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DS > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

Where does the stomach begin?

A

At the gastroesophageal junction where the oesophagus ends.

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2
Q

What is the superior part of the stomach?

A

Fundus. It is the curvature at the top of the stomach. Acts as a chamber.

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3
Q

What is medial to the gastroesophageal junction?

A

Cardia.

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4
Q

What makes up majority of the stomach?

A

The body.

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5
Q

What is towards the distal end of the stomach?

A

The antrum. The antrum feeds into the pylorus (sphincter).

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6
Q

What does the pylorus control?

A

The entry of food into the duodenum.

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7
Q

What does the greater curvature consist of?

A

Rural folds. They aid the digestion of gastric contents.

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8
Q

What is the incisura?

A

The angle that connects the lesser curvature to the antrum.

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9
Q

What are the major functions of the stomach?

A
  1. reservoir for food.
  2. Digests food - has to do this to allow food to become particular consistency before entering the duodenum. Needs to enter small intestine as chyme.
  3. Antrum mixes and grinds up the food.
  4. Pylorus regulates the size of particles, before they move into the small intestine.
  5. Gastric acid secretion - 1.5L per day.
  6. Secretes: mucus, bicarbonate, intrinsic factor, pepsinogen, and prostaglandins.
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10
Q

What happens in gastric motility?

A

The funds acts as a food store, the body and antrum mix the food and the pylorus contracts to limit exit of chyme.

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11
Q

What are the exact steps in the motility of the stomach?

A
  1. Relaxation of fundus (vasovagal reflex). When meal enters it, mediated by the vagus nerve. Vagus nerve causes reflex which tells funds to relax, and food is stored.
  2. Contraction of body and antrum. Allows food to be moved to distal part of the stomach.
  3. Pylorus contracts. Needs to remain shut during physical digestion of the food.
  4. Mixing by retropulsion. Allowing food to digest into smaller particles.
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12
Q

Normal function requires?

A
  1. Intact antrum - as the antrum does a lot of the mixing.
  2. Intact pylorus - things won’t be held in the stomach with digestion if not intact.
  3. Intact duodenum - controls the release of chyme into the small intestine for alter digestion by the pancreas.
  4. Normal vagus nerve.
  5. Normal hormone function.
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13
Q

What is abnormal gastric emptying?

A

Either rapid or delayed.

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14
Q

What causes rapid gastric emptying?

A

People who have had gastric-surgery. People have had their antrum removed and pylorus, they can develop “dumping syndrome”.

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15
Q

What is the “dumping syndrome”?

A

Rapid entry of food from the stomach into the small intestine.

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16
Q

What are the symptoms for “dumping syndrome”?

A

Nausea.
Vomiting.
Cramping.
Diarrhoea.

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17
Q

What causes “dumping syndrome”?

A

No antrum to mix up the food, and no pylorus to control the exit of food. So food is not completely digested [hyperosmolar chyme]. The large particles act as an osmotic pressure. They draw fluid into the small intestine and it causes the stomach to distend.

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18
Q

What does the hyperosmolar chyme cause?

A

Rapid fluid shift into the gut, causing intestinal distension = pain. Diarrhoea due to osmotic effect. Can cause committing as well.

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19
Q

What causes delayed gastric emptying?

A

Diabetic gastroparesis, which is caused by an autonomic neuropathy.

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20
Q

What is gastric secretion common to?

A

All mammals.

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21
Q

What is the main role of gastric acid?

A

It sterilises the food. The stomach environment is hostile to most bacteria except for Helicobacter pylori.

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22
Q

What else can gastric acid do?

A

It can help in absorption of iron and B12.

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23
Q

What happens when people have low or absent gastric acid?

A

Achlorhydia. It is common with people who have pernicious anaemia.

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24
Q

How is acid secreted

in the stomach?

A

Parietal cells are located in the body of the stomach. They secrete acid.

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25
Q

What causes parietal cells to secrete gastric acid?

A

They have proton pumps on the parietal cells which secrete approximately 2L a day of HCl acid.

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26
Q

Describe the H+/K+-ATPase Pump on the parietal cell?

A

It’s known as a proton pump and it requires ATP as energy for reaction.

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27
Q

What does the Parietal pump do?

A

It actively pumps hydrogen ions out of the cell into the stomach:

H2O + CO2 H+ + HCO3-. The reaction is catalysed by carbonic anhydrase.

K+ then enters the cell and HCO2- is transported out of the cell into the bloodstream.

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28
Q

Why is ATP required to drive the reaction?

