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GI/Rheumatology Module > Complications of Alcohol Induced Liver Disease > Flashcards

Complications of Alcohol Induced Liver Disease Flashcards

1
Q

What is the 2nd most common cause of Cirrhosis in the US?

A

Alcohol Liver Disease

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2
Q

Does the liver have the ability to regenerate? Can it do so with repeated hepatocyte damage?

A

Yes, and repeated hepatocyte damage results in a buildup of connective tissue inhibiting regeneration

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3
Q

What is the normal Metabolic Function of the Liver?

A
  1. Gluconeogenesis
  2. Oxidation of Fatty Acids
  3. Formation of Urea
  4. CYP Enzymes
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4
Q

What is the normal Synthetic Function of the Liver?

A

Synthesis of plasma proteins, albumin, and clotting factors

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5
Q

What is the normal Bile Production of the Liver?

A

Produces bile to be stored in the gallbladder and excreted to help with digestion

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6
Q

What liver function tests are performed to monitor Cellular Function of the liver?

A

AST and ALT

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7
Q

What liver function tests are performed to monitor Synthetic/Metabolic Function of the liver?

A
  1. PT
  2. INR
  3. Albumin
  4. Ammonia
  5. Cholesterol
  6. Glucose
  7. Platelets
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8
Q

What liver function tests are performed to monitor Obstruction of the liver?

A
  1. Bilirubin
  2. Alk Phos
  3. GGT
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9
Q

What is responsible for 2/3 of cirrhosis?

A

Alcohol

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10
Q

Are women or men more susceptible to alcoholic liver injury?

A

Women

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11
Q

What are the steps of Alcoholic Liver Disease Progression?

A
  1. Steatosis
  2. Alcoholic Hepatitis
  3. Cirrhosis
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12
Q

Steatosis, Hepatitis, and Cirrhosis mean what in ALD?

A

Steatosis = Really fatty liver
Hepatitis = Inflammation
Cirrhosis = End stage liver disease

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13
Q

Hepatic Steatosis can be seen how?

A
  1. Increased intracellular accumulation of TG
  2. Reversible
  3. No cell death, normal LFTs
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14
Q

Hepatitis can be seen how?

A
  1. Death of hepatocytes, inflammatory infiltrations, cell necrosis
  2. Somewhat Reversible
  3. Collagen production = scar tissue
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15
Q

Cirrhosis can be seen how?

A
  1. Hepatocytes are replaced by fibroblasts
  2. Irreversible
  3. Shrinkage of the Liver
  4. Portal HTN
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16
Q

What are the S/S of Cirrhosis?

A
  1. Ascites
  2. Jaundice/Icterus
  3. Clay Colored Stools
  4. Cola Colored Urine
  5. Palmar Erythema
  6. Altered Mental Status
  7. Asterixis
  8. Abdominal Pain
  9. Spider Angiomas
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17
Q

What is a laboratory test that reveals cellular dysfunction of the liver?

A

INCREASED AST/ALT

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18
Q

What is a laboratory test that reveals synthetic/metabolic dysfunction of the liver?

A
  1. INCREASED PT/INR
  2. DECREASED Albumin
  3. INCREASED Ammonia
  4. DECREASED Platelets
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19
Q

What is a laboratory test that reveals obstruction of the liver?

A
  1. INCREASED Bilirubin
  2. INCREASED All Phos
  3. INCREASED GGT
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20
Q

ALT>AST reveals what?

A

Hepatocellular Injury, more specific to the liver

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21
Q

AST>ALT reveals what?

A

Acute Alcoholic Hepatitis

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22
Q

Why do you seen normal/decreased AST/ALT in Cirrhosis?

A

Too many cells have died off and therefore, they are no more cells that can produce AST and ALT

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23
Q

Why is there decreased albumin in hepatic failure?

A

Decrease synthesis and malnutrition, resulting in serum oncotic pressure and fluid retention

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24
Q

Why is there increased ammonia NH3 in hepatic failure?

