Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Alimentary > Disorders of the equine liver READING > Flashcards

Disorders of the equine liver READING Flashcards

1
Q

How is the liver involved in protein metabolism? 3

A
  • synthesises 90% plasma proteins
  • transamination to produce new amino acid and a new keto acid
  • ammonia elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes urea?

A

2 ammonia molecules + carbon dioxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the liver involved in carbohydrate metabolism? 4

A
  • -synthesis/storage/release of glucose
  • glycogen storage
  • G6P oxidation
  • G6P used to synthesise FAs and cholesterol
  • release glucose into systemic circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Role of liver in lipd metabolism?

A
  • esterify FAs into Tgs which are packaged with protein, carbohydrates and cholestero to from VLDL and HDL
  • use of FFAs for energy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Role of liver in bile secretion?

A
  • bile released from hepatocytes. major component is bile acids, into duodenum, >95% reabsorbed (enterohepatic circulation)
  • bilirubin is a breakdown product
  • liver conjugates bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mononuclear phagocyte system?

A

-hepatic macrophages = Kuppffer cells. These produce many inflammatory mediators and have an important role in filtering portal blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical signs of hepatic dysfunction

A

vary greatly, non-specific, depend on extent and duration of hepatic disease, usually >80% hepatic function must be lost.

COMMON = depression, anorexia, colic, HE, weight loss, icterus

LESS COMMON = photosensitisation, diarrhoea, bilateral laryngeal paralysis, haemorrhagic diathesis, ascites, dependent oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What might the colic be due to?

A

acute hepatocellular swelling or biliary obstruction (cholelithisais)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical signs of HE

A

vary from mild depression, to manic behaviour, head pressing, stupor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathogenesis of HE? 3

A

Likely to be multi-factorial:

  • reduced clearance of ammonia
  • imbalance between AAA and BCAA may result in increased concentration of false NT produced in brain
  • other theories exist too
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When does weight loss occur?

A

most likely with chronic liver disease. due to decreased intake + loss of normal hepatic metabolic activities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 broad causes of icterus

A

hyperbilirubinaemia caused by:

  • increased haemolysis
  • impaired hepatic uptake or conjugation
  • impaired excretion of bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you diagnose increased bilirubin production/haemolysis? 2

A

usually increased unconjugated +/- conjugated if liver capacity exceeded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnosis - impaired hepatic uptake or conjugation

A

increased unconjugated, possible cause is acute hepatocellular disease, also anorexia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most common type of icterus in horses = ?

A

impaired hepatic uptake or conjugation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cause of increased excretion of bilirubin

A

cholangitis, colangiohepatitis etc. if conjugated bilirubin concentration is greater than 30% total, indicates H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is phylloerythrin?

A

photodynamic agent formed by bacteria in gut, absorbed conjugated and excreted by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does phylloerythrin cause photosensitisation?

A

UV light exposure causes activation of electrons within the molecule to an excited state, leading to free radical formation –> cell membrane damage and necrosis. Lesions in non-pigmented skin (UV light absorbed more efficiently).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why might diarrhoea be seen? 3

A

alterations in intestinal microflora, portal hypertension, deficiency of bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is haemorrhagic diathesis? When might it be seen?

A

predisposition to bleeding. Subclinical coagulopathy common, rare to see clinical signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3 specific indicators of liver dyfunction

A

increased bile acids, increased sorbitol dehydrogenase (SDH) and increased gamma-glutamyl transferase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why do hepatic ultrasonography?

A

determines size, changes in hepatic parenchyma, dilated bile ducts, choleliths, can only image 20% liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why liver biopsy? 3 Where?

A

diagnosis, prognosis, treatment, 12-14th ICS, submit for histopathologic evaluation +/- culture, poor prognosis if bridging fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is essential to do before taking a liver biopsy?

A

Evaluate coagulation parameters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

General treatment principles - icterus 8

A
  • primarily supportive
  • maintain animal until liver regenerates sufficiently
  • sedation if HE present (xylazine, detomidine)
  • correct fluid deficits and acid-base imbalances
  • IV glucose
  • treat HE
  • dietary management
  • anti-inflammatories
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Treatment of HE 5

A
  • liquid paraffin, magnesium sulfate (reduce toxin absorption)
  • mannitol (cerebral oedema)
  • oral neomycin (decrease bacterial production of ammonia)
  • oral lactulose (limit ammonia absorption)
  • oral BCAA (no evidence)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Dietary management

A

high carbohydrate, limit protein (but not too much, more important to ensure quality protein to ensure malnutrition doesn’t occur)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is DMSO

A

dimethyl sulfoxide - may help dissolve intrabiliary sludge or small stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Suggest some anti-inflammatories 3

A
  • flunixin meglumine
  • DMSO
  • pentoxifylline - shown to reduce hepatic fibrosis in humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Another name for pyrrolizidine-alkaloid toxicity

A

ragwort poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why might horses ingest ragwort?

A

Accidental (usually unpalatable), contaminated pasture or hay. problems if chronic ingestion (e.g 4-12 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical signs - ragwort poisoning 2

A

HE and photosensitisation (classically)

other signs of chronic liver disease (weight loss etc)

33
Q

diagnosis - ragwort poisoning 2

A

presumptive (history of ingestion and clinical signs of liver disease)
definitive - liver biopsy (megalocytosis, biliary hyperplasia, fibrosis)

34
Q

Treatment of ragwort poisoning

A

no specific but treat for general liver disease. poor prognosis

35
Q

Causes of acute hepatitis

A

Multiple causes:
Theiller’s disease
Bacterial - tyzzer’s, infectious necrotic hepatitis
toxic
viral (EHV in foals, EIA, EVA)
parasites (migration of parascaris equorum , strongylus edentatus/equines/vulgaris

36
Q

Other names for acute hepatitis

A

serum sickness, acute necrotic hepatitis, serum-associated hepatitis

37
Q

Pathogenesis - acute hepatitis

A

small liver, moderate to severe centrilobular to midzonal hepatocellular necrosis with haemorrhage

38
Q

Diagnosis - acute hepatitis 2

A

hisotry+abrupt onset, evidence of hepatic insufficiency

biopsy (supportive)

39
Q

Aetiology of Tyzzer’s disease

A

Infectious hepatitis caused by Clostridium piliformis

40
Q

Clinical signs - tyzzer’s disease

A

foals (7-42 days), may be found dead, non-specific

41
Q

Epidemiology and pathogenesis of tyzzer’s disease

A

organism excreted in faeces of normal horses, bacteria replicate in GIT and reach liver and heart (via blood and lymphatics), causes acute multifocal hepatitis and enteritis

42
Q

Diagnosis - tyzzer’s diesae

A

difficult antemortem and often found dead, otherwise non-specific of liver failure, definitive = by post mortem. ID organism using silver stains

43
Q

Treatment of tyzzer’s disease

A

organism sensitive to penicillin, TCs, and erythromycin

poor prognosis - highly fatal

44
Q

Define cholelithiasis

A

stones in bile ducts

45
Q

Define choledocholithiasis

A

stones in common bile duct, most common cause of biliary obstruction in horse

46
Q

Define hepatolithiasis

A

stones in intrahepatic bile ducts (variation of cholelithiasis

47
Q

Cause of stone formation

A

uncertain - perhaps ascariasis, ascending biliary infection or inflammation, biliary staasis, changes in bile composition, presence of FB. Bacteria - salmonella, e coli, aeromonas hav ebeen cultured from stones

48
Q

Triad of clinical signs associated with cholelithiasis/choledocholithiasis/hepatolithiasis

A

fever+icterus+colic

49
Q

Diagnosis - cholelithiasis/choledocholithiasis/hepatolithiasis

A
  • increased liver enzyme activity (GGT, SDH, AST)
  • ultrasound (dilated bile ducts, evidence of cholelith)
  • biopsy (histopathology and culture)
50
Q

Treatment - cholelithiasis/choledocholithiasis/hepatolithiasis

A

long term antimicrobials, general supportive care, surgery?, prognosis variable depending on fibrosis extent, number/location of choleliths, severity of clinical signs

51
Q

Horses likely to get hyperlipaemia and hepatic lipidosis

A

shetlands, miniature horses, other pony breeds and donkeys (especially if obese).increased risk during pregnancy, lactation or if a primary disease entity exists

52
Q

What happens in hyperlipaemia and hepatic lipidosis?

A

metabolism of fatty acids in peripheral tissues (via action of hormone sensitive lipase), converted to Tg in liver, released into circulation, taken up by peripheral tissues (by lipoprotein lipase).

