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ETATUTWUNI
0911013101
DESCRIPTION
DIPRIVAN (propofol) Injectable Emulsion is a
sterile, nonpyrogenic emulsion containing 10
mg/mL of propofol suitable for intravenous
administration.
Propofol is chemically described as 2,6diisopropylphenol and has a molecular weight of
178.27.
CLINICAL PHARMACOLOGY
General
DIPRIVAN Injectable Emulsion is an intravenous
sedative-hypnotic agent for use in the induction and
maintenance of anesthesia or sedation. Intravenous
injection of a therapeutic dose of propofol produces
hypnosis rapidly with minimal excitation, usually
within 40 seconds from the start of an injection (the
time for one arm-brain circulation). As with other
rapidly acting intravenous anesthetic agents, the
half-time of the blood-brain equilibration is
approximately 1 to 3 minutes, and this accounts for
the rapid induction of anesthesia.
Pharmacodynamics
Pharmacodynamic properties of propofol are
dependent upon the therapeutic blood propofol
concentrations. Steady state propofol blood
concentrations are generally proportional to
infusion rates, especially within an individual
patient.
Undesirable side effects such as cardiorespiratory
depression are likely to occur at higher blood
concentrations which result from bolus dosing or
rapid increase in infusion rate. An adequate interval
(3 to 5 minutes) must be allowed between clinical
dosage adjustments in order to assess drug effects.
Pharmacokinetics
The proper use of DIPRIVAN Injectable
Emulsion requires an understanding of the
disposition and elimination characteristics of
propofol.
The pharmacokinetics of propofol are well
described by a three compartment linear model
with compartments representing the plasma,
rapidly equilibrating tissues, and slowly
equilibrating tissues.
Administration
Oral Administration
Least effective when given orally.b 246 247 245
Higher dosages may be necessary for pain relief, but
the risk of toxicity from metabolite normeperidine is
increased.247 248
Oral therapy is discouraged because of extensive firstpass metabolism in the liver and resultant increased
formation of the toxic metabolite (normeperidine).
IV Administration
Administer by direct IV injection, IV infusion, or IV via a
controlled-delivery device for patient-controlled analgesi
If IV administration is required, decrease dosage and administer
injections very slowly, preferably as a 10-mg/mL injection.
Alternatively, may use the commercially available injection
containing 10 mg/mL intended for use with a compatible
infusion device (does not require further dilution); this 10mg/mL injection is for single use only, and unused portions
should be discarded appropriately.
When given parenterally, especially by the IV route, the patient
should be lying down.
During and immediately following IV administration, an opiate
antagonist and facilities for administration of oxygen and control
of respiration should be available
Demerol Pharmacokinetics
Absorption
Bioavailability
Oral: Undergoes extensive first-pass metabolism
in the liver, with approximately 5060% of a
dose reaching systemic circulation unchanged.
Oral: Bioavailability increases to approximately
8090% in patients with hepatic impairment.
Less than half as effective when given orally as
when given parenterally.
IM: Approximately 8085% of a dose of the drug
is absorbed within 6 hours after intragluteal
injection.
Onset
Oral, peak analgesia: Within 1 hour and declines
gradually over 24 hours.
Sub-Q, peak analgesia: In about 4060.
IM, peak analgesia: In about 3050 minutes.
Duration
Sub-Q or IM: Analgesia is maintained for 24
hours.
Plasma Concentrations
Oral, peak: About 1 hour.
IM, peak: Within 515 minutes.
distribution
Extent
Crosses the placenta; may accumulate in fetus.
Distributes into breast milk
Plasma Protein Binding
Approximately 6080%;246 212 principally
albumin and 1-acid glycoprotein
Elimination
Metabolism
Principally in the liver.
Normeperidine is the active metabolite and exhibits
about half the analgesic potency of meperidine but
twice the CNS stimulant (e.g., seizure-inducing)
potency.
Various toxic effects secondary to CNS stimulation
(e.g., seizures, agitation, irritability, nervousness,
tremors, twitches, myoclonus) have been attributed
to accumulation of normeperidine.
