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Flashcards in GI S5 (Done) Deck (52)
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1

What mechanisms prevent gastric reflux?

Lower oesophageal sphincter (LES):

Usually closed, transiently relaxes to allow bolus through

Stomach:

Angle of His and mucosal flap valve, as well as the postero-lateral location of the fundus all prevent acid reaching the LES and refluxing

Diaphragm:

Right crus of diaphram acts as a sling around the oesophagus serving as an 'extrinsic' sphincter

2

The failure of anti-reflux mechanisms leads to what?

Prolonged contact of gastric juices with oesophageal mucosa

Gastro-oesophageal reflux disease and associated symptoms

3

What are the typical clinical features of Gastro-oesophageal reflux disease (GORD)? 

Dyspepsia

Worsens on lying down, bending over or drinking hot drinks

4

What investigations are indicated by a history that leads you to suspect GORD?

No investigations done in typical clinical presentations

Only if worrying symptoms, such as dysphagia or hiatus hernia are suspected

Endoscopic investigation in this case

5

What are some of the risk factors for GORD?

Pregnancy or obesity

Fat, Chocolate, Coffee or Alcohol

Large meals

Smoking

Hiatus hernia

6

List lifestyle management techniques to prevent/treat GORD

Lose weight

Stop smoking

Reduce consumption of chocolate, coffee, alcohol, fatty foods

7

Outline the types of treatment available for GORD, including their mechanism and an examples of each type

Simple antacids:

Neutralises acid with a base

E.g. Calcium carbonate

Raft antacids (alginates):

Forms a protective raft that sits on top of stomach contents and prevents reflux

E.g. Gaviscon

PPIs:

Reduction of acid secretion by oxyntic cells

E.g. Omeprazole

H2 antagonists:

Blocks H2 receptor which reduces acid secretions

E.g. Ranitidine

 

8

What is a common complication of GORD?

Continual contact of gastric juices and oesophageal mucosa can lead to metaplastic change (Barrett's Oesophagus)

9

What is Gastritis?

Chronic or acute inflammation of the gastric mucosa

10

Differentiate acute and chronic gastritis

Chronic:

Infection with H. pylori

Inflammatory changes to mucosa leadsing to atrophy and metaplasia (possible cancer)

Acute:

NSAIDs, Alcohol, Cocaine

Exfoliation of surface cells and decreased secretion of protective mucus

11

What are the common symptoms of gastritis?

Commonly asymptomatic

Symptoms when they appear include:

- Dyspepia (Pain/Discomfort)

- Nausea

- Vomiting

- Haematemesis

- Melena

12

Outline the complications of Gastritis

Increases risk of Peptic ulcer disease

Chronic gastritis can cause hypergastrinaemia due to increasing gastrin release from G cells, this in turn can lead to Duodenal ulceration (DU)

Chronic Antral H. Pylori gastritis can lead to Gastric cancer and mucosa associated lymphoid tissue lymphoma (MALT Lymphoma)

13

How is gastritis diagnosed?

Endoscopy/Biopsy

Testing for H. Pylori

Blood test (Anaemia due to GI bleed)

Stool test (Blood due to GI bleed)

14

What types of drugs are used to treat gastritis?

Antacids

PPIs

H2 antagonists

General theme is reduction in acid secretion for promotion of healing

Antibiotics

E.g. Clarithromycin/Amoxacillin

Treatment of H. Pylori infection

 

15

What is peptic ulcer disease?

A break in the superficial epithelial cells down to the muscularis mucosa of either stomach (GU) or duodenum (DU)

 

16

Where are peptic ulcers commonly found?

GU:

Lesser curvature and antrum

DU:

Duodenal cap

17

Outline the most common cause of peptic ulcer disease

Give statisitics

NSAIDs:

Inhibit prostaglandins and reduce production of unstirred layer of mucus

50% of patients with long term NSAIDs have mucosal damage

30% when endoscoped have petic ulcer(s)

5% are symptomatic

1-2% have complications such as GI bleed

18

What is the prevlance of the different forms of peptic ulcer disease and how do prevalence rates vary across ages and countries?

DU in 10% adult population

GU is 2-3x less common (3-5%)

Prevalence is lower among younger adults and higher in older

Developing countries have increasing prevalence of NSAID associated DU and decreasing prevalence of H. Pylori associated ulceration

 

19

What are the clinical features of Peptic ulcer disease?

Reccurent, burning epigastric pain:

Worse at night and when hungry in DU

Relieved by eating

Persistent severe pain:

Suggestive of penetrtion of ulcer into other organs

Back pain:

Suggests penetration of ulcer in posterior stomach

Nausea and vomitting:

Less common

Weight loss and anorexia:

GUs only

Sudden haematemesis:

Asymptomatic patients can suddenly present with haematemesis when a blood vessel is erroded

20

What are the common investigations for suspected Peptic ulcer disease?

Investigation of H. Pylori infection

In 55+ patients or those with alarming symptoms an endoscopy can be done to exclude cancer

21

How is peptic ulcer disease managed?

Triple therapy:

PPIs

H2 antagonists

Antibiotics for H. Pylori (Clarithromycin/Amoxicillin)

If taking NSAIDs, review use and perhaps use alternatives

Prevention:

NSAIDs and PPIs used together if NSAIDs are long term

22

What are the complications of peptic ulcer disease?

Haemorrhage of blood vessels: 

Haematemesis 

Melena

Perforation:

More common in DUs, normally into peritoneal cavity

Gastric outlet obstruction:

Can be pre-pyloric, pyloric or duodenal

Occurs due to active ulcers w/oedema or due to healing of ulcer  with associated fibrosis/scarring

Normally presents as vomiting without pain

23

Describe H. pylori bacteria

Gram negatic, Aerobic

Helical

Urease producing

Found in the mucus layer of the stomach or adhered to gastric mucosa

24

What is the significance of H. pylori producing urease?

Urease produces ammonia and CO2

Ammonia:

Used to neutralise surroundings and protect the bacterium

C13 Urea test:

C13 Urea can be ingested by the patient to test for H. Pylori infection

Urease breaks down C13 urea forming C13 CO2 which can be exhaled and detected

25

How does H. Pylori colonisation of the gastric mucosa cause disease?

Secretion of enzymes and other substances that damage mucosa:

Ammonia is toxic to epithelia

Vacuolating cytotoxin A disrupts tight junctions and leads to apoptosis

Phospholipases

Inflammatory response to bacterium (Inflammatory cells and mediators)

26

What are some of the diseases caused by H. pylori infection?

Chronic gastritis

Peptic ulcer disease

Gastric Cancers

MALT lymphoma

27

How does H. pylori colonisation in different areas of the stomach affect clinical outcomes?

Antrum predominant colonisation:

DU risk

Antrum and body colonisation:

Largely asymptomatic

Body predominant:

GU and cancer risk

 

28

How is a bacterium implicated only in the colonisation of the stomach cause DU?

Antral H. pylori infection leads to hypergastrinaemia and hence increased acid production from oxyntic cells

Duodenal cap is inflammed and damaged by excess acid and metaplasia can occur

H. pylori colonises inflammed duodenal cap

Duodenal immune response leads to duodenitis and development of ulceration which is common intermittent

29

How can we test for H. pylori infection?

C13 Urea test

IgG serum levels

Endoscopy:

Gastric biopsy taken and H. pylori detected by histology and culture

 

30

How is H. pylori infection treated?

Same as Gastritis, GU or DU with H. pylori being the cause

PPI, H2 antagonist, Antibiotics (Clarithromycin/Amoxicillin)

90% successful in treatment of H. pylori