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Gastrointestinal > Lecture 7 and 8: The Small Intestine > Flashcards

Lecture 7 and 8: The Small Intestine Flashcards

1
Q

What is the basis for the digestion/absorption of nutrients in the small intestine?

A

intense motility and secretions in the lumen

large surface area of mucosal cells

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2
Q

Gastric emptying occurs after an ________ (increase/decrease) in intraluminal pressure in the proximal portion of the stomach

A

increase

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3
Q

What happens to duodenal segmental contractions during gastric emptying?

A

They are inhibited

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4
Q

What characteristics of the chyme do vagal afferents respond to?

A

1) acidity

2) hyperosmotic content

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5
Q

Which 2 factors contribute to the inhibition of slowing of gastric emptying?

A

1) fat in duodenum
2) H+ in duodenum

Which is mediated by CCK

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6
Q

When is CCK released?

A

when fatty acids are present in the duodenum

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7
Q

What effect does CCK have on gastric emptying?

A

SLOWS it - contracts pylorus to ensure there is sufficient time for fat to be digested/absorbed

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8
Q

What are the 2 main functions of CCK?

A

1) slow gastric emptying (contract pylorus)

2) relax sphincter of Oddi and contract gallbladder (promote bile and pancreatic secretion)

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9
Q

How does the duodenum detect low pH of chyme?

A

H+ receptors in mucosa –> relay message to gastric smooth muscle via interneurons of myenteric plexus

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10
Q

What are the 2 components of the exocrine pancreatic secretions?

A

1) Aqueous (HCO3)

2) enzymatic component

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11
Q

What is the function of HCOs in the aqueous secretion from the pancreas?

A

neutralize the H+ from the stomach

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12
Q

True or false: pancreatic enzymes are active at acidic pH

A

FALSE

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13
Q

Endocrine is __% of pancreas, exocrine is __%

A

2; 90

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14
Q

How does Secretin drive pancreatic ductal secretion?

A

increases cAMP in duct cells

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15
Q

the increase of cAMP in duct cells opens the CFTR ____ channels which allow an outflow of __ into the duct lumen

A

Cl-

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16
Q

The efflux of Cl- into the lumen drives the __________

A

Cl-/HCO3 antiporter

Cl comes back into cell, HCO3 goes out

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17
Q

Where does the ductal intracellular bicarb come from?

A

1) across basolateral membrane via NBC-1 symporter

2) generated intracellularly by carbonic anhydrase

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18
Q

What moves the H+ into the blood from the ductal cell?

A

Na/H exchanger

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19
Q

Since the CFTR transporter is so important in secreting HCO3 to neutralize the acid, what happens in patients with cystic fibrosis?

A

mutated CFTR so HCO3 secretion is defective (decrease in pancreatic ductal secretion so acinar enzymes are not washed out ultimately destroying the gland)

20
Q

Which cells release CCK?

A

I cells

21
Q

What 3 things trigger CCK release?

A

1) direct interaction of fatty acids or amino acids with I cells
2) binding of fatty acids or amino acids or both to sensor paracrine cells that release CCK-RP
3) release of monitor peptide by pancreatic acinar cells

22
Q

What are the 2 ways CCK stimulates acinar secretion in the pancreas?

A

ENDOCRINE: binds to CCK1 receptor

NEURAL reflexes: activate vagovagal reflex leading to release of Ach, GRP, and VIP by enteric neurons

23
Q

How do CCK, Ach, and GRP effect the release of acinar enzymes?

A

mobilize intracellular Ca++ which phosphorylates various structures and moves enzyme-filled granules to the apical membrane where they fuse and release their contents

24
Q

Where are pancreatic enzymes activated from their zymogen form to their active form?

A

lumen of duodenum

25
Q

What else do pancreatic enzymes contain that prevent premature activation of enzymes?

A

Trypsin inhibitors

26
Q

What stimulates secretin release?

A

acidic pH (below 4.5) of the lumen

27
Q

What 4 things can increase pancreatic secretion in the intestinal phase?

A

1) secretin
2) CCK secretion
3) enteropancreatic reflexes (from distention/hypertonicity)
4) vagovagal reflexes (from CCK sensory enteric neurons)

28
Q

Bile is synthesized and secreted by _____________ into the _____ ____________.

A

hepatocytes; bile cannaliculi

29
Q

CCK stimulates the ________ of the gallbladder and ________ pf the sphincter of Oddi

A

contraction; relaxation

30
Q

Major constituents of bile:

A 
65% bile acid
20% phospholipids
5% protein
4% cholesterol
0.3% bile pigments
5-6% electrolytes
31
Q

Bile acids are _________ and form micells

A

detergents

32
Q

The majority of bile acid is recycled from intestine back to liver via ___________ __________

A

enterohepatic circulation

33
Q

True or false: conjugated bile acids can cross the intestinal epithelium

A

FALSE

34
Q

How are conjugated bile acids reabsorbed at the terminal ileum?

A

Na-dependent bile acid transporter (asbt)

it is a symporter

35
Q

What happens to bile that reaches the colon?

A

becomes deconjugated and is passively reabsorbed

36
Q

What are the 2 contractile activities that exist in the small intestine?

A

1) Segmentation

2) Peristalsis

37
Q

What are segmentation contractions?

A

chyme splits and goes both caudad and orad directions, merges again and mixes

38
Q

Where do segmentation contractions occur?

A

small and large intestine

39
Q

Where do peristaltic contractions occur?

A

pharynx, esophagus, gastric antrum, small and large intestine

40
Q

Describe the movement of a peristaltic contraction

A

area orad to the bolus contracts while area caudad to it relaxes, propelling bolus forward

41
Q

What regulates orad contractions in PERISTALSIS

A

Ach and Substance P

42
Q

What regulates caudad relaxation in PERISTALSIS

A

VIP and nitric oxide

43
Q

What is the migrating motor complex?

A

periodic contractions mediated by hormone MOTILIN that occur to clear the remaining gastric and intestinal contents out of the way

44
Q

After a meal, MMC and motilin levels _____ (increase/decrease)

A

decrease

45
Q

What is the function of Brunner glands in the small intestine?

A

secrete mucus and bicarb

46
Q

What do Paneth cells secrete?

A

antimicrobial peptides and enzymes

Gastrointestinal (8 decks)

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