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Gastric 1+2+3 Flashcards

1
Q

What is Dyspepsia?

A

A complex of upper GI tract symptoms which are typically present for 4 or more weeks including upper abdominal discomfort, heartburn, acid reflux, nausea and or vomiting

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2
Q

What is Gastro-oesophageal reflux disease?

A

When contents of the stomach reflux into the oesophagus through the lower oesophageal sphincter

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3
Q

What are the symptoms of Gastro-oesophageal reflux disease?

A

Heart burn
Acidic taste (potential dental erosion)
Cough
Can be asymptomatic

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4
Q

What are the risk factors of developing Gastro-oesophageal reflux disease?

A

Essentially anything that increases Intrabdominal pressure:
-obesity
-pregnancy
-delayed gastric emptying

Lower oesophageal dysfunction
Hiatus hernia

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5
Q

What is a Hiatus hernia?

A

When the Lower-oesophageal sphincter herniates through the diaphragm so it is now in the thorax rather than the abdomen

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6
Q

What 3 components help keep the oesophageal eal sphincter closed?

A

Muscular elements (intrinsic and diaphragm)

Right crus

Angle oesophagus joins stomach

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7
Q

What is the right crus?

A

Derived from intervertebral discs of L1-L3 the wrap around the lower oesopheal sphincter keeping it closed

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8
Q

What are some potential complications of Gastric-oesophageal reflux disease?

A

Oesophagitis
Ulceration
Haemorrhage
Strictures
Metaplastic changes (Barrett’s oesophagus)

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9
Q

What is oesophagitis?

A

Inflammation of epithelium of oesophagus

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10
Q

What layer gets damaged if ulceration?

A

Muscularis mucosa damaged

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11
Q

What complication can occur if haemorrhaging occurs?

A

Anaemia

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12
Q

What are strictures, when do they normally occur, what complications can this lead to with respect to Gastro-oesophageal reflux disease?

A

When continual repair leads to fibrous strictures forming

This can lead to dysphagia

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13
Q

What is Barretts oesophagus?

A

When repeat exposure of gastric contents to the oesophagus occurs leading to metaplastic changes

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14
Q

What cells are normally present in the lower oesophagus?

What cells do these change to in Barrett’s oesophagus?

A

Stratified squamous epithelia -> columnar cells

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15
Q

What is the risk of cells converting to columnar epithelial cells in Barrett’s oesophagus?

A

Columnar cells have increased risk of Dysplasia leading to Adenocariinoma development

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16
Q

What is adenocarcinoma?

A

A cancer of glandular origin

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17
Q

How can Gastro-oesophageal reflux disease be managed?

A

Lifestyle

Drugs

Surgery

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18
Q

What lifestyle changes can be implemented to help with gastro-oesophageal reflux disease?

A

Weight loss
Eat smaller meals
Don’t eat then sleep (prop up while sleeping)
Decrease alcohol and caffeine intake

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19
Q

What drugs can be used to manage Gastro-oesophageal reflux disease?

A

Proton Pump Inhibitor (omeprazole)

H2 receptor antagonists like Famotidine (decreases acid production)

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20
Q

What surgery is done to help treat GORD?

A

Fundoplication

Fundus of stomach wrapped around lower oesophagus to help with sphincter mechanism

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21
Q

What is Gastritis?

A

Inflammation of the stomach mucosa

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22
Q

What are some symptoms of Gastritis?

A

Pain
Nausea
Vomiting
Haemorrhage

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23
Q

What type of cells invade the lamina propria in Gastritis?

A

Neutrophils

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24
Q

What can cause Acute gastritis?

A

NSAIDs
Bare alcohol
Chemotherapy
Bile reflux

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25
Q

What can cause Chronic Gastritis?

A

Infection with H-pylori
Autoimmune cause

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26
Q

What are some pathological changes in gastritis?

A

Epithelial damage
Epithelial hyperplasia
Vasodilation
Neutrophil response

Lymphocyte response (lamina propria)
Glandular atrophy (lamina propria)
Fibrotic changes (lamina propria)

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27
Q

What is the autoimmune cause of chronic gastritis?

A

Autoimmune antibodies attack parietal cells

Leads to decreased acid production and decreased intrinsic factor production

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28
Q

Why is it important that Parietal cells produce Intrinsic factor?

A

Intrinsic factor needed to absorb Vitamin B12

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29
Q

What haematological condition can develop as a result of loss of intrinsic factor production by parietal cells?

A

Pernicious anaemia which is a type of Megaloblastic anaemia

30
Q

What part of the body does Vitamin B12 get absorbed with the hep of intrinsic factor?

A

Ileum (distal part of small intestine)

31
Q

In autoimmune chronic gastritis, what are some symptoms that occur as a result of atrophy of the body of stomach?

A

Megaloblastic anaemia (pernicious anaemia)

Neurological symptoms

Anorexia

Glossitis (symptom of pernicious anaemia)

32
Q

What is Glossitis?

A

Inflammation of tongue

33
Q

What route does H-pylori infect people?

A

Faecal-oral route

34
Q

What type of organism is Helibacter pylori?

A

Gram negative helical bacteria

35
Q

What are the features that help H-pylori infect?

A

Flagella for motility
Chemotaxis (find areas of higher acidity)

Adhesins to fix to gastric epithelia (resist peristalsis)

36
Q

What enzyme is important in helping protect the H-pylori in the stomach?

Why?

