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Small animal medicine final topics > 21. ACUTE LIVER DISEASES IN DOGS. ACUTE HEPATIC FAILURE > Flashcards

21. ACUTE LIVER DISEASES IN DOGS. ACUTE HEPATIC FAILURE Flashcards

1
Q

Clinical signs of acute liver failure

A
  • Sudden onset
  • Good general condition
  • (Ø oedema, ascites, kachexia)

Mild-middle

  • Anorexia, depression, dehydration
  • Vomitus, (diarrhoea), pd
  • Icterus (usually no anaemia)
  • Fever (infection)
  • Coagulopathy (acute cases)
  • Hemorrhagia, petechia, hematemesis, melena, hematochezia
  • He
  • Abdominal pain
  • Liver: normal size, pain - acute liver cell distension
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2
Q

Intrinsic effect

A
  • reproducible
  • dose-dependent, over dose limit
  • Direct toxic effect
  • like paracetamol, xylitol
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3
Q

Idiosyncratic effect

A
  • Unique, can not calculate, not reproducible, unique effect
  • In therapeutic dose also, not dose-dependent
  • rare, only in few cases
  • phenobarbital, lomustin, itraconazole
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4
Q

Influenced by:

A
  • Age, condition, general health, immune system, unique sensitivity, other drugs parallel
  • Genetics?
  • Breed predisposition:
    o Dobermann: sulfonamide, amiodaron
    o Labrador: carprofen (cause more chronic hepatitis)
  • Toxin: type, dose, exposure time
  • Glutathione role (detoxification of toxic metabolits) – cats are very sensitive
  • Drugs/toxin no signs, acute, fulminant, chronic
  • NECROSIS (zone3), centrolobular +- cholestasis, steatosis (fatty), (inflammation)
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5
Q

Main groups of causes of acute hepatic failure:

A

Infections, other( trauma, heat), systemic or metabolic

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6
Q

Infectious causes:

A 
Vírus
Bacterium 
Fungus
Protozoon
Parasites
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7
Q

Oher causes:

A

Trauma
Heat stroke
hypoxia

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8
Q

Systemic or metabolic causes

A

IHL
Acute pancreatitis
Acute hemolytic anaemia

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9
Q

aim of treatment of AHF:

A

stabilization, support of liver function:

  • Stop the indicial cause, antidote
  • Fluid and electrolyte, acid base therapy
  • Treat the Brain oedema, HE, bleeding
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10
Q

Hepatotoxicosis - drugs:

A
  • Diazepam C
  • Phenobarbital D ,phenitoin, primidon D
  • Sulfonamide D
  • Trimetoprim-sulfa
  • Paracetamol (acetaminofen) D,C
  • Amanita mushroom (Amanita phalloides) D,C (very dangerous)
  • Xylitol (sugar – did you use any substitutions)
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11
Q

Short about paracetamol poisoning:

A

Quck depletion of glutathion stores, methaemoglobinaemia, hepatic necrosis (centrolobular hepatic necrosis)

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12
Q

Signs of paracet poison:

A
  • Cyanosis
  • dyspnoe (lung edema)
  • tachycardia
  • tachypnoea
  • brown blood
  • (looks similar to heart failure)
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13
Q

Lab work of paracet:

A
  • Hemolytic anaemia, with methemoglobinaemia,
  • brown blood, nucleated rbc, schistocyta, acanthocyta, heinz body,
  • ALT increased
  • Br increased
  • Hb uria
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14
Q

Treatment of Hepatotoxins in general:

A

N-Acetylcystein NAC

SAMe (Hepapet, Samyilin, Denosyl) -additional treatment after stabilization!

Sylimarin

C-vitamin, E-vit

Cimetidine (Histodyl inj)
- Inhibit the P450 enzyme system – it worsen the condition so we must stop!

Fluid, electrolyte, oxigen, mannit..

