This case study describes the diagnosis and treatment of prostate cancer in an 87-year-old male patient. Key details include: - Cancer was diagnosed via biopsy and confirmed to be adenocarcinoma. Staging investigations found the cancer to be localized. - The patient underwent external beam radiotherapy to the prostate with doses of 78-79.2 Gy over 8 weeks. - Common side effects were managed conservatively. The patient will continue follow-up care and has a good prognosis given the localized stage at diagnosis.

1. CA PROSTATE CASE STUDY

2. • Patient Name: Nashon Kongo Omauna.
• GENDER: MALE
• AGE: 87 YRS
• PATIENT NO. RT 79452

3. Group C. Names.
• Christa Apondi. Hsb 232-0036/2021
• Thaddeus Mukhisa HSB 232-0306/ 2023
• Gregory Barongo. HSB 232-0304/ 2021
• Sharon Murianki HSB 232-0035/ 2021
• Mike Osborn. HSB 232-0549/ 2021
• Mirriam Mulele HSB 232-0042/ 2021

4. INTRODUCTION
Anatomy
The prostate gland lies between the pubis symphysis and the anterior
rectal wall and is closely applied to the bladder neck and seminal
vesicles.
Has 4 surfaces .Anterior .Posterior. Inferior laterals.
APEX Inferior BASE superior.

6. • Histopathology.
• PathologyMore than 95% of prostate cancers are adenocar-cinomas,
and ~4% are transitional cell cancers [6]. Others are neuroendocrine
carcinomas (small cell) and sarcomas. Prostatic intraepithelial neo-
plasia (PIN) is a precursor lesion.
• Acinar adenocarcinoma. Most people get this type. It develops in the
gland cells that line the prostate gland.
•
• Ductal adenocarcinoma. This kind starts in the cells that line the ducts
(or tubes) of the prostate gland. It’s usually more aggressive than the
other type. That means it grows and spreads more quickly.

8. ETIOLOGY
• It is suspected there is inherited or genetic factor involved
EPIDEMIOLOGY
Typically affects males greater than 50yrs of age
Prostate cancer is among the most common can-cers in men worldwide
and the second most common cause of cancer-related mortality in
males with an estimated 1,600,000 cases and 366,000 deaths annually
[1].Black men in the United States and the Caribbean have the highest
documented pros-tate cancer incidence rates in the world.

9. • Signs &symptoms
I. new onset of erectile dysfunction
II. Urge to frequently urinate
III. Dysuria
IV. Heamaturia
V. Inguinal swelling
VI. Bone pain.
VII. Incontinence
VIII. Cord compression.
IX. Lower obstructive edema

10. INVESTIGATIONS DONE Diagnostic work up.
• CT Scan – useful in evaluating lymph nodes and bonny anatomy
• Pelvic MRI
• Ultrasound -Abdominal pelvic USG, Prostate USG.Transrectal ultrasound.
• Lab tests – PSA, full hemogram urinalysis
Findings. A firm and irregular prostate in a digital rectal exam (DRE) is typical of
cancer, but cancer foci may be found in a normal prostate. Cachexia, globe vesicale,
lower extremity lymph-edema, deep venous thrombosis, spasticity, motor
weakness, and supraclavicular lymphadenopathy may be observed during routine
physical examination.Laboratory findings. Anemia may be seen due to metastatic
disease. Bilateral ureter obstruction causes azotemia. Alkaline phosphatase in bone
metastasis and acid phosphatase in extraprostatic extension may increase.
• Ca prostate is confirmed by biopsies under TRS Ultrasound guided
• The extent of primary disease is assessed by MRI of the prostate & MRI or CT scan of the
pelvis and abdomen to detect locoregonal &distant spread.

11. if PSA >20, T2 and PSA >10, GS ≥8, T3–T4, or presence of
symptomsPelvic CT/ MRI: if T3–T4 or T1–T2 and risk of LN involvement
is >10% [17].MR spectroscopy: Role in routine manage-ment is
controversialProstate imaging reporting and data sys-tem (PI-RADS) —
The International Prostate MRI Working Group developed PI-RADS to
standardize prostate MRI examination perfor-mance and reporting. An
update version
PI-RADS 1—Clinically significant cancer is highly unlikely to be present.•
PI-RADS 2—Clinically significant cancer is unlikely to be present.• PI-
RADS 3—The presence of clinically sig-nificant cancer is equivocal.• PI-
RADS 4—Clinically significant cancer is likely to be present.• PI-RADS
5—Clinically significant

12. Roots of possible spread
• 1. lymphatic system
• Lymphatic drain from the prostate to the obturator, presacral, internal
and external common iliac and para-aortic lymph nodes.
• Ca prostate can extent
I. Through Prostate capsule – posteriorly, at the apex & at the
junction between the base and bladder neck & seminal vesicle
II. Spread occurs to the seminal vesicle and lymphnodes with
increasing tumor stage and histological grade.

