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YEAR 5: Histopathology > Histo: Diseases of the Pancreas and Gallbladder > Flashcards

Histo: Diseases of the Pancreas and Gallbladder Flashcards

1
Q

What are the main components of the exocrine part of the pancreas?

A

Acini and ducts

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2
Q

What is the endocrine component of the pancreas called?

A

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

List some causes of acute pancreatitis.

A

Duct obstruction
- Gallstone (50%)
- Trauma
- Tumours

Metabolic/toxic
- Alcohol (33%)
- Drugs (e.g. thiazides)
- Hypercalcaemia
- Hyperlipidaemia

Ischaemia
- Shock
- Hypothermia

Infection/inflammation
- Mumps
- Autoimmune

Idiopathic (15%)

NOTE: gallstones + alcohol are KEY

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5
Q

What is the basic common pathogenesis of gallstone and alcohol-induced acute pancreatitis?

A

Duct obstruction

The rest of the etiologies cause acute pancreatitis via direct acinar injury

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6
Q

Describe how gallstones causes acute pancreatitis

A
  • Gallstones can obstruct the bile ducts distal to where the common bile ducts and pancreatic ducts join
  • This leads to the reflux bile up the pancreatic ducts which can damage the acini
  • Digestive proenzymes are released which then become activated
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7
Q

Describe how alcohol can cause acute pancreatitis.

A

It leads to spasm/oedema of the sphincter of Oddi and the increasing the viscosity of pancreatic secretions. Both of these cause duct obstruction.

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8
Q

Describe the three main patterns of injury in acute pancreatitis

A
  • Periductal - necrosis of acinar cells near ducts (usually secondary to obstruction)
  • Perilobular - necrosis at the edges of the lobules (usually due to poor blood supply)
  • Panlobular - develops as periductal or perilobular inflammation worsens
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9
Q

Outline the pathway of inflammation in acute pancreatitis.

A

Activated enzymes → acinar necrosis → release of more enzymes

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10
Q

What is saponification?

A
  • Lipases break down fats to release free fatty acids
  • Calcium binds to the free fatty acids forming soaps
    (yellow-white foci)
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11
Q

List some complications of acute pancreatitis.

A

Local:

  • Pseudocyst formation
  • Abscesses

Systemic:

  • Sepsis
  • ARDS
  • DIC
  • Shock
  • Hypoglycaemia
  • Hypocalcaemia
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12
Q

Define pseudocyst.

A
  • A collection of fluid lined by fibrous tissue (no epithelial lining)
  • They are rich in pancreatic enzymes and necrotic material

They may resolve, compress adjacent structures, become infected, or perforate

More commonly associated with chronic pancreatitis but can occur with acute

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13
Q

List some causes of chronic pancreatitis.

A

Metabolic/Toxic:
- Alcohol (80%)
- Haemochromatosis

Duct obstruction:
- Gallstones
- Abnormal anatomy
- Cystic fibrosis

Autoimmune

Tumours

Idiopathic

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14
Q

Outline the pattern of injury in chronic pancreatitis.

A
  • Chronic inflammation with parenchymal fibrosis and loss of parenchyma
  • There will be duct strictures with calcified stones with secondary dilatations
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15
Q

Describe the difference between WBCs seen in acute vs chronic pancreatitis

A
  • Acute - neutrophils
  • Chronic - lymphocytes
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16
Q

List some complications of chronic pancreatitis.

A
  • Malabsorption
  • Diabetes mellitus
  • Pseudocysts
  • Pancreatic carcinoma
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17
Q

What radiographic feature is diagnostic of chronic pancreatits?

A

Visible pancreatic calcifications on AXR

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18
Q

What is the cytological feature is characteristic of autoimmune pancreatitis?

A

Large numbers of IgG4 positive plasma cells typically found around the ducts

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19
Q

How is autoimmune pancreatitis treated?

A

Steroids - usually responds well

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20
Q

Name 3 categories of pancreatic neoplasms

A
  • Carcinomas
  • Cystic neoplasm (cystadenomas)
  • Neuroendocrine tumours (islet cell tumours)
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21
Q

What are the two types of pancreatic carcinomas and which is more common?

A
  • Ductal (85% of all pancreatic neoplasms)
  • Acinar

Many ductal carcinomas may actually arise from acini after a process called acini-ductal metaplasia (these ductal carcinomas have a different natural history to truly ductal carcinomas)

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22
Q

Name two types of cystic neoplasm of the pancreas.

A
  • Serous cystadenoma - contains serous secreting epithelium
  • Mucinous cystadenoma - contains mucous secreting epithelium

Usually benign

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23
Q

List some risk factors for pancreatic cancer.

A
  • Smoking
  • BMI and dietary factors
  • Chronic pancreatitis
  • Diabetes mellitus
24
Q

Name two types of dysplastic precursor lesion that ductal carcinoma can arise from.

A
  • Pancreatic intraductal neoplasia (PanIN)
  • Intraductal mucinous papillary neoplasm
25
Q

Which mutation is very common in ductal cancer?

A

K-ras (95% of cases)

26
Q

Describe the macroscopic appearance of ductal carcinoma?

