Pathology & Investigation

Benign Prostatic Hyperplasia

Presented by Dr. Ankur AgarwalSurgical Resident

Introduction Etiology Pathology Clinical findings Investigation MCQ References

Scheme of Presentation

It is a histologic diagnosis characterised by proliferation of the cellular elements of the prostate.

In men 20 to 30 years of age, the prostate weighs about 20 gm and generally weighs more after 50. It is a common problem among older men, aged > 50 however, it is an infrequent cause of death.

BPH is considered to be the most common benign internal neoplasm of the adult male.

Introduction

The prevalence of histologically diagnosed prostatic hyperplasia increases from 8 percent in men aged 31 to 40, 40 to 50 percent in men aged 51 to 60, >80 percent in men older than age 80

BPH is considered a normal part ageing process in men, serum testosterone level decreases slowly but the level of oestrogenic steroids is not decreased equally.

According to theory, this increased levels of oestrogenic steroids cause for prostate enlargement.

The secretion of intermediate peptide growth factors also plays a part in the development of BPH.

Etiology

Androgens are necessary for both normal and abnormal development of the prostate.

Testosterone is converted to a more potent androgen, dihydrotestosterone (DHT), by the enzyme 5-α reductase type 2. The type 1 form of the enzyme is present in liver and skin.

Men who congenitally lack 5-α reductase type 2 enzyme have normal serum testosterone levels but lack dihydrotestosterone.

Those with this disorder have a rudimentary prostate throughout life but rarely experience bladder outlet obstruction secondary to BPH.

These findings suggest that the active androgen, DHT, is important in promoting growth of prostate that would eventually lead to symptomatic BPH.

Prostatic hyperplasia increases urethral resistance causing compensatory changes in bladder function.

Obstruction induced changes in detrusor function, compounded by age related changes in both bladder and nervous system function lead to Urinary frequency Urgency Nocturia

Pathophysiology

McNeal demonstrated that BPH first develops in the peri-urethral transition zone of the prostate.

BPH affects both glandular epithelium and connective tissue stroma.

Pathology

Coronal

Transitional zone surrounds the urethra proximal to the ejaculatory ducts.

Central zone surrounds the ejaculatory ducts and projects under the bladder base.

Peripheral zone constitutes the bulk of the apical, posterior, and lateral aspects of the prostate.

Anterior fibromuscular stroma extends from the bladder neck to the striated urethral sphincter

The zonal anatomy of the prostate is clinically important because most carcinomas arise in the peripheral zone, whereas BPH affects the transitional zone, which may grow to form the bulk of the prostate.

BPH begins as micronodules in the transitional zone which grow and coalesce to form macronodules around the inferior margin of the pre-prostatic urethra, just above the verumontanum.

Macronodules in turn compress the surrounding normal tissue of the peripheral zone postero-inferiorly, creating a ‘false capsule' around the hyperplastic tissue which coincidentally provides a plane of cleavage for its surgical enucleation.

Well-defined nodules compress the urethra (arrowheads) into a slit-like lumen.

As the transitional zone grows, it produces the appearance of ‘lobes' on either side of the urethra. In due course, these lobes may compress or distort the preprostatic and prostatic parts of the urethra and produce symptoms.

The central zone surrounding the ejaculatory ducts is rarely involved in any disease.

BPH typically affects the submucous group of glands in the transitional zone, forming a nodular enlargement.

This overgrowth compresses the PZ glands into a false capsule and causes the appearance of the typical ‘lateral’ lobe.

The unique feature of human prostate is the presence of prostatic capsule- plays an important role in the development of Lower urinary tract symptoms.

The capsule transmits the “pressure” of tissue expansion to the urethra and leads to an increase in urethral resistance.

In the Late Stage of BPH

• When BPH affects the

Central Zone glands, a

‘middle’ lobe develops that

projects up into the bladder

within the internal sphincter

The relationship between

anatomical prostatic enlargement,

lower urinary tract symptoms

(LUTS) and urodynamic evidence

of bladder outflow obstruction

(BOO) is complex

Effects of BPH

Diagram showing the relationship between histologic hyperplasia of the prostate (BPH), lower urinary tract symptoms (LUTS), benign prostate enlargement (BPE), and bladder outlet obstruction (BOO). The size of the circles does not represent actual proportions

but rather illustrates the partial overlap between the different disease definitions.

The pathophysiology of benign prostatic hyperplasia (BPH) involves complex interactions between urethral obstruction, detrusor function and dysfunction, and urine production.

Prostatic hyperplasia increases urethral resistance, resulting in compensatory changes in bladder function.

However, the elevated detrusor pressure required to maintain urinary flow in the presence of increased outflow resistance occurs at the expense of normal bladder storage function.

Chronic bladder outlet obstruction (BOO) secondary to BPH leads to

Urinary retention Renal insufficiency Recurrent UTI Bladder wall thinning and loss of function due to constant

distension Haematuria Vesical calculi

The prostatic urethra is lengthened (twice its normal length), but it is not narrowed anatomically.

The normal posterior curve may be so exaggerated- requires a curved catheter to negotiate it.

When only one lateral lobe is enlarged, distortion of the prostatic urethra occurs.

Effects of BPH on the Urethra

If BPH causes BOO, the musculature of the bladder hypertrophies to overcome the obstruction and appears trabeculated .

BPH is associated with increased blood flow, and the resultant veins at the base of the bladder causes haematuria.

