Stones Flashcards
nephrolithiasis
stone in upper UT or collecting system
calculus
concretion anywhere in the system
bladder stones
stones in bladder
MC in underdeveloped countries
nephrocalcinosis
calcification with renal parenchyma
rare, rarely cortex, uncommon
5 major types of stones
calcium oxalate calcium phosphate uric acid cystine struvite
calcium oxalate monohydrate
whewellitte
calcium oxlate dihydrate
weddellite
struvite
urease stones
infection stones
triple phosphate stones
magnesium ammonium phosphate
supersaturation
ratio of salt/solubility
ss1 crystals
*can be changed by increase or decrease in urine volume
stones result from
phase change (dissolve salt–>ppt)
free particle model
crystal nuclei occur because increase in super saturation in dissolved salts present in ultrafiltrate (colelcting duct)
fixed particle model
crystal nuclei form in lumen of nephron and adhere to tubular epithelial (requires renal cell injury)
jux of CD and papilla
randall’s plaque hypothesis
loss of normal urothelial covering of renal papilla exposes a randall’s plaque (nidus of interstital CaPo4) that urine crystals can attach and grow on
CaOx stone disease and antibitoics
oxalobacter formigenes uses oxalate to make ATP
if these bacteria decrease by antibiotics, oxalate will increase, risk of stones increases
oxalates
coffee tea nuts rhubarb strawberries cranberry juice
metabolic defects taht could lead to CaOx stones
hypercalciuria
hyperoxaluria
hyperuricosuria
inhibitor deficiency
how do you get hyperoxaluria?
increase in production (congenital, too much vit C, glycol)
OR decrease Ca to bind due to malabsorption–>too much oxalate absorbed through intestine
treatmetn of hyperoxaluria
ca or mg supplemetation + treating malabsorption
uric acid crystals and hyperuricosuria
uric acid cyrystals may form nucleus for caox salt ppt–> treat with thiazide and allopurinol
how do you get excess uric acid?
increase in purne–>increase uric acid–>bone buffering along with excess Ca–>crystals
increase purine from meat, gout, post chemo, lesch-nyans
different inhibitor deficiencys
cirtate- complexes with Ca to dissolve (lost in chronic acidosis-RTA 1, CRG, acetazolamide)
Mg- forms sol complex with Ox
oral orthiphosphate-decreases Ca excretion
inorganic pyrophosphate
CaPO4 stone risk factors
hypercalciuria
alkaline urine
uric acid calculi are the
only truly radiolucent stones
tx uric acid cyrstals
k+ cirtate (urine alklakinization)
cystne stones
cystinuria due to an AR disease involving defect in 5 dibasic amino acids (COLA) transport in nephron and gastric mucosa, but only increase cysteine causes clinical manifestations
Clinical cysteine stones
children
mildly radio-opague staghorn nuclei-hexagonal crystals
renal parenchymal dmaage
tx cysteine stones
d-penicilamine-disrupts disulfide bonds in cystine
struvite stones are main cause of
staghorn stones
struvite stones are the MCC of
stones in women and paraplegics
struvite stones form from
supersaturation with Mg-ammonium PO4
patho of struvite stone
form in presence of UTI with a urea-splitting organism
proteus, kleb, serratia, enterobacter
bacteria resides in stone and cause srecurrent UTI
marker of struvite stones
alkaline urine (7.5-8)
dx of struvite stones
stone analysis, cystine crystalluria (hexagons), cyanide nitroprusside test (qualitative), 24hr urine studies (quant)
clinical for struvite stones
staghorn nuclei
recurrent uti
progressive renal insuffiency, urospesis, peripnephric abscess, obstruction
intervene for stone with
uncontrollable pain
fever
1 kidney
treatment for idiopathic hypercalcuria
hydrate, thiazides, diet that restricts Na, Ca, animal protein
treatment of hyperuicosuria
allopurinol
struvite treatment
antibiotics and urease inhibitors
cystine treatment
hydrate, alkalinize, restrict Na, use d-pen to block sulfide bonds
