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48 Cards in this Set

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Antacid
a)mechanism of action
Antacid
a)mechanism of action: neutralize secreted gastric acid thereby reduce gastric aciditiy (increase gastric PH)
Antacid
b)clinical indications
Antacid
b)clinical indications: used as an ADJUNCT to other approaches for relief of PU pain and to promote healing of PUs
Antacid
c)adverse effects
Antacid
c)adverse effects:
1. GI: diarrhea (magnesium salts), constipation (aluminum, calcium salts).
2. HYPOphosphatemia: associated with aluminum-containing antacids
3. HYPERmagnesemia, HYPERaluminemia: in patients with renal failure taking large doses chronically
4. acid rebound: associated with calcium containing antacids
Antacid
d)cautions and considerations
Antacid
d)cautions and considerations:
1. pregnancy: concern only with chronic high doses
2. breast-feeding: no documented problems in neonates
3. pediatrics: NOT recommended < age 6 years, unless proper diagnosis made
Antacid
e)drug interactions
Antacid
e)drug interactions
1. adsorb drugs to surface, thereby decreasing bioavailability: tetracycline; ciprofloxacin, norfloxacin
2. increased gastric PH, thereby altering drug absorption: a) decreased absorption, decreased THERAPEUTIC effect: digoxin, phenytoin, isoniazid, ketoconazole; and b)increased absorption, increased ADVERSE effects: salicylates, levodopa.

NOTE: In general, do not take antacids within 1-2 hours of other oral drugs
Antacid
f)acid neutralizing capacity of antacid products
Antacid
f)antacid neutralizing capacity of antacid products: Delcid (highest), Tums (lowest)
Antacid
g)dosage and administration
Antacid
g)dosage and administration:
*usual duration of therapy: 4-8 weeks; continue therapy for at least 4-6 weeks after all symptoms have disappeared.
*LIQUID forms preferable to tablets- more potent, more effective
*tablets should be chewed well and followed with a glass of water
Histamine H2-Receptor Antagonists (H2As)
a)available agents
Histamine H2-Receptor Antagonists (H2As)
a)available agents:
1. cimetidine (Tagamet)
2. ranitidine (Zantac)
3. famotidine (Pepcid)
4. nizatidine (Axid)
*C.R.F.N.
Histamine H2-Receptor Antagonists (H2As)
b)mechanism of action
Histamine H2-Receptor Antagonists (H2As)
b)mechanism of action: block gastric acid secretion by inhibiting the action of histamine at the histamine H2-receptor sites on the PARIETAL CELL; also inhibit acid secretion stimulated by GASTRIN and ACETYLCHOLINE
Histamine H2-Receptor Antagonists (H2As)
c)pharmacokinetics
Histamine H2-Receptor Antagonists (H2As)
c)pharmacokinetics:
1. metabolism: HEPATIC; RANITIDINE (extensive first-pass metabolism of oral dose)
2. elimination: primarily RENAL
3. distribution: distributed into BREAST MILK; crosses the PLACENTA
Histamine H2-Receptor Antagonists (H2As)
d)clinical indications (FDA-approved)
Histamine H2-Receptor Antagonists (H2As)
d)clinical indications (FDA-approved):
1. treatment and prevention of DU: C.R.F.N.
2. treatment of active benign GU: C.R.F.N.
3. ZOLLINGER-ELLISON SYNDROME: cimetidine, ranitidine, famotidine
Histamine H2-Receptor Antagonists (H2As)
e)adverse effects
Histamine H2-Receptor Antagonists (H2As)
e)adverse effects (udually mild and infrequent):
1. GI: n/v/d, constipation
2. CNS: headache, dizziness, drowsiness, mental confusion, and seizures (with CIMETIDINE)
3. allergic: skin rash
4. endocrine (with CIMETIDINE): gynecomastia, impotence, galactorrhea
5. hematologic: thrombocytopenia
Histamine H2-Receptor Antagonists (H2As)
f)cautions and considerations
Histamine H2-Receptor Antagonists (H2As)
f)cautions and considerations:
1. pregnancy: ALL H2A's CROSS THE PLACENTA
2. breastfeeding: ALL H2A's EXCRETED INTO BREAST MILK
3. pediatrics: consider risk-benefit in children <16 y/o age due to limited clinical experience
4. geriatrics: no problems documented to date
Histamine H2-Receptor Antagonists (H2As)
g)drug interactions
Histamine H2-Receptor Antagonists (H2As)
g)drug interactions: CIMETIDINE inhibits the CYTOCHROME P450 MIXED-FUNCTION OXIDASE ENZYME in the liver, thereby decreasing hepatic metabolism, delaying elimination, and increasing serum concentrations of drugs metabolized by this system. Drugs most frequently implacted are theophylline, phenytoin and warfarin.
Histamine H2-Receptor Antagonists (H2As)
h)dosage and administration
Histamine H2-Receptor Antagonists (H2As)
h)dosage and administration:
1. Cimetidine: oral, IM, IV
2. Ranitidine: oral, IM, IV
3. Famotidine: oral, IV
4. Nizatidine: oral
Histamine H2-Receptor Antagonists (H2As)
i)general administration guidlenines
Histamine H2-Receptor Antagonists (H2As)
i)general administration guidelines:
1. usual duration of therapy for active DU: 4-8 weeks; for benign GU: 6-8 weeks; symptoms may subside within 1-2 weeks of starting therapy, but this does not mean the ulcer has healed
2. a single bedtime dose is very effective
3. when treating gastric acid hypersecretory conditions such as ZES, adjust dosage as needed and continue as long as clinically indicated.
4. with moderate to severe renal function impairment or severe liver disease: dosage reduction (or less frequent administration) recommended.
Sucralfate (Carafate)
a)mechanism of action
Sucralfate (Carafate)
a)mechanism of action: binds to the ulcer site (local action) forming a coating which protects the ulcer site from acid. Adsorbs bile salts and pepsin thereby inhibiting their local destructive action on the mucosa.
Sucralfate (Carafate)
b)pharmacokinetics
Sucralfate (Carafate)
b)pharmacokinetics:
1. absorption: minimal
2. elimination: primarily FECAL
Sucralfate (Carafate)
c)clinical indication
Sucralfate (Carafate)
c)clinical indication: short-term treatment of active DU; maintenance therapy for DU
Sucralfate (Carafate)
d)adverse effects
Sucralfate (Carafate)
d)adverse effects:
1. few systemic adverse effects
2. GI: constipation; dry mouth; metallic taste; nausea; stomach cramps/pain
3. allergic: skin rash; hives; pruritis
4. hypophosphatemia
5. increased serum aluminum levels with compromised renal function
Sucralfate (Carafate)
e)cautions and considerations
Sucralfate (Carafate)
e)cautions and considerations: RENAL FAILURE- with long-term use, aluminum absorption may cause aluminum toxicity
Sucralfate (Carafate)
f)drug interactions
Sucralfate (Carafate)
f)drug interactions:
1. antacids: may interefere with binding of sucralfate to mucosa
2. digoxin; phenytoin; theophylline; quinidine; warfarin; oral tetracyclines; ciprofloxacin, norfloxacin: decreased absorption of these drugs- separate administration times of 2 hrs.
3. vitamin A, D, E, K: decreased absorption; vitamin requirements may be increased
4. levothyroxine: decreased absorption- separate administration times by 8 hours or d/c sucralfate
Sucralfate (Carafate)
g)dosage and administration
Sucralfate (Carafate)
g)dosage and administration:
1. adult/adolescent: 1 g QID (active ulcer); 1 g BID (maintenance)
2. pediatric dose not established
Sucralfate (Carafate)
h)general administration guidelines
Sucralfate (Carafate)
h)general administration guidelines:
1. usual duration of therapy: 4-8 weeks
2. take with water on an empty stomach (1h before meals and at bedtime)
3. antacids can be adminstered 1/2 hr before/after sucralfate
4. suspension for pts unable to take tablets
Misoprostol (Cytotec)
a)mechanism of action
Misoprostol (Cytotec)
a)mechanism of action:
1. mucosal defense effect- increases gastric mucus production and mucosal bicarbonate secretion
2. antisecretory effect- inhibits gastric acid secretion
Misoprostol (Cytotec)
b)pharmacokinetics
Misoprostol (Cytotec)
b)pharmacokinetics: elimination- primarily RENAL
Misoprostol (Cytotec)
c)clinical indication
Misoprostol (Cytotec)
c)clincal indication: prevention of NSAID and aspirin-induced GU in patients at high risk of developing GU or complications thereof.
