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15 Cards in this Set
- Front
- Back
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What are clinical signs of hepatic dz in horses?
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low prevalence in horses
icterus: early acute, late chronic hepatoencephalopathy (HE): depression, lethargy, somnolence, head pressing, yawning, compulsive walking, excitability, mania, seizures, coma potential contributing factors: hyperammonemia, false NTs: ↑ aromatic AAs (methionine, lysine), ↓ branch chain AAs (leucine, isoleucine, valine), biogenic amines, mecraptopurans, SCFA, hypoglycemia: most cases are normoglycemic other neuro signs: peripheral neuro deficits, muscle weakness, truncal ataxia, dysphagia, lar par ↓ appetite or anorexia wt. loss photosensitization fever edema/ascites (usually not present) abdominal pain: recurring colic hemorrhage, ↑ clotting time |
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How are the following serum enzymes interpreted in horses: SDH, AST, GGT, ALP, bilirubin
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SDH, AST, GGT, (ALP):
-marked ↑: acute hepatic necrosis -mild ↑: hypoxemia, endotoxemia, septicemia, intestinal dz, hyperthermia, drugs GGT: biliary epi, cholestasis, short T1/2 ALP: ubiquitous, isoenzymes, cholestasis SDH: liver specific (acute liver dz), short T1/2, unstable AST: not liver specific, ↑ in acute dz, long T1/2 bilirubin: total, direct, indirect (unconjugated) - conjugated bili is a more reliable indicator of hepatic dz -↑ unconjugated bili: anorexia, LI obstruction, hemolysis (ex. red maple toxicosis), drugs (steroids, heparin, halothane) |
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What are some aids to dx of liver dz?
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abdominal U/S
liver bx: do coag panel 1st bilirubinuria bromosulphthalien clearance bile acids: more reliable in chronic active dz ammonia: unstable, process ASAP |
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What is the tx for hepatic insufficiency?
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acute stage: promote liver regeneration
-↓ photodermatitis -correct fluid, electrolyte, acid base abnormalities -↓ toxic protein metabolites (ammonia): oral neomycin, lactulose -sedate if excitatory signs of hepatoencephalopathy -protect from self inflicted injuries -prolonged course of ABs dietary management -feed high carb, low protein ration rich in branch chain AAs: beet pulp, sorghum -frequent small meals: beet pulp mix, grass (oat) hap, pasture grazing |
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Theiler's dz
a. etiology/occurrence b. risk factor c. clinical signs d. tx |
a. etiology: unknown
-sporadic occurrence, effects adults -in 20% of cases, equine origin biologic given 25-120 d. prior (vaccine, antiserum: tetanus antitoxin) b. risk factor: lactating mares given tetanus antitoxin c. clinical course of 1-5 d. -high mortality rate -afebrile, icterus, anorexia, abdominal pain, petechiae, profound HE, photosensitization d. aggressive supportive therapy |
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Tyzzer's dz
a. etiologic agent b. clinical signs c. px |
a. etiologic agent: Clostridium piliformis
b. acute septicemia in foals 7-42 d. old clinical signs: sporadic, non-specific c. invariably fatal |
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chronic active hepatitis
a. etiology b. clinical signs c. dx d. tx |
a. idiopathic: possible autoimmune or hypersensitivity rxn, or manifestation of chronic cholangitis
b. insidious onset, intermittent episodes -clinical signs: progressive hepatic failure, exfoliative coronary dermatitis c. hepatic enzymes, liver bx d. supportive, immunosuppressive dose of corticosteroids, ABs |
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pyrrolizidine alkaloid toxicity
a. etiologic agents b. conditions of poisoning c. clinical signs d. lesions |
a. plant alkaloid: Senecio sp, Amsinckia sp, Crotalaria sp, Heliotrope, Lupinus, Astragalus, etc.
b. usually chronic, but acute episodes can occur -plants are unpalatable: usually exposed when cut or baled in hay mixed in cubes c. signs occur long after removal from toxin source -usually abrupt onset of hepatic failure: HE, icterus (late), photosensitization -chronic liver failure, +/- wt. loss d. megalocytosis, biliary hyperplasia |
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cholelithiasis
a. pathogenesis b. clinical signs c. dx d. tx e. px |
a. calculi consist of calcium bilirubinate
-stones may not form readily unless there is preexisting cholangitis -calculi, sludge, cholangitis, suppurative inflammation --> biliary tract obstruction, intra/extra hepatic cholestasis b. recurrent colic, icterus, fever, depression, wt. loss c. markedly ↑ GGT, ALP, transabdominal U/S, liver bx d. supportive care, long term ABs for cholangitis, sx esp. if common bile duct occluded e. guarded |
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bacterial cholangiohepatitis
a. etiology b. clinical signs c. dx d. tx |
a. usually 2º to other liver/bilary dz or ascending infection from intestinal tract
b. fever, anorexia, icterus c. ↑ GGT, ALP, transabdominal U/S, liver bx d. supportive care, long term ABs |
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hyperlipemia, hepatic lipidosis
a. signalment b. clinical signs c. tx |
a. most common in ponies, miniature horses
-predisposing factors: obesity, late pregnancy/lactation b. clinical signs: anorexia, severe depression, icterus, HE, laminitis c. IV dextrose, correct acid-base imbalances, insulin w/ oral glucose, heparin IV |
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What is the approach to chronic weight loss?
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-assess BCS, hx, PE (incl. thorough oral exam), clin path
-predict outcome: presumptive dx, px -ascertain owner expectations: time, financial -initiate therapy, management |
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What are some ddx for chronic wt. loss?
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respiratory
CV: 1º rare GI: dental disorders hepatobiliary musculoskeletal: arthritis, muscle atrophy urogenital endocrine neurological: motor neuron dz multiple factors -systemic disorders: abscess, sepsis, pain -behavioral: vices, social group -neoplasia (uncommon): U/S, bx, cytology |
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What is the treatment for chronic wt. loss?
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improve nutrition: start w/ small amts. frequently, esp. hay
ID & treat 1º disorder provide supportive therapy enhance immune function deworm recommend preventive measures: parasite control, vaccines, pasture management, toxin avoidance |
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What are some nutritional principles important in treating chronic wt. loss?
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start w/ small amts. frequently, esp. hay
aim: restore BCS ≥ 4 modify ration relative to age & dentition: horses w/ dental problems can chew pellets or extruded feeds softened in water, or eat a soupy mash feed small amts. often feed malnourished horses separately avoid reliance on grazing: soft slurry, energy dense ration (↑ fat content) ↑ energy availability thru concentrate, pelleted, or extruded feed & high energy dense fats in processed feeds or by adding vegetable oil |
