Gastric motility and secretion Flashcards

1
Q

Stores ingested food until it can be emptied into the small intestine.
Located between the esophagus and duodenum

A

Stomach

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2
Q

The 1st area of stomach is covered by the regis called ___

A

Ruga

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3
Q

The stomach is divided into 3 major parts

A

fundus, stomach body, antrum

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4
Q

Between stomach and duodenum, we have the ___ sphincter, which guards the antrum from the stomach into the duodenum

A

pyloric

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5
Q

The stomach stores ___ in the duodenum at a rate that does not exceed in the small intestine functional capacity.
The stomach cells also secrete __ and ___, the enzyme necessary for protein digestion.

A

chyme
HCL
pepsinogen

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6
Q

the stomach contains: ___ __ muscle and ___ smooth muscle layer

A

Circular smooth

longitudinal

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7
Q

oblique smooth muscle cells

A

serves in the complex grinding of the food

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8
Q

Two functional zones of the stomach

A

the proximal stomach and distal stomach

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9
Q

primarily serves as a reservoir and it stores the food before it can move to the distal stomach

A

proximal stomach

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10
Q

has thick muscle layer and is able to perform powerful muscle contraction. Serves to grind, titurate the meal and regulate rate at which partially digested food is emptied into the duodenum

A

distal stomach

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11
Q

During fasting, the entire content of the digestive tube catches undigested materials or ingested foreign substance moves them along the entire length of the digestive tract starting in the stomach. This can be considered a ___ ___ function of the digestive tract

A

house keeping

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12
Q

The house keeping function is accomplished with the help of __, which causes growling

A

migrating myoelectric complex MMC

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13
Q

migrating myoelectric complex MMC occurs in 3 phases

A

the quiescent,
irregular electric motor activity
most powerful contraction

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14
Q

in the absence of MMC – migrating motor complexes, undigested materials or ingested foreign particles can accumulate and form aggregate known as ___, which can obstruct the digestive lumen in particularly in the stomach and lead to ulcers

A

BEZOARS

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15
Q

The migrating myoelectric complexes are induced by peptide gastro-intestinal hormone called ___.

A

MOTILIN

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16
Q

levels of endogenous motilin correlate with the phases of migrating motor complex contractions, and if we inject the exogenous motilin, we can induce phase ___ of the MMC contraction ( the phase with stronger contraction)
Another peptide hormone is ___, which is suspected to regulate this activity

A

3

GHRELIN

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17
Q

___ and several erythromycin analogs known as __ can mimic the effects of motilin and significantly increase the gastrointestinal motility

A

Erythromycin

motilides

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18
Q

lower doses the erythromycin can promote the release the __ from the neurons of myenteric plexus and induce increase motility.

at higher doses erythromycin can directly stimulate the ___ receptors in the smooth muscles cells and induce very strong contraction and increase gastrointestinal motility

A

Ach

motilin

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19
Q

the increase in gastrointestinal motility by erythromycin can be used as a prokinetic agent and can actually be useful in patients that have impaired gastro-motility, like patients with ___ ___

A

DIABETIC GASTROPARESIS

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20
Q

As the stomach receives the food, it relaxes to accommodate the incoming meal known as ___ ___

A

receptive relaxation

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21
Q

triggered when the mechanoreceptor are stimulated in the stomach wall by the incoming food. Its
Mediated by intrinsic and vago-vagal reflexes

Its Mediated by ___ and __ reflexes

A

receptive relaxation response
intrinsic
vago-vagal

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22
Q

when food is going to the stomach, the wall of the stomach stretches and stimulates the mechanoreceptors, this cause the vagal nerve endings to release ___. ___ then acts pre-synpatically to promote the release of additional neurotransmitters, Nitric oxide and vasoactive intestinal peptide VIP

A

acetylcholine

Ach

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23
Q

__ and __ induce the relaxation in proximal stomach, as a result the stomach is able to accommodate the incoming food.

A

NO

VIP

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24
Q

When food moves from the proximal stomach to the distal stomach it is mixed and triturated by the strong contractions of the enteron
Pacemaker cells, the ___ ___ __ ___, which initiate the slow wave potentials and electrical activity of smooth muscle cells.
when slow wave potential reaches threshold, the peristatic wave is initiated and moves from stomach fundus to body, towards the enteron—small portion of chyme is emptied into the duodenum, through partial open pyloric sphincter

A

interstitial cells of cajal

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25
Q

when the perisitic wave of contractions reaches the pyloric sphincter and empties small amounts of chyme, the pyloric sphincter contracts and it seals the exit and chyme goes back into the ___ until the next contraction.

A

enteron

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26
Q

refers to the collection of disorders of different etiology in which gastric emptying is impaired or delayed

A

Gastroparesis

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27
Q

Causes of impaired gastric motility

A

SURGERY
MEDICATIONS
DIABETES

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28
Q

gastro paresis and the delayed gastric emptying can aggravate the symptoms of __, making the symptoms worse

A

diabetes

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29
Q

MEDICATIONS such as ___ or __ drug decrease gastro motility and cause gastro paresis.

A

anticholinergic

opioids

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30
Q

With a delayed gastric emptying, the delivery of nutrients to the duodenum is unpredictable and may influence the ability of the subject to maintain ___ control.

A

glycemic

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31
Q

MOST CLINICALLY CHALLENGING OF GASTRO PERISIS is patients with long standing
___ affects the cellular metabolism and membrane functions thickening of the capillary basement membrane

A

diabetes mellitus

Hyperglycemia

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32
Q

When capillary basement membrane is too thick, it might result is __, destroying the normal neuronal functions and result in neuronal death and disruption of the neuronal pathways which regulate the stomach motility resulting in gastro paresis.

A

hypoxia

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33
Q

causes of gastro paresis

A

damages to the nerve fibers,
loss of the pace maker cells
loss of enzymes Nitric Oxide Synthase

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34
Q

the loss of NO can result in __ spasm, constant contraction of the pyloric sphincter.

A

pyloric

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35
Q

what kind of diet would you recommend to a patient with impaired gastric emptying

A

low fat meals

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36
Q

Overall the function of smooth muscle cells of the stomach is regulated by 3 major types of factors:

A

Gastric factors
Duodenal factors
The factors that are coming from the outside of the duodenum system

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37
Q

factors that originate in the duodenum

A

Duodenal factors

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38
Q

factors that originate in the stomach

A

Gastric factors

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39
Q

The major gastric factors regulates the gastric motility is the presence of large amounts of chyme in the stomach.

when there’s a lot of chyme in the stomach, the gastric motility is stimulated by the action of vagus nerve ending and myenteric plexus. In addition, there’s a hormone release by the enteron endocrine cells of the stomach, and this hormone is called __.

A

GASTRIN

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40
Q

the central hormone produced by the stomach. has a stimulatory effect on both gastric motility and gastric secretion.

A

Gastrin

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41
Q

the __ has the power to inhibit the motility until it is ready to process more nutrients

A

duodenum

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42
Q

The major factors that inhibit the stomach motility in the duodenum are

A

fatty, hypertonic, acidic chyme

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43
Q

the presence of fatty, hypertonic, acidic chyme in the duodenum initiate two types of response:

A

hormonal response

neural response.

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44
Q

Occurs Outside the digestive system

A

emotion, intense pain

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45
Q

The 3 major enterogastrons include

A

SECRETIN, CCK, GIP

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46
Q

The hormonal response of fatty, hypertonic, acidic chyme in the duodenum are collectively known as ___ and inhibit gastric motility

A

ENTERO-GASTRONS

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47
Q

involves the reflexes that are integrated entirely within the enteric nervous system

A

SHORT REFLEXES

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48
Q

reflexes that involve autonomic nervous system

A

LONG REFLEXES

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49
Q

With the presences of fatty, hypertonic, acidic chyme, we decrease the ___ fibers and increase the activity of the ___ fibers (activity). As a result, the gastric motility is inhibited

A

parasympathetic

sympathetic

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50
Q

___ in the duodenum inhibit gastric motility

A

fats

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51
Q

NO is produced by NO synthase. how does the loss of NO synthase affect gastric motility

A

results in impaired gastric emptying

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52
Q

NO is a major inhibitory neurotransmitter, and induces the ___ of smooth muscle cells. Without, we have constant contractions of the pyloric sphincter

A

relaxation

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53
Q

the MMC migrating motor complex accomplishes the ___ functions of the digestive tract.

