Hepatobiliary diseases I Flashcards
(41 cards)
Difference between cat and dog pancreatic duct.
In cats, the pancreatic duct and the common bile duct combine to enter the duodenum together.
In dogs, the pancreatic duct and the CBD remain independent and enter the duodenum on their own.
This is clinically significant in cats because the combined duct can contribute to the development of triaditis. Bile duct inflammation can cause pancreatic inflammation and vice versa.
Also, dogs have an accessory pancreatic duct and only some cats have this.
Triaditis: pancreatitis, inflammatory bowel disease, and cholangiohepatitis.
Which duct comes off the gallbladder itself?
the cystic bile duct
(joins the hepatic bile duct, and they become the common bile duct)
Main diseases of the canine and feline biliary tracts with potential for an infectious etiology are (2)
neutrophilic cholangitis and cholecystitis (CC).
Neutrophilic cholangitis is the most common of the 4 recognized subtypes of cholangitis, occurring commonly in cats and less commonly in dogs.
cholangitis = bile duct system inflammation
cholecystitis = gallbladder inflammation
most common of the 4 recognized subtypes of cholangitis?
neutrophilic cholangitis is most common of the 4 recognized subtypes of cholangitis, occurring commonly in cats and less commonly in dogs. Due to different biliary tract anatomy.
neutrophilic
lymphocytic
chronic (e.g. caused by Platynosomum (liver fluke) infection)
destructive cholangitis
Histologically neutrophilic cholangitis/ cholecystitis looks like…
Neutrophilic periportal and intrahepatic bile duct inflammation with neutrophils in bile duct walls and lumina.
If the inflammation extends into the hepatic parenchyma -> its called cholangiohepatitis.
Acute cholecystitis sees- neutrophilic inflammation within the wall, epithelium, and lumen of the GB, which becomes mixed inflammation with chronicity.
Pathogenesis of Neutrophilic cholangitis/cholecystitis.
Ascending intestinal bacterial infection. Cumulatively due to GI dysbiosis, cholestasis, altered biliary tract anatomy, increased biliary tract pressure, altered immune function.
Confirmed bacteria in only about 69% of cases.
Bacteria most commonly identified in dog and cat neutrophilic cholangitis.
* Enteric organisms Escherichia coli, Enterococcus spp., Bacteroides spp., and Clostridium spp.
In acute cholecystitis, erosion or ulceration of the mucosa may occur.
The less common, severe cholecystitis can result in necrosis of the GB wall or emphysematous cholecystitis.
Clinical signs of Neutrophilic cholangitis/cholecystitis. (8)
Lethargy
Vomiting
Weight loss
Hyporexia/anorexia
Icterus (39% dogs and 63% cats)
Pyrexia (30-40%)
Abdominal pain (32% dogs and 24% cats)
Hepatomegaly (21%)
Laboratory findings in Neutrophilic cholangitis/cholecystitis. (3+4)
Hematology:
* Neutrophilia (36% cats/50% dogs)
* Left shift (34%cats/30% dogs)
* Anemia of chronic or inflammatory disease
Biochemistry:
* Increased liver enzyme activity and bilirubin.
* Variable increase in ALT (83% cats/91% dogs), ALP (58% cats/97% dogs),
AST (82% cats/81% dogs) and GGT.
* Hyperbilirubinemia (77% cats/75% dogs)
* Liver function markers (glu, urea, albumin, cholesterol) infrequently abnormal!
Normal liver enzymes and bilirubin DOES NOT exclude the disease.
Confirmation requires exclusion of other causes if suspected NC/CC.
cholangitis = bile duct system inflammation
cholecystitis = gallbladder inflammation
Ultrasonography in Neutrophilic cholangitis/cholecystitis.
Hyperechoic (cats 23%/dogs 31%),
normal liver echogenicty in cats (58%),
mixed echogenicity in dogs (31%).
Hepatomegaly (36%).
Thickened gallbladder wall (cats 29%/dogs 34%), distended common bile duct (cats 42%/dogs 33%), gallbladder sediment (cats 35%/dogs 51%).
Several studies, where no difference is found between normal liver and inflitrative disease!
Diagnosis of diffuse liver disease based solely on US and laboratory findings should be made with caution.
USe of FNA in Neutrophilic cholangitis/cholecystitis.
FNA (fine needle aspiration)
* Quick diagnostic information
* Cost-effective
* Complications uncommon (thrombocytes need to be >50 000 before proceeding with FNA)
Cons:
* Non-diagnostic samples occur.
* Misdiagnosis occurs.
* FNA does not reflect morpholgy of the parenchymal architecture. Studies show FNA 51% agreement with histology.
Biopsy and culture when Neutrophilic cholangitis/cholecystitis.
Cholecystocentesis (punction of the gallbladder)
* Cytology and bacteriology can be done on the punctate fluid (aerobic + anaerobic culture).
Biopsy and culture
* US-guided
* Laparoscopic vs surgical: Larger and higher quality sample sizes.
Requires general anesthesia, measuring clotting factors and thrombocyte count >80 000.
Increased risk of complications of course.
Tx of Neutrophilic cholangitis/cholecystitis.
Antibiotics ideally based on bacterial culture and sensitivity testing.
* Amoxicillin+clavulanic acid, ampicillin +/- metronidazole for 6-8 weeks
Supportive therapy
* Fluid therapy
* Appetite stimulants
* Antiemetics
* Pain management
* Feeding tube
* Liver supportive medications/food supplements (ursodeoxycholic acid (Ursochol), SAMe/S-adenosyl-L-methionine)
urso-de-oxy-cholic acid
SAMe can be taken orally, IM or by IV.
