Hepatobiliary Flashcards

1
Q

OBJ: Given a patient with a specific hx and/or PE indicative of hepatobiliary disease, be able to determine ddx and create a rational diagnostic plan

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2
Q

OBJ: Be able to create a rational pre-operative and post-operative plan for animals ndergoing hepatobiliary surgery

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3
Q

OBJ: Be able to discuss indications for specific surgical techniques for hepatobiliary disease

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4
Q

PBJ: Be able to discuss complications and prognosis of common surgical hepatobiliary diseases

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5
Q

What are the clinical sing of hepatic parenchymal disease

A
  • Lethargy, anorexia, weight-losss
  • Vomiting/Diarrhea
  • Ascites, abdominal distension - only if severe
  • Collapse/weakness/shock
  • PU/PD
  • Hepatic encephalopathy - only if severe
  • Icterus - only if severe
  • Asymptomatic
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6
Q

What are the clinical signs associated with severe hepatic parenchymal disease

A
  • Ascites, abdominal distension
  • Hepatic encephalopathy
  • Icterus
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7
Q

What findings are seen on CBC/Chemistry with hepatic parenchymal disease?

A
  • Signs of ongoing injury
  • Cholestasis
  • Decreased functional liver capacity (end-stage liver)
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8
Q

What are the ddx for hepatocellular injury?

A
  • Benign (vacuolar hepatopathy, extramedullary hematopoiesis)
  • Secondary effect (trauma, shock)
  • Toxic/infectious
  • chronic active hepatitis
  • Immune-mediated, copper-associated
  • Hepatic lipidosis (cat)
  • Hepatic parenchymal mass/disease
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9
Q

What diagnostic tests can be used to narrow down the cause of hepatocellular injury?

A
  • Abdominal radiographs
  • Abdominal US
  • CT Scan (Sx planning)
  • FNA, Biopsy, Fluid analysis
  • Staging
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10
Q

What are the ddx for a liver mass?

A
  • Abscess
  • Neoplasia
  • Cyst
  • Liver lobe torsion
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11
Q

What are the signs of a hepatic abscess?

How are they diagnosed?

Treatment?

A
  • Vague clinical signs to sepsis
    • Elevated ALP and left shift neutrophilia
  • Dx: Abdominal US and cytology/culture
    • mixed echogenicity +/- gas
  • Tx:
    • Medical (antibiotics)
    • Surgical (lobectomy)
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12
Q

What is the most common neoplasia of the liver?

What is the common primary neoplasia of the liver in dogs? cats?

how are they diagnosed?

A
  • Most common: metastatic
  • Dogs: Hepatocellular carcinoma
    • MST > 1400 days for massive form
    • US and Cytology useful
  • Cats: Biliary Cystadenoma
    • ‘cysts’ with anechoic fluid on ultrasound
    • Cytology less useful unless solid mass
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13
Q

What are the clinical signs of hepatocellular injury?

A
  • Asymptomatic
  • Nonspecific signs
  • Similar signs as hepatic disease
  • Icterus
  • Signs of shock
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14
Q

What diagnostic tests can be done to differentiate the causes of hepatocellular injuries?

A
  • Blood work (increased Bilirubin/ALP)
  • Coagulation disturbances more common
  • Abdominal radiographs
  • Abdominal US
  • Fluid analysis (bilirubin 2x higher than in serum)
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15
Q

What are the differentials for elevated cholestatic enzymes?

A
  • Pre-hepatic: hemolysis
  • Hepatic: severe parenchymal disease
  • Post-hepatic: Gall bladder mucocele, Extrahepatic biliary tract obstruction, Biliary tract rupture
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16
Q

What causes Gallbladder mucocele?

A
  • Cystic mucosal hyperplasia
    • Increased mucus can lead to duct obstruction or gallbladder rupture
  • Hyperadrenocorticism, Hypothyroidism
17
Q

How is a gallbladder mucocele diagnosed?

A
  • US - ‘classic’ stellate/kiwi appearance
18
Q

What breeds are predisposed to gallbladder mucoceles?