A

house keeping

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54
Q

segmentation id observed in the ___ intestine

A

small

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55
Q

during vomiting, the stomach, esophagus and corresponding sphincters are ___

A

relaxed

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56
Q

The main force of expulsion during vomiting comes from the respiratory muscles:

A

diaphragm
major aspiration muscle
abdominal muscle

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57
Q

Vomiting is regulated by the vomiting center which is in the ___ of the brain stem

A

medulla

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58
Q

the stomach is squeezed by diaphragm from ___ and the abdominal muscles from __ which causes the forceful expulsion of the stomach content into the esophagus and into the oral cavity

A

above

below

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59
Q

during vomiting the content of the stomach does not enter the respiratory airways bc the __ is closed

A

glottis

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60
Q

Vomiting is proceeded by:

A

profuse salivation
sweating
rapid heart rate
sensation of nausea due to discharge of the ANS

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61
Q

phayngeal stimulation is delivered to the vomiting center with the help of the ___ NERVE.

A

GLOSSOPHARYNEAL

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62
Q

The irritation of gastric mucosa by various drug, cytotoxic drugs, and the presence of pathogenic bacteria or viruses is transmitted and relayed to the vomiting center and the information is relayed from the gastric mucosa with the help of the ___ NERVE

A

VAGUS

63
Q

the vestibual nuclei and the cerebellum signals mediates the vomiting associated with __ sickness and vertigo

A

motion

64
Q

In this zone we have a specific chemoreptor cells which constantly monitor the blood and the cerebral spinal fluid for the presence of the potentially toxic or harmful compound; lacks a blood brain barrier

A

“chemoreceptor trigger zone”

65
Q

The chemoreceptor trigger zone has a high concentration of

A

serotonin
dopamine receptors
muscarinic receptors
cannabinoid receptors

66
Q

What is the ligand for the neurokinin-1 receptor?

A

Substance P

67
Q

the solitary tract nucleus relays information to the vomiting center from the __, small intestine and pharynx. Contains high concentration of :

A
stomach
cannabinoid receptors.
serotonin
dopaminergic receptors
mucarinic receptors
histamine receptors
neurokinin-1 receptors
68
Q

Information from the vestibular nuclei and cerebellum is transmitted to the vomiting center with the help of histamine receptors H1 and __ receptors.

A

muscarinic

69
Q

anti-emetic class are classified according to their receptors:

A
serotonin antagonists
dopamine antagonists
histamine H1 antagonists
muscarinic antagonists
neurokinin antagonists
cannabinoid agonist
70
Q

Serotonin receptor antagonist inhibit the function serotonin receptors in the ___ and the ___ mucosa. They interfere with the serotonin receptor function in the chemoreceptors trigger zone and the vomiting center

A

gastric

intestinal

71
Q

are widely used drugs that treat emesis associated with cancer chemotherapy – cytotoxic drugs

A

serotonin receptor antagonist

72
Q

most widely used anti-emetic

considered to be the general purpose anti-emetics, and are also effective against the vomiting associated with cancer chemotherapy

A

dopamine receptor antagonist

73
Q

Anti-emetic drugs are considered ___ drugs

A

Neuroleptic

74
Q

Two adverse effects that occur if we inhibit the dopaminergic receptors on the brain/CNS:

A

Parkinsons disease- parkinsonism symptoms can develop

Lethargy dyskinisia – involuntary movement of various parts of the body

75
Q

used to manage the vomiting associated with motion sickness, so they inhibit the transmission of information from the vestibular nuclei to the vomiting center.

A

Histamine H1 antagonist and muscarinic receptors

76
Q

stimulated by substance P, this antagonist is used as the additional therapy for patients experiencing multiple cycles of chemotherapy, and is effective against delayed vomiting

A

neurokinin1 receptor

77
Q

interferes with the vomiting reflex by stimulation that the cannabinoid receptors in the vomiting center

A

Dronabinol

78
Q

The surface of the stomach is covered by the invagination shown above. The upper part of the invagination is called gastric __ and the bottom gastric __.

A

pit

gland

79
Q

Deep below the gastric gland we have chief cells. The chief cells produced ___

A

pepsinogen

80
Q

The pepsinogen is an inactive precursor of the digestive enzyme __, so it is converted into its active form pepsin with the help of __ and the pepsin is a protolytic enzyme, it digest proteins

A

pepsin

HCL (hydrochloric acid)

81
Q

In the middle of the gastric gland we have parietal cells, which secrete __ and intrinsic factors. The intrinsic factor is necessary for successful absorption of ____ in the intestine.

