GORD and Ulcers

Question 1

What is peptic ulcer disease?

Answer 1

Peptic ulcer disease:
- Upper GI disorder due to erosion of the mucosal layer of the GI tract occurring in areas exposed to acid and pepsin.

Question 2

Which site is commonly affected in peptic ulcer disease?

Answer 2

In peptic ulcer disease the most common ulceration site is in the lesser curvature of the stomach and in the proximal duodenum

Question 3

Gastroesophageal reflux disease

Answer 3

Gastroesophageal reflux disease:
* Disease characterized by acid reflux into the oesophagus
* Symptoms: Heartburn- uncomfrotable burning sensation behind the breastbone. (retrostenal pain), regurgitation, sore throat, acid brash, waterbrash(watery sensation in the mouth), nocturnal cough (exacerbation of ashtma)
* Complications:
* Dysphagia, chest pain, oesophageal erosions, oesophageal ulcer, strictures (narrowing of the oesophagus) caused by inflammation, alterations of peristaltic movement.
* Increased risk of oesophageal cancer and Barrett’s oesophagus.
* Risk factors: Obesity, hiatus hernia, pregnancy, GI motility disorders (delayed gastric emptying)
* Behaviours that can worsen it: Smoking, eating large meals, eating late at night, fatty foods, fried foods, alcohol, caffeine, medications (e.g. aspirin)
* Treatment:
* Antacids (neutralize acids)
* Histamine H2 antagonists (target H2 receptors on parietal cells)
* Proton pump inhibitors (irreversibly block the action of the H+/ K+- ATPASE on parietal cells)
* Alginates (Seaweed based, form a protective layer over stomach contents)

Question 4

Which drugs promote gut healing?

Answer 4

Drugs that promote gut healing:
* Misoprostol (promotes healing of NSAID-associated ulcers, acts on G-protein-coupled EP receptors in gastric mucosa, increases mucus and bicarbonate production, reduces acid secretion)
* Sucralfate (forms a protective coating over ulcers and erosions)
* Bismuth chelate (toxic to H.pylori)

Question 5

Gastroesophageal reflux disease treatment

Answer 5

Gastroesophageal reflux disease treatment
* Antacids (neutralize acids)
* Histamine H2 antagonists (target H2 receptors on parietal cells)
* Proton pump inhibitors (irreversibly block the action of the H+/ K+- ATPASE on parietal cells)
* Alginates (Seaweed based, form a protective layer over stomach contents)

Question 6

Gastroesophageal reflux disease symptoms

Answer 6

Gastroesophageal reflux disease symptoms
* Heartburn- uncomfortable burning sensation behind the breastbone (retrostenal pain),
* regurgitation,
* sore throat,
* acid brash,
* waterbrash(watery sensation in the mouth),
* nocturnal cough (exacerbation of ashtma)
* increased salivation
* shortness of breath

Question 7

Gastroesophageal reflux disease complications

Answer 7

Gastroesophageal reflux disease complications
* Dysphagia,
* chest pain,
* oesophageal erosions,
* oesophageal ulcer,
* strictures (narrowing of the oesophagus) caused by inflammation,
* alterations of peristaltic movement.
* Increased risk of oesophageal cancer and Barrett’s oesophagus.

Question 8

Gastroesophageal reflux disease risk factors

Answer 8

Gastroesophageal reflux disease risk factors
* Obesity
* hiatus hernia,
* pregnancy,
* GI motility disorders (delayed gastric emptying)

Question 9

Behaviours that can worsen gastroesophageal reflux disease:

Answer 9

Behaviours that can worsen gastroesophageal reflux disease:
* Smoking,
* eating large meals,
* eating late at night,
* fatty foods,
* fried foods,
* alcohol,
* caffeine,
* medications (e.g. aspirin, calcium channel blockers, nitrates)

Question 10

What is Gastroesophageal reflux disease?

Answer 10

Gastroesophageal reflux disease:
* Disease characterized by acid reflux into the oesophagus
* the backflow of stomach acid (and bile) into the oesophagus.

Question 11

What is Normal gastro-oesophageal reflux (GOR)?

Answer 11

Normal gastro-oesophageal reflux (GOR) is the passage of gastric contents into the oesophagus. It is considered physiological in infants when symptoms are absent or not troublesome.

Question 12

What is GORD in children?

