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MET3b > Urinary Caculus Disease > Flashcards

Urinary Caculus Disease Flashcards

1
Q

Define a urinary calculus

A
  • kidney stone
  • solid conglomeration of mineral salts with or w/o associated urinary proteins
  • form in the kidney
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2
Q

Types of stone

A
  • calcium oxalate
  • urate
  • magnesium ammonium phosphate
  • cysteine
  • others = xanthine, idinavir, matrix
  • most mixed composition = urate and nidus common, calcium oxalate and calcium phosphate v. common
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3
Q

Calcium oxalate Stones

A
  • commonest type
  • insoluble
  • 2 types = dihydrate (softer) and monohydrate (extremely hard(
  • show up on x-rays
  • Randall’s plaques and duct of Bellini plugs
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4
Q

Calcium Phosphate Stones

A
  • associated with = hyperparathyroidism, distal renal tubular acidosis, medullary sponge kidney
  • also associated with urinary stasis and infection
  • show up reasonably well on x-ray
  • quite hard
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5
Q

Urate Stones

A
  • bright yellow
  • from uric acid which has entered urine
  • formation related to urinary pH, 5.4 or 10.3 required for formation (free theory)
  • soft and dissolvable
  • associated with metabolic syndrome
  • urate crystals -> stone formation (fixed theory)
  • part of both theories
  • treat by alkalinisation of urine (drink more liquid)
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6
Q

Magnesium ammonium phosphate stones

A
  • struvite
  • infection related
  • slightly shows up on x-ray
  • relatively soft
  • has some calcium phosphate
  • associated with staghorn calculi
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7
Q

Cysteine Stones

A
  • associated with cysteinuria (genetic)
  • poorly visible on x-ray
  • hard
  • produce white smoke/rotten egg smell when lasered = hydrogen sulphide
  • treat with medical dissolution therapy in specialist centres
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8
Q

Matrix Stones

A
  • proteinaceous material

- chewing gum lik

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9
Q

Idinavir Stones

A
  • do not show up on CT
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10
Q

Hounsfield Units

A
  • CT scan
  • semi quantitative
  • hardness scale based on pixel brightness = x-ray attenuation
  • can predict treatment success
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11
Q

Free Theory

A
  • explains stone formation
  • stone constituents have appropriate amounts but without inhibitors = stones form
  • affected by conc of solutes, urine acidity and presence of formation inhibitors
  • drive the solute conc. down by increasing fluid intake
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12
Q

Fixed Theory

A
  • explains stone formation
  • energy required to make a crystal lattice (enthalpy of formation) lower if surface to form on
  • depends on surface to form lattice on, other crystals present, randall’s plaques (sub urothelial deposits then when urothelium denudes contacts urine so crystals form)
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13
Q

Randall’s plaques

A
  • calcium oxalate
  • calcium phosphate forms in interstitium of kidney
  • urothelium ulcerates exposing plaque to urinary surface
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14
Q

Duct of Bellini plugs

A
  • stones formed within tubules
  • duct of bellini narrows (collecting duct)
  • stones get stuck at papillary surface
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15
Q

Causes of hypercalcaemia

A
  • hyperparathyroidism
  • sarcoidosis
  • excessive vitamin D
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16
Q

Oxalate

A
  • in diet
  • endogenous sources (liver)
  • vitamin C -> oxalate
  • absorbed by colon
  • calcium binds in gut preventing it from being absorbed
  • malabsorption = colitis, crohns, jejunoileal bypass surgery = enteric hyperoxaluria
  • bile salts increase absorption
17
Q

Dietary sources of oxalate

A
  • rhubarb
  • spinach
  • beetroot
  • sweet potato
  • nuts
  • dark chocolate
18
Q

Stone Inhibitors

A
  • THP = tamm Horsfall protein (uromodulin)
  • osteopontin
  • citrate
  • nephrocalcin
    (prevent crystalline structures binding to renal epithelial cells and reduce free calcium on crystal for growth)
19
Q

What do THP mutations lead to?

