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Patho II > Liver > Flashcards

Liver Flashcards

1
Q

What is the functional unit of the liver?

A

lobule

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2
Q

What are the liver cells called?

A

hepatocytes

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3
Q

What run through the hepatocytes?

A

sinusoids

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4
Q

Where is bile secreted from?

A

bile canaliculi

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5
Q

What is the hepatic portal system?

A

One capillary bed is connected by a vein to a second capillary bed; hepatic a. connects with portal v.

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6
Q

Where is the first capillary bed of the hepatic portal system located and what occurs here?

A

Stomach and Intestine

Nutrients and toxins are absorbed

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7
Q

Where is the second capillary bed of the hepatic portal system located and what occurs here?

A

in the liver sinusoids

Nutrients and toxins leave and go to the hepatocytes

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8
Q

What provides 60-70% of hepatic blood flow?

A

portal vein

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9
Q

What supplies 30-40% of hepatic blood flow?

A

hepatic artery

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10
Q

What is blood flow dependent?

A

Hepatic clearance of many drugs and important hormones

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11
Q

What declines with age?

A

hepatic blood flow

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12
Q

What can cause temporary protection of hepatocytes?

A

ischemia or hypoxia

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13
Q

What does cellular acidosis protect the liver from?

A

oxidant chemicals

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14
Q

What does adenosine protect the liver from?

A

hepatoprotector against liver damage induced by CCl4 and ethanol

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15
Q

How does cellular acidosis occur in the liver?

A

When liver is ischemic of hypoxic, lactic acid builds up and causes the pH to decrease in the hepatocytes. This acidic pH keeps the hydrolytic enzymes that are produced from hypoxia and ischemia from detroying hepatocytes

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16
Q

What are the major functions of the liver?

A

1) Detoxification
2) Metabolism of carbs, proteins, and fats
3) Formation of coagulation factors
4) Formation of bile
5) Formation and storage of blood
6) Storage of vitamins and iron

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17
Q

What enzymes can be found in the liver?

A

CYP 450 enzymes

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18
Q

What is Phase I of liver metabolism?

A

drugs are lipophilic and are hydroxylated or oxidized to become hydrophillic

Reactive metabolites are formed

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19
Q

What is Phase II of liver metabolism?

A

the reactive metabolites formed in Phase I are conjugated and become unreactive in order to be excreted

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20
Q

What are found in liver sinusoids as liver macrophages?

A

Kupffer cells

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21
Q

What is the function of Kupffer cells?

A

Removes particulate materials and microbes from circulation

Removes 99% of bacteria from gut that flows to liver through portal system

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22
Q

What is glycogenesis?

A

excess glucose after a meal is converted to glycogen

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23
Q

What is glycogenolysis?

A

Decreased glucose between meals stimulates breakdown of glycogen

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24
Q

What is gluconeogenesis?

A

Exhaustion of glycogen reserves stimulates glucose production from amino acids and sugars

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25
Q

What three things are carried out in the liver in order to maintain blood glucose?

A

Glycogenesis
Glycogenolysis
Gluconeogenesis

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26
Q

How does the liver metabolize protein?

A

1) Deamination of amino acids
2) Removal of ammonia by synthesis of urea
3) Formation of plasma proteins
4) Synthesis of non-essential amino acids

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27
Q

Where does ammonia come from in liver protein metabolism?

A

bacterial degradation of amines, amino acids, purines, and urea in gut

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28
Q

How does the liver metabolize fat?

A

Carbs and proteins must first be converted to fat then:

1) beta oxidation of fatty acids
2) synthesis of lipoproteins, cholesterol, and phospholipids

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29
Q

What coagulation factors does the liver form?

A

Prothrombin

Factors VII, IX, and X

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30
Q

What does the liver require in order to make the coagulation factors?

A

Vitamin K

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31
Q

What factors effect the cause of abnormal hemostasis resulting from abnormal liver function?

A

1) Abnormal coagulation factor synthesis
2) Synthesis of dysfunctional coagulation factors
3) Increased consumption of coagulation factors
4) Platelet disorders

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32
Q

How is bilirubin formed?

A

be the breakdown of heme present in hemoglobin, myoglobin, cytochromes, catalase, peroxidase

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33
Q

What enzyme is responsible for the breakdown of heme and where can it be found?

A

Heme oxygenase

Found in spleen and Kupffer cells in the liver

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34
Q

What is associated with unconjugated bilirubin?

A

very poorly water soluble at physiologic pH

toxic effects

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35
Q

How dose bilirubin get excreted?

A

Unconjugated bilirubin must first be conjugated by glucoronic acid in the liver in order to be excreted in urine

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36
Q

How is urobilinogen produced?

A

by the bacterial breakdown of bilirubin excreted in bile into the bowel

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37
Q

How is urobilinogen excreted?

A

It is partly absorbed by bowel or it enters the general circulation and is excreted in urine

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38
Q

When would urinary urobilinogen excretion be increased?

A

1) excessive bilirubin production
2) Inefficient hepatic clearance of the urobilinogen
3) Excessive exposure of bilirubin to intestinal bacteria

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39
Q

When would urinary urobilinogen excretion be reduced?

A

1) biliary obstruction

2) Severe cholestasis

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40
Q

What are causes of elevated serum bilirubin?

A

1) overproduction of bilirubin
2) Impaired uptake, conjugation, or excretion of bilirubin
3) Backward leakage from damaged hepatocytes or bile ducts

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41
Q

What are the potential beneficial effects of bilirubin?

A

1) Antioxidant
2) Inverse relationship between serum bilirubin levels and risk of ischemic coronary artery disease and cancer mortality
3) Induction/overexpression of heme oxygenase reduces the replication of Hepatitis C virus

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42
Q

What are the physiologic mechanisms that protect against bilirubin toxicity?

A

1) Binding to plasma albumin
2) Rapid uptake
3) Conjugation
4) Clearance

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43
Q

What is urobilinogen excreted in feces?

A

Stercobilin

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44
Q

What is urobilinogen excreted in urine?

A

urobilin

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45
Q

What is the third way that urobilinogen can be excreted

A

By enterohepatic circulation

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46
Q

What is jaundice?

A

Refers to yellowish tint to the body tissues, including a yellowness of the skin and deep tissues

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47
Q

What are common causes of jaundice?

A

1) increased destruction of RBCs, with rapid release of unconjugated bilirubin into the blood
2) Obstruction of the bile ducts or damage to the liver cells so that even the usual amounts of bilirubin cannot be excreted into the GI tract

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48
Q

What are the two types of Jaundice?

A

Hemolytic and Obstructive

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49
Q

What is Hemolytic jaundice?

A

rapid turnover of RBCs and body can’t get rid of them fast enough

Unconjugated bilirubin is majority

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50
Q

What is obstructed jaundice?

A

Bilirubin is conjugated but can’t get to intestine to be converted into urobilinogen to be excreted

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51
Q

What is the normal plasma concentration of bilirubin?

A

0.5 mg/dL of plasma

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52
Q

When does the skin typically appear jaundice?

A

when the concentration of plasma bilirubin is 3X the normal amount

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53
Q

What tests are used to detect liver injury?

A

ALT

AST

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54
Q

What tests are used to test liver capacity to transport organic anions and metabolize drugs?

A

Bilirubin and bile acids

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55
Q

What enzyme when elevated reflects cholestasis?

A

Alkaline phosphatase

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56
Q

What are the liver function markers?

A 
Albumin
Prothrombin Time (PTT)
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57
Q

What is the function of serum aminotransferases?

A

these enzymes are normally intracellular but are released when hepatocytes are injured

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58
Q

What is the function of bilirubin and bile acids?

A

Measure the liver’s ability to clear endogenous or exogenous substances from circulation

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59
Q

What marker is impaired in plasma if heme catabolism isn’t working properly?

A

Bilirubin

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60
Q

What marker is impaired in plasma if carbohydrate metabolism isn’t working properly?

A

Decreased Glucose

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61
Q

What marker is impaired in plasma if protein synthesis isn’t working properly?

A

Decreased Albumin

Prolonged PTT

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62
Q

What marker is impaired in plasma if protein catabolism isn’t working properly?

A

Increased Ammonia

Decreased Urea

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63
Q

What marker is impaired if lipid metabolism isn’t working properly?

A

Increased cholesterol

Increased triglycerides

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64
Q

What marker is impaired if drug metabolism isn’t working properly?

A

Biological half time of a drug

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65
Q

What marker is impaired if bile acid metabolism isn’t working properly?

A

Increased bile acids

66
Q

Where is 50% of body lymph formed?

A

liver

67
Q

What space does porous fenestrations in sinusoidal endothelial cells leak fluid and proteins into?

A

Space of Disse

68
Q

What is LSEC?

A

Liver Sinusoidal Endothelial Cells

69
Q

What is the significance of the LSEC and Space of Disse?

A

increased sinusoidal pressure increases lymph production and fluid will leak out and accumulate in abdominal cavity as ascitic fluid

70
Q

What occurs in regeneration of normal liver?

A

Macrophages, Hepatic stellate cells, and LSECs signal hepatocytes to enter mitosis

Hepatic stellate cells are NOT ACTIVATED

71
Q

What occurs in regeneration of abnormal, chronically damaged liver?

