La Medicine -- Liver Iv

Front 1

Examples of chronic liver diseases?

Back 1

--chronic active hepatitis

--cholangiohepatitis

--cholelithiasis

--toxicoses

Front 2

Differentiating causes of chronic liver disease: tools?

Back 2

--bloodwork may be challenging

--ultrasound can be helpful

--biopsy necessary for accurate diagnosis

Front 3

What is chronic active hepatitis? Where is the inflammation? What kind of infiltrate?

Back 3

--chronic, idiopathic hepatic inflammation

--periportal and/or biliary inflammation with variable fibrosis and inflammatory infiltrate

--lymphocytes and plasma cells in infiltrate

Front 4

Chronic active hepatitis results from an inflammatory or infectious insult that causes what?

Back 4

--promotes biliary proliferation

>> impair bile excretion

>> destroy hepatocytes

>> promote fibrosis

Front 5

Clinical signs of chronic active hepatitis?

Back 5

--weight loss, icterus, depression

--mild colic and intermittent fever

--aseptic vasculitis (occasional)

>> dermatitis of coronary band (horses)

>>focal areas of necrotic leathery skin

Front 6

Diagnosis of chronic active hepatitis?

Back 6

--mild increase in AST, SDH

--marked increase in ALP and GGT

--increased bile acids

--increased bilirubin (esp. conjugated)

--variable increase in white cells, fibrinogen, TP

Front 7

Most effective way to diagnose chronic active hepatitis?

Back 7

--liver biopsy

>> culture and sensitivity

>> histopathology

Front 8

Histo of liver biopsy with chronic active hepatitis?

Back 8

--infiltration with mononuclear cells

--biliary hyperplasia can occur

--hepatocellular necrosis

>> bridging lobules or from portal tract to central v.

>> fibrosis and cirrhosis eventually

Front 9

Treatment of chronic active hepatitis?

Back 9

--antibiotics if CBC/culture/biopsy suggest infection

--corticosteroids if lymphocytic plasmacytic infiltration or fibrosis

>> prednisolone, dexamethasone

Front 10

Antibiotic choices for chronic active hepatitis with infection?

Back 10

--ampicillin and chloramphenicol

--IV penicillin/gentamicin (more severe case)

--TMS (oral, cheap, easy to give, available)

Front 11

Chronic active hepatitis prognosis depends on?

Back 11

--severity of clinical signs

--degree of fibrosis/hepatocellular disruption

Front 12

Chronic active hepatitis prognosis poor if?

Back 12

--severe clinical signs

--severe fibrosis or hepatocellular disruption on biopsy

Front 13

Corticosteroids for chronic active hepatitis: prolong survival time?

Back 13

--do not prolong survival

Front 14

Monitor chronic active hepatitis with?

Back 14

--repeat bloodwork

--potentially repeat biopsy?

Front 15

Suppurative cholangiohepatitis is characterized by? Clinical signs?

Back 15

--neutrophil accumulation within hepatic portal tracts and bile ducts

--fever, colic, icterus, weight loss, inc. GGT

Front 16

Most important sequelae of cholangiohepatitis?

Back 16

--cholelithiasis

--eventual loss of hepatic function

--chronic active hepatitis?

Front 17

Cholangiohepatitis occurs due to (7)?

Back 17

--cholestasis or cholelithiasis

--intestinal inflammation/obstruction

--chronic active hepatitis

--neoplasia

--intestinal parasitisim

--toxins: sporidesmin in cattle and sheep

--often idiopathic

Front 18

Lab work with cholangiohepatitis will show?

Back 18

--elevated hepatic enzymes

--elevated conjugated bilirubin

--inflammatory CBC

Front 19

Ultrasound for cholangiohepatitis will show?

Back 19

--diffuse increase in echogenicity due to cellular infiltrate and fibrosis

--hepatomegaly

--mild biliary distension and biliary wall thickening

Front 20

Biopsy for cholangiohepatitis will show?

Back 20

--severity of disease and degree of fibrosis

--neutrophilic infiltrate and hepatocyte necrosis

Front 21

Bacteria commonly cultured from cholangiohepatitis biopsy?

Back 21

--Salmonella

--E. coli

--citrobacter

--aeromonas

--acinetobacter

Front 22

Cholangiohepatitis treatment? Drug choice? Monitor how?

Back 22

--4-6 wks of antibiotics

--serial measurement of liver enzymes

--TMS, penicillin/gentamicin, ampicillin, chloramphenicol

Front 23

Cholelithiasis means what?

Back 23

--stones in left or right bile ducts or gallbladder

Front 24

Choledocholithiasis means what?

Back 24

--stones in common bile duct

Front 25

Hepatolithiasis means what?

Back 25

--stones in the intrahepatic bile ducts above left and right hepatic bile ducts

Front 26

What is the most common cause of biliary obstruction in large animals? Labwork signs?

