Downloaded 55 times
2016 Sessions: Erectile dysfunction
The document discusses the epidemiology, risk factors, pathophysiology, and treatment options for erectile dysfunction (ED), defining it as the inability to achieve or maintain an erection suitable for sexual performance. It highlights various causes of ED, including psychogenic, organic, neurogenic, and hormonal factors, and lists treatment modalities such as lifestyle changes, pharmacological agents, local therapies, and surgical options. The document emphasizes the importance of considering cardiovascular health in patients with ED and the need for a multidisciplinary approach in managing the condition.
More Related Content
Similar to 2016 Sessions: Erectile dysfunction
More from Sri Lanka College of Sexual Health and HIV Medicine
![CTEV [ clubfoot] DR ARUN LAL ,DR MOHAMED ASHRAF travancore medical college k...](https://cdn.slidesharecdn.com/ss_thumbnails/ctevclubfootdrarunlaldrmohamedashraftravancoremedicalcollegekollamkeralaindia-260208063247-18fc466c-thumbnail.jpg?width=640&height=640&fit=bounds)
![ONFH[AVN HIP] -TRIPLE REGIME -A NOVAL SURGICAL CONCEPT .pptx](https://cdn.slidesharecdn.com/ss_thumbnails/onfhavnhip2026koaconcalicutdrgokuldevdrmashraf-260210064517-213ec005-thumbnail.jpg?width=640&height=640&fit=bounds)
2016 Sessions: Erectile dysfunction
- 1. TREATMENT MODALITIES IN ERECTILE DYSFUNCTION DRHIMALI PERERA CONSULTANT VENEREOLOGIST COORDINATOR TRAINING AND CAPACITY BUILDING NATIONAL STD /AIDS CONTROL PROGRAMME
- 2. ERECTILE DYSFUNCTION ‘The consistent orrecurrent inability of a man to attain and or maintain a penile erection sufficient for sexual performance’
- 3. EPIDEMIOLOGY OF ERECTILE DYSFUNCTION •50% amongst aged 40y-70y, according to Massachusetts Male Ageing Study(MMAS) • 322 million projected cases worldwide by 2025 • Sri Lankan situation unknown
- 4. RISK FACTORS FORED Advancing age Drugs Dyslipidemia Hypertension Diabetes mellitus Atherosclerosis /CAD Alcohol & Smoking Trauma Pelvic surgery Neurological disorders Hormonal disorders Psychological factors Stress/Sedentary life style
- 5. STUDY(MMAS) INCREASING PREVALENCE OFED WITH AGE 0 0.5 1.0 70 65 60 55 50 45 40 Age(years) Probability None Minimal Moderate Complete Feldman HA et al. J Urol 1994;151:54-61
- 6. MASSACHUSETTS MALE AGEINGSTUDY (MMAS) PREVALENCE OF ERECTILE DYSFUNCTION None 48% Minimal 17% Complete 10% Moderate 25% Feldman HA et al. J Urol 1994;151:54–61
- 7. CLASSIFICATION OF ED PsychogenicOrganic (80%)
- 8. ORGANIC CAUSES Therapeutic drugs Endocrinologic Neurogenic structural Peyronie’sdis Arteriogenic eg Atherosclerosis Venogenic E,venogenicVasculogenic /Arteriogenic venogenic Systemic
- 9. 50% OF DIABETESMELLITUS PATIENTS HAVE ED Pathophysiology •Neurogenic Autonomic NS Peripheral NS •Arterial Atherosclerosis Microangiopathy •Endothelial Impaired smooth muscle relaxation •Myogenic Impaired smooth muscle function
- 10. ED INDICATES APOSSIBLE CONCOMITANT HEART PROBLEM • Men with ED, aged >55 Y have a 25% risk of a cardiovascular event and ED patients should be promptly investigated for CV risk. (Tho m pso n IMe t alJAMA 20 0 5; 29 4: 29 9 6 -30 0 2) • The recognition of ED as a warning sign of silent vascular disease has led to the concept that a man with ED but no cardiac symptoms is a cardiac or (vascular) patient until proven otherwise. (Prince to n II: Jackso n G e t al. 20 0 6 . JSe x Me d)
- 11. PHYSIOLOGY OF NORMAL ERECTION •Cerebralcontrol -PVN •Autonomic control-parasympathetic stimulation • Molecular Mechanisms Endothelial dysfunction
- 12. ERECTOGENIC & INHIBITORY STIMULI Cerebral cortex Spinalcord Erectogenic stimuli Inhibitory stimuli – anxiety – fear – depression PRO-ERECTILE neural signalling PVN PVN
- 13. PENILE ERECTION: AN INTEGRATEDRESPONSE Supraspinal control and integration Spinal reflexes and integration Autonomic nervous system ERECTION
- 14.
