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Central nervous system stimulants /certified fixed orthodontic courses by Indian dental academy
1. Central Nervous System Stimulation
-primary action of a diverse group of
pharmacological agents -adverse effect
associated with many drugs
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2. INDIAN DENTAL ACADEMY
Leader in continuing dental education
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3. Behavioral Manifestations of CNS
Stimulation
mild elevation in alertness, decrease in
drowsiness and lessening of fatigue
(Analeptic Effect)
increased nervousness and anxiety
-convulsions.
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4. Molecular Basis of CNS
Stimulation
Imbalance between inhibitory and excitatory
processes as in the brain. This hyper-excitability
of neurons results from:
potentiation or enhancement of excitatory
neurotransmission(e.g. amphetamine)
depression or antagonism of inhibitory
transmission (e.g. Strychnine)
presynaptic control of neurotransmitter release
(e.g. picrotoxin)
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6. Analeptic Stimulants
diverse chemical class of agents
majority can be absorbed orally
have a short duration of action - primary
expression of pharmacological effect is
convulsions (tonic-clonic) uncoordinated
pharmacological effect is terminated through
hepatic metabolism
Possible Common Mechanism of Action -ability to
alter movement of chloride ions across neuronal
membranes
Therapeutic Uses Group as a whole has limited
therapeutic use.
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7. Doxapram and Nikithamide - used to
counteract postanesthetic respiratory depression
and for acute hypercapnia in chronic pulmonary
disease.
Pentylenetetrazole - used clinically as a tool for
screening latent epileptics and experimentally to
screen compounds for anti-epileptic activity.
Picrotoxin - used to study CNS mechanisms; it
interferes with pathways that are strychnine
resistant.
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8. Strychnine is a source of accidental poisoning.
Also used to study CNS mechanism because of
its relatively specific action as a glycine
antagonist.
Adverse Reactions:
Convulsion is characterized by opisthotonos, i.e.,
tonic extension of body and all limbs. Back is
arched and only the back of the head and the
heels are touching the touching the surface. All
sensory stimuli produce exaggerated response
and slight sensory stimulation may trigger
convulsion.
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10. Treatment of Strychnine
Poisoning
(1) Remove/reduce external sensory stimuli
(2) Diazepam or Clonazepam I.V. or nitrous
oxide by inhalation to depress CNS and
stop convulsions which can be fatal
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12. CHARACTERISTICS
all compounds are absorbed well orally
large portion of untransformed amphetamine is
excreted unchanged
in the urine. Consequently, acidifying the urine
with ammonium chloride hastens its clearance,
and thus reduces its reabsorption in the renal
tubules.
Overdose: hyperreflexia, tremors and
convulsions
Fatalities: hyperthermia rather than
cardiovascular effects
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13. Pharmacological Actions
The primary effects of an oral dose are
wakefulness, alertness, decrease fatigue;
mood elevation, increased ability to
concentrate; an increase in motor and
speech activity. Amphetamines also
diminish the awareness of fatigue;
person may push exertion to the point of
severe damage or even death.
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14. Stimulate the respiratory center, especially when
respiration is depressed by centrally acting drugs,
(barbiturates and alcohol).
Amphetamine can reverse the marked sedation
and behavioral retardation resulting from
reserpine-like drug.
Depresses appetite by their action on the lateral
hypothalamus rather than an effect on metabolic
rate.
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15. Mechanisms of Action
Releases monoamines at synapses in
the brain and spinal cord.
Inhibits neuronal uptake of monoamine
Direct agonist of DA and 5-HT receptors
Antagonist at certain adrenreceptors
May inhibit monoamine oxidase.
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20. Mechanisms of Action
Increase cyclic nucleotide concentration
Blocks adenosine receptors
Alters intracellular calcium distribution
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21. Caffeine, the most widely used drug in
the world, is a stimulant. Commonly
found in coffee, tea, soft drinks,
chocolate and a wide variety of overthe-counter medications, it is legal to
buy and easily accessible.
Caffeine is a physically addictive drug
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23. Cardiovascular System: Increase rate
and force of the heart by directly
stimulating myocardium (low doses)
Tachycardia and arrhythmias at higher
doses. Peripheral vasodilation decease
in blood pressure (acute administration)
Hypotension and cardiac arrest (rapid i.v.
theophyline)
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24. Smooth Muscles: Relaxes vascular
smooth muscle (Theophylline »Caffeine)
Kidney: All xanthines are capable of
producing some degree of diuresis in
humans (Theophylline > Caffeine)
Miscellaneous: Xanthines shorten
clotting time by increasing tissue
prothrombin and factor V.
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25. Adverse effects
Stimulate gastric secretions in patients
with ulcer
Dehydration in children due to vomiting
and transient diuretic action (theophyline)
Allergic reaction (aminophylline)
Psychic Dependence (Caffeine)
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26. Therapeutic Uses
Caffeine + plus ergot alkaloid
(Ergotamine): used to treat migraine
headaches
OTC preparations: Theophylline:
Prophylaxis for chronic asthma
Respiratory Stimulant Bronchodilator for
relief of asthmatic symptoms
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27. NICOTINE
CNS Effects:
Powerful CNS stimulant at lower doses;
Large doses produce clonic convulsion, then
depress CNS, compounding postictal
depression
Stimulates respiration
Produces emesis
Tolerance to central actions with chronic use
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28. Cardiovascular Effects
Tachycardia
Increased blood pressure
Pupillary constriction
Cardiovascular collapse - due to CNS
depression
Ganglionic blockade and arrhythmias
Fatalities: Due to respiratory failure
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29. COCAINE
Psychomotor stimulant
local anesthetic
Chemistry- alkaloid from coca plant
alkaloid is highly lipid-soluble
hydrochloride salt is water soluble
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30. Routes of Administration
Chewing: with an-alkaloid material (South
America)
Sniffing: hydrochloride salt -absorption: nasal
mucous membranes -local vasoconstriction slows
absorption and prolongs effect
Oral: large doses are needed for effect rapid onset
Smoking: cocaine is converted to alkaloid
(freebase or "crack") which is readily volatilized
undegraded at lower temperature. I.V. and
smoking: reaches CNS in seconds in high
concentration produces more immediate and
intense effects
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31. Pharmacokinetics
large vol. of distribution
quickly metabolized: half-life 30-90 minutes
principal metabolites: a) Ecogonine
methylester - inactive b) Benzoylecogonine inactive c) norcocaine - active
half lives of metabolites: 4 to 6 hrs. metabolites: Excreted in urine
Drug Testing: BE - detectable for 1-3 days
Cocaine - detectable for a few hours
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