & ADT
◦ Guidelines continue to differ & hence there is a need of more good quality studies for a controversy free
management considering all clinical aspects..!
119

120. 120

121. ◦ TRUS showing hypo echoic lesion in transitional zone, No extraprostatic extension.
• Biopsy showing adeno carcinoma with Gleason score 5
• CT showing no lymph node involvement
• Bone scan –No hot spots(can be omitted).
• Diagnosis - Early prostatic carcinoma.
121

122. Clinical Case 2
122
• Krishna , a 65 year old male patient presented to the OPD with difficulty in passing urine.
• He is having Urinary hesitancy, diminished force of urine stream, intermittency,sense of incomplete
voiding for the last 2 months,
• the symptoms are gradually progressing for the last 2 months.
• He has no other complaints.
• There is no bone pain or tenderness.
• His bowel habits are normal. Not a diabetic or hypertensive.

123. ◦ On further evaluation, he has no pallor, icterus or Lymphadenopathy.
◦ CVS, RS within normal Limits
◦ P/A no organomegaly
◦ •On Digital rectal examination , he has a Hard, nodular, asymmetrical swelling in the prostate gland
raised above the surface of gland and is surrounded by compressible prostatic tissue
◦ His biochemical parameters are normal except PSA .
◦ PSA was 14ng/ml.
123

124. • TRUS showing hypo echoic lesion with seminal vescicle and bladder base involvement.
• Biopsy showing adeno carcinoma with gleason score 7
• CT scan no lymphadenopathy
• Bone scan – No hot spots
• Diagnosis – Locally advanced prostatic carcinoma
124

125. Clinical Case 3
◦ Shiva a 70 year old male patient presented to the OPD with complaints of difficulty in passing urine.
◦ He is having Urinary hesitancy, diminished force of urine stream, intermittency, sense of incomplete
voiding for the last 1 year, the symptoms are gradually progressing for the last 1 year.
◦ He is also having Urgency,frequency, and dribbling for last 6 months.
◦ He is having Hematochezia, Constipation, Intermittent diarrhoea for the last 1 month.
◦ He is also complaining of low back ache and pelvic pain for last 1 month.
◦ O/E He is thin emaciated, has pallor, and inguinal lymphadenopathy .
◦ CVS, RS within normal Limits
125

126. ◦ P/A a firm 3x3 cm mass palpable in the abdomen below umbilicus
◦ On Digital rectal examination , he has a Hard, nodular, asymmetrical swelling in the prostate gland
Firmness extending superior to the prostate gland. There was a mass palpable in the anal canal at 12 o
clock position and the finger stained with blood and mucus.
• He had tenderness at L1 vertebra region.
• His PSA was 30ng/ml.
• He had hyponatremia.
126

127. TRUS showing hypo echoic lesion in transitional zone, with extension to the seminal vesicle, bladder base,
and rectum
• Biopsy showing adeno carcinoma with Gleason score 7
• CT showing internal iliac, para and pre aortic lymph node involvement
• Bone scan –Hot spots at vertebral column, ribs and pelvis.
• Diagnosis - Metastatic prostatic carcinoma.
127

128. 128