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47 Cards in this Set

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What locations can urinary tract obstruction occur in?
*Anywhere throughout the collecting system including:
1) Intratubular (e.g. crystals precipitating in tubules, as seen in IV Acyclovir).
2) Intraluminal (lesion is within the lumen of collecting system, such as a stone).
3) Intramural (lesion arises from wall of collecting system, such as bladder tumor causing obstruction).
4) Extrinsic compression (process outside the collecting system causes compression such as a pelvic tumor, or prostate enlargement).
5) Functional obstruction (e.g. neurogenic bladder).
What is hydronephrosis?
*A stone has caused the obstruction here.
*A stone has caused the obstruction here.
Most common cause of obstruction in men?
*Prostatic enlargement; urethral obstruction.
*Prostatic enlargement; urethral obstruction.
What happens in the early stages of the pathogenesis of urinary obstruction?
1) Increased pressure in Bowman’s space (pressure in this space normally near-zero).

2) Diminished filtration across basement membrane because of smaller pressure gradient.

3) Attempted compensation by increasing blood flow to glomerulus t...
1) Increased pressure in Bowman’s space (pressure in this space normally near-zero).

2) Diminished filtration across basement membrane because of smaller pressure gradient.

3) Attempted compensation by increasing blood flow to glomerulus to raise intraglomerular pressure and favor filtration.
*Dilation of afferent arteriole.
What happens in the middle stages of the pathogenesis of urinary obstruction?
*(4-5 hours).

*Reduced GFR from obstruction leads to gradual reduction in renal blood flow:
1) Likely mediated by decreased distal delivery of sodium from reduced GFR.

2) Thromboxane A2 and other factors (angiotensin II,  decreased endothel...
*(4-5 hours).

*Reduced GFR from obstruction leads to gradual reduction in renal blood flow:
1) Likely mediated by decreased distal delivery of sodium from reduced GFR.

2) Thromboxane A2 and other factors (angiotensin II, decreased endothelium-derived relaxing factor) contribute to afferent vasoCONSTRICTION, further reducing GFR!
What happens in the late stages of the pathogenesis of urinary obstruction?
1) Dilation of urinary collecting system.
2) Increased lymphatic drainage.
3) Reduction in GFR.

*Above factors lead to gradual reduction in tubular pressure back toward normal.
1) Dilation of urinary collecting system.
2) Increased lymphatic drainage.
3) Reduction in GFR.

*Above factors lead to gradual reduction in tubular pressure back toward normal.
What happens to tubular function during obstruction?
*Decrease in GFR and decrease in delivery of filtrate to distal nephron can lead to confusing laboratory studies:
1) Decreased urine Na concentration (often <20meq/L; but this ISN'T volume depletion).
2) Increased urine osmolality (often >500mosm/kg).

*Due to injury in the distal nephron, handling of K, acid-load and water are impaired:
1) Hyperkalemia appears out of proportion to the severity of kidney injury (may be an altered response to aldosterone).
2) You see acidosis (non-anion gap) from impaired distal acidification of urine.
3) In cases of partial obstruction, response to ADH may be impaired, leading to polyuria and excess H2O losses.
What happens to tubular function once a urinary obstruction is corrected?
*Tubular function remains impaired for a time even after relief of obstruction!

*“Post-obstructive diuresis”:
1) You see appropriate mobilization of retained fluid.
2) You see osmotic diuresis from excess solute concentrations (e.g. urea).
3) But there is persistently impaired Na and H2O handling.
4) So you need to watch carefully for volume depletion or electrolyte abnormalities (hypokalemia, H2O depletion).
What happens to the GFR in urinary obstruction?
*GFR in the affected kidney is clearly reduced.

*Overall GFR is usually preserved IF obstruction is UNILATERAL:
1) Remaining kidney increases its filtration (can double) to compensate.
2) Serum laboratory values may be normal or near-normal.
What are the Clinical Features of obstruction?
unilateral--
bilateral--
1) Unilateral:
*Flank pain or fullness.
*Pain may be colicky and severe, especially if from an obtructing stone.
*Hematuria if stone-related.

2) Bilateral:
*History of difficulty urinating.
*Suprapubic fullness/tenderness.
*Decrease in urine output (notoriously unreliable clue).
*Increase in urine output (if partial obstruction).
What are the Lab findings in obstruction?
unilateral--
bilateral--
1) Unilateral:
*All labs usually normal (unless patient only has one kidney).

2) Bilateral:
*Elevated BUN, Creatinine.
*Elevated BUN/Cr ratio, decreased urine sodium, high urine osmolality may all MIMIC volume depletion.
How do you make the diagnosis of obstruction?
What do you look for on history and PE?
Labs?
*History may provide clues (e.g. history of urinary difficulty or flank or pelvic fullness).

*Physical Exam:
1) Flank tenderness.
2) Lower abdominal/pelvic fullness-- bladder can be palpable.
3) Rectal exam (men) to look for enlarged prostate.
4) Pelvic exam (women) to look for pelvic malignancy.

