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M104 T1 > M104 T1 L4 > Flashcards

M104 T1 L4 Flashcards

1
Q

How long is the digestive system in life compared to when fully lengthened?

A

approx 5 - 7m

79m

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2
Q

What three salivary glands are present in the oral cavity?

A

parotid
sublingual
submandibular

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3
Q

What are the accessory organs of the digestive system present in the thoracic cavity?

A

liver
gallbladder
pancreas

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4
Q

In which two places are the accessory organs of the digestive system located?

A

oral cavity

thoracic cavity

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5
Q

What substances does the GI tract extract from ingested products?

A

chemical energy

vitamins, minerals & water

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6
Q

What are the six processes the GI performs on ingested products?

A 
ingestion
secretion
motility
mechanical digestion
chemical digestion
absorption 
elimination of waste
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7
Q

What are the four layers of the GI tract?

A

the inner mucosa
the sub mucosa
the muscularis externa
the outer serosa

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8
Q

What are the three layers of the mucosa?

A

inner epithelial layer
lamina propria
muscularis mucosae

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9
Q

What cells does the lamina propria contain in the gut?

A

lymphatic cells

are associated with lymphoid tissue

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10
Q

What layer is on top of the inner epithelial layer of the mucosa?

A

the lamina propria layer of connective tissue

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11
Q

What is a benefit of having lymphatic cells in the lamina propria of the gut?

A

the cells have immune function
act as an additional protective barrier against pathogenic species which may cross from the gut lumen into the mucosal layer

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12
Q

What structures does the sub mucosa layer contain?

A

blood vessels
lymphatic supply to the gut wall
the sub mucosal nerve plexus

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13
Q

Which muscle types are in the the muscularis externa layer?

A

inner circular muscle

outer longitudinal muscle

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14
Q

What lies in between the inner circular muscle and the outer longitudinal muscle of the muscularis externa layer?

A

the myenteric nerve plexus

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15
Q

What is the layer of the GI tract that comes after the muscularis externa layer?

A

the outer serosa layer

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16
Q

What material is the oesophagus made up of?

A

flat epithelium

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17
Q

What structures are in the inner surface of the stomach and in the inner SI surface?

A

stomach - gastric pits

SI - villi and mv

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18
Q

What does the LI contain?

A

gut microbiota

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19
Q

What is the motility within the GI tract mainly governed by?

A

the contraction of smooth muscle - involuntary control

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20
Q

Which areas of the GI tract is instead governed by the voluntary contraction of striated skeletal muscle?

A

the upper oesophagus

the external anal sphincter

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21
Q

What is a single-unit smooth muscle cell innervated by?

A

an autonomic nerve fiber

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22
Q

How do muscle cells work as a syncytium?

A

the single-unit smooth muscle cells connected to eachother by gap junctions
this allows for the electrical coupling of the cells
so the contraction can occur in peristaltic waves
the cells contract as a functional syncytium

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23
Q

What is the enteric NS responsible for?

A

controlling gut motility

controlling secretion

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24
Q

What does the enteric NS give the gut the ability to do?

A

gives the gut the ability to contract completely independently of external neurostimulation

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25
Q

What does the enteric NS consist of?

A

two interconnected plexuses in gut wall

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26
Q

What are the two types interconnected plexuses in gut wall?

A

Myenteric plexus

Submucosal plexus

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27
Q

What type of innervation allows for the external modification of autonomous motility and secretion occur?

A

extrinsic autonomic sympathetic innvervation

parasympathetic innervation

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28
Q

Which local stimuli might cause the intrinsic enteric NS to undergo reflexive contraction?

A

stretch
nutrients
irritation
hormones

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29
Q

What is the Myenteric plexus primarily responsible for?

A

motility

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30
Q

What is the Submucosal plexus primarily responsible for?

A

secretion

local blood flow

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31
Q

What is the basic activity of the enteric NS controlled centrally by?

A

the autonomic NS

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32
Q

How does the autonomic NS supply the GI tract?