A

Product of amino acid metabolism that is cleared by the liver

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25
Q

Why is there increased prothrombin time PT and international normalized ratio INR in hepatic failure?

A

Due to decreased synthesis of clotting factors by the liver

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26
Q

Why is there decreased platelets in hepatic failure?

A

Due to splenomegaly from portal HTn and decreased hepatic production of thrombopoietin

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27
Q

Why is there increased alkaline phosphatase Alk Phos and gamma-glutamyl transpeptidase GGT?

A

Increase Alk Phos + Normal GGT = non hepatic source
Increase GGT is marker for alcohol abuse

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28
Q

Why is there an increase in total bilirubin in hepatic failure?

A

Result of liver damage or obstruction

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29
Q

What are the lab findings for Cholestatic Jaundice?

A
  1. Moderate AST/ALT elevation <500
  2. Increased bilirubin
  3. Alk Phos >4x normal average
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30
Q

What are the lab findings for Alcoholic Hepatitis?

A
  1. AST at least 2x ALT
  2. Increased bilirubin
  3. Alk Phos normal to <3x average
  4. Decreased albumin
  5. Increased PT/INR
  6. Increased GGT
  7. Thrombocytopenia
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31
Q

What are the lab findings for Acute Liver Toxicity?

A
  1. AST/ALT in the 1000s
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32
Q

In the Model for End Stage Liver MELD Score what score indicates a poor prognosis?

A

> 18

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33
Q

MELD Score is used for what patients?

A

Short term view of survival 3-months, helps prioritize patients for transplant

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34
Q

In the Maddrey Discriminant Function MDF Score what score indicated a poor prognosis?

A

> 32

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35
Q

MDF Score is used for what patients?

A

Alcoholic Hepatitis, short term prognosis

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36
Q

For those with MDF Score >32 what is the treatment recommended in Alcoholic Hepatitis Treatment?

A

Prednisolone

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37
Q

What is the MOA of Prednisolone?

A
  1. Anti-Inflammatory
  2. Anti-Fibrotic
  3. Reduces Cytokine Production
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38
Q

What are the CIs of Prednisolone?

A
  1. Active GI Bleed
  2. Infection
  3. AKI
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39
Q

What is the survival benefit timeline of Prednisolone?

A

Max 28 days

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40
Q

What are Contraindications to treatment for Alcoholic Hepatitis?

A
  1. Uncontrolled infections
  2. Acute kidney injury with serum creatinine >2.5 mg/dL
  3. Uncontrolled upper gastrointestinal bleeding
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41
Q

If the patient is eligible for treatment for Alcoholic Hepatitis, what should be started?

A
  1. Prednisolone
  2. Enteral nutrition
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42
Q

What are the 5 complications of cirrhosis?

A
  1. HE
  2. EVB
  3. HRS
  4. Ascites
  5. SBP
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43
Q

What is Ascites?

A

Accumulation of an excessive amount of fluid within the peritoneal cavity

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44
Q

What is the pathophysiology for Ascites?

A
  1. Fibrotic liver –> portal HTN –> activates vasodilatory mechanisms (NO)
  2. Kidneys sense inadequate renal perfusion and activate the RAAS to retain more Na and H2O
  3. Increase hydrostatic pressure
  4. Decrease oncotic pressure due to decrease albumin production
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45
Q

What are the S/S of Ascites?

A
  1. Protruding abdomen
  2. Pitting edema
  3. Positive fluid wave
  4. Shifting dullness
  5. Abdominal pain
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46
Q

For the very first episode of Ascites, what is the diagnosis/fluid assessment?

A

SAAG Score = Albumin serum - Albumin ascitic fluid

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47
Q

What SAAG Score confirms portal HTN causation?

A

> 1.1 m/dL

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48
Q

What are the grades of Ascites, and the type of therapy considerations?

A
  1. Mild = sodium restriction
  2. Moderate = diuretics
  3. Large = drain tap
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49
Q

What are the goals of therapy for Ascites?

A
  1. Control ascites
  2. Prevent/relieve symptoms
  3. Prevent complications
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50
Q

What are the non-pharmacologic interventions for Grade 1 Mild Ascites?