- 15. THE MOLECULAR BIOLOGYOF ERECTIONS Ca2+ cGMP cAMP Ca2+ Ca2+ Ca2+ K+ Endothelium Smooth muscle tonic contraction: Ca2+ Locking mechanism PDE-5 PDE-2,3,4
- 16. ENDOTHELIAL DYSFUNCTION= ERECTILE DYSFUNCTION Ca2+ cGMP cAMP Ca2+ Ca2+ Ca2+ K+ Na+ Ca2+Ca2+ NO NOEndothelium Smooth muscle relaxation Role of the endothelium PDE-5 PDE-2,3,4
- 17. ENDOTHELIAL DYSFUNCTION= ERECTILE DYSFUNCTION NO cGMP cAMP Adr NA Ca2+ PDE-5 Ca2+ Ca2+ K+ Na+ NO Ca2+ PGE VIPCa2+ PDE-2,3,4 Endothelium Smooth muscle relaxation Neural mechanisms Ca2+ ACh
- 18. CAUSES OF ARTERIOGENICED Causes Examples Atherosclerosis Smoking Hypercholesterolaemia Iatrogenic Aorto-iliac surgery Renal Transplantation Radiotherapy Trauma Pelvic fracture injury Blunt perineal trauma Others Post priapism
- 19. CAUSES OF VENOGENICED Causes Examples Abn venous channels Surgery forpriapism Repeated stricture surgery Veno-occlusive dysfunction Abn smooth muscle function Overactive sympathetic tone Ischaemia Hypercholesterolaemia Loss of smooth muscle Ageing Ischaemia Impaired tunica albuginae function Peyronie’s disease Ageing Ischaemia
- 20. THERAPEUTIC DRUGS CAUSING ED •Antidepressants Tricyclic MAO inhibitors SSRI • Antihypertensives B-blockers Ca channel blockers Diuretics Central acting drugs • Anti-cholinergic : Atropine • Psychotropic : benzodiazepines • Others: Cimetidine, digoxin, metoclopramide, phenytoin, carbamazepine, ketoconazole • HAART
- 21. NEUROGENIC CAUSES OFED SITE CAUSE CNS Injury, Stroke ,encephalitis Multiple sclerosis Parkinson’s disease Alzheimer’s disease Temporal lobe epilepsy Spinal Cord Injury Multiple sclerosis Spina bifida Syringomyelia Subacute combined degeneration Spinal cord compression with tumors
- 22. NEUROGENIC CAUSES OFED SITE CAUSE Peripheral nervous systemPeripheral neuropathy, & e.g.alcohol, diabetes, amyloidosis Radiation injury Pelvic fracture injury Disc Prolapse
- 23. SURGICAL CAUSES OFED SITE SURGERY Neural Cerebral/Spinal surgery control of erection Pelvic Radical cystectomy/prostatectomy parasympathetic nerves Rectal surgery-Ca Bladder& Rectum (S2,3.4) Transpubic urethroplasty TURP Bladderneckincision Penile vasculature Aorto-iliac surgery Renal transplantation Surgery forpriapism Urethroplasty Penis Peyronie’s disease Penile amputation
- 24.