A
  • Shelties
  • cocker spaniels
19
Q

What is the treatment for a Gallbladder mucocele

A
  • Cholecystectomy > medical management
  • Emergent/urgent for symptomatic/icteric dogs, bile peritonitis/ruptured gallbladder, distended bile ducts
20
Q

What is the prognosis for treatment of gallbladder mucoceles?

A
  • Post-operative mortality ~20-30%
  • 5% complication rate for asymptomatic dogs
21
Q

How is a Cholecystectomy completed?

A
  1. Bile duct catheterized and flushed
  2. Gallbladder dissected free of liver
  3. Cystic duct ligated
  4. Can be done laparoscopically
22
Q

What are extrahepatic causes of biliary tract obstruction?

A
  • Pancreatitis/Cholangiohepatitis (cats)
  • neoplasia
  • choleliths
23
Q

How is biliary tract obstruction diagnosed

A

Abdominal US

24
Q

What is the treatment for biliary tract obstructions?

A
  • Surgery
    • remove obstruction if possible
    • +/- place a choledocal stent
25
Why would the biliary tract rupture?
* Disease gallbladder/ducts * Trauma
26
How is biliary tract rupture diagnosed?
* Abdominal US * Fluid analysis
27
What is the prognosis of a ruptured biliary tract?
* Bile peritonitis * usually sterile - 30% mortality * Septic bile peritonitis - 70% mortality
28
What is the pathogenesis of a porto-systemic shunts?
* Congenital - typically single shunting vessels * extrahepatic (outside liver) - small dogs * Intrahepatic (within hepatic parenchyma) - large dogs * Acquired * multiple small shunts due to portal hypertension * often adjacent to the kidneys
29
What are the clinical signs of Porto-systemic Shunts?
* Hepatic encephalopathy * head pressing, circling, stupor after eating * Urate urolithiasis (radiolucent) * Decreased growth * Intermittent vomiting * Hypersalivation “ptyalism” (cats) * Copper colored iris (cats) * Seizures * PD/PU * Asymptomatic
30
How are portosystemic shunts diagnosed?
* CBC/Chemistry * Decreased functional liver capacity * low BUN, albumin, cholesterol, and glucose * With/without elevations in ALT, AST, ALP * UA - urate crystals * Bile acid/ammonia - prolonged * Abdominal imaging: * US, CT, MRI, Portography (IV contrast in portal vein tributary)
31
What is the treatment for porto-systemic shunts?
* Surgery * Medical Management * portal venous hypoplasia, multiple acquired shunts
32
What is a common complication _during_ surgery to fix a porto-systemic shunt?
Occluding shunt too quickly ⇢ **fatal portal hypertension**
33
What are the common complications _following_ surgery to fix a porto-systemic shunt?
* Hypoglycemia - 44% of dogs * Portal hypertension - 2-14% * Shock, abdominal pain, abdominal distension, diarrhea, vomiting * Seizures - up to 20% * often not responsive to diazepam
34
What is the long term management for porto-systemic shunts?
* Recheck bloodwork/bile acids in 6 weeks * if normal ⇢ gradually discontinue medical management * If elevated ⇢ wait additional 6 weeks, then repeat * Chronically elevated bile acids - 40% of dogs * PVH-MVD * Acquired shunt * Incomplete attenuation
35
Why do animals with porto-systemic shunts develop urate urolithiasis?
lack of urate metabolism by the liver
36
What is portal venous hypoplasia?
* a congenital type of shunting * occurs on a microvascular level * **Numerous microscopic shunts at the level of the portal triads**
37
What is portal venous hypoplasia?
* a congenital type of shunting * occurs on a microvascular level * **Numerous microscopic shunts at the level of the portal triads**
38
How are porto-systemic shunts managed medically?
* Moderatly protein restricted diet * mostly branched chain AA * Decreases the production of ammonia⇢ ⇣neurologic signs * Lactulose * trap ammonia in the lumen of the intestines in th form or ammonium * Antibiotic (amoxicillin/metronidazole) * decrease ammonia producing GI flora * Gastroprotectants - Intrahepatic shunts * increased risk of GI ulceration