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Equine medicine > Liver > Flashcards

Liver Flashcards

1
Q

Why does the horse have continuous bile flow into the duodenum

A

horses do not have a gall bladder

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2
Q

what are the function of the liver

A

Metabolic, secretory, excretory & storage

  1. Protein metabolism - AA delivered from the GIT to liver
  2. AA catabolism
  3. Lipid metabolism
  4. detoxification
  5. mononuclear phagocyte system
  6. Vit A,D, B12, cu, Fe
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3
Q

Why is it difficult to pick up liver failure in the early stages of disease

A

Varies greatly and are often non-specific
Hepatic insufficiency
- inability of the liver to maintain adequate normal function
Most functions are not impaired until 80% functional hepatic mass it lost making it very diffcicult to pick up disease in the early stages

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4
Q

What are the main clinical signs seen with hepatic disease in horses

A 
weight loss 
Deppression 
anorexia 
Icterus/jaundice 
Hepatic encephalopathy 
signs of abdominal pain colic
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5
Q

what are some of the less common CS of hepatic disease

A 
Photosensitisation 
Fever; inflammation +/- infection 
haemorrhage: typically only seen in end stage liver disease 
ascites or oedema 
Diarrhoea 
Bilateral laryngeal paralysis
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6
Q

Describe the aetiology of Hepatic encephalopathy

A

Not the primary disease it is a clinical manifestation of a disease
Complex clinical syndrome - CS result in neuronal inhibition
Severity of neurological signs corresponds to degree of hepatic dysfunction but not type or reversibility of hepatic disease

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7
Q

What are the 5 different proposed mechanism for hepatic encephalopathy

A
  1. Gastrointestinal derived neurotoxins (increased plasma ammonia)
  2. Altered amino acid metabolism
  3. Augmented GABA activity in the brain (diazepam contraindicated as enhances the effect of GABA)
  4. Increased permeability of the blood brain barrier
  5. Impaired CNS energy metabolism
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8
Q

What are the liver enzymes that can be used to detect Hepatobiliary

A

Gamma-glutamyl Transferase (GGT)- most sensitive indicator for liver disease

  • Microsomal membrane protein found in epithelial cells of the biliary tract, renal tubules, mammary gland and pancreas
  • Increased in blood GGT - specific for cholestasis - increase in urinary GGT = damage to renal tubular epithelial cells
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9
Q

what is an indicator of hepatobiliary leakage

A

AST - not specific for liver disease (can be very high your muscle trauma)

  • Cystolic enzyme present in all cells in body
  • Highest concentration in skeletal muscles & hepatocytes but also found cardiac mycocytes, erythocytes and enterocytes

Increases are non specific for liver disease

SDH - cytosolic enzyme released during acute hepatocellular necrosis or changes in hepatocyte membrane permeability
==> increases in blood are highly specific for hepatocellular injury

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10
Q

what is the most common cause of indirect reacting Hyperbilirubinaemia

A

unconjugated bilirubin - albumin bound
the most common cause is anoerexia
Liver failure
Haemolytic anaemia

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11
Q

what are the 3 most common reason for unconjugated bilirubin increase

A

increased in production
decrease hepatic uptake
decreased conjugation of bilirubin

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12
Q

increased conjugated bilirubin (direct reacting)

A

intrahepatic cholestasis

Extrahepatic bile duct obstruction

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13
Q

what are the the common causes of increased conjugated bilirubin

A

Liver failure
cholestheiasis
cholangiohepatitis

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14
Q

Blood ammonia

A

Very good indicator of liver functions
Toxic by product of amino acid metabolism produced in all tissues and by microflora in the GIT

Absorbed by hepatocytes and used to synthesise non essential AA - converted into urea in hepatocytes = BUN (excreted by kidneys)
Increased plasma ammonia = reduced liver function

Great in principle need a good lab to run often not possible

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15
Q

Serum bile acid

A

Produced and excreted by hepatocytes from cholesterol
Most sensitive and specific test of liver function: hepatic blow flow, removal from circulation, conjugation, excretion
Increases within 24-48 hours of onset of liver disease- highest in biliary obstructed liver disease

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16
Q

where is the liver located on your right side

A

9-14 intercostal space mid abdoen

surrounded by vital structures

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17
Q

where is the liver located on your left side

A

4-7th intercostal space ventral

on ultrasound liver should be hyopechoic (blacker) compared to the spleen

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18
Q

what are the principles of treatment of liver disease

A

Supportive care - aim to maintain patient until liver regenerated and regains function
antimicrobirals - often due to cholestasis
hepatic encpehalopathy
Nutritional suport
Antiinflammatories

19
Q

what types food should be given to a horse with liver disease

A

Diet high in branches chains of amino acids and readily digestible CHO in multiple small feedings
Minimise intake of proteins and aromatic AA= avoid lucerne hey & legumes

20
Q

what is the prognosis for horses with liver disease

A

Liver has significant ability to regenerate (fibrosis =poorer prognosis)
depends on severity and duration of underlying disease
Trend of decreasing bile Acids & GGT = better prognosis

21
Q

What is the aetiology of theilers disease

A

Acute hepatic necrosis, serum hepatitis

Sporadic cause of acute and rapidly progressing hepatic failure (2-7 days)

22
Q

How do you diagnose theilers disease

A

History of equine-origin biological admin 4-10wks prior (TETANUS)
HistopathOLOGY - centrilobular to midzonal hepatocellular necrosis

23
Q

What is the difference b/w primary and secondary hepatic lipidosis

A

1- no underlying disease present

2- secondary to any other concurrent disease process = more common (any disease that results in negative energy balance)

24
Q

what are the clinical signs of hepatic lipidosis

A

Often acute onset ==> hepatic +/- renal dysfunction
Initial signs are mild and vague - high index of suspicion in susceptible breeds and circumstances
initial - depression, lethargy, inappetance, icterus
mild to progressive - reluctance to move
late - hepatic failure, recumbent, altered mentation

25
Q

How do you diagnose hepatic lipidosis

A

CS
Hyperplipaemis - serum triglyceride > 5.6mmol/L
Increases in GGT, SDH, bile acids, Bilirubin & ammonia
Histopathology - liver biopsy - diffuse infiltration of hepatocytes with lipid

26
Q

How do you treat hepatic lipidosis

A 
Remove stress &/or treat concurrent disease 
Nutritional support 
- reverse negative energy balance 
Voluntary food intake 
involuntary caloric intake
27
Q

How to reverse the energy balance of horses with hepatic lipidosis

A

increase blood glucose concentration
Promote the release of endogenous insulin
Inhibit mobilisation of FFA from adipose

28
Q

What IV fluid therapy can be used in horses with hepatic lipidosis

A

Exogenous insulin
Decreases release of FFA from adipose tissues and enhances peripheral tissue clearance of triglycerides
Frequent monitoring of blood glucose to maintain euglycaemia

29
Q

what is the prognosis with an animal with hepatic lipidosis

A

Prevention is very important - any animal that is in the clinic and need to go off food should go on detrose
Poor to 100% mortality when infiltrate of FFA
Miniature horses have a better prognosis
Dependent on early and aggressive treatment

30
Q

How do you prevent horses from getting hepatic lipidosis

A

Identification of susceptible animals and risk factors
Implementation of management strategies - adequate nutrition and exercise to prevent obessity
close observation/ monitoring peri partum

31
Q

What are the clinical signs of Ascending bacterial cholangitis

A

Anoreia, fever, colic (compression of Si with large size) icterus

32
Q

How do you diagnose Ascending bacterial cholangiohepatitis

A

Liver biopsy and culture

Isolates most commonly enteric organism

33
Q

What the treatment and prognosis of ascending bacterial cholangiohepatitis

A

txm - antimicrobial therapy min 4-6 weeks

Prognosis- far with supportive care

34
Q

Explain the aetiology of tyzzers disease

A

Clostridium piliformis - motile spore forming, intracytoplasmic anaerobe
Foals - 7-42days
Sporadic highly contagious
Oral exposure - primary infection is in the colon - dissemination via blood and lymphatics

35
Q

what are the CS of tyzzers disease

A

Sudden death without premonitory signs

Non specific hepatopathy ==> lethargy, anorexia, icterus, diarrhoea, recumbency, convulsion & death

36
Q

How do you definitively diagnose and treat Tyzzers disease

A

Histopathology: swollen liver with coagulative necrosis, organism identification by silver stain
Fastitidous to culture so cant be relied upon clinically

txm - antimicrobials

37
Q

what is the most common cause of chronic liver failure in horses

A

Ingesting plants containing Pyrrolizidine alkaloids
PA alkylates nucleic acids and protein preventing cellular division and protein synthesis = megalocytes formation = fibrous tissue repleces hepatic parenchyma as megalocytes die

38
Q

what is the difficulty with diagnosis of PA poisoning

A

Chronic low dose consumtion
CS seen 4 months after consumption = can be up to years
Acute development pf HE & photosensitisation occurs late in the disease
Often will not be able to find the plant in the paddock as the animals have eaten them months before

39
Q

How do you diagnosse PA poisoning (chronic megalocytic hepatopathy)

A

History of exposure to PA containing plants
CS and biochemical evidence of hepatic disease
Definition diagNOSIS - histopathological pathognomic findings
- MEGALOCYTOSIS
BRIDING PORTAL FIBROIS
BILIARY HYPERPLASIA

40
Q

What are some of the common PA containing plants

A 
Highly unpalatable - only eats if there is no other feed 
Fireweed 
Lantaan 
Pattersons curse 
heliotropes 
Rattle pods
41
Q

What are the pathognomonic histological findings of PA disease

A

Megalocytosis
Bridging portal fibrosis
Biliary hyperplasia

42
Q

Chronic Active Hepatitis (CAH)

A

idiopathic, chronic progressive hepatopathy - postilated autoimmune or hypersensitive reaction

43
Q

How do you diagnosis Chronic active hepatitis

A

Periportal inflammation with lymphocytes, plasma cells and mononuclear cells
+/- biliary hyperplasia and periportal fibrosis
No megalocytes

Equine medicine (9 decks)

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