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44 Cards in this Set
- Front
- Back
How much of cardiac output does the liver receive? |
1/3-1/2 |
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What are the two general patterns of liver disease? What is each susceptible to? |
Periportal pattern (zone 1) - susceptible to toxins Centrilobar pattern (zone 3) - susceptible to ischemic injury |
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How much of the liver may be damaged before you see signs of hepatic insufficiency? |
80% |
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What are the most common signs of hepatic disease in horses? |
Depression Anorexia Colic Icterus (may have pigmenturia) Hepatic encephalopathy |
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What is icterus? |
An accumulation of bilirubin in the tissues. May be due to failure of uptake, conjugation, or excretion of bilirubin. Other pigments may also cause yellow discolouration. |
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What can cause hepatic encephalopathy? |
Hepatic insufficiency or shunting of blood past the liver (portosystemic shunts are rare in horses). Will have hyperammonemia and aromatic amino acids in the blood (act as neurotransmitters and increase inhibitory NTs at GABA receptors) |
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What are the clinical signs of hepatic encephalopathy? |
Depression Drastic behaviour change Ataxia, paresis Aimless wandering Head pressing Yawning Grimace Stupor/coma |
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What tools are useful to evaluate a suspected hepatic encephalopathy horse? |
Clinical pathology Ultrasound Biopsy (others) |
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What liver enzymes are most useful to measure in horses? |
SDH GLDH (not commonly done) AST Arginase |
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What are the two cholestatic enzymes? |
GGT ALP |
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What is bilirubin? What would tell you that there may be hepatobiliary disease? |
Bilirubin - a normal metabolite of heme formed in macrophages. An increase in conjugated bilirubin to more than 25% of total bilirubin is consistent with hepatobiliary disease (so need to measure conjugated and unconjugated). |
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What test is useful for indicating hepatic function in the horse? |
Bile acids! |
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Describe the expected changes with liver disease for albumin, globulins, clotting time, BUN/ammonia, and glucose. |
Albumin - decreased with very chronic liver disease Globulins - increased (inflammation) Clotting times - prolonged (factors 2, 7, 9 10 made in liver) BUN - decrease Ammonia - increase Glucose - decreased |
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What might you see on ultrasound of a diseased liver? |
Prominent vascular pattern (portal veins with prominent fibrous tissue lining (white circles) vs hepatic veins) Likely won't see bile ducts Limitations: ribs, depth/size of liver, abdominal viscera |
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Describe principles of taking a liver biopsy. |
First: do a pre-biopsy coagulation profile! PT, APTT. Ultrasound-guided biopsy is best Use a 14g TruCut biopsy needle Send it for histopathology and culture. |
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In general, how do you treat liver disease? |
Mostly supportive care. Fluids (dehydration, acid/base abnormalities, electrolytes) Nutritional supplementation Decrease toxin production/absorption from gut Anti-inflammatories Manage hepatic encephalopathy |
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Describe a "traditional liver diet" for a horse. |
Low protein High carbohydrates Rich in branched-chain amino acids + grass hay Fed in multiple small meals (help maintain blood glucose) |
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What can you use to help decrease production and absorption of toxins? |
Mineral oil Magnesium sulfate (these two decrease transit time, and reduce the time for bacteria to produce ammonia, or for the gut to absorb it) Oral antibiotics to decrease NH4 absorption (metronidazole, lactulose? listed but not an abx) |
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Why should you avoid giving diazepam to sedate a horse with hepatic encephalopathy? |
Hepatotoxic Can cause excitation alone ACTIVATES GABA - things will get so much worse!! |
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Name three other supportive medications that can be used to treat liver disease. |
Sam-e Pentoxyfylline Milk thistle |
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What's the best way to determine prognosis for liver disease? |
Severity of clinical signs |
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What causes acute hepatitis in horses? |
Unknown but has been linked to... - Equine serum products - Viruses - Hepatotoxic substances - Type III hypersensitivity |
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What are the clinical signs of acute hepatitis? |
(Typically in adults) Anorexia Acute depression Other CNS signs (including hepatoencephalopathy) Icterus "Colic" |
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How can you diagnose acute hepatitis?