A
  • Gritty and grey
  • Invades adjacent structures
27
Q

How does tumour location affect latency period in ductal carcinoma?

A

Tumours affecting the head of the pancreas present earlier (with biliary obstruction)

28
Q

Describe the microscopic appearance of ductal carcinoma.

A
  • Adenocarcinomas (secrete mucin and form glands)
  • Mucin-secreting glands are set in desmoplastic stroma
29
Q

What is the most common site of ductal carcinoma?

A

Head (60%) > Body > Tail>diffuse

NOTE: opposite for neuroendocrine tumours (more common in the tail)

30
Q

What are the usual sites of metastasis of ductal carcinoma?

A
  • Direct: bile ducts, duodenum
  • Lymphatic: lymph nodes
  • Blood: liver (most common site of metatasis)
  • Serosa: peritoneum

Perineural spread is common

31
Q

List some complications of ductal carcinoma.

A
  • Metastasis
  • Chronic pancreatitis
  • Venous thrombosis (migratory thrombophlebitis) - Trosseau sign of malignancy
32
Q

By what mechanism does pancreatic cancer cause migratory thrombophlebitis?

A
  • Circulating pancreatic cancer cells release mucous which activates the clotting cascade
33
Q

List some key features of pancreatic neuroendocrine neoplasms.

A
  • Usually non-secretory
  • Contains neuroendocrine markers (e.g. chromogranin) - can be measured as a screening test for neuroendocrine tumours
  • May be associated with MEN1
34
Q

What is the most common type of functional (secretory) neuroendocrine tumour?

A

Insulinoma (derived from beta cells)

35
Q

List some factors that increase the likelihood of developing gallstones.

A
  • Obesity
  • Age
  • Gender (females)
  • Ethnic factors
  • Hereditary
  • Drugs (e.g. oral contraceptive)
  • Rapid weight loss
36
Q

What are the two types of gallstone and what are their distinguishing features?

A

Cholesterol (>50% cholesterol)
* May be single
* Mostly radiolucent (NOT seen on AXR)

Pigment
* Often small with multiple stones
* Contain calcium salts of unconjugated bilirubin
* Mostly radio-opaque

37
Q

List some complications of gallstones.

A
  • Bile duct obstruction
  • Acute and chronic cholecystitis
  • Gallbladder cancer
  • Pancreatitis

Most are asymptomatic

38
Q

What is the main cause of acute and chronic cholecystitis

A

Gallstone (associated in 90% of cases)

39
Q

What is the term used to describe diverticula of the gallbladder? How do they form?

A

Rokitansky-Aschoff sinuses - form as a result of the gallbladder contracting against an obstruction

40
Q

Which type of cancer is gallbladder cancer?

A

Adenocarcinoma

NOTE: it is technically a type of cholangiocarcinoma

90% associated with gallstones

41
Q

What cells make up the endocrine part of the pancreas?

A

Alpha cells - release glucagon (increase blood glucose)

Beta cells - release insulin (decrease blood glucose)

Delta cells - releases somatostatin which controls alpha and beta cells

42
Q

What are the components to metabolic syndrome?

A

BP > 140/90
Dyslipidaemia (HDL < 1 in men, 1.3 in women)
Central obesity (>94/80cm in M/F)
Microalbuminaemia
Fasting BG > 6mmol

43
Q

What causes the destruction of beta cells in T1DM?

A

Autoimmune destruction of beta cells by CD4 and CD8 cytotoxic cells

44
Q

What scoring system is used for acute pancreatitis?

A

Glasgow score

> 3 = severe

45
Q

What markers are used in the Ix of acute pancreatitis?

A

Amylase - only transiently elevated
Lipase - more sensitive

46
Q

What would be seen on histology of acute pancreatitis?

A

Coagulative necrosis

47
Q

Who is acinar cell carcinoma more commonly seen in?

A

Older adults - but it is rare

48
Q

What Ca-19 level would be suspicious of pancreatic malignancy?

A

> 70

49
Q

What is the management of pancreatic adenocarcinoma?

A

Usually palliative chemotherapy as most cases present late once metastasis has occured.

Small proportion of patients may be offered surgical resection (Whipple’s procedure) but it is a highly morbid procedure.

50
Q

What is Zollinger-Ellison syndrome?

A

Causes gastronomes in the pancreas or duodenum, resulting in excess gastric acid production and recurrent ulceration.

51
Q

What would a glucagonoma cause?

A

Necrolytic migrating erythema

52
Q

What marker can be used to detect neuroendocrine pancreatic tumours?

A

Chromogranin

53
Q

Which tumours are seen in MEN1?

A

Parathyroid adenoma (or hyperplasia)
Pituitary adenoma
Pancreatic endocrine tumour

54
Q

Which tumours are seen in MEN2a?

A

Parathyroid adenoma
Thyroid adenoma
Phaechromocytoma

55
Q

Which tumours are seen in MEN2b?

A

Medullary thyroid adenoma
Phaechromocytoma
Acoustic neuroma

(Marfanoid phenotype)

YEAR 5: Histopathology (20 decks)

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