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YEAR 2 GI > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Fundus purpose

A

Storage- not for long

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2
Q

The esophagus goes to what part of the stomach

A

The Fundus

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3
Q

Where does receptive relaxation occur?

A

Fundus- food entering from esophagus

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4
Q

Where’s the Antrum? And for what (2)?

A

Near the pyloric sphincter (bottom part of stomach)
For mixing/grinding
And release of gastrin

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5
Q

Three types of cell in gastric pits/glands?

A

Gastric neck cells

(Gland)
Parietal cells
Chief cells

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6
Q

Gastric pit/gland secretions and where they come from?

A

Mucus = surface mucus cells and neck
Pepsinogen = chief cells
Hpl and intrinsic factor = parietal cells
Gastric =

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7
Q

Release of HCL happens how?

A

CO2 then reacts with water IN cytosol of parietal cells
= carbonic acids that quickly dissociated into carbonic acid and hydrogen/proton
Proton pump with potassium coming in
Bicarbonate comes in = blood basic, stomach acidic. So in response chloride moves across into stomach lumen = HCL
And note that a gradient has been created so… water comes in to stomach as well

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8
Q

Proton pump inhibitors inhibit what proton pump?

A

One involved in the secretion of HCL in the GI tract

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9
Q

Example of proton pump inhibitors?

A

Omeprazole eg for heart butn
Lansoprazole

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10
Q

Why is blood after eating more basic?

A

Because proton pump releases protons into the stomach lumen, in response bicarbonate comes from stomach into blood and that’s basic

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11
Q

How is the proton potassium pump controlled? (Gastrin or histamine or acetylcholine)

A

Pump is activated if phosphorylated by kinase enzyme located IN parietal cells.
So inhibit kinase enzyme = inhibit pump.

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12
Q

Way that gastrin encourages HCL production?

A

Gastrin = released into blood
= receptor in parietal cells of gastric pits
= release calcium
= encourages protein kinase c
= pump active

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13
Q

You could never put the whole process on a flash card (which I reckon you’ll need to know) but see the release of more histamine starts a chain reaction that does what to the proton potassium pump?

A

Increase in activation of protein kinase a, which phosphorylates proton pump = more protons = more HCL

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14
Q

How does acetylcholine affect the proton potassium pump?

A

Acetylcholine will be released from enteric or the parasympathetic system, = increase calcium = increase protein kinase a

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15
Q

What’s the effect of Gastrin and acetylcholine basically to release HCL?

A

Increase calcium = activate protein kinase c and increase release of HCL

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16
Q

What works to inhibit protein kinases (considering histamine, Gastrin, and acetylcholine)

A

Prostaglandins

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17
Q

What has gastrin levels got to do with histamine levels and release of HCL therefore?

A

Gastrin and ACh stimulates ecl cells and causes greater release of histamine and thus stimulates parietal cells

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18
Q

Difference in cephalic and gastric stage?

A

Cephalic = vagus/enteric nerve at sight/smell
Gastric = reflexes

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19
Q

Why is the cephalic stage important? (Gastric acid secretion at sight/smell of food)

A

Because before food enters stomach, must have certain amount of acid ready for sterilisation.

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20
Q

Which phase is inhibition of vagal activity when you’re eating etc

A

Intestinal phase

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21
Q

What leads to the intestinal phase (after the gastric phase)?

A

When you stop thinking about food = end cephalic stage = inhibit vagal activity.
Decrease in pH due to HCL, therefore inhibit release of gastrin (negative feedback)

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22
Q

Half way between asis and pubic tubercle and inch above = what

A

Deep ring

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23
Q

Which ring is the aponeurosis of the external oblique muscle?

A

The superficial ring

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24
Q

Of gastric glands, the mucous neck cells, the chief cells and the parietal cells secrete what

A

Mucous

Pepsinogen

Intrinsic factor and HCL

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25
Q

Proton potassium pump is activated when phosphorylated by what enzyme located in parietal cells

A

Protein kinase enzyme

So inhibit this enzyme and you inhibit the pump

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26
Q

Gastrin, histamine and acetylcholine help control the proton potassium pump…which two do this by increasing calcium?

