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45 Cards in this Set
- Front
- Back
Familial amyloidosis has been characterized in these 3 cat breeds |
Abyssinian Siamese Oriental |
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What breed of cats have polycystic kidney disease |
Persian |
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How old are Abyssinian cats with familial amyloidosis when they develope CRF? |
with in the first 3 years of life |
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Besides amyloid depositis in the kidney's, where else can it be deposited with Abyssinian cats? |
adrenal thyroid pancrease colon
- generally not clinical to the syndrome |
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In Siamese and oriental shorthair cats, where is amyoid deposted? |
more commonly liver The amyloid AA protein is a little different than Abyssinian cats and might explain why it prefers the liver |
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PKD in Persians is a ____ trait (inheritance) |
autosomal dominant |
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Where do cysts form in PKD?
What happens over time? |
proximal and distal tubules renal cortex and medulla
increase in number and size |
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How early can PKD be detected in cats? |
6-8 weeks of age U/S but absence of custs does not preclude their developement at a later age |
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Do cats with PKD have hypertension |
no |
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What familial renal disease do samyed dogs get? |
heridatary nephritis abnormal collagen linking of the basement membrane |
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What familial disease do soft coated wheaten terriers get? |
PLE PLN or both immune complex glomerulonephritis
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TX of cystinuria SX Medical RX |
- mechanical removal - dietary dissolution of calculi (dissolve in alkaline urine) - D-penicillamine (make more soluable in urine) - more GI upset 2-mercaptopropinoylglycine (2-MPG) |
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Dogs with DCM have defective biosynthesis of this non-essential AA which generally occurs in dogs that also have cystinuria |
carniturua (carnitine deficiency) |
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What animals get hyperuricosuria? |
Dalmations and primary hepatic disease |
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How do dogs with primary hepatic disease develope hyperuricosuria |
Reduced conversion of uric acid to allantoin and ammonium to urea.
Most common with PSS |
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How does Allpurinol work? What should be avoided? |
reduce the serum and urine uric acid concentrations administered to dogs consuming a purine restricted diet to avoid formation of xanthine calculi |
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How long until urate uroliths are dissolved |
3.5 months |
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What animals will allopurinol not work for? |
hepatic defects possibly will resolve with PSS correction |
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How is primary renal glucosuria diagnosed? |
serial blood glucose measurements or fructosamine R/O hyperglycemia. |
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This is an inherited proximal tubular defcet that results in glucosuria, amonoaciduria, proteinuria, phosphaturia, and phyophosphatemia. |
Fanconi syndrome in humans |
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What breed of dog has inherited fanconi syndrome |
basenji |
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What diseases/drugs can cause acquired Fanconi Syndrome? |
gentamicin ethylene glycol primary hypoparathyroidism |
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What abnormalities does Fanconi Syndrome Cause? |
glucosuria aminoaciduria (cystine) proteinuria abnormal absoroption of HCO3, Na, K, and urate |
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What is the sex prediliction for Fanconi syndrome?
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females 3:1
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Diagnostic testing for Fanconi Syndrome show initially and late disease: |
glucosuria euglycemia isostenuria
as the disease progresses hyperchloremic metabolic acidosis and renal failure |
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TX for Fanconi Syndrome: What breeding enthusiasts want Urinary alkalization option Goals of HCO3 levels and K levels |
Supportive - Administration of sodium bicarbonate - exacerbates bicarbonaturia. - Urinary alkalization with potassium citrate is helpful. - Goal is to keep HCO3 above 12 and potassium 4-6 mEq/L - TX: Renal failure |
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Prognosis for Fanconi Syndrome |
Depends on the degree of azotemia at diagnosis short term - guraded to good long term - poor |
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How do the renal tubules regulate acid base hemostasis (2)? |
1. absorption of 90% of HCO3- in the proximal tubule 2. excretion of H and ammonium in the distal renal tubule |
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What is type II RTA? |
inability of the proximal tubule to prevent loss of HCO3- |
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What is type I RTA? |
inability of the distal tubule to excrete H |
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What is renal tubular acidosis |
rare tubular disorders that lead to hyperchloremic metabolic acidosis |
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What occurs at the cellular level(transporter) that causes proximal RTA. |
defect in the basolateral membrane Na/HCO3- cotransporter with leakage of HC)3- into the tubular lumen resulting in priximal RTA |
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Why is proximal RTA self limiting? |
metabolic acidosis is self-limiting because the distal tubule's ability to excrete acid. If oral sodium bicarbonate is added, the HCO3- presented to the distal tubule overwhelms the distal buffering system and results in bicarbonateuria. |
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How is proximal RTA diagnosed? |
acidic urine pH hyperchloremic metabolic acidosis identification of other tubular defects (euglycemia, glucosuria, aminoaciduria) |
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TX for proximal RTA |
potassium citrate |
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What can the kidneys not do with type 1 RTA in response to systemic acidosis? |
in response to systemic metabolic acidosis, unable to acidify the urine. |
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This type of RTA is associated with hypoaldosteronism |
Type IV distal RTA |
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What occurs at the molecular level of Type IV RTA |
loss of aldosterone stimulated H/ATPase pump and loss of distal Na absorption |
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How is type I RTA diagnosed |
hyperchloremic metabolic acisosis with alkaline urine failure to acidify the urine in response to an ammonium chloride challenge |
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TX for type I RTA |
administration of a alkali source potassium and sodium citrate |
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Under what two situations is ADH released |
hyperosmolality hypovolemia |
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Where dose ADH act in the nephron and what does it do? |
collecting tubules and collecting ducts
makes them become more permable to free water resulting in more concentrated urine |
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What are some causes of acquired NDI? |
E.coli - endotoxin - receptor interference RX - glucocorticoids/chemotherapy low K high Ca tubular injury medullary washout
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What is congential NDI |
rare deficiency of ADH receptors |
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Why dose dietary sodium restriction help with NDI? |
reduces the amount of solute presented to the kidney that must be excreted therefore, decreasing water loss. |