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Semester 4 > Case 2 > Flashcards

Case 2 Flashcards

1
Q

What is the resting volume of the stomach what is it’s maximum capacity?

A

1300m- 1500ml, capacity is 3L

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2
Q

What is the name for the inner concavity of the stomach?

A

The lesser curvature.

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3
Q

What is the name for the outer convexity of the stomach?

A

The greater curvature

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4
Q

What is the name for the angle on the lesser curvature of the stomach?

A

The incisura angularis

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5
Q

What are the four anatomical parts of the stomach?

A

The cardia, fundus, body/corpus and the pyloric part

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6
Q

What part of the stomach surrounds the cardial orifice at the top of the stomach?

A

The cardia

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7
Q

What is the name for the top dilated part of the stomach related to the left dome of the diaphragm?

A

The fundus

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8
Q

What part of the stomach lies between the fundus and the pyloric antrum?

A

The body/corpus

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9
Q

What are the two functional portions of the stomach?

A

the orad and caudad region.

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10
Q

What functional region of the stomach includes the fundus and the superior part of the body?

A

The orad

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11
Q

What functional region of the stomach contains the lower part of the corpus and the antrum?

A

the caudad

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12
Q

What is the name for the coarse in foldings of mucosa and submucosa throughout the inner surface of the stomach? Where are they most prominent?

A

rugae, they are most prominent in the proximal stomach

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13
Q

What is the name of the tall columnar mucous secreting cells which line the the whole gastric mucosa and gastric pits?

A

surface foveolar/mucous cells

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14
Q

What is the role of the mucous secreted by surface foveolar/mucous cells?

A

They protect the stomach lining from acid

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15
Q

Where are mucous neck cells found what is their role?

A

These cells are found deepish in the gastric pits and are thought to be progenitors of both the surface epithelium and cells of the gastric glands.

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16
Q

What type of cell found deepish in the gastric pits are thought to be the progenitors of the surface epithelial cells and gastric glands?

A

Mucous neck cells

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17
Q

Where are delta cells found what do they secrete what effect does this have?

A

they are found in stomach intestines and islets of langerhans, they secrete somatostatin which reduces gastrin and histamine release.

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18
Q

What cells does the somatostatin released by D/Delta cells act on what effect does it have?

A

G cells and ECL reducing gastrin and histamine release.

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19
Q

What are the three main types of gastric glands?

A

Cardiac tubular, main gastrin and pyloric(antral glands.

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20
Q

What is the name for the glands located in the mucosa of the cardia and secrete soluble mucous?

A

cardiac.

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21
Q

What are the three main types of cell in main oxyntic/gastric glands?

A

Chief/peptic cells, mucus neck cells and parietal/oxyntic cells

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22
Q

Where are the main gastric glands found?

A

In the body and fundus of the stomach.

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23
Q

Which cell type in the main gastric gland is basophilic?

A

Chief/peptic/zymogen cells

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24
Q

What do chief cells screte?

A

proteolytic proenzymes, pepsinogen I & II

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25
Q

Which type of cell found in the main gastric glands has a canalicular intracellular structure.

A

Parietal/oxyntic cells

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26
Q

What do parietal/oxytic cells secrete?

A

HCL and intrinsic factor

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27
Q

Where are parietal cells found in main gastric glands?

A

Mostly in the upper half

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28
Q

What are the two cell types of the pyloric/antral glands?

A

Mucus and G cells

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29
Q

pyloric/antral glands mostly contain which type of cell?

A

Mucous cells

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30
Q

What do G cells secrete?

A

gastrin

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31
Q

The serosa of the stomach is part of what structure?

A

The peritoneum

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32
Q

What are the three layers of musculature of the stomach from outer to innermost?

A

longitudinal, circular and inner oblique.

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33
Q

What two plexuses supply the stomach with its intrinsic innervation?

A

myenteric (auerbach’s) and submucoal (Meissener’s) plexuses

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34
Q

Where is the auerbach plexus located?

