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Patho Summer Test #1 > Gastrointestinal Module #1 > Flashcards

Gastrointestinal Module #1 Flashcards

1
Q

What are the layers of the GI tract (from inner to outer layers)?

A

Mucosa

Submucosa

Muscularis

Adventitious (serosa)

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2
Q

What is the muscosa layer made of?

A

Mucosa Epithelium

Lamina Propria

Muscularis Mucosae

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3
Q

What can you find in the submucosa layer?

A

Glands

Associated Ducts

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4
Q

What are the layers of the muscularis layer?

A

Circular Layer

Longitudinal Layer

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5
Q

What is the adventitious (serosa) layer made of?

A

Connective Tissue

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6
Q

What is the enteric nervous system?

A

Intrinsic Nervous System of the GI tract

**considered part of the autonomic nervous system

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7
Q

What influences the enteric nervous system?

A

Parasympathetic = excitatory

Sympathetic = inhibitory

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8
Q

What is unique about the enteric nervous system?

A

Functions autonomously (w/o having to go up to the brain)

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9
Q

What are the 3 Enteric Plexuses?

A

Submucosal Plexus (Meissner Plexus)

Myenteric Plexus (Auerbach Plexus)

Subserosal Plexus

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10
Q

Where is the submucosal plexus located?

A

Located in submucosa

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11
Q

What is the function of the submucosal plexus?

A

Secretion and absorption

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12
Q

Where is the myenteric plexus located?

A

Between circular/longitudinal layers of the muscularis

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13
Q

What is the function of the myenteric plexus?

A

Motility

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14
Q

Where is the subserosal plexus located?

A

Mesentery

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15
Q

What does the subserosal plexus innervate?

A

ANS innervation of blood vessels and connective tissue

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16
Q

What are the 3 general functional components of the enteric plexuses?

A

Sensory

Motor

Interneurons

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17
Q

What do the sensory neurons of the enteric plexuses monitor?

A

Distention and chemical status of GI tract

**Sensory afferents via sympathetic nerves

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18
Q

What do the motor neurons of the enteric plexuses control?

A

Motility of the gut wall

Smooth muscle of GI vasculature

Secretions of the mucosa/submucosa

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19
Q

What does the interneurons of the enteric plexuses do?

A

Communication between sensory and motor neurons

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20
Q

What is the definition (for this class) of appetite?

A

Hunger

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21
Q

What is the definition (for this class) of satiety?

A

Sensation of fullness/satisfied

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22
Q

Where are the 2 centers that control appetite and satiety located?

A

Hypothalamus

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23
Q

What are the names of the centers that control appetite and what are they specifically controlling?

A

Lateral Center = Appetite

Medial Center = Satiety

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24
Q

What are the stimuli of the lateral center (appetite center)?

A

Smell (CN1), Vsiual, Taste (CN7, 9), Hearing (CN8)

Physiological Depletion of nutrient/energy stores

Memory/Fantasy

Gastric Hormone = Ghrelin

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25
Q

Where is ghrelin released from?

A

Stomach

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26
Q

What is ghrelin known as?

A

Hunger Hormone

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27
Q

What is the function of the medial center (satiety center)?

A

Suppress appetite

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28
Q

What are the stimuli of the medial center (satiety center)?

A

GI Hormones released during food ingestion (CCK, GLP-1, etc)

Leptin

PYY

Insulin

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29
Q

Where is leptin released from?

A

Fat Cells

Chief Cells

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30
Q

Where is PYY released from?

A

Small Intestine after meal

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31
Q

What extrinsilically influences the enteric system?

A

Autonomic Nervous Center:

    Sympathetic System = nerves of 
    sympathetic tract in thoracic and upper 
    lumbar regions

    Parasympathetic System = Vagus Nerve 
    and pelvic nerves of sacral plexus
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32
Q

How does the sympathetic system influence the enteric system?

A

Inhibitory effects on the GI tract:

    decrease peristalsis and secretions

    inhibit blood flow to GI tract
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33
Q

How does the parasympathetic system influence the enteric system?

