Erectile Dysfunction and Benign Prostate Hyperplasia

Erectile Dysfunction (ED) and Benign Prostatic Hyperplasia (BPH) are two common conditions affecting men's health. ED involves difficulty achieving or maintaining an erection due to vascular disease, diabetes, hormonal imbalances, nerve damage, or psychological factors, causing symptoms like reduced libido and decreased sexual satisfaction. BPH, on the other hand, is a non-cancerous prostate enlargement causing urinary issues such as frequency, urgency, weak flow, straining, and nocturia, primarily due to hormonal changes, aging, and genetics. Treatment options for ED include medications, vacuum devices, and lifestyle modifications, while BPH management involves medications, minimally invasive procedures, surgery, and lifestyle changes, highlighting the importance of consulting a healthcare professional for personalized guidance and care.

1. Erectile
Dysfunction
Presented by: Kashaf Tahir
Supervised by:Dr. Muhammad Salman

2. Anatomy
•Corpora cavernosa
•Arterial supply
•Venous supply
•Somatic innervation
•Autonomic innervation

3. Mechanism of Erection

4. Erectile Dysfunction
Erectile dysfunction (ED) is defined by the Fourth International
Consultation on Sexual Medicine as:
“the consistent or recurrent inability to attain
and/or maintain penile erection sufficient
for sexual satisfaction”.

5. Etiology
PSYCHOGENIC
•Sudden onset
•Complete immediate loss
•Morning erection +ve
•Age-related (>65 years), anxiety,
depression
•Varies with partner and
circumstances
ORGANIC
•Gradual onset
•Incremental progress
•Morning erection –ve
•Due to vasculogenic, cavernosal
neurogenic, endocrine, drug-
induced, anatomic cause

6. Etiology of Organic Causes
1.Vasculogenic origin
•Pathology interfering with NO signaling, e.g., vascular inflammation
•Atherosclerosis or thrombosis of artery supplying the penile tissue
•Prolonged hypertension
2.Cavernosalorigin
•Peyronie’sdisease
•Venous dilatation
•Elevated smooth muscle tone
•Congenital defects e.g., venous drainage anomaly

7. Cont.
3.Neurogenic origin
a.Corticalimpairment
•Medial preoptic area, paraventricular nucleus, and hippocampus are
responsible for sexual stimuli.
•Demyelinating and neurodegenerative disorders e.g., Multiple sclerosis,
stroke, brain tumors, Parkinson’s disease, Alzheimer’s disease, encephalitis
b.Spinal cord Injury
•Severed connection between pelvic nerves and brain > reflexogenic erection
impairment
•lesions above T11 > psychogenic erection impairment
•Lesions below T11 and above sacral pathway > either reflexogenic or
psychogenic erection impairment

8. Cont.
c.Peripheral damage
•Iatrogenic insults (major pelvic, bladder, prostate, rectal surgery)
•Post radical proctectomy
•TURP
•Radiotherapy and brachytherapy to treat prostate cancer
4.Endocrine origin
•Hypogonadism
Testosterone <300 ng/dL
•Hyperprolactinemia
Prolactin >35 ng/Dl
5.Drug/disease-induced ED

9. Assessment of Erectile Dysfunction
1.International Index of Erectile Function
•15 questions
•Golden standard
2.Erectile Dysfunction Inventory of Treatment Satisfaction
3.Quality of Sexual Life Questionnaire

10. Evaluation of Erectile Dysfunction
•Psychogenic ED and Mental Health
•Blood tests
•CBC, lipid profile, TSH level, HgbA1c, LH and Prolactin levels, TSH levels,
morning testosterone
•Nocturnal tumescence testing
•Penile duplex Doppler ultrasound
•Corpus cavernosometry
•Dynamic infusion cavernosometry (DICC) - > Osinski reflex
•Cremasteric reflex

11. Cont.
•Patient history include vascular risk factors (e.g., hypertension and diabetes),
lifestyle factors (such as smoking, activity level, alcohol intake, and the use of any
recreational drugs), and general medication history
•Referral to cardiologist (ED may be the first symptom of underlying vascular or
heart disease)
•Referral to endocrinologist (For evaluation of hypothalamus-pituitary axis
disorders)

12. Management
Non Pharmacological1.Lifestyle Modification
•Increased physical activity
•Switching to a Mediterranean diet or nutritional counseling
•Stopping smoking, drugs, and alcohol
•Gaining reasonable control of diabetes, lipids, and cholesterol
2.Psychosexual therapy

13. Management
Pharmacologic
1.Oral Phosphodiesterase-5 Inhibitors
•Sildenafil 25-50 mg 1 hour before intercourse
•Vardenafil 5-10 mg 1 hour before intercourse
•Tadalafil 5-10 mg 30 minutes before intercourse
•Commonadverseeffectsareheadache,facialflushing,dyspepsia,nasalcongestion,and
dizziness
•May cause blue/green color blindness, sudden hearing loss, priapism
•Metabolism by CYP3A4
•Contraindicated in patients taking organic nitrates
•should not be administered within 4 hours of an α-adrenergic antagonist

14. Cont.
2.Prostaglandin E1 analog
•Alporstadil
•Intracavernosalalprostadil=10to20mcguptoamaximumof60mcg.
Maximumnumberofinjectionsisoneperdayandthreeperweek.Adverse
effectsincludeinjectionsitepain,priapism.
•Intraurethralalprostadil=125to1,000mcgshouldbeadministered5to10
minutesbeforeintercourse.Beforeadministration,thepatientshouldempty
hisbladderandvoidcompletely.Nomorethantwodosesperdayare
recommended.

