Diseases of the Hepatobiliary System p843-872

Question 1

When is abx therapy indicated in liver failure?

Answer 1

When cholelithiasis, cholangitis and cholangiohepatitis are present, as well as liver dysfunction caused as a secondary problem to sepsis.

Question 2

In animals with hepatoencephalopathy, what drugs should be avoided and why?

Answer 2

Diazepam and other benzodiazepines, due to their ability to ENHANCE GABA on inhibitory neurons, thus ability to worsen HE. Sedation, when necessary in these animals, should be done with small amounts of alpha2-agonists.

Question 3

Why is a low protein/high starch diet, with a high BCAA/AAA ratio important in animals with hepatoencephalopathy?

Answer 3

During hepatic dysfunction, the hepatic metabolism of aromatic amino acids (AAA) is reduced and accumulation occurs. AAA can mimic neurotransmitters, aggravating signs of HE. Branched chain amino acids (BCAA) are metabolized by adipose and muscle.

Question 4

This drug aims to reduce intestinal ammonia absorption by suppressing enteric ammonia production. It is more nephrotoxic than a cousin drug and can be irritating to the intestinal mucosa. It’s used at 10-30 mg/kg PO q6-12hr
A) Lactulose
B) Neomycin
C) Metronidazole

Answer 4

B) Neomycin

Question 5

This drug is used for limiting intestinal ammonia absorption. It is used at 0.2-0.5 mL/kg PO, q6-8hr. It works by being poorly absorbed by the SI, creating an acidic environment and a gradient for ammonia to migrate from the blood stream to the large colon. Here it is trapped and expelled.
A) Lactulose
B) Neomycin
C) Metronidazole

Answer 5

A) Lactulose

Question 6

This drug at 10-15 mg/kg, q12h, can be used in conjunction with acetic acid (0.5 mL/kg, PO q12h) and mineral oil, for limiting intestinal ammonia absorption. This drug is metabolized by the liver and signs of toxicity can mimic hepaticencephalopathy.
A) Lactulose
B) Neomycin
C) Metronidazole

Answer 6

C) Metronidazole

Question 7

What is the purpose of Vit E (10,000 U PO, q24h) and pentoxifylline (8-10 mg/kg PO q12hr) in hepaticencephalopathy?

Answer 7

Vit E acts an antioxidant and anti-inflammatory. Pentoxifylline works as a nonselective phosphodiesterase inhibitor, providing weak inhibition of inflamm cytokines TNF-alpha and IL-6. It also decreases RBC deformability, possibly preventing microthrombosis.

Question 8

This drug is given at 20 mg/kg, PO q24h and can be given in cases of hepaticencephalopathy due to reduced endogenous production. This drug augments glutathione synthase levels in the hepatocyte, stabilization of membrane function, modification of cytokine expression and inhibition of apoptosis in normal cells.
A) DMSO
B) N-acetylcystein (NAC)
C) S-adenoslymethionine (SAMe)

Answer 8

C) S-adenoslymethionine (SAMe)

Question 9

This drug may act as an antioxidant and can aid in dissolving intrabiliary sludge or small calcium bilirubinate stones. Can cause hemolytic crisis in those with already fragile RBCs.
A) DMSO
B) N-acetylcysteine (NAC)
C) S-adenosylmethionine (SAMe)

Answer 9

A) DMSO

Question 10

This drug is though to be cytoprotective, improve hepatic microcirculation and oxygen delivery, enhance hepatic metabolic functions by restoring glutathione levels, block TNF-alpha release and act a free radical scavenger. Typically dosed at 70 mg/kg IV, q6hr, for two days.
A) DMSO
B) N-acetylcysteine (NAC)
C) S-adenosylmethionine (SAMe)

Answer 10

B) N-acytelcysteine

Question 11

I am a disease aka as enzootic hepatitis. I am transmitted by A) _____. I cause abortions in pregnant females and B) _____ in lambs, kids, and calves. My mortality rate in adults is C) < or > in young animals. On necropsy, I will have caused hepatomegaly and hemorrhage, with histopath showing eosinophilic intranuclear inclusion bodies. The state and federal regulatory veterinarian D) does or does not need to be called.

