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CFT II > Exam 2 - Liver Toxins > Flashcards

Exam 2 - Liver Toxins Flashcards

1
Q

what is phase I of drug metabolism? what is the product?

A

oxidation - many drugs use cytochrome p450 for this

metabolites are the product

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2
Q

what are common hepatotoxins we see affecting companion animals?

A

sago palm, xylitol, amanita mushrooms, aflatoxins, & blue green algae (microcystin)

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3
Q

what are some potentially hepatotoxic drugs?

A

acetaminophen, phenobarbital, sulfa drugs, lomustine, carprofen, azole drugs, & herbal remedies

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4
Q

what is the general approach you should take for a patient presenting with acute liver injury?

A

clinical signs are usually very severe - need to identify cause & prevent further exposure

biopsy not typically performed - these animals are at risk for developing acute liver failure

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5
Q

T/F: metabolites of drugs oxidized by cytochrome p450 in the liver is more toxic than the original drug form

A

true

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6
Q

why is the liver susceptible to oxidative damage?

A

positioned between systemic circulation & sphlanic vessels

responsible for handling xenobiotics/drugs

has a lot of resident macrophages

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7
Q

what liver pathology does amanita mushrooms cause?

A

hepatonecrosis!!!!!

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8
Q

what animals are especially susceptible to acetaminophen toxicity?

A

cats

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9
Q

__________ & _______ are both dose-dependent toxicities affecting the liver of companion animals

A

acetaminophen & phenobarbitol

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10
Q

why are sulfa drugs potentially hepatotoxic?

A

idiosyncratic drug reactions in dobermans & other short coated breeds - think twice before giving!!!

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11
Q

what should you give alongside lomustine chemo? why?

A

denamarin & SAMe - lomustine is damaging to the liver

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12
Q

what breeds should you think about prior to giving them carprofen? why?

A

labs - breeds that are especially susceptible to chronic hepatitis

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13
Q

what is the leading cause of drug induced liver injury in humans?

A

herbal remedies

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14
Q

what are some signs that an animal with acute liver injury has progressed into acute liver failure?

A

increased bilirubin, coagulopathies, & hepatic encephalopathy

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15
Q

what are some aspects that go into preventing/reducing exposure to the agent causing liver injury in companion animals?

A

induce emesis/lavage - if within the time period

+/- activated charcoal - only if they are conscious!!!! will decrease & prevent absorption

+/- enemas - need to consider intrahepatic circulation

+/- cholestyramine (cyanobacteria, cycad)

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16
Q

what is the antidote for amanita toxicity?

A

silymarin or penicillin G

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17
Q

what is the antidote for acetaminophen toxicity?

A

n-acetylcysteine (antioxidant)

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18
Q

what is the point of giving an acute liver injury patient lactulose?

A

if hepatic encephalopathy is present - can measure NH3 to make this decision

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19
Q

when may you need to add electrolytes & glucose to iv fluids for a patient with acute liver injury?

A

if liver failure is present!!!

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20
Q

what are the primary toxins of sago palms? what is the pathogenesis?

A

azoglycosides - seed is the most toxic part

converted to methylazoxymethanol by the gi microbiota

enterohepaticaly recirculated - causes gi & hepatic toxicity

2 other neurotoxins - cause seizures, ataxia, weakness, & tremors

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21
Q

when is the incidence of cycad toxicity highest?

A

in the spring - when seeds are out & about

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22
Q

when are clinical signs seen with cycad toxicity? when are lab changes seen?

A

clinical signs - 4 to 24 hours after ingestion

clin path changes - liver dysfunction, typically 24 to 72 hours after ingestion

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23
Q

what are some negative prognostic factors for cycad toxicity?

A

ALT > 125 U/L at presentation

thrombocytopenia

worse clinical signs at the time of presentation

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24
Q

what is the prognosis of cycad toxicity?

A

12-50% mortality

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25
Q

what treatment should be immediately initiated if an animal presents with cycad toxicity?

