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MEN’S HEALTH ISSUES
DR. TAIT FORS
WISCONSIN INSTITUTE OF UROLOGY
OBJECTIVES
Understand Men’s Health Issues:
 Evaluation and treatment options for erectile dysfunction
 Understand indications of when to evaluate for low testosterone levels,
indications for treatment and treatment options.
 Understand the basics of BPH and treatment options
 Indications for PSA testing and causes of elevation
OBJECTIVES
Understand incontinence
 Define incontinence in a male
 Understand the basic evaluation and treatment of incontinence
Erectile
Dysfunction:
Evaluation and Treatment
ERECTILE DYSFUNCTION
Definition:
 Inability to achieve or maintain an erection sufficient for satisfactory
performance
 Sexual desire, ability to have an orgasm and ejaculate may be intact
despite the inability to have an erection
 Cause is often multi-factorial
 More than half of men aged 40-70 years old (in the US) are unable to
attain or maintain an erection sufficient for satisfactory sexual
performance
PHYSIOLOGY OF PENILE ERECTION

Erection involves the integration of neural and vascular functions

Occurs when blood flow into the penis exceeds outflow

3 types of erections:
 Psychogenic: central-stimulated or non-contact
 Stimulated by memory, fantasy, visual or auditory
 Reflexogenic: genital-stimulated or contact
 Genital-stimulated induced by tactile stimulation
 May be preserved in upper spinal cord lesions.
 May be short in duration and poorly controlled by individual
 Central (nocturnal): central-originated
 May occur spontaneously without stimulation or during sleep
 Most occur during rapid eye movement (REM) sleep
PHASES OF ERECTION PROCESS
1.
2.
3.
4.
5.
6.
Flaccid phase: Minimal arterial and venous flow; Blood flowing in and out of spongy
chambers is equal (Corpora cavernosa and corpus spongiosum). The cavernous smooth
musculature and smooth muscles of arteriolar and arterial walls are tonically contracted
Latent (filling) phase: Occurs with psychological or sexual stimulation. Increased flow and
decreased pressure in the internal pudendal artery. Neurotransmitters cause penile smooth
muscles to relax, increasing blood flow to the corporal bodies. Some elongation of the penis
Tumescent phase: Rising intracavernous pressure until full erection is achieved. Penile arteries
expand to accommodate the increased blood flow needed to elongate and expand the penis
Full erection phase: Increased volume of blood within the penis is prevented from draining,
thus expanding the penis to full erection
Rigid erection phase: Maximum rigidity is attained. The glans and spongiosum enlarge until
penile veins are forcefully compressed. This increases engorgement and maintains maximum
penile rigidity. Ejaculation occurs
Detumescent phase: Sympathetic tonic discharge resumes, resulting in contraction of the
smooth muscles around the sinusoids and arterioles. This diminishes the arterial flow to
flaccid levels, expels a large portion of blood from the sinusoidal spaces, and reopens the
venous channels. Penis returns to flaccid length and girth
CLASSIFICATION OF ED
Psychogenic
1. Generalized type
A. Generalized unresponsiveness
a) Primary lack of sexual arousability
b) Aging-related decline in sexual arousability
B. Generalized inhibition
a) Chronic disorder of sexual intimacy
2. Situational
A. Partner-related
a) Lack of arousability in specific relationship
b) Lack of arousability owing to sexual object preference
c) High central inhibition owing to partner conflict or threat
B. Performance-related
a) Associated with other sexual dysfunction/s (e.g. rapid ejaculation)
b) Situational performance anxiety (e.g. fear of failure)
C. Psychological distress- or adjustment-related
a) Associated with negative mood state (e.g. depression) or major life stress (e.g. death of partner)
CLASSIFICATION CONTINUED
II. Organic
1. Neurogenic
2. Hormonal
3. Arterial
4. Cavernosal (venogenic)
5. Drug induced
III. Mixed organic/psychogenic (most common type)
FACTORS THAT CAN DISRUPT THE
NORMAL PHYSIOLOGIC MECHANISM
Most commonly the cause is multi-factorial

Psychological
Performance anxiety, strained relationship, lack of sexual arousal, depression, schizophrenia)

Neurogenic
Spinal cord injury (degree depends on nature, location and extent of lesion)
Dementia, Parkinson’s, stroke, tumors, trauma, Shy-Drager syndrome
Peripheral neuropathy due to diabetes, chronic alcohol abuse, vitamin deficiency
Direct injury to cavernous or pudendal nerves from trauma, radial pelvic surgeries or pelvic irradation
Iatrogenic impotence from radical prostatectomy, abdominal-peroneal resection, extenral
sphincterotomy


Arterial disorders: such as atherosclerotic disease
Hormonal: Hypogonadism, hyperprolactinemia, Cushing’s syndrome, Addison’s disease,
thyroid issues
CLASSIFICATION CONTINUED

Cavernosal disorders: Cavernous veno-occlusive dysfunction resultant of
Peyronie’s , ages, diabetes, etc

