This document discusses male sexual dysfunction and erectile dysfunction (ED). It defines ED and provides prevalence data, noting that the risk of ED increases with age. It describes the anatomy involved in erection, ejaculation, and the arterial and venous blood supply of the penis. The mechanisms and phases of erection are explained. Common risk factors, causes, and medications associated with ED are listed. Methods for diagnosing ED including history, physical exam, the International Index of Erectile Function (IIEF), and potential tests like nocturnal penile tumescence monitoring and duplex ultrasound are outlined.

1. Male sexual dysfunction
Edmond Wong

2. A
B
C
• Name the structures A, B, C and D (0.5 mark each)
D

3. • A : Skin (0.5)
• B : Dartos fascia (0.5)
• C : Buck’s fascia (0.5)
• D : Tunica albuginea (0.5)

4. What is the definition of ED?
• Persistent inability to initiate and maintain
an erection sufficient for satisfactory
sexual activity
• Better not to use “Impotence” as it is less
precisely defined

5. What is prevalence & severity?
• Massachusetts Male Aging Study (MMAS)
• Prevalence –
– Men 40-70yo
• ~50% have ED
• Mild ED: 17%
• Moderate ED : 25%
• Complete ED : 10%
• ED prevalence increases with age
– 50% at age 50, 60% at age 60, 70% at age 70

6. What is innervation of
erection and ejaculation?
• Autonomic
– Sympathetic nerves from T11-L2
– Parasympathetic from S2-4, form the pelvic plexus
– The cavernosal nerves are branches of pelvic plexus
(i.e. parasympathetic) that innervate the penis
– Parasympathetic stimulation causes erection
– Sympathetic activity causes ejaculation and
detumescence (loss of erection)

7. What is innervation of
erection and ejaculation?
• Somatic
– Somatosensory information travels via the pudendal
nerves
– Onuf’s nucleus (S2-4) is the somatic centre for
efferent innervation of the ischiocavernosus and
bulbocavernosus muscles of the penis
• Central
– Medial preoptic area and paraventricular nucleus
(PVN) in the hypothalamus are important centres for
sexual function and penile erection

8. What is the arterial blood
supply of penis?
• Originate from internal pudendal artery
• Three branches of common penile artery which join to form
vascular ring near the glans
• Bulbourethral artery
– Supplying the bulb and corpus spongiosum
• Dorsa penile artery
– Skin, fascia and the glans penis and forms anastomoses with the
bulbourethral artery at he glans. These anastomoses allow division the
the urethra during urethral stricture surgery without compromising the
blood supply to the distal urethral
• The cavernous artery
– Supplies only the cavernosal bodies & gives off many helicine arteries
which supply the trabecular erectile tissue & sinusoid. Does not
anastomose with other 2 penile arteries
• Pulsations absent in penile vessels – likely vascular cause of
ED

9. What is the venous blood
supply of penis?
• Skin and subcutaneous tissue  saphenous
vein
• Emissary veins draining corpus cavernosum and
corpus spongiosum  deep dorsal vein 
periprostatic venous plexus
• Emissary veins draining proximal corpora
cavernosa  nternal pudendal veins

10. Physiology of Erectile ResponsePhysiology of Erectile Response
Complex process
combining
• psychological stimuli
• neurologic event
• smooth muscle relaxation
• arterial dilation
• venous compression

11. What are the five phases of
erection?
Phase Term
0 Flaccid phase
1 Latent (filling) phase
2 Tumescent phase
3 Full erection phase
4 Rigid erection phase
5 Detumescence phase

12. What is mechanism of
erection?
• Neuroendocrine signals from the brain, created by audiovisual
or tactile stimuli
• Signals are relayed via the cavernosal nerve to the erectile
tissue of the copora cavernosa, activating the veno-occlusive
mechanism
• This triggers increased arterial blood flow into sinusoidal spaces
with relaxation of cavernosal smooth muscle, and opening of
the vascular space
• Compressing the subtunical venous plexuses, decreasing
venous outflow
• Both spongiosus and cavernosus are surrounded by tunica
albuginea, which consist of outer longitudinal and inner circular
layers. The sliding of 2 layers over each other during
engorgement lead to occlusion of emissary veins
• Rising intracavernosal pressure and contraction of the
ischiocavernosus muscles produces a rigid erection

13. Mechanism of erection
• Full erection phase:
– Compression of the deep dorsal and
cricumflex vein btw Buck’s fascia & engorged
cavernosa  glanular tumescence
• Rigid –erection phase:
– Ischiocavernosus and bulbocavernosus
muscle forcefully compress the spongiosum
and penile veins  further engorgement and
increase pressure in glans and spongiosum

14. Mechanism of PDE5-i
• nitric oxide is synthesized from L-arginine and released
by neurons, endothelial cells, and possibly corporal
smooth muscle cells of the penis in response to sexual
stimulation
• Nitric oxide enter SM cell
• Activate soluble form of enzyme guanylate cyclase
(sGC)
• sGC convert guanosine triphosphate (GTP) to cyclic
guanosine monophosphate (cGMP) (an active
intracellular 2nd
messenger)
• cGMP lead to SM relaxation thru reduction of
intracellular Ca  erection
• cGMP is metabolize to GMP (inactive) by PDEs
• Thus PDE inhibitor facilitate NO induced SM relaxation
by increase accumulation of intracellular cGMP

17. What is mechanism of
erection?

18. Pathophysiology of Erectile Dysfunction
Inflow Outflow
Failure to initiate
Psychogenic / Neurogenic
Failure to store
Venous leak
Failure to fill
Arterial insufficiency

19. What is the mechanism of
venogenic erectile dysfunction?

20. • What physiological process is this chart describing? (1)
• What are the top and bottom row depicting? (2)
• Can you name the 6 columns? (2)
Q57

21. • Tumescence / erection (1)
• Top row : artist depiction of the state of the
cavernosal arteries during different phases of
erection induced by prostaglandin injection (1)
• Bottom row : Doppler waveform of the
cavernous arteries during this erection (1)
• Flaccid, latent, tumescent, full, rigid,
detumescent
• (2 marks for ALL 6 correct answers)