- 25. SYSTEMIC DISEASES • Hyperlipidemia •Atherosclerosis • Hypertension • Chronic renal failure
- 26. PSYCHOGENIC • Sudden onset •Situational • Relationship problem • Life event • Anxiety, fear, depression
- 27. SPORTS-RELATED ED SITE SPECIFICBLUNT TRAUMA • Cyclist • Gymnastics – bars/projections • Water-ski/water-jet ski • Football • • • Munnariz RMe t al. JUro l1 9 9 5; 1 53: 1 8 31 -40
- 28. HISTORY • Chronic medical/Psychiatric/ Surgical conditions • Sexual • Psychosocial • Drugs • Smoking/alcohol/recreational drugs • Erectile dysfunction questionnaires(International Index of erectile function/IIEF)
- 29. EXAMINATION • Body habitus-BMI • 2ry sexual characteristics • CVS- Pulses /BP • CNS –( lower limbs) • Genitalia
- 30. INVESTIGATIONS U/E/LFT,FBC,FBS HBA1c Lipid profile S testosterone Sprolactin LH/FSH Urinalysis Dip-stick Thyroid function Tests TSH
- 31. TREATMENT OPTIONS Life stylechanges & risk factor modification Phychosexual counselling & education Oral agents Local therapies Surgical therapy New treatment modalities Hormonal
- 32. ORAL AGENTS •May actcentrally - e.g. dopaminergic agonist or •Peripherally - e.g. phosphodiesterase-5 inhibitor
- 33. AVAILABLE ORAL AGENTS Phosphodiesterase-5inhibitor • Sildenafil citrate (VIAGRA ® ) • Tadalafil (CIALIS ® ) • Vardenafil (LEVITRA ® )
- 34. MECHANISM OF ACTIONOF PDE5 INHIBITORS
- 35. PDE5 INHIBITORS Advantages • Effectiveand inexpensive • Non invasive • Require sexual stimulation to be effective • Well tolerated Disadvantages • Contraindicated in patients on nitrate therapy • Cytochrome P450 drug interactions Caution with protease inhibitors
- 36. DRUG INTERACTIONS OFPDE5 INHIBITORS • Nitrates added hypotensive effect Recreational ‘Poppers’ (amyl nitrate) Levels of PDE5 inhibitors Increased by Protease inhibitors erythromycin, itraconazole/ ketoconazole
- 37. SILDENAFIL (VIAGRA,SELAGRA) • Take½ - 1 hour for action • Action last 4 hours • Food delays absorption • Dose 25 mg-100mg • Side effects: Headache, flushing, blocked nose, epigastric discomfort, visual disturbance
- 38. SILDENAFIL & EYEPROBLEM • Colour discrimination (blue-green) • Non-anterior ischaemic optic neuropathy (NAION) – Po m e ranz e t al20 0 2, 20 0 5, Bo shie r e t al20 0 2, Gruhn & Fle de lius 20 0 4 • Anterior ischamic optic neuropathy (AION) – Dhe e r e t al20 0 2 • Central serous chorioretinopathy – Allibhai e t al20 0 4
- 39. VARDENAFIL (LEVITRA) • Rapid onsetof action (<30 mins) • More specific for PDE-5 • Less side effects • Action lasts 9 -12 hours • Dose 10,20,40mg
- 40. TADALAFIL (CIALIS, MEGAFIL) • Longerhalf life • Active for 24 hours Dose 2.5mg -20mg • Side effects- myalgia, back pain • No visual disturbances
- 41. LOCAL THERAPIES Second line •Intra-urethraltherapy •Intra-cavernosal injection therapy •Vacuum device therapy
- 42. INDICATION FOR LOCAL THERAPIES •Failure of oral drug therapy (DM) • Contraindications to oral drugs (Nitrate uses ) • Adverse events from oral drugs • Individual preferences
- 43. TRANSURETHRAL ALPROSTADIL (MUSE/ MEDICATEDURETHRAL SYSTEM FOR ERECTION)
- 44. TRANSURETHRAL APPLICATION OF ALPROSTADIL Advantages • Noneedles • Effective in about 2/3 of men • Suitable/acceptable for most men Disadvantages • 30% incidence of penile pain • Requires dexterity & insertion post-micturition • Slower acting than injection • Patients need to be taught technique • Just prior to sex
- 46.
