Prostate swellings Flashcards

1
Q

Benign nodular hyperplasia:

  • AKA
  • what is the pathology?
  • What is the pathophysiology
A

AKA benign prostatic hyperplasia

Pathology: irregular proliferation of both glandular and stromal prostatic tissue

Pathophysiology: hormonal imbalance causes alteration of androgen/oestrogen causing proliferation of peri-urethral (central) prostatic tissue as this is oestrogen responsive
= disturbance of bladder sphincter mechanism by physical obstruction and by physiological interference of peri-urethral gland at the internal urethral meatus

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2
Q
What are the 
-symptoms
-complications
-management
of BPH?
A

Symptoms: prostatism
-voiding symptoms (obstructive): weak or intermittent urinary flow, straining, hesitancy, terminal dribbling and incomplete emptying
-storage symptoms (irritative) urgency, frequency, urgency incontinence and nocturia
-post-micturition: dribbling
= acute and chronic urinary retention

Complications:

  • bladder hypertrophy = diverticulum formation
  • if left untreated can lead to hydroureter, hydronephrosis, infection but NOT pre-malignant

Management:
-watchful waiting

-1st line Alpha blockers (tamsulosin):
decrease smooth muscle tone (prostate and bladder)
considered first-line, improve symptoms in around 70% of men
adverse effects: dizziness, postural hypotension, dry mouth, depression

-5 alpha reductase inhibitors (prevent synthesis of testosterone - finasteride and dutasteride)
block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH
unlike alpha-1 antagonists causes a reduction in prostate volume and hence may slow disease progression. This however takes time and symptoms may not improve for 6 months. They may also decrease PSA concentrations by up to 50%
adverse effects: erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

-surgery: transurethral resection of prostate (TURP)

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3
Q

Carcinoma of prostate:

  • is this common?
  • what patient demographic is affected?
  • what genetic mutations have been found to be assoc. with this?
A

-common: 11% cancer deaths in males

Epidemiology: caucasians, western world, 60-80yrs, risk increases with affected 1st degree relative

Genetics:

  • mutations on chromosomes 1p/8p/xp
  • mutations of BRCA2 gene
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4
Q

Describe the pathology of carcinoma of prostate

A

->95% are multifocal adenocarcinomas, arises mainly in peripheral ducts and glands

Spread:

  • locally to prostatic capsule, urethra, bladder base and seminal vesicles
  • lymphatic - (pelvic) sacral/iliac/paraaortic nodes
  • Bones - osteosclerotic met.s, lungs, liver
  • perineural invasion along autonomic nerves
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5
Q

Describe the presentation of prostate carcinoma

A
  • asymptomatic (found on DRE/PSA)
  • lower urinary tract symptoms
  • haematuria
  • haematospermia
  • bone pain
  • anorexia
  • weight loss
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6
Q

Describe what is found on DRE of carcinoma of prostate?

A

Asymmetry/nodule/fixed/craggy

-75% arise in the periphery so can be felt

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7
Q

What is PSA?

A

prostate specific antigen, normal levels about 4 but it rises with age

GP’s run checks on at risk patients and do blood tests for PSA – if these are raised, then patients are referred to clinic.
If levels are raised but stable, then patients are normally monitored either every 6 or 12 months.
If levels are raised and increasing, then it is more likely to be cancer.

sensitivity of PSA is high but specificity is low. (if they do have a raised PSA they are likely to have cancer but if they dont could also have cancer)

(5-alpha reductase inhibitor)

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8
Q

What could cause a rise in PSA levels?

A
  • prostate carcinoma
  • BPH
  • prostatits/UTI
  • retention
  • catheterisation
  • DRE
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9
Q

Describe the 4 ways prostate carcinoma is diagnosed?

A
  • DRE
  • Imaging
  • PSA
  • transrectal US biopsy

If they have a positive DRE/positive PSA/clinical suspicion refer for biopsy

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10
Q

What imaging is used to diagnose prostate carcinoma?