A

between the circular and longitudinal layers of the stomach.

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35
Q

Is it the intrinsic or extrinsic innervation that is responsible for peristalsis?

A

Intrinsic.

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36
Q

What aspect of the innervation of the stomach allows peristalsis in the antrum to influence the duodenal bulb?

A

The fact that the system for innervating the duodenum is continuous for those that innervate the stomach.

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37
Q

Where does the sympathetic innervation of the stomach arise how does it affect motility?

A

It arises from the coeliac plexus, it inhibits motility.

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38
Q

Where does the parasympathetic innervation of the stomach arise from, how does it affect motility?

A

It arises from the vagus nerve and stimulates motility.

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39
Q

where is the stomach relative to the peritoneum?

A

Intraperitoneal

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40
Q

What is the name of the specialized pacemaker cells located in the walls of the stomach, small intestine and large intestine?

A

cells of cajal

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41
Q

Where is the duodenum relative the the peritoneum?

A

It is retroperitoneal except at it’s beginning where it is connected to the liver via the hepatoduodenal ligament, a part of the lesser omentum

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42
Q

What are the four parts of the duodenum in order?

A

superior, descending, inferior and ascending.

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43
Q

Where does the superior part of the duodenum start and end? what are it’s relations?

A

It starts at the pyloric orifice and ends at the neck of the gall bladder. It is just right of vertebra L1, passes anteriorly to the gastroduodenal artery, portal vein and inferior vena cava.

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44
Q

Where does the descending part of the duodenum start and finish? What are its relations?

A

It starts at the neck of the gall bladder extending to the lower border of the L3 vertebra, Its anterior surface is covered by the transverse colon, behind it is the right kidney and is lateral to the head of the pancreas

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45
Q

Which of the four sections of the duodenum contains the major and minor duodenal papilla? What opens through these?

A

descending duodenum, the bile and pancreatic ducts open through the major papilla whereas the accessory duct opens to the minor papilla.

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46
Q

Which is the longest section of the duodenum?

A

The inferior part

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47
Q

What are the relations of the inferior part of the duodenum?

A

It crosses over the inferior vena cava, aorta and vetebral column and is crossed anteriorly by the superior mesenteric artery and vein.

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48
Q

What are the relations of the ascending part of the duodenum?

A

It is left of the aorta and alongside the vertebral column to roughly the L2 level.

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49
Q

Where does the duodenum end what surrounds this?

A

The duodenal flexure. It is surrounded by a fold of peritoneum containing muscle fibers know as the suspensory ligament or the ligament of Treitz

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50
Q

What are the cells of cajal attached to the smooth muscle of the stomach, large & small intestines via?

A

gap junctions and the myenteric plexus.

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51
Q

What does BER stand for?

A

Basal electrical rhythm

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52
Q

The cells of cajal undergo a rhythmic de and repolarization, at what voltage? What does this create?

A

From -65mV to -45mV this creates a slow wave known as the BER

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53
Q

What are the three meal related motor functions of the stomach?

A

Storage, mixing and slow emptying.

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54
Q

What are the two phases of a gastric slow wave?

A

Upstroke and plateau.

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55
Q

What is the standard rate of gastric slow waves?

A

3-4 waves per minute.

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56
Q

What are 5 agents that increase the smooth muscle contractile activity of the stomach?

A

ACh, gastrin, histamine, nicotine, barium and K+

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57
Q

What are 5 agents that inhibit stomach smooth muscle activity?

A

enterogastrone, epinephrine, norepinephrine, atropine and Ca2+

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58
Q

What is the name for the process by which the stomach expands as more food enters it? What reflex modulates this?

A

Receptive relaxation, it is mediated partly by the vagovagal reflex

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59
Q

What part of the brain related to swallowing sends a signal to the stomach when sending a bolus towards it?

A

The swallowing center of the medulla

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60
Q

What are the inhibitory neurotransmitters though to be responsible for receptive relaxation?

