HEPATIC SYSTEM

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HEPATIC SYSTEM
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Abnormalities that occur with hepatic disease

• Photosensitization (25)
• Hepatoencephalopathy (80)
• Coagulopathies
• Icterus
• Mild to moderate colic
• Pruritis
• Ascites is fairly infrequent
• Weight loss (w/ chronic)

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CBC

• Mostly nonspecific changes
• Evidence of hemolytic disease (red discoloration
  etc)
• WBC and fibrinogen indicate inflammation

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Chemical profile

• Hypoglycemia
• BUN
• Low values indicate liver disease
• Variable by lab and diet
• Horses rarely have hypoproteinemia associated
  with liver disease
• Increased bile acids
• Sensitive indicator especially in chronic cases
• Can do bile acids anytime (horses dont have a
  gallbladder so there arent any pre or post
  prandial concerns)

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Liver enzymes

• SDH
• Liver specific
• Will increase due to even very mild hepatic
  trauma or in colic despite direct hepatic damage
  (acute)
• ALP
• Not liver specific
• High levels in foal due to anabolism in skeleton
• Associated with biliary system (acute)
• AST (SGOT)
• Not liver specific mostly in hepatocytes
• ½ life is longer so it indicates chronic dz
• GGT
• Fairly liver specific
• Derived from biliary cells
• Increases tend to persist for weeks (chronic dz)

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Icterus

• Evaluated through bilirubin levels
• Unconjugated bilirubin
• Calculated (Indirect)
• Increased levels can be associated with anorexia
• Conjugated bilirubin
• Measured (Direct)
• Ration of direct to total bilirubin gt 25 is
  associated with cholestatic disease

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Photosensitization

• 25 of cases
• 2 types of photosensitizing agents
• Photoallergic
• Phototoxic
• Typically only white areas affected

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Hepatic encephalopathy

• 80
• CS frequent yawning, behavioral change, generic
  CNS signs etc
• Pathophysiology
• Blood ammonia elevated (other toxins may act
  synergistically with ammonia)
• Amino acids (decreased branched chain AA,
  increased aromatic amino acids)
• Increased aromatic AA may lead to formation of
  increased inhibitory neurotramsitteres,
  alterations in catecholamines
• Tx
• Low protein diet and supplement with branch
  chained AA

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IDIOPATHIC ACTIVE HEPATIC DISEASE

• Aka Theilers disease, serum sickness
• Mostly ADULTS
• Most frequently associated with tetanus antitoxin
  but also associated with any equine serum product
• Etiology
• Increased incidence in certain geographic areas
• Possible viral infection

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IDIOPATHIC ACTIVE HEPATIC DISEASE

• CS
• Onset abrupt
• Fever absent
• W TAT onset begins 4-10 weeks post vaccination
• General liver disease signs (hepatic
  encephalopathy, photosensitization etc)
• Dx
• Elevated bilirubin, AST, SDH, GGT
• Necropsy small flaccid liver, icteric carcass

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CHOLELITHIASIS

• Choledocholelithiasis (common bile duct) is the
  most common biliary obstruction in the horse
  (occurs more frequently in the horse than in
  other domestic animals)
• Pathogenesis
• Unknown ascending infection, parasites, foreign
  body etc)
• Composition of stones mixed
• Bilirubin, CaPO4, cholesterol esters, bile
  pigments etc

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CHOLELITHIASIS

• Signalment ADULTS, no breed or sex predilection
• Risk factors enteric Gram infection from SI
• CS
• Intermittent abdominal pain w pyrexia and icterus
  
• Less commonly HE, photosensitization, weight loss
• Lab evaluation
• Increased liver enzymes (GGT, ALP, bile acids)
• Suspect cholestasis if direct is gt30 of total
  bilirubin

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CHOLELITHIASIS

• US definitive diagnosis
• Hepatomegaly and bile duct dilation
• Generally multiple choleliths seen
• Tx
• Medical
• long term broad spectrum ABs (enrofloxacin/
  ceftiofur)
• Fluid therapy
• DMSO helps dissolve Ca glucoronidate calculi
• Bile salt therapy contraindicated in horses
• Surgical relief of obstruction
• Guarded prognosis
• Monitoring
• Repeat US, sequential GGT/ALP

