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Urinary tract stones (Aetiology (Metabolic Hyper Ca Hyperuricosuria…
Urinary tract stones
Aetiology
Metabolic
Hyper Ca
Hyperuricosuria (gout)
Malabsorption
Endocrine
Hyperthyroidism
Hyperparathyroidism
Addison's
Cushing's
RTA
Infection
Recurrent UTI (struvite)
Autoimmune
Crohn's, Coeliac
Sarcoidosis
Iatrogenic
Catheter, stent
Jejunoileal bypass
Congenital/genetic
Hyperoxaluria
Cysteinuria
Drugs
Lithium
Vit D excess
Diuretics
Antacidss
Corticosteroids etc.
Neoplastic
Malignancy (hyper Ca)
Prevention
Oxalate stones
Pyridoxine (Vit B6)
Struvite
UTI tx
Ca stones
Thiazide diuretic if needed
Urate
Urine alkalination (K citrate, Na bicarb)
Allopurinol (per gout)
All stones
Adequate fluids
Normal Ca diet
Cystine
Urine alkalinisation
Cysteine chelation - D penicillamine
Types of
stone
Ca phosphate
Epidemiology
Second commonest
Aetiology
Increased Ca
Renal tubular acidosis
Magnesium
ammonium
phosphate
(struvite)
Epidemiology
<15%
Aetiology
UTI with urease producing bacteria (alkaline)
(proteus, Klebsiella, pseudomonas)
Ca oxalate
Aetiology
Increased Ca (hyperparathyroidism, malignancy, increased intake, excessive bone resorption)
Increased oxalate (primary hyperoxaluria, high intake e.g. spinach, choc, tea, reduced Ca, dehydration)
Primary renal disease
Epidemiology
Commonest
Urate
Epidemiology
10%
Aetiology
Hyperuricaemia (overproduction or reduced secretion)
Ileostomy (reduced bicarb, more acidic urine)
Cystine
Epidemiology
RARE
Aetiology
Renal tubule defect
Cysteinuria (AR)
Risk factors
Foreign bodies
(catheter, stent)
UT abnormalities
Male gender
Age
High oxalate diet, dehydration
Pathophysiology
Normal soluble material supersaturates the urine and precipitates to form a crystal
Also reduced levels of crystal inhibitors in the urine
Commonly deposit at narrowings in ureter
(pelvicoureteric junction, pelvic brim, vesicoureteric junction)
also proximal ureter
Obstruction causes release of PGs and
vasodilatation and smooth muscle spasm
Clinical presentation
Abdo pain
Radiation
Loin to groin (ureteric)
Associated symptoms
N+V
Haematuria
Fever (if infected)
May have LUTS
Character
Colicky (ureteric)
Dull (renal or bladder)
Timing
Intermittent, progressive
Onset
Insidious or sudden
Exacerbating/relieving
Cannot lie still, nothing helps
Site
Loin (large staghorn)
Loin to groin (ureteric)
Pelvic (bladder)
Severity
Severe
Asymptomatic
If infected, fever,
rigors, N+V
LUTS (if lower UT)
Complications
AKI
UTI infection
Ureteric stricture
Sepsis
Epidemiology
Common
Peak 20-40y (F), 40-60y (M)
M>F
Diagnosis
Examination
Abdo - tenderness, guarding
PR - normal
Investigations
Bedside
Obs - fever
Bloods
FBC, CRP, U+Es, glucose,
bone profile, Ca
Urine
Dipstick (haematuria)
MCS and cytology
Stone biochemistry
Imaging
USS KUB (hydroneprosis, stones)
KUB X-radiograph (but urate radiolucent)
CT KUB (can see most stones)
History
Management
Initial ABCDE
Definitive
Medical
Supportive
Analgesia (diclofenac, opioids)
Antiemetic
Abx if infection
Medical expulsion therapy
Indication: stone >5mm, non-resolving pain
E.g. nifedipine (CCB), tamsulosin (a-blocker)
Method: promotes expulsion
Extracorporeal shockwave lithotripsy (ESWL)
Indication: stones 5-10mm if MET unsuccessful
Method: USS shockwave shatters stone, small bits pass
SE: renal injury, HTN
Ureteroscopy
Indication: stone >5mm, MET unsuccessful
Method: ureterscope plus basket
Surgical
Percutaneous nephrolithotomy (PCNL)
Indication: large, multiple or complex stones
Open nephrolithotomy
Rarely used
Conservative
IV fluids (pass small stones <5mm)
Where to treat
Admit if infected, dehydrated, intractable
pain/N+V, diagnostic uncertainty, poor response
Definition
Disorder of caliculi (stone)
formation in the urinary tract