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Year 3 - Met3b > Urinary Calculus Disease > Flashcards

Urinary Calculus Disease Flashcards

1
Q

What is a urinary calculus

A

A kidney stone

- It is a solid conglomeration of mineral salts, with or without associated urinary proteins that form in the kidneys

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2
Q

Name the types of urinary calculus

A 
•  Calcium Oxalate
- calcium phosphate/hydroxyapatite 
•  Urate
•  Magnesium Ammonium Phosphate
•  Cysteine

Others
• Xanthine
• Idinavir
• Matrix

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3
Q

Most kidney stones have a…

A

most kidney stones have a mixed composition.

- Urate crystals forming a nidus are relatively common, and the most common composition is a 80% CaOX:20% CaPO4 mix

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4
Q

What are the common types of urinary calculus

A 
•  Calcium Oxalate
- Calcium phosphate/hydroxyapatite 
•  Urate
•  Magnesium Ammonium Phosphate
•  Cysteine
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5
Q

What are the most common combination of kidney stones

A

most common composition is a 80% CaOX:20% CaPO4 mix

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6
Q

What is the commonest type of urinary calculus

A

Calcium oxalate (80%)

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7
Q

describe calcium oxalate

A
  • it is insoluble

- not forming this type of stone depends upon inhibitors

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8
Q

What are the two types of calcium oxalate

A
  • dihydrate which are softer (700HU)

- monohydrate which are extremely hard (1500 HU)

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9
Q

Does calcium oxalate stone show up on X rays

A

yes

- spikes and radio-opaque

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10
Q

What three conditions does calcium phosphate show up on

A

Classically associated with 3 conditions:
• Hyperparathyroidism
• Distal Renal Tubular Acidosis (Type 1)
• Medullary Sponge Kidney (MSK)

  • also associated with urinary stasis and partly with infection
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11
Q

Describe calcium phosphate

A
  • Show up well on X ray - smooth and large

- usually quite hard 1200 HU

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12
Q

What is urate stone formation related to

A
  • Stone formation is related to urinary pH (acidic urine forms stones)
  • associated with the metabolic syndrome and chemotherapy
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13
Q

Describe urate stones

A
  • Bright yellow stones formed from uric acid that has entered the urine
  • Soft (400 HU)
  • dissolvable - useful as you can dissolve them
  • cannot see them on an x ray
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14
Q

What stone is associated with metabolic syndrome

A

Urate stones

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15
Q

What are magnesium ammonium phosphate stones often called

A

Struvite stones

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16
Q

Describe magnesium ammonium phosphate stones

A
  • Infection related- due to bacteria meeting a surface and producing a low acidic pH such that Mg salts precipitate out of the urine onto the surface
    • Shows up slightly on X-rays - large
    • Usually relatively soft (200-600HU)
    • Often has associated Calcium Phosphate
    • Classically associated with Staghorn Calculi
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17
Q

What stone is often associated with calcium phosphate

A

Magnesium Ammonium phosphate

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18
Q

What are cysteine stones associated with

A

associated with cystinuira a genetic disorder

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19
Q

Describe cysteine stones

A
  • Poorly visible on x-ray & are Hard (1400HU) - yellow and crystalline
  • Produce white smoke and a rotten egg smell when they are lasered (Hydrogen sulphide)
  • Treated with medical dissolution therapy in specialist centres
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20
Q

describe matrix stones

A

proteinaceous material

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21
Q

describe idinavir stones

A

Do not show up on CT

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22
Q

Describe xanthine stones

A

almost anything with crystallise if the concentration is high enough

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23
Q

What stones do not show up on X ray

A

Urate stones

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24
Q

What does HU stand for

A

Hounsfield units

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25
Q

Describe the HU scale

A
  • Air is -1000HU
  • Water is 0HU
  • Bone is +1000HU
  • Soft tissue is +20HU
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26
Q

Name the two theories that are influencing stone formation

A
  • Free theory

- fixed theory

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27
Q

Describe free theory

A
  • The presence of stone constituents in the appropriate amounts and without enough inhibitors will form stones
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28
Q

What is free theory affected by

A
  • concentration of solutes
  • urine acidity
  • presence of formation inhibitors
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29
Q

What inhibits stone forming in free theory

A

inhibitors

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30
Q

Describe fixed theory

A

The energy required to make a crystal lance (enthalpy of formation) is lower if there is a surface to form them on e.g. Randall’s plaques

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31
Q

What does fixed theory depend on

A
  • depends upon a surface to form a lattice on
  • crystals
  • randall’s plaques
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32
Q

