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*MHD Exam 5 > Nephrolithiasis > Flashcards

Nephrolithiasis Flashcards

1
Q

the most common type of kidney stone

A

calcium oxalate

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2
Q

What are some of the causes of calcium oxalate stones?

A
  • too much Ca in blood: hypercalcemia
  • too much Ca in urine: hypercalciuria
  • not enough citrate in urine: hypocitraturia
  • too much oxalate in urine: hyperoxaluria
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3
Q

What do calcium oxalate stones look like on microscopy?

A

envelope and dumbbell-shaped

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4
Q

Which endocrine condition can cause hypercalcemia and hypercalciuria (most common cause)?

A

hyperparathyroidism (elevates serum calcium)

*sarcoidosis can also elevate calcium through overproduction of 1,25-dihydroxy vitamin D

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5
Q

What effect does sarcoidosis have on stone formation?

A

It causes an overproduction of 1,25-dihydroxy Vitamin D, leading to elevated serum calcium.

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6
Q

_________ is an inhibitor of calcium-oxalate stone formation.

A

citrate

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7
Q

What is the relationship between hypocitraturia and metabolic acidosis?

A

Metabolic acidosis causes hypocitraturia. This is because the kidney reabsorbs citrate (alkaline) at the PT to a greater degree to compensate for systemic metabolic acidosis. This leaves less citrate in the urine to alkalinize urine pH and act as a “solvent” for calcium.

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8
Q

What are some of the causes of hypocitraturia?

A
  • metabolic acidosis
  • RTA type I
  • idiopathic
  • high animal protein diet
  • medullary sponge kidney
  • meds (topiramate)
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9
Q

What are the causes of hyperoxaluria?

A
  • Enteric (complication of short bowel syndrome, Crohn’s, Hirschprung’s, CF, ileal resection)
  • Meds (Vit. C abuse)
  • Inherited (autosomal recessive enzymatic defects in glyoxylate metabolism)
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10
Q

Describe the pathophysiology of enteric hyperoxaluria.

A

dietary Ca binds to unabsorbed FFAs in small bowel –> not enough Ca to bind dietary oxalate –> unbound oxalate absorbed in colon and filtered into urine –> in urine, oxalate binds to calcium = calcium oxalate stones

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11
Q

How can vitamin C abuse lead to hyperoxaluria?

A

Excess vitamin C is excreted in the oxalate form, which may bind calcium in the urine and cause formation of calcium oxalate crystals. Taking more than 4-5 tabs/day of vitamin C can precipitate acute calcium oxalate stones.

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12
Q

What is primary hyperoxaluria?

A

autosomal recessive enzymatic defect in glyoxylate metabolism that results in enhanced oxalate overproduction; diagnosed in infants and children; can lead to kidney failure, transplantation, and/or dialysis

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13
Q

Antifreeze poisoning can precipitate which type of stone?

A

Calcium oxalate stones because oxalate is a metabolite of ethylene glycol. Oxalate accumulation in large concentrations in blood –> filtered into kidney –> precipitated with Ca –> calcium oxalate stone

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14
Q

Fluid intake to produce UOP of 2-2.5 L/day reduces the incidence of new stones due to:

A

reduction in supersaturation of crystals

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15
Q

_______ reduces the 5 year risk of CaOx stone formation by 50%.

A

Salt intake of less than 2000 mg/day

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16
Q

Why does reduction of salt intake reduce calcium in the urine?

A

because transporters in the PT are not saturated; thus, more Na+ is reabsorbed in the PT, causing calcium to be passively reabsorbed with it = less calcium in urine

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17
Q

How do you treat calcium oxalate stones when a patient has hypercalciuria?

A
  • Do NOT decrease calcium intake (can have implications on bones)
  • Instead, use a thiazide diuretic to decrease calcium excretion in the urine (HCTZ, chlorthalidone)
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18
Q

How do you treat calcium oxalate stones when a patient has hypocitraturia?

A

Supplementation with citrate:

  • K-Citrate tabs increase urinary pH and calcium solubility
  • lemon juice=effective source of citrate
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19
Q

How do you treat calcium oxalate stones when a patient has hyperoxaluria?

A
  • Low-oxalate diet (avoid green beens, celery, chocolate, green onions, black tea, berries, orange and lemon peel, peanut butter)
  • Increase calcium intake (increased calcium in gut=increased binding to oxalate=less oxalate filtered into kidney)
  • Medications (Tums- calcium carbonate)
  • Increase fluids
  • Restrict vitamin C
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20
Q

Calcium phosphate stones form in ________ urine pH.

A

alkaline

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21
Q

Calcium phosphate stones are a common complication of __________.

A

distal RTA, meds (topiramate)

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22
Q

What do calcium phosphate stones look like on microscopy?

A

wedge-shaped prism and needle crystals

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23
Q

Why are calcium phosphate stones hard to treat?

A

They form in alkaline urine pH; therefore, alkalinization of the urine is not an effective treatment.

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24
Q

the only stones that are radiolucent on X-ray

A

uric acid stones and cystine stones

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25
Q

What do uric acid stones look like on microscopy?

A

rhomboid or rosettes

26
Q

Uric acid stones only form in ________ urine pH.

