Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Gastrointestinal > Physiology of Fluid Balance > Flashcards

Physiology of Fluid Balance Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

contents of faeces

A

water
cellulose
bilirubin
bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

definition of diarrhoea

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

is water ingested and secreted balanced with water absorbed

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how is absorption of water in the GI driven

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how may water move during absorption

A

via transcellular or paracellular routes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how is sodium/H+ exchange stimulated

A

luminal bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

occurs in ileum and proximal colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where do epithelial sodium channels occur

A

occurs in the colon (distally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

describe sodium/H+ exchange

A

occurs in duodenum and jejunum

stimulated by luminal bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe parallel sodium/H+ and Chloride/bicarbonate exchange

A

occurs in ileum and colon

most important in interdigestive period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

describe epithelial sodium channels

A

occurs in the colon (distally)

regulated by aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

occurs throughout small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

how does chloride absorption occur

A

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
Q

secondary messengers that indirectly activate CFTR

A

cAMP
cGMP
calcium

27
Q

chloride absorption in large intestine

A

the driving force is provided by lumen negative potential due to electrogenic movement of sodium through epithelium sodium channels

28
Q

how does chloride secretion occur

A

at a basal rate

usually overshadowed by a higher rate of absorption

29
Q

where does chloride secretion occur

A

from crypt cells

30
Q

processes involved on the basolateral membrane during chloride secretion

A

Na+/K+ATPase
Na+/K+/2Cl- co-transporter (NKCC1)
K+ channels (IK1 and BK)

31
Q

process of chloride secretion

A

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
Q

how is CFTR indirectly activated

A

bacterial enterotoxins
hormones and neurotransmitters
immune cells products
some laxatives

33
Q

secondary messengers that indirectly activate CFTR

A

cAMP
cGMP
calcium

34
Q

where does the chloride conductance mediated by CFTR result from

A

opening of channels at apical membrane

insertion of channels from intracellular vesicles into membrane

35
Q

causes of diarrhoea

A 
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
Q

outcomes of diarrhoea

A

dehydration - loss of sodium and water
metabolic acidosis - loss of bicarbonate
hypokalaemia - loss of potassium

37
Q

treatment of diarrhoea

A

maintenance of fluid and electrolyte balance (first priority)
use of anti-infective agents (if appropriate)
use of non-antimicrobial antidiarrhoeal agents (symptomatic)

38
Q

how may the absorption of NaCl be impaired

A

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
Q

how may excessive secretion be a cause of diarrhoea

A

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
Q

describe rehydration therapy for diarrhoea

A

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

Gastrointestinal (71 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions