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Little clinical use, except methylxanthines
 Can be classified in to:


› Respiratory stimulants ( Analeptics).

› Convulsants
› Psychomotor stimulants
› Psychomimetic drugs
Doxapram :
 MOA not clear, may excite central neurons
 Short acting, high margin of safety.
 Low doses selective for respiratory centre
 ↑ Tidal volume & rate of respiration
Uses :
 Post-anaesthetic resp. depression
 COPD i.e. hypoxemic,hypercapnic res.fail
 Apnoea in premature infants
Dose- 2-5mg/min(max 4mg/kg) slow i.v
infusion.
Contraindications:
 Hypoxaemic, normocapnic resp.failureasthma
 Resp.fail due to neurological & muscular
diseases.
 Epilepsy
Side effect:
 Restlessness
 Tachycardia
 High doses: convulsions & arrhythmias

No clinical use
 Used as research tools
Strychnine:
 Alkaloid, convulsant poison.
 Spinal cord stimulant
 MOA: Blocking the receptors for Glycine
 In poisoning convulsion treated withDiazepam or clonazepam slow i.v

Picrotoxin:
 Blocks the Cl- ion channel of GABAA.
Bicuculline:
 Plant alkaloid, GABAA antagonist.
Pentylenetetrazole (PTZ):
 Direct depolarization of central neurons
 Provides useful animal model for testing
anticonvulsant drugs.
Amphetamine group:
 Amphetamine
 Dexamphetamine
 Methamphetamine
 Methylenedioxy Methampheta(MDMA)
 Methylphenedate
 Fenfluramine
Non-Amphetamine group
 Modafinil
 Atomoxetine
 Sibutramine
 Pemoline
Cocaine
Methylxanthines:
 Caffeine
 Theophylline
 Theobromine
MOA: ↑DA conc. In synaptic cleft by
 Enter N endings by active transport
 Displace DA(also NE) from vesicles
 Also inhibits MOA-B, ↓DA metabolism.
Pharmacological effects: (central)
 ↑ motor activity
 Euphoria & excitement
 Anorexia
 Stereotyped & psychotic behaviour
↑ BP, inhibition of GI motility
 Fatigue both physical & mental reduced.
 Amphetamine psychosis on repeated
use- paranoid ideas, A & T hallucinations.
PK:
 Well absorbed orally
 Freely penetrates BBB
 Unmetabolised drug excreted in urine

ADHD with minimal brain dysfunction:
 Characterised by› Hyperactivity
› Inability to concentrate
› Impulsive behavior
 Dexamphetamine,
 Methylphenedate,
 Atomoxetine quite effective.
Narcolepsy: Characterised by Sleep attacks during day time
 Night mares in awakening state
 Cataplexy-reversible
 Methylphenedate is still used
 Modafinil- devoid of abuse liability
Fenfluramine, dexfenfluramine used
earlier to treat obesity
 Discouraged due to: Tolerance
 Insomnia, pul.htn, abuse potential.
Sibutramine new drug used now
 Blocks neuronal uptake of mainly NE &
5HT (also dopamine) at hypothalamic
site that regulates food intake.

Use:
 Severe obesity with risk factors like DM.
Adverse effects:
 Dry mouth
 Headache
 Insomnia
 Constipation
 ↑in HR & BP
 CI in CVS diseases, withdrawn from
market
Tolerance
 Psychic dependence, rarely physical.
Amphetamine overdose:
 Euphoria, dizziness, tremors, HTN
 Irritability, anorexia, insomnia
 Higher doses- convulsions, psychotic
manifestations, arrhythmias, coma
 Rx –diazepam(slow i.v), haloperidol
 Gastric lavage, acidification of urine
 HTN-nifedipine/labetolol, arry-esmolol

Sudden deaths occurred with MDMA.
 Induces heat stroke like conditionrhabdomyolysis & renal failure
 Inappropriate secretion of ADH
Methylenedioxy amphetamine (love drug)
 75mg- psychotomimetic effects
 150 mg-LSD like effects
 300mg- amphetamine like
 SE: tachycardia, HTN, arrhythmias

