9. the Exocrine Pancreas Flashcards
how is the PANCREAS in relation to PERITONEUM
RETROPERITONEAL
(EXCEPT TAIL - intraperitoneal)
PANCREAS in relation to STOMACH
POSTERIOR (behind)
which NERVES / CHAIN SUPPLY PANCREAS
SYMPATHETIC CHAIN
- SPLANCHNIC NERVE
name of PLEXUS where SYMPATHETIC CHAINS PASS as they go towards PANCREAS (supplies)
COELIAC PLEXUS
(bundle of nerves in the upper abdomen, sits behind the pancreas)
PANCREAS surrounded by lots of LYMPH NODES:
- ANTERIOR PANCREATICODUODENAL lymph node
- POSTERIOR PANCREATICODUODENAL lymph node
- SUPERIOR BODY lymph node (top of body of pancreas)
- INFERIOR BODY lymph node
- SPLENIC lymph node
- HEPATIC lymph node (near hepatic artery)
- PYLORIC lymph node (near pyloris of stomach)
- CELIAC lymph node (close to celiac plexus)
- SUPERIOR MESENTERIC lymph node (above SMA)
ARTERIES that SUPPLY PANCREAS
- SPLENIC ARTERY (top of pancreas, on way to spleen)
- HEPATIC ARTERY (into liver)
(AORTA)
VEINS that drain PANCREAS
- SPLENIC VEIN (from spleen, behind pancreas)
- HEPATIC PORTAL VEIN (to liver)
(VENA CAVA)
what are the EXOCRINE functioning CELLS of the PANCREAS
ACINAR CELLS and DUCT CELLS
what are the ENDOCRINE functioning CELLS of the PANCREAS
ISLETS of LANGERHANS
- ALPHA, BETA, DELTA, PP CELLS
ANATOMICAL PARTS of the PANCREAS
TAIL, BODY, HEAD, UNCINATE PROCESS
what is the MAIN DUCT of the PANCREAS
PANCREATIC DUCT
PANCREATIC DUCT and BILE DUCT (from liver) JOIN and EMPTY into DUODENUM THROUGH the…
AMPULLA OF VATER
PANCREATIC and BILE DUCTS both EMPTY INTO the
DUODENUM
(via AMPULLA)
BRANCH DUCTS lead into the MAIN PANCREATIC DUCT. where do Branch ducts come from
ACINAR UNITS
what is the AUXILIARY DUCT
only in some people
alternative duct to empty Pancreatic juices into Duodenum
EMBRYOLOGY - PANCREAS DEVELOPS FROM which 2 BUDS:
VENTRAL BUD and DORSAL BUD
which FUSE to become whole pancreas
EMBRYOLOGY BUD CELLS develop and DIFFERENTIATE into which CELLS
- ENDOCRINE CELLS: ALPHA, BETA, DELTA, PP
- ACINAR CELLS
- DUCTAL CELLS
what is the ROLE of ENDOCRINE ALPHA CELLS
secrete GLUCAGON
- acts on LIVER
-> Glycogen breakdown for glucose release
what is the ROLE of ENDOCRINE BETA CELLS
Secrete INSULIN
- acts on MUSCLE CELLS,
FAT CELLS (ADIPOCYTES),
ERYTHROCYTES
-> Glucose Uptake
also acts as Mitogen as it promotes CELL DIVISION
what is the ROLE of ENDOCRINE DELTA CELLS
secrete SOMATOSTATIN
- acts on ENDOCRINE SYSTEM as REGULATOR
also acts as Mitogen as it promotes CELL DIVISION
what is the ROLE of ENDOCRINE PP CELLS
secrete PANCREATIC POLYPEPTIDES
- act on PANCREAS ITSELF
for regulation of RELEASE of HORMONES
which ENDOCRINE CELLS help CELL DIVISION
INSULIN and SOMATOSTATIN
PP CELLS secretions ACT ON..
PANCREAS
- regulate release of hormones
BUD CELLS develop into which STEM CELLS that can differentiate into ACINAR and DUCTAL cells
CENTROACINAR CELLS
What do ACINAR CELLS RELEASE
ZYMOGENS - INACTIVE PRECURSOR of ENZYMES
(from ZYMOGEN GRANULES)
What BINDS to ACINAR CELLS for release of ENZYMES
CCK
(acinar cells have CCK Receptors)
MAIN PROTEASES from ACINAR CELLS
ELASTASE, CHYOTRYPSIN
& TRYPSIN
RELEASE of ZYMOGENS from ACINAR CELLS are REGULATED by..
