Session 5 - Function And Pathology Of Stomach Flashcards

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
Q

What happens in the intestinal phase of digestion?

A

10% of acid secretion

Chyme initially stimulates G cells (amino acids in the duodenum)

quickly overtaken by inhibition of G cells (CCK + secretin?)

26
Q

How does the stomach protect itself from acid?

A

Mucus/ HCO3- production
Mucus cells at surface and neck of gastric pits.
Forms thick alkaline viscous layer to protect cells

27
Q

Why are NSAIDs avoided in people with gastric ulcers?

A

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
Q

Name 3 factors which can breach stomach defences?

A

Alcohol
Helicobacter pylori
NSAIDs

29
Q

Define dyspepsia

A

Upper GI symptoms

30
Q

What is Zollinger-Ellison disease?

A

Increase in gastrin production from the pancreas = more parietal cells = more acid

31
Q

What is GORD?

symptoms?

A
Reflux of stomach contents into oesophagus.
Symptoms:
Heartburn 
Cough 
Sore throat 
Dysphagia - difficulty swallowing
32
Q

Causes of GORD?

A

LOS problem
Hiatus hernia
Obesity
Delayed gastric emptying (raised intragastric pressure)

33
Q

Complications of GORD?

A

Oesophagitis
Strictures

Barrett’s oesophagus - stratified squamous metaplasia to simple columnar -> increased risk of adenocarcinoma.

34
Q

Treatment of GORD?

A

Lifestyle:
Lose weight, sleep upright, eating earlier

Drugs:

  • antacids (from a layer of alkaline over acid)
  • H2 antagonists
  • PPIs
35
Q

What is acute gastritis?

A

Acute inflammationof the mucosa.

36
Q

Causes of acute gastritis ?

A

Alcohol
NSAIDs
Bile reflux

37
Q

Symptoms of acute gastritis?

A
None
Pain
Vomiting 
Nausea 
Possibly bleeding
38
Q

What are the causes of chronic gastritis?

A

Bacterial - H. Pylori

autoimmune - autoantibodies to parietal cells -> pernicious anaemia

39
Q

Symptoms of chronic gastritis?

A

None
Pain
Vomiting
Nausea

BUT can progress

Peptic ulcers
Adenocarcinoma
MALT lymphoma

Pernicious anaemia if autoimmune (tiredness, glossitis)

40
Q

What is the defition of an ulcer?

A

Must extend to the muscularis mucosa

41
Q

Where are peptic ulcers most commonly found?

A

First part of duodenum

42
Q

Where is the most common place for ulcers in the stomach?

A

Lesser curve of the stomach

43
Q

Causes of peptic ulcers?

A

H. Pylori
Stomach acid
NSAIDs

44
Q

Symptoms of peptic ulcer disease?

A

Epigastric pain

  • burning/gnawing
  • after meals
  • duodenal ulcer - worse at night

Serious

  • bleeding
  • Weight loss
45
Q

How could you diagnose gastric pathology?

A

Upper GI endoscopy

Urease breath test - h. Pylori

Erect CXR - gas under diaphragm

46
Q

Which antibiotics would you use to treat h. Pylori?

A

Clarithromyocin

Amoxicillin

47
Q

Name a H2 blocker?

A

Cimetidine

Ranitidine

48
Q

Name a PPI?

A

Omeprazole

49
Q

How does h.pylori cause problems?

A

Releases cytotoxins - causing direct epithelial damage

50
Q

What is the spread of H.pylori?

A

Fecal/oral route