Pancreas Physiology Flashcards
Pancreas Exocrine Cells name
Acinar
-> With zymogen granules (enzyme precursors)
Acute Pancreatitis cause
Injury to acinar cells -> autodigestion + immune inflammation
- Itself due to several causes: alcohol, gallstones main
Severity of acute pancreatitis
Spectrum: 30-40% cases are severe with 20-30% mortality (ie quite high)
Autodigestive Proteases cause
Destruction of pancreas acini
Autodigestive Lipases cause
Necrosis of fat in pancreas and other sites
Autodigestive elastases cause
Blood vessel destruction = internal haemorrhage
Why is acute pancreatitis so severe
Standard inflammatory response is compounded by activation of digestive enzymes leading to autodigestion
Clinical signs of acute pancreatitis
Epigastric pain
Nausea, vomiting, fever, abdominal tenderness
(Non specific)
How to diagnose acute pancreatitis
Initially neutrophil count to see if inflammation
Then to specify pancreatitis:
1 Elevated serum amylase and lipase
2 CT scan
How to manage acute pancreatitis
IV fluids
Nasogastric suction to remove the pancreatic enzymes
Chronic Pancreatisis presentation
Fibrotic due to repeated inflammation
Atrophy = smaller pancreas
Chronic Pancreatisis cause
Repeated inflammation of pancreas (often due to heavy alcohol intake)
Chronic Pancreatisis complications
Loss of exocrine function = malabsorption
If very severe spreads from acini to islets of langheran = endocrine complications (diabetes)
Pancreatic Carcinoma deaths
Very high despite actual cancer being uncommon (as high fatality due to late presentation)
Pancreatic cancer, what is the type of cancer
Adenocarcinoma as glandular tissue
Where are pancreatic carcinomas most common
Head of pancreas
Complications of head of pancreas cancer
Biliary obstruction
Diagnosis of pancreatic cancer
Imaging (CT US) confirmed by biopsy
Endocrine pancreatic tumour name
Insulinoma (Rare)
Ductal cell of pancreas secretion
Bicarbonate
Acinar cell secretion
Digestive enzymes
Bicarbonate secretion steps
- HCO3- from blood into ductal cells, and HCO3- made in ductal cells from H2O and CO2
- Secreted via activate transport (CFTR and Cl-/HCO3- exchanger)
How does secretin increase bicarbonate secretion from the pancreas
Secretin -> cAMP -> CFTR -> HCO3-
How does vagal stimulation increase bicarbonate secretion from the pancreas
Vagal afferents -> Calcium -> increased HCO3- secretion
Acinar cells high in which organelle
Endoplasmic reticulum to make lots of enzymes
What mediates release of pancreatic enzymes
CCK
How does CCK stimulate pancreatic enzyme secretion
- Hormone in blood -> acinar cells stimulated
- Activates vagus Efferents next to I cell -> brainstem -> vagus afferents stimulate acinar cells
Trypsinogen -> trypsin enzyme
Enterokinase
Trypsin cleaves which enzymes
Trypsinogen (auto catalytic)
Chymotrypsingen
Carboxypeptidase
+ others
Protease
Enzyme that digests protein
Lipase function
Triglycerides -> monoglycerides / free fatty acids
Amylase function
Starch -> sugar
What pre-empts the pancreas to begin releasing enzymes into the duodenum
Gastrin release during gastric phase of digestion
Inhibitors of pancreatic enzyme secretion
Glucagon
Somatostatin
Pancreatic polypeptide
Peptide YY (from colon ie further down)
What happens with Cystic Fibrosis disease
Defective CFTR -> thick mucus clogs things eg ducts
Impact of defective CFTR on pancreatic secretion thickness
Inc Cl- accumulation in cells -> inc Na+ accumulation from lumen -> inc H2O absorbed from lumen
= Pancreatic secretions less water = thick (hyperviscous)
Impact of defective CFTR on pancreatic enzymes in the pancreas
Accumulation of enzymes in the pancreas (as clogged duct from thick secretion) = autodigestion of pancreas = Pancreatisis
Pancreas divisum
Failure of the pancreatic ducts to fuse = small flow as two ducts but one exit = blockage = Pancreatisis from autodigestion due to accumulation of enzymes
Pancreatic insuffiency how much loss of exocrine function needed
> 90%
Which enzyme is most critically lost during pancreatic insufficiency
Lipase = fat malabsorption
Impacts of fat malabsorption (eg loss of lipase)
Weight loss
Steatorrhoea (fat in stool)