Answer 11

A) Mosquitos
B) Fever
C) Lower, a lot lower; in younger approaches 100%, in adults 20-30%
D) DOES NEED TO BE CONTACTED

Question 12

Telangiectasia is known as “sawdust livers” in the slaughter houses. What histopath changes are seen and what clinical signs are caused by this disease?

Answer 12

Telangiectasia is a focal degeneration of liver lobular ciruclation, with red-brown foci. Causing about 10% of condemnations, this disease has no clinical signs. Proposed pathogenesis is necrotizing hepatitis, ischemia induced by imboli, Vit E-selenium deficicency, immune mediated or reduced density of the reticulin framework.

Question 13

What causes the classic “nutmeg” liver?

Answer 13

Congestion of blood in the sinusoids and central veins.

Question 14

This equine disease causes abortion. The fetus can have hepatocyte necrosis with acidophilic intranuclear inclusion bodies in more than 50% of the hepatocytes.

Answer 14

Equine herpes virus

Question 15

The following characteristics are that of flow-limited drugs or capacity-limited drugs?

1. High hepatic excretion ratio
2. Quick and efficient excretion
3. Rate of elimination only limited by hepatic blood flow
4. Morphine and lidocaine as examples
5. Liver dysfunction causes increased bioavailability and decreased elimination

Answer 15

Flow-limited drugs

Question 16

The following characteristics are that of flow-limited drugs or capacity-limited drugs?

1. Low hepatic extraction ratio
2. Slowly extracted by the liver
3. Elimination is highly dependent on hepatocellular uptake and metabolism
4. Effects on these drugs are variable
5. Clearance seen to be increased with atenolol, decreased with diazepam and chloramphenicol

Answer 16

Capacity-limited drugs

Question 17

What are the two phases of drug metabolism in the liver? What is the purpose?

Answer 17

1. Oxidative phase

2. Glucuronidation These make the drugs water soluble and prepare them for excretion via the kidney

Question 18

What is a common laboratory finding in large animals with hepatocellular neoplasias?

Answer 18

Erythrocytosis because of a paraneoplastic syndrome and increased production of erythropoietin.

Question 19

What is hemochromatosis and how is it differentiated from hemosiderosis?

Answer 19

Hemochromatosis is a disorder caused by deposition of hemosiderin in the parenchymal cells.Hemosiderosis is iron accumulation in the reticuloendothelial cells, not the hepatocytes.

Question 20

What breed of cattle is seen to be affected by hemochromatosis? What is the inheritance pattern?

Answer 20

Salers cattle pass on hemochromatosis through autosomal recessive. There is an inappropriate absorption of iron by the GI tract, with subsequent hepatic storage and overload, ultimately leading to loss of hepatic function.

Question 21

When diagnosing hemochromatosis, what are normal liver iron concentrations in horses? In cattle?

Answer 21

In horses: 100-300 ppmIn cattle: 84-100 ppm

Question 22

Histopath of the liver of an animal with hemochromatosis reveals what?

Answer 22

Iron deposits in the liver, brown pigment stains the hepatocytes and the Kupffer cells.

Question 23

Biliary tract disease is rare in large animals. T/F

Answer 23

True.

Question 24

Match the correct term with the definition.
Cholelithiasis
Choledocholithiasis
Hepatolithiasis

A) The most common cause of biliary obstruction in large animals, occurs more frequently in horses, stones found in the common bile duct

B) Biliary calculi located in either the bile ducts or gallbladder

C) Presence of calculi in the intrahepatic bile ducts above the right and left hepatic ducts

Answer 24

Cholelithiasis - B
Choledocholithiasis - A
Hepatolithiasis - C

Question 25

A triad of these clinical signs cause suspicion of cholelithasis.

Answer 25

Recurrent abdominal pain, intermittent pyrexia and icterus

Hyperammonemic hepatic encephalopathy, photosensitization and weight loss are less common features.

