Q: My son (daughter), sister (brother), boyfriend (girlfriend) is cocaine, crack addicted. How can I help him (her)/ them? |
Q: I am cocaine--crack addicts, how you can help me? |
Q: What are warning signs of cocaine, crack addiction? |
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Q: After ingestinging cocaine through the nose, irregular heart beats can be fast and spasm like. I understand adrenline can be up to 5 times higher...how dangerous are these spasms? how fatal are the possibilities? |
There is a big difference between cocaine and adrenaline. Adrenaline is a natural mediator-hormone of Central Nervous System (CNS). After "adrenaline attack" the rest of the hormone will be utilized and CNS will return to homeostatic status. Cocaine blocks reuptake of dopamine, which produce "adrenaline attack" similar effects, but also it produce euphoria. Therefore, people are not addicted to adrenaline, except those, who are fanatics of rolocoaster ride *smile*.
The rest is from NIDA News Letter...
There are enormous medical complications associated with cocaine use. Some of the most frequent complications are cardiovascular effects, including disturbances in heart rhythm and heart attacks; such respiratory effects as chest pain and respiratory failure; neurological effects, including strokes, seizure, and headaches; and gastrointestinal complications, including abdominal pain and nausea.
Cocaine use has been linked to many types of heart disease. Cocaine has been found to trigger chaotic heart rhythms, called ventricular fibrillation; accelerate heartbeat and breathing; and increase blood pressure and body temperature. Physical symptoms may include chest pain, nausea, blurred vision, fever, muscle spasms, convulsions and coma.
Different routes of cocaine
administration can produce different adverse effects. Regularly snorting
cocaine, for example, can lead to loss of sense of smell, nosebleeds, problems
with swallowing, hoarseness, and an overall irritation of the nasal septum,
which can lead to a chronically inflamed, runny nose. Ingested cocaine
can cause severe bowel gangrene, due to reduced blood flow. And, persons
who inject cocaine have puncture marks and "tracks," most commonly in their
forearms. Intravenous cocaine users may also experience an allergic reaction,
either to the drug, or to some additive in street cocaine, which can result,
in severe cases, in death. Because cocaine has a tendency to decrease food
intake, many chronic cocaine users lose their appetites and can experience
significant weight loss and malnourishment. Research has revealed a potentially
dangerous interaction between cocaine and alcohol. Taken in combination,
the two drugs are converted by the body to cocaethylene. Cocaethylene has
a longer duration of action in the brain and is more toxic than either
drug alone. While more research needs to be done, it is noteworthy that
the mixture of cocaine and alcohol is the most common two-drug combination
that results in drug-related death.
Q: If cocaine is blocking reuptake of dopamine, why it can not be used in treatment of Parkinson Disease? |
Cocaine is indirect agonist
of dopamine, which blocks the reuptake process. The etiology of Parkinson
Disease is include the deficit of dopamine. But this deficit is due to
the low amount of dopamine produced cells; therefore, only direct agonist
of dopamine will work in this situation.
Q: My son, passed away
on July 25, 1999. The cause of death is:
|
Cocaine is a potent central nervous system stimulant. Its effects last
20 minutes to several hours, depending on drug content and purity. The
initial signs of stimulation are increased motor activity, restlessness,
tachycardia, increased blood pressure, and euphoria. The euphoria is quickly
followed by feelings of discomfort and depression and a craving to re-experience
the drug. With excessive dosage the drug can produce hallucinations, paranoid
delusions, itching, and cocaine "bugs" (sensation of insects crawling on
or under the skin). Overdoses cause tachyarrhythmias and a marked elevation
of blood pressure. These can be life threatening, especially if the user
has underlying cardiac disease. Toxicity results in seizures, followed
by respiratory and circulatory depression of medullar origin. Cocaine is
also highly pyrogenic because the stimulation and increased muscular activity
causes greater heat production. Heat loss is inhibited by the intense vasoconstriction.
Cocaine induced hypothermia may cause muscle cell destruction and myoglobinuria
resulting in renal failure.
Fatality
Excessive cocaine use
increases the risk of toxic overdose. The LD50 (fatal to 50% of users)
is believed to be about 500 mg. Most death have been found to be due to
cardiovascular or respiratory collapse immediately following intravenous
injection. Some studies have shown that ingestion or inhalation may result
in a symptom free period as long as an hour which is then followed by a
generalized seizure and death. In many deaths attributed to cocaine overdose,
two or more drugs are often found, including alcohol, barbiturates, amphetamines,
heroin, and methadone.
Cardiopulmonary
Concerns
Loss
of protective airway reflexes The ability to protect the airway
correlates with the level of consciousness. An unconscious individual may
hyperventilate because of loss of upper airway muscle tone. This allows
the tongue to fall back and obstruct the airway.
Aspiration
pneumonitis Loss of motor tone and flaccidly of the upper airway
allow gastric secretions to enter the airway. The low pH of gastric secretions
results in a serious pneumonitis.
Disturbance
of central respiratory drive Possible head injury and cerebral
edema secondary to anoxic insult can increase intracranial pressure. This
can, in turn, affect the respiratory centers in the brain stem. Patients
may hyperventilate or hyperventilate, depending on the severity of the
insult. Adequate alveolar ventilation must be assured by the imposition
of a mechanical ventilator.
Hypoxemiarelated
intracranial pressure increase Hyperemia secondary to anoxic insult causes
dilation of the cerebral blood vessels resulting in edema and increased
intracranial pressure.
Hypercarbiarelated
intracranial pressure increase. Hyperventilation from airway obstruction
or central dysfunction results in hypercarbia. The increased pace causes
dilation of the cerebral vessels and increased increased intracranial pressure.
Hypervolemia
Hypervolemia will result in pulmonary edema.ung compliance is reduced with
pulmonary edema and results in higher ventilating pressures which may have
detrimental effects on the lungs. Hypovolemia increases the susceptibility
of a patient to cardiovascular complications of positive pressure ventilation
such as decreased blood pressure and cardiac output.
Immobilization
Immobility results from the loss of consciousness. Secretions tend to pool
in the dependent areas of the lungs. This promotes the development of atelectasis
and pneumonia.
Myocardial
infarction The vasoconstriction associated with cocaine use
may result in coronary artery spasm, myocardial schema, and arrhythmia's.
Neurologic complications
Manifestations of cocaine
toxicity include tremors, muscle twitching, seizures, stroke, and cerebral
hemorrhage. Neuralgic dysfunction's affect the ability to synchronize the
patient/ventilator interface, and to deliver adequate ventilation with
frequent activation's of the pressure limiting mechanisms of the ventilator.
Hyperthermia
The
increased body temperature associated with the intense muscle contractions
that occur with cocaine overdose, increases oxygen consumption and carbon
dioxide production. This must be taken into account when determining the
set minute volume for mechanical ventilation. Appropriate adjustments in
FOIL and ventilation can be made by monitoring serial arterial blood gases.
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