15. Cont.
3.Testosterone Replacement Therapy
•Testosterone patch 4–6 mg/day; apply to scrotum
•Testosterone gel 5–10 g/day; apply to shoulders, upper
arms, abdomen
•IM Testosterone cypionate200–400 mg every 2–4 weeks
•SC Testosterone implant 50–450 mg every 3–4 months
•Serumtestosteronenormalrange(300-1,100ng/dL)
•Beforestartingtestosteronereplacement,patients40yearsandolder
shouldbescreenedforbenignprostatichyperplasiaandprostatecancer.
•Cancausesodiumretention,whichcancauseweightgainorexacerbate
hypertension,congestiveheartfailure,andedema,gynecomastia,
deleteriousserumlipoproteinchangesandpolycythemia.

16. Cont.
4.Other Agents
•Trazodone 50 to 200 mg/day
•Yohimbine 5.4 mg three times daily
•Papaverine 7.5 to 60 mg [single agent therapy]
•Papaverine 0.5 to 20 mg [combination therapy] intracavernosal
injection
•Phentolamine 1 mg [combination therapy] intracavernosalinjection
•L-arginine 5000 mg PO for 4-6 weeks

17. Cont.
Surgical
•Penile revascularization
•Implantation of prosthetic devices
Other Interventions
•Vacuum erection devices
•Low intensity shockwave therapy
•Kegel exercises
•Acupuncture and acupressure

18. Benign Prostate
Hyperplasia

19. Prostate and BPH
•The prostate is a small, walnut-sized organ located under the bladder,
through which the urethra runs. It is composed of epithelial cells, which are
secretory, and stromal cells, which include smooth-muscle cells and
connective tissue.
•BPH arises due to the loss of homeostasis between prostatic cellular
proliferation and apoptosis or cell death.
•BPH is characterized by the non-malignant proliferation of glandular
epithelial tissue and stromal components of the prostate.
•It is acombinationofintheprostaticstromaandbladderneckaswellas
theincreasedadrenergictoneanatomicaleffectsofanenlargingprostate
leadtolowerurinarytractsymptoms(LUTSs)andbladderoutflow
obstruction(BOO).
•BPHasatypicalagingprocess

20. Pathophysiology
•BPHcommonlyresultsfrombothstatic(gradualenlargementofthe
prostate)anddynamic(agentsincreaseα-adrenergictoneand
constrictthegland’ssmoothmuscle)factors.
•Withintheprostate,testosteroneisconvertedby5α-reductaseto
dihydrotestosterone(DHT)thatisfive-to-tentimesmorepotentthan
testosteroneandisresponsibleforstimulatinggrowthfactorsthat
influencecelldivisionleadingtoprostatichyperplasiaand
enlargement.

21. Symptoms of BPH
•Lowerurinarytractsymptoms(LUTS):
1.Voiding(obstructive)LUTS
Urinaryhesitancy,diminishedstream,straining,incompleteemptying,
interruptionoftheurinarystream,anddribblingarethoughttobeassociated
withobstruction
2.Filling(irritative)LUTS
Urgency,frequency,andnocturiaarebelievedtoarisefrominvoluntary
detrusorcontractions(detrusoroveractivity)
•Complicationsincludechronickidneydisease,grosshematuria,urinary
incontinence,recurrenturinarytractinfection,bladderdiverticula,andbladder
stones

22. Assessment
•International prostate symptom score (IPSS)
•digital rectal examination (DRE)
•Prostatic ultrasound or TRUS
•Urinalysis, urine cultures if infection is suspected
•Measurement of serum prostate-specific antigen (PSA) if DRE reveals
a nodular or hard prostate

23. Treatment
•Pharmacologictherapyinterfereswiththestimulatoryeffectof
testosteroneonprostateglandenlargement(reducesthestaticfactor)or
relaxesprostaticsmoothmuscle(reducesthedynamicfactor).
1.α-AdrenergicAntagonists
•Relaxsthesmoothmuscleintheprostateandbladderneck,increase
urinaryflowratesby2to3mL/secandreducepostvoidresidualurine
volumes
•Adverseeffectsincludefirst-dosesyncope,orthostatichypotension,and
dizziness
•Tamsulosinisselectiveforprostaticα1A-receptors
Pharmacologic

24. Cont.
2.5α-Reductase Inhibitors
•Interferewiththestimulatoryeffectoftestosterone,slowdisease
progressionanddecreasetheriskofcomplications.
•Preferredasinitialtherapyinpatientswithaprostategland>40g
•DutasterideinhibitstypesIandII5α-reductase,whereasfinasteride
inhibitsonlytypeII.
•ReduceserumPSAlevelsby50%
•FDApregnancycategoryXandarethereforecontraindicatedinpregnant
female
3.Combinationtherapy
•Consideredforsymptomaticpatientswithaprostategland>40gandPSA
≥1.4ng/mL.

25. Cont.
4.Anticholinergics
Oxybutynin 5-10mg/dayPO
Tolterodine 2-4mgPOoncedaily
Darifenacin 7.5–15.0mg once a day
•MuscarinicM3receptorantagonistscanbeofferedtopatientswithsymptomsof
anoveractivebladder.
•Side effects include dry mouth, dizziness, constipation and blurred vision
5.Phytotherapy
Sawpalmettoberry(Serenoarepens)
Africanplumtree(Pygeumafricanum)
Stingingnettle(Urticadioica)
Ryegrasspollen
•Anti-inflammatoryeffectbyinhibitionofprostanoidformation

26. Cont.
•Transurethral resection of the prostate (TURP)
•UroLift
•Transurethral needle ablation (TUNA)
•Transrectal high-intensity focused ultrasound (HIFU)
Non-Pharmacologic

27. THANKS!
A
ny
QUESTI N
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