22. What is the mechanism of
ejaculation?
• Tactile stimulation of the glans penis causes sensory
information to travel (via the pudendal nerve) to the
lumbar spinal sympathetic nuclei
• Sympathetic efferent signals (travelling in the
hypogastric nerve) cause contraction of smooth muscle
of the epididymis, vas deferens, and secretory glands,
propelling spermatozoa and glandular secretions into the
prostatic urethra
• There is simultaneous closure of the internal urethral
sphincter and relaxation of the extrinsic sphincter
• Rhythmic contraction of the bulbocavernosus muscle
leads to the pulsatile emission of the ejaculate from the
urethra

23. Risk Factors for ED
• Aging
• Systemic diseases: D.M., hypertension,
atherosclerosis, hyperlipidemia
• Endocrine disorders: hypogonadism,
hyperprotactinemia
• Alcohol abuse or smoking
• Trauma or surgery to pelvis or spine
• Depression or stress
• Drugs: antihypertensives, antidepressants,
hormones

24. What are the causes of ED?
• IMPOTENCE
– Inflammatory – prostatitis
– Mechanical – Peyronie’s disease
– Psychological – depression
– Occlusive vascular factors – arteriogenic, PVD
– Trauma – pelvic fracture
– Extra factors – pelvic surgery/RRP – neuro (cavernosal
nerve)-vascular (to cavernosa) injury
– Neurogenic – stroke/spinal cord defect
– Chemical – alcohol, smoking, drugs (diuretics/anti-HT)
– Endocrine – DM

25. Aetiological Causes
Psychogenic
• anxiety
• depression
Endocrine
• hormonal deficiency
Neurogenic
• surgery or trauma to
pelvis or spine
• diabetes mellitus or
alcohol

26. Aetiological Causes
Arteriogenic
• hypertension, smoking, D.M.
• hyperlipidaemia
• surgery or trauma to pelvis
Venous
• functional impairment of the
veno-occlusive mechanism
Drugs
• antihypertensives,
antidepressants

27. What medication asso with ED?
• Diuretics & antihypertensive
• Antidepressant
• Anti-anxiety
• Anti-epileptic drugs
• Pakinson’s disease med
• Antihistamines
• NSAIDs
• Antiarrhythmics
• H-2 blockers
• Muscle relaxants
• Prostate cancer medication
• Chemotherapy

28. What is the difference between
psychogenic vs organic causes?
• Psychogenic
– Sudden onset
– Situational
– Morning erection +ve
– Rigidity of morning erection
– Other psychological
complaints
– Spouse relationship
– Abnormal sexual
development
• Organic
– Gradual onset
– Always
– Morning erection –ve
– Chronic medical illness
(DM, HT, IHD)
– Pelvis trauma / surgery
– Endocrine / Neurological
disease
– Recreational drugs
– +/- Loss of libido
– +/- Reduced size of penis

29. DiagnosisDiagnosis

30. Scenario
• M/70
• HT/DM
• Worsening erectile function for 1 year
• Affecting relationship with 30-year-old wife

31. What is the specific history for ED?
• Sexual
– Onset (sudden or gradual)
– Duration, severity – IIEF
– Early morning erections?
– Loss of libido, sexual relationship issues (different partners)
– Previous treatment
– Patient’s expectation
• Medical and surgical
– Hypertension; cardiac disease; peripheral vascular disease; diabetes
mellitus; endocrine or neurological disorders; pelvic surgery,
radiotherapy, or trauma
• Drugs
– Antipsychotic drugs, anti-anxiety drugs, diuretics, chemotherapy, etc
• Psychosocial
– Anxiety, depression
• Social
– Smoking, alcohol consumption

32. What is IIEF?
• IIEF (International Index of Erectile
Function) 1997
• For assessment of intensity of ED
• Best description of own situation in last 6
months of sexual activity

33. What is IIEF?
• Five domains
1. Erectile function
2. Orgasmic function
3. Sexual drive
4. Intercourse
satisfaction
5. Overall satisfaction
• Short form: IIEF-5
– Scoring 1-5 for each, Total
25
– No ED: 22-25
– Mild ED: 17-22
– Mild to moderate: 12-16
– Moderate ED: 8-11
– Severe ED 1-7

34. What is IIEF-5?

35. What is the physical
examination?
• Height , weight BMI , BP
• Secondary sexual characteristics to rule out hypogonadism
• Thyroid evaluation
• Cardiovascular system
– LL pulses
• Abdominal
– Waist cricumference
• Neurological system
– Penile Sensatiion, bulbocarvernosus reflex, LL neurology
• Genital-urinary system
– Penile deformity, phimosis, Peyronie's plaques
– Testicular size, consistence and mass
– DRE: anal tone, prostate

36. What is the Ix?
• L/RFT
• PSA
• Fasting glucose
• Lipid profile
• TFT
• Hormone profile
– Testosterone
– Prolactin
• Urinalysis

37. Why should ED be investgiated
ED is associated with other morbidities in 20%
• DM
• Occult cardiac disease
• Dyslipidaemia
• Endocrine disorders: hypogonadism
• CVA – 50%

38. Cardiovascular assessmentCardiovascular assessment

39. What is cardiac evaluation in
ED?
• If happened to men having symptomatic
coronary artery disease ( CAD ), ED
precedes 55 – 65% CAD by 3 – 4 years
• Sex energy expenditure is equal to
15min walk or climbing 2 flights
• Absolute risk that sex can trigger MI is 1-
2 per million

40. Princeton II consensusPrinceton II consensus
ED as warning sign of
vascular / cardiac disease

41. What is Princeton II
consensus?

42. What is Princeton II
consensus?

43. What is Princeton II
consensus?
• Low risk
– Controlled HT, NYHA 1, <3 risk factors for IHD, stable
angina, uncomplicated past MI
• Intermediate risk
– >/= 3 risk factors, NYHA 2, <6 weeks from MI
• High risk
– High risk arrhythmia, unstable angina, recent MI (<2
weeks), HOCM, NYHA 3-4, uncontrolled HT

44. What are the indications for
specific diagnostic tests?
• Primary erectile disorder (not caused by organic
disease or psychogenic disorder)
• Young patients with a history of pelvic or perineal
trauma
• Patients with penile deformities that might require
surgical correction, e.g. Peyronie’s disease, congenital
curvature
• Those unresponsive to medical therapy
• Complex psychiatric or psychosexual disorders
• Complex endocrine disorders
• Medicolegal reasons, e.g. implantation of penile
prosthesis, sexual abuse

