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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 made up of

A

smooth muscle

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2
Q

describe the LES innervation

A

receives direct inhibitory innervation no dilator muscles open the LES

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3
Q

how does the LES open

A

opening is due to the movement of the bolus through the relaxed sphincter

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4
Q

describe how the LES relaxes during a swallow

A

the result of excitation of receptors in the pharynx

the afferent stimulus travels to the sensory nucleus, the nucleus solitarius.

A programmed set of events from teh dorsal vagal nucleus and the nucleus ambiguus mediats eh esophageal peristalsia nd th sphincter relaxation. The vagal efferent fibers communicate with the myenteric neurons that mediate LES relaxation.

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5
Q

how is contraction of the crural diaphragm controlled

A

by the inspiratory center in the brainstem and the nucleus of the prenic nerve. The crural diaphragm is innervated by the right and left phrenic nerves through nicotinic cholinergic receptor Ach + excitatory effects

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6
Q

mechanisms involved in the regulation of basal LES tone

A

excitatory cholinergic nerves ACh and the toni cmyogenic property of the LES favor contraction, wheras the inhibitory nitrergic (NO) pathway favors inhibitions.

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7
Q

describe the LES in advanced achalasia

A

the LES remains contracted owing to its myogenic property when completely de innervation

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8
Q

what does transient relaxation of the LES do and when does this happen

A

allows for gas venting

suppressed in horizontal position

blocked by sleep

lasts about 15s

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9
Q

what is hypotensive LES and what are the causes

A

reduced basal tone of the LES

can result in reflux into the esophagus

may have contractons

most often caused by reduced myogenic tone of LES but can be due to cholinergic suppression or drugs that cause smooth muscle relaxation

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10
Q

what can hypotensive LES lead to

A

GERD, erosive esophagitis, peptic stricture, barretts esophagus

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11
Q

what are 3 mechanisms of LES incompetence in GERD

A

LES may be hypotensive

LES barrier may be overwhelmed by increased intragastric pressure (pregnancy)

LES may exhibit frequent reflex transient LES relaxation (single most important precipitant for reflux)

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12
Q

what is different about the stomach and the esophagus as far as how it handles contact with acid

A

in gastric and duodenual epithelia, hydrogen ions must cross the mucus unstirred water layer-bicarbonate layer before ocntact can be made with surface of the epithelum. The esophagus does not have this layer.

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13
Q

what are structural barriers to H+ ions in epithelial defence against acid injury

A

apical cell membrane and intercellular junctional complex.

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14
Q

what are functional components of the epithelial defense against acid

A

intracellular buffering by negatively charged proteins and bicarb ions, and H+ extrusion

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15
Q

diffusion or refluxed gastric acid into intercellular space can cause what

A

sustained esophageal contraction

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16
Q

describe how sustained esophageal contraction can result from GERD

A

When H+ enters the intercellular space it encounters and activates the chemosensitive nociceptors whose signals are transmitted via the spinal cord to the brain for symptoms receptions (heartburn), activation of the same nociceptors is also capable of initiating a short relfex arc to esophageal smooth muscle (longitudinal)

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17
Q

what do longitudinal muscles of the esophagus do

A

cause shortening of esophagus which may facilitate esophageal transit and help with relaxation of the lower esophageal spincter

activity does not affect manometry readings

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18
Q

sustained contractions of longitudinal muscle of esophagus may be associated with what

A

chest pain

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19
Q

gastric acid can cause longitudinal muscle of esophagus contraction which can cause what

A

sliding hiatal hernia

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20
Q

what is a hiatal hernia

A

displacement of the stomach into the thoracic cavity via diaphragmatic esophageal hiatus

often associated with disruption of the LES

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21
Q

how does displacement of the LES relative to the diaphragm cause hiatal hernia

A

crural diaphragma normally encircles the LES and is thought to help with the sphincter function, thus displacemtn fo the LES eliminates this contribution

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22
Q

what symptoms are associated with hiatal hernia

A

GERD

impaired esophageal emptying

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23
Q

what is schatzkis ring

A

ring forms at the junction which may limit entry of poorly chewed food into the stomach

the mucosal ring is Schatzkis ring or B ring

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24
Q

what is achalasia

A

failure of LES to relax, failure to generate peristalsis due to nerve damage to inhibitory nerves or both inhibitory and excitatory

