IC19 Benign Prostate Hyperplasia Flashcards
description of BPH
Progressive condition; worsens over time
* Lower urinary tract signs & symptoms (LUTS)
* Negative impact on QOL
Non-malignant growth of some components of prostate
physiology - types of tissues
- epithelial (static)
- stromal (dynamic)
physiology: epithelial tissues
Testosterone converted to dihydrotestosterone [DHT] by enzyme type II 5α-reductase, in the prostate
* DHT ⇒ stimulates growth of prostate
physiology: stromal tissues
Innervated by α1 adrenergic receptors
pathophysiology
based on static & dynamic components
static
High levels of DHT ⇒ enlargement of prostate tissue
dynamic
Increased smooth muscle tissue & agonism of α1 receptors
→ vasoconstriction of prostate
⇒ narrowing of urethra outlet (smaller)
overall outcome
Urethral obstruction + signs & symptoms
phases of bladder response to obstruction
- early phase
- middle phase
- late phase
phases of bladder response to obstruction
(1) early
Bladder muscle forces urine through narrowed urethra by contracting more forcefully
Urine able to pass out normally → lesser signs & symptoms
phases of bladder response to obstruction
(2) middle
- Bladder muscles gradually become thicker (hypertrophy) to overcome the obstruction
- Detrusor muscles achieving highest state of hypertrophy ⇒ muscle decompensates (cannot contract strongly)
phases of bladder response to obstruction
(3) late
Detrusor muscle become irritable &/ or overtly sensitive (overactivity/ instability) → contract abnormally in response to small amounts of urine in bladder ⇒ need to urinate frequently
signs & symptoms (general + 2 main types)
Start to occur in ⅓ men >65 years
Most usually remain asymptomatic
Lower urinary tract symptoms (LUTS)
main types
1. obstructive
2. irritative
obstructive symptoms
when + how it occurs & what are the symptoms
- More often in early disease
- Narrowed urethra → difficult to pass urine
- Detrusor muscle not irritable/ overactive YET
Hesitancy, weak stream, sensation of incomplete emptying, dribbling, straining, intermittent flow
irritative symptoms
when + how it occurs & what are the symptoms
- When detrusor muscle decompensates
- Occurs after several years of untreated BPH
Dysuria → pain on urination
Due to bladder continuously contracting
Frequency, nocturia, urgency, urinary incontinence
Assessing BPH
D, U, U, P, P
- Digital rectal exam (DRE)
- Ultrasonography
- Maximum urinary flow rate (Qmax)
-
Postvoid residual (PVR)→ amount of urine left in bladder after urinating
<100 mL = normal; >200 mL = inadequate emptying -
Prostate specific antigen (PSA)
Might be elevated in BPH & positively correlated with prostate volume
Helps predict progression of BPH (>1.5 ng/ mL)
Higher risk for prostate cancer
drug exacerbating BPH + reasons
Anticholinergic: decrease bladder muscle contractility
* Antihistamines, tricyclic antidepressants
α1 adrenergic agonists: contraction of prostate smooth muscles
* Decongestants
Opioid analgesics: increase urinary retention
Diuretics: increase urinary frequency
Testosterone: stimulate prostate growth
management of BPH
when to watch, when to initiate pharmacotherapy
watch
* Mild symptoms (IPSS <8)
* moderate/ severe symptoms (IPSS ≥ 8) who are not bothered by symptoms (IPSS QOL <3)
initiate
symptomatic patients who are bothered by it (IPSS QOL ≥ 3) & those with complications
non-pharmacological methods
- Limited fluid intake in evening
- Minimise caffeine & alcohol intake
- To take time to empty bladder completely & often
- Avoid medications that can exacerbate symptoms
pharmacological therapy
- a1 adrenergic antagonists
- 5a reductase inhibitors
- PDE5 inhibitors
- antimuscarinics
(1) a1 adrenergic antagonists
types
MOA, drugs, titration
non-selective
* Antagonises both peripheral vascular & urinary α1 adrenergic receptors
* Doxazosin, terazosin
* Need to titrate slowly to therapeutic dose (risk of hypotension & syncope)
selective
* Antagonises only urinary α1A adrenergic receptors (predominant in prostate & LUT)
* Alfuzosin, Tamsulosin, Silodosin
* No need for titration (lesser risk of titration)
(1) a1 adrenergic antagonists
indication
general; selective vs non-selective
general
reducing LUTS (moderate/ severe) with SMALL prostate (<40g)
Selective
For patients who don’t require added BP lowering effect
non-selective
* Beneficial in hypertensive patients requiring additional BP lowering effect
* To avoid in patients with hx of syncope
* Not to use as monotherapy with HTN & BPH concurrently
(1) a1 adrenergic antagonists
clinical effects
prostate size, PSA, onset, what happens if discontinue
- Do not reduce prostate size
No prevention for progression of BPH/ need for surgery - No effect on PSA
- Onset → fast; days to weeks
- Signs & symptoms will recur if discontinued
(1) a1 adrenergic antagonists
SE
General
muscle weakness, fatigue, ejaculatory disturbances, headache
To give bedtime administration ⇒ decreases orthostatic effects
(1) a1 adrenergic antagonists
SE (selective)
Low to none peripheral vascular dilation
Less hypotension/ syncope
Ejaculatory disturbances (delayed/ retrograde)
* Silodosin > Tamsulosin > Alfuzosin
* Lesser sexual dysfunction than 5ARIs
(1) a1 adrenergic antagonists
SE (non-selective)
Dizziness
First dose syncope → body not adjusted yet
Orthostatic hypotension
(1) a1 adrenergic antagonists
SE: intraoperative floppy iris syndrome
how it occurs, approach to prevention
- Occurs if patient takes α1 adrenergic antagonists before cataract surgery
Mostly tamsulosin - Due to blockage of α1 receptors in iris dilator muscle ⇒ pupil will constrict (smaller)
- Men should avoid initiation of α1 adrenergic antagonists until surgery completed OR hold at least 14 days before surgery