Medication-induced:
 Meds that interfere with central neuroendocrine or local neurovascular control of penile smooth
muscle. Central neurotransmitter pathways, including serotonergic, noradrenergic and dopaminergic
pathways may be disturbed by antipsychotics, antidepressants and centrally activing antihypertensive
drugs
 Common meds: SSRI’s, beta-adrenergic blocking drugs, thiazide and non-thiazide diuretics,
 May cause decreased libido: spironolactone
 May improve erections: alpha 1 blockers, angiotensin II receptor blockers

Penile structure
CAUSES OF ED
 -High blood pressure, diabetes mellitus, dyslipidemia, CV disease, obesity
 Can lead to a degeneration of the penile blood vessels, leading to restriction of
blood inflow through the arteries.
 Leakage of blood through the veins during erection

-Treatment of many medical conditions
 -Surgery or radiation therapy for cancer of the prostate, bladder, color or rectum
 -Smoking, drug or alcohol abuse
 Compromise blood vessels
 -Sedentary lifestyle
PATIENT HISTORY
• Sexual history: severity, onset, duration
• Presence of concomitant medical or psychosocial factors
• Difficulties obtaining or maintaining an erection
•
Onset? Sudden or gradual?
 Slow onset occurs with age and causes that have gradual effect
 Rapid onset, may indicate a specific event (physical or psychological)
•
Sexual desire on scale 1-10
•
Nocturnal erections
•
Penile curvature or pain with erection/ejaculation
•
Prior treatments and level of response
HISTORY CONTINUED
•
Is the primary sexual problem
• ED
• Premature ejaculation
• Sexual response cycle: desire, ejaculation, orgasm
• Psychosocial assessment of past and present partner relationship
SEXUAL HEALTH INVENTORY FOR
MEN (SHIM)
EVALUATION
Overview of medical, sexual, psychosocial history
Co-morbid conditions that predispose:
 Cardiovascular: HTN, atherosclerosis, hyperlipidemia
 Diabetes
 Depression
Risk factors:
 Pelvic/perineal/penile trauma or h/o radiation
 Neurological disease
 Obesity
 Peyronie’s disease
 Prescription medications
 ETOH/tobacco use/recreational drug use
PHYSICAL EXAMINATION
Cardiovascular
Respiratory
Neurological
 S/S of disease: hemiparesis after stroke, MS
Abdomen/pelvis/GU
 S/S of hormonal dysfunction: lack of facial hair, gynecomastia, hypothyroid facies
 Check for penile plaques
 Check size, position and consistency of testes
Secondary sexual characteristics
Vascular health
 S/S of disease: HTN, ischemic ulcers, angina, lower extremity pulses
MANAGEMENT
Treatment options based in stepwise fashion with increasing invasiveness
and risk based against the likelihood of efficacy
•
Oral phosphodiesterase type 5 inhibitors (PDE-5 inhibitors)
•
Intra-urethral Alprostadil
•
Intra-cavernous vasoactive injection
•
Vacuum constriction device (VED)
•
Penile prosthesis
•
If indicated, counseling
•
If indicated, endocrine therapy for those with definitive
endocrinopathy such as hypogonadism, hyperprolactinemia, thyroid
disorder
INDICATIONS FOR CLEARANCE FROM
CARDIOLOGY
•
Unstable or refractory angina
•
Uncontrolled HTN
•
CHF class III or IV
•
Cardiovascular accident within 2 weeks
•
High risk arrhythmias
•
Hypertrophic obstruction and other cardiomyopathies
•
Moderate to severe valvular disease
Presence of 3+ co-morbidities, there is an increased risk of MI with
sexual activity.
•
HTN
•
Diabetes
•
Dyslipidemia
•
Obesity
•
Smoking
•
Sedentary lifestyle
ORAL PHOSPHODIESTERASE TYPE 5
INHIBITORS (PDE-5 INHIBITORS)
•
•
First line therapy.
•
Sildenafil (Viagra) 50-100 mg
•
Vardenafil (Levitra) 10-20 mg
•
Tadalafil (Cialis) 2.5-5 mg daily dose or 10-20 mg prn dosing
Time of onset:
•
Range of 20-30 minutes
•
If no response in 20 minutes, then delay for 1 hr (sildenafil or vardenafil) or 2
hrs (tadalafil) when serum concentrations have peaked
•
Avoid high fat meal prior as this will delay absorption (sildenafil and vardenafil)
PDE-5 INHIBITORS
Period of efficacy
• Tadalafil 17.5 hours. May work up to 36 hours
• Sildenafil and vardenafil 4-5 hours
Adverse events
• Visual disturbances, flushing, headache, flushing, rhinitis, slight lowering of
blood pressure, dyspepsia
• Nitroglycerin should not be given within 24 hours of sildenafil or vardenafil
and 48 hours of tadalafil
CONTRAINDICATIONS TO PDE-5
INHIBITORS

Vardenafil is contraindicated in those on type-1A antiarrhythmics (quinidine or
procainamide), type-3 antiarrhythmics (sotalol or amiodarone) or with
congenital prolonged QT syndrome

