SASP 2020 Flashcards
A 12-year-old girl has recurrent UTIs. Physical examination is normal. An ultrasound shows a large, thickened bladder wall and bilateral hydroureteronephrosis. A VCUG demonstrates no VUR and a large PVR. The next step is:
A. MAG-3 renogram. B. MRI scan of lumbosacral spine. C. urethral pressure profile. D. uroflow with EMG. E. cystoscopy and urethral dilation.
D: “uroflow with EMG.”
Profound dysfunctional voiding can be quite severe with the presentation of non-neurogenic neurogenic bladder (Hinman-Allen syndrome). The assessment of dyssynergic voiding with uroflow/EMG should identify the etiology. Although invasive urodynamics and MRI scan of the spine may be indicated, these would be second-order evaluations after failed management or when associated with other symptoms of potential spinal cord tethering. Certainly, more invasive procedures such as cystoscopy and urethral dilation will not address this functional issue. The presence of hydroureteronephrosis is not due to upper tract urinary obstruction; therefore, a MAG-3 renal scan is not indicated.
A four-year-old boy with PUV has a vesicostomy. Serum creatinine is 0.6 mg/dL. Ultrasound shows minimal hydronephrosis. Videourodynamics show a bladder capacity of 30 mL with a pressure of 14 cm H2O when leakage occurs from the vesicostomy with no reflux. Undiversion is considered. The best management is resection of the posterior urethral valves and:
A. ileal augmentation cystoplasty. B. ileal augmentation with appendicovesicostomy. C. bladder cycling via the vesicostomy. D. primary closure of the vesicostomy. E. autoaugmentation cystoplasty.
D: “primary closure of the vesicostomy.”
There was at one time concern that a cutaneous vesicostomy caused permanent loss of bladder volume and compliance. However, recent studies show that it does not significantly affect either, and that in fact, the bladder cycles via a properly created vesicostomy. Preoperative videourodynamics showing a small bladder capacity do not predict eventual functional bladder capacity. Approximately 75% of children will have normal bladder function after vesicostomy closure. The need for bladder augmentation is more related to the effects of the primary pathological condition on the detrusor. Augmentation cystoplasty may be needed after undiversion in patients with PUV, based on the effect of the primary obstruction on long-term detrusor function. The eventual need for augmentation should be assessed with sequential follow-up after the vesicostomy has been closed.
A 55-year-old woman on warfarin for recurrent pulmonary emboli has cystitis. The drug least likely to cause enhanced anticoagulation is:
A. tetracycline. B. nitrofurantoin. C. ciprofloxacin. D. trimethoprim. E. sulfamethoxazole.
B: “nitrofurantoin.”
All of the following drugs may ENHANCE the hypoprothrombinemic response to oral anticoagulants: allopurinol, aminoglycosides, aminosalicylic acid, chloramphenicol, cimetidine, ethacrynic acid, fluoroquinolones, indomethacin, isoniazid, metronidazole, miconazole, nalidixic acid, oxyphenbutazone, phenylbutazone, propoxyphene, salicylates, sulfonamides, tetracyclines, trimethoprim/sulfamethoxazole, and Vitamin E. Nitrofurantoin does not interact with warfarin.
The semi-synthetic beta-lactam penicillins, such as carbenicillin, ticarcillin, mezlocillin, and piperacillin, may produce coagulation defects at high doses, especially in the presence of renal impairment. Iodinated contrast material may also produce transient abnormalities in clotting. Broad-spectrum antimicrobials, particularly when administered orally, may disrupt the gut flora and alter Vitamin K synthesis. Drugs such as allopurinol and metronidazole inhibit the hepatic metabolism of oral anticoagulants. Drugs such as ethacrynic acid, nalidixic acid, and sulfonamides displace oral anticoagulants from proteins and increase the amount of circulating anticoagulant.
A 55-year-old woman has flank pain, fever, and malaise. Her serum creatinine is 1.6 mg/dL. Abdominal CT scan is shown. The next step is:
A. long-term antibiotics. B. percutaneous drainage. C. PCNL. D. nephrectomy. E. nephroureterectomy.
D: “nephrectomy.”
The clinical presentation and CT scan are most consistent with xanthogranulomatous pyelonephritis (XGP). The CT scan demonstrates the presence of a calculus and severe distortion of the renal parenchyma. Lipid laden macrophages are commonly identified in renal tissue and urine. Such cells are not seen in the urine of patients with pyelonephritis. In this case, complete removal of the kidney is warranted. Long-term antibiotics or PCNL is not the best solution. There is no abscess fluid to drain. Although RCC and urothelial carcinoma have been reported to occur in such cases, they are rare and the clinical picture is most consistent with an inflammatory, not a neoplastic, disorder. Nephroureterectomy is not indicated.
A 39-year-old woman has dysuria and frequency. Urinalysis shows 30 WBC/hpf and midstream urine culture shows 103 CFU/mL coagulase-negative Staphylococci. The next step is:
A. phenazopyridine. B. repeat midstream culture. C. urine culture for mycobacteria. D. antimicrobial therapy. E. catheterized urine culture.
D: “antimicrobial therapy.”
The standard definition of significant bacteriuria for a clean voided urine is > 105 CFU/mL of a uropathogen. This criterion has stood the test of time for screening and epidemiological studies and for entering patients in clinical trials. However, there are several important exceptions to its rigid use in clinical practice and one is in patients with a pyuria/dysuria syndrome. In these patients, a lower colony count may represent significant bacteriuria. Certain bacterial species such as coagulase-negative Staphylococci grow slowly in urine and significant infections may only have counts of 103 CFU/mL. Since the patient has a symptomatic, culture-proven UTI, treatment with phenazopyridine alone would be inappropriate. Repeat urine culture (midstream or catheterized) is not indicated. Mycobacteria culture is indicated only in sterile pyuria.
A 48-year-old man undergoes radical cystectomy with a Studer orthotopic neobladder. Three months postoperatively, he has urinary frequency and day and nighttime incontinence. A videourodynamic study (image shown) demonstrates a capacity of 300 mL, detrusor pressure at capacity is 10 cm H2O, Valsalva LPP is 130 cm H2O, and PVR is 75 mL. The next step is:
A. observation.
B. alpha-blocker therapy.
C. CIC every two to three hours.
D. placement of an artificial urinary sphincter.
E. augmentation of his orthotopic diversion.
A: “observation.”
