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0112 ceu.pub

National Association for Health Professionals Top 5 Medications Prescribed in the US
A prescription medication is a licensed medicine that is regulated by legislation to require a medical
prescription before it can be obtained. The term is used to distinguish it from over-the-counter drugs
that can be obtained without a prescription. Different jurisdictions have different definitions of what
constitutes a prescription drug. In the United States, the Federal Food, Drug, and Cosmetic Act defines
what requires a prescription.
"Rx" is often used as a short form for prescription drug in North America. It is in fact an abbreviation
for the Latin "recipe," the imperative form of "recipere," meaning "take thus."
Dispensation of prescription drugs often includes a monograph (in Europe, a Patient Information Leaf-
let or PIL) that gives detailed information about the drug.
Hydrocodone
Hydrocodone or dihydrocodeinone is a synthetic opioid derived from either of two naturally occurring
opiates: codeine and thebaine. It is an orally active narcotic analgesic (pain reliever) and antitussive
(cough suppressant). It is available in tablet, capsule, and syrup form, and is often compounded with
other, generally less effective non-opioid compounds such as paracetamol (also known as acetamino-
phen) or ibuprofen, both often added to discourage recreational use (as paracetamol can cause poten-
tially fatal liver toxicity at high doses), and to provide a possible synergy of analgesic effects between
hydrocodone and the non-opioid compounds present. The particular niche in which hydrocodone is
most commonly used is as an intermediate centrally acting analgesic. Abrupt discontinuation of hydro-
codone (Vicodin, Vicodin ES, and Norco) may result in withdrawal symptoms.
Hydrocodone was first synthesized in Germany in 1920 by Carl Mannich and Helene Löwenheim and
was approved by the Food and Drug Administration on 23 March 1943 for sale in the United States.
As a narcotic, hydrocodone relieves pain by binding to opioid receptors in the brain and spinal cord. It
can be taken with or without food as desired. When taken with alcohol, it can intensify drowsiness. It
may interact with monoamine oxidase inhibitors, as well as other drugs that cause drowsiness. It is in
FDA pregnancy category C. Animal reproduction studies have shown an adverse effect on the fetus,
and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use
of the drug in pregnant women despite potential risks. In addition, a newborn of a mother taking the
medication may exhibit breathing problems or withdrawal symptoms.


Studies have shown hydrocodone is stronger than codeine but only one-tenth as potent as morphine at binding to receptors and reported to be only 59% as potent as morphine in analgesic properties. How-ever, in tests conducted on rhesus monkeys, the analgesic potency of hydrocodone was actually found to be higher than that of morphine. Orally administered hydrocodone has a MEDD factor of .4, mean-ing that 1 mg of hydrocodone is equivalent to .4 mg of intravenous morphine. However, because of morphine's low oral bioavailability, there is a 1:1 correspondence between orally administered mor-phine and orally administered hydrocodone. Hydrocodone can be habit-forming, which leads to physical and psychological dependence, but the po-tential for addiction varies from individual to individual depending on unique biological differences. Sales and production of this drug have increased significantly in recent years, as have diversion and illicit use. In the U.S., formulations containing more than 15 mg per dosage unit are considered Sched-ule II drugs, as would any formulation consisting of just hydrocodone alone. Those containing less than or equal to 15 mg per dosage unit in combination with paracetamol or another non-controlled drug are called hydrocodone compounds and are considered Schedule III drugs. Hydrocodone is typically found in combination with other drugs such as paracetamol, aspirin, ibuprofen and homatropine methylbro-mide. The purpose of the non-controlled drugs in combination is often twofold: 1) To provide in-creased analgesia via drug synergy. 