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R - Yr2 Alimentary (Liam Lennox) > H. Pylori & Gastric Disease > Flashcards

H. Pylori & Gastric Disease Flashcards

1
Q

What is Heliobacter Pylori?

A

A gram -ve, spiral shaped, microaerophilic, flagellated bacterium carried by around 50% of the worlds population

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2
Q

Where does Heliobacter Pylori colonise?

A

The mucouse layer of the gastric mucosa only.

It doesnt penetrate into the epithelium or anywhere else

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3
Q

How does Heliobacter Pylori cause a problem?

A

It releases ammonia which can provoke an immune response and is also toxic to the epithelium, as are other chemicals released by Heliobacter Pylori

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4
Q

What does a Heliobacter Pylori cause?

A

Chronic gastritis leading to:
- In most people no significant disease

  • If predominant in the body -> Loss of acid, gastric atrophy and finally gastric cancer
  • If predominantly in the antrum -> Rise in acid -> Duodenal ulcers
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5
Q

What determines the outcome of a Heliobacter Pylori infection?

A
  • Site
  • Environmental factors e.g. smoking
  • Genetic susceptibility
  • Bug characteristics (virulence factors)
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6
Q

Define virulence factors?

A

Molecules produced by certain strains of a micro organism which give it an advantage at colonising or harming the host.

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7
Q

In what ways can we diagnose Heliobacter Pylori infection?

A

Non-Invasive:

  • Stool Antigen Test (ELISA)
  • Urea Breath Test
  • Serology (IgG test)

Invasive (by Upper GI endoscopy):

  • Staining of gastric biopsy
  • Culture of biopsy
  • Rapid slide urease test
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8
Q

Explain the rapid slide urease test?

A

Biopsy of mucosa isplaced in a medium with urea and a pH indicator

> Urease converts urea to ammonia and CO2
pH rises
Indicator changes colour

Urease is an enzyme produced by Heliobacter Pylori

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9
Q

Explain the Urea breath test?

A
  • Urea tagged with an unusual isotope of carbon is breathed in
  • Bacteria converts to ammonia + CO2
  • Unusual isotope of carbon detected in breathed out CO2
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10
Q

What is the best invasive vs non-invasive way of detecting Heliobacter Pylori?

A

Stool Antigen Test (ELISA)

Rapid slide Urease Test

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11
Q

How do we eradicate a Heliobacter Pylori infection?

A

7 days of triple therapy:

  • Clarithromycin
  • Amoxicillin (tetracycline if penicillin allergic)
  • A Proton Pump Inhibitor (PPI) e.g. Omeprazole

Further 2nd line protocols should this fail

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12
Q

Define Dyspepsia?

A

Also known as indigestion.

A condition of impaired digestion causing symptoms such as:
- Upper abdominal pain/discomfort
- Anorexia
- Bloating
- Nausea / Vomiting
- Fullness and early satiety
- Heartburn
Retrosternal pain
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13
Q

How common is dyspepsia?

A

Around 80% of people get it occasionally with no serious underlying disease

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14
Q

Define a functional disorder?

A

One which impairs normal function of the gut without any detectable pathology.

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15
Q

Define an organic disorder:

A

Any disease in which there is detectable pathology. Either micro or macroscopic

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16
Q

Give some examples o dyspepsia causing conditions and whether they are functional or organic?

A

Functional:

  • Psychological (psychological factors are very important in many functional disorders)
  • Non-ulcer Dyspepsia
  • IBS
  • Drugs

Organic:

  • Peptic Ulcer
  • Gastritis
  • Gastric Cancer
  • Coeliac Disease
  • Colonic Cancer
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17
Q

When would an upper GI endoscopy be indicated for dyspepsia?

A

If it came with any of the ALARMS symptoms:

  • Anorexia
  • Loss of Weight
  • Anaemia
  • Recent Onset >55 yrs or Persistant despite Treatment
  • Melaena/Haematemesis or Mass
  • Swallowing problems (Dysphagia/Odynophagia)
18
Q

Define Haematemesis?

A

Vomiting blood

19
Q

Define Odynophagia?

A

PAin when swallowing

20
Q

NAme a few drugs that can cause dyspepsia

A

NSAIDs & Steroids
Ca Antagonists
Theophyllines
Nitrates

21
Q

What is the flow chart approach to dyspepsia?

A

Dyspepsia:

  • Alarms features?
  • > Yes = Upper GI endoscopy
  • No = Age?
  • > Over 55 = UGIE
  • Under 55 = Heliobacter Pylori test
  • > If +ve do eradication therapy and or symptom treatent with antacids (PPIs or H2R antagonists) and change lifestyle factors
22
Q

What are H2R antagonists?

