Transcript drugs of abuse

DRUGS OF ABUSE
DR Feziwe Bisiwe
Department of Internal Medicine
• Case presentation
Ms S, 32yr old female referred from Hoopstad for
Heroin withdrawal.
Has been using heroin,cocaine and alcohol for the
past 15 yrs of her life and now she wanted to
quit.
No other chronic medications and not on any other
medication.
She last used the drugs about 6 hrs prior to
admission.
• On Examination
• BP:90/60mmHG, Pulse :62 b/min regular
• Face flushed ,speech slurred and febrile with a
temperature of 37.9
• She was agitated,anxious and eager to be helped
• Fingers had tar stains
• The rest of examination was essentially normal.
• ECG: showed sinus rhythm,wide QRS complexes
with a prolonged QT time
• Infection markers were all normal
• FBC: Macrocytosis
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LFTs :slightly Raised levels of GGT
HIV: Non –reactive
The rest of blood results were normal.
A diagnosis of Drug withdrawal was made and
the patient was admitted and was managed
according to the detoxification guidelines.
• She made a dramatic improvement but on a
third day she absconded.
DRUGS OF ABUSE
Common drugs of abuse
• Opioids- mostly heroin
• Cocaine
• Amphetamines
• Prescription meds- mostly benzodiazepines
• Codeine containing medications eg
Paracodeine and cough mixtures.
HEROIN
• Is an opioid- it mimics endorphins
• It can either be injected IV, IM, smoked or sniffed.
• Effect :IV: 7-8sec,IMI-5-8min,Smoked/sniffed-1015 min.
• It comes as a white powder in its pure forms but
with mixing with glucose, talcum and brick dust it
ends up as a brownish powder.
• The threshold for development withdrawal
symptoms on discontinuation or toxicity depends
on the tolerance of each patient.
Mechanism of action
• The BBB permeability to heroin is about 10 times
that of morhpine.
• It is hydrolysed into 6-acetylmonomorphine and
morphine which then binds to the mu opioid
receptors.
• This results in GABA release inhibition from the
nerve terminal, thus reducing the inhibitory
effect of GABA on dopaminergic neurons.
• The increased activation of dopaminergic
neurons and release of dopamine to the synaptic
cleft results in a sustained activation of the postsynaptic membrane.
EFFECTS
CNS
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Euphoric rush
Analgesic
Anxiolytic
Slow breathing
Sedation
Dependence and addiction
CVS
 Increases parasympathetic
 Bradycardia
 Hypotension
 Brady arrhythmias
 Prolonged QT time
 Non cardiogenic pulmonary
oedema.
GIT and other effects
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Nausea and vomiting
Constipation
Dry mouth
Bacterial infections and infective endocarditis
Pupillary constriction
High energy followed by psychomotor
retardation.
WITHDRAWAL
SYMPTOMS
• ‘flu-like symptoms
• Abdominal cramps
• Anxiety,irritability
• Cravings
• Fever and chills
• Muscle cramps
• Nausea,sweating
• Restlessness
SIGNS
• High BP
• Tachycardia
• Lacrimation
• Dilated pupils
• Piloerection
• Rhinorrhea
• Muscle spasms
• Vomiting and diarrhoea
Heroin Detoxification
• Methadone- opioid agonist
• Should be started 8-12 hrs after last use
• Start with a dose enough to alleviate withdrawal
signs without causing toxicity ,then taper it down
gradually.
• Symptomatic treatment
• Alternative drug-Buprenorphine-Naloxone
combination
• Clonidine-for migraine.
Mx of heroin toxicity
• Usually activated charcoal and gastric lavage are
not beneficial
• Golytely 2l/hr until stools are watery is used to
irrigate the bowel.
• Naloxone is the definite drug of choice-40mg in 1l
N/S or DW @ 10ml /hr.
• Pulmonary edema- usually resolves in 24-48 hrs,
it only requires supportive Rx.
• Convulsions are not common-Benzodiazepines
• Rhabdomyolysis-crystalloids and diuresis.
COCAINE
• Derived from a coca plant,is a crystalline tropane
alkaloid.
• It come as an off- white powder or ‘rock’
• It modifies the action of dopamine in the brain by
inhibiting its re-uptake from the synaptic cleft and
thus causing prolonged postsynaptic stimulation.
• Mostly act on the ‘reward pathway 'which
consists of ventral segmental area, nucleus
accumbens and caudate nucleus, that is why it
has a strong potential of psychological
dependence.
• It also blocks norepinephrine transporter ;
serotonin transporter and sodium channel
thereby interfering with propagation of action
potentials.
• Its effects are potentiated by concurrent
alcohol abuse, the mortality rate is increased
by 25 %.
• It is metabolized in the liver and its
metabolites are excreted in the urine.
MECHANISM OF ACTION
EFFECTS
CNS
• Euphoria
• Convulsions
• CVA
• Appetite suppression
• Hallucinations and
delusions
• Hyperthermia
CVS
• Activates sympatheticvasoconstriction,tachycardia
• Cathecholamines increase
about 5 fold
• Unpredictable BP
• Impairment of conductionWPW syndrome
• Risk of MIs
• Accelerated atherosclerosis
• Myocarditis and DCMO
• Hypercoagulable states
Other effects
• Hyperkalemia
• Hypersensitivity pneumonitis-cough and
hemoptysis
• Central retinal occlusion and endophthalmitis
• Platelet aggregation and increased
plasminogen activating factor
• Destruction of nasal septum
• Withdrawal symptoms are the same as the
ones mentioned before.
• Detoxification is achieved by tapering the dose
used and symptomatic treatment.
• Toxicity is also managed symptomatically.
• They benefit from beta –adrenergic receptor
blockers like Labetalol
– Phase I - Early stimulation
• CNS findings - Mydriasis, headache, bruxism, nausea,
vomiting, vertigo, nonintentional tremor (eg, twitching
of small muscles, especially facial and finger), tics,
preconvulsive movements, and pseudohallucinations
(eg, cocaine bugs)
• Circulatory findings - Possible increase in BP, slowed or
increased pulse rate (possibly with ventricular ectopy),
and pallor
• Respiratory findings - Increase in rate and depth
• Temperature findings - Elevated body temperature
• Behavioral findings - Euphoria, elation, garrulous talk,
agitation, apprehension, excitation, restlessness,
verbalization of impending doom, and emotional
lability
– Phase II - Advanced stimulation
• CNS findings - Malignant encephalopathy, generalized seizures and
status epilepticus, decreased responsiveness to all stimuli, greatly
increased deep tendon reflexes, and incontinence
• Circulatory findings - Hypertension; tachycardia; and ventricular
dysrhythmias (possible), which then result in weak, rapid, irregular
pulse and hypotension; and peripheral cyanosis
• Respiratory findings - Tachypnea, dyspnea, gasping, and irregular
breathing pattern
• Temperature - Severe hyperthermia (possible)
– Phase III - Depression and premorbid state
• CNS - Coma, areflexia, pupils fixed and dilated, flaccid paralysis,
and loss of vital support functions
• Circulatory - Circulatory failure and cardiac arrest (VF or asystole)
• Respiratory - Respiratory failure, gross pulmonary edema,
cyanosis, agonal respirations, and paralysis of respiration
THE END!!!
1ST YR ON DRUGS
3 YRS LATER.....