A

It shifts hydrogen against the concentration gradient. Cell has to actively increase the concentration, by pumping the ions from a low concentration to a high concentration. The [H+] inside the cell = 4x10^8 M; [H+] outside the cell = 0.5M. Thus the cell needs ATP/energy.

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29
Q

What happens when the parietal cells are active (secreting)?

A

The tubulovesicles fuse with the canaliculus, increased surface area and numbers of H+/K+ - ATPase increases acid secretion into the lumen of the gut. Acid secretion is against a 3 million fold concentration gradient.

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30
Q

How does the stomach protect itself?

A

It secretes a layer of mucus that protects the stomach form exposure to the acid. It secretes bicarbonate to the epithelium to protect it from the acidic environment.

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31
Q

Why is the protection important?

A

It is the basis of why peptic ulcers form. If the layer of protection is destroyed, then ulceration occurs due to acidic environment.

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32
Q

Define neurotransmitter?

A

Molecule that transmits a signal from one neurone to another.

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33
Q

Define autocrine?

A

Molecule released by a cell that targets itself.

34
Q

Define paracrine?

A

Molecule released by a cell that targets adjacent cells.

35
Q

Define endocrine?

A

Molecule (known as hormone) released by endocrine cells into circulation to target distant cells.

36
Q

Where are the ECL (enterochromaffin-like) cells located?

A

Body of the stomach.

37
Q

Where are the G cells located?

A

Antrum of the stomach.

38
Q

What do ECL cells secrete?

A

Histamine (paracrine molecule).

39
Q

What does histamine do?

A

It stimulates acid secretion directly by acting upon adjacent parietal cells.

40
Q

What do G cells secrete?

A

Gastrin (endocrine molecule).

41
Q

What does Gastrin do?

A

It enters the blood circulation, binds to ECL cells stimulating a histamine release. Histamine then stimulates parietal cells to secrete HCL.

42
Q

Where are the D cells located?

A

Antrum of the stomach.

43
Q

What do D cells secrete?

A

Somatostatin (endocrine and paracrine molecule).

44
Q

What does Somatostatin do?

A

Inhibits acid secretion by acting on adjacent G cells and inhibiting Gastrin release.

45
Q

What is acetylcholine?

A

Neurotransmitter.

46
Q

What is it released by?

A

Vagus nerve and enteric neurons.

47
Q

What does acetylcholine stimulate?

A

Parietal cells to release HCL. ECL cells to release histamine -> stimulate parietal cells. G cells to release gastrin -> stimulates parietal cells and ECL cells.

48
Q

What causes increased gastric acid secretion (abnormal)?

A

Tutors that produce gastrin (gastronoma).

H.pylori gastritis.

49
Q

What happens when you have too much gastric acid secretion?

A

Destruction of the gastric mucosa, and the formation of multiple ulcers. They are difficult to treat and manage.

50
Q

What causes decreased gastric acid secretion (abnormal)?

A

Pernicious anaemia - antibodies target parietal cells and intrinsic factor. Destroy the parietal cells or intrinsic factor, reduced acid secretion.
Gastric surgery - remove certain parts of the stomach that contain parietal cells.
Vagotomy - operation performed with certain gastric surgeries; the vagal trunk is cut. Loss of the vagus nerve, leads to reduced ACh. So reduced acid secretion.
Drugs - block acid production in people ho have peptic ulcer disease. Called proton pump inhibitors or histamine receptor antagonists.

51
Q

Where is Pepsinogen secreted from?

A

Chief cells.

52
Q

What happens when pepsinogen comes into contact with HCl?

A

Cleaved into pepsin.

53
Q

What does Pepsin do?

A

It degrades proteins at aspartic amino acids.

54
Q

Where is intrinsic factor secreted from?

A

Parietal cells.

55
Q

Where is prostaglandins secreted from?

A

Stomach.

56
Q

What do prostaglandins do?

A

Repair mucosa.

57
Q

Describe the cephalic phase?

A
  1. Begins when you think about eating, sight of food or smell of food.
  2. Brain then sends signals to the vagus nerve/enteric nerves.
  3. Vagus nerve release ACh.
  4. ACh stimulates parietal cell to release acid.
    ECL cell to release histamine, which stimulate parietal cells to create HCl. Stimulates G cells to release Gastrin, stimulates ECL cells, release Histamine, stimulates Parietal cells to release HCl.
58
Q

Describe the Gastric phase?

