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GI -S > Gastro Duodenal Disease > Flashcards

Gastro Duodenal Disease Flashcards

1
Q

In addition to digestion what role does the stomach also play in the body?

A

Endocrinology

Produces intrinsic factor

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2
Q

What are the three types of Peptic ulcer?

A 
Gastric Ulcers (GU)
Duodenal Ulcers (DU)
NSAID Ulcers
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3
Q

What type of peptic ulcer is most common?

A

Duodenal ulcers are more common than gastric ulcers.

They are more common in the elderly and there is a significant geographical variation.

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4
Q

What are the most common cause of peptic ulcers?

A

H. Pylori

Then NSAIDs/Aspirin

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5
Q

What is Dyspepsia?

A

Dys = bad, Pepsis = digestion

Pain or discomfort in the upper abdomen.

Very common: 40% of people report having had one or more dyspeptic symptoms in the previous year.

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6
Q

What are the symptoms of dyspepsia?

A 
Upper abdominal discomfort
Retrosternal pain if reflux
Anorexia
Nausea
Vomiting
Bloating
Fullness
EARLY SATIETY (alarm symptom)
Heartburn
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7
Q

What are the less common causes of peptic ulceration?

A

Hyperthyroidism
Zollinger-Ellison syndrome
Vascular insufficiency Sarcoidosis
Crohn’s Disease

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8
Q

What are the two classifications of Dyspepsia?

A

Dyspepsia which is investigated can be classified as:

Organic or Functional

Functional more common

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9
Q

What are the causes of organic dyspepsia?

A 
GORD +/- erosive oesophagitis
Gastritis, duodenitis
Peptic ulcers
Gastric Cancer
Liver and pancreatobiliary disease
Non-GI causes (e.g. Medication, ACS)
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10
Q

What is functional Dyspepsia?

A

Non-ulcer dyspepsia.

The presence of symptoms thought to originate in the gastroduodenal region (early satiation, postprandial fullness, epigastric pain or burning) in the absence of any organic, systemic or metabolic disease that is likely to explain the symptoms.

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11
Q

What is FGIDs?

A

Functional Gastrointestinal Disorders.

Dyspepsia is one of the most common.

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12
Q

What is postprandial fullness?

A

Feeling full as soon as you start eating.

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13
Q

How would you approach the presentation of Dyspepsia?

A

Most patients do not require upper GI endoscopy.

  1. Review medication
  2. Consider non-gastro-duodenal causes
  3. Lifestyle advice (weight, alcohol and diet)
  4. Test )for H. pylori) and treat
  5. Trial of acid-suppressing medication (PPI)
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14
Q

What medications would you review in a patient presenting with dyspepsia?

A
  • NSAIDs,
  • Steroids,
  • Biphosphonates (given for osteoporosis, Causes ulceration)
  • Ca antagonists
  • Nitrates
  • Theophylline’s
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15
Q

What non-gastro-duodenal causes would you consider in patients presenting with dyspepsia?

A

Acute coronary syndrome

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16
Q

When should the GP refer patients who present with dyspepsia?

A
  • Unexplained weight loss
  • Iron deficiency anaemia or overt bleeding
  • Progressive dysphagia
  • Persistent vomiting (haemoptemesis)
  • Epigastric mass
  • Abnormal imaging Study
  • Over 55yrs with new persistent dyspepsia
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17
Q

How does the stomach initiate the production of acid?

A

G cells located in the antrum produce gastrim.

Gastrim causes parietal cells to produce hydrochloric acid in the corpus

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18
Q

List the effects of NSAID related large bowel disorder

A

Ulceration and bleeding,
IBD like colitis,
Perforation
Diaphragm like strictures of caecum and ascending colon
Exacerbation of pre-existing IBD or precipitation of relapse
Association with collagenous colitis

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19
Q

What is enteropathy?

A

A disease of the intestine. Especially the small intestine

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20
Q

Define hypoalbuminuria

A

Condition where blood albumin levels are abnormally low

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21
Q

List the effects of NSAID related oesophageal disorder

A

Pill Oesophagitis:

Avoid NSAID digestion in the supine position (affect the oesophagus just before the stomach)

22
Q

List the effects of NSAID related stomach and duodenal disorder

A

Gastroduodenal erosion and ulcers. Can cause GI bleeding

23
Q

List the effects of NSAID related small bowel disorder

A

Ulceration and bleeding. Increased risk of protein and blood losing enteropathy; could lead to iron deficiency anaemia and hypoalbuminuria

24
Q

Why can NSAIDs cause ulcers all over the GI tract?

A

They do not require acid to react so can affect everywhere

25
Q

What are the clinical features of peptic ulcers?

A 
Epigastric pain is the main feature
Nocturnal/hunger pain
Back pain
Nausea and occasionally vomiting
Weight loss and anorexia
Only sign may be epigastric tenderness
If the ulcer bleeds, patient may present with haematemesis and/or malaena or anaemia
26
Q

What treatment may relieve epigastric pain from peptic ulcers?

A

Antacids (PPI)

27
Q

What does back pain suggest in suspected peptic ulcer?

A

Penetration of a posterior DU

28
Q

What investigations are performed for peptic ulcers?

