Session 5 - Function And Pathology Of Stomach Flashcards

(50 cards)

1
Q

How is gastric contents prevented from refluxing?

A

The right crus of the diaphragm wraps around the LOS.

The oesophagus enters at an acute angle

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2
Q

What is the epithelium of the stomach?

A

Simple columnar

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3
Q

How many muscle layers in the stomach

A

3

Extra oblique muscle layer

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4
Q

How does the stomach mechanically digest food?

A

The lower portion of the stomach constricts every 20 seconds - strong peristalsis
The stomach goes from large to small - creating a funnel , so that larger bits remain in the stomach

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5
Q

How is the entrance of food into the duodenum controlled?

A

The pylorus relaxes every 3 minutes or so, releasing liquid chyme into the duodenum

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6
Q

How does the stomach perform its function as a store?

A

Receptive relaxation
Rugae allow distension

Allows food to enter without raising intra-gastric pressure too much

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7
Q

Why do we have acid in our stomach?

A

Disinfect stomach contents.
Activates proteases (pepsinogen->pepsin)
Helps unravel proteins

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8
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

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9
Q

Which cell secretes gastrin?

A

G cells

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10
Q

Which cells secrete histamine?

A

ECL cells

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11
Q

What do the chief cells secrete?

A

Pepsinogen

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12
Q

What do D cells secrete?

A

Somatostatin

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13
Q

Which cells secrete mucus?

A

Mucous cells

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14
Q

What cells make up the surface and neck of the gastric pits?

A

Mucous cells

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15
Q

Which cells are mainly in the fundus and body of the stomach?

A

Parietal cells
ECL cells
Chief cells

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16
Q

Which cells are mainly in the pyloric region of the stomach?

A

D cells

G cells

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17
Q

How is acid production controlled?
Which receptors do they act at?
Which one is endocrine, paracrine, neural?

A

By Histamine from ECL cells - H2 receptors - paracrine
By gastrin from G cells (acts at CCK receptors) - endocrine
By ACh from vagal stimulation - muscarinic receptor - neural

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18
Q

How is Gastrin secretion controlled?

A
Stimulated by:
    Peptides/amino acids
    Vagal stimulation:
           -> ACh + gastrin-releasing peptide 
Inhibited by:
Somatostatin
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19
Q

How is acid secretion inhibited?

A

D cells secrete somatostatin.
Stimulated by low pH. Food pH decreases when food leaves the stomach
Somatostatin acts on G cells. Reduce gastrin production

When food leaves the stomach, the distension decreases reducing vagal stimulation of G cells and parietal cells

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20
Q

Why is there an alkaline tide after meals?

A

Water is broken down to make H+
The OH- joins CO2 to make bicarbonate
Bicarbonate is exported out of the cell on an anion anti port. Cl- is imported into the cell
H+ and Cl- join to make HCl.

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21
Q

What type of transport is used to export hydrogen ions into the stomach?

A

Primary active transport

22
Q

Name the three phases of digestion ?

A

Cephalic (thought of food)
Gastric (food in the stomach)
Intestinal (food in the intestine)

23
Q

What happens in the cephalic phase of digestion?

A

30% of HCl is produced.

Thought of food+tasting+chewing+swallowing => vagal stimulation.
Stimulation of G cells via release of Gastrin releasing protein

24
Q

What happens in the gastric phase of digestion ?

A

Distension of stomach = vagal stimulation
Food acts as buffer = removes inhibitory mechanisms
Amino acids = gastrin release

60% of acid secretion

25
What happens in the intestinal phase of digestion?
10% of acid secretion Chyme initially stimulates G cells (amino acids in the duodenum) quickly overtaken by inhibition of G cells (CCK + secretin?)
26
How does the stomach protect itself from acid?
Mucus/ HCO3- production Mucus cells at surface and neck of gastric pits. Forms thick alkaline viscous layer to protect cells
27
Why are NSAIDs avoided in people with gastric ulcers?
Prostaglandins maintain blood flow to the epithelium - maintaining cell turnover and nutrient supply If you take NSAIDs and prevent prostaglandin formation then blood flow to the epithelium is compromised
28
Name 3 factors which can breach stomach defences?
Alcohol Helicobacter pylori NSAIDs
29
Define dyspepsia
Upper GI symptoms
30
What is Zollinger-Ellison disease?
Increase in gastrin production from the pancreas = more parietal cells = more acid
31
What is GORD? | symptoms?
``` Reflux of stomach contents into oesophagus. Symptoms: Heartburn Cough Sore throat Dysphagia - difficulty swallowing ```
32
Causes of GORD?
LOS problem Hiatus hernia Obesity Delayed gastric emptying (raised intragastric pressure)
33
Complications of GORD?
Oesophagitis Strictures Barrett's oesophagus - stratified squamous metaplasia to simple columnar -> increased risk of adenocarcinoma.
34
Treatment of GORD?
Lifestyle: Lose weight, sleep upright, eating earlier Drugs: - antacids (from a layer of alkaline over acid) - H2 antagonists - PPIs
35
What is acute gastritis?
Acute inflammationof the mucosa.
36
Causes of acute gastritis ?
Alcohol NSAIDs Bile reflux
37
Symptoms of acute gastritis?
``` None Pain Vomiting Nausea Possibly bleeding ```
38
What are the causes of chronic gastritis?
Bacterial - H. Pylori autoimmune - autoantibodies to parietal cells -> pernicious anaemia
39
Symptoms of chronic gastritis?
None Pain Vomiting Nausea BUT can progress Peptic ulcers Adenocarcinoma MALT lymphoma Pernicious anaemia if autoimmune (tiredness, glossitis)
40
What is the defition of an ulcer?
Must extend to the muscularis mucosa
41
Where are peptic ulcers most commonly found?
First part of duodenum
42
Where is the most common place for ulcers in the stomach?
Lesser curve of the stomach
43
Causes of peptic ulcers?
H. Pylori Stomach acid NSAIDs
44
Symptoms of peptic ulcer disease?
Epigastric pain - burning/gnawing - after meals - duodenal ulcer - worse at night Serious - bleeding - Weight loss
45
How could you diagnose gastric pathology?
Upper GI endoscopy Urease breath test - h. Pylori Erect CXR - gas under diaphragm
46
Which antibiotics would you use to treat h. Pylori?
Clarithromyocin | Amoxicillin
47
Name a H2 blocker?
Cimetidine | Ranitidine
48
Name a PPI?
Omeprazole
49
How does h.pylori cause problems?
Releases cytotoxins - causing direct epithelial damage
50
What is the spread of H.pylori?
Fecal/oral route