Describe how free theory produces stones

A
  • unsaturated urine
  • as the concentration increases the solubility product is reached
  • above the solubility product is the metastable region, there is saturated urine but crystals are prevented from forming by inhibitors
  • then as the concentration increases you reach the formation product
  • above the formation product is where crystals form spontaneously (spontaenous region)
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33
Q

in the free theory describe where non stone formers and stone formers sit

A

Non-stone formers
- these sit in the metastable region

Stone formers
- sit in both the metastable and spontaneous regions

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34
Q

Name some inhibitors in the free theory

A

These form soluble complexes with promoting ions

  • Citrate - calcium citrate is soluble
  • Magnesium - magnesium oxalate is soluble
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35
Q

What is the treatment for stones formed by free theory

A

decrease concentration by increasing the fluid intake

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36
Q

Describe the fixed theory

A
  • there is high levels of energy needed to form a crystal lattice
  • but much lower levels of energy is needed to form a crystal lattice on a rough surface

This rough surface can be due to

  • other crystals such as urate
  • can also be due to presence of sub urothelial deposits known as randall’s plaques

example
- calcium phosphate crystals form at the base of the loop of hence which ulcerates the urothelium creating a rough surface for crystal formation

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37
Q

Why is urate stone formation different

A
  • part of both free and fixed theory
  • pH dependent (free theory)
  • presence of urate crystals act as a nidus for stone formation (fixed theory)
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38
Q

When do urate crystals form

A
  • When the urine pH is the same as the pKa value at 5.4, urate cyrstals can form which can be independent of the concentration
  • there is a second pKa value at 10.3
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39
Q

fixed and free theories are not …

A

mutually exclusive

- e.g. urate and calcium oxalate crystals

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40
Q

What is the treatment of urate crystals

A
  • the treatment of urate stone formation is therefore alkalisation of urine - including drinking more liquid
41
Q

What are the two ways in which calcium oxalate stones form

A
  • Randall’s plaque

- Duct of bellini “plugs”

42
Q

Describe the two ways in which calcium oxalate stones form

A

Randall’s plaques:
• CaPhos forms in the intersFFum of the
kidney
• Urothelium “ulcerates” exposing plaque to urinary surface

Duct of Bellini “plugs” • Stones formed within the tubules
• Duct of Bellini narrows
• Stones gets “stuck” at papillary surface

43
Q

Name some causes of hypercalaemia

A
  • Hyperparathyroidism
  • Sarcoidosis
  • Excessive vitamin D
44
Q

Where is oxalate found

A
  • found in our diet from a host of sources
  • oxalate is created from endogenous sources in the liver as part of glycolate metabolism
  • Vitamin C is converted to oxalate
45
Q

Where is oxalate absorbed

A

Primarily from the colon

46
Q

what does calcium prevent oxalate from doing

A
  • calcium binds oxalate in the gut and prevents it from being absorbed
47
Q

What can cause enteric hyperoxaluria

A

Malabsorption from any cause, such as coliFs, especially crohns disease, or jejunoileal bypass surgery, can result in enteric hyperoxaluria

  • free fatty acids bind to and precipitate calcium
  • bile salts increase colonic absorption of oxalate and perhaps decrease bacteria that would otherwise breakdown oxalate
48
Q

What are dietary sources of unopposed oxalate

  • High levels
  • Moderate levels
  • Low levels
A

High

  • Rhubarb
  • Spinach
  • Swiss chard
  • Beetroot

Moderate

  • Okra
  • sweet potato
  • dark chocolate
  • Nuts
  • Pak Choi
  • Parsnips

Low

  • carrots
  • apples
  • sprouts
  • berry fruits
  • leeks
  • brocooli
  • chives
  • green beans
  • cranberries
49
Q

Name a stone inhibitor

A

Tamm Horsfall Protein (uromodulin)

50
Q

How does Tamm Horsfall Protein work

A
  • Prevents it binding to renal epithelial cells = potential nidus ‘flushed away’
  • reduces “free” calcium on crystal for group
51
Q

What does mutation on Tamm Horsfall Protein do

A
  • Leads to familial juvenile hyperuremic nephropathy

- leads to medullary cystic kidney disease 2 (both have increased stone formation/nephrocalcinosis)

52
Q

What does Tamm Horsfall Protein also do

A
  • Prevents some bacterial to attach to epithelium (reduces UTI from E.coli
53
Q

