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FHB GI > 51 Small Intestine > Flashcards

51 Small Intestine Flashcards

1
Q

Generally, what things occur during the small intestinal phase of digestion?

A
  • Increased GB contraction.
  • Relaxation of the sphincter of Oddi.
  • Secretion of pancreatic and biliary juices.
  • Regulation of gastric emptying (control of pylorus).
  • Inhibition of gastric secretion
    (Intense motility and secretions in the lumen and a large surface area of mucosal cells are the basis for digestion/absorption of nutrients).
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2
Q

What is occurring (generally) after gastric emptying, in terms of gastric and duodenal contractions?

A
  • An increase in tone (intraluminal pressure) in the proximal portion of stomach
  • Increased strength of antral contractions
  • Opening of the pylorus
  • Simultaneous inhibition of duodenal segmental contractions
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3
Q

In what two general ways does chyme entering the duodenum inhibit gastric emptying?

A

Hormonal and neural (vagal) pw’s

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4
Q

*During inhibition of gastric emptying, vagal afferents respond to ___________________ of chyme as it enters duodenum.

A

Nutrients (H+ and hyperosmotic content)

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5
Q

What happens to feedback inhibition on gastric emptying after the chyme moves further down the small intestine?

A

It stops (gastric emptying starts again)

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6
Q

*In addition to the vagal inhibition of gastric emptying, the presence of what 2 substances contribute to inhibition/slowing of gastric emptying?

A

Fat and H+ in the duodenum

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7
Q

The effect of fat on slowing gastric emptying is mediated by _____________, which is secreted when fatty acids are present in the duodenum.

A

Cholecystokinin (CCK)

Contracts pyloric sphincter

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8
Q

Besides pyloric contraction, what other effects does CCK have on the GI system distal to the stomach?

A

CCK also regulates gallbladder contraction, relaxation of sphincter of Oddi, and pancreatic secretion.

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9
Q

The effect of H+ on slowing gastric emptying is mediated by ____________________.

A

the ENS (reflexes)

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10
Q

During inhibition of gastric emptying, H+ receptors in the duodenal mucosa detect the low pH of chyme and relay this to gastric smooth muscle via interneurons in the ________________.

A

Myenteric plexus

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11
Q

Why would gastric emptying be inhibited by fat?

H+?

A
  • To make sure there is time for fat digestion/absorption

- To make sure there is ample time is available for neutralization of acid by pancreatic HCO3-

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12
Q

What are the 2 general components of pancreatic secretions?

A
  1. An aqueous component, high in HCO3-

2. An enzymatic component

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13
Q

Secretions from what organ/gland are the largest contributors to enzymatic digestion of the meal?

A

Pancreas (exocrine)

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14
Q

Which contributes the most HCO3- towards digestion:

a. salivary glands of face
b. biliary ductules
c. duodenal epithelial cells
d. exocrine pancreas

A

d. exocrine pancreas

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15
Q

*Why is having HCO3- in pancreatic secretions important?

give pancreatic reason + stomach reason

A

Pancreatic enzymes are not active at acidic pH.

- Also, this neutralization reduces the possibility of intestinal mucosal damage by incoming gastric acid and pepsin

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16
Q

*Describe the general pathway of ducts from the liver + GB + pancreas to the duodenum.

A

R/L hepatic ducts from liver to common hepatic duct (which receives input from GB via cystic duct) to common bile duct (which receives input from pancreatic duct) to sphincter of Oddi

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17
Q

What 4 hormones are released from the endocrine pancreas (2% of pancreatic volume)?

A
  • Insulin
  • Glucagon
  • Somatostatin
  • Pancreatic polypeptide
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18
Q

Name the 3 general cell types along the pathway a secretion will take in a pancreatic exocrine gland.
(hint: it’s similar to salivary gland construction)

A
  1. Acinar cells
  2. Centroacinar cells
  3. Ductal cells
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19
Q

What is the general role of centroacinar cells of the pancreatic ducts?