- 47. INTRACAVERNOSAL INJECTION OF ALPROSTADIL Advantages •Rapidly effective • Good success rates when well motivated • Suitable for most men • Few contraindications & drug interactions Disadvantages • Invasive, not acceptable to some patients/partners • Patients need to be taught technique • Manual dexterity & reasonable eye sight • Local side-effects (e.g. penile pain, bleeding, bruising, fibrosis) • Priapism • Just prior to sex
- 48.
- 49. VACUUM CONSTRICTION DEVICES Advantages • Suitablefor most men with ED • Less side-effects • Few contraindications • Suitable for long term use • Non invasive Disadvantages • Erections can be uncomfortable • Erections may last > 30 minutes • Sensation of ejaculation can be impaired • Lack of spontaneity/cumbersome • Partners may complain the penis is felt cold • Pivoting of penis at base • Just prior to sex
- 50. SURGICAL THERAPY • Penileprosthesis – Implant • Correction of anatomical deformities-Peyronie’s disease • Vascular surgery-may increase arterial inflow & decrease venous outflow young patients with arterial stenosis may be candidates
- 51.
- 52. HORMONAL REPLACEMENT INDICATIONS • Youngpatients with primary hypogonadisam • ED with low testosterone level
- 53. LOW DENSITY EXTRA- COPORALSHOCK WAVE THERAPY(LI-ESWT) Advantages No pain No adverse effects Not on demand basis Non invasive Feasible Tolerable Disadvantages Cost HCWdependent
- 54. METHOD OF APPLICATIONOFMETHOD OF APPLICATION OF LI-ESWTLI-ESWT
- 55.
- 56. INTERNATIONAL PROTOCOLINTERNATIONAL PROTOCOL •2 sessions per week, for 3 weeks • 3 weeks off therapy • Repeat 2 sessions per week for 3 weeks
- 57. ED - THEFUTURE • Alprostadil 0.3% topical cream licensing in Canada and Europe ,Phase iii studies • Gene therapy - based on vascular endothelial growth factor and nitric oxide synthase genes-trails
- 58. TAKE HOME MASSAGE& CHALLENGES •In a steady relationship, involve sexual partner/s in the management. it’s a problem to both partners •Multidisciplinary approach is needed to manage ED patients effectively •Some treatments and investigations are costly and not available in the SL government sector
- 59.
Editor's Notes
- #5 HT –Ed more prevalent with HT than age-matched GP Atherosclerosis –Atheromata-reduce penile perfusion Dyslipedimia –high cholesterol and low HDL
- #6 MAAS shows 15% had ED with hypertension
- #13 PVN-Paraventricular nucleus in hypothalamus
- #16 In the flaccid state Cavernous smooth muscle and penile artery smooth muscle are in tonic contraction. Tonic contraction is maintained by the ca locking mechanism of the smooth muscle. Cavenosal and penile artery smooth muscle relaxation leads to erection. This process is predominantly via neurotransmitter No. NO is released from endothelial cells and parasympatheic non cholinerigic nerve endings. The second messenger system leading to caverous smooth muscle relaxation is mediated via two distinct pathways. C AMP amd CGMP. NO stimulate the formation of CGMP. PGE1 and VIP stimulate cAMP formation. Adnenarlin and noadrenalin inhibit the formation of cyclic AMP. Both cAMP and CGMP promote efflux of ca from the cell, leading to smooth muscle relaxation and vasodilation resulting in erection. CGMP is broken down by enzyme pospodiesterase 5. Other pospodiesterse enzimes involved are PDE 2,3 and 4