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ACVS Phase I Master Deck *Use This* > Chapter 96: Hepatic Vascular Anomalies > Flashcards

Chapter 96: Hepatic Vascular Anomalies Flashcards

1
Q

List the (4) tributaries of the portal vein and what they drain:

A
  • Cranial mesenteric vein (largest tributary, SI)
  • Caudal mesenteric vein (colon +proximal rectum)
  • Splenic vein (spleen and stomach via left gastric vein)
  • Gastroduodenal vein (pancreas, duodenum, stomach (right gastric v) - dogs only)
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2
Q

How many hepatic veins do dogs usually have?
Which is the largest?

A
  • 5-8 hepatic veins
  • The left hepatic vein is the largest and most cranial
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3
Q

What embryonic vessels give rise to the hepatic sinusoids, hepatic portion of the vena cava, and the portal vein?

A

The vitelline vessels.

The portal v. is an anastomosis of the right and left vitelline vv.

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4
Q

What is the ductus venosus?

A

A venous shunt between the left umbilical vein and the cranial segment of the right vitelline vein.

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5
Q

What shunts most likely arise from patency of the ductus venosus?
- When is functional and structural closure expected?
- In which breed can this be delayed?

A

Left-sided intrahepatic PSS
- Functional closure within 2-6 days after birth
- Structural closure within 3 weeks after brith
- Delayed in Irish Wolfhounds - 23% still open at 6 days but all close by 9 days

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6
Q

What substances promote ductus venosus closure?
What substances slow it down?

A

Promote: Endothelin, cytochrome P-450, thromboxane A2

Slows down: Prostaglandin F1alpha, Prostaglandin E2 - cause relaxation of the vessel, modulating the effects of endothelin

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7
Q

What are the three broad categories of hepatic vascular disease?

A
  1. Congenital PSS
  2. Disorders associated with abnormal hepatic bloodflow or portal hypertension (called PVH or primary hypoplasia of portal vein, used to be MVD)
  3. Disturbances in portal outflow
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8
Q

What % of congenital PSS are extrahepatic?

A

66-75%

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9
Q

Where do acquired shunts most commonly enter the systemic circulation?
What are some causes of acquired shunts?

A

At the renal vein or the vena cava near the kidneys

Causes:
- Hepatic fibrosis (cirrhosis)
- PVH with portal hypertension
- Hepatic AV malformations

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10
Q

What % of dogs and cats with PVH-MVD have a concurrent congenital PSS?

A

Dogs 58%
Cats 87%

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11
Q

What breeds are overrepresented for PVH-MVD?

A

Cairn Terrier, Maltese, Yorkie

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12
Q

How much liver function needs to be lost for hepatic encephalopathy to occur?

A

70%

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13
Q

List the various toxins inplicated in hepatic encephalopathy and their mechanisms

A

It’s a long chart. Know that there are 20 and ammonia is #1 and it is excitotoxic (increases glutamate release -> overstimulates NMDA receptors - >seizures, eventual coma)

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14
Q

What usually happens to ammonia in the liver?

A

Converted to urea and glutamine in the urea cycle

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15
Q

What is the role of lactulose in medical management?

A
  • Promotes acidification of colonic contents, resulting in entrapment of luminal ammonia
  • Decrease in colonic bacterial numbers
  • Osmotic effect reduces fecal transit time - gets it out quicker.
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16
Q

What % of dogs will have AV malformations in 2 lobes?

A

20%

17
Q

What medication should patients with intrahepatic shunts recieve for the rest of their lives?

A

Omeprazole to reduce the risk of GI ulceration
- With addition of lifelong antacids, mortality dropped from 25% to 3.2%

18
Q

What percentage of all dogs have congenital portosystemic shunts?

A

0.18%

19
Q

What % of PSS are acquired?

A

20%

20
Q

What is the new term for MVD?

Can MVD be distinguished from PSS on biopsy?

A

Portal vein hypoplasia with portal hypertension OR idiopathic noncirrhotic portal hypertension.

NO - they look the same. Must rely on imaging and response to surgery.

21
Q

What is hepatic AV malformation? What is the prognosis?

A

Rare condition of multiple high arterial pressure - low venous pressure communications in the liver. Congenital.

Prognosis poor.

22
Q

20 different compounds are implicated in hepatic encephalopathy. What (6) things do they generally cause?

A

Impede neuronal function
Cause cell swelling
Impede membrane pumps and ion channels
Elevate intracellular calcium
Depress electrical activity
impair cerebral function

23
Q

What are the metabolic derangements of hepatic insufficiency?

What can make them worse?

A

Hypoglycemia
Dehydration
Hypokalemia
Alkalemia

Worse with NSAIDs, high protein meals, GI ulcers, use of stored blood for transfusion, drugs (benzos, etc)

24
Q

Hepatic encephalopathy occurs with what % of liver function loss?

A

70%

25
Q

The venous system of the liver is derived from what three embryologic veins?

A

Umbilical
Vitelline
Cardinal

26
Q

In what % of dogs does the left portal vein also supply blood to the dorsal part of the right lateral lobe near the porta hepatis?

A

60%

27
Q

The right and left supracardinal veins give rise to what veins?

A

Right: Azygous v.
Left: Hemiazygous v.

28
Q

Describe the most common presentation/morphology of congenital portosystemic shunts?

A

As a single intra- or extrahepatic vessel that provides direct vascular communication between the portal venous supply and the systemic venous circulation, bypassing the liver.

29
Q

Name the six forms of PSS in Tobias’ chart:

A

A. Portocaval
B. Portoazygous
C. Gastrocaval
D. Splenocaval
E. Left gastric, cranial/caudal mesenteric, or gastroduodenal to cava
F. Combinations

30
Q

Portocaval and portoazygous shunts occur through development of communications between which embryologic vein systems?

A

Cardinal and vitelline

31
Q

True or false? More blood flow through a shunt results in clinical signs at a later age?

A

False - earlier age.

32
Q

Where does the left hepatic vein terminate?

A

Just caudal to the diaphragm and is 1/2 covered in liver near left triangular ligament.

33
Q

Bile ducts and branches of the hepatic artery are usually where in relation to the portal vein?

A

Ventral to portal vein.

ACVS Phase I Master Deck *Use This* (88 decks)

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