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Neurological Effects of Heroin Use

May 6, 2011 · Posted in Heroin 

Heroin is derived from the pulp drying opium poppies that have a content of morphine and codeine, which is an effective pain reliever and is widely used in medicine for the treatment of cough and diarrhea drug.

Heroin has been known by humans at least since 6000 years ago, and is known comes from the tree of happiness. In the 7th century or the 8th, suspected Arab traders took it to China and used as a medicine. After that, the English and Portuguese to supply China with opium and put the UK as the world’s largest heroin.

New in 1874 people make heroin and opium poppies. At that time, heroin is sold as a safe substitute for morphine and not addictive. But eventually it was realized that heroin addiction also causes a high, then in England in 1920 prohibited by law, the Dangerous Drug Act.

The use of heroin have been increasing since early 1990 and experienced a boom since 1996. According to the National Household Survey on drug abuse in the USA in 1996 as many as 2.4 million people had used heroin. In Indonesia the number of people with narcotics in 1995 was 130,000 people (0.065%). Narcotics Users are mostly young people aged 26 years.

The death rate due to the use of heroin in Indonesia reached 17.6%. Heroin (diasetilmorfin) including the group of opioid agonists and is a derivative of morphine which is made from morphine which had acetylation of the hydroxyl group at C3 and C6 bond.

Other names of heroin: smack, junk, china ehirte, chiva, black tar, speed balling, dope, brown, dog, Negra, Nod, white hores, stuff.

Pharmacokinetic

Absorption

Heroin is absorbed well in the subcutaneous, intramuscular and mucosal surface of the nose or mouth.

 

Distribution

Heroin with a quick entry into the blood and into the network. High concentration of heroin in the lungs, liver, kidney and spleen, whereas in low concentrations in skeletal muscle. Concentration in the brain is relatively low compared to other organs due to blood brain barrier. Heroin penetrate the blood brain barrier more easily and rapidly than with morphine or other opioids class.

 

Metabolism

Heroin hydrolysis in the brain rapidly became monoasetilmorfin and eventually became the morphine, then experience an advanced glukuronik acid conjugation with morphine 6-glukoronid a stronger analgesic effect than morphine alone. Drug accumulation occurs in patients with renal failure.

 

Excretion

Heroin / morphine diekstresi mainly through the urine (kidney). 90% is excreted within the first 24 hours, although it can still be found in urine 48 hours in the body is converted into heroin and morphine is excreted as morphine.

 

Pharmacodynamic

Working Mechanism.

Opioid agonists cause analgesia due to binding to specific receptors located in the brain and spinal cord, thus affecting the transmission and modulation of pain. There are 3 types of specific receptors, namely μ receptor (mu), δ (delta) and κ (kappa). In the brain there are three kinds of peptides whose activities endogeneus like opiates, yitu enkephalin binding to δ receptors, β endorphin to μ receptors dandynorpin with resptor κ. Μ receptor is the receptor for morphine (heroin). The three types of receptors is associated with G proteins and is paired with adenilsiklase cause a decrease in the formation of cyclic AMP thus inhibited the activity of neurotransmitter release.

 

Inhibitory effects of opiates in the release of neurotransmitters.

The release of noradrenaline.

Opiates inhibit noradrenaline release by activating μ receptors located in the area noradrenaline. Morphine effect is not limited in the cortex, but also in the hippocampus, amygdala, cerebellum, and locus cereleus periaquaductal area.

 

Disposal asetikolin

Asetikolin release inhibition occurs by receptor deltha striatum region, the amygdala and hippocampus region by μ receptors.

Release of dopamine release by dopamine diinhibisi kappa receptor activity.

 

Workplace

There are two places that the main opiate drugs work, namely the central nervous system and visceral. In the central nervous system opiate effect in several regions including cortex, hippocampus, thalamus, hypothalamus, nigrostriatal, mesolimbik system, locus coreleus, periaquaductal region, medulla oblongata and spinal cord. In the visceral nervous system, opiates work on myenterikus plexus and plexus submukous that cause constipation effect.

