Anectine and Weed
Edited by Hugh Soames
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Anectine and Weed
Most people who consume marijuana do so for its mood-altering and relaxing abilities. Weed gives people a high and allows them to relax. However, heavy consumption of weed can cause unwanted results. It can increase the anxiety and depression a person experiences, and it can interact with certain other drugs including Anectine. It is important to remember that interactions do occur with all types of drugs, to a great or lesser extent and this article details the interactions of mixing Anectine and Weed.
Mixing Anectine and Weed
Suxamethonium chloride, also known as suxamethonium or succinylcholine, or simply sux by medical abbreviation, is a medication used to cause short-term paralysis as part of general anesthesia. This is done to help with tracheal intubation or electroconvulsive therapy. It is administered by injection, either into a vein or into a muscle. When used in a vein, onset of action is generally within one minute and effects last for up to 10 minutes.
Common side effects include low blood pressure, increased saliva production, muscle pain, and rash. Serious side effects include malignant hyperthermia, hyperkalemia and allergic reactions. It is not recommended in people who are at risk of high blood potassium or a history of myopathy. Use during pregnancy appears to be safe for the baby.
Suxamethonium is in the neuromuscular blocker family of medications and is of the depolarizing type. It works by blocking the action of acetylcholine on skeletal muscles.
Suxamethonium was described as early as 1906 and came into medical use in 1951. It is on the World Health Organization’s List of Essential Medicines. Suxamethonium is available as a generic medication.
Succinylcholine chloride injection is indicated, in addition to general anesthesia, to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation.
Its medical uses are limited to short-term muscle relaxation in anesthesia and intensive care, usually for facilitation of endotracheal intubation. It is popular in emergency medicine due to its rapid onset and brief duration of action. The former is a major point of consideration in the context of trauma care, where endotracheal intubation may need to be completed very quickly. The latter means that, should attempts at endotracheal intubation fail and the person cannot be ventilated, there is a prospect for neuromuscular recovery and the onset of spontaneous breathing before low blood oxygen levels occurs. It may be better than rocuronium in people without contraindications due to its faster onset of action and shorter duration of action.
Suxamethonium is also commonly used as the sole muscle relaxant during electroconvulsive therapy, favoured for its short duration of action.
Suxamethonium is quickly degraded by plasma butyrylcholinesterase and the duration of effect is usually in the range of a few minutes. When plasma levels of butyrylcholinesterase are greatly diminished or an atypical form is present (an otherwise harmless inherited disorder), paralysis may last much longer, as is the case in liver failure or in neonates.
It is recommended that the vials be stored at a temperature between 2°-8 °C. The multi-dose vials are stable for up to 14 days at room temperature without significant loss of potency. Unless otherwise indicated in the prescribing information, room temperature for storage of medications is 15°-25 °C (59°-77 °F).
Side effects include malignant hyperthermia, muscle pains, acute rhabdomyolysis with high blood levels of potassium, transient ocular hypertension, constipation and changes in cardiac rhythm, including slow heart rate, and cardiac arrest. In people with neuromuscular disease or burns, an injection of suxamethonium can lead to a large release of potassium from skeletal muscles, potentially resulting in cardiac arrest. Conditions having susceptibility to suxamethonium-induced high blood potassium are burns, closed head injury, acidosis, Guillain–Barré syndrome, cerebral stroke, drowning, severe intra-abdominal sepsis, massive trauma, myopathy, and tetanus.
Suxamethonium does not produce unconsciousness or anesthesia, and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. Therefore, administration of the drug to a conscious patient is contraindicated.
The side effect of high blood potassium may occur because the acetylcholine receptor is propped open, allowing continued flow of potassium ions into the extracellular fluid. A typical increase of potassium ion serum concentration on administration of suxamethonium is 0.5 mmol per liter.The increase is transient in otherwise healthy patients. The normal range of potassium is 3.5 to 5 mEq per liter. High blood potassium does not generally result in adverse effects below a concentration of 6.5 to 7 mEq per liter. Therefore, the increase in serum potassium level is usually not catastrophic in otherwise healthy patients. Severely high blood levels of potassium can cause changes in cardiac electrophysiology, which, if severe, can result in arrhythmias and even cardiac arrest.
Malignant hyperthermia (MH) from suxamethonium administration can result in a drastic and uncontrolled increase in skeletal muscle oxidative metabolism. This overwhelms the body’s capacity to supply oxygen, remove carbon dioxide, and regulate body temperature, eventually leading to circulatory collapse and death if not treated quickly.
