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D2 Fall > Gen Path Exam 3 - Liver Disease > Flashcards

Gen Path Exam 3 - Liver Disease Flashcards

1
Q

What does the liver synthesize and secrete?

A

Bile

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2
Q

What does the liver metabolize?

A

Amino acids
CHO
Fats

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3
Q

What does the liver store? (5)

A

Glycogen
Vitamin A
Vitamin B12
Folate
Iron

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4
Q

What else does the liver synthesize?

A

Lipid
Serum protein (albumin, clotting factors, globulins)
Hepcidin

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5
Q

What lowers plasma iron?

A

Hepcidin

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6
Q

Portal vein going into the liver drains from where?

A

GI

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7
Q

What does the liver detox?

A

Blood (1st pass metabolism)

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8
Q

What does the liver breakdown?

A

Estrogen

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9
Q

Organs and ducts that produce, store, and release bile into small intestine

A

Biliary system

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10
Q

What 3 things are part of the biliary system?

A

Liver
Gallbladder
Bile duct

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11
Q

Which part of the biliary system?

Produces bile

A

Liver

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12
Q

Which part of the biliary system?

Storage and release of bile into duodenum when food is eaten

A

Gallbladder

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13
Q

Which part of the biliary system?

Transport bile from liver to duodenum

A

Bile duct

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14
Q

A yellow/green substance synthesized and secreted by the liver

A

Bile

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15
Q

Where is bile stored?

A

Gall bladder

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16
Q

Bile is released into the __________ via the _____________

A

duodenum; common bile duct

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17
Q

What is bile composed of?

A

Bile acids/salts
Bilirubin
Cholesterol
Other waste products/pollutants

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18
Q

Aids in digestion and absorption of fats

A

Bile

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19
Q

Serves as primary pathway for elimination of bilirubin, excess cholesterol, and other toxic substances

A

Bile

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20
Q

What are the 3 main things a Hepatic Panel detects?

A

Synthesis of liver enzymes
Bilirubin processing/bile secretion
Extent of liver damage

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21
Q

Which part of the Hepatic Panel?

Total protein (albumin + globulins)
Albumin
Pro-thrombin time and INR

A

Synthesis of liver enzymes

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22
Q

When measuring the synthesis of liver enzymes in the Hepatic Panel, what detects the presence and function of coagulation factors?

A

Pro-thrombin time and INR

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23
Q

Which part of the Hepatic Panel?

Bilirubin
Alkaline phosphatase
Gamma-glutamyltransferase

A

Bilirubin processing/bile secretion

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24
Q

When measuring the bilirubin processing/bile secretion in the Hepatic Panel, what is released with bile duct damage?

A

Alkaline phosphatase

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25
Q

When measuring the bilirubin processing/bile secretion in the Hepatic Panel, what is released with bile duct damage, but is more specific since it is not present in bones?

A

Gamma-glutamyltransferase

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26
Q

Which part of the Hepatic Panel?

Aspartate aminotransferase
Alanine aminotransferase

A

Extent of liver damage

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27
Q

When measuring the extent of liver damage in the Hepatic Panel, what is more specific for liver damage?

A

Alanine aminotransferase

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28
Q

What panel includes bilirubin, albumin, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase?

A

Comprehensive metabolic panel

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29
Q

The liver has a _________ functional reserve - only 10% normal tissue can sustain life; full regeneration within __________

A

large; 4 months

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30
Q

T/F: Liver diseases are typically silent and insidious

A

True!

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31
Q

What do most patients have at the time of referral?

A

Chronic liver disease

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32
Q

T/F: Signs and symptoms of liver diseases appear weeks, months, or even years after onset of injury (may only be detected by lab abnormalities) with liver injury and healing being subclinical

A

True

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33
Q

Clinical sign of underlying disease

A

Jaundice

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34
Q

Yellow discoloration of skin, mucous membranes, and sclerae of eyes

A

Jaundice

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35
Q

Caused by elevated serum bilirubin

A

Jaundice

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36
Q

Pathogenesis depends on where bilirubin metabolism is altered

A

Jaundice

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37
Q

Yellow breakdown product of RBCs, which becomes a component of bile

A

Bilirubin

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38
Q

What are the 3 reasons a person may have elevated bilirubin?

