Ms. Robinson, 2016). Adverse CNS effects such

Ms. Jones presents
with the classic symptoms of gastroesophageal reflux disease (GERD), and after
ruling out other causes of her symptoms, she should be treated with a histamine-2
receptor antagonist (H2RA) such a famotidine (Pepcid).  Because famotidine can be used as over the
counter treatment of GERD, a self-medication history for treatment of GERD
should be obtained (Woo & Robinson, 2016). 
Treatment with famotidine is appropriate with symptoms of dyspepsia or
mild GERD symptoms with no evidence of erosive disease (Woo & Robinson,
2016).  While there are treatment
indications with H2RAs for individuals with esophagitis due to GERD with mild erosive
components, efficacy is limited due to ineffective treatment in patients with
severe esophagitis (Kahrilas, 2016).

Pharmacodynamics

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The mechanism of
action of famotidine, as well as other H2RAs, is the inhibition of the
histamine-2 receptor on the gastric parietal cell, thereby decreasing the
secretion of acid production by 35% to 50% (Kahrilas, 2016; Woo & Robinson,
2016).  H2RAs are reversible competitive
blockers that do not affect histamine-1 receptors or acetylcholine (Woo &
Robinson, 2016).  H2RAs inhibit gastric
secretion in all phases, including fasting and nocturnal secretions, and
secretions caused by muscarinic agonists, gastrin, food, insulin, caffeine,
pentagastrin, and betazole (Woo & Robinson, 2016).  Famotidine does not affect gastric emptying,
lower esophageal sphincter pressure, and has little or no effect on fasting or
postprandial serum gastrin (Woo & Robinson, 2016).

Pharmacokinetics 

Famotidine is well
absorbed following oral administration; absorption may be decreased by antacids
but can be taken without regard to food (Woo & Robinson, 2016).  The onset of action occurs within 60 minutes
of administration and peak of action takes place between one and four hours
after onset (Woo & Robinson, 2016). 
The half-life of famotidine is between 2.5-3.5 hours and duration of
action lasts one to four hours (Woo & Robinson, 2016).  Between 30% and 35% of the drug is
metabolized into inactive compounds by the CYP450 enzyme system and 25% to 30%
is excreted unchanged in the urine (Woo & Robinson, 2016).  Famotidine is 15% to 20% protein bound and
has a bioavailability of 40% to 45% (Woo & Robinson, 2016). 

Pharmacotherapeutics

Patients with
renal impairment who are prescribed famotidine require dosage adjustments due
to reduced renal clearance, especially those with moderate to severe impairment
with a creatinine clearance of less than 50 mL/min (Lexicomp, 2017; Woo &
Robinson, 2016).  Adverse CNS effects
such as mental confusion, agitation, psychosis, depression, and disorientation
are more common in those with renal impairment and older adults with reduced
renal function (Woo & Robinson, 2016). 
Patients with renal dysfunction have also been reported to have prolonged
QT interval (Lexicomp, 2017).  Famotidine
should be used with caution in these patients. 
Vitamin B12 deficiency may occur with treatment lasting two or more
years due to B12 malabsorption (Lexicomp, 2017).  This is dose-related and has a stronger
association in females and those under the age of 30; discontinuation of
therapy reduces the prevalence of B12 deficiency (Lexicomp, 2017).  The use of H2RAs has not been adequately
studied in pregnant women and should only be used when potential benefits
outweigh risks; they are considered Pregnancy Category B (Woo & Robinson,
2016).  The FDA has approved the use of famotidine
in infants and children, although it is reported that children younger than one
year of age have experienced agitation with its use (Woo & Robinson, 2016).  Other adverse effects with the use of famotidine
include gastrointestinal symptoms such as vomiting, nausea, liver enzyme
abnormalities, and dry mouth; rare hematologic disorders such as
agranulocytosis, pancytopenia, leukopenia, and thrombocytopenia;
hypersensitivity reactions such as rash, urticaria, and angioedema;
musculoskeletal effects such as muscle cramps and rhabdomyolysis; respiratory
issues such as bronchospasm and interstitial pneumonia; sensory effects such as
tinnitus and taste disorders; and other rare cases of impotence and
gynecomastia have occurred (Woo & Robinson, 2016; Lexicomp, 2017).

Drug interactions
of H2RAs are associated with their metabolism by the CYP450 enzyme system (Woo
& Robinson, 2016).  Concurrent
administration of famotidine and ketoconazole may decrease the action of
ketoconazole by reducing its absorption; it is recommended to separate
administration by giving ketoconazole first and famotidine one hour later (Woo
& Robinson, 2016).  Food may increase
the bioavailability of famotidine, but its implications have no reported
clinical significance (Woo & Robinson, 2016).  Patients may take antacids concomitantly with
famotidine; if administration of the antacid interferes with the absorption of famotidine,
the administration should be separated by 30 minutes to one hour (Woo &
Robinson, 2016).  Medications that
decrease lower esophageal sphincter tone and contribute to regurgitation in
GERD include anticholinergics, theophylline, caffeine, meperidine, and calcium
channel blockers (Woo & Robinson, 2016).

