Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
67 Cards in this Set
- Front
- Back
The types of CNS stimulants |
Convulsants, psychomotor stimulants, hallucinogens and antidepressants |
|
The convulsants/respiratory stimulants are also known as |
Analeptics |
|
Classification of CNS stimulants |
a) Convulsants/Respiratory stimulants ( non-addicting drugs) b) Psychomotor stimulants (have high addictive potential) |
|
MOA of CNS stimulants |
1) Potentiation/enhancement of excitatory neurotransmission2) Antagonism/depression of inhibitory neurotransmission3) Affecting pre-synaptic neurotransmitter release |
|
Why are convulsants and respiratory stimulants no longer in use |
(1) dose used to reverse depression is close to dose that can causeconvulsion (2) they are not specific antagonist for depressant drugs (3) there are better orsafer management procedure that are currently adopted e.g. maintenance of patient's airway.
|
|
Classes of convulsants/respiratory stimulants |
1) strychnine 2) picrotoxin 3) bicuculine 4) pentylenetetrazole 5) amiphenazole 6) doxapram 7) nikethamide Ami and Nike, Strike Picro's Bike for Doxa pentylenetetrazole |
|
Source of strychnine |
obtained from seeds of Strychnos nuxvomica. |
|
Use of strychnine |
1) Currently used as a bitterstomachic to increase appetite. 2) Used also as poison for dogs. |
|
Seizure associated with strychnine |
Associated with opisthotonos (spasm of the muscles causing backward arching of the head, neck and spine) |
|
MOA of strychnine |
a selective competitive antagonist and blocks the inhibitory effect of glycine at all glycine neurons or by blocking the post-synaptic inhibition produced by inhibitorytransmitter, glycine.
|
|
Source of picrotoxin |
The fish anamirta cocculus |
|
MOA of picrotoxin |
Blocks pre-synaptic inhibition mediated through GABA A |
|
Why is picrotoxin contraindicated in morphine poisoning |
Both morphine and picrotoxin are spinal stimulants |
|
Drug used in picrotoxin poisoning |
Diazepam |
|
MOA of bicuculine |
Similar in action to picrotoxin. It interferes with GABA A binding |
|
Pentylenetetrazole is also known as |
Metrazol, leptazole and PTZ |
|
MOA of pentylenetetrazole |
Similar action to picrotoxin |
|
MOA of pentylenetetrazole |
Similar action to picrotoxin |
|
Use of pentylenetetrazole |
To induce chemo shock seizures in mice |
|
Use of amiphenazole |
Barbiturates and opiate poisoning |
|
Amiphenazole is used best in combination with? |
Bemegride |
|
Use of doxapram |
1)short acting respiratory stimulant. 2) Initially used to reverse centralrespiratory depression due to barbiturates and inhalant anesthesia. 3) Also used to treat apnea in premature-infants. |
|
Nikethamide is also called |
coramine. (nike left ami for cora) |
|
MOA of nikethamide |
1) similar action to doxapram 2) stimulates chemoreceptors in the aortic and carotid bodies 3) a weak convulsant |
|
General effects of psychomotor stimulants |
1) excitement and euphoria 2) decrease fatigue 3) increase motor activity |
|
Classes of psychomotor stimulants |
1) methylxanthines 2) nicotine 3) cocaine 4) amphetamines 5) methylphenidate 6) ephedrine |
|
Source of methylxanthines |
theophylline (tea), theobromine (cacoa) and caffeine (coffee). |
|
MOA of methylxanthines |
1)inhibit phosphodiesterase thus leading to increase in cAMP & cGMPgiving rise to increased cardiac, contraction. 2)They also block adenosine receptors 3) are involved in translocation of extracellular calcium. |
|
Effect of methylxanthines |
1-2 cups of coffee (100-200 mg) causes a decrease in fatigue & increased mental alertness due to stimulation of the cortex. 12-15 cups (1.5 g) causeesanxiety & tremor. |
|
Uses of methylxanthines |
1)cause relaxation of bronchial smooth muscles thus used in asthma(theophylline). 2)They are used in combination with analgesics (aspirin/paracetamol) to manage headache (caffeine). 3)has a mild diuretic action. |
|
Contraindications of methylxanthines |
1) crosses placenta so contraindicated pregnancy & also secreted in the breast milk. 2)Stimulate gastric acid secret ion thus worsens ulcer |
|
How addictive is nicotine |
It is the API in tobacco. Second to caffeine as most widely used CNS stimulants and 2nd to alcohol as most widely abused drug. |
|
MOA of nicotine |
at lower dose causes ganglionic stimulation by depolarization. At higher dose, causes ganglionic blockade |
|
Effects of nicotine |
appetite suppression. Low dose (in cigarette) produces euphoria, arousal & relaxation. |
|
Contraindications of nicotine |
1) lt is harmful to hypertensive patients because it increases bloodpressure & heart rate. 2) it is also harmful to angina patients because it causes vasoconstriction which reduces coronary blood flow. 3) By inhaling a complete tobaccostick, an average smoker takes in 1-2 mg of nicotine. 4) Acute lethal dose is 60 mg, thus.increases risk of lung Cancer and other cardiovascular diseases. |
|
Uses of nicotine |