The length of time postoperatively after orthotopic diversion influences continence results. The image demonstrates a smooth walled bladder without reflux. The reservoir capacity can and typically does increase over the first six to twelve months, and even longer in patients with anti-refluxing afferent limbs (e.g., Studer type). CIC will decrease incontinence but too frequent CIC will prevent the reservoir from increasing its capacity over time. Alpha-blocker therapy may relax the proximal urethra and exacerbate incontinence. At this point, it is premature to perform interventions such as sphincter placement as well as augmentation
A 28-year-old man with Kallmann syndrome is treated with hCG and FSH injections over two years. His serum testosterone and FSH levels are normal. His semen volume is 1.0 mL, sperm count is six million sperm/mL, and sperm motility is 90%. Well-timed sexual intercourse has not resulted in pregnancy for his wife, whose evaluation is normal. The next step is:
A. intrauterine insemination. B. color Doppler scrotal ultrasound. C. ICSI. D. TRUS. E. testis biopsy.
A: "intrauterine insemination." Intrauterine insemination (IUI) is an effective treatment option for couples when the male partner has a total motile sperm count (ejaculate volume x sperm concentration x % sperm motility) greater than 5 million. IUI involves placing processed sperm into the uterine cavity via a catheter inserted through the cervix and into the uterus. This approach allows the sperm to bypass the vaginal fluid and cervical mucous, and thus, higher numbers of motile sperm are able to reach the fallopian tubes, where fertilization occurs. Semen volume and sperm production are commonly limited in men with Kallmann syndrome, because prostate, seminal vesicle, and testicular size are often decreased as a result of this condition. However, sperm quality tends to be completely normal. In vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) are not indicated at this point. Screening scrotal ultrasound is not indicated in infertile male patients without physical exam findings needing further investigation, and testis biopsy will not be helpful since the patient is not azoospermic. TRUS is useful to evaluate for suspected ejaculatory duct obstruction, which is usually associated with low ejaculate volume (< 1.0 mL) azoospermia. Ejaculatory duct obstruction is not associated with Kallmann syndrome.
The parameter that most accurately measures renal function in a patient with an ileal conduit is:
A. creatinine clearance. B. urinary concentrating ability. C. fractional excretion of sodium. D. acid loading. E. proteinuria.
C: “fractional excretion of sodium.”
Measuring renal function in patients with intestinal diversion may be difficult. Most parameters of renal function will be affected by the intestinal absorption of various substances in the urine, including creatinine and urea (affecting acid loading tests), as well as secretion of alkalinizing substances and alteration in the osmotic content affecting urinary concentrating ability, so creatinine clearance and proteinuria will not be accurate measures. Sodium handling in ileal segments is not markedly altered as ammonium substitutes for sodium in the Na/H antiporter in the bowel lumen.
A four-year-old boy has renal failure due to membranoproliferative glomerulonephritis. He has undergone a bilateral orchiopexy and proximal hypospadias repair as an infant. He is at greatest risk for development of:
A. gonadoblastoma. B. NSGCT. C. Sertoli cell tumor. D. Wilms' tumor. E. RCC.
D: “Wilms’ tumor.” was the correct answer.
A number of recognizable syndromes are associated with an increased incidence of Wilms’ tumor. Three syndromes that are well known to be at high risk for Wilms’ tumor development include: Denys-Drash syndrome (DDS - male pseudohermaphroditism manifested by proximal hypospadias and cryptorchidism, membranoproliferative glomerulonephritis, and nephroblastoma), Beckwith-Wiedemann syndrome (macroglossia, nephromegaly, and hepatomegaly), and WAGR syndrome (Wilms’ tumor, aniridia, gonadoblastoma, and intellectual disability). In patients with DDS, the kidneys need to be monitored carefully and removed as renal failure occurs. With DDS, there is no increased risk of RCC, Sertoli cell tumor or NSGCT of the testis.
A six-year-old boy with left scrotal pain has a tender indurated epididymis and normal testes. Urinalysis is normal. An ultrasound shows normal testes with Doppler evidence of blood flow, an enlarged, hypervascular left epididymis, and normal kidneys. The next step is:
A. scrotal exploration. B. radionuclide testicular scan. C. VCUG. D. oral antibiotic therapy. E. NSAIDS.
E: “NSAIDS.”
This boy most likely has torsion of the left appendix testis or epididymis resulting in reactive epididymitis. This does not require surgical exploration when the diagnosis is clear. Considering the age of the patient, the presentation is very strongly consistent with torsion of an appendix testis, and testicular scan is unlikely to add any useful information. In cases of epididymitis in this age group, antibiotics are not needed as bacterial epididymitis is rare. The most appropriate treatment includes NSAIDS as well as rest and scrotal support. A VCUG is not useful given the normal kidneys on ultrasound and absence of infection.
A 23-year-old man underwent left transscrotal orchiectomy demonstrating a mixed NSGCT (70% embryonal carcinoma, 30% seminoma) with lymphovascular invasion. Tumor markers and metastatic evaluation are negative. In addition to RPLND and excision of the left spermatic cord and left scrotal scar, treatment should include:
A. observation.
B. chemotherapy.
C. left inguinal sentinel lymph node biopsy.
D. left superficial inguinal lymph node dissection.
E. XRT to left hemiscrotum and left inguinal lymph nodes.
A: “observation.”
A meta-analysis including 206 cases with scrotal violation found that the risk of local recurrence increased from 0.4% for patients treated with inguinal orchiectomy to 2.9% with scrotal violation, but there was no difference in systemic recurrence or survival rates. As such, excision of the scrotal scar may be considered at the time of RPLND and removal of the spermatic cord remnant, with no additional treatment necessary. Specifically, prophylactic (given the negative metastatic evaluation) inguinal lymph node biopsy, dissection, or XRT would not be necessary. Likewise, scrotal violation during orchiectomy would not itself represent an indication for systemic chemotherapy.
A 45-year-old man with a history of recurrent UTIs has two days of perineal discomfort, dysuria, and urinary frequency. Urinalysis reveals bacteriuria and pyuria. Physical examination reveals an enlarged prostate. He finished his last course of antibiotics one week ago. Before antibiotic treatment is restarted, the culture that should be obtained is:
A. midstream urine. B. urine by suprapubic aspiration. C. expressed prostatic fluid. D. pre- and post-prostatic massage voided urine and prostatic fluid. E. initial voided urine.
A: “midstream urine.”
This man likely has chronic bacterial prostatitis, which is usually manifested by recurrent UTIs with the same organism. While lower urinary tract bacterial localization is helpful in identifying the prostate as a nidus of infection, localization is useless in the presence of bacteriuria, with all isolation specimens having bacterial growth due to contamination. This man is currently symptomatic with documented bacteriuria, and therefore, should not undergo localization testing. In this situation, preferred treatment is to obtain a midstream urine culture and treat with nitrofurantoin. Nitrofurantoin will clear the urine of bacteriuria and have little to no effect on intraprostatic bacteria. Once the urine has been documented to be sterile, usually in three to five days, bacterial localization studies with initial voided, midstream, expressed prostatic secretions, and post-prostatic massage urinary specimens should be obtained. These tests will allow confirmation of chronic bacterial prostatitis. For chronic prostatitis caused by E. coli, four to six week treatment with fluoroquinolones is superior to the alternative three month therapy with trimethoprim/sulfamethoxazole; however, the risk of fluoroquinolone use should be discussed with the patient. Approximately 20% of the patients will fail the initial therapy and a rescue treatment with a second cycle of therapy with an alternative quinolone has been found to rescue the majority of the relapsing patients.
23-year-old asymptomatic woman has a palpable right-sided abdominal mass with serum creatinine of 0.9 mg/dL. CT scan is shown. The next step is:
A. follow-up CT scan in three months. B. CT-guided biopsy. C. angioembolization. D. right nephrectomy. E. neoadjuvant XRT followed by radical nephrectomy.
D: “right nephrectomy.”
This patient has a massive fat-containing tumor of the right kidney. The primary differential diagnosis is between an angiomyolipoma (AML) and a retroperitoneal liposarcoma. The CT scan demonstrates the tumor arising from within the kidney, not the retroperitoneum, and the tumor does not “push” the kidney as is characteristic of the imaging findings in liposarcoma. Thus, the diagnosis is a very large AML, and with these characteristic radiological findings, a biopsy is not necessary. Given the large size of this AML, it has a significant risk for hemorrhage, particularly in a young woman of childbearing age, so observation is not an appropriate management strategy. Selective renal arterial embolization is the treatment of choice in many instances of AML, especially in the acute situation of spontaneous hemorrhage. In most cases of massive AML, the tumor size precludes effective embolization and the risk of spontaneous hemorrhage persists despite embolization. Thus, surgical resection (or a partial nephrectomy, if technically feasible) is a better choice. In this case, because of the large tumor size and anatomical location, a total nephrectomy is the likely outcome. Neoadjuvant radiation prior to resection may be recommended if this were a liposarcoma, but as AML is a benign tumor, this is not indicated.
A 60-year-old man with erectile dysfunction has an nonpalpable right testicle. Ultrasound reveals a 2 x 2 cm homogeneous ovoid mass at the right internal ring. The next step is:
A. observation. B. hCG therapy. C. percutaneous biopsy. D. orchidopexy. E. orchiectomy.
A: "observation." The presence of cryptorchidism increases the risk of testicular cancer in the cryptorchid testis. Orchiopexy before puberty has been associated with a decreased risk of testicular cancer, and is, therefore, recommended when cryptorchidism is detected in this age group. Management of the postpubertal patient with cryptorchidism has evolved over time, as understanding of the long-term malignancy risks of cryptorchid testes has improved and as perioperative anesthetic risks have decreased. Given the risk of malignancy, orchiectomy of the undescended testes may be considered in healthy postpubertal patients until the risk of operative mortality exceeds the risk of mortality from germ cell cancer, which has been demonstrated to occur at age 50 for ASA class I and II cases. As such, while orchiectomy may be considered for healthy patients with cryptorchidism between age 12 and 50, observation is recommended for postpubertal patients at significant anesthetic risk, as well as all males older than 50 with cryptorchidism (as in this patient). Biopsy would not be indicated in this setting, as a negative biopsy cannot exclude the presence of malignancy elsewhere in the testis. Likewise, although hCG therapy has historically been used to stimulate testicular descent, such hormone therapy is not currently recommended given the lack of rigorous data supporting its efficacy.
A 45-year-old obese man with untreated sleep apnea develops nocturnal enuresis. He has no daytime incontinence. Physical examination is unremarkable except for mild lower extremity edema. Urinalysis is negative, and his PVR is 30 mL. The most likely etiology of the enuresis is:
A. increased secretion of ADH.
B. increased secretion of atrial natriuretic peptide.
C. detrusor overactivity.
D. mobilization of lower extremity edema.
E. hypercarbia induced drowsiness.
B: “increased secretion of atrial natriuretic peptide.”
Sleep apnea is a recognized cause of nocturia and secondary nocturnal enuresis. It causes nocturnal diuresis by a cascade of events which are precipitated by hypoxia which occurs during the intermittent occlusion associated with obstructive sleep apnea. The hypoxia-induced increase in right atrial transmural pressure leads to elevated atrial natriuretic peptide (ANP) and subsequent decreased secretion of ADH, resulting in increased nocturnal urinary output. ANP secretion is induced by elevated intrathoracic pressures due to diaphragmatic contraction against a closed upper airway. Isolated detrusor overactivity at night is unlikely in the absence of daytime symptoms. Mobilization of mild lower extremity edema is unlikely to cause a significant increase in nighttime urine production. Sleep apnea can cause hypercarbia but this is not a known cause of increased urine production. An additional advantage of treatment of sleep apnea with CPAP is improvement in nocturnal enuresis.
A 43-year-old woman has a 3 cm vesicovaginal fistula on the posterior bladder wall, 2 cm above the trigone, three years following pelvic XRT for cervical cancer. CT urogram demonstrates normal upper urinary tracts without evidence of recurrent disease. The next step is:
A. bladder biopsy.
B. bilateral percutaneous nephrostomies.
C. injection of fibrin glue.
D. transvaginal repair with gracilis interposition.
E. transabdominal repair with omental interposition.
A: “bladder biopsy.”
Although less common with improved radiation techniques, radiation-induced fistulas are commonly associated with persistent or recurrent cervical cancer. Fistulas may occur during or shortly following XRT as a result of tumor necrosis in the wall of the vagina or bladder. Fistulas that develop one or more years following XRT are attributed to radiation-induced endarteritis obliterans with subsequent necrosis of the vaginal and bladder wall. The most important aspect in the management of a patient with a fistula following XRT is to rule out recurrent cervical cancer. Locally recurrent cervical cancer following definitive XRT is associated with poor survival despite aggressive multimodal management. Fistula repair would not be indicated in the setting of recurrent disease. While nephrostomy placement would divert some of the urine in the short term, it would not help with the diagnosis of potential recurrence. Fibrin glue could be considered in a small (< 2-3 mm), oblique, non-radiated fistula; this would not be an appropriate option in this patient.
30-year-old woman received a renal transplant two years ago. Her creatinine is 1.1 mg/dL and she has no proteinuria. She is planning a pregnancy and should be advised:
A. to proceed.
B. that a Cesarean section delivery will be required.
C. that a late delivery is expected.
D. that there is a greater risk of birth defects.
E. to reduce immunosuppression during pregnancy.
A: “to proceed.”
There have been many successful pregnancies reported after renal transplantation and vaginal delivery is appropriate without the concern for a pregnancy that extends beyond normative gestational age values. Most women can deliver vaginally without risk to the allograft. The risk of birth defects is not significantly different from age-matched women in the general population. Because the volume of distribution increases during pregnancy, the dose of immunosuppressive medications may be increased to prevent renal allograft rejection. Impaired renal allograft function and proteinuria are significant risk factors for pre-eclampsia, hypertension, rejection, and graft failure.
A 72-year-old man develops dyspnea and hypertension following adrenal-sparing nephrectomy. The preoperative CT scan shows aortic and renal artery calcification. A ventilation perfusion scan shows a low probability of pulmonary emboli. The best agent to treat the hypertension is a(n):
A. diuretic. B. calcium channel blocker. C. alpha-blocker. D. ACE inhibitor. E. angiotensin receptor blocker.
A: “diuretic.”
This patient has a high probability of having renal artery stenosis. By removing one kidney, the situation becomes analogous to the one-kidney, one clip model. In this situation, hypertension is largely maintained by volume and sodium excess. In the face of normal circulating angiotensin II (AII) levels, ACE inhibitors or AII antagonists do not result in marked decrease of blood pressure. Calcium channel blockers and alpha-blockers also are not very effective until the volume overload has been treated. Since the etiology of hypertension is intravascular volume expansion, the best choice is a diuretic.
A 32-year-old woman with a T5 spinal cord injury develops profuse sweating, hypertension, and bradycardia during urodynamic evaluation. The bladder is emptied but her symptoms persist with a blood pressure of 170/100 mmHg. The next step is to administer:
A. oral nifedipine. B. sublingual nifedipine. C. transdermal nitroglycerin. D. I.V. atropine. E. I.V. hydralazine.
C: “transdermal nitroglycerin.”