Nitrates: Life threatening hypotensive episode may occur with concurrent use

Caution vs contraindicated

Severe cardiovascular diseases, left ventricular outflow obstruction, those
with tendency to develop priapism (sickle cell anemia, leukemia, etc)

Unstable angina, cardiac failure, recent MI, uncontrolled or life-threatening
arrhythmia, poorly controlled blood pressure
TRANSURETHRAL THERAPY
•
Alprostadil: synthetic formulation of PGE-1 via intracavernous and transurethral
routes
•
Mechanism: absorption from urethra to the corpus spongiosum and then corpus
cavernosum. Aprostadil stimulates adenyl cyclase to increase intracellular levels of
cAMP and lower levels of intracellular calcium, thereby relaxing arterial and trabecular
smooth muscle.
•
In office test trial
•
Potential side effects:
•
Penile and/or scrotal pain or discomfort
•
Hypotension and syncope (1-5.8% risk)
•
Vaginal discomfort in female partners after ejaculation (10%)
•
Priapism
INTRACAVERNOUS INJECTION
•
Vasoactive injection drug. Considered most effect nonsurgical therapy
•
First line for those that cannot tolerate or not a candidate for oral meds
•
Initial injection in office
•
Benefits: rapid onset of action, reduced incidence of systemic complications
and drug interactions compared to systemic treatments
•
Response >85%
•
Patient discontinuation rate 20-60%
• Lack of patient motivation
• Cost
• Loss/disinterest of partner
• Dissatisfaction with drug-induced erection
•
Combination of agents into injection:
• Bi-mix, Tri-mix, Tri-mix super, Quad mix and various dosing in each combination
• Papaverine: induces relaxation of cavernous smooth muscle and penile vessels
• Phentolamine: alpha-adrenergic antagonist for alpha-1 and alpha-2 receptors
• Alprostadil: causes smooth muscle relaxation, vasodilation, and inhibition of
platelet aggregration
•
Potential adverse effects:
• Priapism, corporal fibrosis, bleeding, hematoma, pain at injection site, penile
fibrosis, burning at injection site, penile curvature or plaque
CONTRAINDICATIONS OR CAUTION
TO INJECTION
•
Patients with sickle cell anemia, schizophrenia or severe psychiatric disorder,
severe venous incompetence
•
Use of anticoagulation or ASA…. Compress injection site for 7-10 minutes after
injection
•
In patients with poor manual dexterity, sexual partner may be instructed to
perform the injection
PRIAPISM
•
Higher incidence with rapid dose escalation by the patient
•
Missed initial injection with second attempt
•
Use among neurogenic or young patients
•
If erection lasts >4 hours, then urgent medical evaluation indicated by Urologist
•
Treatment per Urologist:
•
Diluted phenylephrine 250-500 mg every 3-5 minutes until detumescence.
Monitor BP.
VACUUM ERECTION DEVICE (VED)
•
Plastic cylinder connected directly or by tubing to a vacuum-generating source
(battery or manual)
•
After penis engorged, then a ring placed at base to maintain erection
•
Do not leave ring in place for > 30 minutes
•
Erection produced is different from a normal physiological erection or one
produced via injections
•
Complications: penile pain, numbness, difficult ejaculation, ecchymosis,
petechaie
•
Caution in those taking Coumadin or ASA
PENILE PROSTHESIS
Types:
•
Malleable (semirigid)
•
Mechanical
•
Inflatable devices: 2 piece and 3 piece.
•
The 3 piece inflatable device is the most common. This consists of a paired
cylinder, a scrotal pump and a suprapubic fluid reservoir
Low
Testosterone
Objective:
 Understand indications of when to
evaluate for low testosterone levels
 Understand indications for
treatment of low testosterone
levels
 Understand treatment options
Testosterone
•
Testosterone is an anabolic-androgenic steroid hormone
•
90-95% of testosterone is produced by the Leydig cells in the testes and 10% comes from
the adrenal glands
•
Testosterone is needed to form and maintain the male sex organs and promote secondary
male sex characteristics such as voice deepening and hair growth patterns
•
Facilitates muscle growth, bone development and maintenance
Hypothalamic-pituitary-gonadal axis
Effects of Testosterone
Normal effect of testosterone
 Male sex organs: growth, development, secondary sex





