PT Liver Cirrhosis Flashcards

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1
Q

What are clinical consequences of liver cirrhosis?

A
  • Ascites
  • Spontaneous Bacterial Peritonitis (SBP)
  • Hepatic encephalopathy (HE)
  • Varices and Variceal bleeding
  • Hepatorenal syndrome
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2
Q

What are immediately life‐threatening complications of cirrhosis.

A

Acute variceal bleeding and spontaneous bacterial peritonitis (SBP)

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3
Q

Desired outcome of clinical consequences

liver cirrhosis?

A
  1. Prevention of complication

2. Resolution of acute complication

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4
Q

How to diagnose Ascites?

A
  • Clinical features: protuberant abdomen, fluid wave, bulging flanks, abdominal pain.
  • Abdominal ultrasonography.
  • Paracentesis
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5
Q

What is the main aim in treatment of ascites and how?

A
  • Attainment of negative sodium balance.
  • Dietary sodium restriction (<2000 mg/day), fluid restriction (<1.5 L/day) if serum sodium is less than
    120–125 mmol/L. Goal is sodium excretion greater than 78 mmol/day.
    • Diuretics: combination furosemide and spironolactone is preferred initial therapy in most patients. A
    ratio of 40 mg of furosemide to 100 mg of spironolactone is an appropriate starting regimen.
  • If tense ascites, large‐volume paracentesis can be used. Administer albumin at a dose of 6–8 g/L of
    ascitic fluid removed if more than 5 L is removed at one time.
  • If refractory ascites, consider midodrine 7.5 mg three times daily as add‐on therapy to diuretics.

Dr: treatment of tenses ascites are combination of albumin, furosemide and spirolactone

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6
Q

Why NSAID should be discontinue in treatment of ascites?

A

Because it can cause sodium/water retention, destroy the balance

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7
Q

Explain the pathophysiology of SBP?

A

a. Principal: seeding of the ascitic fluid from an episode of bacteremia.
- Bacteria (enteric gram‐negative pathogens) may enter the blood because of increases in gut permeability secondary to portal hypertension.
B. Reduced opsonic activity of the ascitic fluid and alterations in neutrophil function.

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8
Q

What is clinical presentation of ascites?

A
  • Common symptoms: fever, abdominal pain, nausea, vomiting, diarrhea, rebound tenderness, and exacerbation of encephalopathy.
  • Renal failure (33%, associated with significant increases in mortality).
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8
Q

What is clinical presentation of ascites?

A
  • Common symptoms: fever, abdominal pain, nausea, vomiting, diarrhea, rebound tenderness, and exacerbation of encephalopathy.
  • Renal failure (33%, associated with significant increases in mortality).
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9
Q

What is predictor of poor outcome in SBP treatment?

A

bilirubin > 8 mg/dL, albumin < 2.5 g/dL, creatinine > 2.1 mg/dL, hepatic encephalopathy, hepatorenal syndrome, and upper GI bleeding.

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10
Q

Explain the abx therapy in acute treatment of SBP?

A

I. Empiric therapy should be instituted. Treatment duration: 5–10 days.
II. Third‐generation IV cephalosporins are considered first line: cefotaxime (2 g every 8–12
hours) or ceftriaxone (2 g/day)
III. Ofloxacin 400 mg orally BD in those without prior fluoroquinolones exposure and no
evidence of shock, vomiting, grade II or higher encephalopathy, or SCr > 3 mg/dL.
IV. Avoid aminoglycosides (high risk of renal failure in patients with cirrhosis and SBP).

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11
Q

How to prevent SBP? (explain on the prevention of SBP?)

A

Oral antibiotics (Ciprofloxacin OR Trimethoprim/sulfamethoxazole 1 double‐strength tablet for 5 days/wk)

Oral antibiotics to reduce number of enteric organisms in the GI tract (GI decontamination),
reducing the chance of bacterial translocation to prevent SBP in high‐risk patients. Antibiotic regimens are similar for both primary and secondary prevention:

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12
Q

Differentiate primary and secondary prevention of SBP?

A

Primary prevention
-During acute upper GI bleeding, give 7‐day course of ceftriaxone during hospitalization.
-Long‐term use of ciprofloxacin or trimethoprim/sulfamethoxazole in certain cases.
Secondary prevention
-All patients recovering from an initial SBP episode: oral prophylactic antibiotics indefinitely.
-Consider patient for liver transplantation (2‐year survival is 25%–30% after recovery).