A

NO and VIP

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61
Q

Which of the the functional divisions of the stomach is responsible for the mixing function of the stomach?

A

The caudad region

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62
Q

What happens to the strength of constrictor waves of the stomach as they approach the pyloric antrum? What effect does this have?

A

They become stronger forcing the contents under higher pressure towards the pylorus.

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63
Q

What happens to the pylorus as stomach peristalsis approaches it what does his cause?

A

It contracts impeding emptying causing most antral contents to be retropulsed.

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64
Q

What is the normal mealemptying time of the stomach?

A

2-3 hours.

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65
Q

What mediates the increase of pyloric pump activity in response to stretching of the stomach?

A

local myenteric reflexes.

66
Q

Where and when is gastrin released? What is its effect?

A

It is released by the antral mucosa in response to the presence of certain foods. It stimulates secretion of acidic gastric juice and increases the motor functions of the stomach and pyloric pump activity.

67
Q

How do endogastric reflexes impede stomach function?

A

They inhibit the pyloric pump and increase the tone of the pyloric sphincter.

68
Q

What are the three routes duodenal endogastric resources can take?

A

Directly from the duodenum to the stomach via enteric NS, Through extrinsic nerves that go to prevertebral sympathetic ganglia then back through inhibitory nerve fibers to the stomach and via the vagus nerve to the brainstem where they inhibit the normal excitatory signals transmitted to the stomach via the vagi.

69
Q

What is the effect of cholecystokinin (CCK)

A

Inhibits the effect of gastrin reducing gut motility.

70
Q

Where is secretin released what effect does it have?

A

It is released from duodenal mucosa and inhibits stomach contractions.

71
Q

What is the effect of gastric inhibitory peptide? Where and when is it released?

A

It is released by the small intestine in response to the presence of fat in the chyme and has a general but weak effect on gut motility.

72
Q

What effect do emotions have on gut motility?

A

anger/aggression increase gut motility and depression & fear decrease gut motility.

73
Q

What does MMC stand for?

A

Migrating motor complexes

74
Q

What is the effect of motilin?

A

It increases the strength of MMC

75
Q

What are the main uses of MMC?

A

remove remaining food in the stomach and intestines between meals, and to transport bacteria from the small to large intestine especially preventing migration of colonic bacteria the terminal ileum.

76
Q

Mild peristalsic contractions occur in empty stomachs these increase in size/strength what can this lead to?

A

It can cause the electrical waves to fuse resulting in a tetanic contraction lasting 2-3 minutes.

77
Q

What do oxyntic/gastric glands secrete?

A

HCl, pepsinogen, intrinsic factor and mucous

78
Q

Where are Oxyntic glands located? How much of the stomach do they make up?

A

They are located on the inside surfaces of the body and fundus of the stomach making up 80% of the stomach

79
Q

Where are the pyloric glands located? How much of the stomach do they make up?

A

They are located in the antral part of the stomach making up the distal 20%

80
Q

What do pyloric glands secrete?

A

Mucous and gastrin

81
Q

What is the role of peptic cells?

A

secretion of pepsinogen.

82
Q

What is the role of parietal/oxyntic cells?

A

secretion of HCl and intrinsic factor

83
Q

What is the role of intrinsic factor what secretes it?

A

It is essential for the absorption of vitamin B12 and is secreted by parietal cells mostly in Oxyntic glands but also in pyloric glands

84
Q

What is the role of G cells?

A

They secrete gastrin

85
Q

What are the four types of cells in pyloric glands?

A

Mucous neck cells, Peptic/chief cells, parietal/oxyntic cells and G cells

86
Q

What is the pH of gastric juice?

A

roughly 0.8

87
Q

What is combined with CO2 under the influence of CA to form bicarbonate ions

A

hydroxyl ions

88
Q

What is exchanged so that Cl ions can diffuse into cannaliculi

A

bicarbonate ions

89
Q

What causes the negative potential between parietal cells and the cannaliculi, what effect does this have?

A

Chloride ions are actively transported out of the cytoplasm of the parietal cell and sodium ions are actively transported out of the cannaliculi. This causes positively charged potassium ions and some sodium ions to be attracted from the parietal cells into the cannaliculi.

90
Q

What enzyme catalyzes the pumping of hydrogen ions into the cannaliculi in exchange for potassium? What happens to sodium and potassium still in the cannaliculi?

A

H+ K+ ATPase. It is mostly reabsorbed.

91
Q

What are the three phases of gastric secretion?

A

The cephalic, The gastric and The intestinal phases.

92
Q

What is the effect of gastrin?

A

It stimulates parietal cells to produce HCl

93
Q

What proportion of gastric secretion does the Cephalic phase account for?

A

20%

94
Q

When does the cephalic secretion stage occur?

A

Before food enters the stomach mostly while it is being eaten.

95
Q

Which parts of the brain co-ordinate the signals in the cephalic phase of secretion what nerves do they transmit signals via?

A

The hypothalamus and the amygdala create the signals and then transmit them via the dorsal motor nucleus of vagi then via the vagus nerves

96
Q

What proportion of gastric secretion does the gastric phase account for?

A

70%

97
Q

What are the three pathways that are activated by the presence of food in the stomach that contribute to increased gastric secretion?

A

Long vagovagal reflexes that travel from the stomach to the brain and back, local enteric reflexes and the gastrin mechanism

98
Q

What part of the duodenum is thought to be responsible for the intestinal phase of gastric secretion?

A

The mucosa as it releases a small amount of gastrin

99
Q

What is the primary role of ECL cells?

A

The secretion of histamine

100
Q

What does the ECL in ECL cells stand for?

A

Enterochromaffin-like cells.

101
Q

What are two agents that can trigger ECL cells to release histamine?

A

Gastrin and Acetylcholine

102
Q

Pepsin is released from peptic cells in what form? What activates it?

A

Pepsin is released as pepsinogen. It becomes active one it makes contact with hydrochloric acid

103
Q

What are the glycoproteins in mucus called?

A

Mucins

104
Q

What are the various proportions of the contents of mucous?

A

90% water and ions, 5-10% protein (glycoproteins) and 1-5% mucus glycoproteins

105
Q

What are the two layers of the mucus barrier?

A

A lower adherent layer and a superficial loose layer

106
Q

In which layer of mucus does symbiotic bacteria reside?

A

The loose superficial layer.

107
Q

What are the central regions of Mucins made predominantly of? What is the other name for these?

A

Tandem repeats of serine theronine and proline the other name for these is STP repeats.

108
Q

The long central chain composes what percentage roughly of amino acids within a mucin?

A

60%

109
Q

What is at either end of the long protein chain within a mucin? What function does this serve?

A

at either end a globular protein can be found this allows each mucin to attach to other mucins via disulphide bonds

110
Q

What is the benefit of covering mucins in carbohydrates?

A

It prevents them from being broken down by proteases and causes leptins (surface proteins often found on pathogens) to bind to them impeding pathogen motility.

111
Q

What are the five most common carbohydrates coating mucins?

A

N-acetylgalactosamine, N-acetylglucosamine, fructose, glactose and sialic acid

112
Q

Where are MUC5AC and MUC6 found?

A

In the stomach

113
Q

Where does MUC2 form the mucus gel?

A

In the colon cecum and ileum

114
Q

Most mucosal pathogens have what adaption that allows them to get past the mucus layers of the gut?

A

They produce enzymes that degrade the mucins allowing them to increase the fluidity of the mucus.

115
Q

What type of bacteria is Helicobacter pylori what shape is it and what renders it motile?

A

It is a gram negative microaeophillic bacillus. It is spiral shaped and is motile because of its flagellae

116
Q

H.pylori colonizes stomachs of 50% of the global population in throughout their life times what does this colonization cause?

A

Gastritis along with abdominal pain and nausea and increases the risk of peptic ulcers and gastric MALT lymphoma

117
Q

What are the symptoms of chronic gastritis?

