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JC WCS > Urology JC075: The Penis Does Not Obey The Order Of Its Master: Erectile Dysfunction > Flashcards

Urology JC075: The Penis Does Not Obey The Order Of Its Master: Erectile Dysfunction Flashcards

1
Q

Anatomy of penis

A

Skin
—> Superficial (Dartos) fascia
—> Deep (Buck’s) fascia
—> Tunica albuginea (outer longitudinal + ***inner circular) (weakest at 5 to 7 o’clock position)
—> Corpus cavernosum (with fibres from Tunica albuginea traversing for structural support)
—> Sinusoids containing blood (smooth muscle in between sinusoids)

3 Corporal bodies:

  1. Corpus spongiosum
    - enlarge into ***glans penis —> covering distal part of Corpus cavernosum
    - houses urethra
    - continues into Bulbus penis
    - covered by ischiocavernosus muscle
  2. Corpus cavernosum x2
    - continuous with each other
    - elongate into left + right ***crus

Penis:

  • superficially bound to fascia by ***Fundiform ligament —> invest into Dartos fascia
  • deeper bound to Buck’s fascia by ***Suspensory ligament of penis —> invest into Buck’s fascia —> superiorly connect to Pubic symphysis

Artery supply:
***Internal pudendal artery —> Cavernous artery + Bulbourethral artery + Dorsal artery + Circumflex artery

Venous supply:

  1. ** Subtunical plexus —> **Emissary vein (drain Corpus cavernosa) —> across Tunica albuginea towards surface —> ***Superficial dorsal vein —> Saphenous vein —> External iliac vein
  2. ***Deep dorsal vein —> Internal pudendal vein —> Internal iliac vein
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2
Q

Physiology of erection

A

Detumescence (Flaccid penis)
Tonically contracted:
- Arteriole wall smooth muscle
- Smooth muscle separating sinusoids inside 3 corporeal bodies
—> Minimal amount of arteriolar bloodflow into corporal bodies
—> Subtunical venous plexus + Emissary veins drainage good

Tumescence:
Relaxed:
- Arteriole wall smooth muscle
- Smooth muscle in between sinusoids
—> Rapid ↑ in arterial inflow to sinusoids
—> ***Sinusoids engorged with blood
—> ↑ Size + ↑ Girth + ↑ Length
—> ***Subtunical plexus compressed
—> Tunical covering stretched
—> ***Occluding emissary veins
—> Block venous drainage
—> Trapping blood inside corporal bodies
—> Erection
  • **Main components:
    1. Smooth muscle relaxation (Arteriole wall smooth muscle + Smooth muscle separating sinusoids)
    2. Sinusoidal relaxation + engorgement
    3. Arterial dilatation
    4. Venous compression

Innervation:

  1. Sympathetic (T11-L2) —> Pelvic plexus —> ***Cavernous nerve (neurovascular bundle)
  2. Parasympathetic (S2-S4) —> Pelvic plexus —> ***Cavernous nerve (neurovascular bundle)
  3. Somatic system (Dorsal nerve —> Onuf’s nucleus S2-4 —> Ischiocavernosus (erection) + Bulbospongiosus (***ejaculation)

SM contraction:

  • Sympathetic firing (NE) —> ↑ intracellular Ca —> activate SM contraction —> Detumescence
  • **Parasympathetic firing (ACh) —> ↓ pre-synaptic sympathetic firing + stimulates **NO release from endothelium —> SM relaxation —> Tumescence

Overall process:
Audiovisual / Fantasy stimuli (psychogenic), Tactile (reflexogenic), Nocturnal (REM sleep)
—> **Cavernous nerves to generate NO (nNOS) to initiate erection
—> *Parasympathetic firing to generate NO (eNOS) from **endothelium to **maintain erection
—> **cGMP pathway
—> SM relaxation (Arteriole, Intracorporeal intersinusoidal SM)
—> Blood engorgement + Trapping within corporeal bodies
—> **Ischiocavernosus muscle contraction (Onuf’s nucleus) forcefully compress base of engorged corpora cavernosa, producing “Rigid-phase” of erection