A

Excitatory to GI Tract:

     increase peristalsis and secretions

     relax involuntary sphincters of GI tract

     facilitate blood flow to GI tract
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34
Q

What is the intrinsic regulation of the enteric system?

A

Can feedback on itself and function autonomously = “brain in the gut”

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35
Q

What are the specific functions of the enteric nervous system?

A

Control Motility

Regulation of fluid exchange and local GI blood flow

Regulation of gastric and pancreatic secretion

Regulation of gastrointestinal endocrine cells

Defense reactions

Entero-enteric reflexes

ENS/CNS interaction

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36
Q

How does the enteric nervous system control motility?

A

Peristalsis

Sphincter Control

Etc.

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37
Q

How does the enteric nervous system regulate fluid exchange and local GI blood flow?

A

Regulate permeability to ions thus influence fluid

Influence vasodilation of BV

Influence fluid secretion

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38
Q

How does the enteric nervous system regulate gastrointestinal endocrine cells?

A

Signal release of GI hormones (ie excessive seratonin released from GI walls = nausea/vomiting)

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39
Q

What are the entero-enteric reflexes?

A

Signaling system between regions of the GI tract

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40
Q

What are examples of the entero-enteric reflexes?

A

Gastric activity stimulating Si motility and releaxation of iliocecal valve

Small intestine activity signals release of pancreatic enzymes

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41
Q

What is secreted in the mouth that is important for the GI tract?

A

Saliva

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42
Q

What controls the release of salivia?

A

BOTH parasympathetic and sympathetic systems stimulate salivary glands

NOT CONTROLLED BY HORMONES!

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43
Q

What does saliva contain (8 things)?

A

Water

Mucus

Na+

Bicarbonate

Chloride

K+

Salivary Amylase

Immunoglobulin A (IgA)

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44
Q

What is the function of bicarbonate in saliva?

A

Maintain pH in mouth to neutrolize bacteria (tooth decay)

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45
Q

What does salivary amylase do?

A

Begins first steps to break down (digest) carbohydrates

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46
Q

What is the purpose of IgA in saliva?

A

Prevent Infection

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47
Q

Where is the upper esophageal sphincter located?

A

Junction of lower pharynx and esophagus

Approximately @ level of cricoid cartilage

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48
Q

What is the function of the upper esophageal sphincter?

A

Prevent air from entering esophagus during ventilation

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49
Q

Is the upper esophageal sphincter considered a “true” sphincter?

A

Yes

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50
Q

Where is the lower esophageal sphincter located?

A

Narrowing of esophagus proximal to junction of esophagus and stomach

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51
Q

What is the function of the lower esophageal sphincter?

A

Barrier to reflux (regurgiation) of acidic content of stomach

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52
Q

Is the lower esophageal sphincter a true sphincter?

A

No

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53
Q

So if the lower esophageal sphincter is not a true sphincter, how is it maintained?

A

Increased smooth muscle tone –> 20 mmHg

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54
Q

What happens to the lower esophageal sphincter smooth muscle tone during swallowing?

A

Relaxed by peristaltic waves

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55
Q

What are the 2 phases of swallowing?

A

Voluntary Phase (oropharyngeal phase)

Involuntary phase (esophageal phase)

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56
Q

What happens during the voluntary phase (oropharyngeal phase) of swallowing?

A

Food broken down and tongue pushes bolus posteriorly

Soft palate (superior constrictor muscles) contract to close nasopharynx

Epiglottis closes of larynex/trachea

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57
Q

How long does it take for food to be pushed into the esophagus during the voluntary phase (oropharyngeal phase) of swallowing?

A

1 - 2 seconds

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58
Q

When does the involuntary phase (esophageal phase) of swallowing begin?

A

As bolus enters esophagus

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59
Q

When does the involuntary phase (esophageal phase) of swallowing end?

A

As bolus enters stomach

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60
Q

How long does the voluntary phase (esophageal phase) of swallowing last?

A

5 - 10 seconds

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61
Q

How is the bolus moved toward the stomach in the esophagus?

A

Peristalsis

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62
Q

What is peristalsis?

