VM 575 (Digestive System II) FINAL EXAM
STUDY GUIDE QUESTIONS ACCURATE AND
VERIFIED.
Identify the parameters on routine chemistry profiles that can be markers
for liver function
Bilirubin
Bile acids
BUN
Ammonia
Albumin
Glucose
Cholesterol
Be able to recognize chemistry profiles that suggest liver dysfunction
Hyperbilirubinemia: Unconjugated = hemolysis/prehepatic, conjugated =
cholestasis, mixed = primary hepatic parenchymal disease
Bild acids: increased if liver is not capable of reabsorbing
Cholesterol: decreased in advanced liver disease, increased in severe
cholestasis
Glucose: decreased in 80% of the liver has been compromised
BUN: will decrease if liver is not breaking down ammonia
Ammonia: will increase if liver is damaged
Albumin: will decrease in hepatopathies
Be able to explain the overview of bilirubin and bile acid metabolism and
how these measures can be used to assess liver function.
Bilirubin is a waste product of heme that is from broken down RBCs.
Unconjugated bilirubin is transported to the liver bound to albumin. Once at
the liver it becomes conjugated and excreted into the bile duct and then
through the intestine. If there is an increase in unconjugated bilirubin it could
be due to extravascular hemolysis. An increased conjugated bilirubin could be
,attributed to severe cholestasis where the bile duct is obstructed
Bile acids: synthesized in the liver and excreted into the bile duct. If bile acids
are increased post feeding it is an indicator of liver dysfunction.
List clinical features and physical exam findings that could suggest
hepatobiliary disease is present
Gastrointestinal signs, PU/PD, neurologic signs
Bleeding - increased clotting time, GI ulceration (portal hypertension),
jaundice, ascites, weight loss, dehydration
Hepatomegaly, petechia and ecchymoses, melena, pallor, depression
Be able to select appropriate differentials for chemistry profiles suggestive
of liver disease.
List common historical findings in feline liver disease
Icterus/jaundice
Anorexia, vomiting, muscle waisting
PU/PD
Depression
Understand key differences in the assessment of feline and canine liver
enzymes
GGT is not used in cats
The half life of AST is very short in cats so any elevation should be considered
severe
Be able to formulate a prioritized differential list for an icteric cat
3 common diseases: hepatic lipidosis, cholangitis/cholangiohepatitis, and
lymphoma
1 not uncommon disease: acute pancreatitis
2 uncommon diseases: toxoplasmosis and FIP
Explain the value of ultrasound and fine need aspirates in the assessment
of feline liver disease
,Ultrasound: assessment of hepatic parenchyma and intrahepatic vs. post-
hepatic cholestasis (surgical vs. non-surgical disease)
FNA/cytology: simple, inexpensive, minimally invasive, minimal risk for
bleeding, evaluation of limited number of cells, no architecture
FNA can rule in or out 2 of the most common liver diseases in cats (lipidosis
and lymphoma)
Develop a treatment protocol for a cat with hepatic lipidosis
Fluid therapy is needed to address hydration, electrolyte, and acid-base
disturbances
Anti-emetic therapy can help address nausea
Nutritional support is the single most important factor associated with survival
Nutritional support should be provided by a feeding tube
Pro-motility agents can decrease food intolerance
Vitamin K should be provided to animals with clotting time abnormalities
L-carnitine supplementation can improve beta oxidation lipids and can be
supplemented
Taurine supplementation can promote normal bile acid conjugation and
decrease build up of toxic bile acids
Thiamine deficiency is often present and this can be associated with CNS signs
such as blindness
Antioxidant supplementation should be considered as oxidative liver injury
occurs in affected cats
Cobalamin can promote antioxidant formation
Treatment for encephalopathy is needed in some cats
Explain the pathophysiology of portosystemic shunts (PSS) in the dog
including congenital extrahepatic, congenital intrahepatic, and acquired
shunts.
Congenital: vascular abnormalities that develop due to inappropriate closure
of portions of the fetal vasculature.
