Pathology of obstructive uropathy Flashcards
1
Q
Normal bladder function
A
- Filling: unidirectional peristalsis down ureters to bring urine to bladder
- Bladder stretches (high compliance) and is in a low pressure state
- Normal voiding: First SNS to sphincter decreases and sphincter opens. Then PsNS increases and causes bladder to contract (low pressure)
- If obstruction is btwn bladder and kidney it is upper urotract (must be bilateral to produce renal Sx but still can produce)
- If obstruction is btwn bladder and end of urethra it is lower urotract (anywhere will produce Sx)
2
Q
Etiology of obstructive uropathy
A
- Congenital: atresia of urethra, meatus stenosis, presence of valves in either ureter or urethra
- Acquired: calculi (stones), infection/inflammation, hyperplasia (BPH), pathophysiological, trauma
3
Q
Clinical presentation of upper urinary tract obstruction
A
- Acute: renal colic (groin/ab radiating to flank pain comes in peristalsis), often from stones
- Chronic: dull pain, ache, pressure (recurrent UTI)
4
Q
Clinical presentation of lower urinary tract obstruction
A
- Irritative + obstructive Sx
- Irritative Sx: dysuria, urge incontinence, nocturia, increased frequency and urgency
- Obstructive Sx: decreased force of stream, dribbling, hesitancy, intermittency, incomplete emptying
- See an increase in post-void residual (PVR)
- By far most common is BPH in a man
- If its chronic bladder outlet obstruction: bladder hypertrophy and detrusor (SM part of bladder wall) dysfxn
5
Q
Changes in kidney function w/ obstructive uropathy
A
- Renal insufficiency may be seen either in acute or chronic obstructions, depends on degree of obstruction, presence of bilateral kidneys, and baseline renal function
- Response to obstruction: altered renal blood flow, change in GFR, loss of concentrating ability w/in collecting duct
- Dilation of renal tubules, first in collecting duct then extends proximally (gloms affected last)
- Can see fibrosis, mac infiltrate, hemorrhage/necrosis
- Radiographic changes: bladder trabeculation, diverticuli, calculi, J hooking of ureter, hydronephrosis, thinned parenchyma
6
Q
Effects of urethral and bladder outflow obstruction
A
- Urethral obstruction: bladder dilation and hypertrophy, dilated ureter, dilated renal pelvis and calyces (hydronephrosis) all bilateral
- Outflow obstruction: bladder SM hypertrophy and hyperplasia (bundles of SM form trabeculi)
7
Q
Hydronephrosis
A
- Can be seen in any kind of urinary tract obstruction
- Hydronephrosis is characterized by dilated calyces and dilated pelvis w/ thinning of the medulla and cortex, chronically can lead to HTN
- Micro: early there is dilation of tubules, followed by tubular compression and atrophy
- Can also see interstitial fibrosis and normal gloms
- Hydroureter (seen in hydronephrosis): dilation, hypertrophy and hyperplasia of SM due to chronic increase intraluminal pressure + chronic infl cells
8
Q
Whitaker test
A
- Nephrostomy + bladder catheter and measure pressure difference
- If difference is 22cmH20 there is an obstruction
- Btwn 15-22cm H2O and its undetermined
9
Q
Associated Sx for various obstructions
A
- Calculi: renal colix and hematuria
- BPH: urinary bladder syndrome (hesitancy, straining, dribbling, frequency, dysuria)
- Infection: fever, frequency, urgency, pyuria, leukocytosis, bacteriuria, dysuria, ab pain
- HTN common in longstanding hydronephrosis
- Renal failure (uremia): high BUN, Cr, anemia, lethargy, nausea, vomiting, mental changes
10
Q
Consequences and complications
A
- Infection: stasis of urine promotes infection (urethritis, prostatitis, ureteritis)
- Renal failure: due to suppression of glomerular filtration and ischemic atrophy of the kidney
- Acute complete urinary tranct obstruction causes shut down of renal function and very little or no hydronephrosis
- Intermittent or partial urinary tract obstruction results in hydronephrosis
11
Q
Benign prostatic hyperplasia (BPH) 1
A
- Hyperplasia of stroma and epithelium (usually w/in transition or periurethral zone)
- Most common cause of urinary tract obstruction
- Begins 5-6th decade, hormones play important role
- Prostates have enlarged, nodular surface (normal is smooth)
- BPH tends to affect the medial lobe of the prostate, where as prostate cancer tends to affect the lateral lobes
12
Q
Benign prostatic hyperplasia (BPH) 2
A
- Micro: there is a nodular appearance to the area of hyperplasia
- At a higher mag, BPH is associated w/ tubuloalveolar glands that are dilated or w/in foldings of the epithelium (increased number of folds)
- BPH leads to obstructive and irritative Sx, and Sx are not always related to enlargement
- Signs: bladder hypertrophy, trabeculation
13
Q
Prostatitis
A
- Acute: periglandular-intraglandular infiltrate
- Predominantly PMNS and usual cause is infection
- Chronic prostatitis: largely an interstitial infiltrate w/ mononuclear cells and unknown cause
14
Q
Complications of BPH
A
- Urinary retention
- Infection
- Bladder decompensation
- Calculi (!)
- Hematuria
- Hydronephrosis
- Renal failure
15
Q
Rx of obstructions and post-obstructive response
A
- Rx is remove the obstruction (site and cause of obstruction dictates Rx)
- Post-obstructive diuresis: after relief of unilateral ureter obstruction of solitary kidney or relief of bilateral ureter obstruction
- Physiologic post obstructive diuresis: self-limiting
- Pathologic: impaired concentrating ability or Na reabsorption (rare)