A

Gastrin and acetylcholine. Think gAstrin and Acetylcholine and cAlcium. Vs hIstamine.

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27
Q

What stops the cephalic stage of gastric acid secretion?

A

Stop eating = down vagal activity

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28
Q

What stops the gastric stage of gastric acid secretion?

A

Down pH = up HCL = down gastrin

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29
Q

What stops the intestinal stage of gastric acid secretion

A

Duodenum usually alkaline, so acid in stomach that’s gone past sphincter = enterogastric/ splanchnic reflex to inhibit

S cells in mucosa of duodenum release secretin which will go to blood and reach antrum/ G cells to inhibit directed

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30
Q

Inhibition of gastric acid in the intestinal phase is due to the introduction of what in the duodenum?

A

Acid and fat/carbs in the duodenum

Acid = enterogastric/ splanchnic reflex = secretin from s cells in the mucosa, = inhibit gastrin directly on g cells (travel through the blood)
Fat = GIP gastric inhibitory peptide = inhibit release of gastrin

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31
Q

Secretin is an example of what

A

An enterogastrone, just like GIP

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32
Q

When are enterogastrones released?

A

In response to acid mainly , but also fatty acids and monoglycerides in duodenum and hypertonic solutions I.e. solutions that have lots of molecules

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33
Q

Why are entergastrones released? Eg gastro inhibitory peptide from g cells and secretin from s cells

A

To prevent acid build up in the duodenum

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34
Q

Two methods of enterogastrones?

A

Inhibiting gastric acid secretion by:
Inhibiting gastrin
Inhibiting HCL release from parietal cells

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35
Q

What inhibits motility/contracts pyloric sphincter?

A

Enterogastrones

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36
Q

When does Pepsinogen (secreted by chief cells) become pepsin?

A

When stomach pH below 3 (often)

And if pH increases, becomes Pepsinogen again

We can’t store pepsin, it can degrade protiens

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37
Q

Why does pepsin deactivate when reaching the duodenum?

A

Because it’s inactivated at a neutral pH

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38
Q

What does mucus do? (2)

A

Protects the stomach wall from action of hydrochloric acid and hydrolytic enzymes (neutral pH)
And mechanical injury (slippy)

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39
Q

How come the stomach won’t digest itself?

A

Mucus

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40
Q

Where is the intrinsic factor/B12 complex absorbed?

A

Ileum

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41
Q

What is pernicious anaemia?

A

Defect in intrinsic factor

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42
Q

Why would defect in intrinsic factor cause less oxygen in tissues (that shows up

A

Because no vitamin B12 = no maturation of rbc

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43
Q

Thin or thick muscle, antrum Vs body?

A

Thick for antrum l

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44
Q

More digestion body or antrum

A

More in the antrum, more secretion of enzymes in body

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45
Q

Is there mixing of food in the body of stomach?

A

No

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46
Q

Mixing/ grinding of food into smaller molecules due to which muscles

A

Oblique

Not long and circular

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47
Q

Pyloric sphincter controls against hyper acidity in the intestines

A

True

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48
Q

Why only small amount of chyme (gastric content) in the duodenum?

A

Pancreatic juice/enzymes can’t work in acidic conditions

Hence control of neutralising bicarbonate release

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49
Q

Further mixing happens when pyloric sphincter is shut why?

A

Antral contents, forced back towards the body when closed during contraction

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50
Q

How many waves per minute

A

Like, 3

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51
Q

Where are the pacemaker cells located? That controls peristalsis

A

Longitudinal muscle layer

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52
Q

Depol of pacemaker cells in the longitudinal muscle layer, is that spontaneous?

A

Yes

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53
Q

What is the slow wave (peristaltic wave) rhythm of the stomach called?

A

Basic electrical rhythm

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54
Q

What does sub threshold mean? Of the slow waves caused by the pacemaker cells

A

Not enough to initiate action potential, so need further depol from somewhere else

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55
Q

Further depol for action potentials for small waves comes from what

A

Acetylcholine or gastrin

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56
Q

Distension of stomach causes two different types of reflexes:

A

Long = vagus
Short = enteric nervous system

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57
Q

Distension of stomach causes long reflex (vagus) and short reflex (enteric nervous system)… both of these will increase the release of what?