2) To limit the intake of hydrocodone by causing unpleasant and often unsafe side effects at higher-than-prescribed doses. In the UK, it is listed as a Class A drug under the Misuse of Drugs Act 1971. Hydrocodone is not available in pure form in the United States due to a separate regulation, and is always sold with an NSAID, paracetamol, antihistamine, expectorant, or homatropine. The cough preparation Codiclear DH is the purest US hydrocodone item, containing guaifenesin and small amounts of ethanol as active ingredients. In Germany and elsewhere, hydro-codone is available as single-active-ingredient tablets as Dicodid available in 5- and 10-mg strengths. As with many other opioids, it is quite possible to reduce the amount of hydrocodone needed to stop a certain level of pain by having the patient take the hydrocodone along with one of the medications with analgesic-sparing properties, also known as potentiators. The most common, one of the most effective with hydrocodone, and safest is hydroxyzine (often marketed under the brand name Vistaril). Orphena-drine, nefopam, carisoprodol, and antihistamines also potentiate most opioids. Especially in the case of carisoprodol, it is imperative that the titration and addition of the potentiator be done under strict super-vision of a physician. Hydrocodone also interacts relatively well with most adjuvant and atypical analgesics used for severe and neuropathic pain such as first-generation anti-depressants, anticholinergics, anticonvulsants, cen-trally acting stimulants, NMDA antagonists, etc. Hydrocodone can usually be successfully used with duloxetine (Cymbalta) for neuropathic pain, especially that from diabetic neuropathy, provided that the patient has normal relative and absolute levels of Cytochrome P450-related liver enzymes. Common side effects include dizziness, itching, lightheadedness, nausea, sweating, drowsiness, consti-pation, vomiting, and euphoria. Vomiting in some patients is so severe that hospitalization is required, although this can be due to alcohol consumption before taking the medication. Some less common side effects are allergic reaction, blood disorders, changes in mood, racing heartbeat, mental fogginess, anxiety, lethargy, difficulty urinating, spasm of the ureter, irregular or depressed respiration, and rash. Generic Zocor (simvastatin)
Simvastatin is a hypolipidemic drug used to control elevated cholesterol, or hypercholesterolemia. It is
a member of the statin class of pharmaceuticals.
Simvastatin is a synthetic derivate of a fermentation product of Aspergillus terreus. The drug is mar-
keted under the trade name Zocor, as well as generically.
The primary uses of simvastatin is for the treatment of dyslipidemia and the prevention of cardiovascu-
lar disease. It is recommended to be used only after other measures such as diet, exercise, and weight
reduction have not improved cholesterol levels.
All statins act by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA reductase, the rate-
limiting enzyme of the HMG-CoA reductase pathway, the metabolic pathway responsible for the en-
dogenous production of cholesterol. Statins are more effective than other lipid-regulating drugs at low-
ering LDL-cholesterol concentration but they are less effective than the fibrates in reducing triglyceride
concentration. However, statins reduce cardiovascular disease events and total mortality irrespective of
the initial cholesterol concentration.
The drug is in the form of an inactive lactone that is hydrolyzed after ingestion to produce the active
agent. It is a white, nonhygroscopic, crystalline powder that is practically insoluble in water, and freely
soluble in chloroform, methanol and ethanol.
The development of simvastatin was closely linked with lovastatin. Biochemist Jesse Huff and his col-
leagues at Merck began researching the biosynthesis of cholesterol in the early 1950s. In 1956, mevalo-
nic acid was isolated from a yeast extract by Karl Folkers, Carl Hoffman, and others at Merck; while
Huff and his associates confirmed that mevalonic acid was an intermediate in cholesterol biosynthesis.
In 1959, the HMG-CoA reductase enzyme (a major contributor of internal cholesterol production) was
discovered by researchers at the Max Planck Institute. This discovery encouraged scientists worldwide
to find an effective inhibitor of this enzyme.
By 1976, Akira Endo had isolated the first inhibitor (Compactin, ML-236B) from the fungus Penicil-
lium citrinium in Sankyo, Japan. In 1979, Hoffman and colleagues isolated lovastatin from a strain of
the fungus Aspergillus terreus. While developing and researching lovastatin, Merck scientists syntheti-
cally derived a more potent HMG-CoA reductase inhibitor from a fermentation product of Aspergillus
terreus, which was designated MK-733 (later to be named simvastatin).
Common side effects (>1% incidence) may include abdominal pain, diarrhea, indigestion, and a gen-
eral feeling of weakness. Rare side effects include joint pain, memory loss, and muscle cramps. Choles-
tatic hepatitis, hepatic cirrhosis, rhabdomyolysis and myositis have been reported in patients receiving
the drug chronically.

Lisinopril
Lisinopril is a drug of the angiotensin-converting enzyme (ACE) inhibitor class that is primarily used
in treatment of hypertension, congestive heart failure, and heart attacks and also in preventing renal and
retinal complications of diabetes. Its indications, contraindications and side effects are as those for all
ACE inhibitors. It has been compared with omapatrilat, which is of similar function.
