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Block D - Digestion and Metabolism > Pharmacology -- Antacids, motility and anti-motiliy agents > Flashcards

Pharmacology -- Antacids, motility and anti-motiliy agents Flashcards

1
Q

3 treatments for ulcers

A
  • Proton pump inhibitors
  • H2 receptor blockers
  • Antacids
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2
Q

5 treatable GIT conditions

A
  • Reflux esophagitis
  • Peptic ulcers
  • Delayed gastric emptying
  • Inadequate propulsion of chyme
  • Infections and inflammations
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3
Q

How are peptic ulcers formed?

A

Imbalance favoring the acid pepsin aggression vs. mucosal defense

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4
Q

Describe how helicobacter pylori infection contributes to the formation of peptic ulcers

A
  • Gastrin is a hormone that promotes acid secretion in the stomach
  • Ordinarily, increase HCl inhibits the production of gastrin
  • H. pylori blocks the inhibition of gastrin and instead allows gastrin to keep increasing stomach pH
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5
Q

5 drug targets in ulcer therapy

A
  • Neutralizing acids with antacids
  • H2 receptor blockers (cimetidine, ranitidine)
  • M1 M3 blockers (propantheline)
  • Adenylyl cyclase inhibitors
  • H+/K+ ATPase pump blockers
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6
Q

2 H2 (histamine) receptor blockers

A
  • Cimetidine
  • Ranitidine
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7
Q

3 disadvantages of cimetidine

A
  • Short duration of action
  • Interaction with p450 enzymes
  • Anti-androgenic effects
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8
Q

Alternative to cimetidine

A

Ranitidine (also an H2 receptor blocker)

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9
Q

3 advantages to using ranitidine as an alternative to cimetidine

A
  • Longer duration of action
  • No p450 interactions
  • Weaker anti-adrogenic effects
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10
Q

What is emoprazole

A

An irreversible inactivtor of the H+/K+ pump

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11
Q

Why is it that omeprazole only blocks the H+/K+ pump in the stomach and not anywhere else in the body that needs it?

A
  • Target dependent
  • Can only be activated by low pH
  • i.e. it is a prodrug activated by low pH
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12
Q

Why is it that many NSAIDs are accompanied by omeprazole?

A

NSAIDs are known to cause bleeding and ulcers, so omeprazole is used as an adjunct to prevent damage to the stomach due to its long duration of action

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13
Q

Side effect of omeprazole

A

Gastric mucosal hyperplasia

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14
Q

Possible mechanism for the side effect of omeprazole

A

Excessive gastrin secretion

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15
Q

Mechanisms of action of antacids

A
  • Neutralization of intragastric HCl
  • Increase in intragastric pH

leads to

  • Reduction of pepsin activity
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16
Q

Systemic antacid

A

Sodium bicarbonate

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17
Q

Adverse effect of systemic antacids

A

Increase in blood pH

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18
Q

3 nonsystemic antacids

A
  • Calcium
  • Magnesion
  • Aluminum
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19
Q

Problem with nonsystemic antacids

A

Poorly absorbed

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20
Q

Therapeutic effects of antacids

A

Effective management of peptic ulcers

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21
Q

Disadvatanges of antacids

A
  • Frequent dosing required
  • Disagreeable taste
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22
Q

2 properties of sodium and potassium antacids

A
  • Rapid onset
  • Short duration of action
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23
Q

3 properties of calcium antacids

A
  • Rapid onset
  • Long duration of action
  • Limited effect on pH
24
Q

3 properties of magnesium antacids

A
  • Rapid onset
  • Large effect on pH
  • Laxative
25
Q

2 properties of aluminum antacids

A
  • Slow onset
  • Constipative
26
Q

What is sucralfate?

A

A mucosa protecting drug

27
Q

Explain the mechanism of sucralfate

A
  • Complexes with protein at ulcer site to form a protective layer
  • Binds to pepsin
28
Q

Describe the effects of reflux esophagitis (i.e. the series of events)

A
  1. Inappropriate relaxation of the lower esophageal sphincter
  2. Flow og gastric content into esophagus
  3. Irritation and inflammation of mucosa
29
Q

2 ways to intervene in reflux esophagitis

A

Intervene at the following events:

  • Inappropriate relaxation of LES (by increasing its tone)
  • Flow of gastric content into esophagus (by countering acidity with antacids)
30
Q

Describe the series of events in gastroparesis

A
  1. Damage to gastric nerve or smooth muscle (diabetes)
  2. Delay in gastric emptying
31
Q

How to intervene in the event of gastroparesis

A

Prokinetic drugs to counteract effects of damage to nerves or smooth muscle

32
Q

3 adverse effects of cholinergic drugs

A
  • Stimulation of salivary, gastric, pancreatic and intestinal secretions
  • No coordination of gastroduodenal contraction
  • Cardiac and asthma conditions could be exacerbated
33
Q

5 effects of D2 receptor antagonists

A
  • Block inhibitory presynaptic D2 receptor
  • Increase lower sphincter tone
  • Increase force of gastric contraction
  • Increase coordination of gastroduodenal coordination
  • Increase gastric emptying
34
Q

2 side effects of D2 antagonists

A
  • Parkinson-like side effects
  • Increase in prolactin levels and breast tenderness (gynecomastia, galactorhea)
35
Q

3 effects of 5HT4 agonists

A
  • Increase lower sphincter tone
  • Increase gastroduodenal coordination
  • Increase gastric contractions
36
Q

2 types of activity that ondansteron has

A
  • 5HT3 antagonistic activity
  • Antiemetic acitivity
37
Q

3 causes of constipation

A
  • Functinoal disorders
  • Drug treatments
  • Low residue diets
38
Q

2 causes of diarrhea

A
  • Bacterial or viral infection
  • Chronic inflammatory disease
39
Q

Drug type to treat constipation

A

Laxatives

40
Q

Drug type to treat diarrhea

A

Anti-diarrheal

41
Q

4 laxative mechnisms of action

A
  • Secretory or stimulant
  • Saline
  • Emollient
  • Bulk forming
42
Q

What is castor oil

A

Secretory laxative

43
Q

Mechanisms of castor oil (secretory laxative) action

A
  1. Increased prostaglandins and adenylate cyclase
  2. Increased Cl channels
  3. Increased fluid accumulation
  4. Increased fluid flow and peristalsis

NOTE: Other mechanism = inhibition of water reabsorption in lower intestine

44
Q

2 bulk-forming agents

A

Bran

Psyllium husk

45
Q

Mechanism of action of bulk forming agents

A
  1. Formation of large hydrophilic mass
  2. Increased bulk and water content
  3. Decreased intestinal transit time
  4. Decreased viscosity of luminal content
  5. Increased flow through bowel
46
Q

3 saline laxatives

A
  • Magnesium hydroxide
  • Sodium phosphate
  • Sodium sulfate
47
Q

Mechanism of saline laxatives

A

Drawing water into intestine by osmotic process

48
Q

4 disadvantages of laxatives

A
  • Lead to habituation
  • Damage to myenteric plexus
  • Colonic atony
  • Excessive loss of Ca++
49
Q

Therapeutic priorities in the treatment of constipation

A
  1. Increase fiber in diets and increase fluids
  2. Bulk agents
  3. Osmotic laxatives
  4. Stimulants
50
Q

3 antidiarrheal drugs

A
  • Opioids
  • Morphine
  • Codeine
51
Q

3 mechanisms of antidiarrheal drugs

A
  • Act on interstinal neurons –> increased absorption and reduced fluid secretion
  • Act on CNS
  • Alter pattern of motility to increase resistance to flow
52
Q

What are the motility alterations made by anti-diarrheal drugs?

A
  • Increased segmental contraction
  • Decreased propulsive contractions
53
Q

Mechanism of anti-diarrheal morphine and codeine

A
  • Motility alterations
    • Increased segmental contractions
    • Decreased propulsive contractions
  • Cross the blood brain barrier –> exhibit both CNS and local action
54
Q

2 advantages of using loperamide and diphenoxylate as anti-diarheal agents as opposed to morphine and codeine

A
  • No CNS effects
  • Low abuse potential
55
Q

When should opioids not be used in the treatment of diarrhea?

A

When the diarrhea is induced by enteric infections

56
Q

3 types of prokinetic drugs

A
  • Cholinergic drugs
  • D2 receptor antagonists
  • 5HT4 agonists

Block D - Digestion and Metabolism (29 decks)

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