feline hepatobiliary disorders

Question 1

common clinical presentation of feline hepatobiliary dz

Answer 1

• Clinical signs very similar for most feline hepatobiliary diseases
• Jaundice & hepatomegaly –most common findings
• n.b. nt the case with dogs

Question 2

Yellow cat…………..think:

Answer 2

• Hepatic Lipidosis
• Cholangitis / Cholangiohepatits
• FIP
• Lymphoma (FeLV)

Question 3

t common liver dz in cats

Answer 3

• Primary (idiopathic)
• Most common liver disease in cats***

they stop eating for no apperant reason

• Starvation causes increased lipolysis and mobilization of FA’s to hepatocytes
• Intrahepatic fat build up leads to pronounced intrahepatic cholestasis

Question 4

role of obesity in hepatic lipidosis in cats

Answer 4

Obese cats not able to adapt to metabolism of fat for energy during catabolic stress, starvation
As true carnivores, the unique requirements of cats for protein, essential amino acids, and essential fatty acids may play a role in this susceptibility

Question 5

predisposing factors for hepatic lipidiosis

Answer 5

Obesity

• Obese cats do not adapt to metabolism of fat for energy during periods of starvation
• Triggers for inappetance

Stressful events
Nonhepatic illnesses

• Prolonged anorexia (often >2 weeks)
• Severe weight loss (often >25%)

Question 6

signalment for hepatic lipidiosis

Answer 6

Middle -aged adult cats
Median 7 years, Range 0.5 -20 years
No breed or gender predilection
Obese body condition
Median BW -10 lb

Question 7

cs for hepatic lipidiosis

Answer 7

Persistent anorexia (often > 2 weeks)
Recent weight loss (>25%)
Muscle wasting, weakness
Depression, lethargy
Vomiting (38% of cases)
Diarrhea, constipation
Bleeding (20% of cases)
Jaundice (70%)
Hepatic encephalopathy

Question 8

physical findings in cats with hepatic lipidiosis

Answer 8

• Jaundice (70%)
• Hepatomegaly
• Muscle wasting
• Dehydration
• Seborrhea
• Pallor
• Ventroflexion of head and neck
  
  • ▪Hypokalemia, hypophosphatemia, thiamine

Question 9

chem panel for feline hapatic lipidiosis

Answer 9

Bilirubin (increased) 95%
ALP (increased ) 80%
GGT WNL
ALT (increased) 72%
AST (increased) 89%
Hypoalbuminemia 60%
BUN (decreased) 58%
Low K+, low Mg++ 30%
Hypophosphatemia 17

Question 10

adv of doing fna with hepatic lipidiosis

Answer 10

Safe, quick, easy to perform
Ultrasound guided
Less invasive, less accurate than biopsy
Over 80% hepatocytes vacuolated (“foamy”)
No inflammation
Coag times first!!!!
Pre-treat with vitamin K1 (1 mg/kg SQ q 24 hours)

Question 11

when is cytology helpful with hepatic lipidiosis

Answer 11

not always sufficient
Cytology ONLYdiagnostic if history and other findings consistent with primary hepatic lipidosis

Question 12

bx findings for hepatic lipidiosis

Answer 12

Findings
Tissue floats in formalin
Severe, widespread vacuolation
Imprint cytology: foamy hepatocytes
Minimal inflammation or necrosis
Oil red O: positive for lipid in vacuoles

Question 13

tx for hepatic lipidiosis

Answer 13

Identify and treat underlying cause
Restore fluid and electrolyte imbalances (KCl, Phos, Mg)
Prolonged aggressive nutritional support -hallmark of tx
▪Esophagostomy or PEG tube usually indicated
Dietary supplements
Hepatoprotectives
Control vomiting
Minimize stress
Beware of Refeeding Syndrome

Question 14

methods of feeding for hepatic lipidiosis

Answer 14

Force or coax feeding (difficult)
Naso-gastric (NG)
Esophagostomy
Gastrostomy (PEG)
PPN or TPN (total parental nutrition0- nt the best

Question 15

best choice of food for hepatic lipidiosis

Answer 15

High in protein
Low in carbs

Question 16

px for hepatic lipidiosis

Answer 16

Good for most cats with tx (primary form)
Long term nutritional support REQUIRED!
Do not remove feeding tube too soon!!

Question 17

how to prevent hepatic lipidosis

Answer 17

Balanced diet
▪High protein
▪Low carbs
Regular exercise
Minimize stress
Environmental enrichment

Question 18

characteristics of inflammatory hepatobiliary dz in cats

Answer 18

• Tends to be more biliary in distribution
• Exception –hepatic lipidosis
• they are Acquired hepatobiliary disease in cats

Question 19

cause for inflammatory hepatobiliary dz

Answer 19

Likely due to relationship between common bile duct and major pancreatic duct

Question 20

Primary output for bile and pancreatic secretions in the cat

Answer 20

Major duodenal papilla

Question 21

Primary output for pancreatic secretions in the dog

Answer 21

• Minor duodenal papilla
• Often absent in the cat

Question 22

possible causes of inflamatory hepatobiliary dz

Answer 22

Ascension of substances (bacteria) from duodenum
Ascension of digestive enzymes from subclinical pancreatitis
Lesions in duodenum, pancreas, and biliary tract often seen concurrently (triaditis)

Question 23

Group of diseases characterized by inflammation of the biliary ducts

Answer 23

Cholangitis

Question 24

Group of diseases characterized by inflammation of the biliary ducts and surrounding liver tissue