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History of an equine-origin biologic Clinical signs Bloodwork Biopsy (widespread necrosis, centrilobular) Necropsy |
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How do you treat acute hepatitis? What's the prognosis? |
Treatment: nonspecific, hepatosupportive. May need sedation to control mania. Prognosis: often stabilize within 2 days, with supportive care. Prognosis is poorer if severe HE, hemorrhage, hemolysis, or if mania persists through sedation. |
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What is the causative agent of Tyzzer's disease? |
Clostridium piliformis |
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What are the clinical signs of Tyzzer's disease? |
(Note: typically in foals 9-30 days) Acute depression Icterus Fever Anorexia Diarrhea Seizures/coma Rapid progression to death |
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How can you diagnose Tyzzer's disease? |
Antemortem: - Age, clinical signs - Icterus, increased liver enzymes, bile acids, bilirubin - Biopsy (and maybe RT-PCR) Postmortem: - Hepatomegaly - Multifocal miliary hepatic necrosis - Organisms demonstrated with silver stain |
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How do you treat Tyzzer's disease? |
Antibiotics: tetracycline, penicillin, or TMS Supportive care Parenteral nutrition Note: peracute death common, so treatment is rarely effective |
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What is cholangiohepatitis? |
Inflammation of the bile passages and adjacent liver parenchyma. |
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What are the suspected etiologies of cholangiohepatitis? |
Ascending infection Parasite migration Chronic biliary stasis Biliary reflux |
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What are the clinical signs of cholangiohepatitis? |
Pyrexia Colic Icterus Chronic, significant weight loss |
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How do you diagnose and treat cholangiohepatitis? |
Dx: liver biopsy (histopath, culture) Tx: systemic antibiotics - long course - primarily g- bacteria from the gut - support liver function and treat underlying disease |
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What are some plants that contain pyrrolizidine alkaloids? |
Amsinckia intermedia Senecio spp Crotalaria spp |
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What are the clinical signs of pyrrolizidine alkaloid toxicosis? |
Depression WEight loss Icterus Photodermatitis Hepatoencephalopathy |
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How do you diagnose pyrrolizidine alkaloid toxicosis? |
History (walk the field!) Bloodwork suggestive of liver disease Biopsy (megalocytosis is pathognomonic) |
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How can you treat pyrrolizidine alkaloid toxicosis? What's the prognosis? |
Tx: Supportive treatment, and treat asymptomatic animals. Remove others from the field. Prognosis: poor. Often die 5-10 days after signs appear. |
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What's the toxin in alsike clover? |
Suspected... sooty blotch (Cymadothea trifolii), a fungal plant pathogen. May see black, irregular lesions on the back side of leaves. |
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What are the clinical signs of alsike clover toxicity? |
Photosensitization Liver failure (and associated signs) Nervous/digestive disorders (colic, diarrhea, oral lesions) |
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In what animals is hepatic lipidosis more common? |
Miniature horses Donkeys (mini and normal) Adult horses (esp if obesity, weight loss, stressful events, or anorexia) |
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Describe the pathogenesis of hepatic lipidosis. |
Decreased carbohydrate availability > energy from fatty acid oxidation > overwhelmed liver gluconeogenesis > ^^triglyceride storage Things that increase removal of fatty acids from adipose tissue: increased glucocorticoids, increased glucagon, decreased insulin |
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What are the clinical signs of hepatic lipidosis? |
Icterus Anorexia Weakness/ataxia Severe depression Recumbency Diarrhea Mild abdominal pain Fever Dependent edema |
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How can you diagnose hepatic lipidosis? |
Bloodwork (hepatic panel, lipids/triglycerides) Ketonuria Ultrasound Biopsy |
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How do you treat hepatic lipidosis? |
Improve energy intake and balance Treat hepatic disease Eliminate stress/treat concurrent disease Inhibit fat mobilization from adipose (insulin) Increase triglyceride uptake in tissues (heparin) |