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10. Urolitiasis (1063) > Urolithiasis > Flashcards

Urolithiasis Flashcards

1
Q

What is the two tumb rules when it comes to positioning of laser fibers in the urether?

A

Aim at 1/4 of the diameter of the stone

When you see the fiber your scope is safe

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2
Q

When was ESWL approved for urolithiasis?

A

1986

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3
Q

Indications for ESWL

A

non obese patient
stones ≤ 2 cm
pelvic stones
stone in upper and middle calyceal groups

less effective on ureteral stones

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4
Q

What are “hard stones”?

A

Density >1000 HU

Calcium oxalate
monohydrate
cystine
brushite

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5
Q

Prognostic factors for successful ESWL-treatment:

A 
Number of stones
Lower pole?
Composition (<1000 HU?)
UT Anatomy
BMI >30
Duration of obstruction
Available equpment
Experience of operator
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6
Q

What are the benefit of ESWL for pediatric patients?

A 
minimally invasive
high stone free rates
easier passage of fragments
low complication rate
no renal damage
need for stenting rare
  • general anasthesia in children < 10 years
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7
Q

Contraindications for ESWL:

A 
Preganancy
Anticoagulants
Uncontrolled urinary infection
Severe skeletal anomalies
Morbid obesity
Arterial anerurysm (in the vicinity)
Anatomical obstruction distally to the stone
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8
Q

ESWL-complications:

A 
Steinstrasse 4-7%
Development of the residual stones 21-59%
Renal colic 2-4%
Infection (sepsis 1-2,7%)
Concussion 
Hematuria
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9
Q

What is the use for double J-stents in ESWL?

A

Prevents obstruction and colic

Does not reduce steinstrasse and infections

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10
Q

What is the effect of α1-blockers on ureteral lithiasis?

A

Reduction of time for the expulsion of fragments
Reduction of the renal colic episodes
Increase of SFR

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11
Q

When should antibiotics be used in prophylaxis for ESWL?

A

Internal stent placement
Increased bacterial burden (nephrostomy tube, indwelling catheter, infectious stones)
Positive culture

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12
Q

What are the biggest risk factors for kidney stones?

A

Male
Caucasian
Old age
Overweight/obese

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13
Q

Name 3 non-infectious stones:

A

Calcium oxalate
Calcium phosphate
Uric acid

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14
Q

Name 3 infectious stones:

A

Magnesium ammonium phosphate
Carbonate apatitie
Ammonium urate

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15
Q

Name 3 stones caused by genetic disorders:

A

Cystine
Xantine
2,8-Dihydroxyadenine

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16
Q

How are kidney stones mostly composed (in %)?

A 
calcium-based 78-85%
uric acid 5-10%
struvite 1-4%
cystine 1%
drugs/metabolites <1%
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17
Q

Name 3 kidney stones caused by drugs:

A

Indinavir
amoxicillin
ciproloxacin

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18
Q

When should stone analysis be performed?

A

First stone

and

recurrent stones despite drug therapy
early recurrence after complete stone clearance
late recurrence after long stone-free period because composition may change

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19
Q

What health risk factors is urolithiasis associated with?

A 
diabetes
obesity
metabolic syndrome
osteoporos
cardiovascular pathologies
renal failure
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20
Q

What is the stone recurrence rate at 2, 5, 10 and 15 years?

A

11%
20%
31%
39%

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21
Q

How common is hightly recurrent stone disease?

A

~10%

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22
Q

When taking a medical history of a stone forming patient what should be included?

A

Stone history
Dietary habits
Medication charts

heredity
IBD
malignancies
gout
obesity
diabetes
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23
Q

What diagnostic imaging should be performed on a stone forming patient?

A

Ultrasound
Enhanced helical CT
Determination av Hounsfield units

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24
Q

What blood analysis’ should be performed on a stone forming patient?

A

Creatinine
Calcium
Uric acid

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25
Q

What urine analysis’ should be performed on a stone forming patient?

A 
pH
dipstick test
urine culture
microscopy of urinary sediment
cyanide nitroprusside test (cystine)

2 x 24 hour collection
any time for noobstructing stones, > 6 weeks after stone removal/passage

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26
Q

What should stone forming patientes be adviced when it comes to fluid intake?

