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GI Acid (Akbareli) Flashcards

1
Q

What is the pH at which dental enamel erodes?

A

5.5

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2
Q

What is the pH of stomach acid?

A

2.0

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3
Q

What are some causative agents of ulcers?

A
  1. Acid
  2. Pepsin
  3. Drugs (NSAIDS)
  4. H Pylori
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4
Q

What are some defense mechanisms to prevent ulcers?

A
  1. Mucus
  2. Bicarbonate
  3. Blood flow
  4. Prostaglandins
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5
Q

What are the two goals of acid prevention?

A
  1. Enhance host defense

2. Eliminate causative factors

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6
Q

What 3 types of problems do acid suppression therapy address?

A
  1. GERD
  2. Peptic Ulcers (due to NSAIDS)
  3. Duodenal and peptic ulcers (due to H Pylori)
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7
Q

Did the incidence of peptic ulcer disease increase or decrease during the 20th century?

A

Decreased (lower infection rates with H pylori)

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8
Q

Did the incidence of gastroesophageal reflux disease increase or decrease in the 20th century?

A

Increased (major gastric acid-related disorders)

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9
Q

Who discovered the H2 receptor?

A

Sir James Black, a scottish pharmacologist

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10
Q

How was the H2 receptor discovered?

A

By modifying the structure of histamine to Cimetidine

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11
Q

Histamine stimulates contraction of what type of muscle?

A

Smooth

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12
Q

What blocks histamine?

A

Mepyramine

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13
Q

What are some actions of histamine?

A
  1. Stimulates acid secretion
  2. Increase HR
  3. Inhibits contraction of rat uterus 9not blocked by mepyramine)
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14
Q

Where is histamine produced?

A

Enterochromaffin cells

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15
Q

What stimulates enterochromaffin cells to release histamine?

A
  1. Cholecystokinin receptors are stimulated by gastrin (from the endocrine system)
  2. Muscarinic receptors are stimulated by acetylcholine (vagus X neuronal system) to release histamine
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16
Q

How are gastric parietal cells activated to release gastric acid (three step process)?

A
  1. Histamine activates H2 receptors (GPCR)
  2. cAMP increases
  3. H/K ATPase pumps activated
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17
Q

What is the main mechanism of action of H2 Receptor Antagonists?

A

Competitively antagonize H2 receptors on parietal cells by preventing the action of the H/K ATPase pumps

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18
Q

What are three common forms of peptic ulcers?

A
  1. Helicobacter pylori-associated
  2. Non-steroidal anti-inflammatory drug-induced
  3. Stress-related mucosal damage (SRMD) - critically ill hospitalized patients
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19
Q

What are some lesson common causes of peptic ulcers?

A
  1. Zollinger-Ellison syndrome
  2. Radiation
  3. Chemotherapy
  4. Vascular insufficiency
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20
Q

What are 3 ways peptic ulcers may be treated?

A
  1. Reduce gastric acid secretion from parietal cells
  2. Providing a barrier over the lesion itself, or by stimulating endogenous mucopeptide formation
  3. Eradicating the bacterium Helicobacter pylori
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21
Q

What are some common H2 Receptor Antagonists?

A
  1. Cimetidine (Tagamet)
  2. Ranitidine (Zantac)
  3. Famotidine (Pepcid)
  4. Nizatidine (Axid)
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22
Q

What are FDA indications for H2 Receptor Antagonists?

A
  1. Treatment of gastric ulcer
  2. Duodenal ulcer
  3. Gastroesophageal reflux disease (GERD)
  4. Pathological hypersecretory conditions (e.g. Zollinger-Ellison Syndrome)
  5. Heartburn / avid indigestion / sour stomach - OTC
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23
Q

What are 2 unlabeled uses of H2 Receptor Antagonists?

A
  1. Part of multi-drug regimen to eradicate Helicobacter pylori in the treatment of peptic ulcer
  2. Prevention of NSAID-induced gastric damage
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24
Q

How are the H2 receptor antagonists mainly excreted?