Answer 12

Gastro-oesophageal reflux disease (GORD) in children is the presence of troublesome symptoms or complications arising from GOR.

Question 13

Frequent effortless regurgitation of feeds is common and __________ in infants less than 1 year of age. It may be ____________to differentiate between gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease (GORD) as there is no reliable diagnostic test.

Answer 13

Frequent effortless regurgitation of feeds is common and normal in infants less than 1 year of age. It may be difficult to differentiate between gastro-oesophageal reflux (GOR) and gastro-oesophageal reflux disease (GORD) as there is no reliable diagnostic test.

Question 14

Why are children <1 year susceptible to GOR?

Answer 14

Children< 1 year are susceptible to GOR due to several anatomical and physiological features:
* They have delayed gastric emptying
* They have a short, narrow oesophagus
* Their lower oesophageal sphincter is slightly above the diaphragm

Question 15

When are children more at risk for developing GORD?

Answer 15

Children with increased risk for developing GORD if they have/are:
* Cystic fibrosis
* severe neurological impairment
* gastro-oesophageal abnormalities
* premature
* Parental history of heartburn or acid regurgitation.
* Obesity.
* Hiatus hernia.
* History of congenital diaphragmatic hernia (repaired) or congenital oesophageal atresia (repaired).
* Neurodisability

Question 16

When should GORD be suspected in children?

Answer 16

GORD should be suspected in children with either (but usually both) of the following:
* Frequent and troublesome regurgitation or vomiting (which may occur up to 2 hours after feeding).
* Frequent and troublesome crying, irritability, or back-arching during or after feeding, or feeding or food refusal (despite being willing to suck on a dummy).
* distressed behaviour,
* hoarseness,
* unexplained
* feeding difficulties,
* faltering growth
* chronic cough
* A single episode of pneumonia.

GORD should be suspected in children over 1 year who present with heartburn, retrosternal pain, or epigastric pain.

Question 17

GORD in children: when should same day admission be arranged?

Answer 17

Same-day admission should be arranged if the child has:
Haematemesis (vomiting blood) (not caused by swallowed blood from a nosebleed or ingested from a cracked maternal nipple).
Melaena (black stool, symptom of internal bleeding).
Dysphagia.

Question 18

When should there be specialist assessment by a paediatrician or paediatric gastroenterologist?

Answer 18

Specialist assessment by a paediatrician or paediatric gastroenterologist should be arranged if there is:
An uncertain diagnosis or ‘red flag’ symptoms which suggest a more serious condition.
Persistent faltering growth associated with regurgitation.
Suspected complications, such as recurrent aspiration pneumonia, or unexplained apnoeas.

Question 19

Which complications may arise in children with GORD?

Answer 19

Complications that may occur in children with GORD include:
* Anaemia
* Dysphagia (difficulty in swallowing)
* Respiratory symptoms (such as cough, wheeze, asthma, or reactive airways disease)

Plus other symptoms
* Sleeping difficulties
* Dental erosion.
* Failure to thrive
* Reflux oesophagitis
* Aspiration pneumonia
* Acute otis media

Question 20

GORD infant/children treatment

Answer 20

GORD infant/children treatment:
* Children who have frequent regurgitation only: parents and carers reassured that symptoms are likely to improve over time.
* Breastfed infants with suspected GORD: 1–2 week trial of Gaviscon® Infant
* Formula-fed infants with suspected GORD: sequential 1–2 week trial of:
* reduction of the volume of feeds,
* more frequent feeds,
* thickened feeds (for example Instant Carobel®)
* Gaviscon® Infant.
For breastfed and formula-fed infants:
If treatment with Gaviscon® Infant is successful, continue. Stop treatment every 2 weeks to see if symptoms improve and treatment can be stopped.
If treatment with Gaviscon® Infant is not successful, a 4–week trial of omeprazole or H2 receptor antagonist (H2RA) may be considered.
* If symptoms still persist, the child should be referred for specialist assessment.
* For children aged 1–2 years of age with suspected GORD, a 4–week trial of omeprazole or H2RA may be considered.
If symptoms still persist, the child should be referred for specialist assessment.

Question 21

Red flags: indicative of non-GORD issues

Answer 21

Red flags: indicative of non-GORD issues
* Vomiting –
* bilious
* bloodstained
* very forceful
onset occurs > 6m
* Respiratory symptoms
* Diarrhoea
* Blood in stool
* Lethargy
* Fever
* Abnormal abdominal examination
* Neuro/developmental problems e.g bulging fontanelle
* Dysuria
* High risk of atopy

Question 22

What is there usually misdiagnosis of in children?

