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529 Cards in this Set
- Front
- Back
How much liver function must be lost before clinical signs or abnormal bloodwork is seen?
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80%
|
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In the horse, which liver enzyme is highly specific for hepatocellular damage?
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SDH (sorbitol dehydrogenase)
|
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With cellular injury, SDH is released from where?
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Cytoplasm of hepatocyte
|
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AST is a non-specific liver enzyme since it is also present where in the equine?
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Liver, skeletal and cardiac muscle, RBC
|
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AST can be falsely increased with what conditions?
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Hemolysis and lipemia
|
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ALP is an enzyme that is indicative of what?
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Biliary obstruction of cholestasis
|
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ALP can also be elevated with what condition?
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Neonates with osteoblastic activity
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In horses, which enzyme is the most sensitive indicator of liver disease?
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GGT
|
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GGT is an indicator of what liver condition?
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Biliary tract disease or cholestasis
|
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What do young animals have higher GGT?
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Colostral ingestion
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Is bilirubin a sensitive indicator of liver dz in the horse?
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No
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In the liver, free or indirect bilirubin is conjugated with what?
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glucose
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Direct (conjugated) bilirubin should be how much of total bilirubin?
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< 25% of the total
|
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What other condition can cause hyperbilirubinemia?
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Anorexia, fasting
|
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In fasting hyperbilirubinemia, which portion of bilirubin is elevated?
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Indirect (unconjugated)
|
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What does elevated bile acids indicate?
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Only that hepatobiliary function is abnormal
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When performing a bile acid test, which sample is not needed?
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Fasting
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What is the benefit of measuring bile acids in a horse?
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More sensitive of liver dz than bilirubin
|
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Why would you measure blood ammonia?
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Failure of the liver to process ammonia into urea may result from chronic hepatocellular dz leading to hyperammonia (and hepatocencephalopathy)
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What other 2 heaptic products will decrease with liver dysfunction?
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BUN, coagulation factors (7, ext pathway PT)
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On U/S, the liver should remain within what boundary?
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Costochondral junctions
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What structures of the lover can be seen with endoscopy?
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Distal portion of common bile duct only
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What is the benefit of performing a liver bx?
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Provides definitive dx and allows the clinician top offer a prognosis
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In which pts should a liver bx be performed with extra caution?
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Clinical bleeding diatheses
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What are the indicators for a poor prognosis in a horse with liver dz?
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-hypoalbuminemia <2.5g/dl
-increased globulin level -prolonged PT by 30% -chronic severe elevation of GGT -bridging fibrosis of liver lobules on histopath |
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What are the terminal clinical signs in a horse with a fibrotic liver?
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Hemolytic crisis and marked hepatoencephalopathy
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What is the most classic sign of liver dz?
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Icterus- oral mucus membranes, sclera, aural/vaginal mucosa
|
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What causes icterus?
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Failure to excrete bilirubin
|
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In horses, what condition can cause jaundice without primary liver dysfunction?
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Anorexic hyperbilirubinemia
|
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What are the clinical signs of hepatic encephalopathy?
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-anbnormal mentation, cortical dysfunction
-alterations in behavior -wandering aimlessly -circling/head pressing -inspiratory stertor -yawning |
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What is the cause of dermatitis/photosensitization with liver disease?
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Failure of the liver to excrete phylloerthrin, is transported to the skin, reacts with UV light
|
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Why is diarrhea a sign of liver dysfunction?
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Failure of the liver to recirculate bile acids leads to poor digestion of fat and subsequent diarrhea
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Failures of the liver to metabolize carbs, fats and proteins leads to what clinical signs of liver failure?
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Lethargy/wt loss
|
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Why is peripheral edema a sign of liver dz?
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Liver fails to produce the primary plasma protein albumin, oncotic pressure drops, allowing fluid to leak into the interstitium leading to edema
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What is the cause of ascites in liver patients?
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Portal hypertension and increased hydrostatic pressure along the sinusoidal channels increase lymph production- lymph is high in protein and leaks to the peritoneum and then the peritoneal cavity
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Bleeding diatheses is a result of the liver failing to produce which clotting factors?
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2, 7, 9, 10
|
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Horses with what type of acute liver failure have a better chance for long-term regeneration of the liver?
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Those with no evidence of chronic fibrosis
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CNS dysfunction is most likely due to what?
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Abnormal protein metabolism by the liver
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From the abnormal protein metabolism, levels of what chemical rise in the blood?
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Ammonia
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What is the goal of initial tx for HE?
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-abolishing the abnormal behaviors to prevent the horse for endangering itself and others
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Which class of drugs should be avoided in cases of HE, and why?
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Avoid benzodiazepines, effects of GABA on inhibitory neurons may worsen signs of HE
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What is the drug of choice to use as a sedative for a horse with HE?
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Detomidine- a2 agonist
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Is neomycin a good choice for a drug that will minimize the amount of ammonia in the system?
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Only initially, prolonged use may be toxic to intestinal enterocytes
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Why is the administration of dextrose important, esp since most horses in liver failure aren’t hypoglycemic?
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-provides PPN is horse is anorexic
-decreases ammonia concentration in blood -decreases reliance of catabolic gluconeogenesis -decreases protein catabolism -spares hepatic energy used in gluconeogenesis |
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Blood glucose should be maintained at what level for a horse?
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80-120 mg/dl
|
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Horses with liver should consume a diet comprised of what components?
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-branched chain amino acids
-very low protein fiber -oats and grass hay, avoid alfalfa |
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Horses that have chronic active hepatitis may have cholangiohepatitis as well.. these a usually brought on by what type of infection?
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Ascending infection, gram neg, from the GI tract
|
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When is the use of abx in a horse with liver disease indicated?
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-following liver bx
-histopath results of inflammatory infiltrates -positive results of bx tissues culture and sensitivity |
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What are the useful abx in liver patients?
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-pcn, gentamycin
-enrofloxicin -chlorampehincol -trimethroprim-sulfa |
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What anti-inflammatory drugs should be given to horses with liver dz?
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-Banamine
-pentoxifylline |
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What is the use of DMSO in liver dz?
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May dissolve small biliary stones of sludge within the biliary tract
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When would sx be indicted for a liver pt?
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When there is obstruction to the distal bile duct and no fibrosis is present
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Idiopathic acute hepatitis , the most common cause of acute hepatitis and acute liver failure in horses, is also known as what?
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Theiler’s dz
Serum hepatitis Post-vaccinal hepatitis |
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IAHD is most often associated with what?
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Administration of equine biologic products in adult horses
|
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It has been proposed that IAHD is what type of reactions?
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Type III immune mediated
|
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Which clinical sign of liver failure is NOT seen in IAHD?
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Fever
|
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Diagnosis of IAHD is largely determined by what?
|
-anamnesis
-concurrent clinical signs -abnormalities on serum chem., liver bx, necropsy |
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Confirmation of IAHD requires what?
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Bx or necropsy of the liver
|
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With IAHD, where is the hepatocellular necrosis most severe?
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Centrilobar region
|
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What type of tx is used for IAHD?
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Supportive
|
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What type of dietary changes are made for tx IAHD?
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-low protein
-increase carbs -branched chain amino acids |
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In the US, IAHD is associated with what type of horse and why?
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Brood mare, use of TAT following parturition
|
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Signs of PA toxicity may be seen when after ingestion?
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4 weeks to 1 year
|
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What are the most common clinical signs of PA toxicity?
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-weight loss
-slight to moderate icterus -HE -photosensitization and diarrhea may occur -mares may abort |
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How much of the plant must be ingested to cause toxicity?
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2-5% of the horses body weight
|
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What are the common PA plants in the US?
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-Senecio (tansy ragwort, groundsel)
-Amsinckia (fiddleneck) -Crotalaria (rattlebox) |
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What is the result of ingestion of PAs?
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Carried to the liver, metabolized to pyrrole derivatives, can cross link double stranded DNA which inhibits nuclear acids, cell replication and protein synthesis. Hepatocyte unable to divie, becomes enlarged and forms megalocytes
|
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What happens to megalocytes when they die?
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Replaced by connective tissue and fibrosis
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Hepatocytes located where are first affected by PA toxicosis?
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Surrounding portal triads
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What is the result of venooclusive dz which disrupts blood supply to the liver?
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Regeneration is impossible
|
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Periportal dz from Pas causes which liver enzymes to be persistently elevated?