*Laboratory:
*BUN/Cr and urine indices can be misleading.
*Urinalysis findings of blood and/or crystals can be suggestive of stones (blood and crystals) or malignancy (blood).
What therapeutic maneuver can you do to help make a diagnosis of obstruction?
*Post-void residual:
-Placement of urethral catheter after patient has attempted to void.
-Greater than 100ml retained urine indicates incomplete bladder emptying.
In diagnosing obstruction, what imaging can help?
1) Intravenous pyelogram:
*RARELY, IF EVER, performed because of risk of contrast-related kidney injury.

2) Ultrasound:
*Looks for hydronephrosis, dilated renal pelvis.
*Can sometimes identify stones.

3) CT scan:
*More precisely determines location of obstruction.
*Particularly useful in patients with stones.
IVP showing hydronephrosis. These are rarely done because contrast injures the kidneys.
IVP showing hydronephrosis. These are rarely done because contrast injures the kidneys.
*Top: Normal ultrasound.
*Bottom: Hydronephrosis.
*Top: Normal ultrasound.
*Bottom: Hydronephrosis.
CT scan showing stone causing obstruction.
CT scan showing stone causing obstruction.
How do you treat an obstruction?

How quickly can normal GFR be regained?
*Definitive treatment is relief of obstruction.

*Response to therapy depends on duration and severity of obstruction:
-Expect a return of GFR to normal if obstruction relieved WITHIN A FEW DAYS to a week.
-Complete obstruction UNLIKELY to regain much function after 1-2 weeks.
-Partial obstruction MAY respond favorably even after weeks to months.
Take home points in treating urinary obstruction:
*Timely intervention is necessary to prevent permanent injury.

*Some laboratory features and even clinical signs can be misleading if obstruction is not suspected.

*Tubular function is impaired, even during the initial stages of recovery.
How common are kidney stones?
*Very common, affecting up to 10% of the population (lifetime risk).
*Accounts for 1/1000 hospitalizations (generally for pain control), many more ER visits.
*Substantial cost, both in surgical/medical therapies and in loss of productivity.
*Se...
*Very common, affecting up to 10% of the population (lifetime risk).
*Accounts for 1/1000 hospitalizations (generally for pain control), many more ER visits.
*Substantial cost, both in surgical/medical therapies and in loss of productivity.
*Severe pain!!

*Incidence:
-Around 10% lifetime (white males).
-Appears to be rising.
-Gender, ethnic, regional, and seasonal variations.

*Recurrence:
-40-50% recur within 5 years.
-Recurrence rate as high as 75% over 25 years.
How do stones present?
*Renal colic: Severe flank pain, abrupt onset with radiation to groin.

*Gross or microscopic hematuria.

*Nausea/vomiting, occasional ileus (decrease in intestinal motility).
What are the Clinical Findings in kidney stones?
What do you look for on PE & Labs?
*Exam:
-Mild fever.
-Flank tenderness.

*Lab:
-Hematuria.
-Possibly crystalluria.
-Elevated WBC.
(∆= pyelonephritis)
Epidemiologically, stone formation is more likely in someone who fits what profile?
*Stone formation more likely in:
-White.
-Male.
-Live in the South.
-Summertime (early winter in women).
What's the chemical makeup of kidney stones?
Calcium oxalate 75%
Uric acid 10-15%
Struvite 15-20%
Cystine 1%
What is the Life Cycle of the Stone?
*Supersaturation (for calcium oxalate, this occurs in 50% of adults).

*Nucleation (forms submicroscopic particles): needs to attach to epithelial surface or grow quickly to avoid being flushed out.

*Growth (may take weeks-months-years).
*Supersaturation (for calcium oxalate, this occurs in 50% of adults).

*Nucleation (forms submicroscopic particles): needs to attach to epithelial surface or grow quickly to avoid being flushed out.

*Growth (may take weeks-months-years).
What are the natural Inhibitors of stone formation?
1) Citrate: Binds calcium in urine to form soluble complex.

2) Magnesium.

3) Macromolecules:
-Nephrocalcin.
-Tamm-Horsfall protein.
What are Predisposing anatomic factors to stone formation? 3
1) Horseshoe kidney.

2) Medullary sponge kidney (congenital, mostly women): cystic dilation of ducts-- stagnant urine flow.

3) Polycystic kidney disease.
Calcium oxalate stones. Look like envelopes.
Calcium oxalate stones. Look like envelopes.
What are the 3 causes of calcium oxalate stone formation?
*Crystalloid concentration:
1) Hypercalciuria
2) Hyperoxaluria.
3) Low urine volume.
What are the 3 "promoters" of calcium oxalate stone formation?
1) Hyperuricosuria (Uric acid “seed” crystal can promote calcium oxalate stone).

2) High sodium diet (promotes calcium excretion in urine).

3) Low-carbohydrate (Atkins) diet:
*Presumably from high protein load, increased purine metabolism and uric acid levels, also chronic acidosis and decreased fluid intake.
Discuss hypercalciuria as a risk factor for stone formation?