A

Aim for urine volume >2,5L

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27
Q

What are the dietary recommendations for stone forming patients?

A 
Normal calcium intake
Low sodium (Na(Cl)
Low animal protein intake
Low fat intake
Moderate oxalate intake
Reduce simple sugar intake
Eat vegetables and fruit

Fluids for urine volume >2L

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28
Q

What causes Uric acid stones?

A

LOW URINE PH + HYPERURICOSURIA

insuline resistance excess purine intake
metabolic syndrome proliferative syndromes
obesity gout
type 2 diabetes type 2 diabetes
diarrhea uricosuric drugs

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29
Q

How do you treat Uric acid stones?

A 
Increase fluid intake
Urine alkalinization (Potassium citrate)
Decrease protein intake
Decrease sugar intake
Allopurinol
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30
Q

Why is hypocitraturia bad?

A

Acidic pH consumes citrates and favour calcium oxalate stones

Citrate is a potent inhibitor of cristallization

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31
Q

What can Thiazides cause?

and by what mechanism?

A

Hypoctiraturia

Thiazides –> hypokalemia —> intracellular acidosis—> inhitibs synthesis and promotes citrate reabsorption into the cell

=treat hypokalemia

(Potassium=Kalium)

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32
Q

Name a source of potassium that can lower the risk for stone disease?

A

Orange juice

cranberry and grapefruit juice can increase the risk

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33
Q

What can cause Hyperoxaluria?

A

Increased oxalate intake
High urinary concentration because of low urine volume
Reduced calcium intake (calcium decreases oxalate absorbtion)

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34
Q

How do you treat Hyperoxaluria?

A 
Increase fluid intake
Eat less oxalates and fat
Increase calcium intake
Vitamin B6
Correction of bowel pathology when possible
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35
Q

What can cause Hypercalciuria?

A 
Low diures
High calcium intake
High protein intake 
High salt intake
Metabolism
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36
Q

How do you treat Hypercalciuria?

A

More fluids
Limit calcium intake
Limit protein intake
Limit salt intake

Thiazide diuretics—>
increase calcium reabsorption
OBS give potassium supplementation to prevent Hypokalemia and hypocitraturia

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37
Q

What can cause Cystine stones?

A 
Low diures
Low urinary pH
High urinary cystine levels
-high methionin food (parmesan, eggs, horse-meat...)
-high protein intake
-high salt intake
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38
Q

How do you treat Cystine stones?

A 
Increase fluid intake
Alkalinization (potassium citrate)
Medicate with Tipronine (breaks cystine in two)
Lower intake of methionin
Reduce protein intake
Reduce salt intake
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39
Q

How do you treat infectous stones?

A

Remove stone

Treat UTI

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40
Q

Does position of the patient matter when performing PNL?

A

More a preference of the surgeon

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41
Q

Why is a posterior calyx preferable for acess when perorming PNL?

A

There is an avascular fielt known as Brodels bloodless line between the anterior and posterior divisions

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42
Q

What is the risk when using balloon dilators for access when performing PNL?

A

They can dislocate the stone out of the system

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43
Q

What are the major complications of PCNL?

A 
Rupture of collecting system
Hemorrhage
Pleural injury
Injury to adjacent organs
Fever and sepsis
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44
Q

PCNL stands for:

A

Percutaneous Nephrolithonomy also PNL

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45
Q

What are the indications for open or laparoscopic surgery for stones?

A 
Anatomical abnormalities:
-horseshoe kidneys
-malrotated kidneys
-UPJO with stones
-ectopic kidneys
Stones in symptomatic diverticula
When other treatment options are unavailable or have failed
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46
Q

How often should a stone that has not been treated be checked?

A

Every 6 months initially, than yearly

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47
Q

What is mandatory before endoscopic stone treatment?

A

Urine culture/microscopy
Treatment of UTI
Peri-operative antibiotic prophylaxis

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48
Q

What is the mean ureteral diameter?

A

10F

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49
Q

What is the mean ureteral length?

A

30 cm

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50
Q

How much better are digital systems for endoscopic stone removal?

A

saves 20-25% of time

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51
Q

What is normal renal pelvic pressure (RPP)?

