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Clin Med II - GI > Liver (Washington) > Flashcards

Liver (Washington) Flashcards

1
Q

Define steatosis

A

Fatty infiltration of the liver (TGs and other fats inside hepatocytes)

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2
Q

Define steatohepatitis

A

When inflammation is a/w fatty infiltration of the liver

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3
Q

Define cirrhosis

A
  • Chronic degenerative disease
  • Hepatocytes are damaged and replaced by scar tissue
  • Results in decreased function of the liver
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4
Q

What is AST? What does it test for?

A
  • Aspartate Aminotransferase
  • Enzyme normally found in RBCs, liver, heart, muscle, pancreas, kidneys
  • Tests for liver damage (along with ALT)
  • Formerly called SGOT
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5
Q

What are normal AST levels (generally)?

A

Low

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6
Q

How is the amount of AST in the blood related to tissue damage?

A

Directly - more AST in blood means more tissue damage

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7
Q

What does the ratio of AST to ALT tell us?

A

Whether liver or another organ has been damaged

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8
Q

Which liver lab test component is mainly found in liver tissue?

A

ALT

AST is less specific

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9
Q

Which is more specific to the liver - ALT or AST?

A

ALT

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10
Q

What is ALT? What does it test for?

A
  • Alanine Aminotransferase
  • Enzyme found mainly in liver
  • Tests for liver damage/disease
  • Formerly called SGPT
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11
Q

What are normal values of ALT (generally)?

A

Low

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12
Q

What is ALP? What does it test for?

A
  • Alkaline Phosphatase
  • Enzyme made mostly in liver and bone (some in intestines, kidneys, placenta)
  • Non specific
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13
Q

The liver makes more ____ (ALT, AST, ALP) than other organs or bones

A

ALP

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14
Q

Abnormally elevated levels of ALP could be from:

A
  • Rapid bone growth (puberty)
  • HyperPTH
  • Vit D deficiency
  • Liver damage
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15
Q

What is GGT?

A
  • Gamma glutamyl transpeptidase
  • Enzyme in blood that functions as a transport molecule to help liver metabolize drugs/toxins
  • Found in many places but NOT bone
  • Can help you determine if high ALP is prob due to bone disease
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16
Q

What does a high ALP with a high GGT indicate?

A

Liver or bile ducts damage

high GGT rules out bone as a cause!

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17
Q

What does a high ALP with a normal GGT indicate?

A

Bone disease

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18
Q

Define total bilirubin

A

Amount of bilirubin in a blood sample

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19
Q

How does bilirubin circulate in the blood?

A

In 2 forms:

  • Direct (conjugated)
  • Indirect (unconjugated)
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20
Q

Features of indirect bilirubin

A
  • Unconjugated
  • Insoluble
  • Conjugated in the liver
  • Not measured directly form the blood (need total and direct values)
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21
Q

Which type of bilirubin cannot be measured straight from the blood?

A

Indirect

need total and direct to calculate

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22
Q

Elevated levels of indirect bilirubin indicates:

A
  • Hemolysis

- Failure of liver uptake

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23
Q

Features of direct bilirubin

A
  • Conjugated
  • Soluble
  • Measured directly in blood
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24
Q

Elevated levels of direct bilirubin indicates:

A

Impaired secretion of liver

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25
Q

Define albumin, its functions, and what it evaluates

A
  • Protein made by the liver
  • Helps move bilirubin, Ca, hormones and meds through blood
  • Keeps fluid in blood from leaking out into tissues
  • Used to assess liver and kidney disease
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26
Q

Decreased levels of albumin occurs when?

A
  • When body does not get or absorb enough nutrients

- Crohn’s, after wt loss surgery, low protein diets, Celiac

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27
Q

Increased levels of albumin occurs when?

A
  • Dehydration

- High protein diet

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28
Q

Define alcoholic liver disease

A

-Acute or chronic inflammation
-Parenchymal necrosis of liver
induced by alcohol

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29
Q

What is the MC precursor of cirrhosis in the US?

A

Alcoholic liver disease

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30
Q

Is alcoholic liver disease reversible or irreversible?

A

Reversible in early stages

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31
Q

3 major stages of ALD

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
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32
Q

Features of fatty liver stage of ALD

A
  • Present in 90+% of binge and chronic alcoholics
  • Asymptomatic
  • Reversible w/cessation of alcohol
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33
Q

Features of alcoholic hepatitis stage of ALD

A
  • 10-20% of alcoholics
  • Asymp - symptomatic
  • Reversible w/cessation
  • Precursor to cirrhosis
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34
Q

What stage of ALD is the precursor to cirrhosis?

A

Alcoholic hepatitis

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35
Q

What is the first histologic response to any hepatotoxic stimuli (e.g. ETOH)?

A

Fat accumulation

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36
Q

Where does fat accumulation in the liver occur?

A

At the location of alcohol dehydrogenase (leading to a deficiency of this enzyme)

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37
Q

What is the hallmark of alcoholic hepatitis?

A

Hepatocyte injury (degeneration, necrosis, PMN infiltration, fibrosis)

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38
Q

What is the most important risk factor of ALD?

A

Quantity AND duration of alcohol intake

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39
Q

Who is more susceptible to ALD?

A 
-Females
(lower levels of alcohol dehydrogenase to begin with)
-Concurrent HCV
-Genetics
-Fatty liver from obesity
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40
Q

How does ALD occur in pts w/concurrent HCV?

A
  • Develop at a younger age

- Worse survival

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41
Q

What is the amount of alcohol per day threshold for males vs. females in developing ALD?

A
  • Males: 80+ g/d
  • Females: 30-40+ g/d
  • 1 drink is approx. 12 g
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42
Q

If symptoms are present in early ALD (fatty liver), what would it be?

A
  • Hepatomegaly
  • RUQ tenderness (occasionally)
  • Nausea
  • Jaundice (very rare)
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43
Q

How does advanced (alcoholic hepatitis) ALD present?

A
  • SOME are asymp
  • Fever
  • Spider nevi
  • Jaundice
  • Abdominal tenderness
  • Encephalopathy
  • Portal HTN (ascites, esophageal varices)
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44
Q

What lab abnormalities may be found in early (fatty liver) ALD?

A
  • Modest increase in GGT, AST, ALT
  • High TGs
  • High cholesterol
  • High bilirubin (occasionally)
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45
Q

What lab abnormalities may be found in advanced (alcoholic hepatitis) ALD?

A
  • Severe increase in GGT, AST, ALT, AST:ALT
  • High bilirubin (common)
  • High ALP
  • Low albumin
  • Coagulopathy (increased PT)
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46
Q

What imaging is used to evaluate alcoholic liver disease? What does it detect?

A

Ultrasound:

  • Fatty infiltration
  • Size of liver
  • Biliary obstruction
  • Ascites
  • CANNOT detect fibrosis or inflammation
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47
Q

Liver ultrasound cannot detect:

A

Fibrosis and inflammation

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48
Q

What is needed for definitive diagnosis of ALD?

A

Liver biopsy

U/S cannot detect fibrosis and inflammation

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49
Q

Describe liver biopsy’s role in ALD:

A
  • Needed for definitive diagnosis

- Guides therapy

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50
Q

What does early ALD show on liver biopsy?

A

Macrovesicular fat

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51
Q

What does advanced ALD show on liver biopsy?

A

PMN infiltration w/hepatic necrosis, Mallory bodies, and fibrosis
*Findings are non-specific and identical to those of NASH (non-alcoholic steatohepatitis)

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52
Q

General treatment of ALD

A
  • Abstinence from alcohol
  • Proper nutrition (including potentially folic acid, thiamine, zinc supplements)
  • Psych counseling
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53
Q

Pharmacologic treatment of ALD

A
  • Methylprednisolone with taper MAY reduce short term mortality in alcoholic hepatitis
  • Pentoxifylline (TNF-inhibitor) reduces 1 month mortality rates in alcoholic hepatitis
  • NO benefit to use both
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54
Q

Surgical treatment of ALD

A

Liver transplant for end stage cirrhosis

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55
Q

When is Methylprednisolone used in ALD?