 

Effects to other organ systems

Central nervous system

1. Analgesia

Analgesic efficacy is based on 3 factors:

  • Increase the pain threshold excitatory
  • Affect emotions, in the sense that morphine can alter the resulting reaction accompanies the pain at the time the patient felt pain. After the administration of drugs the patient still feel (realize) there is pain, but fear no longer worried reactions arise. Effects of this drug is relatively larger influence effective component (emotional) than sensory
  • Facilitate sleep onset

2. Euphoria
Administration of morphine in patients experiencing pain, will cause feelings of euphoria in which patients will experience a comfortable feeling free from anxiety. Instead of an equal dose when given to normal people who do not experience pain, often leading to feelings of worry disforia be accompanied by nausea, vomiting, apathy, decreased physical activity and heavy extremities.

3. Sedation

Administration of morphine can cause drowsiness and lethargi effect. The combination of morphine with a drug that affects the central depression as sedative hypnotics will cause very deep sleep.

4. Breathing

Administration of morphine can cause respiratory depression, caused by direct inhibition on the respiratory center in the brain stem. Respiratory depression usually occurs within 7 minutes after intravenous injection or 30 minutes after subcutaneous or intramuscular injection. Respiration returned to normal within 2-3 hours.

5. Pupil

Systemic administration of morphine can cause miosis. Miosis occurs due to stimulation of the Edinger Westphal nucleus N. III

6. Nausea and vomiting

Caused by direct stimulation in the emetic chemoreceptor trigger zone in the brain stem.

 

Peripheral Effects

1. Gastrointestinal tract.

  • In the hull will inhibit gastric acid secretion, gastric mortilitas reduced, but the tone of the antrum rising.
  • In the intestine beasr will reduce peristalsis, which can cause constipation.

2. Cardiovascular System

Does not have significant effects on blood pressure, cardiac frequency and rhythm. Changes that seem only to be secondary to decreased activity and sleep state agencies, hypotension due to peripheral arterial and venous dilatation due to the mechanism of central depression by the stabilization mechanism of vasomotor and release of histamine.

3. Skin

Cause dilation of blood vessels of skin, so skin looks red and feels hot. Often the formation of sweat, probably caused by increased blood circulation in the skin due to central effects and release of histamine.

4. Urinary tract

Ureter and urinary vesika tonus increase, sphinkter increased muscle tone, which can cause urinary retention.

 

Types of Heroin

This type of heroin that is often traded are:

1. White powder

Traded in the bags that have been specially packaged with a size of 3×1, 5 cm, contains 100 mg of powder with high levels of heroin ranged from 1-10%. At present levels of heroin in powder tends rose, averaging around 35%. Usually the powder is mixed with sugar, milk powder or starch. Many bought and sold in the Asian region.

2. Cocoa powder

The shape, packaging and levels similar to white powder heroin, only the brown color. Many found in the area of ​​Mexico.

3. Black Tar

Many bought and sold in Usa. The black color is caused by the processing method. Shape into small pieces like nuts and sticky. Levels of heroin in it ranges from 20-80%. Usage is usually diluted with water and then warmed over the fire. After reconstitution can be inserted into the syringe.

 

How to Use

1. Injection

Injection intravenously, subcutaneously or intra muscular injection is more practical and efficient for low grade heroin. Intravenous injection can cause euphoria effects within 7-8 seconds, while the intra-muscular effect is 5-8 minutes slower.

Losses injection:

  • Can cause other daninf septikemi
  • Can cause hepatitis or HIV
  • Injection nerulang can damage the veins, causing thrombosis and abscess.

2. Inhaled.

Heroin powder is placed in aluminum foil and heated over the fire, then the smoke inhaled through the nose. Peak effect with the use of inhaled / smoked usually felt within 10-15 minutes.

3. Inhaled through a pipe or a rolled cigarette.

The use of heroin with high levels usually by inhaled or smoked. The use of heroin is smoked or inhaled (chasing the dragon) is now increased to avoid the effects caused by injection. Use of inhaled safer than inhaled, and therefore enters the body is gradually making it easier to control.

 

Effects arising from the use of heroin

According to the National Institute of Drug Abuse (NIDA), divided into short-term effects and long-term effects.