Ms. Jones presents
with the classic symptoms of gastroesophageal reflux disease (GERD), and after
ruling out other causes of her symptoms, she should be treated with a histamine-2
receptor antagonist (H2RA) such a famotidine (Pepcid).  Because famotidine can be used as over the
counter treatment of GERD, a self-medication history for treatment of GERD
should be obtained (Woo & Robinson, 2016). 
Treatment with famotidine is appropriate with symptoms of dyspepsia or
mild GERD symptoms with no evidence of erosive disease (Woo & Robinson,
2016).  While there are treatment
indications with H2RAs for individuals with esophagitis due to GERD with mild erosive
components, efficacy is limited due to ineffective treatment in patients with
severe esophagitis (Kahrilas, 2016).

Pharmacodynamics

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The mechanism of
action of famotidine, as well as other H2RAs, is the inhibition of the
histamine-2 receptor on the gastric parietal cell, thereby decreasing the
secretion of acid production by 35% to 50% (Kahrilas, 2016; Woo & Robinson,
2016).  H2RAs are reversible competitive
blockers that do not affect histamine-1 receptors or acetylcholine (Woo &
Robinson, 2016).  H2RAs inhibit gastric
secretion in all phases, including fasting and nocturnal secretions, and
secretions caused by muscarinic agonists, gastrin, food, insulin, caffeine,
pentagastrin, and betazole (Woo & Robinson, 2016).  Famotidine does not affect gastric emptying,
lower esophageal sphincter pressure, and has little or no effect on fasting or
postprandial serum gastrin (Woo & Robinson, 2016).

Pharmacokinetics 

Famotidine is well
absorbed following oral administration; absorption may be decreased by antacids
but can be taken without regard to food (Woo & Robinson, 2016).  The onset of action occurs within 60 minutes
of administration and peak of action takes place between one and four hours
after onset (Woo & Robinson, 2016). 
The half-life of famotidine is between 2.5-3.5 hours and duration of
action lasts one to four hours (Woo & Robinson, 2016).  Between 30% and 35% of the drug is
metabolized into inactive compounds by the CYP450 enzyme system and 25% to 30%
is excreted unchanged in the urine (Woo & Robinson, 2016).  Famotidine is 15% to 20% protein bound and
has a bioavailability of 40% to 45% (Woo & Robinson, 2016). 

Pharmacotherapeutics

Patients with
renal impairment who are prescribed famotidine require dosage adjustments due
to reduced renal clearance, especially those with moderate to severe impairment
with a creatinine clearance of less than 50 mL/min (Lexicomp, 2017; Woo &
Robinson, 2016).  Adverse CNS effects
such as mental confusion, agitation, psychosis, depression, and disorientation
are more common in those with renal impairment and older adults with reduced
renal function (Woo & Robinson, 2016). 
Patients with renal dysfunction have also been reported to have prolonged
QT interval (Lexicomp, 2017).  Famotidine
should be used with caution in these patients. 
Vitamin B12 deficiency may occur with treatment lasting two or more
years due to B12 malabsorption (Lexicomp, 2017).  This is dose-related and has a stronger
association in females and those under the age of 30; discontinuation of
therapy reduces the prevalence of B12 deficiency (Lexicomp, 2017).  The use of H2RAs has not been adequately
studied in pregnant women and should only be used when potential benefits
outweigh risks; they are considered Pregnancy Category B (Woo & Robinson,
2016).  The FDA has approved the use of famotidine
in infants and children, although it is reported that children younger than one
year of age have experienced agitation with its use (Woo & Robinson, 2016).  Other adverse effects with the use of famotidine
include gastrointestinal symptoms such as vomiting, nausea, liver enzyme
abnormalities, and dry mouth; rare hematologic disorders such as
agranulocytosis, pancytopenia, leukopenia, and thrombocytopenia;
hypersensitivity reactions such as rash, urticaria, and angioedema;
musculoskeletal effects such as muscle cramps and rhabdomyolysis; respiratory
issues such as bronchospasm and interstitial pneumonia; sensory effects such as
tinnitus and taste disorders; and other rare cases of impotence and
gynecomastia have occurred (Woo & Robinson, 2016; Lexicomp, 2017).

Drug interactions
of H2RAs are associated with their metabolism by the CYP450 enzyme system (Woo
& Robinson, 2016).  Concurrent
administration of famotidine and ketoconazole may decrease the action of
ketoconazole by reducing its absorption; it is recommended to separate
administration by giving ketoconazole first and famotidine one hour later (Woo
& Robinson, 2016).  Food may increase
the bioavailability of famotidine, but its implications have no reported
clinical significance (Woo & Robinson, 2016).  Patients may take antacids concomitantly with
famotidine; if administration of the antacid interferes with the absorption of famotidine,
the administration should be separated by 30 minutes to one hour (Woo &
Robinson, 2016).  Medications that
decrease lower esophageal sphincter tone and contribute to regurgitation in
GERD include anticholinergics, theophylline, caffeine, meperidine, and calcium
channel blockers (Woo & Robinson, 2016).

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