Hydrocodone

Also known as

Vicodin, Norco, Lortab, Hysingla ER, Zohydro ER, Hycodan, Robidone, vics, hydros, lorris, tabs, watsons, 357s, vicos

Classification

Opioid, analgesic

Overview

Narcotic analgesic related to codeine, but more potent and more addicting by weight. It is used also as a cough suppressant .

Medical usage

Narcotic analgesic .

Source

Doctor shopping, altered or fraudulent prescriptions, bogus call-in prescriptions, diversion by some physicians and pharmacists, and drug theft are all major sources of this drug .

Why take it?

Sought after effects

• improvement of mood,
• reduction of pain,
• euphoria ,
• increased sense of well-being,
• numbness,
• feeling sleepy or lethargic,
• reduced worry and stress .

Undesired effects

• dizziness,
• constipation,
• nausea,
• vomiting .

Dosage

Abuse

• Threshold - 3 - 5 mg,
• Light - 5 - 10 mg,
• Common - 10 - 25 mg,
• Strong - 25 - 40 mg,
• Heavy - 40 mg + .

How long do its effects last?

Onset of effects

• oral - 10 - 60 minutes , 10 - 30 minutes .

Duration of effects

• oral - 4 - 8 hours , 4 - 6 hours .

After-effects

• all ROA's - 1 - 12 hours .

Pharmacology

The euphoria, anxiety suppression and pain relief effects appear to stem from the way in which opioids mimic endogenous endorphins. Endorphins are responsible for analgesia, causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or excitement. This mimicking of natural endorphins results in the drug's effects. It acts primarily on μ-opioid receptors, with about six times lesser affinity to δ-opioid receptors .

Pharmacodynamics

Hydrocodone, a semisynthetic opiate agonist and hydrogenated ketone derivative, is similar to other phenanthrene derivatives, such as codeine. Used as an analgesic, hydrocodone is combined with acetaminophen, ibuprofen, or aspirin to treat pain. Used as an antitussive, hydrocodone is combined with phenylephrine, pseudoephedrine, phenylpropanolamine, guaifenesin, pyrilamine, pheniramine, or chlorpheniramine. Opiate agonists exert their principal pharmacologic effect at specific receptor binding sites in the CNS and other tissues. There are several subtypes of opiate receptors including the mu receptor (localised in pain modulating regions of the CNS), the kappa receptor (localised in the deep layers of the cerebral cortex), the delta receptor (localised in the limbic regions of the CNS), and the sigma receptor (thought to mediate the dysphoric and psychotomimetic effects of some opiate partial agonists). Agonist activity at the mu or kappa receptor can result in analgesia, miosis, and/or decreased body temperature. Agonist activity at the mu receptor can also result in suppression of opiate withdrawal, whereas antagonist activity can result in precipitation of withdrawal. Opiate agonists act at several sites within the CNS involving several systems of neurotransmitters to produce analgesia, but the precise mechanism of action has not been fully determined. Opiate agonists do not alter the threshold or responsiveness of afferent nerve endings to noxious stimuli nor the conduction of impulses along peripheral nerves. Instead, they alter the perception of pain at the spinal cord and higher levels in the CNS and the person's emotional response to pain .

Absorption

Well absorbed from the gastrointestinal tract .

Bioavailability

Oral 70% - 85% .

Metabolism

Hepatic and also in intestinal mucosa .

Half-life

75 - 180 minutes .

Lethal dosage

LD50 = 85.7mg/kg (subcutaneous, in mice) .

Mechanism of action

Hydrocodone acts as a weak agonist at OP1, OP2, and OP3 opiate receptors within the CNS. Hydrocodone primarily affects OP3 receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as hydrocodone also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability .

Signs of usage

• exaggerating pain symptoms or lying about injury to receive prescriptions,
• requesting frequent refills for the drug,
• seeing two or more doctors for additional prescriptions,
• social isolation, or spending more time away from other people,
• going through money quickly,
• focusing more on obtaining and using hydrocodone than taking part in formerly enjoyable or valued activities,
• marked mood changes .

Effects

Physical effects

• physical euphoria,
• pupil constriction,
• appetite suppression,
• cough suppression,
• orgasm suppression,
• pain relief,
• respiratory depression,
• sedation,
• constipation,
• decreased heart rate,
• difficulty urinating,
• itchiness,
• nausea,
• stomach cramps .

Cognitive effects

• cognitive euphoria,
• compulsive redosing,
• dream potentiation,
• anxiety suppression,
• decreased libido,
• sleepiness .

Minor effects

Common

• constipation,
• nausea .

Less common

• abdominal or stomach pain or discomfort,
• back pain,
• bladder pain,
• bloody or cloudy urine,
• difficult, burning, or painful urination,
• dry mouth,
• frequent urge to urinate,
• heartburn,
• itching skin,
• lower back or side pain,
• muscle spasms,
• vomiting .

Mild effects

• anxiety/dysphoria,
• constipation,
• dizziness,
• drowsiness,
• fatigue,
• headache,
• nausea,
• trouble sleeping/nightmares,
• diffuse muscle weakness,
• itchiness .

Serious side-effects

• bowel obstruction,
• breathing problems,
• slowed or irregular heartbeat,
• severe allergic reaction such as rash, hives, itching or swelling,
• trouble urinating,
• vomiting .

Major effects

Less common

• bloating or swelling of the face, arms, hands, lower legs, or feet,
• body aches or pain,
• chills,
• cough,
• depression,
• difficult or laboured breathing,
• ear congestion,
• fear or nervousness,
• fever,
• headache,
• loss of voice,
• nasal congestion,
• rapid weight gain,
• runny nose,
• sneezing,
• sore throat,
• tightness in the chest,
• tingling of the hands or feet,
• unusual tiredness or weakness,
• unusual weight gain or loss .

Positive

• improvement of mood,
• reduction of pain,
• euphoria .

Neutral

• itching,
• light-headedness,
• sedation,
• changes in focus and attention .

Negative

• dizziness,
• constipation,
• nausea and vomiting,
• when insufflated, burning in nose and sinuses .

Overdose

• cyanosis,
• blurred vision,
• change in consciousness,
• chest pain or discomfort,
• cold and clammy skin,
• confusion,
• constricted pupil (black part of the eye),
• coughing that sometimes produces a pink frothy sputum,
• decreased awareness or responsiveness,
• dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position,
• increased sweating,
• irregular, fast or slow, or shallow breathing,
• lightheadedness, dizziness, or fainting,
• pale skin,
• sleepiness or unusual drowsiness,
• slow or irregular heartbeat,
• weak muscle tone ,
• slowed breathing,
• muscle weakness,
• narrowed or widened pupils,
• coma,
• death .

Dangerous interactions

Dangerous

• Ketamine - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.
• MXE - This combination can potentiate the effects of the opioid.
• DXM - CNS depression, difficult breathing, heart issues, hepatoxic, just very unsafe combination all around. Additionally if one takes dxm, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
• Cocaine - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
• Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.
• GBL / GHB - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.
• Tramadol - Concomitant use of tramadol increases the seizure risk in patients taking other opioids. These agents are often individually epileptogenic and may have additive effects on seizure threshold during coadministration. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
• Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Blackouts/memory loss likely .

Caution

• PCP - PCP can reduce opioid tolerance, increasing the risk of overdose.
• Nitrous oxide - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely.
• Amphetamines - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
• MAOIs - Coadministration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe and fatal adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhoea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases .

Withdrawal

• constant shivering,
• diarrhoea,
• insomnia,
• fever,
• anxiety,
• hallucinations,
• body aches,
• intense sweating,
• nausea,
• vomiting,
• rapid or irregular heartbeat,
• depression .

Drug testing

How long does hydrocodone stay in the urine?

Three to four days after a dose . These are capable of detecting hydrocodone in your system for around 2 - 4 days .

How long can a saliva test detect hydrocodone?

These can only detect hydrocodone during the first 12 - 36 hours after the last pill you took .

How long can a hair test detect hydrocodone?

It can be detected for up to 90 days , .

Detox

Withdrawal from long-term hydrocodone use can be very unpleasant. The opiate withdrawal syndrome is frequently described as having flu-like symptoms. Despite the potential for some profoundly uncomfortable moments, the opiate detox process is not typically life-threatening.

Any one of these symptoms may be enough to send a user back to the drug for relief, and that is why inpatient treatment centers are a safe, caring and effective place to deal with hydrocodone withdrawal.

Some treatment programmes administer medications to ease the patient's withdrawal. This form of medical assistance sometimes involves other potentially addictive substances, and is strictly controlled and monitored by addiction treatment professionals.

Treatment focused on the addiction will prove highly valuable moving forward, but another important part of treatment involves discovering why you became addicted and how you can live without the substance in the future.

Mental health treatment, like cognitive-behavioral therapy, can help those addicted to retrain their minds and teach them new ways to deal with pain and other circumstances that led to substance abuse .

Treatment for hydrocodone addiction is similar to heroin addiction treatment in that it utilises many of the same evidence based methods. Methadone, buprenorphine, and naltrexone are all medications that can be used to stabilise the patient and minimise their chance of relapse. Behavioural therapies can be helpful to change the way an individual thinks about their substance abuse as well as to teach them better coping skills for the future.

Any comorbid disorders associated with one's drug abuse should be assessed and treated in addition to their addiction, and depression is extremely common among hydrocodone addicts. Antidepressants can often be used as well as therapy models like cognitive-behavioral therapy that can treat both addiction and mood disorders at the same time. Depending on the severity of the individual's condition, inpatient care might be necessary, but many people receive proper and effective treatment in an outpatient programme .

Statistics

According to the DEA, hydrocodone is the most commonly prescribed (and the most abused) opioid drug in the United States, and the National Institute on Drug Abuse (NIDA) reports that the US consumes nearly 100% of the world's supply of this drug . The following key statistics illustrate the extent of hydrocodone abuse -

• According to the National Survey on Drug Use and Health and Health (NSDUH), 4 million people over the age of 12 reported using hydrocodone for nonmedical purposes in 2013.
• Over 29,000 hydrocodone-related exposures and 36 deaths were reported in the U.S. in 2012, according to the American Association of Poison Control Centers.
• The Drug Abuse Warning Network (DAWN) estimated that there were more than 82,000 emergency room incidents in 2011 related to non-medical abuse of hydrocodone .

The number of prescriptions for hydrocodone written in the United States has increased dramatically in the last 25 years. This increase in prescriptions has, in turn, increased the rate of prescriptions diverted to the illicit market. The availability of hydrocodone on the black market has skyrocketed as a result .

History

Hydrocodone was first synthesised in Germany in 1920 by Carl Mannich and Helene Löwenheim. Hydrocodone is derived from codeine. As a semi-synthetic opioid, it is most often used orally as a narcotic analgesic and antitussive. Used mostly in combination with Acetaminophen (Vicodin) or Ibuprofen .

The first report, that hydrocodone produces euphoria and habituation symptoms, was published in 1923. The first report of hydrocodone dependence and addiction was published in 1961 .

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