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Pathology (Guide) > Histopathology - Pancreatic Disease > Flashcards

Histopathology - Pancreatic Disease Flashcards

1
Q

What is the role of the pancreas?

A
  • Produces 2L a day of enzymic HCO3- rich fluid, stimulated by secretin + CCK
  • Exocrine pancreas composed of ducts and acinar cells
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2
Q

Where is secretin produced and what does it do?

A
  • Produced by s-cells of duodenum
  • Controls gastric acid secretion + buffering with HCO3-
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3
Q

Where is CCK produced and what does it do?

A
  • Made by I-cells in duodenum
  • Responsible for stimulating digestion of fat + protein
  • Causes release of digestive enzymes
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4
Q

What is the function of the exocrine pancreas and its secretions?

A

Function:
- Digestive
- Proteases, lipases + amylase

Secretions:
- Secretes products into ducts (digestive enzymes)

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5
Q

What is the function of the endocrine pancreas and its secretions?

A

Function:
- Endocrine

Secretions:
- Secrets products into bloodstream (e.g. hormones)

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6
Q

What are the Islets of Langerhans within the endocrine pancreas and what are their features?

A

Α cells:
- Glucagon increases blood glucose

Β cells:
- Insulin decreases blood glucose

Delta cells:
- Somatostatin regulates Α + Β cells

D1:
- Vasoactive peptide
- Stimulates secretion of H20 into pancreatic system

PP:
- Pancreatic polypeptide
- Self regulates secretion activities

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7
Q

What is a metabolic syndrome and its features?

A

Collection of conditions that increase risk of IHD

  • Fasting hyperglycaemia >6mmol/L
  • BP >140/90
  • Central obesity
  • Dyslipidaemia (decreased HDL cholesterol + increased TGs)
  • Microalbuminaemia
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8
Q

How is diabetes mellitus diagnosed?

A
  • Fasting glucose >7mmol/L
    OR
  • Random plasma glucose >11.1mmol/L
    OR
    HBA1c >48mmol/L
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9
Q

What is the pathogenesis of T1DM and some features?

A
  • Autoimmune destruction of β cells by CD4+ + CD8+ T lymphocytes
  • May present with DKA
  • Insulin dependent
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10
Q

What is T2DM strongly related to?

A
  • Obesity
  • Insulin resistance
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11
Q

What are some macrovascular complications of diabetes?

A
  • Cardiac (IHD)
  • PVD (Claudication, change in colour/temp, poor healing ulcers)
  • Cerebral (CVA)
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12
Q

What are some microvascular complications of diabetes?

A
  • Glomerulonephritis (renal)
  • Ulcers (peripheral neuropathy)
  • Diabetic retinopathy (ocular)
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13
Q

How is acute pancreatitis scored?

A

GLASGOW Scale
- >=3 = severe pancreatitis

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14
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED
- I: Idiopathic
- G: Gallstones
- E: Ethanol
- T: Trauma
- S: Steroids
- M: Mumps
- A: Autoimmune
- S: Scorpion venom
- H: Hyperlipidaemia
- E: ERCP
- D: Drugs (e.g. thiazides)

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15
Q

What are the most common causes of acute pancreatitis?

A
  • Gallstones
  • Ethanol
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16
Q

How does acute pancreatitis present?

A
  • Severe epigastric (central) pain radiating to back
  • Pain relieved by sitting forward
  • Vomiting prominent
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17
Q

What is seen on blood tests for acute pancreatitis?

A
  • Amylase transiently increase
  • Serum lipase big increase (more sensitive)
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18
Q

What are some complications of acute pancreatitis?

A
  • Formation of pseudocyst (pathological collection of fluid)
  • Shock
  • Hypoglycaemia
  • Hypocalcaemia
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19
Q

What is seen on histology for acute pancreatitis?

A

Coagulative necrosis

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20
Q

What is the pattern of damage in acute pancreatitis?

A

Periductal damage: is necrosis of acinar cells near ducts, leading to obstructive causes

Perilobular damage: is necrosis at the edge of th elobules leading to ischaemic causes

Panlobular damage: is a combination of periductal and perilobular damage

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21
Q

What are some causes of chronic pancreatitis and which is most common?

A
  • Alcoholism (most common)
  • Cystic fibrosis
  • Hereditary
  • Pancreatic duct obstruction (e.g. stones/tumour)
  • Autoimmune (IgG4 produced by plasma cells)
22
Q

How does chronic pancreatitis present?

A
  • Epigastric pain radiating to back
  • Malabsorption (weight loss + steatorrhoea)
  • Secondary DM (malabsorption due to lack of enzymes to digest food)
23
Q

What is seen on histology of chronic pancreatitis?

A
  • Fibrosis
  • Loss of exocrine tissue parenchyma
  • Duct dilatation with thick secretions
  • Calcification
  • Similar to pancreatic cancer
24
Q

What are some complications of chronic pancreatitis?

A
  • Pseudocysts
  • Diabetes
  • Pancreatic cancer
25
Q

What are some features of acinar cell carcinoma?

A
  • Rare
  • Older adults
  • Enzyme production by neoplastic cells
26
Q

How does acinar cell carcinoma present?

A
  • Non-specific Sx
  • Abdo pain
  • Weight loss
  • Nausea
  • Diarrhoea
  • ?multifocal fat necrosis + polyarthralgia due to lipase secretion
27
Q

What is the histopathology of acinar cell carcinoma?

A
  • Neoplastic epithelial cells with eosinophilic granular cytoplasm
  • +ve immunoreactivity for lipase, trypsin + chymotrypsin
28
Q

What is the prognosis of acinar cell carcinoma?

A
  • Median survival = 18mths from diagnosis
  • 5-yr survival <10%
29
Q

What are some RFs for developing gallstones?

A
  • Increasing age
  • F>M
  • OCP
  • Disorders of bile metabolism
30
Q

What are common forms of gallstones?

A
  • Cholesterol (radiolucent)
  • Calcium salts - rarer (radio-opaque)
31
Q

What is cholelithiasis?

A

Presence of gallstones in gallbladder (20% adults in West)

32
Q

What is acute cholecystitis?

A
  • Acute inflammation
  • 90% associated with gallstones
33
Q

What is chronic cholecystitis?

A

Chronic inflammatino leading to fibrosis (90% a/w gallstones)

34
Q

What is cholangiocarcinoma?

A

An adenocarcinoma, 90% a/w gallstones

35
Q

What is pancreatic carcinoma?

A

A ductal adenocarcinoma of the pancreas

36
Q

What is the epidemiology of pancreatic carcinoma?

A
  • 85% of all pancreatic malignancies
  • Average age 60yrs
  • M>F
37
Q

Where is pancreatic carcinoma commonly found?

A
  • Normally head of pancreas
38
Q

What are some RFs for pancreatic carcinoma?

A
  • Smoking
  • Diet
  • Genetic (FAP, HNPCC)
39
Q

What are some clinical features of pancreatic carcinoma?

A
  • Weight loss + anorexia
  • Upper abdo pain + back pain (chronic, persistent, severe)
  • Jaundice (painless), pruritis, steatorrhoea
  • DM
  • Trousseau’s sign
  • Ascites
  • Abdominal masses
  • Virchow’s node
  • Courvoisier’s sign
40
Q

What are some investigation findings for pancreatic carcinoma?

A

Bloods:
- Decreased Hb
- Increased bilirubin
- Increased Ca

CT/MR/ERCP

CA19.9 >70IU/mL

41
Q

What is the management for pancreatic carcinoma?

A
  • Palliative chemotherapy (5-FU)
  • Surgery = Whipple’s procedure (surgical resection)
42
Q

What is the prognosis for pancreatic carcinoma?

A

Very poor
- 5yr survival rate <5%

43
Q

Where are neuroendocrine (islet cell) tumours found?

A

Normally body or tail of pancreas

44
Q

What are some features of neuroendocrine (islet cell) tumours?

A
  • Circumscribed 1-5cm
  • Cells arranged in nests or trabeculae with granular cytoplasm
  • May be MEN 1 pts
  • May be multiple lesions
  • Unpredictable behaviour
45
Q

What are the functional neuroendocrine tumours and how do they present?

A

Present: Sx related to hormone excess

  • Insulinoma: hypoglycaemic attacks
  • Gastrinoma: Zollinger-Ellison syndrome (recurrent ulceration)
  • Glucagonoma: Necrolytic migrating erythema
  • VIPoma: diarrhoea
46
Q

When are non-functional neuroendocrine tumours found?

A

Incidentally on imaging
OR
Grow large enough to produce Sx of local disease or metastasis

47
Q

What are some investigations for neuroendocrine tumours?

A
  • CT/MRI
  • Chromogranin = acts as marker
48
Q

What is the management for neuroendocrine tumours?

A
  • Surgery
49
Q

What is Multiple Endrocrine Neoplasia?

A

A group of genetic syndromes where there are functioning hormone-producing tumours in multiple organs

50
Q

What are some pancreatic malformations?

A
  • Ectopic pancreas
  • Pancreas divisum (failure of fusion of dorsal + ventral buds = increased risk of pancreatitis)
  • Annular pancreas (presents with duodenal obstruction)

Pathology (Guide) (84 decks)

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