Only caffeine if used as CNS stimulant
PK:
 Oral- rapid but irregular absorption
 PPB:<50%
 Distributed all over the body
 Met: in liver by demethylation & oxid.
 Metabolites excreted in urine
 T1/2: 3-6hrs

AE:
 Gastric irritation, N, V
 Nervousness, insomnia, agitation
 Muscule twitch, rigidity
 ↑body temp,delirium, convulsions
 Tachy, extra systoles at high doses
Uses:
 In Analgesic mixture for headache
 Migraine
 Apnoea in premature infants
Produce changes in sensory
perceptions, thoughts, behaviour &
mood.
 Actions mimic psychoses- psychedelics
 Lysergic acid diethylamide (LSD)
 Mescaline
 Phencyclidine
 Cannabinoids

Derived from cereal fungus ergot
 Hofmann synthesized & experimented on
himself.
 Act as agonist at 5HT2 receptors.
 Excitation threshold of retina ↓-visual
hallucinations
 Excitation threshold of RAS↓-hyper
arousal state
 Experiences may be bad or good trip.

Extract of hemp plant-C.sativa, C.indica
 Bhang- paste of powdered dried
leaves, used as drink
 Marijuana- dried leaves & flowering
tops, smoked in pipes or rolled as
cigarettes.
 Charas or hashish- resinous exudates
leaves & flowering tops, potent smoked
inpipe.
 THC content more in hashish

Initial CNS stimulation later sedation.
 Stimulatory phaseeuphoria, ↑talkativeness, ↑appetite
 Felling of confidence, relaxation & well
being
 Other- analgesia, antiemetic
 Peripheral effects- tachy, VD, reddening
of conjunctiva











Two types CB 1& 2 receptors
CB1 in brain CB2 in periphery
Anandamide-endogenous ligand CB1.
Dronabinol, Nabilone- synt.analogues of
THC
Use: CB1 Agonists- ↑appetite in AIDS pts.
Dronabinol-antiemetic in cancer chemo.
Rimonabant : CB1 antagonist, used for
obesity, dose-20mg OD before Breakfast
Smoking cessation
Indications:
 AD, multi infarct dementia
 Mild cognitive impairment
 MR, learning defects, ADHD in children
 TIA, CVA, Stroke
 Organic psychosyndromes
 Sequale of head injury
 ECT, brain surgery
↑ global/regional blood flow
 Direct support of neuronal metabolism
 Enhancement of neurotransmission
 Improvement of discrete cerebral
functions

Main pathological features:
 Amyloid plaque
 Neurofibrillary tangles
 Marked ↓ in choline acetyltransferase &
loss of cholinergic neurons in brain.

ACEs that cross BBB are preferred.
Tacrine:
 Longer acting, reversible ACE
 Palliative for mild to moderate AD
 Orally active
 Improves memory, cognition, well being
 Facilitates Ach release
 AE: hepatotoxicity

Newer reversible Anti cholinesterase
 Better penetration in to CNS
 Better tolerated & less toxic than tacrine
 Clinical results modest & temporary
 Donepezil: 5mg OD orally evening ↑ max
10mg after 4 wks
 Rivastigmine:1.5 mg orally BD ↑ to 3mg
BD after 2 wks
 Galantamine:4mg BD orally ↑to 8mg BD
after 2 wks

Transdermal Rivastigmine patch –
applied every 24hrs
 SE:diarrhoe, N, V, ↑urination
Acetyl-L-carnitine:
 Structural analogue of Ach
 ↓ signs & symptoms of dementia in AD
 ↑ cholinergic transmission
 Also have antioxidant properties, slows
progression of AD

Excitotoxicity due to enhanced
Glutamate transmission via NMDA recp.
 Dose:5mg OD slowly ↑ to 10-20mg/day
 Non-comp. antagonist of NMDA recp.
 Better tolerated, less toxic.
Miscellaneous :
 Nootropics-piracetam, aniracetam
 High doses of vit E(1000 IU B.D)
 Antioxidants-vit
C, A, Zn, Se, bioflavonoids or spirulina ↓
progression even in middle stage AD.