A

sympathetic and parasympathetic pathways

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33
Q

What is the effect of parasympathetic innervation on the GI tract?

A

it is excitatory to motility and secretion

rest and digest - promotes digestion

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34
Q

What part of the GI tract is innervated by the vagus nerve?

A

spans from the anterior part of the GI tract up until the transverse colon

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35
Q

What part of the GI tract is under sacral parasympathetic innervation?

A

the parts of the GI tract beyond the transverse colon

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36
Q

What is the effect of sympathetic innervation on the GI tract?

A

it is inhibitory to motility and secretion
promotes fight or flight portion
represses mechanisms that promote digestion

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37
Q

What two main types of mechanisms are responsible for regulating GI motility?

A

neural mechanisms

endocrine hormones

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38
Q

Where are endocrine hormones secreted from?

A

endocrine cells in the epithelial layer of the GI mucosa

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39
Q

What is the pathway of endocrine hormones to access the GI tract?

A

they leave the endocrine cells in the GI mucosa
they enter the portal blood circulation
they come back round through the vasculature

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40
Q

What is cholecystokinin released by?

A

I cells of the SI

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41
Q

What is the effect of cholecystokinin?

A

it is inhibitory to gastric emptying
allows the deudenum to deal with the contents that are currently present in the lumen
stimulates the digestion of fat and protein

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42
Q

How does cholecystokinin inhibit gastric emptying?

A

it causes gallbladder contraction

it causes the growth of exocrine pancreas and thereby stimulates the secretion of pancreatic enzymes for digestion

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43
Q

What is motilin released by?

A

M cells of the duodenum and jejunum

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44
Q

What is the effect of motilin?

A

it promotes gastric and intestinal motility

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45
Q

What are the two different types of electrical activity in excitable smooth muscle cells?

A

Slow waves and Spike potentials

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46
Q

When are spike potentials generated?

A

once the threshold is reached
causes an influx of Ca2+ influx
smooth muscle contracts

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47
Q

What is the function of slow waves?

A

they provide a basic electrical rhythm via interaction with the Interstitial Cells of Cajal

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48
Q

In waves/min, what is the basic electrical rhythm responsible smooth muscle contraction stimulation?

A

3 - 12 waves/min

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49
Q

In terms of slow waves and spike potentials, what will and won’t lead to a contraction?

A

slow - doesn’t in itself lead to contraction

spike - causes contraction by further depolarisation to threshold levels towards a more +ve membrane pt

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50
Q

What happens when successful spike potentials occur?

A

receptors on the smooth muscle cell are stimulated

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51
Q

What can stimulate smooth muscle cell receptors after a spike potential? (MADD)

A 
endocrine hormones (Motilin)
excitatory NTs (Acetylcholine)
stretch from GI lumen contents (e.g. Duodenal Distension)
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52
Q

Through which methods can smooth muscle contraction be inhibited?

A

symp stimulation - norepinephrine
hormones - secretin
inhibitory enteric NS

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53
Q

How is smooth muscle contraction inhibited?

A

via hyperpolarization - it makes the membrane pt more -ve rather than less -ve
so it’s harder to reach the threshold pt and for an actpt to occur

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54
Q

What are the two main categories of contraction that occur in the GI tract?

A

segmentation

peristalsis

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55
Q

What happens during segmentation contraction in the GI tract?

A

there are bursts of circular muscle contraction and relaxation which pushes the contents back and forth over a short short distances in a pendulum movement allows mixing to occur

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56
Q

What is the effect of segmentation contraction in the GI tract?

A

it allows the mixing the contents of the lumen

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57
Q

What is the effect of peristalsis in the GI tract?

A

it allows the propulsion of the contents of the lumen

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58
Q

What happens during peristalsis contraction in the GI tract?

A

local distention triggers contraction behind the bolus within the GI lumen and relaxation of the muscle in front
causes a wave of contraction to ripple along the gut

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59
Q

What regulates peristalsis?

