La Medicine -- Liver Iii

Front 1

Parasitic liver disease is most often caused by which organism? Most often occurs when?

Back 1

--fasciola hepatica

--most often occurs in lat fall/winter

Front 2

Where does fasciola hepatic occur?

Back 2

--PNW

--South Central US and Florida

--like wet, warm environments

Front 3

How do sheep get infected with fasciola hepatica?

Back 3

--sheep ingest metacercariae on vegetation

Front 4

What is the infectious stage of the fasciola hepatica life cycle?

Back 4

--metacercariae

Front 5

Most damage from fasciola hepatica is due to?

Back 5

--migrating juvenile flukes

Front 6

Antihelmentics don't treat _____ flukes very well.

Back 6

--don't treat juvenile flukes very well

Front 7

Different levels of severity with liver fluke disease?

Back 7

--subclinical disease and production loss

--anemia, ill thrift, hepatic dysfunction

>> fluke migration and feeding

--acute illness & sudden death (Cl. novyi B & D)

Front 8

Clinical signs of fluke infection in cattle?

Back 8

--often subclinical in cattle

--reduced weight gain, feed efficiency, lactation

--weight loss emaciation, depression, anorexia

--anemia, hypoproteinemia, bottle jaw

Front 9

Liver flukes cause disease via?

Back 9

--hyperplastic cholangitis

--plasma protein loss

--blood loss

--proline
>> depression anemia, biliary hyperplasia

Front 10

Liver flukes may cause what in camelids?

Back 10

--endocarditis and RHF

>> right ventricle filled with fibrin

Front 11

Clinical signs in sheep and goats?

Back 11

--fluke entry to bile ducts can be fatal

>> ascites, hemoabdomen, pallor and icterus

>> heavy fluke burden

--chronic disease (more common)

>> edema, ascites, emaciation

>> extensive fibrosis as liver heals tracts

Front 12

Diagnosis of liver flukes: lab findings?

Back 12

--anemia

--hypoproteinemia

--mild eosinophilia

--elevated hepatic enzymes

--fecal sedimentation for ova

Front 13

Correct fecal exam for fluke eggs?

Back 13

--fecal sedimentation

Front 14

Fasciola eggs may look like which rumen fluke spp?

Back 14

--paramphistomum

Front 15

Why might paramphistomum eggs indicate fasciola infection?

Back 15

--transmitted by the same snail

Front 16

The flukecides for Fasciola are effective against Paramphistomum, too. T/F?

Back 16

--False!

Front 17

Flukecides in the US do not kill migrating larvae. T/F?

Back 17

--True!

Front 18

Which two antihelminthic products kill Fasciola?

Back 18

--albendazole

--clorsulon

Front 19

Most important time range to treat for Fasciola?

Back 19

--start when flukes >12 wks old
>> after transmission season ends

--stop when flukes < 6 mo old & less pathogenic

Front 20

Name of large american liver fluke?

Back 20

--Fascioloides magna

Front 21

Fascioloides magna is most commonly found in which spp?

Back 21

--deer, elk, moose

Front 22

One or two fascioloides magna flukes can kill a goat. T/F?

Back 22

--True

Front 23

Why does fascioloides magna have a broader geographic distribution than fasciola?

Back 23

--greater number/variety of snail hosts

>> tolerate wider range of habitat/temperature

Front 24

Cattle are what kind of hosts for fascioloides magna? How do they react to it? Infection is difficult to diagnose because? How does this affect the value of the liver?

Back 24

--dead end hosts

--rapidly encapsulate parasite

--lack of fecal egg production

--can't sell liver >> giant fluke in it

Front 25

Fascioloides magna causes what in sheep and goats? Treatment?

Back 25

--death or severe hepatic insufficiency

--treatment: albendazole

Front 26

Lancet fluke scientific name?

Back 26

--dicrocoelium dendriticum

Front 27

Intermediate hosts of dicrocoelium dendriticum?

Back 27

--snails and ants

Front 28

Where do infectious metacercariae of dicrocoelium develop? How do livestock get infected?

Back 28

--develop in ants

--livestock ingest ants while grazing

Front 29

Pathogenicity of dicrocoelium? Pathogenicity more likely if?

Back 29

--inflammation of biliary tree, cirrhosis, hepatic insufficiency

--pathogenicity more likely with large numbers of flukes

Front 30

Clinical signs of dicrocoelium?

Back 30

--weight loss

--depression

--anemia

--hypoproteinemia

--bottle jaw

Front 31

Diagnosis of dicrocoelium?

Back 31

--fecal sedimentation or float

Front 32

Differential diagnoses for dicrocoelium?

Back 32

--chronic fascioliasis

--Gi helminthiasis

--Johne's, other causes of wasting

Front 33

Treatment of dicrocoelium?

Back 33

--albendazole

Front 34

What is fat cow syndrome?

Back 34

--mobilization of fat to the liver of post-parturient dairy cows in response to negative energy balance and hormonal changes

--ketosis >> hepatic lipidosis

Front 35

When does fat cow syndrome occur?

Back 35

--after calving in over-conditioned cows

--with co-morbidities, e.g. metritis

Front 36

--Clinical signs of fat cow syndrome?