A

Bile isn’t being formed
Breakdown of large amounts of blood
Obstruction of bile flow out of liver (tumor; gallstone)

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39
Q

T/F: Bilirubin alone is highly toxic and insoluble and can’t be excreted; it has to be managed

A

True

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40
Q

In bilirubin metabolism, what are RBCs consumed by?

A

Macrophages

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41
Q

In bilirubin metabolism, what is converted to biliverdin?

A

Protoporphyrin

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42
Q

In bilirubin metabolism, what is unconjugated to bilirubin?

A

Biliverdin

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43
Q

In bilirubin metabolism, what binds tightly to albumin?

A

Unconjugated bilirubin

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44
Q

In bilirubin metabolism, what does albumin carry to the liver?

A

Unconjugated bilirubin

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45
Q

In bilirubin metabolism, what conjugated bilirubin, making it water-soluble and non-toxic?

A

Uridine glucuronyl transferase (UGT)

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46
Q

In bilirubin metabolism, where is conjugated bilirubin transferred to form bile?

A

Bile canaliculi

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47
Q

In bilirubin metabolism, where is bile stored in the gallbladder released into to aid in digestion?

A

Small intestine

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48
Q

In bilirubin metabolism, what converts conjugated bilirubin to urobilinogen?

A

Intestinal flora

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49
Q

In bilirubin metabolism, what is oxidized to stercobilin and urobilin, which are mostly excreted in feces?

A

Urobilinogen

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50
Q

In bilirubin metabolism, what is reabsorbed into blood and filtered by kidney and makes urine yellow?

A

Urobilin

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51
Q

Makes urine yellow

A

Urobilin

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52
Q

Makes stool brown

A

Stercobilin

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53
Q

Steps of bilirubin metabolism

A
  1. Macrophages eat RBCs
  2. Protoporphyrine -> biliverdin -> UCB
  3. Albumin carries UCB to liver
  4. UGT -> CB-> makes it water-soluble and non-toxic
  5. CB goes to bile canaliculi -> forms bile -> stored in gallbladder
  6. Bile released into small intestine to aid digestion
  7. Intestinal flora converts CB -> urobilinogen
  8. Urobilinogen -> stercobilin and urobilin -> excreted mostly in feces
  9. Some urobilin reabsorbed into blood -> filtered by kidney -> urine is yellow
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54
Q

Lab findings in extravascular hemolysis or ineffective erythropoiesis

A

High UCB

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55
Q

Lab findings in physiologic jaundice of newborn

A

High UCB

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56
Q

Lab findings in biliary tract obstruction (obstructive jaundice)

A

Low CB
Low urine urobilinogen
High alkaline phosphatase

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57
Q

Lab findings in viral hepatitis

A

High UCB
High CB

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58
Q

What are the 5 key causes of jaundice?

A

Extravascular hemolysis
Ineffective erythropoiesis
Physiologic jaundice of newborn
Biliary tract obstruction (obstructive jaundice)
Viral hepatitis

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59
Q

Inflammation of the liver

A

Hepatitis

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60
Q

Term that is often used to describe diseases caused by specific viruses that infect the liver (hepatotropic)

A

Hepatitis

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61
Q

A severe, life-threatening form of acute hepatitis

A

Fulminant hepatitis

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62
Q

Six different hepatitis viruses have been identified, but what types cause the majority of problems?

A

A, B, C

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63
Q

Symptoms < 6 months: jaundice with dark urine (due to CB), fever, malaise, nausea and elevated liver enzymes (ALT, AST)

A

Acute Hepatitis

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64
Q

Symptoms > 6 months: risk for progression to cirrhosis

A

Chronic Hepatitis

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65
Q

What viruses are transmitted in in a similar manner and many patients have coinfection, which increases risk for hepatic dysfunction?