A

decontamination of the gi tract!!!!!! activated charcoal is associated with improved survival!!!!

cholestyramine is a resin given orally that may prevent enterohepatic recirculation

26
Q

what are amanita phalloides?

A

death cap mushrooms that contain several toxins including amatoxin - these toxins are not destroyed by cooking or freezing!!!!

27
Q

what are these?

A

death cap mushrooms

28
Q

what are the 4 phases of amanita toxicity?

A
  1. latency
  2. gi signs
  3. recover
  4. fulminant multiorgan failure
29
Q

T/F: toxins from amanita toxicity can be measured in the liver (postmortem) or the stomach contents

A

true

30
Q

what treatments are used for amanita toxicity?

A

penicillin G & silymarin

31
Q

T/F: companion animal commercial diets are regularly tested for aflatoxin contamination

A

true

32
Q

is acute or chronic toxicity more common in aflatoxicosis?

A

acute - rapidly fatal, toxic metabolites of p450 are produced with secondary oxidative injury

chronic exposure - can lead to immunodeficiency & hepatic neoplasia

33
Q

what happens if you have an animal that has aflatoxicosis from their dog food?

A

NOTIFY THE FDA & ISSUE A RECALL

34
Q

how can aflatoxins be measured in the body?

A

urine, food, or liver (postmortem)

35
Q

what is the mortality rate of aflatoxicosis?

A

64-100% - very very bad, no antidote

36
Q

what do you think is likely a problem here?

A

aflatoxins - moldy corn baby

37
Q

what is xylitol?

A

sugar substitute included in human food products

38
Q

what is the pathogenesis of xylitol toxicity?

A

causes acute hypoglycemia followed by hepatotoxicity 1-3 days later (induces an insulin surge & profound insulin resistance)

can cause mild dose-dependent self-limiting disease or idiosyncratic acute liver failure

39
Q

what is a negative prognostic factor for xylitol toxicity?

A

hyperphosphatemia

40
Q

what treatment is used for xylitol toxicity?

A

decontamination & supportive care

41
Q

what is the toxin that is so so bad in algal blooms? what is it produced by? where is it found?

A

microcystin!!!!!

cyanobacterium - found in still fresh water (texas in the summer) because it has warmth, sunlight, & nutrients

42
Q

how long before you see signs associated with cyanobacterium/microcystin toxicity?

A

generally very fast - minutes to hours, bad news

43
Q

what are some common clinical signs seen with microcystin toxicity?

A

seizures, depression, anorexia, vomiting, diarrhea, petechiae/ecchymoses, melena, icterus, ataxia, & collapse

44
Q

you have a patient that ate sago palm 2 days ago that has been treated supprotively for the last day with no improvement - you run labs and see elevated liver enzymes, decreased calcium, phosphate, protein, & albumin, with thrombocytopenia

you run a coag panel, and you see these results - what are you concerned about?

A

liver injury +/- DIC

45
Q

you have a patient that ate sago palm 2 days ago that has been treated supportively for the last day with no improvement - you run labs and see elevated liver enzymes, decreased calcium, phosphate, protein, & albumin, with thrombocytopenia

is this dog in acute liver failure? why?

A

no - bilirubin isn’t increased, but we are likely headed that way

46
Q

you have a patient that ate sago palm 2 days ago that has been treated supprotively for the last day with no improvement - you run labs and see elevated liver enzymes, decreased calcium, phosphate, protein, & albumin, with thrombocytopenia

he is 5 kg & 5% dehydrated - what is your fluid plan for the first 10 hours?

A

maintenance - 5 X 60 = 300 mL/day ~ 12.5 mL/hr

dehydration - 5%, 0.05 X 5 = 0.25 L over 10 hours ~ 25 mL/hr

ongoing losses - 10 mL/hr

total for first 10 hours - 47.5 mL/hr

supplement potassium!!! 40 mEq/L (20 mEq KCl & 20 mEq KPO4)

47
Q

you have a patient that ate sago palm 2 days ago that has been treated supportively for the last day with no improvement & is pukey, yellow, & depressed - you run labs and see elevated liver enzymes, decreased calcium, phosphate, protein, & albumin, with thrombocytopenia

would you give this dog antibiotics? oral liver protectants? plasma products? treatment for hepatic encephalopathy?

