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Gastrointestinal (equine) > Liver disease and hyperlipidaemia > Flashcards

Liver disease and hyperlipidaemia Flashcards

1
Q

what are the functions of the liver?

A

digestive/secretory/metabolic
detoxification/excretion
synthetic (clotting factors/proteins)
storage (vitamins/minerals)

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2
Q

what are some possible signs of liver disease?

A

jaundice
weight loss/inappetence
depression/CNS signs
skin lesions
haemorrhage
colic
oedema
diarrhoea
bilateral laryngeal paralysis

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3
Q

what is jaundice?

A

retention of bilirubin (mainly unconjugated)

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4
Q

what are some differentials for jaundice?

A

anorexia
haemolysis
liver failure

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5
Q

what are some possible CNS signs that can present with liver disease?

A

quiet/dull
yawning
progression to somnolence, blindness, head pressing, compulsive walking

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6
Q

what are some skin lesions associated with liver disease?

A

photosensitisation
pruritus
coronitis

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7
Q

why does liver disease causes hepatic photosensitisation?

A

phylloerythrin accumulation as the liver doesn’t remove it, this is activated by UV light

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8
Q

what is the cause of pruritus associated with liver disease?

A

accumulation of bile acids

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9
Q

why may liver disease cause haemorrhage?

A

decreased production of clotting factors

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10
Q

why can liver disease cause colic?

A

hepatitis leads to stretching of the liver which is painful

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11
Q

why is laryngeal paralysis one of the first neuropathies seen with liver disease cases?

A

recurrent laryngeal nerve is very long so any toxins which effect axons will cause damage to this one first

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12
Q

what do liver enzyme tests tell us about?

A

liver damage (released when liver cells are damaged/break open)

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13
Q

what liver enzymes are of biliary origin?

A

GGT and ALP

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14
Q

what liver enzymes of of hepatocellular origin?

A

SDH, GLDH, AST, LDH

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15
Q

which liver enzymes are liver specific?

A

GGT, SDH, GLDH

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16
Q

what is a non-liver source of AST?

A

muscle

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17
Q

which enzyme is the most sensitive indicator of liver damage?

A

GGT

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18
Q

what form of liver disease can raised GGT and ALP indicate?

A

biliary

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19
Q

what form of liver disease does raised AST, GLDH and LDH indicate?

A

hepatocellular

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20
Q

how does the degree of increase of liver enzymes correlate with the prognosis?

A

very poorly correlated

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21
Q

why does there need to be significant liver damage before function is impaired?

A

has a 70% reserve capacity and the ability to regenerate

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22
Q

what is the most useful test in horses to assess liver function?

A

bile acids

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23
Q

what is the function of bile acids?

A

absorb lipids and lipid soluble vitamins
excretion of cholesterol

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24
Q

what happens to most of the bile acids secreted by the liver?

A

reabsorbed in the small intestine and returns via the enterohepatic circulation

25
Q

what happens to bile acids if the liver begins to fail?

A

they are not reabsorbed after returning through the enterohepatic circulation from the small intestines

26
Q

what are the forms bilirubin can be measured in?

A

total, conjugated, unconjugated

27
Q

what are the possible differential for increased unconjugated bilirubin?

A

liver failure, haemolysis, anorexia, intestinal obstruction

28
Q

where does unconjugated bilirubin come from?

A

breakdown of haemoglobin/myoglobin from macrophages

29
Q

what is the job of the liver in relation to unconjugated bilirubin?

A

conjugate it and secrete it into the intestines

30
Q

what does a very marked increase in conjugated bilirubin suggest?

A

choleostasis

31
Q

what form of bilirubin can be found in urine?

A

conjugated (unconjugated is water soluble)

32
Q

what does the presence of conjugated bilirubin in the urine suggest?

A

increased systemic levels of bilirubin (possible cholestasis or liver failure)

33
Q

what are some tests for liver function?

A

bile acids
bilirubin
ammonia

34
Q

why is ammonia difficult to measure?

A

very volatile so have to test the blood very soon after taking the sample
RBCs also produce it which will change the concentration in the sample

35
Q

what is ammonia turned into in the liver?

A

urea

36
Q

how will urea concentration change if the liver has decreased function?

A

decrease (lack of ammonia metabolism)

37
Q

how will globulin concentration change if the liver has decreased function?

A

increase (kupffer cells failure to remove intestinal antigens)

38
Q

how will triglyceride concentration change if the liver has decreased function?

A

increase (inadequate carbohydrate metabolism and gluconeogenesis)

39
Q

how should the liver appear compared to the spleen?

A

slightly hypoechoic to the spleen

40
Q

what are some possible complications of liver biopsies?

A

haemorrhage
inappropriate sample
negative culture
infections

41
Q

what are liver biopsies usually used for?

A

help to give severity and prognosis of a condition
guide treatment

42
Q

what toxicity is causes by ragwort?

A

pyrrolizidine alkaloid toxicity

43
Q

what is the pathogenesis of pyrrolizidine alkaloid toxicity?

A

alkylates DNA leading anti-mitosis causing megalocytosis as the cells are unable to divide, they then get damaged and die leading to fibrosis

44
Q

how is ragwort usually ingested by the horse?

A

in hay - more palatable when dried

45
Q

when do horses begin to show clinical signs of ragwort poisoning?

A

very late in disease process when they have liver failure just prior to death

46
Q

should ragwort poisoning be treated?

A

depends on severity of clinical signs (mainly supportive)

47
Q

what is chronic active hepatitis?

A

any progressive inflammatory hepatitis

48
Q

what should always be included in the treatment for chronic active hepatitis?

A

corticosteroids - immunosuppressive

49
Q

how should hepatic encephalopathy be treated?

A

reduce neurotoxin production - metronidazole, lactulose
avoid sedation
fluid balance and regulate glucose

50
Q

how can metronidazole be used to treat hepatic encephalopathy?

A

reduces the number of ammonia producing bacteria

51
Q

how does lactulose aid treatment of hepatic encephalopathy?

A

poorly digested/absorbed carbohydrate which will increase the acidity of the colon (increasing H+) to convert ammonia into ammonium

52
Q

how will a blood sample of hyperlipaemia appear?

A

fatty serum (dense white cloudy)

53
Q

what are some risk factors for hyperlipaemia?

A

breed
obesity
females
insulin sensitivity
transport, stress, lactation
starvation

54
Q

what is the pathogenesis of hyperlipaemia?

A

stored fats are broken down and fatty acids are taken to the liver to produce energy which leads to triglycerides accumulating in the liver and plasma

55
Q

what equine in very susceptible to hyperlipaemia?

A

donkeys

56
Q

how does hyperlipaemia present?

A

anorexia, lethargy, weakness (non-specific)

57
Q

how is hyperlipaemia treated?

A

get animal in positive energy balance (tube feed)
correct dehydration and acidosis
symptomatic therapy

58
Q

what is the prognosis for hyperlipaemia?

A

guarded to poor

Gastrointestinal (equine) (12 decks)

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