Final Exam - Food Animal Renal Disease Flashcards

(49 cards)

1
Q

what are your main differentials you should have for azotemia in food animals?

A

dehydration, septic shock, bacteremia, nephrotoxins, pyelonephritis, leptospirosis, & urolithiasis

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2
Q

what defines azotemia?

A

elevation in creatinine & BUN

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3
Q

what defines pre-renal azotemia in food animals? what is seen clinically?

A

decreased glomerular perfusion (dehydration)

characterized by azotemia, USG > 1.025, urine:serum urea > 20:1, & urine: serum creatinine > 30:1

sunken eyes, elevated skin tent time, depression/decreased/absent suckle reflex

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4
Q

what defines renal azotemia in food animals?

A

any hemodynamic or toxic cause that leads to marked hypotension so they kidneys lose the ability to concentrate urine in the face of azotemia

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5
Q

what are some examples of hemodynamic causes of renal azotemia?

A

septic shock, hemorrhage, & severe fulminant diarrhea

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6
Q

what is the pathophysiology of hemodynamic causes of acute renal failure resulting in renal azotemia?

A

marked hypotension and/or release of endogenous pressor agents that have the potential to initiate hemodynamically mediated acute renal failure (starts as pre-renal)

severe hypotension results in the release of renin & activation of AT II which constricts the afferent glomerular arterioles

endotoxins damage the endothelium - promotes the clotting cascade

partial occlusion of renal vasculature decreases renal blood flow (bloat)

erythrocyte aggregation which occurs with high PCV & low blood flow can potentiate local renal hypoperfusion

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7
Q

what are some examples of nephrotoxins that cause acute renal failure in food animals?

A

medications - aminoglycosides/tetracyclines

endogenous - myoglobin/hemoglobin

plants - oak, pigweed, & halogeton

mycotoxins - aflatoxin

heavy metals - mercury, arsenic

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8
Q

what is the pathophysiology of most toxins causing acute renal failure?

A

most nephrotoxins damage kidneys by causing acute tubular necrosis but the basement membrane remains intact

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9
Q

what clinical signs are seen in food animals with acute renal failure?

A

polyuria/oliguria/anuria, depression, & anorexia

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10
Q

what derangements are seen on a chemistry panel of a cow in acute renal failure?

A

azotemia, metabolic alkalosis (low sodium, low chloride, hypo/normokalemia, hypocalcemia, hypo/normophosphatemia, & hypermagnesemia)

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11
Q

how is acute renal failure diagnosed in a cow?

A

low USG, discolored urine, proteinuria, sediment (casts degrade rapidly), & use fractional excretion of sodium to determine renal function

k is low because ruminants lose it in their saliva - metabolic alkalosis

BUN: creatinine ratio < 10:1

urine: serum urea < 20:1 & creatinine < 30:1

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12
Q

is a cbc useful for evaluating a cow for acute renal failure?

A

nope - won’t tell you much

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13
Q

what value on a chemistry panel is a prognostic indicator for a cow with acute renal failure?

A

magnesium - if greater than 3X, is bad!

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14
Q

how is fluid therapy monitored in oliguric/anuric animals with acute renal failure?

A

carefully monitored via CVP’s & daily weight gain

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15
Q

how is oliguria corrected in a cow in acute renal failure? what drugs should be avoided?

A

after fluid therapy & electrolyte replacement - mannitol 20% IV or furosemide 2 mg/kg IV

avoid anti-prostaglandin drugs (banamine)

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16
Q

what therapy is used for cows with acute renal failure?

A

correct the predisposing problem, replace fluid volume deficits, correct electrolyte & acid base imbalances, correct oliguria if present, & caloric support

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17
Q

how many nephrons must be lost before clinical signs are seen in a cow with CKD?

A

at least 75% of nephrons must be lost to get clinical signs

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18
Q

what is the pathophysiology of CKD in cows?

A

may be a result of an initial acute disease/residual damage or glomerular/tubulointerstitial disease

as renal function decreases, there is a decline in GFR - solutes that are normally eliminated from the body are retained (BUN, creatinine)

increased solute filtration filtration & diuresis in surviving nephrons along with concurrent tubular disease impedes normal resorption of water (leads to pu/pd)

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19
Q

what are some examples of causes of CKD in cows?

A

history or previous sepsis, diarrhea, etc

glomerular disease - amyloidosis

tubulointerstitial diseases - pyelonephritis

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20
Q

what are the general clinical signs associated with CKD in cows?

A

weight loss, anorexia, pu/pd, kidney may palpate abnormally on rectal, & severe protein loss may lead to SQ edema

21
Q

what food animals are susceptible to oak toxicosis? which ones aren’t?