Short Term Effects:

  • Fidget
  • Respiratory Depression
  • Function mentally foggy
  • Nausea and vomiting
  • Pressing pain
  • Spontaneous Abortion

Long-term effects:

  • Addiction
  • HIV, hepatitis
  • Collapse vein
  • Bacterial infections
  • lung disease (pneumonia, tuberculosis)
  • Infection of the heart and valve

The influence of heroin to pregnant women:

  • Potential serious complications, spontaneous abortion, premature delivery.
  • Infants born to narcotic addicted mothers are at high risk for the occurrence of SIDS (Sudden Infant Death Syndrome).
  • Infants born to narcotic addicted mothers can suffer with drawl symptoms within 24-36 hours after birth. Symptoms baby added anxiety, agitation, frequent yawning, sneezing and crying, shaking, vomiting, diarrhea and seizures in some cases occur commonly.

Neurological complications that can occur due to use of heroin:

  • Cerebral edema
  • Myelitis
  • Postanoxia encephalopathy
  • Crush injury
  • Impaired coordination, difficulty speaking

 

TOXICITY AND OTHER EFFECTS OF NON-INTEREST HEROIN USERS

Acute intoxication (overdose)

Toxic dose, 500 mg for non-addicts and 1800 mg for narcotic addicts. Symptoms of overdose usually occur shortly after drug administration.

Symptoms of acute intoxication (overdose):

  • - Awareness of decline, sopor – coma
  • - respiratory depression, lower respiratory frequency 2-4 times a minute, and breathing may be Cheyene Stokes
  • Pupil small (pin poiny pupil), symmetric and reactive
  • Looks sianotik, skin redness face unevenly
  • Blood pressure at first either, but can be if respiratory worsening hypotension and shock
  • Low body temperature (hypothermia) and the skin feels cold
  • Bradycardia
  • Pulmonary Edema
  • Seizures
  • Death is usually caused by respiratory depression. Mortality increases when combined with drug addicts drugs that cause cross-reactions such as alcohol, tranquilizer.
  • The death rate of heroin + alcohol → 40%
  • The death rate of heroin + tranquilizer → 30%

 

Chronic Infection

Show various aspects of heroin addiction:

  1. Habituation, ie psycho-emotional changes that patients addicted to the drug.
  2. Physical dependence, namely the need for these drugs because of physiology and biochemistry body can not function anymore without the drug.
  3. Tolerance, namely the increasing need for the drug to get the same effect. Although tolerance arises when the first use of opioids, but the manifest after 2-3 weeks of therapeutic doses of opioid use. Tolerance will happen more quickly when given in high doses and shorter intervals of administration. Opioid cross-tolerance is an important characteristic, whereby if the patient has been tolerant with morphine, he will also be tolerant to other opioid agonists, such as methadone, meperidine and so forth.

The mechanism of drug tolerance and dependence.

The exact mechanism is unknown, possibly by cellular adaptations that lead to changes in enzyme activity, the release of certain biogenic amines or some immune response.

Nucleus locus ceruleus allegedly responsible for inflicting on withdrawal symptoms. The nucleus is rich in opioid receptors places, alpha-adrenergic and other receptors. Stimulation of opioid receptors and alpha-adrenergic give the same response on intracellular. Receptor stimulation by opioid agonists (morphine) will suppress the activity of cyclic AMP adenilsiklase.

When the stimulation was given continuously, will occur in the physiological adaptation of neurons that make normal levels of adeniliklase although binding to opiates. If the bond is terminated with a sudden opiates or replaced with opioid antagonist drug that is, there will be an increase in cyclic AMP adenilsilase effect sudden and is associated with the patient’s symptoms of hyperactivity symptoms.

Drug withdrawal symptoms (symptoms of abstinence or withdrawal syndrome) occurs when a drug addict to stop using the drug abruptly. Symptoms usually occur within 6-10 hours after the last drug administration and peak in 36-48 hours.

Withdrawal can occur spontaneously due to the sudden cessation of drug or can be in precipitation with opioid antagonist administration as naloxono, naltrexone. Within 3 minutes after injection of opioid antagonists, withdrawal symptoms develop, reaching a peak within 10-20 minutes, then disappeared after 1 hour.

