NURSING IN ONE CLICK

spasmo proxy use

2013-01-31T07:26:00.000-08:00

You Are Here: Home » Education » Health Issue » Drug Awareness Education

Some facts of Dextropropoxyphen - A component of Spasmo-proxyvon (SP)

Dr Diamond *

1. Description:

Dextropropoxyphene is classified as an opioid analgesic and is used to treat mild to moderate pain. It can be used to ease pain before, during and after an operation. It is often combined with Acetaminophen and sold in several countries (note: In some countries, compounds containing Dextropropoxyphene are available only with a valid doctor's prescription). Dextropropoxyphene is derived from a much stronger opiate agonist called Methadone. It is approximately 1/2 to 2/3 as potent as Codeine.

Propoxyphene refers to a racemic mixture of both Dextro-Propoxyphene and its optical isomer Levo-Propoxyphene. Dextro-Propoxyphene possesses only mild analgesic activity but no anti-tussive activity. However, with Levo-Propoxyphene, the converse is true (i.e. it possesses only anti-tussive activity but no analgesic activity).

In the United States, Dextropropoxyphene HCI is available as a prescription with Acetaminophen in ratio anywhere from 30 mg/600 mg to 60 mg, 325. mg respectively. These are usually named "Darvocet," "Darvin," or "Darvon." In Australia, dextropoxyphene is available on prescription, both as a combined product (32.5 mg dextropropoxyphene per 325 mg acetaminophen) known as either "Di-gesic", "Capadex", or "Paradex" and in pure form (100 mg capsules) known as "Doloxene". Dextropropoxyphene is marketed in Europe as "Abalgin" amongst other names.

In India, Dextro-Propoxyphene is found in a number of pharmaceutical preparations. The most common are

Brand name ------- Active Ingredients
- Diclofenac Sodium
Buta-PROXYVON - 32.5 mg Dextropropoxyphene HCI
- 400 mg Acetaminophen
PROXYVON - 65 mg Dextropropoxyphene HCI
400 mg Acetaminophen
- 65 mg Dextropropoxyphene HCI
SPASMO- - 400 mg Acetaminophen
PROXYVON 10 mg Dicyclomine

Note: In parts of Southern India, it has come to our attention that the key ingredient in these preparations has changed from bextropropoxyphene HCI to Dextropropoxyphene Napsylate. There are key differences between these formulations:

First, the Napsylate salt form is WATER-IN SOLUBLE. Hence, it cannot be abused by the parenteral route (i.e. by injection);
Second, approximately 100 mg of Dextropro poxyphene Napsylate is equivalent to 65 mg of Dextropropoxyphene Hql.
Third, the onset of action of the Napsylate salt is slightly longer (about an hour) than that of the HCI salt.

2. INDICATIONS:

Analgesia

Dextropropoxyphene, like Codeine, is classified as a "week" opioid. Codeine is more commonly used, however some individuals (approximately 10·20% of the Caucasian population) are unable to metabolize it, due to poor functioning of a hepatic enzyme called CYP2D6. It is in these people that dextropropoxyphene is particularly useful, and does not require CYP2D6 (as it is metabolism is via CYP3A4).

The maximum doses for the constituents of Spasmo Proxyvon (constituents shown above) are as follows:

Acetaminophen: 2-4 grams/day
Dextro-Propoxyphene HCI : 390 mg/day
Dextro-Propoxyphene Napsylate : 600 mg/day
Dicyclomine : No available safety data for dos es above 80 mg/day

Opioid Withdrawal

In pure form, Dextropropoxyphene is commonly used to ease the withdrawal symptoms in people addicted to opioids. However, being very weak in comparison to those opioids which are commonly abused, dextropropoxyphene can only act as a "partial" substitute. It does not have much effect or mental cravings; however it can be effective in alleviating physical withdrawal effects such as muscle cramps.

Dextropropoxyphene is subject to some controversy: whilst many physicians prescribe it for a wide range of mild to moderately painful symptoms as well as in treatment of diarrhoea, many others refuse to prescribe it, citing its highly addictive nature and limited effectiveness (some studies show it to be no more effective as a painkiller than aspirin).

The therapeutic index of dextropoxyphene is relatively small. In the UK, dextropropoxyphene and co-proxamol are now discouraged from general use, and since 2004 preparations containing only dextropropoxyphene have been discontinued. This has been a somewhat controversial decision, since it has caused abusers to switch to the combined product and risk acetminophen toxicity. So far, Australia has declined to follow suit, and opted to allow pure dextropropoxyphene to remain available by prescription.

3. PHARMACOKETICS :

Dextropropoxyphene (DPP) has a 1/2 life of 6 to 12 hours. However, its metabolite, norpropoxyphene (NPP) has a 1/2 life of 30 to 36 hours. After oral ingestion, onset of effects is usually 1 hour, with peak plasma concentrations achieved within 2 - 21/2 hours. Repeated doses (at intervals of 6 hrs.), lead to increasing plasma concentrations, eventually reaching a plateau at/after the 9th dose (at 48 hrs.).

It is worth knowing that due to extensive first-pass metabolism of DPP, the plasma concentrations after a single dose may be four times lower than those found in steady state (achieved with regular dosing at 6 hr. intervals). Also, with repeated dosing, it takes longer for the metabolite to be eliminated. On the whole, the metabolism of DPP takes a lot longer than that of morphine.

4. ADVERSE EFFECTS:

Side effects ( just as with other opiates) include:

impairment of mental performance.
euphoria.
drowsiness.
lethargy.
blurred vision.
miosis (constriction of pupils)
decreased appetite.
inhibition of the cough reflex (antitussive effect)
respiratory depression.
constipation.

Overdose is commonly broken into two categories: liver toxicity (from acetaminophen poisoning) and dextropropoxyphene overdose. Many users experience toxic effects from the acetaminophen in pursuit of the endnessly-increasing dose required to achieve euphoria. They suffer acute liver toxicity, which causes severe stomach pain, nausea, and vomiting (all of which are increased by light or stimulation of the sense of sight).

Dextropropoxyphene also has several other non-opioid side-effects.

Both propoxyphene and its metabolite norpropoxyphene, have local anesthetic effects at concentrations about 10 times those necessary for opioid effects. In this respect, norpropoxyphene is more potent than propoxyphene, and they are both more potent than indocaine.

Both propoxyphene and norpropoxyphene also have direct cardiac effects which include decreased heart rate, decreased contractibility, and decreased electrical conductity (i.e. increase PR, AH, HV and QRS intervals). Norpropoxyphene is several times more potent than propoxyphene in this activity. These effects appear to be due to their local anesthetic activity and are not reversed by naloxone.

Both propoxyphene and norpropoxyphene are potent blockers of cardiac membrane sodium channels and are more potent than lidocaine, quinidine, and procainamide in this respect. They (propoxyphene and nor-propoxyphene) appear to have the characteristics of a Vaughn Williams Class IC antiarrhythmic.

5. TOXICOLOGICAL MECHANISM:

Excessive opioid receptor stimulation is responsible for the CNS depression, respiratory depression, miosis, and gastrointestinal effects seen in propoxyphene poisoning. It may also account for mood/thought altering effects. Local anesthetic activity appears to be responsible for the arrhythmias and cardiovascular depression seen in propoxyphene poisoning. Widening of the QRS complex appears to be a result of a quinidine - like effect of propoxyphene, and sodium bicarbonate therapy appears to have a positive direct effect on the QRS dysrhythmia.

Seizures may result from either opioid or local anesthetic effects. Pulmonary edema may result from direct pulmonary toxicity, neurogenic/anoxic effects, or cardiovascular depression.

6. RECREATIONAL USE:

The general consensus amongst recreational drug-users is that Dextropropoxyphene, when injected, products an amazing rush, on par with heroin. However, there is very little euphoria that occurs after the rush, so users tend to keep on injecting on an hourly basis to continue experiencing the rush throughout the day.

This is in direct contrast with injecting Methadone, where IDUs (Injection Drug Users) describe little to no "rush" upon intravenous administration, but a tremendous euphoria that lasts for quite a long time (in comparison with most shorter-acting opiates like Heroine or Morphine)

7. Question/Answer:

How can I get rid of an addiction to Spasmo-Proxyvon (SP)
Q. I am addicted to SP for the past 2 years. I want to stop taking this drug. Please suggest a few tips. I had tried to stop for about 16 days' during which I could not sleep and I had pain in my legs. The food also tasted bad (question from an SP addict.)
A. Spasmo Proxyvon contains dextropropoxyphene which is a weak opiod (opium-like) agent. You should gradually reduce the dose slowly but steadily and surely over the next few weeks. With a strong will power, it is not difficult. Please keep in mind that the situation will become worse if you do not stop now and you may need to go to a de-addiction centre.

