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The Patient 20300 > Dyspepsia, GORD and Peptic Ulcer Disease > Flashcards

Dyspepsia, GORD and Peptic Ulcer Disease Flashcards

1
Q

What is dyspepsia

A

A persistent or recurrent pain or discomfort in upper abdomen

British Society of Gastroenterologists definition - range of symptoms arsing from upper GI tract including upper abdominal pain or discomfort, heartburn, gastric reflux, nausea or vomiting

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2
Q

What are the causes of dyspepsia

A

Causes include:
Lifestyle factors
Medication
Diseases

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3
Q

What is GORD and what are the symptoms and complications?

A

Gastro-oesophageal reflux disease (GORD). Symptoms/complications resulting from reflux gastric contents into oesophagus, oral cavity or lung

Can cause chronic cough, laryngitis. There is a link to asthma

Can lead to complications such as stricture, Barrett’s oesophagus and oesophageal carcinoma

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4
Q

What causes GORD

A 
Causes:
Obesity
Genetic
Lifestyle
Medication
Age
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5
Q

What physiological phenomena causes gord

A

Lower oesophageal sphincter relaxation causing reflux of gastrix contents into oesophagus

There is also poor peristaltic movement, not enough saliva and delayed gastric emptying

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6
Q

What are peptic ulcers? What complication can they lead to

A

Open sores that develop on the inside lining of oesophagus, stomach or upper portion small intestine

Complications include upper GI bleed

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7
Q

What causes peptic ulcers

A

H Pylori (bacterial infection)
NSAIDS
Lifestyle factors
Genetic

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8
Q

What is the official definition of a peptic ulcer

A

‘ a breach in the continuity of the epithelial lining of more than 5mm in diameter, with associated inflammation’

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9
Q

Why do ulcers develop

A

Ulcers develop where there is an imbalance between the agents that protect the epithelium and those which attack

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10
Q

What are the symptoms of both dyspesia and GORD

A 
Initial symptoms can include:
Upper abdominal pain, tenderness, discomfort
Heartburn/reflux
Bloating
Early satiety
Nausea and vomiting
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11
Q

What are the generalised symptoms of gastric ulcer desease

A

Pain radiates to back

Mainly occurs at night

Aggravated by food

Lose weight

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12
Q

What are the specific symptoms of a duodenal ulcer

A

Epigastric pain

Anytime – empty stomach

Relieved by food/antacids

Gain weight

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13
Q

What are the ALARM warning signs for referral

A 
A- Anaemia
L- Loss of weight (unintentional)
A- Anorexia
R- Recurrent problems*
M- Melaena(blood in stool)/ haematemesis
S- Swallowing problems

*- Only age> 55 with unexplained & persistent recent onset dyspepsia

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14
Q

What does an assessment for the GI diseases include

A 
Includes:
Detailed history – medical and social
*Medication review - many medicines can cause GI disturbances*
NSAIDs
Bisphosphonates
Corticosteroids
Calcium antagonists
Nitrates
Theophyllines
Blood tests 
H Pylori testing – see later
X-ray
Endoscopy
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15
Q

What are the initial management steps

A

Identify potential causative medications and manage appropriately
Lifestyle Measures
Smoking cessation
Healthy eating
Avoid known precipitants that cause dyspepsia:
fatty, acidic or fried foods and chocolate
Reduction or exclusion of alcohol and caffeine
Avoid eating late in the evening
Weight reduction
Reduce stress
Raising the head of the bed (GORD) - reduces night time reflux

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16
Q

What are antacids

A

Medicines that neutralise acid - often used for dyspepsia

Available OTC – liquids and tablets

Simple, cheap, effective

Dose:
when required for symptoms
between meals and at bedtimes
four or more times daily

Liquids more effective than solid dosage forms, but less portable or convenient.

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17
Q

What are the side effects of antacids

A

Antacids usually contain aluminium or magnesium compounds:

Magnesium containing - laxative effect

Aluminium containing - constipating

Also look out for:

Calcium containing - possible rebound acid secretion/hypercalcaemia

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18
Q

Why is the sodium content important with antacids

A

Avoid if patient is on salt restricted diet

High sodium content undesirable in:
patients with liver, renal and cardiac conditions
hypertension
pregnancy

Definition of Low Na+
Sodium content of less than 1mmol per tablet or 10-mL dose.

