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 Central Nervous System Stimulation
-primary action of a diverse group of
pharmacological agents -adverse effect
associated with many drugs

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 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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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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Classification of CNS
Stimulants
 Analeptic Stimulants



Respiratory Stimulants
Convulsants

 Psychomotor Stimulant
 Sympathomimetics or Adrenergic CNS
Stimulants

 Methylxanthines
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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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 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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 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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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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PSYCHOMOTOR
STIMULANTS
 Drugs of Primary Importance
Amphetamine - prototype
Methamphetamine
Methylphenidate

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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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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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 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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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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Therapeutic Uses
 Hyperkinesias - Methylphenidate
 Narcolepsy - Amphetamine or
methylphenidate
 Obesity - Fenfluramine

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Adverse Effects
 CNS: Euphoria, dizziness, tremor, irritability,
insomnia, Convulsion (at higher doses),
hyperthermia and coma
 C.V. Cardiac stimulation leads to headache,
palpitations, cardiac arrhythmias, anginal pain
 Other: Weight loss, Psychotic Reaction which
are often misdiagnosed as schizophrenia.
 Addiction - including psychic dependence,
tolerance and physical dependence.
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 Drug Interactions:




Tricyclic antidepressant
Antihypertensive Agents
Foods high in tyramine content

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METHYLXANTINES
 Caffeine:




Coffee (100-150 mg/cup)
Tea (30-40 mg/cups)
Cocoa (15-18mg/cup)

 Theophylline: Tea and cocoa
 Theobromine: Cocoa

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Mechanisms of Action
 Increase cyclic nucleotide concentration
 Blocks adenosine receptors
 Alters intracellular calcium distribution

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 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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Pharmacological Activity/
Adverse Effects
 Low Doses: 50-250mg/Caffeine (Oral Doses)
Increase mental alertness, decrease
drowsiness Lessen fatigue
 Larger Doses: 250-600mg/Caffeine Irritability,
restlessness, tremor, insomnia, headache,
palpitations and hyperesthesia GIT upset
 Large Doses: > 1000 mg Overt excitement,
delirium and clonic seizures
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 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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 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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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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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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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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 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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COCAINE
 Psychomotor stimulant
 local anesthetic
 Chemistry- alkaloid from coca plant
alkaloid is highly lipid-soluble
hydrochloride salt is water soluble

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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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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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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 www.indiandentalacadmey.com
  • 2. INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacadmey.com
  • 3.  Behavioral Manifestations of CNS Stimulation  mild elevation in alertness, decrease in drowsiness and lessening of fatigue (Analeptic Effect)  increased nervousness and anxiety -convulsions. www.indiandentalacadmey.com
  • 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) www.indiandentalacadmey.com
  • 5. Classification of CNS Stimulants  Analeptic Stimulants   Respiratory Stimulants Convulsants  Psychomotor Stimulant  Sympathomimetics or Adrenergic CNS Stimulants  Methylxanthines www.indiandentalacadmey.com
  • 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.    www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 11. PSYCHOMOTOR STIMULANTS  Drugs of Primary Importance Amphetamine - prototype Methamphetamine Methylphenidate www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 16. Therapeutic Uses  Hyperkinesias - Methylphenidate  Narcolepsy - Amphetamine or methylphenidate  Obesity - Fenfluramine www.indiandentalacadmey.com
  • 17. Adverse Effects  CNS: Euphoria, dizziness, tremor, irritability, insomnia, Convulsion (at higher doses), hyperthermia and coma  C.V. Cardiac stimulation leads to headache, palpitations, cardiac arrhythmias, anginal pain  Other: Weight loss, Psychotic Reaction which are often misdiagnosed as schizophrenia.  Addiction - including psychic dependence, tolerance and physical dependence. www.indiandentalacadmey.com
  • 18.  Drug Interactions:    Tricyclic antidepressant Antihypertensive Agents Foods high in tyramine content www.indiandentalacadmey.com
  • 19. METHYLXANTINES  Caffeine:    Coffee (100-150 mg/cup) Tea (30-40 mg/cups) Cocoa (15-18mg/cup)  Theophylline: Tea and cocoa  Theobromine: Cocoa www.indiandentalacadmey.com
  • 20. Mechanisms of Action  Increase cyclic nucleotide concentration  Blocks adenosine receptors  Alters intracellular calcium distribution www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 22. Pharmacological Activity/ Adverse Effects  Low Doses: 50-250mg/Caffeine (Oral Doses) Increase mental alertness, decrease drowsiness Lessen fatigue  Larger Doses: 250-600mg/Caffeine Irritability, restlessness, tremor, insomnia, headache, palpitations and hyperesthesia GIT upset  Large Doses: > 1000 mg Overt excitement, delirium and clonic seizures www.indiandentalacadmey.com
  • 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) www.indiandentalacadmey.com
  • 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. www.indiandentalacadmey.com
  • 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) www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 28.  Cardiovascular Effects Tachycardia Increased blood pressure Pupillary constriction Cardiovascular collapse - due to CNS depression  Ganglionic blockade and arrhythmias Fatalities: Due to respiratory failure     www.indiandentalacadmey.com
  • 29. COCAINE  Psychomotor stimulant  local anesthetic  Chemistry- alkaloid from coca plant alkaloid is highly lipid-soluble hydrochloride salt is water soluble www.indiandentalacadmey.com
  • 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 www.indiandentalacadmey.com
  • 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    www.indiandentalacadmey.com
  • 33. www.indiandentalacademy.com Leader in continuing dental education www.indiandentalacadmey.com