Back 36

--anorexia, weight loss, depression

--depressed rumen motility and lactation

--signs of metritis, retained fetal membranes, mastitis, hypocalcemia, displaced abomasum

Front 37

Hepatic lipidosis occurs in goats when?

Back 37

--late gestation

Front 38

Diagnosis of fat cow syndrome?

Back 38

--liver enzymes often normal

--hypoglycemia

--ketonuria

Front 39

Fat cow syndrome treatment and prognosis?

Back 39

--prognosis can be guarded

>> mortality 25%

--treat any predisposing disease

--treat negative energy balance and lipidosis

Front 40

Prevention of fat cow syndrome?

Back 40

--appropriate dietary management during late lactation and dry period

>> ideal BCS in late lactation

>> adequate protein & roughage in dry period

>> additional grain 2-4 wks prior to calving

--prompt treatment of periparturient diseases

Front 41

Are liver biopsies indicated with fat cow syndrome?

Back 41

--no

--lipidosis present in normal high-producing post-parturient cows without disease

Front 42

How do you treat negative energy balance in ruminants that are anorexic?

Back 42

--propylene glycol

Front 43

When does pregnancy toxemia occur in ewes/does?

Back 43

--final 2-4 wks of gestation

Front 44

Cause of pregnancy toxemia in ewes/does?

Back 44

--inability to meet energy requirements with rapid fetal growth

--nutritional and physiological stress

>> bad weather, shearing, shipping, etc.

--often fat animals

Front 45

Why are small ruminants with multiple fetuses more predisposed to pregnancy toxemia?

Back 45

--less room in rumen >> can't fit enough foot

Front 46

Clinical signs of pregnancy toxemia?

Back 46

--anorexia, weakness, depression

--separation from the herd

--apparent blindness

--tremors, star gazing, ataxia, circling, bruxism

Front 47

DDX for pregnancy toxemia?

Back 47

--mastitis

--hypocalcemia

--polioencephalomalacia

--enterotoxemia type D

--toxicoses

Front 48

Physical exam and lab findings with pregnancy toxemia?

Back 48

--ketonuria

--acidosis with low K+ and Ca++

--elevated FFAs and betahydroxybutyrate (BHB)

--does may have marked neutrophilia

--friable/fatty liver on necropsy

Front 49

Treatment of pregnancy toxemia?

Back 49

--C-section or induce parturition

--continuous infusion of glucose

--adjunct therapies: B vitamins, transfaunation, propylene glycol

Front 50

How do you induce parturition in ewes? Does?

Back 50

--ewes: dexamethasone

--does: dexamethasone or PGF2

Front 51

Ewes and does are predisposed to pregnancy toxemia if?

Back 51

--enter third trimester over or under conditioned

--have too many fetuses

Front 52

Prevention of pregnancy toxemia?

Back 52

--provide excellent quality forage

--fetal sorting in early pregnancy (day 45 ideal)

>> know how many fetuses

--serial measurement of plasma BHB to assess nutritional adequacy

Front 53

BHB >__mmol/L indicates need for greater energy treatment in ewes.

Back 53

BHB > 0.8 mmol/L

Front 54

Hyperlipemia occurs in ponies, donkeys, and mini horses in response to what sudden change? Which animals are predisposed?

Back 54

--sudden drop in dietary carbs

>> sudden starvation or anorexia

>> history of stress or recent weight loss

>> fat mobilization with hepatic accumulation

--lactating animals predisposed

Front 55

What is hyperlipidemia? Reversible? Occurs when?

Back 55

--mild metabolic dysfunction with mild increase in serum triglycerides (<500 mg/dl)

--usually reversible with inc. in calories

>> need to forcefeed or put on TPN?

--often occurs when animals are azotemic

Front 56

What is hyperlipemia? Signs?

Back 56

--serum triglycerides > 500 mg/dl (much >)

--more severe dysfunction than hyperlipidemia

--anorexia, depression, weakness, incoordination, diarrhea

--white coating of tongue

--concurrent myopathy

--insulin resistant hyperglycemia

Front 57

Hyperlipemia results in which sequelae (4)?

Back 57

--severe metabolic dysfunction and death

--liver rupture (hemoabdomen & sudden death)

--laminitis (frequent)

--lipid accumulation in liver, kidney, heart, and skeletal muscle

Front 58

Diagnosis of hyperlipemia?

Back 58

--measure triglycerides, > 500 mg/dl

--white or yellow opaque plasma

--elevated bilirubin

--metabolic acidosis (severe cases)

--hepatomegaly and inc. echogenicity on US

>> some loss of normal hepatic architecture

Front 59

Treatment of hyperlipemia?

Back 59

--correct primary disease so they'll eat

--correct negative energy balance

>> IV dextrose

>> force feeding

>> IV nutrition (amino acids)

--insulin reduces fat mobilization (glargine)

--heparin: upregulate hormone sensitive lipase

Front 60

Why can't you give very much dextrose?

Back 60

--increases plasma osmolality and urine osmolality (causes dehydration)

--can only give 30%

Front 61

Most important thing about hyperlipemia treatment?

Back 61

--need to correct negative energy balance asap to prevent more lipid mobilization