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25
Q

what are symptoms of achalasia

A

chest pain, regurgitation, difficulty swallowing, heartburn, cough, weight loss

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26
Q

what is a dilated esophagus and birds beak deformity of distal esophagus associated with

A

achalasia

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27
Q
A

achalasia

no peristalsis and LES not opening

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28
Q

what does an achalasia monometry reading look like

A

absent peristalsis, only low amplitude spontaneous activity is present. Intraesophageal pessure is higher than intragastric pressure and esophageal transit time is very slow

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29
Q

what types of cells are in the stomach

A

superficial epithelial cells

mucous neck cells

stem/regenerative cells

parietal cell - acid

cheif cell - pepsinogen

endocrine cell

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30
Q

what are the sections of the stomach

A

fundus

body

antrum

pylorus

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31
Q

what are the hormones involved in regulated gastric acid production

A

gastrin releasing peptide

BLI

gastrin

histamine

somatostatin

GIP

epiderman growth factor

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32
Q

where is gastrin releasing peptide found

A

muscle, mucosa, plexuses

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33
Q

gastrin releasing peptide location and major action

A

GI nerves

gastrin release and acid secretion

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34
Q

gastrin location and major action

A

gastric antrum, duodenum

gastric acid and pepsinogen secretion

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35
Q

histamine location and major action

A

ECL cells

stimulus of gastric acid secretion

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36
Q

somatostatin location and major action

A

gastric D cells

paracrine regulator of acid and gastrin

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37
Q

GRP releases NTs where and what does that do

A

mucosa

acts on G cell that produce gastrin

38
Q
A

gastrin producing G cells

responsive to GRP

39
Q

what family does gastrin belong to

A

cholecystokinin

40
Q

why can gastrin bind to CCK receptors better than many cholecystokinins?

A

it shares a stretch of amino acids in common

41
Q

what induces gastrin release

A

antrum distension

gastrin releasing peptide

fat, proteins, amino acids

beta 2 adrenergic agonists

lumen neutralization

42
Q

suppressors of gastrin release

A

somatostatin

starvation

lumen acid <3

43
Q

what does gastrin do

A

stimulates acid secretion and histamine release

increases tone of LES

regulates antral muscle activity

induces somatostatin relase

induces mucosal growth

44
Q

where are D and G cells found

A

antrum

45
Q

describe how G cells are stimulated to make gastrin

A

the GRP nerve from the mucosa is stimulated by ACh and then sends a signal to the GRP receptor which stimulates the creation and release of gastrin into a nearby capillary bed

46
Q

what happens with gastrin in the oxyntic mucosa (more cranial)

A

gastrin comes from the capillaries and acts on the colocystokinin receptor on the parietal cell inducing acid release and also on Histamine producing cells (ECL cells) stimulating histamine production

47
Q

what are ECL cells

A

histamine producing cells

48
Q

what does histamine do in the oxyntic mucosa

A

activates the histamine receptor 2 on pairetal cells

acts in a paracrine way

49
Q

what is a D cell

A

somatostatin cell

50
Q

function of D cells

A

reduce the production of HCl, Pepsin, histamine and gastrin and affects gastric motility

51
Q

in the antrum what does somatostatin do

A

acts on G cell to shut down gastrin production and release

52
Q

what does the somatostatin produced in the oxyntic mucosa do

A

reduces histamine release

reduces HCl secretion

reduces pepsin secretion

53
Q
A
54
Q

what other than hormones can induce the gastrin/somatostatin pathway

A

stretch receptors in stomach

55
Q

what are the inhibitors of gastric acid secretion from the pancreas and small intestine

A

CCK

Secretin

VIP

GIP

Neurotensin

Peptide YY

Somatostatin

Prostaglandin E2

Urogastrone

56
Q

describe how parietal oxyntic cells stimulate secretion

A

ACh muscarinic receptors, histamine receptors and gastrin CCK-B receptors are activated and cause canuliculi to form to tubulovesicles open to the lumen leading to H+/K+ ATPase pump to be activated

57
Q

what is the primary pump for H

A

H/K ATPase

58
Q

how does the HK ATPase pump get activated

A

adenylate cyclase (histamine) and PLC (gastrin, ACh) activate kinases that in turn activate pump

59
Q

what happens when H+ exits the apical side of the parietal cell

A

HCO3- flows down the electrochemical gradient out the basolateral membraen which draws Cl- into the cell