A

USS, skeletal xrays/bone xrays

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11
Q

What is a transrectal US biopsy? when is this done? what are the complicationS?

A

8-12 needle core biopsies guided by USS - uncomfortable

Indications:

  • abnormal DRE, an elevated PSA
  • previous biopsies showing PIN (prostatic intraepithelial neoplasia), or ASAP (atypical small acinar proliferation)

Complications:

  • haematuria and haematospermia for 2-3weeks after
  • 0.5% sepsis risk
  • 0.5% rectal bleed
  • vaso-vagal syncope
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12
Q

what scoring is used to grade prostate carcinoma? describe this?

A

gleasons scoring - v. good predictor of prognosis and is widely used

  • score based on the architectural appearance of prostate gland
  • 2 most abundant cell patterns assessed and then added together to give a score

Graded using the Gleason grading system, two grades awarded 1 for most dominant grade (on scale of 1-5) and 2 for second most dominant grade (scale 1-5). The two added together give the Gleason score. Where 2 is best prognosis and 10 the worst.

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13
Q

How is prostate carcinoma staged?

A

TNM
Tumour - 1-5
Nodes - 0-1
Met.s - 0-1

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14
Q

What are the different management options for organ confined disease of the prostate?

A

Watchful waiting/deferred treatment/symptomatic treatment:
-conservative then as systemic/local progression treat palliatively

Active surveillance/active monitoring:
-close surveillence and treat at pre-defined thresholds that classify progression - curative

Radical surgery postatectomy (radical/laparoscopic/robotic)
-complications are erectile dysfunction, incontinence, bladder neck stenosis

Radical radiotherapy: EBRT, brachytherapy
-complications are irritative LUTS, haematuria, GI sx, erectile dysfunction, incontinence

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15
Q

What are the different management options for locally advanced disease?

A

Radiotherapy with neo-adjuvant hormonal therapy:
-better 5yr survival compared to EBRT alone

Watchful waiting

Hormonal therapy - symptomatic treatment if unfit for curative

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16
Q

What hormonal therapy is available for prostatic carcinoma?

A

Synthetic GnRH agonist (Leutinising hormone releasing hormone) agonists:
-causes downreg. of LHRH receptors with subsequent suppression of pituitary LH and FSH secretion and testosterone production
- Goserelin (Zoladex)
(cover initially with anti-androgen to prevent rise in testosterone)

Antiandrogen:

  • steroidal - cyproterone acetate (loss libido, ED, gynaecomastia, cardiovascular toxicity and hepatotoxicity)
  • non-steroidal - hillutamide, flutamide, bicalutamide (gynaecomastia, breast pain, hot flushes, hepatotoxicity)
17
Q

Why is it important to use anti-androgen 1 wk before and continure for 2 weeks after the LHRH agonist? what are the other side effects of LHRH agonists?

A

Can cause a testosterone surge (flare-up phenomenon) :
-20% pt.s manifest with acute spinal cord compression

Side effects:
loss libido/ED
hot flushes/sweats
wt gain
gynaecomastia
anaemia
cognitive changes
osteoporosis
18
Q

describe the management of metastatic disease of the prostate?

A

Androgen deprivation therapy:

  • hormonal therapy
  • bilateral subcapsular orchidectomy
  • maximal androgen blockade

Diethylstilbestrol/steroids

cytotoxic chemo

19
Q

What is the treatment in general for prostate

A

Localised prostate cancer (T1/T2)

Treatment depends on life expectancy and patient choice. Options include:

conservative: active monitoring & watchful waiting
radical prostatectomy
radiotherapy: external beam and brachytherapy

Localised advanced prostate cancer (T3/T4)

Options include:

hormonal therapy: see below
radical prostatectomy
radiotherapy: external beam and brachytherapy

Metastatic prostate cancer disease - hormonal therapy

Synthetic GnRH agonist

e.g. Goserelin (Zoladex)
cover initially with anti-androgen to prevent rise in testosterone

Anti-androgen

cyproterone acetate prevents DHT binding from intracytoplasmic protein complexes

Orchidectomy