A

the functional myenteric plexus

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60
Q

What does the law of the intestines state?

A

that peristalsis can only move food along the GI tract aborally

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61
Q

What is Hirschsprung’s disease caused by?

A

the myenteric plexus is missing from the distal portion of the colon

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62
Q

What happens in Hirschsprung’s disease?

A

the pathologic aganglionic section of colon lacks peristalsis
it undergoes continuous spasm
leads to functional obstruction and severe constipation

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63
Q

How is Hirschsprung’s disease treated?

A

surgery is performedto bypass the part of the colon that’s lacking nerve cells

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64
Q

What are the three stages of deglutition?

A

Oral
Pharyngeal
Oesophageal

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65
Q

What happens during the oral stage of deglutition?

A

voluntary initiation of swallowing in the oral cavity

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66
Q

What happens during the pharyngeal stage of deglutition?

A

involuntary passage of food through pharynx into oesophagus

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67
Q

What happens during the oesophageal stage of deglutition?

A

involuntary passage of food from pharynx to stomach

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68
Q

What is the oesophagus lined by?

A

protective, stratified squamous epithelium

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69
Q

What type of muscle is in the muscularis layer of the upper part of the oesophagus?

A

striated skeletal muscle

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70
Q

What is the oral phase of swallowing regulated by?

A

voluntary control

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71
Q

How does the oral stage of deglutition occur?

A

the tongue pushes up and against the hard palate
it contracts to force lubricated bolus into the pharynx
this initiates the pharyngeal stage swallowing through stimulation of sensory receptors

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72
Q

What are the three sections of the pharynx?

A

oropharynx
nasopharynx
larygopharynx

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73
Q

Which three nerves are involved in the pharyngeal stage of deglutition?

A

CN V - trigeminal
CN IX - glossopharyngeal
CN X - vagal

74
Q

What happens to the soft palette during the pharyngeal stage of deglutition?

A

it is elevated over the posterior nares to close nasal pharynx

75
Q

How is the bolus moved from the orpharynx into the oesophagus in the pharyngeal stage of deglutition?

A

the presence of the bolus in the oropharynx signals the swallowing centre in the brain
motor efferents in three nerves (CN V, IX & X) cause a series of muscle contractions, moving the bolus through the oropharynx into laryngopharynx and into oesophagus

76
Q

What happens to the epiglottis during the pharyngeal stage of deglutition?

A

is shuts to close the larynx

77
Q

What happens to the upper oeophageal sphincter during the pharyngeal stage of deglutition?

A

it relaxes

78
Q

What happens to respiration during the pharyngeal stage of deglutition?

A

it is inhibited

79
Q

What happens during the oesophageal phase of deglutition?

A

ther is a slower primary peristaltic wave that moves the bolus downwards towards the stomach

80
Q

What muscle types are involved in the oesophageal phase of deglutition and how?

A

circular muscle contraction behind the bolus

longitudinal muscle contracts in front to shorten the fibres and to push the wall outwards

81
Q

What substance is secreted in the lower oesophageal area during the oesophageal phase of deglutition?

A

mucus IOT lubricate and reduce friction

82
Q

What structures relax during the oesophageal phase of deglutition and why?

A

the lower oesophagus and the lower oesophageal sphincter

IOT allow the bolus to move into the stomach

83
Q

What will happen if the 1o peristaltic wave isn’t successful in moving the bolus into the stomach?

A

a 2o peristaltic wave will be stimulated by stretch within the oesophagus

84
Q

What innervation is responsible for the co-ordination behind swallowing?

A

intrinsic - myenteric innervation

extrinsic - vagal innervation

85
Q

What happens during achalasia?

A

the lower esophagus sphincter muscle fails to relax causing food to remain in the oesophagus

86
Q

What are the harmful effects of achalasia? (DUI.i - driving under influence idiot)

A

distention
ulceration
inflammation
infection

87
Q

Which two conditions are caused by a problem with oesophageal motility?