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13
Q

What is main treatments targeted in HE?

A

at reducing the nitrogen load in the gut

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14
Q

What is dose of lactulose in HE treatment?

A

Oral: Initially, 30‐45 mL 3‐4 times daily, adjusted as necessary to achieve 2 or 3 soft stools daily.
Rectal: Mix 200 g (300 mL) of solution with 700 mL of water or 0.9% NaCl: Administer as a

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15
Q

How abx treat HE?

A

Targeted at reducing the number of intraluminal urease‐producing bacteria that can lead to excess NH3 production.

16
Q

State 3 abx and dose to treat HE?

A

Neomycin (3–6 g/day in three or four divided doses for 1–2 weeks and then 1–2 g/day
maintenance); neomycin is considered as effective as lactulose.
Metronidazole (250 mg orally bid) can be used. Long‐term use (peripheral neuropathy).
- Rifaximin is as effective as lactulose and other nonabsorbable antibiotics.
- Better tolerated & Greater drug cost (offset by fewer hospitalizations and shorter stay lengths).
- Oral 550 mg bid to reduce risk of overt hepatic encephalopathy recurrence.

17
Q

What is preffered agent in management of acute variceal bleeding and the dose?

A

Octreotide

Dosing: 50‐mcg intravenous bolus, then 50 mcg/hour intravenously for 3–5 days.

17
Q

What is preffered agent in management of acute variceal bleeding and the dose?

A

Octreotide

Dosing: 50‐mcg intravenous bolus, then 50 mcg/hour intravenously for 3–5 days.

18
Q

Why vasopressin is less use in management of acute variceal bleeding and how it is used?

A

due to coronary vasoconstriction/
hypertension with vasopressin (nitroglycerin attenuates these effects to some extent). has a worse adverse effect profile than octreotide (risk of ischemia, hypotension, and skin
necrosis limit use)
dose: 0.2–0.4 unit/minute plus nitroglycerin 40–400 mcg/minute for 3–5 days

19
Q

What is Nondrug measures to control bleeding in management of acute variceal bleeding?

A
  • Minnesota or Blakemore tube: Balloon compression applied directly to bleeding varices
  • Transjugular intrahepatic portosystemic shunt: shunting of blood from the portal circulation (associated with complications such as bleeding, infection, and increased risk of HE).
  • Surgery
20
Q

Abx used as prophylaxis in management of acute variceal bleeding?
true or false?
Dose?

A

True. The use of oral or intravenous prophylactic antibiotics in patients with cirrhosis with variceal bleeding reduces short‐term mortality.

Drug : Ceftriaxone IV 1 gram/day for 7 days
Fluoroquinolone can be considered in patients who do not have a high risk of quinolone resistance.

21
Q

Nonselective β‐blockers (propranolol, nadolol, carvedilol): significant reduction in the incidence of first bleed. Therapy should aim for a resting heart rate of 55–60 beats/minute or a 25% reduction from baseline in Prevention of variceal bleeding, Primary prophylaxis. To whom beta blocker should be indicated or consider?

A
- Indicated in patients who have small varices and no history of bleeding but meet the criteria for increased
risk of bleeding (Child‐Pugh class B or C, red wale marks on varices).
- Consider in patients who have small varices and no history of bleeding, but who do not meet the criteria for
increased risk of bleeding ( long‐term benefit is unclear).
- indicated in all patients with medium or large varices and no history of bleeding. An endoscopic variceal
ligation (EVL) can be used if nonselective β‐blockers are contraindicated
22
Q

How to treat Hepatorenal syndrome?

A
  • Albumin in combination with octreotide (200 mcg subcutaneously three times daily) or midodrine (12.5 mg
    three times daily maximum) may be considered for type 1.
  • Albumin plus norepinephrine may be considered if the patient is in the intensive care unit.
23
Q

what are Other possible treatments for HE?

A
  • Benzodiazepine antagonists such as flumazenil can be used in cases of possible benzodiazepine overdose (risk of lowering the seizure threshold often limits their use).
  • Zinc supplementation should be used in patients with documented zinc deficiency.
  • Branched‐chain amino acids and intravenous L‐ornithine L‐aspartate are alternative or additional therapies in patients who are unresponsive to traditional therapies
  • Nutritional interventions include 35–40 kcal/kg/day based on IBW and 1.2–1.5 g/kg/day
    protein intake.
  • Polyethylene glycol 3350 given orally or by nasogastric tube over 4 hours resulted in faster improvement in encephalopathy than lactulose.