A

HCL

vitamin B12

82
Q

Enteroendocrine cells

A

gastrin

83
Q

Parietal cells

A

HCl and intrinsic factor (B12)

84
Q

Mucous neck cells

A

thin watery mucus

85
Q

Surface epithelial cells

A

thick, viscous, alkaline mucus = protective barrier

86
Q

Aids in the breakdown of muscle and connective tissue, reducing large food particles into smaller particles

A

HCl

87
Q

Kills microorganisms ingested with food

Uncoils and denatures the proteins exposing more peptide bonds for digestion

A

HCL

88
Q

Why not produce the pepsin right away?

A

The main building block of the cells is protein. If activated right away it’ll destroy its own proteins.

89
Q

The 3 level barrier of the gastric defense are:

A

Pre-epithelial
epithelial
sub-epithelial

90
Q

this level barrier secretes mucus. its primarily composed of water, phospholipids and glycoproteins. This mucus prevents the diffusion of hydrogen ions and pepsin .

A

pre-epithelial

91
Q

in the pre-epithelial, the mucus gel functions as a non-stirred water layer blocking diffusion of__ and __. __ secreted by surface epithelial cells forms a pH gradient (pH 1-2 in the gastric lumen, and pH 6-7 along the epithelial cell surface).

A

H+
pepsin
Bicarbonate

92
Q

In the gastric mucosa we have a very high level of ___, which can increase the secretion of mucus, and bicarbonate. They can also inhibit the parietal cells, the acid secretion

A

prostaglandins

93
Q

___ are necessary to maintain the normal mucosal blood flow. Overall they are considered one of the most significant factors in the maintenance of the gastro mucosal defense.

A

Prostaglandins

94
Q

____drugs which inhibit the synthesis of prostaglandins in the gastric mucosa are associated with a variety of effects in the gastrointestinal system. Most dangerous of course is gastro intestinal bleeding and hemorrhage

A

non-steroidal inflammatory

95
Q

prostaglandins - functions

A

regulare release of bicarb and mucus
inhibit parietal cell secretion
maintains mucosal blood flow

96
Q

within the gastric submucosal layer supplies micronutrients and oxygen while removing toxic metabolites.

A

Microvascular system

97
Q

The three main stimulants of H+ ion secretion are

A

acetylcholine, gastrin, and histamine

98
Q

Characteristic features of the inactive parietal cell:

A

tubulovesicular network contains inactive proton pumps. When stmulated by HISTAMINE, ACETYLCHOLINE, or GASTRIN, which bind to receptors on the vasolateral membrane, tubulovesicular network is going to fuse with apical membrane of the parietal cells, and as a result the surface area of the membrane can increase up to 100 folds and we have insertion of active proton pumps into the membrane and the acid secretion

99
Q

The main player of of acid secretion is ___

____ ___ is present at high concentrations in the parietal cells

A

H/K ATPase

Carbonic anhydrase

100
Q

Parietal cells contain receptors for acetylcholine, gastrin, and histamine on their basolateral membrane. Stimulation of these receptors promotes ___ ___

A

acid secretion

101
Q

Histamine stimulate ___ receptor
acetylcholine acts on ___ receptor
gastrin stimulates the ___ _ receptor

Activation of these receptors/pathway, is insertion of H/K ATPase into the membrane and secretion of acid

The effect of these 3 pathways are synergistic

A

H2 histamine
cholecystokinin 2
M3 muscarinic

102
Q

The most potent acid suppressor drugs are the ___, which suppress the final step of acid production, the proton pump itself

A

proton pump inhibitor ppi

103
Q

the inhibition of proton pump means that the proton pump inhibitor is going to reduce the __ production independently from pathway stimulating the acid secretion. Except the H2 histamine receptor antagonist bc there effect can be overcome by the __ or __

A

acid
Ach
gastrin

104
Q

All __ are pro-drugs, to become active they need to be activated in the acidic environment of the stomach

A

PPI

105
Q

Acid secretion resumes only after __ pump molecules are synthesized and inserted into the luminal membrane, providing a prolonged (up to 24- to 48-hour) suppression of acid secretion.

