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Gastrointestinal System > Pharmacotherapy of GERD and PUD > Flashcards

Pharmacotherapy of GERD and PUD Flashcards

1
Q

What are the classic symptoms of GERD?

A

Heartburn and regurgitation

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2
Q

What are other symptoms of GERD?

A

Dyspepsia,
Chest pain,
Belching,
Chronic cough

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3
Q

What are the standard treatments for GERD?

A

Medications that suppress gastric acid

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4
Q

What is the most common cause of PUD?

A

H. pylori

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5
Q

What are other causes for PUD?

A

Use of NSAIDs, including aspirin
Bile reflux

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6
Q

What is the treatment for healing the ulcers themselves?

A

PPI for ulcer healing

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7
Q

What is the function of parietal cells?

A

They are the “factory of H+”

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8
Q

What is the direct way of regulating acid secretion?

A

Acetylcholine, gastrin, and histamine stimulate the parietal cells, triggering the secretion of H+ into the lumen

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9
Q

What is the indirect way of regulation acid secretion?

A

Acetylcholine and gastrin also stimulate the ECL cell, resulting in the secretion of histamine which then acts on the parietal cells

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10
Q

What is the etiopathogenesis of peptic ulcer?

A

PUD: chronic mucosal ulceration affecting mostly the duodenum or stomach

It can occur in any part of the GIT

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11
Q

What is the function of the tubulovesicular structures?

A

Increase the apical surface, for instance allowing more space for the cell to produce HCl

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12
Q

What are the aggressive factors of peptic ulcers?

A

H. pylori
NSAIDs
Gastric acid
Pepsin
Smoking

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13
Q

What are the defensive factors of peptic ulcers?

A

Mucus
Bicarbonate
Blood flow
Prostaglandins

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14
Q

What is mucus and how is it a defensive factor?

A

It is a barrier that protects underlying cells from acid and pepsin, mucus is also an alkaline

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15
Q

What is bicarbonate and how is it a defensive factor?

A

Mostly remain trapped in the mucus where it neutralises the H+ (in duodenum, neutralises stomach acid)

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16
Q

What is blood flow and how is it a defensive factor?

A

Ischemia leads to injury, increasing vulnerability to acid and pepsin

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17
Q

What are prostaglandins and how is it a defensive factor?

A

They stimulate to secretion of mucus and bicarbonate and promote vasodilation, also suppresses acid secretion

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18
Q

What is H. pylori and why is it an aggressive factor?

A

It is a gram (-) bacteria which resides between epithelial cells and the mucus barrier

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19
Q

What are NSAIDs and why are they an aggressive factor?

A

They inhibit synthesis of prostaglandins

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20
Q

What is gastric acid and how is it an aggressive factor?

A

An absolute requirement for ulcer generation, however, not sufficient by itself to cause ulcers

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21
Q

What is pepsin and why is it an aggressive factor?

A

Can injure unprotected cells

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22
Q

What is smoking and how is it an aggressive factor?

A

Delays ulcer healing and increase the risk of recurrence

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23
Q

What is the classes of anti-ulcer dugs?

A

Antibiotics
Anti-secretory agents
Mucosal protectants
Antacids
Antisecretory agents that enhance mucosal defence

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24
Q

What are the examples of antibiotics?

A

Clarithromycin, Amoxicillin, Metronidazole, Bismuth

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25
Q

What receptor does acetylcholine bind to?

A

M3 muscarinic receptors

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26
Q

What receptors does CCK bind to?

A

CCK2

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27
Q

What receptors does histamine bind to?

A

H2 receptors

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28
Q

What is the effect of acetylcholine, CCK and H2?

A

Through a Ca2+ or cAMP (histamine) pathway they increase the function of the proton pump (H+/K+ ATPase)

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29
Q

What receptor do prostaglandins bind to? How do they work?

A

EP3 and the inhibit the cAMP pathway and thus inhibit the proton pump, less HCl production

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30
Q

Which is the most efficient treatment for blocking the H+/K+ ATPase?

A

PPIs

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31
Q

What is the function of Clarythromycin?

A

Inhibits protein synthesis of H. pylori

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32
Q

What are the side effects of Clarythromycin?

A

Nausea, diarrhoea, and distortion of taste

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33
Q

What is FDA update for clarithromycin?

A

Increased risk of CV events and death in patients with CAD

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34
Q

What is the function of Amoxicillin?

A

Disrupts cell wall

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35
Q

When is the activity of Amoxicillin ideal?

A

When the pH is neutral; thus reducing gastric acidity will enhance its activity

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36
Q

What can be used to reduce the gastric acidity in combination with Amoxicillin?

A

Omeprazole

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37
Q

What are the side effects of Amoxicillin?

