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sam dr green > feline hepatobiliary disorders > Flashcards

feline hepatobiliary disorders Flashcards

1
Q

common clinical presentation of feline hepatobiliary dz

A
  • Clinical signs very similar for most feline hepatobiliary diseases
  • Jaundice & hepatomegaly –most common findings
  • n.b. nt the case with dogs
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2
Q

Yellow cat…………..think:

A
  • Hepatic Lipidosis
  • Cholangitis / Cholangiohepatits
  • FIP
  • Lymphoma (FeLV)
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3
Q

t common liver dz in cats

A
  • 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
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4
Q

role of obesity in hepatic lipidosis in cats

A

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

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5
Q

predisposing factors for hepatic lipidiosis

A

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%)
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6
Q

signalment for hepatic lipidiosis

A

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

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7
Q

cs for hepatic lipidiosis

A

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

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8
Q

physical findings in cats with hepatic lipidiosis

A
  • Jaundice (70%)
  • Hepatomegaly
  • Muscle wasting
  • Dehydration
  • Seborrhea
  • Pallor
  • Ventroflexion of head and neck
    • ▪Hypokalemia, hypophosphatemia, thiamine
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9
Q

chem panel for feline hapatic lipidiosis

A

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

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10
Q

adv of doing fna with hepatic lipidiosis

A

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)

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11
Q

when is cytology helpful with hepatic lipidiosis

A

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

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12
Q

bx findings for hepatic lipidiosis

A

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

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13
Q

tx for hepatic lipidiosis

A

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

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14
Q

methods of feeding for hepatic lipidiosis

A

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

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15
Q

best choice of food for hepatic lipidiosis

A

High in protein
Low in carbs

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16
Q

px for hepatic lipidiosis

A

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

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17
Q

how to prevent hepatic lipidosis

A

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

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18
Q

characteristics of inflammatory hepatobiliary dz in cats

A
  • Tends to be more biliary in distribution
  • Exception –hepatic lipidosis
  • they are Acquired hepatobiliary disease in cats
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19
Q

cause for inflammatory hepatobiliary dz

A

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

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20
Q

Primary output for bile and pancreatic secretions in the cat

A

Major duodenal papilla

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21
Q

Primary output for pancreatic secretions in the dog

A
  • Minor duodenal papilla
  • Often absent in the cat
22
Q

possible causes of inflamatory hepatobiliary dz

A

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

23
Q

Group of diseases characterized by inflammation of the biliary ducts

A

Cholangitis

24
Q

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

A

Cholangiohepatitis

25
Q

common presentation for feline colangitis complex

A

Dehydration, icterus are common findings

26
Q

Neutrophilsin lumen/epithelium of bile ducts

A
  • neutrophilic cholangitis
27
Q

describe acute nutrophilic cholangitis

A

Edema/inflammation (neutrophils) in portal areas

28
Q

describe chronic cholangitis

A

Neutrophils, lymphocytes, plasma cells
Bile duct hyperplasia

29
Q

etiology for nutrophilic cholangitis

A

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

30
Q

pathophysiology for neutrophilic cholangitis

A

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

31
Q

dx for neutrophilic

A

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)

32
Q

ef. dx for neutrophilic cholangiits

A
  • Definitive diagnosis –HISTOPATHOLOGY
    • Tru-Cut needle biopsy vs. laparoscopic biopsy vs. wedge biopsy
  • Obtain aerobic/anaerobic bacterial cultures
33
Q

tx for neutrophilic cholangitis

A
  • 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
34
Q

explain how ursodiol works in tx for neutrophilic cholangitis

A
  • Replaces “bad” hepatotoxic hydrophobic bile acids
  • Hepatoprotective
    • Anti-inflammatory
    • Immunomodulatory
    • Anti-fibrotic
  • Choleresis for bile sludge
35
Q

px for neutrophilic cholangitis

A
  • 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
36
Q

primary hepatobiliary neoplasia in cat

A
  • Primary hepatobiliary neoplasia rare in cat

Cholangiocellular (bile duct) carcinoma
Hepatocellular carcinoma

37
Q

metastatic neoplasia of the hepatobiliary

A
  • Metastatic hepatic neoplasia more common

Lymphoma
Myeloproliferative disease
MCT
HSA

38
Q

dx for hepatobiliary neoplasia

A
  • Abnormal liver enzymes common
    • May be absent if < 75% hepatic involvement
  • Diagnosis –ultrasound and histopathology
39
Q

tx for hepatobiliary neoplasia

A
  • Surgery
  • Chemotherapy
40
Q

px for hepatobiliary neoplasia

A
  • Good for benign masses
  • Generally poor for malignancies (variable though)
  • Completely resected carcinomas –can have prolonged survival
41
Q

causes of Extraluminal compressive lesions of bile duct

A
  • Neoplasia (biliary, pancreatic, duodenal)
  • Stricture
  • Diaphragmatic hernia
  • Congenital anomalies
42
Q

Intraluminal obstructive lesions of the bile duct

A

Cholelithiasis
Inspissated bile
Liver flukes

43
Q

key dx for extrahepatic bile duct obstruction

A
  • Ultrasound is KEYto diagnosis
    • Dilation of gallbladder
    • Distended bile duct
    • Tortuous bile duct
    • Hepatomegaly
44
Q

tx for extrahepatic bile duct obstruction

A

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

45
Q

signalment for congenital portosystemic shunts

A

Young cats
Predispositions
▪< 3 years old
▪Male

persians, himalayan

46
Q

cs of congenital portosystemic shunts

A

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

47
Q

lab abnormalities for portosystemic shunts

A
  • 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
48
Q

tx for congenital portosystemic shunts

A

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

49
Q

complications for tx of congenital portosystemic shunts

A
  • Portal hypertension / seizures (cats worse than dogs)
  • ▪Hemorrhage
  • Treat and stabilize HE prior to surgery
50
Q

labwork suggestive of acute liver dz

A

Increased ALT
Increased AST

  • Often normal liver size and echogenicity
51
Q

tx for acute liver hepatopathy

A
  • Prevent further absorption
  • Elimination of substance (if possible)
  • Aggressive supportive care
  • N-acetylcysteine for acetaminophen toxicity
52
Q
A

sam dr green (10 decks)

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