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30 Cards in this Set
- Front
- Back
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1. What is the difference between TESTICULAR TORSION and EPIDIDYMITIS? (Age, appearance, Prehn's sign, treatment)
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TESTICULAR TORSION: Age-Under 30 yr (usually prepubertal), Appearance-Testes may be elevated into the inguinal canal; swelling. Prehn's Sign-Pain stays the same or worsens. Treatment-Immediate surgery to salvage testis; suigical orchiopexy for both testes. *EPIDIDYMITIS: Age-over 30 yr. Appearance-Swollen testis, overlying erythema, urethral discharge/urethritis, prostatitis. Prehn's Sign-pain decreseas with testicular elevation. Treatment: antibiotics.
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2. How does testicular cancer usually present? Describe the major risk factors, histology,and treatment.
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Testicular cancer usually presents as a painless testicular mass in a young man (20-40 years old). The main risk factor is cryptorchidism. Roughly 90% are germ cell tumors; the most common type is seminoma. Testicular cancer generally is treated with orchiectomy and radiation; if disease is widespread, use chemotherapy. Alpha-fetoprotein is a marker for yolk sac tumors; human chorionic gonadotropin is a marker for choriocarcinoma. Leydig cell tumors may secrete androgens and cause precocious puberty.
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3. How is renal cell carcinoma diagnosed and treated?
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Patients rarely present with the classic triad of hematuria, flank pain, and a palpable flank mass. Painless hematuria (gross or microscopic) is the most typical presenting sign. CT scan (preferred over intravenous pyelography) is a good initial diagnostic test (see figure). Treatment for disease confined to the kidney or with extension limited to renal vein invasion (classic) is surgical resection. With other organ invasion or distant metastatic disease (usually to lung or bone), chemotherapy (e.g., interleukin-2) is the preferred treatment.
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4. What is the classic cause of orchitis? How is it treated? Does it usually cause infertility?
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Mumps can cause orchitis, which classically presents with a painful, swollen testis in a post-pubertal male. The best treatment is prevention (immunization against the mumps virus). Mumps orchitis rarely causes sterility because it is usually unilateral. Epididymo-orchitis is more common and typically due to spread from adjacent bacterial epididymitis.
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5. What are the symptoms and sequelae of benign prostatic hypertrophy (BPH)?
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BPH can cause urinary hesitancy, intermittency, terminal dribbling, decreased size and force of the urinary stream, sensation of incomplete emptying, nocturia, urgency, dysuria, and frequency. It may result in acute urinary retention, urinary tract infections, hydronephrosis, and even kidney damage or failure in severe cases.**A, Tomogram from an intravenous pyelogram in a 52-year-old man shows a mass in the lower pole of the left kidney (arrows), with lucent central areas. This renal cell cancer was subsequently resected. **B, CT image shows a left renal cell cancer (arrows) in a different patient. Note the detbrmity of the collecting system.
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6. How is BPH treated?
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Medical therapy, which is started when the patient becomes symptomatic, includes alpha blockers (e.g., prazosin, terazosin, doxazosin) and antiandrogens (e.g., gonadotropin-releasing hormone analogs, flutamide, finasteride). Transurethral resection of the prostate (TURP) is used for more advanced cases, especially with repeated urinary tract infections, urosepsis, urinary retention, and/or hydronephrosis or kidney damage due to reflux. Open surgical prostatectomy is used in some patients, but is associated with a higher complication rate.
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7. How do you recognize and manage acute urinary retention?
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Acute urinary retention generally presents with abdominal pain; palpation of a full, distended bladder on abdominal exam; a history of BPH in men; and a lack of urination in the past 24 hours or more. The first step is to empty the bladder. If you cannot pass a regular Foley catheter, do a suprapubic tap to drain the bladder. Then address the underlying cause--usually BPH, which in this setting is generally treated with TURP.
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8. What are the common causes of impotence?
