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Urology Residency Flash Cards > Urolithiasis > Flashcards

Urolithiasis Flashcards

1
Q

What lab work should be ordered for a patient presenting with an acute stone episode?

A

WBC with differential, urinalysis, BUN, Cr, and electrolytes. If patient is febrile do not forget urine C/S

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2
Q

What are imaging options for patients with suspected urolithiasis?

A
  1. CT stone protocol (best test)
  2. KUB XR (not all stones will show)
  3. KUB U/S may detect hydro but more difficult to assess stones in the ureter
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3
Q

What is first line imaging for suspected stones in children?

A

KUB U/S

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4
Q

What are indications for prompt intervention with stones?

A
  1. Septic stones
  2. Stones in a solitary kidney
  3. Stones causing intractable pain
  4. Stones causing bilateral obstruction
  5. Stones causing an inability to tolerates oral intake secondary to nausea/vomiting/pain
  6. Prolonged complete or high grade unilateral urinary obstruction
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5
Q

List changes that occur in the kidney and ureter during acute ureteral obstruction?

A
  1. 0-90mins - increased ipsilateral renal blood flow, and increased intra-ureteral pressure
  2. 90 - 300mins - decreased ipsilateral renal blood flow and increased contralateral renal blood flow with continued increased intra-ureteral pressure
  3. 300mins to 18 hours - decreased intra-ureteral pressure with decreased ipsilateral renal blood flow but increased contralateral renal blood flow.
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6
Q

What are chronic changes that can occur in the ureter as a result of obstruction and what is the timeline?

A
  1. Hypertrophy of ureteral musculature - within 3 days
  2. Scarring and fibrosis of the ureter - may begin within 2 weeks
  3. If a stone is causing complete obstruction - permanent renal damage is thought to occur after approximately one month
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7
Q

How does thiazide work for prevention of stones?

A

Thiazides increase re-absorption of calcium in the proximal and distal tubules of the nephron and inhibit sodium re-absorption in the distal tubules.

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8
Q

How do thiazides prevent stone formation?

A

They decrease the urinary excretion of calcium and correct acidosis. A low sodium diet enhances the hypocalciuric effects of thiazides.

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9
Q

What are side effects of thiazides?

A

Hypokalemia, weakness, fatigue and ED

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10
Q

How does citrate/bicarbonate work for prevention of stones?

A

Citrate (converted to bicarbonate in the liver) and bicarbonate work correcting acidosis and increasing urinary pH and urinary citrate.

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11
Q

What is the preferred urinary alkalizer for preventing calcium oxalate urolithiasis?

A

Potassium citrate (K-citrate)

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12
Q

In patients with renal insufficiency or whom are at risk for hyperkalemia what is preferred to alkalinize urine?

A

Sodium citrate

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13
Q

What are side effects of potassium citrate?

A

Hyperkalemia, peptic ulcers, diarrhea and metabolic acidosis

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14
Q

What is the adult dose of potassium citrate?

A

20meq PO BID or TID (titrate based on urine pH > 5.5)

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15
Q

What is the most common metabolic abnormality in stone formers?

A

Hypercalciuria

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16
Q

What is the most common stone composition in industrialized countries?

A

Calcium oxalate

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17
Q

What is the most common cause of urolithiasis?

A

Dehydration

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18
Q

In what conditions are calcium oxalate stones the most commonly formed?

A

healthy adults, healthy children, intestinal bypass, inflammatory bowel diseases, and renal failure

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19
Q

In what patients are calcium phosphate stones the most commonly formed?

A

hyperparathyroidism, Type I RTA, medullary sponge kidney, and carbonic anhydrase inhibitor use

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20
Q

For patients who form uric acid stones what is their relative serum and urine uric acid levels to normal people?

A

The same, not elevated.

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21
Q

What are 3 unique characteristics of uric acid stones?

A

Form in acidic urine pH<6
Radiolucent
Dissolve with urinary alkalization

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22
Q

What are unique characteristics of struvite stones (magnesium, ammonium phosphate)?

A
  1. Most staghorn calculi are composed of struvite
  2. They are most commonly caused by UTI (urease splitting organisms)
  3. They form in alkaline urine and dissolve with urinary acidification
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23
Q

What are unique characteristics of cystine stones?

A
  1. Cause cystinuria (usually homozygotes)

2. Form in acidic urine and dissolve with urinary alkalization

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24
Q

What are unique characteristics of matrix stones?

A
  1. Most commonly caused by UTI’s (proteus)
  2. Form in alkaline urine
  3. Are radiolucent
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25
Q

What are unique characteristics of ammonium acid urate stones?

A

Common causes include laxative abuse, UTI, urinary phosphate deficiency.

Radiolucent

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26
Q

What are unique characteristics of protease inhibitor stones (indinavir (crixivan), nelfinavir.