A

5-15 mm Hg

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52
Q

When will you damage the fornix with elevated renal pelvic pressure?

A

At 80-100 mm Hg

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53
Q

What does elevated renal pelvic pressure (RPP) cause?

A

epithelial damage
resorption of irrigation fluid (containing bacteria and endotoxins)
pyelo-interstitial or pyelo-lymphatic/pyelo-tubular reflux–> nephrotic damage —> renal scarring

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54
Q

Late complications of URS:

A

ureteral stricture

persistent vesicoureteral reflux

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55
Q

Early complications of URS:

A

ureteral stripping
guidewire under the mucosa
perforation
mucosal injury etc

hypothermia
bleeding
push up of the stone
hematuria
renal colic
fewer or urosepsis
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56
Q

Problems with stents:

A 
Stent related symptoms
Encrustation
Infection
Migration
Hyperplastic reaction
Extrinsic mechanical pressure
Long-term patency
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57
Q

What is different with stents in pregnant women?

A

A higher tendency for ureteral sten ecrustation

Change stent every 2 months

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58
Q

Symptoms from stents:

A

Frequency
Dysuria
Urgency
Suprapubic pain

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59
Q

What is the depth of penetration of a Ho:YAG-laser?

A

0,4 mm

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60
Q

What is true for Retropulsion and stone treatment using Ho:YAG-laser?

A

More energy = more Retropulsion

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61
Q

What are the settings for DUST-vaporisation?

A

Long Pulse 800 µsec
Low Energy 0,5 J
High Frequency 15-10 Hz

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62
Q

What are the settings for Fragments?

A

Short Pulse 200 µsec
High Energy 1,5-2 J
Low Frequency 5 Hz

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63
Q

What is the Moses technology?

A

The laser emits part of the energy to create an initial bubble,
the remaining energy is discharged once the bubble is formed, so that it can pass through the already formed vapor channel

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64
Q

Is bigger laser fibres better?

A

No size does not affect fragmentation efficiency
small fibres gives less retropulsion
small fibres gives more space in the working channel

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65
Q

Should laser fibres be stripped or unstripped?

A

Better performance if stripped

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66
Q

When is the laser fibre most damaged?

A

Hard stones
High energy
Short pulse duration

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67
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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68
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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69
Q

What is first line imaging for suspected stones in children?

A

KUB U/S

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70
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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71
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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72
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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73
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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74
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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75
Q

What are side effects of thiazides?

A

Hypokalemia, weakness, fatigue and ED

76
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.

77
Q

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

A

Potassium citrate (K-citrate)

78
Q

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

A

Sodium citrate

79
Q

What are side effects of potassium citrate?

A

Hyperkalemia, peptic ulcers, diarrhea and metabolic acidosis

80
Q

What is the adult dose of potassium citrate?

A

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

81
Q

What is the most common metabolic abnormality in stone formers?

A

Hypercalciuria

82
Q

What is the most common stone composition in industrialized countries?

A

Calcium oxalate

83
Q

What is the most common cause of urolithiasis?

A

Dehydration

84
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

85
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

86
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.

87
Q

What are 3 unique characteristics of uric acid stones?

A

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

88
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
89
Q

What are unique characteristics of cystine stones?

A
  1. Cause cystinuria (usually homozygotes)

2. Form in acidic urine and dissolve with urinary alkalization

90
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
91
Q

What are unique characteristics of ammonium acid urate stones?

A

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

Radiolucent

92
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

93
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.

94
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
95
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
96
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.

97
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
98
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)

99
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

100
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)

101
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
102
Q

What UTI organisms produce urease?

A
  1. Proteus
  2. Klebsiella
  3. Serratia
  4. Staphylococcus
  5. Morganella
  6. Providencia
  7. Enterobacter
103
Q

What types of stones are associated with UTI?

A

Struvite, matrix, carbonate apatite

104
Q

What changes does acidosis cause in urinary composition?

A
  1. Increased urine calcium
  2. Increased urine phosphate
  3. Decreased urine citrate
105
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

106
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)

107
Q

Which stones form in alkaline urine?

A
  1. Matrix stones
  2. Stones that contain phosphate, carbonate or ammonia)
    [struvite, calcium phosphate, calcium carbonate]
108
Q

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

A

Calcium oxalate, hippuric acid

109
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)
110
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)
111
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.

112
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)
113
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
114
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

115
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
116
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

117
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.

118
Q

When should magnesium be give as a stone formation inhibitor?

A

Most useful in patients with hypomagnesuria and calcium stones

119
Q

What is the main side effect of magnesium supplementation?

A

Diarrhea

120
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.

121
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)

122
Q

What are side effects of AHA?

A

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

123
Q

How do you define hypercalciuria?

A

Urinary calcium > 200mg/day

124
Q

What are the 4 different types of hypercalciuria?

A
  1. Absorptive
  2. Renal
  3. Resorptive
  4. Unclassified
125
Q

What is the pathophysiology of ABSORPTIVE hypercalciuria?

A

Primary mechanism is excess intestinal absorption of calcium

126
Q

What is the pathophysiology in RENAL hypercalciuria?

A

Primary mechanism is impaired renal tubular reaborption of calcium

127
Q

What is the pathophysiology in RESORPTIVE hypercalciuria?

A

Primary mechanism is hypersecretion of PTH. (hyperparathyroidism)

128
Q

What is the definition of hypomagnesuria?

A

Urinary magnesium < 50mg/day

129
Q

How do you treat hypomagnesuria?

A

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

130
Q

How do you define hyperuricosuria?

A

Urinary uric acid > 600mg/24h

131
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.

132
Q

Most common metabolic abnormality, type of stone, and cause of urolithiasis in the US:

A
  1. Metabolic abnormality: hypercalciuria
  2. Type of stone in industrialized countries: calcium oxalate
  3. Cause: dehydration
133
Q

Calcium oxalate stones

A

Most common renal and bladder stones in adults, children, intestinal bypass, IBD, and renal failure
Most common cause = dehydration
Forms in urine with wide range of pH
Radio-opaque

Calcium oxalate monohydrate = whewellite (crystals are ovals and dumbbells)
Calcium oxalate dihydrate = weddellite (crystals are envelopes and octahedrons)

134
Q

Calcium phosphate stones

A

More common in patients with hyperparathyroidism, RTA type 1, medullary sponge kidney, and carbonic anhydrase inhibitor use
Formed in alkaline urine
Radio-opaque
Mineral name = apatite

Crystal shape = powder like and often causes cloudy urine

135
Q

Uric acid (urate) stones

A

Normally have normal serum and urine uric acid levels
Most common cause = dehydration
Forms in acidic urine (usually pH <6.0)
Radiolucent (can’t see)

Dissolves with urinary alkalinization

Stone shape = parallelograms, double headed arrows, some in rosettes

136
Q

Magnesium ammonium phosphate (also called struvite or triple phosphate)

A

Most staghorn calculi are composed of struvite
Most common cause = UTI
Forms in alkaline urine
Radio-opaque
Dissolves with urinary acidification

Crystal shape = coffin lids

137
Q

Stones that form in alkaline urine

A

Struvite
Calcium phosphate
Matrix

138
Q

Cystine Stones

A

Cause - cystinuria (usually homozygotes)
Forms in acidic urine
Radiopaque
Dissolves with urinary alkalinization

Crystals = regular hexagons

139
Q

Matrix Stones

A

Most common cause = UTI (Proteus)
Forms in alkaline urine
Radiolucent

140
Q

Ammonium acid urate

A

Common causes = intestinal malabsorption, UTI, phosphate deficiency,
Radiolucent

141
Q

Protease inhibitor stones

A

Stones from precipitated drug - Indinavir, nelfinavir
Radiolucent and not visible on non-contrast CT scan
Forms in urine with pH of 5 or less

Acidifying urine to dissolve stones not practical because of extremely low pH required

142
Q

List of radiolucent stones

A

Uric acid (urate)
Xanthine
Matrix
Ammonium urate
Protease inhibitor stones
Silica

143
Q

Urine chemistry abnormalities that would PROMOTE stone formation

A

Hypercalciuria
Hypocitraturia
Hyperoxaluria
Hyperuricosuria
Hypomagnesiuria
Xanthinuria