A

Acetylcholine = increase force of contraction by adding extra depol for the small waves

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58
Q

Where is bicarbonate released from?

A

(Activated by acid)
Submucosal glands called brunner’s gland (of the duodenum)

Also liver and pancreas (triggered by a cells/secretin due to acid)

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59
Q

Is there bicarbonate present in bile?

A

Yes
Hence why acid detection = s cells = secretin in blood to pancreas and liver = release bile

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60
Q

Bile duct takes to where

A

The duodenum

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61
Q

What is the pancreatic head surrounded by?

A

The C shaped duodenum

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62
Q

Tail of pancreas touches what

A

The spleen

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63
Q

Is the pancreas exocrine or endocrine?

A

Both
Via blood (endocrine)
And via ducts (exocrine)

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64
Q

What part of the pancreas is responsible for the secretion of hormones? (Endocrine)

A

Pancreatic islets called islets of Langerhans

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65
Q

Where does insulin come from

A

Islets of langerhans in the pancreas

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66
Q

Which two hormones control blood glucose level?

A

Insulin and glucagon

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67
Q

But what hormone controls the secretion of insulin and glucagon?

A

Somatostatin

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68
Q

Where does somatostatin come from?

A

The pancreatic islets called langerhans islets

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69
Q

What does insulin do Vs glucagon

A

Insulin = decreases blood glucose levels
Glucagon = increases blood glucose levels

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70
Q

What cells of the pancreas responsible for exocrine

A

Acinar cells
Which form lobules

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71
Q

Enzymes from pancreas come out from where

A

Acinar cells in the body which form lobules

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72
Q

Enzymes are secreted from Acinar cells which form lobules, in the body of the pancreas. Where else in intestines are enzymes secreted?

A

Duodenum

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73
Q

Is lumen of the gastrointestinal tract considered part of the body?

A

Yea

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74
Q

What are lobules (Acinar cells for exocrine) of the pancreas connected by?

A

Intercalated ducts

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75
Q

Lobules are connected by intercalated ducts. However, we have other ducts, big ones called what

A

Intralobular ducts

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76
Q

The main duct in the pancreas will lead to what

A

Main pancreatic duct will lead to the common bile duct

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77
Q

Go outwards from the lobules to the duodenum if you get what I mean

A

Lobules > intercalated ducts > intralobular ducts > main pancreatic duct > common bile duct > sphincter of oddi

78
Q

What sphincter can control the release of bile and pancreatic juice from the bile duct?

A

The sphincter of oddi

79
Q

What’s the purpose of the accessory pancreatic duct?

A

Plan B duct

80
Q

Common bile duct vs pancreatic duct comes from where

A

Common bile is from the liver and gallbladder, but the pancreatic duct is from the pancreas

81
Q

Alpha cells Vs beta cells Vs acini cells secret what

A

In lobules (exocrine) acini = enzymes

In the islets of langerhans, alpha beta gamma and delta.
Alpha = glucagon
Beta = insulin (no yo glucose therefore inferior like beta)

82
Q

Exocrine function of the pancreas is important for what bodily function

A

Digestion- enzymes directly to the duodenum and also most food components are digested by pancreatic juice

83
Q

Which cells of the pancreas produce the digestive enzymes?

A

Acini

84
Q

Duct cells or Acinar cells in the pancreas exocrine release of bicarbonate?

A

Duct cells

Acinar for the ezymes

85
Q

What is the sphincter of oddi responsible for secreting? (3)

A

Bike from gallbladder
Pancreatic juice
Bicarbonates

86
Q

We know that Acinar cells release/contain digestive enzymes. These are stored as what

A

Inactive zymogen granules, and this is to prevent auto digestion of pancreas

87
Q

Zymogens cause what to all components inside food

A

Hydrokysis

88
Q

What enzyme converts trypsinogen to trypsin?

A

Enterokinase

89
Q

If zymogens are the form of digestive enzymes that are inactive, what activated them?

A

Enterokinase converts trypsin into trypsinogen, then that converts every other zymogen to active forms

90
Q

When does the pancreas secrete bicarbonate?