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3
Q

***SM relaxation

A

Arteriole wall smooth muscle + Smooth muscle separating sinusoids

Via:

  1. K influx into cell (hyperpolarisation of cell)
  2. Ca sequestration into ER
  3. Blocking further Ca influx from outside of cell

2 mechanisms:

  1. cAMP pathway (NO independent)
    - **PGE1 —> adenylyl cyclase —> ATP to cAMP —> PKA —> cAMP degraded by **PDE2-4 (inhibited by Papaverine)
  2. cGMP pathway (NO dependent)
    - **NO (most important molecule to bring about SM relaxation) —> guanylyl cyclase —> GTP to cGMP —> PKG —> cGMP degraded by **PDE5 (inhibited by Sildenafil, Papaverine, Zaprinast)
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4
Q

Phosphodiesterase

A
  • Superfamily of enzymes
  • 11 different types
  • except PDE6 (exclusive in retina), all PDE identified in cavernosal tissue
  • ***PDE5 most important PDE in termination in cGMP-signaling-induced smooth muscle relaxation
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5
Q

Nitric oxide

A
  • Small-sized molecule produced from **endothelium + **nerves
  • freely diffusible across cell membranes

NO synthesis requires NO synthetase (NOS: 3 isoforms)

  1. nNOS (nervous tissue): ***Initiating erection
  2. eNOS (endothelium): ***sustaining erection
  3. iNOS (all other cell types) (little involvement in erection)

When NO is released from nerves (i.e. neurotransmitter)
—> termed non-adrenergic / non-cholinergic (***NANC) neurotransmission

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6
Q

Erectile dysfunction

A
  • Old term: Impotence
  • Part of the ***spectrum of male sexual dysfunction
    —> Erectile dysfunction
    —> Ejaculatory dysfunction (Premature ejaculation, Anejaculation, Retrograde ejaculation)
    —> Reduced libido

Definition:

  • Persistent inability to achieve / maintain erection sufficient to permit satisfactory sexual performance
  • **Repeated + **Chronic

(Most men experienced >=1 episodes of unsatisfactory erections with partner, often associated with anxiety / alcohol / fatigue —> NOT erectile dysfunction + NOT require treatment)

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7
Q

Significance of ED

A
  • Common problem, esp. in aging population
  • Affect physical + psychosocial health —> impair QOL
  • ***Often early (and only) manifestation of CVS disease (arterial supplying penis have similar caliber to coronary arteries —> affected together)

Prevalence of ED:

  • 40-70yo 52% ED
  • ~20% of all adult men (mild / moderate / severe)
  • ↑ with age

Epidemiological trend

  • Strong association between ED and ***DM, DL, obesity, metabolic syndrome, smoking, CVS disease, depression, BPH
  • Prevalence ↑ with age

Diagnosis of ED represents a **barometer of CVS health + shown to associate with **CVS disease mortality

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8
Q

***Causes of ED

A
  1. Organic
    - **Vasculogenic
    —> Arteriogenic (not enough arterial blood to penis)
    —> Cavernosal (venogenic, penis fail to trap blood)
    - **    Neurogenic
    - ***Endocrinologic
  2. ***Psychogenic
    - Generalised
    - Situational
    —> Partner-related
    —> Performance-related
    —> Distress / Adjustment-related
  3. **Drug-induced
    - Antihypertensives (Thiazides, β blockers)
    - Antidepressants (SSRI, TCA)
    - Antipsychotics (Neuroleptic)
    - Recreational drugs (Heroin, Marijuana, Methadone)
    - **    Antiandrogens (directly cause ED, 5α-Reductase inhibitors, LHRHa (Luteinizing Hormone - Releasing Hormone analogue))

Nowadays —> Almost always ***Multi-factorial in etiology

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9
Q

***Investigations of ED

A
  1. ***Nocturnal penile tumescence (NPT)
  2. Penile brachial pressure index
  3. Duplex USG
  4. Pudendal angiography
  5. Pelvic venography
  6. Pharmacologic cavernosometry + cavernosography
  7. Rigiscan
    Etc.

