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10. Urolitiasis (1063) > Kidney Stones > Flashcards

Kidney Stones Flashcards

1
Q

___ weather increases stone formation

A

hot

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2
Q

____% recurrence risk at 5 years

A

50-60

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3
Q

Immobilization leads to hyper____

A

hypercalciuria

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4
Q

_____ imaging prior to PCNL

A

Non-con CT

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5
Q

MUST obtain ____ before intervention to stratify infection risk

A

UA

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6
Q

Ureteral stones <10mm distally should be offered ____

A

alpha-blockers

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7
Q

Re-imaging prior to surgery if stone ____ OR would change management

A

moved/passed

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8
Q

Offer stone treatment if MET is not successful after ____

A

4- weeks

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9
Q

____ is the procedure with lowest morbidity & complication rate

A

ESWL

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10
Q

1st line therapy for mid or distal ureteral stones - ____

A

URS

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11
Q

____ is recommended to treat cystine or uric acid ureteral stones

A

URS

Cystine - not well broken down by ESWL

Uric Acid - radiolucent

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12
Q

Reasons to not stent

  1. No ____ injury
  2. No ____ stricture
  3. _____ contralateral kidney
  4. ____ AKI
  5. No planned 2nd stage URS
A
  1. No ureteral injury
  2. No ureteral stricture
  3. Normal contralateral kidney
  4. No AKI
  5. No planned 2nd stage URS
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13
Q

Pre-stenting should ____ be performed

A

NOT

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14
Q

Meds for stent discomfort

A

alpha-blocker

anti-muscarinics

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15
Q

With infection the first priority is _____

A

decompression of upper tract with stent vs PCN

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16
Q

In patients with <20mm of non-lower pole stones, you can offer ___ OR ____

A

ESWL or URS

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17
Q

Total stone burden >2 cm should be treated with ____

A

PCNL

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18
Q

For symptomatic, non-obstructing stones, you can off ____

A

stone treatment

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19
Q

May perform ____ when stone filled kidney has negligible function

A

nephrectomy

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20
Q

Offer ___ or ___ with symptomatic, <10mm lower pole stones

A

ESWL or URS

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21
Q

NTs are ____ in uncomplicated PCNLs

A

optional

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22
Q

Use ___ for irrigation for PCNL & URS

A

normal saline

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23
Q

May prescribe ____ to facilitate stone passage s/p ESWL

A

alpha-blocker

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24
Q

Do NOT use ____ with pts who have anatomic or functional obstruction

A

ESWL

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25
Q

____ stones should be treated regardless of symptoms

A

Staghorn

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26
Q

Children always need metabolic evaluation with a ____

A

24 hr urine

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27
Q

In pediatrics with total stones >20 mm, you can offer ___ or ____ with pre-stenting

A

PCNL

ESWL with pre-stenting

no distinction between lower pole

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28
Q

In pregnant pts with ureteral stones, you can offer ____ to pts who fail observation

A

URS

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29
Q

Safest time for stone surgery in pregnancy is ____ trimester

A

2nd

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30
Q

When fragments are present, should offer ____ treatment to render stone free

A

endoscopic

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31
Q

Abort procedure and obtain culture if ____ urine is encountered

A

purulent

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32
Q

In anti-coagulated pts, ____ is 1st line stone therapy

A

URS

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33
Q

Skin to stone distance >____cm is associated with SWL failure

A

10

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34
Q

BMI >____ may prohibit ESWL

A

30

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35
Q

Treatment for 1.8cm lower pole stone in horseshoe kidney

A

PCNL

36
Q

With ruptured calyx, you can ____

A

observe

37
Q

Stones resistant to ESWL

A

CaOx Monohydrate
Brushite
Cystine

38
Q

Risk factors for uric acid stone formation

A

T2DM

Obesity

39
Q

Risk factors for hydroxyapatite stone formation

A

RTA
HyperPTH
Medullary sponge kidney
Carbonic anhydrase inhibitor

40
Q

Pharmacologic therapy for hypercalciuria

A

Thiazide diuretic

41
Q

Pharmacologic therapy for hyperuricosuria

A

Allopurinol

in recurrent Ca++ stone formers

42
Q

Pharmacologic therapy for hypocitraturia

A

Potassium Citrate

43
Q

Repeat 24 hr urine s/p ____ of dietary or medical intervention

A

6 months

44
Q

Incidence of kidney stones peaks in the ___________ decades of life.

A

Fourth to sixth

45
Q

What is the concentration product?

A

A mathematical expression of the product of the concentrations of the pure chemical components (ions or molecules) of the salt.

46
Q

What is the thermodynamic solubility product?

A

The point at which the dissolved and crystalline components are in equilibrium for a specific set of conditions.

