Hepatic Dr Yvorchuck Flashcards

1
Q

What is the triad of CS for Cholelithiasis in the horse

A

Colic

Pyrexia

Icterus

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2
Q

What is the triad of CS for Pyrrolizidine Alkaloid toxicity in equines

A

Fibrosis

Bile duct proliferation

megalocytosis

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3
Q

what are bw changes seen in hepatic dysfunction in horses

A

on CBC:

  • RBCs = mostly ACD*
  • WBC = varies but expected to be elevated as almost alway some infectious component*

in acute dz = leukopenia likely

Fibrinogen = varies depending on timeline & severity

likely hyperfibrinogenemic (chronic)

on Chemistry:

  • Glu = possibly hypoglycemic, often hyperglycemic*
  • BUN = <10 considered significant for liver dysfunct.*
  • Protein = rarely hypoalbuminemic or hypoproteinemic, may see hyperglobinemia d/t chron. inflammatory dz*
  • Bilirubin = serum bile aciids (SBA) increased esp chronic/severs dz*

Liver enzymes = SDH, ALP, AST, GGT gives clues as to specific dz process

hepatocellular = SDH -> ACUTE, AST -> Chronic

biliary = ALP -> ACUTE, GGT -> Chronic

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4
Q

what is the most useful indicators of liver injury

A

SDH, GGT & SBA

in the face of significant liver dz at least 1 of the 3 are elevated

SDH = acute liver

SBA = end stage liver

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5
Q

what does GGT mean

A

ductal enzyme denoting biliary dysfunction

also involved in repair phase, not only cell dysfunct. & renal

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6
Q

what does GGT elevations in urine indicate

A

that the GGT is of renal origin not liver (too big to pass through glomerulus)

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7
Q

other than liver dysfunction what other reason might you see an incr in ALP in an equine

A

ALP is also a bone enzyme so it might be elevated in Young Growing horses!

Remember context when interp. BW!

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8
Q

When interpreting SDH what is good to remember

A

That SDH returns to baseline in 3-5 days so can indicate point insult & if shows up again = new insult

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9
Q

will horses likely have just hepatocellular or biliary dysfunction

A

No!

Very rare that will have one or the other exclusively - more likely to have both dz processes concurrently to some degree

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10
Q

What should you suspect when you see a triad of CS referable to coagulation, nervous & cutaneous systems

A

Liver dysfunction

involvement of these 3 systems in a horse think LIVER!

usually not a single horse problem - more likely a “herd” issue think toxins

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11
Q

what are 4 clincal presentations (problems) that can indicate liver dysfunction

A
  1. Icterus
  2. Hepatic encephalopathy
  3. Photosenstization
  4. Clotting disorders
  5. w or w/o Colic
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12
Q

Icterus

A

conjugated bilirubin causes more pronounce icterus than unconjugated

the pattern of bilirubin elevation helps differentiate b/t

Pre & post-hepatic hyperbilirubinemia

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13
Q

how are total bilirubins measure

A

unconjugated (indirect) = calculated

conjugated (direct) = measured

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14
Q

what is elevated direct bilirubin a highly specific indicator or

A

liver failure

if direct >/= 25% of total -> predominantly biliary disease

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15
Q

how commonly is hepatic encephalopathy seen in liver dysfunction

A

80% of case

d/t accumulation of blood ammonia

must differentiate from idiopathic hyperammonemia:

rare complication of severe GI dz

Absence of markers of hepatic dz.

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16
Q

Tx for hepatic encephalopathy

A

supplement BC AAs

Low protein diet

17
Q

photosensitization

A

white areas affected

tx symptomatically

18
Q

clotting disorders

A

not seen frequently compared to other signs

tends to be terminal in horses

PT increases first - shortest T1/2

19
Q

CS of hepatic dz in horses

A

Colic - common

Behavior changes - aggression/depression

Ascites - very rare

Yawning

20
Q

how to classify liver pathology

A

consider acute v chronic = liver insult v liver failure

  • liver damage/insult*
  • more likely when pre-existing septic, hypoxic, neoplastic or metabolic conditon

increases in liver enzymes, normal liver function tests

  • liver failure*
  • rare in horse

increases in liver enzymes AND liver function tests

21
Q

most common liver pathology

cause(s)

A

hepatitis

  • toxins: plants or feeds*
  • infection*
  • choleliths*

most common chronic cause:

megalocytic hepatopathy (PA toxicosis)

22
Q

Tx for liver dx

A

behavior:

sm.doses of alpha2 agonists if sedation necessary

avoid diazepam

correct acid base disturbances

decr enteric ammonia - neomycin or lactulose

  • neomycin can mess up intes. flora use carefully

Decr hepatic workload

dietary mgmt:

  • freq small feedings
  • < 8% protein hay - no alfalfa
  • supplement w/ folic acid, B vits & fat-soluble vits

antimicrobials:

  • broad-spectrum
  • Pen/Gen/Metro or Enro/metro
  • TMS depending on c/s

Pentoxifylline for inflammatory a/o fibrosing liver dz

23
Q

Px for liver dz

A

dependent on dz

poor if:

low alb, incr glob or both

PT 30% longer than normal

lg incr GGT, ALP w/ norm or decr SDH w/ incr SBA

terminal signs: hemolytic crisis, encephalopathy w fibrotic liver

24
Q
A