A

HBV
HCV
HIV

66
Q

When should you get a med consult?

A

Non-specific history of hepatitis and signs/symptoms of jaundice

67
Q

Which hepatitis viruses are spread oral-fecal?

A

HAV
HEV

68
Q

Which hepatitis viruses are spread parenteral (childbirth, unprotected sex, IV drug abuse, needle stick)

A

HBV
HCV

69
Q

Which hepatitis virus is commonly acquired by travelers?

A

HAV

70
Q

Which hepatitis virus is commonly acquired from contaminated water or undercooked seafood?

A

HEV

71
Q

Which hepatitis viruses have the following symptoms?

Fever, jaundice, fatigue, loss of appetite

A

HAV
HEV

72
Q

Which hepatitis virus has the following symptoms?

Most have mild to no symptoms
30% have anorexia, fever, jaundice, RUQ pain

A

HBV

73
Q

Which hepatitis virus has the following symptoms?

85% of acute cases are asymptomatic

A

HCV

74
Q

Which hepatitis viruses are acute only (no carrier or chronic state)?

A

HAV
HEV

75
Q

Which hepatitis virus?

10% develop chronic disease
Of those, 30% develop cirrhosis and 3% develop HCC

A

HBV

76
Q

Which hepatitis virus?

80-90% develop chronic disease
Of those, 33% develop cirrhosis and 2.5% develop HCC

A

HCV

77
Q

Which hepatitis viruses are diagnosed by:

IgM -> active infection
IgG -> protective; indicated prior infection or immunization

A

HAV
HEV

78
Q

Which hepatitis virus is diagnosed by the following diagnostic antibodies:

IgM for HB core antigen (anti-HBc)
HB surface antigen (HBsAg)
AST, ALT, bilirubin may be elevated

A

HBV

79
Q

Which hepatitis virus is diagnosed by recovery:

HbsAg clears and antibodies (anti-HbsAg) appear

A

HBV

80
Q

Which hepatitis virus is diagnosed by immunity:

IgG anti-HBc

A

HBV

81
Q

Which hepatitis virus is diagnosed by HCV RNA (often persistent even if antibodies present)?

A

HCV

82
Q

Which hepatitis viruses have a vaccine?

A

HAV
HBV

83
Q

Which hepatitis virus?

Treated with IFN or nucleotide/nucleoside inhibitors

A

HBV

84
Q

Which hepatitis virus?

Treated with combo antiviral therapy which is very effective - goal is sustained virologic response or “cure” (undetectable RNA within 6 months of tx)

A

HCV

85
Q

Which hepatitis virus?

95% of infections are curable, but tx is very expensive (100k)

A

HCV

86
Q

Which hepatitis virus?

Infection in pregnant women causes fulminant hepatitis (liver failure w/ massive necrosis)

A

HEV

87
Q

Which hepatitis virus?

Only hep virus that is a DNA virus

A

HBV

88
Q

Which hepatitis virus?

Reinfection can occur even after tx

A

HCV

89
Q

Which hepatitis virus?

Dependent on HBV for infection; superinfection upon existing HBV is more severe than coinfection

A

HDV

90
Q

What diagnosis?

Elective dental tx should be deferred until resolution of active disease; emergency tx should be done in hospital dental clinic

A

Acute HBV or HCV

91
Q

What diagnosis?

Elective and emergency dental tx should be done in hospital dental clinic

A

Chronic HBV or HCV with significant hepatic dysfunction

92
Q

What diagnosis?

Can receive elective tx w/o special precautions

A

Chronic HBV or HCV without significant hepatic dysfunction

93
Q

What is the leading cause of liver disease in most Western countries?

A

Alcoholic liver disease

94
Q

Causes damage to hepatocytes due to alcohol consumption (generally binge drinking)?

A

Alcoholic liver disease

95
Q

What is alcoholic liver disease mediated by?

A

Acetaldehyde

96
Q

Alcohol metabolite

A

Acetaldehyde

97
Q

What are the 3 types of damage in alcoholic liver disease?