characteristics, sperm production, erections
Behavior: Improved sexual libido, mood, memory,
energy
Bone: Increased bone mineral density
Fat tissue: Body and visceral fat reduction
Muscle: Anabolic; increased muscle mass and strength
Liver: Stimulates production of serum proteins
Normal effects continued
 Kidney: Stimulates erythropoietin production
 Heart: Coronary vasodilation
 Blood: Suppression of clotting factors, low HDL-cholesterol
 Bone marrow: Stimulates stem cell production
 Hair: Influences body hair growth, especially facial hair
What is Low T?
 No absolute value, different labs have
differing reference range depending on the
assay (ThedaCare T range 132-813 ng/dL)
 Most widely accepted is total T<300 mg/dL
as recommended by the Endocrine Society
Guidelines USA 2006, updated 2010
 Low total and/or free along with symptoms
 A free testosterone level below 65 pg/mL
(calculated) or 0.8 ng/dL (directly
measured) can provide supportive evidence
for testosterone treatment
What is Low T continued
 Blood should be drawn between 6-9 AM to follow the body’s normal circadian rhythm
when screening
 Not all men with low T need treatment as many are not symptomatic
 T decreases naturally as men age (declines approximately 1-2% per year after age 40)
Prevalence
•
Low testosterone (total T<300) affects roughly 39% of men over the age of 45
•
Incidence of low testosterone increases with age:
Approximately 20% of men over age 60, 30% of men over 70 and
50% of men over 80 years will have low T levels
Causes of low T






Primary
(Testicular failure)
Congenital---Klinefelter’s
Acquired --- Mumps and other viruses
Trauma
Aging
HIV/AIDS
Undescended testicles







Secondary
(Pituitary/hypothalamic failure)
Aging
Chronic illness
HIV/AIDS
Certain drus/alcohol
Hyperprolactinemia (micro or macro
adenoma)
Obesity
Medication (opiate pain medication and
some hormones)
Signs and Symptoms of Low T
 Fatigue/Lack of motivation
 Decreased muscle mass/increased body fat
 Decreased libido
 Infertility
 Loss of axillary and pubic hair, decreased shaving
 Erectile dysfunction
 Mood swings
 Depressed mood
 Sleep disturbance (either increased sleepiness or insomnia)
 Decreased bone mineral density
When to refer?
 Male complaining of symptoms of low testosterone
 Considering testosterone replacement
When and Who to treat…
 Low T levels alone is not an indication for T replacement
 Symptomatic men with low T (<300-350) who are interested in treatment
 Not all clinical manifestations of low T need to be present
 Androgen deficiency is diagnosed based on labs and symptoms. You cannot look at one
without the other
 T replacement is contraindicated in prostate and breast cancer
 Use with caution in men with symptomatic BPH or sleep apnea as these could worsen
 Informed discussions with men who desire having children
ADAM Questionnaire
ADAM Flowsheet
Treatment options:
 Many T delivery methods are available






Topical
IM
Implants
Buccal
Transdermal
Aveed
 Not one treatment is right for every man
 Gel formulations require contact precautions
Baseline labs
 Baseline testosterone level x 2 (between 6-9 am)
 Baseline PSA, LFTs, lipids, H/H and DRE
Types of replacement
(Creams, gels, IM, buccal, transdermal, implant)
 Androgel 1.62%, 1 pump=20.25 mg
 Start with 2 pumps 40.5 mg (1 pump each arm)
 Applied to shoulders and upper back once daily in the morning
 Avoid transference to females and children
 Axiron 1 pump=30 mg
 Start 2 pumps 60 mg (1 pump per axilla)
 Easier to avoid transference
 Fortesta 10 mg per pump
 Start with 40 mg (2pumps per thigh)
 Testim 1% 50 mg/5 gram tube, 1 tube=1 dose
 Applied to shoulders and upper back once daily
 Aveed injection
Intramuscular injection
 Initial injection given in the office
 Ideally given in the buttocks, but may be given in thigh or shoulder
 Available as Testosterone cypionate, enanthate, decanoate
 Obtain peak and trough levels to determine dose
 Typical dose 200 mg every 2 weeks, may titrate based on levels
 Testosterone level within 2 days (peak)
 Testosterone level at 2 weeks (trough)
Follow up IM testosterone
 Check labs 6-7 weeks after initial injection with labs
Mid-cycle testosterone level (if on 2 week dosing, then obtain 1 week after injection)
 PSA, LFT, lipids, H/H, repeat DRE

 How do you decide if patient is on correct dose?
Review of labs
 Clinical symptoms

 Typical course of follow up once stable
3 months
 6 months
 Annual with testosterone level, PSA for DRE

Gel testosterone replacement
 Baseline labs
 Follow up

4-6 weeks after initiating medication




3 months



Labs: Testosterone level, LFTs, lipids, H/H, PSA
DRE
Symptom check
Labs: Testosterone level
Symptom check
Every 6-12 months



Labs: Testosterone level, PSA
DRE
Symptom check
Aveed
 Testosterone undecanoate injection which is long-acting
 Injected into the buttocks
 Initial injection, then 4 weeks later, then every 10 weeks
 Monitor patient for 30 minutes after injection

Risk of pulmonary oil microembolism

Caused by tiny droplets of castor oil that travels to the lungs
Other forms of replacement
 Androderm-transdermal patch
 Applied nightly. Prevents transference
 Testopel
 Office procedure
 Implanted pellet in the buttocks
 Every 3-6 months
 Striant SR
 Buccal delivery, on gum just above incisor
 Aveed
 Long acting IM injection every 10 weeks
What is the goal?
 Clinical goal
 Relief of symptoms of hypogonadism (not absolute T level)
 Need to establish normalization or at least an increase of testosterone level
 6 month trial before determining efficacy or lack of efficacy
Risk of testosterone replacement
 Fluid and electrolyte disturbance
 Water retention
 May lead to HTN, peripheral edema, exacerbation of CHF
 Monitor weight and blood pressure for those at risk
 Hematologic reactions
 Polycythemia
Secondary to stimulatory effect on erythropoietin
 Hct levels > 50, risk of stroke
 Hepatotoxicity
 Liver toxicity rare

 Gynecomastia or breast tenderness
 Due to elevated levels of estrogen (metabolite of testosterone)
Risk of replacement continued
 Spermatogenesis and Infertility
 Exogenous testosterone leads to spermatogenic arrest via negative feedback
inhibition of both pituitary LH and FSH secretion
 Azoospermia occurs in >90% of patients within 10 weeks. Sperm levels may rebound
within 18 months of cessation
 Altered cholesterol
 May lower HDL levels
 Generally does not affect total cholesterol or LDL
 Exacerbation of sleep apnea
 May exacerbate existing or those pre-disposed to sleep apnea
Controversies
 Prostate cancer
No increased risk of incidence of prostate cancer in men on testosterone replacement
 Men with lower T were found to have higher grade and stage of disease in some studies
 May consider careful T replacement if NED at 2 years post prostate cancer treatment

Controversy
 Cardiovascular events
Testosterone Therapy and Cardiovascular Risk:
Advances and Controversies
Abraham Morgentaler, MD; Martin M. Miner, MD; Monica Caliber, MSc;
Andre T. Guay, MDy; Mohit Khera, MD; and Abdulmaged M. Traish, PhD
Abstract
Two recent studies raised new concerns regarding cardiovascular (CV) risks with testosterone (T) therapy.
This article reviews those studies as well as the extensive literature on T and CV risks. A MEDLINE search
was performed for the years 1940 to August 2014 using the following key words: testosterone, androgens,
human, male, cardiovascular, stroke, cerebrovascular accident, myocardial infarction, heart attack,
death, and mortality. The weight and direction of evidence was evaluated and level of evidence (LOE)
assigned. Only 4 articles were identified that suggested increased CV risks with T prescriptions: 2
retrospective analyses with serious methodological limitations, 1 placebo-controlled trial with few major
adverse cardiac events, and 1 meta-analysis that included questionable studies and events. In contrast,
several dozen studies have reported a beneficial effect of normal T levels on CV risks and mortality.
Mortality and incident coronary artery disease are inversely associated with serum T concentrations (LOE
IIa), as is severity of coronary artery disease (LOE IIa). Testosterone therapy is associated with reduced
obesity, fat mass, and waist circumference (LOE Ib) and also improves glycemic control (LOE IIa).
Mortality was reduced with T therapy in 2 retrospective studies. Several RCTs in men with coronary
artery disease or heart failure reported improved function in men who received T compared with placebo.
The largest meta-analysis to date revealed no increase in CV risks in men who received T and reduced CV
risk among those with metabolic disease. In summary, there is no convincing evidence of increased CV
risks with T therapy. On the contrary, there appears to be a strong beneficial relationship between
normal T and CV health that has not yet been widely appreciated.
ª 2015 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2015;90(2):224-251
 Understand
the basics of BPH
 Understand
treatment options for BPH


Prevalence

20% in men aged 41-50

50% in men aged 51-60

>90% in med older than 80
Pathology

Develops in the transition zone, hyperplastic process resulting in an
increase in cell number

As transition zone enlarges, the outer zones of the prostate are compressed

Symptoms secondary to:

Obstruction by the prostate

Secondary to bladder response to the outlet resistance

Mechanical obstruction results from intrusion into the urethral lumen or
bladder neck leading to a higher bladder outlet resistance

Dynamic obstruction: The prostatic stroma which is composed of smooth
muscle and collagen is rich in adrenergic nerve supply.

Level of autonomic stimulation sets a tone to the prostatic urethra

Use of alpha blocker decreases this tone which decreases outlet resistance

Voiding complaints are a result of the response of the bladder to the increased
outlet resistance

Bladder outlet obstruction (BOO) leads to detrusor muscle hypertrophy,
hyperplasia, collagen deposition

Obstructive symptoms
 Urinary hesitancy
 Weak stream: Decreased force and caliber of stream.
 Sensation of incomplete bladder emptying: Double voiding
 Straining to void

Irritative symptoms
 Urgency
 Frequency
 Nocturia

Assess with the questionnaire developed by the American Urological
Association (AUA) called AUA Symptom Score
 Quantifies the severity of symptoms on a scale of 0-5.
 Score ranges from 0-35
 Score 0-7 is mild
 Score 8-19 is moderate
 Score 20-35 is severe
Physical examination:
 DRE: Size and consistency
 Size does not always correlate with patient symptoms or degree of
obstruction
 Expected exam of the prostate: smooth, enlarged, elastic
 Focused neurological exam: perineal or lower extremity sensation or
alternations in rectal sphincter tone or the bulbocavernous reflex
Laboratory evaluation:
 Urinalysis


