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*Medicine: Gastrointestinal > GORD and Barrett's Oesophagus > Flashcards

GORD and Barrett's Oesophagus Flashcards

1
Q

What are the symptoms of gastro-oesophageal reflux?

A
  • Heartburn (major feature)
    • aggrevated by bending, stooping, lying down + after meals, but relieved with antacids
  • Regurgitation of acids + foods into mouth (waterbrash, halitosis, enamel erosion)
  • Odynophagia or dysphagia (due to oesophagitis)
  • Belching
  • Nocturnal asthma/cough (due to aspiration of gastric contents on lying)
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2
Q

How do you diagnose GORD?

A
  • Diagnosis is clinical + often requires no futher ix
  • Ambulatory 24hr pH monitoring - gold standard, a pH <4 more than 4% of the time -> abnormal
  • Oeseophageal manometry
  • Combined impedance-pH testing
  • OGD indicated in:
    • >55y/o
    • <55y/o but with alarm symptoms (weight loss, dysphagia, haematemesis, anaemia)
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3
Q

Which GORD patients would you give an urgent endoscopy to?

A

if they have any of: ALARMS

  • Anaaemia
  • Loss of weight
  • Anorexia
  • Recent onset of progressive symptoms
  • Melaena / hametemesis
  • Swallowing difficulties
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4
Q

What are the risk factors for GORD?

A
  • Hiatus hernia
  • Obesity
  • Pregnancy
  • Systemic sclerosis
  • Cigarette smoking
  • Fat, choc, coffee or alcohol ingestion
  • Drugs - antimuscarinics, Ca-ch blockers, nitrates
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5
Q

What constitutes the lifestyle management for GORD?

A
  • Weight loss
  • Smoking cessation
  • Small, regular meals
  • Avoid eating <3h before bed
  • Raise the bed head
  • Reduce hot drinks, alcohol, caffeine, spicy foods, fizzy drinks, citrus fruits, tomatoes, onions, chocolate
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6
Q

What is the pharmacological management of GORD?

A
  • Alginate-containing antacids (magnesium trisilicate, gaviscon)
  • Proton pump inhibitors (-prazole)
  • H2-receptor antagonists (-tidine)
  • Dopamine antagonist prokinetic agents (metoclopramide, domperidone)
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7
Q

What is the surgical management of GORD?

A
  • if symptoms unmanageable by medication or in those whose symptoms return on stopping treatment
  • aim is to increase resting lower oesophageal sphincter pressure
  • open surgery or laproscopic Nissen fundoplication - where fundus of stomach is sutured around the lower oesophagus to produce an ‘antireflux’ valve
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8
Q

What is a hiatus hernia?

A

2 types:

  • Sliding hiatus hernia
    • when the gastro-oesophageal jxn slides through the hiatus and lies above diaphragm, no symptoms unless associated reflux
  • Rolling/para-oesophageal hernia
    • uncommon, where gastric fundus rolls up through the hiatus alongside oesophagus, with the gastro-oesophageal jxn remaining below diaphgram -> can give rise to complications (volvulus, bleeding + resp comps), treated surgically
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9
Q

How does a hiatus hernia give rise to GORD?

A

A hiatus hernia can cause a weakness of the valve between the oesophagus and stomach that normally prevents acid reflux.

Therefore acid and contents are able to reflux into the oesophagus from the stomach as stomach is also sat higher.

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10
Q

What is dyspepsia?

A
  • a common complaint describing a range of non-specific symptoms referring to upper GIT
  • epigastric pain/burning, nausea, heartburn, fullness, belching
  • patients use term ‘indigestion’
  • dyspeptic symptoms are caused by disorders of oesophagus, stomach, pancreas or hepatobiliary system
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11
Q

What is the most common cause of dyspepsia?

A
  • functional dyspepsia
  • used to be called non-ulcer dyspepsia
  • refers to dyspepsia where there is no visible cause on OGD
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12
Q

What are differentials for dyspepsia?

A
  • Functional dyspepsia
  • H. Pylori infection
  • GORD
  • Peptic ulcer disease
  • Malignancy of oesophagus/stomach
  • IBS
  • Gastritis
  • Oesophagitis
  • Duodenitis
  • Coeliac disease
  • Drug-induced (NSAIDs)
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13
Q

How do you investigate dyspepsia?