A
  • For alcoholic hepatitis
  • Given for 1 month w/a taper
  • MAY reduce short term mortality
56
Q

What is Pentoxifylline and when is it used in ALD?

A
  • TNF inhibitor
  • Given for 1 month
  • Reduces 1 month mortality rate in alcoholic hepatitis
  • Decreases hepatorenal syndrome
  • Used when corticosteroids are contraindicated, no benefit to use both
57
Q

What is the most important prognostic factor of ALD?

A

Continued excessive ETOH use

58
Q

What is the MC chronic liver disease in US?

A

Nonalcoholic Fatty Liver Disease (NAFLD)

59
Q

Why is NAFLD increasing in children?

A

Increasing childhood obesity in the US

60
Q

What is the MC cause of NAFLD?

A

Obesity

61
Q

What meds can cause NAFLD?

A
  • Corticosteroids
  • Amiodarone
  • Diltiazem
  • Tamoxifen
62
Q

What conditions can cause NAFLD?

A
  • DM
  • High TGs
  • Cushing’s
  • PCOS
  • OSA
  • Metabolic syndrome
63
Q

What is the pathology of NAFLD?

A

Macrovesicular steatosis

64
Q

What are the biggest risk factors for progression of NAFLD to advanced hepatic fibrosis and cirrhosis?

A
  • Older age
  • Obesity
  • DM
65
Q

How does NAFLD present?

A
  • Most are asymp
  • Mild RUQ discomfort
  • Hepatomegaly (up to 75% of pts)
66
Q

What is the MC presenting sign of NAFLD?

A

Hepatomegaly

67
Q

Is progression of NAFLD to chronic liver disease common or uncommon?

A

Uncommon

68
Q

What abnormal lab findings could present in NAFLD?

A
  • Mildly elevated AST, ALT, or ALP

- Ratio of ALT:AST is almost always greater than 1

69
Q

How is imaging used in evaluating NAFLD?

A

Macrovascular steatosis may be seen on US/CT/MRI, but it will NOT distinguish b/w steatosis or steatohepatitis

70
Q

What is the diagnostic test of choice for NAFLD?

A

Liver biopsy

71
Q

What does liver biopsy assess for NAFLD?

A

Degree of fibrosis and inflammation

72
Q

Who should NOT have liver biopsy performed if NAFLD suspected?

A

Asymp pts w/normal LFTs

73
Q

What must be ruled out in diagnosing NAFLD?

A
  • Hazardous levels of ETOH use

- Hepatotoxic meds

74
Q

General treatment of NAFLD

A
  • Wt loss
  • Dietary fat restriction
  • Exercise
75
Q

Pharmacologic treatment of NAFLD

A

-Thiazolidinediones
-Vit E
-Metformin
-Pentoxifylline
(all currently being studied)

76
Q

Surgical tx of NAFLD

A

Gastric bypass

77
Q

When is gastric bypass indicated in NAFLD?

A

BMI 35+

78
Q

What is the prognosis of NAFLD?

A
  • Benign and reversible
  • Do have increased mortality compared to those without NAFLD
  • CAN progress to NASH
79
Q

Cirrhosis develops in how many NAFLD pts?

A

1-3%

80
Q

If cirrhosis develops in NAFLD, what is the pt at increased risk for?

A

Liver cancer

*New studies showing an increased risk even in NAFLD pts who don’t develop cirrhosis

81
Q

Risk factors for NASH

A
  • Overweight/obese
  • DM
  • NAFLD (25% get NASH)
82
Q

How does the histology of NASH present?

A

Exactly like alcoholic hepatitis

83
Q

How does NASH present in patients?

A
  • Asymp early in disease

- As disease progresses, fatigue, wt loss and weakness

84
Q

What is the definitive diagnostic test of NASH?

A

Liver biopsy

since all imaging cannot distinguish steatosis from steatohepatitis

85
Q

Treatment of NASH

A
  • Lifestyle (wt loss, low fat diet, physical activity)

- Avoid hepatotoxins

86
Q

Does NASH progress to advanced disease?

A
  • May be a/w fibrosis (40% pts)
  • Cirrhosis develops in 9-25%
  • Hepatocellular carcinoma considered a complication in those who develop cirrhosis
87
Q

What is considered a complication of NASH pts who develop cirrhosis?