Answer 24

Cholangiohepatitis

Question 25

common presentation for feline colangitis complex

Answer 25

Dehydration, icterus are common findings

Question 26

Neutrophilsin lumen/epithelium of bile ducts

Answer 26

* neutrophilic cholangitis

Question 27

describe acute nutrophilic cholangitis

Answer 27

Edema/inflammation (neutrophils) in portal areas

Question 28

describe chronic cholangitis

Answer 28

Neutrophils, lymphocytes, plasma cells Bile duct hyperplasia

Question 29

etiology for nutrophilic cholangitis

Answer 29

**Unknown** Ascending bacterial infection suspected May also be immune mediated

Question 30

pathophysiology for neutrophilic cholangitis

Answer 30

Commonly associated with IBD/pancreatitis Reflux of ascending bacteria during vomiting Also associated with EHBDO ▪Cholangitisand pancreatitis are most common causes

Question 31

dx for neutrophilic

Answer 31

Variable CBC findings (\< 33% of cases) ▪Neutrophilia(left shift), poikilocytosis Chemistry findings (mild to severe) ▪Increases in ALT, AST, ALP, GGT (may be absent) ▪Bilirubin increased in most cases ▪Increased cholesterol (EHBDO)

Question 32

ef. dx for neutrophilic cholangiits

Answer 32

* **_Definitive diagnosis –HISTOPATHOLOGY_** * Tru-Cut needle biopsy vs. laparoscopic biopsy vs. wedge biopsy * Obtain aerobic/anaerobic bacterial cultures

Question 33

tx for neutrophilic cholangitis

Answer 33

* Optimal treatment is unknown * Antibiotics are primary treatment (culture) * Aerobic/anaerobic bacteria of enteric origin * E. coli, Enterococcus, Clostridium * Empericabxcombination * Penicillin, fluoroquinolone, metronidazole * How long to treat –unknown, 4-6 weeks recommended

Question 34

explain how ursodiol works in tx for neutrophilic cholangitis

Answer 34

* Replaces “bad” hepatotoxic hydrophobic bile acids * Hepatoprotective * Anti-inflammatory * Immunomodulatory * Anti-fibrotic * Choleresis for bile sludge

Question 35

px for neutrophilic cholangitis

Answer 35

* Typically good (74% survival to discharge) * 29.3 months –median survival time * Chronic and acute cases * EHBDO have worse prognosis * 30 –40% die within a week of surgery

Question 36

primary hepatobiliary neoplasia in cat

Answer 36

* Primary hepatobiliary neoplasia rare in cat Cholangiocellular (bile duct) carcinoma Hepatocellular carcinoma

Question 37

metastatic neoplasia of the hepatobiliary

Answer 37

* Metastatic hepatic neoplasia more common Lymphoma Myeloproliferative disease MCT HSA

Question 38

dx for hepatobiliary neoplasia

Answer 38

* Abnormal liver enzymes common * May be absent if \< 75% hepatic involvement * Diagnosis –ultrasound and histopathology

Question 39

tx for hepatobiliary neoplasia

Answer 39

* Surgery * Chemotherapy

Question 40

px for hepatobiliary neoplasia

Answer 40

* Good for benign masses * Generally poor for malignancies (variable though) * Completely resected carcinomas –can have prolonged survival

Question 41

causes of Extraluminal compressive lesions of bile duct

Answer 41

* Neoplasia (biliary, pancreatic, duodenal) * Stricture * Diaphragmatic hernia * Congenital anomalies

Question 42

Intraluminal obstructive lesions of the bile duct

Answer 42

Cholelithiasis Inspissated bile Liver flukes

Question 43

key dx for extrahepatic bile duct obstruction

Answer 43

* **Ultrasound is KEYto diagnosis** * Dilation of gallbladder * Distended bile duct * Tortuous bile duct * Hepatomegaly

Question 44

tx for extrahepatic bile duct obstruction

Answer 44

Combined surgical and medical approach Fluids, stabilization Surgery to relieve obstruction Cholecystojejunostomy Cholecystoduodenostomy Liver biopsy Gallbladder biopsy Culture Stone analysis (cholelithiasis)

Question 45

signalment for congenital portosystemic shunts

Answer 45

Young cats Predispositions ▪\< 3 years old ▪Male persians, himalayan

Question 46

cs of congenital portosystemic shunts

Answer 46

**_Single, extrahepatic most common_** Hepatic Encephalopathy (worse after meals) Lower urinary tract signs if stones present (urates) PU/PD Copper colored eyes **_Ptyalism is consistent finding_** Underweight cats Prolonged anesthesia recovery Possible renomegaly Microhepatica

Question 47

lab abnormalities for portosystemic shunts

Answer 47

* Microcytosis * Low albumin * Low cholesterol * Low glucose * Low BUN (single digit) * Bilirubin is NORMAL * Liver enzymes normal or MILDLY increased * Biurate crystals on UA * Bile Acids –ELEVATED (often dramatic * most sensitive in detecting shunts.if BA is normal then there is no way they have shunts

Question 48

tx for congenital portosystemic shunts

Answer 48

Treatment Surgical ligation is treatment of choice Ameroid constrictor –gradual occlusion--mostly done

Question 49

complications for tx of congenital portosystemic shunts

Answer 49

* Portal hypertension / seizures (cats worse than dogs) * ▪Hemorrhage * Treat and stabilize HE prior to surgery

Question 50

labwork suggestive of acute liver dz

Answer 50

Increased ALT Increased AST * Often normal liver size and echogenicity

Question 51

tx for acute liver hepatopathy

Answer 51

* Prevent further absorption * Elimination of substance (if possible) * Aggressive supportive care * N-acetylcysteine for acetaminophen toxicity