Week 9: Cirrhosis

Question 1

What does the GI tract include?

Answer 1

From mouth to rectum.

Question 2

What are accessory organs of digestion?

Answer 2

Liver, gallbladder, pancreas.

Question 3

Is Cirrhosis less common now?

Answer 3

Yes, due to less alcohol abuse.

Question 4

What is still a major risk factor?

Answer 4

Hepatitis C, especially from past blood transfusion contamination.

Question 5

What is cirrhosis?

Answer 5

A condition where the liver becomes full of nodules of varying sizes, surrounded by fibrosis (collagen). makes the liver hard and shrunken.

Question 6

Do cirrhotic nodules work properly?

Answer 6

No. They are functionally impaired.

Question 7

What does the hard liver cause in the blood system?

Answer 7

Portal hypertension (increased pressure in portal circulation).

Question 8

What does the portal vein do?

Answer 8

Brings venous blood from intestines, stomach, esophagus, rectum, spleen → liver.

Question 9

What happens in portal hypertension?

Answer 9

Blood backs up because of the hardened liver → pressure builds in the portal vein.

Question 10

What is missing in cirrhotic nodules under the microscope?

Answer 10

Normal lobular architecture.

Question 11

What does a normal lobule include?

Answer 11

Central vein, portal veins, sinusoids lined with hepatocytes.

Question 12

What is the path of blood in a healthy lobule?

Answer 12

Portal vein → sinusoids → hepatocytes → central vein.

Question 13

What do hepatocytes do?

Answer 13

Absorb/process proteins, lipids, drugs, ammonia, bilirubin.

Question 14

Why is the lobular architecture critical?

Answer 14

It allows proper metabolism and detoxification.

Question 15

What happens when lobular structure is lost?

Answer 15

Nutrient processing is impaired.

Question 16

How is bilirubin processed?

Answer 16

Hepatocytes → conjugation → bile canaliculi → bile ducts.

Question 17

What happens to bile flow in Cirrhosis?

Answer 17

Disrupted due to altered architecture.

Question 18

What are the CONSEQUENCES OF CIRRHOSIS?

Answer 18

Both portal system and bile system are compromised.

Leads to portal hypertension and jaundice.

Question 19

What causes liver cell death?

Answer 19

Hepatotoxic agents (alcohol, viruses, drugs).

Question 20

Is moderate alcohol consumption always harmful?

Answer 20

Not necessarily—liver can regenerate if damage is stopped early.

Question 21

How does alcohol cause fatty liver?

Answer 21

Slows metabolism → fat builds up.

Question 22

What does fatty liver look like under a microscope?

Answer 22

White lipid bubbles in hepatocytes.

Question 23

Can fatty liver be reversed?

Answer 23

Yes, if the damaging agent is removed.

Question 24

What happens if damage continues?

Answer 24

Hepatocytes die → enzymes released (transaminases: GOT/AST, GPT/ALT).

Question 25

What do high transaminases indicate?

Answer 25

Liver cell death.

Question 26

Can the liver regenerate?

Answer 26

Yes, but in chronic injury → forms hyperplastic nodules.

Question 27

Do nodules work?

Answer 27

No. They lack portal & bile connections → non-functional.

Question 28

How is END-STAGE CIRRHOSIS

Answer 28

Chronic liver cell death → regeneration attempts → fibrotic nodules → irreversible. Leads to liver failure.

Question 29

What are the common causes of cirrhosis?

Answer 29

Alcohol Hepatitis C Hepatotoxic drugs

Question 30

What is Ascites?

Answer 30

Fluid in the peritoneal cavity (belly).

Question 31

What are the signs and consequences of ascites?

Answer 31

Fluid wave on belly Hernias (increased pressure) Respiratory distress (diaphragm pushed up) Shallow breathing → respiratory acidosis Cyanosis (blue lips) Can lead to respiratory failure

Question 32

What causes ascites?

Answer 32

Increased hydrostatic pressure from portal hypertension Blocked lymph flow Low albumin (hypoalbuminemia → low oncotic pressure)

Question 33

How is ascites managed?

Answer 33

Increase dietary protein Treat underlying hypoalbuminemia Paracentesis (drain fluid if needed)

Question 34

What is jaundice?

Answer 34

Yellow skin/sclera due to high bilirubin.

Question 35

Where does bilirubin come from?

Answer 35

Breakdown of RBCs → heme → biliverdin → bilirubin.

Question 36

What are the roles of bile?

Answer 36

Emulsifies fats Helps digest lipids Gives feces color

Question 37

How does liver handle bilirubin?

Answer 37

Conjugates it with glucuronic acid Makes it water-soluble Sends it to bile → intestines

Question 38

What is unconjugated bilirubin?

Answer 38

Toxic Not water-soluble Binds to albumin Crosses blood-brain barrier in neonates → kernicterus (brain damage)

Question 39

What are 3 ways of jaundice can happen?

Answer 39

1. Hepatocellular damage: Liver can’t conjugate bilirubin and unconjugated builds up 2. Intrahepatic obstruction: Bile blocked inside liver → conjugated bilirubin builds up 3.Extrahepatic obstruction: Bile blocked outside liver (gallstones, tumors) → conjugated bilirubin builds up

Question 40

What are labs/tests that are run for jaundice?

Answer 40

Total bilirubin is increased Direct (conjugated) bilirubin increased if obstruction Indirect (unconjugated) bilirubin increased if liver cell failure or hemolysis

Question 41

What's the process of liver failure?

Answer 41

Necrosis → liver cells die Fibrosis → scar tissue forms Portal hypertension Varices Splenomegaly Ascites Jaundice Hepatic encephalopathy (brain dysfunction)

Question 42

what are the lab findings in liver failure?

Answer 42

High ALT/AST Low albumin Long PT (clotting time) Vitamin K deficiency Elevated ammonia → encephalopathy

Question 43

How can you recognize liver failure?

Answer 43

Jaundice Ascites Bleeding (varices, bruising) Encephalopathy (confusion, coma)