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MS2 GI > 10/21- Liver failure and portal HTN > Flashcards

10/21- Liver failure and portal HTN Flashcards

1
Q

What is seen here?

A

Normal liver (left) vs. cirrhosis (right)

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2
Q

Non-invasive alternatives to liver biopsies?

A
  • Fibroscan
  • Magnetic Resonance Elastography (MRE)
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3
Q

Describe Fibroscan

  • Pros/cons
A

Fibroscan

  • Works best on thin patients
  • Tells you how stiff/soft the liver is (stiffness can indicated cirrhosis)
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4
Q

What do these fibroscan results show?

A
  • Not as steep slope on left (stiffer?)
  • Steep slope on right (softer?)
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5
Q

How do liver diseases compare on fibroscan results (grades of stiffness)?

A

Different diseases cause different fibrotic patterns and different densities. Also happen at different times

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6
Q

Describe Magnetic Resonance Elastography (MRE)

A

Again, indicates stiffness (blue -> red scale)

  • Newer technique
  • Good for saying yes/no to cirrhosis
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7
Q

What are the 3 types of liver decompensation?

A
  • Synthetic failure
  • Portal HTN
  • Hepatocellular Carcinoma (HCC)
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8
Q

What are markers of synthetic failure in terms of liver disease (what symptoms do you see)?

A

Synthetic Failure

  • Jaundice
  • Prolonged INR (low clotting factors)
  • Hypoalbuminemia
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9
Q

What are signs/symptoms of portal hypertension?

A

Portal vein entering the base of the liver; dilates; 3x increase in pressure (4->12 mmHg)

  • Hypersplenism
  • Fluid retention
  • Ascites and peripheral edema
  • Varices
  • With/without bleeding
  • Encephalopathy
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10
Q

What are the cardinal signs of liver failure?

A

If you have any of these, you have liver failure.

Mortality goes up significantly once any of these happen

  • Jaundice
  • Ascites
  • May include SBP
  • May include peripheral edema
  • Variceal bleed
  • Encephalopathy
  • Clinical or subclinical
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11
Q

Other signs of liver failure?

A
  • Spider angiomata
  • Fed from the middle (blanching)
  • Surprisingly common in people with cirrhosis (especially alcoholic)
  • Palmar erythema
  • Dupuytren contracture
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12
Q

Describe bilirubin synthesis

A
  • RBCs -> hemoglobin -> globin + heme
  • Heme is degraded into bilirubin (unconjugated); carried with albumin to liver
  • Bilirubin transported into hepatocyte and binds Ligandin
  • Glucuronidation -> conjugated bilirubin
  • Bilirubin conjugation actually involves clevage site, heme oxygenase conversion into Biliverdin, and then conjugated bilirubin
  • Bile excreted into bile duct In the intestine:
  • Bilirubin glucuronide (conjugated) converted back into bilirubin (unconjugated) by gut bacteria
  • Bilirubin converted into urobilinogen/urobilin
  • Urobilin should be reabsorbed and sent to kidney (yellow color of urine)
  • Urobilinogen converted to stercobilin and excreted by gut (brown color of stool)

**There is no bilirubin in urine or stool!

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13
Q

What are causes of high unconjugated (indirect) bilirubin?

A

Excess bilirubin production

  • Hemolysis

Failure of conjugation (typ hereditary)

  • Gilbert syndrome
  • Neonatal jaundice
  • Crigler-Najjar

(Other lecture also mentioned decreased uptake such as with Rifampin)

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14
Q

What are causes of high conjugated (direct) bilirubin?

A
  • Biliary obstruction
  • Liver damage
  • Failed excretion
  • Dubin-Johnson
  • Rotor

(Other lecture separated this into main liver disease or obstructive causes; important here to also add failed excretion)

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15
Q

How is clinical testing for direct vs. indirect bilirubin done?

A

Uses a color assay (diazo)

  • Conjugated bilirubin is soluble and direct-reacting
  • Unconjugated bilirubin is not soluble and only reacts after alcohol is added

After initial and then alcohol stages, the total amount has reacted

  • Indirect is calculated by subtracting direct from total
  • A small amount of unconjugated reacts without alcohol (5-10% of total), so direct levels might be a tad high
  • Normal unconjugated levels are 0, but will get a low amount using this assay
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16
Q

What is cholestasis?

A

Failure of bile excretion

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17
Q

What are effects of cholestasis?

A
  • Bile contents in the circulation
  • Bilirubin -> jaundice
  • Bile salts -> pruritis
  • Hepatocyte effects
  • Obstruction -> alkaline phosphatase
  • Damage -> ALT and AST
  • Malabsorption of fats and fat-soluble vitamins
  • Absence of stercobilin in stool (clay-colored) and urobilin in urine (colored instead by bilirubin, darker?)
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18
Q

Look at these pictures of dilated bile ducts due to obstruction

A
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19
Q

What is shown here?

A

ERCP

  • Large duct obstruction
  • Can see stone and dilated duct leading into liver
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20
Q

What is seen here? Main features?

A

Normal liver histology

  • Portal tract (triad)
  • Terminal hepatic venule
  • Zones 1-2-3 moving from tract -> venule
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21
Q

What are diseases of small duct obstruction

A
  • Primary biliary cirrhosis (aka non-suppurative
  • Primary sclerosing cholangitis
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22
Q

What happens in primary biliary cirrhosis?

A
  • PBC – cells and lymphocytes destroy bile duct
  • Granulomas
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23
Q

What happens in primary sclerosing cholangitis?

A
  • Primary sclerosing cholangitis
  • Bead signs (dilated and strictured areas
  • Thick onion-skin appearance of fibrous tissue obstruction the duct
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24
Q

What is seen here?

A

Primary biliary cirrhosis

  • PBC – cells and lymphocytes destroy bile duct
  • Granulomas
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25
Q

What is seen here?

A
  • Primary sclerosing cholangitis
  • Bead signs (dilated and strictured areas
  • Thick onion-skin appearance of fibrous tissue obstruction the duct
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26
Q

What is seen here?

A
  • Primary sclerosing cholangitis
  • Bead signs (dilated and strictured areas
  • Thick onion-skin appearance of fibrous tissue obstruction the duct
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27
Q

Look at these key anatomic features of the liver

A
  • Hepatic vein: entering superiorly
  • Sinusoid
  • Portal vein: entering base of the liver
  • Coronary vein: comes int quite high off of the liver
  • Splenic vein
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28
Q

What happens vascularly in cirrhosis (think of key anatomic features just mentioned)

A

Portal HTN- result of increased portal venous inflow and sinusoidal resistance

  • Splanchnic vasodilation and increased flow into mesenteric veins (leading to:)
  • Increased flow into portal vein
  • Distorted sinusoidal architecture -> increased resistance
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29
Q

What is the pathophysiology of ascites and HRS (hepato-renal syndrome)?

A
  • Cirrhosis causes portal HTN and NO overproduction
  • NO overproduction causes splanchnic and arterial vasodilation
  • This splanchnic arterial vasodilation results in both (1) decreased effective BV and (2) splanchnic lymph production
  • Decreased effective blood volume stimulates ADH production, Sympathetic nervous system activation, and the RAAS system
  • All of these cause (1) sodium/water retention and (2) decreased renal blood flow
  • Ascites results from this sodium/water retention (from decreased effective blood volume) and splanchnic lymph production (both of these are a result of splanchnic and arterial vasodilation)
  • HRS results from decreased renal blood flow
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30
Q

What causes hyponatremia?

  • Cirrhosis is the leading cause of ____
  • Indication of outcomes
  • Associations
  • Treatment
A

NOT a shortage of salt

Cirrhosis is the leading causes of dilutional (hypervolemic) hyponatremia

  • Water retention exceeds Na retention
  • Complications and outcomes are worse in pts with hyponatremia
  • May be associated with diuretics
  • Treated with WATER restriction
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31
Q

What sign/symptom is a big turning point?