A

new

106
Q

There may be rebound acid ___ (acid secretion above pretreatment levels) upon discontinuing the PPI therapy

Prolonged treament can significantly increase gastric ph which is a well established stimuli for the G cells, entero-endocrine cells, which secrete hormone ___, which stimulate the enterochromaffin-like cells to produce histamine

A

hypersecretion

gastrin

107
Q

Histamine stimulates the H2 histamine receptors on the parietal to increase the acid production.
which is what leads to hypersecretion after the discontinuation of __ therapy

A

PPI

108
Q

The most common side effects of PPI:

A

nausea, abdominal pain, constipation, flatulence, diarrhea

109
Q

PPIs are linked with 2-3-fold increased risk of _____ among elderly patients with chronic comorbidity and on broad-spectrum antibiotic

A

Clostridium difficile-associated diarrhea (CDAD)

110
Q

. The acidity in the the stomach is not only an important sterilizer but also the absorption of ____

A

calcium

111
Q

acid in the stomach helps to free the ca ions from the insoluble calcium salt in our food. This will decrease calcium plasma concentration and is a stimulus to release ___ hormones which is aimed to restore the normal ca concentration in the blood circulation

A

parathyroid

112
Q

the acid in the stomach is not only important for absorption of Ca but also

A

vitamin B12, iron, and magnesium.

113
Q

potential risks of PPIi

A
infections
enteric infection
community acquired pneumonia
bone fractures
nutritional deficiency: vit b12, iron, Mg2+
114
Q

There are 3 major phases of gastric secretion

A

Cephalic phase
Gastric phase
Intestinal phase

115
Q

its initiated before the food actually enters the stomach. Its initiated by the food anticipation, think, or smelling the food

A

Cephalic phase

116
Q

phase where food enters the stomach itself

A

Gastric

117
Q

this phase starts when 1st portion of chyme enter the duodenum

A

intestinal

118
Q

the neurons in the myenteric plexuses they stimulate the __ of the smooth muscles in the stomach while the submucosal plexuses neurons they promote the secretion of __ and ___

A

contraction
pepsinogen
HCL

119
Q

What occurs in the stomach when the ph drops below 2?

A

it serves as a inhibitory signal and temporarily inhibits the gastric motility and secretion until the ph is elevated again

120
Q

The ___ ___ is the main site for ingestion and absorption of food

A

small intestine

121
Q

Two repsonse occur when the chyme enters the duodenum:

So the information of these receptors act to inhibit the neurons in the myenteric plexuses and submucosal plexuses and we have the inhibition of gastric secretion and gastric motility.

A

1st the chymes stretch the duodenum wall and we have the activation of mechanoreceptors and the partially digested nutrients in the duodenum active various chemoreceptors which are present in the duodenum wall

2nd is the endocrine response

122
Q

So the presence of acidic, hypertonic chyme in the duodenum activates the specialized entero-endocrine cells in the duodenum wall which secrete the hormones collectively known as _____

A

entero-gastron

123
Q

that the major entero-gastron are gastric inhibitory peptide:

A

GIP, secretin, and CCK Cholecystokinin

124
Q

These hormones are released into the blood and they reach the gastric cells through circulation, and they again inhibit gastric motility and secretion

A

GIP, secretin, and CCK Cholecystokinin

125
Q

in an experiment, rabbits are administered a cholinergic agonist, pentagastrin or histamine via iv and the acid secretion is measured. which drug when co-administered with each of these agents would be expected to block gastric acid secretion produced by any of the stimuli?

A

PPI

126
Q

3 pathways that can stimulate the insertion of the proton pump into the membrane and stimulate acid secretion

A

histamine H2 receptor antagonist activated by binding of histamine, the muscarinic M3 receptor activated by Ach, and Cholinestikinin 2 receptors activated by gastrin

127
Q

histamine H2 receptor antagonist activated by binding of histamine, the muscarinic M3 receptor activated by Ach, and Cholinestikinin 2 receptors activated by gastrin are inhibited by the ___

A

proton pump inhibitor PPI

128
Q

disruption of the mucosal integrity of the stomach and/or duodenum, leading to local defector excavation due to active inflammation.

a breakage in the intestinal mucosa or duodenum mucosal

A

Ulcer

129
Q

___ deaths per year occur as a consequence of complicated PUD. (peptic ulver disease)

A

15,000

130
Q

Acid ___ disorders are common in the US, with ~4 million individuals (new cases and recurrences) affected per year.