A

Diarrhea

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38
Q

What is the function of Metronidazole?

A

Degradation of biological macromolecules and DNA chains

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39
Q

Which is the antibiotic which 40% of H. pylori has become resistant to?

A

Metronidazole

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40
Q

What are the adverse effects of Metronidazole?

A

Nausea and headaches
Metallic taste and some neurology effects (seizures)

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41
Q

What are the contraindications of Metronidazole?

A

Avoid alcohol consumption

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42
Q

What has caused the resistance of H. pylori to Metronidazole?

A

The misuse and the overuse

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43
Q

What is the function of Bismuth?

A

Acts topically to disrupt cell wall –> lysis of H. pylori

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44
Q

What are the side effects of Bismuth?

A

Harmless black coloration to the tongue and stool

45
Q

What kind of inhibitor is Clarithromycin?

A

A very potent inhibitor of CYP3A4 and p-glycoprotein

46
Q

What is the effect of taking Clarithromycin with drugs that prologs the QT interval?

A

Increase the risk of QT internal prolongation or tornadoes de pointes

47
Q

What are the drug interactions of Metronidazole?

A

Inhibits CYP2C9 and may increase serum concentrations of drugs metabolised by this isozyme

48
Q

What is an example of a drug metabolised by CYP2C9, and thus interacts with Metronidazole?

A

Warfarin

49
Q

What are the first line regiments for eradicating H. pylori?

A

CLAR-based triple therapy 1
CLAR-based triple therapy 2
Bismuth-based quadruple therapy
Sequential therapy

50
Q

What is CLAR-based triple therapy 1?

A

Standard dose PPI, clarithromycin 500mg, amoxicillin 1g

51
Q

What is the duration of CLAR-based triple therapy 1?

A

10 to 14 days

52
Q

What is the eradication rates of CLAR-based triple therapy 1?

A

70 to 85%

53
Q

Which patients are given CLAR-based triple therapy 1?

A

In non-penicillin-allergi, macrolide negative patients

54
Q

What is CLAR-based triple therapy 2?

A

Standard dose of PPI, clarithromycin 500mg, metronidazole 500mg

55
Q

What is the duration of CLAR-based triple therapy 2?

A

10 to 14 days

56
Q

What is the eradication rate of CLAR-based triple therapy 2?

A

70 to 85%

57
Q

When is CLAR-based triple therapy 2 used?

A

In penicillin-allergic patients who are macrolide negative or unable to tolerate bismuth quadruple therapy

58
Q

What is the Bismuth-based quadruple therapy?

A

Bismuth 525mg, Metronidazole 250mg, Tetracycline 500mg, Ranitidine 150mg, standard dose of PPI

59
Q

What is the duration of the Bismuth-based quadruple therapy?

A

10 to 14 days

60
Q

What is the eradication rate of Bismuth-based quadruple therapy?

A

75 to 90%

61
Q

When is quadruple therapy given?

A

In penicillin-allergic patients

62
Q

What is sequential therapy?

A

PPI + amoxicillin 1mg followed by: Psi, clarithromycin 500mg, tinadazole 500mg

63
Q

What is the duration of sequential therapy?

A

5 days each

64
Q

What is the eradication rate of sequential therapy?

A

> 90%

65
Q

What are the comments regarding sequential therapy?

A

Required validation in North Africa

66
Q

Which is the first line therapy now?

A

Bismuth-based quadruple therapy

67
Q

What are the examples of H2R antagonists?

A

Cimetidine (Tagamet)
Ranitidine (Zantac)

68
Q

What are H2R antagonists used for?

A

PUD
GERD
Heartburn
ZE syndrome

69
Q

What are the side effects of of H2R antagonists?

A

Anti-androgenic effects
Pneumonia

70
Q

What are the ant-androgenic effects caused by H2R antagonists?

A

Gynecomastia and decreases libido, maybe impotence (reversible)

71
Q

How and why is pneumonia an adverse effect of H2R antagonists?

A

When acidity of stomach decreases, chance of bacterial colonisation increases, resulting in secondary increase in colonisation of the respiratory tract

72
Q

What is the effect of cimetidine on hepatic enzymes?

A

It inhibits P450

73
Q

What are the drugs that you should pay attention to when giving Cimetidine?

A

Warfarin, phenytoin, theophylline and lidocaine –> all have a narrow therapeutic index

If the therapeutic window is narrow and you increase the concentration –> more likely to have adverse and toxic effects

74
Q

What is the effect of antacids on absorption of cimetidine?

A

Decrease absorption that is why they have to be given 1 hour apart

75
Q

What is the effect of H2R antagonists on serum concentration of drugs that require gastric acid?

A

It decreases the serum concentrations of drugs which require gastric acid for absorption, such as Itraconazole, Rilpivirine and Atazanavir

76
Q

What are the examples of PPIs?

