CC: Portosystemic Shunts (PSS) Flashcards

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1
Q

What’s wrong with Seamus? What behavior was he exhibiting?

A

He has a Portosystemic Shunt.

Depression, Disorientation, Star-gazing!, Head Pressing!, Blind, Failure to Thrive, Vomits!, poor appetite, Ataxia, Pollakiuria.

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2
Q

What were his CBC results?

A

Anemic, Low hematocrit (anemic), Microcytic (small RBCs), normochromic (normally colored RBCs)

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3
Q

What were his Urinalysis results?

A

SG: 1.010 (little dilute)

Ammonium Biurate crystals (ammonia + uric acid)

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4
Q

What were the biochemical profile results?

A

Hypoglycemia (liver or kidney)
Hypoalbuminemia (liver or kidney)
Hypocholesterolemia (liver or kidney)
Low BUN (liver)

4 impaired functions of the liver, scream liver problem

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5
Q

What were the results of liver function tests?

A

High pre- and post-prandial Bile Acids

Hyperammonemia

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6
Q

If you have a PSS what might be affected?

A

Detoxification, Plasma Proteins, Clotting Factors, Delivery of trophic factors to the liver, decreased protein production, decreased metabolism of nutrients, generalized liver failure, toxin clearance decreased (drugs), altered CNS function (ammonia to the brain)

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7
Q

How does ammonia cause encephalopathy?

A

Ammonia –> increase pH!!! –> fucks everything up

Also inhbits glutaminase –> decreased glutamate (product of glutaminase) –> decreased excitation

Increases GABA, don’t exactly understand how

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8
Q

How does the impaired liver fucntion not sucking up aromatic AAs affect brain function?

A

creates False Neurotransmitters: Tyrosine driven to Tyramine (prevents Dopa, NorE, Epi synthesis)

Fit in the receptor but don’t allow any functionality – blocking catecholamine function

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9
Q

What are clinical signs of hepatic encephalopathy?

A

Ataxia, Weakness, Stupor, Head Pressing, Circling, Star-gazing, disorientation, bizarre behavior, seizure/coma

often symptoms appear worse after meals

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10
Q

What are precipitating factors of hepatic encephalopathy?

A

High Protein Meal and Gastrointestinal hemorrhage will Increase Ammonia generation

Constipation will increase amount of time for gut bacteria to act on urea to increase Ammonia generation

Electrolytes (hypokalemia) and Alkalosis (vomiting) will Increase blood pH = more ammonia (NH4 would rather be NH3 in more alkalotic conditions)

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11
Q

Diagnosing PSS: Classic Laboratory Abnormalities

A
Anemia
Hypoglycemia
Hypoalbuminemia
Hypocholesterolemia
Low BUN
Increased Bile Acids, fasting ammonia
\+/- increased liver enzyme activities
\+/- Urate Crystals in urine
\+/- Prolonged clotting times
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12
Q

Diagnosing PSS: How do confirm diagnosis of PSS?

A
Noninvasive:
Abdominal radiographs
Abdominal ultrasound
Nuclear imaging (scintigraphy)
CT or MRI

Invasive:
Portovenography

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13
Q

(PSS Treatment) Why would you use lactulose for treating a PSS?

A

Lactulose is for acidifying the colon - gut bacteria break it down to organic acids–> converts NH3 to NH4 which cannot pass back into body –> shit it out (may cause animal to shit their brains out)

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14
Q

(PSS Treatment) How do antibiotics help treat PSS?

A

decrease number of ammonia producing bacteria

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15
Q

(PSS Treatment) How can you decrease substrate for NH3 production in a PSS patient?

A

Low Protein Diet and/or Control GI Hemorrhage

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16
Q

(PSS Treatment) What kind of surgical intervention is available for PSS?

A

Ameroid Constrictor - band around shunt, gradually absorbs water and constricts shunt until shut off entirely

Celophane band - gradually absorbs water and constricts shunt until shut off entirely

17
Q

What’s the prognosis with surgery?

A

Extra-hepatic - good 85%-94%

Intra-hepatic - alright, but tough 50%-89%

18
Q

What’s the prognosis with medical treatment?

A

Depends on the extent of the shunt, clinical signs, and biochemical derangements.
HE present - BAD - 50% euthanized within a year
35% may live for 3-8 years

19
Q

Is there a difference between surgery and medical treatment for PSS with regards to prognosis?

A

No. The medical journals differ based on whether the author is a surgeon or internist.