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3. Cat & Dog > hepatobiliary 4: other cholestatic disorders > Flashcards

hepatobiliary 4: other cholestatic disorders Flashcards

1
Q

EHBDO - what is it? what animals does it affect?

A
  • Extrahepatic biliary duct obstruction
  • cats and dogs
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2
Q

EHBDO is secondary to what?

A

Secondary to pancreatitis, choleliths, mass, other

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3
Q

EHBDO can cause what? presentation?

A
  • Can cause acute partial to complete biliary obstruction
  • Presentation: Signs of cholestasis, can be painful
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4
Q

EHBDO ultrasound findings

A

Ultrasound can show biliary dilation (intra and/or extrahepatic)
* Can show cause of obstruction

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5
Q

EHBDO treatment

A
  • Treatment aimed at underlying cause
  • Ursodiol often used
  • Complete obstruction is uncommon
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6
Q

Gall Bladder Mucocele (GBM) - typically in what species? what is it and what can it cause?

A
  • Typically dogs
  • Gall bladder distention by abnormal accumulation of mucoid contents
  • Can cause partial to complete biliary obstruction
  • Varying degrees of organization
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7
Q

Gall Bladder Mucocele (GBM) cause and risk factors

A
  • Cause not known
  • Risk factors:
  • Genetic( Shetland Sheepdog predisposed)
  • Endocrine disease (hypothyroidism, hyperadrenocorticism, hyperlipidemia)
  • Possibly previous biliary inflammation
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8
Q

GBM: what signalment is typical? breeds?

A
  • Middle aged to older dogs, any bred
  • Breeds at risk: Sheltie, Cocker Spaniel, Miniature Schnauzer
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9
Q

GBM: Presentation
- clinical findings?

A
  • Clinical findings range in severity:
  • Incidental finding on AUS
  • Inappetence, lethargy, vomiting, icterus
  • Neutrophilia, left shift
  • Hyperbilirubinemia, elevated liver enzymes (ALP, GGT)
  • GB rupture more likely if fever, tachycardia/tachypnea, left shift
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10
Q

GBM: Diagnosis

A
  • Abdominal radiographs
    > Low sensitivity
  • Abdominal ultrasound
    > Presence of semisolid to immobile mucoid material in gall bladder
    > Highly variable appearance
    > Gall bladder “sludge” might progress to mucocele, can be incidental and non-progressive
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11
Q

GBM: Treatment options

A
  • Surgery (cholecystectomy)
    > Referral procedure
  • Some cases without complete obstruction or GB rupture have resolved with medical management
    > Ursodiol
    > Low fat diet
    > +/- antibiotics
    > +/- antioxidants
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12
Q

GBM - how do we decide what treatment options to follow? what has best prognosis?

A
  • Indications are evolving
  • Mobile sludge > start medical treatment
  • Fixed sludge and no clinical signs > conservative treatment acceptable
  • In both cases monitor progression
  • If any progression > cholecystectomy
  • Surgical removal has better prognosis in a healthy candidate
    > GBM can eventually cause obstruction
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13
Q

GBM Treatment: Dogs with Signs - what is the ideal treatment? second option?

A
  • Ideal treatment is surgery
  • If owner declines and there is not complete obstruction: Medical management acceptable
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14
Q

GBM in dogs: Prognosis? what can affect prognosis?

A
  • Initial perioperative mortality 20-30%
  • If discharge from hospital, good prognosis
  • Variable negative prognostic indicators:
    > Concurrent pancreatitis
    > Complete obstruction
    > Gall bladder rupture
    > Older animal
  • May animals with negative indicators have survived > surgery still indicated
  • Probably better prognosis if uncomplicated
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15
Q

types of Vacuolar Hepatopathies in Dogs

A
  • Steroid hepatopathy – glycogen
  • Idiopathic glycogen deposition
  • Hepatocellular steatosis (lipid)
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16
Q

Steroid hepatopathy caused by what? how bad is it?

A
  • Exogenous glucocorticoids, Cushing’s
  • Reversible, usually not clinically relevant
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17
Q
  • Hepatocellular steatosis is secondary to what?
A
  • Secondary to lipid disorders, diabetes mellitus (reversible)
18
Q

Vacuolar Hepatopathies in Dogs
- what do we see on biochem profile?

A

Cholestatic liver pattern on biochemical profile:
* Elevated ALP (moderate, can be marked - dogs); elevated GGT in parallel
* Mild elevation ALT can be found
* Bilirubin normal

19
Q

hepatic Vascular anomalies - which are there? are they more common in dogs or cats?

A
  • Portosystemic shunt
    > Congenital extrahepatic**
    > Congenital intrahepatic
    > Acquired
  • Portal vein hypoplasia, microvascular dysplasia
  • Dogs&raquo_space; cats
20
Q

normal hepatic bloodflow and what is carries? what does the liver do?

A
  • Blood from GI tract, other abdominal organs normally drains into portal vein
    > Delivers nutrients, toxins, bacteria, other elements to liver
    > Oxygenates liver
  • Liver performs metabolic functions on the blood
    > Extract nutrients
    > Modify toxins
21
Q

what is a portosystemic shunt, generally

A

Abnormal connection between the portal vascular system and systemic circulation

  • Anomalous connection between the portal circulation and systemic venous circulation
  • Bypass of hepatic sinusoids
  • Many anatomic variants
  • ”Shunt fraction” varies
22
Q

CASE:
6-month-old Miniature Poodle
- runt of litter
- one month of intermittent vomiting
- quiet
- walking abnormally and bumping into furniture

  • Problem list:
  • Acute onset neurological signs (suspect ataxia, blindness)
  • Chronic intermittent vomiting
  • Quiet demeanour
  • Poor growth

Primary differential?

A

portosystemic shunt

23
Q

portosystemic shunts are commonly associated with what other condition?

A
  • Commonly associated with hepatic encephalopathy
24
Q

how does congenital PSS arise?

A

All mammalian fetuses have a large shunt called the ductus venosus that carries blood quickly through the fetal liver to the heart. A congenital portosystemic shunt develops if:

  1. The ductus venosus fails to collapse at birth and remains intact and open after the fetus no longer needs it.
  2. A blood vessel outside the liver develops abnormally and remains open after the ductus venosus closes.
25
Q

difference between extrahepatic PSS with small vs large shunt fraction?

A

Small shunt fraction:
* small amount of blood bypassing liver
* most blood still entering portal circulation
* potentially fewer clinical signs

Larger shunt fraction
* large amount of blood bypassing liver
* Small amount of blood entering portal circulation
* Likely more clinical signs

26
Q

Intrahepatic PSS - how common is this form of congenitcal PSS? in what breeds, mostly?

A
  • Approximately 25-33% of congenital PSS are intrahepatic
  • Most occur in larger breed dogs
27
Q

Intrahepatic PSS - do these generally have a large volume of diverted blood? where is the shunt located?

A
  • IHPSS have largest volume of diverted blood
  • Shunt located within the hepatic parenchyma
28
Q

Acquired PSS develop secondary to what?

A

Develop secondary to severe liver disease
* E.g., extensive hepatic fibrosis from CH

29
Q

Acquired PSS effects on blood pressures?

A
  • Increase in portal hypertension
  • Creates high pressure environment for portal circulation
    > Recanalization of previous portosystemic collateral vessels
    > Multiple tortuous anastomotic vessels connecting portal vein & vena cava
    > Path of least resistance
30
Q

Hepatic Encephalopathy - when does this arise? what is the result?

A
  • Caused by >70% liver function lost, or diversion of portal blood flow
  • Results in decreased metabolic & detoxifying functions of liver
    ? Toxins can affect cerebral cortex exposed to toxins and cause neuro signs
  • Most commonly seen with congenital PSS
  • Also seen with:
    > Acquired PSS
    > Cirrhosis/end stage liver failure in CH, other hepatopathies
    > Acute liver failure
    > Hepatic lipidosis
31
Q

Hepatic Encephalopathy: Pathogenesis? toxins and sources?

A
  • Toxins cross blood-brain barrier
  • Most important & well known is ammonia
  • Sources of ammonia = dietary protein, body protein breakdown, metabolism of bacteria in microflora, cell metabolism
    > Not just from dietary protein
  • Other toxins involved in pathogenesis of HE, not well identified
32
Q

Hepatic Encephalopathy: Presentation

A
  • Signs and severity are highly variable
  • Non-localizing CNS signs:
    > Mentation changes: depression, lethargy
    > Trembling
    > Ataxia
    > Circling
    > Head pressing
    > Cortical blindness
    > Seizures
  • Ptyalism in cats common
33
Q

Hepatic Encephalopathy: Diagnosis

A
  • Often presumptive based on clinical signs, presence of PSS or other liver disease that causes dysfunction
  • Can measure ammonia levels but not widely available
34
Q

extrahepatic portosystemic Shunt: Presentation: what breeds?

A
  • Small breeds
  • E.g., Yorkshire Terriers
35
Q

intrahepatic portosystemic Shunt: Presentation: what animals?

A
  • Large breeds
  • German shepherd dogs
  • Irish wolfhound
  • Old English sheepdog
  • Australian cattle dogs,
    Australian shepherds
36
Q

Portosystemic Shunt: Presentation
- age of animal?

A
  • Often young dogs
  • Can present middle-aged to older when shunt fraction is low, clinical signs
    are minimal
  • E.g., present for signs secondary to urate uroliths
37
Q

Portosystemic Shunt: clinical signs summary?

A

Clinical signs often relate to effects of decreased liver function:
* Neurologic (HE)
* Gastrointestinal (increased gastrin or other effects)
* Urinary (urate stones)
* Poor growth, “failure to thrive” (decreased nutrient metabolism)

38
Q

examples of Hepatic encephalopathy / CNS signs from portosystemic shunt? how common are they and when do they arise?

A
  • Star-gazing/staringintospace
  • Abnormalbehaviourincludingaggression
  • Headpressing
  • Intermittentblindness
  • Ataxia
  • Pacing
  • Seizures
  • Stupor
  • 41-90% of patients (high rate especially in cats)
  • Occur shortly after a meal in 30-50% of cases
39
Q

examples of GI signs from portosystemic shunt? how common are they and when do they arise?

A
  • Vomiting, diarrhea
  • GI blood loss (melena) especially in IHPSS
  • 30-50% dogs; less common in cats
40
Q

examples of lower urinary tract signs from portosystemic shunt? how common are they?

A

(urate uroliths, UTI)
* Stranguria, hematuria

  • 25-50% of cases

3. Cat & Dog (33 decks)

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