Hepatobiliary investigations, acute & infectious Flashcards

Investigations, acute and infectious

1
Q

What zones or the liver are effected by metabolic/toxic damage? Are they different to the zones affected by hypoxic damage?

A

Metabolic/toxic damage in zone 1
Hypoxic damage in zone 3

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2
Q

What clinical signs are addociated with liver disease?

A
  • portal hypertension
  • jaundice
  • drug intolerances
  • hepatic encephalopathy
  • ascites
  • coagulopathy
  • lethargy
  • anorexia
  • weight loss
  • PUPD
  • V+/D+
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3
Q

How is portal hypertension linked to fluid retention/ascites?

A
  • blood pools in spleen and GIT
  • this reduces the circulating volume
  • RAAS is then activated to retain fluid
  • ascites develops
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4
Q

Why do we see vomiting and diarrhoea with liver disease?

A
  • Can be due to metabolic derangements or due to portal hypertension.
  • Portal hypertension leads to vascular stasis and venous congestion and oedema -> adverse effect on GI tract.
  • Increases the risk of GI ulceration.
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5
Q

Why does PUPD occur with liver disease?

A
  • Decreseased urea production -> decreased medullary solute gradient -> impaired renal concentrating mechanism -> dilute urine & compensatory polydipsia
  • Psychogenic component? Linked to hepatic encephalopathy
  • Reduced hormone metabolism e.g. cortisol
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6
Q

What is the pathophysiology of hepatic encephalopathy? What clinical signs are associated?

A

Encephalopathic detoxification fails for several reasons:
- Congenital portosystemic shunts (cPSS) - toxins bypass the processing plant of the liver
- Acute liver disease - detoxification processes in the liver are compromised and overwhelmed
- Acquired portosystemic shunts - chronic fibrotic/cirrhotic liver disease leads to multiple tortuous anastomotic vessels opening up to divert blood from the hepatic portal vein to bypass the liver

Clinical signs
- Waxing and waning; non-localising on neuro exam
* May be associated with feeding
* Hyperactive &/or depressed/dull/clumsy
* Circling, pacing, central blindness
* Salivation, especially cats
* Seizures —> coma

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7
Q

How do we diagnose hepatobiliary disease?

A

Diagnosis
- ALT, AST, GLDH
- ALP and GGT
- albumin, urea, glucose, cholesterol, coag factors, bilirubin, bile acids, ammonia
- imaging
- sampling
- urinalysis

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8
Q

How is urinalysis useful to diagnose hepatobiliary disease?

A

Urine specific gravity
Often decreased due to various mechanisms causing PU/PD

Bilirubinuria
Normal to find some bilirubin in dog urine but can be increased.
Always abnormal in cat urine

Sediment analysis
Ammonium biurate crystals sometimes seen with PSS.
Identifies dogs at risk of urate urolithiasis

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9
Q

Is radiography helpful to diagnose hepatobiliary disease?

A

No
- poor sensitivity for detection of liver disease
- some information about liver size
- could see choleliths or mineralisation

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10
Q

Is ultrasound helpful to diagnose liver disease? What should you look for?

A

Poor sensitivity for detection of liver disease unless:
* mass lesion
* nodular disease
* significant change in echotexture

Gives some information about liver ie normal if:
* moderately and uniformly echoic
* less echoic than spleen (“kidney, liver, spleen”)
* coarsely granular parenchyma
* uniform texture

Things to look for:
Ascites

Parenchyma
- focal/diffuse change?
- is the margin irregular?
- can we do a guided biopsy?

Biliary tract
- dilation of bile ducts?
- abnormal gall bladder wall and/or contents?
- can we get a guided aspirate?

Vasculature (Doppler)
- congenital portosystemic shunt?
- acquired portosystemic shunts?

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11
Q

What are positive indicators of liver malignancy in dogs when using CT?

A
  • Size (>4.5cm)
  • Postcontrast enhancement pattern
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12
Q

How can we differentiate primary from secondary liver diseases?

A
  • Careful interpretation of signalment, history, physical exam and results of initial diagnostic investigations
  • Avoiding unnecessary testing if the evidence suggests secondary hepatopathy
  • Assessing response to treatment: secondary disease should resolve with management of the underlying disease.
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13
Q

What are examples of secondary hepatopathies?

A
  • GI disease
  • Pancreatitis
  • Endocrine disease
    • hyperadrenocorticism (very rare in cats)
    • diabetes mellitus
    • hypothyroidism (dogs)/hyperthyroidism (cats)
  • Right-sided congestive heart failure
  • Hypoxia e.g. secondary to shock, trauma, anaemia
  • Toxaemia
  • Sepsis/bacteraemia
  • Drug induced in dogs e.g corticosteroids, phenobarbitone*
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14
Q

What are examples of acute primary hepatopathies?

A

Idiopathic

**Toxin/ drug – induced **
“Acute toxic hepatitis”
* Phenobarbitone
* NSAID eg carprofen
* TMPS
* Azathioprine
* Paracetamol
* Xylitol
* Environmental toxins e.g. blue green algae, mushrooms

**Infection; “Infectious hepatitis” **
* Leptospirosis
* Viruses: CAV-1 ; neonatal canine herpes virus
* Bacteria from the GI tract
* Tyzzer’s disease (clostridium piliformis)

Congenital
* Portosystemic shunt
* Primary portal vein hypoplasia

Metabolic
* Glycogen storage disease
* Hepatic amyloidosis

Sepsis/ endotoxaemia
May be part of progression of sepsis to SIRS and MODS

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15
Q

What should you make sure you do before sampling liver using ultrasound guided FNA?

A

coagulation profile

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16
Q

How do we manage the patient with acute liver disease?

A

Supportive
* Intravenous fluid support; avoid LRS? liver cannot metabolise lactate as the buffer.
* Monitor serum potassium and supplement in iv fluids as necessary
* Monitor blood glucose regularly and supplement if necessary
* Control vomiting
* Maropitant: may need to use with caution due to hepatic metabolism
* Consider CRI metoclopramide
* Treat any gastrointestinal ulceration
* GI bleeding can be aggravated by coagulopathy

Treat the cause
* Antibiotics for leptospirosis
* Stop hepatotoxic drugs if you are sure they are implicated
* N-acetylcysteine for paracetamol toxicity, may help with xylitol toxicity too

Treat hepatic encephalopathy

Manage coagulopathy as necessary
* Fresh frozen plasma
* Vitamin K therapy might help

Liver support
* Ursodeoxycholic acid: choleretic effects
* anti inflammatory/immune modulating properties
* Anti oxidants (SAMe, silymarin)

17
Q

What kind of diet should we give patients with liver disease?

A

Protein
- Adequate, good-quality protein as typically in negative energy balance;
- 15-30% for dogs; 30-45% for cats
- If HE – limit dietary protein to reduce ammonia production

Decreased glycogen storage and decreased gluconeogenesis – often have fasting hypoglycaemia. Provide 30-50% of dietary calories from easily digestible, complex, soluble carbohydrates.

Lipids augment fat-soluble vitamin absorption and make food more palatable; be careful in the case of cholestasis though.

  • Vit K supplementation if cholestasis or increased clotting times
  • B Vit supplementation if anorexic >7d
    • Deficiency in cats: neck ventroflexion, dilated pupils, slow conscious proprioception
    • Deficiency in dogs: neck ventroflaxion and profound muscular weakness, vestibular signs, slow menace.

Consider feeding tube

18
Q

What is the prognosis of liver disease?

A
  • Difficult to predict because varies with extent of damage
  • Full recovery is possible but can progress to chronic disease (hepatitis, fibrosis and cirrhosis)
  • Severe cases can require a high level of intensive care
    • refer to a specialist centre if possible
  • Can take a waxing and waning course despite treatment
19
Q

What are negative prognostic indicators in liver disease?

A
  • ascites and splenomegaly
    • suggests portal hypertension has developed