22. Acute liver diseases in cats, feline hepatic lipidosis. Flashcards

1
Q

Acute hepatic failure (AHF) of cats + clinical signs?

A

Acute Hepatic Failure (AHF) of Cats

As AHF of dogs

Technically a clinical syndrome, not a specific diagnosis; 70% of the liver parenchyma is affected

Acute hepatic failure shows histopathological necrosis, and this

should be remembered! Because of the necrotic nature of the disease,

the following outcomes of the condition are:

§ Recovery

§ Chronic liver disease

§ Death

CLINICAL SIGNS

Mild CSx → Slow progression (tissue regeneration/adaptation)

Severe CSx → Acute AHF (Ø tissue regeneration/adaptation)

§ Depression § Polydipsia

§ Dehydration § Icterus

§ Abdominal pain § Fever

§ Coagulopathy § Vomiting

§ CNS signs (HE) § Anorexia

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2
Q

Diagnosis of acute hepatic failure?

A
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3
Q

AHF caused by hepatotoxins?

A

AHF Caused By Hepatotoxins

The liver is sensitive to toxins and drugs, and plays a central role in their metabolism.

Toxic effects on the liver are divided into the following:

Intrinsic toxic effect

Reproducible

Dose-dependent

Toxic dose limit

Direct toxic effect

E.g. Paracetamol; Xylitol

Extrinsic toxic effect (rare)

Non-reproducible

Unique (non-calculable)

Not dose-dependent

E.g. Phenobarbital; Lomustine; Itraconazole

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4
Q

Paracetamol?

A

PARACETAMOL (ACETAMINOPHEN)

Ø Cats!

Rapidly depletes the body’s stores of glutathione (GSH); Produced

toxic metabolites which have an oxidative effect

Erythrocyte methemoglobinemia & hepatocyte necrosis

Clinical signs:

§ Cyanosis § Tachycardia

§ Dyspnoea § Tachypnoea

§ Facial oedema § Brown blood

Lab. D

§ Haemolytic anaemia; Methemoglobinemia

§ Abnormal RBCs: Nucleated; Schistocyte; Acanthocyte;

Heinz body

§ ALT ↑; Br ↑; Haemoglobinuria

Treatment

§ Flush the stomach & give activated charcoal

§ Stabilise patient: IVFT; Oxygen; Mannitol

§ Apply high amounts of antioxidants

§ Key treatment: N-Acetylcysteine

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5
Q

Diazepam & Clonazepam?

A

DIAZEPAM & CLONAZEPAM

Causes acute hepatic failure with high mortality

Idiosyncratic drug reaction; Particularly in PO drug form

Very poor prognosis

Lab. D: Liver enzymes ↑↑↑, especially ALT

Normal cases: Does not alter liver enzyme parameters

Treatment: Immediate withdrawal of the drug; Intensive support

Pathology: Centrilobular necrosis

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6
Q

Phenobarbital, Phenytoin , Primidone and potentiated sulphonamides ?

A

PHENOBARBITAL

Rarely causes hepatotoxicity; Idiosyncratic reaction

Dx: ↓ Albumin; ↑Br; Enlarged liver (or smaller if chronic)

Tx: ↓ The dose; Supportive therapy

PHENYTOIN

Very hepatotoxic

Causing: Acute/chronic hepatitis; Fatal intrahepatic cholestasis

Short half-life in dogs

PRIMIDONE

Metabolite of phenobarbitone; Must not be used in cats!

Hepatotoxic

Pathology: Liver necrosis; Lipidosis; Cholestasis

POTENTIATED SULPHONAMIDE

Idiosyncratic effect; Common

Forms of toxicosis:

§ Sulphonamide hypersensitivity: Thrombocytopenia;

fever; polyarthropathy

§ Acute hepatopathy: Liver necrosis & cholestasis

§ Destructive cholangitis: Idiosyncratic hypersensitivity →

Severe intrahepatic cholestasis → Acholic faeces

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7
Q

Xylitol toxicosis?