19
Q

What are the interactions associated with antacids

A

May impair the absorption of other drugs if taken at the same time

May damage enteric coatings by raising the pH

Rarely may affect pH dependent renal excretion e.g. increase excretion with possible reduction in serum levels (aspirin, lithium)

20
Q

What are alginates

A

The are used in combination with antacid

Increase viscosity stomach contents

Some form a “raft” that floats on top of stomach contents

21
Q

What do histamine H2 receptor antagonists do (give examples)

A

Reduce gastric acid output by blocking histamine H2-receptor blockade

Heal duodenal and gastric ulcers at higher doses.

Include Ranitidine, Cimetidine, Famotidine

Available OTC (lower doses)

Generally taken twice daily

22
Q

What are histamine H2 receptor antagonists licenced for

A 
Licensed for:
GORD (less effective than Proton Pump Inhibitors)
maintenance treatment (rarely used now)
NSAID prophylaxis 
Functional dyspepsia

Also used for stress ulcer prophylaxis, peri-operatively

23
Q

What are the side effects of histamine H2 receptor antagonists

A

Side effects include: headache, diarrhoea, dizziness, occasionally rash, altered LFTs

24
Q

What do proton pump inhibitors used for (give examples)

A

Block final pathway in production gastric acid

Block gastric H,K-ATPase, inhibiting gastric acid secretion

Include Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, Rabeprazole

Available OTC (lower doses) for dyspepsia

Generally once-twice daily

25
Q

What are the indications for PPIs (7)

A 
Many indications including:
Dyspepsia
GORD 
Treatment of gastric and duodenal ulcers 
Maintenance treatment 
NSAID prophylaxis 
Excessive gastric acid secretion
stress ulcer prophylaxis, peri-operatively
26
Q

What are PPI side effects

A

Side-effects include constipation, diarrhoea, headache, dizziness

MHRA warning - subacute cutaneous lupus erythematosus (SCLE)

27
Q

What does long term PPI therapy carry the risk of

A

Achlorhydria – low gastric acid production is associated with increased risk of:
Gastric cancer
H pylori infection (particularly the elderly)
Pneumonia
Clostridium difficile infection (PPI use was associated with a 42 per cent increase in the risk of recurrent CDI)
bacterial overgrowth and reduced calcium absorption leading to hip fracture.

28
Q

What are the PPI drug interactions

A

Interactions include:
Antiretrovirals
Methotrexate
Citalopram

Omperazole is predicted to decrease efficacy Clopidogrel – manufacturer advises avoid
Clinical significance is debatable!
Recommendations include using an alternative PPI or an H2 Antagonist

29
Q

What does H. pylori do

A

Causes persistent infection in gastroduodenal mucosa
Infection always causes gastritis
Commonest cause PUD - > 90% of duodenal and > 70% of gastric ulcers are found to be infected.
Prevalence increases with age
Linked to gastric cancer

30
Q

How does H pylori get transmitted

A

Transmission unclear – gastro-oral and faeco-oral probable

31
Q

How do we detect h. pylori infection

A

H pylori produces an antibody response detectable in serum, saliva or urine and antigen detectable in stool
Testing:
Urea breath test kits
Patient swallows 13C-labelled urea solution
Urease activity by organism produces labelled carbon dioxide.
Stool antigen test
Mucosal biopsies
CLO test - multiple biopsies of mucosa should be taken
Lab based serology (locally validated)

32
Q

What are the specifics around antimicrobials and H. pylori infection

A

Antibiotics/bismuth salts – may supress H pylori growth and give false negative
Achlorhydria (due to the presence of antacid therapy) – can give false positive

Testing should not be performed within 4 weeks of treatment with antibacterials or 2 weeks with PPI/antisecretory drugs