In animals with hyperliapemia, disease occurs due to overporduction of Tg in liver - lipoprotein lipase activity is high

53
Q

Clinical signs - hyperlipaemia and hepatic lipidosis

A

icterus, anorexia, weakness, severe depression, ataxia, mm weakness, recumbency, diarrhoea, mild colic, fever, oedema. If severe fatty infiltratin of liver, signs of hepatic failure may occur

54
Q

Diagnosis - hyperlipaemia and hepatic lipidosis 3

A

breed, clinical signs,
measurement of Tg in serum
liver biopsy (usually not necessary)

55
Q

Treatment - hyperlipaemia and hepatic lipidosis

A

supportive treatment
reverse NEB (encourage to eat, enteral nutrition, parenteral nutrition)
-eliminate stress/treat concurrent disease
-inhibit furhter fat mobilisation from adipose tissue (restore positive energy balance, insulin inhibits hormone sensitive lipase)
-increase Tg uptake by peripheral tissues (heparin increases activity of lipoprotein lipase - but already maximised in hyperlipaemic ponies)

56
Q

Prognosis - hyperlipaemia and hepatic lipidosis

A

poo r- motality in 60-100%

57
Q

Prevention - hyperlipaemia and hepatic lipidosis 2

A
  • avoid obesity and stress

- monitor Tg levels in sick ponies (early attention to nutritional needs in sick animals)

58
Q

Main cause of pre-hepatic icterus

A

haemolysis (–>increased bilirubin production)

59
Q

Causes of haemolysis in horses 5

A
  • NI
  • Infectious (e.g. EIA)
  • Drugs (penicillin)
  • Toxins (onions –> HA)
  • autoimmune HA - relatively rate in horses, Dx by exclusion
60
Q

What % of normal horses show icterus?

A

10-15% of normal horses will look mildly ictericq

61
Q

What is the most common cause of icterus in the horse?

A

anorexia (thus nothing actually wrong with the liver)

62
Q

What is ligandin? When is it released?

A

a protein responsible for uptake of unconjugated bilirubin into liver. its release is stimulated by eating?

63
Q

Causes of post-hepatic icterus? 4

A

cholangitis, cholangiohepatitis, cholestasis, shunts (v rare)

64
Q

What should you ask when you have an icteric horse?

A

anorexic?
foal?
pale?

If no __> think liver disease

65
Q

Functions of liver

A

protein/carbohydrate/lipid metabolism,
bile excretion
immune system
detoxification

66
Q

4 methods of diagnosing liver disease

A

clinical signs, blood work, ultrasonogaphy, biopsy

67
Q

What might you see on hepatic ultrasonography?

A

general size, changes in echogenicity, dilated bile ducts, choleliths, abscesses, neoplasia, can only image about 20% liver.

68
Q

When is liver regeneration unlikely?

A

if severe fibrosis

69
Q

Recommended diet

A

beet pulp, cracked corn (=maize), molasses, sorghum/bran/milo (instead of beet pulp), oat hay (discourage lucerne/alfalfa)

70
Q

Which anti-inflammatories might you give?

A

NSAIDs - flunixin meglumine
DMSO (rare)
corticosteroids - dexamethasone and prednisolone (to prevent progression of inflammation as this leads to fibrosis)
pentoxifylline (rare)

71
Q

Why should you be careful when you give hroses corticosteroids?

A

they cause an increased risk of laminitis

72
Q

What is the result of the fact that the liver has minimal ways of respondign to insult?

A

aetiologic agent often not seen on biopsy

biopsy chagnes are often not definitive (non-specific lymphocytic/lymphoplasmacytic changes for examples)

73
Q

What law requires land owners to limit ragowrt?

A

Ragwort control act 2003

74
Q

How do pyrroles cause damage?

A

they are anti-mitotic = crosslink DNA and bind to nucleic acid and proteins within hepatocyte. this means cells cannot divide –> megalocyte porduction –> megalocyte death –> fibrosis

75
Q

Why don’t horses get gall stones?

A

The have no gallbladder! Instead bile duct stones form

76
Q

What is the difference between hyperlipidaemia and hyperlipaemia?

A

severity

77
Q

Hyperlipaemia treatment 5

A
  • reverse NEB
  • treat the hepatic disease
  • eliminate stress/treat concurrent disease
  • inhibit further fat mobilisation (insulin inhibits hormone sensitive lipase)
  • increase Tg uptake by peripheral tissues (heparin)
78
Q

Main diseases of horse liver 4

A
  • pyrrolizine alkaloid toxicity
  • hyperlipaemia
  • cholelithiasis
  • unknown cause (probably most common!)

Alimentary (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions