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
Q

Do all the H2 Receptor Antagonists have similar half-lives?

A

Yes

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26
Q

What is / are the main route(s) of H2 receptor antagonist administration?

A
  1. Oral (main)

2. Intravenous (rapid anti-secretory effect for ZE syndrome

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27
Q

What are the adverse effects of H2 receptor antagonists?

A

Few adverse effects at doses used with current multi-drug therapies used to treat ulcers

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28
Q

How much of the H2 receptor antagonist drugs is metabolized by the liver?

A

10 to 35 percent

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29
Q

For how many hours are therapeutic levels of H2 receptor antagonist drugs maintained?

A

Up to 12 hours

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30
Q

Within how many hours do serum concentrations of H2 Receptor Antagonists peak?

A

1 to 3 hours

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31
Q

Within how many days of H2 receptor antagonists drugs is tolerance developed?

A

3 days

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32
Q

What occurs upon discontinuation of H2 receptor antagonist drugs?

A

Rebound response

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33
Q

“Common” Side-effects of H2 Receptor Antagonist Drugs affect what percentage of users?

A

Less then 3%

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34
Q

What are some common side effects of H2 Receptor Antagonist Drugs?

A
  1. Diarrhea
  2. Headache
  3. Drowsiness
  4. Fatigue
  5. Muscular pain
  6. Constipation
35
Q

What are some very rare side effects of H2 receptor antagonists?

A
  1. Confusion, delerium in the elderly
  2. Associated with thrombocytopenia
  3. Cimetidine anti-androgen effects
36
Q

What is the “most important” step in the histamine response?

A

The Hydrogen / Potassium ATPase pump (block that and you can block histamine)

37
Q

What type of drugs not only block the histamine respond but also the downstream effects of histamine?

A

Proton pump inhibitors

38
Q

How long is the half-life for H/K ATPase?

A

About 50 hours

39
Q

What do proton pumps have to do with circadian rhythm and what does this mean for the patient?

A

More pumps are synthesized at night and therefore more acid is released around breakfast

40
Q

What are the MOST potent suppressors of acid secretion?

A

Proton Pump Inhibitors (PPIs)

41
Q

By what percentage do proton pump inhibitors diminish basal and stimulated acid production?

A

About 80-95%

42
Q

How long do the effects of proton pump inhibitors last?

A

24-48 hours

43
Q

What are some common proton pump inhibitors?

A
  1. Omeprazole (Prilosec)
  2. Iansoprazole (Prevacid)
  3. Rebeprazole (Aciphex)
  4. Pantoprazole (Protonix)
44
Q

Where are proton pump inhibitors absorbed?

A

The small intestine

45
Q

Where are proton pump inhibitors converted from their pro-drug form into their active form?

A

Gastric parietal cell through a proton-catalyzed process (becomes frapped and cannot diffuse back across the membrane

46
Q

Do proton pump inhibitors bind reversibly or irreverisbly to inhibit the H/K ATPase pump?

A

Irreversibly

47
Q

Are proton pump inhibitors stable at low pH?

A

No, so they are supplied as enteric coated granules in gelatin capsule, or an enteric coated tablet

48
Q

When does acid secretion resume after administration of proton pump inhibitors?

A

When new molecules of pump are inserted in the parietal cell membrane (resulting in prolonged suppression for about 24-48 hours

49
Q

Why do PPIs require 2 to 5 days of once-a-day dosing to achieve 70% anti-secretory activity?

A

Not all pumps and parietal cells are functional at the same time during digestion

50
Q

PPIs are only activated when the pH decreases below what level?

A

4, which usually accurs with parietal cell activation after meals

51
Q

What are 5 “available” PPIs?

A
  1. Esomprazole (Nexium)
  2. Lansoprazole (Prevacid) (iv)
  3. Omeprazole (Prilosec, generic, OTC)
  4. Pantoprazole (Protonix) (iv)
  5. Rabeprazole (Aciphex)
52
Q

What are some common side effects of proton pump inhibitors?

A
  1. Headache
  2. Diarrhea
  3. Abdominal pain
  4. Constipation
    * B12 malabsorption reported with omeprazole
53
Q

Why would liver disease affect the dosage of Iansoprazole?

A

It reduces the clearance of iansoprazole

54
Q

What system in the liver metabolizes proton pump inhibitors?

A

The P450 system

55
Q

What PPIs interact with Warfarin?

A
  1. Esomeprazole
  2. Lansoprazole
  3. Omeprazole
  4. Rabeprazole
56
Q

What PPIs interact with Diazepam?

A
  1. Esomeprazole

2. Omeprazole

57
Q

How do prostaglandins prevent gastric injury?

A
  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
Q

How can NSAIDs induce an injury in the stomach?

A
  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
Q

What is the name of a methyl prostaglandin analog?

A

Misoprostol (Cytotec)

60
Q

What is the mechanism of action of misoprostal (cytotec)?

A
  1. Reduces basal gastric acid levels

2. Enhances bicarbonate and mucous levels in stomach

61
Q

What is the FDA indication for misoprostol (cytotec) prostaglandin analog?

A

Prevention of NSAID-induced gastric ulcers

62
Q

What are 2 unlabeled uses of misoprostol (cytotec) prostaglandin analog?

A
  1. Treatment of duodenal ulcers

2. Cervical ripening and labor induction for obstetrics

63
Q

What are adverse effects of misoprostol (cytotec) prostaglandin analog?

A
  1. Diarrhea
  2. Exacerbation of inflammatory bowel disease
  3. Abortifacient during pregnancy - contraindicated unless under strict birth control
64
Q

What are some side effects of anti-muscarinic drugs?

A
  1. Drowsiness, confusion and memory loss
  2. Dry mouth
  3. Constipation
  4. Urinary retention
  5. Tachycardia and tachyarrhtyhmias
65
Q

What is the mechanism of action of muscarinic antagonists?

A

Antagonism of muscarinic receptors on gastric parietal cells to reduce gastric acid release (Vagus X release ACh via PNS activation)

66
Q

What are some muscarinic antagonist drugs?

A
  1. Propantheline bromide
  2. Clinigium bromide (Quarzan)
  3. Methscopolamine bromide (Parnine)
  4. Belladonna Tincture
  5. Glycopyrrolate
  6. Atropine sulfate
67
Q

What is the mechanism of sucralfate (carafate)?

A
  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
Q

What are the FDA indications of Scuralfate?

A

Short-term treatment of duodenal ulcer, and preventative maintenance after hearing of ulcer

69
Q

What are some unlabeled uses of Sucralfate?

A
  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
Q

What are adverse effects of sucralfate?

A
  1. Constipation (due to 90% of the drug elimination being through the feces)
  2. Aluminum absorption burden in renal patient (excretion from kidneys)
71
Q

What is the mechanism of action of bismuth salts?

A
  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
Q

What are the effects of calcium carbonate?

A

Rapid, high neutralization, long duration

73
Q

How much calcium carbonate is absorbed?

A

About 15%, depending on formulation

74
Q

What are the effects of magnesium salts?

A

Rapid, high neutralization, moderate duration

75
Q

What are the side effects of magnesium salts?

A

Diarrhea, hypermagnesemia in renal disease

76
Q

What are the effects of aluminum salts?

A

Slow onset, low neutralization, long duration

77
Q

What are the side effects of aluminum salts?

A

Constipation, increased fecal phosphate elimination that could contribute to osteoporosis with extended use

78
Q

What is the effect of a “mixture” antacid?

A

Provides sustained effect with balanced effects on intestinal motility

79
Q

Who ingested a beaker of H Pylori resulting in gastritis?

A

Marshall

80
Q

Is H pylori gram negative or gram positive?

A

Gram negative

81
Q

How does H pylori lead to ulcers?

A

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
Q

What has been the most effective approach to eradicating H pylori infections?

A

Combinations of antibiotics and peptic ulcer drugs

83
Q

What are types of antibacterial combination therapies?

A
  1. Two-drug regimens
  2. Three-drug regimens
  3. Bismuth-based four-drug regimens