144
Q

High sodium intake increases stone risk by:

A

Increasing urinary calcium and decreasing urinary citrate

145
Q

Organic inhibitors of crystallization

A

Citrate - decreases calcium stone formation by complexing with calcium and lowering calcium saturation, also directly inhibits calcium crystallization

Urea - decreases uric acid stone formation by increasing the solubility of uric acid (no influence on calcium stone formation)

Others: nephrocalcin, Tamm-Horsfall protein, calgranulin, GAGs, bikunin and uropontin (a form of osteopontin)

146
Q

Inorganic inhibitors of crystallization

A

Pyrophosphate - no way to increase this in the urine

Magnesium - increases solubility of calcium, phosphate, and oxalate

Trace elements, especially zinc

147
Q

How UTI Increases Stone Risk

A
  1. UTI causes hypocitraturia
  2. Urease producing organisms split urinary urea into ammonia and bicarbonate, which alkalized urine and increases the risk of stones formed in alkaline urine, especially struvite
  3. UTI may decrease ureteral peristalsis
148
Q

Urease producing bacteria

A

Proteus
Klebsiella
Serratia
Staphylococcus
Morganella
Providencia
Enterobacter

149
Q

Stones often associated with UTI

A

Struvite
Matrix
Carbonate apatite
Ammonium urate

150
Q

Acidosis increases stone risk.
Acidosis causes the following changes in urinary composition:

A

Increased urine calcium
Increased urine phosphate
Decreased urine citrate

Prolonged acidosis causes bone demineralization, which increases calcium delivery to the kidney and results in hypercalciuria

151
Q

Medications that may lead to urolithiasis

A

Vitamin C - metabolized to oxalate, increases urinary oxalate

Vitamin D (high doses) - increases calcium absorption, which increases calcium to kidney

Triamterene (diuretic) - precipitates in urine and forms radiolucent stones

Protease inhibitors (Indinavir and nelfinavir) - precipitate and forms radiolucent stones

Furosemide - increases calcium excretion in urine

Acetazolamide - carbonic anhydrase inhibitor creases a renal tubular acidosis and increases risk of calcium stones.
-Can be used to prevent uric acid and cystine stones (when citrate does not adequately alkalinize urine, it can be added to increase the urine pH)

Topiramate - stones composed of calcium phosphate

Zonisamide

152
Q

Type I (distal) renal tubular acidosis

A

Impairment in hydrogen ion secretion in the distal tubule, resulting in a persistently high urine pH (> 5.5) and systemic acidosis

Plasma bicarbonate is frequently < 15 mEq/L (15 mmol/L), and hypokalemia, hypercalciuria, and decreased citrate excretion are often present

Nephrocalcinosis and nephrolithiasis are possible complications of hypercalciuria and hypocitraturia if urine is relatively alkaline

153
Q

Oral medication for urinary alkalinization

A

Citrate and bicarbonate prevent stones by correcting acidosis, increasing urinary pH and increasing urinary citrate

Oral citrate is changed to bicarb ny the liver (doesn’t actually deliver citrate to kidney)

154
Q

Most common stone compositions in patients with gout?

A

Calcium oxalate monohydrate (45%)
Uric acid (52%)

155
Q

Medical conditions that increase risk of overall stone disease

A

Obesity
HTN
Diabetes
Hyperthyroidism
Gout
RTA type I
Bone disease
Primary hyperparathyroidism
Malabsorptive GI states

156
Q

Nutritional factors associated with stone formation

A

Calcium intake below or highly above the recommended dietary allowance
High sodium intake
Low fluid intake
Low fruit and vegetable intake
High intake of animal-derived purines

157
Q

Serum studies to order in screening evaluation of stone formers

A

Electrolytes: sodium, potassium, chloride, bicarbonate
Calcium
Creatinine
Uric acid

158
Q

When to suspect primary hyperthyroidism

A

Serum calcium is high or high normal

Predominantly calcium phosphate stones

Elevated urinary calcium

If suspected, get intact PTH
- Mid-range PTH in the face of higher serum calcium (inappropriately normal PTH)
- High or high-normal PTH when vitamin D levels are low

(The diagnosis of primary hyperparathyroidism (PHPT) is usually made by finding a PTH concentration that is frankly elevated or within the normal range but inappropriately normal given the patient’s hypercalcemia)

159
Q

Calcium phosphate stone composition more likely to be associated with the following medical conditions:

A

RTA Type 1
Medullary sponge kidney
Primary hyperparathyroidism
Use of carbonic anhydrase inhibitors

160
Q

Medical Management of Kidney Stones Guidelines:
For pts with calcium stones and relatively high urinary calcium, what should they do with their diet?

