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Y4 - Small Animals > Liver disease > Flashcards

Liver disease Flashcards

1
Q

What is the function of the liver?

A
  • Intermediate metabolism
  • Storage
  • Protein synthesis
  • Production of bile
  • Detoxification
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2
Q

What are the consequences of hepatic dysfunction?

A

Consequences on…
* Bile production
* Metabolic
* Circulation
* Detoxification
* Coagulation

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3
Q

What can cause jaundice (icterus)?

A

Pre-hepatic
* Haemolysis - yellow/white MM

Hepatic
* Hepatocyte dysfunction
* Intrahepatic cholestasis

Post-hepatic
* Extra-hepatic cholestasis

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4
Q

What is seen with metabolic dysfunction?

A
  • Non-specific signs
  • Loss of condition
  • Weight loss
  • Hypoglycaemia
  • Hypoalbuminaemia
  • Only in chronic disease
  • Can contribute to ascites
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5
Q

What is seen with circulatory disturbances?

A
  • Ascites
  • Hypoalbuminaemia
  • Portal hypertension
  • Sodium and water retention
  • Polyuria / polydipsia - cannot concentrate urine (reversible)
  • Portosystemic shunts
  • cirrhosis
    -portal hypertension
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6
Q

What problems with detoxification occur with liver damage?

A
  • Hepatic encephalopathy
  • defective urea formation from ammonia
  • increase blood NH3 leads to CNS signs
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7
Q

What are signs of hepatic encephalopathy?
What can worsen hepatic encephalopathy?

A
  • Anorexia, V & D, PU/PD
  • Dullness, aggression, staggering,
    blindness, head-pressing, seizures
  • Worse if…
    -High protein meal
    -Gastrointestinal bleed
    -Dehydration, acid-base imbalance
  • Increased sensitivity to anaesthetics
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8
Q

What is the consequence of lack of coagulation?

A
  • Defective production and storage of clotting factors
  • Vitamin K malabsorption
  • Portal hypertension = GI bleeding
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9
Q

What are signs of liver dysfunction in dogs?

A
  • Icterus
  • Faecal changes
    -Grey (acholic)
    -Melaena
  • Hepatic encephalopathy
  • Drug intolerance
  • Ascites
  • Stunted growth (if young)
  • Vomiting and diarrhoea
  • Polyuria & polydipsia
  • Non-specific signs
    -Anorexia
    -Weight loss
    -Weakness
    -Poor coat and skin condition
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10
Q

Where is jaundice most evident?

A
  • Sclera - white part of the eye
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11
Q

How would you classify different hepatopathies?

A

Primary =
*Inflammatory disease (infectious/ non-infectious)
* Non-inflammatory disease (non-infectious)

Secondary =
* Non-specific + reversible changes
- Anorexia
- Toxaemia
- Nutritional imbalance
- Metabolic changes
- Infection

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12
Q

What is reactive hepatopathies?

A
  • Most common liver abnormality
  • Little loss of hepatic function
  • Reversible
  • Treat by correcting underlying disease
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13
Q

What are different results of liver biopsies in order of how common they are?

A
  1. Reactive
  2. Chronic hepatitis
  3. Neoplasia
  4. Toxic
  5. Steroid
  6. Nodular hyperplasia
  7. Cholangitis
  8. PSS
  9. Copper
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14
Q

What can cause reactive hepatopathy?

A
  • IBD
  • Bacterial infections
  • Periodontal disease
  • Rickettsial infections
  • Acute pancreatitis
  • Diabetes mellitus
  • Hyperadrenocorticism
  • Hypoadrenocorticism
  • Hyperthyroidism
  • Haemolytic anaemia
  • Septicaemia
  • Shock
  • Right heart failure
  • PLE
  • Severe protein restriction & starvation
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15
Q

What are infectious inflammatory causes of liver disease?
(bacterial/viral/protozoal)

A

Bacterial
* Leptospirosis
* Bacterial cholangiohepatitis

Viral
* Infectious canine hepatitis
* Canine Herpes virus
* FIP

Protozoal
* Toxoplasma

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16
Q

What are non-infectious inflammatory causes of liver disease?