Answer 22

Misdiagnosis between delayed milk protein allergy and GORD in children

Question 23

What do studies show about elevated pHlevels in the lower oesophageal sphincter?

Answer 23

Studies show elevation of pH in lower oesophagus is therapeutically advantageous..

Question 24

What might future GORD interventions include?

Answer 24

Future GORD interventions may include pro-motility drugs

Question 25

Why are proton pump inhibitors the current drug of choice for GORD treatment?

Answer 25

Proton pump inhibitors current drug of choice due to efficacy over H2RAs

Question 26

How is peptic ulcer disease diagnosed?

Answer 26

Peptic ulcer disease is diagnosed by endoscopy or H.pyloribacter testing

Question 27

Where are CCK2 receptors found?

Answer 27

CCK2 receptors are found on the parietal cells

Question 28

Which receptors are found on the parietal cells?

Answer 28

CCK2 and H2 receptors are found on the parietal cells

Question 29

_________ ________ is the target of non-steroidal antiinflammatory drugs.

Answer 29

**Cyclo-oxygenase** is the target of non-steroidal antiinflammatory drugs.

Question 30

What are the two main types of peptic ulcer disease?

Answer 30

Two types of peptic ulcer disease: * Gastric ulcer: Defective ability of gastric mucosa to protect and repair itself * Duodenal ulcer: Hypersecretion of gastric acid → erosion of mucosa in duodenum

Question 31

Histamine

Answer 31

Histamine * Basic amine * Produced by enterochromaffin like cells * Increases the amount of proton pump molecules on cell surface * Stored in granules * Release is stimulated by: Acetylcholine and Gastrin * Targets H2 receptors on PARIETAL cells * Parietal cells secrete acid * Inhibited by prostaglandin E2

Question 32

Hydrochloric acid

Answer 32

Hydrochloric acid: * Produced by parietal cells * Helps to denature and degrade proteins * Converts pepsinogen to pepsin * Protects against bacteria and microorganisms * Creates an acidic environment in the stomach.

Question 33

Gastrin

Answer 33

Gastrin: * polypeptide endocrine molecule * promotes acid secretion from the parietal cells * secreted by G-cells in the stomach * Release stimulated by: digested protein, fat, stomach distenstion, gastric-releasing peptide * Targets CCK2 receptors on ECL and parietal cells (not as common) * Increases amount of protein pumps on parietal cell * Indirectly promotes acid secretion by stimulating receptors on ECL cells * Promotes mucosal cell lining growth of stomach and small intestine * Promotes gastric emptying

Question 34

What does somatostatin do to acid secretion?

Answer 34

Somatostatin switches acid secretion off.

Question 35

How much acid is secreted per day?

Answer 35

Approx 2 litres of acid is secreted a day

Question 36

What is the pH of Hydrochloric acid?

Answer 36

Hydrochloric acid has a pH of <1.0

Question 37

What is hydrochloric acid produced by?

Answer 37

Hydrochloric acid is produced by the parietal cells

Question 38

Acid secretion

Answer 38

Acid secretion * Approx 2 litre/day * HCl, pH< 1.0 * Produced by parietal cells

Question 39

Mucus production

Answer 39

Mucus production * Prostaglandin induced (PGE2) * Produced by mucus secreting epithelial cells (via EP4 receptors) * Also produce bicarbonate ions (via EP1/4 receptors) which become trapped in mucus * Protective layer 0.2mm thick (can be destroyed by alcohol) * mucus allows the pH of epithelial cells to be maintained at nearly neutral despite a luminal pH of about 2. * Mucus also slows the diffusion of acid and pepsins to the epithelial cell surface

Question 40

Somatostatin

Answer 40

Somatostatin * Peptide hormone * Inhibits acid secretion * Secreted from delta cells in the pancreas and duodenal mucosa * Release stimulated by: high gastric acidity * Acts directly on PARIETAL cells * Acts indirectly on enterochromaffin like cells and G cells

Question 41

Prostaglandins (PGE2)

Answer 41

Prostaglandins (PGE2) * Generated in most gastric mucosa cells via cyclo-oxygenase * Lipid * Autocrine molecule * Stimulates mucus and bicarbonate secretion * Inhibits histamine release from enterochromaffin like cells *

