Disorder of Testes and Erectile Dysfunction – Flashcards

1.HISTORY 2.PHYSICAL EXAMINATION 3.URINALYSIS 4.COLORFLOW DOPPLER ULTRASOUND

-Painful: TORSION EPIDIDYMITIS/INFECTION INCARCERATED INGUINAL HERNIA TESTICULAR TUMOR WITH RUPTURE/HEMMORRHAGE TRAUMA -PAINLESS: TESTICULAR TUMOR HYDROCELE INGUINAL HERNIA SPERMATOCELE VARICOCELE

TWISTING OF THE TESTIS AND SPERMATIC CORD AROUND A VERTICAL AXIS, RESULTING IN VENOUS OBSTRUCTION, PROGRESSIVE SWELLING, ARTERIAL COMPROMISE, AND EVENTUALLY TESTICULAR INFARCTION Extravaginal Testicular Torsion: Occurs in neonates. Incomplete attachment of the tunica vaginalis to the dartos layer (Immature gubernaculum). 70% occur prenatally. Testicular salvage rate is poor

Medial rotation of the testes on the spermatic cord within the tunica vaginalis Bell-clapper deformity=inappropriately high fixation of tunica vaginalis to testes predisposes to torsion Venous occlusion and engorgement, with subsequent arterial ischemia and infarction. Most common in adolescents but can occur at any age

Diagnosis is clinical Sudden onset of acute scrotal pain and swelling Exquisitely tender testicle with a high, horizontal lie Absence of cremasteric reflex -Scrotal ultrasound with Doppler flow Documents absence of arterial blood flow Done only if time permits or diagnosis is unclear!

True vascular emergency: Urgent surgical exploration and detorsion Delay may result in loss of testicle Do not wait for ultrasound or results if diagnosis is seriously considered -Testicular preservation is excellent when corrected within 4-6 hours of onset -Delay greater than 12 hours results in poor testicular salvage rate Testes is detorsed and observed at time of exploration 1.Orchiectomy if testis is not viable If viable, orchiopexy is performed (testicular fixation to overlying fascia) 2.Contralateral orchiopexy is always performed as the predisposing bell clapper deformity is frequently bilateral .3.Manual detorsion—"Open the Book" Rotate testicle in a lateral direction May buy time if operating facility is not immediately accessible Must still follow with immediate exploration and bilateral testicular fixation

Mullerian or Wolffian duct remnants Symptoms mimic acute torsion May see blue dot sign Does not require surgery Pain resolves with antiinflammatories If unable to distinguish between testicular torsion scrotal exploration is required

Typically presents as progressive, gradual onset of pain (often greater than 24 hours) Infectious epididymitis Younger men—STDs (Chlamydia or gonococcal infection) Older men—Bacterial genitourinary infection (enteric gram negative bacteria) Noninfectious/inflammatory epididymitis Adverse effects of medications Urinary reflux within the ejaculatory ducts Sperm and fluid extravasation after vasectomy May have associated fever or irritative voiding symptoms

Tender mass posterior/lateral to testicle May have significant associated swelling/tenderness preventing adequate exam Very important to differentiate from testicular torsion May need scrotal ultrasound to confirm blood flow Treatment is conservative: -Antibiotics -Antiinflammatories -Analgesics -Rest -Scrotal elevation If abscess formation occurs, surgical drainage and/or orchiectomy may be necessary

Thickened, warm, erythematous skin Testicle is palpably normal Treat with broad spectrum antibiotics May be associated with abscess formation requiring incision and drainage

Fasciitis of scrotum, groin, and perineum Often seen in the immunocompromised or diabetic patients Exam 1.Diffuse enlargement 2.Thickening and erythema of the scrotal wall, groin, and perineum 3.Necrotic black or ecchymotic patches 4.Crepitus on palpation If left untreated will progress within hours to overwhelming bacterial sepsis with an associated high mortality rate Treatment Broad spectrum antibiotics that cover aerobic and anaerobic organisms Urgent and repeated surgical drainage and debridement

Fluid collection between parietal and visceral layers of the tunica vaginalis surrounding the testicle Typically painless Transilluminates on exam May conceal underlying tumor (reactive hydrocele) May be congenital or acquired