¡gracias
"thank you" in Spanish

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Cns stimulants & cognition enhancers

  • 1.
  • 2. Little clinical use, except methylxanthines  Can be classified in to:  › Respiratory stimulants ( Analeptics). › Convulsants › Psychomotor stimulants › Psychomimetic drugs
  • 3. Doxapram :  MOA not clear, may excite central neurons  Short acting, high margin of safety.  Low doses selective for respiratory centre  ↑ Tidal volume & rate of respiration Uses :  Post-anaesthetic resp. depression  COPD i.e. hypoxemic,hypercapnic res.fail  Apnoea in premature infants
  • 4. Dose- 2-5mg/min(max 4mg/kg) slow i.v infusion. Contraindications:  Hypoxaemic, normocapnic resp.failureasthma  Resp.fail due to neurological & muscular diseases.  Epilepsy Side effect:  Restlessness  Tachycardia  High doses: convulsions & arrhythmias 
  • 5. No clinical use  Used as research tools Strychnine:  Alkaloid, convulsant poison.  Spinal cord stimulant  MOA: Blocking the receptors for Glycine  In poisoning convulsion treated withDiazepam or clonazepam slow i.v 
  • 6.
  • 7.
  • 8. Picrotoxin:  Blocks the Cl- ion channel of GABAA. Bicuculline:  Plant alkaloid, GABAA antagonist. Pentylenetetrazole (PTZ):  Direct depolarization of central neurons  Provides useful animal model for testing anticonvulsant drugs.
  • 9. Amphetamine group:  Amphetamine  Dexamphetamine  Methamphetamine  Methylenedioxy Methampheta(MDMA)  Methylphenedate  Fenfluramine
  • 10. Non-Amphetamine group  Modafinil  Atomoxetine  Sibutramine  Pemoline Cocaine Methylxanthines:  Caffeine  Theophylline  Theobromine
  • 11. MOA: ↑DA conc. In synaptic cleft by  Enter N endings by active transport  Displace DA(also NE) from vesicles  Also inhibits MOA-B, ↓DA metabolism. Pharmacological effects: (central)  ↑ motor activity  Euphoria & excitement  Anorexia  Stereotyped & psychotic behaviour
  • 12. ↑ BP, inhibition of GI motility  Fatigue both physical & mental reduced.  Amphetamine psychosis on repeated use- paranoid ideas, A & T hallucinations. PK:  Well absorbed orally  Freely penetrates BBB  Unmetabolised drug excreted in urine 
  • 13. ADHD with minimal brain dysfunction:  Characterised by› Hyperactivity › Inability to concentrate › Impulsive behavior  Dexamphetamine,  Methylphenedate,  Atomoxetine quite effective.
  • 14. Narcolepsy: Characterised by Sleep attacks during day time  Night mares in awakening state  Cataplexy-reversible  Methylphenedate is still used  Modafinil- devoid of abuse liability
  • 15. Fenfluramine, dexfenfluramine used earlier to treat obesity  Discouraged due to: Tolerance  Insomnia, pul.htn, abuse potential. Sibutramine new drug used now  Blocks neuronal uptake of mainly NE & 5HT (also dopamine) at hypothalamic site that regulates food intake. 
  • 16. Use:  Severe obesity with risk factors like DM. Adverse effects:  Dry mouth  Headache  Insomnia  Constipation  ↑in HR & BP  CI in CVS diseases, withdrawn from market
  • 17. Tolerance  Psychic dependence, rarely physical. Amphetamine overdose:  Euphoria, dizziness, tremors, HTN  Irritability, anorexia, insomnia  Higher doses- convulsions, psychotic manifestations, arrhythmias, coma  Rx –diazepam(slow i.v), haloperidol  Gastric lavage, acidification of urine  HTN-nifedipine/labetolol, arry-esmolol 
  • 18. Sudden deaths occurred with MDMA.  Induces heat stroke like conditionrhabdomyolysis & renal failure  Inappropriate secretion of ADH Methylenedioxy amphetamine (love drug)  75mg- psychotomimetic effects  150 mg-LSD like effects  300mg- amphetamine like  SE: tachycardia, HTN, arrhythmias 
