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GI Midterm > GI Regulation > Flashcards

GI Regulation Flashcards

1
Q

Neurotransmitters in the ANS

A
  • Preganglionic ALWAYS use Ach and nicotinic receptors
  • Postganglionic PSNS use Ach and muscarinic receptors
  • Postganglionic SNS use norepi or epi, EXCEPT for sweat glands, which use Ach
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2
Q

Acetylcholine as a neurotransmitter causes what in the GI tract?

A

PSNS gets GI tract moving

Contraction of smooth muscle, relaxation of internal sphincters, and increase in secretions from salivary, gastric, and pancreatic glands

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3
Q

Norepi as a neurotransmitter causes what in the GI tract

A

SNS stops the GI tract

Relaxes smooth muscle, contracts internal sphincters, and reduces watery glandular secretions

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4
Q

Gastrin (source, stimulus, action)

A
  • G-cells of stomach antrum; few in duodenum
  • increases H+ secretion from parietal cells, grows gastric mucosa, and increase gastric motility
  • stimulated by AA and vagus (which uses GRP)
  • direct and indirect pathways (indirect being more powerful)
  • binds to CCKb
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5
Q

CCK

Source, stimulus, action

A
  • released from I cells of duodenum and jejunum
  • binds to CCKa (specific for CCK) and CCKb (for CCK and gastrin)
  • causes contraction of gallbladder, relaxation of sphincter of Oddi, stimulation of secretions from exopancreas, promotes growth of exopancreas, and inhibits gastric emptying….secretory trifecta
  • released after gastrin in response to protein and lipids
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6
Q

Secretin

Source, stimulus, action

A
  • released from S-cells of duodenum and jejunum
  • released after gastrin and CCK
  • the “anti-gastrin”
  • released in response to H+ and fatty acids
  • causes release of bicarb from pancreas for protection of duodenum and appropriate pH for pancreatic lipases needed for lipid absorption
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7
Q

Incretins

Types, source, stimulus, response

A
  • GIP released from K-cells of duodenum
  • GLP-1 released from L-cells of ileum and colon
  • released in response to glucose, protein, or fat load
  • only hormone to be released in response to glucose, protein, or fat
  • in response to glucose, causes increased insulin release.
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8
Q

Local GI reflexes

A
  • distention of stool causes contraction behind it and relaxation in front of it
  • mediated by ENS
  • controls secretion, peristalsis, and mixing
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9
Q

Extrinsic Reflexes of GI tract

A
  1. GASTROCOLIC: Signal from stomach causes evacuation from colon
  2. ENTEROGASTRIC: Signal from small intestine inhibits stomach secretion and motility
  3. COLONOIEAL: Signal from colon inhibits emptying of ileum
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10
Q

Motility in mouth, esophagus, stomach, small intestine, large intestine

A

Chewing

Swallowing

Digestive period: receptive relaxation, accommodation, and gastric emptying. Interdigestive: migrating myoelectric complexes

Digestive period: segmentation. Interdigestive: peristalsis (MMC)

Haustral shuttling

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11
Q

Function of secondary peristalsis and mechanism of initiation

A

Distention of esophagus stimulates stretch receptors
Clear esophagus of retained food and refluxed gastric contents
Little/no sensation

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12
Q

Anti-reflux mechanisms

Mechanisms for infant and pregnant mother

A
  1. LES pressure greater than stomach
  2. Diaphragm pinching esophagus (INFANTS)
  3. Secondary peristalsis (PREGNANT)
  4. Reflexes
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13
Q

Neuroendocrine effect on ECAs

A

Excitatory: Ach, gastrin
Increase ERA:ECA

Inhibitory: norepi, VIP, and nitric oxide
Decrease ERA:ECA

Can modulate, but not initiate!

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14
Q

Interstitial cells of Cajal

A

Pacemaker cells that generate ECAs

Determine max rate of contraction

Lie btwn circular and longitudinal muscle layers

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15
Q

What are ERAs? How do they affect contractions?

A

Local events on plateau of ECA that cause muscle contraction

Frequency of ERAs determine frequency of contraction

Multiple allow more Ca2+ into SMCs for a stronger and mores sustained contraction

Number and strength of contractions increased with increased ERA:ECA

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16
Q

Neuroendocrine control of peristalsis

A 
Behind bolus (oral to):
Longitudinal: relaxed (inhibitory neuroendocrines)
Circular: contracted (excitatory neuroendocrines)

In front of bolus (aboral to):
Longitudinal: contracted (excitatory neuroendocrines)
Circular: relaxed (inhibitory neuroendocrines)

Interneurons coordinate muscle contraction and relaxation so bolus follows pressure gradient

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17
Q

Three phases of swallowing

Only phase that is voluntary

A
  1. Oral-voluntary
  2. Pharyngeal
  3. Esophageal
18
Q

Antral systole

A

Simultaneous contraction of terminal antrum and pylorus causes mixing via retrograde movement of contents and shearing of food

Chyme and liquids leave before antral systole

19
Q

Driving forces of gastric empyting

A
  1. Lower stomach peristalsis

2. Upper stomach tone

20
Q

Inhibitors of gastric emptying

A
  1. Pyloric sphincter tone

2. Duodenal contraction

21
Q

Characteristics and functions of MMCs

A

=migrating motor complexes
Strong and intermittent waves of contraction in small intestine
Housekeeping-cleans out residual material and prevents bacterial overgrowth
During interdigestive period
Pylorus is open
Mediated by motilin

22
Q

Affects of somatostatin

What cells release it? What causes its release?

A

Endocrine function: inhibits growth hormone

Paracrine function: suppresses release of gastrointestinal hormones
Inhibit G-cells from secreting gastrin in a negative feedback paracrine loop!

Released from D cells; stimulated by stomach acid to act in negative feedback paracrine loop

23
Q

VIP

A

Vasoactive Intestinal Polypeptide (VIP)-mixed response, causing relaxation of SM but increased secretions (–>watery diarrhea)

24
Q

Neuropeptide Y

A

Neuropeptide Y-acts like norepi, relaxes smooth muscle and

25
Q

GRP

A

Gastrin-releasing peptide (GRP, bombesin)-acts like Ach, causing increased gastrin secretion

26
Q

Enkephalins

A

(opiates)-mixed response, causing contraction of smooth muscle and sphincters and reduction of glandular secretions.
Constipation

27
Q

Substance P

A

Substance P-acts like Ach and is secreted with it, causing contraction of smooth muscle and increase in secretions

28
Q

Neurotransmitters in the ENS

A

PSNS acting: Ach, GRP, and Substance P
SNS acting: Norepi, epi, Neuropeptide Y
Mixed: opiates and VIP

29
Q

Saliva characteristics

A

Hypotonic

Higher K+ and bicarb than plasma

30
Q

Gastric secretion characteristics

What would happen with vomitting?

A

Higher Cl-, H+, and K+ than in plasma

Two major secretions:
Oxyntic: from parietal cells, includes HCl, IF, and K+, which is stimulated by feeding

Non-oxyntic: from chief cells and mucous cells, includes pepsinogen,mucous, and Na+

Blood pH would increase because lose H+

31
Q

Pancreatic Juice Caracteristics

A

High bicarb

Concentration of K+ and Na+ equal to what is in blood

32
Q

Effect of CCK and Ach on Secretin

A

Increase effect by acting on K+ channel through Ca2+, causing more leakage of K+

33
Q

Secretin effect on CFTR

A

Stimulates CFTR and the translocation of the H+ K+ ATPase so more bicarb is released into the lumen (as is Cl-)

Secretin stimulates adenosine cyclase to convert cAMP to PKa, which opens CFTR

34
Q

Hartnup disease

A
  • defective amino acid transporter
  • especially affects tryptophan (which is needed to make serotonin, melatonin, and niacin)
  • similar symptoms to niacin deficiency (pellegra)
  • can partially compensate with PepT1 action
35
Q

Difference between liver and gallbladder bile

A

Cl-, Na+, bicarb, and water are reabsorbed when bile is in gallbladder. Lower concentration of these ions in gallbladder bile as compared to liver bile

36
Q

Hirschsprung Disease

A

failure of neural crest migration leads to megacolon (lack of enteric NS)

37
Q

Patterns of digestion and absorption

A
  1. Glucose is not digested and is absorbed unchanged
  2. Luminal hydrolysis-of polymers to monomers (peptides broken down into amino acids in the lumen before absorption)
  3. Brush border hydrolysis-of polymers to monomers (polysaccharides broken down by brush border enzymes into monomers before absorption)
  4. Intracellular hydrolysis-of di and tri peptides, which can be absorbed as is and broken down into individual amino acids in the enterocyte
  5. Luminal hydrolysis followed by re-synthesis of TAGS, broken down into 2 fatty acids and monoglyceride before absorption, but reassembled in the enterocyte
38
Q

Interdigestive absorption of NaCl

A

Parallel Na-H and Cl-bicarb exchange, which is ELECTRONEUTRAL

Occurs in villous epithelia cells of ileum and colon

CA generates intracellular carbonic acid which dissociates to bicarb and H+; both leave the cell so Cl- and Na+ can come into the cell (Na+ uses NHE channel)

Increase in second messengers inhibit this mechanism

39
Q

Nutrient dependent Na+ absorption

A

Villous epithelial cells of small intestine absorb most Na+ using SGLT1 or Na+/amino acid co-transporters

Cl-, K+ and water will follow Na+ absorption into the cell, passively

40
Q

Electrogeneic Na+ absorption

A

Large intestine

Increased by mineralocorticoids

Uses Na+/k+ pump

41
Q

Electrogenic Cl- Secretion
Where?
Why does it matter?

A

From crypts of large and small intestine

CFTR is the chloride channel

42
Q

Types of Diarrhea

A
  1. Osmotic: non-absorbable substance pulls water and electrolytes with it (ie lactose)
  2. Secretory: electrolytes and fluid actively secreted into the gut (ie cholera)

The B subunit of the cholera toxin causes activation of G-alpha

GI Midterm (6 decks)

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