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Semester 3-GI > Lecture 9-Stomach > Flashcards

Lecture 9-Stomach Flashcards

1
Q

What are the basic functions of the stomach?

A
  • receive food and temporarily store it
  • disrupt food
  • continue digestion
  • disinfect
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2
Q

How does the type of epithelium change as you go down from the oesophagus to the stomach?

A

Stratified squamous -> simple columnar

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3
Q

What are the folds of the stomach called?

A

Rugae

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4
Q

Which epithelial cells cover the surface of the stomach and extend into pits/glands?

A

Mucous cells
Parietal cells
Chief cells
G cells

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5
Q

What is the difference between the muscle of the upper and lower stomach?

A

Lower has more muscle for stronger peristalsis

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6
Q

How does the shape of the stomach aid in movement of food?

A

Larger proximally and smaller distally to accelerate the contents and leave lumps behind so chyme can enter the duodenum

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7
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

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8
Q

What do G cells secrete?

A

Gastrin

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9
Q

What do chief cells secrete?

A

Pepsinogen

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10
Q

What do D cells secrete?

A

Somatostatin

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11
Q

What do mucous cells secrete?

A

Mucous (duh?)

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12
Q

What do enterochromaffin-like cells (ECL) secrete?

A

Histamine

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13
Q

Explain the mechanism of secretion of stomach acid

A
  • Parietal cells are stimulated by gastrin, histamine and ACh from vagus nerve
  • Gastrin binds to CCK receptor on parietal cell -> acid
  • Histamine binds to H2 receptor on p cell -> acid
  • ACh binds to muscarinic receptor on p cell -> acid
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14
Q

What stimulates G cells in the antrum of the stomach to produce gastric acid?

A

Peptides/AA in stomach lumen, vagal stimulation (ACh and gastrin releasing peptide)

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15
Q

How is HCl production inhibited?

A

Low pH of food activates D cells to produce somatostatin which inhibits G cells and ECL cells so vagal activity decreases

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16
Q

What is alkaline tide?

A

After a meal, parietal cells produce HCl and secrete HCO3- across the basolateral membrane to increase pH

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17
Q

What are the three phases of digestion?

A
  • Cephalic
  • Gastric
  • Intestinal
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18
Q

Describe the first stage of digestion

A
  • parasympathetic stimuli such as smell, taste, chewing etc directly stimulates parietal and G cells (vagus nerve)
  • anticipating food can also increase GI motility
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19
Q

Describe the second stage of digestion

A
  • distension of stomach stimulates vagus nerve which stimulates parietal and G cells
  • AA and peptides also stimulate G cells
  • enteric NS and gastrin -> smooth muscle contraction
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20
Q

Describe the third stage of digestion

A
  • chyme stimulates gastrin secretion initially
  • this is soon overtaken by inhibition of G cells - lipids activate the enterogastric reflex which decreases vagal stimulation and chyme stimulates CCK and secretin
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21
Q

How is HCO3- a stomach defence mechanism?

A
  • released by mucous cells

- forms a thick alkaline layer that adheres to the epithelium to increase pH

22
Q

How are stem cells involved in the defence of the stomach?

A

High turnover of epithelial cells

23
Q

How are prostaglandins involved in the defence of the stomach?

A

Maintain mucosal blood flow to supply the epithelium with nutrients

24
Q

How do NSAIDs affect the stomach lining?

A

NSAIDs inhibit prostaglandin release -> less blood flow -> damage to epithelium

25
Q

What is receptive relaxation?

A

Vagally mediated relaxation of upper stomach to allow food to enter without an increased intra-gastric pressure to prevent reflux

26
Q

What is GORD?

A

Gastro-oesophageal reflux disease - reflux of stomach contents into the oesophagus

27
Q

What are the symptoms of GORD?

A

Heartburn, cough, sore throat, dysphagia

28
Q

What are the causes of GORD?

A
  • LOS problems
  • delayed gastric emptying
  • hiatus hernia (stomach into thorax)
  • obesity
29
Q

What are the problems associated with GORD?

A
  • oesophagitis
  • strictures
  • Barrett’s oesophagus
30
Q

What is Barrett’s oesophagus?

A

Metaplasia of squamous -> columnar epithelium which increases the risk of adenocarcinoma

31
Q

How can GORD be treated?

A
  • lifestyle modification
  • antacids
  • H2 antagonists
  • PPIs
  • surgery (rare)
32
Q

What is Zollinger Ellison disease?

A

Gastrin-secreting tumour which upregulates parietal cells -> increased HCl -> ulceration of stomach and small intestine

33
Q

What is acute gastritis?

A

Acute mucosal inflammation

34
Q

What can cause acute gastritis?

A

NSAIDs, lots of alcohol, chemo, bile reflux

35
Q

What are the symptoms of acute gastritis?

A

Asymptomatic OR pain, nausea, vomiting and occasionally bleeding

36
Q

What are the two possible causes of chronic gastritis?

A

H. Pylori infection or autoimmune

37
Q

Describe how the autoimmune cause of chronic gastritis can lead to pernicious anaemia

A

Antibodies to gastric parietal cells can lead to pernicious anaemia because if there are no parietal cells, no intrinsic factor is produced which is needed to digest vitamin B12

38
Q

What are the symptoms of chronic gastritis when caused by H. Pylori?

A

Asymptomatic OR similar to acute (pain, nausea, vomiting)

39
Q

What are the symptoms of chronic gastritis when caused by an autoimmune reason?

A

Glossitis, anorexia, anaemia symptoms, neurological symptoms

40
Q

What is peptic ulcer disease?

A

Defects in gastric/duodenal mucosa which extends through muscularis mucosa

41
Q

Where are peptic ulcers most common?

A

1st part of duodenum and lesser curve of stomach

42
Q

What can cause peptic ulcers?

A

Mucosal injury by stomach acid, H. Pylori, NSAIDs

43
Q

What are the symptoms of peptic ulcers?

A

Epigastric pain, back pain with duodenal ulcers, burning following a meal, worse at night

44
Q

What are the serious symptoms of peptic ulcers?

A

Bleeding, early satiety, weight loss

45
Q

How can peptic ulcers be treated?

A
  • eradicate H pylori: PPI + clarithromycin + amoxicillin
  • stop NSAIDs
  • PPIs
  • H2 blockers
46
Q

How is H Pylori spread?

A

Oral-oral or foecal-oral

47
Q

What is the gram stain for H Pylori?

A

Gram negative

48
Q

How does H Pylori increase pH of the mucosal lining of the stomach?

A

Produces urease which converts urea to ammonium which increases the pH

49
Q

What are the problems associated with H Pylori?

A
  • releases cytotoxins (injures epithelium)
  • enzymes (urease)
  • degrades mucus layer
  • inflammation
50
Q

What can H Pylori cause if colonised in the following locations:

1) antrum
2) antrum and body
3) body

A

1) duodenal ulcer
2) asymptomatic
3) cancer

Semester 3-GI (14 decks)

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