A

Acid from stomach = secretin to blood to pancreas = bicarbonate into small intestine and therefore neutralisation of intestinal acid

91
Q

What is zymogen secretion stimulates by?

A

CCK
Cholecystokinin

92
Q

Where is CCK (cholecystokinin) released from? (It’s secretion stimulates zymogen)?

A

From the duodenum

93
Q

When is CCK released?

A

In response to presence of fatty acids, amino acids etc
So food= CCK = zymogens to digest said food

94
Q

Would the long vagal reflex and short enteric reflex be triggered by what?

A

Arrival of digestive products in the duodenum

95
Q

So you keep talking about the long and short reflex induced by distension of stomach. What happens.

A

Release of acetylcholine

96
Q

Describe steps of how pancreatic enzymes are released

A

Stomach distension
CCK secreted
Go to pancreas
Release enzymes into small intestine

97
Q

Retro sternal pain is pain that happens where

A

Discomfort behind the sternum in the chest

98
Q

Retro sternal pain can either be:

A

Cardiac or GI tract in nature

99
Q

Upper GI tract is what:

A

Esophagus and stomach

100
Q

Could obesity cause weakening to the oesophageal sphincter?

A

Yes
Abdominal pressure = herniate mucosa into oesophagus
= hiatus hernia

101
Q

Oesophagus = what

A

Squamous epithelium lining

Lots of layers = stretch

102
Q

Why might hyperplasia occur in oesophageal reflux?

A

Thickening of squamous epithelium I’d always in contact with acid

103
Q

When might ulceration occur of oesophageal epithelium?

A

When reflux is severe

= surface epithelium stripped off

104
Q

Why might metaplasia occur in acid reflux?

A

Mucus helps to protect from acid

105
Q

Severe acid reflux = fibrosis why?

A

Because mucosal metaplasia, not as resistant to sharp food boluses

106
Q

What is ‘Barrett’s oesophagus’?

A

Change from squamous to glandular eouthelium

107
Q

Metaplasia becomes dysplasia becomes neoplasia ie cancer. When is this reversible?

A

Metaplasia is reversible

108
Q

Why is Barrett’s esophagus a precursor lesion to cancer?

A

Metaplasia could lead to dysplasia (mutations) and finally neoplasia

109
Q

You can have squamous carcinoma or adenocarcinoma of the oesophagus. Which arises from Barrett’s oesophagus?

A

Adenocarcinoma (from metaplasia/mucosal glands that aren’t meant to be there but are, due to the acid)

110
Q

obesity is a risk factor for which type of oesophageal cancer?

A

Adenocarcinoma, not squamous carcinoma

111
Q

Is prognosis for oesophageal cancer okay?

A

No, poor prognosis, like 15%

112
Q

What’s gastritis, and why do I think ‘ABC’?

A

Gastritis is stomach inflammation, and it’s:
Autoimmune
Bacterial
Chemical injury

113
Q

Autoimmune gastritis would lead to what deficiency?

A

B12

114
Q

What happens in bacterial gastritis?

A

H pylori bacteria produces potassium = bonds to pump = more acid

115
Q

What food should be avoided in bacterial gastritis?

A

Potassium rich food like bananas

116
Q

Why B12 deficiency in autoimmune gastritis?

A

Because your body is making antibodies to its own parietal cells incl to intrinsic factor
I.e. loss of specialised gastric epithelium

117
Q

Autoimmune gastritis = up or down acid secretion

A

Down acid secretion

118
Q

Bacterial gastritis = up or down acid production

A

Up acid production

119
Q

Would bacterial gastritis be acute or chronic?

A

Both

120
Q

What do you treat bacterial gastritis with?

A

Protein pump inhibitors
And
Antibiotics

Which you wouldn’t do to A version, that’s why biopsy is important

121
Q

What usually causes chemical gastritis?

A

NSAIDS

So might give them with a proton pump inhibitor?

122
Q

What are the other two things chemical gastritis could be caused by?

A

Alcohol
Or
Bile reflux

123
Q

Would there be more mucous producing cells in chemical gastritis?

A

Ye

124
Q

Imbalance between acid secretion and mucosal barrier is caused by what?