A
  • Toxic hepatic disease
  • Drug-induced hepatic disease
  • All forms of chronic hepatitis
  • Canine chronic hepatitis
  • Feline lymphocytic cholangitis
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17
Q

What are non-inflammatory causes of liver disease?

A
  • Congenital portosystemic shunt
  • Juvenile hepatic fibrosis
  • Feline hepatic lipidosis
  • Neoplasia
  • Telangiectasis and Peliosis
  • Surgical
  • Trauma
  • Liver lobe torsion - Entrapment
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18
Q

What is feline hepatic idiosyncrasies? What can cause it?

A
  • Relative deficiency of glucuronyl transferase

Causes =
* Aspirin
* Paracetamol
* Phenols, pine tars, morphine, benzenes, alcohols, barbiturates

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19
Q

What does paracetamol toxicity cause in cats?

A
  • Relative deficiency of glucuronidation + glutathione conjugation
  • Methaemoglobinaemia
  • Haemolytic anaemia - depression + dyspnoea
  • Facial oedema
  • Hepatocellular damage - liver failure + icterus
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20
Q

How do you treat paracetamol toxicity?

A
  • N-acetylcycsteine
  • Vitamin C
  • Supportive Tx - IV fluids, antibiotics, activated charcoal
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21
Q

What are clinical signs of liver failure in cats? (compared to dogs)

A
  • Anorexia and weight loss most common
  • Icterus relatively common
  • Polyuria / polydipsia - less severe
  • Hepatoencephalopathy, increased hypersalivation
  • Microhepatica & cirrhosis rarely seen
  • Pyrexia common in suppurative cholangitis
  • Chorioretinitis or uveitis (FIP, toxoplasmosis)
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22
Q

What are differential diagnoses for jaundice in cats?

A
  • Cholangitis complex
  • FIP (dry-form)
  • Lymphoma
  • (Cirrhosis)
  • Neoplasia
  • Lipidosis
  • Toxoplasmosis
  • Haemolytic anaemia
  • Toxic hepatopathy
  • Pancreatitis
  • Panleucopenia
  • Biliary obstruction / bile duct rupture
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23
Q

What are the steps to diagnosing liver disease?

A
  1. History & clinical signs
  2. Physical examination
  3. Laboratory evaluation
  4. Diagnostic imaging
  5. Liver biopsy
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24
Q

What would you look for on physical exam of liver disease?

A
  • Icterus - present in serum before eye (can have severe disease without icterus)
  • Ascites
  • Hepatomegaly / microhepatica
  • Pain - abdominal
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25
Q

What lab tests would you do for live rdisease?

A
  • Haematology
  • Serum biochemistry
  • Urinalysis
  • Coagulation (before liver biopsy)
  • Liver function tests
  • Peritoneal fluid cytology (ascites)
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26
Q

Regarding liver enzymes what are the hepatocellular + cholestatic markers?

A
  • Hepatocellular markers = ALT + AST
  • Cholestatic markers = ALP + GGT
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27
Q

With serum biochemistry what will tell you about the liver function?

A
  • Serum proteins (especially albumin)
  • Glucose, urea, cholesterol
  • Bilirubin
  • (Ammonia)
  • Bile acids
  • Not liver enzymes - only tell damage (leakage enzymes)
28
Q

What would happen to biochemistry results as liver failure progresses?

A
  • Acute hepatitis = raised ALT + ALP
  • Chronic hepatitis = raised bile acids
  • Cirrhosis = raised bilirubin + decreased albumin
  • End stage liver failure = increased clotting + decreased glucose
29
Q

What is the difference between chronic hepatitis + cirrhosis?

A
  • No clinical signs with chronic hepatitis
30
Q

What different diagnostic imaging can be done for liver disease?

A
  • Survey radiographs
  • Contrast radiographs - portovenography
  • Ultrasonography
  • Scintigraphy
31
Q

What can ultrasonography tell you with liver damage?

A
  • Liver size
  • Heterogenous parenchyma disease
  • Biliary obstruction
  • Biliary calculi
  • Masses
  • Vasculature
  • portosystemic shunts
  • arteriovenous fistulas
32
Q

What are indications to do a liver biopsy?

A
  • Persistent increases in liver enzymes
  • Altered liver size
  • Monitoring progressive liver disease
  • To evaluate response to treatment
33
Q

What needs to be done before taking a liver biopsy?

A
  • Check clotting profile first
34
Q

What are contraindications for percutaneous biopsy?

A
  • Lack of operator experience
  • Small liver, unless ultrasound available
  • Focal disease
  • Extrahepatic cholestasis
  • Bleeding disorder
  • Severe anaemia
35
Q

What are different techniques for liver biopsy?

A
  • Percutaneous
  • blind
  • ultrasound guided ‘tru-cut’ technique
  • Laparoscopy
  • Coeliotomy
36
Q

What dogs are predisposed to juvenile hepatic fibrosis?
What is the pathology of juvenile hepatic fibrosis?

A
  • GSD
  • Rottweiler
  • Progressive fibrosis
  • Minimal inflammatory reaction
  • Central vein fibrosis + occlusion most common
37
Q

What can be secondary to juvenile fibrosis / cirrhosis?
How do they develop?

A
  • Acquired shunts
  • develop from redundant vessels - between portal vein + CVC, portal hypertension often leads to ascites
38
Q

What are different types of canine chronic hepatitis?

A
  • Idiopathic chronic hepatitis
  • Lobular dissecting hepatitis
  • Drug-induced chronic hepatitis
  • Copper-associated hepatitis
  • all lead to cirrhosis
38
Q

When would survival be shorter with chronic hepatitis?

A

If -
- hypoalbuminaemia
- severity of necrosis and fibrosis in the biopsy
- Bridging fibrosis

39
Q

What breeds are predisposed to hepatic portal hypoplasia?

A
  • Small terrier breeds
  • often have no clinical signs or portosystemic shunts
    + increased bile acids
40
Q

What are the different feline cholangitis complex + what are the difference?

A
  • Suppurative cholangitis - neutrophils
  • Lymphocytic cholangitis - lymphocytes + plasma cells
41
Q

What is idiopathic hepatic lipidosis? What does it lead to?

A
  • Massive hepatic fat accumulation

*leads to
- biliary stasis
- liver failure
- anorexia
- death

42
Q

What are clinical signs of hepatic neoplasia + what are the different types?

A
  • Similar to inflammatory liver disease
  • Hepatomegaly - can be irregular shape
  • Primary tumours
  • Infiltrative
  • Metastatic
43
Q

What are different primary neoplasias?

A
  • Hepatocytes
    -Hepatocellular carcinoma
    -hepatoma
  • Biliary - cholangiocarcinoma
  • Connective tissue
    -fibroma / sarcoma
    -haemangioma / haemangiosarcoma
44
Q

What are the principles of treating liver disease?

A
  1. Eliminate causative agent
  2. Suppress ongoing disease
  3. Optimise regenerative capacity
  4. Control complications
45
Q

What does therapy tailored to the clinical picture consist of?

A
  • Dietary modification
  • Ursodeoxycholic acid (UDCA)
  • Anti-oxidant drugs & glutathione donors
  • Treatment of complications
46
Q

What does therapy tailored to biopsy results consist of?

A
  • Inflammatory cells (Neutrophils/Lymphocytes) = antibiotics / immunosuppressives
  • Fibrosis = anti-fibrotic drugs
  • Copper accumulation = decoppering drugs
  • Positive bacterial culture = appropriate antibiotic
47
Q

What dietary management would be needed for hepatic encephalopathy?

