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GIR Test 1 > B5.006 LES and Stomach > Flashcards

B5.006 LES and Stomach Flashcards

1
Q

what is the LES

A

smooth muscle at junction of esophagus and stomach

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2
Q

how is the LES stimulated to open?

A

direct inhibitory innervation

no dilator muscles, open due to the movement of a bolus through the relaxed sphincter

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3
Q

discuss the neural pathways to the LES

A

relaxation induced by excitation of receptors in the pharynx
afferent stimulus travels to sensory nucleus (nucleus solitaries)
dorsal vagal nucleus and nucleus ambiguous mediate esophageal peristalsis and sphincter relaxation

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4
Q

which postganglionic transmitters play a role in LES relaxation

A

NO

vasoactive intestinal peptide (VIP)

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5
Q

discuss the neural pathway to the crural diaphragm

A

contraction controlled by inspiratory center in brainstem and nucleus of phrenic nerve
innervated by right and left phrenic nerves through nicotinic cholinergic receptor ACh

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6
Q

why does the LES favor contraction?

A

tonic myogenic property present even in absence of innervation

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7
Q

what mechanisms are involved in regulation of basal LES tone

A

excitatory ACh
inhibitory NO
tonic myogenic property

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8
Q

what is TLESR

A

transient LES relaxation

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9
Q

what does TLESR occur

A

allows for gas venting from stomach (belching)

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10
Q

describe the process of TLESR

A

relaxation occurs in absence of swallow
complete LES relaxation for about 20 s
relaxation associated with inhibition of crural diaphragm as well

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11
Q

when is TLESR inhibited

A

sleep

horizontal position

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12
Q

what is reflux and how do you know it occurred?

A

movement of stomach contents back into esophagus through LES during relaxation
indicated by a decrease in esophageal pH and an increase in intraesophageal pressure

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13
Q

what is hypotensive LES

A

reduced basal tone of the LES

hypotensive esophageal contractions may or may not be present

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14
Q

result of hypotensive LES

A

reflux into the esophagus

GERD, erosive esophagitis, peptic stricture, Barrett’s esophagus

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15
Q

cause of hypotensive LES

A

most often reduced myogenic tone of LES

can be due to cholinergic suppression or drugs that cause SM relaxation

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16
Q

what are the 3 primary mechanisms of LES incompetence in gastroesophageal reflux?

A

hypotensive LES
increased intraabdominal pressure
TLESR/ inappropriate LESR

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17
Q

describe how increased intraabdominal pressure can result in reflux

A

the LES barrier may be overwhelmed by increased pressure

often associated with impaired contraction of the diaphragmatic sphincter

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18
Q

what is the single most important precipitant for reflux

A

TLESR/ inappropriate LESR

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19
Q

what is one source of increased intraabdominal pressure

A

pregnancy

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20
Q

discuss preepithelial defense in the esophagus vs the stomach

A

poorly developed in esophagus compared to stomach

stomach: mucus and unstirred water layer containing bicarb on top of epithelium, pH 2 outside of mucus but pH 6-7 in unstirred water over epithelium due to neutralization and physical blockage
esophagus: limited mucus-bicarb barrier to buffer diffusing H+

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21
Q

epithelial defenses against acid injury

A

structural: apical cell membrane, intercellular junctional complex
functional: intracellular buffering, H+ extrusion processes

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22
Q

what happens if refluxed gastric acid (H+) diffuses into the intercellular spaces?

A

can induce a sustained esophageal contraction
H+ encounters and activates chemosensitive nociceptors whose signals are transmitted via the spinal cord to the brain for symptom (heartburn) perception
these nociceptors can also initiate a short reflex arc to esophageal smooth muscle as a means of precipitating a contraction

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23
Q

what are some things that can cause an initial esophageal lesion

A 
delayed gastric emptying
increased frequency of TLESR
increased acidity
loss of secondary peristalsis following TLESR
decreased LES tone
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24
Q

what are potential outcomes of esophageal lesions

A

scarring
incompetent LES
recurrent injury > stricture, pain, obstruction, perforation, Barrett’s, cancer

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25
what is the role of longitudinal muscle of the esophagus
not fully understood | causes shortening of esophagus (may facilitate esophageal transit and help with relaxation of the LES)
26
sustained contractions of longitudinal muscles of esophagus associated with...
chest pain gastric acid causes it can eventually lead to hiatal hernia
27
what is a hiatal hernia
displacement of stomach into the thoracic cavity via diaphragmatic esophageal hiatus
28
why can hiatal hernias be associated with disruption of the LES
crural diaphragm normally encircles the LES and helps with sphincter function displacement of LES eliminates this contribution
29
what symptoms are associated w hiatal hernias
reflux (50% have GERD) | can be associated with impaired esophageal emptying
30
what is Schatzkis ring
ring that forms at the junction of LES and stomach (squamocolumnar junction) which may limit entry of poorly chewed food can be asymptomatic
31
what is the normal appearance of the squamocolumnar junction
normally forms a line without constriction, so lowermost part of LES cannot be identified
32
what is achalasia
failure of LES to relax | failure to generate peristalsis
33
what causes achalasia
nerve damage to inhibitory or inhibitory and excitatory nerves more common in middle aged or elderly
34
symptoms of achalasia
``` regurgitation chest pain difficulty swallowing heartburn cough weight loss dilated esophagus and bird's beak deformity of distal esophagus ```
35
what is seen on barium swallow when achalasia is present
lack of esophageal emptying with time
36
findings on manometry of pt with achalasia
incomplete LES relaxation with swallowing absent peristalsis, only low amp spontaneous activity intraesophageal pressure > intragastric pressure transit time slow insufficient inhibitory nerve action
37
what are 2 types of idiopathic achalasia
loss of inhibitory neurons OR loss of all neurons
38
achalasia resulting from loss of inhibitory neurons
elevation in basal LES pressure absence of swallow induced relaxation of LES aperistalsis: simultaneous esophageal body contractions
39
achalasia with complete loss of myenteric neurons
basal LES pressure is lower than normal due to lack of excitatory neurons LES absence of swallow induced relaxation of LES aperistalsis: complete absence of esophageal body contractions
40
cell types in stomach mucosa
``` superficial epithelia mucus neck stem/regenerative parietal chief endocrine ```
41
layers of stomach wall
inside>outside mucosa w/ glands muscularis mucosae submucosa
42
primary hormones regulating gastric acid production
gastrin releasing peptide gastrin histamine somatostatin
43
location and major action of gastrin-releasing peptide
location: GI nerves | action gastrin release and acid secretion
44
location and major action of gastrin
location: gastric antrum, duodenum action: gastric acid and pepsinogen secretion
45
location and major action of histamine
location: ECL cells action: stimulation of gastric acid secretion
46
location and major action of somatostatin
location: gastric D cells action: paracrine regulator of acid and gastrin
47
gastrin releasing peptide nerves
muscle: circular (high conc) and longitudinal (low conc) mucosa: oxyntic (high conc) and antral (low conc) plexuses: myenteric and submucosal
48
function of GRP nerves in muscle
motor function
49
function of GRP nerves in oxyntic mucosa
regulation of gastric acid via somatostatin
50
function of GRP nerves in antral mucosa
gastrin release
51
function of GRP nerves in myenteric plexus
regulation of motor activity
52
function of GRP nerves in submucosal plexus
gastrin release
53
what are G cells
human gastrin producing cells
54
where are G cells located
within basement membranes of glands
55
what do G cells look like on histo
red stain on outside of glands
56
what family of peptides does gastrin resemble
CCK (cholecystokinin) | gastrin binds tighter to gastric CCKB receptor than does actual CCK
57
inducers of gastrin release
``` antrum distention gastrin releasing peptide fat, proteins, AAs B2 adrenergic agonist lumen neutralization ```
58
function of gastrin
``` stimulates acid secretion stimulates histamine release increase tone of LES regulate antral muscle activity induce somatostatin release weak stimulation of pepsinogen secretion induce mucosal growth ```
59
suppressors of gastrin release
somatostain starvation lumen acid (
60
discuss the function of G cells in the antrum
stimulated by vagus nerve via GRP nerves in mucosa produce gastrin gastrin released into capillary bed to exhibit endocrine function gastrin stimulates neighboring D cells to produce somatostatin somatostatin production inhibits further gastrin release from G cells
61
how does gastrin work as a hormone
travels through blood stream to stimulate parietal cells in oxyntic mucosa to produce acid
62
what other stimuli affect production of acid by parietal cells
``` stimulate: vagus nerve action gastrin histamine inhibit: somatostatin ```
63
what cells produce histamine
enterochromaffin-like cells | contain granules surrounded by halo and secretory vesicles
64
describe the regulation of histamine release
ECL cells in oxyntic mucosa produce histamine somatostatin reduces production gastrin and vagus nerve can stimulate production histamine then upregulates acid production in parietal cells and somatostatin production in D cells
65
how do somatostatin positive D cells in the antrum appear on histo
misshapen brown cells
66
somatostatin function in the stomach
reduces secretions reduces hormone/neurotransmitter release stomach motility food consumption
67
what secretions does somatostatin reduce
HCl | pepsin
68
which hormones do somatostatin reduce
histamine | gastrin
69
how does somatostatin affect stomach motility
inhibits late phase of emptying and the migrating motor complex promotes early phase of gastric emptying
70
how does somatostatin affect food consumption
in fed animals- inhibitory | in fasted animals- excitatory
71
where are D cells present
both antral and oxyntic mucosa
72
cell types in base of antral mucosa
ECL cell G cell D cell mucous cell
73
cell types in base of oxyntic mucosa
ECL cell D cell base cell
74
main function of somatostatin in antrum
reduce gastrin release
75
main functions of somatostatin in oxyntic mucosa
reduce histamine release reduce HCl secretion reduce pepsin secretion
76
how is gastrin released from G cells
explosive exocytosis
77
what receptor does gastrin interact with to modulate histamine production
CCK2 receptor on ECL cells
78
how does somatostatin inhibit gastric acid secretion
local diffusion through the intercellular space or local mucosal circulation
79
GRP nerve function opposing actions
GRP nerves can have a positive effect on gastrin production from G cells GRP can have a negative effect on gastrin production by increasing somatostatin production in D cells
80
what is an example of a local neural pathway that regulates gastric acid secretion
stretch receptors in body of stomach stimulate G cells and oxyntic glands
81
how can feedback from the small intestines and pancreas inhibit gastric acid secretion
digestive products in the duodenum trigger release of neuropeptides that inhibit acid secretion
82
examples of neuropeptides that inhibit acid secretion
``` CCK secretin VIP GIP neurotensin peptide YY somatostatin prostaglandin E uragastrone ```
83
how do parietal (oxyntic) cells secrete acid
tubulovesicles fuse with membrane of intracellular canaliculi, which are open to the lumen tubulovesicles secrete H+ and Cl-
84
what parietal cell receptors are present to stimulate secretion
M3- cholinergic (via Ca2+) H2- histamine (via cAMP) CCKB- gastrin (via Ca2+)
85
what proteins are contained in the tubulovesciles that facilitate secretion
H+, K+ ATPase
86
how does ion transport work within the parietal cells
H+ is pumped against a concentration gradient via H+, K+ ATPase Cl- diffuses into lumen via an anion channel when H+ exits apical side, HCO3- flows down electrochemical gradient and draws Cl- into cell
87
where is vitamin B12 found
animal products | produced by bacteria in the gut
88
what are R proteins
made in salivary glans and protect B12 from degradation
89
what is intrinsic factor
made by parietal cells in stomach but is outcompeted for B12 by R proteins eventually associate with B12 when R proteins are digested by pancreatic enzymes
90
how is B12 moved into blood
complex of B12 and IF binds to epithelial cells in terminal ileum transcobalamin II moves B12 into blood
91
function of chief cell
contains zymogen granules that contain pepsinogens | acid converts pepsinogens to pepsin
92
what are pepsins