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CHRONIC ACTIVE HEPATITIS

• Eiology
• Unknown (maybe toxins or bacteria from GIT)
• CS
• Progressive weight loss, intermittent fever and
  icterus
• Some develop peculiar cutaneous lesions
• Lab Evaluation
• ALP, GGT, bile acids increased
• Liver biopsy cholangiohepatitis on histopath

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CHRONIC ACTIVE HEPATITIS

• Tx
• Supportive care
• Corticosteroids where lymphocytic-plasmacytic
  infiltrates
• AB if bacterial infection
• Prognosis
• Based on liver biopsy and response to therapy
• Poor if functional liver failure and fibrosis
• Fair to good if early lesions

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PYRROLIZIDINE ALKALOID TOXICITY

• Risk factors
• Ingestion of PA containing plants (dose
  cumulative)
• Not usually very palatable
• Pathophysiology
• Antimitotic effect on DNA -gt hepatocytes cannot
  divide -gt die replaced by fibrosis
• CS
• Chronic liver failure signs
• Occasionally pruritis
• Abortion

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PYRROLIZIDINE ALKALOID TOXICITY

• Lab evaluation
• Liver enzymes elevated
• Liver biopsy
• Triad of fibrosis, bile duct proliferation, and
  megalocytes
• Prognosis
• End stage fibrosis grave

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TYZZERS DISEASE

• Signalment 7-40 days of age FOALS
• EA Clostridium piliformis
• Risk factors parturition
• Pathophysiology
• Fecal-oral route of transmission
• Carrier state may exist ????
• Not a highly contagious disease
• CS
• Often found dead w no history of signs
• Fever, depression and anorexia
• Icterus, hypoxia, coma, seizures etc

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TYZZERS DISEASE

• Dx
• Lab evaluation
• elevated enzymes, severe hypoglycemia
• Definitive dx only at post mortem
• Organism not readily id in routine stains
• Tx
• No reports of successful tx
• Antimicrobial therapy (pen, tetracyclines,
  erythromycin)

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HEPATIC FAILURE IN FOALS

• CS
• Hepatoencephalopthy w icterus
• Some die peracutely
• Etiology
• Precolostral iron, perinatal herpes, lepto,
  tyzzers, duodenal ulcers, ascarid migration,
  hepatotoxicities
• PSS infrequent
• Dx
• Increased bilirubin, ammonia and prolonged PT
• SDH often normal most foals normally have
  elevated GGT

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GENERAL TREATMENT OF LIVER DISEASE

• Agitation/convulsing xylazine/ AVOID diazepam
• Low glucose give 10 glucose IV
• Decrease blood ammonia
• Oral lactulose, mineral oil/oral neomycin
• Metronidazole
• Correct acidosis
• only if moderate to severe, correct very slowly
  or HE will worsen

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GENERAL TREATMENT OF LIVER DISEASE

• Decrease Hepatic workload
• 5-10 dextrose drip
• Dietary management
• Small meals frequently
• Force feed if not eating
• Branched chain AA supplement
• Bactericidal Abs
• Ampicillin/gentamicin, TMS, ceftiofur

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GENERAL PROGNOSIS IN LIVER DISEASE

• Typically poor if
• Low albumin levels
• PT which is 30 longer than normal
• Large increase in GGT/ ALP w normal or decreased
  SDH
• Marked fibrosis that bridges liver lobules

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ENDOCRINE DISEASES
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PHEOCHROMOCYTOMA

• Benign unilateral tumor of the adrenal medulla
• Signalment gt12 years old
• CS excessive sweating, PU/PD, tachycardia,
  dilated pupils, hyperglycemia
• Dx difficult antemortem
• Blood and urine levels of catecholamines
• Tx
• Surgical removal
• Grave prognosis often too ill to be treated