A

stomach pains, nausea, bloating, belching and in some cases vomiting and black stool.

118
Q

What are the benefits of lifelong H.pylori colonization?

A

It provides protection against the complications of gastroesophageal reflux disease (GERD) including oesophageal adenocarcinoma

119
Q

What is the lifetime risk of peptic ulcers and carcinomas for those infected with H.pylori?

A

10-20% risk of peptic ulcers and 1-2% risk of stomach cancer

120
Q

Inflammation because of H.Pylori can effect the pyloric antrum or the corpus. How does this effect the likelihood of different complications?

A

Inflammation of the corpus most likely will lead to gastric ulcers and gastric carcinoma while inflammation of the pyloric antrum is more likely to lead to duodenal ulcers.

121
Q

What is the coccoid form of H.pylori? What does it allow?

A

The coccoid form is a dormant form of the H.Pylori bacterium that allows it to survive in adverse conditions.

122
Q

What is the cag island?

A

A group of genes that encode for a bacterial secretion system that can be present in H.pylori

123
Q

How does H.Pylori counteract the acidity of the stomach, what is the issue with this?

A

H.Pylori express urease which catalyses the hydrolysis of urea to form ammonia however this ammonia is toxic to epithelial cells

124
Q

How does cag island increase the severity of gastritis?

A

The cag island causes soluble components of the H.pylori cell wall to be translocated to the gastric epithelium, this is recognised by the Nod1 receptor which then stimulates a proinflammatory response which enhances gastric inflammation.

125
Q

How does the presence of the cag island effect H.pylori prognosis?

A

Those infected with cag island possitive strains are more likely to develop peptic ulcers or gastric adenocarcinomas

126
Q

Name three bacterial factors apart from the presence of the cag island that increase the risk of peptic ulcers and gastric adenocarcinomas in H.pylori related gastritis

A

VacA protein secretion, adhesins (e.g.BabA & SabA) and genes such as dupA

127
Q

Name three non bacteria associated factors that increase the risk of gastric adenocarcinomas

A

polymorphisms in the IL1 gene that cause increased production of IL1, smoking and diets high in salt and preserved foods.

128
Q

What is the main non bacteria related factor that increases the risk of peptic ulcers in those with H.pylori relatd gastritis?

A

Smokking

129
Q

How does H.pylori infection contribute to the formation of protective gastric metaplasia? What does this lead to?

A

H.pylori leads to inflammation that reduces the number of somatostatin producing D cells. Somatostatin inhibits gastrin release which means less somatostatin causes increased meal stimulated acid secretion. This increased meal related acid secretion contributes to the production of protective gastric metaplasias which can be colonized and subsequently ulcerated by H.Pylori

130
Q

How does MUC5AC impede H.Pylori infection?

A

They bind to the pathogen trapping it.

131
Q

How does MUC6 impede H.Pylori infection?

A

H.Pylori uses the mucins surface carbohydrates as a food source leading to the production of the 1-4GlcNAc sugar that interupts with cell wall synthesis in the bacteria and acts as a toxin towards it.

132
Q

Ommeprazole is in what class of medications?

A

PPI’s

133
Q

Name 6 alarm features that are indicative of serious disease in dyspepsia?

A

Dysphagia, Weight loss, Protracted vomiting, Anorexia, haematemesis and melaena

134
Q

What is haematemesis?

A

vomiting of blood

135
Q

How can one change their diet in order to prevent dyspepsia?

A

They can omit caffeine, rich, spicy, fatty foods and/or reduce alcohol intake

136
Q

How can alginates help dyspepsia?

A

They form a foam barrier on the surface of the stomach contents that helps keep stomach acid in the stomach.

137
Q

Why are magnesium and aluminium salts used together to help treat dyspepsia?

A

magnesium salts cause diarrhea and aluminium salts cause constipation so using them together cancels out the negative effects.

138
Q

What type of medication is rantidine?

