Disorders of the Liver Part 1 Flashcards

1
Q

What are the 4 lobes of the liver and what separates them?

A
  • Anteriorly: Right lobe and left lobe by falciform ligament.
  • Posteriorly: Anterior and posterior caudate via porta hepatis
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2
Q

What are the 3 components of the porta hepatis?

A
  • Hepatic portal vein
  • Hepatic artery
  • Common Hepatic duct

Not the same as a portal triad

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3
Q

What are the two vessels that supply hepatocytes?

A
  • Venous blood via portal vein
  • Oxygenated blood via hepatic arteries
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4
Q

What is the flow of blood beginning at a portal vein?

A
  1. Portal veins
  2. Sinusoids
  3. Central Veins
  4. Hepatic Veins
  5. IVC
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5
Q

What two lipoproteins are made by hepatocytes?

A
  • VLDL
  • HDL
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6
Q

What is bilirubin from?

A

End product of the breakdown of an RBC, created as unconjugated/indirect/lipid soluble bilirubin

Breakdown of heme to protoporphyrin to bilirubin

UCB = unconjugated bilirubin

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7
Q

What binds to UCB and takes it to the liver?

A

Albumin

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8
Q

What enzyme is used to conjugate bilirubin?

A

Uridine glucuronyl transferase = UGT

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9
Q

What happens to bilirubin once it is conjugated?

A
  1. Transported down bile canaliculi to bile ducts
  2. Deposited within the gallbladder at direct/conjugated bilirubin

It is now water soluble.

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10
Q

What converts CB to urobilinogen and what happens to it?

A
  • Microbes convert it to UBG.
  • UBG can either become stercobilin into your poop (giving it color)
  • It can also become urobilin and get excreted via the kidneys or goes back to the liver
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11
Q

What is jaundice?

A
  • Product of heme metabolism
  • Accumulation of bilirubin
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12
Q

How elevated is serum total bilirubin to give skin a yellow discoloration?

A

Usually greater than 2.5mg/dL

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13
Q

Would pre-hepatic jaundice present with higher UCB or CB?

A

UCB

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14
Q

How do bilirubin levels look in pre-hepatic jaundice?

A

Increased UCB in serum due to RBC hemolysis

aka hemolytic anemias

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15
Q

How can bilirubin levels vary in hepatic jaundice?

A
  • Increased UCB in serum due to hepatocyte impairment
  • Increased CB in serum due to hepatic duct obstruction
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16
Q

How do bilirubin levels look in post-hepatic jaundice?

A
  • Increased CB in serum due to biliary tract obstruction
  • Decreased bilirubin in gut = pale/acholic stool and no UB in urine
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17
Q

What clinical findings are most suggestive of elevated UCB?

A
  • Normal stool and urine color
  • Mild jaundice
  • No bilirubin in urine
  • Splenomegaly (Except in SCD)
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18
Q

What clinical findings are most suggestive of elevated CB?

A
  • Pruritis and jaundice
  • Light colored stools
  • Malaise, anorexia, low-grade fever, RUQ, Dark urine
  • Hepatomegaly, spider telangiectasias, palmar erythema, ascites, gynecomastia, sparse body hair
  • Varies based on liver dysfunction
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19
Q

What is the term for light colored stool?

A

Acholic stool

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20
Q

What clotting factors are NOT affected in liver disease?

A
  • III
  • IV
  • VIII
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21
Q

What does Vit K require to be absorbed from the GI tract?

A

Bile

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22
Q

What CBC count will be lower in liver disease?

A

Thrombocytopenia

TPO is made in the liver

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23
Q

What are the 3 common CBC abnormalities seen in liver disease?

A
  • Thrombocytopenia
  • Leukopenia
  • Anemia

EPO is made in both the kidneys and liver

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24
Q

What carrier protein does the liver make?

A

Albumin

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25
Q

What is the underlying mechanism behind portal HTN?

A

Blockkage in blood flow through the liver, resulting in cirrhosis most commonly.

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26
Q

What is the gold standard to diagnose portal HTN?

A

IVC catheter to measure hepatic venous pressure

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27
Q

What are the clinical manifestations of portal HTN?

A
  • Splenomegaly
  • Esophageal varices
  • Hemorrhoids
  • Caput Medusae
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28
Q

What are the main veins implicated in portal HTN?

A
  • Esophageal veins
  • Paraumbilical veins
  • Superior mesenteric veins
  • Inferior mesenteric veins
  • Middle rectal veins
  • Inferior rectal veins
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29
Q

What are the ABCDEs of Portal HTN?

A
  • Ascites
  • Bleeding
  • Caput Medusae
  • Diminished liver function
  • Enlarged spleen
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30
Q

What is the MCC of ascites?

A

Cirrhosis

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31
Q

What are the underlying mechanisms of ascites?

A
  • Underfill due to lack of albumin and shift of fluid
  • Overflow due to increased pressure
  • Impairment of RAAS
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32
Q

What is the MC organism that causes spontaneous bacterial peritonitis?

A

E. Coli

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33
Q

Why does hepatorenal syndrome occur?

A
  1. Arterial vasodilation in splanchnic circulation due to Portal HTN
  2. More NO is made, vasodilating more and causes a fall in CO
  3. Kidneys become poorly perfused
  4. Acute renal failure ensures
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34
Q

What causes pruritis in liver disease?

A

Bile salts

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35
Q

What are spider nevi and palmar erythema due to?

A

Excess estrogen

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36
Q

What can happen specifically to males with liver disease? Females?

A
  • Males: testicular atrophy & gynecomastia due to impaired cholesterol synthesis
  • Females: Menstrual irregularities due to excess estrogen
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37
Q

What is the severe manifestation of liver disease?

A

Hepatic encephalopathy due to buildup of ammonia

Confusions, tremors, coma

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38
Q

What are the components of a LFT/hepatic panel?

A
  • Total protein
  • Albumin
  • Total bilirubin
  • Direct bilirubin
  • AST/SGOT
  • ALT/SGPT
  • ALP
  • GGT
  • PT/PTT
  • Cholesterol
  • BUN
  • Hepatitis Panel

Bolded are addons

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39
Q

What are the two serum aminotransferases?

A
  • Alanine aminotransferase (ALT/SGPT)
  • Aspartate aminotransferase (AST/SGOT)
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40
Q

What liver enzymes measure hepatocyte damage?

A
  • AST/ALT
  • LDH
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41
Q

Which liver enzyme is most specific for hepatocellular damage if markedly elevated?

A

ALT

AST is found in heart and skeletal muscle too.

ALT has a L, so its the most Liver specific
Acute Liver Trouble

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42
Q

What do significant elevations of ALT and AST associate the most with?

A

Hepatocellular damage

8-25x = acute damage

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43
Q

In general, what does an acute liver damage present as in terms of the aminotransferases enzymes? Chronic?

A
  • Acute: ALT > AST (8-25x ULN)
  • Chronic: AST > ALT (< 8x ULN)

ALT = Acute Liver Trouble

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44
Q

What does a moderate elevation of AST > ALT of around 2 or more suggest?

A

Chronic alcoholic liver disease

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45
Q

What does a moderate elevation of AST > ALT of around 1-1.99 suggest?

A

Chronic NASH/non alcoholic cirrhosis

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46
Q

What elevates LDH?

A

Any cellular damage in general. Non-specific test.

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47
Q

What liver enzymes are used to measure cholestasis?

A
  • ALP
  • GGT (both)
  • 5’-nucleotidase (liver specific)
48
Q

What does a elevation of ALP > 4x ULN suggest? < 4x ULN?

A
  • More than 4x ULN = hepatic cholestasis
  • Less than 4x ULN = non-hepatic/non-cholestatic cause
49
Q

What might elevated ALP and GGT suggest?

A

Hepatobiliary obstruction

50
Q

What is one of the first enzymes to increase in an obstructive disease of the biliary tract?

A

ALP

51
Q

What might elevated GGT without elevated ALP suggest?

A

Alcohol or medications

52
Q

What is GGT not elevated in?

A

Bone disease

53
Q

What LFTs suggest hepatocellular damage?

A
  • Marked elevation of AST/ALT compared to ALP
  • Elevated total and direct bilirubin
54
Q

What LFTs suggest obstructive disease of the liver?

A
  • Elevated ALP compared to AST/ALT
  • Elevated GGT
  • Elevated/normal total bilirubin
  • Elevated direct bilirubin
55
Q

In summary, what does elevated direct bilirubin suggest?

A

Hepatobiliary disease

56
Q

What are the tests for hepatic synthetic function?

A
  • Albumin
  • PT
57
Q

What affects albumin level?

A
  • Liver damage
  • Poor nutrition
  • Kidney disease causing increased excretion(Nephrotic)
58
Q

If PT is prolonged but LFTs remain normal, what does this suggest?

A

Liver function is fine and not the cause

59
Q

What characterizes autoimmune hepatitis?

A

Circulating auto-antibodies and elevated serum globulin levels

60
Q

What demographic is autoimmune hepatitis MC in?

A

Young to middle aged women

61
Q

How does autoimmune hepatitis present?