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GGT, ALP
|
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What is the pathognomonic sign of PA toxicosis?
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-megalocytes
-biliary hyperplasia -periportal fibrosis |
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What is the tx for PA toxicity?
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There is none- death occurs within 10 days of clinical signs of liver failure
|
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Which liver enzyme is the most reliable indicator of subclinical PA?
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GGT
|
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What are the causes of intrahepatic biliary tract disease?
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-cholangitis
-cholelithiasis -choledocholiththiasis (cbd) -foreign body |
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What are the extrahepatic causes of biliary tract disease?
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-abscess formation
-inflammatory dz near the CBD -neoplasia |
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Which is the most common cause of biliary obstruction in the horse?
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Choledocholelithiasis (CBD)
|
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What are bile stones comprised of?
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Precipitates or aggregates of biliary components: bilirubin, bile pigments, cholesterol, carboxylic acid, calcium phosphate, sodium taurodeoxycholate
|
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What are the triad of clinical signs of cholelithiasis in a horse?
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Colic (intermittent but recurrent, fever, jaundice
|
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What additional signs may be seen?
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-HE
-photosensitization -weight loss |
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Cholelithiasis should be suspected when direct (conjugated) bilirubin is at what level?
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>30% of total bilirubin
|
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What effect does obstruction to flow have on bile acids?
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Bile acids are elevated
|
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What other parameters are elevated with cholelithiasis?
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-GGT, ALP, AST, SDH,
-neutrophilic leukocytosis -elevated fibrinogen and globulins |
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How is cholelithiasis dx?
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-abnormal hepatic enzymes
-U/S |
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What is the appearance of a liver with cholelithiasis?
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Echogenicity of the liver parenchyma is increased (comparable to the spleen), bile ducts are tortuous
|
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Hyperlipidemia, hyperlipemia and hypertriglyceridemia are all characterized by what classical clinical signs?
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-anorexia
-depression -lethargy |
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How would you describe hyperlipidemia?
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Mild to moderately elevated serum triglycerides (TGs) with no evidence of lipemic serum or hepatic dysfunction
|
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What is hyperlipemia?
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Moderately elevated TGs with milky serum and fatty infiltrates within the liver
|
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Which animals are known for having hyperlipemia?
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Ponies, donkeys, miniature horses
|
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What is hypertriglyceridemia?
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Mod to severly elevated TG, no evidence of lipemia (no milky serum) and no evidence of fatty liver
|
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What are the risk factors for developing excess circulating TGs?
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-mini horse, donkey, pony
-female -obese animal -endotoxemia -enterocolitis -azotemia -preg (late) -lactation -stress -anything that predisposes the animal to a negative energy balance |
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When glycogen stores from the liver are used up, where does energy come from?
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Fatty acid oxidation
|
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What triggers the mobilization of fat as energy?
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Stress or inability to maintain energy homeostasis
|
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What underlying diseases can trigger fatty oxidation?
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-enterocolitis
-endotoxemia -azotemia -infection -parasitism -neoplasia -transport -weaning |
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Exogneous fat sources are acquired from where?
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Dietary intake
|
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How are short chain fatty acids transported to the liver?
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Incorporated into phospholipids or TGs by the intestinal epithelium and sent to the liver via portal blood
|
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Larger fatty acids are broken down with the small intestinal lumen by what?
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Bile acids- which surround the FAs
|
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What is the role of lipases from the pancreas?
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Cleave the bile acid into 2 FFAs and 1 monoglyceride- bile acid continues down SI lumen and is resorbed
|
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What is a micelle?
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The 2 FFAs and 1 monoglyceride combine to make a water soluble micelle which is absorbed into the enterocytes (absorbed across the brush border via the unstirred layer)
|
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What happens to the micelle once it is in the endoplasmic reticulum?
|
Re-esterified into triglycerides with phospholipids, cholesterol and proteins
|
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What are chylomicrons?
|
The rough ER packages the re-esterified micelles into chylomicrons (water soluble) and expels them into the lateral space (between 2 enterocytes)
|
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How do the chylomicrons get to the liver?
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Picked up by the lymphatic circulation, dumped into the vena cava and then into the liver for processing
|
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What is the source of endogenous TGs mobilized for oxidation?
|
Adipose tissue
|
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Which hormones control the mobilization of adipose tissue?
|
-glucagon
-norepinephrine -epinephrine |
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Once in the liver, what determines the fate of the lipids?
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The energy requirements of the animal and the amount of fat and glucose absorbed from the daily diet.
|
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What 5 products can be made by the liver from lipids?
|
1. Oxidation to acetyl CoAATPenergy
2. Esterification into TGs for storage in the liver 3. Used for gluconeogenesis 4. Made into ketone bodies 5. FFAs used to make TGs that are released into sinusoidal blood as VLDLs |
|
VLDLs are transported to where?
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Adipose tissue
|
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What is the rate limiting step of storing VLDLs into adipose tissue?
|
Lipoprotein lipase (LPL)- activity is stimulated by insulin
|
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True or false…the overproduction of VLDLs by the liver is the cause of hyperlipemia in ponies, mini horses and donkeys?
|
True
|
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Why is it unlikely for horses to suffer ketoacidosis?
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Hepatic efficiency of synthesizing TGs and VLDLs and exporting them back to the bloodstream
|
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What is the effect of hepatic lipidosis?
|
Fatty infiltrates of the hepatocytes disrupt normal function and may result in hepatic rupture and/or failure
|
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What effect does insulin have on adipose tissue?
|
Less mobilization of FAs to the liver
Stimulates LDL to remove VLDLs from circulation |
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What effect do high levels of LPS from endotoxemia have on VLDLs?
|
Interferes with LPLs ability to removes VLDL from circulation
|
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Hyperlipemia should be considered in any obese pony or donkey with what clinical signs?
|
-anorexia
-depression -lethargy |
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What should you suspect in a horse with decreased attitude and appetite in the face of critical illness?
|
Hypertriglyceridemia
|
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What is the appearance of serum in the case of hyperlipemia?
|
Opalescent
|
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What chemistry results would you expect with end stage liver failure?
|
Decreased glucose, BUN, albumin
|
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The presence of elevated TG’s leads to what vicious cycle?
|
Inappetance and further elevations in TGs
|
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How can hepatic lipidosis, hyperlipidemia, hyperlipemia/triglyceridemia be resolved?
|
Assessment and resolution of the underlying disease process
Endotoxemia / enterocolitis resolution -Pregnant mares may require abortion -Lactating mares should have foals weaned |
|
Alternate energy sources can be provided by what means?
|
-enteral
-parenteral Dextrose CRI Enteral feeding of 10% of energy reqs Insulin to counteract hyperglycemia from dextrose |
|
During the PE of the horse, where is the mitral valve located?
|
Left 5th intercostal space, midway between the shoulder and olecranon
|
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Where is the aortic valve located?
|
Left 3rd to 4th intercostal space, just below the shoulder
|
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Which valve is located on the left at the 3rd ICS just below the aortic valve?
|
Pulmonic
|
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How would you localize the tricuspid valve?
|
On the right at the 4th ICS midway between the shoulder and olecranon
|
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The normal S1 heart sound is caused by what?
|
Ventricles contract, AV valves close, pulse occurs
|
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What is the cause of the normal S2 heart sound?
|
Semilunar valves close, diastole
|
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What causes the normal S3 heart sound?
|
Rapid ventricular filling
|
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How often might you hear S3 in the horse?
|
50% of horses, often mistaken for a murmur or split heart sound
|
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S4 may be heard in horses and is caused by what?
|
Atrial contraction
|
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What are non-pathologic murmurs?
|
Murmurs that occur without organic heart disease
|
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What are some examples of non-pathologic murmurs?
|
-increased velocity in blood (excitement)
-changes in blood viscosity (anemia or dehydration) -66% of horses have systolic functional murmurs -< grade III -aortic or pulmonic -most common in neonates |
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What is the range of the normal resting heartbeat of the horse?
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24-44 beats/min
|
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Which heart rhythm is the most common in horses?
|
Regular sinus rhythm
|
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Which is the most common, non-pathologcal arrhythmia in horses?
|
2 degree AV block
|
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What are the conditions seen with 2 degree AV block?
|
-increased vagal tone
-easily eliminated with excitement -heart rate should remain > 24 bpm -S4 should be the only sound during block -confirm with ECG |
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What block would you suspect if S4 cannot be ascultated
|
Sinus block (rare in horse)
|
|
How is sinus block characterized?
|
Long pauses in sinus beat/eliminated with exercise
|
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What causes a sinus block?
|
Increased vagal tone in which SA node does not fire
|
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When is sinus arrhythmia normal?
|
After exercise
|
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What arrhythmia may be heard in a horse esp. after light exercise, and are considered normal?
|
Occasional atril or ventricular premature contraction
|
|
When is it normal to have 3rd degree complete heart block?
|
NEVER!
|
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What general clinical signs might be seen in a horse with cardiac disease?
|
-exercise intolerance
-lethargy or depression -anorexia or weight loss |
|
A less common sign of heart dz is dependent edema which may be seen with what type of heart dz?
|
Right heart failure
|
|
Where does dependent edema occur?
|
ventral thorax and abdomen, distal limbs in severe cases
|
|
How do you determine edema from inflammation?
|
edema should by cool , pitting, nonpainful and symmetrical
|
|
What general respiratory signs are seen with cardiac dz?
|
-tachypnea from hypoxia or pulmonary edema
|
|
What respiratory sounds might you hear with cardiac dz?
|
-cough and audible crackles from pulmonary edema with left heart failure
|
|
What is a common cause of pulmonary edema in horses?
|
Ruptured chordae tendinae of the mitral valve
|
|
When aucultating the heart, what 3 factors do you consider
|
-rate
-rhythm -murmurs |
|
What conditions are you concerned about when assessing heart rate?
|
-tachycardia and bradycardia (sustained)
|
|
When might you be concerned about a normal rhythm with premature contractions?
|
When the rate is increased or occur more frequently than a few per hour
|
|
Pathologic murmurs are associated with what conditions?
|
-valvular abnormality
-shunts -altered contractility -altered blood viscosity |
|
When characterizing a mumur, a systolic murmur is heard when?
|
Between S1 and S2 (audible during palpation of peripheral pulse)
|
|
When is a diastolic murmur heard?
|
Between S2 and S1
|
|
What is meant by a murmur's point of maximum intensity?
|
Select valve or area where murmur is loudest
|
|
The quality of sound of a murmur is subjective without what tool?
|
A phonogram
|
|
Pathologic murmurs are commonly which grade?
|
>Grade 3
|
|
What are the 3 factors useful for determining the cause of a murmur?
|
-PMI
-Timing -valvular activity at the time murmur is asculted: is the valve open or closed? |
|
What is a general sign of increased cardiac pressure?
|
Generalized venous distension
|
|
Jugular pulses seen above the lower 1/3 of the neck can be a sign of what type of heart failure?
|
-tricuspid regurgitation and right heart failure
|
|
Jugular pulsations can be confused buy what other pulse?
|
Referred from carotid artery
|
|
Jugular distension without pulsation is a sign of what condition?
|
Obstruction- thrombosis of jugular vein
|
|
Aortic valve insufficiency is often associated with what change in the pulse?
|
Bounding pulses
|
|
Why is an EC the most useful diagnostic tool for rate and rhythm of the horse heart?
|
Due to large size of equine heart and extensive Purkinje network
|
|
In horses, an ECG provides less information regarding what?
|
heart size
|
|
Which lead is used for an ECG of a horse?
|
1- base lead
|
|
How are the ECG leads positioned for a base lead of a horse?
|
-white lead on right shoulder
-black lead on heart apex -red lead on neck -run on lead 1 |
|
What normal difference might you see in the P wave of a horse ECG?
|
Often bipolar and may change configuration
|
|
In which direction is the QRS in a base lead ECG of a horse?
|
usually negative
|
|
True or false....in a base lead ECG of a horse, the T is usually positive
|
true
|
|
On an ECG 15 big boxes equals how many seconds?
|
3
|
|
What type of probe is needed to perform echocardiograms?
|
2.5 MHz
|
|
Majority of echo imaging is done on which side of the heart?
|
Right
|
|
What structural info can be gained from an echo?
|
-size of heart chambers and outflow vessels
-shape of valves -thickness or walls -confirm presence of pericarditis or endocarditis |
|
What functional information is gained from an echo?
|
-motion of walls and valves
-fractional shortening |
|
What is the normal fractional shortening in a large animal?
|
34-45 %
|
|
What does fractional shortening of <25% indicate?
|
Failure
|
|
Serum chemistry might show what results with heart dz?
|
-azotemia
-increased liver enzymes |
|
Which cardiac enzyme might be increased with mycarditis?
|
Serum cardiac troponin I
|
|
What conditions might a decreased PaO2 indicate?
|
hypoxemia and shunts
|
|
An indirect blood pressure on a horse is taken from where?
|
Coccygeal artery
|
|
When using exercise tests to detect heart disease, normally a the heart and respiratory rates should return to what levels in what timeframe?
|
Return to within 15% of resting value within 15 minutes of the end of exercise
|
|
What technique is used to detect transient or intermittent arrhythmias?
|
Holter monitor
|
|
Pathologic murmurs in horses are of what two types?
|
-congenital
-acquired |
|
What is the msot common congenital abnormality of the horse?
|
Interventricular septal defect (VSD)
|
|
In which direction does blood flow in the heart with a VSD?
|
Left to right
|
|
VSD leads to what conditions within the circulatory system?
|
Pulmonary hypertension and left sided overload, may eventually lead to pulmonary edema and left sided failure
|
|
What are the clinical size of a larger (>2.5cm) VSD?
|
-poor growth, exercise intolerance
-pulmonary hypertension and heart failure -signs develop over days to months |
|
A VSD will produce a > Grade III murmur on what side?
|
Right
|
|
Often there is another murmur, where?
|
Systolic over the mitral or aortic valve
|
|
What tests are used to confirm a VSD?
|
-Echo
-bubble test or color flow Doppler |
|
What characteristic of a VSD dictates the prognosis?
|
Size of the defect
|
|
What is the course of action it the horse is symptomatic?
|
Euthanasia
|
|
What drugs might be used for medical management of VSD?
|
-furosemide (Lasix)
-digoxin |
|
What are the components of the tetralogy of Fallot?
|
-VSD
-aorta displace to right -pulmonic stenosis -right ventricular hyperplasia |
|
What are the clinical signs of TOF?
|
-cyanosis
-poor growth, exercise intolerance in young animals -right to left shunting of blood across VSD |
|
The right to left shunt through the VSD causes what additional complications?
|
-obstruction of outflow of right ventricle through the stenotic pulmonary artery
-leads to inadequate oxygenation of blood |
|
How is TOF diagnosed?
|
-left sided heart base systolic murmur (grade III or >)
-may also be asculted on the right in a young animal -confirm with 2D echo |
|
What is the prognosis of TOF?
|
Poor to grave
|
|
True or False....PDA is just as common in horses as in small animals
|
False, no common
usually subclinical not treated |
|
Are valvular lesions congenital or acquired?
|
Acquired
|
|
Valvular lesions include what types of conditions?
|
-degenerative changes
-valvular changes -myocarditis -endocarditis -ruptured chordae tendinae -congenital valve defects |
|
Do abnormal valves lead to insufficiency/leakage or stenosis?
|
Leakage
|
|
Large leaks of a valve lead to what changes?
|
-regurgitation back into the preceding heart chamber
-enlargement of proximal chamber and subsequent volume overload |
|
Severe volume overload leads to what?
|
Heart failure
|
|
Where are the most common acquired valvular insufficiencies in the horse?
|
Aortic and mitral
|
|
Aortic and mitral insufficiency lead to what problems?
|
Left sided volume overload and pulmonary hypertension
|
|
True or false, horses usually do not develop pulmonary edema unless pulmonary hypertension occurs rapidly
|
True
|
|
In the horse, left sided overload and pulmonary hypertension usually lead to what?
|
Right sided failure
|
|
If atrial enlargement occurs (from regurg) the horse is predisposed to what arrhythmia?
|
atrial fib
|
|
What are the clinical signs of aortic/mitral insufficiency?
|
-exercise intolerance
-reduced performance -mumurs -tachycardia -cough |
|
What sign might be seen in the case of a rupture chordae tendonae?
|
pulmonary edema
|
|
What clinical signs might be seen in a case of tricuspid insufficiency?
|
-jugular distension w/ pulsdation
-subcu edema -venous distension -murmur over tricuspid valve |
|
Color flow Doppler can give what information in the case of aortic or mitral insufficiency?
|
Degree of regurgitation
|
|
The prognosis for an aortic or mitral insufficiency is good with what conditions?
|
-asymptomatic
-regurg jet is small -no evidence of left heart enlargement |
|
What conditions make an aortic or mitral insufficiency a guarded or poor prognosis?
|
-exercise intolerance
-fractional shortening < 30% -pulmonary artery larger than aorta -evidence of endocarditis or myocarditis -left atrial enlargement |
|
True of False, the intensity of a murmur is NOT a reliable indicator of prognosis.
|
True
|
|
When would you treat a cardiac condition in a horse?
|
Only when signs of heart failure are present
|
|
What drug is used in a left sided heart failure?
|
Hydrazaline
|
|
What is the cause of endocarditis?
|
An acquired condition- focus of infection any where in the body that embolizes to the heart
|
|
Which organisms are the common causes of endocarditis?
|
-Pastuerella
-Actinobacillus -Streptococcus |
|
What condition may predispose a valve to bacterial colonization?
|
Pre-existing valve lesion
|
|
What are the possible clinical signs of endocarditis?
|
-may be sub clinical
-may cause heart failure -tachycardia -murmur of valvular insufficiency -fever -anorexia -decreased performance -younger animals (<4 years) -shifting leg lameness |
|
His is endocarditis diagnosed?
|
-visualization of abnormal valve of echo
-inflammatory leukogram -hyperfibrinogenemia -hyperglobulinemia -blood culture (difficult) -identif primary infection |
|
How do you tx endocarditis?
|
-long term abx
-treat for heart failure if present -treat primary focus of infection |
|
What is the prognosis for endocarditis?
|
Good i tx before significant valvular lesions develop
|
|
If the valves have significant lesions, what is the prognosis?
|
Poor to grave - 80% of horse with aortic/mitral valve endocarditis die
|
|
Cardiac inflammation, degeneration or myocyte electrolyte changes from myocaridal dz can lead to what?
|
-altered conduction and arrhythmias
-reduced mycardial function, chamber dilation, insufficient AV valves and heart failure -may lead to arrhythmias and murmurs |
|
What type of murmurs are heard with myocardial dz?
|
systolic (AV valves)
|
|
Which arrhtyhmias are seen with myocardial dz?
|
-ventricular tachycardia
-premature atrial or ventricular contractions -atrial fibrillation |
|
Diagnosis of myocarditis can be difficult, but it is important to indentify what?
|
The underlying cause
|
|
What tx steps are taken for myocarditis?
|
-tx underlyin cause
-provide electrolyte support -NSAIDs -steroids if viral -abx if bacterial -tx symptomatic heart failure if present -tx arrhythmias if present -Mg, lidocaine if ventricular -quinidine with atrial fib -strict rest |
|
What is the prognosis of myocarditis?
|
-good if caused by an electrolyte abnormality
-guarded if myocardial degeneration or inflammation |
|
In general, pericarditis can be caused by what?
|
-septic
-non-septic -neoplastic -idiopathic |
|
What bacteria are common causes of pericarditis?
|
Streptococcus
Gram negative bacteria +/- anaerobes |
|
Horses with what other conditions may develop pericarditis?
|
Pleuropneumonia
EHV-1 |
|
How does pericarditis affect the heart?
|
Thickened and inflammed pericardium cause cardiac tamponade and restrictive pericarditis--interfers with diastolic filling, results in cardiac insufficiency
|
|
What are the clinical signs/physical findings of pericarditis?
|
-fever, depressionm anorexia
-pleurodynia -colic -cardiac tamponade -jugular distension, edema -pleural effusion -muffled heart sounds +/- plerual friction rubs +/- arrhythmias |
|
Which physical finding is the most specific for pericarditis?
|
Tamponade
|
|
What dx test is most specific for pericarditis?
|
Echo
|
|
What would you expect to see on an echo of pericarditis?
|
Pericardial fluid and collapsed right atrium
|
|
What other diagnostic steps can be taken?
|
-aspirate of pericardial fluid for cytology and culture
-electrical alternans on ECG -Non-specific evidence of infection or inflammation (leukocytosis, hyperfibrinogenemia, hyperglobulinemia) |
|
How can pericarditis be treated?
|
-pericaridal drainage and lavage
-abx tx -anti-inflammatory and anlgesic tx -tx arrhythmias and cardiac failure if present |
|
Which heart rate is more common in horses with pathologic arrhythmias?
|
Tachyarrhythmia
|
|
Where does a supraventricular arrhythmia originate?
|
-SA node
-atrium -AV node or junction |
|
From where else can an arrhythmia originate?
|
Ventricle
|
|
Do large animals premature timing arrhythmia or escape timing (occurs later than expected)?
|
Premature arrhythmia
|
|
Arrhythmia frequency can be classified as what 3 types?
|
-isolated abnormal complexes
-paroxysmal -sustained |
|
What is the most common acquired pathologic arrhythmia in horses?
|
Atrial fibrillation (supraventricular)
|
|
What are the predisposing factors of atrial fibrillation?
|
-atrial enlargement
-valvular regurgitation -heart failure -myocarditis -slow atrial rate and high parasympathetic tone |
|
Is exercise intolerance a sign of atrial fibrillation?
|
Yes but only present in 60% of cases
|
|
What causes the clinical signs of atrial fibrillation?
|
Reduced filling of atria
|
|
What other clinical can be seen?
|
-dyspnea
-epistaxis -colic |
|
Only 12% of horses with atrial fib show signs of what condition?
|
heart failure
|
|
What type of rhythm is ausculted in atrial fib?
|
irregularly irregular w/o audible S4
-variable intensity heart sounds from beat to beat -rate is usually normal |
|
In cases of atrial fib, what is the most common murmur that might be heard?
|
Mitral regurgitation
|
|
What would you expect to see on an ECG of a horse with atrial fibrillation?
|
-absence of P waves
-irregularly irregular R-R interval -normal ARS -baseline F waves |
|
What 2 drugs are given to convert the atrial fib?
|
-Quinidine
-Digoxon |
|
Once the arrhythmia converts, which drug do you discontinue?
|
Quinidine- toxic signs may develop
|
|
What are the signs of quinidine toxicity?
|
-colic, diarrhea
-nasal mucosa edema leading to respiratory obstruction -ataxia, behavior change, seizure -tachycarida, other arrhythmias, prolongation of QRS -hypotension and collapse |
|
How do you tx quinidine toxicity?
|
-bicarb
-digoxin if tachycardia -lidocaine if ventricular tachycardia |
|
What is the prognosis for atrial fibrillation?
|
-good to excellent of iopathic A-fib with a normal heart and acute.recent onset
-good if chronic A fib and no sign of failure on echo -guarded to grave with underlying heart dz |
|
What is the cause of Atrial premature contractions (APC)?
|
Impulse originating in the atria but outside the SA node or from the AV junction
|
|
True or false...30% normal horses have 1 APC per minute.
|
False...1 per hour
|
|
When are APC's considered abnormal?
|
-if frequent
-occur in groups -multi-focal in origin |
|
APC may occur in horses with what other conditions?
|
-myocardial dz (esp following EHV1 or other respiratory dz)
-abnormal electrolytes -toxemia or septicemia -cardiac dz causing atrial enlargement |
|
What is meant by atrial tachycardia?
|
More than 4 premature complexes in a row or a sustained atrial tachycardia
|
|
What would you expect to auscult on a horse with APCs?
|
-heart beat earlier than expected, followed by a normal diastolic interval
-if runs of APCs or atrial tachycardia- increased rate |
|
An ECG of APCs will show what?
|
-premature P wave of different conformation than those that originate from SA node
-normal QRS -P wave of APC may be buried in previous T wave -if single, P-P interval normal following APC -increased rate with atrial tachycardia |
|
What is the treatment for APCs?
|
-corticosteroids if suspicious of viral myocarditis
-Atrial tachycardia (>100 bpm) requires quinidine, digoxin (if heart failure) |
|
What are ventricular premature contractions?
|
VPCs are ectopic beats originating from a ventricular focus and occur earlier than expected
|
|
What defines ventricular tachncardia?
|
4 or more VPCs in a row or sustained
|
|
What are the causes of VPCs?
|
-electrolyte abnormality
-myocarditis |
|
Are occasional VOCs and ventricular tachycardia normal or abnormal?