A

gastro-oesophageal reflux

achalasia

88
Q

How does gastro-oesophageal reflux occur?

A

the lower oesophageal sphincter loses its tone

AAR the acidic gastric contents flow into the oesophagus

89
Q

What might gastro-oesophageal reflux be linked to?

A

hiatus hernia

90
Q

What are the harmful effects of gastro-oesophageal reflux?

A

inflammation

ulceration

91
Q

What anatomical defects could cause achalasia?

A

anatomical defects of the vagal or myenteric nerves

92
Q

What can hiatus hernia cause?

A

gastric reflux

93
Q

What happens during a hiatus hernia?

A

a portion of the stomach protrudes through diaphragm into thorax

94
Q

What are the five regions of the stomach?

A 
cardia
fundus
main body
antrum
pylorus
95
Q

How is the stomach adapted to motility?

A

a third inner oblique muscle layer

rugal folds

96
Q

When do rugal folds appear and disappear?

A

appear - when the stomach is empty / contracted

disappear - when stomach is full

97
Q

What is the role of rugal folds?

A

they allow the stomach to stretch out

98
Q

What are the three primary functions of the stomach?

A

to act as a reservoir for boluses
mixing process
emptying process

99
Q

How is the stomach allowed to store boluses?

A

via the vagovagal reflex

100
Q

What is the function of the vagovagal reflex?

A

it allows the reservoir function in the stomach so that it can store boluses
it mediates receptive relaxation in which the muscle tone in the stomach relaxes

101
Q

What happens during the process of mixing in the stomach?

A

slow peristaltic waves
leads to the fragmentation of food
which is mixed with secreted gastric juice for digestion

102
Q

What happens during the process of emptying in the stomach?

A

slow release of contents into the duodenum at a controlled rate

103
Q

What is the primary function of the fundus?

A

as a reservoir

it stretches out IOT accommodate the contents from the oesophagus

104
Q

How does food get ready to leave the stomach?

A

grinding - mixing of contents in the body of the stomach
propulsion - stomach contents are propelled towards the pyloric antrum and towards the pyloric sphincter
retropulsion - it is then forced back for further mixing and digestion
repeats - this process continues over time
chyme - until chyme is produced, ready for expulsion from the stomach

105
Q

What is gastric emptying regulated by?

A

hormonal

neuronal (enteric NS & parasymp ANS)

106
Q

How does gastric emptying occur?

A

peristaltic contractions increase in strength to force contents through the pyloric sphincter and out into the jejunum
the jejunum starts to secrete regulatory hormones as a way of providing regulatory feedback
initiates segmental mixing

107
Q

What is the effect of hormones such as motilin on gastric emptying?

A

cause further excitation and gastric emptying

108
Q

What can inhibitatory gastric emptying be stimulated by?

A

ANS - sympathetic
duodenal enterogastric reflexes
jejunal hormones

109
Q

What is the process by which enterogastric reflexes occur?

A

parasympathetic impulses are sent to the stomach
they inhibit peristaltic waves
inhibits the gastric emptying function

110
Q

What are enterogastric reflexes triggered by?

A

duodenal distension

111
Q

What are examples of hormones from the jujenum that inhibit gastric emptying?

A

CCK

secretin

112
Q

What type of cells produce endocrine hormones that slow gastric emptying?

A

S cells - secretin
K cells - GIP & CCK
I cells - CCK

113
Q

What factors makes duodenal receptors aware that gastric chyme has entered?

A

increased acidity
increased levels of fat digestion products
changes in the osmotic potential of the duodenum

114
Q

What happens to the rate of gastric emptying when physiological changes are detected in the duodenum?

A

triggers receptors within the duodenal wall
activates short reflexes by the enteric NS
decreases the rate of gastric emptying

115
Q

What receptors are present in the duodenal wall? (MOC)

A

mechanoreceptors
osmorereceptors
chemoreceptors

116
Q

What are two examples of gastric motility dysfunctions?

A

dumping syndrome

gastroparesis

117
Q

What might dumping syndrome be caused by physiologically?

A

hypertonic duodenal contents causing rapid entrance of fluid into the duodenal lumen

118
Q

What might dumping syndrome be associated with?

A

the ingestion of a large meal for patients who’ve had a gastrectomy

119
Q

What symptoms are associated with dumping syndrome?

A

nausea, cramps
pallor, sweating
vertigo, fainting

120
Q

When does gastroparesis occur?

A

when the stomach fails to empty properly

prevents proper digestion

121
Q

What symptoms are associated with gastroparesis?

A

bloating and nausea

122
Q

What conditions might cause gastroparesis?

A

gastric cancer

peptic ulcers

123
Q

When might gastroparesis be observed in severely diabetic patients?

A

impaired vagal stimulation to the stomach, will develop autonomic neuropathy

124
Q

Where does the majority of digestion and absorption of nutrients occur and for how long?

A

in the SI over a period of 3 - 5 hrs

125
Q

What structures give the SI a large SA?

A

plicae circulares
villi
‘brush border’ microvilli

126
Q

What are the two types of motility that occur in the SI?

A

mixing & circulation

propulsive peristalsis

127
Q

What does mixing & circulation motility allow for?

A

the maximum exposure and circulation of digesting products for absorption via epithelial cells

128
Q

What is motility in the SI controlled by?

A

intrinsic motor patterns modified by hormonal and ANS neural stimuli

129
Q

How does mixing occur in the SI?

A 
chyme leaves the stomach
enters the SI
stretch receptors respond to its presence 
triggers myenteric innervation 
causes muscle contraction - segmentation
130
Q

What is the effect of segmentation in the SI?

A

mixing and churning of chyme

it doesn’t cause peristaltic movement

131
Q

What does GoldSIMCard stand for?

A

Serotonin, Insulin, Motilin

CCK, Gastrin

132
Q

What do the substances listed in GoldSIMCard have in common?

A

they’re all propulsive peristalsis causing hormones (excitative, SI)

133
Q

What are examples of inhibitory hormones from the SI that reduce propulsive peristalsis?

A

secretin and glucagon

134
Q

What are the three propulsive peristaltic reflexes?

A

Gastroenteric reflex
Gastroileal reflex
Migrating motor complex

135
Q

When do migrating motor complexes occur?

A

in between meals

136
Q

How often do migrating motor complexes occur?

A

every 90 mins - sweeps SI contents into the LI

137
Q

What are gastroenteric and gastroileal reflexes triggered by?

A

gastric distention of the gastric wall

138
Q

What is the effect of gastric distention in a gastroenteric reflex?

A

the myenteric plexus is activated to promote SI peristalsis

139
Q

What is the effect of gastric distention in a gastroileal reflex?

A

distension promotes peristalsis in the ileum to force chyme through ileocecal valve into caecum

140
Q

What are migrating motor complexes regulated by?

A

Intrinsic enteric control

motilin hormone

141
Q

What can happen if migrating motor complexes don’t occur?

A

bacterial overgrowth in the SI

142
Q

What is the role of the iIleocecal valve?

A

prevents backflow contents from the colon back into the SI
responds to pressure to relax the sphincter
promotes peristalsis through the SI into the LI

143
Q

What causes a peristaltic rush?

A

mucosal irritation
it stimulates the ENS and ANS neural reflexes
they rapidly sweep contents of SI into colon

144
Q

What causes paralytic ileus?

A

a loss of peristalsis following mechanical trauma

145
Q

When might paralytic ileus occur?

A

after surgery

146
Q

What structures cause vomiting?

A

SI receptors

two brain centres (VC, CTZ)

147
Q

What type of receptors in the distal SI are triggered that then cause vomiting ?

A

chemical sensory receptors

148
Q

How can the brain cause vomiting?

A

the vomiting centre in the brain causes reverse peristalsis to expel intestinal and gastric contents

149
Q

Why is motility in the LI more sluggish?