  • Prognosis?
A

Ascites

  • 50% mortality at 2 yrs
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32
Q

What causes ascites?

  • Complications
  • Treatment
A
  • Requires 10 mm transhepatic pressure gradient
  • May be infected- spontaneous bacterial peritonitis (SBP)

Treatment: paracentesis

  • Direct aspiration of fluid
  • Bleeding is not related to coagulopathy
  • Fluid shift after paracentesis
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33
Q

What is the Serum-Ascites Albumin Gradient (SAAG)?

A
  • Hydrostatic pressure pushes fluid out
  • Osmotic pressure pulls fluid in
  • The difference is SAAG (>1.1 g/dL)
  • Serum and ascites on the same day
  • > 97% accuracy in predicting portal hypertension
34
Q

How does paracentesis of someone with ascites change the body volume compartments?

A
  • In ascites, there is much flow from blood compartment into body water and ascites
  • With paracentesis, you remove the fluid from ascites compartment, but also blood volume (poor perfusion of kidney)
  • Want to add albumin to move fluid from body water and maintain blood volume
35
Q

How does diuretic use of someone with ascites change the body volume compartments?

A
  • Decrease blood volume in an attempt to decrease amount of fluid causing ascites?
  • Diuretics are dangerous, because they remove fluid from your most vulnerable compartment (blood), causing decreased perfusion to kidneys
36
Q

What do diuretics do?

  • How to use
A
  • Promote excretion of salt in urine
  • Combination is more effective
  • Spironolactone 100 – 400 mg/day
  • Furosemide 40 – 160 mg/day
  • Peripheral edema provides a buffer
  • Patients without edema are at risk of renal failure
  • May cause hyponatremia
37
Q

What is refractory ascites?

  • Prevalence
  • Prognosis
A

Failure to respond to optimal dosing of diuretics and sodium restriction

  • Assuming compliance with 2g Na
  • Not taking NSAIDs Happens in under 10% of pts 75% mortality at 1 yr
38
Q

What are options for treating refractory ascites?

A
  • Serial paracentesis
  • TIPS
  • Liver transplantation
  • Perinovenous shunt (LeVeen, Denver)
39
Q

How is serial paracentesis used to treat refractory ascites?

What do different amounts of ascites indicate/require?

A

Pts who require paracentesis >6L every 10 days are not compliant with sodium restriction

  • Ascites [sodium] is the same a serum
  • 10d oral intake amount = 6 L ascites fluid amount

Albumin infusion

  • Prevents renal injury
  • Given for paracentesis > 5L TIPS makes ascites easier to control
40
Q

How does TIPS work?

A

Transjugular Intrahepatic Porto-systemic Shunt

  • Expandable shunt from hepatic vein to portal vein
  • Immediately solves the pressure problem
  • Downside is that this shunted blood is no longer filtered… -> encephalopathy and confusion
41
Q

What is Hepatorenal syndrome (HRS)?

A
  • Caused by advanced chronic or acute liver failure with portal hypertension
  • Serum creatinine >1.5 mg/dL or clearance under 40 mL /min
  • No shock, bacterial infection, nephrotoxic drugs, or massive gastrointestinal or renal fluid losses
  • No sustained improvement in renal function following diuretic withdrawal and expansion of plasma volume with 1.5 L of isotonic saline
  • Less than 500 mg/dL proteinuria and no ultrasonographic evidence of obstructive uropathy or parenchymal kidney disease
42
Q

What are the types of hepatorenal syndrome?

A

Type 1: rapidly progressing

  • Doubling of the initial serum creatinine to a level > 2.5 mg/dL OR
  • 50% reduction in initial creatinine clearance to a level lower than 20 mL/min in under 2 wks

Type 2: slow course

43
Q

What is hepatorenal management?

A
  • Triple therapy
  • Albumin
  • Octreotide (SS analog)
  • Midodrine
  • TIPS
  • Liver transplantation
44
Q

What is seen here?

A

Esophageal bleed on endoscopy

45
Q

Portal hypertension can lead to varices where?