|
Abnormal
|
|
What do you expect to hear on auscultation of VPCs?
|
-regular rhythm with a beat occuring earlier than normal, followed by a compensatory pause
|
|
Clinical signs of underlying myocarditis or electrolyte disturbances are most common with what disease in horse?
|
Endotoxemia= GI disease
|
|
Sustained ventricular tachycardia is most likely to be associated with what condition?
|
Heart failure
|
|
1) What does a Viruses lack.
|
Viruses do not have:
1. a nucleus 2. organelles 3. ribosomes 4. cytoplasm 5. only a few have enzymes |
|
How would you treat an occasional VOC with a normal rate?
|
Stall rest
|
|
At what heartrate do you consider ventricular tachycardia to be associated with disease?
|
> 60 bpm
|
|
What are the indications of a dangerous ventricular tachycardia that needs immediate attention?
|
HR > 120 bpm
R on T configuration Multifocal origin of QRS |
|
How is ventricular tachycardia treated?
|
-mag sulfate IV
-lidocaine -quinidine -treat underlying dz |
|
Bradycardia may accompany what conditions?
|
-myocardial dz
-cerebral dz |
|
What is the heary rate seen with bradycardia?
|
< 24 bpm
|
|
What changes do you see on an ECG of a horse with bradycardia?
|
Normal complexes, slow rate
|
|
How do you treat bradycardia?
|
Treat underlying cause
|
|
What is third degree AV block?
|
Acquired abnormality of the junctional myocardium that does not allow impulses from the atria to conduct to the ventricles
|
|
What is the order of depolarization of the atria and ventricles wtih 3rd degree block?
|
Atria and ventricle depolarize separately under control of their own pacemakers
|
|
Third degree AV block is more commonly associated with what condtions?
|
-myocarditis
-degenerative changes in the AV node or electrolyte changes |
|
What are the clinical signs/ physical findings of 3rd degree Av block?
|
-exercise intolerance and collapse
-occasional signs of heart failure -slow heart rate <24 bpm, typically regular rhythm |
|
What would you see on an ECG of a 3rd degree AV block?
|
-no relationship between P and QRS
-QRS look slightly abnormal |
|
What is the tx for 3rd degree AV block if caused by non-septic myocarditis
|
Corticosteroids
|
|
What other steps are taken for tx fo 3rd degree AV block?
|
-check electrolytes
-stall rest -resolution requires implantation of a pacemaker |
|
What are the common causes of acute blood loss?
|
-trauma
-guttural pouch mycosis -hemoabdomen -hemothorax |
|
What are the clinical signs of hypovolemia?
|
-tachycardia
-decreased pulse pressure -reduced jugular fill -tachypnea -cold extremities -decreased urine output -depressed mentation |
|
How do you tell evidence of regeneration in an anemic horse?
|
-no reticulocytes so look for MCV (bigger RBCs)
|
|
Does a horse with acute blood loss show hyper or hypoproteinemia?
|
Hypoproteinemia
|
|
What value is U/S in diagnosing acute blood loss?
|
-visualization of an active bleed
-fluid within the abdomen/thoracic compartments |
|
Class 1 category of blood loss is a loss of hoe much of the blood volume?
|
15% or less
|
|
Class 1 blood loss is fully compensated by what mechanism?
|
Transcapillary refill--pulls from the interstitium
|
|
How much is 15% of the blood volume in a 500 kg horse?
|
6 liters
|
|
What clinical signs are seen with 15% blood loss?
|
Few clinical signs are observed
|
|
Category 2 blood loss is a loss of how much volume?
|
15-30% total blood volume
|
|
What is orthostatic hypotension?
|
Blood pressure falls when the horse stands, causing dizziness
|
|
Class 2 blood loss shows increased HR and what kind of MAP?
|
Normal
|
|
What other effects are seen in class 2?
|
-decreased urine output
-compromised splanchnic perfusion (bacterial and endotoxin translocation, sepsis, sever sepsis, septic shock, MODS, death) |
|
Class 3 of blood volume loss is 30-40% of total blood volume, what happens to compensatory mechanisms?
|
-vasoconstrictor response to hemorrhage is no longer able to sustain perfusion of vital organs
-homeostatic mechanisms fail -decompensated hypovolemic shock |
|
Why is hypotension exaggerated in class 3?
|
-loss of vasoconstriction
-increased adenosine due to loss of ATP production (adenosine=vasodilator) |
|
What occurs in class 4 blood loss?
|
> 40% volume loss
-irreevsible decompensation |
|
In compensatory shock, all is well if what parameter is maintained?>
|
MAP
|
|
What is the goal of the homeostatic response?
|
Move interstitial volume into vascular space
-support blood volume/pressure -provide O2 |
|
Which organs get perfused first in compensatory shock?
|
-brain
-heart -lung -kidney |
|
At what point does the RAAS system initiate?
|
Decreased perfusion of renal arteriole
|
|
What 2 other homeostatic mechanisms help to increase volume?
|
-Arginine vasopressin (ADH)
-sympathetic nervous system activation |
|
What are the clinical signs of early decompensated shock?
|
-altered mentation
-prolonged CRT -tachycardia -hypotension -oliguria |
|
What are the signs of late decompensated shock?
|
-prolonged tissue hypoxia
-autoregulatory failure (vasodilation, pupils fixed and dilated, hypothermia, sever acidosis) |
|
In hypovolemia, mortality and morbidity are related to what?
|
volume and duration of blood loss
|
|
What factor is the enemy of the bleeding patient?
|
Time
|
|
What steps should be taken as the first line of defense/treatment in the case of traumatic blood loss?
|
-rapid intervention to prevent further loss: ligation of arterial vessels, application of pressure bandages
|
|
In the case of traumatic blood loss, the 2nd step is initiating fluid tx, what fluid should you use?
|
-crystalloids at shock dose (hypertonic saline)
-40-80 ml/kg (give 10 L to start and evaluate) |
|
When should blood products be given?
|
In the case of sever loss
|
|
What are the indications for whole blood transfusion?
|
PCV < 20% acutely
PCV < 12% for 12-24 hours following blood loss |
|
True or False, PCV is the sole transfusion trigger?
|
False- should also include blood gas information (SaO2 should be 95-100%)
|
|
How much whole blood can you transfuse?
|
20-40%, then marrow replacement should be started
|
|
How do you calculate the amount of blood needed for a transfusion?
|
PCV desired - PCVpatient x .08 Bwt
______________________________ PCV donor |
|
How much blood can a horse safely donate?
|
25% of blood volume
|
|
What are the causes of hemoabdomen?
|
-trauma
-post-op sx hemorrhage -neoplasia -complications from foaling and preg -visceral organ rupture -mesenteric injury -coagulopathy -ovarian hematoma -systemic amyloidosis -idiopathic |
|
What are the clinical signs of hemoabdomen?
|
-colic
-lethargy -hypovolemic shock -anorexia -reluctance to move -weakness/trembling -abdominal distension |
|
Hemoabdomen is a mature horse dz seen more in which breeds?
|
-arabs
-TB |
|
How is hemoabdomen diagnosed?
|
-anemia
-increased lactate -decreased CVP -abd U/S -peritoneal fluid |
|
What is are the primary goal when treating hemoabdomen?
|
-control hemorrhage
-control hypotension (MAP > 60, maintenance fluids only) |
|
Why isn't hypertonic saline given in a case of hemoabdomen?
|
Would increase blood pressure too much
|
|
What steps are taken to tx hemoabdomen?
|
-tranquilizer (ACE)
-quiet environment -no forced movements -blood transfusion when life threatening anemia -O2 if not stressful -anti-fibrinolytics -pro-coagulants |
|
What is the survival rate of hemoabdomen?
|
51-74%, 84% for periparutient hemorrhage in mares
|
|
The short term outcome of hemoabdomen is related to what?
|
The underlying cause
-ability to control hemorrhage -restore effective circulating volume |
|
What are the causes of hemothorax?
|
-trauma
-neoplasia -coagulopathy -iatrogenic |
|
What is vasculitis?
|
Clinicopathologc process that involves inflammation and necrosis of blood vessel walls
|
|
Is vasculitis usually a primary dz?
|
No, typically and 2ndary manifestation of a primary infectious, toxic or neoplastic disorder
|
|
What is the hallmark sign of vasculitis?
|
Predominant involvement of small vessels in skin
|
|
What are the clinical signs of vasculitis?