A
  1. Alcohol Abstinence
  2. Sodium Restriction <2 g/day
  3. Fluid Restriction if Na <120-125 mEq/L
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51
Q

What is the first line treatment option for Grade 2 Moderate Ascites?

A

Spironolactone + Furosemide + Nonpharmacologic

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52
Q

What is the MOA of Spironolactone?

A

Inhibits the action of aldosterone in the distal convoluted tubule; K+ sparing

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53
Q

What is the MOA Furosemide?

A

Inhibits reabsorption of Na and Cl in the ascending loop of Henle and distal renal tubule

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54
Q

What is the dosing ratio of Spironolactone and Furosemide?

A

Spironolactone 100 mg/day PO
Furosemide 40 mg/day PO

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55
Q

Why is the dosing ratio so important for Spironolactone and Furosemide?

A

Keep Potassium within NORMAL range

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56
Q

If you can only do one drug between Spironolactone and Furosemide, which one would be better?

A

Spironolactone, because of RAAS inhibition

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57
Q

What is the treatment titration for Spironolactone and Furosemide?

A
  1. Double dose to response every 3-5 days
  2. MAINTAIN 100 mg: 40 mg ratio for normokalemia
  3. MAX Dose: Spironolactone 400 mg + Furosemide 160 mg
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58
Q

What is the goal of the dual diuretic?

A

Make patient comfortable, will note completely eliminate ascites

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59
Q

HOLD diuretic therapy if what has occurred during monitoring?

A
  1. Uncontrolled or recurrent encephalopathy
  2. Sodium <120 mEq/L
  3. Acute change in baseline renal function AKI
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60
Q

Paracentesis is the manual removal of large volume, and is indicated when?

A

First line treatment for tense ascites/refractory ascites Grade 3 Severe

61
Q

When performing paracentesis, what must be added?

A

If removing >5 liters, give 6-8 albumin per liter of fluid removed to maintain oncotic pressure

62
Q

What is considered Grade 3 Severe Ascites?

A
  1. Unresponsive to optimized treatment (high dose diuretics and sodium restricted diet)
  2. Recurs rapidly after therapeutic paracentesis
63
Q

What are drugs to avoid in Grade 3 Ascites?

A
  1. NSAIDs
  2. ACE/ARBs
  3. All Nephrotoxins
  4. Non-Selective BB
64
Q

Why avoid NSAIDs?

A

Can reduce urinary sodium excretion, AKI
Bleed risk

65
Q

Why avoid ACE/ARBs?

A

AKI, hypotension

66
Q

Why avoid Non-Selective BB?

A

Can cause hypotension in those with refractory ascites, worsening the condition
-NOT an absolute contraindication but take caution in those with hypotension, hyponatremia, or AKI

67
Q

What is Esophageal Varices/Variceal Bleed EVB?

A

Medical Emergency
Enlarged collateral blood vessels that form in the esophagus secondary to portal HTN

68
Q

What is Portal HTN?

A

Gradient of >5 mmHg between the portal and central venous pressure

69
Q

What is the pathogenesis of Portal HTN?

A

Cirrhotic Liver is Less Compliant –> More Resistance to passage of blood flow –> Blood backs up into. the portal vein
HTN = the body tries to release NO vasodilator but it does nothing for the portal HTN, but it DOES dilate the vessels leading into the portal vein so it leads to increased backup of vessels = engorged = varices

70
Q

What is the Root Cause for many of the complications of cirrhosis?

A

Portal HTN

71
Q

What is the most common lethal complication of Cirrhosis?

A

EVB

72
Q

What are concerns of EVB?

A
  1. Recurrence rates very high within first 6 months after initial bleed –> Increased risk of Infection
  2. Increased the risk of developing encephalopathy HE and spontaneous bacterial peritonitis SBP
73
Q

What are the risk factors for EVB?

A
  1. Large varices
  2. Endoscopic Red Signs: red wale marks
  3. Advanced Child Pugh Score
  4. Medications that Increase Bleeding
  5. Coagulopathies –> HIGH INR, LOW PT, LOW Platelets
74
Q

What are the symptoms of EVB?

A
  1. Severe hematemesis
  2. Melena
  3. Upper GI Bleed
  4. Hypotension/Shock
75
Q

What are the labs that demonstrate EVB?

A
  1. Decreased Hgb/Hct
  2. Increased INR
  3. Increased PT
  4. Decreased Platelets
76
Q

What lab value drops during ACTIVE Bleeding?

A

HEMOGLOBIN

77
Q

What is used to diagnosis EVB, and should be done in all cirrhosis patients to screen for varices?

A

Esophagogastrodudodenscopy EGD

78
Q

What are the goals of therapy for EVB?

A
  1. Primary Prophylaxis: prevention of first bleeding episode
  2. Acute Variceal Hemorrhage Treatment: stop active bleeding
  3. Secondary Prophylaxis: prevent re-bleed
79
Q

What type of patients have an indication for primary prophylaxis for EVB?

A
  1. Small Varices + Risk Factors = Nonselective BB
  2. Medium/Large Varices = Nonselective BB if NO hemorrhage risk factors present
80
Q

What is the main treatment option for primary prophylaxis of EVB?

A

Nonselective Beta Blockers:
1. Propranolol
2. Nadolol
3. Carvedilol

81
Q

What is the MOA of Nonselective BB in EVB primary prophylaxis?

A

Decreased portal pressure by reducing portal venous inflow
B1: decreased cardiac output
B2: splanchnic vasoconstriction
A1: intrahepatic vasodilation

82
Q

How do you titrate the 3 main nonselective BB for primary prophylaxis?

A

Titrate to max tolerated dose until you reach a heart rate of 55-60 BPM

83
Q

What is EVL, and when is it used?

A

Endoscopic Variceal Ligation aka placing rubber bands around varices until they are obliterated, used in active bleed

84
Q

If primary prophylaxis has failed, Active Variceal Bleed is occurring what has to be done first?

A

DC BB, patient is hypotensive due to blood loss, STOP BB immediately before starting first line treatment

85
Q

What class of drugs are utilized in Active Variceal Bleed?

A

Splanchnic Vasoconstrictors

86
Q

What is the MOA of splanchnic vasoconstrictors?

A

Decrease portal blood flow and pressure

87
Q

What is the first line therapy option for Splanchnic Vasoconstrictors?

A

Octreotide

88
Q

What is the MOA of Octreotide?

A

Somatostatin analogue that inhibits release of vasodilatory peptides

89
Q

What is another splanchnic vasoconstrictor that is rarely used due to more adverse effects?

A

Vasopressin

90
Q

What is the MOA of Vasopressin

A

Antidiuretic hormone, nonselective vasoconstrictor, systemic effects

91
Q

EVB increases the risk of what?

A

Bacterial Infection SBP

92
Q

What is the agent of choice that is a prophylactic antibiotic that can decrease mortality and decrease recurrent bleeding?

A

Ceftriaxone

93
Q

What is the duration of Ceftriaxone for prophylactic dosing in active variceal bleeds?

A

7 days MAX

94
Q

What is an alternative to Ceftriaxone for prophylactic dosing in active variceal bleeds?

A

Ciprofloxacin

95
Q

What is TIPS can when should it be used?

A

Transjugular Intrahepatic Portosystemic Shunt, salvage therapy if failed to control bleed with EVL

96
Q

TIPS has an increased incidence of what?

A

Hepatic Encephalopathy

97
Q

What does the TIPS Shunt cause?

A

Bypass the portal vein/liver completely = buildup of toxins
1. Decreased portal pressure
2. Increased Ammonia levels = encephalopathic

98
Q

What is the treatment of choice for Secondary Prophylaxis of EVB?

A

Nonselective BB + EVL

99
Q

When do you start Secondary Prophylaxis of EVB?

A

After octreotide is DC’d
Do NOT start after TIPS or Shunt Surgery –> they do not require secondary prophylaxis

100
Q

What is the Nonselective BB of choice for Secondary Prophylaxis of EVB?

