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Gastrointestinal > Cirrhosis And Liver Transplant > Flashcards

Cirrhosis And Liver Transplant Flashcards

1
Q

Hepatic fibrosis

A

1 cause of hepatic fibrosis = alcohol

Is caused by overly exuberant wound healing in which excessive connective tissue builds up

Medical disorders:

  • autoimmune hepatitis
  • certain storage diseases and inborn errors of metabolism
  • congenital hepatic fibrosis
  • chronic infections of bacterial/viral/parasitic
  • nonalcoholic steatohepatitis (NASH)
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
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2
Q

Does hepatic fibrosis by itself cause symptoms?

A

No but the resulting portal HTN and hepatocyte death will

Symptoms include

  • fatigue
  • anorexia
  • muscle cramps
  • disturbed sleep
  • hematemesis/melena or hematochezia
  • spider telangiectasia/palmer erythema/contracture
  • vitamin deficiencies
  • jaundice
  • hepatosplenomegaly
  • gastric/rectal varices
  • hepatic encephalopathy w/ asterixis
  • ascites and peripheral edema
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3
Q

How to diagnose ascites and edema

A

Paracentesis and send to lab:

  • get CBC, gram stain, culture and albumin
  • **if albumin gradient of (serum:ascites) is greater than 1.1 = portal HTN
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4
Q

Treatment for liver cirrhosis symptoms

A

Ascites and edema

  • diuretics
  • trans jugular intrahepatic portosystemic shunt (TIPS) (usually only if refractory presents)
  • large volume paracentesis

Peritonitis = 2nd/3rd gen cephalosporin or fluroquinolone are 1st line

Thrombocytopenia/coagulopathy

  • phytonadione 5mg PO/IV daily
  • FFP only for severe hemorrhage cases

Esophageal/gastric varices

  • 30% of patients with varices will bleed and mortality worsens with only one bleeding incidence
    1) goal is to prevent bleed first if possible = endoscopy and BBs/banding if large
    2) actual treatment is antibiotics/octerotide/ infusion and band ligation or sclerotherpy (usually use both though)
  • can also give vitamin K if elevated PT/INR and lactulose if patient is encephalopathic
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5
Q

What are options to use if chronic bleeding occurs and you can’t get to surgery?

A

Balloon tube tamponade
- usually 1st line and controls acute hemorrhages

Portal decompressive procedures

  • transvenous intrahepatic Portosystemic shunt surgery (TIPS)
  • emergency portosystemic shunt surgery
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6
Q

Hepatorenal syndrome

A

Occurs 10% of patients with advanced cirrhosis

  • always shows the following 4 things:
    1) azotemia (creatinine rises 0.3 points in 48hrs or an increase of 50% or more from baseline

2) macroscopic signs of structural kidney injuries
3) shock
4) failure of kidney function to improve following 2 days of diuretic withdrawal and volume expansion with albumin

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7
Q

Spectrum of Neurocognitive Impairment in cirrhosis (SONIC)

A

A revised staging system for encephalopathy

1) absent
2) covert
3) drowsiness
4) stupor
5) coma

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8
Q

How to treat hepatic encephalopathy

A

1) low protein diet

2) give lactulose and rifaximin and zinc supplements

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9
Q

Hepatopulmonary and portopulmonary HTN

A

Occurs in 5-32% of cirrhosis patients

Have significant SOB with a triad of:

1) liver cirrhosis
2) increased alveolar + arterial gradients while patient is breathing room air
3) AVMs or intrapulmonary vascular dilations

  • *there is no good medical treatment**
  • after confirmation usually give epoprostenol, bosentan or ambrisentan and sildenafil or tadalafil combination to lower pulmonary HTN
  • DONT give BBs or CBBs they worsen it

being female and having autoimmune hepatitis are extreme risk factors

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10
Q

Child-Pugh scoring system

A

Estimates the severity of liver cirrhosis and the potential mortality rate

Based off the following 5 factors:

