Flashcards
Icterus in the Horse
Cards in this deck (41)
- 1What is SHED CSignalment
Health and maintenance
Environment
Diet
Complaint - 2What is a kind of colic that is caused by liver disease?Recurrent colic
swelling of the liver and distension of the biliary tract can cause signs of colic - 3How is fever related to liver disease?liver is responsible for removing antigens from the GIT - but if failing, all of these antigens are then presented to the rest of the body stimulating a fever
- 4How does liver disease cause photosensitisation?horses eat green grass containing chlorophyll which is converted in the liver
when the liver is not functioning this cholorphyll is converted to a compound called phylloerythrin which then circulates through the body and absorbs UV light and causes burning to the skin
-these lesions are seen though the non-pigmented areas of the face - 5What are clinical signs of liver disease - but w/o liver failure yet?significant weight loss, colicing horse
photosensitisation
icterus in the sclera (unusual) - 6Why is hepatic disease confused for other things?not recongized until hepatic failure occurs (at this point 50-60% of liver function is lost)
most horses w/ hepatic failure present w/ hepatic encephalopathy - 7What are the 4 stages of HE?Stage 1: subtle mental impairment
Stage 2: impaired motor function and consciousness
Stage 3: somnolence and aggressive blindness
Stage 4: coma - 8What other clinical signs are often seen w/ hepatic failure?inspiratory dyspnoea
coagulopathies
pruritis
haemolytic crisis/DIC
Recumbency and depression due to decreased glucose
gastric impactions, faecal changes - 9What do serum enzymes suggest in terms of liver function?hepatic disease can be temporarily diagnosed through:
-release from the cytoplasm or membranes of damaged hepatocytes
-increased production/degradation of enzymes
DOES NOT suggest liver functionality --> liver disease and liver function are 2 different things - 10which liver enzyme is not useful in the horse?ALT - the horse does not produce it in significant quantities
- 11What is significant about liver enzyme gamma glutamyl transferase (GGT)only the liver produces it - highest sensitivity test that is released during liver injury
GGT cannot differentiate b/w hepatocellular and biliary disease - but does tell us if there is a liver problem - 12What about sorbital dehydrogenase (SDH) and glutamate dehydrogenase (GLDH)both are fairly liver specific and indicate active hepatocellular necrosis
short half life and should be analysed w/in 12 hours - if analysis is delayed, separate the serum and refridgerate or freeze)
if they are high then you know for sure that the horse has liver damage - 13What are 2 liver non-specific enzymes?Aspartate aminotransferase (AST)
-this is produced by both the muscle and the liver so need to rule out muscle -> run w/ creatinine kinase
Alkaline phosphate (ALP)
-produced by a variety of tissues -- if very elevated assocaited w/ biliary disease/obstruction
glucocorticoids can also elevate ALP - 14What do bile acids indicate?most sensitive test that we have for hepatic disease and predicts long term survivability
post prandial increase is not important as no gallbladder and bile acids are continually released
use caution as bile acids also increase in fasting horses
only produced in the liver - occurs due to shunting or decreased blood flow to the liver, failure of the liver to remove bile acids from enterohepatic circulation or conjugate for excretion
biliary obstruction - back up of bile in to the blood b/c the liver can't process it - 15Is ammonia a useful thing to look for in terms of hepatic disease?produced by bacterial degradation of dietary proteins
normally absorbed from intestine and removed by the liver (SUN/BUN)
w/ hepatic insufficiency MAY have high resting NH4 due to decreased ammonia clearance which contributes to HE
however need to be close to a lab in order to process this - 16Why is biliruben not a good thing to test for?other factors elevate biliruben therefore not a sensitive test
- 17Is it possible to have liver disease w/o icterus?YES
need >75% of loss of functional mass b/f hyperbilirubinea occurs - 18How does anorexia cause icterus?if the horse doesn't eat, a protein called ligandin (has a short half life) drops very quickly and the liver is not able to conjugate biliruben properly
if a horse does not eat for 24 hours - the horse will start to get icteric - 19Why is albumin a poor indicator of liver disease?horses rarely have low albumin but w/ chronic disease might see hypoalbumnia - this is b/c horse albumin has a long half life of 19.5 days
- 20Why are coagulation panels common in horses w/ hepatic disease?b/c these are all produced by the liver
- 21What will you see in a serum biochem in a horse w/ liver disease?• Hypokalemia, hyponatremia, hypochloremia, hypoglycemia
• ↑Triglycerides primarily related to the fact that they are not eating
Metabolic acidosis common - 22What are 2 other useful ways to diagnose liver disease?US and biopsy: histopath and culture
biopsy good for toxicities and masses - but avoid if you suspect a liver abscess - 23What causes pyrrolizidine alkaloid toxicity?ragwort
jaagsiekte
Senecio latifolius
most common cause of hepatic failure in the UK - happens 6 months after ingestion - 24What is cholangiohepatitis?Chronic active hepatitis
implies sustained inflammatory process w/in liver and biliary system
likely an ascending bacterial infection from a previous SI disease - overall unknown - 25What causes acute hepatitis aka Theiler's disease?administration of biologics (tenanus antitoxin, plasma, blood) - maybe viral?