Elimination Route
Excreted in urine as metabolites and unchanged
drug.
Acidifying the urine enhances excretion of the
unchanged drug and normeperidine.
Half-life
Distribution phase half-life, meperidine: 211
minutes
Terminal elimination half-life, meperidine: 35
hours.
Terminal elimination half-life, normeperidine:
Approximately 821 hours
Special Populations
Elimination half-life in hepatic dysfunction,
meperidine: Prolonged.
Cirrhosis207 213 215 or active viral hepatitis:207
216 Averages about 711 hours.
Terminal elimination half-life in renal impairment,
normeperidine: May be prolonged (e.g., 3040
hours).
Renal or hepatic impairment: Accumulation of
normeperidine may occur with repeated, high doses
of the drug
CONTRAINDICATIONS
Hypersensitivity to meperidine(demerol).
Patients who are receiving MAO inhibitors or
those who have received MAO inhibitors in the
past 14 days (ex. selegline, carbex, eldepryl, and
others).
Patients with renal insufficiency (creatine
clearance less than 50 mL/min).
Patients with untreated hypothyroidism,
Addisons disease, benign prostatic hypertrophy,
or urethral stricture.
dilaudid
difinition
Dilaudid (hydromorphone) belongs to a group of
drugs called narcotic pain relievers, also called
opioids. It is similar to morphine.
Dilaudid is prescribed for the relief of moderate to
severe pain. It works by binding to certain
receptors in the brain and nervous system to
reduce pain.
Dilaudid may also be used for other purposes not
listed in this medication guide.
structure
Absorption
After oral administration of DILAUDID 8 mg
liquid or tablets, peak plasma
hydromorphone concentrations are
generally attained within to 1-hour
Distribution
At therapeutic plasma levels, hydromorphone is
approximately 8-19% bound to plasma proteins. After an
intravenous bolus dose, the steady state of volume
distribution [mean (%cv)] is 302.9 (32%) liters.
Metabolism
Elimination
vicodin
structure
CLINICAL PHARMACOLOGY
Hydrocodone is a semisynthetic narcotic
analgesic and antitussive with multiple actions
qualitatively similar to those of codeine. Most of
these involve the central nervous system and
smooth muscle. The precise mechanism of action
of hydrocodone and other opiates is not known,
although it is believed to relate to the existence of
opiate receptors in the central nervous system. In
addition to analgesia, narcotics may produce
drowsiness, changes in mood and mental
clouding.
Pharmacokinetics
Acetaminophen
Acetaminophen is rapidly absorbed from the
gastrointestinal tract and is distributed throughout
most body tissues. The plasma half-life is 1.25 to 3
hours, but may be increased by liver damage and
following overdosage. Elimination of
acetaminophen is principally by liver metabolism
(conjugation) and subsequent renal excretion of
metabolites. Approximately 85% of an oral dose
appears in the urine within 24 hours of
administration, most as the glucuronide conjugate,
with small amounts of other conjugates and
unchanged drug. See OVERDOSAGE for toxicity
information.
ZOLOFT
Pfizer
Sertraline HCl
Antidepressant - Antipanic Antiobsessional Agent
Pharmacokinetics
Following multiple oral once-daily doses of 200
mg, the mean peak plasma concentration (Cmax)
of sertraline is 0.19 g/mL occurring between 6 to
8 hours post-dose. The area under the plasma
concentration time curve is 2.8 mg h/L.
For desmethylsertraline, Cmax is 0.14 g/mL, the
half-life 65 hours and the area under the curve 2.3
mg h/L. Following single or multiple oral once-daily
doses of 50 to 400 mg/day the average terminal
elimination half-life is approximately 26 hours.
Linear dose proportionality has been
demonstrated over the clinical dose range of 50 to
200 mg/day.
Contra-Indications
In patients with known hypersensitivity to
the drug.
MAO Inhibitors: Cases of serious, sometimes
fatal, reactions have been reported in
patients receiving sertraline in combination
with an MAO inhibitor, including the
selective MAO inhibitor, selegiline and the
reversible MAO inhibitor (reversible
inhibitor of MAO-RIMA), moclobemide.