A

acidic

27
Q

Uric acid stones are a complication of which diseases?

A

obesity and diabetes

28
Q

How is obesity related to kidney stone formation?

A

Obesity is associated with a more acidic urine pH and increases in urinary uric acid excretion; thus, obesity increases the risk of developing uric acid stones.

29
Q

What are the predisposing factors of uric acid stones?

A
  • hot and arid climate (dehydration, low urine volume)
  • chronic diarrhea (systemic acidosis and low urine pH, as well as dehydration and low urine output)
  • hyperproduction of uric acid (gout, conditions with high cell turnover like AML and tumor lysis syndrome)
30
Q

Most uric acid stone formers have a urine pH of _____.

A

<6

31
Q

How does uric acid solubility change with urine pH?

A

solubility increases >10x when urine pH increases from 5 to 7

32
Q

What is the treatment for uric acid stones?

A
  • increase urine volume
  • reduce salt
  • reduce animal protein
  • treat metabolic syndrome
  • medications (first-line= potassium citrate to alkalize urine; second line= allopurinol or losartan to decrease production of uric acid)
33
Q

Struvite stones are made of what?

A

ammonium magnesium phosphate

34
Q

What do struvite stones look like on X-ray vs. microscopy?

A
  • X-ray: staghorn

- Microscopy: coffin lid

35
Q

Uric acid stones can only be visualized on:

A

CT and US (radiolucent on X-ray)

36
Q

What is the common cause of struvite stones?

A

Chronic upper UTI with urease-producing bacteria (Proteus, Haemophilus, Klebsiella, Ureaplasma, Staph saprophyticus) –> hydrolyze urea to ammonia, leading to persistently alkaline urine

37
Q

Struvite stones are more common in ______.

A

women

38
Q

How can future struvite stones best be prevented?

A

1) Eradicate infection of urease splitting bacteria w/ antibiotics
2) Completely remove all stones (including residual fragments)
3) Prevent future UTIs

39
Q

Struvite stones form in ______ urine.

A

alkaline

40
Q

How are cystine stones visualized on X-ray vs. CT?

A
  • X-ray: radiolucent

- CT: radiopaque

41
Q

What do cystine stones look like on microscopy?

A

hexagonal crystals

42
Q

Cystine stones are a result of which genetic condition?

A

Cystinuria, an autosomal recessive condition causing PCT dysfunction of reabsorption of cystine, as well as ornithine, lysine, and arginine (COLA). Cystine is poorly soluble, leading to precipitation as stones.

43
Q

What are the 2 main treatments of cystine stones?

A

1) Reduce supersaturation (by increasing fluid intake, restricting protein, reducing sodium, and alkalinizing urine)
2) Chelating agents (contain thiol, which reduces the disulfide bond of cystine and makes it more soluble)

44
Q

Cystine is only soluble under which 2 conditions?

A
  • low concentrations (of cystine)

- alkaline urine

45
Q

Chelating agents are an effective treatment option for which type of stone?

A

cystine stones

46
Q

What is the main chelating agent used to treat cystine stones (especially for refractory cases)?

A

Tiopronin

47
Q

When is a conservative approach to kidney stone management reasonable?

A
  • small stones (<5 mm)
  • distal urethral location
  • adequate pain control w/ analgesics
  • no associated UTI or obstruction
48
Q

What is the 3-part regimen to conservative management of stones?

A
  • analgesia w/ NSAIDs
  • oral fluid intake of 2-3 L/day
  • tamsulosin (alpha-1 antagonist that relaxes ureteral tone)
49
Q

When should there be procedural intervention for a stone?

A
  • larger stones (>5 mm)
  • not passing after 4 weeks of medical therapy
  • intractable pain
  • associated UTI or localized obstruction
50
Q

What are the surgical treatment options for kidney stones?

A
  • ESWL (lithotripsy - US wave crushes stones into smaller pieces that are easier to pass)
  • Ureteroscopy (better for stones that are far up, closer to bladder)
51
Q

What are the 2 key processes that make stones?

A
  • Supersaturation: when urine is supersaturated with stone constituents, stones form; free ion activity that determines supersaturation can be affected by many things, the most important of which is urine volume
  • Nucleation: process by which ions join together to form a solid phase; heterogeneous and homogeneous
52
Q

True or false: Imaging of stones requires contrast dye.

A

False!

53
Q

_______ is the body’s urine alkalinizer.

A

Citrate

54
Q

Losing weight helps decrease formation of which type of stone?

A

uric acid stones

55
Q

Incidence of kidney stones peaks at what age?

A

30s-40s

56
Q

Are kidney stones more common in men or women?

A

men (13%, compared to 5% of women)

*struvite stones are the exception (more common in women)

57
Q

Which race/ethnicity is more prone to developing kidney stones?

A

whites

58
Q

Baby formula contaminated with melamine was responsible for an epidemic of kidney failure in babies due to _______ stone formation.

A

uric acid

59
Q

Where in the renal parenchyma do stones form?

A

renal papillae

60
Q

a microscopic plaque of calcium deposited in the interstitial tissue of the renal papilla, thought to serve as a nidus for urinary stone formation (particularly CaOx stones)

A

Randall’s plaque

*MHD Exam 5 (14 decks)

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