Effects of BPH on the Urinary Bladder

Not all symptoms of disturbed voiding in ageing men should therefore be attributed to BPH causing BOO.

Pathophysiologically, BOO may be caused in part by increased smooth muscle tone, which is under the control of a-adrenergic agonists

Lower Urinary Tract Symptoms (LUTS)

The following conditions can coexist with BOO:o Idiopathic detrusor overactivity. oNeuropathic bladder dysfunction as a result of diabetes,

strokes, Alzheimer’s disease or Parkinson’s disease.oDegeneration of bladder smooth muscle giving rise to

impaired voiding and detrusor instability;oBOO due to BPH.

Hesitancy (worsened if the bladder is very full) Poor flow (unimproved by straining) Intermittent stream – stops and starts Dribbling (including after micturition) Sensation of poor bladder emptying Episodes of near retention

Voiding symptoms

Frequency Nocturia Urgency Urge incontinence Nocturnal incontinence (enuresis)

Storage symptoms-Overactive Bladder Syndrome

This is a urodynamic concept based on the combination of low flow rates in the presence of high voiding pressures.

Diagnosed definitively only by pressure-flow studies.

Bladder Outflow Obstruction

Flow rates provide a useful guide for everyday clinical management.

Urodynamically proven BOO may result from: BPH Bladder neck stenosis Bladder neck hypertrophy Prostate cancer Urethral strictures Functional obstruction due to neuropathic conditions

Effects of BOO on the Bladder

Decrease in urinary flow rates :For a voided volume > 200 ml, a peak flow rate of > 15 ml/s is normal, 10–15 ml/s is

equivocal and < 10 ml/s is low.

Increase in voiding pressures :

Pressures > 80 cmH2O are high, pressures between 60 and 80 cmH2O are equivocal and pressures < 60 cm H2O are normal.

Acute retention of urine

Chronic retention

Impaired emptying of bladder

Haematuria

Complications of BOO

Other than pain from retention, pain is not a symptom of BOO

Its presence should prompt the exclusion of acute retention, urinary infection, stones, carcinoma of the prostate and carcinoma in situ of the bladder

It is critical to exclude causes of LUTS other than BPH before medical or surgical treatment.

The differential diagnosis of lower urinary tract symptoms in addition to BPH includes the following:

Urethral stricture Bladder neck contracture Carcinoma of the prostate Carcinoma of the bladder Bladder calculi Urinary tract infection and prostatitis Neurogenic bladder

History: Symptom assessment:

The International Prostate Symptom Score (IPSS) is recommended scoring system for the baseline assessment of symptom, severity in men presenting with LUTS

Assessment of the Patient with LUTS

0-7 Mildly symptomatic8-19 Moderately symptomatic20-35 Severely symptomatic

Generally WNL

Chronic retention- distended bladder

Loss of the transverse supra pubic skin crease

Examination of the external urethral meatus is done to exclude stenosis or a palpable urethral mass

Epididymides are palpated for signs of inflammation

Abdominal Examination

The posterior surface of the prostate is smooth, convex and firm in consistency.

The rectal mucosa can be made to move over the prostate.

Residual urine may be felt as a fluctuating swelling above the prostate.

Considerable amount of residual urine if present, pushes the prostate downwards, making it appear larger than it is.

Digital Rectal Examination

To eliminate neurological conditions like diabetes mellitus, tabes dorsalis, disseminated sclerosis, cervical spondylosis, Parkinson’s disease may mimic prostatic obstruction.

Examination of perianal sensation and anal tone is useful in detection of an S2 to S4 cauda equina lesion.

Nervous System

A urinalysis should be done either by using a dipstick test or microscopic examination of the spun sediment to rule out UTI and haematuria, either of which strongly suggest a non-BPH pathologic process as a cause of symptoms.

Urine cytology should always be requested in men with severe irritable symptoms and dysuria, especially if they have a smoking history. Carcinoma in-situ of the bladder is a diagnosis that may have serious consequences if overlooked.

Urinalysis

Postvoid residual urine volume is the amount of fluid remaining in the bladder immediately after the completion of micturition.

Studies indicate that PVR urine volume normally ranges from 0.09 to 2.24 mL, with the mean being 0.53 mL (Hinman and Cox, 1967).

Seventy-eight percent of normal men have PVR volumes of less than 5 mL, and 100% have volumes of less than 12 mL(DiMare et al, 1963).

USG & Postvoid Residual Urine Volume

Traditionally, urologists have assumed that increasing amounts of PVR urine denote BPH progression and are thus an “indication” for surgery.

Normally present in Serum but if > 2.5–4 nmol/L, then transrectal ultrasound scanning (TRUS) plus multiple transrectal biopsies (10 biopsies) should be considered.

Serum Prostate – Specific Antigen

Special flow rate clinic. Coupled with ultrasound

measurement of post-void residual urine

Flow Rate Measurement

A, Normal cystoscopic appearance of the prostate in a young man. B, Moderate BPH, viewed cystoscopically

A B

Q- In which zone of the prostate does hypertrophy beginA) Peripheral zone B) Central zoneC) Transitional zoneD)Fibromuscular Stroma

MCQ

Answer- C) Transitional zone

Reference- Bailey & Love’s Short Practice of Surgery, 26th edition, page #1342.

Bailey and Love’s Short Practice of Surgery, 26th Edition Sabiston Textbook of Surgery, 19th Edition Campbell – Walsh Urology, 10th Edition Robbins Basic Pathology, 9th Edition Gray’s Anatomy, 40th Edition

References

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