Susceptibility to malignant hyperthermia is often inherited as an autosomal dominant disorder, for which there are at least six genetic loci of interest, the most prominent being the ryanodine receptor gene (RYR1). MH susceptibility is phenotype and genetically related to central core disease (CCD), an autosomal dominant disorder characterized both by MH symptoms and by myopathy. MH is usually unmasked by anesthesia, or when a family member develops the symptoms. There is no simple, straightforward test to diagnose the condition. When MH develops during a procedure, treatment with dantrolene sodium is usually initiated; dantrolene and the avoidance of suxamethonium administration in susceptible people have markedly reduced the mortality from this condition.
The normal short duration of action of suxamethonium is due to the rapid metabolism of the drug by non-specific plasma cholinesterases. However plasma cholinesterase activity is reduced in some people due to either genetic variation or acquired conditions, which results in a prolonged duration of neuromuscular block. Genetically, ninety six percent of the population have a normal (Eu:Eu) genotype and block duration; however, some people have atypical genes (Ea, Es, Ef) which can be found in varying combinations with the Eu gene, or other atypical genes (see Pseudocholinesterase deficiency). Such genes will result in a longer duration of action of the drug, ranging from 20 minutes up to several hours. Acquired factors that affect plasma cholinesterase activity include pregnancy, liver disease, kidney failure, heart failure, thyrotoxicosis, and cancer, as well as a number of other drugs.
If unrecognized by a clinician it could lead to awareness if anesthesia is discontinued whilst still paralyzed or hypoxemia (and potentially fatal consequences) if artificial ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed.
Mivacurium, a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity.
Deliberate induction of conscious apnea using this drug led to its use as a form of aversion therapy in the 1960s and 1970s in some prison and institutional settings. This use was discontinued after negative publicity concerning the terrifying effects on subjects of this treatment and ethical questions about the punitive use of painful aversion.[citation needed]
There are two phases to the blocking effect of suxamethonium.
Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor’s monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum.
In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by acetylcholinesterase. The muscle cell is then ready for the next signal.
Suxamethonium has a longer duration of effect than acetylcholine, and is not hydrolyzed by acetylcholinesterase. By maintaining the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization.
Calcium is removed from the muscle cell cytoplasm independent of repolarization (depolarization signaling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculations.
The results are membrane depolarization and transient fasciculations, followed by flaccid paralysis.
While this phase is not abnormal and is a part of its mechanism of action, it is undesirable during surgery, due to the inability to depolarize the cell again. Often, patients must be on a ventilator for hours if Phase 2 block occurs. It is caused by the blood concentration of suxamethonium exceeding the therapeutic window. Desensitization occurs at the nerve terminal, and the myocyte becomes less sensitive to acetylcholine; the membrane repolarizes and cannot be depolarized again.
Suxamethonium is an odorless, white crystalline substance. Aqueous solutions have a pH of about 4. The dihydrate melts at 160 °C, whereas the anhydrous melts at 190 °C. It is highly soluble in water (1 gram in about 1 mL), soluble in ethyl alcohol (1 gram in about 350 mL), slightly soluble in chloroform, and practically insoluble in ether. Suxamethonium is a hygroscopic compound. The compound consists of two acetylcholine molecules that are linked by their acetyl groups. It can also be viewed as a central moiety of succinic acid with two choline moieties, one on each end.
Suxamethonium was first discovered in 1906 by Reid Hunt and René de M. Taveau. When studying the drug, animals were given curare and thus they missed the neuromuscular blocking properties of suxamethonium. Instead in 1949 an Italian group led by Daniel Bovet was first to describe succinylcholine induced paralysis. The clinical introduction of suxamethonium was described in 1951 by several groups. Papers published by Stephen Thesleff and Otto von Dardel in Sweden are important but also to be mentioned is work by Bruck, Mayrhofer and Hassfurther in Austria, Scurr and Bourne in UK, and Foldes in America.
Dubai authorities deem that the murder of Hamas operative Mahmoud al-Mabhouh was carried out on their soil by Mossad agents with the use of suxamethonium chloride injection. Entering Dubai under false passports in 2010, the Mossad agents found al-Mabhouh at a hotel, immobilized him with the drug, electrocuted him, then suffocated him by pillow in an assassination. A high concentration of suxamethonium chloride was found in al-Mabhouh’s body post-mortem. The incident triggered significant diplomatic crises in the Middle East, Europe, and Australia.
It was used by serial killer Efren Saldivar (1988-1998), and in the murder of Kathy Augustine (2006).