A

In the kidney

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25
Do all the H2 Receptor Antagonists have similar half-lives?
Yes
26
What is / are the main route(s) of H2 receptor antagonist administration?
1. Oral (main) | 2. Intravenous (rapid anti-secretory effect for ZE syndrome
27
What are the adverse effects of H2 receptor antagonists?
Few adverse effects at doses used with current multi-drug therapies used to treat ulcers
28
How much of the H2 receptor antagonist drugs is metabolized by the liver?
10 to 35 percent
29
For how many hours are therapeutic levels of H2 receptor antagonist drugs maintained?
Up to 12 hours
30
Within how many hours do serum concentrations of H2 Receptor Antagonists peak?
1 to 3 hours
31
Within how many days of H2 receptor antagonists drugs is tolerance developed?
3 days
32
What occurs upon discontinuation of H2 receptor antagonist drugs?
Rebound response
33
"Common" Side-effects of H2 Receptor Antagonist Drugs affect what percentage of users?
Less then 3%
34
What are some common side effects of H2 Receptor Antagonist Drugs?
1. Diarrhea 2. Headache 3. Drowsiness 4. Fatigue 5. Muscular pain 6. Constipation
35
What are some very rare side effects of H2 receptor antagonists?
1. Confusion, delerium in the elderly 2. Associated with thrombocytopenia 3. Cimetidine anti-androgen effects
36
What is the "most important" step in the histamine response?
The Hydrogen / Potassium ATPase pump (block that and you can block histamine)
37
What type of drugs not only block the histamine respond but also the downstream effects of histamine?
Proton pump inhibitors
38
How long is the half-life for H/K ATPase?
About 50 hours
39
What do proton pumps have to do with circadian rhythm and what does this mean for the patient?
More pumps are synthesized at night and therefore more acid is released around breakfast
40
What are the MOST potent suppressors of acid secretion?
Proton Pump Inhibitors (PPIs)
41
By what percentage do proton pump inhibitors diminish basal and stimulated acid production?
About 80-95%
42
How long do the effects of proton pump inhibitors last?
24-48 hours
43
What are some common proton pump inhibitors?
1. Omeprazole (Prilosec) 2. Iansoprazole (Prevacid) 3. Rebeprazole (Aciphex) 4. Pantoprazole (Protonix)
44
Where are proton pump inhibitors absorbed?
The small intestine
45
Where are proton pump inhibitors converted from their pro-drug form into their active form?
Gastric parietal cell through a proton-catalyzed process (becomes frapped and cannot diffuse back across the membrane
46
Do proton pump inhibitors bind reversibly or irreverisbly to inhibit the H/K ATPase pump?
Irreversibly
47
Are proton pump inhibitors stable at low pH?
No, so they are supplied as enteric coated granules in gelatin capsule, or an enteric coated tablet
48
When does acid secretion resume after administration of proton pump inhibitors?
When new molecules of pump are inserted in the parietal cell membrane (resulting in prolonged suppression for about 24-48 hours
49
Why do PPIs require 2 to 5 days of once-a-day dosing to achieve 70% anti-secretory activity?
Not all pumps and parietal cells are functional at the same time during digestion
50
PPIs are only activated when the pH decreases below what level?
4, which usually accurs with parietal cell activation after meals
51
What are 5 "available" PPIs?
1. Esomprazole (Nexium) 2. Lansoprazole (Prevacid) (iv) 3. Omeprazole (Prilosec, generic, OTC) 4. Pantoprazole (Protonix) (iv) 5. Rabeprazole (Aciphex)
52
What are some common side effects of proton pump inhibitors?
1. Headache 2. Diarrhea 3. Abdominal pain 4. Constipation * B12 malabsorption reported with omeprazole
53
Why would liver disease affect the dosage of Iansoprazole?
It reduces the clearance of iansoprazole
54
What system in the liver metabolizes proton pump inhibitors?
The P450 system
55
What PPIs interact with Warfarin?
1. Esomeprazole 2. Lansoprazole 3. Omeprazole 4. Rabeprazole
56
What PPIs interact with Diazepam?
1. Esomeprazole | 2. Omeprazole
57
How do prostaglandins prevent gastric injury?
