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endo y3s1 > IC19 Benign Prostate Hyperplasia > Flashcards

IC19 Benign Prostate Hyperplasia Flashcards

1
Q

description of BPH

A

Progressive condition; worsens over time
* Lower urinary tract signs & symptoms (LUTS)
* Negative impact on QOL

Non-malignant growth of some components of prostate

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2
Q

physiology - types of tissues

A
  1. epithelial (static)
  2. stromal (dynamic)
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3
Q

physiology: epithelial tissues

A

Testosterone converted to dihydrotestosterone [DHT] by enzyme type II 5α-reductase, in the prostate
* DHT ⇒ stimulates growth of prostate

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4
Q

physiology: stromal tissues

A

Innervated by α1 adrenergic receptors

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5
Q

pathophysiology

based on static & dynamic components

A

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

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6
Q

phases of bladder response to obstruction

A
  1. early phase
  2. middle phase
  3. late phase
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7
Q

phases of bladder response to obstruction
(1) early

A

Bladder muscle forces urine through narrowed urethra by contracting more forcefully
Urine able to pass out normally → lesser signs & symptoms

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8
Q

phases of bladder response to obstruction
(2) middle

A
  • Bladder muscles gradually become thicker (hypertrophy) to overcome the obstruction
  • Detrusor muscles achieving highest state of hypertrophy ⇒ muscle decompensates (cannot contract strongly)
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9
Q

phases of bladder response to obstruction
(3) late

A

Detrusor muscle become irritable &/ or overtly sensitive (overactivity/ instability) → contract abnormally in response to small amounts of urine in bladder ⇒ need to urinate frequently

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10
Q

signs & symptoms (general + 2 main types)

A

Start to occur in ⅓ men >65 years
Most usually remain asymptomatic
Lower urinary tract symptoms (LUTS)

main types
1. obstructive
2. irritative

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11
Q

obstructive symptoms

when + how it occurs & what are the symptoms

A
  • 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

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12
Q

irritative symptoms

when + how it occurs & what are the symptoms

A
  • 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

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13
Q

Assessing BPH

D, U, U, P, P

A
  • 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
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14
Q

drug exacerbating BPH + reasons

A

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

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15
Q

management of BPH

when to watch, when to initiate pharmacotherapy

A

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

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16
Q

non-pharmacological methods

A
  • Limited fluid intake in evening
  • Minimise caffeine & alcohol intake
  • To take time to empty bladder completely & often
  • Avoid medications that can exacerbate symptoms
17
Q

pharmacological therapy

A
  1. a1 adrenergic antagonists
  2. 5a reductase inhibitors
  3. PDE5 inhibitors
  4. antimuscarinics
18
Q

(1) a1 adrenergic antagonists
types

MOA, drugs, titration

A

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)

19
Q

(1) a1 adrenergic antagonists
indication

general; selective vs non-selective

A

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

20
Q

(1) a1 adrenergic antagonists
clinical effects

prostate size, PSA, onset, what happens if discontinue

A
  • 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
21
Q

(1) a1 adrenergic antagonists
SE

General

A

muscle weakness, fatigue, ejaculatory disturbances, headache
To give bedtime administration ⇒ decreases orthostatic effects

22
Q

(1) a1 adrenergic antagonists
SE (selective)

A

Low to none peripheral vascular dilation
Less hypotension/ syncope
Ejaculatory disturbances (delayed/ retrograde)
* Silodosin > Tamsulosin > Alfuzosin
* Lesser sexual dysfunction than 5ARIs

23
Q

(1) a1 adrenergic antagonists
SE (non-selective)

A

Dizziness
First dose syncope → body not adjusted yet
Orthostatic hypotension

24
Q

(1) a1 adrenergic antagonists
SE: intraoperative floppy iris syndrome

how it occurs, approach to prevention

A
  • 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
25
Q

(2) 5ARIs
drugs

A

Finasteride, dutasteride

26
Q

(2) 5ARIs
indications

A
  • reducing LUTS (moderate/ severe) with LARGE prostate (>40g)
  • Alternative for patients who want to avoid surgery OR cannot tolerate α1 antagonist
  • Decreases PSA levels → use in patients with initial PSA > 1.5 ng/mL
    Important to obtain PSA levels before initiating therapy ⇒ cannot be interpreted after initiation
27
Q

(2) 5ARIs MOA

A

Inhibits 5α reductase (Type II) → decrease conversion from testosterone to DHT ⇒ reducing the size of prostate

28
Q

(2) 5ARIs SE

A
  • Ejaculatory disorders (reduced semen during ejaculation or delayed ejaculation)
    higher risk than α1 antagonist
  • Decreased Libido (3 -8%)
  • Erectile Dysfunction (ED) (3-16%)
  • Gynecomastia and breast tenderness (1.0%)
29
Q

(3) PDE5i
background

drug, effect on prostate size, onset

A

Tadalafil
Does not affect prostate size
Onset: days to weeks

30
Q

(3) PDE5i indications

A
  • Add on therapy for patients with concomitant ED
  • Monotherapy for patients with BPH-LUTS with or without concurrent ED
    Younger age, low BMI, higher baseline symptoms
31
Q

(3) PDE5i MOA

A

(unknown) Likely smooth muscle relaxation

32
Q

(3) PDE5i SE

A

Significant hypotension

33
Q

(4) antimuscarinics indications

PVR requirement

A
  • Add on therapy for patients with irritative voiding symptoms (mimic overactive bladder)
  • PVR must be <250 mL
34
Q

(4) antimuscarinics MOA

A

Block muscarinic receptors in detrusor muscles ⇒ decrease involuntary contraction of bladder

35
Q

combination therapy

A
  1. a1 antagonists + 5ARIs
  2. 5ARIs + PDE5i
  3. a1 antagonists + PDE5i (rare)
35
Q

combination therapy
purpose

A

Better effects than monotherapy; long term use is safe with mild AE
Beneficial for individuals with moderate symptoms & prostate size > 25g
* IPSS 8-19, IPSS QOL 5-6 (must be affected by the symptoms)

36
Q

(1) a1 antagonists + 5ARIs

effect onset, indication, possible combi

A
  • α1 blockers provide benefit within weeks + 5ARI require months for optimal effects
  • For symptomatic patients with enlarged prostate
  • Possible combinations
    MTOPS: doxazosin + finasteride
    CombAT: tamsulosin + dutasteride
  • After 6 months of combination therapy → can discontinue α1 blockers in moderate BPH
37
Q

(2) 5ARIs + PDE5i

indication, note for cardiac patients

A
  • To mitigate sexual AE: from 5ARI/ concomitant ED
  • Take note in people with cardiac comorbidities (along BPH & ED → very common)
    Unstable angina: should not initiate PDE5I → contraindicated with concomitant use of nitrates
38
Q

(3) a1 antagonist + PDE5i

reasons for rarity, dosing requirements, prostate size

A
  • Rarely used; can cause severe life threatening hypotension
    Need to use uro-selective α1 instead
  • Important to optimise/ stabilise α1 antagonist dose FIRST before adding PDE5I
    PDE5I to use lowest effective dose
  • Does not help with large prostate size

endo y3s1 (16 decks)

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