A

XYLITOL TOXICOSIS

Tolerated well in cats

May lead to hypoglycaemia; liver necrosis & acute liver failure

Lab. D

§ Hypoglycaemia

§ Hypokalaemia

§ ↑↑↑ Liver enzymes

§ ↑↑↑ Br

§ Hypophosphataemia → Hyperphosphataemia

Clinical signs

§ Vomiting § Lethargy

§ Weakness § Ataxia

§ Tremor § Seizure

§ AHF: Icterus; HE; Coagulopathy

Treatment

§ Emesis (unless ingestion was >30 mins ago)

§ Ø Activated charcoal → Ineffective

§ Monitor & maintain blood glucose

§ Coagulopathy: Fresh frozen plasma; Blood transfusion

§ Palliative therapy

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8
Q

Acute hepatic failure caused by pathogens (Feline Infectious peritonitis)?

A

AHF Caused By Pathogens

FELINE HERPESVIRUS

FELINE INFECTIOUS PERITONITIS (FIP)

Coronavirus infection

Multisystemic so lesions may be seen in: Peritoneum; Pleura;

Brain; Eyes; Parenchymal organs

Clinical signs

§ Ø CSx

§ Mild upper respiratory symptoms

§ Mild diarrhoea

Diagnosis: Ø Definitive test

Pathology: Pyogranulomatous hepatitis; Multifocal hepatic necrosis;

Immune-complex vasculitis; Liver is covered by a thick layer of

fibrin

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9
Q

Leptospirosis ( Zoonotic)?

A

LEPTOSPIROSIS [ZOONOTIC]

Cats are relatively resistant

Acute disease; Primarily acute renal failure + cholestatic hepatic

disease; Found in stagnant water and other hosts; Shedding via urine

§ L. icterohaemorrhagie → Icterus; Hepatic damage

§ L grippotyphosa → Chronic hepatitis; Fibrosis

§ L. canicola → Renal failure

Toxin causes:

§ Lysis of tight junctions

§ Intrahepatic cholestasis

§ Vascular damage → Bleeding tendancies

Lab. D

§ ALP ↑↑

§ ALT ↑

§ BA ↑

§ Br ↑

Clinical signs

§ Fever § DIC

§ Myalgia § Oedema

§ Jaundice § Haematemesis

§ Haematochezia § Vomiting

§ Vascular injury § Melena

§ Renal dysfunction § Epistaxis

§ Oliguria/anuria § Uveitis

Diagnosis

§ US: Double layer of the gallbladder: Thickened

§ Serology: Microscopic agglutination test (MAT)

§ PCR

§ Isolation from fresh urine (dark field microscopy)

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10
Q

Clostridium Piliformis (Tyzzers disease)?

A

CLOSTRIDIUM PILIFORMIS (TYZZER’S DISEASE)

Gram negative; Fusiform bacteria; Immunosuppression

Seen in dogs too

Clinical signs

Acute onset; Rapidly fatal (within 24-48 hours)

§ Anorexia

§ Lethargy

§ Abdominal discomfort

Diagnosis → Biopsy

§ Multifocal periportal hepatic necrosis

§ Hepatocyte & intestinal epithelium necrosis

Treatment: Ø Treatment; Palliative

Pathology: Multifocal hepatic necrosis; Necrotising ileitis

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11
Q

Hepatic abscess?

A

HEPATIC ABSCESS (EXTRAHEPATIC LIVER INFECTION)

Focal abscess → Hepatobiliary infection; Ischaemia

Multi-focal abscess → Systemic infection

Bacteria of concern (Cat): Streptococcus spp.; E. coli; Salmonella

spp.; Clostridium spp.

Immunosuppression

Haematogenous spread via: Bile duct; Umbilicus

Hypoxic conditions allow the proliferation of anaerobic bacteria

from normal flora

Clinical signs

§ Anorexia § Ascites

§ Depression § Weight loss

§ Vomitus § Hepatomegaly

§ Fever

Lab. D: Neutrophilia (left shift); Liver enzymes ↑; Br ↑↑

Treatment: Surgery →Drainage →Antibiotics (penicillin +

fluroquinolone)

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12
Q

Mycotic infection, protozoal and parasitic infection ?

A

MYCOTIC INFECTION

Systemic mycosis → Mononuclear phagocytosis → Hepatic signs

Clinical signs

§ Hepatomegaly

§ Ascites

§ Icterus

§ CSx: from inhalation: Cough; Dyspnoea

Lab. D: Liver enzymes ↑/-; SBA ↑; Br ↑; Albumin↓; DIC

Pathology: Granulomatous/pyogranulomatous inflammation

Histoplasmosis: Affecting: Bone marrow; Lymph nodes; GIT

Coccidiomycosis: Affecting: Bones; Joints; Lymph nodes;

Abdominal organs

PROTOZOAL INFECTION

Toxoplasmosis (Toxoplasma gondii) + Immunosuppression

Affecting: Lungs; Eye; Lymphoid tissue; Spleen; CNS; Heart

Clinical signs

§ Icterus

§ Abdominal pain

§ Fever

§ Uveitis

Pathology: Widespread multifocal necrosis; AHF

Treatment: Clindamycin

PARASITIC INFECTION

Dirofilaria immitis

Post caval syndrome/vena cava syndrome (heartworm disease)

Affecting: RA of heart, v. hepatica or vena cava

Clinical signs

Acute onset:

§ Anorexia § Haemoglobinuria

§ Weakness § Anaemia

§ Dyspnoea § Icterus

Lab. D: Intravascular haemolysis

Pathology: Acute, passive congestion of the liver; Necrosis

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13
Q

Feline hepatic lipidosis and clinical signs?

A

Feline hepatic lipidosis

↑ Hepatocellular accumulation of lipids & cholestasis, leading to hepatic failure.

The most common primary hepatopathy in Europe

Indoor, domestic shorthairs; Middle-aged; Obese cats that then undergo prolonged anorexia.

CLINICAL SIGNS

§ Anorexia § Hepatomegaly

§ Depression § Depression (HE)

§ Dehydration § Salivation (HE)

§ Icterus § GI signs (D & V)

§ Coagulopathy § Ventroflexion of head & neck

Two types of FHL exist:

§ Idiopathic hepatic lipidosis (IHL)

§ Secondary hepatic lipidosis

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14
Q

Idiopathic hepatic lipidosis?

A

IDIOPATHIC HEPATIC LIPIDOSIS

Multifactorial/unknown cause

Pathogenesis

Cats are obligate carnivores → High resting protein catabolism,

because of this, they can’t stop their postprandial enzyme activity and essential amino acid catabolism (Arginine, Methionine, Taurine and Carnitine) → These are therefore constantly lost Fasting during anorexia, illness, or stress → ↑ Fat mobilisation from

fat stores & ↓ lipoprotein synthesis → Lipid accumulation

Simultaneously:

↓ Arginine → ↓NH3 metabolism → HE; ↑Ammonia

Summary: Lipid accumulation & ↑Ammonia

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15
Q

Secondary hepatic lipidosis?

A

SECONDARY HEPATIC LIPIDOSIS

Most common type

Caused by metabolic/infective disease:

§ Cholangiohepatitis § DM

§ Cardiomyopathy § IBD

§ Pancreatitis § FORL

§ CKF § FIP

§ Neural diseases § Neoplasia

§ Toxins § Drugs (tetracycline)

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16
Q

Lab D of FHL?

A

LAB. D OF FHL

Acute liver function loss; Non-regenerative anaemia

Intrahepatic cholestasis

§ ↑/- GGT § ↑ TBr § ↑ Glucose

§ ↑ SBA § ↓ K § ↑ NH3

§ ↑ ALT § ↓ P

§ ↑↑ ALP § ↓ Mg

17
Q

Diagnosis and treatment of feline hepatic lipidosis?

A

DIAGNOSIS

Liver biopsy: Definitive diagnosis

Early biopsy may lead to death

Vit. K depletion-coagulopathy: Dangerous to perform!

Histopathology: Hepatocyte vacuolisation; Necrosis; Ø Inflammation

Ultrasound: Hepatomegaly (hyperechogenic)

FNA & Cytology

§ Sudan III stain: “Foamy” cytoplasm

§ Important to differentiate mild-moderate lipid

accumulation from severe lipidosis.

TREATMENT

Glucocorticoids are contraindicated

§ Stabilisation

§ Intensive force feeding: NG tube

§ Avoid re-feeding syndrome

§ Treat background causes

§ Treatment of HE

§ Treatment of coagulopathy

§ Good quality diet; Ø Protein restriction