A

Hepatocellular carcinoma

88
Q

Is cirrhosis reversible or irreversible?

A
  • May be reversible if cause is removed early in the disease

- Irreversible in advanced stages

89
Q

How do s/s of cirrhosis correlate to severity of disease?

A

Regardless of cause of cirrhosis, s/s present the same and indicate severity of disease

90
Q

What are the 2 MC causes of cirrhosis in the US?

A
  • Alcohol

- HCV

91
Q

Pathology of cirrhosis

A
  • Fibrosis leads to physical changes of liver
  • Formation of regenerative nodules
  • Decreased function and an alteration of blood flow
92
Q

Stages of cirrhosis

A
  1. Compensated (no complications, liver can still compensate and manage)
  2. Compensated (w/varices)
  3. Decompensated (w/complications)
93
Q

How do labs present in cirrhosis?

A
  • Macrocytic anemia
  • WBC low OR high
  • Thrombocytopenia
  • Prolonged PT
  • Elevated AST, ALT, ALP
  • Elevated bilirubin
  • Low albumin
94
Q

How is Doppler US used in evaluating possible cirrhosis?

A
  • Liver size
  • Presence of nodules, ascites
  • Patency of blood vessels
95
Q

How is CT/MRI used in evaluating possible cirrhosis?

A

Assess suspicious nodules for malignancy

96
Q

How is esophagogastroduodenoscopy used in evaluating possible cirrhosis?

A

Confirms presence of varices and can detect causes of bleeding

97
Q

What is the gold standard for diagnosis of cirrhosis?

A

Liver biopsy

98
Q

How is liver biopsy used in evaluating cirrhosis?

A
  • 80-100% sensitivity depending on method and size/number of specimens obtained
  • Can sometimes suggest actual cause of cirrhosis
99
Q

When is liver biopsy not necessary in evaluating possible cirrhosis?

A

If clinical, lab, radiologic data strongly suggest presence of cirrhosis

100
Q

General treatment of cirrhosis

A
  • Tx underlying cause if known
  • ETOH cessation
  • Proper diet
  • Psych
  • Vaccines (HAV, HBV, pneumococcal, annual influenza)
101
Q

Pharmacologic treatment of cirrhosis

A

NO meds currently available to halt progression or reverse cirrhosis

102
Q

What is the MC complication of cirrhosis?

A

Ascites and edema

103
Q

Why does ascites/edema occur with cirrhosis?

A

Portal HTN

104
Q

How do you treat ascites?

A
  • Na restriction
  • Diuresis (Spironolactone first THEN add a loop)
  • Paracentesis
  • Transjugular hepatic portosystemic shunt (TIPS)
105
Q

What does the onset of ascites with cirrhosis indicate?

A

Poor prognosis

less than 50% survival in 2 yrs

106
Q

When treating ascites, what is the 1st line diuretic?

A

Spironolactone

*then Loop diuretic

107
Q

When is paracentesis performed in cirrhosis pts?

A

Pts with:

  • Massive ascites
  • Respiratory compromise
  • Not responding to diuretics
108
Q

What is spontaneous bacterial peritonitis?

A
  • Complication of cirrhosis
  • Infection of pre-existing ascitic fluid W/O evidence of a secondary source
  • MC organism is E. coli
109
Q

What is the MC organism of spontaneous bacterial peritonitis?

A

E. coli

d/t bacterial translocation of GI flora through lymph system causing bacteremia which then gets into ascitic fluid

110
Q

How does spontaneous bacterial peritonitis present?

A

Fever, abdominal pain, tenderness, altered mental status

111
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Paracentesis showing:

-Positive ascitic fluid culture and/or elevated PMN count

112
Q

What is the treatment of spontaneous bacterial peritonitis?

A

2nd generation Cephalosporin (MC cefotaxime)

*These pts are on proph abx for live to prevent recurrent infection

113
Q

What is the most life threatening complication of cirrhosis?

A

Variceal hemorrhage

114
Q

How to treat variceal hemorrhage?