Peritoneal fluid passes freely between peritoneal cavity and scrotum through patent processus vaginalis Size may fluctuate throughout the day as fluid passes back and forth May also develop inguinal hernia through patent processus vaginalis Surgical intervention should be delayed for 1-2 years in anticipation of spontaneous closure If persists, surgical correction via inguinal exploration to close patent processus vaginalis and correct possible coexisting inguinal hernia

Usually idiopathic but may be secondary to tumor, infection, or systemic disease Imbalance of fluid secretion and absorption suggested as etiology Does not require treatment unless associated with pain/discomfort Definitive treatment is surgical drainage and excision of the hydrocele sac via scrotal incision

Inguinal hernia may presents as a scrotal mass due to loops of bowel within the scrotum Diagnosis can be confirmed with scrotal/groin US or pelvic CT scan Peristalsis may be seen on US Bowel sounds may be heard on auscultation Incarcerated or strangulated bowel is a surgical emergency

Cyst arising from the epididymis which contains spermatozoa Presents as a painless, cystic mass that lies above and posterior to the testes May be difficult to differentiate from hydrocele Ultrasound may confirm diagnosis Does not require surgical excision unless becomes large and causes discomfort Young men should be advised that surgery may result in obstruction of the spermatic ducts affecting fertility

Abnormal dilation of the pampiniform plexus in the spermatic cord due to elevated venous pressure and/or incompetent valves Occurs in 10-15% of men Identified in 40% of men evaluated for infertility May results in testicular atrophy, poor sperm motility, and decreased sperm count

90%) Left gonadal vein inserts into left renal vein at a right angle Increased incidence of incompetent valves Unilateral right sided varicocele is rare (<2%) Suggests possible compression or obstruction of the right spermatic vein, vena cava, or venous malformation Tumor Retroperitoneal Lymphadenopathy Venous thrombosis Situs inversus

PHYSICAL EXAM Large/Grade 3 - visible on inspection alone Moderate/Grade 2 - Palpable at rest Identified by palpation without bearing down (Valsalva maneuver) Small/Grade 1 - palpable only with Valsalva maneuver Subclinical—Identified on ultrasound only INDICATIONS FOR SURGERY: Painful symptomatic varicocele Significant testicular atrophy Infertility Improves semen parameters in 40-70% 40-60% of couples become pregnant within 1 year of repair

Testicular rupture=laceration of the tunica albuginea which may allow extrusion of testicular parenchyma Higher incidence of rupture with penetrating versus blunt trauma Penetrating trauma as a rule should be explored Scrotal Ultrasound for blunt trauma unless exam is grossly abnormal Indications for exploration after blunt trauma Disruption of tunica albuginea Marked loss of internal homogeneity Large intratesticular hematoma or hematocele Conservative management for nonrupture Rest Ice analgesics

Incidence 3% of full term infant boys up to 30% if premature 75% descend spontaneously by 6 months Palpable (80%) Inguinal Ectopic Nonpalpable (20%) Intraabdominal Absent/vanishing

Infertility Normal spermatogenesis is impaired Cancer Hernia Patent processus vaginalis in 90% Torsion Abnormal mesenteric attachment

Diagnosis by physical exam Imaging is unreliable and does not change management Optimal treatment at age 6-12 months Reexamine under anesthesia Surgical exploration and placement of testicle in scrotal position

-One of the most curable solid neoplasms -Drastic improvement in mortality with the advent of effective chemotherapeutic agents -Mortality In 1970s > 50% After 1990s < 5% Most common solid tumor ages 15-35 Peak incidence: ages 20-40

1.Cryptorchidism History of cryptorchidism in 7-10% (40x increased risk) 5-10% of these in contralateral testicle 50% of bilateral tumors have h/o cryptorchidism Orchiopexy aids diagnosis but does not change malignant potential 2.Hormone exposure (DES treated mother) 3.Atrophy

Local Painless Mass (most common) Swelling, Firmness, Heaviness Pain can occur due to bleeding or infarction Often detected by partner Metastatic Back or abdominal pain (retroperitoneal metastasis) Cough or SOB (pulmonary metastasis) Gynecomastia/breast tenderness (hormonal) Lower extremity edema (iliac/IVC thrombus or compression) Neck mass (supraclavicular nodes)

Seminoma—30-60% Non-Seminomatous Embryonal—3-4% pure, (in 40% of mixed) Teratoma—5-10% Choriocarcinoma—1% Yolk-Sac—rare in adults Mixed—40-60%

AFP, bhCG, LDH Obtain prior to treatment Should resolve after orchiectomy Persistence indicates metastatic disease Used to monitor treatment of advanced disease or to detect recurrence

Present in pure embryonal, yolk sac tumor, teratocarcinoma, or mixed GCTs Never pure seminoma Elevated in 50-70% of NSGCTs Half-life—5-7 days False positive—hepatitis, cirrhosis, ETOH, cocaine, hepatocellular, pancreatic, stomach, and lung CA

Produced by syncytiotrophoblastic cells All Choriocarcinomas 40-60% of embryonal/mixed 10-15% of seminomas Half-life—24-36 hours False positive—hypogonadal state (cross reactivity with LH) Elevated with other malignancies (liver, lung, stomach, pancreas, breast, bladder, renal) and marijuana abuse

Elevated with advanced, bulky metastatic disease Marker for advanced seminoma Low specificity

1.Initial Treatment: All tumors initially receive a radical orchiectomy 2.Inguinal Approach 3.High ligation of the spermatic cord at internal inguinal ring 4Trans-scrotal biopsy is to be CONDEMED!!!! Staging Work-Up: 1,.Chest X-Ray - Initially 2.CT of the Abdomen and Pelvis 3.Chest CT if abnormal CXR or Abdomen/pelvis CT Basic Labs-CBC, BUN, Cr, LFT's, tumor markers

-Retroperitoneal Lymph Nodes First site of metastasis Right—interaortocaval Left—para-aortic Right to left cross-over common -Supraclavicular and mediastinal nodes -Inguinal/Pelvic Nodes Invasion of scrotum/epididymis Disruption of normal lymphatics (prior groin surgery) Extralymphatic distant metastasis Vascular dissemination, tumor emboli from lymphatic's Lung, Liver, Bone, Brain

Dependent on tumor cell type and stage Surveillance Must have highly motivated, reliable patient Radiation Therapy (Stage I and II) Seminoma only Non-seminomatous tumors are not radiosensitive Retroperitoneal Lymph Node Dissection (Stage I and II) Non Seminomatous Chemotherapy (Stages I-III) All tumor types sensitive Bleomycin, Etopiside, Cisplatin

Understanding anatomy is important in evaluating intrascrotal disease Presence or absence of pain is an important piece of history in developing the differential diagnosis of a scrotal mass Testicular cancer is very responsive to therapy even when presenting with metastatic disease

Definition: "...the consistent or recurrent inability to attain and/or maintain a penile erection sufficient for sexual activity." Multifactorial—may impact total health and quality of life About 30 million men in US affected Major risk factor: aging

Depends on intact central, peripheral, and autonomic nervous system The autonomic nervous system is responsible for mediating flaccidity (sympathetic) and erection (parasympathetic) Erection involves 3 necessary processes: Neurologically mediated increase in penile arterial flow Relaxation of cavernous smooth muscle Restriction of venous outflow

In the flaccid state the penile smooth muscle cells are tonically contracted and there is a balance of penile blood inflow and outflow Sexual stimulation if required to initiate the cascade of events leading to penile erection Signals from the brain travel to the autonomic nervous system centers in the spinal cord Signals then travel via the cavernosal nerves to the penis Stimulation of nitric oxide (NO) release from the parasympathetic nerves and penile endothelium at the level of the penile smooth muscle NO stimulates production of cGMP cGMP causes decrease in intracellular Ca2+ resulting in relaxation of vascular smooth muscle Relaxation of vascular smooth muscle results in increased penile blood flow Cavernous sinusoids fill with blood causing the cavernous bodies to compress the traversing emissary veins against the tunica albuginea The combination of increased inflow and decreased outflow of blood leads to a rapid increase in intracavernous pressure, penile rigidity, and erection Following ejaculation the release of catecholamines and the rapid breakdown of cGMP by phosphodiesterase Type 5 isoenzyme (PDE5) returns the penis to a flaccid state

Vasculogenic Neurogenic Hormonal Drug-Induced Anatomic/Structural Psychogenic

Organic: gradual onset, incremental progression, lack morning erections, lack of erection in most stimulating sexual circumstance. Psychogenic; sudden onset, complete immediate lose, morning errections present, varies with partner and circumstance