A

Steatosis
Alcohol hepatitis
Fibrosis-cirrhosis

98
Q

Fat accumulation in hepatocytes

A

Steatosis

99
Q

Which type of damage in alcoholic liver disease?

Liver is large, soft, yellow, and greasy (“fatty liver”)

A

Steatosis

100
Q

Which type of damage in alcoholic liver disease?

Often asymptomatic or mild RUQ discomfort, fatigue, weight loss

A

Steatosis

101
Q

Which type of damage in alcoholic liver disease?

Hepatocyte swelling with necrosis and acute inflammation

A

Alcohol hepatitis

102
Q

Which type of damage in alcoholic liver disease?

Painful hepatomegaly
Elevated liver enzymes (AST > ALT)
Jaundice
Portal hypertension (splenomegaly, ascites)
Malnutrition and vitamin deficiencies (thiamine, B12)
Malaise, weight loss, fever, nausea, vomiting

A

Alcohol hepatitis and fibrosis-cirrhosis

103
Q

What is the tx for alcoholic liver disease?

A

Stop drinking
Supportive care
Liver transplant in later stages

104
Q

What is the prognosis of alcoholic liver disease for those who quit drinking?

A

5 yr survival rate = 90%

105
Q

What is the prognosis of alcoholic liver disease for those who continue to drink?

A

5 yr survival rate = 50-60%

106
Q

Same clinical symptoms and gross/histologic changes as noted in alcohol-related liver disease, but without alcohol exposure

A

Non-alcoholic fatty liver disease

107
Q

Is non-alcoholic fatty liver disease common?

A

Yes!

108
Q

What is non-alcoholic fatty liver disease associated with?

A

Obesity w/ insulin resistance
Type 2 DM

109
Q

In non-alcoholic fatty liver disease, free fatty acids from adipose tissue accumulate in _____________, stimulating more fatty acid production

A

hepatocytes

110
Q

What is the most common cause of incidental elevation of serum transaminases?

A

Non-alcoholic fatty liver disease

111
Q

Diagnosis of exclusion; ALT > AST

A

Non-alcoholic fatty liver disease

112
Q

Major drug metabolizing and detoxifying organ - very susceptible to injury

A

Liver

113
Q

What are the 3 mechanisms of drug-induced liver damage?

A

Direct toxicity
Hepatic conversion to active toxin (metabolite)
Drug or metabolite acts as hapten -> binds to cellular protein, making it immunogenic

114
Q

In drug-induced liver damage, drug rxns can be what 2 things?

A

Predictable (dose-dependent)
Idiosyncratic (unpredictable)

115
Q

What type of drug rxn?

Acetaminophen converted to toxic metabolite

A

Predictable (dose-dependent)

116
Q

What type of drug rxn?

Immediate or delayed (weeks to months)

A

Idiosyncratic (unpredictable)

117
Q

Progressive, diffuse fibrosis/scarring of the liver

A

Cirrhosis

118
Q

Regenerative nodules surrounded by fibrous bands

A

Cirrhosis

119
Q

Focal nodules of viable liver parenchyma remain between the bands of scar tissue

A

Cirrhosis

120
Q

What are the causes of cirrhosis in the US?

A

HCV
Alcoholic liver disease
Non-alcoholic steatohepatitis (NASH)

121
Q

What are the causes of cirrhosis in the developing world?

A

HBV
HCV

122
Q

Pt may be clinically silent without symptoms; only elevated AST and ALT

A

Cirrhosis

123
Q

If symptomatic, pt will present with anorexia, weight loss, weakness, debilitation, signs of liver failure and portal hypertension

A

Cirrhosis

124
Q

What is the tx for cirrhosis?

A

Transplant

125
Q

Is fibrosis of the liver reversible?

A

NO

126
Q

What do many patients with cirrhosis die from?

A

Liver failure
Hepatocellular carcinoma (HCC)

127
Q

What are the 3 potential complications of cirrhosis in regard to dental tx?

