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Gastrointestinal System > Pharmacotherapy of GERD and PUD > Flashcards

Pharmacotherapy of GERD and PUD Flashcards

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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
What receptor does acetylcholine bind to?
M3 muscarinic receptors
26
What receptors does CCK bind to?
CCK2
27
What receptors does histamine bind to?
H2 receptors
28
What is the effect of acetylcholine, CCK and H2?
Through a Ca2+ or cAMP (histamine) pathway they increase the function of the proton pump (H+/K+ ATPase)
29
What receptor do prostaglandins bind to? How do they work?
EP3 and the inhibit the cAMP pathway and thus inhibit the proton pump, less HCl production
30
Which is the most efficient treatment for blocking the H+/K+ ATPase?
PPIs
31
What is the function of Clarythromycin?
Inhibits protein synthesis of H. pylori
32
What are the side effects of Clarythromycin?
Nausea, diarrhoea, and distortion of taste
33
What is FDA update for clarithromycin?
Increased risk of CV events and death in patients with CAD
34
What is the function of Amoxicillin?
Disrupts cell wall
35
When is the activity of Amoxicillin ideal?
When the pH is neutral; thus reducing gastric acidity will enhance its activity
36
What can be used to reduce the gastric acidity in combination with Amoxicillin?
Omeprazole
37
What are the side effects of Amoxicillin?
Diarrhea
38
What is the function of Metronidazole?
Degradation of biological macromolecules and DNA chains
39
Which is the antibiotic which 40% of H. pylori has become resistant to?
Metronidazole
40
What are the adverse effects of Metronidazole?
Nausea and headaches Metallic taste and some neurology effects (seizures)
41
What are the contraindications of Metronidazole?
Avoid alcohol consumption
42
What has caused the resistance of H. pylori to Metronidazole?
The misuse and the overuse
43
What is the function of Bismuth?
Acts topically to disrupt cell wall --> lysis of H. pylori
44
What are the side effects of Bismuth?
Harmless black coloration to the tongue and stool
45
What kind of inhibitor is Clarithromycin?
A very potent inhibitor of CYP3A4 and p-glycoprotein
46
What is the effect of taking Clarithromycin with drugs that prologs the QT interval?
Increase the risk of QT internal prolongation or tornadoes de pointes
47
What are the drug interactions of Metronidazole?
Inhibits CYP2C9 and may increase serum concentrations of drugs metabolised by this isozyme
48
What is an example of a drug metabolised by CYP2C9, and thus interacts with Metronidazole?
Warfarin
49
What are the first line regiments for eradicating H. pylori?
CLAR-based triple therapy 1 CLAR-based triple therapy 2 Bismuth-based quadruple therapy Sequential therapy
50
What is CLAR-based triple therapy 1?
Standard dose PPI, clarithromycin 500mg, amoxicillin 1g
51
What is the duration of CLAR-based triple therapy 1?
10 to 14 days
52
What is the eradication rates of CLAR-based triple therapy 1?
70 to 85%
53
Which patients are given CLAR-based triple therapy 1?
In non-penicillin-allergi, macrolide negative patients
54
What is CLAR-based triple therapy 2?
Standard dose of PPI, clarithromycin 500mg, metronidazole 500mg
55
What is the duration of CLAR-based triple therapy 2?
10 to 14 days
56
What is the eradication rate of CLAR-based triple therapy 2?
70 to 85%
57
When is CLAR-based triple therapy 2 used?
In penicillin-allergic patients who are macrolide negative or unable to tolerate bismuth quadruple therapy
58
What is the Bismuth-based quadruple therapy?
Bismuth 525mg, Metronidazole 250mg, Tetracycline 500mg, Ranitidine 150mg, standard dose of PPI
59
What is the duration of the Bismuth-based quadruple therapy?
10 to 14 days
60
What is the eradication rate of Bismuth-based quadruple therapy?
75 to 90%
61
When is quadruple therapy given?
In penicillin-allergic patients
62
What is sequential therapy?
PPI + amoxicillin 1mg followed by: Psi, clarithromycin 500mg, tinadazole 500mg
63
What is the duration of sequential therapy?
5 days each
64
What is the eradication rate of sequential therapy?
>90%
65
What are the comments regarding sequential therapy?
Required validation in North Africa
66
Which is the first line therapy now?
Bismuth-based quadruple therapy
67
What are the examples of H2R antagonists?
Cimetidine (Tagamet) Ranitidine (Zantac)
68
What are H2R antagonists used for?
PUD GERD Heartburn ZE syndrome
69
What are the side effects of of H2R antagonists?
Anti-androgenic effects Pneumonia
70
What are the ant-androgenic effects caused by H2R antagonists?
Gynecomastia and decreases libido, maybe impotence (reversible)