Addition of further crystals to the saturated solution will cause the crystals to precipitate unless the conditions of the solution, such as pH or temperature, are changed.

47
Q

Citrate: inhibitor MOA

A

Inhibits calcium oxalate and calcium phosphate stone formation:

  • Complexes with calcium, thereby reducing the availability of ionic calcium to interact with oxalate or phosphate
  • Directly inhibits the spontaneous precipitation of calcium oxalate
  • citrate prevents heterogeneous nucleation of calcium oxalate by monosodium urate
48
Q

Magnesium: inhibitor MOA

A

Complexation with oxalate, which reduces ionic oxalate concentration and calcium oxalate supersaturation

49
Q

Nephrocalcin: inhibitor MOA

A
  • Strongly inhibits the growth of calcium oxalate monohydrate crystals
  • Inhibit nucleation and aggregation of calcium oxalate crystals
50
Q

Tamm-Horsfall protein: inhibitor MOA

A
  • MOST ABUNDANT PROTEIN in urine

- Potent inhibitor of calcium oxalate monohydrate crystal aggregation, but not growth

51
Q

Osteopontin/uropontin: inhibitor MOA

A

Inhibit nucleation, growth, and aggregation of calcium oxalate crystals, as well as to reduce binding of crystals to renal epithelial cells in vitro

52
Q

Bikunin: inhibitor MOA

A

Strong inhibitor of calcium oxalate crystallization, aggregation, and growth in vitro

53
Q

What is the matrix in renal calculi?

A

Renal calculi consist of crystalline and noncrystalline components. The noncrystalline component is termed matrix, which typically accounts for about 2.5% of the weight of the stone.

Composed of a combination of mucoproteins, proteins, carbohydrates, and urinary inhibitors.

54
Q

What percent of dietary Ca is absorbed in the intestine?

A

Between 30% and 40% of dietary calcium is absorbed from the intestine, with MOST being absorbed in the small intestine and only approximately 10% absorbed in the colon

55
Q

Most POTENT stimulator of intestinal Ca absorption

A

CALCITRIOL 1,25(OH)2D3 - Active form of vitamin D

Decrease in serum Ca –> PTH secretion –> conversion of 25-hydroxyvitamin D3 to calcitriol –> enhancement of Ca absorption

56
Q

Calcitriol acts on the ____ and ____, in addition to its action in increasing intestinal calcium absorption.

A

Bone: along with PTH, promotes the recruitment and differentiation of osteoclasts that subsequently mobilize calcium from the bone.

Kidney: Calcitriol modulates parathyroid function by inhibiting synthesis of PTH through enhanced vitamin D receptor and calcium- sensing receptor (CaSR) expression in the parathyroid glands –> PTH increases renal Ca reabsorption and enhances phosphate secretion

57
Q

PTH action on the bone and kidneys

A

PTH: stimulates mobilization of calcium from bone through the action of osteoclasts, further raising serum calcium and phosphorus.

Kidneys: enhances renal calcium reabsorption and reduces renal tubular reabsorption of phosphate

58
Q

Primary regulator of renal phosphate handling

A

Regulation of renal phosphate handling is primarily by way of PTH, which inhibits renal tubular reabsorption of filtered phosphate.

59
Q

Oxalate is absorbed in the _______

A

Oxalate absorption occurs throughout the intestinal tract, with about half or more occurring in the small intestine and half in the colon.

60
Q

Most potent oxalate-degrading bacterium

A

Oxalibacter formigenes

61
Q

Most common component of urinary calculi

A

Calcium: a major constituent of nearly 80% of stones

62
Q

Most common abnormality in calcium stone formers

A

Hypercalciuria:

  • Greater than 200 mg of urinary calcium/day after adherence to a 400-mg calcium, 100-mg sodium diet for 1 week
  • Greater than 4 mg/kg/day or greater than 7 mmol/ day in men and 6 mmol/day in women
63
Q

What are the types of hypercalciuria?

A

ABSORPTIVE: Increased intestinal absorption of Ca –> transient increase in serm CA –> suppressed PTH –> increased renal filtration of Ca –> hypercalciuria

RENAL: Impaired renal tubular reabsorption –> elevated urinary Ca –> secondary hyperparathyroidism (serum Ca levels remain normal)

RESORPTIVE: Primary hyperparathyroidism (parathyroid adenoma) –> excess PTH –> excess bone resoprtion –> increase renal calcitriol –> enhanced intestinal absorption of calcium –> elevated serum and urine Ca and reduced Phos levels

64
Q

Malignancy-related hypercalcemia

A

Tumors in patients with humoral hypercalcemia produce a PTH-related protein (PTHrP).