A

Peptic ulceration

125
Q

Why might there be bleeding, perforation and healing by fibrosis (leading to obstruction) in a peptic ulceration?

A

Because stripping surface epithelium = exposing underlying nerves, blood vessels etc, leads to complications

126
Q

How could a peptic ulceration lead to hematemesis? What do you do?

A

Vomiting blood
Blood vessel exposed due to ulceration

Ulcers ablated, or, elastic bands put on the blood vessels

127
Q

Cancer in the oesophagus can be squamous or adenocarcinoma. What about in gastric cancers?

A

Just adenocarcinoma because it’s all glandular epithelium

128
Q

What’s transcoelomic spread?

A

Spread within the peritoneal cavity

129
Q

Where does the esophagus start and end

A

Cricoid cartilage at C6, and ends at T11-12

130
Q

Walls of the intra-abdominal section of the oesophagus are compressed when there is what

A

Positive intea-abdominal pressure

131
Q

During oesophageal peristalsis, the sphincter is what

A

Relaxed to allow food to enter the stomach

132
Q

Mucosal rosette is formed by what

A

Acute angle between oesophagus and the stomach

133
Q

How might food like alcohol or nicotine result in increased amount of reflux/heart burn?

A

It relaxes the o sphincter

134
Q

What’s GORD?

A

Persistent reflux and heartburn can lead to ‘gastro-oesophageal reflux disease’

135
Q

Odynophagia meaning?

A

Pain with swallowing

136
Q

Odynophagia (pain with swallowing) has what associated features?

A

Weight loss
Regurgitation
Cough

137
Q

What is the commonest cause of dysphasia?

A

Benign structure (narrowing)
Sometimes malignant as well

138
Q

Would you ever investigate oesophageal disease with looking at pH?

A

Yes
PH-metry

139
Q

What does manometer do?

A

Measure pressure waves in oesophagus with catheter

140
Q

Hypermotility disorders look like what

A

Corkscrew appearance on Ba swallow

Let’s be honest,you’ll need to look this up.

141
Q

Do people with gord always experience symptoms eg heart burn, water brash etc?

A

NO! Not always!!!

142
Q

When would an endoscopy be performed in GORD?

A

When alarm symptoms such as

Dysphagia
Weight loss
Vomiting

143
Q

Is presentation of oesophageal cancer late or early?

A

Late saldy

144
Q

Where does h pylori of gastritis live?

A

Surface mucosa, not penetrating the epithelial layer

145
Q

CLO test is what and involves what

A

Is a urease-dependant diagnostic test
Taking biopsy from stomach, putting it into test with urea to see if ammonia if formed, if so h pylori bacteria

146
Q

Eradication of h. Pylori looks like what?

A

Triple therapy for 7 days:
Clarithromycin
Amoxicillin
Omeprazole

147
Q

When endoscopy? (ALARM)

A

• Anorexia
• Loss of weight
• Anaemia - iron deficiency
• Recent onset >55 years or persistent despite treatment
• Melaena/haematemesis (GI bleeding) or mass
• Swallowing problems - dysphagia

148
Q

When do we move dyspepsia patients to secondary care?

A

If symptoms persist and bacteria is gone
So start PPI trial for. Few weeks

149
Q

What’s a jejunostomy?

A

Feeding tube into jejunum (rather than stomach eg if stomach has moved due to surgery- pulled up into chest and reattached)

150
Q

Resp. fitness is affected after oesophageal resection?

A

True
They deflate the lungs
So go on cardiorespiratory fitness regimes couple of months

151
Q

Can you do keyhole surgery for paraesophageal hiatus hernia?

A

Yes
The entire stomach could actually be in the chest, so could take longer, but yes

152
Q

For patients struggling with chemotherapy regime before surgery, what about their fitness for surgery?

A

Maybe be worried tbh

153
Q

Which side do we cut for esophagus? Remembering you’ve got the sternum and heart right there. Meaning what:

A

Posterior mediastinal, so we’d have to deflate the right lung

154
Q

What is the largest gland AND the largest organ or the body?

A

The liver

155
Q

Does the liver have only endocrine or only exocrine functions?

