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
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
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
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
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)
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
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
8
Q
Matrix Stones
A
- proteinaceous material
- chewing gum lik
9
Q
Idinavir Stones
A
- do not show up on CT
10
Q
Hounsfield Units
A
- CT scan
- semi quantitative
- hardness scale based on pixel brightness = x-ray attenuation
- can predict treatment success
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
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)
13
Q
Randall’s plaques
A
- calcium oxalate
- calcium phosphate forms in interstitium of kidney
- urothelium ulcerates exposing plaque to urinary surface
14
Q
Duct of Bellini plugs
A
- stones formed within tubules
- duct of bellini narrows (collecting duct)
- stones get stuck at papillary surface
15
Q
Causes of hypercalcaemia
A
- hyperparathyroidism
- sarcoidosis
- excessive vitamin D
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
Significance of infection
- 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
Haematuria Significance
- only 20% colic has haematuria
- any inflammatory condition near urinary tract causes microscopic haematuria
- pneumonia can cause it
27
Investigations
- urine dip (leucocytes, nitrates, urine pH)
- MSU
- Bloods (U&Es, FBC, CRP, calcium & urate)
28
Radiology
```
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
What does management of stone depend on?
site
size
hardness
30
Treatment
```
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
Treatments to Remove
- semi rigid ureteroscopy
- flexible ureterorenoscopy (FURS)
- observe/medical expulsive therapy
- percutaneous nephrolithotomy (PCNL, through abdomen, anaesthetic)
- lithotripsy (ESWL)
32
Metabolic Testing Indications
- multiple stone attacks
- bilateral stone disease
- solitary kidney (increased risk)
- urate, cysteine, calcium stones
33
Metabolic Testing How?
- 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
Prevention Lifestyle
- 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
Prevention with drugs
- thiazides (reduce calcuria)
- potassium citrate (v. poorly tolerated)
- sodium bicarbonate
- allopurinol for urate stones
- penicillamine & thiola for cysteinuria
36
Monitor treatment
- 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
Prognosis
- 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