|
Primary distal limb edema
-hyperemia -P/E hemorrhage -ulceration of mucus membranes |
|
Limb edema may lead to what other complications?
|
skin infarction, necrosis, exudation
|
|
Are hemorrhage and vascular necrosis from vasculitis limited only to the limbs?
|
No, can affect any organ system (lameness, colic, dyspnea, ataxia)
sequelae: cellulitis, thrombophlebitis, laminitis, pneumonia |
|
What are the 4 main causes of vasculitis?
|
-equine purpura hemorrhagica
-equine viral arteritis -equine infections anemia -idiopathic |
|
Is equine purpura hemorrhagica a contagious dz?
|
No
|
|
EPH is a squealae to what other diseases?
|
-systemic dz
-strep equi (esp following vaccination for strangles) -strep zooepidemicus -rhodococcus equi -corynebacterium pseudotuberculosis |
|
What are the signs of EPH?
|
-young to middle age horses
-signs develop 2-4 weeks following respiratory infection -vasculitis syndrome: subcu edema distal limbs, lethargy, anorexia, P/E hemorrhage, fever |
|
What lab results would you expect to see with EPH?
|
-anemia
-neutrophilia -hyperproteinemia -hyperfibrinogenemia -elevated muscle enzymes -TCP (rare) |
|
What will a skin bx show in a case of EPH?
|
Classic, leukocytoclastic vasculitis with necrosis of blood vessels
-immune complexes of IgM/IgA -strep M proteins |
|
What is the TX for EPH?
|
-tx underlying dz
-PCN (hx of strep) -hydrotherapy -distal limb bandages -steroids (prolonged course 2-4 week min) -continue abx |
|
The prognosis for recovery form EPH depends on what?
|
-early recognition
-early aggressive therapy -extent of organ involvement |
|
What are the potential complications from prolonged recovery from EPH?
|
-laminits
-cellulitis -pneumonia -diarrhea |
|
The virus that causes Equine Viral Arteritis is in which family?
|
Arteriviridae
RNA virus, enveloped |
|
Which arthropod carries EVA?
|
None-it's a non-arthropod borne virus
|
|
Is EVA an infectious dz?
|
Yes
|
|
How soon do clinical signs develop after infection with EVA?
|
1- 10 days following inmfection
|
|
What are the clinical signs of EVA/
|
-fever
-lethargy -anorexia -vasculitis/edema (of mammary gland, scrotum, limbs, periorbital, ventral edema) -stiffness -rhinorrhea -abortion (10-60% between 3-10 months gestation) |
|
Do mares become chronic carriers of EVA?
|
No
|
|
What lab results do you expect in the dx of EVA?
|
Results are variable and not diagnostic for EVA
|
|
What is the target organ for the EVA virus?
|
Blood vessels- localizes in the endothelium
|
|
What is the histologic appearance of the vasculitis caused by EVA?
|
-fibrinoid necrosis or tunica media with perivascular lymphocytic/granulocytic infiltration, thrombi are present
|
|
How is EVA transmitted?
|
Aerosolized particles from infected horses
-respiratory secretions -urinary tract secretions/urine -abortive tissues Semen |
|
How quickly can mares eliminate the virus?
|
60 days
|
|
Stallions can be life-long carriers, and show what clinical signs?
|
None
|
|
How is EVA diagnosed?
|
-4 fold increase in Ab titer
-serum positive stallions require semen testing |
|
What type of virus cause Equine Infectious Anemia?
|
Retroviradae, Lentivirus
Rna, reverse transcriptase |
|
How is EIA transmitted?
|
-by blood, from Tabanid insects (horsefly, deerfly)
-fomites -vertical transmission |
|
What are the 3 stages the EIA can occur as?
|
-acute
-chronic -inapparent |
|
What are the signs of the acute stage?
|
-burst of viremia
-fever -TCP -malaise -P/E hemorrhages |
|
What characterizes the chronic stage of EIA?
|
-anemia
-recurrent episodes of viremia -horses are sick ("swampers") -episodes decrease in duration/severity |
|
Any horse experienceing clinical EIA may also develops signs of what conditions?
|
DIC (may die)
|
|
What situations can induce recrudesence of EIA?
|
-stress from
-transport -racing -extreme temps Steroids |
|
Which test is used for EIA?
|
Coggins
also Elisa for screening |
|
EIA is a reportable dz in the US and there is no vaccination, what is the size of the quarantine area for infected horses?
|
200 yards (180m)
|
|
Ingestion of what can cause Heinz Body Hemolytic Anemia?
|
-red maple leaf
-onions -brassica -phenothiazines |
|
Red maple leaf toxicosis can occur in which species?
|
-horse
-pony -zebra -alpaca |
|
When does red maple leaf toxicity tend to occur?
|
Late summer - fall
|
|
How soon do signs of toxicity develop and what causes the anemia?
|
2-3 after ingestion (1.5 - 3 pounds of leaves)
Gallic acid denatures Hbg |
|
Ingestion of the wilted leaves leaves to what lab values?
|
-hemoglobinemia
-hemglobinuria -methemoglobinemia (denatured Hbg unable to carry or transport O2) |
|
What are the clinical signs of Heinz body hemolytic anemia?
|
-anemia (tachycardia/tachypnea)
-chocolate colored mucus membranes -brown/red urine -ARF -colic |
|
Why would heinz body anemia cause ARF?
|
Pigment nephropathy- Hbg filtered at the kidney
|
|
On clinpath results, what is seen with heinz body anemia?
|
-acute,severe anemia (heinz bodies, eccentrocytes)
-azotemia -hemoglobinemia -pigmenturia -increased methemoglobin |
|
What is the tx regimen for heinz body anemia?
|
-IV fluids
-address colic pain as necessary -whole blood transfusion often indicated NO steroids! (associated with non-survival) |
|
What is one of the most common neoplasms in horses?
|
Lymphoma
|
|
Does equine lymphoma have a viral etiology like bovine lymphoma?
|
No
|
|
What characterizes multicentric/generalized lymphoma in the horse?
|
-end-stage dz
-leukemia |
|
The alimentary form of lymphoma occurs in what age and breed of horse?
|
< 5 years of age
-Arabians |
|
Which form of lymphoma is the most common?
|
Splenic
|
|
Which form of lymphoma is primary for metastatic dz?
|
Thoracic (mediastinal/thymic)
|
|
Which type of cutaneous lymphoma has a poor prognosis?
|
Deeper tissue involvement
|
|
What are the clinical signs of lymphoma?
|
-lymphadenoapthy
-lethargy -weight loss -edema -pyrexia |
|
What changes in lab values would you expect with lymphoma?
|
-anemia (suppression of erythropoiesis, bone marrow infiltration, blood loss, immune-mediated
-lymphocyte count typically normal -hyperglobulinemia/hypoalbuminemia |
|
What is the tx for equine lymphoma?
|
Limted- complications are considerable
|
|
What is the function of mitochondria?
|
Use oxygen to provide energy to the muscles
|
|
What is the VO2 max of a horse compared to a human?
|
Human: 50 ml/kg/min
Horse: 140 ml/kg/min |
|
Air is comprised of what percentage of oxygen?
|
21%
|
|
Horses are what type of breathers?
|
Obligate nasal breathers
|
|
How many pairs of sinuses does the horse have?
|
6 pairs
|
|
Which paranasal sinuses are most often diseased?
|
Frontal
Maxillary |
|
What is the most common cause of primary sinusitis in the horse?
|
Streptococcus spp
may occur following a respiratory tract infection |
|
What is the most common cause of secondary sinusitis?
|
Tooth root infection (tooth roots of molars within maxillary sinus)
|
|
What are the other causes of sinusitis?
|
-sinus cyst
-tumors -facial bone fractures |
|
What are the clinical signs of sinusitis?
|
-unilateral or bilateral nasal dischargs (can be foul smelling)
-ocular discharge -malaise -facial deformity if chronic |
|
How do you diagnose sinusitis?
|
-PE, palpation and percussion of face
-endoscopic exam -oral exma -skull rads -sinoscopy -CT -MRI |
|
How do you tx sinusitis?
|
Like an abscess
-tx inciting cause -abx -repeated lavage with balanced polyionic solution |
|
What is an ethmoid hematoma?
|
Benign, progressively expansive soft tissue mass
|
|
In what age of horse do ethmoid hematomas occur?