45. What are the special Test?
1. Nocturnal penile tumescence (NPT)
2. Caverject Trial
3. Vascular imaging
4. Duplex USG
5. Cavernosometry
6. Penile arteriography

46. What is nocturnal penile
tumescence testing?
• 80% Noctural Penile Tumescence (NPT) occurs during
REM sleep
• Rigiscan device contains 2 rings which are placed
around base and distal penile shaft to measure
tumescence and number, duration, and rigidity of
nocturnal erections
• Should be done on at least two nights.
• A functional erectile mechanism is indicated by an
erectile event of
– at least 60% rigidity recorded on the tip of the penis
– that lasts for 10 min or more
• Gold Standard
– Organics vs Psychogenic

47. What is nocturnal penile
tumescence testing?

48. What is intracavernous
injection test?
• A positive test is a rigid erectile response (unable to
bend the penis) that appears within 10 min after the
intracavernous injection and lasts for 30 min
• This response indicates a functional and rule out
veno-occlusive dysfunction, although co-exist with
arterial insufficiency
• If inconclusive as a diagnostic procedure and Duplex
ultrasound of the penile arteries should be requested
• Assisted in Ix including Duplex USG / DICC / penile
arteriogram
• Positive test shows that a patient will respond to the
intracavernous injection program

49. What is duplex ultrasound of
penile arteries?
• Assess cavernosal arterial inflow to corpora
cavernosa
• Normal value
– Peak systolic blood flow >35 cm/s
– End diastolic velocity <5 cm/s and
– Resistance index >0.8
• Further vascular investigation is unnecessary when
a Duplex examination is normal

50. • Name this
investigation (1)
• In investigating
what condition is
this used? (1)
• What is the
finding shown? (1)
Q27

51. • Pharmacologic cavernosography (1)/
Dynamic infusion cavernosgraphy &
cavernosometry (DICC) (1)
• ED (1)
• Venous leakage along pelvic veins
suggestive of veno-occlusive dysfunction
(1)

52. Cavernosography
• Indication:
1. evaluate venous problems in men with ED
2. Investigation of priapism (high flow)
3. Assessment of penile fractures/injury to
assess cavernosal damage
4. Assessment of Peyronie’s disease (rarely
used)
• Contraindication:
– Hx of contrast allergy

53. Carvernosography
• Two 19–22 G butterfly needles inserted into the corpora
• 60-100ml Omnipaque or urograffin infused slowly to
obtain penile pressure 90mmHg
• If penis not erection , contrast leakage
• Fluoroscopy: AP , Rt, Lt oblique view
• Normal: no contrast visualized outside the 2 corpora
cavernosa
• Abnormal: Contrast leakage or significant curvature
• Patient asked to squeeze penis for 5min to ensure
complete emptying

54. • Advantage: more sensitive and accurate
compare to doppler USG for venous
leakage
• Disadvantage:
– Invasive
– Can be painful
– Risk of infection
– Contrast related fibrosis within corpora
– Risk of priapism

55. Dynamic Infusion Cavernosometry &
Cavernosography
• 4 phases
– Injection of vasoactive agents (alprostadil,
Bimix, Trimix) into one corpus cavernosum to
relax the corporeal smooth muscles
– Pharmacologic cavernosometry (infusing the
penis with heparinized saline whilst monitoring
the intracavernosmal pressure)
– Cavernosal artery systolic occlusion pressure
(CASOP) reached as intracavernosal pressure
drops
– Pharmacologic cavernosography (infusing
contrast into the corporeal tissue and
obtaining radiographic images of the penis
and perineum to see if there is venous
leakage
• Normal:
– A gradient between the CASOP and the
brachial artery pressures of <35mmHg
– an equal pressure between the right and the
left cavernous arteries
Venous leakage:
-Inability to occlude systolic pressure
-Large gradient between CASOP & brachial
systolic pressure
-Rapid drop of intracavernosal pressure
upon stopping of infusion

56. What is the indication of arteriography
and dynamic infusion cavernosometry or
cavernosography?
• Arteriography and DICC: dynamic infusion
cavernosometry or cavernosography
should be performed only in patients to
rule out venous leakage who are being
considered for vascular reconstructive
surgery

57. TreatmentTreatment

58. Treatment of Erectile Dysfunction
• Treat underlying disease to preserve health
• Elimination of modifiable risk factors
• Disorders that need treatment as part of ED
management
- relationship conflict
- depression, psychogenic ED
- hypogonadism, hyperprolactinaemia

59. Treatment of Erectile Dysfunction
• Cardiovascular status of the patient
• Is the patient able to resume sexual activity?
- if not, cardiovascular assessment and
intervention may be appropriate
• Patient and partner choices play important
role in identifying successful treatment

60. What are the treatment
options?
• First-line therapies
– Lifestyle modification,
psychosexual therapy
– PDE5i
• Second-line therapies
– Intraurethral injection of
alprostadil
– Intracavernosal injection of
alprostadil
– Vacuum constriction
devices
• Third-line therapy
– Surgical implantation of
prosthesis
– Penile vascular
reconstruction

61. What is the lifestyle
modification to improve ED?
• Smoking
• Alcohol
• HT, DM
• Obesity (BMI), exercise
• A multicentre, randomised study
– In obese men with moderate ED compared 2 years of intensive
exercise and weight loss
– Significant improvements in body mass index (BMI) and physical
activity scores, as well as in erectile function
• Esposito K, et al. Effect of lifestyle changes on erectile dysfunction in obese men: a
randomized controlled trial. JAMA 2004 Jun;291(24):2978-84

62. What is pyschosexual
therapy?
• Identify and treat underlying psychological
diseases
• Provides information and treatment in the
form of sex education, instruction on
improving partner communication skills,
cognitive therapy, and behavioral therapy

63. What is the general efficacy of
various treatment?
• PDE5i - 80% success
– DM 60%, NSRRP 70%
• ICI - 90%
• VCD - 90%
• MUSE - 50%

64. Phosphodiesterase type-5Phosphodiesterase type-5
(PDE5) inhibitors(PDE5) inhibitors

65. What is Phosphodiesterase
type-5 (PDE5) inhibitors?
• sildenafil (Viagra) – half-life 4h
• tadalafil (Cialis) – half-life 17.5h
• vardenafil (Levitra) – half-life 4h
• All have similar effect and outcome
• Enhance cavernosal smooth muscle relaxation and erection by
blocking the breakdown of cGMP to 5GMP. Sexual stimulus is still
required to initiate events
• Make sure no Contraindications
– Concomitant use of nitrates
– Hx of retinitis pigmentosa
– Princeton high risk group
– Severe liver function impairment
• IC50 is the concentration of drug required to produce 50% inhibition
of target enzyme. Vardenafil has the lowest IC50 0.7nM compared
to 0.9 for tadalafil and 3.5 for sildenafil

66. Character of PDE5-i
Sildenafil
(Viagra)
Vardenafil
(Levitrat)
Tadalafil
(Cialis)
Onset of action 15 min -1hr 15min -1hr 15min -2 hr
Effect of food Reduced absorption
with fatty food
Reduced absorption
with fatty food
NONE
Dosage 20,50,100mg 5,10,20mg 5,10,20mg
Side effects Headache,
dyspepsia, facial
flushing,
blurred/blue vision,
backache, myalygia
Headache,
dyspepsia, facial
flushing,
blurred/blue vision,
backache, myalgia
Prolong QT
Headache,
dyspepsia, facial
flushing , blurred/
blue vision ,
backache, myalgia
Contraindications Nitrates Nitrates, anti-
arrhythmics
Nitrates

67. How to counsel patient for PDE5-i?
• No data comparing the efficacy for sildenafil,
tadalafil and vardenafil
• Choice of drug will depend on the patient
preference
– Unplanned sex: tadalafil
– Planned sex: Sildenafil & verdenafil
• Taken at least 30min to 1hr before sex, with
empty stomach
• Medication need appropriate sexual stimulation
• Explained potential side effect

68. Adverse effect
• Headache (20%)
• Flushing (15%)
• Dyspepsia (10%)
• Rhinitis (6%)
• Blurred/ blue vision (6%) (Chromatopsia)
– Cross activity with PDE6 (retinal phototransduction
enzyme)
• Myalgia and back pain (5%)
• Dizziness (5%)
• Priapism (rare)

69. What to do if failed PDE5-i
• 20% do not respond to any PDE5 inhibitors
• Can change to another if one ineffective
• Exclude fake drug
• Should at least try 4 times for at least 2 drug with maximal dosage
before considering failure
• Re-education:
– Dose , timing of med
– Alcohol, interaction with fatty food
– Adequate sexual arousal
– Try few more times
• Check testosterone: make sure not hypogonadal
• Addition testosterone if hypogonadal:
– General improvement in sexual function
– Improved erection
– Enhanced responsiveness of PDE5-I
• Lipitor (Atorvastatin) improve response to sildenafil (Hermann JSM
2005)

70. What is non-arteritic anterior
ischaemic optic neuropathy?
• FDA alert 7/2005: small number of men had lost of eyesight
after taking Levitra, viagra and cialis. This non arteritic ischemic
optic neuropathy cause sudden painless loss of eyesight
because blood flow to the optic nerve is blocked. (disc edema)
• It is not known whether these drugs cause NAION, as the
condition also occur in men not taking such drugs
• High risk patients for NAION include
– Over 50
– DM
– Hypertension
– High cholesterol
– Smoker
– Certain eye problem

71. How about Cardiovascular safety?
• No increase in myocardial infarction rates
• Nitrates are totally contraindicated with PDE5 inhibitors
– cGMP accumulation and unpredictable falls in blood
pressure
– If PDE5I is taken and the patient develops chest pain,
nitroglycerine must be withheld for at least 24 hours
for viagra and levitra, and for at least 48 hours for
cialis

72. What is the evidence of Changing
the PDE5 inhibitor in non-
responder?
• A randomized, open-label, crossover trial
comparing sildenafil and tadalafil
• Some patients might respond better to
one PDE5 inhibitor than to another and
vice versa
• Might be explained by variation in drug
pharmacokinetics
– Eardley I, et al. Factors associated with preference for sildenafil citrate and tadalafil for
treating erectile dysfunction in men naive to phosphodiesterase 5 inhibitor therapy: post hoc
analysis of data from a multicentre, randomized, open-label, crossover study. BJU Int 2007
Jul;100(1):122-9

73. What is the evidence of regular dosing of
PDE5 inhibitor in non-responder?
• No randomized trials to support this
intervention
• Although tadalafil is licensed for daily
dosing at a dose of 2.5 mg and 5 mg,
neither sildenafil nor vardenafil are
licensed for use in this way

74. What is the difference between on-
demand and chronic use of PDE5
inhibitors?
• Double-blind, placebo-controlled,
multicentre, parallel-group study
• Mild-to-moderate ED randomised to
receive once-daily vardenafil 10 mg plus
on-demand vardenafil
• Once-daily dosing does not offer any
sustainable effect after cessation of
treatment

75. What is the evidence of PDE5
inhibitors in post-RRP?
• Early use of a high dose of sildenafil after
RP is associated with the preservation of
smooth muscle within the human corpora
cavernosa
• The response rate to sildenafil treatment
for ED after RP in different trials up to 70%
among those who underwent bilateral
NSRP and up to 15% among those who
underwent non-NSRP
• Daily sildenafil also resulted in a greater
return of spontaneous normal erectile
function post RP compared to placebo
following bilateral nerve-sparing RP in
patients who were fully potent before
surgery

76. What is the evidence of PDE5
inhibitors in post-RRP?
• A randomized, double-blind, multicentre
study
• Compared on- demand and nightly dosing
of vardenafil in men with ED following
bilateral NSRP
• Vardenafil was efficacious when used on
demand, supporting a paradigm shift
towards on-demand dosing
Montorsi F, et al. Effect of nightly versus on-demand vardenafil on recovery of erectile
function in men following bilateral nerve-sparing radical prostatectomy. Eur Urol
2008;54(4):924-31

77. What is the precaution with
anti-hypertensive drugs?
• Small additive drops in blood pressure,
which are usually minor
• Even when the patient is taking several
antihypertensive agents

78. How about Alpha-blocker
interactions?
• Viagra: 50, 100mg not to be taken within a 4
hour window of an alpha blocker
• Levitra: safe to use with tamsolusin. (label
changed in US from previous total
contraindication with alpha blockers)
• Cialis: safe to use with tamsolusin 0.4mg