Serum creatinine


Exclude infection, hematuria
Assess renal function. If renal insufficiency, then upper tract imaging may be warranted
PSA
Imaging:
 Upper tract imaging if presence of concomitant urinary tract disease or
complications from BPH (hematuria, UTI, renal insufficiency, urolithiasis)


Cystoscopy

This is a look into the bladder with a scope/camera to evaluate for bladder
outlet obstruction

Potential findings include:
 Bladder outlet obstruction
 Trabeculation: thickened detrusor muscle bundles
 Diverticulum: mucosal herniation between bundles
Uroflow or Urodynamic studies

Further evaluate etiology of symptoms

Measure of flow rate, obstruction, post void residual, pressure flow,
detrusor contractility

Urethral stricture

Bladder neck contracture

Bladder stone

Bladder cancer

Prostate cancer

Urinary tract infection

Neurogenic disorders

History of neurologic disease, stroke, diabetes or back injury

OAB

Watchful waiting


Mild symptoms
Pharmacological management

Alpha blockers: Mediate the contractile properties of the bladder neck and prostate
 Alpha-1a selective: Fewer side effects as receptors more localized to the prostate
and bladder neck
 Rapaflo
 Tamsulosin
 Alfuzosin
 Alpha-1 long acting:
 Doxazosin
 1 mg daily for 7 days then increase 2 mg po daily for 7 days. May titrate up to
4 mg po daily
 Terazosin with dose titration:
 1 mg for 3 days and then increase 2 mg po daily for 2 weeks. If tolerates then
5 mg po daily up to 10 mg daily
 Side effects: orthostatic hypotension, dizziness, tiredness, retrograde ejaculation,
rhinitis, headache

Pharm continued

5-alpha-reductase inhibitors
 Dutasteride, Finasteride
 Blocks the conversion of testosterone to dihydrotestosterone which
result in a reduction is size of the prostate
 Effects 6 months
 Side effects: decreased libido, decreased ejaculatory volume, ED, breast
tenderness
 PSA reduction 50%

Combination therapy: Both alpha blockers and 5-ARI

Herbal therapy: Saw Palmetto

Transurethral resection of the prostate (TURP)

Methods: TURP, laser PVP, Bipolar

Length of hospital stay 1-2 days

Risks: Retrograde ejaculation, impotence, low risk incontinence

Complications: Bleeding, urethral stricture, bladder neck contracture, perforation of
the prostate capsule with extravasation



TUR syndrome results from a hypervolemic, hyponatremic state due to absorption of the hypotonic
irrigating soln

Clinical manifestations: nausea, vomiting, confusion, hypertension, bradycardia, visual disturbances

Increases with prolonged OR time, > 90 minutes

Treatment: diuresis and if severe hypertonic saline
Transurethral incision of the prostate (TUIP)

Incision of the prostate at 5 and 7 o’clock position starting just distal to the ureteral
orifices and extending outward to the verumontanum

Risks: Retrograde ejaculation
Open simple prostatectomy

Large prostate ~ > 100 grams

Suprapubic or retropubic approach

Indications for PSA testing

Causes of PSA elevation


Glycoprotein
produced primarily
by the epithelial
cells that line the
acini and ducts of
the prostate
Concentrated in
prostatic tissue


Levels normally very low
Disruption of the
normal prostatic
architecture (prostatic
disease, inflammation,
trauma) allows greater
amounts to enter
circulation

Can Increase PSA Levels: Prostatitis, BPH, Urethral or

Can Decrease PSA Levels: Surgical or medical

Lab variability: 25% difference between
prostatic trauma, CaP, Ejaculation(72hrs), and Recent
PBx/surgery
castration, 5 alpha reductase inhibitors (lower PSA by ~
50%)
WHO/Hybritech standards, ambulatory


PSA cut off of 4.0 ng/ml (sensitivity = 20%
and specificity= 60-70%)
Age-adjusted PSA, Free/Total PSA Ratio, and
PSAV will improve both sensitivity and
specificity
Age Range
African American
Whites
40-49 yr
0-2.0 ng/ml
0-2.5 ng/ml
50-59 yr
0-4.0 ng/ml
0-3.5 ng/ml
60-69 yr
0-4.5 ng/ml
0-4.5 ng/ml
70-79 yr
0.55 ng/ml
0-6.5 ng/ml
Improves likelihood of detecting cancers, including aggressive
tumors that are present at PSA levels below 4.0 ng/ml, but risks
identifying clinically insignificant tumors



PSA exists in blood in two
fractions, one bound to
plasma proteins and the
other in a free state.
Pts with PCa tend to have
lower free/total ratios,
whereas men with benign
disease have higher
free/total PSA, except in
the case of
prostatitis(<17%).
Only valid with PSA
between 4-10 ng/ml