A

Histamine H2 receptor antagonists

23
Q

What lifestyle factors affect dyspepsia?

A

Smoking
Drinking
Diet
Lack of exercise

Loss of weight is an indicator

24
Q

Define Gastritis

A

Inflammation in the gastric mucosa

25
Q

How is gastritis diagnosed?

A

The clincal features can be seen on endoscopy then its confirmed histologically wiht a biopsy

26
Q

What are the 3 typs of Gastritis?

A

A - Autoimmune (attacking parietal cells -> low HCl)
B - Bacterial (Heliobacter Pylori)
C - Chemical (Bile/NSAIDs)

27
Q

What types of peptic ulcer are more common and with who?

A

Duodenal over gastric
Men more than women
Older more than younger

28
Q

What can cause a peptic ulcer?

A 
Heliobacter Pylori
NSAIDs
Smoking
In rare cases:
- Zollinger-Elison Syndrome
- Hyperparathyroidism
- Crohn's Disease
29
Q

What are the symptoms of a peptic ulcer?

A
  • Epigatric pain which may be relieved by antacids (point tenderness over diffuse)
  • Pain at night or when hungry (more often a DU)
  • Back Pain (may be a penetrating DU)
  • Nausea or vomiting
  • Weight loss/anorexia

If it bleeds you might get haematemesis or melaena

It often appears as just epigastric pain or tenderness

30
Q

How is a peptic ulcer treated?

A

Antibiotics if its Heliobacter Pylori

Antacids:

  • PPIs (omeprazole)
  • H2 receptor antagonist (ranitidine)

Stop any NSAIDs

Surgery - but only if complicated

31
Q

Complications of a peptic ulcer?

A

Acute Bleeding:

  • Melaena
  • Haematemesis

Chronic Bleeding:
- Iron deficient anaemia

Perforate

Gastric outlet Obstruction:

  • Oedema
  • Fibrotic Stricture
32
Q

What is gastric outlet obstruction?

A

Gastric outlet obstruction is not a single entity; it is the clinical and pathophysiological consequence of any disease process that produces a mechanical impediment to gastric emptying.

Clinically it appears:

  • Vomiting, fermented foodstuffs not bile
  • Early Satiety
  • Abdominal Distension
  • Weight Loss
  • Gastric Splash
  • Dehydration
  • Loss of HCl in vomit -> Metabolic Alkalosis
33
Q

What tests can we do for gastric outlet obstruction?

A

Bloods:

  • Low Cl, Na, K
  • Renal Impairment

Upper GI endoscopy:

  • Prolonged Fast First or aspirate gastric contents
  • Then identify if its a stricture, ulcer or cancer
34
Q

How do we treat gastric outlet obstruction?

A

Treat the underlying cause:

  • If its a stricture use Endoscopic Balloon Dilatation
  • Otherwise it often requires surgery
35
Q

How common is gastric cancer and what histological types is it?

A

Second most common GI cancer
5 yr survival <20%
Most are adenocarcinomas in the glandular epithelium. Can also be a lymphoma (MALT) or sarcoma (GIST)

36
Q

MALT and GIST?

A 
MALT = Mucosa Associated Lymphoid tissue
GIST = GastroIntestinal Stromal Tumour
37
Q

How do patients with gastric cancer present?

A
  • Dyspepsia
  • Early Satiety
  • Nausea & Vomiting
  • Weight Loss
  • GI bleeding (haematemesis/Malaena)
  • Fe deficient anaemia
  • Gastric Outlet obstruction
38
Q

Explain the aetiology of gastric cancer?

A

None of these are a direct cause but all are associated with gastric cancer:

  • Diet
  • Genes
  • Heliobacter Pylori
  • Smoking
  • Previous Gastric pathology or resection
  • Biliary Reflux
  • Family History
39
Q

Explain the inheritance of gastric cancer?

A
  • Most are actually sporadic with no demonstratable inherited component
  • <15% show familial clustering
  • 1-3% of cases are a heritable gastric cancer syndrome
40
Q

How do we investigate a case of gastric cancer?

A

An upper GI endoscopy with biopsy to confirm using a histological diagnosis.

Then stage with a chest and abdominla CT checking:

  • Lymph nodes
  • Lungs
  • Liver
  • Peritoneum
  • Marrow
41
Q

How do we treat gastric cancer?

A

Surgery
Chemotherapy

DUH!

R - Yr2 Alimentary (Liam Lennox) (37 decks)

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