A
  1. Propranolol
  2. Nadolol
101
Q

What is Hepatic Encephalopathy?

A

Worsening of cognitive function that occurs when the liver is no longer able to remove toxic substances from the blood

102
Q

What lab value is seen with Hepatic Encephalopathy?

A

Increase Ammonia NH3 levels

103
Q

Why does Hepatic Encephalopathy cause worsening of cognitive function?

A

Increased ammonia levels cause mental status changes because it crosses BBB

104
Q

What medications are precipitating factors in hepatic encephalopathy?

A
  1. Sedatives
  2. Neuropleptics
  3. Analgesics
  4. Antidepressants
  5. CNS depressants
  6. Diuretics
105
Q

What are a precipitating factors in hepatic encephalopathy?

A
  1. GI Bleeds
  2. Infection
106
Q

What are S/S of hepatic encephalopathy?

A
  1. Altered mental status
  2. Asterixis
107
Q

Diagnosis of hepatic encephalopathy can be seen with elevated NH3, but it does not correlate with what?

A

How the treatment is progressing

108
Q

What are the non-pharmacologic interventions of hepatic encephalopathy?

A
  1. Reduce ammonia production: dietary protein restrictions
  2. Avoidance and prevention of precipitating factors
109
Q

What do you monitor in hepatic encephalopathy?

A
  1. Electrolytes
  2. Mental Status
  3. NOT Ammonia
110
Q

What is the first line prevention and treatment of hepatic encephalopathy?

A

Lactulose

111
Q

What is the MOA of Lactulose?

A

Ion trapping, NH3 –> NH4 –> Excreted in stool

112
Q

How do you titrate Lactulose in Hepatic Encephalopathy?

A

TID dosing titrated to 2-3 soft stools per day

113
Q

What is an alternative to Lactulose if first line treatment failure, or can be add on therapy to Lactulose for hepatic encephalopathy?

A

Rifaximin/Xifaxan

114
Q

What is the MOA of Rifaximin?

A

Decreased urease-containing bacteria in the intestine –> Decrease the production of NH3 from proteins and amino acids

115
Q

What is the titration regimen of Rifaximin for hepatic encephalopathy?

A

BID: prevention/treatment
TID: treatment
NOT titrated to stools

116
Q

What drug has Disulfiram-Like Reactions and has limited use in hepatic encephalopathy?

A

Metronidazole

117
Q

What is SBP?

A

Spontaneous Bacterial Peritonitis
Acidic Fluid + Bacteria = Infection

118
Q

What is the pathophysiology of SBP?

A

Bacterial Translocation, migration from the intestines to mesenteric lymph nodes

119
Q

What are common organisms that can cause SBP?

A
  1. E. coli = -
  2. Klebsiella Pneumoniae = -
  3. Staphylococcus = +
  4. Streptococcus Pneumonia = +
  5. Enterococcus = +
120
Q

What are the SPECIFIC S/S of SBP?

A
  1. Fever
  2. Leukocytosis
  3. Abdominal pain with rebound tenderness
121
Q

What confirms SBP diagnosis in terms of Cell Count?

A

Absolute PMN >250 cells mm^3 indicates SBP

122
Q

If you have PMN >250 and Positive S/S, but a negative culture what should you do?

A

Continue to treat, PMN >250 = SBP

123
Q

If patient presents with positive S/S of SBP, but culture results are not completed what should you do?

A

Do NOT wait for culture results before initiation of antibiotics if SBP is suspected

124
Q

What is the first line treatment of choice for SBP?

A

Third Generation Cephalosporin
1. Cefotaxime
2. Ceftriaxone
Either one for 5-7 days

125
Q

When do you give Albumin in SBP?

A

ALL PATIENTS but especially those with:
1. Screen > 1 mg/dL
2. BUM > 30 mg/dL
3. t.Billi > 5 mg/dL

126
Q

When do you dose Albumin in SBP?

A

Day ONE and Day THREE

127
Q

What is the role of Albumin in SBP?