A

no - not based on the info given

no - dog is vomiting, no oral drugs, do SQ injections of vitamin k

no plasma - dog isn’t bleeding

no treatment for hepatic encephalopathy - no obvious signs & normal ammonia levels

48
Q

you have a patient that ate sago palm 2 days ago that has been treated supportively for the last day with no improvement - you run labs and see elevated liver enzymes, decreased calcium, phosphate, protein, & albumin, with thrombocytopenia

how often are you rechecking labs on this patient?

A

mentation & vitals every 4-8 hours

electrolytes & phosphate 12 hours after starting treatment

liver enzymes/bilirubin/chemistry - after 24 hours

platelet count & coagulation panel after 24 hours

49
Q

what is the most common liver toxin for dogs in texas?

A

sago palm - cycad toxicity

50
Q

what is the general prognosis for acute liver failure?

A

poor

51
Q

what differentiates acute liver failure from acute liver injury?

A

acute liver injury - acute hepatocellular damage & necrosis with retained hepatocellular function

acute liver failure - occurs once hepatocellular damage is so extensive that it compromises hepatic synthetic, excretory, & regulatory functions

52
Q

what are 5 common toxins that cause liver injury in dogs & cats?

A
  1. sago palm - cycad
  2. blue-green algae (microcystins)
  3. amanita phalloides
  4. aflatoxins
  5. xylitol
53
Q

what are 6 drugs that are commonly implicated in causing liver injury in dogs?

A
  1. carprofen
  2. acetaminophen
  3. sulfonamides
  4. lomustine
  5. zonisamide
  6. phenazopyridine
54
Q

what drug, when given orally, may cause an idiosyncratic hepatotoxicity in cats?

A

oral benzodiazepines - diazepam!!!

55
Q

what are 6 potential complications of acute liver failure in dogs & cats?

A
  1. sepsis
  2. hypoglycemia
  3. hepatic encephalopathy
  4. cerebral edema/intracranial hypertension
  5. coagulopathies
  6. icterus
56
Q

what electrolytes & acid base abnormalities may precipitate hepatic encephalopathy?

A

hypokalemia can precipitate HE by stimulating renal ammoniagenesis leading to hyperammonemic states in the body

many of them - hypokalemia, hypophosphatemia, hyperphosphatemia, hyponatremia, hyperlactemia, & refractory metabolic acidosis

57
Q

a dog presents comatose with hepatic encephalopathy - how would you immediately manage it?

A

mannitol or hypertonic saline - elevate their heads & avoid kinking their neck/obstructing their jugular vein

provide adequate sedation & analgesia

avoid hypotension, hypoxemia, hyponatremia, & hyperthermia

minimize spikes in intracranial pressure from agitation or painful stimuli

58
Q

when would you consider using fresh frozen plasma in a dog with acute liver failure?

A

patient has prolonged PT/aPTT with clinical evidence of hemorrhage or those undergoing an invasive procedure

use fresh frozen because it provides all coagulation factors including labile factors V & VIII

59
Q

what is the antidote for acetaminophen toxicity?

A

n-acetylcysteine & SAMe

60
Q

what are the 2 antidotes used for amanita toxicity?

A

penicillin G & silymarin

61
Q

is there an antidote for sago palm toxicity?

A

no :( no specific treatment

62
Q

when would you consider using antimicrobials in a dog with acute liver failure?

A

controversial use - empirical therapy is recommended when there is suspicion of infection or the likelihood of sepsis is high for example when there is progression of HE, refractory hypotension, or the presence of SIRS

3rd generation cephalosporin - good coverage for gram positive & negative

CFT II (28 decks)

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