|
Middle age, 8-10 years
usually unilateral |
|
What are the clinical signs of an ethmoid hematoma?
|
-uni or bilateral epistaxis
-respiratory stridor -facial deformity -decreased airflow through affected nostril |
|
What other upper airway conditions can cause epistaxis?
|
-trauma
-neoplasia -coagulopathy |
|
What lower airway conditions can cause epistaxis?
|
Pulmonary hemorrhage
-neoplasia -pulmonary infarction -atrial fib and pulmonary hypertension |
|
In addition to a PE, what other diagnostics are used for ethmoid hematomas?
|
-endoscopy
-biopsy -rads -CT |
|
What is the appearance of an ethmoid hematoma on a histo slide from a bx?
|
angioma, cappilary, fibrous tissue
|
|
What are the tx options for an ethmoid hematoma?
|
-sx removal, sharp or laser
-formaldehyde injections (intralesional) |
|
Lymphoid hyperplasia syndrome can occur in what areas of the nasopharynx?
|
-dorsal and lateral walls
-soft palate -epiglottis -guttural pouch lining |
|
Grare 3-4 lymphoid hyperplasia is seen in which age of horse?
|
Younger, 2-3 y/o
|
|
What are the causes of pharyngeal lymphoid hyperplasia?
|
Infection
-bacterial -viral Environmental contaminants -endotoxin -ammonia -dust -metals |
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How is lymphoid hyperplasia distinguished from pharyngitis?
|
Lymphoid hyperplasia:
-young horse -not systemically ill -afebrile -normal appetite -BAR |
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What is the response of the lymphoid tissue to antigens?
|
-mucus production
-immunoglobulin secretion |
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What is the key component of respiratory dz?
|
Inflammation
|
|
What occurs in the condition of dorsal displacement of the soft palate?
|
Soft palate displaces dorsally to the epiglottis
|
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How is DDSP diagnosed?
|
-exercise intolerance
-abnormal respiratory sounds during exhalation -resting endoscopy (insensitive unless ulcer) -treadmill endoscopy (better but not perfect? |
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What is the cause of DDSP?
|
Not known, possible neuromuscular dysfunction
|
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What are the non-surgical tx for DDSP?
|
-rest
-tongue tie -steroids -Cornell collar |
|
What is the best sx tx for DDSP?
|
Tie forward
-thyrohyoideus prosthesis (suture) moves larynx rostral and dorsal |
|
What effect does thermopalatoplasty with a laser have?
|
Stiffens the palate
|
|
Dysphagia in foals can be a result of what conditions?
|
-cleft palate
-vit E/selenium deficiency -neonatal nasopharyngeal dysfunction -over zelous lactator |
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What are the clinical signs of nasopharyngeal dysfunction in foals?
|
During first month of life:
-respiratory distress -respiratory stridor -dysphagia/aspiration pneumonia |
|
What might be seen during an endoscopic exam for nasopharyngeal dysfunction in a foal?
|
-nasopharyngeal edema
-laryngeal edema -persistent DDSP -mild in trahea |
|
What are the clinical signs of cleft palate?
|
-milk dripping from nose/mouth
-coughing -aspiration |
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How do you dx cleft palate?
|
-endoscopic exam
-palpation/examination of soft palate |
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What are the causes of cleft palate?
|
-genetics
-teratogens -nutrition -trauma (uncommon congenital defect if foals) |
|
What is the sx approach to tx cleft palate?
|
Mandibular symphisiotomy
|
|
When does a dynamic laryngeal obstruction become apparent?
|
-at exercise
-induced by nasal occlusion |
|
What is the cause of idiopathic laryngeal hemiplasia?
|
Distal axonopathy of the left recurrent laryngeal nerve
|
|
What muscles does ILH affect?
|
Intrinsic laryngeal muscles, adductors, abductors NOT cricothyroid muscles
|
|
Which horse are at risk for ILH?
|
-large horse, > 18 hands
-TB 8% -Draft 35% |
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What are the clinical signs of ILH?
|
-exercise intolerance
-respiratory noise -coughing (eating) |
|
How does ILH cause poor performance?
|
-incr inspiratory resistance
-decr minute volume -decr PaO2, incr PaCO2 -decr VO2 -alteration in Fs:Fr coupling -increased work of breathing |
|
During exercise, a grade 3 ILH collapse how much?
|
70%
|
|
How do you Dx ILH?
|
History of:
-exercise intolerance -respiratory noise Endoscopic exam: -resting -treadmill |
|
Overall, what is the goal of Tx for ILH?
|
Increase the diameter of the airway
|
|
what is the function of IL-5? (2)
|
1. B cell proliferation
2. Helps B cells switch to IgE production |
|
What other procedures are recommended for ILH?
|
-maximize size of rima glottidis
-laryngoplasty + ventriculocordectomy or ventriculectomy or cordectomy -best airway function -resolution of noise? -avoid complication of vocal fold collapse |
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What are the potential complications of Tx ILH?
|
-coughing
-aspiration -continued exercise intolerance -noise |
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What is arytenoid chondritis?
|
Inflammation of the cartilage with abscess
|
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What tissues can trap the epiglottis?
|
Aryepiglottic tissue, when inflammed
|
|
What is the tx for epiglottic entrapment?
|
Transection of the aryepiglottic membrane
-anti-inflammatories or nothing |
|
What is guttural pouch tympany?
|
-excessive accumulation of air and sometimes fluid in the guttural pouch
(foal < 1 year old) |
|
What are the clinical signs of guttural pouch tympany?
|
-swelling in parotid region
-dyspnea -dysphagia -aspiration penumonia |
|
How is GP tympany dx?
|
-rads
-endoscope |
|
How is GP tympany treated?
|
2 sx options
-guttural pouch fenestration -modify the nasopharyngeal opening (resection of salpingo membrane) |
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What is guttural pouch empyema?
|
Suppurative inflammation of the guttural pouch
|
|
When does guttural pouch empyema occur?
|
Following upper airway infection involving Strep
|
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What are the clinical signs of guttural pouch empyema?
|
-mucopurulent nasal discharge
-swelling in parotid region -dsypnea -dysphagia (mass effect, neurogenic) |
|
How doe you Dx guttural pouch empyema?
|
-rads
-U/S -endoscopic examination -culture and sensitivity |
|
What is the Tx for guttural pouch empyema?
|
-irrigate the guttural pouch with balanced electrolyte solution
-systemic abx (PCN) -drain guttural pouch via Viborg's triangle or modified Whitehouse |
|
What type of med should never be used in the guttural pouch?
|
No caustics i.e. iodine
|
|
Guttural pouch mycosis is a result of what type of infection?
|
Aspergillus spp
|
|
What is the primary clinical sign of Guttural pouch mycosis?
|
Epistaxis
|
|
Other clinical signs of Guttural pouch mycosis include what?
|
-horner's
-dysphagia |
|
What would you expect to see on an endoscopic exam of Guttural pouch mycosis?
|
-blood from the guttural pouch opening
-blood within the pouch -fungal plaques |
|
What is the tx for Guttural pouch mycosis?
|
-occlude the affected arteries
(internal carotid is most commonly affected) |
|
Bleeding from the guttural pouch and what in the history would lead you to suspect an avulsion of the rectus and longus capitus muscles?
|
Hx of trauma
|
|
What causes temporohyoid osteoarthopathy?
|
Following otitis media/interna or some inflammatory episode, the stylohyoid bone fuses with the petrous temporal bone
|
|
What is the sequlae of temporohyoid osteoarthopathy?
|
Can impinge on Cn 7 and 8 or the bone fractures- vestibular dz and facial nerve paralysis results.
|
|
What are the clinical signs of temporohyoid osteoarthopathy??
|
-acute onset of vestibular dz
-facial nerve paralysis -head shaking -pain associated with palpation of ear |
|
What are the signs of CN VII damage?
