Unit I herbs as raw materials, biodynamic agriculture.ppt
Cocaine
2. WHAT IS COCAINE?
• Cocai ne (benzoyl -m hyl -ecgoni ne) (C 21N 4) i s
et 17H O
a cr yst al l i ne al kal oi d pr epar ed f r omt he l eaves
of t he Er yt hr oxyl on coca pl ant .
• Cocai ne i s a bi t t er , w t e, odor l ess, cr yst al l i ne
hi
dr ug.
• A ccor di ng t o t he N i onal I nst i t ut e of D ug A
at r buse
(N D ), cocai ne i s:“A pow f ul l y addi ct i ve dr ug
I A er
t hat can be sni f f ed, i nj ect ed, chew or sm
ed oked.”
3. CO NE HAS BEEN CLASSI FI ED AS A SCHEDU I I DRUG BY THE
CAI LE
UNI TED STATES.
4. FORMS OF COCAINE
1. C ocai ne hydr ochl or i de (pow ) : pr epar ed by
der
di ssol vi ng t he al kal oi d i n hydr ochl or i c aci d,
f or m ng a w er sol ubl e sal t .
i at
2. C ack cocai ne : pr oduced w
r hen cocai ne
hydr ochl or i de i s m xed w t h sodi umbi car bonat e
i i
and w er , and t hen heat ed.
at
5. ROUTE OF ADMINISTRATION
• C ocai ne can be adm ni st er ed as a dr ug of abuse i n t he
i
f ol l ow ng w
i ays :
• 1. Cocai ne hydr ochl or i de :
• Sni f f ed (i nt r anasal ),
• sm ng,
oki
• i nt r avenous i nj uct i on (i ncl udi ng bei ng m xed w t h her oi n
i i
or i ngest i on)
6. • 2. C ack cocai ne : i nhal at i on of vapour f r omheat ed
r
f oi l or pi pe.
8. O SET & D R TI O O A TI O
N UA N F C N
FO C C I N D
R O A E EPEN S O TH R U O
D N E O TE F
A M N STR TI O .
DI I A N
Route onset Duration
inhalation 7S 20 min
IV 15 S 22-30 min
Nasal 3 min 45-90 min
oral 10 min 60 min
9. COCAINE MECHANISM OF ACTION
• Cocaine binds to dopamine re-uptake transporters on the pre-
synaptic membranes of dopaminergic neurones.
• This binding inhibits the removal of dopamine from the synaptic
cleft and its subsequent degradation by monoamine oxidase in
the nerve terminal.
10. COCAINE MECHANISM OF ACTION
• Dopamine remains in the synaptic cleft and is free to bind to its
receptors on the post synaptic membrane, producing further
nerve impulses.
• This increased activation of the dopaminergic reward pathway
leads to the feelings of euphoria and the ‘high’ associated with
cocaine use.
11. WHEN GIVEN LOCALLY
• Cocaine produces anesthesia by inhibiting excitation of nerve
endings or by blocking conduction in peripheral nerves.
• This is achieved by reversibly binding to and inactivating sodium
channels.
• Sodium influx through these channels is necessary for the
depolarization of nerve cell membranes and subsequent
propagation of impulses along the course of the nerve.
• When a nerve loses its ability to propagate an impulse, the
individual loses sensation in the area supplied by the nerve.
12. THERAPEUTIC USES OF COCAINE
• Cocaine is used by health care professionals to temporarily numb the lining
of the mouth, nose, and throat (mucous membranes) before certain medical
procedures (e.g., biopsy, stitches, wound cleaning).
• It is an anesthetic that works quickly to numb the area about 1-2 minutes
after application.
• Cocaine also causes blood vessels to narrow, an effect that can decrease
bleeding and swelling from the procedure.
• It is also sometimes used in palliative care of terminally ill patient.
13. METABOLISM OF COCAINE
Serum half life of 45-90 minutes
Only 1% of the drug is recovered in urine after ingestion
Cocaine can be detected in blood or urine only for several
hours after its use
Cocaine metabolites are detectable for 2-5 days
Hair analysis provides a very sensitive marker for cocaine use
within the preceding weeks to months
14. EFFECTS OF COCAINE
1. Initial Low Doses :
A. Physical Effects :
1. Tachycardia, tachypnoea,
2. hypertension,
3. Dilated pupils (& flattened lenses),
4. sweating
5. reduced appetite, reduced need for sleep, reduced lung function,
6. dry mouth,
7. impaired motor control & performance of delicate skills and driving.
15. B- Psychological Effects :
1. Euphoria, sense of well being,
2. impaired reaction time and attention span,
3. impaired learning of new skills.
20. SYSTEMATIC FINDINGS
CARDIOVASCULAR SYSTEM :
Acute Cardiovascular Pathology
Cocaine is directly toxic to cardiac myocytes, and this cardiotoxic
effect does not depend on the
route of administration, and may not necessarily have to occur
at large doses. Neither does it
appear that pre-existing cardiovascular pathology is a pre-
requisite for cocaine toxicity
21. Acute Myocardial Infarction
• The mechanism of cocaine related myocardial infarction is
likely to be multifactorial in nature, and could be related to focal
vasoconstriction of coronary arteries, or spasm of these
arteries.
• Cocaine acts both directly and indirectly on vascular smooth
muscle, via-adrenergic
stimulation (noradrenaline) and an independent, dose-related
effect.
• Cocaine also increases coronary vascular resistance at a time
when it is increasing heart rate and myocardial oxygen demand
22. • Cardiac Arrhythmias
• Cocaine is a Class II antiarrhythmic agent, and exerts its actions
by blocking sodium channels.
• In large doses it is arrhythmogenic, possibly due to it’s effects
on catecholamines rather than any direct effect, or due to
secondary arrhythmias following cardiac
ischaemia due to prolonged coronary artery vasoconstriction.
• A cocaine-induced rise in
intracellular calcium may also be responsible.
23. RESPIRATORY SYSTEM
Non-specific findings at autopsy include pulmonary edema and
congestion, possible due to excess catecholamine release.
Specifically, cocaine use has been associated with :
granulomas in the lungs, and this may represent either
impurities in the drug, or more likely poly drug abuse
Spontaneous pneumothorax or pneumopericardium
Haemoptysis
Pulmonary hypertension
24. GASTROINTESTINAL TRACT
The pathological findings in the gastrointestinal tract of a
cocaine abuser are similar to those found in experimental
animals treated with high levels of catecholamines, i.e.:
Ulceration and perforation
Ischaemic colitis
Severe bowel ischaemia and gangrene (vasoconstriction of
mesenteric vasculature)
Peptic ulcer perforation (due to a disruption of the internal
elastic lamina of the small
vessels supplying the ulcerated area
25. URINARY SYSTEM
Cocaine use is known to have caused:
• Renal infarction
• Renal thrombosis
• Haemolytic uraemic syndrome
• Rhabdomyolysis with myoglobinuric renal failure
26. CENTRAL NERVOUS SYSTEM
• Due to cocaine’s ability to produce hyperpyrexia, combined with
it’s effects on neurotransmitters, the drug may contribute to
seizure formation as well as hyperthermia. Seizures may be
‘primary’, due to cocaine lowering the seizure threshold, or
‘secondary’ to cardiac effects such as ventriculartachycardia
and fibrillation.
27. 11 WAYS TO DIE FROM COCAINE DRUG
ADDICTION
1. Acute hypertensive crises - quickly elevating blood pressure - blows out a
weak blood vessel in brain causing cerebral hemorrhage.
2. Hypertension chronic users may weaken blood vessels in their brain. Die
from strokes or complications after.
3. Acute hypotension - no blood with oxygen to the brain causing an
anaphylaxis - allergic reaction.
4. Status epilepticus - repeated convulsions - increased EEG activity.
5. C.N.S. Rebound - physical and emotional depression - depressed
medullary/respiratory centers of the brain knock you OUT - this is the most
common cause of cocaine death.
28. 6. Hyperpyrexia - Cocaine can raise the body to an extremely high
temperature. May feel cold on the outside. Shows bruising easily - temp 106
degrees (anal)
7. Pulmonary insult - heat fumes and chemicals in lungs cause lungs to
collapse.
8. Paranoid miscalculation - accidental death due to delusions and
hallucinations.
9. Suicide - during post-cocaine depression
10. Needle borne - infections from needle use.
11. Allergic Reaction - anticholinesterase (enzyme) deficiency 10-20 mg. of
cocaine will kill them - the drug never gets destroyed and recycles continuously
throughout the body.
29. COCAINE RISK FOR ABUSE OR DEPENDENCE
Community-based interview surveys suggest that up to one in six persons
who use cocaine will become dependent.. Users
Heavier users and users who take the drug Intravenously or by smoking
are more likely to become dependent than lighter users or intranasal and
oral users..addicts
The greater abuse potential of intravenous or smoked cocaine is attributed
to the faster rate of drug delivery to the brain (within 10 seconds), & faster
onset of psychological effects . Route
This faster onset is associated with a more intense pleasurable response
(the so-called "rate hypothesis" of psychoactive drug action
30. COCAINE ADDICTION
• Why is cocaine so highly addictive?
• Next to methamphetamine,* cocaine creates the greatest
psychological dependence of any drug. It stimulates key
pleasure centres within the brain and causes extremely
heightened euphoria.
• The addictive properties of cocaine are thought to be due to
brain dopamine D2-receptor stimulation.
31. Cycle of Cocaine Addiction
This addiction has biological, behavioral & psychological aspects
Cocaine
Use
EUPHORIA
Positive Reinforcement
Brain Reward Neuroadaptations
Cocaine
Seeking
Behavior CRAVING
Negative Reinforcement
Treatment interventions are designed to reduce euphoria & craving