Like PTH, PTHrP increases renal calcium absorption and stimulates osteoblasts

65
Q

Hyperoxaluria

A

Urinary oxalate greater than 40 mg/day, leads to increased urinary saturation of calcium oxalate and subse- quent promotion of calcium oxalate stones

66
Q

Primary hyperoxaluria

A

Autosomal recessive inherited disorders in glyoxylate metabolism by which the normal conversion of glyoxylate to glycine is prevented, leading to preferential oxidative conversion of glyoxylate to oxalate, an end product of metabolism

67
Q

Enteric hyperoxaluria

A

Most common cause of acquired hyperoxaluria

Chronic diarrheal states –> fat malabsorption results in saponification of fatty acids with divalent cations such as Ca and Mg –> reduced CaOx complexation –> increased pool of oxalate for reabsorption

68
Q

Dietary hyperoxaluria

A

Overindulgence in oxalate-rich food: nuts, chocolate, brewed tea, spinach, potatoes, beets, rhubarb

Severe Ca restriction –> reduced intestinal binding of oxalate, increased intestinal oxalate absorption

69
Q

Hyperuricosuria

A

Urinary uric acid >600mg/day

Increases levels of monosodium urate –> promote CaOx crystallization through heterogenous nucleation or epitaxial crystal growth

Sodium urate: adsorbs inhibitors of crystallization!

70
Q

Hypocitraturia

A

Urinary citrate <320mg/day
Acid-base state = primary determinant of urinary citrate excretion

Metabolic acidosis: reduces citrate levels secondary to enhanced renal tubular reabsorption and decreased synthesis of citrate in peritubular cells

71
Q

Causes of hypocitraturia

A

Pathologic states associated with ACIDOSIS:

  • Distal RTA
  • Chronic diarrheal states
  • Excess animal protein
  • Diuretics
  • ACE
  • Strenuous exercise - lactic acidosis
72
Q

RTA

A

Metabolic acidosis resulting from defects in renal tubular hydrogen ion secretion or bicarbonate reabsorption

73
Q

Type 1 (distal) RTA

A

Most common form of RTA , associated with STONE FORMATION

Dysfunction of the α-type intercalated cells, which secrete protons into the urine via an apical H+-ATPase –> failure to acidify urine

HYPERCALCIURIA
HYPOCITRATURIA
INC. URINARY pH

CALCIUM PHOSPHATE most comon

74
Q

Type 2 (proximal) RTA

A

Defect in HCO3− reabsorption associated with initial high urine pH that normalizes as plasma HCO3− decreases and the amount of filtered HCO3− falls –> bicarbonaturia –> reduced net acid excretion + metabolic acidosis

Stones: UNCOMMON because of normal urinary citrate excretion

75
Q

Type 4 (distal) RTA

A

Associated with chronic renal damage: usually in interstitial renal disease and diabetic nephropathy.

Reduced glomerular filtration –> hyperkalemic hyperchloremic met acidosis

Can still generate acidic urine in response to acid challenge

76
Q

Hypomagnesiuria

A

Magnesium complexes with oxalate and calcium salts, and therefore low magnesium levels result in reduced inhibitory activity.
Low urinary magnesium is also associated with decreased urinary citrate levels, which may further contribute to stone formation

77
Q

Uric acid stone formation: LOW or HIGH pH?

A

LOW urine pH is thought to be a risk factor for uric acid, calcium oxalate, and mixed calcium and uric acid stones.

At pH 5, even modest amounts of uric acid exceed uric acid solubility

78
Q

Three main determinants of URIC ACID stone formation

A

Low urine pH
Low urine volume
Hyperuricosuria

79
Q

Infection stones are primarily composed of ______ and _____.

A

Infection stones are composed primarily of magnesium ammonium phosphate hexahydrate (MgNH4PO4 • 6H2O) but may in addition contain calcium phosphate in the form of carbonate apatite (Ca10[PO4]6 • CO3)

80
Q

Struvite stones (MAP) occur only with infection by _____

A

Urea-splitting bacteria

81
Q

Most common urease-producing pathogens (4)

A 
Proteus
Klebsiella
Pseudomonas
Staphylococcus
E. coli: only rare species produce urease
82
Q

Most common organism associated with infection stones

A

Proteus mirabilis

83
Q

TRUE or FALSE: Struvite stones are more common in women than men

A

TRUE.

Because infection stones occur most commonly in those prone to frequent urinary tract infections, struvite stones occur more often in women than men by a ratio of 2 : 1

84
Q

Ammonium urate stones

A

Radiolucent!

Patients with chronic diarrhea, inflammatory bowel disease, ileostomy bowel diversions, laxative abuse, recurrent urinary tract infection, and recurrent uric acid stone formation

85
Q

Renal stones in pregnancy

A

Renal blood flow increases, leading to a 30% to 50% rise in glomerular filtration rate, which subsequently increases the filtered loads of calcium, sodium, and uric acid.

10. Urolitiasis (1063) (8 decks)

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