Extrahepatic: broadly classified as portocaval (terminating in the caudal vena
cava) or portoazygous (terminating within the thoracic cavity in the azygous
vein)
, Intrahepatic: result of a patent ductus venosus
Acquired: multiple shunts will be present; connect the portal tributaries to the
CVC, usually near the renal veins. Develop as a consequence of portal
hypertension (elevated pressures in the portal venous sytsem)
Describe congenital portal vein hypoplasia and how it compares to
congenital portosystemic shunts in regard to pathophysiology, clinical
signs, bloodwork findings (including protein C activity and bile acid
concentrations), management and prognosis.
PVH: condition in which the microscopic portal vessels are incompletely
developed. This results in diminished hepatic perfusion. Because hepatic blood
flow is overall diminished, the liver responds by duplicating arterioles in an
attempt to restore blood supply.
PVH is historically asymptomatic where PSS is symptomatic
Liver function tests are usually normal in PVH and abnormal in PSS
Liver enzymes are normal to increased in PVH and PSS
Fasting bile acids is often normal in PVH and usually abnormal in PSS
Fed bile acids is usually <70 in PVH and >70 in PSS
Protein C activity is usually >70% in PVH and <70% in PSS
The only definitive way to differentiate the two disorders is by ruling out a
macroscopic shunt with imaging modalities.
Most dogs with PVH are asymptomatic and have a normal life expectancy
without the need for treatment; if portal hypertension occurs these dogs are
treated with medical management for HE and portal hypertension and can
live for many years following the onset of signs
Recognize breed predilections, clinical signs, physical exam findings,
bloodwork and urine abnormalities, and imaging findings in patient's with
portosystemic shunts.
Extrahepatic shunts are usually found in small breed dogs - pug, miniature
schnauzer, maltese, shih tzu, yorkshire terrier, cairn terrier
Intrahepatic sunts are usually found in medium to large breed dogs -
australian cattle dog, australian shepherd, old english sheepdog, labrador
retriever, golden retriever, and irish wolfhound
STUDY GUIDE QUESTIONS ACCURATE AND
VERIFIED.
Identify the parameters on routine chemistry profiles that can be markers
for liver function
Bilirubin
Bile acids
BUN
Ammonia
Albumin
Glucose
Cholesterol
Be able to recognize chemistry profiles that suggest liver dysfunction
Hyperbilirubinemia: Unconjugated = hemolysis/prehepatic, conjugated =
cholestasis, mixed = primary hepatic parenchymal disease
Bild acids: increased if liver is not capable of reabsorbing
Cholesterol: decreased in advanced liver disease, increased in severe
cholestasis
Glucose: decreased in 80% of the liver has been compromised
BUN: will decrease if liver is not breaking down ammonia
Ammonia: will increase if liver is damaged
Albumin: will decrease in hepatopathies
Be able to explain the overview of bilirubin and bile acid metabolism and
how these measures can be used to assess liver function.
Bilirubin is a waste product of heme that is from broken down RBCs.
Unconjugated bilirubin is transported to the liver bound to albumin. Once at
the liver it becomes conjugated and excreted into the bile duct and then
through the intestine. If there is an increase in unconjugated bilirubin it could
be due to extravascular hemolysis. An increased conjugated bilirubin could be
,attributed to severe cholestasis where the bile duct is obstructed
Bile acids: synthesized in the liver and excreted into the bile duct. If bile acids
are increased post feeding it is an indicator of liver dysfunction.
List clinical features and physical exam findings that could suggest
hepatobiliary disease is present
Gastrointestinal signs, PU/PD, neurologic signs
Bleeding - increased clotting time, GI ulceration (portal hypertension),
jaundice, ascites, weight loss, dehydration
Hepatomegaly, petechia and ecchymoses, melena, pallor, depression
Be able to select appropriate differentials for chemistry profiles suggestive
of liver disease.