A

Guideline Statement 9:
Clinicians should counsel patients with calcium stones and relatively high urinary calcium to limit sodium intake and consume 1,000-1,200 mg per day of dietary calcium

Target of <2,300 mg sodium daily

161
Q

Med Mgmt Guideline Statement 10:
Clinicians should counsel patients with calcium oxalate stones and relatively high urinary oxalate to…

A

…limit intake of oxalate rich foods and maintain normal calcium consumption

162
Q

Med Mgmt Guideline Statement 13:
Clinicians should counsel patients with cystine stones to limit…

A

…sodium and protein intake

High fluid intake is particularly important for cysteine stone formers

Need to decrease urinary cysteine concentration to below 250 mg/L

163
Q

Med Mgmt Guideline Statement 14:
Clinicians should offer ————– to patients with high or relatively high urine calcium and recurrent calcium stones

A

Thiazide diuretics
(HCTZ, chlorthalidone, indapamide)

May need to supplement potassium as these cause hypokalemia

Should still restrict sodium in the diet

164
Q

Med Mgmt Guideline Statement 15:
Clinicians should offer ———— therapy to patients with recurrent calcium stones and low or relatively low urinary citrate

A

Potassium Citrate

Potassium citrate is preferred over sodium citrate as the sodium load may increase urine calcium excretion

Sodium bicarb or sodium citrate can be considered if patient is hyperkalemic

165
Q

Med Mgmt Guideline Statement 16:
Clinicians should offer allopurinol to pat

A
166
Q

Primary hyperparathyroidism:

A. Is more common in male patients
B. Is diagnosed with ultrasound of the neck
C. Has its peak incidence at about 50 years of age
D. Is combined with renal stones in more than 50% of patients

A

C. Has its peak incidence at about 50 years of age

167
Q

What is the next step after percutaneus nephrolithotomy (PNL) when bleeding occurs from the nephrostomy tract?

A. Endoscopic exploration
B. Continous irrigation from the nephrostomy tube
C. Insertion of a larger nephrostomy catheter
D. Closure of the nephrostomy catheter allowing tamponade

A

D. Closure of the nephrostomy catheter allowing tamponade

168
Q

A young woman is diagnosed with acute uncomplicated bacterial cystitis. Which pathogen is considered to be the most likely?

A. Escherichia coli
B. Proteus vulgaris
C. Enterococcus faecalis
D. Staphylococcus aureus

A

A. Escherichia coli

169
Q

Which organisms produce urease?

A. Proteus mirabilis, Klebsiella pneumonia, Pseudomonas aeruginosa
B. Escherichia coli, Proteus mirabilis, Klebsiella oxytoca, Candida humicola
C. Enterococcus faecalis, Proteus vulgaris, Providencia stuartii, Escherichia coli
D. Staphylococcus epidermis, Klebsiella oxytoca, Proteus vulgaris

A

A. Proteus mirabilis, Klebsiella pneumonia, Pseudomonas aeruginosa

170
Q

Which of the following Stones are radiolucent?

A. Uric acid, Amonium urate, Xanthine, 2.8-dihydroxyadenine
B. Uric acid, cystine, ammonium urate, Xanthine
C. Xanthine, Uric acid, Cystine, Apatite
D. Calcium phosphates, Apatite, Cystine, Uric acid

A

A. Uric acid, Amonium urate, Xanthine, 2.8-dihydroxyadenine

171
Q

Which kidney stone situation is the best indication for laparoscopic surgery?

A. Pelvic kidney
B. Horseshoe kidney
C. Ureteropelvic junction obstruction
D. Congenital megaureter

A

C. Ureteropelvic junction obstruction

172
Q

Which statement regarding general prevention of kidney stone recurrence is correct?