Autonomic hyperreflexia or dysreflexia (AD) is most commonly seen in patients with spinal cord injury levels above T6. It is an exaggerated sympathetic nervous system response to afferent visceral stimulation that manifests with sweating, headache, hypertension, reflex bradycardia, and flushing above the level of the spinal cord lesion. The normal systolic blood pressure (SBP) in paraplegics and tetraplegics is low, usually 90-110 mmHg. Elevation of SBP with AD symptoms classically begins with a 20 mmHg rise above baseline, well within normal range for a neurologically-intact individual. If the SBP is > 120 mmHg and the patient is symptomatic, presumed AD is present. Initial therapy should focus on the removal of inciting factors. In this case, that would include emptying of the bladder and removal of all urodynamic catheters. If the symptoms persist and SBP remains elevated, but lower than 150 mmHg, then evaluation and treatment of fecal impaction (second-most common cause of AD after bladder distension) are recommended. However, if the systolic pressure remains above 150 mmHg after bladder emptying and catheter removal, then use of a rapid-onset, short-acting anti-hypertensive is recommended while the cause of AD is investigated. One-half to 1 inch of nitropaste 2% should be applied above the level of the lesion (vasoconstriction occurs below the level of the lesion and may interfere with drug absorption) and is preferred due to its ability to be wiped free if rebound hypotension occurs. Nifedipine had been recommended as a primary treatment or prophylactic agent for AD; however, because of several adverse, rebound hypotensive crises resulting in stroke or MI after its use, the Joint Commission for Treatment of High Blood Pressure and National Spinal Cord Injury committees have discouraged its use and it has been banned for treatment or prevention of AD in some hospitals. If the blood pressure remains elevated and does not respond to transdermal or oral therapy, I.V. hydralazine is an option; however, blood pressure may be quite labile after its use with both hypotension and/or rebound hypertension, and the patient will require hospital admission with further monitoring. After the patient is stabilized, additional monitoring may be required. Atropine is not indicated for treatment of this condition.
A 32-year-old man desires a biological child. Both testes are 4 cm long and soft. Two semen analyses reveal azoospermia with volumes of 3.0 mL and 3.1 mL. Testosterone is 280 ng/dL, LH is 7.5 IU/L, and FSH is 8.5 IU/L. The next step is:
A. repeat semen analysis. B. clomiphene citrate. C. beta-hCG and recombinant FSH. D. testis biopsy. E. epididymovasostomy.
B: “clomiphene citrate.” was the correct answer.
The aim of clomiphene citrate therapy in an infertile patient with low serum testosterone levels is to increase intratesticular testosterone levels and thus optimize the intratesticular environment for spermatogenesis. The clomiphene citrate dosage should be titrated to increase the serum testosterone levels to the mid-normal range, when possible. A third semen analysis is unlikely to aid in the diagnosis given that both prior semen tests revealed normal ejaculate volume azoospermia. While exogenous hCG might help optimize his low testosterone levels, recombinant FSH is not indicated given that his FSH levels are not abnormally low. A diagnostic testis biopsy is not required to establish the presence of spermatogenic dysfunction, as the likelihood of non-obstructive azoospermia in a man with testis longitudinal axis less than 4.6 cm and FSH greater than 7.6 IU/L is 89%. Microsurgical reconstruction with epididymovasostomy will not result in ejaculated sperm because his azoospermia is caused by impaired spermatogenesis, not obstruction.
During a left laparoscopic pyeloplasty, the inferior mesenteric artery is accidentally ligated. Blood supply to the left colon will be primarily maintained by the:
A. left colic artery.
B. left colic artery and inferior hemorrhoidal arteries.
C. middle colic artery and superior hemorrhoidal arteries.
D. marginal artery and superior hemorrhoidal arteries.
E. middle colic and middle hemorrhoidal arteries.
C: “middle colic artery and superior hemorrhoidal arteries.” is incorrect.
E: “middle colic and middle hemorrhoidal arteries.”
The inferior mesenteric artery supplies the main blood supply to the left colon via the left colic artery and superior hemorrhoidal arteries. When this is injured or ligated, blood supply is maintained proximally via the middle colic artery which is a branch of the superior mesenteric artery, and distally via the middle and inferior hemorrhoidal arteries. The middle colic and hemorrhoidal arteries connect with each other via the marginal artery of Drummond. This artery runs parallel to the wall of the colon. It is important to maintain this artery during any dissection of the left colon in cases where injury to the inferior mesenteric artery may occur.
A 31-year-old man sustains complete scrotal skin avulsion from a machinery accident. The skin is placed in ice saline and transported to the hospital with the patient. The next step is:
A. saline wet to dry dressings and delayed grafting.
B. reapplication of avulsed skin as a full thickness skin graft.
C. immediate split thickness skin grafting to the scrotum.
D. bilateral testicular thigh pouch creation.
E. thigh flap reconstruction of scrotum.
A: “saline wet to dry dressings and delayed grafting.”
Genital skin avulsion may result from machinery accidents, high-speed blunt trauma, or bizarre sexual practices. The classic mechanism is entrapment of clothing and scrotal skin in the power takeoff apparatus of farming tractors. The underlying testicular structures are often spared. Complex avulsions are best managed with initial judicious debridement, close observation, and delayed reconstruction via primary re-approximation or skin grafting. Immediate grafting of a potentially contaminated wound offers little advantage and may risk graft loss if infection ensues. While avulsed skin from blunt degloving injuries may be preserved and used as either split or full-thickness grafts, machinery accidents in which skin is entrapped and avulsed are likely to damage the intrinsic vascular structures of the skin and make it unsuitable for grafting. Wet to dry dressings allow for granulation tissue to develop with its associated neovascularity, and also cleansing and debridement of the wound bed. Thigh pouches are a reasonable alternative for temporary or permanent management of exposed testes, but immediate creation of pouches may risk infection if the wound is contaminated. Likewise, thigh flap reconstruction is an elective definitive approach to scrotal skin absence, but is not appropriate in the acute injury setting. Finally, the scrotum is uniquely amenable to primary reconstruction because of its excellent vascularity and elasticity; primary closure is possible even when up to 60% of scrotal tissue is lost.
A 49-year-old man with diabetes and hypertension has an 8 cm solid renal mass. Preoperative cardiac angiography reveals a 90% occlusion of the right coronary artery and he undergoes bare metal stenting across the blockage. The minimum delay before surgery is:
A. two weeks. B. four weeks. C. three months. D. six months. E. 12 months.
B: “four weeks.” was the correct answer.
Perioperative coronary stent thrombosis is a catastrophic complication that can occur in patients receiving both bare-metal and drug-eluting stents. Non-cardiac surgery and most invasive procedures increase the risk of stent thrombosis, especially when the procedure is performed early after stent placement. Reasons for an increased risk of stent thrombosis include: incomplete stent endothelialization early after placement, discontinuation of antiplatelet therapy during the peri-procedural period, and the prothrombotic state often created during surgery. Avoidance of preoperative stent implantation, selection of optimal stent type when stent implantation cannot be avoided, delay of non-essential, non-cardiac surgery, a continuation of antiplatelet therapy in the perioperative period, and increased collaboration between different disciplines (surgery, anesthesiology, and cardiology) can all help minimize the risk of perioperative stent thrombosis. Numerous clinical guidelines advise that elective, non-cardiac surgery be delayed for at least four weeks after bare-metal stent implantation and 12 months after drug-eluting stent placement in order to minimize the risk of stent thrombosis. Furthermore, if surgery will need to be performed within 12 months of stent placement, then bare-metal stent implantation is typically preferred over drug-eluting stents, because bare-metal stents endothelialized more rapidly and may, therefore, carry a lower risk of stent thrombosis.
