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31 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: GFR is maintained;
Increase in PT due to obstruction is balanced by increase in RBF (afferent arteriolar vasodilation mediated by PGE2 and NO Next 3‐4 hours: GFR decreases Pt remains high from obstruction; RBF declines due to a shift from afferent arteriolar vasodilation to vasoconstriction mediated by Angiotensin II, Thromboxane A2 and Endothelin 5‐6 hours post‐obstruction: the collecting system pressure begins to fall as well so that both RBF and PT 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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Initial increase in RBF is shorter (90 min) and less profound than in UUO.
Decrease in RBF that follows is much more rapid. The increase in tubular pressures in BUO is greater and more prolonged (24 vs. 5-6 hrs). High elevation in pressure accounts for the big decrease in whole kidney GFR seen in BUO. Greater post-obstructive diuresis with BUO due to volume expansion, urea and other osmolytes, and secreted atrial natriuretic peptide (ANP) |
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What explains the difference seen in the two patterns?
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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 including urinary concentrating ability, sodium and potassium transport, and urinary acidification?
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Urinary concentrating ability: Decreased. Caused by disruption of the hypertonic medullary interstitial gradient and dysregulation of vasopressin-mediated aquaporin water channels. Results in profound post‐obstructive polyuria.
Sodium Transport – decreased sodium transport = inability to concentrate urine. The FeNa is higher after relief of BUO than of UUO (med by ANP) Potassium Transport – Potassium wasting occurs along with the profound natriuresis after release of BUO (stimulated by high ANP). However, after UUO, potassium excretion is decreased. Urinary Acidification – decreased ability to acidify urine. Likely due to deficits in H+ transport at the collection duct not in bicarb reclamation at the proximal tubule. |
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What is thought to be the main mediator of tubulointerstitial fibrosis and how has it been attenuated experimentally?
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Angiotensin II is thought to be an important initiator of fibrosis and ACE-I’s and ARB’s (losartan and candesartan) have been shown to blunt the fibrotic process.
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What is the earliest that the phenomenon of compensatory renal growth has been observed? What factors affect this?
Does it cause an increase in the number of nephrons or glomeruli? |
has been detected ultrasonographically in utero when hydronephrosis or unilateral renal agenesis is present.
decreases progressively with increasing age at which the obstruction occurs The amount of growth is directly proportional to the duration of obstruction no. |
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What are some factors that influence renal recovery after relief of obstruction
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Duration - full recovery after 1 week UUO, 70% after 2 weeks, 30% after 4 weeks, and no recovery after 6 weeks - this was in DOGS, less predictable in humans.
• Higher degree of obstruction, older age, decreased renal cortical thickenss and poor baseline renal function are predictors of diminished recovery greater compliance of collecting system, and pyelolymphatic backflow (pop-off valve) predict greater recovery |
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What studies may be useful in predicting residual function/likelihood of renal recovery after obstruction?
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CT Scan - Renal parenchymal thickness on CT has been used to estimate the renal function. Renal surface areas have been reported to have a strong correlation with DMSA scans.
Cortical phase nuclear renograms (eg DMSA scans specifically, not DTPA or MAG3). |
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What predictive tool can be used with U/S to make it predictive of obstruction?
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the measurement of renal resistive index (RI), which can be used to diagnose obstruction. Typically, RIs > 70% are thought to be indicative of an obstructive process. Controversy remains on clinical utility of this measure.
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Indications to relieve obstruction?
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1. Sepsis
2. Refractory pain. N/V 3. Elev BUN/Cr, hyper-K 4. Multiple trips to ER |
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After sufficient time to allow recovery (6-8 weeks), what cutoff in differential renal function is typically used in the determination of nephrectomy versus renal reconstruction?
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15-20% - reconstruction may be preferable (still debated)
<10% - nephrectomy is indicated |
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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. They have been shown in some studies to be more effective than opioids. Also, 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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BUO or Solitary Kidney - The diuresis is physiologic and represents the excretion of accumulated free water and solutes while obstructed.