A
  • clinical history and physical examination
    • help exclude non-GI causes (drugs)
    • lifestyle/dietary factors identified (GORD)
  • bloods - anaemia, hepatobiliary/pancreatic disease
  • OGD + CLO if >55y/o or ALARM(s) signs - H. Pylori (invasive), malignancy, dysplasia
  • C-urea breath test - H. Pylori (non-invasive)

Depending on test results, it is then best to manage the underlying cause. For functional/uninvestigated dyspepsia, often will involve cutting out drugs causing dyspepsia, implementing over the counter antacids/lifestyle changes. If persistent, then can trial on PPI for 4wks.

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14
Q

What is an OGD/gastroscopy?

A
  • a camera test
  • where doctor looks into upper part of gut
  • consists of oesophagus, stomach, duodenum
  • endoscope is a thin flexible telescope (thickness of a little finger)
  • it is passed through the mouth, down the oesophagus, through the stomach and to the duodenum
  • the endoscope has a light, camera and opening for instruments to be passed through to take biopsies
  • it is both diagnostic and interventional
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15
Q

What happens during an OGD?

A
  • local anaesthetic sprayed to back of mouth
  • lay down side ways
  • option of light sedation with midazolam
  • patient must fast for ~6hrs prior to procedure
  • must not drive for 24hrs post-sedation
  • mouth guard put in place + endoscope passed through
  • you have to swallow it and it passes through - this is most uncomfortable part of procedure
  • air might be passed through to open up stomach
  • whole procedure only takes ~10mins
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16
Q

Are there any side-effects of gastroscopy?

A
  • sore throat
  • slight inc risk of pneumonia
  • occasional damage -> bleeding, infection + perforation
  • small # of people have a heart attack or stroke during/soon after (however, these tend to be older ppl who are already in poor health)
17
Q

What drug(s) is an example of H2 receptor antagonists?

A

Ranitidine

18
Q

What are the indications for H2-receptor antagonists?

A
  1. Peptic ulcer disease: for treatment + prevention of gastric and duodenal ulcers and NSAID-associated ulcers, although PPIs are more effective and therefore usually preferred
  2. GORD + dyspepsia: for relief of symptoms. PPIs are main alternative, and are preferred in more severe cases
19
Q

What is the mechanism of action of H2-receptor antagonists?

A
  • reduce gastric acid secretion
  • acid is normally produced by proton pump of gastric parietal cell
  • which secretes H+ into stomach lumen in exchange for drawing K+ into cell
  • proton pump is regulated by histamine
  • histamine released by local paracrine cells
  • histamine binds to H2-receptors on gastric parietal wall
  • via a second-messenger system, this activates proton pump
  • blocking H2-receptors therefore reduces acid secretion
  • however as proton pump can be stimulated by other pathways, H2 blockers cannot completely suppress gastric acid production
  • in this respect they differ from PPIs which tend to have a more complete suppressive effect
20
Q

What are important adverse effects of H2-receptor antagonists?

A
  • generally well tolerated w/ few side effects
  • bowel disturbance - diarrhoea or less often constipation
  • headache
  • dizziness
21
Q

What are the warnings/contraindications for H2-receptor antagonists?

A
  • excreted by kidneys
  • so dose should be reduced in those w/ renal impairment
  • like PPIs, they can disguise the symptoms of gastric cancer - important to investigate cause
22
Q

Give examples of alginates/antacids

A
  • Gaviscon
  • Peptac

(trade names)

23
Q

What are alginates/antacids indicated for?

A
  1. GORD: for symptomatic relief of heartburn
  2. Dyspepsia: for short-term relief of indigestion
24
Q

What is the mechanism of action of alginates and antacids?

A
  • most often taken as compound preparations
  • containing an alginate with 1+ antacids (eg. sodium bicarb, calc carb, magnesium or aluminium salts)
  • antacids work by buffering stomach acids
  • alginates act to increase the viscosity of stomach contents, which reduces reflux of stomach acid into oesophagus
  • after reacting w/ stomach acid they form a floating ‘raft’
  • this separates the gastric contents from G-O jxn to prevent mucosal damage
  • some evidence suggests they also inhibit pepsin production
  • antacids alone (usually Al or Mg compounds) can be used for short-term relief of dyspepsia
25
Q

What are the important adverse effects of alginates and antacids?

A
  • compound alginates -> few side effects
  • magnesium salts -> diarrhoea
  • aluminium salts -> constipation
26
Q

What are the warnings/contraindications of alginates and antacids?

