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28 Cards in this Set

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stones precipitate when

urine concentration of stone components is too high



solid objectsi nurine can act as nuclei to start crystallization

what are the stone types

Calcium*


Ca Oxalate**


Ca Phosphate


mix of Ca types



uric acid


struvite


cystine

what are risk factors for stone risk?

too water (inadequate intake or too much loss)


nuclei for cystallization



or specifically


too much stone component


not enough inhibitor

what plaque does Ca phosphate concretion in renal tubule make? what happens

Randall's plaque



it erodes through urothelium.


then stone deposits on the exposed plaque (goes from tubule into pelvis)

so risk factors for Ca Oxalate stones specifically

hypercalciuria: can be urine only (filtered out fast enough: GI absorption, high vit D activity, renal leak of Ca out, met acidosis) or secondary to hypercalcemia



hyperoxaluria: excess absorption from GI**, vit C-> ox in alkaline urine, primary hyperoxaluria: AR, enzyme defect



not enough inhibitor: citrate for Ca, Mg for oxalate



hyperuricemia: CaOx stones form on uric acid crystals

how does oxalate absorption in GI become too high?

idiopathic



excess ingestion of high-oxalate foods



low levels of oxalobacter bacteria which degrades oxalates



low binding of oxalate in gut, so more is free to be absorbed (Ca usually does this, so more Ca means less Ox absorbed. Mg can also do this. So Ca Ox stone pts should not lower Ca intake**)

what are some high oxalate food?

dark tea


dark beer


chocolate


nuts


dark leaf


dark berries

why would there be enteric hyperoxaluria

ox binds to Ca and Mg in colon normally and is eliminated.



But in fat malabsorption, fatty acids bind Ca and Mg (celiac, GI resection, cystic fibrosis, Crohn's disease)

So pt has stone. Lab says >20% Ca Phos.



What is differential?

hyperparathyroidism: bone resorption -> HCO3 and phosphate, and then excess Ca HCO3 and Phos excreted in urine. Urine will have high pH, Ca, phos.

What is uric acid a metabolite of?



Why are uric acid crystals common?



What is the obvious tx?



Why don't other animals have this problem?

Adenosine and guanosine -> xanthine --xanthine oxidase-> uric acid



Uric acid isn't very soluble.



Block xanthine oxidase



They have uricase which uric acid -> allantoin which is soluble

what are the biggest risk factors for getting uric acid stones?

excess uric acid production



pH too low******


at low pH, there is a lot of free uric acid (pKa 5.4) so it precipitates out. At pH 6.5 >90% of uric acid is soluble

what factors would lead to excess uric acid levels?

high red meat intake



idiopathic gout


myeloproliferative disorder


chemotherapy (dead cells -> purines to metabolize)


genetic metabolic disorders: hypoxan-guan transferase deficiency; glycogen storage dz

struvite



what pH favors it?


so what else is sometimes in the stones?



how bacteria can cause these?


what does this form?

Mg NH4 PO4



not soluble at high pH


so Ca-P sometimes in stone



proteus: has urease enzyme so urea -> ammonium (part of stone and raises pH which pulls out PO4). So that with the normal Mg -> struvite = staghorn stone since grows and fills collecting system

which bacteria are urea splitters?

Proteus mirabilis*** other Proteus too



klebsiella



pseudomonas



rare species of e. coli

so what are the risk factors for struvite stones?

UTI's with urea-splitters, so any UTI risk factors (female, catheter)

what's the difference between cysteine and cystine?

cysteine is the aa



cystine is two cysteine's that are linked by covalent bond between their S's

so how do people get cystine stones?

AR defect in GI and kidney tubule so tubular reabsroption is imparied so cystine levels become high and stones form



worse in homozygotes than heterozygotes



can also form staghorns

how do you keep from making cystine stones?

keep cystine in solution by diluting with lots of water to have nocturia at least once per night



thiol groups replace a cysteine in cystine and are more soluble: 6-mercaptoproprionyl glycine, D-penicillamine, captopril

what diet recommendations could you give in general to prevent stones?

drink more water


drink more citric juices (Ca stones inhibitor)



eat less animal protein (ups Ca absorb in GI and has purines -> uric acid)



decrease Na intake: kidneys reabsorb more Na and so more Ca too

acute severe pain in flank, can move lower over time or can radiate to labium/testis/glans


intermittent, in waves


nausea/vomit


CVA tenderness


pt moves to try to relieve pain

renal colic = kidney stone

severe pain


nausea/vomit


tenderness in abdomen


guarding or rebound tenderness


hurts to move

peritonitis

how do you do imaging in a renal colic case?

non-contrast CT "stone protocol"


unless pregnant, had too many CT's already



alternatives then:


US


MRI

if pt has stone, what is the thing you can't miss?



how do you check this?

if there is also a UTI



the obstruction and infection can be a life-threatening emergency so missing it can be fatal:



judge based on urinalysis (tx if nitrities or leukocyte esterase or microscope: WBC or bacteria) and clinical scenario. not enough time for culture.

again. When checking for infection in colic pt: if the UA is negative, what would make you suspect infection?

fever


systemic inflammation


unusually severe pain


perinephric stranding on CT (inflammation sign)

what do you give pt with renal colic for rx?

NSAID- a potent one. Might have to IV since vomiting.



Opiod- IV for faster since these hurt so bad



anti-emetic if they need it

what tx do you use to help someone pass the stone "medical expulsive therapy"? like medicine, not surgery or stone laser

α-blocker which relaxes smooth muscle which ureteral spasm will block the stone



tamsulosin has less HTN risk, more literature


terazosin or whatever is cheapter but cross rxn with sulfa allergy



any of these drugs raises chance of passing stone to 79% instead of 50%

what treatment will you do for stones if



infection is suspected


intractable pain


solitary kidney or bilateral obstruction

immediate stent/percutaneous nephrostomy

what treatment will you do for stones if


pain


stone increasing in size


recurrent UTI's with same organism


lower kidney function due to stone

elect to do definitive stone treatment