A

A H2 receptor antagonist

139
Q

What is the usual structure of an ulcer

A

It be sharply demarkated with a zone of eosinophilic necrosis with surrounding fibrosis.

140
Q

Where are type I gastric ulcers found what is thought to be their cause?

A

They occur in the gastric body and are thought to be caused by low gastric acid secretion.

141
Q

Where are type II gastric ulcer found what amount of gastric acid are they associated with?

A

They are found in the antrum and are associated with normal to low amounts of gastric acid

142
Q

Where are type III gastric ulcers found? What are they usual accompanied by? What conc of gastric acid are they associated with?

A

They occur within 3cm of the pylorus and are often accompanied by duodenal ulcers.

143
Q

Where are type IV gastric ulcers found? what are they associated with?

A

They are found in the cardia of the stomach and are associated with low gastric acid secretion.

144
Q

What is the difference in the pain that people with gastric and duodenal ulcers experience?

A

People with gastric ulcers often feel pain right after eating whereas those with duodenal ulcers typically feel pain 2-3 hours after eating.

145
Q

What are Brunners glands? What purpose do they serve?

A

Bruner’s glands are large glands in the first few cm of the duodenal wall that secrete bicarbonate ions that serve to neutralize the acidity of the chyme that leaves the stomach.

146
Q

Alkaline secretions from the pancreas, bile and Brunner’s glands serve to protect the duodenum by neutralizing the acidity of chyme leaving the stomach. How apart from preventing the acidity of the chyme itself damaging the duodenum does this provide protection?

A

Pepsin’s function is reduced as it needs a low pH to function efficiently.

147
Q

How does alcohol aid the formation of GI ulcers?

A

It breaks down the mucosal barrier of the GI

148
Q

How can NSAIDs contribute to the formation of gastric ulcers?

A

NSAIDs are COX-2 selective inhibitors which are acidic themselves. The inhibition of the COX-2 enzyme reduces the levels of protective prostaglandins; this reduction in protaglandins also causes increased gastric acid secretion, diminished bicarbonate and mucus secretion.

149
Q

How does smoking contribute to the formation of ulcers?

A

It increases the nervous stimulation of stomach secretory glands.

150
Q

What type of medication are clarithromysin, amoxillin, metronidazide and tetracycline?

A

antibiotic.

151
Q

what type of medication are cimetidine/tagmet and rantidine/zantac?

A

H2 antagonist

152
Q

How do H2 antagonists help those with stomach ulcers?

A

They prevent histamines released by ECL cells in the stomach from binding to H2 receptors on parietal cells reducing stomach acid secretion.

153
Q

In what two scenarios is surgery used to treat ulcers and what is done?

A

In ulcers with recurrent uncontrolled haemorrhage the bleeding vessel is ligated. In perforated ulcers oversewing is required.

154
Q

Where can particularly damaging narrowing due to ulcers occur what can result from this?

A

Near the end of the stomach swelling and scaring can cause narrowing in the intestinal opening this can result in vomiting of the contents of the stomach.

155
Q

What are the three types of peritonitis?

A

Spontaneous/primary, secondary and chemical.

156
Q

What causes spontaneous/primary peritonitis? Who is particularly at risk?

A

An infection in the fluid of the peritoneal cavity. which can result from liver or kidney failure. People on peritoneal dialysis for kidney failure are at risk.

157
Q

What causes secondary peritonitis?

A

An infection traveling from the digestive tract to the peritoneal fluid.

158
Q

What is allowed to happen when nerve fibers from areas of low sensory input and high sensory input converge on the same levels of the spinal chord?

A

referred pain

159
Q

Irritation of the diaphragm is usually felt as what?

A

Pain in the right shoulder.

160
Q

Which spinal nerves are relevant to pain in the shoulder felt due to irritation in the diaphragm?

A

C3 and C4

161
Q

What are the three stages of vomiting?

A

nausea, retching and emesis

Semester 4 (10 decks)

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