Urinary Tract Obstructions

Question 1

most common cause of prenatal hydronephrosis

Answer 1

ureteropelvic junction (UPJO)

Question 2

urinary tract obstruction - general concepts

Answer 2

*can occur anywhere in the urinary tract
*can be from the inside or the outside
*may constitute a surgical emergency

Question 3

urinary tract obstructions - variable presentations

Answer 3

*flank pain
*suprapubic pain
*nonspecific symptoms
*incidental lab findings
*urinary tract infection (UTI)
*urinary incontinence (overflow)
*anuria

Question 4

ddx for urinary obstructions

Answer 4

*congenital (UPJO, posterior urethral valves)
*ureteral strictures from trauma
*stones
*retroperitoneal fibrosis
*extrinsic compression (tumor, pregnancy)
*BPH
*urethral strictures
*bladder dysfunction

Question 5

key findings for upper vs. lower tract obstructions

Answer 5

*upper tract obstruction: HYDRONEPHROSIS on ultrasound or CT
*lower tract obstruction: distended bladder

Question 6

methods for treating obstructions

Answer 6

*relieve acute obstruction with a tube
*urethral catheter
*suprapubic catheter
*ureteral stent
*nephrostomy catheter
*workup when stable and treat accordingly

Question 7

unilateral ureteral obstructions (UUO) - 3 phases of changes in renal blood flow (RBF) and ureteral pressure

Answer 7

phase 1) hours 1-2: tubular pressure rises from obstruction and RBF INCREASES
phase 2) hours 3-4: RBF starts to decline and shifted to INNER CORTEX
phase 3) after 5 hours: RBF declines further and tubular pressure starts to decrease

Question 8

unilateral ureteral obstructions (UUO) - phases of changes in GFR

Answer 8

phase 1) GFR decreases (because tubular pressure is up), but this is offset somewhat by the rise in RBF
-rise in RBF facilitated by afferent vasodilation from PGE2 and NO

later phases) GFR decreases further because of a decrease in RBF due to vasoconstriction of the afferent arteriole
-vasoconstriction related to activation of RAAS, likely via Angiotensin II

Question 9

bilateral ureteral obstructions (BUO) - phases of changes in renal blood flow (RBF) and ureteral pressure:

Answer 9

*very little rise in RBF early, followed by much more profound decrease in RBF (compared to UUO)
*in BUO, blood flow goes from INNER to OUTER CORTEX
*ureteral pressure higher in BUA and persists longer

note - if someone has a solitary kidney that is obstructed, that is effectively a bilateral obstruction

Question 10

difference in blood flow between unilateral and bilateral ureteral obstructions

Answer 10

*in UUO, blood flow goes from outer to inner cortex
*in BUO, blood flow goes from inner to outer cortex

note - blood flow goes in OPPOSITE directions

Question 11

unilateral vs. bilateral ureteral obstructions (summary)

Answer 11

*both have increases in vascular resistance and ureteral pressure, but with different timing and regulation

1. UUO: early vasodilation via PGs and NO, followed by prolonged vasoconstriction and normalized tubular pressure
2. BUO: little early vasodilation, more profound vasoconstriction, more profound postobstructive diuresis (i.e. after obstruction is relieved)

Question 12

postobstructive diuresis (POD) - overview

Answer 12

*washout after obstruction releases
*may see urine output of 200 mL/hr or greater
*can have profound losses of Na+ and H2O
*mainly after BUO (or UUO in solitary kidney)
*usually ends with homeostasis, but may be pathologic due to multiple factors

Question 13

postobstructive diuresis (POD) - mechanisms

Answer 13

*volume expansion
*urea buildup (and other osmolytes)
*increases ANP production
*downregulation of Na+ transporters in TAL and LOH leads to impaired Na+ reabsorption (LOSE MEDULLARY GRADIENT)
*downregulation of aquaporin channels in collecting duct (less response to ADH)

Question 14

postobstructive diuresis (POD) - management

Answer 14

*assess risks: edema, HTN, CHF, > 1 L in bladder
*monitor if BUO or UUO in solitary kidney
*follow vitals, urine output, BMP
*if stable, free access to oral fluids
*if really sick, follow urine osmolarity (may have initial salt wasting followed by a water diuresis); replace fluids and electrolytes as needed

Question 15

bladder pharmacology - general concepts

Answer 15

*nerve endings in detrusor release ACh that stimulates muscarinic receptors (M1-M5) in the detrusor that cause muscle CONTRACTION in response to ACh
*M2 predominates, M3 more responsible for contractions
*there are also beta adrenergic receptors (beta 2 and beta 3) that allow RELAXATION when stimulated by NE
*beta 3 predominates (activated by mirabegron)

Question 16

antimuscarinics used in bladder problems

Answer 16

*oxybutynin: nonselective
*tolterodine: nonselective
*solifenacin: M3 selective
*darifenacin: M3 selective
*trospium: nonselective; quartenary amine
*fesoteridine: nonselective

Question 17

side effects of muscarinic receptor blockade

Answer 17

*M1: impaired memory/cognition
*M2: prolonged QT interval
*M3: constipation, dry mouth, blurred vision
*M4: impaired cognition
*M5: unclear

Question 18

prostate pharmacology - general concepts

Answer 18

*alpha receptors exist within the prostate (alpha1 predominates)
*alpha agonists → increased muscle tone and increased ureteral resistance (sudafed induces urinary difficulties)
*alpha BLOCKERS → relax the smooth muscle within the prostate, facilitating urination (ex. tamsulosin, terazosin, doxazosin)

Question 19

uses of botulinum toxin in urology

Answer 19

*blocks ACh release at presynaptic terminals and inhibits striated and smooth muscle contractions, as well as afferent nerve activity
*used for refractory overactive bladder, neurogenic bladder, other

Question 20

drugs that cause hemorrhagic cystitis

Answer 20

*cyclophosphamide & ifosfamide
*prevent by co-administering MESNA