Liver Diseases Flashcards
When are horses naturally slightly icteric?
when off feed
What are the major functions of the liver?
- production of plasma proteins, coagulation factors, and acute phase proteins
- glycogenolysis
- gluconeogenesis
- intermediate metabolism of carbohydrates, proteins, and lipids
- stores fat-soluble vitamins
- detoxifying organ
- first pass metabolism
What are some acute and chronic signs of liver disease? When do signs start?
ACUTE - most common; hepatic encephalopathy, abnormal behavior, icterus, jaundice
CHRONIC - weight loss, intermittent fever or colic, diarrhea, ascites, pruritus, photosensitization
> 60-80% of parenchyma nonfunctional
What are the 2 most common causes of hepatic encephalopathy? What is the most common sign?
- hepatic dysfunction
- portosystemic shunt
behavioral changes - depression, incoordination, aimless wandering, blindness, yawning, stridor, head pressing
What are the 3 main aspects of the pathophysiology of hepatic encephalopathy?
- buildup of neurotoxic ammonia
- release of false neurotransmitters (serotonin)
- imbalanced neurotransmission caused by GABA and glutamate
What 2 induction liver enzymes are used for diagnosing liver disease in horses? What specificity do they have?
(biliary!)
- GGT - liver (screening), kidney, pancreas
- ALP - liver, bone, intestine, macrophages, placenta
What problems are most commonly associated with increased GGT and ALP?
(biliary!)
GGT - biliary hyperplasia and cholestasis, naturally high in young animals (found in colostrum) and racehorses, right colonic displacement, proximal enteritis
ALP - biliary hyperplasia, cholestasis, increased synthesis
What 3 leakage enzymes are used to diagnose liver disease in horses? What specificity do they have?
(liver cytosol!)
- IDH (SDH) - liver
- AST - liver, muscle, heart
- LDH - isoenzymes
What problems are associated with increased IDH (SDH), AST, and LDH?
(liver cytosol!)
IDH (SDH) = acute insult (short life, not stable)
AST = inflammation, infection, metabolic disease, toxins, neoplasia
LDH = acute insult (short life, not specific)
Other than liver enzymes, what biochemistry diagnostics are used to diagnosing liver disease?
- direct (conjugated), indirect (unconjugated) bilirubin
- bile acids
- triglycerids
- clotting factors
- ammonia
What is the purpose of using ultrasound when diagnosing liver disease? Where is the probed placed to locate the equine liver?
- determine size, location, vessel diameter, and texture
- abscess, cholelithiasis, neoplasia, and fibrosis location
right last rib to 10th ICS
What must be checked before performing liver biopsies? How are they used? How are they performed?
clotting times
diagnosis and etiology —> culture, prognosis
ultrasound guided - at 14th ICS, measure from tuber coxae to point of shoulder
Hepatic failure in horses:
What are 4 causes of viral liver disease in horses? How are they most commonly diagnosed?
- Equine parvovirus hepatitis - acute, 33% of horses have antibodies, STRONG association with Theiler’s disease
- nonprimate equine Hepacivirus - like huma hepatitis C, acute and chronic, 80% of horses have antibodies, NOT associated with Theiler’s
- Equine pegivirus 1 and 2
- Equine hepatitis B
PCR
What is Theiler’s disease? What is thought to be the etiology?
common cause of acute liver failure in adult horses - aka serum hepatitis, post-vaccinal hepatitis
VIRAL - Equine Parvovirus Hepatitis (EqPV-H)
What are some expected transmission pathways of Theiler’s disease?
- product recipients
- in contact with product receipients
- no known contact possible!
What are 4 risks to developing Theiler’s disease?
- biologic product administration (TAT)
- broodmares
- recent castration
- seasonal - Summer to Fall
What clinical signs are most commonly seen with Theiler’s disease? What are 4 atypical signs?
- acute hepatic failure within 2-3 months after biologic product contact
- anorexia
- hepatoencephalopathy - pica, yawning
- icterus
- fever
- dermatitis
weight loss, edema, icterus, ARDS
What 6 lab results support Theiler’s disease diagnosis? What other tests can be done?