A

Cause = precipitated drug
Stones are radiolucent (not visible on CT scan)
Form in urine with pH > 5

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27
Q

What are types of hard stones and what considerations should be given to managing these?

A

Calcium oxalate monohydrate, and cystine stones are very hard.

Hard stones can be resistant to ESWL, and pulsed dye laser. Holmium laser is effective against both these types of stones.

28
Q

List the radiolucent stone types?

A
  1. Uric acid
  2. Xanthine
  3. Matrix
  4. 2,8 - dihydroxyadenine
  5. Triamterene
  6. Protease inhibitor stones (not visible on XR or CT)
  7. Silica
29
Q

List 12 disease states that that increase the risk of urolithiasis?

A
  1. Obesity
  2. DM
  3. Gout
  4. Metabolic acidosis
  5. Hypertension
  6. Type I RTA
  7. Sarcoidosis (leads to hypercalciuria)
  8. Cystinuria
  9. Inflammatory bowel disease
  10. Chronic diarrhea
  11. Medullary sponge kidney (calcium stones)
  12. Adult polycystic kidney disease
  13. Hypokalemia (causes intracellular acidosis)
  14. Anatomic factors causing urinary stasis or obstruction
  15. Low urine volume (poor hydration)
  16. UTI
30
Q

What abnormalities in urine composition lead to increased risk of stone formation?

A
  1. Hypercalciuria
  2. Hypocitraturia
  3. Hyperoxaluria
  4. Hyperuricosuria
  5. Hypomagnesiuria
  6. Xanthinuria

balance of: urinary pH, crystal inhibitor and crystal promoters.

31
Q

What dietary factors promote formation of urolithiasis?

A
  1. Potential renal acid load (PRAL) - foods that generate circulating acid and lead to decreased citrate ex. eggs, cheese (high PRAL), fruits and veggies (low PRAL)
  2. High sodium intake - increased urinary calcium, decreased urinary citrate
  3. Low fibre diet
  4. High oxalate diet
  5. Carbonated drinks that contain phosphoric acid
32
Q

What are the two categories of stone formation inhibitors and what are some agents in each category?

A

Organic: citrate, urea, nephrocalcin, tamm-horsfall proteins, calgranulin, glycosaminoglycans, bikunin, and uropontin

Inorganic: pyrophosphate, magnesium, trace elements, (zinc)

33
Q

How does citrate work to decrease stone formation?

A

Decreases calcium stone formation by:

complexes with calcium to lower urinary calcium concentration and directly inhibits calcium crystallization

34
Q

How does urea work to decrease stone formation?

A

Decreases uric acid stone formation by increasing solubility of uric acid (no influence on calcium stones)

35
Q

How do UTI’s increase stone risk?

A
  1. Cause hypocitraturia
  2. Urease producing organisms split urinary urea into ammonia and bicarbonate which alkalinizes the urine
  3. UTI may decrease ureteral peristalsis
36
Q

What UTI organisms produce urease?

A
  1. Proteus
  2. Klebsiella
  3. Serratia
  4. Staphylococcus
  5. Morganella
  6. Providencia
  7. Enterobacter
37
Q

What types of stones are associated with UTI?

A

Struvite, matrix, carbonate apatite

38
Q

What changes does acidosis cause in urinary composition?

A
  1. Increased urine calcium
  2. Increased urine phosphate
  3. Decreased urine citrate
39
Q

Through what mechanism does a prolonged acidosis cause hypercalciuria?

A

Leads to bone demineralization, which increases calcium delivery to the kidneys and results in hypercalciuria

40
Q

Which stones form in acidic urine?

A
  1. Amino acid stones (cystine, leucine, tyrosine)

2. Uric acid stones (usually form at a pH < 6)

41
Q

Which stones form in alkaline urine?

A
  1. Matrix stones
  2. Stones that contain phosphate, carbonate or ammonia)
    [struvite, calcium phosphate, calcium carbonate]
42
Q

Which stones can form over a variety of pH’s?

A

Calcium oxalate, hippuric acid

43
Q

What medications increase ones risk for urolithiasis?

A
  1. Vitamin C (gets metabolized to oxalate)
  2. Vitamin D (high doses) - leads to increased calcium absorption and hence hypercalciuria
  3. Triamterene (precipitates in the urine)
  4. Protease inhibitors
  5. Furosemide (increases calcium excretion in the urine)
  6. Acetazolamide
  7. Agents that increase uric acid in urine (salicylates, probinecid)
44
Q

What patients should undergo a metabolic stone workup?