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HYPOTHYROIDISM

• Overdiagnosed dz
• Clinical manifestations
• Skinny, poor-doers, poor performance
• Exertional rhabdomyolysis
• CS
• Decreased food intake
• Dull hair coat, scaly, hypothermia, lethargic,
  thyroid enlargement
• Dx
• Baseline T3 and T4
• Do TRH or TSH stim to verify

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HYPOTHYROIDISM

• Tx
• Supplementation very controversial
• Many report the absence of any response to
  thyroid supplements, some conditions are thyroid
  responsive w/o being hypothyroid

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HYPERTHYROIDISM

• There are no reported cases of equine
  hyperthyroidism

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PIPD

• Pars intermedia dysfunction
• Signalment
• Most common disease associated with advancing age
• No sex predilection
• Ponies more frequently affected than horses
• Pathophysiology
• Loss of dopaminergic control w/I Pars intermedia
• Secretion of POMC by melanotrophs is regulated by
  inhibition via dopamine
• Produce large amounts of alpha MSH and beta
  endorphins

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PIPD

• CS
• Coat abnormalities (85) Hairy
• Chronic or recurrent laminitis (low grade)
• 52 of cases (33 in geriatric population)
• Sole abscesses are a major problem
• PU/PD
• Type 2 diabetes (38)
• Hyperhydrosis
• Muscle wasting
• Weight loss in very advanced cases

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PIPD

• Lab evaluation
• CBC
• typically normal (may have stress leukogram or
  mild anemia)
• Chemistries
• Hyperglycemia (33), Hyperinsulinemia (62),
  cortisol often normal, high ACTH
• Special diagnostics
• Cortisol (future gold standard) one sample in AM,
  second sample 8-10 hours laterin PIPD les than
  30 variation
• Dex suppression (gold standard)
• Give dex and draw post samples at 5 different
  times
• May worsen or cause laminitis

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PIPD

• Tx
• Excellent management w exercise to maintain
  muscle tone
• Cyproheptadine
• Little evidence that the drug should be
  efficacious but it appears to be effective
• Pergolide
• Treatment of choice
• Dopamine receptor agonist decreases POMC
• Clinical improvement expected in 6-8 weeks
• Prognosis predicted by the degree of
  hyperglycemia

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HYPERLIPIDEMIA/ HYPERLIPEMIA

• Hyperlipidemia serum triglyceride is increased
  but less than 500 mg/dl
• Hyperlipemia serum triglyceride in excess of 500
  mg/dl
• Signalment pony and pony crosses, mini horses,
  donkeys and mini donkeys
• Risk factors
• Obesity
• Lactation/ pregnancy
• Stress/ transportation
• Can be a complication of any primary disease when
  a severe energy dietary imbalance occurs in high
  risk breed

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HYPERLIPIDEMIA/ HYPERLIPEMIA

• Pathophysiology
• Negative energy balance results in FA
  mobilization from adipose tissue
• Ketone pathway poorly developed in horses
  therefore TGs get stuck in the blood
• May exacerbate malaise and may prolong recovery
  from the primary disease
• CS
• CS of primary disease
• Lethargy, ADR, depression and anorexia
• CS often nonspecific

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HYPERLIPIDEMIA/ HYPERLIPEMIA

• Dx
• Serum triglyceride levels
• Evaluation of hepatic and renal function
• Diagnosis of primary disease
• Monitor serum to catch early (visualize serum)
• Tx
• Most important factor- nutritional support
• Reverses negative energy balance
• Try to get them to eat anything (give a variety
  and let them nibble each thing)
• Glucose drip to aid in increasing appetite
• Resolve the primary disease

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HYPERLIPIDEMIA/ HYPERLIPEMIA

• Tx
• Heparin therapy
• Used to be recommended but not much improvement
  with heparin b/c its not typically a problem with
  peripheral utilization of FFA
• Contraindicated in individuals with impaired
  coagulation from decreased hepatic function (d/t
  fatty infiltration)
• Insulin therapy
• Blocks mobilization of adipose tissue
• Increases peripheral uptake and use of TGs from
  the blood
• Prognosis
• Grave (mortality 43)
• Prognosis worse in cases of renal involvement
  rather than just hepatic involvement