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Semester 3-GI > Lecture 9-Stomach > Flashcards

Lecture 9-Stomach Flashcards

(50 cards)

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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?

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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?

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A

High turnover of epithelial cells

23
Q

How are prostaglandins involved in the defence of the stomach?

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A

Maintain mucosal blood flow to supply the epithelium with nutrients

24
Q

How do NSAIDs affect the stomach lining?

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A

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

25
What is receptive relaxation?
Vagally mediated relaxation of upper stomach to allow food to enter without an increased intra-gastric pressure to prevent reflux
26
What is GORD?
Gastro-oesophageal reflux disease - reflux of stomach contents into the oesophagus
27
What are the symptoms of GORD?
Heartburn, cough, sore throat, dysphagia
28
What are the causes of GORD?
- LOS problems - delayed gastric emptying - hiatus hernia (stomach into thorax) - obesity
29
What are the problems associated with GORD?
- oesophagitis - strictures - Barrett's oesophagus
30
What is Barrett's oesophagus?
Metaplasia of squamous -> columnar epithelium which increases the risk of adenocarcinoma
31
How can GORD be treated?
- lifestyle modification - antacids - H2 antagonists - PPIs - surgery (rare)
32
What is Zollinger Ellison disease?
Gastrin-secreting tumour which upregulates parietal cells -> increased HCl -> ulceration of stomach and small intestine
33
What is acute gastritis?
Acute mucosal inflammation
34
What can cause acute gastritis?
NSAIDs, lots of alcohol, chemo, bile reflux
35
What are the symptoms of acute gastritis?
Asymptomatic OR pain, nausea, vomiting and occasionally bleeding
36
What are the two possible causes of chronic gastritis?
H. Pylori infection or autoimmune
37
Describe how the autoimmune cause of chronic gastritis can lead to pernicious anaemia
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
What are the symptoms of chronic gastritis when caused by H. Pylori?
Asymptomatic OR similar to acute (pain, nausea, vomiting)
39
What are the symptoms of chronic gastritis when caused by an autoimmune reason?
Glossitis, anorexia, anaemia symptoms, neurological symptoms
40
What is peptic ulcer disease?
Defects in gastric/duodenal mucosa which extends through muscularis mucosa
41
Where are peptic ulcers most common?
1st part of duodenum and lesser curve of stomach
42
What can cause peptic ulcers?
Mucosal injury by stomach acid, H. Pylori, NSAIDs
43
What are the symptoms of peptic ulcers?
Epigastric pain, back pain with duodenal ulcers, burning following a meal, worse at night
44
What are the serious symptoms of peptic ulcers?
Bleeding, early satiety, weight loss
45
How can peptic ulcers be treated?
- eradicate H pylori: PPI + clarithromycin + amoxicillin - stop NSAIDs - PPIs - H2 blockers
46
How is H Pylori spread?
Oral-oral or foecal-oral
47
What is the gram stain for H Pylori?
Gram negative
48
How does H Pylori increase pH of the mucosal lining of the stomach?
Produces urease which converts urea to ammonium which increases the pH
49
What are the problems associated with H Pylori?
- releases cytotoxins (injures epithelium) - enzymes (urease) - degrades mucus layer - inflammation
50
What can H Pylori cause if colonised in the following locations: 1) antrum 2) antrum and body 3) body
1) duodenal ulcer 2) asymptomatic 3) cancer

Semester 3-GI (14 decks)

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