1) ascites
- none = 1
- slight = 2
- moderate/severe = 3

2) Encephalopathy
- none = 1
- slight/moderate = 2
- severe = 3

3) bilirubin count
- <2.0 = 1
- 2-3 = 2
- > 3 = 3

4) albumin
- >3.5 = 1
- 2.8-3.5 = 2
- <2.8 = 3

5) prothrombin time (PT)
- 1-3 sec = 1
- 4-6 sec = 2
- > 6 sec = 3

Scores:

1) 5-6 = A (1yr = 100%; 2yr = 85%)
2) 7-9 = B (1yr = 80%; 2yr = 60%)
3) 10-15 = C (1yr = 45%; 35%)

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11
Q

What auto antibodies are present for types 1-3 autoimmune hepatitis/?

A

Type 1 = ANA/SMA/anti-FLAG/L-PAG

  • safest and mild type
  • liver cirrhosis chance = 45%
  • treatment is usually successful
  • **most common
  • easy to diagnose

Type 2 = Anti-LKM1/anti-LC1

  • worst type
  • liver cirrhosis chance = 80%
  • treatment is usually not successful and the disease often remits
  • easy to diagnose

Type 3= Anti-SLA

  • 2nd worst type but usually doesnt fail treatment
  • liver cirrhosis chance = 75%
  • treatment is usually successful
  • hard to diagnose
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12
Q

AUDIT-C score

A

Determines the likelihood that drinking is negatively affecting the patients health

In men = score > or equal to 4 is positive

In women = score > or equal to 3 is positive

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13
Q

Liver transplantation indications

A

End stage cirrhosis
- or hep C cirrhosis

Fulminant hepatic necrosis

Hepatocellular carcinoma

Biliary atresia

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14
Q

What are absolute contraindications to liver transplant?

A

Elevated intracranial pressures (>40mmHg)

Low cerebral perfusion pressure (<60 mmHg)
- common in fulminant liver failure

Severe pulmonary HTN
- Mean pulmonary arterial pressure > 50mmHg

Sepsis is present

Metastatic HCC is present

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15
Q

What are risk factors for graft failure in transplants?

Patients body will reject the transplant

A

Age > 50 or <13

Hepatic steatosis

Elevated LFTs/bilirubin or both

Prolonged stay in the ICU

Hypotension requiring vasopressors

Hypernatremia

Liver being donated is from older patient

HLA mismatching is high

Autoimmune disorders

possible female -> male donating (low evidence on this though)

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16
Q

How does immunosupression work for liver transplant patients?

A

1) Anti-IL2 receptor monoclonal antibodies (daclizumab/basiliximab)
- given day of transplant surgery

2) calcineuin inhibitor (cyclosporine or tacrolimus)
- varies time frame but starts after transplant is finished

3) mycophenolate mofetil

4) corticosteroids
- taper off after 3-4 weeks except in autoimmune hepatitis (permanent)

17
Q

What are the 4 categories of liver rejection?

A

all show fever except chronic

all show jaundice

1) Hyper acute = presents with VERY high AST/ALT and bilirubin and coagulopathy
2) accelerated = same as #1 but also ascites
3) acute = pain, anorexia, very dark urine and very light stools
4) chronic = presents with ascites and vanishing bile duct syndrome (everything is elevated and DEAK deficiencies are present)

18
Q

Liver transplant rejection differential diagnosis

A

1) viral hepatitis
- can be hep B/C, CMV, Epstein Barr

2) calcineurin inhibitor toxicity
3) Cholestasis

19
Q

Treatment for liver rejection

A

IV corticosteroids (1st line)

Anti-thymocyte globulin (2nd line)

retransplantation when immunosuprresants do not work

20
Q

Early complications of liver rejection

A

all occurs within 2 months usually

Most common = biliary dysfunction

Hepatic artery thrombosis

Hepatic artery mycotic aneurysm

Hepatic artery rupture

Primary nondysfunction

21
Q

Late complications of liver rejection

A

Cholestasis or cholangitis caused by intrahepatic or anastomatic bile duct structures

Most late complications end up requiring retransplant

  • strictures are pretty common and seen in 25-30% of patients*
  • more common in deceased donor grafts

Survival rates are slightly lower in deceased donors and grants are lower than actual tissue across the board

22
Q

What is the most common virus to recur after transplant?

