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Pharmacology > Gastro-oesophageal reflux disease > Flashcards

Gastro-oesophageal reflux disease Flashcards

1
Q

Clinical presentation of dyspepsia

A

Epigastric pain/burning
Early satiation
Postprandial fullness
Belching, bloating, nausea, discomfort

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2
Q

Synonym for dyspepsia?

A

Indigestion

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3
Q

Epidemiology of dyspepsia

A 
Common worldwide (42%)
Only 5% will go to GP
1% referred for endoscopy

40-50% have functional/non-ulcer dyspepsia
40% have GORD
10-13% have some form of ulcer
1-3% have oesophageal/gastric cancer

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4
Q

Heartburn

A

A major symptom of GORD
Burning sensation in the chest just behind sternum/in epigastrium -> pain often rises in the chest and may radiate to the neck, back, shoulder, throat or angle of jaw

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5
Q

How many patients with GORD will present with chest pain?

A

50%

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6
Q

Which condition must be excluded in a patient with unexplained chest pain?

A

Ischaemic heart disease (acute MI, angina)

Only 0.6% of heartburn cause

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7
Q

Aggravating factors of GORD

A

After eating or at night
Worse when lying down/bending over
Common in pregnancy
Consuming food in large quantities or specific foods (certain spices, high fat content, high acid content)

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8
Q

Heartburn/chest pain after eating/drinking combined with difficulty swallowing may indicate?

A

Oesophageal spasms

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9
Q

What are the symptoms that give warning when combined with dysphagia?

A

Weight loss
Proven anemia
Vomiting
Haematemesis

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10
Q

High risk factors accompanying dyspepsia?

A

> 55yo pt

  • onset of dyspepsia <1y previously
  • continuous symptoms since onset
  • family history of upper GI cancer in > 2 1st degree relatives
  • Barrett’ oesophagus
  • pernicious anemia
  • peptic ulcer surgery >20y previously
  • palpable Virchow’s node
  • jaundice
  • upper abdominal mass
  • longstanding change in bowel habit
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11
Q

Which symptoms require endoscopy in heartburn and indigestion?

A 
Weight loss
Haematemesis
Melaenia
Dysphagia
Anemia
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12
Q

Which symptoms allow for empiric treatment w/o endoscopy in heartburn and indigestion?

A

No weight loss
No haematemesis
<45yo

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13
Q

Which cells in the gastric mucosa are responsible for gastric acid secretion?

A

Parietal cells

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14
Q

Parietal cells are stimulated by?

A

Acetylcholine
Histamine
Gastrin

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15
Q

How does acetylcholine stimulate the parietal cells to secrete gastric acid?

A

Induces increase in intracellular calcium -> activation of protein kinases -> stimulate H+/K+ ATPase proton pump to secrete H+ ions in exchange for K+ into stomach lumen

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16
Q

How does histamine stimulate the parietal cells to secrete gastric acid?

A

Activation of adenylyl cyclase -> activation of protein kinases -> stimulate H+/K+ ATPase proton pump to secrete H+ ions in exchange for K+ into stomach lumen

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17
Q

How does gastrin stimulate the parietal cells to secrete gastric acid?

A

Induces increase in intracellular calcium -> activation of protein kinases -> stimulate H+/K+ ATPase proton pump to secrete H+ ions in exchange for K+ into stomach lumen

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18
Q

Gastric acid secretion is diminished by?

A

Prostaglandin E2

Somatostatin

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19
Q

How does prostaglandin E2 diminish the secretion of gastric acid by the parietal cells?

A

Inhibits adenylyl cyclase -> protein kinases not activated

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20
Q

How does somatostatin diminish the secretion of gastric acid by the parietal cells?

A

Inhibits adenylyl cyclase -> protein kinases not activated

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21
Q

Causative factors of peptic ulcer disease

A

NSAIDs esp aspirin
Infection w/ H.pylori (90% duodenal; 70% gastric)
Increased HCl and pepsin secretion
Inadequate mucosal defence against gastric acid

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22
Q

Principles of peptic ulcer disease management

A

Symptomatic relief
Promoting ulcer healing
Prevention of recurrence once healing has occurred
Prevention of complications

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23
Q

Peptic ulcers may occur and disappear spontaneously

True or false?

A

True

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24
Q

Non-pharmacological approaches to peptic ulcer disease

A 
Stop smoking
Avoid ulcerogenic drugs
Reduce caffeine intake
Healthy diet
Test for H.pylori
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25
Q

Name ulcerogenic drugs

A

Alcohol
NSAIDs
Glucocorticosteroids

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26
Q

Pharmacological approaches to peptic ulcer disease

A 
Eradicate H.pylori infection 
- antimicrobial therapy + PPI
Reduce gastric acid secretion
- PPI
- H2 receptor antagonists
Protect the gastric mucosa
- misoprostol
- sucralfate
- alginates
- bismuth
Neutralize gastric acid with non-absorbable antacids
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27
Q

Drug classes used to treat peptic ulcer disease

A 
Antimicrobial agents
Mucosal protective agents
H2 histamine receptor blockers
Proton pump inhibitors
Antacids
Prostaglandins
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28
Q