Historically, lisinopril was the third ACE inhibitor (after captopril and enalapril) and was introduced
into therapy in the early 1990s. Lisinopril has a number of properties that distinguish it from other ACE
inhibitors: It is hydrophilic, has a long half-life andtissue penetration, and is not metabolized by the
liver.
Side effects, some or all of which are serious and require immediate medical attention, include:
Chills, signs of infection
Dark urine, decreased urination (oliguria)
Difficulty swallowing or breathing (signs of angioedema), allergic reaction (anaphylaxis)
Hoarseness
Itching
Yellowing of skin or eyes (jaundice)
Abdominal pain, bloating, vomiting
Chest pain or tightness, dizziness, lightheadedness, fainting (syncope)
Dry cough
Fever
Joint pain
Rash
Diarrhea, nausea
Drowsiness, headache, tiredness
Muscle cramps
Fainting/blackouts
Serious (possibly fatal) liver problems
For adult patients, following oral administration of lisinopril, peak serum concentrations occur within
about 7 hours, although there was a trend to a small delay in time taken to reach peak serum concentra-
tions in acute myocardial infarction patients. Declining serum concentrations exhibit a prolonged termi-
nal phase which does not contribute to drug accumulation. This terminal phase probably represents
saturable binding to ACE and is not proportional to dose. Lisinopril does not appear to be bound to
other serum proteins.
Lisinopril does not undergo metabolism and is excreted unchanged entirely in the urine. Based on uri-
nary recovery, the mean extent of absorption of lisinopril is approximately 25 percent, with large inter-
subject variability (6-60 percent) at all doses tested (5–80 mg). Lisinopril absorption is not influenced
by the presence of food in the gastrointestinal tract. The absolute bioavailability of lisinopril is reduced
to about 16 percent in patients with stable NYHA Class II-IV congestive heart failure, and the volume
of distribution appears to be slightly smaller than that in normal subjects.
The oral bioavailability of lisinopril in patients with acute myocardial infarction is similar to that in
healthy volunteers.
Upon multiple dosing, lisinopril exhibits an effective half-life of accumulation of 12 hours.
Impaired renal function decreases elimination of lisinopril, which is excreted principally through the
kidneys, but this decrease becomes clinically important only when the glomerular filtration rate is be-
low 30 mL/min. Above this glomerular filtration rate, the elimination half-life is little changed. With
greater impairment, however, peak and trough lisinopril levels increase, time to peak concentration in-
creases, and time to attain steady state is prolonged. Older patients, on average, have (approximately
doubled) higher blood levels and area under the plasma concentration time curve (AUC) than younger
patients.
Generic Synthroid (levothyroxine)
Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of
thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems. The
natural hormone is chemically in the chiral L-form, as is the pharmaceutical agent. Dextrothyroxine
(D-thyroxine) briefly saw research as an anticholesterol agent but was pulled due to cardiac side-
effects.
Dosages vary according to the age groups and the individual condition of the patient, body weight and
compliance to the medication and diet. Monitoring of the patient's condition and adjustment of the dos-
age is periodical and necessary. Levothyroxine is taken on an empty stomach approximately half an
hour to an hour before meals.
Dosing must be carefully controlled to achieve TSH levels within the normal reference range. Long-
term suppression of TSH values below normal values will frequently cause cardiac side-effects and
contribute to decreases in bone mineral density (high TSH levels are also well known to contribute to
osteoporosis).
Patients prescribed too high a dose of levothyroxine may experience effects that mimic hyperthyroid-
ism. Overdose can result in heart palpitations, abdominal pain, nausea, anxiousness, confusion, agita-
tion, insomnia, weight loss, and increased appetite. Allergic reactions to the drug are characterized by
symptoms such as difficulty breathing, shortness of breath, or swelling of the face and tongue. Acute
overdose may cause fever, hypoglycemia, heart failure, coma and unrecognized adrenal insufficiency.
Acute massive overdose may be life-threatening; treatment should be symptomatic and supportive.
Massive overdose may require beta-blockers for increased sympathomimetic activity.
The effects of overdosing appear 6 hours to 11 days after ingestion.
