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PCTH 325 > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

What is the basic mechanism of gastric acid release under constitutive conditions?

A
  1. Paracrine release of histamine from ECL cells
  2. Histamine binds to H2 histamine receptors on parietal cells
  3. Stimulate H+/K+ ATPase -> produces basal (constitutive) rate of acid secretion
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2
Q

What is the basic mechanism of gastric acid release under induced (food-related stimulus) conditions?

A

Same as constitutive, but rate of acid secretion increased by:
1. (Neurocrine) release of acetylcholine
-parasypathetic, enteric nervous systems
-acetylcholine binds to M receptor
2. (Endocrine) release of gastrin
-enteric nervous system peptide
Both stimulate ECL cells -> increase His release

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3
Q

What mechanisms protect the stomach against gastric autodigestion? (2)

A
  1. Mucous secretion: resist acid/enzyme action on gastric mucosa
  2. Bicarbonate (HCO3-) ion secretion: trapped in mucus layer (stomach lumen), neutralizes acid (pH mucus =6-7)
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4
Q

What are prostaglandins?

A

Class of locally acting drugs derived from membrane phospholipids that have a net protective effect on stomach

PGE2 produced in gastric mucosa

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5
Q

MOA of Prostaglandins

A

Bind to PGE2 receptors on:
1. Parietal cells: Reduce H+/K+ ATPase activity
2. Mucous cells: stimulate production/release of mucous and HCO3- ions

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6
Q

What causes Peptic Ulcer Disease?

A

Dysequillibrium in stomach (increased acid, or decreased mucous)
Causes acid-induced erosion of stomach lining

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7
Q

How are ulcers treated generally?

A
  1. Neutralize/reduce acid
  2. Strengthen/enhance protective forces (mucus layer, exogenous/artificial support)
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8
Q

What are the 3 primary drugs used for acid neutralization/lowering to treat ulcers +GERD?

A
  1. Antacids
  2. Histamine H2 receptor antagonists
  3. Proton pump inhibitors (PPIs)
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9
Q

Antacids: MOA, 3 examples, side effects, conditions for when they’re useful

A

MOA:
1. Direct chemical neutralization of excess acid
2. Increase gastric pH
no receptors required
Examples:
1. Gaviscon - Al(OH)3
2. Milk of Magnesia - Mg(OH)2
3. Tums - CaCO3
Side Effects:
1. Pharmokinetic drug interaction
-altered pH -> affect solubility/absorption of other drugs, alter weak acid/base equillibrium
2. Carbonate-based salts -> belching
3. Al3+ salts -> constipation, Mg2+ salts -> diarrhea
When they’re useful:
-mild cases, symptomatic relief
-maintenance therapy (b/w meals)

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10
Q

Histamine H2 Receptor Inhibitor: MOA, example, side effects, conditions for when they’re useful

A

MOA:
1. Competitive antagonists blocks histamine H2 receptors in epithelial parietal cells
2. Reduced acid secretion
Example:
1. Cimetidine (the -tidine’s)
Side effects: (low side effect profile)
1. Diarrhea
2. Headache
3. Drowsiness
When they’re useful:
-Most effective for constitutive/nocturnal acid secretion

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11
Q

Proton Pump Inhibitors: MOA, example, side effects, conditions for when they’re useful

A

MOA:
1. Prodrug, activated in areas of concentrated acid
2. Binds to ATPase
3. Irreversible inactivation of H+/K+ ATPase
4. Decrease gastric acid release
Example:
1. Omeprazole (the “-prazoles”)
Side Effects:
1. Diarrhea, headache, abdominal pain
2. Long-term -> increase risk of gastric polyps
When they’re useful:
-Most effective suppressor, lengthy effect (18-24hrs)
-long-term treatment

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12
Q

What are the 2 drugs used for strengthening/enhancing protective forces to treat ulcers +GERD?