Antimicrobial agents used for peptic ulcer disease

A

Amoxicillin
Clarithromycin
Metronidazole
Tetracycline

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29
Q

Mucosal protective agents used for peptic ulcer disease

A

Bismuth subcitrate
Sucralfate
Alginates

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30
Q

H2 histamine receptor blockers used for peptic ulcer disease

A

Cimetidine

Ranitidine

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31
Q

Proton pump inhibitors used for peptic ulcer disease

A 
Esomeprazole
Lanzoprazole
Omeprazole
Pentoprazole
Rabeprazole

Most potent suppressors of gastric acid secretion

  • begins 1-2hrs after 1st dose
  • effect for 2-3 days because of accumulation in gastric canaliculi
  • preferred to H2 antagonists
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32
Q

Antacids used for peptic ulcer disease

A

Aliminium hydroxide
Calcium carbonate
Magnesium
Sodium bicarbonate

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33
Q

Prostaglandins used for peptic ulcer disease

A

Misoprostol

34
Q

Mechanism of action of proton pump inhibitors in peptic ulcer disease

A

Irreversibly inhibit the K+/K+ ATPase proton pump -> hydrogen ion secretion into gastric lumen suppressed

35
Q

Which proton pump inhibitor is in danger of drug interactions?

A 
Omeprazole (inhibits CYP450)
Warfarin
Phenitoin
Diazepam
Cyclosporine
Digoxin
36
Q

Indication for proton pump inhibitor use?

A

Short term PUD and GORD management
Long term GORD relapse prevention
H.pylori eradication in combination w/ ABs
Zollinger-Ellison syndrome treatment
NSAID-associated erosions + ulcers treatment and prevention
IV PPI in high risk bleeding peptic ulcers

37
Q

Amelioration of GORD/PUD symptoms may delay diagnosis of…?

A

Gastric carcinoma

38
Q

Which drug class is indicated for short term PUD and GORD management

A

PPI

39
Q

Which drug class is indicated for long term GORD relapse prevention

A

PPI

40
Q

Which drug class is indicated for H.pylori eradication in combination w/ ABs

A

PPI

41
Q

Which drug class is indicated for Zollinger-Ellison syndrome treatment

A

PPI

42
Q

Which drug class is indicated for NSAID-associated erosions + ulcers treatment and prevention

A

PPI

43
Q

Which drug class is indicated for high risk bleeding peptic ulcers?

A

PPI

Increasing gastric pH stabilises the ulcer clot -> reduced rebleeding risk

44
Q

Adverse effects of proton pump inhibitors

A 
Hypomagnesemia (prolonged use)
Increased fracture risk
Headaches
Skin rashes
Raised LFTs
Diarrhoea (C.difficile)
Drowsiness + impaired concentration (aggravated in CNS depressant use)
45
Q

Which drugs will have inhibited metabolism with omeprazole use?

A 
Warfarin
Phenitoin
Diazepam
Cyclosporine
Digoxin
46
Q

Clinical presentation of hypomagnesemia?

A 
Weakness
Muscle cramps
Cardiac arrythmias
Confusion
Seizures
Hallucinations
47
Q

What can prolonged proton pump inhibitor use result in?

A

Low vitamin B12

Acid required for absorption

48
Q

Proton pump inhibitors cause … of calcium carbonate products?

A

Incomplete absorption

49
Q

H2-receptor antagonists

Mechanism of action

A

Reversibly block the action of histamine at H2 receptors in parietal cells of stomach -> reduce intracellular cyclic adenosine monophosphate concentration -> reduced gastric acid secretion
Gastric acid secretion in response to secretagogues e.g Ach, gastrin also reduced

50
Q

H2-receptor antagonists are very efficient with what type of secretion?

A

Nocturnal acid secretion

51
Q

Indications for H2-receptor antagonists use?

A

Largely replaced by PPIs
Peptic ulcers
Oesophagitis
Effective in healing gastric + duodenal ulcer but high recurrence >60%
Acute stress ulcers
GORD
Heartburn prevention + treatment (50% effective)
Hypersecretory states e.g Zollinger-Ellison syndrome
Prevent aspiration during anasthesia before emergency surgery e.g Mendelson’s syndrome

52
Q

Adverse effects of H2-receptor antagonists

A 
Antiandrogenic effect esp cimetidine (0.1-0.2%)
- impotence
- gynecomastia
- galactorrhoea
Headache
Dizziness
Diarrhoea
Muscular pain
Confusion
Hallucinations
Slurred speech
53
Q

Cimetidine drug interactions

A

Inhibits P450
Increases effects of - warfarin, theopylline, phenytoin, amiodarone, quinidine, fluorouracil, metformin, diazepam, imipramine
Increases absorption of - ketoconazole

54
Q

Why is ranitidine considered superior to cimetidine?