A

Help in contracting the surrounding acinar cells to move pancreatic juice through the ducts.

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20
Q

What is an acinus of a pancreatic duct?

What do acinar cells secrete, generally?

A

The blind end of a branching ductular system – lined by acinar cells.
- Secrete the enzymatic component of pancreatic secretions.

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21
Q

What do centroacinar cells of a pancreatic duct secrete, generally?
What about the ductal cells?

A

They both secrete the aqueous component of pancreatic secretions.

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22
Q

What hormone stimulates the acini of pancreatic ducts?

A

CCK (acinar fluid)

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23
Q

What hormone stimulates the ductal part of pancreatic ducts?

A

Secretin (ductal fluid)

24
Q

Does CCK or secretin influence pH regulation more in the pancreas?
Explain the general process, including where the hormone comes from, what pH triggers hormone release, and how the system stops.

A

Secretin

  • The ducts are the effectors of a pH regulatory system
  • When luminal pH is below ~4.5, the S cells (in the small intestinal epithelium) are triggered to release Secretin
  • Secretin stimulates secretion of HCO3-
  • Negative feedback stops secretin release
25
Q 
*Secretin increases what second messenger in pancreatic duct cells?
What intracellular (ductal cell) changes occur w/secretin stimulation?
A

cAMP

  • CFTR Cl- channels: Cl- flows to lumen, driving HCO3- via Cl-/HCO3- antiporter
  • Recall: Cl- generated via alkaline tide from gastric phase
26
Q

What are the 2 ways which HCO3- gets into a pancreatic ductal cell (so that secretin can eventually trigger its release)?

A
  1. NBC-1 (Na+/HCO3- cotransporter)

2. CO2 diffusion in + CA

27
Q

How is H+ absorbed (after HCO3- is created via CO2 diffusion and secreted) in pancreatic ductal cells?

A

NHE-1 (Na+/H+ exchanger)

28
Q

What is the net result of acidic/basic changes via secretin stimulation on pancreatic ductal cells?

A
  • Secretion of HCO3- in the lumen

- Absorption of H+, acidification of pancreatic venous blood

29
Q

Explain the changes in the pancreas w/r/t cystic fibrosis, and how this occurs on the cellular level.
(CF is a genetic disease that affects function of various epithelial organs – lung, intestine, biliary system and pancreas)

A
  • *CFTR (cystic fibrosis transmembrane conductance regulator) is mutated. As a result, the bicarbonate secretory process is defective
  • Results in a decrease in pancreatic ductal secretion, high concentration and precipitation of the acinar enzymes in the duct, ultimately destroying gland.
30
Q

*What are the 3 ways that CCK (from I cells) is triggered (to eventually affect acinar cell stimulation in the pancreas).

A
  1. Direct interaction of FAs or AAs or both with I cells themselves.
  2. Binding of FAs or AAs or both to sensor paracrine cells that release CCK-RP (CCK-releasing factor or peptide) from duodenal cells
  3. By the release of monitor peptide by pancreatic acinar cells.
31
Q

In what 2 ways does CCK stimulate acinar cell secretion in the pancreas?

A
  1. As an endocrine factor, binds to acinar cell CCK1 receptor.
  2. Stimulates neural reflexes that impinge on the pancreas – activates vagovagal reflex that leads to the release of ACh, GRP and VIP by pancreatic enteric neurons.
32
Q

When CCK, GRP, and ACh act on pancreatic acinar cells, what is the intracellular 2nd messenger?
*What eventually happens?

A

Ca2+

- Pre-synthesized enzymes (stored in zymogen granules) will be exocytosed and washed away by ductal secretions

33
Q

Pancreatic proteases are secreted in inactive forms and converted to their active forms in the lumen of duodenun. This is initiated by _____________.

A

Trypsin

34
Q

Premature activation of pancreatic proteases before reaching appropriate site can result in what dz?
Pancreatic enzymes contain ______________________ to prevent this.

A

Pancreatitis

- Trypsin inhibitors (Trypsin can be inhibited by other trypsin molecules)

35
Q

Some people have genetic mutations where trypsin is resistant to degradation, which can lead to what major dz?

A

Pancreatitis

36
Q

Do pancreatic secretions occur during the cephalic phase of digestion? *How?

A

Yes (via vagal and enteric nerves)

37
Q

*How do pancreatic secretions occur during the gastric phase of digestion?

A

Via stomach distension leads to vagovagal and gastropancreatic reflexes

38
Q

Name 4 ways by which pancreatic secretions are stimulated during the intestinal phase.

A
  1. pH less than 4.5 in lumen causes secretin release, leads to ^ pancreatic secretion
  2. Peptides, AAs, FAs stimulate ^ CCK secretion, leads to ^ pancreatic secretion
  3. Distention/hypertonicity leads to enteropancreatic reflexes which leads to ^ pancreatic secretion
  4. CCK sensory enteric neurons leads to vagovagal reflexes which leads to ^ pancreatic secretion
39
Q

Bile is synthesized and secreted by ____________ into the bile canaliculi that drain into the bile ducts.

A

hepatocytes

40
Q

Where is bile stored + concentrated?

What does bile help digest?

A

GB

- lipids

41
Q

What hormone stimulates the contraction of GB and relaxation of the Sphincter of Oddi.

A

CCK

42
Q

What are the 2 largest components of bile?

A
  1. Bile acids – 65%

2. Phospholipids (mainly lecithins = PC) – 20%

43
Q

What does bile form in order to aid in lipid digestion??

A

Bile acids are detergents and form micelles.

- These micelles shield the hydrophobic fats from the aqueous environment of lumen.

44
Q

What happens after bile is used and continues flowing down the intestinal tract? (be specific)

A

The majority of the bile acid pool is recycled from the intestine back to the liver via enterohepatic circulation. (reaches terminal ileum mostly, w/some at colon)

45
Q

Which bile reaches the terminal ileum, how is it reabsorbed?
What if some of it makes it to the colon?

A

Actively via Na+ -dependent bile acid transporter (asbt)

- At colon, there is minimal passive reabsorption

46
Q

What 2 contractile activities occur in the small intestine?

A

Peristalsis and segmentation

47
Q

Segmentation contractions occur predominantly in what 2 organs?

A

The small and large intestine

48
Q

(Review) In peristaltic contraction on the small intestine, orad contraction is regulated by ________ and _______, and caudad relaxation is regulated by ________ and _______.

A
  • Orad contraction: ACh + Substance P

- Caudad relaxation: VIP + NO

49
Q

*What is the Migrating Motor Complex (MMC) of the small intestine?
What hormone mediates it?

A

Contracts that occur at 90 min intervals to clear any remaining gastric and intestinal contents out into the colon.

  • Motilin mediates it
  • After a meal, motilin levels fall, MMC is suspended.
50
Q

What 3 major glands would you find in the small intestine?

A
  1. Brunner’s glands
  2. Lieberkühn glands (crypts)
  3. Paneth cells
51
Q

What do Brunner’s glands secrete?

A

Mucus + bicarbonate

52
Q

What do crypts of Lieberkühn secrete?

A

Peptidases + carb-digesting enzymes

53
Q

What do Panneth cells secrete?

A

Antimicrobial peptides and enzymes (ribonuclease, esterase, etc.)

54
Q

Where are Panneth cells located?

A

Bottom of villi (in submucosa of duodenum)

55
Q

Describe the general structure of the small intestine’s villi and crypts.

A

Long villi, short crypts

  • Simple columnar epithelium w/brush border
  • Increased SA
56
Q

Do EEC’s release substances to the luminal side or basolateral side?

A

Basolaterally towards the blood (hormones)

57
Q

What types of cells are found directly above Panneth cells in the small intestine?

A

Stem cells

FHB GI (10 decks)

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