Lecture 26 Flashcards

1
Q

What are cholestatic diseases of the liver?

A

Agents that directly damage hepatocytes or conditions where there is obstruction biliary outflow.

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2
Q

What is intra-hepatic cholestatic disease of the liver?

A

The obstruction occurs to the bile ducts or bile canaliculi within the liver.

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3
Q

What is extra-hepatic cholestatic disease of the liver?

A

Obstruction to the common bile duct (outside the liver).

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4
Q

What are autoimmune cholangiopathies?

A

Autoimmune damage to either the bile ducts or bile canaliculi. These are uncommon but not rare disorders.

1) Primary biliary cirrhosis - autoimmune disorder leading to destruction of bile canaliculi.
2) Primary sclerosing cholangitis - autoimmune disorder leading to scarring of bile ducts.

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5
Q

What occurs in cholestasis of sepsis?

A

Sepsis can affect the liver through:

1) Direct affects of intrahepatic infection e.g. liver abscess, bacterial cholangitis.
2) Ischaemia related to hypotension.
3) Circulating microbial products - aprticulary in context of gram-negative infection i.e. this is the most likely thing to lead to cholestatic picture.

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6
Q

What happens when there is impaired blood inflow?

A

Portal vein obstruction, intra/extrahepatic thrombosis will cause:

1) varices
2) splenomegaly
3) intestinal congestion.

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7
Q

What happens when there is impaired intrahepatic blood flow?

A

Cirrhosis, and sinusoid occlusion will cause:

1) Ascites (cirrhosis).
2) Oesophageal varices (cirrhosis).
3) Hepatomegaly.
4) Elevated aminotransferases.

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8
Q

What happens when there is hepatic vein outflow obstruction?

A

Hepatic vein thrombosis (budd-chiari syndrome), sinusoidal obstructive syndrome will cause:

1) Ascites
2) Hepatomegaly
3) Elevated aminotransferases
4) Jaundice.

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9
Q

What are benign neoplasms of the liver?

A

1) Cavernous haemangiomas

2) Hepatocellular adenomas.

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10
Q

What are malignant neoplasms of the liver?

A

1) Hepatocellular carcinoma - see in patients with cirrhosis of the liver.
2) Hepatoblastoma
3) Cholangiocarcinoma
4) Hepatic metastases.

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11
Q

What is the function of the pancreas?

A
Exocrine = 80-90%
Endocrine = 10-20%.
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12
Q

What is the exocrine function of the pancreas composed of?

A

Composed of acing cells and ducts. Acing cells contain zymogen granules.

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13
Q

What are zymogen granules?

A

Inactive enzyme precursors for trypsin, chymotrypsin, amylase, lipase, nuclease and elastase.

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14
Q

What is the endocrine function of the pancreas composed of?

A

Islets of Langerhans. These secrete insulin, glucagon and other hormones.

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15
Q

Describe pathology of the pancreas?

A
Congenital/genetic = cystic fibrosis.
Inflammatory/infective = acute and chronic pancreatitis.
Malignant = carcinoma of the pancreas.
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16
Q

What is acute pancreatitis?

A

Inflammation of the pancreas - associated with acing cell injury.

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17
Q

What is the spectrum of severity duration and severity of acute pancreatitis?

A
Mild = 60-70% cases, low mortality.
Severe = 30-40% of cases, 20-30% mortality.
18
Q

What are the four major categories of acute pancreatitis?

A

1) Metabolic - alcohol.
2) Mechanical - gallstones, trauma.
3) Vascular - shock, vasculitis.
4) Infection - mumps.

19
Q

How do the causes induce pancreatitis?

A

This is due to damage to acing cells. Releases pancreatic enzymes which damage the tissue and damage further acing cells. Secondary inflammatory response, with release of number of cytokines. This will induce massive reaction.

20
Q

What is the consequence of enzyme release?

A

1) Proteases - destruction of acini, ducts and islets.
2) Lipases - fat necrosis of pancreas and other sites.
3) Elastase - blood vessel destruction leading to intestinal haemorrhage.
4) Cell injury response - inflammation and oedema.

21
Q

What are the key events to trigger pancreatitis?

A

Obstruction of the pancreatic ducts or direct injury to acinar cells.

22
Q

Describe pancreatic duct obstruction by gallstones and ductal concretions present in alcoholics?

A

1) Increased intrapancreatic ductal pressure.
2) Accumulation of enzyme rich interstitial fluid.
3) fat necrosis as lipase already active.
4) Promotes oedema and local inflammation.
5) Oedema compromises blood flow.

23
Q

Describe primary acinar cell injury?

A

Viruses, drugs, trauma and iscahamia can be cause the release of enzymes.

24
Q

What are the clinical features of acute pancreatitis?

A

1) Acute abdominal pain - usually upper abdominal and will show in the epigastric region.
2) Nausea and vomiting.
3) Fever, tachycardia.
4) Marked abdominal tenderness - may have ileum and rarely will be shock.

25
Q

How do you make the diagnosis of acute pancreatitis?

A

1) High white cell count - increase in the cells involved in acute inflammatory response, however not specific.
2) Elevated serum amylase (lipase) - measure enzymes that are released from the pancreas, these will be significantly elevated.
3) CT scan - oedema, necrosis and pseudocysts of the pancreas. .
4) Rarely may need laparotomy to confirm diagnosis.

26
Q

How do you manage an acute pancreatitis?

A

“Rest the pancreas”

1) IV fluids - nil by mouth, not eating food.
2) NG suction - nasogastric tube to remove the secretions from gastric.
3) Analgesia.
4) Close monitoring - looking for the complications that may arise with pancreatitis.

27
Q

What is chronic pancreatitis?

A

Defined as repeated bouts of pancreatic inflammation its loss of pancreatic parenchyma and replacement by fibrous tissue.

Majority have heavy alcohol intake (60-70%).

28
Q

What is the pathology of chronic pancreatitis?

A

1) Fibrotic organ - very hard.
2) Atrophy of the exocrine component but relative sparing of the islets.
3) Mild chronic inflammatory infiltrate.
4) Calcification.

29
Q

What causes chronic pancreatitis?

A

1) 60-70% have heavy alcohol intake - intraductal plugs (proteins, cell debris).
2) Previous acute pancreatitis, severe malnutrition and hereditary/CFTR mutations.

30
Q

What are the clinical features of chronic pancreatitis?

A

1) Repeated attacks of abdominal pain - often bought on by alcohol.
2) Can be more persistent pain.
3) If ongoing: loss of exocrine function (malabsorption), pseudocysts, and rarely diabetes mellitus.

31
Q

How do you make the diagnosis of chronic pancreatitis?

A

1) Clinical suspicion.
2) Serum amylase - may not be elevated.
3) CT imaging.

32
Q

Describe pancreatic carcinoma?

A

4th most common cause of cancer death.
Males slight > Females.
Most aged >50 (peak aged 60-80).
Prognosis remains poor (

33
Q

What are the risk factors for pancreatic carcinoma?

A

1) Tobacco smoking - smokers have a higher incidence.
2) Havy alcohol intake.
3) High BMI.
4) Rare hereditary cases.
5) Alcohol and coffee suggested but not confirmed.

34
Q

Where do adenocarcinoma (of the pancreas) form?

A

1) 60-70% will occur in the head of the pancreas.
2) 5-10% will occur in the body of the pancreas.
3) 10-15% will occur in the tail.
3) 20% will diffuse.

35
Q

What happens when there is an adenocarcinoma in the head of the pancreas?

A

The tumour will invade the ampulla and biliary obstruction will occur.

36
Q

What happens when there is an adenocarcinoma in the body and tail of the pancreas?

A

It will remain silent, often large and disseminated at presentation, spread to nodes, adjacent organs, liver, bones and lungs.

37
Q

What are the clinical features of pancreas adenocarcinoma?

A

1) Obstructive jaundice.
2) Pain.
3) Weight loss.
4) Pancreatitis.
5) Thrombophlebitis/venous thrombosis.

38
Q

How do you make the diagnosis of pancreas adenocarcinoma?

A

Made on imaging - followed by CT or Ultrasound guided FNA and core biopsy. No tumour marker identified.

39
Q

Describe pancreatic endocrine tumours?

A

Can get tumours arising from the islet cells. These are rare and can secrete pancreatic hormones.

40
Q

What are endocrine tumours? (examples)

A

Insulinoma - the tumour will secrete insulin. The patient will present with hypoglycaemia. Most benign, 10% malignant. Treat with resection.