A. Calcium intake should be restricted
B. High intake of animal protein should be encouraged
C. A vegetarian diet decreases urinary pH because it is usually more acidic
D. Vegetable intake should be encouraged because of the beneficial effects of fibre

A

D. Vegetable intake should be encouraged because of the beneficial effects of fibre

173
Q

What is the main side effect of the antituberculosis drug Ethambutol!

A. Ototoxicity
B. Optic neuritis
C. Hepatotoxicity
D. Renal insufficiency

A

B. Optic neuritis

174
Q

Which of the following is NOT a complication of epididymo-orchitis?

A. Abscess formation
B. Testicular infarction
C. Testicular atrophy
D. Testicular torsion

A

D. Testicular torsion

175
Q

Chemolysis is an effective means of therapy for the following stones EXEPT:

A. Calcium phosphate stones
B. Cystine stones
C. Uric acid stones
D. Infection stones

A

A. Calcium phosphate stones

176
Q

Wich is the best method of imaging for renal tuberculosis?

A. Choline PET CT
B. CT urography
D. Renogram
C. Retrograde pyelography

A

B. CT urography

177
Q

A 19-year-old man presents with acute pain and swelling of his left scrotum. Which is the most common cause?

A. Viral epididymitis
B. Bacterial epididymitis
C. Viral orchitis
D. Bacterial orchitis

A

B. Bacterial epididymitis

178
Q

Thiazide diuretics are indicated in renal lithiasis to correct:

A. Hyperoxaluria
B. Idiopatic hypercalciuria
C. Hyperuricemia due to underexcretion
D. Hyperuricemia due to overproduction

A

B. Idiopatic hypercalciuria

179
Q

Which type of stone is related to Sarcoidosis?

A. Xanthine
B. Uric acid
C. Calcium oxalate
D. Magnesium ammonium phosphate

A

C. Calcium oxalate

180
Q

Hypercalciuria in primary hyperparathyroidism shows:

A. High serum calcium, high urine cyclic AMP, high intestinal calcium absorption
B. High serum calcium, high urine cyclic AMP, normal intestinal calcium absorption
C. High serum calcium, normal urine cyclic AMP, normal intestinal calcium absorption
D. High serum calcium, normal or low urine cyclic AMP, high intestinal calcium absorption

A

A. High serum calcium, high urine cyclic AMP, high intestinal calcium absorption

181
Q

A 45-year-old female patient comes to the emergency departement suffering right flank pain. A stone of 12 mm is identifiera in the renal pelvis of the right kidney. Which is the preferred approach for this patient?

A. PNL
B. ESWL
C. ESWL + PNL
D. Ureteroscopy

A

B. ESWL

182
Q

Which statement about Pyelonephritic scarring is correct?

A. It always progresses to end-stage renal failiure
B. It is a risk in patients with sterile low-grade vesico-ureteric reflux
C. It is a high-risk for patients with recurrent urinary tract infection (UTI)
D. It is most commonly developed in early childhood in the presence of reflux and UTI

A

D. It is most commonly developed in early childhood in the presence of reflux and UTI

183
Q

Which di-basic amino acid is the least soluble in urine?

A. Lysine
B. Cystine
C. Arginine
D. Ornithine

A

B. Cystine

184
Q

Which is the most effective treatment for calcium oxalate 3 cm stone in the renal pelvis?

A. Flexible ureteroscopy
B. Percutaneous nephrolithotripsy
C. Shock wave lithotripsy
D. Chemolysis

A

B. Percutaneous nephrolithotripsy

185
Q

Which antibiotic is contraindicated for prophylaxis in a newborn with prenatal hydronephrosis?

A. Amoxycillin
B. Trimethorprim sulfamethaxazole
C. Nitrofurantoin
D. Cefaclor

A

B. Trimethorprim sulfamethaxazole

186
Q

Which sign is indicative for SIRS (severe inflammatory response syndrome)?

A. WBC 11/nL
B. PCO2 30 mmHg
C. Respiration 18/min
D. Temperature 36.6C

A

B. PCO2 30 mmHg

10. Urolitiasis (1063) (8 decks)

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