Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Surgery I > Hepatobiliary > Flashcards

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical signs associated with severe hepatic parenchymal disease

A
  • Ascites, abdominal distension
  • Hepatic encephalopathy
  • Icterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the ddx for a liver mass?

A
  • Abscess
  • Neoplasia
  • Cyst
  • Liver lobe torsion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical signs of hepatocellular injury?

A
  • Asymptomatic
  • Nonspecific signs
  • Similar signs as hepatic disease
  • Icterus
  • Signs of shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Why would the biliary tract rupture?

A
  • Disease gallbladder/ducts
  • Trauma
26
Q

How is biliary tract rupture diagnosed?

A
  • Abdominal US
  • Fluid analysis
27
Q

What is the prognosis of a ruptured biliary tract?

A
  • Bile peritonitis
    • usually sterile - 30% mortality
    • Septic bile peritonitis - 70% mortality
28
Q

What is the pathogenesis of a porto-systemic shunts?

A
  • 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
Q

What are the clinical signs of Porto-systemic Shunts?

A
  • 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
Q

How are portosystemic shunts diagnosed?

A
  • 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
Q

What is the treatment for porto-systemic shunts?

A
  • Surgery
  • Medical Management
    • portal venous hypoplasia, multiple acquired shunts
32
Q

What is a common complication during surgery to fix a porto-systemic shunt?

A

Occluding shunt too quickly ⇢ fatal portal hypertension

33
Q

What are the common complications following surgery to fix a porto-systemic shunt?

A
  • 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
Q

What is the long term management for porto-systemic shunts?

A
  • 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
Q

Why do animals with porto-systemic shunts develop urate urolithiasis?

A

lack of urate metabolism by the liver

36
Q

What is portal venous hypoplasia?

A
  • a congenital type of shunting
    • occurs on a microvascular level
  • Numerous microscopic shunts at the level of the portal triads
37
Q

What is portal venous hypoplasia?

A
  • a congenital type of shunting
    • occurs on a microvascular level
  • Numerous microscopic shunts at the level of the portal triads
38
Q

How are porto-systemic shunts managed medically?

A
  • 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

Surgery I (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions