Physiology of digestion

Question 1

stomach: acid features

Answer 1

2.5L of secretions per day
hydrochloric acid
oesophageal and duodenal sphincters to prevent acid from going either way
mucus barrier

Question 2

stomach: cellular features

Answer 2

parietal cells secrete HCl
neuroendocrine cells:
- enterochromaffin cells > histamine
- G cells > gastrin
- D cells > somatostatin (inhibitor)
other cells:
- mucus cells > mucus!! (barrier)
- chief cells > pepsinogen (digestion)

Question 3

food digestion: amylase

Answer 3

amylase acts on carbohydrates
found in mouth and pancreas
glucose absorbed in stomach and small intestine with help of insulin

Question 4

food digestion: proteases

Answer 4

proteases act on proteins
pepsinogen (from chief cells) > pepsin
trypsinogen (from pancreas, activated by enteropetidase) > trypsin
chymotrypsinogen (from pancreas, activated by trypsin) > chymotrypsin
absorption in small intestine

Question 5

food digestion: lipase

Answer 5

lipase acts on fats
pancreatic lipase and pancreatic lipase related protein 2
bile salts emulsify fats and allow lipases to act
enterohepatic circulation

Question 6

hey clinical pathways for nutrient absorption

Answer 6

B12 absorption
folate absorption
iron absorption

Question 7

B12

Answer 7

liberated from protein binding by acid and pepsin from stomach
binds to R factor (cobalamin-binding protein-haptocorrin secreted saliva, bile and the pancreas)
pancreatic proteases release this complex in the duodenum where it is then bound to intrinsic factor which is produced by gastric parietal cells
IF-B12 complex absorbed in terminal ileum

Question 8

B12 - clinical, deficiency

Answer 8

deficiency:
- poor dietary intake (alcoholics, elderly)
- gastric causes (pernicious anaemia, atrophic gastritis - chronic HP infection, PPI use)
- small bowel (coeliac disease, bacterial overgrowth, surgical resection)
- medication (metformin, nitrous oxide)

Question 9

B12 clinical - 3 main to remember

Answer 9

pernicious anaemia (antibodies to parietal cells)
poor dietary intake
small bowel Crohn’s disease/post surgery

Question 10

folate

Answer 10

animal products and leafy green veg in polyglutamate form
cleaves to monoglutamate form in jejenum
key role in DNA synthesis and repair
**increased use in pregnancy

Question 11

causes of folate deficiency

Answer 11

poor dietary intake
small bowel diseases - coeliac, Crohn’s, resection
drugs - methotrexate (inhibits dihydrofolate reductase), trimethoprim, phenytoin

Question 12

iron

Answer 12

2 forms:
- ferrous (Fe2+) - soluable
- ferric (Fe3+) - insoluable
absorbed in duodenum by enterocytes
transported around blood by transferrin

Question 13

types of iron in blood

Answer 13

heme iron:
- complexed to heme
- found in meats
- in ferrous form
- well absorbed
non-heme iron:
- vegetables, cereals etc
- typically ferric form
- not well absorbed

Question 14

iron supplementation

Answer 14

oral iron poorly absorbed (10-15%)
unabsorbed iron > side effects

Question 15

why is iron absorption so inefficient?

Answer 15

hepcidin - degrades ferroportin
high circulating iron is toxic - body limits increase in plasma iron
high plasma iron > high hepcidin > impairs further iron absorption (up to 48hrs)
argument to give alternate day oral iron

Question 16

importance of gastric acid

Answer 16

ferrous iron can be absorbed at low or high pH - patients with achlorhydria (PPI use) don’t absorb ferric iron
gastric acid releases ferric iron complexes, reduces to ferrous form and promotes formation of chelates
vitamin C can reduce ferric to ferrous > promoted absorption