13. Histology and tumor classification
• Tumour describes the size or area of the cancer. This is a
simplified description of the T stage.
• There are 4 main T stages of prostate cancer – T1 to T4.
• T1
• T1 means the cancer is too small to be seen on a scan, or felt
during an examination of the prostate. It’s divided into T1a, T1b
and T1c.

14. • T1a means that the cancer is in less than 5% of the removed
tissue
• T1b means that the cancer is in 5% or more of the removed
tissue
• T1c cancers are found by biopsy
T2
• T2 means the cancer is completely inside the prostate gland. A
new classification no longer divides T2 into 3 sub stages - T2a,
T2b and T2c.
– T2a: Tumor involves 50% or less of one lobe – T2b: Tumor
involves more than 50% of one lobe but not both lobes – T2c:
Tumor involves both lobes

15. T3
T3 means the cancer has broken through the capsule (covering)
of the prostate gland. It’s divided into T3a and T3b.
• T3a - means the cancer has broken through the capsule
(covering) of the prostate gland.
• T3b - means the cancer has spread into the tubes that carry
semen (seminal vesicles).
•

17. T4
T4 means the cancer has spread into other body
organs nearby, such as the back passage, bladder,
or the pelvic wall.

18. NODE (N)
• ode (N) describes whether the cancer has spread to the lymph
nodes.
• N is split into N0 and N1.
• N0 means that the nearby lymph nodes don’t contain cancer
cells
• N1 means there are cancer cells in lymph nodes near the
prostate

20. METASTASIS (M)
• Metastasis (M) describes whether the cancer has spread to a
different part of the body.
• There are 2 M stages – M0 and M1.
• M0 means the cancer hasn’t spread to other parts of your body.
• M1 means the cancer has spread to other parts of the body
outside the pelvis. It is split into M1a, M1b and M1c

21. Metastasis (M)
• M1a means there are cancer cells in lymph nodes outside the
pelvis
• M1b means there are cancer cells in the bone
• M1c means there are cancer cells in other parts of the body
such as the lungs.

23. Gleason score.
• Grading. The most commonly used histo-logical grading system is that of
Gleason, which evaluates major growth patterns and glandular
differentiation [8].• The Gleason grade varies between 1 and 5. The most
commonly seen major pat-tern is combined with the secondary pat-tern,
and the total is used to derive the Gleason score• The Gleason score varies
between 2 and 10. Grade 1 is similar to normal, while grade 5 corresponds
to no glandular pattern.
• • Score: 2–6 = well-differentiated;
• 7 = moderately differentiated;
• 8–10 = poorly differentiated.
• 8 Genitourinary System Cancers

28. TREATMENT OPTIONS
• Surgery
• Radiotherapy
• Brachytherapy
• Immunotherapy.
• Hormonal therapy.
• CHEMOTHERAPY.
• Active surveillance
• Particle therapy
• Gene therapy

29. • Disseminated Metastatic Disease
• HORMONALTHERAPY.• Androgen ablation ± palliative RT ±
bisphosphonates
• • Chemotherapy (docetaxel + cabazi-taxel/carboplatin or estramustine•
Stronsium
• • Immunotherapy (sipuleucel, pembrolizumab)• Residual disease or
recurrent.
• Surgery- Radical prostatectomy.
• Active surveillance-surveillance is a way of monitoring localised (early)
prostate cancer, rather than treating it straight away. You might hear it
called active monitoring.

30. Chemotherapy mechanism of action.
• Docetaxel is a complex diterpenoid molecule and a semisynthetic
analogue of paclitaxel. Docetaxel reversibly binds to microtubulin with
high affinity in a 1:1 stoichiometric ratio, allowing it to prevent cell
division and promote to cell death.
• Mechanism of action
• Carboplatin undergoes activation inside cells and forms reactive
platinum complexes that cause the intra- and inter-strand cross-
linkage of DNA molecules within the cell. This modifies the DNA
structure and inhibits DNA synthesis. This may affect a cell in all the
phases of its cycle.