Nowadays: Goal-directed approach, avoid traditional exhaustive + unreliable investigations —> just treat the patient according to their wish

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10
Q

***Treatment of ED

A
  1. Psychosexual therapy
  2. Penile revascularisation
  3. Penile prosthesis
  4. Intracavernosal injection
  5. Vacuum constriction device
  6. Intraurethral medication (intraurethral PGE)
  7. ***Oral PDE5 inhibitor

Step-wise approach:

  1. Lifestyle changes
    - stop smoking, DM control
  2. 1st line
    - Oral PDE5 inhibitor
    - Vacuum constriction device
    - Low intensity SWL (shockwave lithotripsy)
    (- Topical / Intraurethral Alprostadil (PGE1))
  3. 2nd line
    - Intracavernosal injections
  4. 3rd line
    - Penile prosthesis
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11
Q

***History taking of ED

A

Sometimes history from partner also important

  1. Sexual history / HPI of ED
    - Onset
    - Duration of ED
    - Precipitating events
    - **Global / Situational
    - **    Severity of ED (ability to penetrate)
    - **Libido, ejaculation, orgasmic response
    - **    Presence of morning erection
  2. Medical history
    - **DM, DL, CAD
    - **    Neurologic disease / Neuropathy
    - History of urologic procedure / RT
  3. Social history
    - Smoking, Drinking history
  4. Drug history
    - ***Nitrates (TNG, oral nitrates)
    - Recreational use of drugs

Aim:

  1. Elicit underlying causes of ED
  2. Look for CI for treatment
  3. Uncover possible underlying associated medial illness
  4. Identify patient’s expectation + readiness for invasive treatment if necessary (most patients: to have adequate rigidity for penetrative intercourse for reasonable amount of duration before ejaculation)
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12
Q

Psychogenic vs Organic ED

A

Psychogenic:

  • Sudden onset
  • Complete immediate loss
  • Situational dysfunction
  • Waking erections present

Organic:

  • Gradual onset
  • Incremental progression
  • Global dysfunction
  • Waking erections poor / absent
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13
Q

***P/E of ED

A
  1. General
    - Stature / Gait (indicate neurologic / endocrinopathy)
    - ***Gynaecomastia
    - Lower limb neurology
  2. Abdomen
    - **Secondary sexual characteristics (pubic hair distribution)
    - **    Femoral pulses (vascular diseases)
  3. External genitalia
    - Phallus deformity
    - ***Testes, Genital / Perineal sensation
    (- Bulbocavernosus reflex (S2-S4, squeezing of glans —> contraction of anal sphincter))
  4. Questionnaire to quantitatively define severity of ED
    - International Index of Erectile function (IIEF) questionnaire (15 questions)
    - Abridged version (IIEF-5)
    —> No ED: 22-25
    —> Mild: 17-21
    —> Mild - Moderate: 12-16
    —> Moderate: 8-11
    —> Severe: 5-7
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14
Q

***Investigations of ED

A

Aim: Uncover underlying associated serious medical conditions

  1. FBS
  2. ***Lipid profile
  3. ***Testosterone / LH (if also have reduced libido)
  4. CVS assessment + stratification
    - Risk factors of CAD
    - Angina presence
    - Previous MI
    - LVD / CHF
    - HT
    - Valvular disease
    —> Low risk: Start treatment for ED + Resume sexual activity
    —> High risk: Defer sexual activity until cardiac condition stabilised
    —> Indeterminate risk: refer to cardiologist for assessment

