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24 Cards in this Set
- Front
- Back
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Describe the pattern over time of Renal Blood Flow (RBF) and Collecting System Pressure (PT) after Unilateral Ureteral Obstruction (UUO).
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*First 1-2 hours: both RBF and PT increase. GFR maintained at first by increased blood flow to the obstructed kidney (Increased P_GC). This is affected by afferent arteriolar vasodilation which is mediated in part by Prostaglandin E2 and Nitric Oxide.
*Next 3-4 hours: RBF declines and PT elevated, GFR decreased. The decrease in RBF is affected mainly by a shift from afferent arteriolar vasodilation to vasoconstriction which reduces GFR in the affected kidney. Angiotensin II, Thromboxane A2 and Endothelin have all been show to be mediators of this vasoconstriction. *Next 5-6 hours: RBF and PT both decline. |
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How does this pattern differ with regards to Bilateral Ureteral Obstruction (BUO) or a solitary kidney?
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*In BUO, the initial increase in RBF is shorter and the decrease in RBF that follows is much more rapid and profound. Also BUO has a shift of blood flow to the outer cortex (whereas UUO has shift to the inner cortex)
*The tubular pressures in BUO remain elevated for about 24 hours whereas in UUO the PT begins to decrease after 5-6 hours. This prolonged elevation in pressure accounts for the profound decrease in whole kidney GFR seen in BUO. When the obstruction is released, the postobstructive diuresis is greater with BUO because of volume expansion, urea and other osmolytes, and secreted atrial natriuretic peptide (ANP) |
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What explains the difference between unilateral ureteral obstruction and bilateraly ureteral obstruction?
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In UUO, the contralateral unobstructed kidney prevents the accumulation of vasoactive substances such as ANP that contribute to the preglomerular vasodilation and postglomerular vasoconstriction seen in BUO.
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How does obstruction affect kidney function during and after obstruction?
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*Urinary concentrating ability – obstruction may cause a profound decrease in the kidney’s ability to concentrate urine and lead to a profound post-obstructive polyuria. This is mediated by disruption of the medullary interstitial gradient by dysregulation of aquaporin water channels.
*Sodium Transport – decreased sodium transport also contributes to the obstructed kidney’s inability to concentrate urine. The FENA is higher after relief of BUO than of UUO secondary to the retention of Na, water, and urea that occurs with BUO, and the natriuresis is mainly mediated by atrial naturetic peptide (ANP) in BUO. *Potassium Transport – Potassium wasting occurs along with the profound natriuresis after release of BUO. However, after UUO, potassium excretion is decreased. *Urinary Acidification – Obstruction decreases the kidney’s ability transport H+ and acidify urine. This is likely related to deficits in H+ transport at the collection duct not in bicarb reclamation at the proximal tubule. |
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What effect does obstruction have on the structure of the kidney?
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*Urinary tract obstruction leads to progressive and eventually permanent changes in the structure of the kidney including the development of tubulointerstitial fibrosis, tubular atrophy and apoptosis, and interstitial inflammation, all seen on pathology.
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What factors affect the nature of compensatory renal growth? Does it cause an increase in the number of nephrons or glomeruli?
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Compensatory growth decreases progressively with increasing age at which the obstruction occurs
The amount of growth is directly proportional to the duration of obstruction No increase in number of nephrons or glomeruli – although an increase in the length of the proximal tubule has been described |
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What are some factors that influence renal recovery after relief of obstruction?
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Duration of obstruction – when acute, complete ureteral obstruction is promptly relieved, there is full recovery of GFR
Higher degree of obstruction, older age, and poor baseline renal function are predictors of diminished recovery |
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What is the main limitation of RUS in diagnosis of obstruction? When performing a renal ultrasound, what additive study may be helpful in determining severity of obstruction?
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*RUS is an anatomic and NOT a functional study
*RI = PSV-PDV/PSV *RI > 0.7 can be indicative of obstruction, especially helpful in distinguishing mild from severe obstruction (RI > 0.7 with 93% sensitivity in severe obstruction) |
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What study do we most commonly use to identify renal obstruction? What is the radiotracer that we use and how does it work/how do you interpret the study? Which patients are poor candidates for this study?
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*Lasix scan (DTPA or MAG3) – radiotracer taken up by kidney and measured
*Half-time < 10 minutes is normal, 10-20 equivocal, >20 minutes obstructed *Renal insufficiency, VUR, and some say neonates (b/o renal immaturity) |
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hen relief of an obstruction is indicated, what factors make percutaneous drainage more appropriate than retrograde stenting?
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Obstruction due to external compression especially from cancer or metastatic disease is associated with high rates of stent failure making percutaneous drainage more attractive. Also, stenting typically requires more x-ray radiation compared to percs. Therefore, percutaneous drain placement may be more desirable in pregnant patients. Finally, patients with suspected pyeonephrosis should be percutaneously drained.
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What cutoff in differential renal function is typically used in the determination of nephrectomy versus renal reconstruction?
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The decision to remove a previously obstructed kidney should only be made after adequate time for complete recovery (usually 6 to 8 weeks). If at that time one kidney is contributing less than 10% to global renal function, nephrectomy is usually indicated. However, this decision may be altered in patients with global renal insufficiency since nephrectomy may then hasten the need for dialysis.