A

Urease

Urea converted to ammonia using water

Ammonia is basic and it coats the outer membrane helping protect the bacteria from the acidic conditions

37
Q

How does H-Pylori cause gastritis?

A

Produces digestive enzymes like Mucinase, Protease, and lipases

Ammonia they produce damages the stomach epithelium

Produces Cytotoxin associated Gene A (CAG.A)
Produces Vacuolting Toxin A (VacA)

38
Q

How does CAG.A made by H-pylori cause Gastritis?

A

Stimulates interleukin 8 production leading to inflammation of stomach epithelia

39
Q

How does Vacuolating Toxin A (VacA) produced by H-pylori cause Gastritis?

A

Directly toxic to the stomach epithelia

40
Q

What affect do h-pylori have on G cells in the antrum?

A

Leads to increased activity increasing amount of Gastrin
Leading to the chyme become very acidic

41
Q

What affect does increased acidity if chyme have on h-pylori movements?

A

Can colonise duodenum

42
Q

What happens if h-pylori infects stomach body?

A

Atrophy of parietal cells

Leads to increased cancer risks

43
Q

How do you diagnose infection with H-pylori?

A

Urea breath test

44
Q

How does the urea breath test work?

A

Gastric urea contains C12

Give patients C13, urea gets injected and if H pylori present the urea gets broken down to ammonia

You can then detect a high level of C13 in the CO2 exhaled

45
Q

How do we treat H-pylori infection?

A

Proton Pump Inhibitor (PPI) Omeprazole

2 x antibiotics (clarithromycin + metronidazole)

46
Q

What is peptic ulcer disease?

A

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

47
Q

Where is peptic ulcer disease most common?

A

Duodenum

48
Q

If a peptic ulcer disease occurs in the stomach, where s the most common location?

A

Lesser curve/antrum

49
Q

Go to last slide of gastric disease 3 and label the image of the peptic ulcer disease:

A

1 = epithelium
2 = lamina propria
3 = muscularis mucosa
4 = sub mucosa
5 = muscularis externa

50
Q

What is the ratio of gastric ulcer to duodenal ulcer incidence?

A

Gastric 1: 3 duodenal

51
Q

What is the most common blood group for gastric ulcers?

What is the most common blood group for duodenal ulcers?

A

Gastric = A

Duodenal = O

52
Q

What are the levels of acid like for gastric ulcers?

What are the levels of acid like for duodenal ulcers?

A

Gastric = Normal/low

Duodenal =Normal/high

53
Q

Why do duodenal ulcers lead to high levels of acid?

A

Chyme is more acidic which overwhelms the intestines ability to neutralise it

54
Q

Which type of ucler normally always is associated with H-pylori infection?

A

Duodenal (95-100%) (the H-pylori increase G cell activity meaning more Gastrin made so more parietal cells stimulated to make stomach acid)

Gastric = 70%

55
Q

What is the alkaline layer of the stomach defences?

A

Mucus layer + HCO3- secretion

56
Q

What medication inhibits production of prostaglandins which then leads to reduced support to the protective mucus layer?

A

NSAIDs

57
Q

What are the risk factors for peptic ulcer disease?

A

H-pylori
NSAIDs (inhibits prostaglandins)
Smoking (leads to ulcer relapse)
Massive physiological stress (burns)

58
Q

How do Acute ulcers develop?

A

They develop as part of acute gastritis (transient with healing)

59
Q

Where do chronic ulcers occur?

A

Mucosal junctions like where the antrum meets the curve

60
Q

How can peptic ulcer diseases lead to Pyloric stenosis?

A

Ulceration thought the Muscularis mucosa that extends to the muscularis externa leads to the muscularis externa being replaced by fibrous scar tissue

This scar tissue can build up leading to narrowing of the pyloric sphincter

61
Q

How can peptic ulcer disease lead to peritonitis?

A

The peptic ulcer can go all the way through the Musculariating the stomach wall leading to leakage of contents into peritoneum

62
Q

What is malaena?

A

Relatively slow upper GI bleed

63
Q

What artery can be ruptured if a peptic ulcer perforates posteriorly in the stomach?

A

Splenic artery

64
Q

What happens as result of a peptic ulcer perforating into the gastroduodenal artery?

A

Duodenum or stomach can fill with blood

65
Q

What often happens pyloric stenosis?

A

Vomiting

66
Q

What is haematemesis?

A

When someone bleeds internally leading to them vomiting

67
Q

What region is pain experienced in Peptic Ulcer Disease?

A

Epigastric pain (burning or gnawing pain)

68
Q

What are symptoms of Peptic Ulcer Disease?

A

Epigastric pain

Haematemesis from bleeding

Anaemia due to Malaena

Early satiety
Weight loss

69
Q

How does the onset of pain differ between Duodenal ulcers and gastric ulcers?

A

Duodenal ulcers = food stops pain since pyloric sphincter contracts preventing chyme getting into duodenum

Gastric ulcer = pain made worse straight away with food

70
Q

How do you manage a peptic ulcer disease that isn’t actively bleeding with H-pylori present?

A

PPI + x2 Antibiotics

71
Q

How do you manage a peptic ulcer disease that isn’t actively bleeding without H-pylori present?

A

Stop the meds worsening it like NSAIDs

72
Q

How do you manage a peptic ulcer disease that is actively bleeding?

A

Endoscopic injection
Injecting adrenaline and cauterising

GI (35 decks)

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