Withdrawal symptoms:

  • 6 – 12 hours, lakrimasi, rhinorrhea, multilevel, frequent yawning, restless o 12-24 hours, restless sleep, iritabel, tremors, pupillary dilatation (midriasi), anorexia
  • 24-72 hours, all symptoms increase in intensity accompanied by weakness, depression, nausea, vornitus, diarrhea, abdominal cramps, pain in muscles and bones, alternating cold and heat, increasing blood pressure and heart rate, involuntary movements of arms and leg, dehydration and electrolyte disturbances
  • Furthermore, autonomic hyperactivity symptoms begin gradually reduced within 7-10 days, but people still depend strongly on the drug. Some mild symptoms can still be detected within 6 months. In infants with maternal drug addicts will be a delay in the development and growth that can be detected after age 1 year.

 

DIAGNOSIS

Diagnosis is based on:

1. Diagnose

  • Auto diagnose (honest recognition of patients)
  • Alo diagnose (from families who can be trusted)

2. Physical examination

Intoxikasi acute:

  • Impairment of consciousness
  • Autonomic disturbances, bradycardia, hypothermia, hypotension, cyanosis, pin point pupils
  • Respiratory Depression
  • Pulmonary edema
  • Seizures (rare)
  • Eye, sclera jaundice due to complications in the use of IV opiates
  • Talk to be rigid, dismetri.

Symptoms abstinensia

  • Nervousness, insomnia, sweating, frequent yawning, pupillary dilatation, tachycardia, abdominal cramps. Both the intoxication and abstinensia, found on the skin injection site (hyperpigmentation) along the arm veins.

3. The discovery of objects associated with the use of drugs such as syringes, pipes, aluminum foil, powdered heroin and others around the patient

4. Laboratory tests

  • Urine (drug screening)

To find a substance that is used by the patient. Urine should be obtained not more than 24 hours after last use of substances. Inspection methods such as by way of paper chromatography,

Thin Layer Chromatography, enzyme immunoassay

  • Hair

Liquid chromatography method using ultraviolet dspat determined the existence of opiates in hair pexcandu heroin (opiates). someone said to heroin addicts, when the hair of heroin found in the content of 10 ng / mg hair.

 

MANAGEMENT

Acute intoxication (overdose)

  • Improve and maintain airway as possible.
  • Oxygenation of adekua.
  • Naloxone injection, an initial dose of 0.4 to 2.0 mg IV (children 0.01 mg / kg) naloxane effect seen in 1-3 min and reached its peak in 5-10 minutes. If no response naloxane 2 mg can be repeated every 5 minutes up to a maximum of 10 mg. Naloxone effectively to improve the degrees of consciousness, respiratory depression, pupil size. Patients still must be observed to the effects of naloxone in 2-3 hours. Because of the short duration of action. To prevent rekulensi opiates effects can be given intravenous naloxone 0.4 to 0.8 mg / hour up to minimal symptoms (disappear).

 

Chronic intoxication

Hospitalization

Performed for patient hospitalization patient substance addiction, primarily intended for:

  1. Therapy withdrawal conditions
  2. Detoxification therapy
  3. Maintenance therapy (maintenance)
  4. Therapeutic complications
  5. Aftercare therapy

With the entry of patients into hospital addiction, physical medical evaluations should be given priority. Besides the examination of urine drug screen (to see if patients use other substances that do not admit), routine laboratory tests (including the function of liver function, kidney, danjantung), also performed thoracic images. Detoxification therapy aims for patients to decide the use of his substance and restore cognitive abilities. No other form of therapy that must be done before the second goal was achieved.

Other hospitalitation goal is to help patients to identify the consequences obtained as a result of substance use and understand the risks in case of relapse. In terms of mental hospitalization to control the atmosphere felt like a stony depression, paranoia, feeling quilty because regrets his actions in the past, and acts of self destruction violence.

Short-term hospitalization is recommended for substance addiction which they will be getting treatment for his condition. During the short-term treatment, patients are prepared to follow the maintenance therapy. For adiksinya condition, the patient is never recommended for long-term care.

