Hepatobiliary Vascular Disorders and Hepatic Encephalopathy (Rudinsky - Feb 7th - In Class) &Cholestatic Liver Disease (Rudinsky February 9th - In Class) Flashcards

1
Q

List your treatment options for Congenital PSS:

A
  • Medical management of HE
    • Protein- restricted diet
    • Lactulose, antibiotics
    • Correct precipitating events
  • Shunt attenuation (Surgery)
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2
Q

Congenital PSS
- Extrahepatic PSS
- Hygroscopic casein
- Stainless steel ring
- Fluid absorption
- Shunt occlusion
- Rapid phase (14 d)
- Gradual (up to 60 d)
This is describing …

A

Ameroid Constrictor

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3
Q

List some complications with Ameroid Constrictor:

A
  • Portal Hypertension
  • Seizure
  • Hemorrhage
  • Hypoglycemia
  • Treatment failure
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4
Q

All surgical shunt corrections should be pre-treated with what?

A

Antiepileptics (eg Keppra)

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5
Q

List Clinical Findings for Microvascular Dysplasia (Portal Vein Hyperplasia):

A
  • Small breed dogs
  • Most are asymptomatic
  • “PSS lite”
  • Older at diagnosis
  • Increase SBA; liver biopsy same as congenital PSS
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6
Q

(T/F) There are surgical options for Microvascular Dysplasia

A

False

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7
Q

What are the Diagnoses for Hepatic microvascular dysplasia?

A
  • Lab Findings
    • Increase SBA
    • Mild Increase ALT
    • No synthetic failure or microcytosis
  • Imaging (no shunt)
  • Scintigraphy (no shunt) = specific and sensitive
  • Liver biopsy (same as PSS)
    (ultrasound = specific not sensitive)
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8
Q

EXTRA CARD

A

Highly Sensitive tests will lead to positive findings for patients with a disease, whereas highly Specific tests will show patients without a finding having no disease.

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9
Q

What are the Lab Findings for Microvascular Dysplasia (Portal Vein Hyperplasia)?

A
  • Increase SBA
  • Mild Increase ALT
  • No synthetic failure or microcytosis
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10
Q

(T/F) Microvascular Dysplasia tends to be asymptomatic because the shunt fraction is smaller

A

True

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11
Q

Treatment and Prognosis:
Microvascular Dysplasia (Portal Vein Hyperplasia)
- No treatment required
- Recognition of pre-existing Increase SBA

A

Asymptomatic

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12
Q

Treatment and Prognosis:
Microvascular Dysplasia (Portal Vein Hyperplasia)
- Medical management of HE

A

Symptomatic

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13
Q

(T/F) Hepatic Microvascular Dysplasia (MVD) has a good long term prognosis in most

A

True

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14
Q
  • Plasma protein ANTIcoagulant
    - ** Synthesized in the liver **
    - Vitamin K dependent
  • Primarily used to differentiate MVD and PSS
    • Low protein activity is a characteristic finding in dogs with clinical signs of PSVA
    • Dogs with MVD typically have protein C values > 70%
      • > 70% does not differentiate
      • < 70% likely PSS
        This is describing …
A

Protein C

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15
Q

(T/F) High serum bile acids are a sensitive screening test for both PSS and MVD, the finding of high bile acids does not differentiate between these 2 syndromes

A

True

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16
Q

(T/F) Animals with large shunting portosystemic vascular anomalies (PSS) often require surgical correction, whereas microvascular dysplasia (MVD) is not a surgical problem

A

True

17
Q

What is a sensitive screening test for both PSS and MVD, but the finding does not differentiate between these 2 syndromes?

A

High serum bile acids

18
Q

List consequences of PSS:

A
  • Hepatic encephalopathy (Big one to worry about)
  • Urate urolithiasis
  • Hepatic atrophy
19
Q

(T/F) Hepatic Encephalopathy is not reversible

A

False, is reversible

20
Q
  • Pathogenesis unresolved
  • Ammonia toxicity is key BUT other factors play a role
    • Synergistic toxins
    • Altered neurotransmitters
    • Oxidative stress
    • Inflammatory mediators
  • Astrocytes are the target
    This is describing …
A

Hepatic Encephalopathy

21
Q

Fill in the blanks for Ammonia Metabolism:
- NH3 produced in the colon by bacterial action on dietary protein, protein by-products, and endogenous urea
- NH3 absorbed from colon –> ______(1)______
- Portal blood carries NH3 to ___(2)____
- NH3 –> urea in _____(3)____ (urea cycle)
- NH3 ___(4)___ in peripheral blood

A
  1. portal blood
  2. Liver
  3. hepatocytes
  4. low
22
Q

List causes for Hepatic Encephalopathy:

A
  • PSS
  • Severe liver disease
    • Massive necrosis
    • Cirrhosis
  • Urea cycle enzyme deficiency (uncommon)
23
Q

List treatments for Hepatic Encephalopathy:

A
  • Correct precipitating events
    • High protein meal *
    • GI Bleeding *
    • Blood transfusion
    • Constipation
    • Dehydration
    • Azotemia
    • Infection
    • Alkalosis/ decrease K+
  • Restrict dietary protein
    - Modify protein: Soy>White>Red>Organ Meat
  • Decrease colonic NH3 absorption
  • Alter intestinal bacteria
24
Q

Hepatic Encephalopathy:
With what drug therapies do you want to be careful?

A

Precipitating Events
- Corticosteroids
- NSAIDs
- Tranquilizers
- Anticonvulsants
- Anesthetics
- Diuretics

25
Q
  • Synthetic disaccharide
  • Not digested or absorbed in the gut
  • Metabolized by colonic bacteria to organic acids –> decrease luminal pH (acid)
  • Decrease NH3 absorption from the colon
    This is describing …
A

Lactulose
- Can be given as an enema

26
Q

Hepatic Encephalopathy:
What are the drugs used to alter intestinal bacteria?

A
  • Neomycin (Less systemically absorbed)
  • Amoxicillin
  • Metronidazole (people go to)
27
Q

(T/F) High serum bile acids are a sensitive screening test of both PSS and MVD, the finding of high bile acids does not differentiate between these 2 syndromes

A

True