Gastrointestinal Physiology (con'd) Flashcards

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1
Q

What is the cephalic phase?

A

Vagus nerve (thinking about, smelling, or tasting food) stimulates the ENS to produce acid, gastrin and HCl, and Histamine
this occurs before you eat
Prepartory process

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2
Q

what is the negative feed back mechanism if pH is too low?

A

causes D cells to release somatostatin which inhibit G cells, ECL cells, and parietal cells

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3
Q

what is the gastric phase?

A

when food is present in stomach triggers gastointestinal reflex. Baroreceptors detect enlargment of stomach and chemoreceptors respond to food (sent via vagus nerve), stimulating goblet cells, parietal cells, G cells and chief cells

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4
Q

what happens to food when the pH gets too low?

A

movement of food slows down

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5
Q

what is the intestinal phase?

A

signal coming from the intestine to prepare for incoming food

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6
Q

what is the enterogastric reflex?

A

signal from intestine snt to stomach. chemoreceptors detect pH and good contents, causing hormone secretin to be secreted.

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7
Q

what does secretin do?

A

inhibits gastric function via parietal/chief cell

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8
Q

what other molecules inhibit stomach function which is stronger

A

gastric inhibitory peptide (GIP) - stronger

cholecystokinin

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9
Q

what does the D cell do?

A

secretes somatostatin in response to H+ which acts on G cell, parietal cell, and ECL cells

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10
Q

what are the two classes of drugs that prevent acid secretion? which is irreversible?

A

H2 blockers

proton pump inhibitors (irreversible)

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11
Q

why are NSDAIDs bad for the stomach?

A

prevents prostaglandin synthesis

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12
Q

why are NSDAIDs bad for the stomach?

A

prevents prostaglandin synthesis which regulated gastric secretion

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13
Q

what are two 2 COX enzymes?

A

constitutive COX 1

inducible cox 2

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14
Q

what is the difference between cox 1 and cox 2?

A

cox 1 - works all the time and makes a low, protective dose of PG
cox 2 - makes no PG when turned off, but makes a lot when turned on (pro inflammatory)

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15
Q

what is the difference between 1st and 2nd generation NSAIDs?

A

1st - non specific (block both cox 1 and cox2)

snd - block cox 2 only

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16
Q

what is a downside to 2nd generation NSAIDs?

A

can cause heart attack

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17
Q

what are NO-NSAIDs?

A

Nitric oxide NSAIDs (modified NSAID)
have nonselective COX inhibition and NO release causes vasodilation (protective)
CINODs are also non-specific

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18
Q

what is the difference between endocrine and exocrine pancreas?

A

endo - pancreatic islets

exo - pancreatic duct

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19
Q

how much pancreatic juice is secreted a day?

A

1500ml/day

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20
Q

what are the two components of pancreatic juice?

A

1) aqueous which has Na-HCO3 solution (buffer stomach pH)

2) enzyme - proteolytic enzymes (zymogens), pancreatic amylase/lipases

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21
Q

what 3 things control pancreatic secretion?

A

vagus nerve
cholecystokinin
secretin

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22
Q

how does the vagus nerve control pancreatic secretion?

A

activates Ach? (parasym) which is excitatory and promote excretion or NE (sym) which inhibits secretion

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23
Q

how does cholecystokinin control pancreatic secretion?

A

detects lipids and has positive effect on pancreas but negative effect on stomach
also decreases gastric emptying

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24
Q

how does cholecystokinin control pancreatic secretion?

A

detects lipids and has positive effect on pancreas but negative effect on stomach
also decreases gastric emptying

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25
Q

how does secretin affect pancreatic secretion?

A

when acidic contents reach the stomach, it causes secretin release which acts on pancreas to increase aqueous secretion
also decreases gastric emptying

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26
Q

what is the function of the liver?

A

continually produce bile

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27
Q

what is the function of bile?

A

neutralization via HCO3

emulsification via bile salts to solubilize oils

28
Q

what 3 things control gall bladder emptying?

A

cholecystokinin (gall bladder contraction and relaxation of sphincter of Oddi)
parasym Ach (weak)
secretin

29
Q

when is cholecystokinin (CCK) released?

A

when fats are released into duodenum

30
Q

what are crypts of lieberkuhn?

A

look similar to gastric glands in stomach but are in small intestine
they secrete by young cells at bottom of crypt

31
Q

what is the function of the villi?

A

absorption site

32
Q

what are the 2 kinds of secretion from the small intestine?

A
watery secretion (containing electrolytes)
mucoid secretion
33
Q

what is the difference between immature and mature epithelial cells?

A

immature - secrete within crypt (watery usually)

mature - absorb

34
Q

why have lots of watery secretion?

A

to keep openings clean from bacteria

35
Q

what pump does secretion work though in small intestine? how does it work?