A

Both
Hormones into blood
And
Enzymes for digestion eg in bile

156
Q

Examples of disaccharides

A

1) lactose = glucose + galactose (lactase)

2) sucrose = glucose + fructose (sucrase)

3) maltose = glucose + glucose (Maltase)

157
Q

Pepsin catalysed the hydrolysis of peptide bonds in proteins. What environment does it require

A

Acidic

158
Q

Does the duodenum ever secrete digestive enzymes

A

No

159
Q

What does CCK stimulate the release of

A

Zymogens from pancreatic acini

160
Q

In micelles of fats, where do the polar portions face

A

Outside

161
Q

What does conjugation of bile acids with amino acids do

A

Increase solubility

162
Q

Does peristalsis ever stop

A

No

163
Q

Secretion from brunners glands is stimulated by what

A

Secretin

164
Q

CCK stimulates what

A

Pancreatic enzyme secretion and bile secretion

165
Q

Segmentation contractions in the small intestine are initiated by what?

A

The arrival of food in the stomach

166
Q

Bicarbonate is secreted into bile by duct cells in the liver

A

Treu

167
Q

What does trypsin do?

A

Starts the digestive process of protein molecules by cutting long chains of amino acids into smaller pieces

168
Q

If trypsin Starts the digestive process of protein molecules by cutting long chains of amino acids into smaller pieces, what coverts trypsinogen to trypsin?

A

Enterokinase

169
Q

What are Pepsinogen secreted by

A

Chief cells

170
Q

T or f, secretin is released from a cells in response to acid in the duodenum

A

T

171
Q

The arrival of chyme in the duodenum, triggers a reflex activity in the splanchnic nerve that does what

A

Inhibit gastric secretion and emptying

172
Q

Bike pigments are derived from what

A

Haemoglobin

173
Q

Does sympathetic activity decrease or increase the intensity of segmentation contractions?

A

Decrease

174
Q

Can fructose be absorbed passively across the colonic epithelium?

A

Yes bc it’s a monosaccharide. The only hexose sugars that can be absorbed are fructose, glucose and galactose

But if disaccharides- nah mate

175
Q

Secretions from brunners glands aid in neutralisation. Of gastric acid

A

True
Cuz it’s mucus

176
Q

Where is fructose absorbed?

A

Across epithelium of small intestines

177
Q

So we know that pancreas releases digestive enzymes… but we don’t want to digest the pancreas. So how are they stored?

A

As zymogens

178
Q

Example of zymogen?
which is the inactive form of digestive enzyme, stored safely in the pancreas.

A

Trypsinogen

(which becomes trypsin and converts all other zymogens to active forms)

179
Q

What does the brush border Enterokinase do

A

Concerts released pancreatic trypsinogen into trypsin

(Which converts all other zymogens into active forms)

180
Q

What part of the gastric put secretes bicarbonate rich fluid to neutralise gastric acid?

A

Brunner’s glands

181
Q

What produces vitamin k

A

Colonic bacteria

182
Q

Stomach distension leads to the inhibition or stimulation of gastric secretion?

A

Stimulation obvs

183
Q

When are Pepsinogens from chief cells secreted?

A

By parietal cells in response to lowering pH

184
Q

Where in the small intestine is the intrinsic factor/vitamin B12 complex absorbed?

A

In the terminal ileum

185
Q

What stimulates the secretion of bicarbonate from brunners glands

A

Secretin

186
Q

Bile salts are reabsorbed and recycled to the liver via the hepatic portal vein. Where about is the bile salt reabsorbed in the small intestine?

A

Distal ileum

187
Q

Lysozyme in saliva does what

A

Cleave a component of bacterial cell walls ie it’s bactericidal

188
Q

Proteins are broken down into amino acids, how are these co-transported?

A

With Na

189
Q

Intensity of segmentation contractions increase follow increase in what activity, para or not

A

Parasympathetic

190
Q

What nervous stimulation leads to profuse watery saliva

A

Facial and glossopharyngeal nerves

191
Q

CCK causes gall bladder contraction, leading to bile expulsion. Therefore guess what sphincter is also caused to relax?

A

Sphincter of oddi
To permit bile entry into the duodenal mucosa

YEAR 2 GI (7 decks)

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