A

peptic

131
Q

The pain in the stomach is aggravated by the ___ while the pain in the duodenum ulcer is relieved by the ___.

A

meals

meals

132
Q

the integrity of the gastro intestinal mucosa depends on the balance between the ___ factors and the ___ factors

A

hostile

protective

133
Q

Hostile factors included:

A

H. pylori infections, gastric acid, pepsin, NSAIDs

134
Q

Protective factors include

A

Bicarbonate, prostaglandins, mucus production, blood flow to mucosa

135
Q

Three major causes of peptic ulcer are

A

chronic helicobacter pylori infection, NSAIDs, and Acid hypersecretory states (such as zollinger-Ellison syndrome)

136
Q

a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of peptic ulcer disease. It is associated with up to 70%- 80% of duodenal ulcers.

A

H. pylori

137
Q

colonize the deep layers of the gel that coats the mucosa and disrupt its protective properties causing release of certain enzymes and toxins. It makes the underlying tissues more vulnerable to damage by digestive juices causing injury to the stomach and duodenum cells.

A

-H. pylori

138
Q

H pylori penetrate the ___ layer which cover the gastric epithelial cells. At this level the ph is neutral compared to the lumen which is about 2.

A

mucin

139
Q

pylori can further increase ph in its micro environment through the production of the enzyme ___. Urease produces ammonia, which helps to further increase ph

A

UREASE

140
Q

The two major toxins secrete by H. pylori are

A

Vac A

Cag toxin

141
Q

collapse the endocytic compartment of the cells which causes the appears of large non-functional vacuole

A

VacA

142
Q

disrupts the normal function of the cytoskeleton

A

Cag

143
Q

In fact the chronic infection with ___ is the strongest known risk factor for gastric cancer development. Gastric cancer is the __ leading of cancer related worldwide

A

h pylori

2nd

144
Q

H pylori increase risks or another type of cancerous tumor called

A

MALT LYMPHOMA (mucosal associated lymphoid tissue)

145
Q

The current gold standard for h pylori eradication is a triple combination of drug:

A

first line
second line
third line therapy

146
Q

In 1st line therapy: we have admin of the proton pump inhibitor, with two antibiotics __ and __ or sometimes the PPI with ___ and ___

A
clarithromycin
amoxicillin
or 
clarithromycin
metronidazole
147
Q

2nd line of defense we have admin of PPI with :

or PPI and

or PPI

A

bismuth
metronidazole
tetracycline

or metronidazole
tetracycline

or metronidazole and amoxicillin

148
Q

third line results in ___ rescue therapy or treatment tailored to individual _____ sensitivity

A

emperic

antibiotic

149
Q

H. pylori oscillates between a replicating state (pH ___,antibiotic sensitivity) and nonreplicating state (____, antibiotic insensitivity) according to the pH in the microenvironments

So the administration of proton pump inhibitors only helps to increase the ½ life of antibiotics but it also helps to switch the h pylori into the ___ cycle where its sensitive to antibiotics.

A

6-8
pH 4-6
replication

150
Q

In ___ syndrome, the endocrine tumor develops in the pancreas and secretes very high levels of hormone gastrin. This increase of gastrin stimulates stomach cells to produce the excessive amounts of acid and pepsin which are deposited in the duodenum overwhelming the protective properties of the duodenum mucosa and lead to the development of duodenal ulcers

A

Gastrinoma (Zollinger-Ellison syndrome

151
Q

in Gastrinoma (Zollinger-Ellison syndrome) If the tumor cannot be removed it is managed with ___.

A

proton pump inhibitor

152
Q

PPI can also be used to prevent and treat gastro intestinal ulcerations associated with ___ administration.

A

NSAIDs

153
Q

Since NSAID inhibit the ___ synthesis and this is the major reason of increase risk of gastric intestinal ulceration and peptic ulcer disease, so the introduction of the synthetic ____ analogs together with NSAIDs seem to be a logical approach to prevent the adverse effects in the gastrointestinal tract associated with NSAIDs

A

prostaglandin

prostaglandin

154
Q

the synthetic prostaglandin E2 (PGE2) analog and it has been shown to reduce the risk of peptic ulcers in patients who high doses of NSAIDs

it’s associated with a number of adverse effects and its not used very often. Usually the proton pump inhibitor is preferred in those patients

A

MISOPROSTOL