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JJ > GI Medicine - Liver Disease > Flashcards

GI Medicine - Liver Disease Flashcards

1
Q

what is failure of liver detoxification due to?

A

hepatic dysfunction and/or abnormal blood supply (PSS)

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2
Q

what does build up of ammonia lead to?

A

hyperammonaemia

hepatic encephalopathy

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3
Q

what is caused by hepatic dysfunction and/or abnormal blood supply (PSS)?

A

failure of conversion of ammonia to urea

failure of drug detoxification

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4
Q

what is a key effect of the failure of drug detoxification in the liver?

A

anaesthetic agents have a prolonged effect

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5
Q

what is the effect of encephalopathic toxins?

A

forebrain dysfunction

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6
Q

when is hepatic encephalopathy made worse?

A

following high protein meal

GI haemorhage

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7
Q

why is hepatic encepalopathy worse after a high protein meal?

A

increased ammonia produced due to bacterial fermentation and enterocyte glutamine metabolism

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8
Q

what are the precipitating events for hepatic encepalopathy?

A

feeding high protein meal
vomiting diarrhoea
diuretics (lead to dehydration)

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9
Q

what laboratory tests are used to diagnose liver disease?

A 
liver enzymes (may be primary or reactive)
bilirubin 
bile acids
blood glucose
blood clotting parameters
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10
Q

what is bilirubin a marker of?

A

jaundice

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11
Q

what are bile acids a measure of?

A

liver function

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12
Q

what diagnostic tests are used in liver disease?

A

laboratory tests
imaging
liver cytology (FNA)/biopsy

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13
Q

what are the most common causes of acute liver disease?

A

toxins or infections

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14
Q

what are the most common toxins which cause liver disease?

A

xylitol
mushrooms
blue green algae
aflatoxins

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15
Q

what are the most common drugs which cause acute liver disease?

A 
phenobarbitone
paracetamol
azathioprine
doxycycline
lomustine (CCNU)
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16
Q

what are the most common bacteria which cause acute liver disease?

A

leptospirosis

ascending biliary infection

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17
Q

what are the most common viruses which cause acute liver disease?

A

canine adenovirus

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18
Q

what happens during ascending biliary infection?

A

bacteria from the gut move into bile duct and cause infection

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19
Q

what are the main nursing considerations associated with acute liver disease?

A 
management of hepatic encephalopathy
anti-emetics for nausea
manage hypoglycaemia
consider implications for venepuncture due to coagulopathy risk
specific therapies 
barrier nursing?
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20
Q

how is hepatic encephalopathy managed in acute liver failure?

A

lactulose
seizure management if needed
maintain and monitor hydration and electrolytes (esp. K+)

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21
Q

how may lactulose be administered?

A

oral

retention enema

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22
Q

how does retention enema work?

A

foley catheter used to introduce and hold Lactulose in the colon

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23
Q

what must be remembered about drug dosing in patients with acute liver disease?

A

dose will need to be reduced due to reduced liver function

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24
Q

how can hypoglycaemia be managed?

A

glucose infusion

feed complex carbohydrates little and often

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25
Q

what are the specific therapies for acute liver disease?

A

antioxidants

antibiotics

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26
Q

describe nutritional management of acute liver disease

A

restricted animal protein diet
copper restricted diet
antioxidant supplementation

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27
Q

what si the best diet for acute liver disease?

A

replete protein, plant or soy based (e.g. Purina HA)

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28
Q

why is reduced or alternative to animal protein diet needed in liver disease patients?

A

to reduce ammonia

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29
Q

what diet can be used if plant (soy) based diets cannot be used?

A

hepatic (or less ideally renal) prescription diets are appropriate
cottage cheese added to give more, safe protein

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30
Q

what are the overarching causes of inflammatory liver disease?

A

sterile

infectious

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31
Q

what are the sterile causes of inflammatory liver disease?

A 
chronic hepatitis (dogs)
lymphocytic cholangitis (cats)
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32
Q

what causes chronic hepatitis?

A

idiopathic

copper

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33
Q

why does copper cause inflammatory liver disease?

A

toxic to hepatocytes

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34
Q

what happens during lymphocytic cholangitis (cats)?

A

immune system attacks bile ducts

35
Q

what are the infectious causes of inflammatory liver disease?

A

cholangitis / cholangiohepatitis (chronic and acute)
leptospirosis
chronic FIP

36
Q

what are the specific treatments for inflammatory liver disease?

A

de-coppering therapy for copper excess

antibiotics - if indicated

37
Q

what are the general treatments for inflammatory liver disease?

A 
dietary moification
liver supportive therapies (anti-oxidants)
steroids
choleretics
hepatic encephalopathy therapies
ascites management (spironolactone)
38
Q

what do choleretics do?

A

support bile flow

39
Q

what is involved in de-coppering therapy?

A

chelating agent

restrict copper intake

40
Q

what chelating agents may be given during de-coppering therapy?

A

D-penicillamine

zinc therapy - long term use

41
Q

how does zinc aid de-coppering?

A

competes with copper for uptake into liver

42
Q

how can copper intake be restricted?

A

diet (prescription and avoid red meat, offal, eggs and cereals)
check water source doen’t have copper pipes

43
Q

what is the role of antioxidants?

A

facilitate repair and recovery of hepatocytes

44
Q

what are the main antioxidants given to inflammatory liver disease patients?

A

Silymarin / silibinin / sylibin

S-Adenosyl-L-methionine (SAMe)

45
Q

what is the most commonly used choleretic?

A

ursodeoxycholic acid (UDCA)

46
Q

what is UDCA?

A

hydrophilic, beneficial bile salt

47
Q

how is UDCA derived?

A

synthetic

48
Q

how does UDCA work as a choleretic?

A

stimulates bile flow (reduces viscosity)

modulates inflammatory response in liver

49
Q

what animal should not be given UDCA?

A

rabbits - not safe

50
Q

what are 2 examples of metabolic liver disease?

A

gall bladder mucocoeles

feline hepatic lipidosis

51
Q

what happens in the gall bladder during gall bladder mucocoeles?

A

gall bladder is full of inspissated bile and mucus

52
Q

what does the gall bladder of a patient with gall bladder mucocoeles look like?

A

kiwi fruit

53
Q

what are the signs of gall bladder mucocoeles?

A

asymptomatic
obstruction of bile flow
rupture of gall bladder

54
Q

how are gall bladder mucocoeles managed?

A

medical

surgical

55
Q

what happens during feline hepatic lipidosis?

A

triglyceride deposition within hepatocytes leading to liver failure

56
Q

what are the reasons for feline hepatic lipidosis?

A

primary

secondary

57
Q

what predisposes a cat to feline hepatic lipidosis?

A 
obesity
high fat diet
high carbohydrate diet
systemic illness
DM
58
Q

what does feline hepatic lipidosis lead to?

A

massive intracellular fat accumulation
liver failure
death

59
Q

what are the risks associated with diagnosis of feline hepatic lipidosis?

A

coagulopathies may mean that clotting is slow - risk of bleeding during FNA

60
Q

how can risk of bleeding in a patient with coagulopathy be reduced?

A

check clotting
provide vitamin K therapy (aid clotting factor production)
monitor CVS parameters closely during and after procedure

61
Q

how is feline hepatic lipidosis treated?

A

treat underlying cause (primary vs secondary)
lipidosis treatment
6-8 weeks of home tube feeding

62
Q

what is the most essential part of FHL treatment?

A

nutritional support

63
Q

how should cats never be fed?

A

syringe or force

64
Q

what nutritional support may be needed for FL patients?

A 
tube feeding
high protein
antioxidants
UDCA
L-carnitine
65
Q

how much food should FHL patients receive per day?

A

40-60 kcal/kg/day

66
Q

what are the signs of congenital PSS?

A 
small
dull
lethargic
inappetant
history of waxing and waning GI signs
picky eater
67
Q

what abnormal liver findings would you expect in a patient with congenital PSS?

A

low albumin
low cholesterol
high bile acids
high ammonia

68
Q

what is a portosystemic shunt?

A

bypassing of liver by blood due to a shunt (extra vessel)

69
Q

what are the 2 types of PSS?

A

single congenital

multiple aquired

70
Q

how are multiple PSS acquired?

A

chronic hepatitis leads to increased resistance to blood flow in portal vein leading to opening of shunts

71
Q

what is happening in portovascular anomalies?

A

blood from GI tract bypasses liver and goes straight into systemic circulation
toxins are not removed and liver does not receive nutrients

72
Q

what does lack of nutrient supply to the liver during PSS lead to?

A

liver dysfunction

73
Q

what is the result of blood from GI tract not being filtered by the liver if a PSS is present?

A

toxins will accumulate

hepatic encephalopathy and so brain dysfunction

74
Q

how is PSS treated?

A 
ensure hydration
ensure serum K+ normal
restricted protein or plant based protein diet
Lactulose
antibiotics
anti seizure
surgical closure of shunting vessel
75
Q

how does lactulose work?

A

traps ammonia in the colon

76
Q

what are the signs of hepatic neoplasia?

A

asymptomatic
primary hepatic or obstructive signs
rupture leading to haemoabdomen

77
Q

what may be obstructed by a hepatic tumor?

A

vessels or ducts

78
Q

what are the 3 main types of liver neoplasia?

A

primary tumors
inflitrative
metastatic

79
Q

how are primary liver tumors treated?

A

surgery

80
Q

what is an example of infiltrative liver neoplasia?

A

lymphoma

81
Q

how is infiltrative liver neoplasia treated?

A

chemo

82
Q

what is an example of metastatic liver neoplasia?

A

carcinoma

83
Q

how is metastatic liver neoplasia treated?

A

no treatment as secondary to tumor elsewhere

JJ (33 decks)

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