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
Q

What therapy is not recommended to prevent varices in cirrhosis patients without varices?

A

Pharmacologic therapy

26
Q

What should be given to patients with small varices and no history of bleeding but at increased risk?

A

Nonselective β-blockers

Agents include propranolol, nadolol, and carvedilol.

27
Q

What is the mechanism of action of nonselective β-blockers in treating varices?

A

Blockade of β1-receptors reduces cardiac output; blockade of β2-receptors prevents splanchnic vasodilation

28
Q

What is the target resting heart rate for patients on nonselective β-blockers?

A

55–60 beats/minute

29
Q

What constitutes β-blocker response for primary and secondary prophylaxis?

A

Reduction in hepatic-vein pressure gradient (HVPG) of at least 10% for primary, 20% for secondary

30
Q

What is the role of long-acting nitrates in primary prophylaxis?

A

Should not be used

Increased incidence of adverse effects when used as monotherapy.

31
Q

What is the preferred method for secondary prophylaxis of variceal bleeding?

A

Combination of endoscopic variceal band ligation and nonselective β-blockers

32
Q

What are the common adverse effects of nonselective β-blockers?

A

Light-headedness, fatigue, shortness of breath, sexual dysfunction, bradycardia

33
Q

What is the definition of spontaneous bacterial peritonitis (SBP)?

A

Infection of previously sterile ascitic fluid without an apparent intraabdominal source

34
Q

What is the principal theory for the pathophysiology of SBP?

A

Seeding of ascitic fluid from an episode of bacteremia

35
Q

What are the common bacteria causing community-acquired SBP?

A

Escherichia coli, Klebsiella spp.

Most SBP infections are monobacterial.

36
Q

What is the diagnostic criterion for SBP based on polymorphonuclear cells?

A

More than 250 polymorphonuclear cells/mm3

37
Q

What is the recommended treatment duration for acute SBP?

A

5–7 days

38
Q

What is the rationale for using albumin in SBP treatment?

A

Improves survival in patients with cirrhosis and SBP

Helps with hemodynamics and renal perfusion.

39
Q

What are the antibiotic regimens for primary and secondary prevention of SBP?

A

Fluoroquinolones or trimethoprim/sulfamethoxazole

40
Q

What is the definition of hepatorenal syndrome?

A

Acute kidney injury in patients with cirrhosis and ascites

41
Q

What is recommended for treatment of hepatorenal syndrome?

A

Vasoconstrictor therapy along with albumin

Norepinephrine is preferred in the ICU.

42
Q

What is the prognosis for patients with alcoholic hepatitis with an MDF score greater than 32?

A

Poor prognosis

43
Q

What corticosteroid regimen is suggested for patients with alcoholic hepatitis and an MDF score greater than 32?

A

40 mg/day for 4 weeks, followed by a 2-week taper

44
Q

What is the role of intravenous acetylcysteine in alcoholic hepatitis?

A

Considered for its survival benefit and reduction of early complications