A
  • Familial Juvenile Hyperuremic Nephropathy
  • Medullary Cystic Kidney disease 2
    (increased stone formation in both)
20
Q

THP role

A
  • prevents some bacteria attaching to epithelium
21
Q

How does a ureteric colic present?

A
  • sudden severe right loin pain
  • radiates towards groin
  • agony
  • tender loin
  • blood in urine
22
Q

Investigations

A
  • rule out infection -> pyrexia?
  • Urinalysis
  • FBC
  • U&E = elevated creatinine
23
Q

Differentials for ureteric colic

A
  • biliary colic
  • leaking AAA (older patient consider)
  • ectopic pregnancy if female
  • pneumonia
  • MI
  • pancreatitis
  • pyelonephritis
  • bleeding tumours = renal cell carcinoma
24
Q

Difference between ureteric colic and biliary colic

A 
Ureteric = pain comes and goes with background of pain, radiates to groin
Biliary = pain comes and goes going away completely between bouts, also right upper quadrant radiating under ribs up to shoulder tip
25
Q

Significance of infection

A
  • infection with stone kills!
  • monitor temp!
  • dip urine for nitrates and white cells
  • CRP most sensitive blood marker for infection and ureteric colic inflammatory anyway
26
Q

Haematuria Significance

A
  • only 20% colic has haematuria
  • any inflammatory condition near urinary tract causes microscopic haematuria
  • pneumonia can cause it
27
Q

Investigations

A
  • urine dip (leucocytes, nitrates, urine pH)
  • MSU
  • Bloods (U&Es, FBC, CRP, calcium & urate)
28
Q

Radiology

A 
CTKUB (ultra low dose no staining)
- position, size, hardness
- urate stones lucent, sensitivity and specificity = 50%
US
- if pregnant or children
- non irradiating
- 75% sensitivity = look for acoustic shadow/twinkle
MRI
- poor for stones
- if 2nd/3rd trimester of pregnancy
29
Q

What does management of stone depend on?

A

site
size
hardness

30
Q

Treatment

A 
Should come out naturally
Analgesia
- NSAIDs (acute, can deteriorate renal function)
- opiates
Hydration
- IV fluids if patient vomiting
Medical Expulsive Therapy
- tamulosin relaxes lower ureter increasing passage for stone
Remove Stone
31
Q

Treatments to Remove

A
  • semi rigid ureteroscopy
  • flexible ureterorenoscopy (FURS)
  • observe/medical expulsive therapy
  • percutaneous nephrolithotomy (PCNL, through abdomen, anaesthetic)
  • lithotripsy (ESWL)
32
Q

Metabolic Testing Indications

A
  • multiple stone attacks
  • bilateral stone disease
  • solitary kidney (increased risk)
  • urate, cysteine, calcium stones
33
Q

Metabolic Testing How?

A
  • 2 x 24hr urine collections (calcium, oxalate, urate, volume, sodium & citrate)
  • spot nitroprusside test for cysteine
  • blood tests for calcium, urate, bicarb, U&Es
34
Q

Prevention Lifestyle

A
  • increase urine flow >2L per day
  • reduce sodium intake
  • increase potassium intake
  • restrict high oxalate foods
  • reduce fatty foods (reduce oxalate absorption)
  • calcium with high protein meals (do not restrict, reduces oxalate absorption)
  • reduce animal protein intake (promote urate)
  • not more than 1000% vitamin C per day (1 tablet)
  • take vitamin D and calcium supplementation at meal times
35
Q

Prevention with drugs

A
  • thiazides (reduce calcuria)
  • potassium citrate (v. poorly tolerated)
  • sodium bicarbonate
  • allopurinol for urate stones
  • penicillamine & thiola for cysteinuria
36
Q

Monitor treatment

A
  • 24 urine (volume, sodium intake <5g/d, urate monitor therapy effectiveness)
  • blood urate in users of allopurinol
  • consider help from endocrinologist if metabolic syndrome, hyperparathyroidism and distal RTA
37
Q

Prognosis

A
  • 50% chance of another stone within 10years if no dietary changes
  • increase fluid intake 40% reduces risk
  • consider 6 monthly/yearly KUB to follow known/asymptomatic stones
  • in primary care

MET3b (20 decks)

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