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Are NSAIDs an effective choice in managing renal colic? How do they work? When should they not be used?
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Yes, shown in some studies to be more effective than opioids in relieving pain. Associated with less emesis, sedation, and risk of addiction. They work by preventing the synthesis of prostaglandins that potentiate nociceptors. They also have been demonstrated to reduce collecting system pressure by reducing RBF. NSAIDs should not be used in patients with renal insufficiency as this could be exacerbated by the decreased RBF.
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What patients are at risk for a post-obstructive diuresis? What causes a pathologic diuresis? What are risk factors for development of a pathologic diuresis? How should it be managed?
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Patients with BUO or obstruction of a solitary kidney are at greatest risk for a clinically significant post-obstruction diuresis. The diuresis is physiologic and represents the excretion of accumulated free water and solutes during the obstruction
Pathologic diuresis is due to derangement of the medullary solute gradient, downregulation of sodium transporters and aquaporins, increased ANP Risk factors for development of this pathologic diuresis include history of edema, heart failure, and hypertension Post-obstructive diuresis should be managed with careful monitoring of vital signs and daily electrolytes with repletion of lytes and fluid as needed until the diuresis subsides. |
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What is the classic radiographic finding in retroperitoneal fibrosis?
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Before the wide-spread used of cross-sectional imaging, the classic finding was medially displaced dilated ureters in the setting of hydronephrosis.
CT typically reveals a well-demarcated retroperitoneal mass with variable degrees of contrast enhancement which generally centers around the distal aorta at L4-L5 wrapping around the ureters |
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How should retroperitoneal fibrosis be managed?
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*Relieve any obstruction with stenting or percutaneous drainage.
*Next, biopsy the lesion to rule out malignancy, which is present in up to 10% cases *Then, attempt medical management using some combination of steroids, tamoxifen, and immunotherapy. *If this fails, surgical intervention in the form of ureterolysis should be attempted. |
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What is pelvic lipomatosis? Who is afflicted by it? How does it present? What is the classic finding on excretory urography? How should they be followed and why?
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It is a benign condition marked by exuberant pelvic overgrowth of nonmalignant infiltrative adipose tissue.
African American > Whites. Men >> Women 18:1. Unknown etiology, but half of patients present with LUTS; 25% present with bowel symptoms, usually constipation. Abdominal obesity may present in over 50% cases. The classic finding on excretory urography is a pear-shaped bladder with elevated bladder base. Cysto and RUS (75% have proliferative cystitis, 40% with cystitis glandularis) |
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hat is the prevalence of hydronephrosis of pregnancy by trimester? What is its typical course and which side is usually affected more? What are the symptoms? When and how should it be managed?
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The prevalence by trimester is 15%, 20%, and 50%.
Typically it is asymptomatic and resolves quickly postpartum. R>>L When they do occur, symptoms include flank pain, pyelonephrosis, or renal failure. Normally can be managed conservatively with intravenous hydration, analgesics, and antibiotics. However, stenting may be necessary when conservative management fails, especially with signs of sepsis or compromised renal function. |
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What are the two hypothesized etiologies for hydronephrosis of pregnancy?
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Hormonal – the 10%-15% incidence in the 1st trimester before the uterus reaches the pelvic brim supports a non-mechanical mechanism. Progesterone is hypothesized to promote ureteral dilatation.
Mechanical – the increased incidence after the 20th week when the uterus is large enough to compress the ureters supports a mechanical etiology. |
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What must be kept in mind when hydronephrosis of pregnancy is managed with stenting?
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Rapid stent encrustation may be problematic as urinary calcium excretion increases during pregnancy, necessitating more frequent stent changes.
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Where in the urinary tract is endometriosis found most commonly? How often is the ureter involved?
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Bladder in 70-80%
Ureter involved in 15-20% of the urinary tract cases |
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How does urinary tract endometriosis present? How often can ureteral obstruction and loss of renal function be observed? What imaging must be included in the workup?
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Classic signs and symptoms: cyclical flank pain, dysuria, urgency, UTI’s, and hematuria
Ureteral obstruction can be silent in approximately 40% of patients with ureteral endometriosis, and silent loss of renal function has been reported in 25-40% cases Upper tract imaging, initially with ultrasound, is recommended in all patients with pelvic endometriosis |
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What are some vascular causes of ureteral obstruction?
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AAAs, iliac artery aneurysms, ovarian and testicular vein thrombophlebitis, and circumcaval and retrocaval ureters.
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How is ureteral obstruction after vascular graft placement managed?
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If the hydro is found early and renal function isn’t compromised, observation.
Stenting or perc drains may be required for renal impairment or severe symptoms. Steroids or tamoxifen may be considered if obstruction is due to perigraft fibrosis. |
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A 40 year old obese Caucasion man is evaluated for irritative voiding symptoms. IVP demonstrates a teardrop-shaped elevated bladder, and medial deviation with fullness of the right ureter but no hydronephrosis. CT scan shows an extensive pelvic mass effect surrounding the bladder of fat density. The next step is what?
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*This could be pelvic lipomatosis, but could also be a lipoma or liposarcoma and this diagnosis cannot be excluded wihtout pelvic laparotomy. Especially in the assymetric finding that this patient has with mass effect on the right ureter
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