Pathologic diuresis is the --derangement of the medullary solute gradient caused by downregulation of sodium transporters and impaired sodium reabsorption --downregulation of aquaporins and resultant poor responsiveness of the collecting duct to ADH --increased ANP Post‐obstructive diuresis should be managed with careful monitoring of vital signs and electrolytes with repletion of lytes and fluid as needed until the diuresis subsides. Urinary osmolarity will determine if physiologic solute diuresis or pathologic primary water diuresis (hypo-osmolar urine). Obtain baseline urine osmol and monitor for change from solute to water diuresis. No pharmacologic manipulation of diuresis is useful. |
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What are Retroperitoneal Fibrosis (RPF) and Idiopathic RPF?
What conditions need to be ruled out before diagnosing idiopathic RPF? |
• Predominantly inflammatory mass envelops and potentially obstructs retroperitoneal structures, including either or both ureters.
Idiopathic RPF is a fibrosclerotic disorder thought to be auto-immune in origin that is a diagnosis of exclusion (70%). Predominantly 40-60 yr olds. Males 2-3 times more likely to be affected. Usually isolated entity. --Cancer 8-10% (Lymphoma is the most common, but think about testicular as well) --Urinary extravasation (especially infected) --Repeated cholangial infections or an organizing retroperitoneal hematoma --radiotherapy or operations may have a similar appearance. --A variety of chemicals and medication exposures |
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What are the two stages of the disease?
What is the clinical presentation? |
Inflammatory (early)
Fibrotic plaque formation (late) Most often symptomatic urinary obstruction --Early symptoms may include vague, flank or abd pain, or nonspecific complaints, such as malaise, anorexia, wt loss, moderate pyrexia, N/V, HTN in 50%. Most develop a characteristic pain, described as dull and noncolicky, and occurring in a girdle distribution. - in more than 90%. Relieved by NSAIDS more than narcotics probably due inflammatory effect of the lesion. |
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What is the classic xray presentation for RPF & current imaging modalities of choice?
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On IVP, the classic finding was **medially displaced** and extrinsic compression of ureters in the setting of proximal hydronephrosis.
CT - typically reveals a well‐demarcated retroperitoneal mass with variable degrees of contrast enhancement. Centers around the distal aorta and IVC at L4‐L5. Extends from aortic bifurcation up to renal pedicle and from aorta laterally beyond edge of the psoas muscle and wrapping around the ureters MRI – theoretically allows superior soft tissue discrimination to more accurately distinguish plaque from the great vessels compared to unenhanced CT |
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How should it be managed?
Med/Surg? |
First, relieve any obstruction with stenting or perc.
Next, biopsy the lesion to rule out malignancy, which is present in up to 10% cases Some suggest unnecessary in pts with classic radiographic features, no peripheral adenopathy, and no history of malignancy. Then, attempt medical management using some combination of steroids, tamoxifen, and immunotherapy. ROIDS: prednisolone administered at an oral dose of 30mg daily or 60mg on alternate days (can do for 2 months, then taper (slowly) to 5 mg daily, do this long term. TAMOX: 20 mg of tamoxifen per day, avg tx 9 mo.. 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 it be evaluated? |
benign condition marked by exuberant pelvic overgrowth of nonmalignant infiltrative adipose tissue.
AAs > Whites. M >> W 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, extrinsically compressed and elongated with elevated bladder base. • Cystoscopy – 75% with proliferative cystitis (40% with cystitis glandularis which require surveillance due to reports of adenocarcinoma in these patients). Anatomy can make cystoscopy difficult. Long term follow up advocated because of potential for ureteral obstruction (39% require operative intervention for upper tract obstruction) |
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What is the prevalence of hydronephrosis of pregnancy by trimester?
What is its typical course? What are the symptoms? When and how should it be managed? |
The prevalence by trimester is 15%, 20%, and 50%.
Typically it is asymptomatic and resolves quickly postpartum (within 6 weeks). When they do occur, symptoms include flank pain, pyelonephrosis, or renal failure. Left-sided colic was more likely to indicate presence of stone (64.9% vs 46.6%) Normally can be managed conservatively with intravenous hydration, analgesics, and antibiotics. However, stenting may be necessary especially with signs of sepsis or decr 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 by slowing peristalsis
Mechanical – the increased incidence after the 20th week when he uterus is large enough to compress the ureters supports a mechanical etiology |
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What radiographic finding should make you think of another cause of obstruction (stone) in the setting of hydronephosis during pregnancy?
What must be kept in mind when hydronephrosis of pregnancy is managed with stenting? |
Dilation of the ureters below the pelvic brim.