A
  • minimise ammonia production =
    -protein restriction + modification
  • high biological value = dairy + vegetable
48
Q

What dietary management would be needed for chronic active inflammation?

A
  • Reduce inflammation
  • Prevent copper accumulation=
    • low copper + high zinc
    • fat soluble vitamins = A, D, E, K,
    • Taurine + L-carnitine for cats
  • Add cottage cheese to a standard hepatic diet - high in protein
49
Q

What antibacterial therapy would be needed for hepatic encephalopathy?

A
  • Use based on clinical picture
  • Ampicillin
  • Metronidazole
50
Q

What antibacterial therapy would be needed for bacterial cholangiohepatitis?

A
  • Need culture + sensitivity (bile + tissue)
51
Q

What are advantages of glucocorticoids?

A
  • Improved well-being
  • Appetite stimulation
  • Anti-inflammatory
  • Immunosuppression
  • Anti-fibrotic
52
Q

What are disadvantages of glucocorticoids?

A
  • Steroid hepatopathy
  • Predispose to infection
  • Fluid retention
  • Catabolic
53
Q

What are breeds affected by copper associated hepatopathies?

A
  • Bedlington terriers
  • WHWT
  • Skye terrier
  • Dalmatian
  • Labrador
  • Doberman
54
Q

What are different decoppering agents?

A
  • Copper chelators
    -d-penicillamine
    -2,2,2-tetramine (trientine)
  • Copper absorption blocker
    -oral zinc (give 1hr before feeding)
55
Q

What are the advantages / disadvantages of using adjunctive therapy?

A

Advantages
* Do not need biopsy results
* Broad spectrum of activity
* Wide safety margin
* Combination therapy used

Disadvantages
* Cost
* Worse compliance if given many drugs

56
Q

What are different examples of adjunctive therapy?

A
  • Ursodeoxycholic acid (UDCA)
  • S-Adenosyl methionine (SAMe)
  • Milk thistle
  • Vitamin E
57
Q

What is ursodeoxycholic acid?

A
  • Hydrophilic ‘beneficial’ bile salt
  • alters bile composition
  • stimulates bile flow - contraindicated if complete biliary obstruction
  • modulates inflammatory/immune response
58
Q

What is S-adenosyl methionine?

A
  • ‘Glutathione (GSH) donor’
    = endogenous molecule central to =
  • hepatic metabolism
  • detoxification
59
Q

What benefit does Silybum mariarnum have? (milk thistle)

A
  • Free-radical scavenger
  • Inhibits inflammation
  • Inhibit lipid peroxidase
  • Inhibit collagen deposition
  • Increase glutathionine
60
Q

What are the advantages / disadvantages milk thistle?

A

Advantages
* Wide safety margin
* No absolute contraindications
* Broad spectrum of activity

Disadvantages
* Cost
* Evidence for efficacy

61
Q

What are complications of liver disease?

A
  • Hepatic encephalopathy + coma
  • Ascites + oedema
  • Haemorrhage + anaemia
62
Q

With hepatic encephalopathy, what should be done?

A
  • Identify + treat precipitating cause
    -Dehydration
    -Diuretics
    -Alkalosis
    -Hypokalaemia
    -Gastrointestinal bleeding
  • Reduce ammonia concentrations
    -low protein diet
    -Lactulose
    -Antibiotics (ampicillin / metronidazole)
  • Lactulose retention enema if coma
63
Q

What can be done to treat ascites + oedema?

A
  • Low sodium diet
  • Diuretics
  • spironlactone
  • occasionally add in furosemide
  • Paracentesis
  • drain a minimal volume for patients comfort
  • Could worsen bodywide protein status
64
Q

What can be done to treat hemorrhage and anaemia?

A
  • Vitamin K injections
  • Fresh blood transfusions
  • B vitamin injections
  • H2 blockers if GI haemorrhage
65
Q

What is high cobalamin associated with in cats?

A
  • Hepatic + neoplastic disease

Y4 - Small Animals (105 decks)

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