Question 26

Cholestasis should be suspected in the horse if more than 25-30% of the total bilirubin is

A) Indirect
B) Direct

Answer 26

B) Direct

Question 27

What are some ultrasonographic changes seen in animals with cholelithiasis?

Answer 27

Hepatomegaly, bile duct dilation, parallel channel sign (dilation of interhepatic biliary radicals adjacent to the portal vein), stones themselves, Cholelithiasis can accurately be diagnosed by US in at least 75% of horses if adequate scanning of the liver is obtained and bile duct dilation and choleliths are visualized.

Question 28

Which of the following is incorrect regarding to treatment of cholelithiasis?

A) Broad-spectrum abx aimed at gram (+) enteric bacteria or anaerobes
B) Continuation of abx 6 weeks past time when GGT values return to normal
C) DMSO for aid in dissolving intrabiliary sludge or small calcium bilirubinate stones
D) Fluid therapy to thin secretions and promote bile flow

Answer 28

A) Broad spectrum abx should be aimed at Gram (-) bacteria. IV abx great, and then switch to orals. Chloramphenicol great choice in horses, due to good spectrum against most bacteria, BUT metabolized by liver. If hepatic function is NO BUENO, DO NOT USE.

Question 29

Which of the following describes the animal MOST likely to develop hepatic lipidosis?

A. Late, dry, dairy cow, who is being slowly introduced to the lactation diet
B. BCS 4.5 beef cow that has had her calf and is on good quality pasture
C. Early lactation, high producing dairy cow that went through a long calving interval
D. BCS 3.0 beef cow, with twins, who has maintained an adequate appetite through the transition period

Answer 29

C. Early lactation, high producing dairy cow that went through a long calving interval
Breed differences: Dairy cattle seen to have fatty liver in the first 4 weeks after calving, while in beef cattle, this disease is seen in late lactation, overweight, well-fed cattle that have had a drop in feed (due to feed shortage, or in cattle that are so over-conditioned that they are unable to consume enough energy for themselves)
The primary PRE-partum risk factors for developing hepatic lipidosis are : BCS > 4.0, severe feed restrictions, feeding excess energy and long calving interval
The primary POST-partum risk factors for developing hepatic lipidosis are: concurrent diseases, anorexia or fasting, feed restriction, sudden feed changes

Question 30

What are some concurrent disease that can be seen with hepatic lipidosis?

Answer 30

Metritis, displaced abomasum, retained fetal membranes, parturient paresis, mastitis

Question 31

Ultrasound changes can be subjective, but what might indicate hepatic lipidosis?

Answer 31

ncreased echogenicity, brighter, liver may be larger and more rounded

Question 32

What is the gold standard for diagnosing hepatic lipidosis? How are the results interpreted?

Answer 32

Liver biopsy is gold standard. Identifying fatty infiltration, by percentage of hepatocytes varies. In apparently health, high producing post-partum cattle, there will be a moderate amount of fat present in the liver. Once the fat is more than 34% wet weight, this correlates with signs of disease. This is determined by the tissue sample floating in distilled water with SG of 1.000. The liver, on necropsy, will appear to be swollen, with rounded edges, pale yellow in color and can flow. The fatty infiltrate occurs in the centrilobular and intermediate areas.

Question 33

What is the basic pathogenesis behind hepatic lipidosis?

Answer 33

There is an overwhelming amount of triglycerides formed that that exceeds oxidation capacity and the formation and release of VLDLs into the periphery. Ruminants already have a poor ability to export excess lipids from he liver.

Question 34

What are some management tools to prevent hepatic lipidosis from occurring?

Answer 34

Preventing over-conditioning of late lactation cattle, making sure the cattle are fed, but NOT OVERFED. Supplementation with cobalt, a Vit B12 precursor, can help provide precursors for gluconeogenesis. Treating cattle aggressively for the other concurrent diseases.

Question 35

When does pregnancy toxemia occur in small ruminants?

Answer 35

This occurs 2-4 weeks prior to parturition. Seen in ewes that have more than one fetus and in does with 3-4 feti. The ewes can be seen to be overly fat.

