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ALCOHOLIC liver Disease And Cirrhosis Flashcards

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1
Q

What is a leading cause of liver disease in most western countries, and what percentage of global deaths is it associated with?

A

Excessive alcohol consumption. It’s associated with 3.8% of global deaths.

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2
Q

What is the rank of excessive alcohol consumption as a risk factor for death?

A

Eighth highest risk factor for death.

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3
Q

At what blood alcohol concentration (BAC) does drowsiness typically occur?

A

Drowsiness occurs at 200 mg/dL.

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4
Q

At what blood alcohol concentration (BAC) does stupor typically occur?

A

Stupor occurs at 300 mg/dL.

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5
Q

What serious conditions can occur at higher BAC levels beyond stupor?

A

Coma and/or respiratory arrest.

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6
Q

What are the three forms of alcoholic liver disease (ALD)?

A

(1) Hepatic steatosis (fatty liver disease), (2) Alcoholic (steato) hepatitis, (3) Cirrhosis.

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7
Q

According to the diagram on page 1 (‘Types of ALD’), what is the initial stage of ALD if alcohol exposure continues from a normal liver?

A

If alcohol exposure continues from a normal liver, the initial stage is 1. Alcoholic steatosis (Fatty liver). [Reference Diagram: ‘Types of ALD’ on Page 1]

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8
Q

According to the diagram on page 1 (‘Types of ALD’), what can reverse alcoholic steatosis or alcoholic hepatitis?

A

Abstinence can reverse alcoholic steatosis or alcoholic hepatitis, potentially leading back to a normal liver or a less severe state. [Reference Diagram: ‘Types of ALD’ on Page 1]

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9
Q

According to the ‘Types of ALD’ diagram on page 1, how can fibrosis and cirrhosis develop, and what percentage of alcoholics are affected?

A

Continued exposure from either alcoholic steatosis or alcoholic hepatitis can lead to 3. Fibrosis and cirrhosis. This affects 10-15% of alcoholics. [Reference Diagram: ‘Types of ALD’ on Page 1]

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10
Q

Where is most ingested alcohol absorbed unchanged?

A

In the stomach and small intestine.

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11
Q

How is approximately 10% of ingested alcohol excreted from the body?

A

10% is excreted by the lungs (basis of the Breathalyzer test), kidneys, and sweat.

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12
Q

Which organs are primarily responsible for metabolizing most of the absorbed alcohol?

A

The liver and stomach.

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13
Q

What two enzyme systems involved in alcohol metabolism are induced by alcohol itself?

A

Microsomal Ethanol Oxidizing System (MEOS) and Alcohol dehydrogenase (ADH) (and catalase enzymes).

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14
Q

Describe the metabolic pathway of alcohol involving Alcohol Dehydrogenase (ADH) as depicted in the ‘Fate of alcohol in the body’ diagram on page 2, including products and byproducts.

A

Ingested alcohol is converted by Alcohol Dehydrogenase (ADH) in the cytoplasm to Acetaldehyde. This reaction produces NADH. Acetaldehyde is then converted to Aldehyde, and further to Acetic Acid. [Reference Diagram: ‘Fate of alcohol in the body’ on Page 2, showing Alcohol –(ADH, Cytoplasm)–> Acetaldehyde (produces NADH) –> ALDEHYDE –> ACETIC ACID]

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15
Q

According to the ‘Fate of alcohol in the body’ diagram on page 2, what is the role of Cytochrome P450 (MEOS) in alcohol metabolism, and what potentially harmful substance does it generate besides acetaldehyde?

A

Cytochrome P450 (MEOS), located in the endoplasmic reticulum, metabolizes alcohol to Acetaldehyde. It also generates Reactive Oxygen Species (ROS). [Reference Diagram: ‘Fate of alcohol in the body’ on Page 2, showing Alcohol –(Cytochrome P450 MEOS, Endoplasmic Reticulum)–> Acetaldehyde + Reactive oxygen species]

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16
Q

What are two gender-related factors predisposing to alcoholic liver disease?

A
  1. Differences in alcohol pharmacokinetics and metabolism. 2. Women are more susceptible to alcohol-induced hepatic injury than men.
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17
Q

Why are women generally more susceptible to alcohol-induced hepatic injury?

A

Due to increased gut permeability of endotoxins by oestrogen and increased production of pro-inflammatory cytokines and chemokines.

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18
Q

What ethnic and genetic differences are noted for cirrhosis risk in alcoholics?

A

Cirrhosis is higher in blacks > whites. This is associated with low Aldehyde dehydrogenase in blacks and Asians.

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19
Q

How do co-morbid conditions like HCV and HBV infections affect alcoholic liver disease?

A

Infections with HCV and HBV increase the severity of alcoholic liver disease.

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20
Q

In the pathogenesis of alcoholic steatosis, what important molecule is produced from alcohol oxidation?

A

NADH.

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21
Q

List three key pathogenic mechanisms that contribute to alcoholic steatosis.

A
  1. Increased lipid biosynthesis. 2. Impaired secretion of lipoproteins. 3. Increased catabolism of fat from the periphery. (All influenced by increased NADH).
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22
Q

Explain the mechanisms contributing to alcoholic steatosis, based on the ‘Pathogenesis Mechanisms contributing to Alcoholic steatosis’ diagram on page 3.

A

Alcohol is converted to Acetaldehyde by Alcohol Dehydrogenase, using NAD+ and producing NADH. The increased NADH leads to: increased Lipid biosynthesis, Decreased fatty acid oxidation, and Decreased transport of lipoproteins. Additionally, there’s an increase in Peripheral catabolism of fat. These factors collectively cause Alcoholic steatosis. [Reference Diagram: ‘Pathogenesis Mechanisms contributing to Alcoholic steatosis’ on Page 3]

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23
Q

What is the typical weight range for an enlarged liver in alcoholic steatosis (macroscopy)?

A

4-6 kg.

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24
Q

Describe the macroscopic appearance (color and texture) of the liver in alcoholic steatosis.

A

Yellow and greasy.

