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CAEM Pt. 2 > Exam 3: Equine Hepatic Dz > Flashcards

Exam 3: Equine Hepatic Dz Flashcards

1
Q

Common liver diseases with adult and foals

A
  • Adults = Theiller’s disease, cholangiohepatitis, chronic active hepatitis, pyrrolizidine alkaloid toxicities
  • Foals = Tyzzer’s, EHV-1, sepsis, hepatic abscess
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2
Q

Clinical signs of equine hepatic disease and common associated diseases

A

+ COMMON = vague signs like weight loss, ADR (chronic active hepatitis)
+ Jaundice (cholangiohepatitis)
+ Photosensitization, seasonal (toxic)
+ Hepatic encephalopathy, seizures, mental alterations (Theillers in adults, Tyzzers in foals)

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3
Q

What happens with fasting in horses?

A

Can see a mild hyperbilirubinemia (unconjugated) if off feed or anorexic

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4
Q

Equine hepatocellular enzymes (2)

A

1) Most helpful = SDH = hepatocyte SPECIFIC
2) AST, can also be elevated with musculoskeletal dz

  • SDH = hospital setting, doesn’t keep for long
  • ALT = not helpful in horses
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5
Q

Equine cholestatic enzymes (2)

A

1) GGT: SPECIFIC, easiest and most helpful, may help you gauge disease progression and treatment efficacy
2) ALP = not specific (increased with bone, placenta, intestines, etc)

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6
Q

What is the ONLY condition that produces a conjugated hyperbilirubinemia?

A

Hepatobiliary disease like cholangiohepatitis (not hemolytic dz)

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7
Q

Most helpful biochem test for equine liver disease

A

Serum bile acids - doesn’t require fasting

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8
Q

Equine hepatocellular enzymes (2)

A

1) Most helpful = SDH = hepatocyte SPECIFIC
2) AST, can also be elevated with musculoskeletal dz

  • SDH = hospital setting, doesn’t keep for long
  • ALT = not helpful in horses
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9
Q

Equine cholestatic enzymes (2)

A

1) GGT: SPECIFIC, easiest and most helpful, may help you gauge disease progression and treatment efficacy
2) ALP = not specific (increased with bone, placenta, intestines, etc)

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10
Q

What is the ONLY condition that produces a conjugated hyperbilirubinemia?

A

Hepatobiliary disease like cholangiohepatitis (not hemolytic dz)

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11
Q

Most helpful biochem test for equine liver disease

A

Serum bile acids - doesn’t require fasting

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12
Q

Dx? depression, somnolence (drowsiness), mania, hyperexcitability, seizures

A

> Hepatic encephalopathy due to hyperammonemia

  • Associated with fulminant acute or chronic liver failure = POOR prognosis
  • Non-hepatic = idiopathic (concurrent GI disease), Morgan weanlings (heritable urea cycle defect)
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13
Q

When does Theiller’s disease most commonly occur?

A

Late summer, early fall (DDx: arthropod viruses like WNV, EEE, WEE)

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14
Q

Common hypothesis for causes of Theiller’s disease

A

Recent tetanous antitoxin administration (last 4-6 weeks) to commercial equine plasma (NOT NECESSARY)

*Thought to be viral = flavivirus (bloodborne)

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15
Q

Common clinical presentation of Theiller’s disease

A

Adult with acute onset of signs of hepatic encephalopathy or jaundice

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16
Q

Dx of Theiller’s disease

A
  • History, time of year, clinical signs
  • Chem = VERY HIGH SDH, AST, mild GGT/ALP
    +/- Hyperammonemia
  • Hypoglycemia
  • Metabolic acidosis
  • Low BUN, low albumin
    **Liver biopsy
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17
Q

Tx of Theiller’s dz

A
  • Sedation
  • Hydration = IV fluids = strong alkalizing ions (bicarb) and dextrose
  • K+ in fluids
  • Oral neomycin, metronidazole, lactulose
  • Later = colchicine, prednisolone (anti-fibrotics)
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18
Q

Why don’t we use LRS with liver disease tx?

A

Liver patients can’t clear the L-lactate that is normally metabolized by healthy patients

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19
Q

Common clinical presentation of Theiller’s disease

A

Adult with acute onset of signs of hepatic encephalopathy or jaundice

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20
Q

Cause and diagnosis of chronic active hepatitis

A
  • Path: inflammatory disease with progressive fibrosis (thought to be autoimmune)
  • Dx: U/S guided biopsy (unusual to see U/S changes), histo that is lymphoctyic and plasmacytic, periportal fibrosis
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21
Q

Chem findings with chronic active hepatitis

A

Cholestatic&raquo_space; hepatocellular

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22
Q

Why don’t we use LRS with liver disease tx?

A

Liver patients can’t clear the L-lactate that is normally metabolized by healthy patients

23
Q

Common presentation of chronic active hepatitis

A

+ Weight loss, ADR animal, poor performance

  • Common relapses
  • Adult animal
24
Q

What is a sequelae to cholangiohepatitis?

A

Cholelith formation within biliary passages (bilirubinate stones)

25
Q

Chem findings with chronic active hepatitis

A

Cholestatic&raquo_space; hepatocellular

26
Q

Does cholangiohepatitis commonly progress to liver failure?

A

No

27
Q

Pathology and etiologic agents of cholangiohepatitis

A
  • Ascending infection from proximal small intestine

- E. coli, Aeromonas, Peptococcus, Citrobacter

28
Q

What is a sequelae to cholangiohepatitis?

A

Cholelith formation within biliary passages (bilirubinate stones)

29
Q

Typical presentation of cholangiohepatitis

A

BIG THREE = colic, fever, jaundice

Rare = hepatic encephalopathy, photosensitization

30
Q

Does cholangiohepatitis commonly progress to liver failure?