What are the usual causes of hypercalciuria?
*Present in 50% of stone formers (5% have primary hyperparathyrodisim).

*Hypercalcemia + hypercalciuria should raise suspicion for primary hyperparathyroidism.

*Other rarer causes: RTA, sarcoidosis.
Discuss Hyperoxaluria as a risk factor for stone formation:

What all causes Hyperoxaluria?
*Normal excretion is 15-40mg daily.
*If someone has excess excretion, it is a result of either increased synthesis or dietary absorption.

*Increased synthesis in:
1) Congenital disorders (primary hyperoxaluria types 1 and 2).
2) Excess vit C intake enhances oxalate synthesis in some individuals.

*Increased absorption:
-Normally forms an insoluble complex with Ca in the gut.
-Dietary calcium restriction can actually lead to enhanced oxalate absorption.
-High oxalate diets lead to increased absorption.
-Intestinal malabsorption syndromes (requires an intact colon to absorb the oxalate) like Crohn’s disease, ileal bypass can increase absorption,
Discuss the role of urine volume in calcium oxalate stone formation:
*“Stone clinic effect”: activity of nephrolithiasis appears to diminish during treatment regardless of therapy.

*Saturation of all crystalloids falls with increased urine volume.

*>2L/day urine output is goal, including at night.
Describe the treatment of calcium oxalate stones:
-Universally
-In hypercalciuria
-In hyperoxaluria
*Universal: Increase fluid intake (>2L per day urine volume).

*Hypercalciuria:
1) Diet (reduce sodium, reduce animal protein, moderate calcium intake).
2) Thiazide diuretics (reduce urinary calcium excretion).
3) Potassium citrate (increase urinary citrate – stone inhibitor).

*Hyperoxaluria:
1) Low oxalate diet (avoid tea, colas, rhubarb, spinach, chocolate).
2) Calcium supplements (to bind dietary oxalate).
Uric Acid stones.
Uric Acid stones.
Discuss uric acid stones:

How do we treat them?
*Radiolucent (do not appear on regular X-rays).

*Apart from uric acid stones, also predisposes to calcium stones (may serve as nidus for stone formation).

*Much more soluble at higher pH, so urinary alkalinization (pH 6-7) is treatment.

*Gout + kidney stones is indication for allopurinol.

*Can dissolve spontaneously with treatment.

*Treatment also with purine restricted diet (can add allopurinol if production is excessive).

*Do not use Probenecid!!! (enhances renal excretion of uric acid).
Infection stones (struvite). "Coffin lid" stones. Cats get these.
Infection stones (struvite). "Coffin lid" stones. Cats get these.
Discuss Infection stones:
When do we see these?
How do we treat these?
*Struvite (Magnesium ammonium phosphate) or apatite (calcium phosphate).

*Forms during infection with urease positive bacteria (Proteus or Providencia). The stones themselves become infected.

*Urine pH is elevated to 8 (urea cleaved to ammonia).

*Difficult to clear.

*Antibiotics first, usually followed by stone removal (may need combination percutaneous and ESWL approach).

*All stone fragments need to come out, or the patient may require chronic suppressive antibiotics.
Discuss Cystine stones:
Who gets these?
How do we treat? 2
*Rare associated with inherited disorder (COAL) with reduced tubular absorption of cystine, ornithine, arginine, lysine.

*Very poorly soluble (250mg/L) so requires high urine volumes.

*If concentration too high, can use pharmacotherapy with penicillamine or tiopronin.
Cystine stones
Cystine stones
What drugs may cause cystine stones? 3
*Indinavir, sulfadiazine, triamterene.
*Shown: Indinavir crystals.
*Indinavir, sulfadiazine, triamterene.
*Shown: Indinavir crystals.
What's the workup for stones?
1) First stone--> Stone analysis, U/A, calcium, phosphate, uric acid, BUN/Cr.

2) Imaging to make sure only one stone.
*Enormous struvite stone. Surgery indicated.
*Enormous struvite stone. Surgery indicated.
What's the workup for someone who is having recurrent stones?
*24h collection of calcium, phosphate, oxalate, citrate, uric acid, creatinine, volume, pH, urea nitrogen, sodium, magnesium.

*Gives you all the variables of stone formation.
Who needs a urologist for stones?
*90% of stones pass spontaneously.

*Ureteral stones <4mm likely to pass within a year (70%).

*>8mm unlikely to pass (<10%).
What are the Indications for removal of a stone? 3
*Complete obstruction needs relief in 2 weeks to prevent permanent renal injury.

*Partial obstruction in 4-6 weeks.

*Fever (emergency decompression with stent or percutaneous nephrostomy, remove stone after infection clears).
Take home points regarding stones:
*Nearly everyone has risk factors for stone formation.

*Stones frequently recur.

*Increasing fluid intake is appropriate management for all types of stones.

*Larger stones, or stones causing obstruction require surgical removal.