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Histopathology > Pancreas and Gall Bladder > Flashcards

Pancreas and Gall Bladder Flashcards

1
Q

Describe Pancreatic Microanatomy

A
  • Centroacinar cells - at the end of the ducts
  • Pancreatic acinar cells → make all the enzymes
  • Islets of Langerhans - alpha and beta cells
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2
Q

Left

A

Left: Exocrine component

  • Duct
  • Acinar cells

Right: Endocrine component

  • Islets of Langerhans
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3
Q

Define acute pancreatitis.

A

Acute inflammation of the pancreas caused by aberrant release of pancreatic enzymes

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4
Q

How common is acute pancreatitis?

A

Relatively common, incidence increasing.

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5
Q

What are the causes of acute pancreatitis?

A
  • Duct obstruction
  • Metabolic/toxic
  • Poor blood supply
  • Infection/Inflammation
  • Autoimmune
  • Idiopathic (15%)
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6
Q

What causes duct obstruction in acute pancreatitis?

A
  • Gall stones (50%)
  • Trauma
  • Tumours
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7
Q

What are the metabolic/toxic causes of acute pancreatitis?

A
  • Alcohol (33%) - 5% of alcoholic develop acute pancreatitis
  • Drugs (e.g. thiazides)
  • Hypercalcaemia)
  • Hyperlipideamia
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8
Q

What are the causes of poor blood supply of acute pancreatitis?

A

Shock and Hypothermia

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9
Q

What are the infectious/inflammatory causes of acute pancreatitis?

A

Viruses (e.g. mumps)

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10
Q

Describe the pathogenesis of acute pancreatitis in response to duct obstruction and alcohol.

A
  • Gallstone stuck distal to where the common bile duct and pancreatic ducts join leads to: reflux of 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 a protein rich pancreatic fluid which obstructs the pancreatic ducts
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11
Q

What are the different pattern of injury in acute pancreatitis?

A
  • Periductal
  • Perilobular
  • Panlobular
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12
Q

Describe periductal injury.

A

necrosis of acinar cells near ducts (usually secondary to obstruction)

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13
Q

Describe perilobular injury.

A

Perilobular – necrosis at the edges of the lobules (usually due to poor blood supply)

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14
Q

Describe panlobulr injury.

A

Panlobular – develops from 1. and 2.

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15
Q

How do lipase act in acute pancreatitis?

A

Lipasesè fat necrosis (calcium ions bind to free fatty acids forming soaps which are seen as yellow- white foci)

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16
Q

What is the pathway of inflammation of acute hepatitis?

A
  • Activated enzymes  acinar necrosis  enzyme release
  • Ranges from stromal oedema to haemorrhagic necrosis
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17
Q

What are the complications of acute pancreatitis?

A
  • Pancreatic: pseudocyst formation (collection of fluid without epithelial lining), abscess
    • Pseudocysts can become infected leading to abscess formation
    • Systemic: shock, hypoglycaemia, hypocalcaemia
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18
Q

What is the prognosis of acute pancreatitis?

A
  • Dependent on severity
  • Mortality of 50% for haemorrhagic pancreatitis
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19
Q
A

Lots of fat

Calcified deposits

ACUTE PANCREATITIS

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20
Q

What is chronic pancreatitis associated with? How common are they? What is the mortality?

A
  • Relapsing or persistent - Associated with acute pancreatitis in about half of cases
  • Relatively uncommon
  • Mortality of 3% per year
  • With mild acute pancreatitis, the pancreas can return to normal. However, with severe acute pancreatitis, you are likely to get some degree of scarring which increases your risk of developing chronic pancreatitis
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21
Q

What are the causes of chronic pancreatitis?

A
  • Metabolic/toxic
  • Duct Obstruction
  • Tumours
  • Idiopathic - AI
    *
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22
Q

What are the metabolic/toxic causes of chronic pancreatitis?

A

Alcohol (80%)
Haemochromatosis

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23
Q

What causes duct obstruction in chronic pancreatitis?

A

Gallstones
Abnormal pancreatic duct anatomy

Cystic fibrosis (“mucoviscoidosis”)

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24
Q

What is the pathogenesis of chronic pancreatitis?

A

same as acute pancreatitis

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25
Q

What is the pattern of injury in chronic pancreatitis?

A
  • Chronic inflammation with parenchymal fibrosis and loss of parenchyma (ascini become atrophic)
  • Duct strictures with calcified stones with secondary dilatations
    • Pancreatic calcifications are diagnostic of chronic pancreatitis
26
Q

What are the complications of chronic pancreatitis?

A
  • EARLY: Malabsorption (occurs much earlier as lipases, etc. are not produced)
  • LATE: Diabetes mellitus (late stage as endocrine parts survive much longer than exocrine components)
  • Pseudocysts
  • Carcinoma of the pancreas (?) – unsure of cancer  pancreatitis or pancreatitis  cancer
27
Q
A

Calcified mass - pancreatitis

28
Q
A

Dilated ducts

Fibrous tissue

29
Q
A

No longer acing cells

30
Q

What are pancreatic pseudocysts? Describe the histology and the outcomes?

A
  • Associated with acute and chronic pancreatitis
  • Histology:
    • Lined by fibrous tissue (no epithelial lining)
    • Contains fluid (rich in pancreatic enzymes or necrotic material)
    • Connects with pancreatic ducts
  • Outcomes:
    • Resolve
    • Perforate
    • Compress adjacent structures
    • Infected
31
Q
A

Pancreatic pseudocyst - no epithelial lining

32
Q

What is IgG4-Related Disease? What is it characterised by?

