Liver Flashcards

1
Q

What is ascites?

A

Free fluid in the abdominal cavity owing to increased resistance within the liver and reduced osmotic pressure within the bloodstream

Develops at a 5-year cumulative rate of 30% in compensated liver disease.

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2
Q

What are the complications of liver disease?

A
  • Variceal hemorrhage
  • Hepatic encephalopathy
  • Spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Alcoholic liver disease
  • Viral hepatitis

These complications reflect the severity of liver dysfunction.

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3
Q

What is the Child-Turcotte-Pugh classification used for?

A

To assess the severity of liver disease

Scores range from 5 to 15 based on clinical parameters.

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4
Q

What variables are scored in the Child-Turcotte-Pugh classification?

A
  • Encephalopathy
  • Ascites
  • Bilirubin
  • Albumin
  • Prothrombin time

Each variable is assigned points based on severity.

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5
Q

What does a MELD score indicate?

A

The severity of liver disease and helps prioritize patients for liver transplantation

Higher scores indicate more severe disease.

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6
Q

What is the formula for calculating the original MELD score?

A

9.57 × ln(creatinine) + 3.78 × ln(total bilirubin) + 11.2 × ln(INR) + 6.43

This formula is used to predict mortality.

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7
Q

What is the significance of the MELD-Na score?

A

Incorporates sodium concentration into the MELD score to improve risk discrimination

Hyponatremia is a marker of cirrhosis severity.

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8
Q

What are common clinical features of ascites?

A
  • Protuberant abdomen
  • Shifting dullness
  • Fluid wave
  • Bulging flanks
  • Abdominal pain

These signs help in the diagnosis of ascites.

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9
Q

What dietary restrictions are recommended for patients with ascites?

A
  • Sodium restriction (<2000 mg/day)
  • Fluid restriction (<1.5 L/day) if serum sodium is <120–125 mmol/L

These restrictions aim to reduce fluid retention.

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10
Q

What is the goal for sodium excretion in patients with ascites?

A

Sodium excretion greater than 78 mmol/day

A random spot urine sodium concentration greater than potassium correlates with this goal.

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11
Q

What is hepatic encephalopathy?

A

Brain dysfunction caused by liver insufficiency or portosystemic shunting

It manifests as a spectrum of neurological or psychiatric abnormalities.

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12
Q

What are the West Haven Criteria used for?

A

To classify and grade the severity of hepatic encephalopathy

Includes assessments from unimpaired to coma.

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13
Q

What are the grades of hepatic encephalopathy according to West Haven Criteria?

A
  • Grade I: Minimal
  • Grade II: Moderate
  • Grade III: Severe
  • Grade IV: Coma

Each grade indicates increasing severity of symptoms.

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14
Q

What is the first-line treatment for overt hepatic encephalopathy?

A

Lactulose

It is a nonabsorbable disaccharide that reduces NH3 absorption.

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15
Q

What alternative treatments can be used for hepatic encephalopathy?

A
  • Rifaximin
  • Neomycin
  • Metronidazole
  • Branched chain amino acids (BCAA)

These may be used in patients unresponsive to traditional therapies.

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16
Q

What is the primary management for acute variceal bleeding?

A
  • Fluid resuscitation and hemodynamic stabilization
  • Endoscopy to assess and intervene

Maintaining hemoglobin concentration around 8 g/dL is crucial.

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17
Q

What is the role of vasopressin in variceal bleeding management?

A

Causes splanchnic vasoconstriction to reduce portal pressure

It is used less frequently due to adverse effects.

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18
Q

What is the preferred agent for medical management of variceal bleeding?

A

Octreotide

It has a more favorable adverse effect profile compared to vasopressin.

19
Q

What are the complications associated with sclerotherapy for variceal bleeding?

A
  • Perforation
  • Ulceration
  • Stricture
  • Bacteremia

Sclerotherapy is effective but carries risks.

20
Q

What is the main adverse effect of endoscopic interventions in combination with agent therapy?

A

Hyperglycemia

Adverse effects include abdominal cramping and increased risk of hepatic encephalopathy.

21
Q

What does a Transjugular intrahepatic portosystemic shunt do?

A

Shunts blood from the portal circulation

Associated complications include bleeding and infection.

22
Q

What is the dosing regimen for the intravenous agent mentioned?

A

50-mcg intravenous bolus, then 50 mcg/hour for 3–5 days

23
Q

What should be prescribed to patients with cirrhosis to prevent variceal bleeding?

A

Oral or intravenous prophylactic antibiotics

Reduces short-term mortality.

24
Q

What is the recommended antibiotic regimen for primary prophylaxis in patients with cirrhosis?

A

Ceftriaxone 1 gram/day for 7 days

Especially when quinolone-resistant bacteria are prevalent.

25
What therapy is not recommended to prevent varices in cirrhosis patients without varices?
Pharmacologic therapy
26
What should be given to patients with small varices and no history of bleeding but at increased risk?
Nonselective β-blockers ## Footnote Agents include propranolol, nadolol, and carvedilol.
27
What is the mechanism of action of nonselective β-blockers in treating varices?
Blockade of β1-receptors reduces cardiac output; blockade of β2-receptors prevents splanchnic vasodilation
28
What is the target resting heart rate for patients on nonselective β-blockers?
55–60 beats/minute
29
What constitutes β-blocker response for primary and secondary prophylaxis?
Reduction in hepatic-vein pressure gradient (HVPG) of at least 10% for primary, 20% for secondary
30
What is the role of long-acting nitrates in primary prophylaxis?
Should not be used ## Footnote Increased incidence of adverse effects when used as monotherapy.
31
What is the preferred method for secondary prophylaxis of variceal bleeding?
Combination of endoscopic variceal band ligation and nonselective β-blockers
32
What are the common adverse effects of nonselective β-blockers?
Light-headedness, fatigue, shortness of breath, sexual dysfunction, bradycardia
33
What is the definition of spontaneous bacterial peritonitis (SBP)?
Infection of previously sterile ascitic fluid without an apparent intraabdominal source
34
What is the principal theory for the pathophysiology of SBP?
Seeding of ascitic fluid from an episode of bacteremia
35
What are the common bacteria causing community-acquired SBP?
Escherichia coli, Klebsiella spp. ## Footnote Most SBP infections are monobacterial.
36
What is the diagnostic criterion for SBP based on polymorphonuclear cells?
More than 250 polymorphonuclear cells/mm3
37
What is the recommended treatment duration for acute SBP?
5–7 days
38
What is the rationale for using albumin in SBP treatment?
Improves survival in patients with cirrhosis and SBP ## Footnote Helps with hemodynamics and renal perfusion.
39
What are the antibiotic regimens for primary and secondary prevention of SBP?
Fluoroquinolones or trimethoprim/sulfamethoxazole
40
What is the definition of hepatorenal syndrome?
Acute kidney injury in patients with cirrhosis and ascites
41
What is recommended for treatment of hepatorenal syndrome?
Vasoconstrictor therapy along with albumin ## Footnote Norepinephrine is preferred in the ICU.
42
What is the prognosis for patients with alcoholic hepatitis with an MDF score greater than 32?
Poor prognosis
43
What corticosteroid regimen is suggested for patients with alcoholic hepatitis and an MDF score greater than 32?
40 mg/day for 4 weeks, followed by a 2-week taper
44
What is the role of intravenous acetylcysteine in alcoholic hepatitis?
Considered for its survival benefit and reduction of early complications