endopeptidases that digest proteins into oligopeptides
93
main stimulator of chief cells
ACh secretin maybe histamine and gastrin too?
94
what stimulates local cholinergic reflex and secretin release
H+ release by parietal cells
95
inhibitor of chief cells
somatostatin
96
3 anatomic regions of stomach
fundus corpus antrum
97
2 functional regions of stomach
``` gastric reservoir (tonic contractions) gastric pump (phasic contractions) ```
98
function of proximal stomach
reservoir
99
function of distal stomach
grinding of solids
100
function of pyloric sphincter
sieving of particles
101
describe gastric accommodation
proximal stomach actively relaxes to accommodate meals | NO dependent inhibition of muscles
102
what happens to the proximal stomach during gastric emptying
restoration of fundic tone and volume | ACh dependent tonic contraction
103
3 types of relaxation of gastric reservoir
receptive adaptive feedback-relaxation
104
receptive relaxation
mechanical stimuli in the pharynx stimulate vagus center to inhibit tone and induce relaxation
105
adaptive relaxation
tension receptors on corpus stimulate vagus center to inhibit tone and induce relaxation
106
feedback relaxation
nutrients in duodenum stimulate vagus center
107
what causes the digesta from the gastric reservoir to move into the antral pump
tonic contraction and peristaltic waves in gastric corpus
108
muscle layers of GI smooth muscle
inner > outer oblique circular longitudinal
109
discuss slow wave propagation around stomach
corpus pacemaker 1. fundus 2. corpus 3. orad antrum 4. terminal antrum propagate rapidly around stomach and more slowly down the stomach propagate as a band towards the pylorus, activating contraction as smooth muscle cells depolarize
110
what types of cells develop and propagate slow waves
interstitial cells: network in pacemaker region that allow for electrotonic conduction of slow waves into smooth muscle cells via gap junctions ICC cells: intramuscular cells with enteric neural input via varicosities
111
what are intramuscular interstitial cells of cajal (ICC-IM)
interposed between nerve terminals and smooth muscle cells may be innervated communicate verve stimulation to smooth muscle cells
112
role of slow waves in muscle contractions
membrane potential must reach a threshold to stimulate contractions potential a combo of stretch + ACh + parasympathetic stimuli
113
3 phases of gastric pump
A: phase of propulsion B: phase of emptying C: phase of retropulsion
114
phase of propulsion
contraction of proximal antrum propulsion of chime into relaxing terminal antrum duodenal contractions
115
phase of emptying
contraction in middle antrum transpyloric and retrograde flow duodenal relaxation
116
phase of retropulsion
contraction of terminal antrum jet like backflow with grinding duodenal contraction
117
how are solid particles ground in stomach
forceful jet like retropulsion through the small orifice of the terminal antral contraction
118
what is meant by sieving function
liquids and small particles leave the stomach more rapidly than large particles phase A: rapid flow of liquid and small particles toward pylorus phase B: emptying of liquids and small particles and retention of large particles phase C: retropulsion of large particles
119
discuss the coordination of anto-duodenal contractions
duodenal contractions cease when pylorus is open duodenum can contract 3-4 times during an antral wave pylorus open when middle antrum contracts and closed when terminal antrum contracts
120
discuss the different velocities of gastric emptying
emptying of liquids is exponential emptying of large solid particles only begins after sufficient grinding (lag phase) afterwards viscous chime is mainly emptied in a linear fashion
121
rapid gastric emptying
``` caused by: tonic contractions of reservoir deep peristaltic waves along gastric body deep constriction of the antral waves wide opening of pylorus duodenal receptive relaxation peristaltic duodenal contractions ```
122
delayed gastric emptying
due to feedback inhibition and caused by: prolonged reservoir relaxation shallow peristaltic waves along gastric body shallow antral waves small pyloric opening lacking duodenal relaxation segmenting duodenal contractions
123
which molecules slow gastric emptying
CCK | GLP-1

GIR Test 1 (24 decks)

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