CCK
TRYPSINOGEN is ACTIVATED BY … into TRYPSIN
ENTEROKINASE
WHERE is TRYPSINOGEN ACTIVATED by ENTEROKINASE into TRYPSIN
in the DUODENUM
where should we have ACTIVE TRYPSIN
DUODENUM
NOT in acinar cells (Pancreatitis)
what do DUCTAL CELLS RELEASE
BICARBONATES
what BINDS and REGULATES RELEASE of BICARBONATES from DUCTAL CELLS
SECRETIN
what does SECRETIN BIND to
DUCTAL CELLS (bicarbonates)
what does CCK BIND TO
ACINAR CELLS (zymogens)
HOW does SECRETIN BINDING CAUSE BICARBONATE RELEASE from DUCTAL CELLS
- ACTIVATES cAMP and PKA
- CL- RELEASE
- CL- REABSORBED back IN and HCO3- TRANSPORTED OUT
what ION ALLOWS HCO3- RELEASE from DUCTAL CELLS
CHLORIDE
(RELEASE AND REABSORPTION)
what does HCO3- EXCRETION from DUCTAL CELLS also cause to be RELEASED INTO LUMEN
H2O
- PASSAGE between cells into LUMEN of duct
CHRONIC PANCREATITIS caused by BUILD UP of..
FIBROSIS
from INFLAMMATION
ACUTE PANCREATITIS is the RESULT of what process
NECROSIS
what is the EARLY RESPONSE to NECROSIS and ACUTE INFLAMMATION
SYSTEMIC INFLAMMATORY RESPONSE (SIRS)
(lots of cytokines released)
-> death
what is the LATER RESPONSE to NECROSIS and ACUTE INFLAMMATION
MULTI-ORGAN DYSFUNCTION SYNDROME (MODS)
(organs closing down)
-> death
what is LIKELY to cause ENDOCRINE FAILURE (DIABETES MELLITUS) and/or EXOCRINE FAILURE (MALABSORPTION)
FIBROSIS (CHRONIC PANCREATITIS)
from acute pancreatitis (&necrosis) or other factors
(endocrine failure can lead to cancer)
what usually CAUSES PANCREATITIS and NECROSIS
when there is ACTIVE TRYPSIN IN ACINAR CELLS (activation in acinar and not in duodenum)
-> leads to CELL DAMAGE
-> CYTOKINE RELEASE
-> Pancreatitis & Necrosis
(causes MORE trypsinogen activation in acinar cells, more cell damage etc.)
what can CAUSE the ACTIVATION of TRYPSINOGEN and so ACTIVE TRYPSIN IN ACINAR CELLS
(pancreatitis)
CA2+ SPIKES in ACINAR CELLS
What are in ACINAR CELLS that INACTIVATE/INHIBIT ACTIVE TRYPSIN and ACTIVATION of more
SPINK1/PSTI
PANCREATIC ENZYME INHIBITORS
(activated in the presence of trypsin in acinar cells)
what does SPINK1 do
INACTIVATE ACTIVE TRYPSIN / INHIBIT TRYPSINOGEN ACTIVATION in ACINAR CELLS
- prevent pancreatitis & necrosis
CAUSES of ACUTE PANREATITIS
’’ I GET SMASHED’’
- IDIOPATHIC (unknown) & HERIDATORY
- GALLSTONES (MAIN)
- ETHANOL (ALCOHOL)
other
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion Stings (venom)
- Hypercalcaemia, Hyperlipidaemia, Hyperthermia
- ERCP (endoscopic retrograde cholangiopancreatogrophy)
- Drugs
MAIN CAUSE of ACUTE PANCREATITIS
GALLSTONES
MAIN CAUSE of CHRONIC PANCREATITIS
ALCOHOL
(gallstones can be removed)
how can GALLSTONES cause ACINAR DAMAGE
- Excess CCK
- Excess Trypsinogen release
- LESS SPINK1 (inhibitor)
- MORE active TRYPISIN in acinar cells
what is the CURRENT ASSUMED Model of how GALLSTONES lead to activation of trypsinogen
- enter common bile duct
- BLOCK BILE RELEASE from Ampulla
- BILE enters Pancreatic duct and activates trypsinogen
CAUSES of PANCREATITIS
- FIBROSIS - STIMULATION of STELLATE CELLS
- PROTEOLYTIC CLEAVAGE (activation trypsin)
(CYSTIC FIBROSIS - defects in CL- transporter, LESS HCO3- Release, less H2O, LOW pH, HIGH VISCOSITY and LOW FLOW) - PROTEIN PLUGS (block ducts)
- CALCIFICATION
by which METABOLIC PATHWAY does ALCOHOL CAUSE PANCREATITIS and how
NON-OXIDATIVE METABOLISM
-> release FATTY ACID ETHYL ESTERS
-> CALCIUM SPIKE - PANCREATITIS
what is RELEASED in NON-OXIDATIVE METABOLISM of ALCOHOL that causes CALCIUM SPIKE / PANCREATITIS
FATTY ACID ETHYL ESTERS
what is RELEASED in OXIDATIVE METABOLISM of ALCOHOL that does NOT cause pancreatitis
ACETATE
INCREASED CA2+ causes what to FUSE
LYSOZYME with CATHEPSIN B (PROTEASE)
and
ZYMOGEN - TRYPSINOGEN
hence ACTIVATES
what ENZYME can CLEAVE / ACTIVATE TRYPSINOGEN
CATHEPSIN B