It is available in German-speaking countries under the trade name Lysthenon among others.
It is sometimes used in combination with pain medications and sedatives for euthanasia and immobilization of horses.
Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between Anectine and Weed and an increase in anxiety.
Anyone mixing Anectine and weed is likely to experience side effects. This happens with all medications whether weed or Anectine is mixed with them. Side effects can be harmful when mixing Anectine and weed. Doctors are likely to refuse a patient a Anectine prescription if the individual is a weed smoker or user. Of course, this could be due to the lack of studies and research completed on the mixing of Anectine and Weed.
Heavy, long-term weed use is harmful for people. It alters the brain’s functions and structure, and all pharmaceuticals and drugs including Anectine are designed to have an impact on the brain. There is a misplaced belief that pharmaceuticals and medication work by treating only the parts of the body affected yet this is obviously not the case in terms of Anectine. For example, simple painkiller medication does not heal the injury, it simply interrupts the brains functions to receive the pain cause by the injury. To say then that two drugs, Anectine and Weed, dol not interact is wrong. There will always be an interaction between Anectine and Weed in the brain11.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/.
One of the milder side effects of mixing Anectine and Weed is Scromiting. This condition, reportedly caused by mixing Anectine and Weed, describes a marijuana-induced condition where the user experiences episodes of violent vomiting, which are often so severe and painful that they cause the person to scream. The medical term for Scromiting by mixing Anectine and Weed is cannabinoid hyperemesis syndrome, or CHS. For these reasons, some people choose to quit smoking weed.
It was first included in scientific reports in 2004. Since then, researchers have determined that Scromiting is the result of ongoing, long-term use of marijuana—particularly when the drug contains high levels of THC, marijuana’s main psychoactive ingredient. Some experts believe that the receptors in the gut become overstimulated by THC, thus causing the repeated cycles of vomiting.
In the long run, a person can become even more depressed. There is a belief that marijuana is all-natural and not harmful to a person’s health. This is not true and Anectine and weed can cause health issues the more a person consumes it.
How does Weed effect the potency of Anectine?
The way in which the body absorbs and process Anectine may be affected by weed. Therefore, the potency of the Anectine may be less effective. Marijuana inhibits the metabolization of Anectine. Not having the right potency of Anectine means a person may either have a delay in the relief of their underlying symptoms.
A person seeking Anectine medication that uses weed should speak to their doctor. It is important the doctor knows about a patient’s weed use, so they can prescribe the right Anectine medication and strength. Or depending on level of interactions they may opt to prescribe a totally different medication. It is important for the doctor to know about their patient’s marijuana use. Weed is being legalized around the US, so doctors should be open to speaking about a patient’s use of it.
Sideffects of Anectine and Weed
Many individuals may not realize that there are side effects and consequences to mixing Anectine and Weed such as:
- Dizziness
- Sluggishness
- Drowsiness
- Shortness of breath
- Itching
- Hives
- Palpitations
- Respiratory Depression
- Cardiac Arrest
- Coma
- Seizures
- Death
Interestingly, it is impossible to tell what effect mixing this substance with Weed will have on an individual due to their own unique genetic make up and tolerance. It is never advisable to mix Anectine and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing Anectine and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of Anectine and Weed is not recommended.
Taking Anectine and Weed together
People who take Anectine and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of Anectine and weed depend on whether you consume more weed in relation to Anectine or more Anectine in relation to weed.
The use of significantly more weed and Anectine will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.
People who take both weed and Anectine may experience effects such as:
- reduced motor reflexes from Anectine and Weed
- dizziness from Weed and Anectine
- nausea and vomiting due to Anectine and Weed
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Anectine leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Mixing weed and Anectine
The primary effect of weed is influenced by an increase in the concentration of the inhibitory neurotransmitter GABA, which is found in the spinal cord and brain stem, and by a reduction in its effect on neuronal transmitters. When weed is combined with Anectine this primary effect is exaggerated, increasing the strain on the body with unpredictable results.
Weed and Anectine affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of Anectine and weed have a greater adverse effect yet leading medical recommendation is that smaller does of Anectine can be just as harmful and there is no way of knowing exactly how Anectine and weed is going to affect an individual before they take it.
Taking Anectine and weed together
People who take Anectine and weed together will experience the effects of both substances. The use of significantly more Anectine with weed will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.
People who take both weed and Anectine may experience effects such as:
- reduced motor reflexes from Anectine and weed
- dizziness from weed and Anectine
- nausea and vomiting of the Anectine
Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Anectine leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.