  • Stop the toxic drugs, toxins
  • Antidote (if exist……)
  • Gastric lavage, charcoal < within 2 hours
  • Stabilization (fluid-electrolite therapy, oxygen…)
  • Antioxidant treatment
    o N-acetilcystein, SAMe, E vitamin, syilimarine
  • Refilling the glutathion stores
    o NAC, SAMe
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15
Q

Phenobarbital poisoning:

A

Normal: liver enzyme induction common
- cytochrome P450 enzyme induction,
- Mild-middle↑: ALP, ALT, GGT, Normal albumin, Br, BA!
o 3-4 times higher liver enzymes but liver function tests are still normal
- Swallowed ER→ enlarged hepatocytes→ ↑liver, smooth
- Always check liver parameters before administering this drug for epileptic patient
Hepatotoxicity rare
- Acute necrosis or chronic hepatitis, cirrhosis
- Idiosyncratic reaction
- Minimum 5-12 month in high dose (upper range of therapeutic dose)
- ALP, ALT (>5x), GGT ~ acute / chronic hepatitis
- Abnormal liver function tests: ↓albumin, ↑Br, BA !
- Enlarged liver (acute) or smaller, irregular (chronic toxicity)
Treatment:
- Dose (decrease or stop) + (KBr, or Levatiracetam)
- Supportive therapy (SAMe!!)
- Rutin labor 4-6 months in case of chronic Pb treatment

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16
Q

PHENYTOIN poison

A 
Hepatotoxicosis
-	very hepatotoxic (especially + Phe)
-	Acute or chronic hepatitis / fatal intrahepatic cholestasis
-	In dogs short half life time
-	Do not use as antiepileptic drugs !!!
Primidone 
-	Metabolits of Phe
-	Very hepatotoxic
-	Liver necrosis, lipidosis, cholestasis
-	Never use in cats
17
Q

Primidone poison

A

Primidone

  • Metabolits of Phe
  • Very hepatotoxic
  • Liver necrosis, lipidosis, cholestasis
  • Never use in cats
18
Q

PotSA poisoning:

A
  • Idiosyncratic effect (also dose-dependent)
  • Quite common
  • Especially in dogs
  • In Dobermann mostly Poly arthropathy, not the liver form
    Sulphonamide hypersensitivity
  • Missing the gene that codes the important enzyme which detoxifying the reactive metabolites
  • Oxidative sulphonamide metabolite indicate the T-cell mediated immune response
  • Thrombocytopenia, fever, Poly arthropathy
  • Common in dobbermann
    acute hepatopathy
  • Acute hepatic necrosis + cholestasis / ly, pl inflammation
    DESTRUCTIVE CHOLANGITIS – new disease
  • Idiosyncratic hypersensitivity
  • Destruction of bile ducts in portal region + inflammation (macrophage, ngr, eo) + portal fibrosis
  • Severe intrahepatic cholestasis → acholic faeces
19
Q

Infectious diseases: viral

A
  • Rubarth CAV-1 (canine adenovirus)
  • Canine, feline herpesvirus
  • FIP (feline infectious peritonitis)
  • Suspected other viruses in the pathomechanism of hepatitis!!!
20
Q

Infectious diseases: BACTERIAL

A

BACTERIAL

- Leptospirosis - Clostridium piliformis (Tyzzer’ diseases) - Helicobacter canis  - Extrahepatic infection, liver abscess (sepsis) - Acute bacterial cholangiohepatitis
21
Q

Infectious diseases: FUNGUS

A

FUNGUS

- Histoplasmosis - Coccidiomycosis
22
Q

Infectious diseases: PROTOSOON

A

PROTOSOON - Toxoplasmosis

23
Q

Infectious diseases: PARASITES

A

PARASITES - Dirofilaria immitis

24
Q

HEPATITIS CONTAGIOSA CANIS (RUBARTH)

A

HEPATITIS CONTAGIOSA CANIS (RUBARTH)
Exposure → viraemia → lymphoid/other tissues → cytotoxic injury
- Canine adenovirus 1 (CAV-1) - vaccination against it, rarely seen these days
- Acute hepatic necrosis, GB-edema, dark, mottled appearance of liver
- Tropism: vascular endothel cell, hepatocyte (cytotoxic injury)
o 1: 500 → ø clinical signs
o 1: 4 → centrilobular to bridging hepatic necrosis
o 1:16-500 → chronic hepatitis , cirrhosis
- Complication: HE, DIC, G, GN (ic), GI, vasculitis, tonsillitis „blue eye disease”: uveitis, cornea edema, glaucoma, keratopathy
- Diagnosis: inclusion bodies, direct fluorescent antibody, biopsy
- Treatment: widespread use of vaccine (cross-reacting CAV-1, 2)
- atropine → anterior uveitis, - iv fluid therapy, blood transfusion
- topical corticosteroid →minimize inflammation in acute stage

