Helicobacter pylori and Gastric Disease Flashcards

1
Q

Upper GI Tract

A

Oesophagus
Stomach

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2
Q

Lower GI Tract

A

Small intestine
Large intestine

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3
Q

dyspepsia symptoms

A

Epigastric pain
Burning
Fullness
Bloating
Satiety
Nausea
Sickness
Heartburn
Reflux
Discomfort

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4
Q

Dyspepsia greek meaning

A

dys = bad, pepsis = digestion

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5
Q

what are the collective group of symptoms for dyspepsia

A

Pain or discomfort in the upper abdomen

upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomiting, bloating, fullness, early satiety and heartburn

For 4 weeks ( 12weeks Rome criteria)

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6
Q

is dyspepsia common

A

80 % of people, most have no serious underlying disease

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7
Q

GP consultations percentage for dyspepsia patients

A

When broadly defined, dyspepsia occurs in 40%, leads to GP consultation in 5% and referral for endoscopy in 1% of the population annually.

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8
Q

what can cause symptoms of dyspepsia for upper GI

A

GORD
Peptic ulcer
Gastritis
Non ulcer dyspepsia
Gastric cancer

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9
Q

What can cause the symptom of dyspepsia in lower GI

A

Gallstones
Pancreatic disease
IBS
Colonic cancer
Coeliac disease

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10
Q

what may be other causes of dyspepsia

A

Other systemic disease – metabolic, cardiac

Drugs

Psychological

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11
Q

what do you do if a patient presents with dyspepsia

A

History & examination are key!!

Drug history – NSAIDs, steroids, bisphosphonates, Ca antagonists, nitrates, theophyllines, remember OTT

Lifestyle – alcohol, diet, smoking, exercise, weight reduction

Examination including BMI

Bloods – FBC, ferritin, LFTs, U&Es, calcium, glucose, coeliac serology/serum IgA

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12
Q

what bloods need to be done for dyspepsia

A

FBC, ferritin, LFTs, U&Es, calcium, glucose, coeliac serology/serum IgA

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13
Q

when do you refer for endoscopy

A

ALARMS

Anorexia
Loss of weight
Anaemia – iron deficiency
Recent onset >55 years or persistent despite treatment
Melaena/haematemesis (GI bleeding) or mass
Swallowing problems - dysphagia

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14
Q

what is an upper GI endoscopy

A

Diagnostic and therapeutic upper GI endoscopy

Local anaesthetic (throat spray) or sedation

Day case

Fasted

Consent

Risks - 1:2000 risk perforation, bleeding, reaction to drugs given

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15
Q

what is helicobacter pylori

A

Gram negative, spiral-shaped, microaerophilic, flagellated Gram –ve bacteria

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16
Q

how common is helicobacter pylori

A

Infects 50% world population

Acquired in childhood

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17
Q

what can H.pylori only colonise

A

only colonise gastric type mucosa

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18
Q

where does H.pylori reside

A

in the surface mucous layer and does not penetrate the epithelial layer

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19
Q

what does an H.pylori infection do

A

Evokes immune response in underlying mucosa – dependent on host genetic factors

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20
Q

what is the infection pathway and pathogenesis for Helicobacteria

A
  • enters host and aurvives
  • motility and chemotaxis
  • adhesin receptor interaction (establish colony)
  • toxin release and damage to host
  • intracellular replication
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21
Q

what is the clinical outcome of helicobacter pylori for >80%

A

asymptomatic or chronic gastritis

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22
Q

what is the C

A

chronic atrophic gastritis
intestinal metaplasia
gastric or duodenal ulcer

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23
Q

what is the the clinical outcome of helicobacter pylori for 1%

A

gastric cancer
MALT lymphoma

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24
Q

what is the clinical outcome of H.Pylori dependent on

A

site of colonization

characteristics of bacteria

host factors e.g. genetic susceptibility

environmental factors e.g. smoking

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25
Q

what are the three different types of gastritis caused by chronic H.Pylori infection

A

Antral predominant Gastritis

Mild Mixed Gastritis

Corpus predominant Gastritis

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26
Q

what does Corpus predominant Gastritis mainly affect

A

the body of the stomach

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27
Q

Corpus predominant Gastritis effect on acid secretion

A

decreased acid secretion and Gastric Atrophy

28
Q

what condition will Corpus predominant Gastritis lead to

A

gastric cancer

29
Q

what part of the stomach is predominantly affected by Antral predominant Gastritis

A

antrum

30
Q

what effect does Antral predominant Gastritis have on acid secretion

A

increased acid secretion

low Risk of Gastric Ca

31
Q

what condition will Antral predominant gastritis lead to

A

Duodenal ulcer

32
Q

Mild Mixed Gastritis

A

Normal Acid producing No significant disease

33
Q

what are the non invasive diagnostic methods of H.Pylori

A

Serology: IgG against H. pylori

13C /14C Urea Breath Test

Stool antigen test – ELISA - need to be off PPI for 2 weeks

34
Q

what are the invasive methods for H.Pylori

A

requires endoscopy
Histology: gastric biopsies stained for the bacteria
Culture of gastric biopsies
Rapid slide urease test (CLO)

35
Q

Rapid slide urease test (CLO)