Stents must be changed frequently!! |
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Where in the urinary tract is endometriosis found most commonly? How often is the ureter involved?
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? |
Bladder in 70‐80%
Ureter involved in 15‐20% of the urinary tract cases. Classic signs and symptoms: cyclical flank pain, dysuria, urgency, UTI’s, and hematuria 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? How do you diagnose an iliac artery aneurysm on physical exam?
How is ureteral obstruction after vascular graft placement managed? |
AAAs, iliac artery aneurysms, ovarian and testicular vein thrombophlebitis, and
circumcaval and retrocaval ureters. Pulsatile mass on rectal exam. --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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What is the most frequent cause of congenital UPJ obstruction?
What are other causes of intrinsic UPJ obstruction? |
--Intrinsic aperistaltic segement of ureter. Loss of spiral musculature and replaced by longitudinal muscle bundles or fibrous tissue. May appear grossly normal.
Kinks, valves, bands, or adhesions produced by infoldings of the ureteral mucosa and musculature, “High insertion” of the ureter |
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Do “aberrant” crossing vessels really cause UPJ obstructions? Why are they significant?
How can you differentiate UPJ obstruction and VUR? How do we diagnose UPJ obstructions in neonates/infants? In adults? |
Probably not. Likely there is an intrinsic lesion at UPJ or proximal ureter that causes dilation at the crossing vessel. Supported by studies showing the transition point doesn’t correspond to the location of the crossing vessel. They make minimally invasive endopylotomy more difficult.
Diuretic renography. --During evaluation of flank pain, hematuria, azotemia, frequent UTI in older children/adults – ultrasound or CT scan |
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Describe the general concept of endoscopic treatment of UPJ obstructions. Where should the incision in the ureter be made and why?
What factors would make you less likely to fix UPJ obstruction endoscopically? Does failed endoscopic procedure compromise success of subsequent open/lap surgery? |
General concept is to make full thickness incision through obstructing proximal ureter from the ureteral lumen out to the peripelvic and periureteral fat. Stent placed across incision and allowed to heal. Laterally (?posterior) to avoid crossing vessels.
>2cm stricture, crossing vessels, high-grade obstructions, presence of renal calculi....No |
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What is a retrocaval ureter? How is it diagnosed and treated?
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Rare congenital anomaly that occurs as a consequence of persistent posterior cardinal veins during embryologic development.
Diagnosed on CT scan or pyelography (characteristic S-shaped deformity) Pyelopyelostomy – transect the dilated renal pelvis and transpose ureter anterior to vena cava |
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What are the endoscopic treatments options for ureteral strictures and their characteristics?
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--Retrograde stents – useful in acute,intrinsic (not extrinsic) causes of strictures
--Percutaneous drainage – used to temporize extrinsic strictures --Retrograde/antegrade balloon dilation – most successful (85%) in short, iatrogenic, non-anastomotic strictures (ie those following ureteroscopic instrumentation). Often require repeat dilations --Endoureterotomy (retrograde or antegrade) – cut stricture from inside. Often re-stricture. Can’t be done close to great vessels (near iliacs) |
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Surgical options? Where on ureter and what length of defect?
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--Ureteroureterostomy – ideal for short (<2-3 cm) defects in upper/mid ureter
--Ureteroneocystotomy – distal 3-4 cm of ureter (4-5 cm defect) --Psoas hitch – lower 1/3 of ureter (6-10 cm defect) --Boari flap – 12-15 cm defect, sometime can even reach the right renal pelvis --Renal descensus – upper ureter. (5-8cm defect) caudal mobilization of kidney --Transureteroureterostomy – when length is only sufficient to reach contralateral ureter --Ileal ureteral substitution – only if you are a UNC GYN surgeon |
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What is the incidence of ureteroenteric anastomotic strictures? What are factors?
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--4-8% in urinary conduits, 4-25% in continent diversions
--Technique of dissection - preservation of blood supply --Type of anastomosis – non-refluxing anastomoses have higher stricture rate (13% vs 1.7%) |
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What are indications for intervention? What are the interventions?
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--Pain, infections, renal insufficiency associated with functional obstruction
--Antegrade percutaneous drainage/stent preferred – despite 50% long term patency, still preferred as initial intervention --Open repair – reserved for failed endoscopic attempts |