A
  1. Misoprostol
  2. Sucralfate
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13
Q

Misoprostol: MOA, side effects, conditions for when they’re useful

A

MOA:
1. Prostaglandin E1 (PGE1) analogue, EP receptor agonist
2. Simulate parietal cell EP receptors -> inhibit H+ release
Simulate mucous cell receptors-> increase HCO3- secretion
3. Artificially restore PGE function in body
Side Effects:
-PGE is a contractile agent of smooth muscle:
1. Intestine: Diarrhea/cramping
2. Uterus: Induce labor
When they’re useful:
-NSAID-induced ulcers

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14
Q

Sucralfate: MOA, side effects

A

MOA:
1. Acid releases sulfated sucrose molecules
2. Binds/links charge groups (proteins, glycoproteins, etc.)
3. Viscous, sticky protective gel prevents further damage
-Frequent dosing required
Side Effects:
- Constipation (due to Al3+ ions)

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15
Q

Triple therapy: MOA/Example, when they’re useful

A

MOA/Example:
1. PPI + 2 of clarithromycin/amoxicillin/metronidazole for 14 days
-historically standard therapy
When they’re useful
- H.Pyroli-related ulcers

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16
Q

Quadruple therapy: MOA/Example, when they’re useful

A

MOA/Example:
1. PPI + 2 of clarithromycin/amoxicillin/metronidazole + 3rd antibiotic or bismuth subsalicylate for 14 days
-combat antibiotic resistance
When they’re useful
-H. Pyroli-related ulcers

17
Q

What causes GERD (Gastroesophageal Reflux Disorder)?

A

Retrograde stomach acid reflux movement to esophagus

18
Q

How is GERD treated?

A
  1. Neutralize/reduce gastric acid release
  2. Alginate-containing antacids (reduce acid)
19
Q

What are 2 intestinal disorders?

A
  1. Constipation (Rate of residue flow too slow ->increased H2O absorption)
  2. Diarrhea (Rate of residue flow too fast -> decreased H2O absorption)
20
Q

What causes constipation?

A

-Diet, stress, drug side effects
-reduction/absence of propagating colonic contractions -> reduced frequency/difficulty of defecation

21
Q

How is constipation treated (3)?

A
  1. Diet management
  2. Tweak current pharmacological regime (avoid side effects)
  3. Laxatives (stimulate enteric nervous system -> bowel movement)
22
Q

Types of laxatives (3)

A
  1. Bulk
  2. Osmotic
  3. Stimulant/Contact
23
Q

Bulk laxatives: MOA, side effects, types (+1 example each)

A

MOA:
1. Indigestible, H2O-absorbing molecules produce intestinal disgestion in colon through their H2O retention properties
2. Stimulate GI tract
3. Bowel movement
Side effects:
-no serious adverse effects
Types/Examples:
1. Altered dietary intake (fibre)
-Bran
2. Supplements
-Methylcellulose (citrucel)

24
Q

Osmotic Laxatives: MOA, side effects, example

A

MOA:
Similar to bulk laxatives, use poorly absorbed salts, fatty acids and/or carbohydrates (rather than fibre)
1. Osmosis -> increase colon fluid volume
2. Increase H2O retention -> stimulate peristalsis
Side Effects:
-Abdominal cramps, diarrhea
Example:
-Saline puratives (MgSO4)

25
Q

Stimulant Laxatives: MOA, example

A

MOA:
1. Released anthracene compounds that directly simulate myenteric plexus (enteric nervous system)
2. Smooth muscle activity 3. Defecation
Example:
-Sennosides (Ex-lax)

26
Q

What causes diarrhea?

A

-chronic disease, toxins, stress, anxiety, drugs, infectious agents (acute=viral, bacterial, parasites/protozoa)
-stimulate GI tract to move move indigestible residue too fast for adequate H2O absorption-> excess/frequent loose/liquid bowel movements

27
Q

How is diarrhea treated (2)?

A
  1. Fluid/Electrolyte Management
  2. Anti-motility agents (Opiates)
28
Q

Fluid/Electrolyte Management: MOA

A
  1. Ensure proper hydration with H2O
  2. Oral sodium/glucose solution -> ions help facilitate re-uptake once absorbed
29
Q

Anti-Motility Agents (Opiates): MOA, Example, Side Effects

A

MOA:
1. Act on u receptors of enteric nervous system in myenteric plexus
2. Diminish propulsive activity
3. Allow more time for H2O absorption
Example:
Ioperamide (more selective for digestive tract receptors than other opioids for analgesia)
Side Effects:
-Constipation

PCTH 325 (19 decks)

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