31. Genetherapy
• Corrective gene therapy, which is already being used by many
investigators in the treatment of patients with prostate cancer,
involves the replacement or inactivation of a defective gene, such as a
mutated tumor suppressor gene, or a dominant oncogene that has
been found to play a role in the pathogenesis or progression of
prostate cancer.

32. Brachytherapy.
• Prostate brachytherapy. Used for Early stages of tumour.
• Low risk disease; or boost after EBRT
• Permanent seeds; LDR I-125
• Perineal template Pd-103; HDR

33. EXTERNAL BEAM RADIOTHERAPY
SIMULATION
Patient is supine position – to allow less prostate motion & for patient
comfortability especially with well distended bladder.

35. CONSIDERATIONS/ PREPARATIONS
• Completely full bladder – to displace small bowel away from the
region of interest.
• Empty rectum- full rectum leads to variations in prostate position

36. CT SCANNING
• With the patient immobilized in the treatment position following
bladder &rectal protocols a RT CT scan is performed.
• Skin reference tattoos were placed anteriorly on the midline of the
symphysis pubis and laterally over the hips and aligned with lasers to
prevent lateral rotation.
• Radio-opaque markers were placed on the skin to locate the tattoos on
the CT scans
• The CT scan of the entire pelvis was taken.
• CT data was the transferred to planning enabled computer for
outlining and target volume definition

37. Organs at risk
• Bladder-65Gy.Dmax.
• Rectum- V50<50%
• Penile bulb‐mean dose 50Gy.
• Femoral heads –V50<5%
• Nerves of prostatic plexus lying adjacent to the penile bulb.Dmax
66Gy

38. BEAM PLANNING
• Using forward planning an optimal dose distribution is
calculated.beams with MLC are chosen
• Beam 1 PA 1800
• Beam 2. 2LAT 90⁰,270⁰
• Beam 3. AP 0⁰

39. PRESCRIPTION
• Dose per #1.8-2 Gy
• Energy 6-18MV
• Whole pelvis-45-50 Gy
• Prostate field 78-79.2 Gy
• Prostate bed 64- 66 Gy for postoperative RT
• Palliative-30Gys 10 fractions

40. TREATMENT DELIVERY
• Patient was always treated in supine lie with a comfortably full
bladder after rectal voiding.
• The isocentre was marked with reference to the anterior tattoo over
the pubis symphysis.
• IGRT was used through out the treatment sesion

41. CARE OF PATIENTS
• Monitored for side effects
• Advised the pt on adequate nutrition
• Managed the pain
• Encouraged mobility
• Provided emotional support
• Formulate and follow up plans

42. Effects prostate cancer treatment
• 1. fatigue –Recommend adequate rest.
• 2. skin reaction. Dermatitis and hyperdigmentation. –Oilments.
• 3. loose stools –in take of high roughage
• 4. diarrhoea-Drink plenty of liquids, including water, broths and juices.
Avoid caffeine and alcohol.
• 5. mild proctitis & tenesmus-Medications are given in pill, suppository or
enema form. They include sucralfate (Carafate), mesalamine (Asacol HD,
Canasa, others), sulfasalazine (Azulfidine) and metronidazole (Flagyl).
These medications can help control inflammation and reduce bleeding.
• 6. urgency to urinate

43. Management of side effects
a) Loperamide hydrochloride for diarrhoea cases
b) Low residue diet for loose stools
c) Local anaesthesic suppositories for severe proctitis and tenesmus

44. Follow up and prognosis
• A follow up was scheduled TCA after 2 months with abdominal pelvic
MRI results for post RT Work out.
• Advised the patient to visit the department incase of any unusual
experience in the general body health or bowel and urine behavior

45. Prognosis.
• The 5 year survival rate for the 89% of men diagnosed with local or
regional prostate cancer approaches 100% but drops to 30% for those
diagnosed with metastatic disease.
• Prognosis factors.

46. REFFERENCES
• 1. Radiotherapy planning Fourth Edition by Jane ODDS, Tom Roques,
• 2. CT & MRI pathology Michael L. Grey, Jagan M. Ailnani
• 3. eclipse anatomy atlas