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Regulation of GI functions Flashcards

1
Q

What are the four functional layers of the GI tract?

A

mucosa, submucosa, muscularis, and serosa

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2
Q

What is the plexus in the submucosa? What is its main function?

A

Contains submucosa plexus (Meissner’s). More about glandular secretion (function of the submucosa plexus)

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3
Q

What is the plexus in the muscularis layer? What is its main function?

A

Contains the myenteric plexus (Auerbach’s). More about muscle movement (function of the myenteric plexus)

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4
Q

How is the innervation of the GI tract divided?

A

(1) intrinsic innervation

(2) extrinsic innervation

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5
Q

What is the extrinsic innervation of the GI tract?

A

extrinsic innervation is via the autonomic nervous system; ANS innervates the ENS

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6
Q

What is the intrinsic innervation of the GI tract?

A

enteric nervous system

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7
Q

What is the enteric nervous system?

A

enteric nervous system is the inter-connected submucosal and myenteric plexuses; contains the PSNS ganglion and postganglionic neurons

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8
Q

Where is the enteric nervous system derived from?

A

Like ANS, the ENS is derived from migrating neural crest cells

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9
Q

What are the prevertebral ganglia (sympathetic innervation)?

A

Celiac (innervates stomach, small intestine), superior mesenteric (innervates distal portion of the small intestine, large intestine and ascending and transverse colon), inferior mesenteric (innervates transverse colon, distal colon, rectum)

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10
Q

What portion of the GI tract does the vagus nerve innervate?

A

Up to the splenic fixture (up to the transverse colon). Sacral portion of the nervous system innervates the remainder

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11
Q

What is the parasympathetic innervation to the transverse colon, distal colon, and rectum?

A

Postganglionic neurons in Auerbach’s and Meissner’s plexuses

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12
Q

How is visceral pain related to dermatoes?

A

referred pain; visceral pain will be located in the related dermatome of the same spinal segment.

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13
Q

Where are the cell bodies of the sympathetic prepanglionic neurons located?

A

Lateral horn of the spinal cord (between T1-L2)

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14
Q

Landmark for T4 dermatome?

A

Nipples

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15
Q

Landmark for T10?

A

Belly but-ten

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16
Q

Landmark for L1?

A

L1 is IL (inguinal ligament)

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17
Q

S2, S3, S4?

A

keep the penis off the floor

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18
Q

Describe the somatic motor system

A

single neuron, releases Ach which binds to a nicotinic receptor

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19
Q

Describe the parasympathetic nervous system

A

pre and postganglion; preganglion (long) releases Ach which binds to a nicotinic receptor; postganglion (short) releases Ach which binds to a muscarnic receptor

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20
Q

Describe the normal (forget the expections) sympathetic nervous system

A

pre and postganglion; preganglion (short) releases Ac which binds to a nicotinic receptor; postganglion releases norepi. which binds to adrenergic receptors

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21
Q

What the exceptions to the normal sympathetic nervous system (2 exceptions)?

A

(1) Sweat glands; the postganglion of sweat gland releases Ach.
(2) Adrenal medulla releases epi. after Ach is released by preganglionic neurons

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22
Q

What is the affect of Ach on the GI tract?

A

contracts smooth muscle, relaxes internal sphincter, increases salivary, gastric, and pancreatic secretion

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23
Q

What is the affect of Norepi. on the GI tract?

A

relaxes smooth muscle, contracts internal sphincters, reduces watery glandular secretions

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24
Q

How to interpret questions involving the GI tract?

A

Remember, the enteric nervous system can and does function autonomously. Loss of ANS innervation will not cause prevent GI motility completely. If you are given a question with a patient who is unable to poop, first chose the question that is related to decrease enteric function. if that is not an option, then focus on ANS related answers

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25
Q

Definition of protuberate

A

to swell or bulge (a patient with a protuberate abdomen is constipated)

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26
Q

What is hirschsprung disease?

A

Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses in distal segment of colon. Due to failure of neural crest cell migretion. Associated with mutations in RET

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27
Q

What is RET?

A

Mutations in the RET gene are the most common known genetic cause of Hirschsprung disease. The RET gene provides instructions for producing a protein that is involved in signaling within cells. This protein appears to be essential for the normal development of several kinds of nerve cells, including nerves in the intestine. Mutations in the RET gene that cause Hirschsprung disease result in a nonfunctional version of the RET protein that cannot transmit signals within cells. Without RET protein signaling, enteric nerves do not develop properly. Absence of these nerves leads to the intestinal problems characteristic of Hirschsprung disease.

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28
Q

Treatment for Hirschsprung disease?

A

Resection

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29
Q

What is meant by the term neurocrine?

A

specialized paracine (subdivision of paracrine comunication) involving a neuron; occurs in the gut

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30
Q

What is paracine communication? What are some examples?

A

No blood travel and act locally; somatostatin and histamine

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31
Q

What is endocrine communication? What are some examples?

A

Must travel in blood and act at a distance; gastrin, CCK, secretin, GIP and GLP-1

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32
Q

Nae an example of a substance that acts as both a hormone and paracrine substance?

A

Somatostatin (paracrine substance in GI tract/hormone in the endocrine system - inhibits GnRH #tbt)

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33
Q

What nerves innervate the enteric nervous system, in terms of sympathetic and parasympathetic fibers?

A

sympathetic - mainly postganglionc, parasympathetic - preganglionic

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34
Q

Name all 5 neurotransmitters in the ENS

A

vasoactive intestinal polypeptide, substance p, enkephalins (opiates), neuropeptide y, gastrin-releasing peptide (GRP)

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35
Q

Hey! What’s a cool way to remember the 5 neurotransmitters in the EMS?

A

VIP Opiates GSN (game show network)

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36
Q

What is the function of vasoactive intestinal polypeptide?

A

relaxes smooth muscle but increases salivary, gastric, and pancreatic secretion

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37
Q

What is the function of substance p?

A

(co-secreted with Ach) contracts smooth muscle and increases salivary glands secretions. “Think of it as a helper to Ach”

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38
Q

What is the function of enkephalins (opiates)?

A

contract smooth muscle and sphincters, reduces glandular secretions. Overall, however, opiates cause constipation because they disrupt the normal contraction and relaxation cycles require for propulsion

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39
Q

What is the function of neuropeptide y?

A

relaxes smooth muscle and reduces glandular secretions

40
Q

What is the function of gastrin-releasing peptide (GRP) aka bombesin?

A

increases gatrin secretion

41
Q

What is VIPoma?

A

a disease resulting from an islet cell tumor of the pancreas, which leads to increased production and secretion of vasoactive intestinal polypeptide

42
Q

What are the symptoms of VIPoma?

A

watery diarrhea, hypokalemia

43
Q

I didn’t understand the reasoning behind the second challenge question Mechanism explaining how excess VIP leads to watery diarrhea and hypokalemia

A

VIP is a potent stimulator of gut cyclic adenosine monophosphate (cAMP) production, which leads to massive secretion of water and electrolytes (mainly potassium).

44
Q

4 main GI hormones

A

gastrin, cholecystokinin (CCK), secretin, incretins (GIP and GLP-1)

45
Q

Where is gastrin secreted?

A

secreted by G cells in the antrum of the stomach; some G cells in duodenum, and pancreatic islets

46
Q

What are the two forms of gastrin?

A

17-aa peptide (little form) and 34-aa version which is secreted at low levels between meals

47
Q

Function of gastrin?

A

acts to increase gastric H+ secretion, grow gastric mucosa, increase gastric motility

48
Q

What causes the release of gastrin?

A

dietary pepties and vagal stimulation

49
Q

What is unique about vagal innervation on G cells?

A

Vagal innervation uses gastrin-releasing peptide (GRP) not acetylcoline as the neurotransmitter

50
Q

What is the negative feedback on G cells?

A

Acid in antrum stimulates D cells to release somatostatin, which acts in a paracrine fashion to inhibit the G cell

51
Q

Which cells can gastrin bind to?

A

Gastrin can bind to parietal cells (directly stimulate H+ secretion) or ECL (indirectly stimulate H+ secretion)

52
Q

How do ECL cells (Enterochromaffin-like cells) cause H+ secretion?

A

When gastrin binds to CCK-B receptors on ECL cells, histamine is released. Histamine binds to histamine receptors on parietal cells to stimulate H+ secretion into the lumen.

53
Q

Which pathway, indirect or direct, is more powerful in causing H+ secretion?

A

indirect pathway (amplification effect)

54
Q

What are the two classes of medicine to reduce stomach acid?

A

H2 blockers (block histamine binding to H2 receptor on parietal cell) and proton pump inhitiors (proton pump on luminal surface of the parietal cell)

55
Q

Which works faster - H2 blocker or Proton pump inhibitor?

A

H2 blocker

56
Q

Which is more powerful - H2 blocker or proton pump inhibitor?

A

Proton pump inhibitor

57
Q

What is atropine?

A

Ach receptor blocker (more specifically a muscarnic receptor blocker)

58
Q

Why doesn’t atropine inhibit the production of stomach acid?

A

Gastrin-Releasing Peptide is used as a neurotransmitter by the vagus nerve; not Ach

59
Q

What are the phases of gastric secretion?

A

Cephalic, gastric and intestinal

60
Q

What happens during the cephalic phase of gastric secretion?

A

In the cephalic phase, the
taste or smell of food, tactile sensation
of food in the mouth, or though of food
sends nervous impulses to the medulla oblongata.
These impulses cause parasympathetic
neurons via the vagus nerves to stimulate
secretion of hydrochloric acid and pepsin
in the stomach. The parasympathetic stimulation also results in secretion of gatrin from the lower part of the stomach. This hormone travels through th bloodstream and further stimulates hydrochloric acid and pepsin scretion in the upper and middle parts of the stomach.

61
Q

What happens in the gastric phase of gastric secretion?

