IP-5 Liver disease and cirrhosis review Flashcards

1
Q

What is acute alcoholic hepatitis?

A

Occurs after decades of heavy EtOH consumption and rarely in people who binge drink that results in liver failure and death 40% of the time. AST/ALT > 2 X ULN. Use the DF or MELD score

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2
Q

Signs and symptoms of cirrhosis

A

Jaundice, spider angiomata, nodular liver, splenomegaly, ascites, caput medusa, palmar erythema, gynecomastia, asterixis, anorexia, T2DM.

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3
Q

How do we diagnose cirrhosis?

A

The only definitive way is by liver biopsy. Because this isn’t feasible, we use characteristic symptoms, ultrasound and laboratory values to diagnose cirrhosis.

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4
Q

Which lab values are helpful in the diagnosis of cirrhosis or liver disease in general. What are the reference ranges?

A

Total protein (6-8.5), albumin (3.1-4.3), AST: (10-40 male, 9-25 female), ALT (10-55 male, 7-30 female), CBC and the inverted fishbone of LFTs (TP, Alb, AST/ALT, DBILI, TBILI, ALP)

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5
Q

List the complications of cirrhosis

A

Portal hypertension (increased pressure within the portal venous system), esophageal varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy

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6
Q

How can we tell if portal hypertension is present?

A

HVPG > 5 mmHg and is even more significant if HVPG > 10 mmHg OR through calculation of a SAAG score. (above 1.1 is diagnostic for portal hypertension)

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7
Q

How do you calculate a SAAG score?

A

SAAG= serum albumin - ascites albumin (>1.1 = portal hypertension)

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8
Q

What is esophageal varices and what factors determine the presence of varices

A

Blood back ups result in the formation of varices, which are alternate routes of blood flow. The higher the portal HTN, the higher the risk of varix formation (usually HVPG > 10)

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9
Q

What is ascites?

A

An accumulation of fluid in the peritoneal cavity cause by lymph leakage from the capillaries into the peritoneal cavity.

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10
Q

What is spontaneous bacterial peritonitis (SBP)?

Which microbes mostly present?

A

Infection in the ascitic fluid without a primary intra-abdominal source. The ascitic fluid allows overgrowth of bacteria such as E. coli and K. pneumoniae (most common)

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11
Q

What is hepatic encephalopathy?

A

Disturbance in the CNS as a result of accumulation of nitrogenous substances present in bloodstream due to haptic insufficiency and liver failure. This substance alters neurotransmission leading to decreased cognition, confusion and behavioral changes.

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12
Q

Treatment for acute alcoholic hepatitis

A

A DF score > or = 32 means you should initiate prednisolone 40mg daily x 28 days, then taper. Pentoxifylline and nutritional support are also recommended.

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13
Q

Two options for primary prophylaxis of vatical bleeding

A

Surgical intervention or medication (Propranolol 20mg BID or nadolol 40mg once daily)

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14
Q

Treatment for acute vatical bleeding

A

3 procedures: endoscopic procedures (band ligation, endoscopic injection sclerotherapy), pharmacotherapy, and interventional procedures (balloon tamponade).
7 day course of ABX therapy as prophylaxis against SBP.
Octreotide works by selectively constricting splanchnic vessels.

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15
Q

Secondary prophylaxis of vatical bleeding

A

Most common regimen consists of non-selective B blocker plus serial endoscopic variceal ligation.

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16
Q

Treatment for portal hypertension

A

Propranolol 20mg BID or nadolol 40mg daily

17
Q

Treatment for ascites

A

Aldosterone antagonist (spironolactone 100mg daily up to max 400mg daily). Furosemide (20mg BID up to max 80mg BID) is added to this regimen to minimize the risk of hyperkalemia and enhance diuresis to a target weight loss of 0.5kg/day

18
Q

Treatment for SBP

A

Most common empiric regiment is ceftriaxone 1gm Q 12 H x min of 5 days (14 days if confirmed with positive blood cultures)

19
Q

How to treat macrocytic anemia related to cirrhosis

A

BANANA bag (Folic acid, thiamine, and MultiV) in maintenance fluid

20
Q

Treatment for hepatic encephalopathy

A

Lactulose 20-30 grams PO Q 1 hour until BM, then 20-30 grams PO 3-4 X daily (titrated to 2-3 BM/day). Used to treat and prevent hepatic encephalopathy.
Rifaximin: Decrease the number of bacteria in the gut that produce the enzyme urease which prevents the conversion of urea to ammonia.
Metronidazole and neomycin are other options but not well studied.

21
Q

How does lactulose work?

A

Osmotic laxative that makes the patient excrete ammonia before it is able to be absorbed in the GI tract, thereby lowering systemic ammonia levels. Secondly, is that lactulose converts ammonia to ammonium which are not absorbed from the GI tract and thus excreted from the body.

22
Q

Monitoring parameters for patients with SPB

A

SCr and BUN should be monitored daily to asses for hepatorenal syndrome.

23
Q

Monitoring parameters for patients receiving B blocker for portal hypertension/varix formation

A

Patients taking non-selective B blockers should have their HR monitored (goal: 55-60 BPM or 25% reduction in resting HR)

24
Q

Monitoring parameters for patients with acute encephalopathy and hepatic encephalopathy

A

Restrict dietary protein intake to 10-20 g/day until acute episode resolves. Bowel movements and mental status should be monitored multiple times per day.