Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which postganglionic transmitters play a role in LES relaxation

A

NO

vasoactive intestinal peptide (VIP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why does the LES favor contraction?

A

tonic myogenic property present even in absence of innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what mechanisms are involved in regulation of basal LES tone

A

excitatory ACh
inhibitory NO
tonic myogenic property

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is TLESR

A

transient LES relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does TLESR occur

A

allows for gas venting from stomach (belching)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when is TLESR inhibited

A

sleep

horizontal position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is hypotensive LES

A

reduced basal tone of the LES

hypotensive esophageal contractions may or may not be present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

result of hypotensive LES

A

reflux into the esophagus

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

hypotensive LES
increased intraabdominal pressure
TLESR/ inappropriate LESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the single most important precipitant for reflux

A

TLESR/ inappropriate LESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is one source of increased intraabdominal pressure

A

pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

epithelial defenses against acid injury

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are potential outcomes of esophageal lesions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the role of longitudinal muscle of the esophagus

A

not fully understood

causes shortening of esophagus (may facilitate esophageal transit and help with relaxation of the LES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

sustained contractions of longitudinal muscles of esophagus associated with…

A

chest pain
gastric acid causes it
can eventually lead to hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is a hiatal hernia

A

displacement of stomach into the thoracic cavity via diaphragmatic esophageal hiatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

why can hiatal hernias be associated with disruption of the LES

A

crural diaphragm normally encircles the LES and helps with sphincter function
displacement of LES eliminates this contribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what symptoms are associated w hiatal hernias

A

reflux (50% have GERD)

can be associated with impaired esophageal emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is Schatzkis ring

A

ring that forms at the junction of LES and stomach (squamocolumnar junction) which may limit entry of poorly chewed food
can be asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the normal appearance of the squamocolumnar junction

A

normally forms a line without constriction, so lowermost part of LES cannot be identified

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is achalasia

A

failure of LES to relax

failure to generate peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what causes achalasia

A

nerve damage to inhibitory or inhibitory and excitatory nerves
more common in middle aged or elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

symptoms of achalasia

A 
regurgitation
chest pain
difficulty swallowing
heartburn
cough
weight loss
dilated esophagus and bird's beak deformity of distal esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is seen on barium swallow when achalasia is present

A

lack of esophageal emptying with time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

findings on manometry of pt with achalasia

A

incomplete LES relaxation with swallowing
absent peristalsis, only low amp spontaneous activity
intraesophageal pressure > intragastric pressure
transit time slow
insufficient inhibitory nerve action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are 2 types of idiopathic achalasia

A

loss of inhibitory neurons
OR
loss of all neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

achalasia resulting from loss of inhibitory neurons

A

elevation in basal LES pressure
absence of swallow induced relaxation of LES
aperistalsis: simultaneous esophageal body contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

achalasia with complete loss of myenteric neurons

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

cell types in stomach mucosa

A 
superficial epithelia
mucus neck
stem/regenerative 
parietal 
chief
endocrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

layers of stomach wall

A

inside>outside
mucosa w/ glands
muscularis mucosae
submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

primary hormones regulating gastric acid production

A

gastrin releasing peptide
gastrin
histamine
somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

location and major action of gastrin-releasing peptide

A

location: GI nerves

action gastrin release and acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

location and major action of gastrin

A

location: gastric antrum, duodenum
action: gastric acid and pepsinogen secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

location and major action of histamine

A

location: ECL cells
action: stimulation of gastric acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

location and major action of somatostatin

A

location: gastric D cells
action: paracrine regulator of acid and gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

gastrin releasing peptide nerves

A

muscle: circular (high conc) and longitudinal (low conc)
mucosa: oxyntic (high conc) and antral (low conc)
plexuses: myenteric and submucosal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

function of GRP nerves in muscle

A

motor function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

function of GRP nerves in oxyntic mucosa

A

regulation of gastric acid via somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

function of GRP nerves in antral mucosa

A

gastrin release

51
Q

function of GRP nerves in myenteric plexus

A

regulation of motor activity

52
Q

function of GRP nerves in submucosal plexus

A

gastrin release

53
Q

what are G cells

A

human gastrin producing cells

54
Q

where are G cells located

A

within basement membranes of glands

55
Q

what do G cells look like on histo

A

red stain on outside of glands

56
Q

what family of peptides does gastrin resemble

A

CCK (cholecystokinin)

gastrin binds tighter to gastric CCKB receptor than does actual CCK

57
Q

inducers of gastrin release

A 
antrum distention
gastrin releasing peptide
fat, proteins, AAs
B2 adrenergic agonist
lumen neutralization
58
Q

function of gastrin

A 
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
Q

suppressors of gastrin release

A

somatostain
starvation
lumen acid (

60
Q

discuss the function of G cells in the antrum

A

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
Q

how does gastrin work as a hormone

A

travels through blood stream to stimulate parietal cells in oxyntic mucosa to produce acid

62
Q

what other stimuli affect production of acid by parietal cells

A 
stimulate:
vagus nerve action 
gastrin 
histamine
inhibit:
somatostatin
63
Q

what cells produce histamine

A

enterochromaffin-like cells

contain granules surrounded by halo and secretory vesicles

64
Q

describe the regulation of histamine release

A

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
Q

how do somatostatin positive D cells in the antrum appear on histo

A

misshapen brown cells

66
Q

somatostatin function in the stomach

A

reduces secretions
reduces hormone/neurotransmitter release
stomach motility
food consumption

67
Q

what secretions does somatostatin reduce

A

HCl

pepsin

68
Q

which hormones do somatostatin reduce

A

histamine

gastrin

69
Q

how does somatostatin affect stomach motility

A

inhibits late phase of emptying and the migrating motor complex
promotes early phase of gastric emptying