79. ApomorphineApomorphine

80. What is Apomorphine?
• Dopamine receptor agonist
• Sublingual (Uprima SL)
– Erections are achieved within 20 min
• Efficacy rates (erections sufficient for intercourse) range from 30%
to 55%)
• Acts centrally on dopaminergic receptors in the paraventricular
nucleus of the hypothalamus to enhance and co-ordinate the effect
of sexual stimuli
• Adverse effects: nausea; headache; dizziness
• Apomorphine is not contraindicated in patients taking nitrates or
antihypertensive drugs
• Used in patients with certain contraindications for the use of PDE5
inhibitors, e.g. nitrates
• Multiple daily dosing possible: once / 8 hours

81. Intraurethral therapyIntraurethral therapy

82. What is the mechanism of
prostaglandin E?
• Prostaglandin E binds to PGE receptor,
activating adenylate cyclase which
converts ATP to cAMP
• cAMP activate PKA which brings about
the relaxation of the smooth muscle
directly without NO pathway

84. What is intraurethral therapy?
• Alprostadil
• Synthetic prostaglandin E1 (PGE1) pellet administered
into the urethra via a specialized applicator
• Once inserted, the penis is gently rolled to encourage
the pellet to dissolve into the urethral mucosa, from
where it enters the corpora
• Efficacy – 50%
• Side-effects: penile pain; priapism; local reactions

85. Intracavernosal therapyIntracavernosal therapy

86. What is Intracavernosal
therapy?
• Alprostadil
• Increase cAMP within corporal smooth muscle
 relaxation of SMC
• Right angle at lateral mid-penile shaft
• Efficacy rates for intracavernous alprostadil -
90%
• Adverse effects: pain; priapism; haematoma
• Contraindications: men at risk of priapism (1%)
and men with bleeding disorders

87. What is Intracavernosal
therapy?

88. What is Intracavernosal
therapy?
Locate the area of injection. Wipe off with an alcohol swab. Grasp the head of the
penis, not the skin. Position the penis along your inner thigh. Maintain traction on the
head after cleaning the side of the penis.

89. What is Intracavernosal
therapy?
• Most long-term injection users can switch
to sildenafil despite underlying
pathophysiology
• Almost one-third of long-term
intracavernous injections users who
subsequently responded also to sildenafil
preferred to continue with an
intracavernous injection programme

90. What is combination therapy?
• Papaverine – combination therapy today
due to its high incidence of side-effects as
monotherapy
• Phentolamine - in combination therapy to
increase efficacy. As monotherapy, it
produces a poor erectile response

91. What is combination therapy?
• Papaverine plus phentolamine plus alprostadil
have never been licensed for ED
• Combination had similar side-effects as
alprostadil monotherapy, but a lower incidence
of penile pain due to lower doses of alprostadil
• Fibrosis and priaprism were more common when
papaverine was used. In addition, mild
hepatotoxicity has been reported with
papaverine

92. What is the action to be taken
with a prolonged erection?
• 19-gauge needle is used to aspirate blood
• If failed, an intracavernous injection of
phenylephrine, starting at a dose of 200
μg every 5 min and increasing to 500 μg if
necessary

93. Vacuum erection deviceVacuum erection device

94. Vacuum Constriction Device

95. • What is this device? (0.5)
• Name one condition it is used for (0.5)
• Name one complication from its use? (1)

96. • Vaccum constriction device (0.5)
• ED, Peyronie’s disease (0.5)
• Cold penis, difficulty with ejaculation,
bruising, penile numbness (1 max)

97. Vaccum constriction device
• Erections with these do not use physiological erection pathways
• Plastic cylinder connected directly or by tubing to a vacuum-
generating source (manual or battery-operated pump)
• Penis is engorged by the negative pressure
• Constricting ring is applied to the base to maintain the erection
 should not be left in place > 30 minutes
• Can be used successfully by men with a malfunctioning penile
prosthesis in place
• Used after explanation to prevent shortening
• Disadvantage: cold numb penis, no ejaculation, discomfort in
orgasm
• Patients taking aspirin or warfarin should exercise caution when
using these devices
• Erections satisfactory for intercourse, is as high as 90%, but
decreases to 50-64% after 2 years. Most men who discontinue
within 3 months

98. Penile prosthesisPenile prosthesis

100. What is Penile prosthesis?
• Third-line therapy
• Surgical implantation into the corpora to provide penile rigidity
and sufficient erectile size for sexual intercourse
• Two types of prosthesis exist: malleable (semi-rigid) and
inflatable (two- or three-piece)
• Most patients prefer the three-piece inflatable devices due to
the more ‘natural’ erections obtained.
• Two-piece inflatable prosthesis can be a reliable option with
fewer mechanical complications and is easier to implant
• A semi-rigid prosthesis provides a constantly rigid penis and
may be suitable in older patients with infrequent sexual
intercourse with less mechanical failure but erosion and chronic
pain

101. • AMS 700
• 5YS 90%
• Side-effects: mechanical failure (5% per year); erosions (5%);
infections (2%)
• Reservoir in abdomen
• Pump in scrotum, pair of cylinders implant into penis
• Infection rate may be reduced to 1% by implanting an antibiotic-
impregnated prosthesis
• Infection rate is similar between primary VS revision, DM VS
non-DM
• Staphylococcus epidermidis- commonest
• Mulcahy technique has been described in an attempt to
salvage the situation and insert a new prosthesis at the time of
the infected one. It involves copious wound irrigation with
kanamycin, bacitracin, iodine, hydrogen peroxide, vancomycin
and gentamycin. The success rate is 80% at 3 years

102. Surgical penileSurgical penile
revascularizationrevascularization

103. What is surgical penile
revascularization?
• Post-traumatic arteriogenic ED in young patients
• In young patients with pelvic or perineal trauma,
surgical penile revascularization has a 70% long-
term success rate
• The lesion must be demonstrated by Duplex
ultrasound and confirmed by selective internal
pudendal arteriogram
• Corporeal veno-occlusive dysfunction is a
contraindication to revascularization and must be
excluded by DICC
• Vascular surgery for veno-occlusive dysfunction is
no longer recommended because of poor long-
term results

104. Androgen deficiencyAndrogen deficiency

105. hypogonadism
• 95% testosterone is produce by Leydig cells
• Serum level peak at 7-8am and lowest at midnight. Clinically
serum testosterone is best estimated in the morning
• Incidence of late-onset hypogonadism: 20% of men over 70
• <10% ED due to hypogonadism
• Serum testosterone is loosely bound to albumin in 50% and
50% to sex hormone binding globulin (SHBG). Whereas 2% is
free. The bioactive testosterone refers to free and albumin
bound serum testosterone (~50%)
• Estimation of the bioavailable testosterone is a more accurate
test than total serum testosterone when investigating
hypogonadism
• SHBG is increase in: ageing , cirrhosis, hyperthyroidism ,
anticovulsants, oestrogen, HIV infection

106. Approach
• History:
– loss of libido, low mood, lethargy
– Change in sexual function
• Physical examination:
– Loss of muscle mass & hair loss
– regression of secondary sexual characteristics
– softer and smaller testis,
– gynaecomastia (aromatisation of testosterone in fatty
tissue to oestrogen)
• Investigation:
– fasting glucose, lipid,
– total testosterone, free testosterone, FSH and LH
– Oestradiol, TFT & prolactin in selected case

107. Late-onset male hypogonadism
• Symptom complex resulting from age-
related decline in testosterone level in
men
• Cause:
– Primary: Testicular failure
– Secondary:
• Pituitary or hypothalamic disorder (Kallman’s
syndrome)
• Conbined hypogonadism

108. Treatment
• Weight loss
• Clomiphene citrate
• Androgen replacement therapy
–CI: polycythemia, fluid retention, Ca prostate
and breast , sleep apnoea, heart failure,
severe renal and liver failure
–Oral – first pass to liver for metabolism > too
fast to have an effect
–Transdermal, subcutaneous, intramuscular

109. Monitor
• Serum testosterone level
• Clinical signs and symptoms
• Assess bone mineral density
• Adverse effect:
– Excessive rise in hematocrit (>54%)
– Raised PSA or abnormal DRE
– Ance
– Increase oliness of skin
– Gynaecomastia
– Suppression of fertility
– Some testicular atrophy

110. Testosterone & Ca Prostate?
• No positive correlation btw testosterone
level and Ca Prostate in prospective
epidemiological studies
• Small clinical trails have not shown
increase in clinical prostate cancer in the
testosterone group compared with the
placebo groups
• But no sufficient data to drawn conclusion

111. Ejaculatory disorder

112. Ejaculatory disorder
• Hematospermia
• Retrograde ejaculation
• Premature ejaculation
• Ejaculatory failure

113. Hematospermia
• Commonly seen after prolonged period of sexual
abstience, always resolved spontaneously
• Investigation if beyond several weeks
• History:
– Exclude hematuria
– Recent trauma
– Infection (STD)
– Bleeding disorder
– PMH: TB, Ca prostate
• Three important point need evaluation:
– Patient age
– Duration & recurrence
– Associated hematuria

114. • Physical examination:
– Blood pressure
– Genital: TB, bead cord vas
– Penis
– DRE: prostate
• Investigation:
– Bld, PSA
– MSU : sterile pyuria
– Urethral swab for younger pt
– Cytology
– FR + RU if slow stream

115. Cause
• Infection (40%): TB, HIV, CMV
• STD: herpex, chlamydia, ureaplasma
• Prostatitis (30%)
• Post-TRUS + bx
• Prostate cancer
• Urethritis and urethral stricture
• Acquire or congenital cyst of the seminal vesicle
• Systemic disorder: HT, liver disease, lymphoma

116. Further investigation
• TRUS: reveal abnormalities in 95%
– Prostatic calcification (40%)
– Ejaculatory duct calculi (40%)
– Dilated ejaculatory duct (30%)
– Ejaculatory duct cyst (10%)
– BPH (30%)
– Dilated or clacified SV (20%)
– Mullerian duct remnants (7%)
• Treatment:
– Reassurance
– Antibiotics ?

117. Retrograde ejaculation
• History:
– Low ejaculate volume
– Post- ejaculate urine cloudy
• Investigation : post-ejaculate urine examination for
sperm
• Cause :
– Post- RPLND
– DM
– Bladder neck surgery, TURP
– Trauma
– Alpha- blockers
– Urethral stricture
– Spinal cord injury

118. Treatment
• Medication: to close the bladder neck
– Sympathomimetic : pseudoephedrine & ephedrine
– TCA: imipramine
– Efficacy : 50%
• IVF:
– Sperm retrived from alkalinised post-ejaculate urine
– Fertilization rate: 50%
• How to alkalinise urine?
– Sodium bicarbonate: 1gm at night before & 1mg in
the morning of sperm collection
– Or use Liverpool solution : NaCl + NaHCO3
– Empty bladder before masturbation
– Obstain post-ejaculated urine & send to lab ASAP

119. Premature ejaculationPremature ejaculation

120. Premature Ejaculation
• Most important point:
1. Short ejaculatory latency time
2. Lack of ejaculatory control
3. Decreased satisfaction with sexual
intercourse
• Interpersonal distress
• Negative man’s self-esteem
• Reduced sexual function and QOL
Patrick DL et al ,J Sex med 2005
Giuliano F et al, Eur Urol 2008
Rowland DL et al, J Urol 2007

121. DSM-IV-TR 2000
• Persistent or recurrent ejaculation with
minimal sexual stimulation;
–Before, on , or shortly after penetration
–Before the person wishes it;
• Must also cause marked distress or
interpersonal difficulty;
• Cannot be due exclusively to the direct
effects of a substance.

122. The International Society for Sexual
Medicine (ISSM)
• The first evidence-based definition
• ‘Premature ejaculation is a male sexual
dysfunction characterized by ejaculation which
always or nearly always occurs prior to or within
about one minute of vaginal penetration; and
inability to delay ejaculation on all or nearly all
vaginal penetrations; and negative personal
consequences, such as distress, bother,
frustration and/or the avoidance of sexual
intimacy

123. Classification
• Lifelong condition
• Acquired condition
• Natural variable PE
• Premature –like ejaculatory dysfunction
Cooper AJ et al, J Sex Maritla Ther 1993
Waldinger MD et al, Drugs 2007

124. What is the prevalence?
• Major problem in assessing the
prevalence of PE is the lack of an
accurate (validated) definition
• The most common male sexual
dysfunction, with prevalence rates of 20-
30%
• Prevalence of PE is not affected by age

125. Etiology
Psychogenic:
• Anxiety
• Early sexual
experience
• Infrequent sexual
intercourse
• Poor ejaculatory
control technique
• Negative conditioning
Biological cause:
• Penile
hypersensitivity
• Hyperexcitable
ejaculatory reflx
• Endocrinopathy
• Genetic
predisposition
• 5HT- receptor
dysfunction

