Physiology of Fluid Balance Flashcards
how is water absorbed in GI tract
passive process driven by transport of solutes (sodium) from lumen of intestines to the bloodstream
contents of faeces
water
cellulose
bilirubin
bacteria
definition of diarrhoea
loss of fluid and solutes from GI tract in excess of 500ml per day
is water ingested and secreted balanced with water absorbed
yes
how is absorption of water in the GI driven
mainly by reabsorption of sodium - provides osmotic force fo reabsorption of water
how may water move during absorption
via transcellular or paracellular routes
how is sodium/H+ exchange stimulated
luminal bicarbonate
where does parallel sodium/H+ and Chloride/bicarbonate exchange occur
occurs in ileum and proximal colon
where do epithelial sodium channels occur
occurs in the colon (distally)
how is parallel absorption of chloride driven by odium/glucose co-transport and sodium/amino acid co-transport
collectively the overall transport of sodium generates a transepithelial potential in which the lumen in negative - driving parallel absorption of chloride
describe sodium/glucose co-transport and sodium/amino acid co-transport
most important in postprandial period in jejunum
secondary active transport and electrogenic
describe sodium/H+ exchange
occurs in duodenum and jejunum
stimulated by luminal bicarbonate
describe parallel sodium/H+ and Chloride/bicarbonate exchange
occurs in ileum and colon
most important in interdigestive period
describe epithelial sodium channels
occurs in the colon (distally)
regulated by aldosterone
where does sodium/glucose co-transport and sodium/amino acid co-transport take place
occurs throughout small intestine
how is parallel absorption of chloride driven by odium/glucose co-transport and sodium/amino acid co-transport
collectively the overall transport of sodium generates a transepithelial potential in which the lumen in negative - driving parallel absorption of chloride
action of aldosterone in epithelial sodium channels
opens channel
inserts channels into membrane from intracellular vesicle pool
increases synthesis of channels and NA+/K+-ATPase
describe NHE1
cellular pH housekeeper
how is Na+/H+ exchange stimulated
by the alkaline environment of the lumen due t presence of bicarbonate from the pancreas
describe parallel sodium/H+ and Chloride/bicarbonate
primary mechanism of sodium absorption in the interdigestive period - absorption is electroneutral
does not contribute greatly to postprandial absorption
how is parallel sodium/H+ and Chloride/bicarbonate regulated
via intracellular cAMP, cGMP and calcium - all reducing NaCl absorption (a cause of diarrhoea due to infection of E.Coli)
describe epithelial sodium channels
mediates electrogenic sodium absorption in the distal colon;
highly efficient and important in sodium conservation
how is epithelial sodium channels increased
via aldosterone;
not regulated by cAMP or cGMP
action of aldosterone in epithelial sodium channels
opens channel
inserts channels into membrane from intracellular vesicle pool
increases synthesis of channels and NA+/K+-ATPase
how does chloride absorption occur
passively via transcellular or paracellular routes
other;
Cl–HCO3- exchange (ileum, proximal and distal colon)
parallel Na+-H+ and Cl–HCO3- exchange (ileum and proximal colon)
secondary messengers that indirectly activate CFTR
cAMP
cGMP
calcium
chloride absorption in large intestine
the driving force is provided by lumen negative potential due to electrogenic movement of sodium through epithelium sodium channels
how does chloride secretion occur
at a basal rate
usually overshadowed by a higher rate of absorption
where does chloride secretion occur
from crypt cells
processes involved on the basolateral membrane during chloride secretion
Na+/K+ATPase
Na+/K+/2Cl- co-transporter (NKCC1)
K+ channels (IK1 and BK)
process of chloride secretion
Low intracellular Na+ drives inward movement of Na+, K+ and Cl- via NKCC1
K+ recycles via K+ channels, but intracellular concentration of Cl- increases providing electrochemical gradient for Cl- to exit cell via CFTR on the apical membrane
Lumen negative potential develops providing voltage-dependent secretion of Na+ through paracellular pathway
how is CFTR indirectly activated
bacterial enterotoxins
hormones and neurotransmitters
immune cells products
some laxatives
secondary messengers that indirectly activate CFTR
cAMP
cGMP
calcium
where does the chloride conductance mediated by CFTR result from
opening of channels at apical membrane
insertion of channels from intracellular vesicles into membrane
causes of diarrhoea
infectious agents - viruses and bacteria impaired absorption of NaCl chronic disease toxins drugs psychological factors hypermotility non-absorbable or poorly absorbable solutes in intestinal lumen (lactase deficiency) excessive secretion
outcomes of diarrhoea
dehydration - loss of sodium and water
metabolic acidosis - loss of bicarbonate
hypokalaemia - loss of potassium
treatment of diarrhoea
maintenance of fluid and electrolyte balance (first priority)
use of anti-infective agents (if appropriate)
use of non-antimicrobial antidiarrhoeal agents (symptomatic)
how may the absorption of NaCl be impaired
congenital defects (e.g. congenital chloridorrhoea – absence of Cl–HCO3- exchanger)
inflammation
infection (e.g. enterotoxins from some strains of E.coli and campylobacter sp.)
excess bile acid in colon
how may excessive secretion be a cause of diarrhoea
cholera;
cholera toxin (CTX) enters enterocyte
enzymatically inhibits GTPase activity of the Gs subunit
increased activity of adenylate cyclase
increased concentration of cAMP
cAMP stimulates CFTR
hypersecretion of Cl-, with Na+ and water following
describe rehydration therapy for diarrhoea
exploits SGLT1;
2 Na+ bind
Affinity for glucose increases, glucose binds
Na+ and glucose translocate from extracellular to intracellular
2 Na+ dissociate, affinity for glucose falls
Glucose dissociates
Cycle is repeated