PSAV of >0.75 ng/ml in pts with PSA of 4-10
ng/ml (3 values over >18 mo)

PSAV not independent predictor of +Pbx

Some recommend threshold be lowered
◦ 0.25 ng/ml/yr in men 40-59
◦ 0.5 ng/ml/yr in men 60-69
◦ 0.75 ng/ml/yr for men > 70




Screening at ages 50-75, 40 if +FH (1st
degree) or African-American race
2008 USPSTF recommended stopping
screening at age 75(insufficient evidence <75)
75 corresponds to typical age when US men
have < 10 year life expectancy
Comorbidities factor in screening decision


2011 USPSTF recommends against screening.
Grade D: There is moderate or high certainty
that the service has no net benefit or that the
harms outweigh the benefits.
AUA/ACS: USPSTF recommendations not
supported by literature and a disservice to
men.




Goal: reduce the morbidity/mortality of CaP
Regionally advanced/metastatic CaP have
considerably diminished long-term survival
CaP stage migration: pre-1990 35% chance for
potentially curative intervention vs. 90% today
SEER Data: 41% reduction in CaP mortality
between 1990 and 2008 (36% in blacks) , 10-yr
CaP survival rates: 80.7% in 1990 vs 97.2% in
1998

Studies suggest PSA screening responsible for
CaP dx at earlier stages when active tx may
reduce mortality

European Randomized Study of Screening for
Prostate Cancer (ERSPC)

PLCO NCI Cancer Screening Trial (PLCO)

Goteborg Randomized Population-Based CaP
Screening Trial

162,000 men, 7 countries, 14 yr f/u

71% increase in CaP incidence

41% reduction in advanced disease

27% reduction in CaP mortality

Similar to 30% mortality reduction seen in
breast ca screening



Similar to 33% reduction in CaP mortality seen
from 1994 to 2003 following intro of PSA
screening
1,410 men needed to screen(NNS) and 48
needed to treat(NNT) to prevent 1 CaP death
Mortality curves begin to diverge at 7 yrs and
become statistically sig at 9 yrs f/u

@14 yrs f/u 44% predicted reduction in CaP
mortality, 293 NNS/12 NNT(J Clinical Oncology
2011; 29: 464)

# needing to be screened similar to
mammography and fecal occult blood testing

Criticized many exposed to Tx SE’s to save lives

landmark study proving PSA screening saves lives

N Engl J Med 2009; 360: 1320.

77,000 men screened (1/2 size), PSA cutoff 4.0,
no PSA velocity

No benefit for CaP screening @ 7 yrs f/u

Same result in European Study @ 7 yrs

Received much press

N Engl J Med 2009; 360: 1310.

17% increase CaP incidence/no reduction adv
stage

Really compared less to more screening rather
than screening to no screening

44% had already been screened; therefore
screened group at a lower risk for CaP

Explains why such a low # of CaP deaths in both
groups

PSA cutoff of 4.0 outdated and PSA velocity
(predicts CaP mortality when PSA<4) not used

Only 30% of screened with elev PSA underwent a
Pbx!

Criticisms not reported; hence, conclusions of
limited value.

Factored heavily in USPSTF draft
recommendations 2011

Asked what the benefit for screening would be in
men with minimal or no co-morbidity

Found a 44% decrease in CaP mortality

Only had to screen 5 men to eliminate 1 death

Why? Pts with co-morbidities more likely to die
of another cause before dying of CaP


Conclusion: PSA screening for men in good
health reduces prostate cancer specific
mortality with minimal overtreatment.
J Clin Oncology; 2011, 29: 355-361.


Received much less press than ERSPC/PLCO
despite superior methodology
Median 14 yr f/u with 50% cumulative relative
risk reduction in screened group

293 men NNS/12 NNT/1 CaP death prevented

More favorable screening #’s than ERSPC

Younger median age, 56 yr

PSA threshold for pbx lower than PLCO

Higher pbx rate if elevated PSA(93% vs 3040% PLCO)

Pre-screening less common (3% vs 44%
PLCO)



Much longer median f/u: 14 yrs vs 9 ERSPC
vs 11.5 PLCO
Not all men dx’ed with CaP underwent tx,
showing screening can reduce mortality
without requiring tx in all men dx’ed with
CaP
Lancet Oncol 2010; 11: 725

3 elements for screening to be successful

Adequate informed consent


Avoid over diagnosis and over treatment in those
unlikely to experience a survival benefit (<10 yr
life expectancy)
Improve tx quality to reduce morbidity



Prostate Cancer Prevention Trial-no “safe”
PSA value
Risk continuum: 10% bx + if PSA 0-2, 1525% if PSA 2-4, 17-32% if PSA 4-10, and
43-65% if PSA >10
No single threshold PSA value which
should prompt a PBx



A baseline PSA above the median for age is a
stronger predictor of future CaP risk than
FH/race
Goal: ID men at higher risk by obtaining a
PSA at age 40 and follow them closer
Urology. 2006; 67: 316