A 72-year-old man with a large RCC has right hip pain. Bone scan shows multiple metastases and plain films of the right femur show a 4.0 cm lytic cortical lesion. The next step is:
A. XRT to the femur. B. strontium-89. C. open stabilization of the femur. D. pazopanib. E. ipilimumab and nivolumab.
C: “open stabilization of the femur.”
Surgical treatment of bony metastases from RCC is indicated in patients who are at high risk of fracture, particularly those with large (> 3 cm) lytic lesions, involving the cortex of weight-bearing bones. Although the patient has a poor long-term prognosis, should he develop a femur fracture, the quality of his remaining survival will be markedly diminished. Since the risk of fracture is relatively high (given the size and characteristics of the lesion), systemic therapy should be delayed until the femur has been stabilized. Tyrosine kinase inhibitors (pazopanib) or checkpoint inhibitors (ipilimumab and nivolumab) would both be reasonable choices following stabilization of the femur. XRT and strontium-89 would help control pain but would not be adequate to prevent fracture in this case.
A five-year-old girl is wet within the first few minutes after voiding. She has mild perineal erythema. The next step is:
A. repositioning on the toilet. B. use a timer to assure five minutes on toilet. C. uroflow and PVR. D. oxybutynin and timed voiding. E. VCUG.
A: “repositioning on the toilet.”
Postvoid dribbling is most commonly due to vaginal pooling of urine which leaks out once the patient stands or walks. Vaginal reflux is seen by VCUG in many young girls. Immediate improvement may be seen by undertaking maneuvers to facilitate vaginal drainage while still on the toilet; this includes straddling the toilet seat, sitting backward on the toilet seat, leaning forward after voiding, suprapubic compression before getting up, and careful tissue drying after the above maneuvers. Medications and the other studies are not necessary. Five minutes on the toilet will not ensure drainage of urine trapped in the vagina.
A six-year-old asymptomatic boy with PUV had neonatal valve ablation. He has worsening bilateral hydronephrosis and his serum creatinine has increased from 0.6 to 1.0 mg/dL over the past nine months. Videourodynamics reveal no VUR or evidence of residual valves, and filling pressures of 15 cm H2O at 220 mL and 32 cm H2O at 280 mL. The next step is:
A. voiding diary. B. antimuscarinic. C. alpha-blocker. D. nocturnal indwelling catheter. E. initiate CIC every four hours.
A: “voiding diary.”
Children with correction of severe obstructive uropathy will sometimes demonstrate a persistent decrease in renal concentrating ability. This tends to worsen with growth and may lead to very high obligate urine output. This output can, at times, be so high that children cannot void frequently enough to maintain safe intravesical pressures; hydronephrosis and rising creatinine will ensue. This boy appears to void without obstruction. He does have reduced bladder compliance (as many valve patients do), and his safe zone for filling is equal to 220 mL. However, if his urine output is very high, then he will reach this capacity very quickly after voiding. While he may eventually need timed voiding, antimuscarinic medication, CIC, or a nocturnal indwelling catheter, none of these can be used in a logical way without first knowing more about the patient’s daily urine volume. An alpha-blocker is not indicated in this patient.
A four-year-old girl voids normally but is continuously wet. A renal ultrasound shows normal-appearing kidneys bilaterally. The next step is:
A. MAG-3 renal scan. B. VCUG. C. MRI scan. D. cystoscopy and vaginoscopy. E. retrograde pyelogram.
C: “MRI scan.”
The clinical scenario of dribbling despite normal voiding creates suspicion of an ectopic ureter. Often the ectopic upper pole moiety of the duplex kidney is very small and not easily identified on ultrasound. In these cases, an MRI scan or MR urogram are the best imaging tests to localize the difficult to identify small, dysplastic upper poles and their ureters. MR urogram is not always required since the T2-weighted images of a standard MRI are particularly suited for finding and defining fluid-filled structures like an ectopic ureter. Sagittal imaging may demonstrate the exact termination of the ectopic ureter. DMSA scan is most useful in the identification of small ectopic kidneys but is unlikely to be useful when the renal ultrasound is normal. If the moiety is small, a MAG-3 renal scan will appear normal because the upper pole often has no function and the lower pole will not deviate. VCUG will sometimes show VUR into an ectopic ureter depending on the location of the orifice. Cystoscopy and vaginoscopy can identify the ectopic orifice, but the orifice is often difficult to identify endoscopically and is not as sensitive as an MRI scan. Retrograde pyelogram is also limited due to difficulty in identifying the ectopic ureteral orifice.
In a man with high risk prostate cancer undergoing radical prostatectomy, the primary landing zone for nodal metastases is:
A. external iliac. B. obturator. C. internal iliac. D. common iliac. E. presacral.
C: “internal iliac.”
The internal iliac lymph nodes (hypogastric) have the highest independent risk of being positive. The external iliac, obturator, common iliac, and presacral areas are all regions with potential for lymph node metastases but at lower rates.
Three months following a CVA, a 67-year-old woman develops urgency urinary incontinence. Videourodynamic testing will most likely show detrusor overactivity and simultaneous:
A. involuntary smooth and striated sphincter contraction.
B. involuntary smooth sphincter contraction and striated sphincter relaxation.
C. involuntary smooth sphincter relaxation and striated sphincter contraction.
D. involuntary smooth and striated sphincter relaxation.
E. sphincter bradykinesia.
D: “involuntary smooth and striated sphincter relaxation.”
Typically, CVA is associated with neurogenic detrusor overactivity (DO) with appropriate relaxation of the bladder outlet (both smooth and striated sphincteric mechanisms) during involuntary bladder contractions. External sphincter contractions may be seen with DO as a voluntary normal guarding reflex. DO associated with detrusor external sphincter dyssynergia is commonly seen with suprasacral spinal cord injury and in 25-40% of patients with multiple sclerosis. Sphincter bradykinesia is not typically seen with CVA and is associated with Parkinson’s disease.
A 13-year-old girl with spina bifida was augmented five years ago and is on CIC and antibiotic prophylaxis. She recently developed incontinence and has had two UTIs. The next step is:
A. change antibiotic prophylaxis.
B. instill antibiotics into bladder during CIC.
C. observe CIC technique and obtain catheterization diary.
D. bladder ultrasound.
E. videourodynamic evaluation.
C: “observe CIC technique and obtain catheterization diary.”
The new onset of a UTI and incontinence in an augmented patient with a neurogenic bladder raises concerns. The first concern in a patient at this age, going through puberty, should be determining whether she is doing CIC as she has been instructed. It is very common for teenagers at this developmental stage to become non-compliant with CIC due to peer pressure and the desire to be “normal”. Their attitude toward authority and supervision is also changing. Teenagers are commonly untruthful when questioned about CIC. For this reason, it is very important to first determine whether CIC is really being done appropriately. If CIC is not a problem, then the evaluation for bladder stones, changing bladder storage dynamics, and other issues should be addressed.