A
  • Characterised by large numbers of IgG4 positive plasma cells
    • NOTE: as part of a polyclonal response you would expect to have mixed levels of the different IgGs
    • May involve the pancreas, bile ducts and almost any other part of the body
  • IgG4 related disease is a relatively new phenomenon and is thought to have explained most cases of what has been previously, wrongly, described as ‘autoimmune pancreatitis’
33
Q
A
  • Histology:
    • Duct is surrounded by loads of IgG4 expressing plasma cells
    • These patients respond very well to steroids
34
Q

What are the tumours of the pancreas?

A

Carcinomas

Cystic neoplasms

Pancreatic neuroendocrine tumours (islet cell tumours)

35
Q

Where do the carcinomas arise from?

A
  • Ductal* (85% of all neoplasms)
  • Acinar
36
Q

Where do the cystic neoplasms arise from?

A
  • Serous cystadenoma
  • Mucinous cystic neoplasm
37
Q

Describe the epidemiology of ductal carcinomas.

A
  • 5% of cancer deaths
  • Increasingly common with age, 2M: 1F

•5 year survival: 5%

38
Q

What are the RFs for pancreatic carcinomas?

A
  • Smoking
  • BMI and dietary factors
  • Chronic pancreatitis
  • Diabetes
39
Q

Where do ductal carcinomas arise from? What mutations are found?

A
  • Ductal carcinoma arises from two types of dysplastic (i.e. pre-cancerous) ductal lesions:
    • Pancreatic Intraductal Neoplasia (PanIN)
    • Intraductal Mucinous Papillary neoplasm
    • These do NOT invade through the BM
  • K-Ras mutations are present in 95% of cases
40
Q
A

Raised nucleus-cytoplasmic ratio

PanIN

41
Q

How do ductal carcinomas look macro/microscopically?

A
  • Macroscopic Appearance:
    • Gritty and grey
    • Invades adjacent structures
    • Tumours in the head present earlier
  • Microscopic Appearance:
    • Adenocarcinomas:
      • Secrete mucin (stain for mucin)
      • Form glands
      • Set in desmoplastic stroma (i.e. tumour induces fibrous tissue growth around it- to the tumour)
42
Q
A

Ductal carcinoma

43
Q
A

Adenocarcinoma

Perineural invasion

44
Q

What are the sites of ductal carcinomas?

A
  • Sites of ductal carcinoma (neuroendocrine tumours are most common tail > body > head – i.e. the reverse)
    • Head (60%)
    • Body
    • Tail
    • Diffuse
45
Q

How to ductal carcinomas spread?

A
  • DIRECT: bile ducts, duodenum
  • LYMPHATIC: lymph nodes
  • BLOOD: liver
  • SEROSA: peritoneum
46
Q

What are the complications of ductal carcinomas?

A
  • Due to spread
  • Chronic pancreatitis
  • Venous thrombosis (migratory thrombophlebitis) – CHARACTERISTIC
    • Circulating pancreatic cancer cells releasing mucous which activates the clotting cascade
47
Q

What do cystic tumours contain? How malignant are they?

A
  • Cystic tumours (serous cystadenoma; mucinous cystic neoplasm)
    • Contain serous or mucin secreting epithelium (like ovarian tumours)
    • Usually benign
48
Q
A

Cystic tuour

Mucinous

Benign

Well demarcated

49
Q

What are pancreatic endocrine neoplasms? What are the types What are they associated with?

A
  • General facts:
    • Usually non-secretory
    • Stained by neuroendocrine markers (chromogranin stain)
    • Behaviour is difficult to predict
    • Associated with MEN1
    • Types:
      • Insulinomas (most common type of functional tumour)
        • Derived from beta cells
        • Whipple’s triad (glucose <50mg/dL, S/S hypo, relief on glucose administration)
50
Q
A

Pancreatic Endocrine neoplasms

51
Q

How common are gallstones? What are the RFs?

A
  • 20% of adults in the West have gallstones
  • Risk factors:
    • Female, 40yo
    • Ethnicity (e.g. Native Americans)
    • Hereditary factors (e.g. disorders of bile metabolism)
    • Drugs (e.g. oral contraceptive)
    • Acquired disorders (e.g. rapid weight loss)

Female, Fair, Fat, Fertile, Forty

52
Q

What are the types of gallstones?

A
  • Cholesterol (>50% cholesterol)
    • May be single
    • Mostly radiolucent (you will NOT see them on a plain abdominal X-ray  hence, USS
  • Pigment (contain calcium salts of unconjugated bilirubin)
    • Often multiple
    • Mostly radio-opaque (because they contain calcium)
53
Q

What are the complications fo gallstones?

A
  • MOST PEOPLE do not have any problems
  • Bile duct obstruction
  • Acute and chronic cholecystitis
  • Gallbladder cancer
  • Pancreatitis
54
Q

What is the histology of acute and chronic cholecystitis?

A
  • Acute cholecystitis:
    • Acute inflammation (neutrophils, oedema)
    • 90% are associated with gallstones
  • Chronic cholecystitis
    • 90% contain gallstones
    • Fibrosis, small, neoangiogenesis
    • Diverticula (Rokitansky-Aschoff sinuses) – gallbladder contracting against obstruction → diverticula
55
Q
A

Cystic spaces - diverticula

Gall bladder wall -thick

56
Q
A

Diverticula (Rokitansky-Aschoff sinuses)

Fibrosis in wall

57
Q
A

Advanced gall bladder cancer

58
Q

What are the gall bladder cancers? What are they associated with?

A
  • Adenocarcinoma
  • 90% associated with gallstones
  • This is UNCOMMON
  • It is technically a type of cholangiocarcinoma
59
Q
A

Ductal adenocarcinoma

60
Q
A

option 4

61
Q
A

Haemolytic anaemia

Histopathology (14 decks)

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