How does it alter blood flow?

A

High pressure in portal vein reverses direction of blood through coronary veins to stomach and esophagus

  • Esophageal varices
  • Stomach
46
Q

What are the different stages of varices/pressures?

A
  • Expansion: HPVG > 10 mmHg (hepatic portal vein gradient?)
  • Bleeding: HPVG > 12 mmHg (mean 20 mmHg)
47
Q

What characteristics of varices is related to risk of bleed?

A
  • Location (gastric > esophageal)
  • Risk of bleed is related to the SIZE of varices (directly proportional to wall tension; LaPlace)
  • Appearance: red sign (mucosa starting to split apart)
  • Variceal pressure > 12 mmHg (not direct ratio, just 12 threshold)
48
Q

The risk of bleeding with varices is due to ___ NOT ____

A

The risk of bleeding with varices is due to location (and underlying pressure) NOT coagulopathy!

49
Q

What are the relative bleeding risks for different variceal locations?

A

1. Esophageal (most common)

2 .Gastroesophageal (higher risk)

  • Lesser curve (GOV type 1)
  • Greater curve (GOV type 2)- bleed more than lesser

3. Isolated gastric varices (less common but higher bleeding risk than GOV for type 1. Basically all IGV type 1 bleed)

  • Fundus (IGV type 1)- bleed more than other
  • Other (IGV type 2)
50
Q

What is seen here?

A

Red sign (Red Wales) of varices

51
Q

What is primary prophylaxis for varices?

A
  • Hepatic venous pressure gradient (HVPG) is affected by inflow and outflow
  • No bleeding if HVPG under 12 mm Hg

Treatment:

- Non-selective beta-blockers: reduce splanchnic blood flow

  • Vasoconstriction (unopposed alpha)
  • Decreased cardiac output

- TIPS

- Variceal ligation (+/- B blocker)

Not:

  • Nitrates – higher mortality
  • Angiotensin II blockers not helpful
52
Q

T/F: Most cirrhotics have true clotting defect

A

False?

53
Q

What can be done to evaluate in vivo coagulation?

A

Thrombin generation assay is pretty close

  • Measures both procoagulant and anticoagulant activities
  • “ETP—endogenous thrombin potential”
54
Q

What conclusions were found in regards to coagulopathy in cirrhotics?

A
  • Routine coagulation tests (PT, PTT) are inadequate to assess bleeding risk in cirrhotic patients
  • Thrombin generation assays incorporating anticoagulant factors provide a more relevant indicator of bleeding risk
  • Coagulation is “rebalanced” in cirrhosis
  • Abnormal coagulation in cirrhosis is less important than portal hypertension in increasing bleeding risk!
55
Q

T/F: There is a concern about thrombosis in cirrhosis

A

True!

May be shifting from worried about bleeding (coagulation defect) to thrombosis

  • One study found an increased risk of VTE in patients with cirrhotic and non-cirrhotic liver disease
  • An imbalance in coagulation was found favoring procoagulant activity
  • Looks like Protein C deficiency
56
Q

What are different encephalopathy symptoms seen in cirrhotics (more/less common)?

A

More common:

  • Confusion or coma
  • Asterixis
  • Loss of fine motor skills
  • Hyperreflexia

Less common:

  • Cognitive deficits detected by special testing
  • Babinski sign
  • Slow, monotonous speech
  • Extrapyramidal-type movement disorders
  • Clonus
  • Decerebrate posturing
  • Decorticate posturing
  • Hyperventilation
  • Seizures*
57
Q

What are the symptoms of encephalopathy: stage 0?

A
  • No changes in personality or behavior
  • No asterixis
58
Q

What are the symptoms of encephalopathy: stage 1?

A
  • Trivial lack of awareness
  • Shortened attention span
  • Impaired addition or subtraction.
  • Hypersomnia, insomnia, or inversion of sleep pattern
  • Euphoria or depression
  • Asterixis may be present
59
Q

What are the symptoms of encephalopathy: stage 2?