List common historical findings in feline liver disease
Icterus/jaundice
Anorexia, vomiting, muscle waisting
PU/PD
Depression
Understand key differences in the assessment of feline and canine liver
enzymes
GGT is not used in cats
The half life of AST is very short in cats so any elevation should be considered
severe
Be able to formulate a prioritized differential list for an icteric cat
3 common diseases: hepatic lipidosis, cholangitis/cholangiohepatitis, and
lymphoma
1 not uncommon disease: acute pancreatitis
2 uncommon diseases: toxoplasmosis and FIP
Explain the value of ultrasound and fine need aspirates in the assessment
of feline liver disease
,Ultrasound: assessment of hepatic parenchyma and intrahepatic vs. post-
hepatic cholestasis (surgical vs. non-surgical disease)
FNA/cytology: simple, inexpensive, minimally invasive, minimal risk for
bleeding, evaluation of limited number of cells, no architecture
FNA can rule in or out 2 of the most common liver diseases in cats (lipidosis
and lymphoma)
Develop a treatment protocol for a cat with hepatic lipidosis
Fluid therapy is needed to address hydration, electrolyte, and acid-base
disturbances
Anti-emetic therapy can help address nausea
Nutritional support is the single most important factor associated with survival
Nutritional support should be provided by a feeding tube
Pro-motility agents can decrease food intolerance
Vitamin K should be provided to animals with clotting time abnormalities
L-carnitine supplementation can improve beta oxidation lipids and can be
supplemented
Taurine supplementation can promote normal bile acid conjugation and
decrease build up of toxic bile acids
Thiamine deficiency is often present and this can be associated with CNS signs
such as blindness
Antioxidant supplementation should be considered as oxidative liver injury
occurs in affected cats
Cobalamin can promote antioxidant formation
Treatment for encephalopathy is needed in some cats
Explain the pathophysiology of portosystemic shunts (PSS) in the dog
including congenital extrahepatic, congenital intrahepatic, and acquired
shunts.
Congenital: vascular abnormalities that develop due to inappropriate closure
of portions of the fetal vasculature.
Extrahepatic: broadly classified as portocaval (terminating in the caudal vena
cava) or portoazygous (terminating within the thoracic cavity in the azygous
vein)
, Intrahepatic: result of a patent ductus venosus
Acquired: multiple shunts will be present; connect the portal tributaries to the
CVC, usually near the renal veins. Develop as a consequence of portal
hypertension (elevated pressures in the portal venous sytsem)
Describe congenital portal vein hypoplasia and how it compares to
congenital portosystemic shunts in regard to pathophysiology, clinical
signs, bloodwork findings (including protein C activity and bile acid
concentrations), management and prognosis.
PVH: condition in which the microscopic portal vessels are incompletely
developed. This results in diminished hepatic perfusion. Because hepatic blood
flow is overall diminished, the liver responds by duplicating arterioles in an
attempt to restore blood supply.
PVH is historically asymptomatic where PSS is symptomatic
Liver function tests are usually normal in PVH and abnormal in PSS
Liver enzymes are normal to increased in PVH and PSS
Fasting bile acids is often normal in PVH and usually abnormal in PSS
Fed bile acids is usually <70 in PVH and >70 in PSS
Protein C activity is usually >70% in PVH and <70% in PSS
The only definitive way to differentiate the two disorders is by ruling out a
macroscopic shunt with imaging modalities.
Most dogs with PVH are asymptomatic and have a normal life expectancy
without the need for treatment; if portal hypertension occurs these dogs are
treated with medical management for HE and portal hypertension and can
live for many years following the onset of signs
Recognize breed predilections, clinical signs, physical exam findings,
bloodwork and urine abnormalities, and imaging findings in patient's with
portosystemic shunts.
Extrahepatic shunts are usually found in small breed dogs - pug, miniature
schnauzer, maltese, shih tzu, yorkshire terrier, cairn terrier
Intrahepatic sunts are usually found in medium to large breed dogs -
australian cattle dog, australian shepherd, old english sheepdog, labrador
retriever, golden retriever, and irish wolfhound