  • 19. Only caffeine if used as CNS stimulant PK:  Oral- rapid but irregular absorption  PPB:<50%  Distributed all over the body  Met: in liver by demethylation & oxid.  Metabolites excreted in urine  T1/2: 3-6hrs 
  • 20. AE:  Gastric irritation, N, V  Nervousness, insomnia, agitation  Muscule twitch, rigidity  ↑body temp,delirium, convulsions  Tachy, extra systoles at high doses Uses:  In Analgesic mixture for headache  Migraine  Apnoea in premature infants
  • 21. Produce changes in sensory perceptions, thoughts, behaviour & mood.  Actions mimic psychoses- psychedelics  Lysergic acid diethylamide (LSD)  Mescaline  Phencyclidine  Cannabinoids 
  • 22. Derived from cereal fungus ergot  Hofmann synthesized & experimented on himself.  Act as agonist at 5HT2 receptors.  Excitation threshold of retina ↓-visual hallucinations  Excitation threshold of RAS↓-hyper arousal state  Experiences may be bad or good trip. 
  • 23. Extract of hemp plant-C.sativa, C.indica  Bhang- paste of powdered dried leaves, used as drink  Marijuana- dried leaves & flowering tops, smoked in pipes or rolled as cigarettes.  Charas or hashish- resinous exudates leaves & flowering tops, potent smoked inpipe.  THC content more in hashish 
  • 24. Initial CNS stimulation later sedation.  Stimulatory phaseeuphoria, ↑talkativeness, ↑appetite  Felling of confidence, relaxation & well being  Other- analgesia, antiemetic  Peripheral effects- tachy, VD, reddening of conjunctiva 
  • 25.         Two types CB 1& 2 receptors CB1 in brain CB2 in periphery Anandamide-endogenous ligand CB1. Dronabinol, Nabilone- synt.analogues of THC Use: CB1 Agonists- ↑appetite in AIDS pts. Dronabinol-antiemetic in cancer chemo. Rimonabant : CB1 antagonist, used for obesity, dose-20mg OD before Breakfast Smoking cessation
  • 26. Indications:  AD, multi infarct dementia  Mild cognitive impairment  MR, learning defects, ADHD in children  TIA, CVA, Stroke  Organic psychosyndromes  Sequale of head injury  ECT, brain surgery
  • 27. ↑ global/regional blood flow  Direct support of neuronal metabolism  Enhancement of neurotransmission  Improvement of discrete cerebral functions 
  • 28. Main pathological features:  Amyloid plaque  Neurofibrillary tangles  Marked ↓ in choline acetyltransferase & loss of cholinergic neurons in brain. 
  • 29. ACEs that cross BBB are preferred. Tacrine:  Longer acting, reversible ACE  Palliative for mild to moderate AD  Orally active  Improves memory, cognition, well being  Facilitates Ach release  AE: hepatotoxicity 
  • 30. Newer reversible Anti cholinesterase  Better penetration in to CNS  Better tolerated & less toxic than tacrine  Clinical results modest & temporary  Donepezil: 5mg OD orally evening ↑ max 10mg after 4 wks  Rivastigmine:1.5 mg orally BD ↑ to 3mg BD after 2 wks  Galantamine:4mg BD orally ↑to 8mg BD after 2 wks 
  • 31. Transdermal Rivastigmine patch – applied every 24hrs  SE:diarrhoe, N, V, ↑urination Acetyl-L-carnitine:  Structural analogue of Ach  ↓ signs & symptoms of dementia in AD  ↑ cholinergic transmission  Also have antioxidant properties, slows progression of AD 
  • 32. Excitotoxicity due to enhanced Glutamate transmission via NMDA recp.  Dose:5mg OD slowly ↑ to 10-20mg/day  Non-comp. antagonist of NMDA recp.  Better tolerated, less toxic. Miscellaneous :  Nootropics-piracetam, aniracetam  High doses of vit E(1000 IU B.D)  Antioxidants-vit C, A, Zn, Se, bioflavonoids or spirulina ↓ progression even in middle stage AD. 