it has no therapeutic use except in-smoking cessation therapy which could be nicotine replacement product such as nicotine patch combined with nicotine gum orVarenicline (the most effective) + behavioural conselling |
|
Varenicline is also called |
Cytisine |
|
Natural analogue of varenicline |
Cytisine |
|
Dose of varenicline |
day 1-3- 0.5 mg OD orallyday 4-7- 0.5 mg bd orallyDay 8 end of treatment- 1mg bd orally If quitting is successful after 12 weeks, continue another 12 weeks at 1mg bd |
|
Withdrawal symptoms of nicotine |
Withdrawal syndrome: irritability, anxiety, restlessness, insomnia, headaches, difficulty in concentrating. |
|
MOA of varenicline |
Varenicline is a partial agonist at nicotine Ach receptors thus produces less euphoric effects than nicotine (since nicotine is a full agonist at this receptor) |
|
MOA of cocaine |
blockade of reuptake of monoamines (dopamine, 5-HT &Norepinephrine) in the presynaptic terminal. This results in prolongation ofdopaminergic effect in the brains pleasure system (limbic system) leading to the intense euphoria associated with cocaine. |
|
Mode of administration of cocaine |
It has minimal bioavailability when taken via oral route thus it is snorted, solubilized and injected, smoked (crack i.e. the alkaloid form). |
|
Why is cocaine addictive |
Upon smoking, there is intenseeuphoria (rush) followed by intense dysphoria (crash) thus making this drug addictive. |
|
Effects of cocaine |
1)depression due to dysphoria, 2)agitation 3)paranoia 4) hyperthermia due to increased heat production coupled with vasoconstrictive effects that minimize ability to dissipate heat, 5) chestpain due to vasoconstriction of coronary arteries or pulmonarydamage 6)and finally convulsion. |
|
Treatment of cocaine toxicity |
1)toxicity can be treated by cooling and calming the patient.2) Benzodiazepines (lorazepam) help to calm agitated persons and prevent convulsion. This helps cool the patients and manage hyperthermia. 3)short acting anti-hypertensives, anti-convulsants and symptomatic supportive care. |
|
Uses of cocaine |
1) in ophthalmology for pupillary dilation 2) anesthetic in surgery, 3)experimental tool to study cathecholamine release |
|
Why is amphetamine different from cocaine |
similar effects with cocaine but longer lasting euphoria effect. |
|
Examples of amphetamines |
1) Dextroamphetamine (major member of this class) 2)methamphetamine which is aderivative of amphetamine3)methylenedioxymethamphetamine or Ecstasy (MDMA) which is a derivative of methamphetamine with both stimulant and hallucinogenic properties 4) lisdexamfetamine which is a pro-drug converted toand dextroamphetamine. |
|
MOA of amphetamines |
1) has indirect effect on CNS. 2) releases intracellular stores of catecholamines thereby increasing its level and inhibits MAO as well as weak reuptake transportinhibitor. |
|
Uses of amphetamines |
1) ADHD in children 2) narcolepsy 3) appetite suppression |
|
Which amphetamine is used in ADHD |
Atomoxetine; it is a non-stimulating drug. It is a selective norepinephrine reuptake inhibitor |
|
Symptoms of narcolepsy |
a sleep disorder characterized by uncontrolled bouts of sleepinessduring the day, a loss in muscle control (catalepsy) and paralysis due to Strong emotions like laughter |
|
Amphetamines used to treat narcolepsy |
Modafinil and armodafinil |
|
Amphetamines used to suppress appetite |
Phentermine and Diethylpropion; structurally related to amphetamines |
|
Contraindications of amphetamines |
1) hypertension 2) cardiovascular disease 3) glaucoma 4) hyperthyroidism 5) patients on MAO inhibitors |
|
Pharmacological active isomer of methylphenidate |
Dexmethylphenidate |
|
Effect of methylphenidate |
Similar to that of amphetamines |
|
MOA |
a dopamine and norepinephrine transport inhibitor thus increases levels of dopamine and norepinephrine in the synaptic space. |
|
Advantage of methylphenidate |
Has less potential for abusecompared to cocaine/amphetamine because it enters the brain more slowly |
|
Use of methylphenidate |
1) ADHD- Methylphenidate and dexmethylphenidate 2) narcolepsy- methylphenidate |
|
Adverse effects of Methylphenidate |
Abdominal pain and nausea |
|
Contraindications of Methylphenidate |
1)in seizure because increases seizure frequency (especially if patients on anti-depressant) 2) glaucoma. |
|
MOA of ephedrine |
It is an indirect acting and resistant to monoamine oxIdase and catechol-o-methyltransferase. It acts on part of the sympathetic nervous system and indirectly stimulates adrenergic receptor by increasing the activity of norepinephrine at the postsynaptic alpha and beta receptors |
|
Adverse effects of ephedrine |
cardiovascular toxicities, flushing, Sweating, acne, nausea, decreased urination, restlessness, confusion, insomnia |
|
Contraindications of ephedrine |
1)patients on NDRIS(Bupropion) and MAOIs 2) glaucoma |
|
Uses of ephredine |
1) weight loss 2) asthma(acts as a bronchodilator) 3) nasal decongestant |