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Cology 2 Exam 4 > GI Pharmacology 1 > Flashcards

GI Pharmacology 1 Flashcards

1
Q

What are the three bases of therapy for acid-peptic disease?

A

Neutralize excess acid
Reduce gastric acid secretion
Enhance gastric mucous defense

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2
Q

How do we neutralize excess acid?

A

Antacids

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3
Q

How do antacids work?

A

They neutralize acid directly in the stomach

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4
Q

How are different antacids different from eachother?

A

They have different neutralizing capacity, different solubilities, and different palatability

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5
Q

Describe sodium bicarbonate

A

Baking soda
Quickly neutralizes acid
Produces sodium and alkali load
Can cause fluid retention, produce gas (belching)
Increased pH will increase gastrin release

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6
Q

Describe calcium carbonate

A 
Works rapidly
Moderate neutralizing ability
CaCl2 - absorb 10-15%
Increased kidney pH can cause kidney stones
May induce rebound acid secretion
Can cause constipation
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7
Q

Describe aluminum hydroxide

A 
Amphogel
Decreases phosphate absorption, increases stomach emptying which can increase acid secretion
Cytoprotective effect on mucosa
Can cause constipation
Chelates other drugs
Contraindicated in appendicitis
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8
Q

Describe magnesium hydroxide

A

Milk of Magnesia
Good neutralizing ability
MgCl2 - low solubility, some Mg absorption
Can cause diarrhea
Contraindicated in renal failure, appendicitis, intestinal obstruction

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9
Q

What two antacids are combined? How do they work?

A

Magnesium hydroxide + Aluminum hydroxide
Liquid suspension - insoluble
Used together counteracts the GI motility

Liquids better than tablets
Take 1-3 hours after meal and at bedtime for 6-8 weeks for peptic ulcer

Doesn’t control noctural acid secretion!

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10
Q

How do we reduce gastric acid secretion?

A

H2 receptor antagonists, proton pump inhibitors

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11
Q

How do H2 receptor antagonists work?

A

They decrease acid secretion by blocking H2 receptors on parietal cells
This blocks basal, nocturnal, AND stimulated acid secretion (so no rebound decrease in pH)
Reduces volume and H+ concentration in secretion
Also reduces pepsin so they will have effects on digestion

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12
Q

Describe the structure of antihistamines?

A

Structural analogs of histamine with a bulky side chain

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13
Q

Indications for H2 receptor antagonists

A

Peptic ulcer disease
GERD
Zollinger-Ellison syndrome

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14
Q

Describe the pharmacodynamics of H2 receptor antagonists?

A

Well absorbed from GI tract
Hepatic metabolism and secreted by renal tubules
Renal impairment dosage adjustment required

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15
Q

Adverse effects of cimetidine?

A 
Headache
CNS: Confusion, seizures*****
Rash
Diarrhea
Decreased metabolism
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16
Q

Adverse effects of ranitidine?

A

Diarrhea
Constipation
Headache
Blood dyscrasias

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17
Q

Adverse effects of famotidine?

A 
Headache
Constipation
Diarrhea
Dizziness
Blood dyscrasias
18
Q

Adverse effects of Nizatidine?

A 
Somnolence*****
Fatigue
Headache
Rash*****
Blood dyscrasias
Tachycardia****
19
Q

How to proton pump inhibitors work?

A

They are prodrugs activated by stomach acid
Irreversible inhibitors of proton pumps, they form sulfate bonds with the pumps

Acid secretion requires a new pump!

Up to 95% inhibition after 7 days

20
Q

Indications for PPI’s?

A

Pts not controlled by H2 antagonists
Hypersecretory states - Zollinger Ellison, systemic mastocytosis
Severe GERD
Short term ulcers

21
Q

Adverse effects of PPI’s?

A

Hyperplasia of parietal cells in experimental animals (not yet seen in humans, this could be risk for tumor)
Elevated stomach pH, bacterial infections, hypergastrinemia, decreased calcium absorption, rebound hypersecretion upon drug removal

22
Q

What anticholinergics are used for gastric-peptic disease? How do anticholinergics work?

A

Pirenzepine, Telenzepine
M1 antagonists, they decrease basal secretion 40-50%
They have limited effects on stimulated pumps(?)

23
Q

Toxicities with anticholinergics?

A

Worry about antimuscarinic side effects

24
Q

True or False: Anticholinergics are approved for use in gastric-peptic disease in the US

A

False, only in Japan/Europe/Canada

25
Q

What is Octreotide?

A

Gastrin inhibitor

It is a somatostatin analog that blocks gastrin release

26
Q

What is Octreotide used for?

A

Gastrinomas

Zollinger-Ellison

27
Q

Toxicities with Octreotide?

A

Severe diarrhea

28
Q

How is Octreotide administered?

A

IV

29
Q

What mucosal protecting agents do we have?

A

Sucralfate
Colloidal bismuth (Pepto bismol)
Misoprostol

30
Q

Why do we use mucosal protecting agents?

A

They promote healing of epidermal layer damaged in ulcer disease

31
Q

What is Sucralfate?

A

A mucosal protecting agent, an aluminum salt with sugars attached
Binds to ulcerated spots to form a protective layer/barrier to acid and pepsin
Also promotes PG synthesis

32
Q

Toxicities with Sucralfate?

A

Can cause constipation
Avoid in renal failure
Patients at risk of aluminum overload
Can inhibit the absorption of other drugs

33
Q

How does Colloidal bismuth work?

A

Coats the stomach lining
Enhances cytoprotective factors
Inhibits pepsin activity

34
Q

Toxicities with colloidal bismuth?

A

Imparts black color to oral cavity and feces

Contains salicylates, can induce acid secretion

35
Q

How does misoprostol work?

A

It is a PGE1 analog
It enhances mucous production
Decreases acid production

36
Q

Indications for Misoprostol?

A

Ulcers caused by NSAIDs

37
Q

Toxicities with Misoprostol?

A

Diarrhea
Abdominal cramps
CI in pregnancy
Use with caution in renal failure

38
Q

What is Helicobacter pylori?

A

Causes inflammatory gastritis
Involved in 60% of peptic ulcers
Associated with gastric lymphoma, adenocarcinoma
Common, many asymptomatic - increases incidence with age

39
Q

What is the H. pylori triple therapy regimen?

A 
Proton pump inhibitor (or H2 antagonist)
plus
Clarithromycin 500 mg BID
plus
Amoxicillin (1g) or Metronidazole (500 mg)

Take for 14 days

40
Q

What is the H Pylori quadruple regimen?

A

Proton pump inhibitor BID (or H2 antagonist)
Metronidazole (500 mg TID)
Tetracycline (500 mg QID)
Bismouth subsalicylate (525 mg QID)

Cology 2 Exam 4 (16 decks)

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