Absorption of Ions and Water Flashcards
What are the relative functions of an intestinal villous and crypt? What are the cell types present in each area?
villous = absorption.
- absorptive cells
- mucous secreting cells –> mucous production
crypt = secretion.
- stem/progenitor cell –> crypt-villous axis
- paneth cell –> defence against microbes
- enteric endocrine cell –> hormone secretion
In the colon the surface epothelial cells are primarily responsible for ………….. ………….., whereas colonic gland cells mediate ……. …………..
electrolyte absorption
ion secretion
Small intestine surface area is increased by:
1.
2.
3.
- macroscopic folds of Kerckring (plicae circulares)
- Villi
- microvilli on apical surface of the epthelial cells and crypts
Total surface area of small intestine?
200m^2
tennis court
What is the relative volume of fluids in and out in a day:
- Food
- Saliva
- stomach
- Pancreas and bile
- small intestine
- large intestine
In - food 2L - saliva 1.5L - stomach 2L - pancreas and bile 2L - small intestine 1L Out - small intestine 6.5L - large intestine 1.9L
What is the difference between transcellular and paracellular secretion/absorption?
Transcellular = the solute must cross the two cell membranes in series. Active transport implicated Paracellular = the solute moves passively between adjacent epithelial cells via the tight junctions
How is water absorbed?
Paracellularly!
Depends on the absorption of Ion, principally Na+ and Cl-
Transport of Na, Cl and bicarb into the lateral intercellular spaces. Resulting high NaCAl near the apical end of the space causes it to be hypertonic which causes an osmotic flow of water from the lumen, and via the tight junctions into the intercellular spaces
List the four ways Na+ is transported.
Where do these take place and when?
Entire length of the intestine
- Na/Glucose transport (SGLT-1) or Na-Amino transport JEJUNUM, FED STATE
- Na-H exchanger, JEJUNUM, ALL TIME
- Parallel Na-H and Cl-HCO3- exchange, ILEUM/LI, FASTED STATE
- Epithelial Na+ channels - ENaC, DISTAL COLON,
- Na/Glucose tranport or Na-Amino transport
- Na+ crosses membrane down an electrochemical gradient (Na-K pump)
- Co-transoprt with glucose via SGLT-1
- Co-tranpsort with amino acids via IMINO, B0 and EAAT3
- Na-H exchanger
Na+ uptake, H+ extrusion into lumen
Energy comes from Na-K pump
- Parallel Na-H and Cl-HCO3- exchange (electroneutral)
How is this process regulated?
How do enterotoxins induce secreotory diarrhoea’s?
- Primary route of absorption in the fasted state
Carbonic anhydrase produces bicarb and H+
Bicarb leaves in exchange for Cl-
H+ leaves in exchange for Na+
Gradient maintained by Na-K pump - Increased cAMP and cGMP as well as intracellular Ca2+ with reduce NaCl absorption.
- Enterotoxins elevate cAMP and inhibit NaCl absorption
- Epithelial Na+ channels
Where does this take place?
In what 3 ways do mineralocorticoids increase Na+ absorption?
entry occurs across the apical membrane via ENaC channels that are highly specific fro Na+
Mainly in distal colon
Mineralocorticoids increase Na+ absorption by
1. increase opening of apical Na+ channels
2. insertion of channel from vesicle
3. increased synthesis of apical pumps
Describe Cl- transport
What are the 3 models proposed?
occurs throughout the small and large intestine and is often closely linked to Na+ absorption
- passive Cl- absorption
- parallel Na-H and Cl-HCO3 exchange
- Cl-HCO3 exchange
- Passive Cl- absorption
What are 2 the driving forces?
- A passive process driven by the electrochemical gradient for Cl- either by a paracellular of transcellular route
- The driving force for both is derived from either Na+glucose transport in the small intestine and epithelial Na+ channels in the distal end of the colon
- Parallel Na-H and Cl-HCO3 exchange
electroneutral NaCl absorption also mediates Cl- absorption in the ileum and proximal part of the colon
- Cl-HCO3 exchange
In the absence of Na-H exchange occurs in the ileum and in surface epithelial cells in the large intestine
What is congenital chloridorrhea?
What is the potential treatment?
The congenital absence of an apical Cl-HCO3 exchanger is an autosomal recessive disorder
Affected children have diarrhoea with an extremely high Cl-
Because secretion of HCO3 is reduced, patients are alkalitic
PPI is a pontential treatment, gets rid of alkaline tide
Absorptogogues promote absorption
Give some examples
Where and how does it act?
Angiotensin and aldosterone
Increase BP by stimulating Na+ absorption
Small intestine - enhances electroneutral NaCl ansorption by upregualting Na-H exchange
Colon - stimlates absorption through ENaC
What are the 4 categories of secretagogues?
- bacterial enterotoxins
- hormones and neurotransmitters
- products of the immune system
- laxatives
How does cholera cause secretory diarrhoea?
What is an effective treatment and why?
increases cAMP
increases Cl and K secretion and inhibits electroneutral NaCl absorption
Second messengers do not alter the function of nutrient-coupled Na+ absorption, oral rehydration solution containing glucose and Na+ is effective
What is Verner-Morrison syndrome?
Affects hormone/NT mediated secretogogues
mostly pancreatic tumours that produce VIP which increases cAMP –> diarrhoea
How do immune products cause diarrhoea?
What are the treatments?
Histamine and prostaglandins released from mast cells induce diarrhoea through cAMP e.g. in IBD
Treatments
1. opiod receptor against acts on myenteric plexus
2. somatostatin analogues
Describe how calcium is absorbed?
Passive
- paracellular pathway, not under control of VDR
Active
- active transcellular uptake via apical Ca2+ channels, binds to calbindin which acts as a buffer to keep conc low.
- Basolateral Na-Ca exhanger extrude Ca2+ from cells
- Active VitD activates all three steps
