pancreas lecture Flashcards
pancreatic development
foregut and midgut join in developing embryo; ventral (part of hepatobiliary bud become liver and gall bladder) and dorsal buds form; duodenum rotates to form a C-shape - ventral bud swings round to lie adjacent to dorsal bud; both fuse and ventral bud duct becomes main pancreatic duct
where is islet tissue most abundant
tail
where does pancreas lie
mainly on posterior abdominal wall to hilum of spleen
close relations with and supply from
coeliac and superior mesenteric arteries
angiography
blush forms (tumour) as stimulates own angiogenesis
somatostatin
endocrine cyanide - suppress release of most other hormones and other biological functions
cystic fibrosis
effects both exocrine and endocrine effects
islets
lose connection from branching duct system and become islets; tail > head
duct cell, centroacinar and acinar cells form what functional unit
blind endotubules
bicarbonate secretions
prevents damage to duodenal mucosa, raises pH to optimum range for enzymes in pancreas, washes low volume enzyme secretion out of pancreas into duodenum
as empty more stomach contents into duodenum (low pH)
raise in bicarbonate secretion up to pH 5 (other mechanisms also help neutralise acid to raise pH further - Brunner’s glands, bicarbonate in bile)
exchange driven by electrochemical gradients
high EC (blood) Na+ vs IC (duct cell); high Cl- in lumen vs IC (duct cell)
K+ to blood via K+ channel and Cl- to lumen via Cl-channel
facilitated diffusion
what do lipases require presence of for effective action
bile salts
pancreatic secretions
adapt to diet (high protein, low carbs increases prportion of proteases and decreases proportion of amylases)
pancreatic enzymes and bile
essential for normal digestion; lack can lead to malnutrition even if dietary input okay
orlistat
inhibits pancreatic lipases to treat obesity, but causes steatorrhoea
cephalic phase
reflex response to sight/smell/taste/thought; enzyme rich component only, low volume mobilises enzymes by vagus nerve
gastric phase
stimulation of pancreatic secretion originating from food arriving in stomach; same mechanisms as cephalic
intestinal phase
70-80% secretions; hormonally mediated when gastric chyme enters duodenum; both compounds of pancreatic juice stimulated (enzymes, HCO3- and juice flows into duodenum)
CCK
also stimulates bile secretion (on top of lipases)
control of enzyme secretion: peptides and fat
C-cells - CCK in blood, vagus - acinus - proenzymes and trypsin inhibitors cause negative feedback
switch off CCK
cephalic phase ends when meal eaten, absorption of fats and peptides removed local luminal stimulus for CCK release from mucosa (possibly other mechanisms)
stimulus interaction
CCK alone - no effect on HCO3-; secretin can markedly increase HCO3- secretion; if both together then marked increase in HCO3- secretion (secretin acts as switch so stops duodenum having too much HCO3- before food enters); vagus nerve has similar effect to CCK; secretin has no effect on enzyme secretion
CCK potentiated effects of secretin
don’t want low pH in duodenum