2013-01-31T06:48:00.001-08:00

Unbound MEDLINE

Clinical evaluation of cefotaxime versus gentamicin plus clindamycin in the treatment of polymicrobial peritonitis.

Abstract

One hundred fifty-one patients with presumed aerobic-anaerobic mixed peritoneal infections were treated in a prospective, randomized trial with either cefotaxime alone (76) or the combination of gentamicin-clindamycin (75). Primary and complicating foci of sepsis were cultured for both aerobic and anaerobic pathogen identification and antibiotic susceptibility. In vitro aerobic disk sensitivities (114 isolates) to cefotaxime were 82% and to gentamicin, 88%; anaerobic agar-diffusion sensitivities (227 isolates) to cefotaxime were 87% and to clindamycin, 98%. Only enterococci and Pseudomonas sp were consistently resistant to cefotaxime. Infection was eliminated in 82% of those treated with cefotaxime and in 87% of those treated with the gentamicin-clindamycin combination, yet sepsis recurred in 11% of those treated with cefotaxime and in 13% for those given gentamicin-clindamycin. Five patients (7%) demonstrated nephrotoxicity for gentamicin. (Serum creatinine increased greater than 1.5 mg/100 ml over pretreatment levels.) Otherwise, incidence and severity of adverse reactions were identical for the two groups and consisted primarily of phlebitis and diarrhea. One patient in each treatment group died of uncontrolled sepsis. Although results suggested a laboratory superiority of gentamicin-clindamycin, there was a clinical equality in therapeutic benefit and a greater safety following the use of cefotaxime alone.

Authors

Stone HH, Geheber CE, Kolb LD, Strom PR

Source

Clinical therapeutics 5 Suppl A: 1982 pg 1-9

MeSH

Adolescent
Adult
Aged
Bacterial Infections
Cefotaxime
Clindamycin
Drug Therapy, Combination
Female
Gentamicins
Humans
Male
Microbial Sensitivity Tests
Middle Aged
Peritonitis

Pub Type(s)

Clinical Trial
Comparative Study
Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

6293712

2013-01-02T23:16:00.001-08:00

Definition of tuberculosis

noun

[mass noun]

an infectious bacterial disease characterized by the growth of nodules (tubercles) in the tissues, especially the lungs.
- The disease is caused by the bacterium Mycobacterium tuberculosis or (especially in animals) a related species; Gram-positive acid-fast rods

The most common form, pulmonary tuberculosis (formerly known as ‘consumption’), is caused by inhalation of the bacteria. It was widespread in 19th-century Europe, and still causes millions of deaths each year in developing countries. The disease can affect other parts of the body, notably the bones and joints and the central nervous system. Its spread is countered by vaccination and by the pasteurization of milk to prevent transmission from cattle. It was once considered incurable, but early X-ray diagnosis permits its arrest by drugs and surgery

Origin:

Causes of Tuberculosis

Cases of tuberculosis are caused by a bacterium called Mycobacterium tuberculosis. This bacterium typically attacks the lungs but may also attack other parts of the body such as the kidney, spine, and brain. Tuberculosis may also be linked to certain risk factors, including alcoholism, IV drug abuse, and homelessness.

Know the Risk Factors

Research has shown that people with certain risk factors are more likely to develop tuberculosis. A risk factor is anything that increases a person's chance of developing a disease.

Specific tuberculosis risk factors include:

Alcoholism
IV drug abuse
Crowded living conditions
Homelessness
Poverty
Immigration from certain countries
Low body weight
Certain medical treatments (such as corticosteroid treatment or organ transplants)
Certain medical conditions, such as:

HIV or AIDS
Diabetes mellitus
Silicosis
Cancer of the head or neck
Leukemia or Hodgkin's disease

Severe kidney disease
Certain treatments for rheumatoid arthritis or Crohn's disease.

2013-01-02T23:01:00.000-08:00

Coronary heart disease

Coronary artery disease; Arteriosclerotic heart disease; CHD; CAD

Last reviewed: June 22, 2012.

Coronary heart disease (CHD) is a narrowing of the small blood vessels that supply blood and oxygen to the heart. CHD is also called coronary artery disease.

Causes, incidence, and risk factors

Coronary heart disease (CHD) is the leading cause of death in the United States for men and women.

Coronary heart disease is caused by the buildup of plaque in the arteries to your heart. This may also be calledhardening of the arteries.

Fatty material and other substances form a plaque build-up on the walls of your coronary arteries. The coronary arteries bring blood and oxygen to your heart.
This buildup causes the arteries to get narrow.
As a result, blood flow to the heart can slow down or stop.

A risk factor for heart disease is something that increases your chance of getting it. You cannot change some risk factors for heart disease, but others you can change. See: Heart disease - risk factors

Symptoms

Symptoms may be very noticeable, but sometimes you can have the disease and not have any symptoms. This is especially true in the early stages of heart disease.

Chest pain or discomfort (angina) is the most common symptom. You feel this pain when the heart is not getting enough blood or oxygen. How bad the pain is varies from person to person.

It may feel heavy or like someone is squeezing your heart. You may feel it under your breast bone (sternum), but also in your neck, arms, stomach, or upper back.
The pain usually occurs with activity or emotion, and goes away with rest or a medicine callednitroglycerin.
Other symptoms include shortness of breath and fatigue with activity (exertion).

Women, elderly people, and people with diabetes are more likely to have symptoms other than chest pain, such as:

Fatigue
Shortness of breath
General weakness

Signs and tests

Your doctor or nurse will examine you. Your doctor will often order more than one test before making a diagnosis.

Tests may include:

Coronary angiography -- an invasive test that evaluates the heart arteries under x-ray
Echocardiogram stress test
Electrocardiogram (ECG)
Electron-beam computed tomography (EBCT) to look for calcium in the lining of the arteries -- the more calcium, the higher your chance for CHD
Exercise stress test
Heart CT scan
Nuclear stress test

Treatment

You may be asked to take one or more medicines to treat blood pressure, diabetes, or high cholesterol levels. Follow your doctor's directions closely to help prevent coronary artery disease from getting worse.

Goals for treating these conditions in people who have coronary artery disease:

Blood pressure less than or equal to 140/90 (even lower for patients with diabetes, kidney disease, or heart failure)
HbA1c levels if you have diabetes at a level recommended by your doctor
LDL cholesterol level less than or equal to 100 mg/dL (even lower for some patients)

Treatment depends on your symptoms and how severe the disease is. Your doctor may give you one or more medicines to treat heart disease, blood pressure, diabetes, or high cholesterol. Follow your doctor's directions closely to help prevent coronary artery disease from getting worse.

Never stop taking your medicines without talking to your doctor first. Stopping heart medicines suddenly can make your angina worse or cause a heart attack.

Your doctor may refer you to a cardiac rehabilitation program to help improve your heart's fitness.

Procedures and surgeries used to treat CHD include:

Angioplasty and stent placement, called percutaneous coronary interventions (PCIs)
Coronary artery bypass surgery
Minimally invasive heart surgery

Expectations (prognosis)

Everyone recovers differently. Some people can maintain a healthy life by changing their diet, stopping smoking, and taking medications exactly as the doctor prescribes. Others may need medical procedures such as angioplasty or surgery.

Although everyone is different, early detection of CHD generally results in a better outcome.

Calling your health care provider

If you have any risk factors for CHD, contact your doctor to discuss prevention and possible treatment.

Immediately contact your health care provider, call the local emergency number (such as 911), or go to the emergency room if you have:

Angina or chest pain
Shortness of breath

2013-01-02T23:00:00.001-08:00

2012-12-25T22:18:00.000-08:00

2012-12-12T12:53:00.001-08:00

2012-12-12T12:46:00.001-08:00

2012-12-12T12:43:00.001-08:00

2012-12-12T12:34:00.001-08:00

by this super camera in minimum rate

2012-12-12T12:27:00.002-08:00

2012-12-12T12:23:00.000-08:00

2012-12-02T23:09:00.001-08:00

2012-12-02T23:01:00.002-08:00

2012-11-20T05:30:00.000-08:00

2012-11-13T07:20:00.001-08:00

2012-11-13T01:01:00.003-08:00

2012-11-13T01:01:00.001-08:00

2012-11-13T01:00:00.002-08:00

jernal pharmacology

2012-11-10T22:07:00.002-08:00

"ltr" style="text-align: left;" trbidi="on">

Add capkkkiijhhtion

Add caption

2012-11-10T11:57:00.001-08:00

2012-10-11T10:18:00.001-07:00

about interview ppt

2012-10-09T19:27:00.002-07:00