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3. Cat & Dog > hepatobiliary 2: acute hepatitis > Flashcards

hepatobiliary 2: acute hepatitis Flashcards

1
Q

infectious causes of acute hepatits?

A

Canine adenovirus-1
Leptospirosis
Clostridium spp.
Ehrlichia canis

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2
Q

toxins that can cause acute hepatitis

A
  • Mycotoxins, aflatoxicosis
  • Blue green algae (cyanobacteria)
  • Amanita mushrooms
  • Xylitol
  • Organic solvents
  • Cycad / sago palms
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3
Q

deugs that can cause acute hepapitis

A

Carprofen
Acetaminophen (cats&raquo_space; dogs)
TMS
Azathioprine
Diazepam (oral – cats)
Ketoconazole
Methimazole (cats)
Antiepileptics (phenoparbital, zonisamide)

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4
Q

Acute Hepatic Injury: Presentation

A

Clinical signs related to hepatic cell necrosis & inflammation
* Non-specific: anorexia, vomiting, PU/PD
* More specific: abdominal pain, ascites
* Liver-specific: icterus

  • Signs of coagulopathy, hepatic encephalopathy can be present
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5
Q

Acute Hepatic Injury: Diagnosis - biochem and lab findings

A

Biochemical profile:
* Marked elevations ALT, AST occur early in the process
* Signs of cholestasis often present
* Possibly azotemia (pre-renal, or renal from shared etiology)

Otherlaboratoryfindings
* Anemia (blood loss, other causes)
* Coagulopathy
* Signs of DIC

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6
Q

Leptospirosis testing methods

A
  • Point-of-care antibody tests ( Zoetis Witness)
  • PCR
  • Microscopic agglutination test (MAT)
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7
Q

Point-of-care antibody tests ( Zoetis Witness) for lepto; what may occur in acute disease?

A
  • IgM Can be negative in acute disease
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8
Q

PCR lepto test; what do we sample? when? cuation with antibiotics?

A
  • Performed on blood and urine
  • Typically positive in blood in first 10 days of infection, urine thereafter
  • Antibiotics cause negative result
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9
Q

lepto Microscopic agglutination test (MAT); how does it work/ what is detected? how does vaccination affect this?

A
  • Antibodies to several serovars
  • 4-fold increase in acute and convalescent (2-weeks later) supportive of diagnosis
  • Vaccination can cause positive titres
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10
Q

Serovars covered in North American leptospirosis vaccination

A
  • ‘CPIG’
  • Canicola, Pomona, Icterohaemorrgiae, Grippotyphosa
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11
Q

Acute Hepatic Injury: Diagnosis - what do we see with imaging?

A

Abdominal imaging
* Liver can be large, presence of ascites
* Hepatic parenchyma diffusely altered echogenicity
* Ultrasound can be normal

  • Ultrasound findings not specific, do not define extent of injury
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12
Q

Acute Hepatic Injury: Treatment

A

Treatment of underlying cause, if known
* Toxin: gastric decontamination
* Empirical treatment Leptospirosis if risk in your area (doxu

Liver supportive treatment
* Antioxidant (SAMe and others, N-acetylcysteine as an IV option)
* Ursodiol if cholestatic

Intensive care support
* GIulceration, coagulopathy

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13
Q

why is the liver prone to oxidative damage?

A
  • Central role in metabolism of drugs, toxins
  • Large population of macrophages (Kuppfer cells)
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14
Q

purpose of glutatione? when may it be reduced?

A
  • Essential anti-oxidant in hepatocytes
  • Reduced levels found in bile duct obstruction, lipidosis, inflammatory liver disease
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15
Q

is oxidative injury often important in canine /. feline hepatobiliary disease?

A
  • Oxidative injury likely important in canine & feline hepatobiliary disease
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16
Q

Commonly used anti-oxidants for liver

A
  • SAMe
  • Silymarin (Milk thistle)
  • Vitamin E
  • N-Acetylcysteine

SAMe & silymarin available together in some commercial products

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17
Q

reccomended antioxidant for liver support, and why

A

Recommend to use veterinary grade SAMe products
* Over the counter products might not contain appropriate amounts despite label

18
Q

Evidence-based indications for antioxidants for liver support, for amanita, Acetaminophen toxicity, aflatoxins, Lomustine

A
  • Amanita toxicity – silymarin improved outcomes
  • Acetaminophen toxicity, aflatoxins – N-acetylcysteine improved outcomes
  • Lomustine – SAMe/silymarin protective
19
Q

Suggested indications for anti-oxidants for liver

A
  • Acute liver injury
  • Canine chronic hepatitis
  • Feline hepatic lipidosis
20
Q

can or should we combine antioxidants for liver treatments?

A
  • Ideal agent / combination of agents unknown
    > Generally safe
21
Q

Choleretics; what do they do?

A
  • Modulates bile acid pool (less toxic to hepatocytes)
  • Anti-inflammatory and anti-oxidant properties
22
Q
  • Only absolute contraindication for choleretics? when are they often used?
A

Only absolute contraindication is complete biliary obstruction
* Often added to patients with cholestasis as part of their condition * Limited evidence

23
Q

choleretic which is given for liver support

A

Ursodeoxycholic acid (ursodiol)
* Synthetic hydrophilic bile acid

24
Q

what animal is hepatic nodular hyperplasia common in? how many nodules?

A
  • Hepatic nodular hyperplasia very common in older dogs
  • Single o rmultiple nodules
25
Q

nodular hyperplasia presentation; enzymes, signs

A

Presentation
* Mild to moderate elevations in liver enzymes, typically found incidentally
* No clinical signs

26
Q

Nodular Hyperplasia; can we see it on ultrasound? what type of liver change is this?

A

Can appear on ultrasound as a neoplastic process but is a benign, regenerative change

27
Q

CASE:
* Problem list:
* Pyrexia
* Icterus
* Recent decrease appetite, now anorexia
* Decreased MCS and BCS
* Dehydrated
* Chronic vomiting

> what are our initial plans?

A
  • Biochemical profile
  • Complete blood count
  • Urinalysis
  • FeLV/FIV
28
Q

Cholangitis - what is this? where can it extand? what animal is this common in?

A

Inflammation of the biliary tract
* Can extend into hepatic parenchyma (“cholangiohepatitis”)

  • Cholangitis affects cats&raquo_space; dogs
29
Q

Feline Cholangitis - what liver values do we expect to be high?

A
  • Serum ALP, GGT
  • Serum bilirubin
  • (ALT, AST elevation if cholangitis extends into hepatic parenchyma)

> BUT remeber cats have such short enzyme half lives that we may not see these elevated values

30
Q

why may serum ALP and GGT be elevated? how do these enzymes differ in cats vs dogs?

A
  • Biliary epithelium react to inflammation, other stimuli
  • Increased in intrahepatic or extrahepatic cholestasis, drug effect (dogs)
  • Shorter half-life in cats vs dogs
31
Q

what can cause a rise in serum bilirubin levels? what will PCV look like? what mix will we see in most hepatobiliary disease?

A
  • Pre-, hepatic, and post-hepatic causes
  • Normal PCV = intra- or extra-hepatic cholestasis present
  • A mix of conjugated and unconjugated bilirubin in most hepatobiliary diseases
32
Q

diseases that are commonly concurrent with feline cholangitis? why?

A
  • Concurrent pancreatitis and/or intestinal disease common
    > “Triaditis”

Shared pathophysiology:
* Anatomy: pancreatic & bile duct proximity; sphincter of Oddi spasm in IBD
* Common triggers / causative agent
* Likelymultifactorial

33
Q

Neutrophilic (Suppurative) Cholangitis - what is the likely cause of this? is it usually acute or chronic?

A
  • Likely ascending bacterial infection from intestine
    > E.coli, Streptococcus, Klebsiella, Pseudomonas, Enterococcus, Clostridium, etc
    > Neutrophilic inflammation of bile lumen, ducts, edema
  • Typically acute in nature
    > A more chronic, mixed inflammatory stage also recognized
34
Q

Neutrophilic Cholangitis: Presentation - what signalment? clinical signs?

A
  • Any signalment of cat, but typically young to middle-age
  • Clinical signs usually <1 month
    > Pyrexia, lethargy, icterus, other non-specific signs
    > Signs of pancreatitis or intestinal disease can be present and overlap
35
Q

Neutrophilic Cholangitis: Diagnosis - labwork and ultrasound results?

A
  • Labwork and imaging results not sensitive or specific
  • Often:
    > Neutrophilic inflammation on CBC
    > Elevated bilirubin, ALT (sometimes ALP)
    > Labwork can be normal
  • Ultrasound:
    > Enlarged liver, dilated biliary tracts, gall
    bladder debris might be present
    > +/- Pancreatitis, intestinal disease
36
Q

Neutrophilic Cholangitis: how do we get a difinitive diagnosis? risks and contraindications?

  • do we have some other options that might be helpful, aside from imaging, labwork?
A

Definitive diagnosis requires cholecystocentesis & bile culture
* Risks (overall low): GB rupture, hemorrhage
* Contraindicated if noted GB wall devitalization

  • Liver fine needle aspirate
    > Neutrophilic inflammation, non-specific
  • Hepatic biopsy
    > Portal and biliary duct neutrophilic inflammation
37
Q

Neutrophilic Cholangitis - can we always get a diagnosis? how do we often proceed?

A

can be difficult to get difinitive diagnosis
* Often: empirical treatment after presumptive diagnosis

38
Q

when is sampling for neutrophilic cholangitic contraindicated?

A
  • Sampling contraindicated if uncontrolled coagulopathy
39
Q

Neutrophilic Cholangitis: Treatment

A
  • Antibiotics for 4-6 weeks: ideally based on culture and sensitivity
  • Empirical choices targeting gram positive & negative, aerobe and anaerobe (E coli most
    common); bile secretion; bactericidal
    > Fluoroquinolone (+/- potentiated penicillin/ clindamycin)
    > Penicillin + metronidazole
    > No enrofloxacin in cats! (Prado, marbofloxacin appropriate)
  • IV antibiotics if signs of sepsis or systemic illness
  • Hospitalization for IV fluids, nutritional support usually required
  • Anti-emetics, appetite stimulants
  • Vitamin K if coagulopathy (plasma in severe cases)
  • Consider:
    > S-adenosylmethionine, silybin, and
    ursodeoxycholic acid (ursodiol)
  • Treatment for concurrent disease (e.g., pancreatitis)
    > Analgesia with opioids
    > If signs of intestinal disease, eventually consider diet suitable for IBD
40
Q

Neutrophilic Cholangitis - what should we consider doing prior to discontinuing antibiotic treatment? what other disease might we want to investigate?

A
  • Consider rechecking hepatic values prior to discontinuing antibiotics
  • Patients might require further investigation for other diseases
    > IBD, chronic pancreatitis
41
Q

Neutrophilic Cholangitis: Prognosis

A
  • Most cats recover with treatment, recurrence not common
  • Concurrent disease a factor in prognosis
  • Complications rare
    > GB obstruction with cholelith, abscessaction

3. Cat & Dog (33 decks)

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