Misoprostol (Cytotec)
d)adverse effects
Misoprostol (Cytotec)
d)adverse effects:
1. GI: diarrhea and mild abdominal/stomach cramping (dose-related;self-limiting, usually resolves after 8 days); constipation; flatulation; nausea; vomiting
2. CNS: headache
Misoprostol (Cytotec)
e)cautions and considerations
Misoprostol (Cytotec)
e)cautions and considerations:
1. contraindicated during PREGNANCY; risk of miscarraige via uterine stimulation
2. breast-feeding: NOT recommended due to possibility of significant diarrhea in nursing infant
Misoprostol (Cytotec)
f)drug interactions
Misoprostol (Cytotec)
f)drug interactions: magnesium-containing antacids- may aggravate misoprostol-induced diarrhea
Misoprostol (Cytotec)
g)dosage and administration
Misoprostol (Cytotec)
g)dosage and administration:
1. adults: 200mcg (0.2mg) QID or 400mcg (0.4mg) BID
2. pediatric and adolescent dose not established
Misoprostol (Cytotec)
h)general administration guidelines
Misoprostol (Cytotec)
h)general administration guidelines:
1. take WITH or AFTER meals and at bedtime
2. intitiate misoprostol therapy when NSAID therapy started
3. renal impairment: dosage reduction NOT usually required
Omeprazole (Prilosec)
a)mechanism of action
Omeprazole (Prilosec)
a)mechanism of action: IRREVERSIBLY inhibits the H+/K+ ATPase enzyme system (the acid/proton pump of the gastric mucosa) of the parietal cells, thereby profoundly inhibiting gastric acid secretion
Omeprazole (Prilosec)
b)pharmacokinetics
Omeprazole (Prilosec)
b)pharmacokinetics:
1. metabolism: hepatic (first pass metabolism)
2. elimination: primarily RENAL
Omeprazole (Prilosec)
c)clinical indications (FDA-approved)
Omeprazole (Prilosec)
c)clinical indications (FDA-approved):
1. short-term treatment of active DU and GU
2. treatment of gastric acid hypersecretory conditions such as ZES
3. erosive esophagitis
4. GERD poorly responsive to other treatment
Omeprazole (Prilosec)
d)adverse effects
Omeprazole (Prilosec)
d)adverse effects:
1. GI: n/v/d, abdominal pain, constipation
2. CNS: headache, dizziness, unusual drowsiness or tiredness
3. allergic: skin rash; pruritis
4. hematologic: anemia, leukocytosis, neutropenia, thrombocytopenia
5. hypoglycemia: in diabetic patients
Omeprazole (Prilosec)
e)cautions and considerations
Omeprazole (Prilosec)
e)cautions and considerations:
1. breast-feeding: may be excreted in breast milk
2. pediatrics/geriatrics-lack of info
3. chronic hepatic disease: may require dosage reduction due to decreased elimination
Omeprazole (Prilosec)
f)drug interactions
Omeprazole (Prilosec)
f)drug interactions:
1. ampicillin; iron salts;ketoconazole: decreased absorption of these medications due to increased gastric PH
2. phenytoin, diazepam, warfarin: omeprazole INHIBITS CYTOCHROME P450 ENZYMES in liver; therefore, concurrent use may caused decreased hepatic metabolism, delayed elimination and increased blood concentrations of these drugs
3. bone marrow depressants
Omeprazole (Prilosec)
g)dosage and administration
Omeprazole (Prilosec)
g)dosage and administration
*for DU, GU, and ZES
*oral therapy
*pediatric dose not established
Omeprazole (Prilosec)
h)general administration guidelines
Omeprazole (Prilosec)
h)general administration guidelines:
1. take BEFORE a meal, preferably in the morning
2. can be taken with antacids for relief of pain
3. swallow capsule WHOLE
4. geriatric patients: daily dose should not exceed 20mg
5. renal impairment of hepatic dysfunction: dosage adjustment not required.
Lanzoprazole (Prevacid)
a)mechanism of action
Lanzoprazole (Prevacid)
a)mechanism of action: irreversibly inhibits the H+/K+ ATPase enzyme system (the acid/proton pump) of the PARIETAL CELL, thereby profoundly inhibiting gastric acid secretion
Lanzoprazole (Prevacid)
b)pharmacokinetics
Lanzoprazole (Prevacid)
b)pharmacokinetics:
1. metabolism: hepatic
2. elimination: BILIARY and RENAL
Lanzoprazole (Prevacid)
c)clinical indications (FDA-approved)
Lanzoprazole (Prevacid)
c)clinical indications (FDA-approved):
1. short-term treatment of active DU
2. short-term treatment of erosive esophagitis
3. gastric acid hypersecretory conditions such as ZES
Lanzoprazole (Prevacid)
d)adverse effects
Lanzoprazole (Prevacid)
d)adverse effects:
1. GI: n/d, abdominal pain
2. CNS: headache, dizziness
3. allergic: skin rash, pruritis
Lanzoprazole (Prevacid)
e)drug interactions
Lanzoprazole (Prevacid)
e)drug interactions:
1. ketoconazole, ampicillin, iron salts, digoxin: decreased absorption of these drugs due to increased gastric PH
2. theophylline: decreased metabolism, delayed elimination and increased serum theophylline levels since LANSOPRAZOLE INHIBTS CYTOCHROME P45O ENZYMES
Lanzoprazole (Prevacid)
f)dosage and administration
Lanzoprazole (Prevacid)
f)dosage and administration:
1. adult dose:
*for DU (4 wks)
*for ZES
Lanzoprazole (Prevacid)
g)general administration guidelines
Lanzoprazole (Prevacid)
g)general administration guidelines:
1. take BEFORE eating
2. swallow capsule WHOLE
3. severe hepatic disease- dosage reduction
PHARMACOTHERAPY TO ERADICATE HELICOBACTER PYLORI INFECTION
A. FDA-approved regimens:
1. Clarithromycin and Omeprazole
2. Clarithromycin and Tritec (ranitidine bismuth citrate)