How does meat increase the risk of stones

A
  • Meat contains huge levels of oxalate but also contains a lot of calcium
  • meta increases the risk of stones via its high levels of urate
54
Q

is tea a high level of oxalate

A
  • tea is cited as asource of oxalate but added milk contains calcium and its associated volume makes it a risk reducer
55
Q

What are the differential comapred to urinary colic

A

Abdominal Pathology

  • abdominal aortic aneurism
  • bowel colic
  • biliary colic
  • ectopic pregnancy in females

Medical causes

  • pneumonia and MI
  • pancreatitis

Other urinary tract causes

  • pyelonephritis
  • bleeding tumours such as renal cell carcinoma or transitional cell carcinoma of the renal pelvis
56
Q

What is the difference between ureteric colic and bowel colic

A

Ureteric colic
- pain usually comes and goes with a background of pain

Bowel colic
- comes and goes, going away completely between bouts

57
Q

describe what the infection signs are

A
  • temperature
  • dip the urine to look for nitrates and white cells
  • presence of blood does not matter (20% of colic has no haematuria) and any inflammatory condition near the urinary tract will cause microscopic haematuria including pneumonia
  • CRP is the most sensitive blood marker for infection as ureteric colic is inflammatory in nature
58
Q

What investigations should you do if you suspect urinary colic

A
  • Examination
  • urine MSU
  • Bloods - U%Es, FBC &CRP, Calcium, urate, phosphate, bicarbonate, glucose
  • Imaging - spiral non contrast CT-KUB, KUB X RAY, USS, IV urogram, MRI
59
Q

What is the main imaging that is used in renal colic

A
  • Ultra low dose CTKUB is the mainstay of imaging
60
Q

what does ultra low dose CTKUB tell you in imaging

A
  • 99% of stones diagnosed
  • Not operator dependant
  • Position, size and hardness
61
Q

What do you do if the CTKUB is positive

A
  • Perform a KUB to look at the stone position
  • scout film of the CTKUB is not good enough
  • Dont try to diagnose a stone on a plain KUB - sensitivity and specificity is 50%
62
Q

What is the alternative for imaging

A

Ultrasound used in:

  • pregnancy
  • children
63
Q

What are the downside of using ultrasound

A
  • 75% sensitivity
  • misses very big and small stones
  • overcalls renal sinus fat as stones
64
Q

describe the use of IVU for imaging on stones

A
  • dying out
  • operator dependent
  • 1:120,000 risk of death from contrast allergy
  • multiple films give surrogate for obstruction
65
Q

How can you tell the ultrasound is look at a stone

A
  • need to look for an acoustic shadow or twinkle
66
Q

describe the use of MRI for stones

A
  • poor for stones

- used in the 2nd and 3rd trimester of pregnancy

67
Q

What does the management of stones depend on

A
  • site
  • size
  • hardness of the stone
68
Q

What is the treatment of stones

A

Analgesia

  • NSAIDS - useful in acute situation but may deteriorate renal function
  • Opiates - sometimes needed

Antibiotics if infection

  • Hydration - IV if necessary as patient may be vomiting, but this will not push out the stone

Medical expulsive therapy

  • tamsulosin is used to relax the lower ureter and increase stone passage
  • there are few alpha receptor in the upper ureter so MET is not used here
  • removal of stone if necessary
69
Q

Name some ways to remove stones

A
  • Semirigid urethroscopy (urs)
  • flexible ureterorenoscopy (FURS)
  • Percutaneous nephrolithotomy (PCNL)
  • Lithotripsy
70
Q

How does semirigid urethroscopy (urs) work?

A
  • Involves passing a teloscope into the ureter through the penis into the bladder to break up the stone
71
Q

How does flexible ureterorenoscopy (FURS) work

A
  • involves using a similar scope but is more flexible, this allows full access to stones in the kidney
72
Q

How does a Percutaneous nephrolithotomy (PCNL) work

A
  • key hold surgery for large multiple or complex stones
73
Q

What is the majority of treatment of stones

A
  • observed/medicial expulsive therpay
74
Q

How does Lithotripsy work

A
  • involves using sound waves to break the stone up
75
Q

How do you treat stones in the lower ureter

A
  • 95% of these stones under 10mm will pass from this location with medical expulsive therapy
  • patients have had lithotripsy but less effective
  • usually end up having a semirigid urethroscopy (urs)
76
Q

How do you treat middle ureter stones

A
  • medial expulsive therapy
  • semirigid urethroscoy
  • Percutaneous nephrolithotomy
77
Q

How do you treat stones in the upper ureter

A
  • due to lack of alpha receptors watching them is poor choice
  • lipthroscopy - stone has to be soft enough to work
  • urethroscopy
  • Percutaneous nephrolithotomy
78
Q

How do you treat stones in the kidney

A
  • Medical expulsive therapy and watching but anything over 4mm has a chance at causing damage
  • lipthroscopy - stone has to be soft enough to work
  • urethroscopy
  • Percutaneous nephrolithotomy
79
Q

What is metabolic testing indicated in

A
  • Multiple stone attacks
  • Bilateral stone disease
  • Solitary kidney (increased risk)
  • Urate / cysteine / calcium stones
80
Q

How do you carry out metabolic testing

A
  • 2 x 24 hour urine collections measuring: Calcium, Oxalate, Urate, Volume, Sodium & Citrate
  • Spot Nitroprusside test for Cysteine
  • Blood tests: Calcium, Urate, bicarbonate, U&Es
81
Q

What is the biggest single win in metabolic testing

A

fluid volume increase

82
Q

How do you prevent stones

A
  • increase urine flow to greater than 2L per day
  • reduce sodium intake
  • increase potassium intake (citrus fruits)
  • restrict high oxalate foods
  • reduce fatty foods
  • calcium with high protein meals ( do not restrict calcium this increases risk of net calcium loss and osteoporosis)
  • reduce animal protein intake (urate promoter)
  • not more than 1000% of vitamin C per day
  • take vitamin D and calcium supplementation at meal times
83
Q

What happens if you reduce calcium intake

A
  • increases risk of net calcium loss

- increases osteoporosis

84
Q

What drugs can you take to prevent stones

A

• Thiazide = reduces calcuria (but no strong evidence that they are effective)

  • Potassium citrate
  • very poorly tolerated

• Sodium bicarbonate

  • pyridoxine - oxalate stone prevention
  • Allopurinol for urate stones prevention
  • Penicillamine & Thiola for Cysteinuria
85
Q

How do you monitor treatment

A
  • 24hr urine
  • esp. for urine Vol, Na intake (< 5g/d)
  • Urate useful in urate stones
  • Monitor if specific therapy working (eg citrate, oxalate restriction etc)
  • Spot urine for Na/K as an alternative
  • Blood urate in users of allopurinol
  • Consider help from an endocrinologist in metabolic syndrome, hyperparathyiodsm and distal RTA
86
Q

there is a 50% chance of…

A

50% chance of another stone within 10 years if no dietary changes happen

87
Q

How much does a increase in fluid intake reduces risk of stone by

A

40%

88
Q

when should you use a follow up ultrasound

A
  • Consider a 6 monthly or yearly KUB to follow known, asymptomatic stones
  • In stone free formers, a 6 monthly to yearly USSKUB is reasonable
  • This can happen in primary car
89
Q

What is the presentation of stones

A
  • renal colic
  • renal obstruction
  • mid-ureter obstruction
  • lower ureter obstruction
  • bladder/uretra obstruction
  • co-exisiting UTI
  • haematuria
  • proteinuria
  • sterile pyuria
  • anuria
90
Q

What are the symptoms of renal colic

A
  • loin to groin spasmodic pain with background level
  • ipsilateral loin tenderness
  • nausea and vomitting
  • cannot stay still
91
Q

What are the symptoms of renal obstruction

A
  • pain in loin between rib 12 and lateral edge of lumbar muscles
92
Q

What are the symptoms of lower ureter obstruction

A
  • bladder irritability

- pain in the scrotum/penile tip in males or labia major in females

93
Q

What are the symptoms of bladder/urethra obstruction

A
  • pelvic pain
  • dysuria
  • straining/inability to void and interrupted flow
94
Q

What would you expect in a physical examination of someone with renal colic

A
  • usually no tenderness on palpation

- may be renal angle tenderness especially to percussion if there is retroperitoneal inflammation

95
Q

What would you see on urine MSU in renal colic

A
  • dipstick (usually and for blood 90%) - leucocytes and nitrites for infection
96
Q

what would you normally see rise in bloods for renal colic

A
  • rise in creatinine is normal but beware a stone in a solitary kidney
97
Q

describe the size of the stone that usually pass spontaneously

A
  • Stones <5mm in lower ureter - 90-95% pass spontaneously

- increase in fluid intake to help them pass

98
Q

What are the indications for urgent intervention

A
  • glomerular death
  • infection and obstruction
  • urosepsis
  • intractable pain or vomiting
  • impending ARF
  • obstruction in a solitary kidney
  • bilateral stone obstruction
99
Q

What is the first line investigation in stones

A

non contrast CT KUB

Year 3 - Met3b (26 decks)

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