Weed Vs Anectine
Taking Anectine in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of Anectine and weed may have difficulty forming new memories. With weed vs Anectine in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of Anectine when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of Anectine and weed can lead to permanent changes in the brain22.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741114/.
Anectine Vs Weed
Studies investigating the effects of drugs such as Anectine and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when Anectine and weed are combined. Severe and dangerous side effects can occur when medications are mixed in the system, and sleep disorders are a common side effect of taking weed and Anectine together.
When a small to medium amount of weed is combined with Anectine, sleep disorders such as sleep apnea can occur. According to the latest data from the US Centers for Disease Control and Prevention (CDC) most ER visits and hospitalizations caused by too much weed were associated with other substances such as Anectine.
How long after taking Anectine can I smoke weed or take edibles?
To avoid any residual toxicity it is advisable to wait until the Anectine has totally cleared your system before taking weed, even in small quantities.
Overdose on Anectine and weed
In the case of Overdose on Anectine or if you are worried after mixing Anectine and weed, call a first responder or proceed to the nearest Emergency Room immediately.
If you are worried about someone who has taken too much Anectine or mixed weed with Anectine then call a first responder or take them to get immediate medical help. The best place for you or someone you care about in the case of a medical emergency is under medical supervision. Be sure to tell the medical team that there is a mix of Anectine and weed in their system.
Excessive Weed intake and result in scromiting, chs, and anxiety disorder. It is advisable to quit vaping weed if you are feeling these symptoms.
Mixing Anectine and weed and antidepressants
Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use Anectine and weed. These individuals may not realize that there are side effects and consequences to consuming both Anectine, marijuana and a range of antidepressants.
Studies on weed, Anectine and antidepressants is almost nil. The reason for so little information on the side effects of the two is mostly down to marijuana being illegal in most places – although a number of states in the United States have legalized the drug.
Self-medicating with Weed and Anectine
A lot of people suffer from depression caused by weed and Anectine. How many? According to Anxiety and Depression Association of America (ADAA), in any given year, it is estimated that nearly 16 million adults experience depression. Unfortunately, that number is likely to be wrong due to under reporting. Many people do not report suffering from depression because they do not want to be looked at as suffering from a mental illness. The stigmas around mental health continue and people do not want to be labeled as depressed.
Potential side effects from mixing Anectine and weed
Quitting weed to take Anectine
Medical professionals say an individual prescribed or taking Anectine should not stop using weed cold turkey. Withdrawal symptoms can be significant. Heavy pot users should especially avoid going cold turkey. The side effects of withdrawal from weed include anxiety, irritability, loss of sleep, change of appetite, and depression by quitting weed cold turkey and starting to take Anectine.
A person beginning to use Anectine should cut back on weed slowly. While reducing the amount of weed use, combine it with mindfulness techniques and/or yoga. Experts stress that non-medication can greatly improve a person’s mood.
Weed and Anectine can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and Anectine may include:
- loss of motor skills
- poor or lack of coordination
- lowered blood pressure
- short-term memory loss
- increased heart rate
- increased blood pressure
- anxiety
- paranoia
- increased energy
- increased motivation
Mixing Anectine and weed can also produce hallucinations in users. This makes marijuana a hallucinogenic for some users. Weed creates different side effects in different people, making it a very potent drug. Now, mixing Anectine or other mental health drugs with weed can cause even more unwanted side effects.
Mixing drugs and weed conclusion
Long-term weed use can make depression and anxiety worse. In addition, using marijuana can prevent Anectine from working to their full potential33.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/. Weed consumption should be reduced gradually to get the most out of prescription medication. Marijuana is a drug and it is harmful to individual’s long-term health. Weed has many side effects and the consequences are different to each person who uses it, especially when mixed with Anectine.
If you take Anectine, and also drink Alcohol or MDMA, you can research the effects of Anectine and Alcohol , Anectine and Cocaine as well as Anectine and MDMA here.
To find the effects of other drugs and weed refer to our Weed and Other Drugs Index A to L or our Weed and Other Drugs Index M-Z.
Or you could find what you are looking for in our Alcohol and Interactions with Other Drugs index A to L or Alcohol and Interactions with Other Drugs index M to Z , Cocaine and Interactions with Other Drugs index A to L or Cocaine and Interactions with Other Drugs index M to Z or our MDMA and Interactions with Other Drugs Index A to L or MDMA and Interactions with Other Drugs Index M to Z.
Anectine and Weed
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