Session 11b Prostate Flashcards
Epidemiology of prostate cancer
Commonest cancer in men
2nd commonest cause of death from cancer in men
1/8 men diagnosed in their lifetime
Rare in men under 50
Risk factors for prostate cancer
Increased age
FH (BRACA2 gene mutation)
Ethnicity- black>white>asian
Label
Prostate cancer lesions are commonly found in the
Periphery of posterior part of prostate
Prostate cancer lesions are more commonly found in the
Periphery of the posterior part
BPH usually found
Central
Presentation of prostate cancer
Symptoms of UTI, prostatism, metastatic disease in bone (spine) causing bone pain
Increasingly, carcinoma of prostate is found following
Investigation of elevated prostate-specific antigen (PSA) in otherwise asymptomatic men
Differential diagnoses:
65 y/o, hesitancy, nocturia, weight loss, lower back pain
BPH
Prostate cancer
Prostatitis
Urethral stricture
Multiple myeloma
Neurological: CVA, Parkinson’s, spinal cord compression
questions to identity BPH or prostatic cancer
Family history
hormone use- increased testosterone
Haematuria
Bone pains elsewhere
Examination for BPH or prostate cancer
Digital rectal examination
DRE of prostate cancer
Enlarged prostate, hard and irregular, obliteration of median sulcus
(should be smooth and plum sized, feel 2 different lobes)
DRE in BPH
A lot larger and maybe firmer
Causes of a raised PSA
Prostate cancer
Infection
Inflammation
Large prostate
Urinary retention
PSA comes back as 35, what does this mean
Normal range is less than 40 for a 60-69 year old
More than 80% chance of prostate cancer as so high
Doing DRE can cause
Raised PSA
What else can cause elevated PSA
UTI
Inflammation
Large prostate BPH
Urinary retention
Presentation of prostate cancer
Urinary symptoms
Bone pain
Raised PSA,biopsy
Opportunistic finding from DRE
Incidental finding at transurethral resection of prostate
Grading of prostate cancer
Gleason classification grades 1-5
TNM system
Diagnosis of prostate cancer
DRE
Ultrasound
Increased PSA?
Biopsy
Radiographs and bone scans- osteoslcerotic lesions on radiographs and increased isotope uptake on both scans are seen if there is metastatic spread
Patients in advanced prostate cancer stages can develop
Sclerotic bone legion- hot spots on bone scan
Treatment for localised prostate cancer
Surgery, hormone therapy, radiotherapy
Surveillance
Treatment of T1/T2 prostate cancer
Radical surgical resection maybe curative, TURP may be required
Treatment of advanced prostate cancer
Hormonal manipulation is beneficial since testosterone promotes tumour growth (testosterone, dihydrotestosterone)
Surgical castration, medical castration (LNRH or GnRH agonist)
Palliative care
Prognosis for prostate cancer
5 year survival for T1 = 75-90%
5 year survival falls to 30-45% if local of metastatic spread
Side effects of castration
Hot flushes
Impotence
Thinning of bones
Diminished muscle mass
Increase in breast size
Weight gain
Mood changes
features of Polycystic kidney disease
8-10% of CKD
Most common inherited nephropathy
Presentation of Polycystic kidney disease
30-40 years of age with hypertension, acute loin pain, haematuria or bilateral palpable kidneys
Pathology of Polycystic kidney disease
Cysts develop anywhere in kidney, compress surrounding parenchyma and impair renal function
Tubule cannot properly drain into CD
Autosomal dominant and recessive Polycystic kidneys
Dominant: 1/500-1000
Recessive: 1/20000-40000
Cysts are seen in kidneys and
Liver/ovaries
Macroscopic findings Polycystic kidney disease
Large with yellow fluid-filled cysts replacing the parenchyma
Haemorrhage into cysts can occur
Microscopic findings Polycystic kidney disease
Cysts lined with cuboidal epithelium
USS or CT scan in Polycystic kidney disease
Bilateral enlarged kidneys with multiple cysts
What is the most likely cause of pain and macroscopic haematuria
Adult Polycystic kidney disease
Cysts can begin to form in childhood but not clinically evident until adulthood
Cysts can fill with blood following trauma, resulting in severe abdominal pain and macroscopic haematuria
Cysts can become infected
Further aspects of history to explore with APKD
Can cause hypertension and CKD, cysts in other organs, inherited (family member dying of berry aneurysm/brain haemorrhage, kidney problems etc)
Associated with valvular heart disease, diverticular disease, berry aneurism. Any history of stroke/cerebral haemorrhage should be sought
Outcomes in APKD
Morbidity and mortality result of hypertension, e.g. MI and cerebrovascular disease
Condition also leads to progressive CKD
Treatment involves controlling BP
Dialysis and renal transplant needed in end stage renal failure develops
Immediate management of APKD
Pain control- clots in the renal collecting system causes renal colic
IV fluids to increase urine output, attempt to wash clot out
Information given to APKD
Possibility of recurrent episodes of macroscopic haematuria, given advice on management at home with simple analgesia and oral hydration
Advise to avoid contact sports in which abdominal trauma may occur (Rugby, boxing)
What issues need to be addressed in follow up of APKD
Hypertensive, ECG changes consistent with LVH
treatment of bp recommended for adults with BP >130/80, ACEI preferred, can preserve renal function in patients with APKD
Is genetic screening useful for PKD
Genetic screening not useful unless large number of family members with disease
Screen on annual basis for elevated BP or urine dipstick abnormalities
Late teens: ultrasound, absence of cysts at this stage would make disease unlikely
Repeated when >30 years, still no cysts = APKD virtually excluded