CN VIII? |
CN VII: drooped muzzle, ear
CN VIII: vestibular signs |
|
What are the txs for temporohyoid osteoarthopathy?
|
-sulfa abx
-nsaids sx: -stylohyoid osteotomy -ceratohyoid osteotomy -tarsorhaphy (sx closure of eye) |
|
In terms of lung dz, what is a bleeder horse?
|
Exercise induced pulmonary hemorrhage
|
|
What characterizes EIPH?
|
-evident following intense exercise
-characterized by blood in the airways -associated with poor racing performance |
|
What is the potential etiology of EIPH?
|
Pulmonary capillary disruption
-high pulmonary artery pressure -very negative inspiratory pressure |
|
Which horse breeds are affected by EIPH?
|
-all TB racehorses
-most SB racehorses -62% racing quarter horses Western pleasure horse- safe, slower speed |
|
What are the clinical signs of EIPH?
|
-5% will have epistaxis
-blood in the trachea 45-60 mins post exercise -hx of poor performance |
|
On post mortem of EIPH, where is bleeding seen?
|
Caudal dorsal lung fields
|
|
What is the Tx for EIPH?
|
There is none, can give furosemide to decrease pumonary arterial pressure
|
|
What can be done for EIPH?
|
Reduce components of transmural pressure
-insp. driving pressure -pulmonary capillary pressure Inspiratory obstructions -ILH |
|
Inflammation of the respiratory system can have what effects?
|
-constriction
-mucus, edema -tissue damage -remodeling,fibrosis |
|
What are the clinical signs/findings of inflammatory airway dz?
|
-mucus
-inflammatory cells -/+ cough -no fever -normal appetite -not sick |
|
What percentage of racehorses have inflammatory airway dz?
|
33%
|
|
What are the infectious causes of inflammatory airway dz?
|
Viral:
-influenza -herpes virus -rhinovirus Bacteria -strep |
|
What are the non-infections causes of inflammatory airway dz?
|
-allergy
-particulates -endotoxin |
|
What are the major contributors to particulates that can cause inflammatory airway dz?
|
-bedding
-hay -barn activites |
|
Which horses are more at risk for inflammatory airway dz?
|
Younger <4
-recently entered race training -feeding hay vs pasture |
|
What is the importance of the affect of inflammatory airway dz?
|
Amount of mucus can affect the way a horse finishes a race.
|
|
What is the tx for inflammatory airway dz?
|
-Anti inflammatories ( be careful w. abx), steroids
-abx -improve the enivronment |
|
What is another name for reactive airway obtsruction?
|
Heaves
|
|
How is heaves characterized?
|
-Inflammatory condition of the lower airway characterized by the presence of bronchospasm, mucus plugs and chronic changes to the bronchiolar walls leading to terminal airway obstruction
|
|
heaves is thought to caused by what?
|
Allergy to inhaled antigens such as dust from feed and beeding
|
|
What are the clinical signs of heaves?
|
-older horse
-coughing -exercise intolerance -increased respiratory rate and effort -flared nostrils -double expiratory effort |
|
What will you hear when ausculting the chest on a horse with heaves?
|
-crackles
-wheezes |
|
In dx heaves, the horse is typically > 10 yrs of age with a cough that is worse, when?
|
In the barn
|
|
What would you expect to find on PE?
|
-no fever
-good appetite -abnormal tracheal and pulmonary auscultation |
|
How is heaves dx?
|
-rads
-BAL (>15% neutrophils) -endoscopy -atropine test -ABG |
|
Thoracic auscultation may be normal during normal tidal breathing, what method can you use to increase the respiratory rate?
|
Re-breathing bag
|
|
What are the goals of tx for heaves?
|
-prevent exposure to offending antigens
-decrease pulmonary inflammation -supportive care (no nsaids- leukotriene pathway) Give steroids |
|
What is the most effective tx for heaves?
|
Environmental change- turn your horse out
|
|
What additional steps can be take for heaves?
|
-feed pellets, bed on shavings
-soak hay or feed hay cubes -steroids -bronchodilators |
|
What is the genus/species for the equine lungworm?
|
Dictyocaulus arnfieldi
|
|
What is the role of the donkey in the infection of the horse with lungworm?
|
Donkey is the asymptomatic source
|
|
In the horse, the lungworm life cycle is arrested in which stage?
|
Adult stage, burrows into lungs
|
|
What clinical signs are seen the horse with lungworm?
|
-parsitic bronchitis
-copius mucus production -cough -crackles, wheezes caudal and dorsal -2ndary bacterial infection -pulmonary edema -coughin -increased respiratory effort |
|
How is lungworm dx and tx?
|
-history of contact with donleys or mules
-eosinophils and larvae on tracheal aspirate or tracheal wash |
|
What are the 2 most common causes of viral respiratory dz in the horse?
|
-influenza A
-herpes 1,4 virus |
|
Equine influenza A is what type of virus?
|
-SS RNA, orthomyxoviridae
|
|
Equine influenza A virus has tropism for which cells?
|
Epithelium of the respiratory tract
-ciliated epithelium of the trachea and bronchi -impairs the mucociliary clearance |
|
What are the clinical signs of Equine influenza A? (#1 cause of URTD)
|
-highly contagious (1-5 days)
-serous nasal discharge -cough -fever -inappetence -muscle soreness -lymphadenopathy |
|
How is Equine influenza A dx?
|
-nasopharyngeal swab
(virus isolation, elisa, pcr) -serology |
|
What is the tx for Equine influenza A?
|
-supportive care (access to food/water)
-rest (no training) -anti-pyretic meds (banamine) |
|
What is the in vaccinating against Equine influenza A?
|
Decreases the severity of infections, does not prevent it
|
|
Which horses are at risk for Equine influenza A?
|
-naive horses
-neonates -geriatric, immunosuppressed 2ndary complications: -pneumonia -bacterial infection of upper airway -viral cardiomyopathy/myocarditis |
|
What type of virus is equine herpes virus 1 and 4?
|
-DS DNA, herpesviridae
|
|
What effects does herpes 1,4 have on the respiratory tract?
|
-local lymph nodes infection
-leukocyte associated viremia -disseminates to distant organs including gravid uterus and CNS |
|
What effect does herpes 1,4 have on vascular enodthelium?
|
Viral replication causing vascultitis, hemorrhage, thrombosis, necrosis
|
|
Where does the latent herpes 1,4 virus hide?
|
In the trigeminal ganglion and leukocytes of the lymphoreticular system
|
|
What are the clinical signs of upper respiratory tract infection of herpes 1,4?
|
-serous or purulent nasal discharge
-ocular discharge -fever, malaise -limb edema |
|
What other major complications can arise from herpes 1,4?
|
-abortion, last trimester
-myeloencephalopathy -pulmonary vasculotropic infection |
|
How are respiratory viruses spread?
|
Fomites
|
|
What is the TX for EHV 1,4?
|
-supportive care
-analgesia, anti pyrexic --access to food/water -warmth -acyclovir (EHV1) -no exercise |
|
Can EHV be prevented/
|
vaccine offers some protection against respiratory signs and abortion, but not encephalopathic dz
|
|
What causes the development of bacterial pleuropneumonia?
|
-bacteria colonize the lung resulting in pneumonia, abscessation and inflammation of the pleura with accumulation of pleural fluid
|
|
What are the risk factors for developing bacterial pleuropneumonia?
|
-viral infection
-transport with head tied up -post anesthesia or stress |
|
Dx of bacterial pleuropneumonia should include what components?
|
-Hx and pE
-thoracic auscultation -thoracic rads -thoracic U/S -thoracocentesis -tracheal wash -CBC/fibrinogen |
|
What finding would you expect on PE of a horse with bacterial pleuropneumonia?
|
-depressed/lethargic/inappetent
-fever -tachycardia -tachypnea/cough -pleurodynia -auscultation: crackles, wheezes, pleural friction rubs -cyanosis |
|
What are the DDX's for bacterial pleuropneumonia?
|
-fungal pneumonia
-granulomatous lung dz -EHV 5 -neoplasia |
|
What is the Tx for bacterial pleuropneumonia?
|
-Abx
-thoracic drainage -IV fluids -plasma -nsaids -O2 |
|
What Abxs should you consider in tx bacterial pleuropneumonia?
|
Mitronidazol (for anaerobes) and PCN
|
|
Which analgesics are considered for tx of bacterial pleuropneumonia?
|
-Nsaids
-lidocaine infusion (somatic) -intercostal anesthesia -ketamine infusion |
|
When would colloids be given to a horse with bacterial pleuropneumonia?
|
-with hypoproteinemia
-vasculitis -inflammation |
|
What additional complications can arise from bacterial pleuropneumonia?
|
-laminitis
-thrombophlebitis -enterocolitis -chronic abscessation -bronchopleural fistula |
|
What are the clinical signs of thoracic trauma?
|
-shallow, fast breathing
-ventral increase in lung sounds -dorsal decrease in sound or nothing heard |