Potential causes of negative bacterial growth when sampling for Neutrophilic cholangitis/cholecystitis.
- Previous antimicrobial therapy
- Dysregulated immune response to bacteria or bacterial products, without colonization.
How to treat in these cases?
* Assess response to antimicrobial therapy
* Ursodeoxycholic acid and antioxidants (SAMe) theoretically indicated.
* Corticosteroids in cats with refractory disease.
Based on the theory that biliary inflammation reflects ongoing, up-regulated immune responses to bacteria/bacterial proteins.
urso-de-oxy-cholic acid
Explain antioxidant (SAMe) S-adenosyl-L-methionine.
an antioxidant with hepatoprotective properties, particularly in the management of liver disorders such as cholangitis, hepatic lipidosis, and chronic hepatitis.
SAMe acts by enhancing the synthesis of glutathione, a critical antioxidant in liver cells, thereby protecting hepatocytes from oxidative damage and supporting liver function.
It may also have anti-inflammatory and antifibrotic effects.
In veterinary use, SAMe is typically administered orally, and IV administration is not common practice. This is mainly because SAMe is unstable in aqueous solutions.
SAMe (S-adenosyl-L-methionine) is not an amino acid itself, but it is derived from the essential amino acid methionine. In the body, methionine combines with ATP to form SAMe, which then acts as a key methyl donor in various biochemical reactions. SoSAMe is a methylating agent.
Uncommon biliary tract conditions (2)
Toxoplasma gondii diagnosed in immunosuppressed cats with cholecystitis.
Helicobacter pylori-specific DNA fragments detected by PCR analysis of bile from cats with lymphocytic cholangitis.
Currently insufficient information to determine if these organisms are pathogenic in this settings.
Describe Lymphocytic cholangitis.
1 of the 4 subtypes of cholangitis.
Chronic progressive inflammation centered in the biliary tree in CATS (not dogs).
Infiltration of small lymphocytes into portal areas with variable portal fibrosis and biliary hyperplasia.
- Any age can be affected
- No breed or sex predisposition
Etiology:
* Possible immune-mediated
* Based on lymphocyte markers and histological features, e.g., bile duct destruction.
Possible trigger from bacterial infection.
In most cats evidence does not support a role of infectious agents.
Clinical signs of Lymphocytic cholangitis.
Gradual weight loss over months to years.
* Polyphagia or anorexia
* Vomiting
* Lethargy
* PU/PD
Poor body condition
Often bright on physical examination
In contrast to neutrophilic cholangitis:
* Jaundice, hepatomegaly, ascites may be present.
Laboratory findings in Lymphocytic cholangitis.
Marked hyperglobulinemia
Mild elevations of ALT and ALP activity
Ultrasonographic findings in Lymphocytic cholangitis.
Ascites, hepatomegaly, and/or lymphadenomegaly may be identified.
Liver echogenicity may be normal, increased, decreased, or heterogeneous.
Gallbladder and extra-hepatic biliary tree abnormalities are uncommon, In contrast to neutrophilic cholangitis.
Normal abdominal U/S DOES NOT exclude a diagnosis of lymphocytic cholangitis!
Diagnosis of lymphocytic cholangitis requires?
Liver biopsy is required for the definitive diagnosis.
The most consistent histologic features include infiltrating aggregates of small lymphocytes into the portal region, portal fibrosis, and biliary ductular proliferation.
Treatment and prognosis of lymphocytic cholangitis.
Immunosuppressive doses of prednisolone and/or ursodeoxycholic acid.
Supportive care
* E.g., therapeutic abdominocentesis
Treatment with antibiotics is not indicated unless supported by bacterial culture and sensitivity testing.
Prognosis with treatment is good in some reports.
E.g., resolution of ascites and median and mean survival times of 26 to 36 months.
Lymphocytic cholangitis Suspected disease, but
Owner doesn’t want to have biopsies which would be necessary for confirmation of diagnosis. What do you do?
Recommendation to at least exclude bacterial inflammation (so culture from liver/biliary tract).
Often treated with antibiotics until culture, cytology/histology results are back. Assess the response to antibiotics until results are back.
When infectious causes are excluded you can start with prednisolone. Gradual dose tapering if possible.
If no response to prednisolone, consider small cell lymphoma.
Next, Try Azathioprine, cyclosporine (in case its just prednisolone resistant disease).
If the Owner doesn’t want to do ANY sampling.
Start with broad spectrum antibiotics +/- ursodeoxycholic acid, and assess the response.
If No improvement within 1-2 weeks -> start with prednisolone.
Case: 10y 5m, DSH, FN
Indoor, deworming once a year, not vaccinated.
Increased appetite during 1-2 years, weight loss.
Vomiting hairballs twice a week.
BCS 3/9. Breathing normal. HR 160x/min, regular, no murmur. Temp 37,9. Mild icterus. MM moist. Palp lnn WNL. Soft abdomen on palpation, no pathologies detected. BP 139/113 (121) - normotensive.
Diagnosis?
Tx?
cholangiohepatitis
Treatment at first:
SAMe (S-adenosyl-L-methionine) and ursodeoxycholic acid
Later tx:
added prednisolone
Increased cobalamine, folic acid can indicate? (4)
incidental,
neoplasia,
liver disease,
dysbiosis/IBD/EPI