126. Neurophysiology of ejaculation

127. Neurophysiology
• Ejaculatory control centers in spinal cord
• Received peripheral afferents and
supraspinal influences
• Coordinate sympathetic , parasympathetic
and somatic outputs to pelviperineal
structrues

128. 5-HT neurons
• Activation of 5-HT1A autoreceptors  decrease
5-HT release by presynaptic neurons (-ve
feedback)
• Activation of 5-HT1A decrease ejaculatory
latency
• Activation of postsynaptic 5-HT2C or 5-HT1B
receptors prolongs ejaculatory latency
• PE may be due to imbalance btw 5-HT1A
(hypersensitivity) and 5-HT2C or 5-HT1B
(hyposensitivity)
• Increase central 5-HT  delay ejaculation

129. What is the approach to PE?
• History and physical examination
– Intravaginal ejaculatory latency time (IELT)
• Clinical use of self-estimated IELT is adequate, stopwatch-
measured IELT is necessary in clinical trials
– Patient-reported outcomes (PROs) have the potential to identify
men with PE
• Patient-reported outcomes (PROs) have the potential to
identify men with PE
• Further research is needed before PROs can be
recommended for clinical use
– Duration time of ejaculation, degree of sexual stimulus, impact
on sexual activity and QoL, and drug use or abuse
– It is also important to distinguish PE from ED
– ED develop secondary PE caused by the anxiety
– Examination of the vascular, endocrine and neurological
systems
• Routine laboratory or neurophysiological tests are not
recommended

130. Measurement of response
• Intravaginal ejaculatory latency time
(IELT)
– Time between vaginal intromission &
ejaculation
• Perceived controlled over ejaculation
• Improvement of personal distress

131. What are behavioural therapy?
• ‘Stop-start’ programme developed by Semans
• ‘Squeeze’ technique, proposed by Masters and Johnson
• Masturbation before anticipation of sexual intercourse
• Success rates of 50-60% in short term
• Time intensive, require the support of a partner and can
be difficult to do
• Recurrence is likely after treatment cessation

132. Pharmacotherapy for PE
• Anti-depressant:
–TCA: Clomipramine
–SSRIs: paroxetine, fluoxetine, sertraline, etc
• Phosphodiesterase-5 inhibitors (PDE-5i)
• Tramadol
• Topical agents: lidocaine/prilocaine

133. SSRI
• Increase synaptic 5-HT concentration via blockade of 5-HT
transporters
• Paroxetine (20-40mg), Clomipramine (10-50mg) or fluoxetine (20-
40mg)
• Meta-analysis: Paroxetine produce strongest delay in ejaculation
• Daily txn, effect start on 2 week
• Need to withdrawn gradually over 4 week (except fluoxetine)
• SE:
– Psychiatric and neurological
– Dermatological reaction
– Anticholinergic SE
– Change in body weight
– Cognitive impairment
– Drug-drug interactions
– Sexual SE: ED and loss of libido

134. SSRI discontinuation syndrome
• Especially in paroxetine
• 1-3 days after drug discontinuation
• Median duration: > 1 week
• Reversible when SSRI reintroduced
• Dizziness, nausea and emesis, headache,
gait instability, lethargy, agitation , anxiety
and insomnia
Black K et al, J Psy Neurosci 2000
Haddad P et al, J psychopahrmacol 1998
Tamam L et al, Adv ther 2002

135. Serotonin syndrome
• SSRI with long half-lives
• Interactions with agents that enhance 5-
HT CNS activity
• Myoclonus, hyper-reflexia, sweating,
shivering , lack of coordination and mental
status changes
Nelson EB et al, J Clin Psychiatry 1997
Lane R et al, J Clin Psychopharmacol 1997

136. Dapoxetine
• New agents under development
• Rapid onset (1.29hr) and short half-live
(1.49hr)
• On-demand dapoextine 30 or 60mg
significantly improved outcome vs placebo
• IELT increase 3.6x from baseline
• SE: nausea, diarrhoea, headache,
dizziness and insomnia
Pryor JL et al, Lancet 2006

137. PDE-5i
• Results has been conflicting
• No pharmacological rationale
• Paroxetine + sildenafil vs paroxetine:
increased IELT and satisfaction but with
more SE (headaches and flushing)
Salonia A et al, J Urol 2002
• No effect in men without coexiting ED,
cause decrease in post-ejaculatory
refractory period
Chen J et al, Urology 2002

138. Tramadol
• Centrally acting synthetic opioid
• Inhibit nor-adrenaline and serotonin
reuptake
• Rapidly absorbed and eliminated
• Increased IELT, sexual satisfaction and
ejaculatory control vs placebo (p<0.05)
Safarinejad MR et al, J Clin Psychopharmacol 2006
Salem EA et al, J Sex Med 2008

139. Topical agents
• Topical lidocaine/prilocaine cause
desensitization
• Increase mean IELT by 2.4x vs placebo
(p<0.01)
Dinsmore WW et al, BJU Int 2006
• SE: local numbness(12%), loss of erection
• Severance Secret cream: increase IELT
and sexual satisfaction vs placebo
Choi HK et al, Urology 2000
Choi HK et al, Int J impot Res 1999

140. Conclusion
• PE is an under-treated condition due to
lack of understanding of its cause and
potential therapy, and because of its
sensitive nature
• 5-HT has been implicated as a key
mediator of ejaculatory control

141. Conclusion
• Available therapy include off-label use of
SSRIa and PDE-5i , as well as topical
anaesthetics
• New on-demand agents like tramadol and
dapoxetine are currently under evaluation
• Role of other central neurotransmitter as
future targets to delay ejaculation needs
further investigation

142. Ejaculatory failure
• Cause: Post SCI, RPLND , psychogenic
• History: what level , bowel and bladder fxn
• Investigation:
– SA: azzospermia
– Post-orgasmic urine  no fructose
• Treatment: Electro-ejaculator
– Seager electro-ejaculator
– Rectal probe to stimulate perirectal, periprostatic sympathetic
nerves
– May require GA
– Watch out for autonomic dysreflexia in above T6 lesion
– Sperm: poorere quality & mobility
• Alternative: sperm retrieval technique (pregnancy rate
70%)

