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LSS 2 - Alimentary > The Oesophagus and Stomach > Flashcards

The Oesophagus and Stomach Flashcards

1
Q

State the basic plan of the gut wall from the lumen outwards.

A

Epithelium, lamina propria, submucosa, muscularis, serosa/adventitia
There are nerve plexuses in the submucosa and muscularis
Serosa is a mixture of connective tissue and epithelium
Adventitia is only connective tissue

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2
Q

What vertebral level does the oesophagus start at?

A

C5

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3
Q

How long is the average oesophagus?

A

25-30 cm

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4
Q

At what vertebral level does the oesophagus pierce the diaphragm?

A

T10

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5
Q

Describe the cell type in the upper oesophagus and the reason for having this cell type.

A

Non-keratinising stratified squamous - this is good for protection - acts as a barrier and prevents the loss of water through the epithelium

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6
Q

What are the two important sphincters in the oesophagus?

A

Upper oesophageal sphincter and the lower oesophageal sphincter

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7
Q

Describe the difference in structure of the lower and upper oesophageal sphincters.

A

The upper oesophageal sphincter is made up of only skeletal muscle whereas the lower oesophageal sphincter consists of both skeletal and smooth muscle.

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8
Q

What state are the sphincters in when there is no food in the mouth?

A

They are tonically active meaning that they are both closed.

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9
Q

What happens when food goes into the mouth?

A

When food goes into the mouth, a reflex is set up by the swallowing centre in the brain leading to peristalsis.

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10
Q

How does muscle type change as you pass down the oesophagus?

A

You go from skeletal to smooth muscle as you move down the oesophagus.

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11
Q

How does the innervation change as you pass down the oesophagus?

A

It goes from motor neurones to autonomic nervous system as you move down the oesophagus.

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12
Q

What two types of muscle are in the oesophagus?

A

Circular and longitudinal

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13
Q

What is the difference between the primary and secondary peristaltic waves?

A

Secondary peristaltic wave is initiated after the primary if the food gets stuck.

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14
Q

The lower oesophageal sphincter is not considered a true anatomical sphincter. What is it formed by?

A

Diaphragm (muscular part), greater curvature of the stomach folding inwards, difference in pressure between the thorax and abdomen

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15
Q

What are the gastric folds in the stomach lining called and what is the point in them?

A

Rugae - they increase surface area

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16
Q

Describe the transition in epithelium from the oesophagus to the stomach.

A

Oesophagus is made up of non-keratinising stratified squamous epithelia and the stomach epithelium is made up of simple columnar epithelium

17
Q

What are the 4/5 regions of the stomach?

A

Cardiac, Fundus, Body, Pylorus and Pyloric Antrum

18
Q

Certain substances are produced in certain regions of the stomach.
State which substances are produced in which regions.

A

Cardiac and Pyloric regions - mucus only
Fundus and Body - pepsinogen, HCl, mucus
Antrum - gastrin

19
Q

What feature do the mucus secreting cells of the stomach have that protects them from the acidity of the stomach?

A

They secrete HCO3- that sits on top of these cells and neutralises the acid that comes into contact with its surface

20
Q

How much acid is produced by the stomach per day and what is the concentration of protons?

A

2 L

150 mM

21
Q

What do Gastric Chief Cells produce?

A

Gastric Chief Cells produce pepsinogen
State some histological features of Gastric Chief Cells.
They have a lot of RER
They have Golgi apparatus for packaging and modifying for export
They have a lot of vesicles at the apical membrane

22
Q

State three structural features of the resting parietal cell.

A

Numerous mitochondria - provide energy for the active transport of protons into the lumen of the stomach
Cytoplasmic Tubulovesicles - contain H+/K+ ATPase channels
Internal Canaliculi - fluid filled reservoirs present within the resting parietal cell

23
Q

What is the role of parietal cells?

A

Parietal cells pump protons into the lumen of the stomach and make it more acidic

24
Q

Describe the mechanism by which active parietal cells increase the proton concentration in the stomach.

A

Carbon dioxide diffuses into the cell from the blood and reacts with water with the action of carbonic anhydrase to produce bicarbonate and a proton. A sodium-potassium exchanger bring one potassium in and one sodium out. The K+ follows the concentration gradient and diffuses into the canaliculi. HCO3- is exchanged for Cl- - the Cl- then moves down the concentration gradient into the canaliculi. Then, ATP is used to actively transport H+ into the canaliculi with K+ moving out. There is a massive ATP driven movement of protons into the stomach lumen.

25
Q

What is the effect of inhibiting carbonic anhydrase?

A

This reduces the acid producing ability of the parietal cells because it is no longer able to convert water and carbon dioxide into H2CO3 (so H+ and HCO3- isn’t generated)

26
Q

What two proteins do you need a lot of to increase the acidity of the stomach?

A

Carbonic Anhydrase and H+/K+ ATPase

27
Q

How does pepsinogen turn into pepsin?

A

The acid makes the pepsinogen unfold and this causes autocatalysis (pepsinogen metabolises itself) of pepsinogen to produce pepsin.

28
Q

What are the two stimuli for gastrin production?

A

Acid production itself

Local peptide hormones that are being produced by pepsin

29
Q

What is the effect of gastrin?

A

Gastrin is produced in the pyloric antrum and passes into the bloodstream before returning to the lumen of the stomach where it causes an increase in acid secretion by the stomach epithelium.

30
Q

How can gastrin indirectly increase acid secretion?

A

Gastrin stimulates the release of histamine from chromaffin cells (in the lamina propria) - this stimulates acid secretion

31
Q

What are the three phases of gastric secretion?

A

Cephalic, Gastric, Intestinal

32
Q

Describe the cephalic phase of gastric secretion.

A

This is before the food even enters your mouth. The vagus nerve from the medulla stimulates the enteric nervous system to increase the production of acid and pepsin. You also get an increase in gastrin production (which causes further increase in acid production).

33
Q

Describe the gastric phase of gastric secretion.

A

Once the food is in the stomach, stretch and chemoreceptors send messages to the brain. The brain then activates the vagus nerve and increases pepsin and acid production. Once the process has been started, the enteric nervous system will take over and cause churning of the stomach.

34
Q

Describe the intestinal phase of gastric secretion.

A

Chyme enters the small intestine and if the pH is < 2 or the chyme has a high lipid content, this acts as a stimulus that goes up to the brain and switches off acid and pepsin production.

35
Q

What are the three hormones produced in the enterogastric reflex? What is the name given to this group of hormones?

A

Gastric Inhibitory Peptide, Cholecystokinin and Secretin
These are enterogastromes
They decrease the production of acid and pepsin
The enterogastric reflex is a reflex that is controlled by hormones

36
Q

Describe the excitatory process when chyme has a high protein content.

A

If the chyme entering the small intestine has a high protein content it will stimulate the release of gastrin so that more acid is produced hence more pepsinogen is converted to pepsin so the proteins will be better digested.

37
Q

State two drugs that decrease acid secretion and their targets.

A

Omeprazole - proton pump inhibitor

Ranitidine - histamine receptor antagonist

38
Q

Which of the following structures within the

parietal cell contains the most H+/K+ ATPase?

A 
Canaliculi
Carbonic anhydrase
Golgi body
Mitochondria
Tubulovesicles -->
39
Q

Which of the following stimuli would be most likely to

decrease acid secretion in the stomach?

A 
Chyme fatty acid content -->
Increased acetylcholine secretion
Increased gastrin secretion
Protein content of the meal
Stomach distension

LSS 2 - Alimentary (18 decks)

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