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Module 16 > Managing Canine and Feline Liver Disease > Flashcards

Managing Canine and Feline Liver Disease Flashcards

1
Q

how are acute hepatopathies treated (3)

A
  1. largely supportive (manage c/s, complications, fluids, antioxidants, antiemetics)
  2. address underlying cause if known (withdrawal/emesis of hepatotoxic drug, doxycycline if leptospirosis)
  3. steroids not indicated
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2
Q

how are chronic hepatopathies treated (3)

A
  1. specific therapy should be based on biopsy (steroids and colchicine should only be administrated after biopsy)
  2. even without biopsy, non specific therapy is warranted (antioxidants, ursodeoxycholic acid)
  3. many drugs undergo hepatic metabolism so carefully consider meds
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3
Q

what are hepatoprotection mechanisms

A

glutathione (GSH) is an antioxidant and free radical scavenger

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4
Q

what is gultathionine synthesized from

A

its synthesized from cysteine, glutamate, and glycine

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5
Q

what do decreased GSH indicate

A

severe liver disease

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6
Q

what are commonly used nutraceuticals used in liver disease (4)

A
  1. antioxidants: s-adenosylmethionine (SAMe)
  2. vitamin E
  3. silybin
  4. zinc
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7
Q

what is s-adenosylmethionine (SAMe)

A

precursor of GSH

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8
Q

what effects does s-adenosylmethionine (SAMe) have

A

anti-inflammatory and antioxidant effects

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9
Q

when is s-adenosylmethionine (SAMe) used

A

acute toxic hepatopathies

adjunctive treatment in inflammatory disease, cholestatic hepatopathies

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10
Q

what are the side effects of s-adenosylmethionine (SAMe)

A

low incidence of side effects

  1. nausea
  2. GI signs
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11
Q

what does of s-adenosylmethionine (SAMe) is used

A

20 mg/kg/day PO

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12
Q

what is silymarin

A

derived from milk thistle plant

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13
Q

what effects does silymarin have

A

anti-fibrotic

anti inflammatory

anti oxidant

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14
Q

when is silymarin used

A

mushroom toxicity (amanita phalloides)

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15
Q

what are the funcitons of vitamin E

A

protect phospholipids membrane from oxidative damage when free radicals are formed

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16
Q

is there a benefit of vitamin E in liver disease

A

unclear

increase in GSH, but no improvement in clinical or histological findings

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17
Q

what are the functions of n-acetylcysteine (NAC)

A

pro drug of cysteine that helps replenish hepatic intracellular cysteine and GSH concentrations

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18
Q

when is n-acetylcysteine (NAC) used

A

in acute liver injury due from drugs/toxins

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19
Q

how does n-acetylcysteine (NAC) help with paracetamol toxicity in cats

A

toxic intermediate (NAPQI) is formed in cats which is detoxified by conjugation to glutathione

cats are deficient in the glucuronidation pathway or if GSH reserves inadequate with toxic dosage

NAPQI can cause hepatic and RBC injury

cysteine is needed for glutathione production

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20
Q

what is ursodeoxycholic acid (UDA)

A

synthetic hydrophilic bile acid

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21
Q

what is the function of ursodeoxycholic acid (UDA) (3)

A
  1. may displace toxic hydrophibic bile acids
  2. increases glutathione production in hepatocytes
  3. promotes bile flow
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22
Q

when is ursodeoxycholic acid (UDA) contraindicated

A

contraindicated in biliary obstruction because it promotes bile flow

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23
Q

what are the uses of ursodeoxycholic acid (UDA) (2)

A
  1. medical management of GB mucocele
  2. acute and chronic hepatopathies –> particularly where cholestasis plays a role
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24
Q

what is vitamin K required for

A

hepatic synthesis of II, VII, IX, X

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25
Q

what is the dosage of vitamin K

A

2.5 mg - 5 mg/kg SC or PO

IV admin risk of anaphylaxis

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26
Q

how should vitamin K be administrated in biliary disease or anorexia

A

fat soluble vitamins are not absorbed

so need to give vitamin K SC

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27
Q

when are antibiotics in liver disease indicated

A

when bacterial infection is primary or secondary complication and in treatment of hepatic encephalopathy