A

allows for sufficient water and electrolyte absorption

allows for the formation and storage of faeces

150
Q

Where does water and electrolyte absorption occur?

A

the proximal portion of the LI

151
Q

Where does the formation and storage of faeces occur?

A

the distal portion of the LI

152
Q

What type of bacteria does the LI contain?

A

commensal microbiota

153
Q

Why are the commensal microbiota in the LI beneficial?

A

they aid digestion

they synthesise vitamins B and K

154
Q

What are the structural adapatations of the LI?

A

the formation of the muscularis into the taenia coli

155
Q

What does the taniae coli do?

A

it tonically contracts to form haustral bulges

156
Q

How often do mass movements of peristalsis occur?

A

2-3x per day

157
Q

What is the effect of forceful peristaltic contractions?

A

they force LI contents into sigmoid colon and rectum

158
Q

What are the two types of reflexes in the LI responsible for mass movements of peristalsis?

A

the gastro-colic reflex

the duodeno-colic reflex

159
Q

What are the two types of peristalsis that occur in the LI?

A

slow waves of peristalsis

mass movements of peristalsis

160
Q

What are the reflexes responsible for mass movements of peristalsis triggered by?

A

stretch in the stomach and duodenal walls via the ANS

161
Q

What substances does faeces contain the residues of?

A

digestion
bacteria
bile pigment
mucosal debris

162
Q

What is the defaecation reflex initiated by?

A

when mass movements push faecal matter into the normally empty rectum

163
Q

What happens once faecal matter enters the rectum?

A

the afferent nerve fibres are stimulated by stretch receptors
they activate the enteric NS and parasympathetic ANS

164
Q

What happens once the defaecation reflex is triggered?

A

the longitudinal muscle in the rectum involuntary contracts
opening the internal anal sphincter
the constricted external anal sphincter is voluntarily relaxed to allow defecation

165
Q

How does the constricted external anal sphincter voluntarily relax?

A

via the skeletal motor neuron innervation

166
Q

What are the nerves of the submucosal plexus derived from?

A

the myenteric plexus

167
Q

What are the nerves of the myenteric plexus derived from?

A

the plexuses of parasymp nerves around the superior mesenteric artery

168
Q

What do slow waves involve?

A

cyclical oscillations of membrane pt

169
Q

What are the two 1o lymphoid tissues?

A

bone marrow and thymus

170
Q

What are the three examples of 2o lymphoid tissues?

A

lymph nodes, spleen, tonsils

171
Q

Why are they called inclusion cells?

A

bc they are abnormal fibroblasts with lots of dark inclusions in the central area of the cytoplasm

172
Q

What is the role M cells have in immunity?

A

they transport antigens from the GI lumen to immune cells, thereby initiating an immune response or tolerance.

173
Q

Where are M cells located?

A

lymphoid tissues in the mucosa

174
Q

What are the three extrinsic reflexes that can occur in the GI tract? (ICE)

A

gastroileal, gastroColic and Enterogastric

175
Q

What are two pancreatic proteases?

A

trypsin and chymotrypsin

176
Q

What four digestive enzymes are produced by the exocrine pancreas?

A

lipase, amylase, chymotrypsin, trypsin

177
Q

What is the pH of chyme in the duodenum (emerging from the stomach)?

A

~pH2

178
Q

What does the duodenum do in response to acidic chyme entering from the stomach?

A

secretes CCK < gallbladder contraction < alkaline bile released into the duodenum

179
Q

What is the difference between the basolateral and apical membranes?

A

baso - the membrane away from the lumen and close to the serosa (external tubing)
apical - the membrane lining the lumen and away from the serosa

180
Q

What is the difference between trypsin and chymotrypsin?

A

they hydrolyse bonds on different parts of the proteins they’re lysing

181
Q

What cells release gastrin and where?

A

G cells in the pyloric antrum of the stomach, duodenum, and the pancreas

M104 T1 (15 decks)

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