Absorption/secretive/digestive stuff

Question 1

How does NA get absorbed in SI?

Answer 1

Actively absorbed
Via SGLT1 - Na/glucose transporter. Takes up Na alongside glucose - useful when lots of glucose
Na-H exchanger - swaps Na for H. Useful when low pH or when high HCO3 as H+ wants to get out of cell
Enac - this is increased by aldosterone

Question 2

Electroneutral exchange

Answer 2

Used to absorb Na + Cl
Na-H exchanger alongside Cl-HCO3 exchanger
H+ and HCO3 are secreted

Question 3

Chloride absorption

Answer 3

Passive Cl transport

Parallel Na-H and Cl-HCO3 (electroneutral)

Question 4

Absorptagogues

Answer 4

e.g. angiotensin + aldosterone
Released when BV drops (dehydration) or drop in BP - RAAS
Na absorption
Angiotensin - enhances electroneutral NaCl absorption
Aldosterone in colon - enhances Enac

Question 5

Secretagogues

Answer 5

Bacterial enterotoxins e.g. cholera
Hormones + NTs
Product of cells of the immune system
Laxatives 
(the first 3 all increase cAMP)
Cholera increases cAMP which increases Cl and K secretion and blocks electroneutral transport of Na and Cl. Treatment takes advantage of SGLT1 transporter so alongside glucose

Question 6

Loperamide

Answer 6

This decreases gut motility as it is an opioid receptor antagonist. So increases amount of time faeces spends in the LI to absorb more h2o out of it

Question 7

Carbohydrate absorption

Answer 7

Only monosaccharides are absorbed so everything has to be broken down into this. It is a 2 step process:

1. Intraluminal hydrolysis of starch to oligosaccharides by salivary + pancreatic amylases (stimulated by CCK)
2. Brush border digestion of oligosaccharides - hydrolysis, lactase/maltase/sucrose-isomaltase with peak activity in jejunum

Absorption is also a 2 step process
Transport across apical membrane: glucose + galactose transported via SGLT1 (secondary AT alongside Na)
Fructose is transported by FD through GLUT5
Then on basolateral side - all go through GLUT2

Question 8

Protein absorption

Answer 8

4 major pathways:

1. Proteins get digested luminary to release AAs
2. Digestion in the brush border of oligopeptides to AAs
3. Oligopeptides get taken up by PEPT1 and then broken down in cytoplasm
4. Oligopeptides get taken up by PEPT1 and transported straight into blood

Luminal digestion = gastric + pancreatic peptidases. Chief cells stimulated by Ach release pepsinogen - pepsin. Can be exopeptidase or endopeptidases

Brush border digestion = also an endopeptidase or exopeptidase

There are loads of transport systems for AAs e.g. imino for glycine, some are Na dependent, some are Na independent

Question 9

Digestion of fat

Answer 9

Dietary lipids disrupted mechanically in mouth/stomach + resulting lipid particles stabilised as an emulsion. Emulsion by: cooking/blending, chewing/gastric churning, + intestinal peristalsis. This increases SA:vol ratio so lipase have a big surface to work on. Lipid digestion in mouth + stomach by lingual/gastric lipase (chief cells in response to gastrin/Ach). They release a FFA: if this is small then protonated in stomach + absorbed across mucosa. If large then remains in core of a triglyceride. When gets to duodenum, I cells stimulated to release CCK - causes bile release + pancreatic enzyme release. The surface of the triglycerides gets hydrolysed which leads to budding off and formation of a micelle. Micelles transport the lipids to the enterocyte surface where they meet an acidic enviro from Na-H exchange. Fatty acids get protonated + leave micelle to enter enterocyte by diffusion, active transport or incorporation. Remaining bile gets reabsorbed at terminal ileum + colon + into enterohepatic circulation + back to liver. Short chain fatty acids can go straight across into blood. Long chain form chylomicrons in the enterocyte then are transported into the lymph system. They find their way back to endothelial cells that express lipoprotein lipase to break fat down into glycerol + FA which go in liver. FA stored as fat. Glycerol used for gluconeogenesis.

Question 10

Glucose channel Km values

Answer 10

Low Km = high affinity
Glut 1 and 3 = low km as have high affinity for glucose as they control basal level on all cells so always need to take up glucose
Glut 2 = high km as they are glucose sensor cells on pancreatic beta cells and hepatocytes
glut 4 = on muscle + adipocytes - insulin dependent