 

Fermakoterapi

Opioid withdrawal therapy

  • Opioid withdrawal is not life-threatening, but associated with fisikologis disorders and physical distress is quite heavy.
  • Most patients with mild withdrawal symptoms which only requires a supportive environment without requiring them drug.
  • Klonidin can be used to reduce withdrawal symptoms with suppress feelings of anxiety, lakrimasi, rhinorrhea and excessive sweating. The initial dose given 0.1 to 0.2 mg every 8 hours. Then can be increased if necessary to 0.8 -1.2 mg / day, next to ditappering off after 10-14 days.

Non-specific therapy (symptomatic).

  • Sleep disturbance (insomnia) may be given sedative hypnotics
  • Pain can be given analgesic
  • Nausea and vomiting can be given class metoklopamide
  • Colic can be given antispasmolitika
  • Anxiety can be given antiansietas
  • Rhinorrhea can be given class fenilpropanolamin

 

Opioid addiction detoxification therapy

  • Methadone is the drug of choice in addiction detoxification therapy opioids. But when the methadone dose is lowered, the possibility of relapses are common. Another obstacle is to take a long time in detoxification therapy, and when using opioid antagonists will have to wait abstinensia symptoms for 5-7 days. The recommended dose of methadone detoxification treatment for heroin (morphine) is 2-3 x 5-10 mg per day orally. After a stable dose of 2-3 days starting ditappering off within 1-3 weeks.
  • Low dose buprenorphine (1.5 to 5 mg sublingual every 2-3 x per week) reported more effective and lighter than the withdrawal effects metadone.
  • Another alternative therapy that is suggested that rapid detoxification shorten the time of detoxification therapy and allows patients to be included in the opiate antagonist therapy. Types of rapid techniques detoxification among others klinidin naltrexon.

Maintenance therapy (maintenance) of opioid addiction.

  • Methadone and left-handed alpha-acetyl; methadol (Lam) is a standard maintenance therapy opioid addiction. Methadone given every day, while Lam only 3 times a week. Providing methadone maintenance therapy and Lam on a very helpful suppress criminal behavior. For maintenance therapy, methadone dose may be increased (usually 40-100 mg / day). To keep the patient still fun and lowered slowly.
  • Buprenorphine can also be used as a traditional therapy with a dose of 2 mg-20 mg / day.
  • Naltrexone is used for opioid addiction who have high motivation to quit. Naltrexone given orally 50-100 mg daily for 2 – 3 times a week.

After-care therapy

Covers the stabilization efforts in the field of physical, mental, religious, communication, social interaction, educational, aiming to achieve better conditions of behavior and function better than a former substance abusers. The role of the family at this time is necessary.

 

CLOSING

Heroin is a powerful narcotic in the cause of tolerance, physical dependence and fsikis. Discontinued drug suddenly may cause symptoms abstinesia (medication discontinuation). The use of heroin can also cause symptoms of acute intoxication (overdose), short-term complications and long term.

To control drug addict patient required an integrated management between doctors, patients and patients’ families because it takes a long time to restore the patient’s body.

 

REFERENCES­­

Cohan SL. Central nervous system disturbances Narcotics and brain death in clinical management of poisoning and drug overdose, ed. By Haddad LM. 2nd ed. Philadelphia: WB Saunders, 1990 (11): 223-7

Hubbell KC. Opiats and Narcotics in clinical management of poisoning and drug overdose, ed. By Haddad LM. 2nd ed. Philadelphia: WB Saunders, 1990 (38): 706-16

Kriegstein. Chasing the dragon heroin use cans brain damage. New York: Reuteut Health, 1999.

Olson KR. Management of Poisoned patient in Basic and Clinical Pharmacology. Katzung BG (ed). 7th ed. Stamfort: Appleton, 1998 (59): 970-77

Ruttenberg AJ. Etiology of heroin, related death. Journal of Forensic Science, 35 (4) July 1990: 890-900

Way EL. Drugs of abuse in Basic and Clinical Pharmacology. Katzung BG (ed). 7th ed. Stamfort: Appleton, 1998 (32): 518-9

Way WL. Analgosics opioids and antagonists in Basic and Clinical Pharmacology. Katzung BG (ed). 7th ed. Stamfort: Appleton, 1998 (31): 496-514

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