GORD and Ulcers Flashcards

1
Q

What is peptic ulcer disease?

A

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.

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2
Q

Which site is commonly affected in peptic ulcer disease?

A

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

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3
Q

Gastroesophageal reflux disease

A

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)

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4
Q

Which drugs promote gut healing?

A

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)

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5
Q

Gastroesophageal reflux disease treatment

A

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)

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6
Q

Gastroesophageal reflux disease symptoms

A

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

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7
Q

Gastroesophageal reflux disease complications

A

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.

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8
Q

Gastroesophageal reflux disease risk factors

A

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

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9
Q

Behaviours that can worsen gastroesophageal reflux disease:

A

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)

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10
Q

What is Gastroesophageal reflux disease?

A

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

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11
Q

What is Normal gastro-oesophageal reflux (GOR)?

A

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.

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12
Q

What is GORD in children?

A

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

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13
Q

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.

A

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.

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14
Q

Why are children <1 year susceptible to GOR?

A

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

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15
Q

When are children more at risk for developing GORD?

A

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

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16
Q

When should GORD be suspected in children?

A

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.

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17
Q

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

A

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.

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18
Q

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

A

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.

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19
Q

Which complications may arise in children with GORD?

A

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

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20
Q

GORD infant/children treatment

A

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.

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21
Q

Red flags: indicative of non-GORD issues

A

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

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22
Q

What is there usually misdiagnosis of in children?

A

Misdiagnosis between delayed milk protein allergy and GORD in children

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23
Q

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

A

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

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24
Q

What might future GORD interventions include?

A

Future GORD interventions may include pro-motility drugs

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25
Q

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

A

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

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26
Q

How is peptic ulcer disease diagnosed?

A

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

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27
Q

Where are CCK2 receptors found?

A

CCK2 receptors are found on the parietal cells

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28
Q

Which receptors are found on the parietal cells?

A

CCK2 and H2 receptors are found on the parietal cells

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29
Q

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

A

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

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30
Q

What are the two main types of peptic ulcer disease?

A

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

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31
Q

Histamine

A

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

32
Q

Hydrochloric acid

A

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.

33
Q

Gastrin

A

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

34
Q

What does somatostatin do to acid secretion?

A

Somatostatin switches acid secretion off.

35
Q

How much acid is secreted per day?

A

Approx 2 litres of acid is secreted a day

36
Q

What is the pH of Hydrochloric acid?

A

Hydrochloric acid has a pH of <1.0

37
Q

What is hydrochloric acid produced by?

A

Hydrochloric acid is produced by the parietal cells

38
Q

Acid secretion

A

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

39
Q

Mucus production

A

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

40
Q

Somatostatin

A

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

41
Q

Prostaglandins (PGE2)

A

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
*

42
Q

Bicarbonate ions

A

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

43
Q

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

A

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

44
Q

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

A

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

45
Q

What does gastric epithelium protection depend on?

A

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

46
Q

Which 3 routes can acid secretion be stimulated by?

A

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

47
Q

Which cells secrete the protective secretions?

A

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

48
Q

ENS/CNS acid secretion

A

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

49
Q

Acid secretion:
Gastrin
Histamine
ENS/CNS

A

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)

50
Q

What do NSAIDs do?

A

NSAIDs block the production of prostaglandins

51
Q

Gastic ulcers

A

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)

52
Q

Duodenal ulcers

A

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)

53
Q

Which lifestyle factors can contribute to peptic ulcer formation?

A

Stress, smoking, alcohol can contribute to peptic ulcer formation

54
Q

What are 5 red flags in peptic ulcers?

A

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

55
Q

What does epigastric mean?

A

Epigastric:
relating to the central upper part of the abdomen

56
Q

Peptic ulcer symptoms

A

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

57
Q

Why are proton pump inhibitors one of the best treatments?

A

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

58
Q

Peptic ulcer diagnosis

A

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)

59
Q

H Pylori breath test

A

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

60
Q

Peptic ulcer disease treatment

A

Peptic ulcer disease treatment

Acid controlling agents
* Antacids
* H2 antagonists
* Proton pump inhibitors

Protective agents
Bismuth, Sucralfate, Misoprostol

H. pylori eradication
Antibiotics

61
Q

ANTACIDS

A

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

62
Q

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

A

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

63
Q

H2 receptor antagonists

A

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

64
Q

What is gynaecomastia?

A

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

65
Q

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

A

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

66
Q

Proton pump inhibitors

A

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

67
Q

Proton Pump Inhibitor Side effects

A

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

68
Q

What can proton pump inhibitors do to other drugs?

A

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

69
Q

Which 3 compounds can be protective and promote ulcer healing?

A

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
* Misoprostrol: Prostaglandin analogue (PGE1)
Inhibits acid secretion & promotes protective mucosal secretions. Contraindicated in pregnancy. SE include menorrhagia

70
Q

Bismuth

A

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

71
Q

Sucralfate

A

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
72
Q

Misoprostol

A

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

73
Q

Helicobacter pylori

A

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

74
Q

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

A

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

75
Q

H.pylori erradication

A

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

76
Q

H.pylori erradication pharmacy issues

A

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

77
Q

H.pylori quadruple therapy

A

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