A

A biopsy is taken from the stomach and is put into the well where the gel is impregnated with urea if there is bacteria in the specimin the ureas reacts with the urea and forms ammonia changing the ph of the well and the colour to pink (positive) yellow (negative)

36
Q

what colour will a positive Rapid slide urease test (CLO) show

A

Pink

37
Q

what colour will a negative Rapid slide urease test (CLO) show

A

Yellow

38
Q

what is gastritis

A

Inflammation in the gastric mucosa
Histological diagnosis
Clinical features seen at endoscopy

39
Q

what are the causes of Gastritis

A

Autoimmune (parietal cells)
Bacterial (H. pylori)
Chemical (bile/NSAIDs)

40
Q

what age groups are most commonly affected by peptic ulcers

A

Both GU and DU commoner in elderly people

41
Q

what are the majority of peptic ulcers caused by

A

Helicobacter pylori infection (50% GU 80% DU)

42
Q

what are peptic ulcers also caused by

A

NSAIDs, smoking

Rarely they are caused by other conditions such as Zollinger-Ellison syndrome, hyperparathyroidism, Crohn’s disease

43
Q

what symptoms are associated with peptic ulcer

A

pigastric pain is the main feature (pointing sign, may be relieved by antacids)

Nocturnal/hunger pain (more common in DU)

Back pain (may suggest penetration of a posterior DU)

Nausea and occasionally vomiting

Weight loss and anorexia (chronic ulcer)

Only sign may be epigastric tenderness

If the ulcer bleeds, patients may present with haematemesis and/or melaena, or anaemia

44
Q

If the peptic ulcer bleeds what will the patient present with

A

haematemesis and/or melaena, or anaemia

45
Q

how do you treat a peptic ulcer caused by H.Pylori

A

Ulcers caused by H. pylori are treated by eradication therapy to get rid of the bacteria

Complications are treated as they arise

46
Q

what are pharmalogical treatments for peptic ulcers

A

Antacid medication – proton pump inhibitors (omeprazole)or H2 receptor antagonists (ranitidine)

If NSAIDs are also involved, these have to be stopped if possible, or should continue to receive other protective agents following eradication therapy

47
Q

when is surgery indicated for a peptic ulcer

A

In a complicated PUD

48
Q

How do you eradicate H.Pylori

A

Triple therapy for 7 days
Clarithromycin 500mg bd
Amoxycillin 1g bd (or Metronidazole 400mg bd)
Tetracycline is given if penicillin allergy

PPI: e.g. omeprazole 20mg bd

49
Q

is eradication of H.pylori effective

A

In 90% of cases

50
Q

what are the complications of a peptic ulcer

A

Acute bleeding – melaena and haematemesis
Chronic bleeding – iron deficiency anaemia
Perforation
Fibrotic stricture (narrowing)
Gastric outlet obstruction – oedema or stricture

51
Q

gastric outlet obstruction symptoms

A

Vomiting – lacks bile, fermented foodstuffs

Early satiety, abdominal distension, weight loss, gastric splash

Dehydration and loss of H+ and Cl- in vomit

Metabolic alkalosis

52
Q

blood results for gastric outlet obstruction

A

low Cl, low Na, low K, renal impairment

53
Q

diagnosis for gastric outlet obstruction

A

UGIE (prolonged fast/aspiration of gastric contents), identify cause – stricture, ulcer, cancer

54
Q

how do you treat gastric outlet obstruction

A

endoscopic balloon dilatation, surgery

55
Q

Gastric cancer

A

Second commonest malignancy worldwide
Large geographical variation – genetic and environmental factors
Very poor prognosis (5 yr survival <20%)
Presents late in Western countries
Majority are adenocarcinomas (epithelial cells)

56
Q

what are types of gastric tumours

A

MALT, GIST

57
Q

how do patients present with gastric cancer

A

Dyspepsia, early satiety, nausea & vomiting, weight loss, GI bleeding, iron deficiency anaemia, gastric outlet obstruction

58
Q

Aetiology of gastric cancer

A

Smoking has a definite positive association as has some food groups e.g. high salt diet, foods high in nitrates. The major aetiological factor in GC is HP.

Other factors to consider – family history, previous gastric resection, biliary reflux, premalignant gastric pathology

59
Q

characteristics of majority of gastric cancer

A

sporadic with no demonstrable inherited component

60
Q

characteristics of <15% of gastric cancer

A

familial clustering, most not associated with definitive germline mutation

61
Q

characteristics of 1-3% of gastric cancer

A

heritable gastric cancer syndromes
HDGC;AD, CDH-1 gene (E-cadherin)

62
Q

how do you make a histological diagnosis of gastric cancer

A

Endoscopy and biopsies

63
Q

what investigations are done for gastric cancer

A

Staging investigations – has it spread elsewhere?
CT chest/abdo – lymph nodes and liver/lungs/peritoneum/bone marrow

MDT discussion – imaging/histology/patient fitness

64
Q

MDT discussion for gastric cancer

A

imaging/histology/patient fitness

Who is present? gastroenterologist, pathologist, radiologist, upper GI surgeons, oncologists, specialist nurses

65
Q

treatment of gastric cancer

A

surgical and chemotherapy