PSS and PVH

Question 1

What historical findings can differentiate between an infectious/toxic cause of hepatic dysfunction vs. PSS?

Answer 1

(Chronicity, usually infectious/toxin is acute vs. PSS is chronic; also having a hx of exposure to an infectious agent/toxin)

Question 2

What is provided to the liver via the portal vein?

Answer 2

(Trophic hormones, nutrients/oxygen, bacterial products, and intestinal derived toxins)

Question 3

What is ammonia converted to in the liver?

Answer 3

(Urea, this is why BUN low with PSS/liver dysfunction)

Question 4

What can occur secondarily to the decreased delivery of trophic factors (such as insulin and glucagon) to the liver that is associated with PSS?

Answer 4

(Poor hepatic development, decreased protein production, alter metabolism (of fats, proteins, and carbs), and hepatic failure)

Question 5

What effects does ammonia have on the brain?

Answer 5

(Induces an imbalance between the inhibitory and excitatory neurotransmitters of the brain (more GABA primarily), causes edema (usually acute cases but can be see in chronic), and increase pro-inflammatory cytokines levels)

Question 6

What clinical signs can be associated with HE?

Answer 6

(Ataxia, weakness, stupor, head pressing, circling, star gazing, disorientation, bizarre behavior, seizures, coma; sometimes can be worse after meals)

Question 7

For the following factors, explain how they can precipitate signs of HE:

• High protein meal, GI hemorrhage
• Constipation
• Hypokalemia, alkalosis

Answer 7

• High protein meal, GI hemorrhage (Increased NH3 generation by metabolism of excess protein)
• Constipation (Longer GI transit time = bacteria have more fuel to make more NH3)
• Hypokalemia, alkalosis (Increased blood pH, NH3 happier in basic environment compared to ammonium so will be more ammonia)

Question 8

(T/F) There is no such thing as an acquired intrahepatic shunt.

Answer 8

(T, can only acquire extrahepatic shunts secondary to end stage liver dz)

Question 9

How does the presentation differ for an animal with PSS vs. PVH?

Answer 9

(PSS → younger, more severe clinical signs and biochemical abnormalities; PVH → older, typically incidental finding on routine blood work, less severe clinical signs)

Question 10

Why is the anemia associated with PSS typically microcytic?

Answer 10

(Liver produces iron carrier proteins = microcytic)

Question 11

How can a diagnosis of PSS be confirmed?

Answer 11

(Imaging (CT is best) and/or measuring protein C activity)

Question 12

(T/F) Protein C testing can be used to differentiate between PSS and PVH.

Answer 12

(T, typically < 70% in PSS and > 70% in PVH)

Question 13

What is the main medical treatment for PSS?

Answer 13

(Lactulose (traps ammonia in colon as ammonium, modulates bacterial flora (?), and is a cathartic); can also do antibiotics, cleansing enemas, low protein diets)

Question 14

Gradual occlusion of PSSs via surgery is necessary to prevent what from occurring secondarily?

Answer 14

(Portal hypertension)