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GI > Water Balance in the G.I. tract > Flashcards

Water Balance in the G.I. tract Flashcards

1
Q

describe the absorption of water in the GI tract

A

a passive process driven by the transport of solutes (especially Na+0 from the lumen of the intestines into the bloodstream

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2
Q

what is faeces made of

A

100ml water, 50ml cellulose, bilirubin, bacteria

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3
Q

what is diarrhoea in terms of fluids

A

loss of fluid and solutes from GI tract in excess of 500ml per da

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4
Q

what is interstitial fluid movement always coupled to

A

solute movement

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5
Q

what are the two routes water can travel via

A

transcellular- move across membranes via aquaporins

paracellular- through tight cell junctions between enterocytes

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6
Q

how does the re-absorption of Na+ allow the re-absorption of water

A

creates as osmotic pressure

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7
Q

what stimulates proton excretion

A

Na+/H+ exchange in the duodenum and jejunum stimulated by bicarbonate

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8
Q

what is the most important mechanism in the fasting state

A

Na+ co transport in the small intestine- inward movement of Na+ coupled to the movement of a monosaccharide (glucose of individual amino acid)

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9
Q

what is the post prandial period

A

time after eating

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10
Q

what is the most effective mechanism in the fasting state

A

parallel exchangers: Na+/H+ and Cl-/HCO3-

occurs in the ileum and colon

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11
Q

what epithelial channels are regulated by aldosterone

A

epithelial Na+ channels (ENaC)

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12
Q

what type of transport is the Na+ co transporters

A

secondary active transport

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13
Q

how are the Na+ co transporters electrogenic

A

as overall transport generates a transepithelial potential in which the lumen is negative (drives the parallel absorption of Cl-

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14
Q

how many Na for each glucose or amino acid

A

2

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15
Q

where does Na+/H+ exchange happen

A

in jejunum and proximal colon at apical membrane via NHE2 and NHE3

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16
Q

does the parallel exchange of Na+/H+ and Cl-/HCO3- create a a potential across the membrane

A

no is electroneutral

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17
Q

what regulates the parallel absorption of Na+ and Cl-

A

intracellular cAMP, cGMP and Ca2+ = all reduce NaCl absorbtion

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18
Q

in parallel absorption what goes out when Na+ and Cl- comes in

A

Na+/H+

Cl-/HCO3-

19
Q

what does a reduction in NaCl absorption do

A

causes diarrhoea- secretory diarrhoea

20
Q

what causes secretory diarrhoea

A

infection (e.coli) can increase intraceluular cAMP

21
Q

what do ENaC channels do

A

mediate electrogenic Na+ absorption in the distal colon

22
Q

what are ENaC channels regulated by

A

increased by aldosterone, not mediated by cAMP/GMP (the cyclic nucleotides)

23
Q

how does aldosterone increase ENaC activity

A

opens then, puts more of them into the membrane, increases synthesis of them and Na+/K+-ATPase

24
Q

why are ENaC ion channels not transporters

A

as the sodium travels down its electrical gradient

25
Q

what happens if the ENaC channels are defective

A

lot of sodium in the colon which holds onto water= diarrhoea

26
Q

how is Cl- absorbed in the colon

A

passively via trans-cellular or para-cellular routes

or

Cl–HCO3- exchange (ileum, proximal and distal colon) and (ii) parallel Na+-H+ and Cl–HCO3- exchange (ileum and proximal colon)

27
Q

how is Cl- passively absorbed in the small intestine

A

driving force= lumen negative potential due to electrogenic transport of Na+ (Na+/glucose and Na+/amino acid) – negative lumen pushing cl out

28
Q

how is Cl- passively absorbed in the large intestine

A

driving force= lumen negative potential due to electrogenic movement of Na+ through ENaC

29
Q

when healthy, is there net Cl- absorption or secretion

A

absorption

30
Q

where does Cl- secretion occur and at what rate

A

from crypt cells at a basal rate

31
Q

how does Cl- leave the cell

A

via CFTR (cystic fibrosis) on the apical membrane down an electrochemical gradient

32
Q

what does the secretion of Cl- lead to

A

creates negative lumen potential which leads to secretion of Na+ paracelullarly and K+ vis K+ channels (ions that came in with Cl_ via the NKCC1 channel)

33
Q

what increases the activity of CFTR

A 
bacterial endotoxins,
calcium, cGMP and cAMP,
hormones and neurotransmitters,
immune cell products (prostaglandins, histamine),
some laxatives
34
Q

what is the overall effect of the opening of CFTR channels

A

secretory diarrhoea

35
Q

what metabolic ion problems can diarrhoea cause

A

dehydration (Na+ and H2O loss)
metabolic acidosis (HCOs- loss)
hypokalaemia

36
Q

what can cause impaired absoprtion of NaCl which results in diarrhoea

A

congenital defects, inflammation, infection, excess bile acid in colon

37
Q

what are the biochemical causes of diarrhoea

A

impaired absorption of NaCl, non absorbable or poorly absorbable solutes in intestinal lumen (sugar substitutes,
hypermoblity, excessive secretion, lactase deficiency

38
Q

why does hypermotility cause diarrhoea

A

not enough time to finish absorption

39
Q

how does the cholera toxin cause diarrhoea

A

inhibits GTPase which increases cAMP which stimulates CFTR which causes secretory diarrhoea

40
Q

how does lactase deficiency cause diarrhoea

A

as un-absorbed lactose acts osmotically and retains water in the lumen

41
Q

how do rehydration therapies work

A

Absorption of Na+ and glucose by SGLT1 cause accompanying absorption of H2O

SGLT1 on apical membrane of enterocyte

42
Q

what drugs are used as anti motility agents to treat diarrhoea

A

opoid drugs e.g. codeine, diphenoxylate and loperamide(last two low CNS penetration so less change of abuse),

43
Q

how do opioids cause reduced motility

A

inhibit enteric neurones, decrease peristalsis, increased segmentation, increased fluid absorption, constriction of pyloric, ileocaecal and anal sphincters, increase tone of large intestine

GI (64 decks)

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