A

In the gastric phase of gastric secretion, food has entered and distended the stomach. This distention activates a parasympathetic reflex via the medulla oblongata, and also has a direct stimulatory effect on the gastric glands. The result is continued secretion of hydrochloric acid and pepsin.

62
Q

What happens in the intestinal phase of gastric secretion (according to our notes)?

A

Food (chyme) in the duodenum stimulates G cells to produce gastrin

63
Q

What happens in the intestinal phase of gastric secretion (in actuality)

A

In the intestinal phase of gastric secretion, chyme has entered the duodenum, so gastric secretion is no longer needed. When the chyme contains lipids from the digestion of fats or contains enough hydrochloric acid to bring its pH below 2, gastric secretion is inhibited.

64
Q

How many major forms does CCK exist in?

A

CCK exists in three major forms

65
Q

Which is more selective for CCK - CCKa or CCKb?

A

CCKa receptors are selective for CCK, while CCKb binds CCK and gastrin

66
Q

Which cells secrete CCK? Where are they located?

A

CCK is secreted from I cells in the duodenum and jejunum

67
Q

Secretion of CCK is in response of what?

A

In response to fat and protein

68
Q

Function of CCK?

A

Contract the gallbladder, relaxes the sphincter of oddi, stimulates secretion of primarily enzyme from the exocrine pancreas, promotes growth of exocrine pancreas and gallbladder, and inhibits gastric emptying

69
Q

What is the secretory trifecta caused by CCK?

A

contraction of the gallbladder, relaxation of the sphincter of oddi, stimulation of pancreatic enzyme secretion

70
Q

What cells secrete secretin?

A

S cells in the duodenum and jejunum

71
Q

What causes the release of secretin?

A

H+ and fatty acids

72
Q

Function of secretin?

A

promotes secretion of HCO3- from pancrease and bile, which neutralizes stomach acid

73
Q

Importance of acid neutralization in duodenum?

A

Acid neutralization in the duodenum is necessary for luminal protein and fat absorption because pancreatic lipases are denatured at low pH

74
Q

When are incretin released?

A

Released from the intestine after a glucose, protein or fat load (responds to any nutrient)

75
Q

What are the two main incretins?

A

Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1)

76
Q

What cells secrete GIP?

A

K cells in the duodenum

77
Q

What cells secrete GLP-1?

A

L cells in the ileum and colon

78
Q

Function of incretins?

A

Incretins augment insulin release from the pancreatic beta cell but only when glucose is present in the lumen of the GI tract

79
Q

Excess of what enzyme can be linked to ulcers?

A

Gastrin

80
Q

What causes an ulcer?

A

Decreases in the stomach’s mucus lining (too acidic an environment or too little mucus released)

81
Q

Why are H2 blockers ineffective treatment options with someone who has excess gastrin?

A

Gastrin can still lead to H+ secretion via direct stimulation of parietal cell by binding to CCKb

82
Q

What causes Zollinger Ellison syndrome?

A

Zollinger Ellison syndrome is due to a G-cell tumor in the wall of the duodenum

83
Q

What are the three types of GI reflexes?

A

local reflexes, extrinsic reflexes, reflexes involving cognitive awareness

84
Q

What do local reflexes control in the GI tract?

A

Control secretion, peristalsis and mixing contractions; entirely within the ENS

85
Q

What are the three extrinsic reflexes of the GI tract?

A

gastrocolic, enterogastric, colonoileal

86
Q

Describe the gastrocolic reflex

A

signals from the stomach (from distension) cause evacuation of the colon
(stimulates GI motility)

87
Q

Describe the enterogastric reflex

A

signals from the small intestine inhibit stomach motility and stomach secretion
(inhibits GI motility)

88
Q

Describe the colonoileal reflex

A

signals from the colon inhibit emptying of ileal contents into the colon
(inhibits GI motility)

89
Q

What are the GI reflexes involving cognitive awareness?

A

vomiting reflex, pain reflex, defecation reflex

90
Q

What is the result of the pain reflex?

A

Causes general inhibition of the entire GI tract

91
Q

What is the defecation reflex?

A

The defecation reflex is an involuntary response of the lower bowels to various stimuli thereby promoting or even inhibiting a bowel movement.

92
Q

What substance stimulates “vomiting centers”?

A

Morphine

93
Q

What stimulates food intake?

A

ghrelin from an empty stomach, appetizing sight/smell/taste of food signals from cerebral cortex

94
Q

What inhibits food intake?

A

afferents from stoach relaying fullness, gastrointestinal hormones (insulin, pyy - pancreatic peptide y, cck), adipose tissue releasing leptin

95
Q

What is leptin?

A

the “satiety hormone” (the feeling or state of being full); inhibits hunger; a hormone made by adipose cells; opposed by the actions of the hormone ghrelin

96
Q

What part of the brain controls food intake?

A

Hypothalamus; it is subject to positive and negative influences fro the CNS, stomach, and hormones

97
Q

What are the two major paracrine substances?

A

Histamine and somatostatin

GI (27 decks)

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