A
  1. Large stone burden
  2. Recurrent stone formers
  3. Nephrocalcinosis
  4. Pediatric stone formers
  5. Uncommon stone composition (cystine, uric acid)
  6. Stone arising from UTI
  7. Family history of stones
  8. Medical, genetic, or anatomic condition that increases stone forming risk)
  9. Solitary kidney
  10. Professionals whom if developed renal colic while working could be deleterious to others (pilots, bus drivers, truck drivers, surgeons)
45
Q

When should you perform a metabolic stone workup?

A

At least one month after stones have been treated, or if stents present they have been removed or if infection present it has been eradicated.

46
Q

What is the initial metabolic workup that all patients with urolithiasis should have?

A
  1. Hx and Px
    Ask about fluid consumption, diet, UTI, medications, prior urolithiasis, and family history of urolithiasis
  2. Analyses stone composition
  3. Urinanalysis including urine pH
  4. Serum chemistries: Na, K, Cl, HCO3-, uric acid, calcium, and creatinine. (If Ca elevated or stone predominantly calcium phosphate order a serum PTH)
47
Q

What should a 24 hour urine study test include?

A
  1. pH measurement
  2. Total urinary volume
  3. Urinary calcium
  4. Urinary oxalate
  5. Urinary citrate
  6. Urinary uric acid
  7. Urinary sodium
  8. Urinary potassium
  9. Urinary creatinine
48
Q

How do you know if the 24 hour urine study is incomplete?

A

If the 24 hour urinary creatinine excretion is abnormally low.

Normal urinary creatinine excretions are:
M 14-26mg/kg/day
F 11-20mg/kg/day

49
Q

What are general recommendations to make to patients for stone prevention?

A
  1. Oral fluid intake should be sufficient to generate 2.5L of urine per day.
  2. Fluids containing citrate are ideal (lemon, orange, lime etc)
  3. Encourage low sodium diet (<100meq/day) - decreases urinary calcium and increases urinary citrate
  4. Reduce PRAL (potential renal acid load) foods
    - reduce intake of non-dairy animal protein
    - reduce intake of cheese and eggs
    - increase intake of fruits and vegetables
  5. Low oxalate diet
  6. Avoid high doses of vitamin C (>500mg/day)
  7. Moderate calcium intake (1000-1200mg/day)
  8. High fibre diet
  9. Weight loss in obese patients
50
Q

When should citrate medications be considered? What are your two options for dietary citrate supplementation?

A

Urinary alkalinizer used for calcium oxalate stones.

K-citrate is first choice, sodium citrate is another option but increased sodium can promote stone formation

51
Q

How does allopurinol work as a stone formation inhibitor and when should it be prescribed?

A

Decreases serum uric acid by inhibiting xanthine oxidase (enzyme responsible for converting hypoxanthine to xanthine and xanthine to uric acid.

Allopurinol prevents uric acid stones ONLY when there is hyperuricosuria, this is REGARDLESS of hyperuricosemia.

52
Q

When should magnesium be give as a stone formation inhibitor?

A

Most useful in patients with hypomagnesuria and calcium stones

53
Q

What is the main side effect of magnesium supplementation?

A

Diarrhea

54
Q

When can pyridoxine (vitamin B6) be given as a stone formation inhibitor?

A

Used to treat primary hyperuxaluria - needs to be given with thiols to prevent neurologic side effects.

55
Q

What is acetohydroxamic acid (AHA) used for as a stone formation inhibitor?

A

AHA - inhibits urease and reduces the growth of struvite stones (its use is restricted to patients whom which have residual or recurrent struvite stones after surgical therapies have been exhausted)

56
Q

What are side effects of AHA?

A

nausea/vomiting, anorexia, tremor, anxiety, headache (30%), hemolytic anemia (15%) alopecia, DVT, rash after drinking EtoH

57
Q

How do you define hypercalciuria?

A

Urinary calcium > 200mg/day

58
Q

What are the 4 different types of hypercalciuria?

A
  1. Absorptive
  2. Renal
  3. Resorptive
  4. Unclassified
59
Q

What is the pathophysiology of ABSORPTIVE hypercalciuria?

A

Primary mechanism is excess intestinal absorption of calcium

60
Q

What is the pathophysiology in RENAL hypercalciuria?

A

Primary mechanism is impaired renal tubular reaborption of calcium

61
Q

What is the pathophysiology in RESORPTIVE hypercalciuria?

A

Primary mechanism is hypersecretion of PTH. (hyperparathyroidism)

62
Q

What is the definition of hypomagnesuria?

A

Urinary magnesium < 50mg/day

63
Q

How do you treat hypomagnesuria?

A

Dietary magnesium (magnesium oxide 400-500mg PO BID) watch out for diarrhea

64
Q

How do you define hyperuricosuria?

A

Urinary uric acid > 600mg/24h

65
Q

What are the TWO types of stones that one is at increased risk of forming if they have hyperuricosuria?

A

Uric acid stones, and calcium oxalate stones.

Urology Residency Flash Cards (8 decks)

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