Trade name: dramamine

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, insomnia, itch, motion sickness

Side effects:

Heavy sedation (***)

Trade name: Benadryl

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, insomnia, itch, motion sickness

Side effects:

Heavy sedation (***)

Trade name: Atarax

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, insomnia, itch, motion sickness, vertigo, nausea, vomiting

Side effects:

Heavy sedation (***)

Trade name: poly-Histine-D

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, motion sickness, vertigo, nausea, vomiting

Side effects:

Moderate sedation (**)

Trade name: Phenergan

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Insomnia, motion sickness, anti-emetic

Side effects:

Heavy sedation (***)

Trade name: perlactin

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, migraine, Cushing's syndrome

Side effects:

Moderate sedation (**)

Trade name: Dimetapp

Mechanism of action:

1st generation H₁ receptor antagonist

Clinical Use:

Allergy, common cold, rhinitis, potentiate analgesia

Side effects:

LOW sedation (*)

Trade name: Allegra

Mechanism of action:

2nd generation H₁ receptor antagonist

Clinical Use:

Allergy, insomnia, itch, motion sickness, potentiate opioid analgesia

Side effects:

NON-sedating

Trade name: Allegra

Mechanism of action:

2nd generation H₁ receptor antagonist

Clinical Use:

Allergy, insomnia, itch, motion sickness, potentiate opioid analgesia

Side effects:

NON-sedating

Class of drug:

Proton pump inhibitors in parietal cell (irreversible) --> have to synthesize new pump

Mechanism of action:

Taken as a prodrug --> acid resistant capsule (acid labile drugs) --> dissolve in intestinal lumen --> absorbed --> released where gastrin/somatostatin are released --> protonated in canaliculi --> bind channel and exert action

Clinical Use:

heartburn, GERD, peptic ulcer from NSAID or H. pylor

Side effects:

Vitamin B₁₂ deficiency, Ca²⁺, Iron and zinc absorption issues. Take a supplement with them.

Class of drug:

Mucosal protective agent (use with PPI or H1 antagonist)

Mechanism of action:

Reacts with HCl in stomach --> forms viscous paste & acid buffer --> complexes with albumin/fibrinogen creating protective barrier

Clinical Use:

gastric/dudenal ulcers, stress related GI bleeding

Side effects:

Constipation, flatulence

Class of drug:

Mucosal protective agent (use with PPI or H1 antagonist)

Mechanism of action:

PGE₁ analogue --> increases mucus/bicarbonate secretion, increase mucosal blood flow (activates PG-E3/E4 receptors on parietal cells --> G_i -->decrease cAMP --> counter histamine effects

Clinical Use:

NSAID induced ulcers, gastric/dudenal ulcers using NSAIDs

Side effects:

Diarrhea, abdominal pain

Class of drug:

Bismuth protective antacid

Mechanism of action:

Unknown, but decreases inflammation and irritation of GI lining via protective coat action

Clinical Use:

H. pylori cocktail, dyspepsia, acute diarrhea

Side effects:

Black tongue/stools; Reyes Syndrome

Class of drug:

Pro-kinetic agent

Mechanism of action:

5-HT4 receptor antagonist --> ACh release in myenteric plexes --> stimulate gastric emtying.

It also inhibits D2 receptor (blocks ACh release)

Clinical Use:

GERD, IBS syndrome, gastritis, dyspepsia

Side effects:

Significant CNS effects (D2 is site for antisychotic drugs)

Cimetidine (Tagament)

Ranitidine (Zantac)

Famotidine (Pepcid)

Nizantidine (Axid)

Class of drug:

H₂ receptor antagonists

Mechanism of action:

Blocks H₂ receptor on the parietal cell --> no signal to increase HCl secretion

Clinical Use:

heartburn, GERD, peptic/gastric ulcers, stress related GI bleeding

Side effects:

Diarrhea, headache, fatigue, myalgias, constipation, gynecomastia at high concentrations --> increased estradiol effects

Potency:

famotidine > nizatidine =ranitidine > cimetidine

1. Parietal cell --> secretes HCL in response to H₂ binding (little also in response to ACh from vagus)

2. Enterochromaffin-like cell --> secretes Histamine onto parietal cell

3. G-cell --> in response to food in stomach secretes gastrin --> through antrum/fundis blood vessels --> gastrin binds receptor on ECC --> H2 release

4. D-cell --> releases somatostatin --> acts on G cell & stops gastrin release, aslo enters blood vessel and acts on ECC --> prevents H⁺ secretion

Acetylcholine can also activate --> ACh --> M₃ on ECC (that releases histamine) and on parietal cell --> HCl release

Acute:

1. Beta₂ agonists

2. Muscarinic antagonists

3. Theophylline

Chronic:

1. Long-acting Beta₂ (improve response to steroids)

2. Corticosteroids

3. Inhibitors of mast cell mediator release

4. Anti-IgE antibodies

Prophylaxis:

1. Leukotriene antagonists