Well established relationship between vascular disease and ED ED may be the first identified symptom of vascular disease The smaller cavernosal arteries make them more susceptible to occlusion This is why discussing ED is important May detect early vascular disease that is otherwise not clinically evident Begin early treatment and lifestyle modification before disease becomes severe or life threatening events occur

Atherosclerosis and asst risk factor: dylipidemia, smoking, obesity, sedentary lifesyle

Phase 1: Unhealthy lifestyle factors increase oxidative stress in endothelial cells, causing early injury. Leads to impaired NO production at endothelial cell. Phase 2: Endothelial cell: Early endothelial and vascular damage leds to atherosclortic changes Phase 3: Continued endothelial damage can lead to worsening ED and serious, life-threatening disease

Neurogenic Factors: Radical pelvic surgery (cavernous nerve injury), Pelvic/spinal cord injury, Multiple sclerosis or demyelinating conditions, Diabetic neuropathies, Pudendal nerve injury, Stroke, Alzheimer's disease, Parkinson's disease Hormonal Factors: Hypogonadism, Hypothyroidism, Pituitary disease or tumor Penile Injury or Disease: Trauma, Priapism, Peyronie's Disease, Anatomic abnormalities Medications: Cardiovascular drugs, SSRIs, hormonal agents, recreational drugs, cytotox agents, H2 agents, prtoease inhibitors

Targeted Medical History Is it ED, or something else? If it is ED, is it a problem? Is it clearly psychogenic or organic? Assessment of risk factors Targeted physical exam Genital exam Neurologic exam Perineal sensation, rectal tone, cremasteric and bulbocavernosal reflexes Cardiovascular exam Blood pressure, groin and peripheral pulses Laboratory tests Testosterone, lipid profile, glucose

-Lifestyle modification: Stop smoking, Limit or avoid alcohol, Follow healthy diet, Exercise regularly -Drug therapy modifications -Psychosocial Counseling -Androgen Replacement Therapy -Oral Medications: phosphodiesterase type 5 inhibitors

Inhibits degradation of cGMP by PDE 5 Works synergistically with NO to increase intracellular cGMP concentration Facilitates cavernous smooth muscle relaxation Does not work on the penis in the absence of sexual stimulation because NO and cGMP levels are low in the flaccid state

Sildenafil (Viagra) Vardenafil (Levitra) Tadalafil (Cialis) All 3 are similarly efficacious (65-70%) No head to head trials for direct comparison Variability in pharmacokinetics (t ½, onset of action, duration of action, etc.)

Headache Flushing Rhinitis Dyspepsia Visual changes (due to cross reactivity with PDE 6—seen primarily with sildenafil) Back pain (seen with tadalafil likely due to inhibitions on PDE 11)

-Absolute contraindication: patients taking concomitant nitrates(isosorbide dinitrate, nitropaste, etc.)!!! -Heart attack, stroke, or life-threatening arrhythmia in the last 6 months or current uncontrolled cardiovascular disease -Retinitis pigmentosa - drugs like sildenafil can affect a phosphodiesterase sub-type which is active in the retina. -Caution is advised in use with α blockers !!

Increases intracellular cAMP to induce smooth muscle relaxation and vasodilation Lack of response to oral therapy Contraindications to specific oral drugs Adverse reactions/intolerance to oral drugs More reliable, instant, predictable erection Patient preference

Penile Prosthesis -Intolerance or lack of response to other treatment modalities Irreparably damaged erectile tissue Specific concomitant medical conditions such as vascular or neurologic disease, chronic renal disease, and genital trauma

ED is a highly prevalent and undertreated disease that can significantly impact men's total health Aging is strongly associated with ED as a risk factor Lifestyle factors (such as sedentary lifestyle, obesity, and smoking) are associated with an increased risk of ED ED is associated with comorbid conditions, such as cardiovascular disease, hypertension, diabetes, and depression Vascular disease and ED have many shared risk factors that lead to endothelial cell damage ED frequently has both organic and psychogenic origins Initiate first-line therapy including lifestyle modifications and oral medications The unique mechanism of PDE 5 inhibitors have revolutionized ED treatment Contraindications to or failure of first line therapy should trigger urology referral to discuss second and third line therapies