71
How and why is pneumonia an adverse effect of H2R antagonists?
When acidity of stomach decreases, chance of bacterial colonisation increases, resulting in secondary increase in colonisation of the respiratory tract
72
What is the effect of cimetidine on hepatic enzymes?
It inhibits P450
73
What are the drugs that you should pay attention to when giving Cimetidine?
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
What is the effect of antacids on absorption of cimetidine?
Decrease absorption that is why they have to be given 1 hour apart
75
What is the effect of H2R antagonists on serum concentration of drugs that require gastric acid?
It decreases the serum concentrations of drugs which require gastric acid for absorption, such as Itraconazole, Rilpivirine and Atazanavir
76
What are the examples of PPIs?
Omeprazole, Esomeprazole (Nexium), Rabeprazole, Lansoprazole, Dexlansoprazole, Pantoprazole
77
What is the function of the Omeprazole?
Irreversibly inhibits the H+/K+ ATPase Inhibit CYP2C19
78
What are the uses of Omeprazole?
Used for ulcers, GERD, acid hyper secretion
79
What is the function of Esomeprazole?
Nearly identical to omeprazole; however, it is metabolised less slowly --> longer-lasting effects compared to omeprazole Inhibit CYP2C19
80
What are the drug interactions of Omeprazole and Esomeprazole?
Reduces adverse and beneficial effects of clopidogrel (anti-platelet agent) Inhibition of CYP2C19 --> inhibition of conversion of clopidogrel to its active metabolite (Plavix)
81
In what kind of patients do you not give Omeprazole/ Esomeprazole as a PPI?
The ones who you prescribe Clopidogrel to You give alternative PPI
82
What is the function of Rabeprazole (Pariet)?
Reversible inhibits H+/K+ ATPase, effects are less durable Also has antibacterial effects (helps eradicate H. pylori)
83
How are PPIs metabolised?
Partially by CYP2C19
84
What happens if patients have very active CYP2C19?
May have a decreased response to PPI treatment
85
What are the PK of PPIs?
PPIs are a prodrug; enteric coating removed in the alkaline environment of the duodenum
86
What is the half-life of PPIs like?
Short serum half-lives but duration of action is longer than H2R antagonists, allowing for once a day use
87
What is the tolerance of PPIs like?
Unlike H2RAs, tolerance to PPIs does nit occur with continuous use
88
What are the side effects of PPIs?
Headache, nausea, diarrhoea (increased risk of C. difficile infection), abdominal pain, vomiting, pneumonia, fractures
89
What is long term PPI use associated with?
Hypomagnesia and vitamin B12 deficiency
90
What is the function of Sucralfate ?
Promotes ulcer ealing by creating a protective barrier against pepsin and acid
91
What is Sucralfate used for?
Acute therapy and maintenance therapy of duodenal ulcers Not as frequently used anymore
92
What is Misoprostol?
A prostaglandin E1 analogue
93
What is the function of Misoprostol?
Suppresses secretion of gastric acid, Promotes secretion of bicarbonate and mucus Maintains submucosal blood flow Prevents NSAID-induced ulcers
94
How does Misoprostol prevent NSAID-induced ulcers?
By serving as a replacement for endogenous prostaglandins
95
What are antacids?
Alkaline compounds that neutralise stomach acid
96
What are examples of antacids?
Al(OH)3 Mg(OH)2 Ca(CO)3 NaHCO3
97
In what cases are antacids used?
Peptic ulcers, GERD, heartburn
98
What is the margin of safety of antacids like?
Wide margin of safety
99
What are the effects of antacids?
Decrease destruction of the gut wall Reduces pepsin activity, if pH > 5 Enhances mucosal protection by stimulation production of prostaglandins
100
Which is the exception of antacids which is not poorly absorbed?
NaHCO3
101
What is the advantage of antacids being poorly absorbed?
Do not alter the pH
102
What are the adverse effects of antacids?
Al & Ca --> constipation Mg & Na --> diarrhoea
103
What are some precautions when using antacids?
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
Which drugs' absorption is affected by antacids?
Cimetidine and Ranitidine
105
What is Vonoprazan ?
Potassium-competitive acid blocker
106
Which diseases in Vonoprazan approved for?
Erosive and non-erosive GERD and heartburn
107
What are the side effects of Vonoprazan?
Indigestion Stomach upset Tenderness in stomach region Burning feeling in stomach or chest
108
How is Vonoprazan metabolized?
Mainly by CYP450, CYP3A4 and to some extent by CYP2B6, CYP2C19, CYP2D6, and SULT2A1
109
How is Vanoprazal eliminated?
In urine (67%) and feces (31%)

Gastrointestinal System (29 decks)

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