Question 36

What blood work changes are noted in small ruminant pregnancy toxemia?

Answer 36

Serum BHB is typically > 1 mmol/L. Ketonuria typically occurs before ketonemia.

Question 37

What are the two principles of treatment of ketosis?

Answer 37

1. Administering exogenous energy source

2. Remove factors requiring energy demand on the email

Question 38

How can parturition be induced in ewes and does?

Answer 38

15-20 mg of dexamethasone/ewe 10 mg of dexamethasone/doe

Question 39

How much propylene glycol or IV glucose can be given to support small ruminants with pregnancy toxemia?

Answer 39

Oral propylene glycol - 150-200 mL given q12 for the first two doses then 60 mL/dose for 3-6 additional days

IV glucose 150-200 mL of 10-20% as a bolus followed by a drip of 5-10%

Question 40

Pancreatitis in cattle and in horses is a rare finding. How is it best diagnosed?

A) Laboratory findings
B) Ultrasonographic findings
C) Histology from necropsy
D) Antemortem biopsy

Answer 40

C) Histology on necropsy

Question 41

List some causes of pancreatitis in cattle and horses.

Answer 41

Migrating parasites, bacterial or viral infections, immune-mediated damage, biliary or pancreatic duct inflammatory disease, vitamin D tox, Vit A or E deficiencies. Drugs known to cause pancreatitis in humans, that are used in horses are: furosemide, tetracycline, estrogen, corticosteroids

Question 42

Clinical signs of pancreatitis are non-specific. What are they?

Answer 42

Mod-severe abdominal pain, gastric reflux, hypovolemic shock, cardiovascular compromise.

Question 43

If laboratory work is done to diagnosis pancreatitis, what are some values of importance?

Answer 43

Serum amylase 14-35 IU/L
Serum lipase23-87 IU/L
Peritoneal fluid amylase 0-14 IU/L
Peritoneal fluid lipase 0-36 IU/L
Trypsin 28.5 ng/mL

Question 44

This laboratory finding is most specific to the pancreas and its activity was significantly higher in horses with pancreatic damage than in healthy horses.

A) Serum amylase
B) Serum lipase
C) Serum trypsin
D) Serum GGT

Answer 44

C) Serum trypsin This enzyme is specific to the pancreas, as amylase originates from the salivary gland and lipase originates from the liver. GGT levels are not a sensitive indicator of pancreatic disease. Trypsin activates its own zymogen and those of other pancreatic enzymes as well.

Question 45

Management of pancreatitis consists of what?

Answer 45

This is symptomatic. Gastric decompression is often needed, as well as control of abdominal pain, IV fluids to correct hypovolemia, Abx due to secondary bacterial infections

Question 46

Chronic interstitial pancreatitis has been known to be correlated with what parasites in cattle and horses?

Answer 46

In horses: Strongylus equinus and Strongylus edentatus, one report of Parascaris equorumIn cattle: Eurytrema pancreaticum and Eurytrema coelomaticum, but these have not been isolated in the US

Question 47

Pancreatitis in cattle occurs most frequently with what disorder?

Answer 47

Type I diabetes mellitus

Question 48

What does histopath usually find in examination of cattle with pancreatitis?

Answer 48

Absence of beta cells in the islet tissues

Question 49

What is the clinical significance of finding pancreatic calculi in older cattle? > 5 yrs

Answer 49

Usually an incidental finding on necropsy. Generally made of calcium carbonate and calcium phosphate. Predisposing factors are silica-rich soil, vit A deficiency or chronic inflammation of pancreatic ducts

Question 50

Icterus is caused by 3 failed processes involving bilirubin. What are they?

Answer 50

1. Failure of bilirubin uptake
2. Failure of conjugation of bilirubin
3. Failure to excrete of bilirubin

Question 51

In ruminants, icterus is less likely due to acute liver disease and more attributed to what?

Answer 51

Hemolysis, as seen in anaplasmosis or copper toxicity, for example

Question 52

Diarrhea can be seen in ruminants with chronic liver failure. Why is this?

Answer 52

Portal hypertension and increased hydrostatic pressure can lead to diarrhea in ruminants with chronic liver failure.

Question 53

What is the mechanism behind how portal hypertension, due to chronic liver failure, leads to ascites?

Answer 53

Venous blockage produces increased hydrostatic pressure, which causes portal hypertension. Protein leakage occurs into the peritoneal cavity. This leakage comes from the increased production of hepatic lymph, which is high in protein. The lymph leaks into the interstitial space and then into the peritoneal cavity.

Question 54

Why does hepatic photosensitization occur in animals with liver failure?

Answer 54

Bacterial degradation in the rumen, of chlorophyll, creates a photodynamic agent called phylloerythrin. This is typically conjugated in the liver and excreted in the bile. With liver failure, the phylloerythrin is transported to the skin, reacts with sunlight and emits an energy that causes lesions to the white areas.

Question 55

Which clotting factors are produced in the liver?

Answer 55

I, II, V, VII, IX, X

Question 56

What are some speculations as to the pathophysiology of hepatic encephalopathy?

Answer 56

1. Synergistic neurotoxins pass excretion through the kidney
2. Manganese deposition in the globes pallidus region of the brain; increased levels due to lack of excretion by the liver
3. Neurosteroids with GABA-agonist properties, i.e. ammonia plays a role in the metabolism of GABA and could act synergistically
4. Increased concentrations of branched chain amino acids compete for entry into the CNS and may lead to increased production of inhibitory neurotransmitters

Question 57

What are some liver leakage enzymes?

Answer 57

SDH, LDH, GDH, AST

Question 58

What are some liver enzymes that are seen with cholestasis?

Answer 58

GGT, ALP

These are more likely to elevate in chronic hepatic disease than leakage enzymes.

Question 59

What other tissues can GGT come from?

Answer 59

Pancreases, mammary gland, lung, kidney tubules

Question 60

What other sources can ALP come from?

Answer 60

Bone, intestines, placenta, and macrophages

Question 61

Why is ammonia a good assessment of liver function?

Answer 61

The liver is responsible for converting ammonia to urea by the hepatic urea cycle. The ammonia comes from degradation of protein and amino acids in the GI and is carried to the liver in the portal circulation.

Question 62

Match the location of a liver biopsy with the following species:
Equine, bovine, small ruminants

A) Horizontal line cranial from middle of paralumbar fossa to where line crosses 11th ICS on the right side
B) Line drawn from tuber coxae to point of the shoulder, intersection of 14th ICS
C) Line level with ventral end of last rib, intersecting with 9th or 10th ICS

Answer 62

Bovine A) Horizontal line cranial from middle of paralumbar fossa to where line crosses 11th ICS on the right side
Equine B) Line drawn from tuber coxae to point of the shoulder, intersection of 14th ICS
Small ruminants C) Line level with ventral end of last rib, intersecting with 9th or 10th ICS

Question 63

What are indications of a poor prognosis in liver disease, for equine?

Answer 63

Low albumin, less than 2.5 g/dL
Increased globulin level
Prothrombin time greater than 30% of normal
Greatly elevated GGT and ALP

Question 64

A recently parturient lactating mare presents to the hospital with depression, jaundice, pica and behavioral changes consistent with hepatic encephalopathy. Blood reveals elevated bile acids, decreased BUN, hyperammonemia and prolonged clotting times. What drug should be avoided, when attempting to sedate this mare for a liver biopsy?

A) Xylazine
B) Ketamine
C) Butorphanol
D) Midazolam

Answer 64

D) Midazolam

With suspicion of liver disease, benzodiazepines should be avoided, as they have a GABA like behavior and will exacerbate inhibitory neuron activity.

Question 65

A recently parturient lactating mare presents to the hospital with depression, jaundice, pica and behavioral changes consistent with hepatic encephalopathy. Blood reveals elevated bile acids, decreased BUN, hyperammonemia and prolonged clotting times. A liver biopsy is retrieved, revealing widespread necrosis of hepatocytes and the centrilobular and midzonal areas replaced by eosinophilic granular mass. What is the most likely etiology for this mare’s liver failure?

A) Ingestion of tansy ragwort
B) Administration of tetanus antitoxin
C) Overdose of tetracyclines
D) Lymphoma

Answer 65

B) Administration of TAT. This mare likely has Theiler’s disease, aka idiopathic acute hepatic disease (IAHD). Equine plasma is also associated with IAHD. A viral etiology has been shown to be present, now called Theiler’s disease-assoc virus. 2-3 mths after admin of blood products, acute hepatic failure can occur.

Question 66

What diet changes should occur in a mare suspected to have Theiler’s disease?

A) Decrease carbohydrates and protein
B) Decrease carbohydrates and increase protein
C) Increase carbohydrates and protein
D) Increase carbohydrates and decrease protein

Answer 66

D) Decreasing quantity of proteins and increasing carbohydrates will help in lessening degree of abnormal behavior assoc with hepatic encephalopathy. Diets high in branched chain amino acids will also help.

Question 67

This is the etiologic agent for Black Disease.

A) Clostridium chauveoi
B) Clostridium sordelli
C) Clostridium novyi type B
D) Clostridium hemolyticum

Answer 67

C) Clostridium novyi type B

Question 68

How do animals acquire the Black disease etiologic agent and how does it cause Black disease?

Answer 68

C. novyi type B can be ingested from the soil and found in the GI system and livers grazing on affected pasture. Once ingested, the bacteria becomes disseminated throughout the macrophage system. Once anaerobic conditions become available, the spores will germinate and enter a vegetative state. As proliferation occurs, necrosis of the liver occurs, due to the exotoxins produced.

Question 69

What are the exotoxins produced by the etiologic agent of Black Disease?

Answer 69

There is an alpha- and beta-toxin released from C. novyi Type B. The alpha-toxin enters the cell by receptor-mediated endocytosis and inhibits triphosphatases. The beta-toxin is a necrotizing and hemolytic phospholipase C.

Question 70

What clinical sign of Black Disease gave its name and how does this occur?

Answer 70

The exotoxins fro C. novyi Type B causes venous congestion, thus blackening the skin.

Question 71

What’s the most common clinical sign of Black Disease?

A) Peracute death
B) Icterus
C) Hepatic encephalopathy
D) Venous congestion

Answer 71

A) Peracute death due to the destruction of the exotoxins to vascular endothelium and then organ failure.

Question 72

What is the primary lesion of Black Disease seen on necropsy?

Answer 72

Multiple areas of hepatic necrosis, appearing yellow to white and surrounded by a broad zone of hyperemia.

Question 73

What is the predisposing agent that destroys the liver and allows Black Disease and Bacillary hemoglobinuria to occur?

Answer 73

Fasciola hepatica

Question 74

Bacillary hemoglobinuria or Redwater disease is caused by what?

A) Clostridium chauveoi
B) Clostridium sordelli
C) Clostridium novyi type B
D) Clostridium hemolyticum

Answer 74

D) C. hemolyticum, or C. novyi type D

Question 75

What is the most important exotoxins of C. hemolyticum and how does it’s destructive properties differ from that of Black Disease?

Answer 75

The beta-toxin from C. hemolyticum is a phospholipase C, which ultimately causes hepatocyte necrosis, hemolysis and damage to vascular epithelium. It differs from C. novyi Type B because it causes hemoglobinuria.

Question 76

What is the pathognomonic lesion of bacillary hemoglobinuria?

Answer 76

Ischemic hepatic infarct, which has a zone of hyperemia at its interface with viable liver tissue. Coagulation necrosis, partially liquified at its center.

Question 77

What is the causative organism for Tyzzer’s disease and what age of horse does it affect?

Answer 77

Typically found in foals 7-42 days old, Clostridium piliforme is the causative agent.

Question 78

What is the prognosis for Tyzzer’s disease?

Answer 78

C. piliforme in foals in highly fatal.

Question 79

This mineral toxicity is the best documented of the toxic causes of liver failure and can occur following administration of nutritional supplements.

Answer 79

Iron toxicity can occur with supplements containing ferrous fumarate. Clinical signs start with hepatoencephalopathy and icterus.

Question 80

What are several congenital/inherited disease that are the cause of liver disease in equine or farm animals?

Answer 80

Congenital portosystemic shunts can occur infrequently in both equine and bovine patients.

Hepatic failure can be seen in Morgan foals and is fatal, often ending in a terminal hemolytic crisis.

Glycogen branching enzyme deficiency is found in QH and Paint horses. This is a autosomal recessive mutation in the glycogen branching enzyme I. Foals are unable to store and mobilize glycogen to maintain normal glucose homeostasis.

Question 81

What is kernicterus?

Answer 81

This is a bilirubin encephalopathy that occurs in foals with neonatal isoerythrolysis. Neurologic signs are caused by the neurotoxic effects of unconjugated bilirubin.

Question 82

Why might Vit E might be needed in chronic active hepatitis (CAH)?

Answer 82

CAH is an idiopathic progressive hepatopathy. Similar to an autoimmune or hypersensitivity in humans, this is often diagnosed by a liver biopsy with a mononuclear cell infiltrate located along the portal/periportal areas, along with biliary hyperplasia and fibrosis or cirrhosis.

Vit E may aid in protection of membrane phospholipids from oxidative damage and suppress activation of inflammatory cells.

Question 83

What are the primary plants containing pyrrolizidine alkaloids?

A) Astragalus and Oxytropis
B) Senecia and Crotalaria
C) Perilla frutescens
D) Pteridium aquilinum

Answer 83

B) Senecia and Crotalaria

Astragalus and Oxytropis are known as locoweeds
Perilla frutescens is perilla mint
Pteridium aquilinum is bracken fern

Question 84

When do clinical signs show up in animals that have been ingesting pyrrolizidine alkaloids? How do PAs cause clinical signs?

Answer 84

Signs occur when hepatocytes are lost and replaced by fibrous tissue. PAs are metabolized by liver to a more toxic pyrrole. These can cause cross-linking of double stranded DNA and become antimitotic. Megalocytes are created since hepatocytes cannot divide, and the liver becomes replaced with connective tissue.

Question 85

This liver fluke is the most common, in the south-central states, Florida and the PNW.

A) Fascioloides manga
B) Fasciola gigantica
C) Paramphistomum
D) Fasciola hepatica

Answer 85

D) Fasciola hepatica is the common liver fluke in the south-central states, Florida, and the PNW.

Fascioloides manga is the large American liver fluke and is not as common. F. gigantica is present in the tropics. Paramphistomum is a species of non pathogenic rumen flukes. These eggs on a fecal can be mistaken with F. hepatica and treatment for F. hepatica will result in continued fecal egg burden.

Question 86

Economic loss is probable with a liver fluke load of over 40 flukes. Clinical disease is seen with a load over ___ flukes.

A) 75
B) 150
C) 200
D) 300

Answer 86

C) 200

Question 87

Sheep and goats are a) MORE/LESS susceptible that cattle to Fasciola hepatica.

Answer 87

a) More

Question 88

What is the important vector of Fasciola hepatica? What stage affects cattle and small ruminants when ingested?

Answer 88

The mud snail is the vector for liver flukes. Intramolluscan development occurs, followed by the release of cercariae that encyst as infective metacercariae on pasture vegetation.

Question 89

Which of the following drugs is an effective flukecidal?

A) Ivermectin
B) Albendazole
C) Fenbendazole
D) Sulfadimethoxine

Answer 89

B) Albendazole 10 mg/kg

Question 90

Fusobacterium necrophorum has several virulence factors that contribute to development of liver abscesses. What is the major virulence factor? How do these factors cause pathogenesis?

Answer 90

Leukotoxin of subspecies necrophorum and subspecies funduliforme allow the pathogen to survive, proliferate and set up infection of the ruminal wall and liver.

The combination of effects are dermonecrotic, cytotoxic, survival in high oxygen concentrations, and phagocytic mechanisms.