60
Q

how does Cl get into the lumen

A

Cl- diffuses into thelumen via anion channel

61
Q

how is B12 prevented from being degraded in the stomach

A

R protein made by salivary gland

62
Q

what is IF

A

helps protect B12 in the lower part of the intestine

63
Q

how does B12 get into the blood

A

transcobalamin 2 moves vitamine B12 into the blood

64
Q

what is a cheif cell

A

contain zymogen granules that contain pepsinogen –>acid–> pepsin that breaks down proteins

65
Q

how does pepsinogen production get stimulated

A

somatostatin at the level of the cheif cell

66
Q

what is the main patwhay

A

that cheif cells are stimulated

through ACh reflex activated by acid production in stomach

67
Q

acid produced by the parietal cell stimulates production of what

A

secretin

68
Q

what does secretin do

A

acts back on cheif cell to stimulate pepsinogen production

69
Q

what are parts A and B of stomach

A

A - storage

B - grinding of solids

70
Q

how does gastric emptying occur generally

A

restoration of fundic tone and volume from ACh dependent tonic contraction

71
Q

what are 3 kinds of relaxation of the gastric reservoir

A

receptive

adaptive

feedback relaxation

72
Q

what do NO, VIP and ACh do in gastric emptying

A

ACh stimulates tonicity

VIP and NO stimulate relaxation

73
Q

what cranial nerve is key in stomach relaxation/contraction

A

vagus nerve

74
Q

what are the muscle laters of the stomach

A

oblique

circular

longitudinal

75
Q

what is the corpus pacemaker

A

that is in the body of the stomach that initiates the contraction moving across the stomach and then sweeping down

76
Q

how does a slow propagating wave in the stomach begin

A

interstitial cells have a natrual fluxuation fo membrane potentials

linked to eachother via gap junctions with eachother and smooth muscle cells

the enteric motor neuron has varicosities that releases NTs to the smooth muscle cells and interstital cells

77
Q

what component of the production of a slow propagating wave in the stomach is requrired for the fluxuating membrane potential to be stimulated to the point that it creates a contraction

A

neurotransmitters released from varicosities

stretch

ACh

parasympathetic

78
Q

what are the 3 phases of the gastric pump

A

phase of propulsion

phase of emptying

phase of retropulsion

79
Q

what happens in the phase of propulsion in the antrum

A

contraction of proximal antrum

propulsion of chyme into relaxing terminal antrum + duodenal contraction

80
Q

what happens in the emptying phase of the antrum

A

contraction of the middle antrum

transpyloric and tretrograde flow + duodenal relaxation

81
Q

what happens in the retropulsion phase of the antrum

A

contraction of the terminal antrum

jet like back flow with grinding + duodenal contraction

82
Q

what phase is the pylorus open and why

A

the mid antrum is contracting, emptying phase

the peristaltic contractions in the duodenum are stopped as well because if they didnt the contraction would block the entry of those contents into the small intestine

83
Q

what is the function of retropulsion

A

grinding of solid particles is caused by the forceful get like retropulsion through the small orifice of the terminal antral contraction

84
Q

what is sieving function

A

liquids and small particles leave the stomach more rapidly than large particles because the bulge of the terminal antrum retains the larger particles

85
Q

what is emptied faster liquids or solids and why

A

liquieds

large solid particles only begins after sufficient grinding, afterwards viscous chyme is mainly emptied in a linear fashion

86
Q

what is the lag phase

A

the grinding of solid particles that delays it from being emptied

87
Q

what is rapid emptying

A

caused by tonic contraction of the resivoir, deep peristaltic waves along the gastric body, deep constrictions of the antral waes, a wide opening of hte pylorus, a duodenal resceptive relaxation and peristaltic dodenal contractions

88
Q

what is delayed emptying

A

due to feedback inhibition caused by a prolonged relaxation fo the reservoir , shallow peristaltic waves along the gastric body, shallow antral waves, a small pyloric opening, a lacking duodenal relaxation and segmenting duodenal contractions

89
Q

what mechanisms help slow the gastric emptying

A

I cell - in duodenum CCK comes out and activates receptors to send singals to slow emptying

L cells - in ileum, secrete GLP, CPR to stimulate the delay of gastric emptying

90
Q

what stimulates I cells and L cells

A

free fatty acid

91
Q

is a phase 3 contraction

A

a very strong contraction with pylorus being open to get residual things out of your stomach

GIR Test 1 (15 decks)

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