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Boards: Hepatobiliary > Liver Failure > Flashcards

Liver Failure Flashcards

1
Q

How is acute liver failure defined in people?

A
  • decreaed liver function
  • coagulopathy
  • no preexisting liver disease
  • signs consistent with HE
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2
Q

List 4 functions of the liver

A
  • carbohydrate, fat, protein metabolism
  • metabolism and detoxification
  • bile production
  • coagulation factor production + other proteins
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3
Q

What part of the hepatic lobule is most sensitive to toxins and why?

A

central vein - because lowest O2 cc and highest cytochrome P-450 (i.e., more toxic metabolites accumulate here)

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4
Q

How does ammonia lead to cerebral edema?

A

enters astrocytes
together with glutamate –> forms glutamine –> osmotically active

also inserts aquaporine-4 channels - enhances this water movement intracellularly

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5
Q

How is the coagulation system affected by liver failure (4 points)

A
  • less procoagulation factor
  • less anticoagulant factors
  • derangements of fibrinolysis
  • less and dysfunctional platelets
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6
Q

What is the most common sign of hepatic encephalopathy in cats?

A

ptyalism

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7
Q

List 9 precipitating factors of hepatic encephalopathy

A
  • hypokalemia
  • hyponatremia
  • GI bleed
  • constipation
  • renal disease/azotemia
  • high protein meal/diet change or indiscretion
  • sepsis/SIRS
  • furosemide administration
  • alkalosis
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8
Q

What are the grades for hepatic encephalopathy?

A

0 - normal
1 - mild impairment or apathy
2 - severe apathy, mild ataxia
3 - severe ataxia, head pressing, circling etc.
4 - seizures, stupor/coma

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9
Q

Explain how acetaminophen causes liver toxicity

A

acetaminophen –> oxidized by cytochrome P-450 –> NAPQI –> free radical, i.e., cytotoxic (destroys cell membranes, including liver and RBC especially)

zone 3 centrilobular hepatocellular necrosis

NAPQI can be detoxified by conjugation with glutathione –> when depleted –> cell damage

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10
Q

What is the mechanism of toxicity of aflatoxin-induced liver failure?

A

aflatoxin B1

DNA-polymerase inhibition –> cells cannot produce needed proteins and die

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11
Q

What are the 3 phases of amanita mushroom toxicity?

A

GI phase
latent phase
hepatorenal phase

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12
Q

What is the mechanism of action of sago palm toxicity?

A

cycasin toxin

toxic compund of cycasin decreases mitochondrial ATP activity and glucose-6-phosphatase –> centrilobular and midzonal coagulation necrosis and hepatocellular death

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13
Q

How soon after exposure to oral diazepam can cats develop hepatic necrosis?

A

5-13 days

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14
Q

How is leptospirosis thought to induce hepatotoxicity?

A

indirectly through cholestasis of sepsis

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15
Q

What type of crystals occur in dogs with PSS?

A

urate crystals, ammonium-biurate

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16
Q

What are the recommended antibiotics to reduce ammonia load in PSS/HE?

A
  • Ampicillin
  • metronidazole
17
Q

What is cimetidine and how does it work?

A

cytochrome P-450 inhibitor - will reduce load of toxic metabolite (NAPQI) from acetaminophen, has to be given within 16 hours of exposure

18
Q

What is the primary toxin in sago palm, and what part of the plant is it most concentrated in?

A

cycasin
seeds

19
Q

What is the toxin in Cyanobacteria?

A

blue green algae
microcystins

20
Q

What is the treatment for Amanita mushroom toxicity?

A

Silamaryn
Penicillin G

21
Q

How is xylitol suspected to cause hepatotoxicity?

A

ATP depletion leading to hepatocellular necrosis
oxidative injury from ROS production

22
Q

What are the 3 main serovar causing leptospirosis disease in dogs?

A

gryppothyphosa
pomona
icterohemorrhagica

23
Q

A single leptospirosis titer > ________ in an unvaccinated dog with classical clinical signs provides a presumptive diagnosis

A

1.800

24
Q

A ______-fold increase in paired leptospirosis titer is consistent with a previous infection

A

4-fold

25
Q

What are the best samples for leptospirosis antigen detection and what are their time frames for sampling?

A

first 10 days - blood
after 10 days - urine - carrier stage

26
Q

What are the recommended treatments for the active infection versus carrier stage for leptospirosis in dogs?

A

active infection - ampicillin/sulbactam
carrier stage - doxycycline

27
Q

How does acute liver failure cause high bilirubin

A
  • intrahepatic cholestasis from:
  • leakage of tight junctions that separate bile canaliculi from blood
  • hepatocyte swelling - bile canalicular flow obstructed
  • necrosis of hepatocytes
28
Q

What are the 3 main causes of thrombocytopenia in acute liver failure?

A
  • less thrombopoietin production
  • blood loss
  • consumption - primary hemostasis activation
29
Q

Why are patients with acute liver failure hyperfibrinolytic?

A

decreased tPA and uPA clearance by the liver –> accumulate in blood and increase fibrinolysis

30
Q

What are the 3 types of hepatic encephalopathy?

A

A - from acute liver failure
B - PSS
C - chronic liver disease and cirrhosis

31
Q

Where in the cell are ALT and AST found?

A

ALT - cytoplasm
AST - cytoplasm and mitochondria

32
Q

How does hypokalemia precipitate hepatic encephalopathy?

A

increases renal ammoniagenesis

less potassium –> leads to K absorption in exchange for H+ secretion –> more acidic intraluminal environment –> enhances ammonia absorption

33
Q

Is hypophosphatemia or hyperphosphatemia a negative prognostic indicator in acute liver failure?

A

hyperphosphatemia

hypophosphatemia develops from increased cell regeneration - good sign

34
Q

How do arterial and venous ammonia concentrations compare?

A

similar in healthy individual

arterial higher in patients with HE

35
Q

Why is vasopressin not recommended in patients with acute liver failure?

A

causes cerebral vasodilation –> inceases ICP

Boards: Hepatobiliary (5 decks)

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