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25
What are two notable macroscopic characteristics of a liver with alcoholic steatosis regarding its consistency and behavior in water?
It is easily ruptured and floats in water.
26
What is the early microscopic finding in alcoholic steatosis, and where is it typically located?
Early steatosis is microvesicular and centrilobular.
27
What is the late microscopic finding in alcoholic steatosis, and what is its extent?
Late steatosis is macrovesicular and involves the entire lobule.
28
What is another term for alcoholic steatosis?
Fatty liver disease.
29
What do rounded edges signify in the macroscopic description of alcoholic steatosis?
This is one of the macroscopic features indicating an enlarged liver, often due to fat accumulation.
30
In what percentage of alcoholics does alcoholic hepatitis occur, and typically after how many years of alcohol abuse?
In 35% of alcoholics(not majority), typically after 3-5 years.
31
What are the three ways acetaldehyde induced damage contributes to alcoholic hepatitis pathogenesis?
1. Increased lipid peroxidation. 2. Acetaldehyde-protein adduct formation. 3. Disruption of cytoskeletal and membrane function.
32
How do Reactive Oxygen Species (ROS) generated by Cytochrome P450 contribute to alcoholic hepatitis?
ROS react with cellular proteins, damage membranes by lipid peroxidation, and alter hepatocellular function and drug toxicity.
33
Explain the role of impaired hepatic production of methionine in alcoholic hepatitis pathogenesis.
Impaired hepatic production of methionine leads to oxidative injury, contributing to decreased intrahepatic glutathione levels.
34
According to the 'Mechanisms contributing to hepatocyte injury' diagram for alcoholic hepatitis on page 4, how does decreased methionine production by the liver contribute to hepatocyte injury?
The diagram indicates that alcohol metabolism can lead to decreased methionine production by the liver. This results in decreased glutathione levels. Reduced glutathione impairs the liver's defense against free radical-induced injury (from sources like MEOS/Cytochrome P450), thereby contributing to damage to cell membranes, proteins, organelles, and increased apoptosis of hepatocytes, all features of alcoholic steatohepatitis. [Reference Diagram: 'Mechanisms contributing to hepatocyte injury' in Alcoholic Hepatitis on Page 4]
35
What are other contributing factors to alcoholic hepatitis besides direct liver damage mechanisms?
Malnutrition and deficiencies of vitamins (due to alcohol supplying calories, impaired digestion, pancreatitis), release of bacterial endotoxin from the gut into the portal circulation, and release of endothelins from sinusoidal endothelial cells (causing vasoconstriction and decreased perfusion).
36
Describe the macroscopic appearance of the liver in alcoholic hepatitis.
The liver can be normal or enlarged, often bile stained, and features of steatosis may be present.
37
What is hepatocyte swelling and necrosis in the microscopy of alcoholic hepatitis?
Cells undergoing swelling (ballooning) and necrosis due to accumulation of fat, water, and proteins.
38
What are Mallory bodies, and what are they composed of?
Mallory bodies are eosinophilic cytoplasmic clumps in hepatocytes, representing an accumulation of cytokeratin filaments.
39
Describe the neutrophilic reaction seen in alcoholic hepatitis.
Neutrophils accumulate around degenerating hepatocytes, especially those with Mallory bodies. Lymphocytes and macrophages are also present.
40
Define cirrhosis.
A condition involving the entire liver in which the parenchyma is changed into a large number of nodules separated by fibrous septa.
41
List three acquired aetiologies of cirrhosis.
Alcohol, Post-Viral, Metabolic syndrome and NAFLD (others include Biliary causes, Autoimmune, Drugs and toxins).
42
List three congenital aetiologies of cirrhosis.
Haemochromatosis, Wilson's Disease, Alpha 1 anti-trypsin deficiency.
43
What is the initial step in the pathogenesis of cirrhosis after an injurious agent?
Inflammation.
44
Which cells are primarily responsible for producing cytokines like IL1, TNFα, and TGFβ in the pathogenesis of cirrhosis?
Inflammatory cells, Kupffer cells, endothelial cells, hepatocytes, and bile duct epithelial cells.
45
According to the pathogenesis flow diagram on page 5, what is the central cellular event in cirrhosis pathogenesis that is triggered by cytokines and other factors?
Stimulation of stellate cells. This stimulation is caused by inflammation (TNF, IL), cytokines, direct damage by toxins, and reaction to extracellular matrix disruption. [Reference Diagram: Pathogenesis flow on Page 5]
46
List four factors that can lead to the stimulation of stellate cells in cirrhosis pathogenesis.
1. Inflammation (TNF, IL). 2. Cytokines. 3. Direct damage by toxins. 4. Reaction to extracellular matrix disruption.
47
Describe the progression from fibrosis to cirrhosis as depicted in the pathogenesis flow diagram on page 5.
Stimulation of stellate cells leads to Fibrosis. Fibrosis causes the Formation of fibrous septa. This results in Ischaemia, leading to Cell Necrosis. Subsequent Regeneration in the presence of fibrous septa leads to the Formation of nodules (Hyperplasia), which characterizes Cirrhosis. [Reference Diagram: Pathogenesis flow on Page 5]