Indications for specialised testings (e.g. NPT, Angiogram)

  1. ***Primary ED (ED since puberty)
  2. Young ED with history of pelvic / perineal trauma
  3. ***Complex psychiatric / psychosexual disorder
  4. Penile deformities
  5. ***Complex endocrinopathies
  6. Medico-legal reasons (e.g. rape)
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15
Q

PDE5 inhibitor

A

Result in SM relaxation from inhibiting cGMP degradation

***NOT initiators of erection —> still require sexual stimulation to produce NO for initiating erection

4 drugs available:

  1. Sildenafil (Viagra)
  2. Tadalafil (Cialis)
  3. Vardenafil (Levitra)
  4. Avanafil (Spedra)

Efficacy:

  • similar onset of action
  • similar % of successful intercourse
  • achieves successful intercourse ***~70% (50% in DM / post-radical prostatectomy patients)

Sildenafil vs Vardenafil vs Tadalafil:

  • Onset of action: 25, 25, 30mins
  • Duration: 5, 5, ***36hours
  • Starting dose: 50mg, 10mg, 20mg
  • Take before sex: 1 hour, 25-60 mins, 30min-36hours
  • Max dosing frequency: all ***1 per day

SE:

  1. ***Headache
  2. ***Flushing
  3. ***Nasal congestion
  4. Abnormal vision (PDE6 ∵ cross reactivity between PDE5 and 6 —> see blue tint) (Sildenafil, Vardenafil only)
  5. Back pain / Myalgia (PDE11) (Tadalafil only)

Administration:

  1. Check of absolute CI (concomitant intake of ANY form of ***Nitrates —> converted to NO —> cGMP accumulation —> profound hypotension + possible death)
  2. 1 hour before sexual intercourse
  3. Sexual stimulation necessary
  4. Must NOT take >=1 dose in a day
  5. Warn about SE
    - avoid driving / operating machinery after taking

Warn against:

  1. ***MI, stroke, life threatening arrhythmia within previous 6 months
  2. ***New York Heart Association class 2 or higher HF / CAD causing unstable angina
  3. ***Resting hypotension (<90/50 mmHg) or HT (>170/100 mmHg)
  4. Known hereditary degenerative retinal disorders including retinitis pigmentosa
  5. Severe hepatic impairment (Child-Pugh C) / ESRD requiring dialysis
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16
Q

Alprostadil injections

A
  • Synthetic form of PGE1
  • Elicits SM relaxation using cAMP pathway (**independent of NO)
    —> cause erection **    without any sexual stimulation
  • Topical / Intraurethral Alprostadil no longer available in HK

Intracavernosal injection (ICI) still available (***Caverject)

  • inject directly into Corpus cavernosum (2 / 10 o’clock)
  • only approved form of injectable for ED
  • efficacy: 70-80% patients (even in DM / post-RP patients)
  • need titration of dosage (5-20ug)

SE:

  1. Painful erection
  2. ***Prolonged erection
  3. ***Priapism
  4. Penile fibrosis
17
Q

Vacuum constriction device (VCD)

A

Unpopular form of treatment (may be suitable for elderly who have infrequent sex)

Advantages:
- Non-invasive

Disadvantages:

  • Unnatural “cold” (blue) penis
  • Inability to ejaculate
  • ***Bruising + numbness

CI:
- Patients on anticoagulants

18
Q

Penile prosthesis

A

3rd line treatment

Indication:

  • ED refractory to all other treatment
  • Patients who want a “permanent” solution

2 main types:

  1. ***Malleables (semirigid rods)
  2. ***Inflatables

Advantages:

  • High success rate (90-95%)
  • High satisfaction rate (80-90%)

Disadvantages:

  • Cost
  • Irreversible damage to corporeal bodies
Complications
- Infection
- Erosion (out of penis)
- ***Mechanical failure
—> usually require removal of whole set-up followed by new one

JC WCS (134 decks)

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