Pancreas and Gall bladder pathology Flashcards

1
Q

What does the following image show? (Hint: it’s healthy tissue)

A

Exocrine component of the pancreas

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2
Q

What does the image show? (Hint: it is healthy tissue)

A

Endocrine component of the pancreas

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3
Q
  1. What is acute pancreatitis?
  2. Risk factors
A
  1. Acute inflammation of the pancreas caused by aberrant release of pancreatic enzymes.
  2. Alcohol and drugs
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4
Q

What are the causes of acute pancreatitis?

A

Duct obstruction:

  • Gall stones (50%)
  • Trauma
  • Tumours

Metabolic/toxic:

  • Alcohol (33%) - 5% of alcoholics develop acute pancreatitis
  • Drugs e.g. thiazide
  • Hypercalcemia (acute pancreatitis with other causes can cause hypocalcaemia)
  • Hyperlipidemia

Poor blood supply:

  • Shock
  • Hypothermia

Infection/inflammation:

  • Viruses (Mumps, which is a virus that affects glands, so can affect glands in the pancreas)
  • Autoimmune
  • Idiopathic (15%)
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5
Q

Describe the pathogenesis of duct obstruction, and how it can lead to acute pancreatitis

A

Gallstone stuck distal to where the common bile duct and pancreatic duct joins leads to reflux of the bile up the pancreatic duct followed by damage to acini and release of proenzymes which then become activated.

Alcohol leads to spasm/oedema of Sphincter of Oddi and the formation of the protein rich pancreati fluid which obstructs the pancreatic ducts

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6
Q

What type of injury to the pancreas does infection/inflammation cause? (everything apart from duct obstruction)

A

Direct acinar injury

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7
Q

Acute pancreatitis: patterns of injury:

Describe the patterns of injury ofthe following and what causes it

  1. Periductal
  2. Perilobular
  3. Panlobular
A
  1. Periductal - necrosis of acinar cells near ducts (usually secondary to obstruction)
  2. Necrosis at the edges of the lobules (usually due to poor blood supply
  3. Panlobular - develops from 1 and 2
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8
Q

Describe the pathogenesis of injury to the periductal and periorbital areas of the pancreas

A

Activated enzymes –> acinar necrosis –> enzyme release etc.

Ranges from stromal oedema, to haemorrhagic necrosis

e.g. Lipases –> fat necrosis - calcium ions bind to free fatty acids forming soaps wihc are seen as yellow-white foci

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9
Q

Describe the following regarding acute pancreatitis:

  1. Complications
  2. Prognosis
A

1.Complications:

  • Pancreatic - pseudocyst (an accumulation of fluid without an epithelial lining), abscess
  • Systemic - shock, hypoglycemia, hypocalcemia
  1. Prognosis:
    * Overall mortablity up to 50% for haemorrhagic pancreatitis
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10
Q

What does this image show?

A

Fatty deposition in the pancreas in acute pancreatitis

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11
Q

What is chronic pancreatitis?

A

Relapsing or persistent inflammation of the pancreas, associated with acute pancreatitis

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12
Q

Why are many cases of chronic pancreatitis linked to acute pancreatitis?

A

Mild acute pancreatitis can heal itself and regenerate. Very bad acute pancreatitis can lead to chronic pancreatitis and long term damage leading to persistent/chronic pancreatitis

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13
Q

What are the causes of chronic pancreatitis?

A

Metabolic/toxic:

  • Alcohol (80%)
  • Haemachromatosis - Fe desposited in the pancreas, affecting both exocrine and endocrine components

Duct obstruction:

  • Gallstones
  • Abnormal pancreatic duct anatomy
  • Cystic fibrosis “mucoviscoidosis”

Tumours

Idiopathic - autoimmune

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14
Q
  1. What is the pathogenesis of chronic pancreatitis?
  2. What is the pattern of injury for chronic?
A
  1. Same as acute pancreatitis - obstruction or metabolic components can lead to release of enzymes causing necrosis and inflammation of the pancreas
  2. chronic inflammation, as in 1, with parenchymal fibrosis and loss of parenchyma. Duct strictures withe calcified stones occur, causing secondary dilatations
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15
Q

What are the complications of chronic pancreatitis?

A
  • Malabsorption
  • Diabetes mellitus
  • Pseudocysts (which can lead to abscess formation so need to be removed)
  • Carcinoma of the pancreas
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16
Q

What does this image show?

A

Pancreatic calcifications - diagnostic of chronic pancreatitis

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17
Q

What does this image show?

A

Chronic pancreatitis: only islets left behind, everything else has been destroyed. Fibrosis and loss of parenchymal tissue

18
Q

What is a pancreatic pseudocyst?

A
  • Associated with acute and/or chronic pancreatitis
  • Lined by fibrous tissue (no epithelial lining), contain fluid rich in pancreatic enzymes or necrotic material
  • Connect with pancreatic ducts
  • May resolve, compress adjacent strctures, become infected or perforate
19
Q

What is IgG4 related disease?

A

`Autoimmune pancreatitis

Characterised by a large numbers of IgG4 positive plasma cells

May involve the pancreas, bile ducts and almost any other part of the body

Responds very well to steroid therapy

20
Q

What tumours can develop in the pancreas and what cellss are affected?

A

Carcinomas:

  • Ductal (85% of all neoplasms) - most cancers are ductal
  • Acinar

Acinar ductal metaplasia - is an important pathway for pancreatic cancer - derived from acinar but become ductal tissue

Cystic neoplasms:

  • Serous cystadenoma
  • Mucinous cystic neoplasm

Pancreatic neuroendocrine tumours - Islet cell tumours

21
Q

What is the epidemiology of Ductal carcinoma of the pancreas?

A
  • 5% of cancer deaths
  • Increasingly common with age, 2:1 male:female
  • 5 year survival: 5%
22
Q

What are the risk factors for Pancreatic carcinoma?

A
  • Smoking
  • BMI and dietary factors
  • Chronic pancreatitis
  • Diabetes
23
Q

Describe the pathogenesis of Ductal carcinoma

A

Ductal carcinomas arise from dysplastic ductal lesions:

  • Pancreatic Intraductal Neoplasia (PanIN)
  • K-ras mutations in 95% of cases
24
Q

Describe the pathology of Ductal carcinomas

  1. Macroscopic appearance
  2. Microscopic appearance
A

Macroscopic appearance:

  • Gritty and grey
  • Invades adjacent structures
  • Tumours in the head present earlier

Microscopic appearance

Adenocarcinomas:

  • Mucin secreting glands set in desmoplastic stroma
25
Q

What does this image show? What in this is characteristic of this condition?

A
  • Adenocarcinoma of the pancreas
  • Nerve wrapping itself around the tumour, which is peri-neural invasion - very characteristic of pancreatic cancer
26
Q

What are the main sites for ductal carcinomas?

A
  • Head (60%)
  • Body
  • Tail
  • Diffuse

Follows the anatomy

This is the reverse for neuroendocrine tumours

27
Q

Describe the spread/where the spread of ductal carcinoma is for the following:

  1. Direct
  2. Lymphatic
  3. Blood
  4. Serosa
A
  1. Direct –> Bile ducts. duodenum (movement of pancreatic secretions)
  2. Lymphatic –> lymph nodes
  3. Blood –> liver (portal system)
  4. Serosa –> Peritoneum
28
Q

What are the complications of Ductal carcioma?

A
  • Commonly complications are due to spread - e.g. liver and Jaundice
  • Chronic pancreatitis
  • Venous thrombosis (migratory thrombophlebitis) - pancreatic cancer cancer diagnosed late, lots of cancer cells causes mets are in the blood. These produce mucin/mucous which trigger the coagulation cascade in the blood causing clotting
29
Q

What are cystic tumours?

A

Tumors that contain serous or mucin secreting epithelium

Usually benign

30
Q

Describe Pancreatic endocrine neoplasms

A
  • Usually non-secretory
  • Contain neuroendocrine markers e.g. chromogranin - which is a blood screening test for NETs
  • Behaviour is difficult to predict
  • May be associated with MEN1
31
Q

What is an insulinoma?

What is there a high risk of?

A
  • Insulinomas - tumors deriving from the beta cells of the pancreas - which secrete insulin causing increased secretion of insulin
  • commonest type of secretory tumor
  • High risk of hypoglycemia
32
Q

Where are NETs most commonly found in the pancreas?

A

The tail of the pancreas (opposite to carcinomas of the pancreas)

33
Q

What does this image show?

What are they commonly seen in?

A

Rosette cells

Common pathological presentation of NETs

34
Q

What are the main problems that can occur in the gall bladder (3)?

A
  • Gall stones
  • Inflammation
  • Cancer
35
Q

What percentage of adults in the West have cholelithaiasis?

A

20% of adults in the West have gallstones

36
Q

What are the risk factors for gall stones?

A
  • Age and gender- increasing age, F>M
  • Ethnic and geographic e.g. Native Americans
  • Hereditary e.g. disorders of bile metabolism
  • Drugs e.g. Oral contraceptive pill
  • Acquired disorders e.g. rapid weight loss
37
Q

What are the different types of gall stones?

Which ones are radiolucent, and which ones are radioopaque?

A
  • Cholesterol - more than 50% of all gall stones. These may be single, mostly radiolucent
  • Pigment - containing calcium salts of unconjugated bilirubin. There are often multiple, and most of them are radioopaque
38
Q

What are the complications of Gall stones?

A
  • Bile duct obstruction
  • Acute and chronic cholecystitis
  • Gall bladder cancer
  • Pancreatitis

However, many with gallstones are asymptomatic

39
Q

What is acute cholecystitis?

Most common cause?

A

Acute cholecystitis is acute inflammation of the gall bladder

90% associated with gall stones

40
Q

What is chronic cholecystitis?

What happens/forms?

A
  • Chronic inflammation of the gall bladder
  • Development of fibrosis and diverticula - called Rokitansky-Aschoff sinuses. These diverticula develop due to obstruction and overworking - same as diverticula develop in the colon
  • 90% contain gall stones
41
Q

What cancer occurs in the gall bladder?

What are 90% of gall bladder cancer associated with?

A

Adenocarcinomas

90% associated with gall stones

42
Q

What is cholangiocarcinoma?

Where is it common?

A

Cholangiocarcinoma is cancer of the bile ducts, and can develop from advanced gallbladder cancer

Not so common in the UK, but commonest in South America