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Impotence is caused most commonly by vascular problems and atherosclerosis. Medications are also a common culprit (especially antihypertensive and antidepressant agents). Diabetes can cause impotence through vascular (increased atherosclerosis) or neurogenic (diabetic autonomic neuropathy) compromise. Patients undergoing dialysis are often impotent. Remember "point and shoot": parasympathetics mediate erection: sympathetics mediate ejaculation. The history often gives you a clue if the cause of impotence is psychogenic (fairly common). Look for a normal pattern of nocturnal erections, selective dysfunction (the patient has normal erections when masturbating but not with his wife), and a history of stress, anxiety, or fear.
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9. What are the signs of urethral injury?
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Usually urethral injury occurs in the context of pelvic trauna. The four hallmark warning signs are a boggy, movable prostate on exam, blood at the urethral meatus, severe pelvic fracture, and scrotal/perineal ecchymosis.
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10. True or false: Urethral injury is a contraindication to passing a Foley catheter.
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True. Always look for the four warning signs of urethral injury. If even one of these signs is present, do not attempt to pass a Foley catheter. Order a retrograde urethrogram to rule out urethral injury in this setting (see figure). Image from a retrograde urethrogram performed on a young man after trauma. There is disruption of the posterior urethera, with significant contrast extravasation.
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11. Distinguish between hydrocele and varicocele.
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A hydrocele represents a rennant of the processus vaginalis (remember enbryology?) and transilluminates. It generally causes no symptoms and needs no treatment. A varicocele is a dilatation of the pampiniform venous plexus ("bag of worms," usually on the left). It does not transilluminate, disappears in the supine position, and becomes prominent with standing or the Valsalva maneuver. Varicoceles may cause infertility or pain; in either case, they can be treated surgically.
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12. Describe the classic findings of nephrolithiasis.
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Nephrolithiasis (kidney stones) can cause severe flank pain that often radiates to the groin and is colicky in nature. It may cause hematuria (gross or microscopic), and usually an abdominal radiograph reveals the stone (85% of stones are radiopaque).
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13. What are the different types of stones? What causes them?
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Roughly 75-85% of stones contain calcium. Look for hypercalcemia (usually due to hyper-parathyroidism) or small bowel bypass, which increases oxalate absorption and thus calcium stone formation. Roughly 10-15% of stones are struvite (magnesium-ammonium-phosphate) stones, which are caused by urinary tract infection (usually with Proteus species). The classic example is the staghorn calculus (a stone that fill the entire calyceal system). About 5-10% of stones are uric acid. Look for gout or leukemia. The remaining 1-3% are cystine stones, which suggest hereditary cystinuria.
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14. How is nephrolithiasis treated?
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The cornerstones of nephrolithiasis treatment are large amounts of fluid hydration,narcotics for pain, and observation, because most stones pass spontaneously. If they do not pass, treat with lithotripsy, uteroscopy with stone retrieval, or open surgery (last resort).
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15. Define cryptorchidism. When does it occur?
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Cryptorchidism is arrested descent of the testicle(s) between the renal area and the scrotum. The more premature the infant, the greater the likelihood of cryptorchidism. Many arrested testes eventually descend on their own within the first year. After I year. surgical intervention (orchiopexy) is warranted in an attempt to preserve fertility as well as to facilitate future testicular exams. Affected testes have an increased risk for testicular cancer.
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16. True or false: It is important to place abdominal testes in the scrotum surgically to decrease the risk of cancer.
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False. Cryptorchidism is a major risk factor for tesficular cancer (40 times increased risk), but bringing the testis into the scrotum probably does not alter the increased risk. The high testicle is found (the further away from the scrotum), the higher the risk of developing testicular cancer and the lower the likelihood of retaining fertility.
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17. Where do the left and right ovariatfftesticular veins drain?
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The right ovarian/testicular vein drains into the inferior vena cava, whereas the left ovariardtesticular vein drains into the left renal vein.
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18. When is kidney transplant considered for patients with renal disease?
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Kidney transplant is an option for patients with end-stage renal disease (creatinine clearance <10-15 rag/rain), unless they have active infections or other life-threatening conditions (e.g., AIDS, malignancy). Lupus erythematosus and diabetes are not contraindications to transplantation.
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19. Who makes the best donor for patients who need a kidney transplant?
