Histopathology 9: Pancreas & Gall Bladder Flashcards
Which 2 mediators control enzyme and alkali release from the pancreas ?
Secretin - released by S cells in the duodenum causes pancreatic HCO3- secretion
Cholecystokinin (CCK) - released by I cells in the duodenum causes pancreatic release of digestive enzymes
Which cells release glucagon ?
Alpha cells
Which cells release somatostatin ?
Delta cells
What type of hypersensitivity reaction is T1DM ?
Type 4 delayed T cell mediated
List the causes of Acute pancreatitis ?
I GET SMASHED
Duct obstruction -> gallstones, trauma, tumours (MAIN SO REMEMBER)
Metabolic -> alcohol, drugs (thiazides), hypercalcaemia (COMES UP IN EXAMS), hyperlipidaemia
Poor blood supply -> Shock and hypothermia
Infection -> Mumps
AI
Idiopathic
Which blood test is most sensitive for Acute pancreatitis ?
Serum Lipase
List 4 causes of chronic pancreatitis ?
Cystic fibrosis
Alcoholism
Pancreatic duct obstruction - stones /cancer
Auto-immune
Describe the histology of chronic pancreatitis ?
- Dilated ducts
- Fibrosis
- calcification
- loss of exocrine tissue
A patient presents with significant weight loss, abdominal pain, multifocal fat necrosis and polyarthralgia. Histopathology: Eosinophilic granular cytoplasm, immune reactivity for lipase
Most likely diagnosis ?
Acinar cell carcinoma
neoplasm that releases lots of lipase
A patient presents with epigastric pain that radiates to the back, he’s jaundiced and appears cachectic. An abdominal mass is felt on examination.
Most likely diagnosis ?
Ductal adenocarcinoma of the pancreas
Where in the pancreas do Ductal adenocarcinomas tend to occur ?
Head of the pancreas
What is covosiers law ?
Presence of a palpable enlarged gallbladder, with painless jaundice means gallstones are unlikely.
What is the tumour marker for pancreatic cancer ?
CA19-9
Histopathology: Cells arranged in nests or trabecular with granular cytoplasm.
Most likely diagnosis ?
Characteristic feature?
Islet cell tumour- Insulinoma
Hypoglycaemic attacks.
Which syndrome is associated with gastrinomas
Zollinger ellison syndrome
What are Rokitansky-Aschoff sinuses ?
Cholecystitis causes fibrosis which means the gallbladder is contracting against an obstruction.
This pressure causes diverticula of the gallbladder to form which are known as Rokitansky-Aschoff sinuses.
What is the endocrine /exocrine aspect of the pancreas?
What do they produce?
Endocrine - Islet of Langerhands:
Insulin
Glucagon
Somatostatin
Exocrine - Acini + ducts:
Protease
Lipase
Amylase
Define acute pancreatitis
Acute inflammation of the pancreas caused by aberrant release of pancreatic enzymes
How do alcohol, gallstones and other causes of acute pancreatitis cause it?
Note this is also how chronic pancreatitis works
Alcohol: (Duct obstruction)
Spasm/oedema of the sphincter of Oddi + formation of protein-rich pancreatic fluid which is thick and causes an obstruction
Gallstones: (Duct obstruction)
Get stuck distal to where CBD and pancreatic duct join
→ bile reflux up pancreatic duct → damage to acini → release of proenzymes which then become activated
All other causes:
Via direct acinar injury
Describe the three main patterns of injury in acute pancreatitis and describe what they result from.
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 – results from worsening periductal or perilobular inflammation
Outline the pathway of inflammation in acute pancreatitis
Activated enzyme reflux 🡪 acinar necrosis 🡪 release of more enzymes
Release of lipases 🡪 fat necrosis 🡪 saponification w/ calcium (soaps formed when ca binds w/ free fatty acids)
Complications of acute pancreatitis v chronic pancreatitis? (4)
Acute:
- Pseudocyst formation, abscesses
- Shock
- Hypoglycaemia
- Hypocalcaemia (due to saponification)
Chronic:
- Malabsorption
- Diabetes mellitus
- Pseudocysts
- Pancreatic carcinoma
What are pseudocysts?
What happens to pseudocysts?
A collection of fluid in a dilated space without an epithelial lining (has fibrous lining)
They are rich in pancreatic enzymes and necrotic material
They are lined by fibrous tissue
NOTE: they may resolve, compress adjacent structures, become infected or perforate (if they perforate → necrotic material rich in activated enzymes leaks into peritoneal cavity = acute peritonitis)
What is the characteristic feature of autoimmune pancreatitis?
How is this treated?
Large numbers of IgG4 positive plasma cells typically found around the ducts
Steroids - usually responds well