A

Structurally different to cimetidine but as effective
Less CNS symptoms because does not cross BBB as easily
Little/no anti-androgenic effect
No effect on P450 therefore fewer drug interactions

55
Q

Mechanism of action of prostaglandins

A

Inhibit secretion of HCl + stimulate mucus and bicarbonate secretion + submucosa vasodilation
Less effective than PPIs/H2 receptor agonists

56
Q

In what cases are prostaglandins routinely used?

A

NSAID induced ulcers

57
Q

Adverse effects of prostaglandin use

A

Uterine contractions
Nausea
Diarrhoea

58
Q

In which patients is prostaglandin use in peptic ulcer disease contraindicated?

A

Pregnancy

59
Q

Mechanism of action of sucralfate

A

A sucrose hydrogen sulphate-aliminium complex that forms paste-like gel when in contact w/ HCl -> local protective action on ulcer base + protect ulcer epithelium from gastric acid and directly absorbs pepsin and bile

60
Q

Indications for use of sucralfate

A

Benign gastric ulceration
Benign duodenal ulceration
Chronic gastritis
Administer frequently and at least 2 hours apart from other medications (30min from other antacids)

61
Q

Side effects of sucralfate use

A 
Constipation
Diarrhoea
Vomiting
Serum phosphorus reduction (binds phosphorus)
Raised calcium levels
62
Q

Drug interactions of sucralfate?

A

Tetracycline

Phenytoin

63
Q

Mechanism of action of bismuth subcitrate

A

Precipitates at acid pH w/ high affinity for damaged tissue -> visible coating at ulcer base -> protection against acid + pepsin digestion AND mucous production stimulation

64
Q

Adverse effects of bismuth subcitrate

A 
Blackening of tongue, teeth + stools
Renal failure (prolonged treatment)
65
Q

Mechanism of action of alginates

A

Extracted from algae

Increase viscosity and adherence of mucus to oesophageal mucosa -> protective barrier

66
Q

Indications for alginate use

A

Dyspepsia
Symptomatic peptic ulcer relief
Symptomatic oesophageal reflux relief
Used in pregnancy

67
Q

Mechanism of action of antacids

A 
Directly neutralise intaluminal acid -> reduce acid delivery into duodenum after meal
Doesn't block production
May increase oesophageal sphincter tone
May reduce oesophageal pressure
Take 1hr after meal + at bedtime
68
Q

At what pH does peptic enzyme activity stop?

A

5

69
Q

Which ulcers are antiacids more effective with?

A

Duodenal ulcers (>gastric ulcers)

70
Q

Which antacids must you use with caution

A

Na+ containing antacids w/ cardiovascular disorders

71
Q

Does adding local anaesthetic add advantage to antacid efficacy?

A

No

72
Q

Aluminium hydroxide antacid

Mechanism of action

A

Forms AlCl in stomach + raises pH to 4 -> absorbs pepsin + binds bile
Increases phosphorus excretion (forms complexes) - useful as phosphate binding agent in renal impairment

73
Q

Magnesium (hydroxide + trisilicate) antacid

Mechanism of action

A

Forms magnesium chloride in the stomach

Mg2+ poorly absorbed from gut -> does not cause systemic alkalosis

74
Q

Aluminium hydroxide antacide

Side effects

A

Constipation/faecal impaction
Safe in pregnancy if renal fx normal
Can cause haemorrhoids

75
Q

Magnesium (hydroxide + trisilicate) antacid

Side effects

A 
Hypermagnesemia in severe renal impairment (accumulation)
N+V
Diarrhea
ECG changes
Respiratory depression
Safe in pregnancy
76
Q

Calcium antacid

Mechanism of action

A

Neutralises gastric acid + bonds phosphate

77
Q

Calcium antacid

Side effects

A

Rebound acid hypersecretion
Milk-alkali (Burnette) syndrome - hypercalcaemia causing metastatic calcification + renal failure
Bones, stones, groans + moans

78
Q

Burnett’s syndrome

A

A far-advanced milk-alkali syndrome due to long-standing calcium and alkali ingestion. It is characterised by severe hypercalcaemia, irreversible renal failure, and phosphate retention.
The patient is treated by withdrawal of excessive calcium and alkali intake.

79
Q

Mendelson’s syndrome

A

A chemical pneumonitis or aspiration pneumonitis caused by aspiration during anaesthesia, especially during pregnancy.
Aspiration contents may include gastric juice, blood, bile, water or an association of them.

80
Q

Sodium bicarbonate

Side effects

A

Systemic alkalosis

Belching + flatulence due to released CO2

81
Q

H.pylori therapy

A 
Triple therapy
- 7-14 day regimen for eradication therapy
- PPI plus 2 of the following
a) Clarithromycin 500mg bd
b) Amoxicillin 1g bd
c) Metronidazole 400mg bd
d) Tetracycline (resistance cases)
Continue the PPI for 1 month or until ulcer has healed

Quadruple therapy

  • if PPI contraindicated
  • Ranitidine 300mg daily for 7 days plus bismuth subcitrate 120mg 6hrly for 7 days plus 2 of the following
    a) Clarithromycin 500mg bd
    b) Amoxicillin 1g bd
    c) Metronidazole 400mg bd
    d) Tetracycline (resistance cases)

Pharmacology (32 decks)

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