1. Stimulate secretion of mucous and bicarbonate in superficial epithelial cells and by increasing mucosal blood flow 2. Inhibit acid production by binding the EP3 receptor on parietal cells
58
How can NSAIDs induce an injury in the stomach?
1. Systemic and localized inhibition of COX-1 which decreases regulation of acid release and decrease mucous and bicarbonate secretion 2. Aspirin and NSAIDs can directly injure or irritate the stomach lining
59
What is the name of a methyl prostaglandin analog?
Misoprostol (Cytotec)
60
What is the mechanism of action of misoprostal (cytotec)?
1. Reduces basal gastric acid levels | 2. Enhances bicarbonate and mucous levels in stomach
61
What is the FDA indication for misoprostol (cytotec) prostaglandin analog?
Prevention of NSAID-induced gastric ulcers
62
What are 2 unlabeled uses of misoprostol (cytotec) prostaglandin analog?
1. Treatment of duodenal ulcers | 2. Cervical ripening and labor induction for obstetrics
63
What are adverse effects of misoprostol (cytotec) prostaglandin analog?
1. Diarrhea 2. Exacerbation of inflammatory bowel disease 3. Abortifacient during pregnancy - contraindicated unless under strict birth control
64
What are some side effects of anti-muscarinic drugs?
1. Drowsiness, confusion and memory loss 2. Dry mouth 3. Constipation 4. Urinary retention 5. Tachycardia and tachyarrhtyhmias
65
What is the mechanism of action of muscarinic antagonists?
Antagonism of muscarinic receptors on gastric parietal cells to reduce gastric acid release (Vagus X release ACh via PNS activation)
66
What are some muscarinic antagonist drugs?
1. Propantheline bromide 2. Clinigium bromide (Quarzan) 3. Methscopolamine bromide (Parnine) 4. Belladonna Tincture 5. Glycopyrrolate 6. Atropine sulfate
67
What is the mechanism of sucralfate (carafate)?
1. When pH goes below 4, aluminum is released and it forms a viscous gel that adheres to epithelial cells and ulcer craters 2. Inhibits the breakdown of mucosal proteins by pepsin
68
What are the FDA indications of Scuralfate?
Short-term treatment of duodenal ulcer, and preventative maintenance after hearing of ulcer
69
What are some unlabeled uses of Sucralfate?
1. Acelreated healing of gastric ulcers 2. Long-term treatment of gastric ulcers 3. Treatment of NSAID-and aspirin-induced mucosal damage 4. Prevention of stress ulcers and GI bleeding in critically ill patients 5. May be useful in prophylaxis of stress ulcers
70
What are adverse effects of sucralfate?
1. Constipation (due to 90% of the drug elimination being through the feces) 2. Aluminum absorption burden in renal patient (excretion from kidneys)
71
What is the mechanism of action of bismuth salts?
1. Forms an insoluble complex at pH below 3.5 with possible gastroprotective effects 2. May stimulate prostaglandin formation 3. May suppress H pylori growth
72
What are the effects of calcium carbonate?
Rapid, high neutralization, long duration
73
How much calcium carbonate is absorbed?
About 15%, depending on formulation
74
What are the effects of magnesium salts?
Rapid, high neutralization, moderate duration
75
What are the side effects of magnesium salts?
Diarrhea, hypermagnesemia in renal disease
76
What are the effects of aluminum salts?
Slow onset, low neutralization, long duration
77
What are the side effects of aluminum salts?
Constipation, increased fecal phosphate elimination that could contribute to osteoporosis with extended use
78
What is the effect of a "mixture" antacid?
Provides sustained effect with balanced effects on intestinal motility
79
Who ingested a beaker of H Pylori resulting in gastritis?
Marshall
80
Is H pylori gram negative or gram positive?
Gram negative
81
How does H pylori lead to ulcers?
Produces urease, leading to the formation of CO2 and NH3 which neutralizes the acidic environment. Ammonia is toxic to epithelial cells and leads to ulcers.
82
What has been the most effective approach to eradicating H pylori infections?
Combinations of antibiotics and peptic ulcer drugs
83
What are types of antibacterial combination therapies?
1. Two-drug regimens 2. Three-drug regimens 3. Bismuth-based four-drug regimens

xD3 Pharm Exam 3 (8 decks)

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