A
  • Lethargy or apathy
  • Disorientation
  • Inappropriate behavior
  • Slurred speech
  • Obvious asterixis
60
Q

What are the symptoms of encephalopathy: stage 3?

A
  • Gross disorientation
  • Bizarre behavior
  • Semistupor to stupor
  • Asterixis generally absent
61
Q

What are the symptoms of encephalopathy: stage 4?

A

Coma

62
Q

What are goals of therapy in treating encephalopathy?

A

Identify and eliminate precipitating factors

  • Infection
  • GI Bleeding
  • Constipation
  • Hypokalemic metabolic alkalosis
  • Drugs: benzodiazepines, barbiturates, opiates

Inhibit noxious neurotransmitters

  • Reduce production and absorption of nitrogenous substances from the gut
  • Increase excretion of nitrogenous substances
63
Q

What drugs can be used to treat encephalopathy?

A
  • Lactulose

Antibiotics

  • Rifaximin
  • Neomycin
  • Metronidazole
64
Q

Characteristics of Lactulose?

  • Drug class
  • Indications
A

Poorly absorbed disaccharide; changes colon pH and bacterial growth environment

  • Prevention and treatment of HE
  • Diarrhea (esp), dehydration, hypernatremia
65
Q

Characteristics of Rifaximin?

  • Drug class
  • Indications
A

Non-aminoglycoside, semi-synthetic, nonsystemic antibiotic

  • Reduction in risk of recurrence of overt HE in patients 18+ years old
66
Q

Characteristics of Neomycin?

  • Drug class
  • Indications
A

Aminoglycoside antibiotic

  • Adjuvant in hepatic coma or intolerance other antibiotics
  • Ototoxicity and nephrotoxicity
67
Q

Characteristics of Metronidazole?

  • Drug class
  • Indications
A

Synthetic antiprotozoal and antibacterial agent

  • Not FDA approved for HE May cause peripheral neuropathy and DDI with alcohol
68
Q

Fun fact: on an individual basis, ammonia levels aren’t that indicative of risk of HE event (although there is some broad correlation)

A

Merp

69
Q

How to manage PSE?

A
  • Serum ammonia is not usually helpful
  • Maintain protein intake as tolerated
  • We no longer recommend protein restriction
  • Lactulose
  • Non-absorbable antibiotics
  • Neomycin
  • Metronidazole
  • Rifaximin
  • Experimental therapy – GPB
70
Q

How to assess liver failure (for possible surgery?)?

A

Child-Turcotte-Pugh (CTP)

71
Q

What are the Child-Turcotte-Pugh (CTP) classes based on point score?

A
72
Q

What scoring system is better than CTP for evaluating liver failure?

A

MELD- Model of End Stage Liver Disease

73
Q

What does MELD measure? Predict?

A
  • Formula based on bilirubin, INR, creatinine; no subjective component
  • Predicts mortality at 90 days
  • Adopted for liver allocation in 2002
  • Sickest get transplanted first
  • Avoids certain problems with CTP
  • Accurate in about 80% of patients – requires certain exceptions
74
Q

What is the MELD formula?

A

6.3 + ([0.957 x log creat] + [0.378 x log bili] + [1.12 x log INR] + 0.643) x 10

75
Q

When should MELD be renewed? Exceptions?

A
  • 25+ – every 7 days
  • 19-24 – every 30 days
  • 11-18 – every 90 days
  • < 10 – every year

Exceptions:

  • Tumors
  • Biliary sepsis
  • Lung diseases
  • Metabolic diseases
  • Bleeding
76
Q

What is the prognostic significance of MELD scores?

A
77
Q

Prognostic evaluations of MELD score are affected by what?

A

Serum sodium!

  • With lower sodium, MELD score doesn’t have quite such a bad prognosis (modulated)
78
Q

Summary of Cirrhosis Complications

A
79
Q

Summary of Ascites and HRS

A
80
Q

Summary of Variceal Bleeding

A
81
Q

Summary of PSE

A
82
Q

Summary of Risk Assessment

A

MS2 GI (26 decks)

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