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Living, related donors are best (siblings or parents), especially when human leukocyte antigens (HLA) are similar, but cadaveric kidneys are more commonly used because of availability. Before transplant, perform ABO blood typing and lymphocytotoxic (HLA) cross-matching to ensure a reasonable chance at success.
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20. Describe unacceptable kidney donors.
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Unacceptable kidney donors include newborns, people over the age of 60, and patients with a history of generalized or intraabdominal sepsis, malignancy, or any disease with possible renal involvement (e.g., diabetes, hypertension, lupus erythematosus).
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21. Where is the transplanted kidney placed? What happens to the native kidneys?
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A transplanted kidney is placed in the iliac fossa or pelvis (for easy biopsy access in case of later problems as well as for technical reasons). Usually the recipient's kidneys are left in place to reduce the morbidity of the surgery.
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22. What are the three basic types of rejection with kidney transplantation?
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Hyperacute, acute, and chronic.
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23. What causes hyperacute rejection? What is the classic clinical description?
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Hyperacute rejection is due to preformed cytotoxic antibodies against the donor kidney; it occurs with ABO blood-type mismatch as well as other preformed antibodies. In the classic clinical description, the surgery is completed, the vascular clamps are released to allow blood flow, and the transplanted kidney quickly turns bluish-black. Treat by removing the kidney.
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24. What causes acute rejection? How does it present? How is it treated?
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Acute rejection is T-cell-nediated. It presents days to weeks after the transplant with fever, oliguria, weight gain, tenderness and enlargement of the graft, hypertension, and/or laboratory derangements. Increases in creatinine are more reliable than increases in blood urea nitrogen. Treatment involves increasing corticosteroids or using antithymocyte globulin and other immunosuppressants. Accelerated rejection occurs over the .first few da's and is thought to reflect reactivation of previously sensitized T cells.
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25. What causes chronic rejection?How does it present?How is it treated?
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Chronic rejection can be T-cell- or antibody-mediated. This late cause (months to years after transplant) of renal deterioration presents with gradual decline in kidney function, proteinuria, and hypertension. Treatment is supportive and not effective, but the graft may last several years before it gives out completely. A new kidney can be transplanted if this occurs.
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26. Discuss the mechanism of action of the commonly used immunosuppressant drugs in transplant medicine.
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* Steroids inhibit intefleukin-I production. * Cyclosporine inhibits interleukin-2 production * Azathioprine is an antineoplastic that is cleaved into mercaptopurine and inhibits DNA/ RNA synthesis (which causes decreased production of B cells and T cells) * Anfithymocyte globulin is an antibody against T cells. * OKT3 is an antibody to the CD3 receptor on T cells.
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27. How do you distinguish the nephrotoxicity of cyclosporine from rejection?
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Cyclosporine is a well-known cause of nephrotoxicity that can be difficult to distinguish from graft rejection clinically. When in doubt, a percutaneous needle biopsy of the graft should be done if the patient is taking cyclosporine, because in most cases the two can be distinguished histologically. Renal ultrasound also helps. Practically speaking, if you increase the immunosuppressive dose, acute rejection should decrease, whereas cyclosporine toxicity stays the same or worsens.
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28. What risks are associated with immunosuppression?
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hnmunosuppression carries the risk of infection (with common as well as strange bugs that infect patients with AIDS) and an increased risk of cancer (especially lymphomas and epithelial cell cancers).
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29. Define epispadias and hypospadias. How are they treated?
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Both are congenital penile anonalies. In hypospadias the urethra opens on the dorsal (under) side of the penis (see figure). In epispadias the urethra opens on the ventral (top) side of the penis. Epispadias is associated with exstrophy of the bladder. Both are treated with surgical correction.**A, Distal hypospadias. B, Severe proximal hypospadias in the midscrotal area.
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30. Define Potter's syndrome. With what is it associated?
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Potter's syndrome is bilateral renal agenesis, which causes oligohydramnios in utero (because the fetus swallows fluid but cannot excrete it). It is also associated with limb deformities, abnornal facies, and hypoplasia of the lungs. It is inconpatible with life because of the severe associated lung hypoplasia.
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