- increased AST, LDH, SDH, and GGT
- increased total and unconjugated bilirubin
- increased bile acids
- decreased BUN, hyperammonemia
- increased PT, PTT
- decreased albumin
PCR, biopsy (hepatocyte necrosis - dish rag liver)
What is the focus of treating Theiler’s disease? In what 7 ways is this done?
controlled hepatoencephalopathy
- dextrose and balanced electrolytes
- diet low in protein and high in carbohydrates - sorghum, milo, beet pulp
- antioxidants and antiinflammatories
- systemic antimicrobials
- Neomycin, lactulose, mineral oil
- sedation
- corticosteroids
What is Tyzzer disease? What is its etiology?
common cause of acute hepatitis in foals 7-42 days old (also affects intestines and heart)
Clostridium piliforme - spore-forming intracellular anaerobe, multiple strains found in the environment
How is Tyzer disease transmitted? What are the 2 most common risk factors?
colonization in the GIT and liver allows fecal-oral transmission from carriers
- time of year - Spring = mare on lush pasture
- resident status
What is the pathophysiology of Tyzzer disease?
- overgrowth of C. piliforme in the gut of the mare following exposure
- foal ingests mare feces
- bacteria is absorbed by portal circulation and reaches the liver
(sporadic or outbreaks seen)
What are the 2 most common clinical signs of Tyzzer disease? What else is seen?
septic shock and liver failure
- severe depression, fever
- icterus,
- coma, sudden death —> foal commonly found dead without prior signs
What are the 4 most common laboratory signs of Tyzzer disease?
- overwhelming sepsis = leukopenia, hemoconcentration, hyperfibrinemia
- hypoglycemia
- severe acidosis
- increased IDH, AST, LDH, GGT, and ALP
How is Tyzzer disease diagnosed?
- post-mortem: acute multifocal hepatitis, lytic necrosis, enteritis and intrahepatocellular filamentous bacteria seen with silver stain
- culture (difficult!)
- PCR
How is Tyzzer disease treated?
- supportive care
- high doses of Penicillin, Gentamycin, or Metronidazole
- septic shock treatment
(highly fatal)
What are the 2 major causes of chronic liver disease? What signs are most common with each?
- cholangiohepatitis - jaundice, fever, occasional colic, anorexia
- cholestasis (lithiasis) - recurrent colic and weight loss
What are the most common causes if cholangiohepatitis?
- bacteremia
- ascending infection
(causes chronic liver disease)
What are the 2 most common presentations of cholestasis? What are the 3 most common risk factors?
- biliary obstruction and liver disease
- incidental findings
- middle-aged horses
- cholangiohepatitis
- stasis of bile
What are the 4 most common clinical findings seen with chronic liver disease?
- recurrent colic
- intermittent pyrexia
- icterus
- weight loss
What laboratory findings are indicative of chronic liver disease?
- increased GGT and ALP
- increased bilirubin
- increased IDH, LDH, and AST
- increased bile acids
- inflammatory profiles
How is ultrasound used to diagnose chronic liver disease? Where are choleliths most commonly found?
- hepatomegaly
- bile duct dilation = increased echogenicity
- biopsy for histopath and culture
cranioventral part of the right liver - 6-8th ICS
What broad-spectrum antimicrobials are most commonly used for chronic liver disease? How long?
Penicillin, Gentamycin, 3rd gen Cephalosporins, Trimethoprim/Sulfamethoxazole, Enrofloxacin + Metronidazole
6 weeks past normalization of GGT
Other than antimicrobials what treatments are recommended for chronic liver disease?
- DMSO
- fluids
- NSAIDs
- bile salts - anti-inflammatory, choleretic
- cholelithotomy or cholelithotripsy
prognosis based on fibrosis, clinical signs, and location
What causes pyrrolizidine alkaloid toxicity? What does it cause?
ingestion of Senecio or Crotalaria plants, most common when horses have sparse access to food, hay, or pellets
chronic, progressive, often delayed liver disease
What is the pathophysiology of pyrrolizidine alkaloid toxicity?
- PA is activated into pyrrols in liver
- pyrrol is absorbed, reach portal circulation, and reaches the liver again
- pyrrols then cross-link DNA (dose-dependent), having an antimitotic and megalocytic effect
- hepatocytes then no longer divide and are replaced by connective tissue
- this causes liver failure, veno-occlusive disease, nad portal hypertension
What clinical signs are seen with pyrrolizidine alkaloid toxicity?