Question 42

Bicarbonate ions

Answer 42

Bicarbonate ions * Neutralize effect of hydrochloric acid (allows for helicobacter pylori to thrive at mucosal layer surface)

Question 43

Acetylcholine acts on Gq-couple M3 receptors on parietal cells. Increased Ca2+ results in increased acid secretion

Answer 43

Acetylcholine acts on Gq-couple M3 receptors on parietal cells. Increased Ca2+ results in increased acid secretion

Question 44

The mucus gel layer, which is about 0.2 mm thick, effectively separates the HCO3--rich secretions of the surface epithelial cells from the _________ contents of the gastric lumen

Answer 44

The mucus gel layer, which is about 0.2 mm thick, effectively separates the HCO3--rich secretions of the surface epithelial cells from the acidic contents of the gastric lumen

Question 45

What does gastric epithelium protection depend on?

Answer 45

Protection of the gastric epithelium depends on both mucus and HCO3- secretion.

Question 46

Which 3 routes can acid secretion be stimulated by?

Answer 46

Acid secretion can be stimulated by: * Gastrin binding to CCK2 receptors on Enterochromaffin like cells * Gastrin binding to CCK2 receptors on parietal cells * Histamine binding to H2 receptor on parietal cells

Question 47

Which cells secrete the protective secretions?

Answer 47

The epithelial cells of the mucosa secrete the protective secretions of mucus and bicarbonate ions

Question 48

ENS/CNS acid secretion

Answer 48

ENS/CNS acid secretion * Target M3 receptor on parietal cells * Suffalic reflex * Prepares stomach for environment with food

Question 49

Acid secretion: Gastrin Histamine ENS/CNS

Answer 49

Acid secretion: * Gastrin: targets CCK2 receptors on eneterchromaffin like cells and parietal cells * Histamine: targets H2 RECEPTOR on parietal cells * ENS/CNS: targets M3 receptor on parietal cells (suffalic reflex)

Question 50

What do NSAIDs do?

Answer 50

NSAIDs block the production of prostaglandins

Question 51

Gastic ulcers

Answer 51

Gastic ulcers * Defective ability of gastric mucosa to protect and repair itself * Often caused by long term NSAID use * Occur more frequently in older people (f~>m)

Question 52

Duodenal ulcers

Answer 52

Duodenal ulcers * Hypersecretion of gastric acid leads to erosion of mucosa in duodenum * Often caused by H. pylori infection (inhibits delta cells, production of ulcer promoting agents such as urease) * 80% of all peptic ulcers * Occur more frequently in young people (m>f)

Question 53

Which lifestyle factors can contribute to peptic ulcer formation?

Answer 53

Stress, smoking, alcohol can contribute to peptic ulcer formation

Question 54

What are 5 red flags in peptic ulcers?

Answer 54

5 red flags for peptic ulcers: * Weight loss * Vomiting * Development of back pain * Blood in stools * Lack of efficacy with acid control therapy

Question 55

What does epigastric mean?

Answer 55

Epigastric: relating to the central upper part of the abdomen

Question 56

Peptic ulcer symptoms

Answer 56

Peptic ulcer symptoms * Epigastric discomfort (pain): * 30 min -1 h after meal (gastric). Food intake increases pain * 2- 3 h post meal (duodenal). Food intake temporarily decreases pain

Question 57

Why are proton pump inhibitors one of the best treatments?

Answer 57

Why are proton pump inhibitors one of the best treatments? * They are the final step

Question 58

Peptic ulcer diagnosis

Answer 58

Peptic ulcer diagnosis * Endoscopy to determine site of lesion: stomach, duodenal or gastric **H. Pylori tests** * Carbon-13 (13C) urea breath test – under fasting conditions (NICE recommended) Non-invasive Citric acid solution with 13C containing urea Bacterial urease hydrolyses urea into 13CO2 + 2NH3 Increase in 13CO2 indicates presence of H. pylori Others? Stool antigen test (NICE recommended) Laboratory-based serology Biopsy based tests during endoscopy(NICE recommended)

Question 59

H Pylori breath test

Answer 59

H Pylori breath test * Person ingests a citric acid labelled carbon atom 13C solution containing urea * Bacterial urease hydrolyses urea into 13CO2 + 2NH3 * If H pylori is present an enzyme called urease is produced and hydrolyses urea into 13CO2 + 2NH3 * Increase in carbon dioxide 13CO2 indicates H pylori presence