48
What is the outcome of regeneration in the context of established fibrous septa during cirrhosis development?
Formation of nodules (Hyperplasia).
49
What injurious agents can initiate the pathogenic cascade leading to cirrhosis?
Alcohol, Viral (e.g., HBV, HCV), Toxins, Autoimmune processes, Metabolic/NAFLD conditions, or inherited factors.
50
Describe the typical macroscopic appearance of a cirrhotic liver.
The liver is diffusely nodular, often shrunken and fibrotic. It may be yellow (in alcoholic cirrhosis) or green (in biliary cirrhosis).
51
What are the two main microscopic features of cirrhosis?
1. Loss of lobular architecture and vascular architecture. 2. Parenchyma separated into nodules by fibrous septa.
52
What microscopic evidence of aetiology might be seen specifically in alcoholic cirrhosis?
Fat (steatosis) and Mallory's hyaline.
53
According to the 'Cirrhosis - Pathogenesis' schematic diagram on page 6, what key cell type is activated in the Space of Disse, and what influences its activation?
The Stellate/Ito Cell, located in the Space of Disse, is activated. It is influenced by Cytokines released from inflammatory cells and hepatocytes. [Reference Diagram: 'Cirrhosis - Pathogenesis' schematic on Page 6]
54
According to the 'Cirrhosis - Pathogenesis' schematic diagram on page 6, what is depicted being released from inflammatory cells and hepatocytes, acting on Stellate cells in the Space of Disse?
Cytokines. These are shown originating from inflammatory cells within the sinusoids and also near hepatocytes, influencing the Stellate/Ito cell. [Reference Diagram: 'Cirrhosis - Pathogenesis' schematic on Page 6]
55
For alcoholic steatosis (as a clinical feature, not necessarily cirrhosis stage), what is a common finding regarding liver size?
Hepatomegaly (enlarged liver).
56
In alcoholic steatosis, what is typically observed for serum bilirubin levels?
Mild elevation of serum bilirubin.
57
How common is severe hepatic dysfunction in the stage of alcoholic steatosis?
Severe hepatic dysfunction is unusual.
58
What are the structural components that separate the liver parenchyma into nodules in cirrhosis?
Fibrous septa.
59
What color might a cirrhotic liver be, depending on the underlying cause (e.g., alcoholic vs. biliary)?
May be yellow in alcoholic cirrhosis or green in biliary cirrhosis.
60
When does alcoholic hepatitis typically manifest in relation to alcohol consumption?
Usually after bouts of alcohol ingestion.
61
List three common symptoms of alcoholic hepatitis.
Malaise, Anorexia, Weight loss (due to release of cytokines), and Upper abdominal discomfort.
62
Why might tender hepatomegaly occur in alcoholic hepatitis?
Due to stretching of the liver capsule because of liver enlargement.
63
What is the characteristic pattern of serum AST/ALT elevation in alcoholic hepatitis?
Elevated serum AST/ALT, with AST > ALT, indicating liver cell damage.
64
How does loss of detoxification in ALD and cirrhosis manifest clinically, and what biochemical change is associated with it?
It can lead to Encephalopathy, associated with increased serum ammonia levels.
65
What are the clinical and biochemical consequences of liver cell damage in ALD and cirrhosis?
Jaundice (due to increased serum bilirubin) and increased Serum aminotransferases (ALT, AST).
66
How does cholestasis due to the fibrosis and obstruction manifest in ALD and cirrhosis?
It leads to Jaundice (increased serum bilirubin) and increased serum alkaline phosphatase.
67
What are the clinical manifestations of loss of synthetic function in ALD and cirrhosis?
Ascites (due to decreased serum proteins like globulins, albumin), and Coagulopathy/Bleeding manifestations (due to decreased synthesis of clotting factor, leading to increased Prothrombin time).
68
List three major causes of death in patients with alcoholic liver disease and cirrhosis.
Hepatic coma/encephalopathy, Massive gastrointestinal haemorrhage, Intercurrent infection (Others: Hepatorenal syndrome, Hepatocellular carcinoma (In 1-6%)).
69
What is the five-year survival prognosis for patients with alcoholic liver disease who stop alcohol intake versus those who continue?
90% in patients who stop alcohol intake; 50% - 60% in patients with continued intake of alcohol.
70
Besides alcohol-related and post-viral causes, list two other causes of cirrhosis mentioned on page 8.
Biliary cirrhosis, Haemochromatosis (also Wilson's disease).
71
What are three recommended reading topics related to advanced liver disease?
Pathogenesis of liver failure, portal hypertension, jaundice.
72
What specific instruction is given for understanding Post viral cirrhosis?
Please see note.
73
What specific instruction is given for understanding Biliary cirrhosis as a cause of cirrhosis?
Please refer text book.
74
What specific instruction is given for understanding Haemochromatosis as a cause of cirrhosis?
Please refer text book.
75
What specific instruction is given for understanding Wilson's disease as a cause of cirrhosis?
Please refer text book.
76
What is the general theme of the 'Reading topics' suggested on page 8?
Complications and consequences of severe liver disease and dysfunction, specifically liver failure, portal hypertension, and jaundice.

Pathology GI (7 decks)

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