A
  • Insidious onset
  • Often precipitated by a viral illness/drug exposure or postpartum
  • Otherwise healthy with multiple spider nevi, cutaneous striae, acne
  • Extrahepatic features like arthritis or thyroiditis
62
Q

What lab findings are associated with autoimmune hepatitis?

A
  • AST/ALT elevations of 1.5x-50x ULN
  • Elevated total bilirubin
  • Positive ANA
  • pANCA
  • Anti-SLA (soluble liver antigen)
63
Q

How is autoimmune hepatitis definitively diagnosed?

A

Liver biopsy

64
Q

What conditions are autoimmune hepatitis co-existing with sometimes?

A
  • Primary biliary cirrhosis
  • Sclerosing cholangitis
65
Q

How do we treat autoimmune hepatitis?

A
  • Prednisone
  • May add azathioprine
  • Liver transplant last resort
66
Q

What medications can induce hepatitis?

A
  • Acetaminophen with alcohol
  • Isoniazid with rifampin
  • ABX (tetracyclines)
  • Herbal supplements
67
Q

How does drug/toxin induced hepatitis present?

A
  • Hepatomegaly
  • Jaundice
  • Fatigue
  • N/V
68
Q

How do the transaminases present in drug/toxin induced hepatitis?

A

ALT > AST

Acute Liver Trouble

69
Q

How much acetaminophen can cause hepatitis?

A

4g in adults or 80mg/kg in kids

Found in more than just tylenol!!!!!!

70
Q

When does stage 1 of acetaminophen induced hepatitis occur and what happens?

A
  • Timing: 30 minutes - 24 hours
  • N/V, diaphoresis, pallor, lethargy, malaise
  • Normal labs
  • Could be asymptomatic
71
Q

When does stage 2 of acetaminophen induced hepatitis occur and what happens?

A
  • Timing: 24-72 hours
  • Stage 1 symptoms resolve, but then the patient worsens
  • AST/ALT elevations occur
  • RUQ pain with hepatomegaly and tenderness
  • PT and bilirubin elevations
72
Q

When does stage 3 of acetaminophen induced hepatitis occur and what happens?

A
  • Timing: 72-96 hours
  • Stage 1 symptoms reappear + hepatic encephalopathy
  • AST/ALT > 10k
  • Prolong PT/INR
  • Hyperammonemia
  • Hypoglycemia
  • Acute renal failure
  • Death usually occurs d/t multi organ failure
73
Q

When does stage 4 of acetaminophen induced hepatitis occur and what happens?

A
  • Timing: 4 days to 2 weeks
  • Only occurs if you survive stage 3
  • If you do recover, complete recovery is seen
74
Q

How do you diagnose acetaminophen induced hepatitis?

A
  • Serum level of acetaminophen
  • treat above the line for the graph
75
Q

How do you treat acetaminophen induced hepatitis?

A

N-acetylcysteine

Activated charcoal also helps

76
Q

What is considered excessive alcohol intake and how long do you have to do it for have high risk?

A
  • Males: 2+ drinks a day
  • Females: 1+ drinks a day
  • 10 years of this
77
Q

What are the stages of alcoholic liver disease?

A
  1. Fatty liver/steatohepatitis (hepatomegaly)
  2. Alcoholic hepatitis (acute/chronic inflammation and parenchyymal damage)
  3. Cirrhosis (Non-reversible)
78
Q

How much do you have to drink to have a higher frequency of alcoholic liver disease?

A

50g of alcohol daily for 10 years

79
Q

Why does alcohol cause damage?

A

Acetaldehyde is a metabolite of ethanol that causes cellular damage

80
Q

In steatohepatitis, how do labs look?

A
  • Mild AST/ALT elevations
  • Macrocytic anemia
81
Q

In alcoholic cirrhosis, how do labs look?

A
  • AST/ALT elevations
  • Elevated total bilirubin > 10mg
  • Hypoalbuminemia
  • PT/INR prolongation
  • Anemia (iron and folate)
  • Later: Lyte abnormalities and elevated BUN/Cr
82
Q

In alcoholic hepatitis, how do labs look?

A
  • AST > ALT by 2x or more
  • ALP elevated up to 3x
  • Elevated total bilirubin
  • Leukopenia and thrombocytopenia

Not an acute process, so AST elevates more

83
Q

How do you definitively diagnose alcoholic liver disease?

A

Biopsy showing macrovesicular fat and PMN infiltration with hepatic necrosis

84
Q

How do alcoholic steatohepatitis and NASH present?

A

Identical

85
Q

What is the #1 treatment for alcoholic steatohepatitis?

A

Not drinking

Reversible at steatohepatitis stage.

86
Q

What are the pharmacotherapy options for alcoholic hepatitis?

A
  • Methylprednisolone x1 month
  • Pentoxifylline if severe (vasodilator) x1 month
87
Q

What are the unfavorable prognostic factors for alcoholic hepatitis?

A
  • Prolonged PT/PTT
  • Bilirubin > 10mg
  • Hepatic encephalopathy
  • Azotemia
88
Q

What is the MC risk factor for NA fatty liver disease?

A

Obesity

89
Q

What is the difference between Non-alcoholic fatty liver and non-alcoholic steatohepatitis?

A
  • NAFL has NO inflammation
  • NASH has inflammation
90
Q

When is NAFLD typically diagnosed?

A

40s-50s

91
Q

How do AST/ALT appear for NASH?

A

< 2

ETOH would make it higher

92
Q

How do you definitively diagnose NASH?

A

Liver biopsy

93
Q

NAFLD Spectrum Image

A
94
Q

What medications can help treat NAFLD?

A
  • Vit E
  • TZDs
  • Metformin
  • Wt loss agents

Insulin sensitizing agents

95
Q

What are the poor risk factors for NASH to become cirrhosis?

A
  • Old
  • Male
  • Obesity
  • DM
96
Q

What is seen throughout the liver in cirrhosis?

A
  • Fibrosis
  • Nodular regeneration replacing functional hepatocytes with nonfunctioning fibrotic nodules
97
Q

How does cirrhosis typically present?

A
  • N/V
  • Abd pain
  • S/S of Portal HTN
  • Spider angiomas, palmary erythema
  • Menstrual abnormalities, ED, gynecomastia
  • Anemia
  • Glossitis
  • Jaundice (later)
  • Ascites (later)
  • Encephalopathy (later)
98
Q

How do labs appear early in cirrhosis?

A

Minimal changes

99
Q

What is the first-line test for cirrhosis?

A

US to assess size and ascites and other stuff

100
Q

How is cirrhosis definitively diagnosed?

A

Liver biopsy

101
Q

What other imaging is highly useful in cirrhosis evaluation?

A

EGD to check for esophageal varices

Since Portal HTN is v common w/ cirrhosis

102
Q

How do we treat ascites/edema?

A
  • Na restriction
  • Spironolactone
  • Lasix
  • Paracentesis (new onset, unable to tolerate diuretics, or respiratory issues)
  • TIPS placement for variceal bleeding, but also treats ascites
103
Q

What suggests bacterial peritonitis from ascites?

A
  • Worsening abd pain
  • Fever
  • Leukocytosis
104
Q

What is the MCC of bacterial peritonitis and the treatment and prophylaxis?

A
  • MC organism: E. coli
  • Tx: Cefotaxime 2g IV q8-12h x 5-7d
  • Prophylaxis: Oral FQ
105
Q

What secondary organ system can be affected by liver disease?

A

Renal

106
Q

How do you treat hepatic encephalopathy?

A
  • Less protein
  • Lactulose to get rid of ammonia organisms
  • ABX (Rifamixin or metro)
107
Q

What infusions may help with anemia and coagulopathies due to cirrhosis?

A
  • Ferrous sulfate
  • Folic acid
  • Vit K
  • FFP
  • Oral thrombopoietin (maybe)
108
Q

What are the components of a MELD score and what is it?

A
  • Model for End Stage Liver Dz
  • Bilirubin, creatinine, and INR
  • 14 or higher needed to qualify for transplant
109
Q

What everyday things can help reduce the risk of rapid decompensation from cirrhosis?

A
  • Coffee
  • Tea
  • Statins
110
Q

What is primary biliary cirrhosis/cholangitis?

A

Chronic, autoimmune destruction of intrahepatic bile ducts and cholestasis

111
Q

Who is primary biliary cholangitis MC in?

A

Women aged 40-60

Often with other autoimmune conditions

112
Q

What lab finding is incidentally found that suggests primary biliary cholangitis?

A

Elevated ALP

113
Q

What are the MC early s/s of primary biliary cholangitis?

A

Fatigue and pruritis

114
Q

What labs are elevated in primary biliary cholangitis?

A
  • Early: ALP and cholesterol
  • Later: Bilirubin
  • Antimitochondrial Ab in 95% of pts
  • Positive ANA and IgM
115
Q

How is primary biliary cirrhosis diagnosed?

A

US and labs only

116
Q

What is the treatment for Primary biliary cholangitis?

A
  • Ursodeoxycholic acid (FDA approved)
  • For itchin: Cholestyramine (bile salt binder)
117
Q

What does primary biliary cirrhosis increase your risk of?

A

Hepatobiliary carcinoma