A

cattle & sheep!!!

goats aren’t affected!!!

22
Q

what is the pathophysiology of oak toxicosis?

A

metabolites of gallotannins cause precipitation of proteins into the gi tract & kidneys

23
Q

what are the predisposing factors of oak toxicosis?

A

weather changes, shortage of forage, & younger animals

24
Q

what are the clinical signs associated with oak toxicosis?

A

anorexia, depression, ruminal atony, & dehydration

constipation with hemorrhagic diarrhea after

hematuria, polyuria, oliguria

ascites, hydrothorax, tenesmus, & swollen peri-anal area

25
what is seen on cbc, chemistry, & urinalysis of a animal with oak toxicosis?
cbc - indicates dehydration chemistry - azotemia, low sodium, chloride, calcium, & normal to hyperkalemia urinalysis - low USG, hematuria, & casts
26
how is a diagnosis of oak toxicity made?
presumptive based on oak containing pastures & acute renal failure
27
what treatment is used for animals with oak toxicity?
reduce injury, remove them from the source NaCl isotonic fluids remove oak from the rumen - transfaunation, vitamin B, & propylene glycol
28
what animals are most commonly affected by pyelonephritis?
females way more than males!!!!! days to months after parturition, ascending infection from c. renale or e. coli
29
what clinical signs are seen with pyelonephritis?
non-specific chronic signs, painful (mimics hardware), tenesmus, pollakiuria, hematuria, tomato noodle soup urine rectal exam - large kidney/ureter, very painful
30
what is seen on cbc, chemistry, & urinalysis of an animal with pyelonephritis?
cbc - neutrophilia, mild to moderate anemia, & elevated globulin/fibrinogen chemistry - renal failure, but sometimes only one kidney, & may not see signs urinalysis - isosthenuria, proteinuria, hematuria, pyuria, WBC casts, bacteriuria, so use a gram stain to differentiate
31
how is pyelonephritis diagnosed?
renal dysfunction, history that is supportive, rectal exam, urine culture, & ultrasound
32
what treatment is used for pyelonephritis?
antibiotics, supportive care, & surgery if there is a remaining kidney
33
what is the most common cause for post-renal azotemia in food animals?
obstruction of the urinary tract that leads to hydronephrosis
34
how is post-renal azotemia in a food animal diagnosed?
ultrasound & abdominocentesis
35
where are obstructions typically located in cattle? what about sheep & goats?
cattle - distal sigmoid flexure sheep & goats - urethral process or the distal sigmoid flexure
36
what type of stones do feedlot cows or show steers/lambs get in the late feeding period?
struvite/calcium carbonate stones
37
what animals are predisposed to getting silicious stones causing a urinary obstruction?
cattle & sheep on pasture in fall & winter or dry lot fed hay & grain after weaning
38
what is the treatment for urinary obstructions in food animals? what is the prognosis for these animals?
guarded for urethral obstruction - need surgery if there is an obstruction & urethral rupture!!!! ruptured bladder requires surgical management or a drain in the abdomen
39
what therapy is recommended for urethral obstruction?
medical or surgical medical - extend penis & pass a catheter
40
what is seen on pathology that is pathognomonic for oak toxicosis?
eosinophilic staining solid material in the lumen of the proximal convoluted & ascending tubule
41
concentration of the urine is important for what urinary stone formation?
important for silicious calculi formation
42
what is the basic pathogenesis of stone formation?
struvite - Ca:PO4 imbalance & mucoprotein silicious - low water intake, calculi are formed early
43
how are silicious stones prevented?
increase animal's water consumption
44
how are struvite stones prevented?
decrease urinary P levels by supplementing concentrate rations with 1.5-2% limestone acidify the urine - Ca:P ratio > 2:1 increase urine volume - 4% salt in the diet & provide fresh water all the time
45
what is ulcerative posthitis? what causes it?
pizzle rot - condition of sheep & goats characterized by ulcerations on the prepuce of males & the vulva of females interaction of corynebacterium renale & high levels of urea in urine
46
what are some differentials for pizzle rot?
ulcerative dermatitis & urolithiasis
47
what is the pathogenesis of pizzle rot?
high levels of urinary urea interact with the organism high protein diets = alkaline urine with high urea c. renale hydrolyzes urea to ammonia which accumulates in preputial/vulva regions causing necrosis of cells leading to ulceration
48
what animals are more commonly affected by pizzle rot?
mostly castrated males angora & merino breeds due to increased amounts of hair/wool around the prepuce
49
how is pizzle rot treated & prevented?
ulcerated area is debrided & a triple antibiotic ointment is applied change the animal's diet to reduce protein clip the hair/wool around the area