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28
Q

why should tetracycline, sulphonamides, erythromycin not be used in liver disease

A

because they are metabolized in the liver

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29
Q

how does hepatic fibrosis occur

A

with chronic hepatic inflammation myofibroblasts are activated which cause fibrosis

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30
Q

how does fibrosis lead to portal hypertension

A

collagen impedes blood flow

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31
Q

what does bridging fibrosis lead to

A

causes permanent hepatic distortion and as fibrosis advances it leads to cirrhosis (end stage liver failure)

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32
Q

what are anti-fibrotic drugs (5)

A
  1. prednisolone
  2. penicillamine
  3. vitamin E
  4. SAMe
  5. silibyn
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33
Q

what is the most common steroid used in chronic hepatitis

A

prednisolone

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34
Q

what are the effects of prednisolone (4)

A
  1. anti-inflammatory
  2. immunomodulatory effects
  3. anti fibrotics
  4. choleretic effects (increase volume of secretion of bile from liver)
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35
Q

what is the ideal dosage and duration for chronic hepatitis

A

1-2 mg/kg PO q24, gradually taper

look at liver enzymes and evaluate

ideally want to repeat biopsy but often owners don’t want to put dog through it again

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36
Q

what are the indications of steroids in hepatic disease (5)

A
  1. biopsy evidence of ongoing inflammation
  2. infection has been ruled out
  3. lymphocytic cholangitis (cats)
  4. chronic hepatitis (dogs)
  5. no or only early mild fibrosis associated with inflammatory infiltrate
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37
Q

what are the contraindications of steroids in hepatic disease (5)

A
  1. hepatic encephalopathy (will cause protein breakdown)
  2. known or suspected infection
  3. if portal hypertension, gastric ulceration or ascites (will make worse)
  4. advanced, bridging fibrosis or non inflammatory fibrosis (suggesting a risk of portal hypertension)
  5. acute hepatopathy
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38
Q

what effect do steroids have on hepatic enzymes

A

they can increase

increase in ALP

+/- ALT/AST

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39
Q

if steroids are being given how should you monitor to find the correct dosage for the individual

A

monitor for signs of glucocorticoid excess

polyuria, polydipsia, polyphagia, alopecia, lethargy, hepatomegaly

40
Q

what is primary copper toxicosis

A

defect in biliary copper excretion

progressive accumulation results in chronic hepatitis

41
Q

what is secondary copper deposition in chronic liver disease caused by

A

cholestasis causes a defect in copper excretion through the bile

42
Q

how can a biopsy differentiate between primary and secondary copper storage disease

A

primary: copper accumulation is in zone 3 (centrilobular)
secondary: copper accumulation in zone 1 (periportal parenchyma)

43
Q

how is copper storage disease diagnosed

A

the magnitude of increase of liver enzymes and diagnostic imaging are very similar then dogs with chronic hepatitis

so biopsy is needed

44
Q

how is copper storage disease treated (4)

A
  1. D-penacillamine
  2. trientine (2,2,2-tetramine)
  3. dietary management low copper diet with added zinc
  4. oral zinc
45
Q

what is D-penacillamine

A

chelating agent that binds copper and excretes it via the kidneys

46
Q

what other effects does D-penacilliamine have

A

immunomodulatory and anti fibrotic properties

47
Q

what is trientine

A

chelating agent of copper

used when D-penacillamine causes GI side effects

48
Q

how does zinc help in copper storage disease

A

produces metallothionein in intestinal mucosa which prevents uptake into the circulation

which binds copper in the diet

49
Q

how is leptosirosis treated

A

barrier nursing

supportive care for different organ systems

antibiotics: doxycycline 10mg/kg PO 2 weeks, penicillin derivative IV if cannot tolerate doxycycline

50
Q

what is portal hypertension

A

increases in blood pressure within the portal venous system

51
Q

what is the relationship between portal blood flow, intrahepatic venous resistance and portal vein pressure

A

portal vein pressure = portal blood flow x intrahepatic venous resistance

52
Q

what are the consequences of portal hypertension (4)

A
  1. ascites
  2. GI ulceration
  3. multiple acquired shunts
  4. hepatic encephalopathy
53
Q

how is ascites treated

A

diuretics

54
Q

what type of diuretic is spironolactone

A

aldosterone receptor antagonist –> decreases Na and water absorption from the kidneys so it they are excreted into the urine

conserves K+

55
Q

what type of diuretic is furosemide

A

loop diuretic

inhibits luminal Na/K/Cl cotransporter

causes loss of Na/K/Cl so you need to monitor them and make sure you don’t dehydrate the aptient (monitor electrolytes, urea and creatinine)

56
Q

what are the benefits of an abdominocentesis

A

comfort and improves respiration

57
Q

what are the risks of abdominocentesis

A

hypoalbuminemia, hypovolemia

promote dehydration

58
Q

what does portal hypertension increase the risk of in the GI tract

A

ulceration

59
Q

what can GI hemorrhage result in with hepatobillary disease

A

hepatic encephalopathy

60
Q

what is hepatic encephalopathy

A

neurological abnormalities that may occur with liver dysfunction

accumuluation of toxins (ammonia) leads to altered neurotransmission in the brain

61
Q

what is hepatic encephalopathy associated with

A

portosystemic shunt

cirrrhosis

acute fulminant hepatic failure

62
Q

what are the clinical signs of hepatic encephalopathy (8)

A
  1. lethargy
  2. head pressing
  3. blindness
  4. seizure
  5. abnormal behaviour
  6. ptyalism (cats)
  7. ataxia
  8. coma
63
Q

how is hepatic encephalopathy treated (6)

A

aim is to reduce ammonia

  1. diet
  2. antibiotics
  3. lactulose
  4. fluid therapy
  5. gastro protective medication
  6. siezure medication
64
Q

how can the diet manage hepatic encephalopathy

A

small frequent meals

protein restriction –> minimize demand on urea cycle

65
Q

what diet changes can be made in young animals to treat hepatic encephalopathy

A

can’t restric protein completely

will break down endogenous protein

so feed as much protein as can be tolerated (hepatic prescription diets, add tofu, low fat cottage cheese, no red meat)

purina HA a soya based may be better

66
Q

what antibiotics are used to treat hepatic encephalopathy (4)

A
  1. ampicillin
  2. neomycin
  3. metronidazole (low dose 7.5 mg/kg BID)
  4. amoxicillin and clavulanic acid
67
Q

what is the purpose of using antibiotics to treat hepatic encephalopathy

A

to decrease GI ammonia producing bacteria

68
Q

why is lactulose used to treat hepatic encephalopathy

A

soluble fibre that acidifies colonic contents which will reduce ammonia absorption and also increase colonic bacterial cell growth which will incorperate ammonia into their cell walls

it also decreases intestinal transit time so there are less opportunities to absorb ammonia

69
Q

why should hartmann’s be avoided as a fluid therapy in hepatic encephalopathy

A

because it contains lactate

70
Q

what is the fluid of choice for hepatic encephalopathy

A

0.9% NaCl

supplement with maintainence KCl

add glucose to fluids if low (liver makes glucose)

71
Q

how can the seizures caused by hepatic encephalopathy be managed

A

dizepam or midazolam for immediate control

levetiracetam is preferable

propofol CRI

72
Q

what are portosystemic shunts

A

vascular anomalies that redirect blood from the portal vein to the systemic circulation bypassing the hepatic sinusoids and liver parenchyma

73
Q

how does portosystemic shunting lead to hepatic encephalopathy

A

toxins, proteins and nutrients are absorbed by the intestines enter the circulation

74
Q

what are the types of portosystemic shunts

A

congenital or acquired with portal hypertension

75
Q

how do congenital portosystemic shunts occur

A

fetal liver has large shunting vessels (ductus venosus) to byoass the hepatic circulation which should normally close at birth

76
Q

what are the types of macroscopic congenital portosystemic shunts

A
  1. extrahepatic
  2. intrahepatic
77
Q

what breeds are susceptible to congenital extrahepatic shunts

A

smaller dogs

yorkies, matlese

78
Q

what breeds of dogs are more susceptible to intrahepatic shunts

A

larger dogs

labs

79
Q

what are microscopic congenital portosystemic shunts

A

portal vein hypoplasia (also known as microvascular dysplasia)

80
Q

what are the clinical signs of congenital portosystemic shunts (5)

A
  1. neurological signs: hepatic encephalopathy, seizuring
  2. urinary (PUPD, urate urinary stones)
  3. GI (vomiting, diarrhea)
  4. failure to thrive, poor coat, “runt” of liver
  5. copper irises (cats only)
81
Q

how are congenital portosystemic shunts diagnosed (4)

A
  1. increase in bile acids, ammonia
  2. decrease in urea, albumin
  3. ultrasound (consider referral)
  4. biopsy liver if no macroscopic shunt on imaging
82
Q

how is congenital PSS treated

A
  1. medical: stabilize HE (diet, lactulose, antibiotics)
  2. surgery (treatment of choice)
  3. long term medical management if surgery not feasible
83
Q

how does an aquired portosystemic shunt occur

A

develop from opening of embyronic vessels

compensatory mechanism to chronic portal hypertension

84
Q

how are acquired shunts treated

A

medically managed

cannot be ligated

85
Q

describe the general contents of liver diets (3)

A
  1. restricted in protein
  2. low in copper, high in zinc
  3. vitamins B and E, antioxidants
86
Q

what are the indications for a liver diet (2)

A
  1. hepatic encephalopathy
  2. copper storage disease
87
Q

when are liver diets not indicated

A
  1. acute hepatopathies
  2. ascites
  3. if you don’t know, but the liver enzymes are up
88
Q

what is hepatic lipidosis

A

cholestatic liver disorder

89
Q

what is hepatic lipidosis caused by

A

negative energy balance caused by anorexia leads to enhanced mobilization of fat stores in the liver

abnormal accumulation of lipids in the hepatocytes –> severe intrahepatic cholestasis, hepatic dysfunction

90
Q

what is the signalment of hepatic lipidosis

A

typically middle aged overweight cats

91
Q

what are predisposing factors to hepatic lipidosis (3)

A
  1. obesity
  2. anorexia
  3. stress
92
Q

what can hepatic lipidosis be secondary to (4)

A
  1. pancreatitis
  2. cholangitis
  3. IBD
  4. neoplasia
  5. obesity, prolonged anorexia and stress
93
Q

what will be seen on biochem with hepatic lipidosis

A

increase in ALP

normal GGT

94
Q

what will the liver appearnce be on US with hepatic lipidosis

A

hyperechoic hepatic parenchyma and hepatomegaly

95
Q

how is hepatic lipidosis treated (6)

A
  1. IV therapy
  2. treat underlying causes
  3. feed the cat ASAP
  4. mintor glucose and electrolytes (esp K+ and PO43-)
  5. vitamin K
  6. supportive treatment (anti emetics, anti oxidants, pain relief)
96
Q

what type of diet should you feed a cat presenting with hepatic lipidosis

A

feeding tube if needed

high quality diet, high protein (+/- taurine, B vitamins)

gradually delivery –> day 1 33% RER, day 2 66% RER, day 3 100%

Module 16 (26 decks)

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