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Clinical signs associated with liver disease in horses. (11)
icterus, anorexia, depression, weight loss, colic, diarrhea, fever, encephalopathy, ptyalism, photosensitization, death
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Where does each enzyme come from:
ALP
SDH
AST
GGT
LDH
- ALP- biliary tract
- SDH-hepatic parenchyma
- AST- hepatic parenchyma
- GGT- biliary tract
- LDH- hepatic parenchyma
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What is the only enzyme that is specific to the liver in horses?
sorbitol dehydrogenase (SDH)
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Hepatocellular disease markers. (4)
increased SDH, AST, LDH, unconjugated bili> conjugated bili
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What are cholestatic disease markers? (3)
increased GGT, ALP, conjugated bili
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What are the acute phase proteins of horses? (2)
fibrinogen, serum amyloid A
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The hepatic functional residual capacity (FRC) is __________.
high [ie. when an animal is showing clinical signs, the disease is advanced/severe]
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What are the species susceptibilities to pyrrolizidine alkaloid (PA) toxicity (most to least)?
pigs> chickens> cattle/horses> sheep/goats
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Animals of __________ are more susceptible to PA toxicity; PA toxicity causes ______(2)______.
poor nutrition; chronic fibrosing hepatopathy and hepatic failure
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Animals get chronic fibrosing hepatopathy associated with PA toxicity from... (2)
chronic cumulative exposure and ingestion of 2-5% of body weight of toxic plant
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To become toxic, pyrrolizidine alkaloids must...
be bioactivated by P450 to toxic pyrroles.
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PA alkaloids are __(2)__, causing disease.
cytotoxic and antimitotic [mitotic spindle inhibition]
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How do you diagnose PA toxicity? (4)
clinical findings, increased GGT, hyperbili, liver biopsy
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What are the 3 classic histologic findings on liver biopsy with PA toxicity?
megalocytic hepatopathy, bridging periportal fibrosis, biliary duct hyperplasia
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How do you treat PA toxicity? (3)
supportive/ non-specific, treat hepatic encephalopathy, keep out of direct sunlight (photosensitization)
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What is the prognosis of PA toxicity?
poor
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How do you prevent PA toxicity? (3)
remove from pasture, plant control, herd assessment of GGT
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What pathology is associated with acute cases of PA toxicity? (3)
enlarged liver, hemorrhages, icterus
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What pathology is associated with chronic cases of PA toxicity? (2)
atrophied, small liver, fibrous
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How can hepatic encephalopathy occur? (3)
decreased synthesis of substances required for brain function (glucose), increased synthesis of encephalopathogenic products (ammonia), decreased metabolism of encephalopathogenic precursors [accumulation of toxic products]
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Hepatic encephalopathy is a(n) ____________; therefore, you must address...
secondary disease; address the underlying disease.
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What are potential causes of hepatic encephalopathy? (10)
PA toxicity, Theiler's dz, Tyzzer's dz, Cholangiohepatitis, Cholelithiasis, iron toxicity, neoplasia, PSS, lipidosis/ amyloidosis, necrosis
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What are the theories of how hepatic encephalopathy arises? (4)
toxic metabolite, hyperammonemia, false neurotransmitter/AA imbalance, benzodiaepine-like substances (valium/diazepam, midazolam)
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What are the 3 parts of the toxic metabolite theory of hepatic encephalopathy?
- accumulation of toxic products not metabolized first pass through the liver or bypass the liver
- anatomic defects (PSS)
- nitrogenous metabolites implicates
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With the hyperammonemia theory of HE, there is dysfunction of ___(2)__, leading to an increase in __(3)__, causing... (3)
Na+K+ATPase pump and Kreb's cycle; CNS nitric oxide, free radicals, altered ion dynamics; cell swelling, abnormal ion gradient, demyelination.
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False neurotransmitters are produced from __________; they are thought to cause HE by... (3)
aromatic amino acids; competing for binding sites, activating CNS receptors, altering neuronal function and mentation.
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Describe the benzodiazepine theory of HE.
increased inhibitory GABA, increased production of endogenous GABA, increased inhibition, causing altered mentation, depression, head pressing, aggressive behavior, seizures.
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How do you treat/manage HE in horses? (8)
lactulose (decreases pH and promotes ammonia trapping in the gut), mineral oil, sodium sulfate, activated charcoal, diuresis (decrease cerebral edema), antioxidants, neomycin, supportive therapy, +/- other antibiotics
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How is diagnosis of hepatic inflammatory disease achieved? (3)
liver biopsy, histopathology, tissue culture (determine if bacterial etiology)
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Cholangitis is ______ in horses and is most often associated with ____________.
rare; gram negative enteric organisms
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Tyzzer's disease occurs in __________ horses and is...
young; severe, acute, fulimnant, necrotizing bacterial hepatitis caused by Clostridium piliformis [ingestion].
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Theiler's disease occurs in _________ horses with a....
adult; history of biological products, like an antitoxin or blood transfusion.
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Clinical signs of Tyzzer's disease. (6)
icterus, depression, encephalopathy, diarrhea, colic, acute death
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What is the prognosis for Tyzzer's disease?
grave
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If you attempt treatment for Tyzzer's disease, what will you do? (5)
penicillin, cephalosporins, metronidazole, oxytet, supportive care
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What is the etiology of Theiler's disease?
equine adenovirus, gaining entry from administration of biological products
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What are clinical signs of Theiler's disease? (9)
anorexia, icterus, pigmenturia, fever, edema, colic, photodermatitis, HE, 4-10 weeks after receiving biological products
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What is the prognosis for Theiler's disease?
guarded
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How do you diagnose Theiler's disease? (3)
history, ultrasonography (small liver), histopath (centrilobular and midzonal necrosis/ hemorrhage)
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How do you treat Theiler's disease? (3)
supportive care, minimize stress, treat HE
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