centrilobular necrosis, hepatocellular necrosis - 26What is cholelithiasis?Calculi in the bile ducts
etiology unknown but probably ascending infection from the SI
invariably associated w/ concomitant cholangiohepatitis
look for ALP b/c this indicates a liver component - 27What is equine hyperlipaemia?metabolic disorder
characterised by opaque serum or plasma, serum triglycerides and fatty infiltration of the liver (and other organs)
obesity increases the risk - 28What is a subclinical elevation of triglycerides called?hyperlipidaemia
subclinical elevations of triglycerides - no fatty liver, no hepatic dysfunction
normal response to a negative energy balance - 29What are the 3 options for handling free fatty acids?oxidative pathway - complete oxidation by the Kreb's cycle + glycerol
ketogenic pathway: partially oxidized - ketone bodies
reesterification to TG - TG stored in liver or returns to circulation
--> so either get too many TG in the liver, and too many in the circulation when it is really bad - 30What are TG exported into the blood by?VLDL - very low density lipoproteins
- 31Why are cattle more likely to have fatty livers?cattle cannot handle VLDLs and thus are more likely to have fatty livers
ketone body pathways are less developed in horses so also not as likely to develop ketosis
horses also have a greater hepatic exporting (as VLDLs) which is why they get a hypolipaemia - 32what does lipoprotein lipase do?catalyzes uptake of VLDL to peripheral tissues
heparin increases activity and release and is required as a cofactor - insulin does to
inhibited by azotaemia - 33What does hormone sensitive lipase do?catalyzes breakdown of TG in the adipose tissue
insulin inhibits activity (glucose indirectly via insulin)
glucocorticoids stimulate activity - 34Is hyperlipaemia a primary disease?NO
has an underlying cause that you need to look for
most common cause is inadequate nutrition leading to a negative energy balance - 35what points horses at risk of hyperlipaemia?ponies do not tolerate fasting as well as horses (fat ones esp)
stress, systemic illness
can have a seasonal occurrence - poor pastures and pregnant/lactating - 36What are the clinical signs of hyperlipaemia?non-specific - anorexia, depression,
icterus
diarrhea
others - ventral edema, fetid breath, grey coating on tongue
clinical signs can progress rapidly w/ death occurring in 6-10 days - 37How is hyperlipaemia diagnosed?blood
enzymes
triglycerides levels > 500 mg/dl
function tests - bile acids, ammonia
others - hypoglycemia, azotemia, metabolic acidosis - 38What are the main therapeutic objectives?determine underlying cause and treat
restore energy balance
supplement and monitor glucose
monitor hydration status, acid base and electrolytes
heparin therapy
insulin therapy - 39How do you prevent hyperlipaemia?Prevention:
• MONITOR TGs - prevent a negative energy balance
• Be on ALERT for hyperlipaemia in ANY SICK PONY, DONKEY or MINIATURE HORSE, ICELANDIC HORSE etc.
• Ensure adequate nutritional intake during illness
NOTE: Leptin as a biomarker?? → leptin concentrations inversely related to insulin sensitivity - 40What do owners need to be aware of in regards to treatment of acute liver failure?requires intensive and expensive therapy
currently equine liver disease = poor prognosis even if diagnosed - and high costs - 41What are some things you can do to treat acute liver failure?sedation - lowers seizure threshold and augments GABA receptors by toxins
fluid therapy
glucose supplementation
decrease further GIT toxin production - dietary changes (low protein)
GIT drugs: mineral oil and activated charcoal, lactulose, and others
broad spectrum antibiotics
protect from sunlight
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- BVetMed 3: Alimentary Flashcards on Icterus in the Horse , created by Erin Loogman on 02/04/2019.
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