Median PSA 0.7 between 40-50/0.9 between 5060
Baseline PSA between median for age and 2.5
associated with a 14.6/7.6 increased risk for
future risk of CaP
Higher baseline PSA levels are associated with
greater PSAV, more aggressive tumors, and
greater CaP specific mortality

PSA is a more specific CaP test in younger men
because of less BPH

Less frequent testing in low risk pts might reduce
CaP M/M and cost of screening


Given relationship between PSAV/CaP death,
ID’ing aggressive CaP pts early might make cure
possible
Chemoprevention

Elevated age-adjusted PSA

PSA Velocity of > 0.75 ng/ml/yr

% free PSA < 17%

Abnormal DRE (induration, nodule,
firmness)




Prostate cancer screening allows the detection of potentially lethal
cancer at a point in time when it is more likely to be curable. This comes
at the expense of treatment nonaggressive cancers and morbidity of
dx/tx. Therefore, satisfactory informed consent to screen includes a
discussion of the harms and benefits of PCa screening with each patient
so they understand all the factors to be considered in the shared
decision-making about screening.
Allows men the right to decide whether tx is right for them rather than
not being offered the option for early detection of prostate cancer.
We believe that the evidence supports that prostate cancer screening
should be offered to all men 50 years of age with at least a 10-year life
expectancy. If there is a higher risk of PCa, such as family history of PCa
or if the patient is of African descent, screening should be offered at age
40 years.
There is also evidence that a single PSA at age 40 has a high predictive
value for the future risk for developing prostate cancer.
INCONTINENCE:
The Basics
OBJECTIVES

Define incontinence in a male

Understand basic evaluation and
treatment
Causes of incontinence
Urge
 Neuropathic
 Stress urinary incontinence
 Congenital
 Overflow
 Posttraumatic
 Fistulous connection

Evaluation

Voiding diary

Cystoscopy

Urodynamics
Urge incontinence


Involuntary loss of urine accompanied by strong sense of
urgency
Detrusor instability
 Irritative voiding symptoms: urgency, frequency, nocturia, urge
incontinence
 Differential causes:
○ Neuropathic injury: spinal cord injury
○ Obstruction
○ Inflammation: Interstitial cystitis
○ Diabetes
○ BPH
Overflow incontinence

Loss of urine secondary to full bladder
 Secondary to bladder outlet obstruction or acontracile
bladder

Evaluation
 Check US for post void residual (PVR) or cathed PVR
Stress incontinence
Causes of Male
Stress Incontinence
Prostate surgery
 Radical Prostatectomy / TURP
 Other pelvic surgery or trauma


Spinal disease

Neurologic disease
Behavioral Modifications
Decrease fluid intake
 Void frequently or timed voiding
 Avoid bladder irritants such as caffeine,
alcohol
 Avoid activity that increases
intraabdominal pressure for stress
incontinence

Management

OAB
 Pharmacological management with bladder relaxants
 Surgical procedures: Interstim, Intravesical botox, PTNS

Overflow incontinence
 Clean intermittent catheterization or indwelling foley
catheter
 Determine etiology to treat appropriately

Stress incontinence
 Kegel exercises
 External catheter or penile clamp
 Surgery: Sling
True or False:
72 year old male with a history of MI 10 years
ago. He carries NTG SL but has never used it.
He is on anticoagulants. It is most appropriate
to start him on oral medication.
True:
His history of MI was 10 years ago. He has never used his NTG SL.
It is most appropriate to start him on PDE-5 inhibitors with the
understanding he cannot use his NTG SL and risks involved. It is
important to review with patient absence of chest of pain, ability to
climb 2 flights of stairs.
He is on anticoagulation which is contraindicated in using a VED and a
precaution in using injectable medications
The best time of day to draw a total
testosterone level is:
a.
b.
c.
d.
Early in the morning as a fasting lab
Anytime of the day as long as they are fasting
In the evening
After abstaining from intercourse for 3 days
The best time of day to check a total
testosterone level is between 6-9 am.
The total testosterone level will be lower in the
evening secondary to diurnal variation.
The PSA test is the blood test that is important
to abstain from ejaculation for 3 days prior to
test.
The current guidelines for PSA testing:
a.
b.
c.
d.
If positive FHx of prostate cancer then start screening 10 years
prior to their diagnosed prostate cancer
Between the ages of 50-75 years of age or 40 years old if a FHx of
prostate cancer
Screen PSA starting at 50 years old and if stable, then stop
screening at age 60
Based on recent guidelines, stop checking PSA for prostate cancer
screenign
The recommended ages for prostate cancer screening are from 50-75
years of age.
Prostate cancer screening is recommended at 40 years old if there is a
positive family history of prostate cancer.
True or False:
BPH is a risk factor for prostate cancer?
False:
The diagnosis of BPH is not correlated with risk
of prostate cancer, but can elevate the PSA.
Fill in the blank:
The basic work up for male incontinence
includes history, physical exam, voiding diary
and __________.
In a male with lower urinary tract symptoms, it
is important to determine any post void
residual.
Thank you