143. Peyronie’s diseasePeyronie’s disease

144. What is Peyronie’s disease?
• Fibrous plaque within tunica albuginea of
penis
• associated with DM, antiepileptic drugs
and beta blockers
• Curvature, penile pain or shortening
• Erectile dysfunction

145. What is the cause?
• Trauma to tunica albuginea
• Wound healing > excessive fibrotic plaque
• Dorsal plaque more common
• Penile curvature as corpus cavernosum can’t
lengthen fully on erection limited by plaque
• Associated with Dupuytren’s contracture 30%
• Incidence <5%, men aged 40-70 years

146. What is natural course of the
disease?
• Active phase 6 months, painful erection
with changing deformity
• Quiescent phase 9-12 months stable
deformity, painless
• Natural Hx over 18 m
– 13% improved
– 40% stable
– 47% progress

147. How to make diagnosis?
• By history and P/E
– History
• Disease Duration
• Pain
• Penile deformity –angle, direction
• Stability
• Penile length
• Erections , able to penetrate
• IIEF
• Risk factor for ED
– P/E
• Assess degree of curvature by 1 photogragh, 2 IC PGE1
• Exam for plaques, location, size
• Penile length, stretched & flaccid state
• Extremeties for Dupuytren’s contracture

148. What is the treatment?
• Early disease <3m consider medical Tx /
injection / ESWL, low successful rate
– Oral vit E
• 200mg tds for 3 months
• In a randomized trial vitamin E has been shown to
improve pain in 75% of patients and improves the
deformity in 10%
– Oral colchicine x3m (limited evidence for efficacy)
– Intralesional verapamil, steroid x 6m

149. Photograph taken during a procedure
• What is being done? (1)
• What procedure is this? (0.5)
• Name 3 complications from this procedure (0.5 each)
Q45

150. • Artificial erection from injection of saline into
corpus cavernosum (1)
• Correction of penile curvature eg. in Peyronie’s
disease (0.5)
• Shortening of penis, erectile dysfunction,
deformity recurrence, palpable suture through
penile shaft skin, altered/decreased penile
sensation (0.5 each, total 1.5)

151. Is ESWL useful?
• Initiating an inflammatory reaction thru
direct damage to plaque and result in
plaque resorption
• No study has demostrate any
improvement in plaque size or curvature
• NICE do not recommend

152. What are the indications for
Surgery?
• Disease present for at least 12m
• stable for at least 3m
• Deformity makes intercourse difficult
• Quality of erection important
• ED > ? Prosthesis

153. Surgery: Penile shortening
• Indicated in pt: no ED , <60degree curvature, no
hourglass demormities or hinge effect
• Must warn pt of Penile shortening effect
• Nesbit
– Penis degloved via circumglandular incision
– Artificial erection with NS
– ellipitcal incision: 1mm for 10 degree deformity
curvature on convex side
– Complication: all penile shortening, 1% ED rate,
recurrence of deformity
– Success rate 80%

154. Surgery: Penile maintaining
• Lue’s procedure
– By incising the plaque and interposing a graft (fascia lata / vein graft/ Gortex
graft)
– Do cause penile shortening but not to the extent that corporal plication
– More ED – 15%
– Not recommended for complete excision of the plaque due to compromising veno-occlusive
mechanism and causing ED
• Surgery in general
– Success rate: 80%
– Risk: bleeding, infection , bruising
– Loss of 1cm in 26%
– ED in 15%
– Recommend penile traction device or penile rehab with PDE5-i
• About 10% of patients will subsequently require circumcision due to secondary
phimosis

155. When is prothesis required?
• Penile prosthesis is indicated in patients
with both Peyronie’s disease and severe
ED
• After insertion and inflation of penile
prosthesis, the penis is bent in opposite
direction to break the plaque (modelling)
– 90% successful rate

156. PriaprismPriaprism

157. Priapism
• Definition:
– Persistent erection > 4 hours
– Not related to sexual desire
• Two age group:
– 5-10 yo
– 20-50 yo
3. Stuttering priaprism – repeated, shorter self-

158. Presentation
• FOUR Main questions:
1. Duration of erection > 4 hours?
2. Painful / non painful ? (Ischemic vs nonischemic)
3. Previous history of priapism
4. Predisposing factors
• Physical examination:
– Rigid corpora cavernosa
– Flaccid Corpus spongiosum and glans penis

160. Investigation
• Blood: CBP, Hb/electrophoresis (SSD)
• Urine: C/ST , toxicology
• Penile blood gas:
– Aspirate blood directly from either corpora
• Duplex USG of carvernosal arteries:
– Ischemic ( inflow low or absent)
– Non ischemic (inflow normal or high)
• Penile pudenal arteriography: not readily available
Appearance pH PO2
(mmHg)
PCO2
(mmHg)
Low flow Dark red <7.25 <30 >60
High flow Bright red = 7.4 >90 <40

161. Treatment
• Conservative
• Medical
• Minimally invasive
• Surgical treatment
• Always warn patient about the possibility
of impotence due to cavernosal fibrosis

162. Doppler USG can differentiate high or low flow priaprism

164. Treatment for Priapism
• Cavernosal aspiration successful rate: 1/3
• Distal shunt
– Winter (large biopsy needle , corporo-glanular)
– Ebbehoj (Scalpel, corporo-glanular)
• Lue’s modification “T-Shunt” (scalpel, corporo-glandular)
– El-Ghorab: piece of tunic albuginea excised at tips of coprora via a
dorsal transverse incision just distal to corona
• Proximal shunt:
– For failed distal shunt or severe distal penile edema
– 80% successful rate, but ED > 90%
– Quackels /Sacher (corporo-spongiosal)
– Grayhack (corporo-saphenous)
• Supra-selective embolisation of common penile artery – successful rate 80%
– Absorbable materials like clots and gel cause less ED than coils or
permanent chemical

166. El-Ghorab

167. Quackels /Sacher

168. Grayhack

169. A procedure for a urologic emergency is about to be
performed
• What is the name of this procedure? (2)
• What is it used for? (1)
Q20

170. • Ebbehoj shunt, a type of distal
cavernoglandular shunt (2, 1 mark for
mentioning just “shunt” without name)
• Ischemic priapism not responsive to
injectional medical treatment (1)

171. How about high-flow
priaprism?
• Not a urological emergency
• Duplex USG can confirm diagnosis
• Selective internal pudendal embolisation, better with
absorbable material including clots or gels
• Successful rate up to 80%
• If failed > open exploration and direct ligation