Physiology of Fluid Balance Flashcards

(40 cards)

1
Q

how is water absorbed in GI tract

A

passive process driven by transport of solutes (sodium) from lumen of intestines to the bloodstream

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2
Q

contents of faeces

A

water
cellulose
bilirubin
bacteria

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3
Q

definition of diarrhoea

A

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

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4
Q

is water ingested and secreted balanced with water absorbed

A

yes

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5
Q

how is absorption of water in the GI driven

A

mainly by reabsorption of sodium - provides osmotic force fo reabsorption of water

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6
Q

how may water move during absorption

A

via transcellular or paracellular routes

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7
Q

how is sodium/H+ exchange stimulated

A

luminal bicarbonate

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8
Q

where does parallel sodium/H+ and Chloride/bicarbonate exchange occur

A

occurs in ileum and proximal colon

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9
Q

where do epithelial sodium channels occur

A

occurs in the colon (distally)

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10
Q

how is parallel absorption of chloride driven by odium/glucose co-transport and sodium/amino acid co-transport

A

collectively the overall transport of sodium generates a transepithelial potential in which the lumen in negative - driving parallel absorption of chloride

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11
Q

describe sodium/glucose co-transport and sodium/amino acid co-transport

A

most important in postprandial period in jejunum

secondary active transport and electrogenic

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12
Q

describe sodium/H+ exchange

A

occurs in duodenum and jejunum

stimulated by luminal bicarbonate

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13
Q

describe parallel sodium/H+ and Chloride/bicarbonate exchange

A

occurs in ileum and colon

most important in interdigestive period

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14
Q

describe epithelial sodium channels

A

occurs in the colon (distally)

regulated by aldosterone

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15
Q

where does sodium/glucose co-transport and sodium/amino acid co-transport take place

A

occurs throughout small intestine

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16
Q

how is parallel absorption of chloride driven by odium/glucose co-transport and sodium/amino acid co-transport

A

collectively the overall transport of sodium generates a transepithelial potential in which the lumen in negative - driving parallel absorption of chloride

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17
Q

action of aldosterone in epithelial sodium channels

A

opens channel
inserts channels into membrane from intracellular vesicle pool
increases synthesis of channels and NA+/K+-ATPase

18
Q

describe NHE1

A

cellular pH housekeeper

19
Q

how is Na+/H+ exchange stimulated

A

by the alkaline environment of the lumen due t presence of bicarbonate from the pancreas

20
Q

describe parallel sodium/H+ and Chloride/bicarbonate

A

primary mechanism of sodium absorption in the interdigestive period - absorption is electroneutral
does not contribute greatly to postprandial absorption

21
Q

how is parallel sodium/H+ and Chloride/bicarbonate regulated

A

via intracellular cAMP, cGMP and calcium - all reducing NaCl absorption (a cause of diarrhoea due to infection of E.Coli)

22
Q

describe epithelial sodium channels

A

mediates electrogenic sodium absorption in the distal colon;

highly efficient and important in sodium conservation

23
Q

how is epithelial sodium channels increased

A

via aldosterone;

not regulated by cAMP or cGMP

24
Q

action of aldosterone in epithelial sodium channels

A

opens channel
inserts channels into membrane from intracellular vesicle pool
increases synthesis of channels and NA+/K+-ATPase

25
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)
26
secondary messengers that indirectly activate CFTR
cAMP cGMP calcium
27
chloride absorption in large intestine
the driving force is provided by lumen negative potential due to electrogenic movement of sodium through epithelium sodium channels
28
how does chloride secretion occur
at a basal rate | usually overshadowed by a higher rate of absorption
29
where does chloride secretion occur
from crypt cells
30
processes involved on the basolateral membrane during chloride secretion
Na+/K+ATPase Na+/K+/2Cl- co-transporter (NKCC1) K+ channels (IK1 and BK)
31
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
32
how is CFTR indirectly activated
bacterial enterotoxins hormones and neurotransmitters immune cells products some laxatives
33
secondary messengers that indirectly activate CFTR
cAMP cGMP calcium
34
where does the chloride conductance mediated by CFTR result from
opening of channels at apical membrane | insertion of channels from intracellular vesicles into membrane
35
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 ```
36
outcomes of diarrhoea
dehydration - loss of sodium and water metabolic acidosis - loss of bicarbonate hypokalaemia - loss of potassium
37
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)
38
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
39
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
40
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