CHRONIC liver failure due to insult over many years —> signs seem acute
- weight loss
- icterus
- abnormal behavior
- ohotosensitization
- stridor, diarrhea
How is pyrrolizidine alkaloid toxicity diagnosed with bloodwork? U/S? Biopsy?
increased GGT, ALP, bile acids, and bilirubin
increased echogenicity
chronic hepatitis - fibrosis, bile duct proliferation, megalocytosis
What treatment is recommended for pyrrolizidine alkaloid toxicity? What also needs to be considered?
- supportive therapy for liver failure
- Pentoxifylline
- SAMe
- may improve with treatment and relapse once stopped (still ingesting!)
other horse on pasture need to be checked for toxicity on blood work, look out for toxic plants
What are some other toxicities that can cause chronic liver failure?
- alsike clover poisoning
- panicum toxicity
- iron toxicity
- drug-induced hepatotoxicity
What causes hyperlipemia/hepatic lipidosis? What are 3 risk factors?
high caloric need, but low intake results in life-threatening, fatty liver disease with cloudy serum
- well-conditioned, middle-aged
- ponies and donkeys
- early lactation, late pregnancy
What is the pathophysiology of hyperlipemia?
high caloric need and stress with low intake cause a negative energy balance, resulting in….
- fat mobilization
- TG synthesis
- secretion VLDL
- fat accumulation and deposition
What clinical signs are associated with hyperlipemia?
- anorexia, depression, weakness
- incoordination
- diarrhea, colitis
- colic
What are 4 ways hyperlipemia is diagnosed?
- opaque plasma due to TG > 500 mg/dL
- increased bilirubin
- azotemia
- fatty liver infiltration (biopsy)
How is hyperlipemia treated?
emergency!
- treat negative energy balance
- IV fluids
- enteral/parental nutritional support - small volume q2-4hr with critical care meals
- heparin
- insulin for hyperglycemia
When are antimicrobials used to treat liver disease? Which IV and long-term oral ones are most commonly used?
cholelithiasis, cholangitis, cholangiohepatitis
IV - Pen/Gen, Enrofloxacin, Metronidazole
PO - TMS, Enrofloxacin + Metronidazole, Chloramphenicol (careful - liver metabolism!)
What is the most important aspect to hepatic encephalopathy treatment?
avoid self-trauma, minimize stress and neurological damage
- sedation (careful with respiratory distress)
- BZD antagonists - Flumazenil, Sarmazenil
- antioxidants - SAMe, Acetylcysteine, Pentoxifylline
What dietary management is recommended for hepatic encephalopathy?
low protein with high BCAA/AAA —> grass/oat hay, beet pulp, cracked corn
- may need forced enteral or partial parenteral
How can ammonia absorption and cerebral edema be decreased in cases of hepatic encephalopathy?
Neomycin, Lactulose, Acetic acid, mineral oil, Metronidazole
Furosemide, hypertonic saline, Mannitol 20% solution over 20-30 mins
What fluid therapy is recommended for chronic liver disease? What is avoided?
- hydration —> NaCl (0.9%) + Ca + dextrose + KCl, bicarbonate, glucose
- colloids
whole blood or hetastarch
What are 5 treatments used for inflammation and fibrosis associated with chronic liver disease?
- corticosteroids - Dexamethasone, Prednisolone
- NSAIDs
- vitamin E
- Pentoxyfyllin
- Colchicine
What antioxidants are recommended for chronic liver disease?
- SAMe
- N-acetylcysteine
- DMSO
Which enzymes are increased with bile duct obstruction?
a. IDH, AST, LDH
b. GGT, ALP
What other parameters will be elevated?
B
- conjugated BILI > 30% of total
- bile acids
Does the horse have a gallbladder?
NO
What is the most important treatment in a horse with hepatic encephalopathy?
a. prevent self-trauma and stress, fluid therapy with dextrose
b. antimicrobials and antioxidants
c. fluid therapy alone
A
Which of the following indicates cholestasis?
a. total BILI 5 mg/dL, conjugated BILI 2 mg/dL
b. total BILI 5 mg/dL, conjugated BILI 1 mg/dL
c. total BILI 5 mg/dL, conjugated BILI 0.5 mg/dL
A