A
  1. Food has made its way into the stomach.
  2. Gastric distension. Stimulates enteric nerves to release more ACh.
  3. ACh does the same thing in the cephalic phase.
  4. Amino acids stimulate the G cells, gastrin released, stimulates ECL cells, histamine released, Parietal cells stimulated and HCl released.
59
Q

Describe the Intestinal phase?

A
  1. Food is leaving the stomach, and fats are sitting in the duodenum. Stomach fills with HCl.
  2. Excessive HCl (low pH) stimulate the D cells, releases somatostatin. Somatostatin inhibits the G cells and stops further production of Gastrin.
  3. Gastric acid secretion turned down.
  4. The fats with HCl stimulate Cholecystokinin and secretin.
  5. Cholecystokinin and secretin inhibit gastric acid secretion and emptying.
  6. Secretin stimulates the pancreas and bile ducts to release bicarbonate. Needs to be secreted to counteract acidic chyme in the duodenum.
  7. Cholecystokinin stimulates the pancreatic enzymes and gall bladder to release bile.
60
Q

What can Helicobacter pylori cause?

A
  1. Gastritis - inflammation in the stomach that may or may not be symptomatic. Non-specific inflammatory response in the stomach.
  2. Peptic ulcer disease - if the mucosal barrier is broken. Crater is formed, as the ulceration becomes deeper bleeding may occur.
  3. Gastric cancer - can increase risk of gastric cancer.
  4. Gastric MALtoma - short for Mucosa-associate lymphoid tissue lymphoma. Not n aggressive cancer, confined just to the stomach. Can be treated by eradicating H.pylori, can lead to control of the MALtoma.
61
Q

What can H.pylori only infect?

A

Humans. Prefers the gastric antrum.

62
Q

How is H.pylori transmitted?

A

From person-person, mainly in childhood. Transmission pathway is unknown.

63
Q

Describe when a person gets infected with H.pylori?

A

The bacteria sits in the antrum of the stomach.

64
Q

Describe the inflammations stage of a H.pylori infection?

A

The bacteria starts to invade the mucosa of the antrum. Inflammation occurs over a long period of time. Gastritis.

65
Q

Describe the ulceration stage of a H.pylori infection?

A

Due to inflammation, inflammatory cells cause destruction of mucosa. An ulcer is formed, H.pylori ulcers cause in gastric or duodenum. If ulcer progresses it essentially causes bleeding.

66
Q

How do you treat H.pylori?

A

Cannot be treated with single antibiotic. Commonly use “Triple Therapy”: Omeprazole (lower the acid environment - proton pump inhibitor); clarithromycin (antibiotic)
amoxycillin (antibiotic). These are used for 14 days.

67
Q

What are second line regiments?

A

Drugs used when the standard therapy has not been successful.

68
Q

How do you detect H.pylori?

A

Stool test or blod test.

69
Q

What is the recurrence rate?

A

It is low. Main risk of infection is during the first 5 years of life.

70
Q

What are the other causes of Peptic ulcers?

A

Aspirin.

NSAIDs (non-steroidal anti-inflammatory drugs).

71
Q

What is a gastrectomy?

A

Surgery to remove the antrum (gastrin stimulus). Inhibits acid secretion.

72
Q

What is a vagotomy?

A

Surgery to remove part of the vagus nerve to reduce acid secretion. Sometimes performed with a pyloroplasty.

73
Q

What is a pyloroplasty?

A

Surgery to cut the pylorus out and stitch it back together so that it is more lax, sphincter not as tight. Food can leave stomach quicker, less stimulation of gastric acid.

74
Q

What year was H.pylori isolated?

A

1986.

75
Q

What are the symptoms of Peptic ulcer disease?

A

Pain - non-specific epigastric pain.
Bleeding.
Perforation.
Obstruction (in pylorus or duodenum) from: swelling, scarring causing stricture.

76
Q

What is a common way to diagnose peptic ulcer disease?

A

Endoscopy.

77
Q

Describe intestinal gastric cancer?

A

Well differentiated cancer - when the pathologist looks at the tissue under the microscope can see different stricture.
Cells arranged in a tubular/glandular pattern.

78
Q

Describe diffuse gastric cancer?

A

Poorly differentiated. Lack glandular formation, and can infiltrate the gastric wall - linitis plastica.

79
Q

Is there an association between H.pylori and Gastric cancer?

A

Yes. A stronger effect for the intestinal type of cancer.

80
Q

What is the reason for increased risk of H.pylori and intestinal gastric cancer?

A

H.pylori can produce non-specific inflammation in gastric mucosa. Can damage parietal cells, gastric acid secretion reduced. Promote certain bacteria which can produce carcinogens.

DS (32 decks)

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