A 60-year-old healthy woman with recurrent UTIs has free air in the bladder and a thickened bladder wall adjacent to a loop of thickened colon seen on CT scan. Cystoscopy demonstrates erythema in the bladder wall with no clear fistula. The next step is:
A. antibiotic suppression.
B. cystogram.
C. CT scan with small bowel follow through.
D. MRI scan.
E. general surgery consult/exploratory laparotomy.
E: “general surgery consult/exploratory laparotomy.”
Cross-sectional imaging, especially CT scan, has become the imaging modality of choice to demonstrate a vesicoenteric fistula. CT or MRI scans may localize the fistula tract as well as the involved segment of bowel. The triad of findings on CT that are suggestive of colovesical fistula consists of (1) bladder wall thickening adjacent to a loop of thickened colon, (2) air in the bladder (in the absence of previous lower urinary tract manipulation), and (3) presence of colonic diverticula. Cystoscopy has the highest yield in identifying a potential lesion, with some type of abnormality noted on endoscopic examination in more than 90% of cases. However, the findings on cystoscopy are often nonspecific and include localized erythema and papillary or bullous changes; a definitive diagnosis by cystoscopy can be made in only 35% to 46% of cases. This patient has clear evidence of a vesicoenteric fistula and further diagnostic studies are not indicated. Should she be a poor surgical risk, long-term antibiotics could be used. Definitive colonic resection of presumed diverticulosis and repair of fistula is indicated with exploratory laparotomy. General surgery may wish to proceed with colonoscopy/barium enema to evaluate the extent of the affected segment or rule out malignancy.
A 33-year-old man with history of depression treated with a monoamine oxidase inhibitor complains of premature ejaculation. The recommended treatment is:
A. topical anesthetic spray prior to coitus. B. tramadol prior to coitus. C. daily clomipramine. D. daily sertraline. E. daily paroxetine.
A: “topical anesthetic spray prior to coitus.”
Selective serotonin reuptake inhibitors (SSRIs) such as paroxetine, sertraline, clomipramine, and tramadol have all been shown to improve premature ejaculation. However, all four of these medications are contraindicated with the use of a monoamine oxidase inhibitor (MAOI). The only pharmacological option for this patient is topical anesthetic spray. Behavioral therapy would be an alternative to pharmacological management.
A 60-year-old man is referred by his internist for evaluation of an elevated PSA. He has no voiding symptoms and his DRE is normal. The laboratory results are not in your chart. You should:
A. call the internist and ask for the results.
B. ask the patient to reschedule and return with his results.
C. obtain a release of information and fax to the internist’s office.
D. assure that the patient signed a protected health information form at registration.
E. draw a PSA.
A: “call the internist and ask for the results.”
A referring health care provider is permitted to disclose protected health information about an individual to a health care provider for that provider’s treatment of the individual. A release of information is not required. Professionalism precludes the inconvenience of rescheduling the patient for another appointment. Redrawing the PSA is potentially more efficient (although results will not be immediately available) but is not cost-effective. The protected health information form that is signed in your office only affirms that the patient is aware of your privacy policies and does not give permission for release of information.
A 47-year-old man has a 3 cm hyperechoic renal lesion on ultrasound. The MRI sequence most likely to confirm the diagnosis of angiomyolipoma is:
A. T1-weighted image without gadolinium.
B. T1-weighted image with gadolinium enhancement.
C. T2-weighted image with fat suppression.
D. T2-weighted image with gadolinium enhancement.
E. magnetic resonance angiography.
C: “T2-weighted image with fat suppression.”
For a fat-containing tumor, a T2-weighted image with fat suppression is most likely to identify macroscopic fat and confirm the diagnosis of an angiomyolipoma (AML). A T1-weighted image without gadolinium is insufficient to confirm the diagnosis of AML. Lesions that enhance with gadolinium on T1-weighted images are typically consistent with malignant lesions. Enhanced T2-weighted imaging is rarely obtained. Magnetic resonance angiographs are rarely necessary for the diagnosis of a renal mass and would not be helpful in this situation.
A 72-year-old woman has urgency urinary incontinence. Examination demonstrates minimal prolapse, no leakage with cough, and vaginal atrophy. In addition to timed voiding and dietary modification, the next step is:
A. pelvic floor muscle training. B. vaginal estrogen. C. oral estrogen. D. duloxetine. E. periurethral injection.
A: “pelvic floor muscle training.”
Pelvic floor muscle training has been shown to be effective for the treatment of both stress urinary incontinence (SUI) and urgency urinary incontinence (UUI) in women and is considered first-line therapy. Vaginal estrogen may improve her vaginal atrophy and genitourinary symptoms of menopause; however, neither oral nor vaginal estrogen has been shown to improve incontinence (even in the setting of vaginal atrophy). Duloxetine, a serotonin reuptake antagonist, may have a positive impact on SUI, but has not been shown be effective for UUI. Duloxetine is not approved for use in the United States for the treatment of SUI. A periurethral injection may be useful in elderly patients (or others looking to avoid surgery) with SUI but would not treat this patient’s symptoms.
A 27-year-old man with a C5 spinal cord injury has recurrent problems with sediment and clogging of his indwelling urethral catheter despite frequent catheter changes. The next step is:
A. urine culture to identify urease producing organism.
B. daily acetic acid irrigation.
C. placement of a large lumen suprapubic tube.
D. non-contrast CT scan.
E. cystoscopy.
A: “urine culture to identify urease producing organism.”
Simple measures, such as catheter irrigations (e.g., acetic acid) and placement of a larger diameter suprapubic tube, may temporize but not completely address the underlying problem of recurrent catheter encrustation with sediment. Catheter encrustation is attributed to bacterial biofilm, particularly biofilms made by urease producing bacteria such as Proteus mirabilis. Urine culture is the appropriate next step. If a urease producing organism is identified, both treatment of the offending organism and evaluation for the presence of bladder or upper tract stones (e.g., with cystoscopy, non-contrast CT scan) that may serve as a nidus for bacterial infection is necessary.
A 55-year-old woman with a history of ovarian cancer is evaluated for gross hematuria. She has a family history of intestinal cancer. CT scan is shown. Genetic testing is most likely to reveal a mutation in:
A. BRCA1. B. MSH2. C. PTEN. D. TP53. E. VHL.
B: “MSH2.”
The patient has evidence of a right upper tract urothelial carcinoma, causing obstruction with resultant hydronephrosis and renal atrophy. Her personal and family history of cancers along with an upper tract tumor are suggestive of Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC). This is caused by mutations in mismatch repair genes which include MLH1, MSH2, MSH6, and PMS2. These patients are at risk of developing colorectal cancer, endometrial carcinoma, digestive adenomas, and ovarian serous cystadenocarcinoma. The other genes listed are associated with other heritable cancers: breast and ovarian cancer (BRCA1); hamartoma, endometrial, and kidney (PTEN, Cowden syndrome); breast cancer, osteosarcoma, and soft tissue sarcoma (TP53, Li-Fraumeni syndrome); renal cell carcinoma, pancreatic neuroendocrine, hemangioblastoma, and pheochromocytoma (Von Hippel-Lindau syndrome).
A 65-year-old man has symptoms of cystitis, left flank pain, and fever to 39°C. Urinalysis reveals pyuria and culture shows a pan-sensitive E. coli. One month after appropriate antimicrobial therapy, he is asymptomatic and repeat urinalysis and mid-stream culture are negative. PVR is 45 mL. The next step is:
A. observation. B. complete urodynamic studies. C. prostatic localization cultures. D. trimethoprim/sulfamethoxazole prophylaxis. E. CT urogram and cystoscopy.