A

1) Hepatocytes are very senescent and unable to divide efficiently
2) The hepatic stellate cells are ACTIVATED to myofibroblasts and excessive scar tissue inhibits regeneration
3) excessive cellular debris inhibits efficient liver regeneration

72
Q

What is the function of hepatic stellate cells?

A

to Store Vitamin A

73
Q

What are the major primary diseases of the liver?

A 
Viral Hepatitis
Nonalcoholic fatty liver disease (NAFLD)
Alcoholic liver disease
Hepatocellular carcinoma (HCC)
Secondary to heart failure and metastatic cancer
74
Q

What is liver disease?

A

an insidious process, except for acute

75
Q

What is acute liver failure?

A

development of severe acute liver injury with encephalopathy and elevated PTT in a patient without cirrhosis or preexisting liver disease

76
Q

What is the cutoff to define acute vs. chronic liver disease?

A

Illness duration less than or greater than 26 weeks

77
Q

What is the major cause of acute liver failure?

A

Viral and drug induced hepatitis caused by APAP

78
Q

What are the clinical manifestations of acute liver failure?

A 
Hepatic Encephalopathy
Severe acute liver injury, leading to liver test abnormalities
Prolonged PTT/INR
Jaudice
Hepatomegaly
RUQ tenderness
Coagulopathy
Increased portal hypertension
79
Q

What is hepatic Encephalopathy (HE)?

A

reversible syndrome of impaired brain function occurring in patients with advanced liver failure

80
Q

What is the pathogenesis of HE?

A

Hyperammonemia
Oxidative stress
Oxindole

81
Q

What occurs with hyperammonemia?

A

Increase in brain uptake of neutral amino acids altering the synthesis of Dopamine, NE, and serotonin

Increase in intracellular osmolarity in astrocytes causign astrocyte swelling

Altered neural electric activity

82
Q

What is oxindole and what does it cause in HE?

A

Tryptophan metabolite formed by gut bacteria that causes sedation, muscle weakness, hypotension, and coma

83
Q

What are the three major pathways of APAP metabolism?

A

1) conjugation and excreted in urine by glutathione (90%)
2) Small portion is excreted in urine without being metbaolized
3) 10% is oxidized and forms NAPQUI

84
Q

What is the substrate for alcohol metabolism in the liver?

A

CYP 2E1

85
Q

What does acute alcohol ingestion cause?

A

NOT risk factor for hepatotoxicity and is actually protective by competing with APAP for CYP450 and therefore decreasing NAPQUI

86
Q

What does chronic alcohol ingestion cause?

A

increased CYP 450 activity two fold and reduces glutathione levels

87
Q

Liver damage from APAP ingestion can happen in what 3 circumstances?

A

Excessive intake of APAP
Excessive cytochrome P450
Decreased capacity for glucuronidation or sulfation

88
Q

What are key processes of hepatocyte necrosis in humans?

A

Cellular Swelling
Inflammation
Release of ALT

89
Q

What is most associated with chronic liver disease?

A

cirrhosis

90
Q

What is cirrhosis?

A

Late stage of progressive hepatic fibrosis characterized by distortion of the hepatic architecture

Considered irreversible in its advanced stages and treatment would be liver transplant

91
Q

What are the causes of cirrhosis?

A

Chronic viral hepatitis (Hep b or c)
Alcoholic liver disease
Hemochromatosis
Nonalcoholic fatty liver disease

92
Q

What is the principle source of ECM in hepatic fibrosis?

A

stellate cells

93
Q

What happens to stellate cells in liver injury?

A

They undergo activation in which they lose vitamin A, proliferate, and become fibrogenic

94
Q

What is portal hypertension?

A

Result of resistance to portal blood flow and may lead to complications such a variceal bleeding and ascites

95
Q

When does portal hypertension often develop?

A

when a patient has cirrhosis

96
Q

What are the structural changes that occur that cause portal hypertension?

A

Distortion of the liver microcirculation by fibrosis
Angiogenesis
Vascular Occlusion

97
Q

What are the dynamic changes that occur that cause portal hypertension?

A

Increased production of vasoconstrictors and reduced release of endothelial vasodilators

98
Q

What are the main clinical consequences of portal hypertension?

A

Ascites
Congestive splenomegaly
hepatic Splenomegaly

99
Q

What is Ascites?

A

accumulation of excess fluid in the peritoneal cavity

100
Q

What is ascites caused by?

A

85% of the time = cirrhosis

101
Q

What does portal hypertension cause profound changes in?

A

splanchnic circulation

102
Q

What are the Circulatory abnormalities seen in patients with cirrhosis or ascites?

A 
Reduced systemic vascular resistance
Reduced arterial pressure
Increased HR
Increased cardiac index
Increase plasma volume
reduced renal blood flow
Increased portal blood flow
103
Q

What are the vascular abnormalities seen in patients with cirrhosis or ascites?

A

Splanchnic vasodilation
Renal artery vasoconstriction
Pulmonary vasodilation

104
Q

What are the functional abnormalities seen in patients with cirrhosis or ascites?

A

Activation of systemic vasodilator factors
Activation of systemic vasoconstrictor factors
Activation of renal vasodilator factors
Reduced glomerular filtration rate

105
Q

What are the biochemical abnormalities seen in patients with cirrhosis or ascites?

A 
Sodium retention
Water retention
Increased systemic prostaglandins
Increased systemic nitric oxide
Increased renal nitric oxide and prostaglandins
106
Q

What two places in the body is alcohol metabolized?

A

Liver and stomach

107
Q

What enzyme converts alcohol to acetaldehyde?

A

Alcohol dehydrogenase (ADH)

108
Q

What enzyme converts acetaldehyde to acetate?

A

Acetaldehyde dehydrogenase (ALDH)

109
Q

What metabolizes the alcohol in the stomach?

A

Alcohol dehydrogenase

110
Q

What infections can reduce the activity of gastric ADH?

A

Helicobacter pylori

Gastritis

111
Q

What is alcoholic steatosis?

A

Reduced oxidation of hepatic fatty acids
Increased lipogenesis
Chronic consumption

No inflammation associated; increased fat production

112
Q

What is alcoholic steatohepatitis?

A

Cytokines and inflammation
Antigenic adduct formation
Immunolgic

113
Q

Where is iron normally stored?

A

Hemoglobin in RBCs
Iron containing proteins other than hemoglobin
Iron bound to transferrin in plasma
Storage iron in the form of ferritin or hemosiderin

114
Q

How does the body eliminate iron excess?

A

Intake
Loss
Recycling

115
Q

What are the causes of iron overload?

A

Increased intake = transfusions

Increased absorption with normal intake = Hereditary hemochromocytosis due to HFE mutation or chronic liver disease

116
Q

What is the clinical consequence of excess iron stores?

A

organ damage from ROS

117
Q

How does excess iron storage cause organ damage?

A

Transferring becomes saturated causing iron to bind to other proteins and molecules

These non-transferring bound iron (NTBI) are taken up parenchymal cells of the liver, heart, and endocrine organs

The excess iron in these organs interact with hydrogen peroxide to cause a fenton reaction which created fenton reagant (ROS)

118
Q

What is hereditary hemochromatosis?

A

caused by HFE mutation in which there is increased intestinal iron absorption

119
Q

What are the mechanisms of liver injury in HH?

A

1) lipid peroxidation
2) interaction of ROS and iron with DNA
3) Stimulation of collagen formation by activation of stellate cells

120
Q

What is the clinical consequence of HH?

A

fibrosis and cirrhosis which occurs when hepatic iron concentration is greater than 3X its normal limit

121
Q

What is the pathogenesis of Hemochromatosis?

A

HFE gene mutation causing hepcidin transcriptional activity to be reduced

decreased hepcidin causes unchecked iron-export by ferroportin in the macrophage which is responsible for excess plasma iron load, tissue iron accumulation, and tissue damage

122
Q

What is Hepatitis A Virus (HAV)?

A

Self limited illness that does not become chronic

Infection confers lifelong immunity

123
Q

How to you prevent HAV?

A

Vaccination
Immune Globulin
Attention to hygienic practices

124
Q

How is HAV spread?

A

Ingestion of contaminated water and foods and is shed in the stool

Consumption of raw or steamed shellfish

125
Q

What is the pathogenesis of HAV?

A

Viral replication occurs in hepatocyte cytoplasm

Hepatocellular damage and destruction of infected hepatocytes is mediated by HAV specific CD8+ lymphocytes and NKCs

Interferon-gamma have a central role in promoting clearance of infected hepatocytes

126
Q

What is the incubation period of HAV?

A

28 days

127
Q

What is are the physical findings of HAV?

A 
Fever
Jaundice
Scleral icterus
Hepatomegaly
Abdominal Pain
128
Q

What are the laboratory abnormalities found in HAV?

A

Increased serum aminotransferase, serum bilirubin, and alkaline phosphatase

129
Q

What are the clinical manifestations of HAV?

A

Sudden onset of nausea, vomiting, anorexia, fever, malaise, and abdominal pain

130
Q

How long are individuals infected for?

A

Contagious during incubation period (3 weeks) and remain so for about a week after jaundice appears

131
Q

How long until patient has full recovery of HAV?

A

6 months

132
Q

What is Hepatitis B Virus (HBV)?

A

global public health concern

Spectrum of clinical manifestations of infection varies in both acute and chronic disease

Clinical outcome of HBV infection depends upon the age at infection, level of HBV replication, and immune status of the host

133
Q

How is HBV spread?

A

Blood
Semen
Other bodily fluids

134
Q

What is the pathogenesis of infection of HBV?

A

Immune mediated liver injury caused by cytotoxic T cell-mediated lysis of infected hepatocytes

Direct cytotoxic liver injury

HBV mutations affect severity

Development of CHRONIC infection

135
Q

What is associated with HBV?

A

cccDNA which serves as template for virus to trasncribe and translate

136
Q

What is the clinical course of acute hepatitis?

A

Mainly have subclinical or anicteric hepatitis

More sever inpatients co-infected with other hepatitis viruses or with underlying liver disease

137
Q

What are the phases of chronic HBV infection?

A

1) Immune tolerance
2) Immune clearance = HBeAG-positive chronic hepatitis
3) Inactive carrier
4) reactivation = HBeAg-negative chronic hepatitis

138
Q

Is there a vaccine for Hepatitis C (HCV)?

A

No

139
Q

What are the hallmarks of HCV?

A

Persistent infection

Chronic hepatitis

140
Q

How is HCV spread?

A

blood-borne virus

Sharing needles to inject drugs

141
Q

What causes hepatocellular carcinoma?

A

Combination of indirect-host mediated and direct HCV-mediated mechanisms

Persistent immune-mediated inflammation which causes ROS to trigger oxidative DNA damage

HCV infection impairs DNA repair pathways

Repeated cycles of hepatocellular destruction with regenerative proliferation and progressive fibrosis within this pro-mutagenic environment results in “cancer field”

142
Q

What is Nonalcoholic Fatty Liver Disease (NAFLD)?

A

represents a spectrum of disorders that have in common the presence of hepatic steatosis in individuals who do not consume alcohol

143
Q

What are the two types of NAFLD?

A

NAFL

NASH

144
Q

What is nonalcoholic fatty liver (NAFL)?

A

hepatic steatosis is present without evidence of inflammation

145
Q

What is nonalcoholic steatohepatitis (NASH)?

A

NAFLD that may progress to cirrhosis; NAFLD with evidence of inflammation

146
Q

Which patients are at a lower risk of developing significant fibrosis?

A

Those with simple steatosis (NAFL)

147
Q

What causes the inflammation seen in NASH/NAFLD?

A

Free cholesterol accumulates causing liver injury by the activation of Kupffer cells, Stellate cells, and Hepatoctyes

148
Q

What do Kupffer cells cause when activated in NAFLD?

A

Causes secretion of proinflammatory mediators and pro-fibrotic factors

149
Q

What do stellate cells cause when activated in NAFLD?

A

Increase liver fibrogenesis

150
Q

What do hepatocytes cause when activated in NAFLD?

A

induces itself lipid peroxidation and lipotoxicity leading to cellular dysfunction and death

151
Q

What happens in NAFLD when free cholesterol accumulates in mitochondria?

A

Mitochondrial dysfunction and an increase in ROS

152
Q

How does insulin resistance cause hepatic steatosis?

A

Insulin resistance causes hyperglycemia and hyperinsulinemia which in turn further increases heptic lipogenesis which increases free fatty acids and keeps the process of liver damage going

153
Q

What symptoms do patients with simple steatosis have?

A

they are asymptomatic

154
Q

What clinical features are found in patients with NASH?

A

Serum AST and ALT are elevated
CVD is a frequent cause of death
Metabolic Syndrome

155
Q

What is cholestatic disease?

A

decrease in bile flow

156
Q

What are the two mechanisms that cause cholestatic disease?

A

hepatocellular

Obstructive

157
Q

What is hepatocellular cholestatic disease?

A

An impairment of bile formation causes decreased bile flow

158
Q

What is obstructive cholestatic disease?

A

An abnormal bile flow occurs after it is formed causine decreased bile flow

159
Q

What does tissue deposition of bile look like in patients with cholestatic disease?

A

yellow discoloration of skin = jaundice

sclera due to retention of bilirubin = icterus

160
Q

What symptoms are associated with cholestatic disease?

A

Pruritus

161
Q

What is the pathogenesis of pruritus?

A

Bile Acids
Endogenous Opioids
Lysophosphatidic acid and autotaxin

Patho II (16 decks)

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