A
  • Vasoconstricting agents
  • Balloon tamponade
  • Endoscopic therapy w/sclerotherapy
  • TIPS
115
Q

What is the primary prophylaxis treatment of esophageal varices?

A

Routine endoscopy screening for all pts with cirrhosis (every 6-12 months)

116
Q

What should pts with cirrhosis be screened for and how often?

A

Routine endoscopy screening for esophageal varices every 6-12 months

117
Q

What is hepatorenal syndrome?

A
  • Complication of cirrhosis
  • Renal failure in pts w/advanced liver disease
  • Functional renal failure w/o renal pathology
  • POOR prognosis unless liver transplanted
118
Q

What is hepatic encephalopathy?

A
  • Complication of cirrhosis
  • Change in mental status
  • Gut derived neurotoxins are not removed by the liver and get to the brain (causing encephalopathy)
119
Q

How is hepatic encephalopathy diagnosed and treated?

A
  • Clinical diagnosis
  • Hydration w/IV fluids
  • Lactulose
  • Mannitol
  • Rifaximin or Metronidazole + Neomycin (if pt does not tolerate Lactulose)
  • Zinc supplement
120
Q

How does lactulose help treat hepatic encephalopathy?

A
  • Removes GI nitrogenous products

- Goal is 2-3 BM/day

121
Q

How does mannitol help treat hepatic encephalopathy?

A

Decreases brain swelling

122
Q

If a pt does not tolerate lactulose, what can be given for tx of hepatic encephalopathy?

A

Rifaximin OR Metronidazole with Neomycin

123
Q

What is hepatopulmonary syndrome and how does it present?

A
  • Complication of cirrhosis
  • Intrapulmonary vascular dilatations OR AV communications/fistulas (R-L shunt)
  • Dyspnea, drop in O2 sat (worse in upright position)
124
Q

What is portopulmonary hypertension and how is it diagnosed?

A
  • Complication of cirrhosis
  • Pulmonary HTN in pts w/portal HTN
  • Rare
  • Diagnose by echo and cardiac cath
125
Q

What is coagulopathy?

A
  • Universal complication of cirrhosis

- Decreased synthesis of clotting factors and impaired clearance of anticoagulants

126
Q

How to treat coagulopathy in cirrhosis pts?

A

Vit K supplementation
*If synthesis/production of clotting factors is diminished then Vit K will NOT help - need FFP (fresh frozen plasma) if active bleeding or before a required procedure only

127
Q

What is the ultimate treatment of decompensated cirrhosis?

A

Liver transplant

5 yr survival is as high as 80%

128
Q

What is hemochromatosis?

A
  • Inherited disorder of iron metabolism
  • Progressive increase in hepatic iron deposition which can lead to cirrhosis
  • Increased risk of hepatocellular carcinoma
129
Q

How can hemochromatosis be diagnosed and how is it treated?

A
  • Elevated fasting transferrin saturation and ferritin level
  • Genetic testing
  • Liver biopsy
  • Tx = regular phlebotomy
130
Q

What is Wilson’s disease and who does it affect?

A
  • Rare autosomal recessive disorder of copper (failure to excrete excess copper leading to liver damage)
  • Young adults and adolescents
131
Q

How is Wilson’s disease diagnosed?

A
  • Low serum cerulosplasmin concentration

- Increased hepatic copper on liver biopsy

132
Q

Treatment of Wilson’s disease?

A

Copper-chelating agents indefinitely

133
Q

MC presenting sign of Wilson’s disease?

A

Kayser-Fleischner ring (around iris of eye)

134
Q

What is alpha-1 antitrypsin deficiency?

A
  • Autosomal recessive disorder that causes abnormal folding of the protein
  • Failure of secretion from liver leads to liver disease
135
Q

How is alpha-1 antitrypsin deficiency diagnosed?

A

Phenotype testing and alpha-1 antitrypsin levels

136
Q

Treatment of alpha-1 antitrypsin deficiency

A

Liver transplant is curative

137
Q

Inherited metabolic liver diseases:

A
  • Hemochromatosis
  • Wilson’s disease
  • Alpha-1 antitrypsin deficiency

Clin Med II - GI (17 decks)

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