Generic Norvasc (amlodipine besylate)

Amlodipine (Norvasc, Pfizer, and generics) (as besylate, mesylate or maleate) is a long-acting calcium
channel blocker (dihydropyridine (DHP) class) used as an anti-hypertensive and in the treatment of an-
gina. Like other calcium channel blockers, amlodipine acts by relaxing the smooth muscle in the arte-
rial wall, decreasing total peripheral resistance and hence reducing blood pressure; in angina it in-
creases blood flow to the heart muscle (although DHP-class calcium channel blockers are more selec-
tive for arteries than myocardium, as the cardiac calcium channels are not of the dihydropyridine-type).
Pfizer patent protection on Norvasc lasted until 2007. Total patent expiration occurred later in 2007. A
number of generic versions are available.
In the United Kingdom tablets of amlodipine from different suppliers may contain different salts. The
strength of the tablets is expressed in terms of amlodipine base, i.e., without the salt. Tablets containing
different salts are therefore considered interchangeable.
The efficacy and tolerability of a fixed-dose combination of amlodipine 5 mg and perindopril 4 mg, an
angiotensin converting enzyme (ACE) inhibitor, have recently been confirmed in a prospective, obser-
vational multicentre trial of 1250 hypertensive patients.
In patients with severe coronary artery disease, amlodipine can increase the frequency and severity of
angina or actually cause a heart attack on rare occasions. This phenomenon usually occurs when first
starting amlodipine, or at the time of dosage increase.
Excessive lowering of blood pressure during initiation of amlodipine treatment can occur, especially in
patients already taking another medication for lowering blood pressure. In rare instances, congestive
heart failure has been associated with amlodipine, usually in patients already on a beta blocker.
Health Information websites:
- www.cdc.gov
- www.medicalnewstoday.com
- www.nih.gov
- www.mayoclinic.com
CEU QUESTIONNAIRE
Complete the questions below to receive 10 continuing education credits. All questions must be answered 1. What is a prescription medication? __________________________________________ _________________________________________________________________________ 2. Rx is the Latin abbreviation meaning what? ___________________________________ _________________________________________________________________________ 3. What is a monograph? ____________________________________________________ _________________________________________________________________________ 4. What two types of opiates does hydrocodone contain? ___________________________ _________________________________________________________________________ 5. Name the 3 forms in which hydrocodone is given. ______________________________ _________________________________________________________________________ 6. In what year was hydrocodone created? And by whom?__________________________ _________________________________________________________________________ 7. Hydrocodone is typically found in combination with what other drugs? _____________ _________________________________________________________________________ 8. What is the most common and safest form of hydrocodone? ______________________ _________________________________________________________________________ 9. What are the most common side effects of taking hydrocodone? ___________________ _________________________________________________________________________ 10. Simvastatin, or Zocor, is used to control what? _______________________________ _________________________________________________________________________ 11. What 3 measures are recommended before prescribing Zocor? ___________________ _________________________________________________________________________ 12. What form is the drug Zocor given?_________________________________________ _________________________________________________________________________ 13. What are the most common side effects of Zocor? _____________________________ __________________________________________________________________________ 14. Name the possible side effects that may result from chronic use of Zocor. ___________ __________________________________________________________________________ 15. What is lisinopril used to treat? _____________________________________________ __________________________________________________________________________ 16. In what year lisinopril introduced into therapy? ________________________________ __________________________________________________________________________ 17. List 3 side effects of lisinopril. _____________________________________________ __________________________________________________________________________ 18. How does the body metabolize lisinopril? ____________________________________ __________________________________________________________________________ 19. What is the half-life of accumulation of lisinopril? ______________________________ 20. Levothyroxine is a synthetic form of what? And what is it used for? _______________ __________________________________________________________________________ 21. What factors determine the dosage of levothyroxine given? ______________________ __________________________________________________________________________ 22. What happens if TSH levels are suppressed long term? _________________________ _________________________________________________________________________ 23. Name 5 results of levothyroxine overdose. ___________________________________ _________________________________________________________________________ 24. What is amlodipine? And what is it used for? _________________________________ _________________________________________________________________________ 25. What effect does amlodipine have on patients with severe coronary artery disease? ___ _________________________________________________________________________ Please mail this CEU back to the NAHP. DO NOT FAX IT IN. Any CEUs
received via fax will be discarded without credit being awarded.
_________________________________________________ _________________________________________________ ____________________ State _______ Zip _____________ Member ID / SSN ___________________________ ISSUE #0112

Source: http://www.nahpusa.com/userfiles/file/ceu/0112%20CEU.pdf

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