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)
16
Q
Epidemiology of calculi
A
- Men and women roughly equal incidence, prevalence increasing
- Relapse associated w/: young age of onset, family Hx, infection stones, underlying condition (hTPH)
17
Q
Types of stones
A
- 80% are Ca oxalate
- CaPO4
- Struvite (infection stones for proteus)
- Uric acid
- Cystine
18
Q
Stone formation
A
- Ca stone are most common and often form when there is hypercalcuria (not necessarily hypercalcemia)
- Supersaturation (normal) may worsen due to an increase of solute or decrease in urine volume
- At some point, spontaneous nucleation and homogenous nucleation (crystal growth) occur
- Heterogenous nucleation: a crystal of one type serves as a nidus on which another compound precipitates (commonly seen as uric acid nidus precipitating CaOx stone)
19
Q
Crystallization inhibitors
A
- Citrate (! most important)
- Mg
- Pyrophosphates
- Proteins
- pH of urine
- Uric acid and cystine will precipitate and form crystal in acidic urine
- Ca stone will form crystals in alkaline pH urine
20
Q
Pathogenesis of stone disease
A
-Predisposing factors: dehydration, hypercalcemic conditions (hyperparathyroidism, cushings, sarcoidosis), bladder obstruction (stasis), congenital d/o (PKC, MSK, calyceal diverticuli)
21
Q
Types of CaOx
A
- Monohydrate: very hard crystals
- Dihydrate: more soft
- Risk factors: hypercalcuria, dehydration, hypocitraturia
- Form in alkaline urine
22
Q
CaPO4 crystals
A
- “metabolic stones”
- Can be due to hyperparathyroidism, RTA, sarcoidosis
- Form in alkaline urine
23
Q
Struvite crystal
A
- Mg ammonium phosphate
- Forms in alkaline urine
- Caused by bacteria (proteus) w/ ukase nz
- soft and may conform to shape of collecting system (stag horn)
- More common in women and in men w/ prostatitis
24
Q
Uric acid crystals
A
- Can be due to hyperuricosuria and/or gout
- Risk factors: dehydration, gout, uricosuric drugs
- Forms in acidic urine
- Hyperuricosuric states: gout, lesch-nyhan syndrome, myeloproliferative (tumor lysis)
25
Q
Cystine crystals
A
- Due to genetic inability to reabsorb cystine, ornithine, lysine, arginine in PT
- Very hard stones
- Forms in acidic urine
- Cystine in urine reacts w/ nitroprusside
- Most important for Rx: increase fluid intake
26
Q
Pathogenesis of CaOx stones
A
- First there is accumulation of crystal deposits around LOH
- Then there are crystal deposition in papillary tissue
- The stones form on a plaque (randall’s plaque)
- The plaque corresponds to urine Ca level and urine volume
- Amount of plaque corresponds to number of CaOx stones
27
Q
Distal RTA (RTA 1)
A
- Inability to excrete acid, acidosis leads to loss of Ca from bones
- Hypocitraturia occurs due to acidosis of urine
- Hypercalcuria + hypocitraturia + alkaline urine = Ca stones
- Can lead to recurrent disease and nephrocalcinosis
- Rx using Kcitrate
28
Q
Nephrocalcinosis
A
- Calcifications of renal papilla/tubules
- Distal RTA and MSK can cause stones and nephrocalcinosis
29
Q
Presentation of kidney stones
A
- Sx: pain, hematuria, UTI, sepsis
- Ab tenderness, on UA there is RBC, WBC, crystals
- Dx best is CT (can also ultrasound
- Hx/PE: family Hx, prior stone Hx, recurrent UTI, systemic disease
- Rx: anlagesia, hydration, hospitalization if systemic infection
- 80-90% of stones pass
- Alpha blockers and Ca blockers an option if stone doesn’t pass
- May have to be removed if: infection, solitary kidney, intractable pain, renal failure
30
Q
Rx of hypercalcuria
A
- Thiazides stimulate Ca reabsorption in PT/DT and decrease Ca excretion by 30%
- Decrease recurrence of stone formation
- SEs: hypercalcemia, hyperuricemia, hypokalemia, hyponatremia, dehydration, hypomagnesia
31
Q
Medical Rx for uric acid stones
A
- Fluids, alkalization of urine w/ K citrate
- Allopurinol if hyperuricosuria
32
Q
Preventing stones
A
- Fluid intake >2 L /day
- Decrease Na intake
- Do not restric Ca
- Avoid carbs/sugar
- Moderate protein (esp. animal protein)
- Increase citrate consumption
33
Q
Rx of struvite stones
A
-Acetohydroxamine (urease inhibitor) to prevent recurrence