A

Omeprazole,
Esomeprazole (Nexium),
Rabeprazole,
Lansoprazole,
Dexlansoprazole,
Pantoprazole

77
Q

What is the function of the Omeprazole?

A

Irreversibly inhibits the H+/K+ ATPase
Inhibit CYP2C19

78
Q

What are the uses of Omeprazole?

A

Used for ulcers, GERD, acid hyper secretion

79
Q

What is the function of Esomeprazole?

A

Nearly identical to omeprazole; however, it is metabolised less slowly –> longer-lasting effects compared to omeprazole

Inhibit CYP2C19

80
Q

What are the drug interactions of Omeprazole and Esomeprazole?

A

Reduces adverse and beneficial effects of clopidogrel (anti-platelet agent)

Inhibition of CYP2C19 –> inhibition of conversion of clopidogrel to its active metabolite (Plavix)

81
Q

In what kind of patients do you not give Omeprazole/ Esomeprazole as a PPI?

A

The ones who you prescribe Clopidogrel to
You give alternative PPI

82
Q

What is the function of Rabeprazole (Pariet)?

A

Reversible inhibits H+/K+ ATPase, effects are less durable
Also has antibacterial effects (helps eradicate H. pylori)

83
Q

How are PPIs metabolised?

A

Partially by CYP2C19

84
Q

What happens if patients have very active CYP2C19?

A

May have a decreased response to PPI treatment

85
Q

What are the PK of PPIs?

A

PPIs are a prodrug; enteric coating removed in the alkaline environment of the duodenum

86
Q

What is the half-life of PPIs like?

A

Short serum half-lives but duration of action is longer than H2R antagonists, allowing for once a day use

87
Q

What is the tolerance of PPIs like?

A

Unlike H2RAs, tolerance to PPIs does nit occur with continuous use

88
Q

What are the side effects of PPIs?

A

Headache, nausea, diarrhoea (increased risk of C. difficile infection), abdominal pain, vomiting, pneumonia, fractures

89
Q

What is long term PPI use associated with?

A

Hypomagnesia and vitamin B12 deficiency

90
Q

What is the function of Sucralfate ?

A

Promotes ulcer ealing by creating a protective barrier against pepsin and acid

91
Q

What is Sucralfate used for?

A

Acute therapy and maintenance therapy of duodenal ulcers

Not as frequently used anymore

92
Q

What is Misoprostol?

A

A prostaglandin E1 analogue

93
Q

What is the function of Misoprostol?

A

Suppresses secretion of gastric acid,
Promotes secretion of bicarbonate and mucus
Maintains submucosal blood flow
Prevents NSAID-induced ulcers

94
Q

How does Misoprostol prevent NSAID-induced ulcers?

A

By serving as a replacement for endogenous prostaglandins

95
Q

What are antacids?

A

Alkaline compounds that neutralise stomach acid

96
Q

What are examples of antacids?

A

Al(OH)3
Mg(OH)2
Ca(CO)3
NaHCO3

97
Q

In what cases are antacids used?

A

Peptic ulcers, GERD, heartburn

98
Q

What is the margin of safety of antacids like?

A

Wide margin of safety

99
Q

What are the effects of antacids?

A

Decrease destruction of the gut wall
Reduces pepsin activity, if pH > 5
Enhances mucosal protection by stimulation production of prostaglandins

100
Q

Which is the exception of antacids which is not poorly absorbed?

A

NaHCO3

101
Q

What is the advantage of antacids being poorly absorbed?

A

Do not alter the pH

102
Q

What are the adverse effects of antacids?

A

Al & Ca –> constipation
Mg & Na –> diarrhoea

103
Q

What are some precautions when using antacids?

A

Some contain substantial amounts of sodium, avoid in patients with hypertension or CHF

Do not use Ca2+ with renal calculi

By raising gastric pH, they reduce the absorption of many drugs, allow for 1 between them

104
Q

Which drugs’ absorption is affected by antacids?

A

Cimetidine and Ranitidine

105
Q

What is Vonoprazan ?

A

Potassium-competitive acid blocker

106
Q

Which diseases in Vonoprazan approved for?

A

Erosive and non-erosive GERD and heartburn

107
Q

What are the side effects of Vonoprazan?

A

Indigestion
Stomach upset
Tenderness in stomach region
Burning feeling in stomach or chest

108
Q

How is Vonoprazan metabolized?

A

Mainly by CYP450, CYP3A4 and to some extent by CYP2B6, CYP2C19, CYP2D6, and SULT2A1

109
Q

How is Vanoprazal eliminated?

A

In urine (67%) and feces (31%)

Gastrointestinal System (29 decks)

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