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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