A

chloride pumps
Cl is moved from one side of epithelium to the other which is turned on by cAMP
Na ions are involved in another pump (water follows) to balance charge

36
Q

what are two epithelial cell types in the small intestine? what do they release?

A

paneth - cryptdins and defensins

goblet cells - mucus

37
Q

what 3 things control small intestinal secretion?

A

1) local distension (when food is present)
2) secretin/CCK (minor)
3) secretagogues

38
Q

what 3 things control small intestinal secretion?

A

1) local distension (when food is present)
2) secretin/CCK (minor)
3) secretagogues

39
Q

what is the function of the mucus in the large intestine?

A

lubrication

adhesive medium for conversion of chyme into feces

40
Q

what 4 things control large intestine secretion?

A

1) tactile stimulation
2) local distension
3) parasym NS (incr production)
4) emotions, stress (diarrhea)

41
Q

what causes cholera?

A

vibrio cholerae in contaminated food/water

42
Q

what does cholera do to the body?

A

causes severe gastroenteritis in children, leading to severe diarrhea, dehydration, and death

43
Q

what are the two subunits of cholera toxin and how do they enter the cell?

A

B and A subunits

1) B subunit binds to enterocyte membrane with high affinity
2) A subunit releases towards the membrane and enters cell membrane

44
Q

what does cholera toxin (A subunit) do once it’s entered the cell?

A

1) splits into two smaller subunits (A1 and A2)
2) activates adenylate cyclase
3) converts ATP to cAMP, which is a potent Cl secretagogue

45
Q

what effects does the cholera toxin have once cAMP is produced?

A

increased Cl secretion, which affects Na and water

Hypersecretion of H2O leading to severe dehydration

46
Q

how do you treat cholera?

A

oral rehydration therapy, making intake more than output

47
Q

what is cystic fibrosis caused by? what effect does this have? why is this significant

A

caused by disfunctional CFTR, which causes little Cl and water secretion, and creates a thick mucus
CF can offer some protection against cholera

48
Q

where does enzymatic digestion start and end?

A

mouth

small intestine

49
Q

what 4 structures secrete digestive enzymes?

A

salivary glands
gastric pits
exocrine pancreas
liver

50
Q

what is the difference between simple and complex carbs?

A

complex: polysaccharides (starch, glycogen, cellulose)
simple: disaccharides (sucrose, lactose, maltosE) and monosaccharides (glc, fru)

51
Q

what structures secrete amylase?

A

salivary gland
gastric pits
pancreas
luminal?

52
Q

what are 2 brush border enzymes?

A

sucrase-isomaltase (sucrase, maltase)

lactase

53
Q

what are 2 brush border enzymes?

A

sucrase-isomaltase (sucrase, maltase)

lactase

54
Q

what receptors are located on the Apical membrane? Basolateral membrane?

A

Apical:SGLT1 (Glu and Gal), GLUT5 (Fru)
Basolateral: GLUT2 (Monosaccharides)

55
Q

how does each receptor transport carbohydrates across the membrane?

A

SGLT1: secondary active transport
GLUT5: facilitated diffusion
GLUT2: facilitated diffusion

56
Q

what are glucose levels in the blood, cytoplasm, and lumen?

A

blood: 4-7mM
cytoplasm: 10mM
lumen: 1-40mM

57
Q

what processes break down protein?

A

1) mastication
2) denaturation
3) acid hydrolysis (activation of pepsinogen)
4) enzymatic breakdown (break peptide bonds)
5) proteolytic enzymes (non specific)
6) endopeptidases (pepsin, trypsin, chymotrypsin)
7) exopeptidases

58
Q

what is the end result of protein digestion?

A

AAs and short peptide chains

59
Q

what is the end result of protein digestion?

A

AAs and short peptide chains

60
Q

how are small peptides carried across the cell?

A

carried intact via transcytosis

61
Q

what happens to tri- and di-peptidases in the cell?

A

proton pumps pump peptide inside
peptidases in cytoplasm break them down into AAs
single AAs are transferred into cell with Na

62
Q

what 3 enzymes break down lipids?

A
salivary lipase
gastric lipase
pancreatic lipase (monoglycerides and FFAs)
63
Q

what 3 enzymes break down lipids?

A
salivary lipase
gastric lipase
pancreatic lipase (monoglycerides and FFAs)
64
Q

how much water is absorbed in the small intestine and large intestine?

A

small - 92% (osmosis)

large - 6-7%

65
Q

what is giardia lamblia?

A

common intestinal parasite transmitted via fecal-oral

66
Q

how does G. lamblia affect the body?

A

disrupts cytoskeleton
and causes MLCK activation to increase paracellular permeability?
leading to decreased digestion, reduced absorption and diffuse microvillus shortening