Question 60

Peptic ulcer disease treatment

Answer 60

Peptic ulcer disease treatment **Acid controlling agents** * Antacids * H2 antagonists * Proton pump inhibitors **Protective agents** Bismuth, Sucralfate, Misoprostol **H. pylori eradication** Antibiotics

Question 61

ANTACIDS

Answer 61

ANTACIDS: * Antacids neutralise gastric acid * Secrete: mucus, bicarbonate and prostaglandins * Dose: take after meal (~1 h pp) * DO NOT suppress acid secretion * Quick onset of relief but last for a short duration * They are weak bases aluminium hydroxide (causes constipation) magnesium hydroxide (cause diarrhoea) may include other agents to help alleviate condition; for example, alginates * Antacids promote gastric mucosal defence by secreting: mucus: protective barrier against HCl Bicarbonate: helps buffer acidic properties of HCl Prostaglandins: prevent activation of proton pump which results in ⇓HCl production * Examples: Rennie * Side effects: diarrhoea, constipation

Question 62

Alginates are scaffolding polysaccharides produced by brown seaweeds react with ________________________ to produce a viscous layer

Answer 62

Alginates are scaffolding polysaccharides produced by brown seaweeds react with acid to produce a viscous layer

Question 63

H2 receptor antagonists

Answer 63

H2 receptor antagonists * Act as competitive antagonists on H2 receptors (reversible) * Targets H2 receptors on parietal cells * All available OTC in lower dosage forms. * Inhibit acid secretion simulated by histamine, gastrin and meals. * Not so good at blocking neuronal mediated acid secretion Examples: cimetidine (Tagamet): blocks P450 famotidine (Pepcid) nizatidine (Axid) Side effects: Diarrhoea. Gynaecomastia (cimetidine) Lethargy, confusion, depression, hallucinations (more likely in elderly or with renal or hepatic impairment) Histamine stimulates acid secretion in parietal cells. Mast cells also produce a basal level of histamine which increases in response to acetylcholine and gastrin

Question 64

What is gynaecomastia?

Answer 64

Gynaecomastia: * enlargement of a man's breasts, usually due to hormone imbalance or hormone therapy.

Question 65

Why are PPIs a better treatment choice than H2 receptor blockers?

Answer 65

PPIs are a better treatment choice than H2 receptor blockers because: * H2 antagonists poor at suppressing acid secretion mediated by acetylcholine or gastrin alone. * Acid is produced by proton pumps in parietal cells, PPIs inhibit acid secretion at site of production * H2 antagonists now largely replaced by PPI

Question 66

Proton pump inhibitors

Answer 66

Proton pump inhibitors * Blocks H+/K+- ATPASE irreversibly. Covalently binds to cysteine residue in proton pump * PPIs are lipophilic weak bases * Absorbed in duodenum and delivered to parietal cells via blood. * Pro drugs: PPIs are inactive at neutral pH, protonated in acidic environment of canaliculae of parietal cells. Protonated form binds covalently to cysteine residue in proton pump. Blocks pump irreversibly. * Almost total inhibition of gastric acid secretion for up to 48 h (p cells have to express new pumps!!) * Delivered by blood Examples: Omeprazole, lansoprazole Side effects: Headaches, diarrhoea, N, V, abdominal pain (normal in GI upset) High doses + long term therapy → risk of gastric cancer (rare), Osteoporotic fractures . Warning → increased risk of hip, wrist, or spine fractures (especially over 50 years of age) (especially in women). Also decreases magnesium levels. C. difficile infections. Warning increased risk of c.diff infections

Question 67

Proton Pump Inhibitor Side effects

Answer 67

Proton Pump Inhibitor Side effects * Headaches, * diarrhoea (osmotic effects), * Nausea, * Vomiting, * abdominal pain (normal in GI upset) * High doses + long term therapy → risk of gastric cancer (rare) (G cells think something is wrong and produce more), * Osteoporotic fractures . Warning → increased risk of hip, wrist, or spine fractures (especially over 50 years of age) (especially in women). Also * decreases magnesium levels. * C. difficile infections. Warning increased risk of c.diff infections> due to elevated pH breeding ground for toxins

Question 68

What can proton pump inhibitors do to other drugs?

Answer 68

Proton pump inhibitors can: * Affect drug absorption due to ↑gastric pH * Increase absorption of ↑absorption of warfarin, diazepam, phenytoin * Increased absorption can lead to→ ↑drug toxicity

Question 69

Which 3 compounds can be protective and promote ulcer healing?

Answer 69

3 compounds that can be protective and promote ulcer healing: * **Bismuth**: Protects the ulcer crater and allows healing Some activity against H. pylori * **Sucralfate**: Can be used to prevent & treat PUD It requires an acid pH to activate Forms sticky polymer in acidic environment and adheres to the ulcer site, forming a barrier May bind with other drugs and interfere with absorption * **Misoprostro**l: Prostaglandin analogue (PGE1) Inhibits acid secretion & promotes protective mucosal secretions. Contraindicated in pregnancy. SE include menorrhagia

Question 70

Bismuth

Answer 70

Bismuth * Protects the ulcer crater and allows healing * Some activity against H. pylori, like an antibacterial * Side effects: black stools, constipation, turn tongue black * Shouldn't be used for more than 2 months

Question 71

Sucralfate

Answer 71

Sucralfate * Can be used to prevent & treat PUD * Complex of aluminium hydroxide and sulphate sucrose * It requires an acid pH to activate * Promotes healing by: Forms sticky polymer in acidic environment and adheres to the ulcer site, forming a barrier * Like a bandaid * No neutralizing ability or effect on acid secretion * can interrupt the results of PPIs since theres not enough contact with the lining * May bind with other drugs and interfere with absorption * Side effects: constipation, bezoar (stomach obstruction) * Not recommended for longer than 2 months * Used for: duodenal ulcers * Shouldn't be used with: Antacids (by raising the pH above 4 → ↓effects of sucralfate) ,Phenytoin, theophylline, digoxin, warfarin, ciprofloxacin → ↓drug absorption *Renal failure (drug contains aluminum that can lead to toxicity) * Give approximately 2 hours before or after other drugs Take on an empty stomach before meals sucralfate

Question 72

Misoprostol

Answer 72

Misoprostol * Prostaglandin analogue (PGE1) * Mimics prostaglandins: increases mucus and bicarbonate production, decreases acid secretion * Inhibits acid secretion & promotes protective mucosal secretions. * Not taken if pregnant can induce early labour * Side effects: menorrhagia (menstrual bleeding that lasts more than 7 days), diarrhoea

Question 73

Helicobacter pylori

Answer 73

Helicobacter pylori * Gram negative, urease positive bacteria * Inhabits antrum of stomach where there is lower acidity * Produces urease which buffers acidity: converts urea to ammonia * Can cause gastritis or hyperacidsecretion due to delta cell decrease * Evidence strongly implicates H. pylori in development of gastric ulcer and gastritis * Developing countries * Incidences of infection increase with age * Increased risk of developing gastric adenocarcinoma

Question 74

What is the 1st line treatment for H.pylori?

Answer 74

H.pylori 1st line treatment: 1st line treatment: Triple therapy - PPI + 2x antibiotics * PPI plus amoxicillin, or clarithromycin * PPI plus clarithromycin and metronidazole * PPI plus amoxicillin and metronidazole

Question 75

H.pylori erradication

Answer 75

H.pylori erradication * 1st line treatment: Triple therapy - PPI + 2x antibiotics PPI plus amoxicillin, or clarithromycin PPI plus clarithromycin and metronidazole PPI plus amoxicillin and metronidazole * Also: Quadruple therapy Bismuth + PPI + 2x antibiotics Pharmacy issues: - antibiotic resistance -> eradication can be difficult - difficulty in delivering antibiotics at therapeutic concentrations - Side effects of therapy: diarrhoea, abdominal pain, fever, increased white blood cell count, rectal bleeding, pseudomembranous colitis

Question 76

H.pylori erradication pharmacy issues

Answer 76

H.pylori erradication Pharmacy issues: - antibiotic resistance -> eradication can be difficult - difficulty in delivering antibiotics at therapeutic concentrations - Side effects of therapy: diarrhoea, abdominal pain, fever, increased white blood cell count, rectal bleeding, pseudomembranous colitis

Question 77

H.pylori quadruple therapy

Answer 77

H.pylori quadruple therapy * Bismuth + PPI + 2x antibiotics