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LA DX & TX II > Final Exam - Food Animal Renal Disease > Flashcards

Final Exam - Food Animal Renal Disease Flashcards

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
Q

what is seen on cbc, chemistry, & urinalysis of a animal with oak toxicosis?

A

cbc - indicates dehydration

chemistry - azotemia, low sodium, chloride, calcium, & normal to hyperkalemia

urinalysis - low USG, hematuria, & casts

26
Q

how is a diagnosis of oak toxicity made?

A

presumptive based on oak containing pastures & acute renal failure

27
Q

what treatment is used for animals with oak toxicity?

A

reduce injury, remove them from the source

NaCl isotonic fluids

remove oak from the rumen - transfaunation, vitamin B, & propylene glycol

28
Q

what animals are most commonly affected by pyelonephritis?

A

females way more than males!!!!!

days to months after parturition, ascending infection from c. renale or e. coli

29
Q

what clinical signs are seen with pyelonephritis?

A

non-specific chronic signs, painful (mimics hardware), tenesmus, pollakiuria, hematuria, tomato noodle soup urine

rectal exam - large kidney/ureter, very painful

30
Q

what is seen on cbc, chemistry, & urinalysis of an animal with pyelonephritis?

A

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
Q

how is pyelonephritis diagnosed?

A

renal dysfunction, history that is supportive, rectal exam, urine culture, & ultrasound

32
Q

what treatment is used for pyelonephritis?

A

antibiotics, supportive care, & surgery if there is a remaining kidney

33
Q

what is the most common cause for post-renal azotemia in food animals?

A

obstruction of the urinary tract that leads to hydronephrosis

34
Q

how is post-renal azotemia in a food animal diagnosed?

A

ultrasound & abdominocentesis

35
Q

where are obstructions typically located in cattle? what about sheep & goats?

A

cattle - distal sigmoid flexure

sheep & goats - urethral process or the distal sigmoid flexure

36
Q

what type of stones do feedlot cows or show steers/lambs get in the late feeding period?

A

struvite/calcium carbonate stones

37
Q

what animals are predisposed to getting silicious stones causing a urinary obstruction?

A

cattle & sheep on pasture in fall & winter or dry lot fed hay & grain after weaning

38
Q

what is the treatment for urinary obstructions in food animals? what is the prognosis for these animals?

A

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
Q

what therapy is recommended for urethral obstruction?

A

medical or surgical

medical - extend penis & pass a catheter

40
Q

what is seen on pathology that is pathognomonic for oak toxicosis?

A

eosinophilic staining solid material in the lumen of the proximal convoluted & ascending tubule

41
Q

concentration of the urine is important for what urinary stone formation?

A

important for silicious calculi formation

42
Q

what is the basic pathogenesis of stone formation?

A

struvite - Ca:PO4 imbalance & mucoprotein

silicious - low water intake, calculi are formed early

43
Q

how are silicious stones prevented?

A

increase animal’s water consumption

44
Q

how are struvite stones prevented?

A

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
Q

what is ulcerative posthitis? what causes it?

A

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
Q

what are some differentials for pizzle rot?

A

ulcerative dermatitis & urolithiasis

47
Q

what is the pathogenesis of pizzle rot?

A

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
Q

what animals are more commonly affected by pizzle rot?

A

mostly castrated males

angora & merino breeds due to increased amounts of hair/wool around the prepuce

49
Q

how is pizzle rot treated & prevented?

A

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

LA DX & TX II (44 decks)

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