E: “CT urogram and cystoscopy.” was the correct answer.
This man presents with symptoms of pyelonephritis. While uncomplicated cystitis in a young sexually active male may not require investigation beyond a follow-up urine culture, a complicated UTI in an older male warrants urologic evaluation, such as CT urogram and cystoscopy due to the higher incidence of associated urologic abnormalities, such as obstruction from either urethral or ureteral strictures, tumor, or stones. Observation is incorrect. Localization cultures might be considered as part of a urologic evaluation but are not sufficient as isolated tests in the presence of a complicated febrile UTI. There is no justification for antimicrobial prophylaxis or urodynamic studies at this time.
Two years after mid-urethral synthetic sling, pelvic examination of a 75-year-old woman reveals extrusion of a small amount of mesh along her anterior vaginal wall. She is continent and denies any other urinary or vaginal complaints. She is not sexually active. Urinalysis is normal. The next step is:
A. observation. B. removal of extruded mesh. C. removal of entire mid-urethral sling. D. oral estrogen. E. removal of exposed mesh and simultaneous sling replacement.
A: “observation.”
As the patient is asymptomatic, intervention is not required at this time. Extrusions that are larger or symptomatic should be treated. Transvaginal estrogen is thought to promote vaginal healing. Oral estrogen therapy, however, is not helpful in this scenario. Removal of the entire mid-urethral sling is not required for a small exposure of mesh, may be technically challenging, and may lead to recurrent stress urinary incontinence. With partial sling excision, continence is typically maintained in the majority of patients; therefore, replacement of another sling would not be indicated. When a mid-urethral sling is eroded into or involves the urinary tract, it should be treated with removal.
Erythropoiesis is stimulated by:
A. hypoxia.
B. increased serum CO2.
C. cardiac erythropoietin production.
D. decreased afferent arteriolar pressure.
E. stimulation of renal medullary collecting duct cells.
A: “hypoxia.”
Red blood cell production is controlled primarily by erythropoietin production in the kidney. Hypoxia is the primary stimulant of erythropoietin production. This occurs in the renal interstitial fibroblasts and possibly in renal proximal tubular cells. Erythropoietin stimulates maturation of erythroid burst-forming units, which eventually leads to increased production of RBCs. Erythropoietin production is not stimulated by either increased CO2 or decreased afferent arteriolar pressure. Neither the heart nor the renal medullary collecting duct cells produce erythropoietin.
In primary hyperaldosteronism, most patients have:
A. hypokalemia. B. hypernatremia. C. increased angiotensin II levels. D. decreased renin levels. E. significant volume expansion (> 1.5 kg).
D: “decreased renin levels.”
Although hypokalemia has been classically described as a common finding in primary hyperaldosteronism, in contemporary series, up to 90% of newly-diagnosed patients are normokalemic at the time of diagnosis. In primary hyperaldosteronism, aldosterone increases sodium reabsorption and potassium secretion in the distal nephron. Hypernatremia does not occur as sodium reabsorption is accompanied by water uptake maintaining isotonicity. At the same time, the resultant volume expansion is limited by mineralocorticoid escape - the result of which limits volume expansion to approximately 1.5 kg or less. In primary hyperaldosteronism, aldosterone secretion is independent of the renin-angiotensin-aldosterone system, and plasma renin levels will be suppressed. This finding is in contrast to patients with secondary hyperaldosteronism, where elevated renin levels are the cause of elevations in aldosterone secretion. This distinction between plasma renin levels in primary and secondary hyperaldosteronism is a critical concept used when screening for primary aldosteronism. Suppression of renin results in decreased levels of angiotensin II. This is formed when renin cleaves angiotensinogen to angiotensin I, which in turn is cleaved by angiotensin-converting enzyme to angiotensin II.
An MRI scan of the head (1.5-Tesla) is recommended for a 44-year-old woman with an InterStim II sacral nerve stimulator. The next step is:
A. tell the patient she cannot have the MRI scan.
B. proceed with MRI scan with neurostimulator turned off.
C. proceed with MRI scan after the magnet switch has been disabled.
D. proceed with MRI scan after removal of lead.
E. proceed with MRI scan following removal of lead and generator.
B: “proceed with MRI scan with neurostimulator turned off.”
Patients with an InterStim II can have an MRI scan of the head using a 1.5-Tesla machine with the stimulator turned off. In general, patients with older InterStim generators may have an MRI scan of the head with the stimulator turned off and the magnet switch turned off. However, certain serial numbers should not have an MRI scan and this information is readily available on the Medtronic website. MRI scan evaluations of the body are not recommended, though reports have shown this to be safe with the implantable pulse generator and magnet turned off using both 0.6 and 1.5-Tesla machines. This is an emerging technology and new products may be available in the near future with improved MRI compatibility.
Following PCNL for recurrent calcium-based stone disease, a 3 mm residual fragment is seen in a lower pole calyx on ultrasound. The next step is:
A. observation. B. 24-hour urine. C. stone protocol CT scan. D. ureteroscopy. E. SWL.
B: “24-hour urine.”
Lower pole residual fragments have a low chance of spontaneously passing. They are also less likely to require intervention as they have a greater tendency to remain asymptomatic in the kidney. A 24-hour urine stone risk profile will help direct medical therapy, especially in a recurrent stone former. In patients with residual fragments after PCNL, those treated with medical therapy had a significantly better stone remission rate (77%) as compared to the control (observation) group (21%). Additionally, residual fragments greater than 2 mm located in the renal pelvis or ureter are independent predictors of a stone event. Ultrasound tends to over-size small renal stones, so there is no need to confirm the presence or size of a small stone in the lower pole, since prevention is the next key step. Further treatment (ureteroscopy or SWL) in the postoperative period for a small residual fragment is not necessary at this time; however, long term follow-up is recommended. Additionally, SWL is typically not recommended for very small stones.
A 34-year-old man with sickle cell trait and hypertension has recurrent erections lasting two to three hours. He has tried oral sildenafil and baclofen with no improvement. He wishes to remain sexually active. The next step is:
A. oral pseudoephedrine. B. oral estrogen. C. oral bicalutamide. D. daily intracavernous phenylephrine. E. penile implant.
C: “oral bicalutamide.”
Recurrent prolonged erections (stuttering priapism) in patients with sickle cell disease and trait eventually progress to more significant episodes. Many therapies have been proposed to include oral alpha-adrenergic agents, hormonal therapy with LH-RH agonists/antagonists, and antiandrogens. Intracavernous alpha-agents (phenylephrine) can be used at the time of a prolonged episode but are not used on a daily basis. Oral estrogens have unacceptable adverse effects, including cardiovascular risks, and are not recommended in this setting. Alpha-adrenergic agents should be used with caution in patients with hypertension. Oral antiandrogens will also allow this patient to continue to have erections and remain sexually active.
A transperitoneal exposure of the right renal hilum requires mobilization of the:
A. stomach. B. duodenum. C. hepatocolic ligament. D. superior mesenteric artery. E. inferior mesenteric vein.
B: "duodenum." The second (descending) portion of the duodenum is of most importance to the urologist because it lies immediately anterior to the right renal hilum and pelvis. This portion of the duodenum is frequently mobilized (referred to as a Kocher maneuver) to expose the right kidney during a transperitoneal approach. The second portion also receives the common bile duct and surrounds the head of the pancreas. Stomach mobilization is not necessary for the right renal hilar exposure. Neither the superior mesenteric artery nor inferior mesenteric vein need to be mobilized to expose the right renal hilum. Mobilization of the hepatocolic ligament will provide exposure to the upper pole of the right kidney, but does not provide access to the hilum of the right kidney.
A 58-year-old man is treated with brachytherapy for a T1c, Gleason 7 (4+3) prostate cancer. His pre-treatment PSA was 9 ng/mL. His PSA nadir at two years is 1.0 ng/mL, and his PSA subsequently rises to 4.5 ng/mL over the next year. The factor most predictive of prostate cancer mortality is:
A. PSA nadir. B. pre-treatment PSA. C. PSA doubling time. D. primary Gleason pattern. E. time interval to recurrence.
C: “PSA doubling time.”
This patient has met the criteria for failure of his brachytherapy (nadir + 2 ng/mL). Although a PSA nadir of 1.0 ng/mL is associated with a higher chance of failure, it does not necessarily predict survival. The pre-treatment PSA, in this case, is favorable and would not predict a poor outcome. Although Gleason score has been associated with prostate cancer-specific mortality, most of the time it has been associated with Gleason scores of 8-10. Short time to recurrence is also unfavorable but not as predictive as PSA doubling time. The short doubling time has been shown in multiple studies to be the factor most predictive of prostate cancer-specific mortality in patients who have a recurrence after definitive local treatment.
Four years after successful placement of a sacral neuromodulation device, a 45-year-old woman has recurrence of her voiding symptoms. Interrogation of the device reveals an abnormal impedance in one of four electrodes on the lead and a battery life of eight months. The next step is:
A. add mirabegron. B. re-program device. C. place new lead. D. replace entire device. E. intradetrusor onabotulinumtoxinA.
B: “re-program device.”
Impedance is an indication of the integrity of a circuit. The range of impedances is generally 400-1500 ohm. High impedances (> 4000 ohms) suggest a disruption in the circuit, called an “open” circuit, and suggest that the electrons are unable to flow. Fractures in the leads or loose connections can create an open circuit. In this case, since the other electrodes have acceptable impedances, reprogramming the device using the other electrodes would be the next step. Although the addition of medications or onabotulinumtoxinA injection may be helpful, neither may be necessary if reprogramming provides symptom relief. Surgical revision is not indicated unless all attempts at reprogramming have failed.
A one-year-old girl with spina bifida has new onset grade 2 hydronephrosis. VCUG demonstrates bilateral grade 4 VUR. CMG is shown. The next step is prophylactic antibiotics and:
A. observation. B. oxybutynin. C. CIC. D. intradetrusor onabotulinumtoxinA. E. bilateral ureteral reimplant.
C: “CIC.”
This child is at risk for upper urinary tract deterioration due to the elevated detrusor LPP. Intervention with CIC is required. The child has a reasonable bladder capacity and anticholinergics are not necessary initially. Reassessment with a catheterization diary after starting CIC is needed to determine the bladder pressure at the patient’s typical catheterized urine volume. This is most predictive of outcome for success with conservative management and to determine the need for antimuscarinics or more aggressive therapy such as onabotulinumtoxinA injections. Antimuscarinic therapy (oxybutynin) without CIC would not provide adequate drainage, especially with high-grade VUR. Reimplantation is not warranted at this point without a trial of non-operative management.
A 55-year-old healthy man diagnosed with prostate cancer is considering active surveillance. His PSA is 9 ng/mL and his prostate volume is 45 mL with normal DRE. Two of 12 biopsy cores are positive, with 25% of each core demonstrating Gleason 6 (3+3) prostate cancer. The factor that classifies his disease as National Comprehensive Cancer Network (NCCN) low risk as opposed to very low-risk is:
A. age. B. number of cores with cancer. C. PSA density. D. PSA. E. extent of cancer on biopsy.
C: “PSA density.”
The NCCN guidelines include a “very low-risk prostate cancer” group that is similar to common inclusion criteria for active surveillance. The criteria include: clinical T1c, PSA less than or equal to 10 ng/mL, PSA density under 0.15 ng/mL/cc, Gleason 6 (3+3) (Grade Group 1), and up to 3 positive biopsy cores with no core greater than 50% involvement. PSA density is one of the strongest predictors of upgrading for men with low-grade prostate cancer undergoing radical prostatectomy or for progression while on surveillance. The PSA density of this patient is 0.2 ng/mL/cc, which places him the the low-risk group, as opposed to the very low-risk group.
Neurons in Onuf’s nucleus are responsible for:
A. bladder sensation. B. bladder relaxation. C. bladder contraction. D. internal sphincter contraction. E. external sphincter contraction.
E: “external sphincter contraction.”
Onuf’s nucleus resides in the anterior horn of the S2 through S4 regions of the sacral spinal cord and contains the pudendal motor neurons that innervate the external striated urethral sphincter. Bladder sensation and bladder contraction involve parasympathetic neurons in the dorsal and ventral portions of the sacral spinal cord, respectively. Coordination between bladder contraction and external sphincter contraction involves neurons in the pontine micturition center.
According to the 2013 AUA Guideline on follow-up for clinically localized renal neoplasms, the recommended surveillance for a pT2NxMx RCC after nephrectomy includes:
A. annual chest x-ray only.
B. abdominal CT scan and chest x-ray at one year only.
C. annual abdominal CT scan and chest x-ray for two years.
D. abdominal CT scan and chest x-ray every six months for three years.
E. annual abdominal CT scan for five years.
D: “abdominal CT scan and chest x-ray every six months for three years.”
The 2013 AUA Guideline for follow-up for clinically localized renal neoplasms recommends in Statement 12 that patients at moderate- to high-risk for recurrence (which includes pT2-4 and any N+ patients) undergo “baseline chest and abdominal scan (CT or MRI) within three to six months following surgery with continued imaging (US, CXR, CT or MRI) every six months for at least three years and annually thereafter to year five. (Recommendation; Evidence Strength. Grade C).”
A 52-year-old woman has bothersome urinary frequency and urgency incontinence. Examination reveals stage 1 anterior vaginal wall prolapse and loss of urine with cough. Urinalysis and PVR are normal. The next step is:
A. behavioral modification and antimuscarinics.
B. transurethral bulking agent.
C. mid-urethral sling.
D. cystocele repair.
E. mid-urethral sling and cystocele repair.
A: “behavioral modification and antimuscarinics.”
Although this patient has a positive cough stress test, the main complaint is urgency urinary incontinence and frequency. Therefore, according to the 2014 AUA/SUFU OAB Guidelines, behavioral modification and pelvic floor muscle training are recommended as first-line treatment, with or without pharmacotherapy (antimuscarinics or beta-3-agonist). Despite the fact that she has a positive cough-stress test, she is not reporting subjective stress urinary incontinence (SUI). Thus, therapy such as a bulking agent or sling aimed at treating SUI should not be part of the initial treatment plan. Stage 1 anterior vaginal wall prolapse is a normal finding and should not cause any signs of a vaginal bulge; therefore, there is no role for a prolapse repair at this time.
