pancreas lecture Flashcards

1
Q

pancreatic development

A

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

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2
Q

where is islet tissue most abundant

A

tail

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3
Q

where does pancreas lie

A

mainly on posterior abdominal wall to hilum of spleen

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4
Q

close relations with and supply from

A

coeliac and superior mesenteric arteries

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5
Q

angiography

A

blush forms (tumour) as stimulates own angiogenesis

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6
Q

somatostatin

A

endocrine cyanide - suppress release of most other hormones and other biological functions

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7
Q

cystic fibrosis

A

effects both exocrine and endocrine effects

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8
Q

islets

A

lose connection from branching duct system and become islets; tail > head

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9
Q

duct cell, centroacinar and acinar cells form what functional unit

A

blind endotubules

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10
Q

bicarbonate secretions

A

prevents damage to duodenal mucosa, raises pH to optimum range for enzymes in pancreas, washes low volume enzyme secretion out of pancreas into duodenum

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11
Q

as empty more stomach contents into duodenum (low pH)

A

raise in bicarbonate secretion up to pH 5 (other mechanisms also help neutralise acid to raise pH further - Brunner’s glands, bicarbonate in bile)

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12
Q

exchange driven by electrochemical gradients

A

high EC (blood) Na+ vs IC (duct cell); high Cl- in lumen vs IC (duct cell)

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13
Q

K+ to blood via K+ channel and Cl- to lumen via Cl-channel

A

facilitated diffusion

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14
Q

what do lipases require presence of for effective action

A

bile salts

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15
Q

pancreatic secretions

A

adapt to diet (high protein, low carbs increases prportion of proteases and decreases proportion of amylases)

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16
Q

pancreatic enzymes and bile

A

essential for normal digestion; lack can lead to malnutrition even if dietary input okay

17
Q

orlistat

A

inhibits pancreatic lipases to treat obesity, but causes steatorrhoea

18
Q

cephalic phase

A

reflex response to sight/smell/taste/thought; enzyme rich component only, low volume mobilises enzymes by vagus nerve

19
Q

gastric phase

A

stimulation of pancreatic secretion originating from food arriving in stomach; same mechanisms as cephalic

20
Q

intestinal phase

A

70-80% secretions; hormonally mediated when gastric chyme enters duodenum; both compounds of pancreatic juice stimulated (enzymes, HCO3- and juice flows into duodenum)

21
Q

CCK

A

also stimulates bile secretion (on top of lipases)

22
Q

control of enzyme secretion: peptides and fat

A

C-cells - CCK in blood, vagus - acinus - proenzymes and trypsin inhibitors cause negative feedback

23
Q

switch off CCK

A

cephalic phase ends when meal eaten, absorption of fats and peptides removed local luminal stimulus for CCK release from mucosa (possibly other mechanisms)

24
Q

stimulus interaction

A

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

25
Q

CCK potentiated effects of secretin

A

don’t want low pH in duodenum