Diseases of the Renal System p873-916 Flashcards
(35 cards)
List some nephrotoxins.
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Aminoglycosides Pigment nephropathies NSAIDs Vitamin D Heavy metals Acorn poisoning
Where in the kidney do aminoglycosides accumulate?
Proximal tubular epithelial cells
What follows after a toxic dose of aminoglycosides accumulates in the epithelial cells?
Cellular metabolism is disrupted and tubular cell swelling, death and sloughing into the tubular lumen occurs.
What electrolyte abnormality can drive the occurrence of amingoglycoside nephrotoxicity?
A) Hyponatremia
B) Hypomagnesemia
C) Hypokalemia
D) Hypochloremia
C) Hypokalemia, as well as low calcium intake, can cause decreased urine output, leading to nephrotoxicity.
What are two common causes of pigment nephropathy?
Myoglobin pigment and hemoglobin
What is the primary renal lesion caused by NSAID toxicity?
Medullary crest necrosis, leading to gross hematuria.
How does the inhibition of prostaglandin production by NSAIDs lead to renal necrosis?
Prostaglandins play an important role in vasodilation when renal blood flow is decreased due to redistribution of cardiac output, in cases of dehydration. NSAID inhibition of PGI2 and PGE2 decreases the ability of these mediators to properly perfuse the cortical and medullary portion of the kidney.
What heavy metals can cause nephrotoxicosis?
What is a chelating agent used in animals that have suspect toxicosis?
Mercury, cadmium, zinc, arsenic and lead can all be nephrotoxic, but are rare causes of renal failure in horses.
Dimercaperol is a chelating agent for heavy metals and can be given IM initially at 3 mg/kg, q6hr for the first day and then 1 mg/kg q6h for two or more additional days.
What part of acorns can cause nephrotoxicity?
The immature leaves and green acorns cause more toxicity than the mature acorns, due to the higher levels of tannins. This toxicity is seen less in horses than cattle.
What is the underlying cause of vasomotor acute renal failure?
Sustained marked hypotension or release of endogenous pressor agents can initiate hemodynamically mediated ARF.
What are some risk factors for vasomotor ARF?
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Sepsis, hemorrhagic shock, severe intravascular volume deficit, septic shock, coagulopathy
Acute glomerulopathy should be considered in horses with severe ARF that do not have a primary predisposing disease leading to vasomotor ARF and have not been exposed to nephrotoxins. What are several bacterial agents that have been isolated in the rare cases of acute glomerulopathy?
E. coli O103:H2S and Streptococcus mitis
Patients with what clinical signs should have ARF as a suspected diagnosis?
Marked depression, anorexia, failure to produce urine in 6-12 hours after initiating fluid therapy.
List some biochemical changes that occur in ARF.
Hyponatremia, hypochloremia, hypocalcemia, azotemia with a BUN:creatinine ratio often less than 10:1
What is the most important assessment of renal function?
Glomerular filtration rate
How is GFR determined?
Timed urine collections or assessing plasma disappearance of several compounds (eg. radiolabled substances)
When treating a horse with ARF, how is a patient characterized with oliguria?
If, after fluid treatment is initiated, a horse has not produced urine in 12-24 hours, oliguria is present.
In patients with oliguria, what secondary side effects can occur?
Edema, noted in the conjunctiva; subcutaneous swelling of dependent areas tachypnea and altered mental states
Blood pressure changes, especially those with vasomotor nephropathy, occur in patients with ARF. Which is more common, hypo or hypertension? What can be done to correct this problem?
Hypotension is seen in patients with ARF, and may not be corrected with just administration of large amounts of IV fluids. Extra vascular accumulation or third spacing can be the cause. Hypertonic saline, dobutamine or other pressor agents can be employed.
Once a patient with ARF continues being oliguric, despite fluid resuscitation and restoration of systemic BP, what drug treatment should be initiated?
Furosemide, at 1 mg/kg, IV q2h. A CRI can be started as well, 0.12 mg/kg/h. If urination does not occur, mannitol or a dopamine infusion can be started.
In the first 1-3 days of life, creatinine concentration in newborns foals is ___% higher than their dams.
A) 10-20
B) 20-30
C) 30-40
D) 40-50
C) 30-40%, likely related to inability of creatinine to equilibrate rapidly across placental membranes
Are BUN levels typically high or low in foals, during the first few months of life?
BUN levels are typically low, due to the anabolic state of the growing foal.
What is the most common bacterial pathogen causing renal abscesses in foals?
Actinobacillus equii
Chronic renal failure in horses is irreversible, progressive process that can be divided by clinical and pathological findings into two broad categories. What are these?
1) Primary glomerular disease
2) Primary tubulointerstitial disease