CAL: prescription diets Flashcards
What are therapeutic options for managing urolithiasis in dogs?
- reduce supersaturation of urine - change urine pH - UTIs if applicable - tx other conditions that increase the risk of urolithiasis
Describe dietary management for struvite urolith
-general principles: decrease urine concentration, increase diuresis and water intake - calculolytic diets (dissolve crystals) - reduce urine concentration of urea, phsophorous and magnesium - moderate protein (to decrease urea for urease-producing bacteria), highly digestible, low fibre - use for 1 months beyond removal of struvite - not meant for long term - don’t forget AB tx for UTI
What is supersaturation?
As the relative supersaturation (RSS) increases >1, the risk of urolith formation increases
What to look for with UA?
whether there are detectable amounts of blood, protein, white blood cells, visible bacteria and to know the urine pH and specific gravity
How to monitor struvite dietary management
persistence of CS, serial abdominal radiographs, urine pH, USG and evidence of crystals in urine.
What emergency stabilisation is given for hyperkalaemia induced ECG abnormalities?
- Ca IV or administration of glucose and/or insulin - calcium gluconate = cardioprotective - insulin regulates K+ levels in blood (insulin –> reduces K+ in blood). Presumably giving glucose –> increased endogenous insulin –> reduces K+ in blood. - fluids containing glucose = help dilute the blood with non-K+ containing fluids
Classic ECG signs with hyperkalaemia
- tented t waves - lack of p waves - QRS widening
What is this type of crystal?
Crystals are v distinct and consistent with calcium oxalate dihydrate
Prevention of reoccurence/tx of calcium oxalate dihydrate crystals
- diets promoting production of understaturation with calcium oxalate - avoid excess dietary calcium and oxalate - don’t restrict dietary phosphorous (i.e. don’t use low protein/renal diets) - manipulating urinary pH not helpful - specific prescription veterinary diets (some change pH, others increase diuresis and water intake) - manage any wt issues
What is the reason so many Dalmations develop urate stones?
In most animals, the by-product of purine metabolism are converted first to hypoxanthine, then to xanthine, then uric acid and finally to allantoin. In affected Dalmations, the enzyme responsible for converting uric acid into allantoin has reduced activity, causing a build up of uric acid and leads to formation of urate uroliths.
What are the nutritional strategies recommended for treating Dalmations with urate uroliths?
• Aimed at increasing urine pH and lower urine concentratons of uric acid, ammonium and/or hydrogen ions. • Calculolytic diets will also require a decrease in purine content – this requires severe protein restriction. • If commercial diets are not used, important ingredients to avoid include fish or offal. Alternate protein sources that are relative low in purines precursors include vegetable proteins, eggs and dairy products. • Other strategies such as switching to canned diets, and increasing diuresis via increasing salt content are also useful. • Protein restricted diets have an alkalinising effect on urine pH however sometimes it is still necessary to use alkalinising agents.
Other than dietary manipulation, what else can be done to aid resolution of clinical disease in dalmations with uroliths?
• Like other uroliths, UTIs need to be appropriately treated. • In addition to diet, administering xanthine oxidase inhibitors (eg, allopurinol) can lower (most effectively) the concentration of uric acid in urine – however this will increase xanthine and hypoxanthine concentrations in urine and sometimes lead to xanthine urolith formation – in order to treat these, allopurinol use should be discontinued and a low purine-diet should be used
What imaging is recommended for cystolith evaluation?
plain radiography usually adequate and sufficient
What are these crystals?
cystine crystals (relatively uncommon versus other uroliths)
Cause of cystine uroliths
an inborn error of metabolism characterised by a defective proximal tubular reabsorption of cystine and other amino acids. In dogs with this particular problem, only a small fraction of cystine is reabsorbed, leading to increased cystine excretion and urolith formation.