Retest using urea breath test if required

33
Q

How do we eradicate H. pylori

A

Triple therapy - 7 day, twice-daily course of a PPI plus two antibiotics

Check allergy status and confirm previous antibiotic exposure

If PUD and H pylori positive- timing of eradication will depend on if PUD also associated with NSAID

34
Q

Which drugs do we use to get rid of h. pylori (first line)

A

First Line – Triple therapy, twice daily for 7 days
PPI full dose BD, Amoxicillin 1g BD, Clarithromycin 500mg BD or Metronidazole 400mg BD

Penicillin allergic – PPI full dose BD, Clarithromycin 500mg BD and Metronidazole 400mg BD

*PPI choice depends on the hospital trust

35
Q

What is a second line treatment for h pylori

A

Alternative regimens available if penicillin allergic and previous clarithromycin exposure or treatment failure

These contain full dose PPI BD plus a combination of two or more of the following antibacterials:
Bismuth 
Tetracycline
Quinolone e.g ciprofloxacin
Metronidazole
Clarithromycin
36
Q

What is the pharmacists role in the treatment of h. pylori (5)

A

Patient education – adherence to regimen and importance of completing course as prescribed

Counsel on side-effects

Interactions e.g.
Clarithromycin + Statins
Metronidazole + alcohol

Ensure regimens prescribed correctly – can be confusing

Appropriate referral if ALRAM symptoms, recurrence

37
Q

What link is there between nsaids and GI disturbances

A

NSAIDs can cause a variety of GI injuries including PUD, bleeding and ulceration

NSAIDs are one of the common causes of PUD

38
Q

What are the risk factors for NSAID bleeds

A 
Risk factors for NSAID bleed include:
Age > 60
Multiple NSAIDs 
Smoker (increased risk PUD)
H pylori infection (increased risk PUD)
Concurrent medication including steroids, anticoagulants (which also affect GI tract)
Higher dose/longer duration
39
Q

How do NSAIDS cause ulcers (both directly and indirectly)

A

Direct mechanisms: Inhibition of prostaglandin synthesis impairs mucosal defences – erosive breach of epithelial barrier allows acid to enter

Acid attack deepens breach into frank ulceration

Low pH encourages passive absorption of NSAID so trapped in mucosa

Indirect mechanisms of NSAID damages include:
Reduce gastric blood flow
Reduce mucus and bicarbonate production
Leads to decreased cell repair

40
Q

How do we manage NSAID-induced PUD

A

Stop NSAID if possible (sometimes not possible for things like arthritis)

Test for H pylori

Treat with full dose PPI (or H2-receptor) antagonist for 8 weeks

If H pylori also present – give eradication therapy after above treatment

41
Q

What steps do we take if the NSAIDS need to be continued after the peptic ulcer has healed

A

Discuss potential harm
Regular review (at least 6 monthly) appropriateness
Reduce dose, Rx PRN, switch to Ibuprofen
Alternative agent e.g. cyclooxygenase-2-selective NSAID
Prescribe gastroprotection

(Gastroprotection:
PPI
H2-receptor antagonist
Misoprostol)

42
Q

What is Misoprostol

A

Effective at preventing NSAID induced PUD (although less effective than PPIs in preventing duodenal ulcers)

Prostaglandin analogue - antisecretory and cytoprotective effects.

Less well tolerated than PPIs. Side-effects include diarrhoea

Contra-indicated in pregnancy (uterine stimulant)

43
Q

won’t be examined Dyspepsia and GORD in Pregnancy: what are the management steps we can take

A

Dyspepsia in pregnancy commonly due to GORD – mechanical and hormonal factors
Symptoms include heartburn and acid reflux

Management can include:
Dietary and lifestyle changes – first line
Antacid or alginate (avoid preparations containing sodium bicarbonate or magnesium trisilicate)
If symptoms severe or persist – Ranitidine or Omeprazole

44
Q

won’t be examined GORD and Reflux in Infants and Children: what are the management steps we can take

A 
Change frequency and volume of feed
Feed thickener or thickened formula feed
Use an alginate instead of thickened feeds
H2-receptor antagonist 
Proton pump inhibitor
(nb, it is common in 12-18 month olds)

The Patient 20300 (24 decks)

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