Stomach And Gastric Disease Flashcards

1
Q

What are the three main functions of the stomach?

A

Storage facility,
Start digestion of protein, carbohydrates and fat,
Destroy pathogens in food

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2
Q

What are the three anatomical divisions of the stomach from superior to inferior?

A

Fundus,
Body,
Antrum

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3
Q

What aids the function of the lower oesophageal sphincter?

A

Right crus of the diaphragm constricts in high IAP
Acute angle of entry
Intrinsic smooth muscle

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4
Q

What change in epithelium is seen between the oesophagus and the stomach?

What is Barrett’s oesophagus?

A

Stratified squamous to simple columnar

Metaplasia of stratified squamous oesophageal tissue to columnar gastric mucosa

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5
Q

What is receptive relaxation?

A

Peristalsis causes reflex relaxation of the proximal stomach, distending the fundus and allowing the stomach to fill without a significant rise in pressure

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6
Q

What types of cells reside within the gastric pits?

A

Gastric gland cells
Parietal cells
Chief cells
G cells near antrum

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7
Q

What protective mechanisms does the stomach have?

A

Stomach mucosa secretes bicarbonate ions to buffer acidic conditions in local environment.

High turnover of epithelial cells.

Prostaglandins increase blood flow and support mucus layer

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8
Q

How do parietal cells secrete stomach acid?

A
  1. Carbonic anhydrase catalyses breakdown of carbonic acid into hydrogen ions and bicarbonate ions.
  2. Chloride ions anti ported into the cell against bicarbonate ions
  3. Hydrogen and chloride ions facillitated diffusion out of the cell and combine to form HCl
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9
Q

What is alkaline tide?

A

Bicarbonate ion secretion into venous blood causing a detectable increase in pH

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10
Q

What characterises the resting state of a parietal cell?

A

Tubulovesicles containing proton pumps remain separate from the apical membrane

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11
Q

What characterises the active state of a parietal cell?

A

Tubulovesicles containing proton pumps fused to cannaliculi of the apical membrane, allowing hydrogen ion secretion

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12
Q

What stimulates the production of stomach acid?

A

Senses - smell, sight, taste.
Stretch receptors in stomach,
Presence of amino acids or peptides,
Chyme sensed in duodenum

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13
Q

What stimulates a parietal cell?

A
Gastrin receptors (G cells)
Histamine receptors (enterochromaffin cells)
Muscarinic receptors (acetylcholine)
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14
Q

How is acid secretion inhibited?

A

D cells secrete somatostatin as a result of a sensed decrease in pH.

These bind to somatostatin receptors and inhibit secretion of gastrin

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15
Q

What is dyspepsia?

A

A complex of upper GI tract symptoms which are typically present for four or more weeks, including upper abdominal discomfort, nausea, heartburn, acid reflux and/or vomiting

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16
Q

What characterises Gastro-oesophageal reflux disease?

A

Heartburn
Acidic taste
Cough
(Sometimes asymptomatic)

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17
Q

What is a hiatus hernia?

A

Lower oesophageal sphincter herniates into thorax through the diaphragm.

Increases risk of GORD and LOS dysfunction

18
Q

What complications of GORD are there?

A
Oesophagitis,
Ulceration,
Haemorrhage,
Strictures,
Metaplastic change.
19
Q

What lifestyle managements are there for GORD?

A

Weight loss,
Avoiding trigger foods,
Smaller meals,
Decrease alcohol and caffeine consumption.

20
Q

What drug management options are there for GORD?

A

PPIs,

H2 receptor antagonists.

21
Q

What surgical management is there for GORD?

What does this involve?

A

Fundoplication - fundus is wrapped around the back of the oesophagus and secured by sutures to aid the LOS

22
Q

What is gastritis?

What symptoms characterise it?

A

Inflammation of stomach mucosa.

Pain,
Nausea,
Vomiting,
Haemorrhage.

23
Q

What causes acute gastritis?

A

NSAIDS,
Bile reflux,
Alcohol consumption risk factor.

24
Q

What causes chronic gastritis?

A

H-pylori infection,

Autoimmune.

25
Q

What complications are associated with chronic autoimmune gastritis?

A

B12 deficiency and pernicious anaemia

26
Q

What features of H-pylori make the gut a suitable place for it’s growth?

A

Microaerophilic
Adhesions to resist preistalsis
Urease to create ammonia and neutralise local environment.

27
Q

How does H-pylori cause gastritis?

A

Cytotoxin associated gene A stimulates IL8 responses,
Vacuolating toxin is toxic to epithelia,
Urease produces ammonia which is toxic to cells.

28
Q

What features would be seen in a H-pylori infection of the antrum?

A

Overactivity of G cells,
More acid secretion from parietal cells,
Duodenal damage and metaplasia - ulceration

29
Q

What features would be seen in a H-pylori infection of the stomach body or fundus?

A

Atrophy of parietal cells,
Less stomach acid,
This is likely asymptomatic but causes an increased risk of cancer.

30
Q

What is the urease breath test?

A
  1. Carbon 13 rich urea is ingested
  2. Urease enzyme converts this to CO2 and Ammonia
  3. C13 is detected in exhaled CO2 to confirm H-pylori infection.
31
Q

How is H-pylori infection treated?

A

triple therapy - PPI plus 2 antibiotics (usually Clarithromycin as one) for 7 to 14 days. Urea breath test afterwards to check success.

32
Q

What is peptic ulcer disease?

A

Defect in gastric or duodenal mucosa that extends through the muscularis mucosa

33
Q

Which areas of the stomach/foregut do peptic ulcers affect?

A

Lesser curve of the stomach, antrum and proximal Duodenum

34
Q

What acidity levels are found in gastric ulcers?

What acidity levels are found in duodenal ulcers?

A

Normal - high in gastric

Low - normal in duodenal

35
Q

What risk factors are there for peptic ulcer disease?

A

H-pylori infection,
NSAID use,
Smoking,
Massive physiological stress eg burns

36
Q

Where do chronic ulcers occur?

A

At mucosal junctions eg antrum to proximal duodenum

37
Q

Scarring secondary to peptic ulcers leads to what complications?

A

Pyloric stenosis,

Perforation and peritonitis.

38
Q

What is Malaena and what is it indicative of?

A

Oxidised haemoglobin in blood found in stool causing a black discolouration.
Indicative of upper GI bleed.

39
Q

What are common symptoms of PUD?

A
Epigastric pain,
Gnawing or burning back pain,
Pain follows meals or at night.
Early satiety,
Weight loss.
40
Q

How do you manage PUD with no active bleeding?

A
  1. Test for H-pylori
  2. If positive - begin triple therapy
  3. If negative, consider stopping exacerbating medications or add PPIs.
41
Q

How do you manage PUD with active bleeding?

A

Inject adrenaline locally to promote clotting,

Treat with cautery and clip application. Then consider managements for no active bleeding.