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FHB - GI/Metabolism - Exam 3 > Lecture 7 - Integrated Response to a meal > Flashcards

Lecture 7 - Integrated Response to a meal Flashcards

1
Q

The following describes what area:

  1. Most significant site for digestion and absorption of nutrients in the GI system
  2. Intense motility and secretions & large surface area of mucosal cells
  3. Gallbladder contraction
  4. Relaxation of sphincter of Oddi
  5. Secretion of pancreatic/bile juices
  6. Regulation of gastric emptying
  7. Inhibition of gastric secretion
A

SMALL INTESTINE

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2
Q
  1. Emptying the gastric contents into the duodenum is slow or fast?
  2. What empties faster: liquids or solids?
  3. What empties more rapidly: Isotonic, Hypertonic, or Hypotonic?
  4. What size must particles be reduced to? Via what mechanism?
A
  1. SLOW –> 3 hours
  2. Liquids
  3. Isotonic is more rapid
  4. Must be smaller than 1 mm3
    - via RETROPULSION
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3
Q

What are the 4 requirements for gastric emptying to occur?

A
  1. Increase in TONE of proximal portion of stomach (more pressure!!!)
  2. Increased strength of astral contractions
  3. Opening of the PYLORUS
  4. Inhibition of duodenal segments
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4
Q

Feedback inhibition of gastric emptying occurs when what occurs?

What are the pathways of control? (2)

What is the affect of the following on gastric emptying?:

  1. Vagal Afferents
  2. Vagal Efferents (3)
A
  1. Inhibition of emptying occurs when the food enters the duodenum
  2. Neural & Hormonal
  3. Afferents –> stimulated by nutrients (H+ and hyper osmotic contents) as it enters duodenum

Efferents:
-decrease the strength of ANTRAL contractions

  • CONTRACTS the pylorus
  • and decrease proximal gastric motility
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5
Q

When does feedback inhibition stop/is reduced?

Why does this occur?

A

When the chyme moves further down the small intestine
- therefore gastric emptying starts again

** duodenum has balanced the chyme from hyper osmotic to isosmotic chyme, and stomach has neutralized acid components thus the food can move on**

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6
Q

What are the 2 major factors that contribute to inhibition/slowing of gastric emptying?

What mediates this affect?? When is this secreted?

A
  1. Presence of fat in duodenum
  2. Presence of H+ (low pH) in duodenum
  3. CCK!!!
    - secreted when FATTY acids are present in the duodenum
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7
Q

What is the function of CCK on:

  1. Gastric emptying
  2. Pylorus tone
A
  1. Slows gastric empyting
  2. Pyloric contraction
    * CCK slows so that there is enough time to digest the FAT and absorb it

ALSO regulates gallbladder contraction & relaxation of sphincter of do and pancreatic secretion!!!

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8
Q

The presence of the following in the duodenum stimulate what?

  1. Fat
  2. Protein
  3. Partially digested protein
A

CCK!

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9
Q

What mediates the effect of H+?

The receptors in the duodenal mucosa detect the low pH and relay this Where??
Via what?

A
  1. Reflexes in the ENTERIC nervous system

2. Relay to the GASTRIC smooth muscle via interneurons of MYENTERIC plexus

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10
Q

What does the H+ reflex from the duodenal mucosa to the gastric smooth muscle ensure?

A

That gastic contents are slowly delivered to duodenum

  • time for neutralization of acid by pancreatic HCO3-
  • critical for proper enzymatic function
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11
Q

What do the following have in common:

  1. Hormonal system (CCK)
  2. Neural System (Enteric System)
A

CCK and Enteric system can both INHIBIT gastric emptying

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12
Q

What is the difference between endocrine & exocrine function of the pancreas?

A

Endocrine:
- releases hormones like insulin & glucagon

Exocrine:
-releases all enzymes responsible for digestion

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13
Q

What are the two components of Pancreatic Secretion?

A
  1. Aqeuous component (HCO3-)
    - neutralizes the H+ delivered to duodenum
  2. Enzymatic Component
    - digests carbs, proteins, and lipids
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14
Q

Secretions from WHERE are the LARGEST contributors to enzymatic digestion of the meal?

Why are these specific secretions important?

A

PANCREATIC secretions

  • also largest contributor of Bicarb ions for neutral pH
    (biliary ductules & duodenal epithelial cells contribute to this)

Pancreatic enzymes are not active at acidic pH
- neutralization also reduces possibility of intestinal mucosal damage by incoming gastric acid & pepsin

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15
Q

What are the 2 functions of bicarbonate?

A
  1. Protect gastric mucosal cells

2. maintain NEUTRAL pH
pepsin has high activity at acidic pH

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16
Q

The following are released from where: (specifically)

  1. Insulin
  2. Glucagon
  3. SOMATOSTATIN
A

Endocrine Pancreas

  • Islets of Langerhans
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17
Q

What is the function of somatostatin?

A

Initiates feedback mechanism when pH drops too low by inhibiting G stomach cells

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18
Q

Describe the structure of the EXOCRINE PANCREAS. (3)

What is it similar in structure to?

A
  1. Ducts & Acini & Centroacinar cells (ducts that extend into the acinus)
  2. Similar to SALIVARY glands
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19
Q

What do the following secrete:

  1. Acinar Cells
  2. Ductal Cells

What is the importance of ductal secretions?

A
  1. Acinar = ENZYMATIC
  2. Centroacinar & Ductal cells secrete aqueous component
    - ductal secretions need to wash out the enzymes so they are not concentrated
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20
Q

If enzymes are concentrated in the acinus due to the lack of ductal cell secretions, what can become activated?

Why is this a concern?

A

TRYPSIN!

  • a concern because it is activated in the PANCREAS instead of the duodenum
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21
Q

What stimulates the following:

Pancreatic

  1. Acinar Cells
  2. Ductal Cells
A

Pancreatic
1. Acinar Cells = CCK!

  1. Ductal Cells = SECRETIN!
22
Q
  1. What are the EFFECTOR arms of a pH regulatory system?
  2. Which cells are activated in the small intestine when luminal pH is below 4.5?
  3. What do these cells release?
A
  1. DUCTAL cells
  2. S cells sense low pH
  3. S cells trigger the release of SECRETIN
23
Q

Describe the following for SECRETIN:

  1. Stimulus
  2. Function
  3. Feedback?
A
  1. low pH in ductal cells of pancreas, S cells of small intestine release Secretin
  2. Secretin secreted BICARBONATE from DUCTAL cells
    - increases the pH
  3. Negative feedback to stop secretin release
24
Q

Where are S cells found?

A

DUODENUM (small intestine)

25
Q

What stimulates the DUCTAl bicarbonate secretion from the pancreas?

A

Secretin!

26
Q
  1. Secretin increases ______ in duct cells.
  2. This opens ______ channels and causes an outflow of ___ into the duct lumen.
  3. This drives the antiporter that exchanges _____ ions for _______.
A
  1. cAMP!
  2. CFTR Cl- channels (diffuse out into the lumen)
  3. Cl goes in, Bicarbonate exchanged OUT
27
Q

What are the 2 sources for bicarbonate in pancreatic Ductal Secretion?

A

Two sources for bicarbonate:

  1. taken across basolateral membrane via symporter NBC-1 (Na-bicarbonate cotransporter type 1).
  2. generated intracellularly by carbonic anhydrase.
28
Q

What is the NET RESULT of secretin on ions?

  1. Secretion
  2. Absorption
A
  1. Secretion of HCO3-
    (stored from previous absorption during alkaline tide)
  2. Absorption of H+, acidification of pancreatic venous blood
    - secretin’s main goal is to INCREASE cAMP in ductal cells! which stimulates the CFTR Cl- channels
29
Q

What channel is mutated in Cystic Fibrosis patients? How does this affect the pancreatic ductal cells?

How does this lead to acute/chronic pancreatitis?

What else do these patients suffer from?

A
  1. CFTR Cl-
  2. No Cl coming out, thus none exchanged for bicarbonate –> NO BICARBONATE to increase pH

no bicarbonate secretion and thus no water secretion
* DUCTAL SECRETION IS AFFECTED

-the enzymes in the acinar cells are not being transported out they build up and suffer from ACUTE PANCREATITIS or chronic pancreatitis due to activated TRYPSIN via ductal secretions

SUFFER FROM: Steatorrhea (fatty stool) and malabsorption

30
Q

Secretin increases cAMP which opens what channels?

A

opens CFTR Cl-

31
Q

What are two purposes of the Secretin test?

A
  1. Assess normal function of pancreas to see if ductal cells produce bicarbonate
  2. Used to detect Gastrinoma (Zollinger-Ellison)
    - -secretin levels cause the increase in gastrin, so if these levels are extremely HIGH this is a positive test
32
Q

Define the following for CCK:

  1. Released from what cells
  2. Direct stimulation
  3. Indirect stimulation
  4. Neurally stimulation of CCK?
A
  1. I cells in duodenum & jejunum
  2. Direct: small peptides/amino acids and fatty acids
  3. Indirect: BINDING of fatty acids or amino acids to sensor PARACRINE cells that release CCK-RP!
  4. release of Monitor Peptide by pancreatic acing cells stimulates CCK
    (vagus/enteric stimulation via Ach or GRP)
33
Q

The following are both negatively regulated by what?

  1. CCK-RP
  2. Monitor Peptide
A

TRYPSIN

  • competes with the monitor peptide & CCK-RP for the bolus of food
34
Q

When trypsin has digested all the CCK-RP and Monitor peptide, what is inhibited??

When is trypsin active and inactive?

A

CCK release is inhibited!

  • nothing stimulating the I cells

Active trypsin: when all the proteins & peptides have been digested

Inactive: when plenty of proteins are available for trypsin it is less active since CCK is stimulated

35
Q

CCK has both endocrine and paracrine function,

Describe the two.

What is activated in the paracrine function? Which NT’s specifically?

A
  1. Endocrine:

CCK binds to acinar cell CCK-1 receptor
(transported in blood)

  1. PARACRINE: Stimulates the NEURAL reflexes
  • activates vasovagal reflex to release
    1. Ach
    2. GRP
    3. VIP
  • stimulates enzyme secretion by acing cells & potentiates the effect of secretin on HCO3- secretion (like CCK)
36
Q

The following are receptors for what?

  1. CCK-B
  2. CCK1
A
  1. Gastrin receptor!

2. CCK receptor!

37
Q

What are the effects of CCK, ACh, and GRP in the pancreas?

A

Stimulate enzyme secretion by ACINAR cells

  • mobilize intracellular calcium
  • phosphorylate proteins
  • zymogen granules move to apical membrane, fuse
  • and then exocytosed into the lumen to be washed by DUCTAL secretions
38
Q

What is the mechanism by which acinar cells secrete enzymes?

A

EXOCYTOSIS of zymogen granules

39
Q

What initiates the conversion of pancreatic proteases into their active forms?

Where does this occur?

What does premature activation of proteases result in?

A
  1. Trypsin
  2. lumen of duodenum
  3. Results in PANCREATITIS (since the proenzymes are secreted from the pancreas)
  • pancreatic enzymes have trypsin inhibitors to prevent premature inactivation
  • there are some genetic mutations that also result in trypsin resistant to degradation, leading to pancreatitis
40
Q

Histologically, what occurs in pancreatitis?

A

Acute pancreatitis : enzymes build up & you start to see FAT NECROSIS

  • lipase destroys the membranes of the fat cells, which causes necrosis of the cells
    • initiates strong inflammatory process
41
Q

What increases Pancreatic secretion in the following phases:

  1. Cephalic Phase
  2. Gastric Phase
  3. Intestinal phase (4 & associated hormones if relevant)
A
  1. Cephalic
    - sight, smell, and taste of food via VAGAL & enteric nerves
  2. Gastric:
    - distension of stomach = VASOVAGAL/gastropancreatic reflex)

3.
- pH vagovagal reflex

ALL INCREASE PANCREATIC SECRETIONS

42
Q

Where is bile:

  1. Synthesized/Secreted
  2. Stored
A
  1. Hepatocytes into the bile canaliculi that drain into bile ducts
  2. Gallbladder
43
Q

How does CCK affect Bile?

What is the main function of bile?

A
  1. CCK:
    - stimulates contraction of Gallbladder
    - relaxation of sphincter of Oddi

Fx: digestion/absorption of lipids

-BILE has no enzymatic activity but is very important for LIPID digestion (pre-processing)

44
Q

65% of bile is made up of what?

What is their function?

A

Bile Acids

  • prepares the lipids for digestion
45
Q

What are bile acids? What specific structure do they form?

A
  1. Detergent
  2. micelles
    - shield hydrophobic products of lipid digestion from aqueous environment of the lumen
46
Q
  1. What recycles bile acids?
  2. What specific attribute of Bile Acids makes them not able to cross the intestinal epithelial lining?
  3. Which apical simperer reabsorbs conjugate bile acids when the chyme reaches the TERMINAL ILEUM?
A
  1. Enterohepatic Circulation
  2. Conjugated Bile acids
  3. ASBT
    - apical Na dependent bile acid transporter

-A minor fraction of bile acids enters the colon –become deconjugated and is reabsorbed passively.

47
Q

Where is the main reabsorption of bile occurring? Which transporter?

A
  1. Terminal ileum

3. ABST

48
Q

What are the two contractile activities in the small intestine?

A
  1. Segmentation
    - small and large intestine
  2. Peristalsis
    - pharynx, esophagus, gastric antrum, small and large intestine.

segmentation = while digestion occurs

peristalsis = once digestion has finished

49
Q

Which of the following regulate Orad Contraction, and which regulate Caudad relaxation in peristalsis?

  1. Ach & Substance P
  2. VIP and NO
A
  1. Ach & Substance P
    - Orad contraction
  2. VIP and NO
    - caudad relaxation
50
Q

When does Migrating Motor Complex or MMC come into play?

Where does this occur?

What hormone mediates these periodic contractions?

A

During fasting!

  • in the duodenum and jejunum

Motilin!
- contractions at 90 minute intervals to clear any remaining gastric contents out of the intestine & into the colon

  • after meal MOTILIN levels fall, MMC stops
51
Q

Name the glands/cells that do the following in the SMALL INTESTINE:

  1. Brunner glands
  2. Lieberkuhn Glands
  3. Paneth Cells
A
  1. Brunner glands
    - secrete mucus and bicarbonate
  2. Lieberkuhn Glands
    - secrete peptidases and enzymes that digest carbs
  3. Paneth Cells
    reside at the bottom of villi & secrete antimicrobial peptides and enzymes

FHB - GI/Metabolism - Exam 3 (21 decks)

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