cocaine ppt

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Cocaine:

Cocaine Ala’a al sharife

overview:

overview Introduction History Forms of cocaine Pharmacokinetics Mechanism of action Clinical toxicity Theraphy Laboratory aspects Theraputic uses

introduction:

introduction Cocaine = methyl benzoyl ecgonine - weak base. Potent CNS stimulant. Cocaine has replaced heroin in some areas as the most commonly abused of the hard drugs.

history:

history history goes back at least several thousand years.(2500 B.C.) Coca leaves (of the plant Erythroxylon coca).

Forms of cocaine:

Forms of cocaine Salts cocaine hydrochloride Water-soluble Snorted Free base Dissolved in water, titrated with ammonia, and extracted into ether. Uncharged smoked Crack cocaine identical chemically – preparation slightly different (free base vs. crack) cocaine hydrochloride titrated with sodium bicarbonate (baking soda) Craking sound when heated Smoked Coca leaf infusions (coca tea)

Slide 7:

So what’s the difference?(salt vs. freebase/crack) Freebase/crack are: Uncharged Lower melting and boiling point Smoked portal of entry - vast surface of the lungs Vasoconstriction at nose eliminated Higher blood levels of cocaine reaches the brain within seconds So, smoked cocaine is more popular But, more dangerous

Slide 9:

Routes of adminstration Insufilation Inhalation Oral IV ‘Speedballs’ = cocaine + heroin

Pharmacokinetics-1:

Pharmacokinetics-1 Nasal application results in peak levels of approximately 100 ng/mL in about 50 to 60 minutes. Smoking crack cocaine results in peak levels of 200 to 400 ng/mL in about 5 to 10 minutes

Pharmacokinetics-1:

Pharmacokinetics-1 Lipophilic – cross blood-brain-barrier Short half life – 60 min Very little cocaine is excreted unchanged in urine. So, unchanged cocaine in urine –drug used recently Screening is for cocaine metabolites in urine Main metabolites: Benzoylecgonine Ecgonine methyl ester In the presense of alcohol ….

Slide 13:

…. Cocaethylene Similar pharmacological properties. half-life about three times that of cocaine. low cocaine blood levels but significant toxic symptoms. More pentration to the blood–brain - greater high much more mortality and morbidity

Mechanism of action:

Mechanism of action CNS Block re-uptake of the neurotransmitters into the presynaptic vesicles (esp. dopamine transporter DAT) Intense euophoria nicotine increases the levels of dopamine in the brain -chain smoking Prolonged exposure Down regulation of dopamine receptors – depression Mesolimbic system – Activation of reward center!! – addiction PNS Block NE transporter – sympathetic activation Increase BP Tachycardia Dilated pupils Block Na+ channels –interfere with AP – local anasthesia

Clinical toxicity-1:

Clinical toxicity-1 intense euphoria, but also agitation, seizures, and occasional cardiovascular accidents (strokes). It increases mental awareness and alertness with an associated feeling of well-being and euphoria. Fatigue is decreased and motor activity is increased, but coordination decreases at the same time. Profound physical and emotional depression, after prolonged use of cocaine.

Clinical toxicity-2:

Clinical toxicity-2 Cardiac effects are common, including tachycardia and other arrhythmias, hypertension, and myocardial ischemia or infarction. Other effects, such as sweating and hyperthermia, are often noted. The toxic dose of cocaine is estimated to equal 2 mg/kg body weight. Many deaths have resulted from cocaine abuse. When fatalities occur the immediate cause is usually intracranial hemorrhage, arrythmia,myocardial infarction, seizures, and/or trauma

Clinical toxicity-3:

Clinical toxicity-3 Ulceration of the nasal septum is always recorded as a complication of long-term nasal abuse of cocaine but this is, in fact, a rare phenomenon. Addictive after only few exposures Withdrawal reported – not severe as opiates Tolerance

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In addition chronic cocaine abuse casuses: Weight loss General fatigue Malnutrition Anemia Increased risk for infections

therapy:

therapy NO antidote. Decontamination usually is not possible(unless oral) General supportive care ,eg: Benzodiazepines – extreme agitation , seizures Vasodilators – lower BP B-blocker (labetalol)- arrhythmias

Laboratory aspects:

Laboratory aspects Immunoassay – screening Gas chromatography – confirmation, quantification Window of detection- variable [ 3 days ] If the urine screen is negative for cocaine metabolites, the blood will also be negative. Blood level – time consuming, no value in therapy Other tests (Acid-base, blood gas, myoglobin ,…)

Therapeutic uses:

Therapeutic uses Historically, local anesthetic in eye and ENT. now predominantly used for nasal and lacrimal duct surgery. The only local anesthetic causing vasoconstriction. The major disadvantages intense vasoconstrictor activity potential for cardiovascular toxicity. largely replaced synthetic local anesthetics . If vasoconstriction is desired for a procedure ,the anesthetic is combined with a vasoconstrictor such as phenylephrine or epinephrine.

Slide 25:

Any question? Thank you!

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