Back 26

--choledocholithiasis

(not common, but most common cause)

>> horses are often incredibly painful

--increased GGT and bilirubin

Front 27

Acute biliary obstruction can occur in horses with?

Back 27

--colonic displacements >> cholestasis

Front 28

Pathogenesis of cholelithiasis?

Back 28

--ascending inflammation or infection

--Salmonella, E coli, Aeromonas, Citrobacter, group D Strep

Front 29

Triad of clinical signs for cholelithiasis?

Back 29

--fever

--colic

--jaundice

Front 30

Cholelithiasis most often causes problems in which spp? Age at occurrence?Signs indicate what? Stones may result in? Obstruction of common duct can produce?

Back 30

--horses, >5y

--signs indicate multiple stones in liver or occluded bile duct

--photosensitization, encephalopathy, weight loss

--CBD block: severe icterus and profound colic

Front 31

Chemistry profile with cholelithiasis?

Back 31

--increased ALP, GGT, AST, SDH

--total bilirubin elevated

--elevated serum bile acids, ammonia

--bilirubinuria

--prolonged clotting times

--neutrophilia

--increased globulins and fibrinogen

Front 32

Profound increase in ____ if common bile duct is block.

Back 32

--ALP

Front 33

>25-30% of bilirubin is ____ with cholelithiasis bilirubin increase.

Back 33

--direct or conjugated

Front 34

Diagnosis of cholelithiasis requires which signs?

Back 34

--fever + colic + jaundice

--elevation of GGT, ALP, bilirubin

--signs of cholelithiasis on ultrasound

>> dilation and thickening of bile ducts on US
>> hepatomegaly on US

>> diffuse increase in echogenicity on US

>> choleliths on US

Front 35

Most common site to view choleliths?

Back 35

--cranioventral right hepatic lobe (6th - 8th ICS)

Front 36

Are choleliths always visible on US?

Back 36

--no

Front 37

Can you image the common bile duct?

Back 37

--no

Front 38

If you see hepatoliths on ultrasound, does that mean they're causing liver disease?

Back 38

--no, look at clinical signs and bloodwork

Front 39

DDX for cholelithiasis?

Back 39

--other forms of chronic liver disease

--causes of mild recurrent colic

Front 40

Treatment of cholelithiasis?

Back 40

--long-term antibiotics and anti-inflammatories

--surgery indicated for choledocholithiasis

Front 41

Liver is often ___ organ to encounter toxins.

Back 41

--first

Front 42

Chemical toxins may be most problematic in which spp?

Back 42

--cattle and sheep

>> do things like suck on batteries

Front 43

Drugs that may cause hepatic injury in horses?

Back 43

--erythromycin

--rifampin

--diazepam

--sulfonamides

--aspirin

Front 44

Mycotoxins cause what kind of hepatic injury? Most common in which spp?

Back 44

--hepatocellular necrosis

--fatty liver changes

--biliary hyperplasia

--megalocytosis

--more common in ruminants

>> accept moldy feed

Front 45

Pyrrolizidine alkaloids cause what kind of toxicosis?

Back 45

--chronic, delayed hepatic failure

Front 46

Pyrrolizidine alkaloid toxicosis occurs when?

Back 46

--forage is parse

--dried plants in hay or silage

--seeds accidentally included in ration

Front 47

Lethal dose of pyrrolizidine alkaloid for horse, cattle, sheep/goats?

Back 47

--200-250 mg/kg bw

-- ~5% bw of dried plants in horses

-- 2-5 % bw toxin in cattle

-- 150% bw in goats and sheep

Front 48

Common plants containing pyrrolizidine alkaloids?

Back 48

--ragwort

--groundsel

--salvation jane

--common heliotrope

--lantana

--tansy

Front 49

Pathophysiology of pyrrolizidine alkaloids?

Back 49

--hepatically metabolized to pyrroles

--pyrroles crosslink dsDNA (anti-mitotic)

>> cells can't divide and form megalocytes

>> chronic megalocytic hepatopathy

--cells die and are replaced by fibrosis

>> marked portal hypertension (diarrhea/ascites) in ruminants

Front 50

Why might foal be at risk of pyrrolizidine alkaloid toxicosis?

Back 50

--pyrroles are rapidly excreted in body fluids

>> milk

Front 51

Clinical signs of pyrrolizidine alkaloid toxicosis in horses?

Back 51

--weight loss

--icterus

--hepatic encephalopathy

--photosensitization

--diarrhea

--abortion

--secondary gastric impaction in ponies

Front 52

Clinical signs of pyrrolizidine alkaloid toxicosis in cattle?

Back 52

--diarrhea, weight loss, tenesmus, prolapsed rectum, ascites

--subtle neurologic or behavioral changes

Front 53

Pyrrolizidine alkaloid toxicosis is a chronic liver injury, but may present?

Back 53

--acute presentation of hepatic failure

>> sudden onset of photosensitization and HE

Front 54

Diagnosis of pyrrolizidine alkaloid toxicosis?

Back 54

--clinical signs

--history of exposure to toxic plants

Front 55

What if SDH, LDH, GLDH are normal with pyrrolizidine alkaloid toxicosis? What do you expect GGT and ALP to do?

Back 55

--elevated during acute hepatocyte destruction

>> may be normal by the time signs present

>> no hepatocellular mass left

--GGT and ALP should be consistently elevated (periportal lesions)

Front 56

How do you differentiate pyrrolizidine alkaloid toxicosis from other chronic liver diseases?

Back 56

--biopsy

>> look for megalocytosis, biliary hyperplasia, periportal fibrosis

Front 57

Treatment of pyrrolizidine alkaloid toxicosis? Improvement unlikely if? Horses that may survive?

Back 57

--supportive until the end (probably euthanasia)

--control of hepatic encephalopathy

--improvement unlikely if substantial fibrosis

--horses that retain an appetite may survive if protected from further exposure

--low protein, high energy diet

Front 58

Establishing pyrrolizidine alkaloid toxicosis prognosis?

Back 58

--consecutive measurement of hepatic enzymes and serum bile acids in conjunction with serial biopsy

Front 59

General principles of treating hepatic disease?

Back 59

--eliminate further exposure

--control abnormal behavior

>> sedation, reduce ammonia, analgesia, reduce cerebral edema

--appropriate nutritional support >> need to eat

--protein and clotting factor support

--treat dehydration, shock, acidosis, and electrolyte derangements

Front 60

What type of liver failure is more likely to result in a good prognosis if treated? Examples?

Back 60

--acute liver failure

>> no severe chronic changes or fibrosis

>> good prognosis for regeneration

Front 61

Poor prognostic indicators for liver disease?

Back 61

--hemolysis

--encephalopathy

--severe acidosis

--diarrhea

--bridging necrosis or fibrosis on biopsy

--high serum bile acids

--long PT

--hypoalbuminema

Front 62

Sedation for hepatic encephalopathy?

Back 62

--sedate with alpha 2s (e.g. detomidine)

Front 63

Methods to reduce blood ammonia?

Back 63

--oral neomycin

--metronidazole?

--lactulose or acetic acid to decrease colonic pH

--mineral oil

--MgSO4

Front 64

How does lactulose work?

Back 64

--reduces pH, increases bacterial assimilation of ammonia, decreases production of ammonia, traps ammonia in lumen, changes microflora

Front 65

Addressing metabolic derangements with liver disease? Fluid rate? Advantages of fluid therapy?

Back 65

--continuous IV fluids with 5-10% dextrose

--50ml/kg/day

--decrease blood ammonia

--address dehydration and shock

--may improve bile flow

Front 66

When should you correct metabolic acidosis?

Back 66

-- if pH <7.1

Front 67

Why might animals with liver disease require potassium supplementation? Why is this important?

Back 67

--reduced appetite >> reduced K+ intake

--low potassium increased production and absorption of ammonia from kidney

Front 68

What should you do if the animal has coagulopathy?

Back 68

--plasma transfusion

Front 69

What additional therapies should be considered for liver disease patients? Which vitamins should be supplemented?

Back 69

--anti-oxidants: DMSO, mannitol, vitamin E

--anti-inflammatory therapy: banamine

--vitamin B1, folic acid, A, D, E, K3

Front 70

Which type of vitamin K should be avoided in horses?

Back 70

--vitamin K3 can cause renal failure in horses!

Front 71

Bacterial cholangitis/cholelithiasis and liver abscesses should be treated with? Length of therapy?

Back 71

--penicillin and gentamicin superior

--cetiofur, chlorampheicol, enrofloxacin, TMS, metronidazole

--long term therapy up to 12 wks

Front 72

Horses with chronic active hepatitis and bridging necrosis with no bacterial etiology, you may consider what treatment?

Back 72

--corticosteroids

>> not desirable in overt liver failure (gluconeogenic, stim. protein catabolism, lipolysis)

Front 73

Things that may decrease fibrosis?

Back 73

--colchicine, cyclosporine, pentoxyfilline, SAM-E

Front 74

Diet for animals with milder liver disease and good appetite?

Back 74

--feed small meals frequently >> maintain blood glucose, stabilize insulin regulation

--palatable meals

--high carbohydrate, moderate protein (~10%)

--protein source rich in branched chain amino acids, e.g. leucine, valine, isoleucine

>> sorghum, milo, beet pulp, bran

Front 75

It's important to avoid excessive ____ in animals with hepatic disease. Why? Avoid which feed? Preferred hay?

Back 75

--avoid excessive protein

--don't want to make more ammonia

--avoid alfalfa and legumes

--oat and grass hay preferable