A
  • well tolerated + safe in pregnancy
  • paediatric formulations are safe for use in infants
  • but compound alginates not to be given in combo w/ thickened milk preparations -> lead to excessively thick stomach contents -> cause bloating + abdo discomfort
  • sodium and potassium containing preparations should be used in pts with fluid overload or hyperkalaemia (eg. renal failure)
27
Q

Give examples of proton pump inhibitors

A
  • lansoprazole
  • omeprazole
  • pantoprazole
28
Q

What are the indications for proton pump inhibitors?

A

first line treatment for:

  1. prevention + treatment of peptic ulcer disease, including NSAID-associated ulcers
  2. symptomatic relief of dyspepsia + GORD
  3. eradication of H. Pylori infection, in which they are used in combo w/ antibiotic therapy
29
Q

What is the mechanism of action of PPIs?

A
  • reduce gastric acid secretion
  • act by irreversibly inhibiting H+/K+-ATPase in gastric parietal cells
  • this proton pump is responsible for secreting H+ and generating gastric acid
  • advantage of targeting final stage of gastric acid production is that they are able to suppress acid production almost completely
  • in this respect, they differ from H2-receptor antagonists
30
Q

What are important adverse effects of PPIs?

A
  • GI disturbances
  • headache
  • increase gastric pH -> reduce body’s host defence against infection; some evidence of inc C. difficile infection in pts taking PPIs
  • prolonged treatment -> hypomagnesaemia -> can lead to tetany + ventricular arrhythmia
31
Q

What are the warnings/contraindications that need to be considered for PPIs?

A
  • PPIs may disguise symptoms of gastric cancer
  • should enquire about alarm symptoms before + during treatment
  • can increase risk of fracture in elderly
  • caution in osteoporosis
32
Q

What is Barrett’s oesophagus?

A
  • squamous epithelium (white) lining oesophagus is replaced
  • by abnormal specialised glandular/columnar mucosa (red)
  • this is a metaplastic change
  • occurs in distal oesophagus
  • develops due to long-standing acid reflux stimulus
  • diagnosed by endoscopy + biopsy
33
Q

What is the management of Barrett’s oesophagus?

A
  • continuous therapy with PPIs
  • surveillance OGD 2yrs w/ multiple biopsies looking for dysplasia or carcinoma
  • if low-grade dysplasia -> surveillance OGD every 6-12 months, radiofrequency ablation +/- endoscopic mucosal resection
  • if high-grade dysplasia -> radiofrequency ablation +/- endoscopic mucosal resection, oesophagectomy
34
Q

Describe the factors that influence a GP’s decision to refer a patient with dyspepsia for endoscopy

A

Any patient with ALARMS symptoms of dyspepsia or is aged over 55 with unexplained + persistent dyspepsia

  • Anaema
  • Loss of weight
  • Anorexia
  • Recent onset of progressive symptoms
  • Melaena or haematemesis
  • Swallowing difficulty
35
Q

What is meant by ‘dysphagia’?

A
  • difficulty in swallowing
  • should prompt urgent investigation
  • need to exclude malignancy
  • (unless of short duration + associated w/ sore throat)
36
Q

What are five key questions to ask a patient presenting with dysphagia?

A
  1. Was there difficulty in swallowing solids and liquids from the start?
  2. Is it difficult to initiate a swallowing movement?
  3. Is swallowing painful (odynophagia)?
  4. Is the dysphagia intermittent or is it constant and getting worse?
  5. Does the neck bulge or gurgle on drinking?
37
Q

What is meant by ‘reflux’?

A

Return of stomach contents into the oesophagus, mouth and potentially lungs that causes symptoms, namely heartburn

38
Q

What is meant by ‘achalasia’?

A
  • motility disorder
  • characterised by oesophageal aperistalsis
  • and impaired relaxation of lower oesophageal sphincter
  • LOS pressure elevated in 50%+ of patients
39
Q

When we swallow, why does food go into the oesophagus and not the trachea?

A
  • when we swallow, food bolus in mouth passes back to oropharynx
  • pressure receptors stimulate centres in medulla
  • this initiates swallowing reflexes
  • uvula goes back and up closing off nasopharynx
  • simultaneously, vocal folds close + epiglottis covers trachea
  • this completely closes airways allowing food to pass into oesophagus

*Medicine: Gastrointestinal (29 decks)

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