A

Coordinated contraction/relaxation of the longitudinal/circular muscles

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63
Q

How does the esophageal muscular pressure range?

A

Ranges from 35 - 85 mmHg

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64
Q

What is the esophageal pressure in the upper and lower esophagus?

A

60 - 80 mmHg

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65
Q

What is the esophageal pressure in the middle esophagus?

A

30 - 45 mmHg

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66
Q

What happens to food in the esophagus if contractions are < 30 mmHg?

A

Food residue may get stuck

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67
Q

What is the nervous system that controls peristalsis?

A

Vagus Nerve for both excitatory and inhibitory pathways (works to coordinate contraction/relaxation)

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68
Q

What are the bodily chemicals that control peristalsis?

A

ACh = excitatory

NO = inhibitory

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69
Q

What is secondary peristalsis?

A

Involuntary wave

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70
Q

What would cause secondary peristalsis?

A

Food residue from ineffective primary peristalsis

OR

Bolus that is “stuck”

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71
Q

Describe what happens when bolus/food residue gets stuck in the esophagus and causes a distention

A

Feedback to:

  Constrict esophagus above distention

   Relax esophagus below distention

   Which pushes residue/bolus along
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72
Q

What happens when you are swallowing food?

A

Single swallow initiates esophageal peristaltic contraction that lasts 5 - 10 seconds follwed by short refractory period

73
Q

After swallowing a bite of food, what does the short refractory period following peristaltic contraction do?

A

Inhibits ability to swallow second bite of food more frequently than 10 - 15 seconda

74
Q

How often do you swallow when drinking a liquid?

A

Every 1 - 2 seconda

75
Q

What is the name of the inhibitory reflex in your esophagus and what does that reflex do when you’re drinking a liquid?

A

Deglutitive Inhibition (made w/ quick subsequent swallows)

Prevents esophagus from ongoing contraction –> esophagus stays relaxed to allow more liquid to descend = gulping

76
Q

What are the 3 factors that create the basal tone of the lower esophageal sphincter?

A

Myogenic Tone (independent of neural input)

Excitatory Vagal Tone (Cholinergic - ACh)

Inhibitory Vagal Tone (Nitrergic - NO)

77
Q

What are some factors that increase lower esophageal sphincter pressure?

A

Vagus Nerve –> excitatory pathways of vagus nerve

Gastrin

Meds for GERD

78
Q

Why does gastrin increase lower esophageal sphincter pressure?

A

Gastrin promotes acid secretion/motility so you need to keep LES closed to prevent acid reflex in esophagus

79
Q

What are some factors that decrease lower esophageal sphincter pressure?

A

Vagus Nerve –> inhibitory pathways

Hormones: progesterone, secretin, glucagon

Fried fatty foods

Tomatoes

Citrus

High Protein Diet

Chocolate

Peppermint

Tobacco

Alcohol

Caffeine

80
Q

What happens to cause GERD?

A

Decreased LES pressure and ineffective clerance mechanism of secondary peristaltic waves

Chronic acid reflux reslts in in flammation/pain and eventual destruction of esophageal wall (esophagitis)

81
Q

What are some causes of decreased lower esophageal pressure/risk factors for GERD?

A

Hiatal Hernia

Pregnancy

Excessive ETOH

Tobacco

Obesity

82
Q

What is achalasia?

A

Rare disease in which lower esophageal sphincter fails to relax

Causes pain with eating and drinking

83
Q

What happens to cause achalasia?

A

Unknown exactly but it is a mechanical result of peristalsis of the esophageal musculature and the failure of the lower esophageal sphincter to relax

84
Q

What is esophageal varices?

A

Severely dilated sub-mucosal veins in the esophagus

**usually d/t portal hypertension

85
Q

What can esophageal varices lead to?

A

Bleeding –> Chronic GI bleeding –> severe systemic consequences

86
Q

What is Barrett’s Esophagus?

A

Condition in which normal mature cells (esophageal squamous epithelium) lining the esophagus are replaced w/ abnormal cells (metaplastic columnar mucosa) d/t exposure to stomach acids

87
Q

What is metaplasia?

A

1 mature adult cell type is replaced by another

88
Q

What are the symptoms of Barrett’s Esophagus?

A

“Heart Burn”

**metaplasia = histologic reflexion of esophagus being exposed to stomach acid

89
Q

Will all patients with GERD develop Barrett’s esophagus?

90
Q

What can Barrett’s esophagus develop into?

A

Adenocarcinoma of the esophagus

91
Q

Will all patients with Barrett’s esophagus develop esophageal cancer?

A

No!

Risk = 1:3000

**amount of dysplasia present increases risk of cancer

92
Q

What id dysplasia?

A

Abnormal development/maturation of cells

Delay/abnormal differentiation of cells results in # of immature cells

Indication of early neoplastic process

93
Q

What are the regions of the stomach?

A

Cardiac = region where esophagus enters stomach

Fundus = area above cardiac region

Pyloric = area near duodenum

Lesser and Greater curvature

94
Q

What is the gastric function?

A

Digestion = secretion and some absorption

Motility = propel food into duodenum

95
Q

What is partially digested food called?

96
Q

How is food digested in the stomach?

A

Gastric juices

97
Q

Which foods are absorbed in the stomach?

A

Aspirin

NSAIDs

Alcohol

98
Q

What relaxes the stomach musculature?

A

Swallowing (prepares stomach for bolus)

99
Q

What stimulates the motility of the stomach?

A

Vagus (cholinergic)

Hormones: Gastrin and Motilin

100
Q

Describe the sequence of gastric motility

A

Series of alternating small waves travel toward the pylorus

4 or 5 sequential peristaltic waves push chyme back and forth (churn)

Last wave forces pyloric sphincter to open and chyme is pushed into duodenum (pylorus is open about 1 - 2 cm which is not enough to regurgitate back into stomach)

101
Q

What is the average total time to empy the stomach?

A

50% after 2 - 3 hours

Total emptying after 4 - 5 hours

102
Q

What are the factors that increase rate of gastric emptying?

A

Larger food volume

103
Q

What are the factors that decrease gastric emptying?

A

Hyper/hypotonic fluid

Fatty Foods

Increased rate of acids entering the duodenum

104
Q

Why do you need decreased rate of gastric emptying when ingesting a hyper/hypotonic fluid?

A

Allow time to create/facilitate isoosmotic environment for the duodenum

105
Q

When ingesting fatty foods what is the hormone that inhibits gastric motility and where is it released?

A

CCK (cholecystokinin)

Synthesized/released by duodenum/SI

**also decreases acid production)

106
Q

Where are fats digested?

107
Q

What happens if too much fat enters the small intestine?

A

Feedback loop slows down rate to allow time to properly digest fats

108
Q

Where is acid neutralized?

109
Q

What happens if too much acid enter the small intestine?

A

Feedback loop inhibits gastric emptying to decrease acid entering duodenum

110
Q

What is pyloric stenosis also know as?

A

Infantile Hypertrophic Pyloric

Stenosis (IHPS)

111
Q

What is going on with pyloric stenosis?

A

Muscles of pyloric sphincter are
hypertrophied which impairs
gastric emptying

112
Q

How is pyloric stenosis treated?

A

Surgery = Pyloromyotomy

113
Q

What is gastric juice?

A

Acid

Mucous

Pepsinogen

114
Q

What are the major secretions of the stomach?

A

Mucus

Acid

Proteases

Hormones

Intrinsic Factor

115
Q

What is the function of mucus?

A

Protect mucosal layer from acid and pepsin (protease)

**stomach acid pH = 1.5

116
Q

How does mucus protect the mucosal layer from stomach acid?

A

Provides transitional layer to protect the epithelium

Contains high levels of bicarbonate (HCO3-) to neutralize the H+ –> pH of stomach = 1.5 and pH @ epithelial layer = 7

117
Q

What are some stimuli of mucus secretion?

A

Prostaglandins (pathway = disrupted by NSAIDs)

Nitric Oxide

118
Q

What are some things that disrupt the mucus barrier?

A

Aspirin

NSAIDs

Alcohol

Bile Salts (regurgitated from SI)

Helicobacter pylori (bacteria)

119
Q

What is the function of stomach acid?

