24 - Pancreatic and gall bladder pathology Flashcards
What do I need to know
- acute and chronic pancreatitis
- pancreatic adenocarcinoma
- cholelithiasis
- acute and chronic cholecystitis
- GB adenocarcinoma (rare)
What are the symptoms of pancreas injury like and why?
They are non-specific and tend to present late in disease progression as it is a hidden organ
What cells make up the exocrine pancreas?
Acinar cells and ductal cells
Acinar cells contain …
Zymogen granules that contain inactive enzyme precursors for trypsin, chymotrypsin, elastase, nuclease, amylase, lipase (proenzymes)
What does damage to cells cause?
Damage to acinar cells causes release of pancreatic digestive enzymes
What activates the pancreatic enzymes?
Trypsin (activated form trypsinogen by enterkinases)
Why is inflammation of the pancreas usually increased compared to other organs?
Initial injury can cause damage to acinar cells causing release and premature activation of pancreatic enzymes that further damage the pancreas
How much of the pancreas function does the endocrine component make up and what does it consist of?
- Islets of Langerhan
- secretes insulin and glucagon
- pathology is diabetes
- only 10-20% of liver
Main pathologies of the pancreas
- pancreatitis
- cystic fibrosis
- carcinoma
Are most cases of acute pancreatitis fatal?
60-70% are mild and most recover
30-40% are severe and 20-30% mortality rate
What are the 4 main mechanisms of pancreatitis?
- Metabolic
- Mechanical
- Vascular
- Infection
Metabolic mechanism of pancreatitis?
Alcohol
Mechanical pancreatitis?
Gallstone (cholelitiasis) and trauma
Obstruct and damage the pancreatic duct
Vascular pancreatitis?
Shock - low BP and organ perfusion, sepsis, trauma
Vasculitis
Infection pancreatitis?
Especially viral i.e. mumps
Most common causes of pancreatitis?
Alcohol and gallstones
What is the pathology of pancreatitis?
- initial injury stimulus and body’s inflammatory response/cytokines damage pancreatic glands and acinar cells
- release of pancreatic enzymes
- autodigestion of pancreatic tissue
- further increases inflammatory response, cytokine release and ongoing tissue damage
Consequence of pancreatic enzymes release?
Proteases - proteolytic destruction of acini, ducts, islets
Lipases - fat necrosis and pancreas and other sites
Elastases - damage BVs leading to interstitial bleeding and bleeding into glands
Cell Injury response - inflammation, oedema, ischaemia
What are the 2 main initial injury events that occur in the pancreas?
- Obstruction of the pancreatic duct
2. Direct injury to acinar cells
- Obstruction of the pancreatic duct
- i.e. gall stones and ductal concretions
- block enzyme (and HCO3-) release
- pressure increase in pancreas and ducts
- increase pressure
- interstitial oedema and local inflammation
- oedema compromises local blood flow leading to ischemia
- fat necrosis as lipase active
- damage to acinar cells and enz release
- Direct injury to acinar cells
- alcohol, drugs, trauma, viruses, ischemia
- inflammatory response
- enzyme release
Clinical features of pancreatitis?
Non-specific
- Acute epigastric pain (LUQ)
- Nausea and vomitting (close to stomach)
- Fever and tachycardia - cytokine response
- Abdominal tenderness
How is pancreatitis diagnosed?
- high WBC (generic to all inflammation)
- MAIN: high serum amylase/lipase due to enzyme release into peripheral blood
- CT scan (edema, pseudocysts, necrosis)
- rarely laparotomy
- epigastric tenderness
Management of acute pancreatitis?
- conservative to rest pancreas to stop further enz secretion and further inflammation so it can start to heal
- may include IV and NG suction to avoid stimulation of enzyme secretion
Chronic pancreatitis definition
Repeated occurrences of pancreatic inflammation leading to chronic inflammation with damage and eventual loss of parenchymal tissue (pancreas functional cells) that is REPLACED by fibrous tissue