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Semester 3-GI > Lecture 12-Liver and Pancreas Pathology > Flashcards

Lecture 12-Liver and Pancreas Pathology Flashcards

1
Q

Where are RBCs broken down?

A

Macrophages in spleen and liver

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2
Q

What is bilirubin a product of ?

A

Heme breakdown

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3
Q

Why does bilirubin have to be bound to albumin in the blood?

A

Because it is hydrophobic

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4
Q

In the liver, what is bilirubin conjugated with and which enzyme does this?

A

Glucoronic acid by UDP glucuronyl transferase

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5
Q

True or false: conjugated bilirubin is water soluble

A

TRUE

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6
Q

How is failure of anabolism of the liver measured?

A
  • albumin and coagulation factors(failure to produce -> prolonged INR)
  • glycogen and haematopoeisis
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7
Q

How is failure of catabolism of the liver measured?

A
  • drugs
  • hormones
  • Hb
  • poisons
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8
Q

What is pre-hepatic jaundice?

A

Too much bilirubin due to excessive breakdown of heme

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9
Q

What is intra-hepatic jaundice?

A

Failure of hepatocytes to conjugate and/or secrete bilirubin

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10
Q

What is cholestasis?

A

Bile stuck in liver

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11
Q

What is post-hepatic or obstructive jaundice?

A

Failure of biliary tree to convey conjugated bilirubin to the duodennum

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12
Q

Describe the presentation of pre-hepatic jaundice

A
  • mild yellow
  • dark stools because lots of bilirubin is converted to stercobilin
  • normal urine colour
  • no pruritis
  • increased serum bilirubin, increased urobilinogen, no conjugated bilirubin in urine
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13
Q

Describe the presentation of intra-hepatic jaundice

A
  • normal stools
  • dark urine because conjugated bilirubin in blood moves to urine as it is not excreted into bile
  • no pruritis
  • increased serum bilirubin, normal urobilinogen, conjugated bilirubin in urine
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14
Q

What can cause intra-hepatic jaundice?

A

Hepatitis and cirrhosis

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15
Q

Describe the presentation of post-hepatic jaundice

A
  • severe jaundice: green tinge
  • pale stools
  • dark urine
  • pruritis because can’t secrete bile salts
  • increased serum bilirubin, decreased urobilinogen, conjugated bilirubin in urine
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16
Q

What can cause post-hepatic jaundice?

A

Pancreatic carcinoma, gallstone in bile duct

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17
Q

What are the three markers of hepatocyte damage/dysfunction?

A
  • alanine aminotransferase (ALT)
  • alkaline phosphatase (Alk Phos)
  • gamma glutamyl transferase (Gamma GT)
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18
Q

Where is ALT released from?

A

Damaged hepatocytes

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19
Q

Where is Alk Phos released from?

A

Liver canaliculi, bile ducts and bone

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20
Q

Where is gamma GT released from?

A

Bile duct cells and to a lesser extend, hepatocytes

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21
Q

What can cause increased ALT levels?

A

Hepatitis: viral, acute alcohol intake, fatty liver disease, drugs

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22
Q

What can cause increased Alk Phos levels?

A
  • Bile duct/liver disease with cholestasis: biliary obstruction, cirrhosis, liver mets, drugs
  • Bone: mets, fratures, osteomalacia, hyperparathyroidism, growing bones
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23
Q

What can cause increased Gamma GT levels?

A

Biliary duct obstruction, cholestasis, cirrhosis, liver mets, drugs, alchoholism

24
Q

Why can ultrasonography be used to diagnose liver conditions?

A

Detects biliary obstruction, hepatic fibrosis, fatty liver disease, portal hypertension, ascites, gallstones and liver mets

25
Q

What happens to hepatocytes in hepatitis?

A

Become inflamed and can’t function properly

26
Q

True or false: hepatitis increases serum NH3 which is produced by colonic bacteria and deamination of AA

A

TRUE

27
Q

What are the symptoms of hepatitis?

A

Unwell, anorexia, fever, RUQ pain, dark urine, jaundice

28
Q

What are the blood test findings in hepatitis?

A
  • normal albumin/INR
  • increased serum bilirubin
  • conjugated bilirubin in urine
  • very high serum ALT
  • normal Alk Phos and gamma GT
29
Q

What is liver cirrhosis?

A

Liver fibrosis -> shrunken, hard, nodular liver

30
Q

What can fibrosis lead to?

A
  • Pressure and occlusion or hepatic sinusoids -> portal hypertension -> diverts nutrient-rich blood away from liver -> ascites
  • pressure on bile canaliculi decreases its ability to excrete toxins
  • hepatocytes replaced by fibrous tissue which decreases albumin production
31
Q

What are the causes of liver cirrhosis?

A

Alcohol, viral, hepatitis, fatty liver disease, idiopathic

32
Q

What are the complications of cirrhosis?

A
  • oesophageal varices
  • haemorrhoids
  • caput medusa (blood flows in the wrong direction through ligamentum teres)
33
Q

What are the symptoms of cirrhosis?

A

Fatigue, bleeding easily, ascites, swollen legs, weight loss, jaundice, haematemesis, melaena, confusion, drowsiness and slurred speech

34
Q

What are the blood test findings in cirrhosis?

A
  • may all be normal
  • decreased albumin/prolonged INR
  • increased bilirubin
  • increased ALT
  • normal Alk Phos
  • raised gamma GT if alcoholic
35
Q

What is the treatment for cirrhosis?

A

No treatment but can deal with complications/have liver transplant

36
Q

What causes biliary duct obstruction?

A

Gallstones from gallbladder blocking common bile duct and carcinoma of the head of the pancreas

37
Q

What is cholangitis?

A

Infection in bile ducts due to E Coli (most common)

38
Q

What are the triad of symptoms (Charcot’s triad) of cholangitis?

A

Fever
RUQ pain
Jaundice

39
Q

What are the two main things leading to the formation of gallstones?

A

Excess cholesterol crystallising or excess bilirubin

40
Q

Why is biliary colic not a true colic?

A

The pain is constant

41
Q

Where is pain felt in biliary colic?

A

RUQ but can radiate to tip of right scapula/shoulder

42
Q

What can precipitate biliary colic?

A

Fatty meal

43
Q

How long can biliary colic last for?

A

6 hours

44
Q

What is acute cholangitis?

A

If gallstone obstructs cystic duct, it can lead to stasis of gallbladder contents which can cause infection

45
Q

What are the symptoms of acute cholangitis?

A

Gallbladder pain, unwell, pyrexia, tender over gallbladder

46
Q

What are the lab findings in liver metastases?

A
  • increased bilirubin
  • conjugated bilirubin in urine
  • raised Alk Phos
  • ALT and gamma GT slightly raised
  • normal albumin and INR
47
Q

What is acute pancreatitis?

A

Due to premature activation of pancreatic proteases in pancreas rather than duodenum -> autodigestion

48
Q

What is chronic pancreatitis due to?

A
  • Due to repeated low grade pancreatitis -> fibrosis

- Alcohol abuse

49
Q

What happens in chronic pancreatitis?

A

Pancreas becomes calcified and patients suffer severe epigastric and back pain -> opiate addiction and suicide

50
Q

What can cause acute pancreatitis?

A
  • alcohol

- gallstones -> outflow obstruction, pancreatic duct hypertension and toxic effect of bile salts can activate enzymes

51
Q

What are the symptoms of acute pancreatitis?

A

Epigastric pain through back, vomiting

52
Q

What are the lab findings for acute pancreatitis?

A

Increased serum amylase/lipase

CT for necrosis/pseudocyst (=fluid collection pushing through lesser sac)

53
Q

What is the treatment of acute pancreatitis?

A

Analgesia and fluids

54
Q

What is the most common type of carcinoma in the pancreas?

A

Ductal adenocarcinomas in the head of the pancreas

55
Q

Why does pancreatic carcinoma present late?

A

It is retroperitoneal (therefore low survival)

56
Q

What are the symptoms of pancreatic carcinoma?

A

Anorexia, malaise, fatigue, epigastric/back pain, dark urine, pale stools, pruritis, weight loss

Semester 3-GI (14 decks)

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