A

Dissolve Food

Inactivate bacteria/microorganisms that have been ingested

Convert pepsinogen to pepsin

120
Q

What cells secrete stomach acid?

A

Parietal cells in the body/fundus of the stomach

121
Q

What molecule is “exchanged” for acid formation in the stomach?

A

Bicarbonate into the plasma

**can lead to Alkaline Tide or Wave”

122
Q

What stimulates acid secretion in the stomach?

A

ACh via vagus nerve (parasympathetic)

Gastrin

Histamine

123
Q

What inhibits acid secretion in the stomach?

A

Gastrin inhibitory peptide (GIP)

Somatostatin

Secretin

Prostaglandin

124
Q

Where is somatostatin secreted from in the gastrointestinal tract?

A

Stomach

Intestine

Pancreas

125
Q

What does secretin do?

A

Works synergistically w/ CCK to inhibit gastric motility

126
Q

What cells produce and secrete pepsinogen?

A

Chief Cells

127
Q

What does pepsinogen need to be converted to pepsin?

A

Acidic Environment (pH < 2)

128
Q

What is the function of pepsin?

A

Proteolytic enzyme that breaks down proteins in the stomach

129
Q

Where is pepsin inactivated?

A

Small Intestine (more alkaline environment)

130
Q

What are the gastric hormones?

A

Gastrin

Motilin

Gastrin Inhibitory Emptying Peptide (GIP)

Grehlin

131
Q

What does gastrin do?

A

Promote gastric juice (acid) secretion and gastric motility

132
Q

What cells secrete gastrin?

A

G Cells in stomach (located in antrum)

133
Q

What does motilin do?

A

Promote stomach/SI motility

134
Q

Where is motilin secreted?

A

From endocrine cells located in the small intestine

135
Q

What does gastric inhibitory emptying peptide do?

A

Inhibit gastric juice (acid) secretion and gastric motility

136
Q

Where is gastric inhibitory emptying peptide secreted?

A

Endocrine cells in the small intestine

137
Q

What is Grehlin?

A

The “hunger hormone”

Plays role in appetite sensation/feeding behavior

**levels rise just before meals

138
Q

Where is grehlin secreted?

A

Endocrine cells mostly located in the stomach

Also from: kidneys, hypothalamus, pituitary, placenta

139
Q

What is Intrinsic Factor?

A

Necessary for Vitamin B12 absorption in the small intestine

140
Q

Where is intrinsic factor secreted?

A

Parietal Cells of the stomach

141
Q

What are the epithelial folds of the stomach called?

142
Q

What are the cell types that are found at the surface of the folds of rugae?

A

Mucous Cells

143
Q

What do the mucous cells in the rugae do?

A

Produce thick mucous = protection from abrasion of food and from pH levels in stomach

144
Q

What cells are found at the base of the folds of rugae?

A

Gastric Glands (vary by stomach region)

145
Q

Which cell type is found in the gastric glands in the body/fundus region of the stomach?

A

Mucous cells –> located @ neck of gastric glands

Parietal Cells

Chief Cells

Enterochromaffin-like Cells

146
Q

What do mucous cells do in the gastric glands @ the body/fundus of the stomach?

A

Secrete thin, watery mucus to liquefy stomach contents

147
Q

What do parietal cells do in the gastric glands @ the body/fundus of the stomach?

A

Secrete acid (HCl)

Secrete intrinsic factor

148
Q

What do chief cells do in the gastric glands @ the body/fundus of the stomach?

A

Secrete pepsinogen (promote protein digestion)

149
Q

What do enterochromaffin-like cells do in the gastric glands @ the body/fundus of the stomach?

A

Secrete histamine (promote acid secretion)

150
Q

Which cells are found in the gastric glands in the cardiac region of the stomach and what do they do?

A

Mucous Cells –> secrete thin, watery mucus to liquefy stomach contents

151
Q

Which cells are found in the gastric glands in the pyloric (antrum) region of the stomach?

A

Mucous Cells

G cells

152
Q

What do mucous cells do in the do in the gastric glands @ the pyloric region of the stomach?

A

Secrete thin, watery mucous to liquefy stomach contents

153
Q

What do G cells do do in the gastric glands @ the pyloric region of the stomach?

A

Secrete gastrin (promote acid secretion/motility)

154
Q

What are the 3 types of weight loss procedures?

A

Adjustable gastric band (LAP Band)

Ventrical Banded Gastroplasty (VBG) –> stomach stapling w/ lap band”

Gastric Bypass

155
Q

Describe the adjustable gastric band procedure

A

Placement of band creates small pouch @ top of stomach

Small pouch “fills” w/ food quickly and passage of food from top to bottom of stomach is slowed

Upper part of stomach experiences sensation of fullness

156
Q

Describe the Vertical Banded Gastroplasty (VBG)

A

Both band and staples are used to create a small stomach pouch

Small opening in bottom of pouch through which food can pass through to rest of the stomach

**smaller pouch helps person eat smaller portions and lose weight over time

157
Q

What are the initial outcomes seen with VBG?

A

Vary from:

“complete” weight loss

some weight loss

poor weight loss

158
Q

What are the longterm outcomes seen with VBG?

A

Many patients will regain weight by gradually stretching small pouch

159
Q

Describe gastric bypass procedures

A

Physically redirects anatomy of GI tract –> bypass created so chyme bypasses proximal small intestine

Point is to limit absorption of calories (and nutrients) in small intestine

160
Q

What are the outcomes of gastric bypass?

A

Long/short term outcomes suggested to be better than banding/stapling procedures

161
Q

What is the most common restrictive operation for weight control?

A

Vertical Banded Gastroplasty (VBG)

162
Q

What are the complications of gastric bypass?

A

Nutritional deficiencies –> need long term supplementation plan

Dumping syndrome –> rapid gastric emptying

Direct complications to GI tract –> bleeding, infections, etc

163
Q

What exactly is dumping syndrome?

A

Jejunum rapidly fills w/ undigested food from stomach?

164
Q

What are the signs/symptoms of dumping syndrome?

A

Cramping

Bloating

Nausea

Vomitting

Diarrhea

Shortness of Breath

165
Q

What is gastritis?

A

Inflammation (diffuse through lining) of gastric mucosa)

166
Q

When would you see acute gastritis?

A

W/ injury to the gastric mucosa

167
Q

What are some causes of acute gastritis?

A

Drugs/Chemicals –> NSAIDs

H. pylori infection

Alcohol

Smoking

168
Q

How long will acute gastritis last?

A

A few days but want to remove offending facotr ASAP

169
Q

What is chronic gastritis?

A

Degenerative gastritis –> Chronic inflammation, mucosal atrophy and epithelial metaplasia

170
Q

When do you see chronic gastritis?

A

More common in elderly

171
Q

What are the 2 types of chronic gastritis?

A

Type A = chronic fundal gastritis –> in fundus/body

Type B = chronic antral gastritis

172
Q

Which type of chronic gastritis is more common?

A

Type B = 4x more common than A

173
Q

Which type of chronic gastritis is considered autoimmune dysfunction?

A

Type A –> antibodies attack parietal, chief cells and intrinsic factor

174
Q

If Type A chronic gastritis is autoimmune, what is the problem with Type B?

A

Seems to be more of motiltiy problem; no loss of acid secretion, parietal cels, intrinsic factor

175
Q

Where in the stomach do you see most gastric ulcers?

176
Q

What kind of feedback is involved w/ gastric uclers?

A

(+) feed back:

Chronic exposure to various substances –> breakdown of protective mucosal lining of stomach

Damaged mucosa releases histamine –> increased release of acids/pepsinogen, increased capillary permeability

177
Q

Do gastric ulcers possess higher risk of cancer?

A

Yes (vs. risk for duodenal ulcer)

178
Q

What are the 2 major risk factors for benign gastric ulcers?

A

Chronic use of aspirin, NSAIDs

H pylori infection

179
Q

What are the clinical signs and symptoms of a gastric ulcer?

A

Food provoking pain pattern –> pain immediately after eating

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