A

Blood tests:

  • H. Pylori serology
  • Hb (anaemia?)
  • Fasting gastrin (Zollinger-Ellison syndrome)

Urea Breath Test:
-H. Pylori

Upper GI endoscopy

  • Visualisation of upper GI mucosa
  • Biopsy gastic ulcers to exclude malignancy
  • Biopsies for H. Pylori

Barium Studies

29
Q

Why does fasting gastrin diagnose zollinger-ellison syndrome?

A

Zollinger-Ellison syndrome = gastrin secreting tumour in pancreas.

Normal G cells stimulated by Vagus (parasympathetic)

During fast shouldn’t produce much gastrin

30
Q

Do you biopsy ulcers in duodenum?

A

No because they are always benign.

Biopsy gastric ulcers always to rule out cancer

31
Q

When would a barium study be carried out?

A

Patient may be unfit for invasive test like endoscopy.

May have severe dysphagia and cannot fit scope down

32
Q

As a GP what tests could you carry out suspecting peptic ulcers?

A

Blood tests

Urea breath test

33
Q

Describe Helicobacter pylori

A

Gram negative, spiral shaped, microaerophilic bacterium

Commonest chronic bacterial infection world wide

Uniquelly adapted to survive in the harsh gastric environment

Acquired in childhood

34
Q

Why is H. Pylori acquired in childhood but not in adulthood?

A

Acid secretion is lower when you are young compared to the adult stomach.

This allows the bacterium to spread by the focal oral route and establish in the less acidic stomach

35
Q

What are the clinical associations with H. Pylori?

A

Gastritis (acute and chronic)
Peptic Ulcer Disease
Gastric Neoplasia (adenocarcinoma and MALT lymphoma)
Non-Ulcer dyspepsia (small proportion of patients)

36
Q

Describe the non invasive tests for H. Pylori Infection

A

Serology: IgG against H. Pylori

^13C/^14C Urea Breath Test

37
Q

Why is ^13C used over ^14C?

A

^14C is radioactive

38
Q

Describe the Invasive Test for H. Pylori infection

A

Endoscopy
Gastric biopsies taken for histology
Gastric biopsies are also cultured
Rapid slide urease test (CLO)

39
Q

how does the Urease Breath Test work?

A

Give drink with urea.
Carbon marked ^13C.
If H. Pylori urea will be broken down and CO2 and ammonia released as products.
If the CO2 you breath out is marked then you know H. Pylori is present

40
Q

How does the CLO test work?

A

Put gastric biopsy in CLO well. pH change detected and H. Pylori can be detected

41
Q

What mucosa can H. Pylori colonise?

A

Gastric type only.

It doesn’t penetrate the epithelium and resides in the mucous layer.

42
Q

What kind of reaction does H. Pylori cause in the body?

A

Induces a powerful inflammatory reaction, which becomes chronic (Chronic gastritis)

43
Q

What are the outcomes of H. Pylori infection?

A

There are 3 outcomes

Antral Predominant Gastritis:

  • This causes an increased acid production
  • There is a low risk of gastric cancer
  • Causes duodenal ulcers

Mild Mixed Gastritis:

  • Normal acid
  • No significant disease

Corpus Predominant Gastritis:

  • Decreased acid production
  • Gastric atrophy
  • Gastric cancer
44
Q

What is the pathophysiology of duodenal ulcer disease?

A

Antrum is infected.
G cells produce extra gastrin because they are tricked into thinking stomach is more alkali than it is.
Acid enters duodenum
Duodenum trie stop protect itself by changing cells from duodenal to gastric cells.
Duodenum wall is weakened as a result
Ulcers occur

45
Q

How can you cure DU?

A

Eradication of H. Pylori will nip the condition in the bud.

Ulcers can be treated to heal and won’t return

46
Q

What is the management of peptic ulcers?

A

Ulcers caused by H. Pylori are simply treated by eradication therapy.

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

Complications are treated as they arise

Surgery only indicated in complicated PUD

47
Q

What is the eradication treatment for H. Pylori?

A

Triple therapy for 7 days.

Acid inhibitor along with 2 antibiotics at least.

Clarithromycin 500mg bd (twice daily)
Amoxycillin 1g bd (or metronidazole 400mg bd)
-Tetracyclin if penicillin allergy
PPI (omeprazole 20mg bd)

This is effective in 90% of cases.

Resistance to antibiotics and poor compliance main reasons for failure

48
Q

What are the indications for H. Pylori eradication?

A

Peptic ulcer disease
MALT lymphoma
Following curative resection of primary gastric cancer

Non ulcer dyspepsia (no sinister signs)
FDR of gastric cancer patient

Long term use of PPI therapy

49
Q

What are the complications of peptic ulcers?

A

Gastric outlet obstruction (scarring in tight junction)

Acute bleeding

Perforation

50
Q

Give a brief introduction to gastric cancer

A

Second commonest GI malignancy
Large geographical variation
Predicted increase in incidence due to population growth
Very poor prognosis (5yr survival

51
Q

What are the clinical features of gastric cancer?

A

Symptoms similar to PUD: Epigastric pain
N&V, anorexia, weight loss
Dysphagia with proximal tumours

Sign’s:
Epigastric mass, weight loss, hepatomegaly if metastatic, Virchow’s node

Investigation:
Endoscopy and biopsy
CT scan of abdomen

52
Q

What is virchow’s node?

A

Lymph node in the left supraclavicular fossa.

Will be visibly enlarged

GI -S (29 decks)

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