A

No

31
Q

Chem findings with cholangiohepatitis

A
  • Infection = mature neutrophilia, hyperfibrinogenemia, hyperglobulinemia
  • Cholestatic = high GGT, elevated ALP, hyperbilirubinemia
  • Usually have normal hepatocellular enzymes
32
Q

Dx of cholangiohepatitis

A
  • Suggestive inflam and cholestatic bloodwork
  • U/S and biopsy (see echogenic changes) - dilated bile ducts, intrahepatic calculi (Ca+ bilirubinate)
  • Histopath = suppurative cholangiohepatitis, minimal fibrosis
  • Culture - aerobic and anaerobic
33
Q

Treatment of cholangiohepatitis

A
  • Antimicrobials = penicillin and gentamicin
  • IV fluids with DMSO (solubilizes Ca++ bilirubinate crystals)
  • *CONTINUE TREATMENT UNTIL GGT NORMALIZES
34
Q

Etiologic agents for hepatic abscesses

A

RARE - Strep equi, Rhodococcus equi

35
Q

Presentation and dx of abscess

A
  • Younger horses = weaning/yearlings

- Dx: bloodwork, U/S

36
Q

Dx? Acute and fulminant liver failure in a foal (7-42 days old), anorexia, encephalopathy, seizures, marked icterus

A

Tyzzer’s disease

37
Q

Etiology of Tyzzer’s disease

A

Hepatocellular necrosis, due to Clostridium piliformis (may be endemic on some farms)

38
Q

Lab findings of Tyzzer’s disease (enzymes, chem findings)

A

> > Peracute presentation, with signs of liver failure

  • Marked elevation of hepatocellular (SHD, AST)&raquo_space; mild elevation of hepatobiliary (GGT, ALP)
  • Marked unconjugated hyperbilirubinemia
  • Hyperammonemia
  • Prolonged clotting times
  • Metabolic acidosis
  • Hypoglycemia
39
Q

Diagnosis of Tyzzer’s disease

A
  • History and signalment = age and clinical signs (any sudden death, 7-42 days old)
  • Chem findings of acute liver failure
  • Definitive dx = demo organism in liver with silver stains (necropsy or biopsy)
  • Fecal PCR
40
Q

Treatment of Tyzzer’s disease

A
  • Intensive fluid therapy: fix dehydration, acidosis, hypoglycemia
  • Antibiotics = crystalline penicillin or metronidazole
    +/- Total parenteral nutrition or plasma
41
Q

DDx of hepatic failure in foals (5)

A

1) Tyzzer’s disease - Clostridia
2) Perinatal EHV-1
3) Iron fumarate toxicity (RARE these days, not injected anymore)
4) Septicemia = MOST COMMON due to FPT
5) Lepto (uncommon)

42
Q

Nutritional management of liver disease in horses (4)

A

1) KEEP THEM EATING (no matter the protein content, etc)
2) Feed small and frequent meals (grazing is best)
3) Branched chain amino acids, not aromatic amino acids (less NH3 production)
4) Vit-E, B, K supplementation

Ex: beet pulp, cracked corn with molasses

43
Q

Common geographic location of toxic pyrrzolidine alkaloid exposures

A

Common in southern and western US, Ex: ransy tagwort, snakeroot, fiddleneck, etc.

*Usually unpalatable = consumed when there’s little else to eat

44
Q

Common toxic exposures of horses

A

1) Pyrrolizidine alkaloid plant and other plants (Ex: alsike clover)
2) Mycotoxins
3) Iron overload

45
Q

Diagnosis of toxic exposure

A

Clinical signs, history, biopsy

46
Q

Treatment of toxic hepatopathies

A
  • Withdrawal of the cause
  • Specific treatment if fibrosis is present
  • Treat ALL horses on premises (either symptomatic or not)
47
Q

Pathophys of pyrrolidizidine alkaloid toxicity

A
  • Most common = chronic and small amounts are ingested
  • Plant is metabolized by hepatic cytochrome P450 to highly toxic pyrroles
  • Pyrroles = anti-mitotic agents, cause DNA cross linking = form giant hepatocytes (megakaryocytosis)
  • Megakaryocytosis = diminished life span, replaced by fibrous connective tissue = fibrosis = liver failure
48
Q

Treatment of pyrrolizidine alkaloid toxicosis

A
  • Remove all horses from exposure
  • Manage their diet = small frequent meals, low protein if possible
  • Manage hepatic encephalopathy = low protein, neomycin/metronidazole, lactulose
49
Q

What breeds are prone to hyperlipemia or hyperlipidemia?

A
  • Ponies
  • Mini horses
  • Donkeys
  • Rare in conventional horses
50
Q

Difference between hyperlipidemia and hyperlipemia

A
  • Hyperlipidemia = serum triglycerides > normal reference, but < 500 mg/dL
  • Hyperlipemia = serum triglycerides > 500 mg/dL = MORE SERIOUS, opaque serum
51
Q

Cause (pathophys) of fatty liver

A

Secondary to other primary disease processes that put the animal in a NEGATIVE ENERGY BALANCE, common with OVERWEIGHT animals

Ex: colic, peritonitis, pneumonia

52
Q

Common sequelae of end stage fatty liver

A

Fat infiltration of liver and kidneys = fatty liver and kidney failure (azotemia)

53
Q

Treatment of fatty liver

A
  • Correct the primary disease
  • GET THEM EATING = establish feed intake quickly
  • Rx: dextrose, insulin, heparin, oral galactose, glucose
  • Monitor renal and hepatic function

CAEM Pt. 2 (27 decks)

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