A
  1. Unpredictable drug metabolism (only occurs with severe disease)
  2. Impaired hemostasis and bleeding (thrombocytopenia and low coagulation factors)
  3. Increased risk of infection
128
Q

Most important and severe consequence of
liver disease

A

Liver failure

129
Q

Will not occur until 80-90% of the liver cells
(hepatocytes) are destroyed

A

Liver failure

130
Q

What are the potential causes of liver failure?

A

Acute - drugs (50% acetaminophen), HAV, HBV

Chronic liver diseases that cause cirrhosis

131
Q

Clinical features include:

Jaundice- when severe leads to pruritis (itching)
Peripheral edema
Spider angioma formation
Multiple organ system failure
Coagulopathy (Bleeding)
Encephalopathy (confusion, stupor)
Coma

A

Liver failure

132
Q

What is the tx for a pt with liver failure that has sufficient residual viable tissue?

A

Regeneration with supportive care

133
Q

What is the tx for a pt with liver failure that has insufficient viable tissue?

A

Transplant

134
Q

Prognosis is poor - pts die within weeks to months

A

Liver failure

135
Q

Where does all gastrointestinal, splenic, and pancreatic venous blood drain?

A

Portal vein

136
Q

Regulates nutrients and filters toxins

A

Portal vein

137
Q

Where does hepatic vein drain into?

A

IVC

138
Q

What are the 3 portal collaterals?

A

Esophageal veins
Hemorrhoidal veins
Periumbilical veins

139
Q

What is the dual blood supply of the liver?

A

Hepatic artery
Portal vein

140
Q

What causes impaired venous return BEFORE the liver?

A

Portal vein obstruction
Thrombosis

141
Q

What causes impaired venous return IN the liver?

A

Cirrhosis

142
Q

What causes impaired venous return AFTER the liver?

A

Hepatic vein obstruction
Chronic passive congestion (R sided heart failure, lung disease)

143
Q

Pathogenesis is impeded venous return from right heart causes blood stasis in liver

A

Chronic passive congestion

144
Q

Caused most often by COPD or restrictive pulmonary disease leading to R heart failure

A

Chronic passive congestion

145
Q

Gross pathology is nutmeg liver

A

Chronic passive congestion

146
Q

Malignant tumor of hepatocytes

A

Hepatocellular carcinoma (HCC)

147
Q

Risk factors are:

Chronic hepatitis (HBV, HCV)
Cirrhosis
Aflatoxins from aspergillus (induce p53 mutations) -> synergistic w/ HBV

A

Hepatocellular carcinoma (HCC)

148
Q

Why are tumors of the liver often detected late?

A

Symptoms masked by cirrhosis

149
Q

Where do tumors of the liver commonly metastasize?

A

Lung

150
Q

All cancers drained by the _______ system
metastasize to _______: lower esophagus,
stomach, intestine, gallbladder, pancreas

A

portal; liver

151
Q

Most often represents crystallized cholesterol in the bile

A

Cholelithiasis (gallstones)

152
Q

Risk factors:

Increasing age
Female
Obesity
Family history
Living in an industrialized society

A

Cholelithiasis (gallstones)

153
Q

Gallstones may be present for _________ before symptoms develop

A

decades

154
Q

Is Cholelithiasis (gallstones) usually symptomatic or asymptomatic?

A

Asymptomatic

155
Q

If symptomatic, what will a person with Cholelithiasis (gallstones) experience?

A

Biliary colic
Acute cholecystitis
Chronic cholecystitis

156
Q

Stone in cystic duct; wax/wane RUQ pain may resolve if stone passes

A

Biliary colic

157
Q

Impacted stone in cystic duct with bacterial infection; severe RUQ abdominal pain, fever, nausea, vomiting

A

Acute cholecystitis

158
Q

Vague RUQ pain especially after meals

A

Chronic cholecystitis

159
Q

What is the tx for Cholelithiasis (gallstones)?

A

Cholecystectomy

160
Q

Surgical removal of gall bladder

A

Cholecystectomy

161
Q

Is the prognosis for Cholelithiasis (gallstones) good or bad?

A

Good

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