Liver Flashcards

1
Q

Kidney is to nephron as liver is to

A

Lobule (acinus)

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2
Q

How much lymph is made in the liver and where is it made?

A

About 50% of the body’s lymph is made there by hepatocytes, and drain into the space of Disse before emptying into the lymphatic duct

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3
Q

Hemoglobin to Bilirubin metabolism

A
  • Old RBCs are cleared by the spleen
  • In the spleen = Hgb -> Heme -> Bilirubin (Unconjugated)
  • Unconjugated bilirubin is lipophilic and neurotoxic. Travels bound to albumin to liver.
  • Liver conjugates it with glucuronic acid to increase it’s water solubility
  • This is now CONJUGATED bilirubin and is excreted in the bile
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4
Q

PT and liver function

A

Good for detecting ACUTE liver injury.

This is because factors V and VII have short 1/2 lives (

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5
Q

Albumin and liver function

A

Not very specific for liver disease because many things can cause albumin levels to decrease
- Not good indicator of acute liver disease (1/2 life of albumin is 21 days)

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6
Q

AST/ALT ratio > ___ suggests cirrhosis or alcoholic liver disease

A

2

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7
Q

This is the MOST sensitive lab indicator of biliary tract obstruction

A

5-NT

5-NT > GGTP > AP

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8
Q

In hepatocellular injury, will you see a rise in conjugated or unconjugated bilirubin

A

Conjugated

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9
Q

This clotting factor is made by the liver but NOT by hepatocytes

A

Factor VIII

It’s made by sinusoidal cells

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10
Q

How liver handles Tylenol

A
  • Tylenol produces a toxic metabolite called NAPQI
  • This is normally conjugated with glutathione so be excreted in the bile
  • In this case, all the glutathione gets used up and NAPQI starts harming the liver
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11
Q

Risk factors for halothane hepatitis

A

Fat females > 40 with multiple exposures.

  • Genetics
  • CYP2E1 induction (from alcohol, ionized, and phenobarbital)
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12
Q

How does alcohol affect the liver

A

Impairs fatty acid metabolism, head to fat buildup within the liver –> hepatomegaly

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13
Q

Why is propranolol good in liver failure?

A

It’s a NONSELECTIVE BB
- B1 = decreased CO
- B2 = splanchnic vasoconstrition
Remember that splanchnic vasoconstriction will reduce portal venous pressures and treat esophageal varies

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14
Q

How does amiodarone affect the liver?

A

It’s hepatotoxic

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15
Q

Main 2 considerations for patients with liver injury presenting for surgery

A

1) Maintain hepatic BF

2) Avoid any drugs that are hepatotoxic or suppress the CYP450

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16
Q

Anesthesia considerations for pt with acute hepatitis

A

1) Maintain hepatic BF
- Use Iso (preserves BF the best)
- Avoid PEEP (increases resistance to hepatic drainage, and remember that increased hepatic venous pressure will decrease hepatic perfusion pressure)
- Ensure normocapnia
- Lots of IV fluids
- Regional OK as long as no coag defects

2) Avoid hepatotoxic drugs or those that suppress the CYP450
- Tylenol
- Halothane
- Amiodarone
- Antibiotics (PCN, tetracycline, and sulfonamides)

17
Q

Effects of alcohol on GABA and NMDA receptors

A

Agonist at GABA

Antagonist at NMDA

18
Q

Early and late signs of alcohol withdrawl

A

Early: tremors and distorted perception (hallucinations and nightmares)

Late: Increased SNS activity (oh fuck, where’s my alcohol??), N/V, insomnia, confusion, and agitation

19
Q

Treatment of alcohol w/d

A

Alcohol, BBs, and A-2 agonists

20
Q

When do DTs present?

A

2-4 days without alcohol

- Grand mal seizures and combativeness

21
Q

Treatment of DTs

A

Diazepam or other benzos

BBs

22
Q

Consequence of portosystemic shunts

A

These shunts occur as blood tries to bypass the liver in high portal pressures.
This blood does not get filtered or processed by the liver, resulting in them remaining in circulation for a longer period of time

23
Q

MELD score looks at

A

3 things:

  • Serum bilirubin
  • Serum creatinine
  • INR
24
Q

What are hepatopulmonary syndrome and portopulmonary HTN?

A

Hepatopulmonary syndrome
- Pulmonary vasodilation leads to increased R–>L shunting and hypoxia

Portopulmonary HTN

  • Portal HTN + Pulmonary HTN
  • PAP > 25