70
Q

how does somatostatin affect food consumption

A

in fed animals- inhibitory

in fasted animals- excitatory

71
Q

where are D cells present

A

both antral and oxyntic mucosa

72
Q

cell types in base of antral mucosa

A

ECL cell
G cell
D cell
mucous cell

73
Q

cell types in base of oxyntic mucosa

A

ECL cell
D cell
base cell

74
Q

main function of somatostatin in antrum

A

reduce gastrin release

75
Q

main functions of somatostatin in oxyntic mucosa

A

reduce histamine release
reduce HCl secretion
reduce pepsin secretion

76
Q

how is gastrin released from G cells

A

explosive exocytosis

77
Q

what receptor does gastrin interact with to modulate histamine production

A

CCK2 receptor on ECL cells

78
Q

how does somatostatin inhibit gastric acid secretion

A

local diffusion through the intercellular space or local mucosal circulation

79
Q

GRP nerve function opposing actions

A

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
Q

what is an example of a local neural pathway that regulates gastric acid secretion

A

stretch receptors in body of stomach stimulate G cells and oxyntic glands

81
Q

how can feedback from the small intestines and pancreas inhibit gastric acid secretion

A

digestive products in the duodenum trigger release of neuropeptides that inhibit acid secretion

82
Q

examples of neuropeptides that inhibit acid secretion

A 
CCK
secretin
VIP
GIP
neurotensin
peptide YY
somatostatin
prostaglandin E
uragastrone
83
Q

how do parietal (oxyntic) cells secrete acid

A

tubulovesicles fuse with membrane of intracellular canaliculi, which are open to the lumen
tubulovesicles secrete H+ and Cl-

84
Q

what parietal cell receptors are present to stimulate secretion

A

M3- cholinergic (via Ca2+)
H2- histamine (via cAMP)
CCKB- gastrin (via Ca2+)

85
Q

what proteins are contained in the tubulovesciles that facilitate secretion

A

H+, K+ ATPase

86
Q

how does ion transport work within the parietal cells

A

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
Q

where is vitamin B12 found

A

animal products

produced by bacteria in the gut

88
Q

what are R proteins

A

made in salivary glans and protect B12 from degradation

89
Q

what is intrinsic factor

A

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
Q

how is B12 moved into blood

A

complex of B12 and IF binds to epithelial cells in terminal ileum
transcobalamin II moves B12 into blood

91
Q

function of chief cell

A

contains zymogen granules that contain pepsinogens

acid converts pepsinogens to pepsin

92
Q

what are pepsins

A

endopeptidases that digest proteins into oligopeptides

93
Q

main stimulator of chief cells

A

ACh
secretin
maybe histamine and gastrin too?

94
Q

what stimulates local cholinergic reflex and secretin release

A

H+ release by parietal cells

95
Q

inhibitor of chief cells

A

somatostatin

96
Q

3 anatomic regions of stomach

A

fundus
corpus
antrum

97
Q

2 functional regions of stomach

A 
gastric reservoir (tonic contractions)
gastric pump (phasic contractions)
98
Q

function of proximal stomach

A

reservoir

99
Q

function of distal stomach

A

grinding of solids

100
Q

function of pyloric sphincter

A

sieving of particles

101
Q

describe gastric accommodation

A

proximal stomach actively relaxes to accommodate meals

NO dependent inhibition of muscles

102
Q

what happens to the proximal stomach during gastric emptying

A

restoration of fundic tone and volume

ACh dependent tonic contraction

103
Q

3 types of relaxation of gastric reservoir

A

receptive
adaptive
feedback-relaxation

104
Q

receptive relaxation

A

mechanical stimuli in the pharynx stimulate vagus center to inhibit tone and induce relaxation

105
Q

adaptive relaxation

A

tension receptors on corpus stimulate vagus center to inhibit tone and induce relaxation

106
Q

feedback relaxation

A

nutrients in duodenum stimulate vagus center

107
Q

what causes the digesta from the gastric reservoir to move into the antral pump

A

tonic contraction and peristaltic waves in gastric corpus

108
Q

muscle layers of GI smooth muscle

A

inner > outer
oblique
circular
longitudinal

109
Q

discuss slow wave propagation around stomach

A

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
Q

what types of cells develop and propagate slow waves

A

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
Q

what are intramuscular interstitial cells of cajal (ICC-IM)

A

interposed between nerve terminals and smooth muscle cells
may be innervated
communicate verve stimulation to smooth muscle cells

112
Q

role of slow waves in muscle contractions

A

membrane potential must reach a threshold to stimulate contractions
potential a combo of stretch + ACh + parasympathetic stimuli

113
Q

3 phases of gastric pump

A

A: phase of propulsion
B: phase of emptying
C: phase of retropulsion

114
Q

phase of propulsion

A

contraction of proximal antrum
propulsion of chime into relaxing terminal antrum
duodenal contractions

115
Q

phase of emptying

A

contraction in middle antrum
transpyloric and retrograde flow
duodenal relaxation

116
Q

phase of retropulsion

A

contraction of terminal antrum
jet like backflow with grinding
duodenal contraction

117
Q

how are solid particles ground in stomach

A

forceful jet like retropulsion through the small orifice of the terminal antral contraction

118
Q

what is meant by sieving function

A

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
Q

discuss the coordination of anto-duodenal contractions

A

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
Q

discuss the different velocities of gastric emptying

A

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
Q

rapid gastric emptying

A 
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
Q

delayed gastric emptying

A

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
Q

which molecules slow gastric emptying

A

CCK

GLP-1

GIR Test 1 (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions