Pancreatic & Gall Bladder Pathology Flashcards
Is the pancreas usually palpable? What does this mean for symptoms?
No. It is ‘hidden’, sits deep, tucked behind duodenum. Therefore symptoms are late & nonspecific
How is the pancreas a dual function organ?
It has both exocrine (80-90%) and endocrine (10-20%) components.
Exocrine function of the pancreas…
- Acinar cells and ducts
- Acini contain Zymogen granules
- release proenzymes that are activated by trypsin
Zymogens are? what are they for?
Inactive precursor enzymes (travel in zymogen granules) for trypsin, chymotrypsin, amylase, lipase, elastase
Prevent digestion of pancreas»_space; inflammatory response
Endocrine function of pancreas?
Islets of langerhans secrete insulin, glucagon
Involved in diabetes mellitus
The main pathologies of the pancreas?
1) Acute & chronic pancreatitis (inflamm/infect)
2) Pancreatic Adenocarcinoma (malignant)
3) Cystic Fibrosis (genetic)
What is acute pancreatitis, how is it classified?
Inflammation of the pancreas
Mild: 60-70% (low mortility rates)
Severe: 30-40% (20-30% mortility) due to multiorgan failure
Etiology of Pancreatitis
Mainly (80-90% due to these)
Alcohol (metabolic)
Gallstones (mechanical)
also
shock/vasculitis
What happens in pancreatitis?
- autodigestion by pancreatic enzymes (damaged cells release enzymes > further damage)
- This lead to a 2’ inflammatory response (cytokines)
What are the consequences of inappropriate pancreatic enzyme release?
Protease: proteolysis of acini, ducts, islets
Lipase: fat necrosis in pancreas + other sites
Elastase: BV destruction»_space; haemorrhage
Cell injury response»_space; inflammation, oedema, impaird blood flow, ischaemia
Key triggers of ACUTE pancreatitis
1) Obstruction : gall stones, ductal concentrations, ampullary obstruction, alcholism.
obstruction > High intrapancreatic ductal pressure > accumulation of enzyme rich fluid > fat necrosis > oedema/ inflammation > impaired BF > ischemia > acinar cell injury
2) Direct injury to acinar cells: enzyme release
Clinical symptoms/features of ACUTE pancreatitis?
- acute abdo pain (epigastric)
- nausea & vomiting
- Fever, tachycardia (inflammatory response)
- marked abdo tenderness (ileus or shock)
How can we diagnose ACUTE pancreatitis?
- Elevated WBC count (non-specific)
- Elevated serum amylase or lipase (non-specific)
- CT scan - oedema, necrosis, pseudocysts
- Rarely laparotomy
Management and treatment of pancreatitis…
“REST THE PANCREAS” (decrease stimulation/secretions)
- IV fluids (no food = no secretions)
- NG suction (remove gastric/ duodenal )
- Anaglasia
- Monitoring
Define CHRONIC pancreatitis
“repeated bouts of pancreatic inflammation with loss of pancreatic parenchyma and replacement by fibrous tissue)
If you were looking at chronic pancreatitis in a microscopic slide, what would you see?
Macrophagal tissue, necrosis, scarring
Etiology/causes of CHRONIC pancreatitis
-60-70% due to heavy alcohol intake (damage to pancreatic tissue)
also
-previous acute pancreatitis
-severe malnutrtion
Pathology of CHRONIC pancreatitis
- Fibrotic (can be rock hard)
- Atrophy of exocrine, but endocrine relatively spared (low risk of diabetes)
- Often calcified (seen in CT scan)
Clinical symptoms/ features of CHRONIC pancreatitis
- repeated attacks of abdominal pain, brought on by ALCOHOL
- persistent pain can also occur
if its ongoing you can see
- loss of exocrine function (rarely endocrine > diabetes)
- pseudocysts (scarring > cavities formed)
Diagnose CHRONIC pancreatitis by
serum amylase (not as prominant as acute) CT imaging
Pancreatic Carcinoma is
4th most common form of cancer death M>F most 50+ years, (peak 60-80) -poor prognosis (due to late presentation) -
Risk factors of adenocarcenoma
- smoking
- rare hereditary cases
- alcohol & coffee
- High BMI
% of adenocarcinoma
60-70% head
5-10% body
10-15% tail
20% diffuse
carcinoma of the head of pancreas
- invade ampulla, bilary obstruction (jaundice, pale stool, dark urine)
- Body and tail: remain silent, spreads to nodes, adjacent organs, liver, bones, lungs