A
  1. Decreases mortality and renal impairment
  2. Prevent AKI and SHOCK
128
Q

When is prophylaxis of SBP necessary?

A
  1. Short term primary prophylaxis in the setting of GI BLEED (variceal bleed)
  2. Long term (indefinite) prophylaxis for History of SBP
129
Q

What is the preferred agent for LONG TERM prophylaxis of SBP?

A

Quinolone Antibiotics
1. Ciprofloxacin Preferred

130
Q

What are the disadvantages of long term prophylaxis?

A
  1. Increased risk of resistance organisms
  2. Increased risk of antibiotic side effects
  3. No proven mortality benefit with long-term prophylaxis
131
Q

What is Hepatorenal Syndrome HRS-AKI?

A

Functional renal failure in the setting of cirrhosis in the absence of intrinsic renal disease

132
Q

What is the pathophysiology of HRS-AKI?

A
  1. Portal HTN, RAAS
  2. Sodium and Water Retention
  3. Increased renal vasoconstriction and decrease renal blood flow leads to reduced renal function over time
133
Q

What is the diagnosis for HRS-AKI?

A
  1. Acute Rise in SCr by >0.3 mg/dL within 48 hours or a percent of >50% within 7 days
  2. No response to 2 days of diuretic withdrawal and albumin infusion
134
Q

Diagnosis of KRS-AKI must exclude what?

A
  1. Hypovolemia
  2. Shock
  3. Nephrotoxic Agents
  4. Structural Kidney Disease CKD
135
Q

What is the stepwise approach to HRS-AKI management?

A
  1. Give albumin 1 g/kg x 2 days
  2. If kidney improves after albumin, just monitor
  3. If no response to albumin, they meet full HRS-AKI criteria and need VASOCONSTRICTORS
  4. Treat with IV Vasoconstrictors NE + Albumin = ICU
  5. If IV vasoconstrictors cannot be used, use oral vasoconstrictors + albumin (less effective)
136
Q

What are the oral vasoconstrictors used in HRS-AKI when IV NE is NOT an option?

A

Midodrine + Octreotide TID

137
Q

What is the MOA of Midodrine and Octreotide?

A

Midodrine = Alpha 2 Agonist
Octreotide = Splanchnic Vasoconstrictor

138
Q

For HRS-AKI where must they be treated and with what?

A

ICU
1. Albumin
2. IV NE + Albumin
3. (PO Midodrine + Octreotide) + Albumin

139
Q

Albumin administration is not indicated for what complication?

A

HE hepatic encephalopathy

140
Q

What are the changes in PK affecting ALD/Cirrhosis?

A
  1. Decreased blood supply to liver an increase metabolic activity
  2. Decrease protein binding secondary to decreased albumin
  3. Accumulation of intestinal fluid
141
Q

Decreased blood supply to liver an increase in metabolic activity leads to what?

A
  1. Decrease drug clearance
  2. Increase drug half life
142
Q

Decrease protein binding secondary to decreased albumin lead to what?

A
  1. Increase free fraction = active drug
143
Q

Accumulation of interstitial fluid leads to what?

A
  1. Increased volume of distribution
  2. Increased drug half life
144
Q

What are examples of Hepatic Biotransformation>

A

Phase I and II Reactions

145
Q

What are Phase I Reactions?

A
  1. CYP450
  2. Drug metabolism by these reactions is affected
  3. Consider medications that do not undergo phase I
  4. Hydrolysis, Oxidation, Dealkyation, and Reduction
146
Q

What are Phase II Reactions?

A
  1. Conjugation
  2. Drug metabolism by these reactions are usually UNaffected
  3. If possible use drugs that undergo phase II
147
Q

It is safer to use a drug that undergoes what phase in hepatic considerations?

A

Phase II

148
Q

What are the treatment options for Alcohol Withdrawal?

A
  1. Replete with thiamine
  2. Replete with folate
  3. Replete electrolytes
  4. Benzos given PRN based on symptoms

GI/Rheumatology Module (18 decks)

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