A

Hepatitis C

23
Q

How is acetaminophen metabolized

A

90% is metabolized in the liver by glucuronidation and sulfation pathways
- produces glucuronide and sulfate moiety respectfully (these are both nontoxic)

8% is oxidized in CYP-P450 system (especially 2E1)

  • generates NAPQI which is a TOXIC metabolite unless it is bound to glutathione
  • if bound to glutathione = gets degraded into cysteine and mercapturic acid (both non toxic)
24
Q

What happens to acetaminophen toxicity?

A

Clearance and metabolism shifts towards CYP450 metabolism

  • NAPQI levels increase dramatically
  • glutathione stores cant keep up = toxic to liver and causes fulminant liver failure
25
Q

Clinical findings in acetaminophen fulminant liver failure

A

Stage 1 (first 24hrs)

  • asymptomatic Or mild N/V
  • AST/ALT will be through the roof (AST > ALT)
  • INR and Creatinine are normal

Stage 2 (2-3 days)

  • RUQ pain/tenderness
  • vomitingand nausea
  • AST/ ALT will be through the roof (ALT = AST)
  • INR is increased and bilirubin is super high
  • creatinine is slightly elevated

Stage 3 (3-4 days)

  • extreme N/V and jaundice
  • metabolic lactic acidosis
  • coagulopathy
  • ARDS/SIRS
  • cerebral edema
  • hepatic encephalopathy
  • **this is usually were death occurs
Stage 4 (4 days+) 
- either the patient survives (either through reversal or liver transplant)and is recovery or they have died

**creatinine is usually only really elevated in end stage liver failure

26
Q

High risk populations to acetaminophen poisoning

A

Age over 40

Chronic alcoholic

Currently infected with hepatitis C

Malnourished

27
Q

What is the cut off for toxic dose in both peds and adult patients?

A

Pediatric = 150 mg/kg

Adult = 7.5 gm total

28
Q

What labs do you need to get in suspect acetaminophen OD or acute liver failure patients

A

Acetaminophen levels
- if caused by acetaminophen levels are still high after 4 hrs = OD attempt

Liver enzymes

Salicylate levels

CBC

Alcohol

EKG

29
Q

Treatment for acetaminophen poisoning

A

Activated charcoal of 1g/kg up to 50g total
- can be given up to 2hrs post ingestion

N-acetylcysteine (NAC)

  • give when toxic levels are present higher than the Rumack line or after 2hrs regardless since you cant give charcoal at this point
  • if given within 8hrs of ingestion = very low chance of liver failure

Also give psychiatric consultation

if presents later than 8hrs and NAC doesnt stop elevated liver enzyme , consult toxicologist (but still start a NAC infusion)

30
Q

What is the Rumack-matthew Nomogram?

A

A nomogram that plots serum acetaminophen concentration over hrs post-ingestion

Helps determine the risk of liver toxicity based on the time and acetaminophen concentration
- also helps the physician determine if they should proceed with N-acetylcystine or not

only useful in single acute ingestion and not intended for extended-release acetaminophen

*** if the point comes out to being above the Rumack line = skip charcoal and go straight to N-acetylcystine

31
Q

How does N-acetylcystine work?

A

Acts as a synthetic glutathione precursor which can bind to NAPQI and allow it to be metabolized into non-toxic compounds

Can give oral or IV

1) oral: 18 doses every 4hrs for 72hrs
- some patients cant tolerate taste/smell however and can projectile vomit

2) IV: 21 hr infusion
- easier to give acutely, however 20% chance of severe anaphylaxis can occur (non-IgE mediated)

is safe in pregnancy

Gastrointestinal (71 decks)

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