25
Q

CANINE HERPESVIRUS

A
  • Acute, afebrile, rapidly fatal in neonatal puppies (die within 1 -3 weeks)
  • Older dogs: mild upper respiratory signs
  • Multiorgan necrosis? (liver, kidney, lung, other organs)
  • Acute, systemic necrosis and hemorrhage
  • Liver necrosis, necrotizing vasculitis, petechia, vesicles, sc edema
  • Eosinophilic intranuclear inclusion bodies in hepatocytes, bile duct epithelium
26
Q

Leptospirosis

A

Acute disease, primarily ARF + cholestatic hepatic disease
Leptospira interrogans / gryppotyphosa
- L. icterohaemorraghie → icterus, hepatic damage
- L. grippotyphosa → chronic hepatitis, fibrosis
- L. canicola → renal failure
o (L. pomona, L. bratislava, australis)
- Cats are relatively resistant
o Reservoir of spirochetas in stagnant water, contact with nondomestic maintenance hosts (skunk, rats, racoons). Shedding via urine
- Toxin: lysis of tight junctions between hepatocytes (dissociation, separation of hepatocytes); intrahepatic cholestasis; vascular damage,
- Laboratory findings: Br increased ,ALP increased ,ALT increased ,BA increased
- Clinical signs:
- fever, myalgia, jaundice, vomiting, vascular injury, uveitis, DIC, edema, oliguria, anuria, uremia
- Hematemesis, hematochezia, melena, epistaxis
- Fever of unknown origin + unexplained renal dysfunction: serology!
Diagnosis:
- Silver (Wartin-Starry)- /Giemsa-stain (stain and cut in lumen!)
- Serology: igg and igm response. Serology titer may be negative during first week, (repeat in 2 weeks) antibody paired serum titers microscopic agglutination test MAT
- PCR: identification of L. DNA
- Isolation from fresh urine (dark-field microscopy)

27
Q

TYZZER’S DISEASE RARE

A
  • Clostridium piliformis (Bacillus p.) Gr - fusiform bacteria + immunsuppression!
  • multifocal hepatic necrosis, necrotizing ileitis
    Clin: dogs, cats
  • acute onset: anorexia, lethargy, abdominal discomfort
  • rapidly fatal, 24-48 h dying. No treatment
    Dg:
  • Biopsy: multifocal periportal hepatic necrosis, C.p within hepatocytes
  • surrounding areas of necrosis and intestinal epithelial cells
  • Routine culture techniques are not effective for isolation
  • Wartin Starry or Giemsa stain
28
Q

HELICOBACTER CANIS

A

HELICOBACTER CANIS

  • Multifocal hepatic necrosis
  • Mostly in young dogs
  • It presents at periphery of the lesions, located in bile canaliculi
  • Suggesting ascending infection along bile duct
29
Q

MYCOSIS

A

MYCOSIS
- systemic mycosis→mononuclear phagocytosis→liver signs (no acute)
- Clin: hepatomegaly, ascites, icterus. inhalation: cough, dyspnoe
- Liver: granulomatous or pyogranulomatous inflamm.(Giant cell, ly, pl)
HISTOPLASMOSIS
- Bone marrow, lymph nodes, GI
COCCIDIOMYCOSIS
- Bones, joints, lymph nodes, abdominal organs
- Labor: enzymes are slightly elevated or normal

30
Q

PROTOZOAL

A

PROTOZOAL
Toxoplasma gondhii + immunosuppression
- Widespread multifocal necrosis, AHF (rapid multiplication of tachyzoites)
- Lungs, eye, lymphoid tissue, spleen, CNS, heart
- Clin: icterus, abdominal pain, fever, uveitis, concomitant lung involvement
- Cats: FeLV/FIV/CCH + Dogs: Fc+
- Treat: clindamycin

31
Q

PARASITE

A

PARASITE
- post caval syndrome or vena caval syndrome (heartworm disease)
DIROFILARIA IMMITIS
- D.i.→right atrium or v.cava or v.hepatica →acute, passive congestion of the liver
Clin: acute onset:
- anorexia/weekness/dyspnoe/Hburia/anaemia/icterus
- Abrupt loss of venous blood flow→ infarction→ necrosis
- Intravascular hemolysis
- No history of cardiopulmonary signs

Small animal medicine final topics (16 decks)

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