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PDA Block 3 > Central Nervous System Stimulants > Flashcards

Central Nervous System Stimulants Flashcards

1
Q

What do CNS stimulants do

A
  • increase the activity of CNS neurons
  • can be the produced either through enhancement of excitation or suppression of inhibition
  • in sufficient doses, all CNS stimulants can cause convulsions
  • CNS stimulant have clinical usefulness in treatment of ADHD and Narcoplesy
  • and they are used ( and abused) for non-therapuetic purposes
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2
Q

Caffeine

A
  • a methylxanthine, similar structurally to purines

- theophylline and theobromine are very similar in structure and mechanism

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3
Q

MOA caffeine

A
  • primary effect at normal caffeine doses: competitive antagonist of adenosine receptors
  • postsynaptic adenosine receptors produce IPSPs (hyperpolarize)
  • presynaptic adensosine receptors inhibit glutmate release

-caffeine inhibits these inhibitory effect (dis-inhibition) resulting in CNS stimulation

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4
Q

What does caffeine do at higher doses

A
  • inhibits cAMP phosphodiesterase
  • results in increased cAMP; responsible for its beneficial effects in the treatment of asthma (not as efficacious as other methylxanthines)
  • induces the release of calcium from intracellular (ER) stores
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5
Q

pharmacological action of caffeine

A
  • CNS stimulant

- peripheral effects

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6
Q

Caffeine as a CNS stimulant

A
  • increased alertness; increased attention during sustained tasks
  • decreased fatigue and drowsiness
  • can cause nervousness, restlessness and tremors
  • high doses stimulate medullary respiratory and cardiovascular centers
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7
Q

Caffeine peripheral effects

A
  • positive inotropic and chronotropic effects (direct effects on the myocardium)
  • dilates coronary and systemic blood vessels; constricts cerebral blood vessels (this may underlie the beneficial effects of caffeine in headache)
  • produces diuresis
  • increases gastric secretions
  • modest bronchodilation
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8
Q

Therapeutic usefulness of caffeine

A
  • primarily used to stay awake (various over the counter prescriptions)
  • added to some aspirin preparations to treat headache (excedrin)
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9
Q

caffeine overdose

A

-excessive CNS stimulation: nervousness, insomnia, excitement

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10
Q

consequences of chronic use of caffeine

A
  • tolerance: develops to the stimulant effects of caffeine
  • physical dependence: develops to caffeine at the dose of two cups of coffee per day

-withdrawal symptoms include feelings of fatigue and sedation; headaches and nausea; vomiting (rare)

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11
Q

Sympathomimetic stimulants

A
  • act through the enhancement of catecholaminergic neurotransmission
  • cocaine
  • amphetamine
  • methylphenidate
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12
Q

Cocaine

A
  • extracted from coca plant
  • local anesthetic
  • illicit use
  • cacoaine is a weak base; therefore, unionized it is in the unprotonated form (B) which predominates at alkaline pH (native people chew leaves with soda lime
  • 3 major forms: hydrochloride salt, purified free base, and impure base “crack”
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13
Q

How are free base cocaine and crack cocaine made

A
  • extracting the hydrochloride salt from an alkaline solution into an organic solvent
  • crack is made by adding bicarbonate to the hydrochloride salt
  • both crack and free base are absorbed more quickly across membrane; but more importantly they are more volatile than the salt form and can be smoked
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14
Q

pharmacokinetics of coaine

A
  • well absorbed through any mucous membrane
  • time to peak effect and duration of action are depndent upon the route of administration (shortest are iv and smoke)
  • metabolized in plasma and liver
  • short plasma half life (50 min) even shorter CNS half life (10-30 min)
  • urine screens detect metabolites
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15
Q

MOA cocaine

A
  • potent inhibitor of the reuptake of NE, DA, 5-HT
  • cocaine binds to the transporter itself and inhibits the binding of the neurotransmitter
  • reinforcing effects are due to increased dopamine in the synapse
  • increases the activity of tyrosine and tryptophan hydroxylase (due to loss of end product inhibition) -increase NT synthesis
  • is a local anesthetic and vascosontrictor
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16
Q

Pharmacological effects of cocaine

A
  • peripheral sympathomimetic effects (due to inhibition of NE reuptake in periphery)
  • vasoconstriction, tachycardia
  • increased alertness and vigilance (due to inhibition of NE reuptake in CNS synapses)
  • euphoria elation, feeling of well being (due to inhibition of DA reuptake in the mesolimbic circuit
  • as a result, cocaine has a high abuse liability
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17
Q

toxic effect of cocaine

A
  • tolerance and physical dependence occur with heavy use, but they are mild
  • mild withdrawal symptoms
  • neurotoxicologic consequences to long term use: due to damage of dopaminergic neurons
  • overdose can cause seizure;CV effect (myocardial infarction and arrhythmias)
  • effects on developing fetus-more significant than alcohol
  • premature labor, low birth weights, many learning and emotional problmes, attaachment disorder
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18
Q

Cocaine and its psychological dependence

A
  • profound psychological dependence
  • drug craving and seeking
  • users crave the drug even 10 minutes after last dose
  • abuse liability is greater with dosage forms that deliver drug rapidly to the CNS (smoking or iv)
  • withdrawal symptoms: dysphoria, depression, sleepiness, fatigue
  • cocaine cravings can be reduced by drugs that increase GABA including ganapentin, vigabatrin, baclofen
19
Q

Amphetamine and methamphetamine

A
  • structurally similar to Norepinephrine
  • weak bases
  • well absorbed orally; the free bas methamphetamine can be smoke (crystal meth)
  • amphetamine is metabolized to a variety of metabolites and about 50% is excreted unchanged; methamphetamine is metabolized to amphetamine
  • relatively long half lives (much longer than cocaine)
20
Q

MOA for Amphetamine and Methamphetamine

A
  • Potentiate NE, DA and 5HT signaling
  • via actions at the trace amine associated receptor (TAAR1)
  • TAAR1 is a GPCR, via cAMP/PKA phosphorylates reuptake carriers (DAT, NET, SERT( and VMAT2
  • results in inhibition of uptake and reversal (release of the amines) from terminal or vesicles (VMAT2)
  • partial agonist of alpha receptors
  • MAO inhibitor at high doses
  • more NE-like effects than cocaine
21
Q

Pharmacological properties of amphetamine and methamphetamine

A
  • arousal; increased wakefulness; decreased fatigue
  • enhance athletic and intellectual performance (quantity is improved, not quality)
  • elevated mood, increased self-confidence
  • respiratory stimulant
  • decreases appetite
  • peripheral sympathomimetic
22
Q

pharmacological properties amphetamine

-what is the active form

A

mixture of steroeisomers; active form is dextroamphetamine

23
Q

pharmacological properties methylphenidate

A

-not technically an amphetamine, but structurally and mechanistically very similar

24
Q

pharmacological properties methamphetamine

A

-gets into brain better, higher abuse liability

25
Q

pharmacological properties lisdextrofetamine

A

-prodrug of dextroamphetamine

26
Q

clinical uses amphetamine and methylphenidate

A
  1. Narcolepsy- use is complicated by risk of abuse and tolerance development
  2. Attention Deficit Hyperactivity Disorder: excessive motor activity, racing thoughts, difficulty in sustained attention; academic underachievement. is effective in many children
  3. exogenous obesity: obesity that is considered to be outside the control of the individual
27
Q

side effects of amphetamine and metylphenidate taken at therapeutic doses

A
  • insomnia
  • abdominal pain
  • anorexia, weight loss
  • suppression of growth
  • high body temperature
  • facial tics
28
Q

toxicity of amphetamines and methylphenidate (occurs at much higher doses than used for ADHD)

A
  • acute toxicity: sympathomimetic effects; restlessness, dizziness, tremor
  • psychosis due to excessive DA
  • neurotoxicity: permanent intellectual problems; neuronal degeneration
  • meth mouth: sever tooth decay, cause by a combination of dry mouth, lack of oral hygiene, increased consumption of sugared drinks, and teeth clenching and grinding
  • abuse liability: esp iv or smoked methamphetamine; worse long term than cocaine
  • sudden cardia death due to sympathetic activation
29
Q

Nicotine-what is it and what is the mechanism of action

A
  • naturally occurring alkaloid in tobacco products
  • MOA: agonist of nicotinic cholinergic receptors

*NMJ: initially activates muscle contraction, but then desensitizes

  • autonomic ganglia:
  • sympathetic: release of epinephrine form adrenal
  • parasympathetic: GI effects
  • receptors in CNS:
  • found in many brain regions; including nucleus accumbens (target of dopamine in the mesolimbic reward circuit)
  • are monovalent cation channels; activation produces a membrane depolarization, thus produces excitation
30
Q

Pharmacological actions of nicotine

A
  1. CNS stimulant-increases alertness
  2. Increases dopamine release in limbic, reward centers-is reinforcing
  3. muscle relaxant
  4. activates the chemoreceptor trigger zone and causes nausea (common with first exposure)
31
Q

Explain why smoking is highly reinforcing

A
  1. reaches the brain very rapidly (lungs to brain in 7 sec)
  2. Increases dopamine signaling in the nucleus accumbens reward pathway
  3. each puff of smoke is a separate opportunity for the brain to associate smoking with reward; therefore it is highly addicting even though a single administration of nicotine is not as rewarding as a single administration of cocaine
32
Q

what is the relationship between environmental factors or cues and smoking

A

Environmental factor or cues become associated with the reward as well

  • setting (“I only smoke in bars”)
  • time of day (“I only smoke after dinner”)
  • preparation (“seeing an ashtray makes me want to smoke”)
33
Q

can people really only be a social smoker

A

-not really because the number of administration perday (STRONG association between smoking and euphoria) and the environmental cues give it a high dependence liability

34
Q

Describe nicotine tolerance`

A
  • occurs over a very short period of time (hours: tachyphylaxis)
  • therefore the first cigarette of the day is the best
35
Q

nicotine withdrawal symptoms

A
  • irritability, hostility, impatience
  • anxiety
  • depression
  • difficulty concentrating
  • increased appetite, weight gain
36
Q

treatment of nicotine dependence

A
  1. Nicotine replacement: most widely used and there are many preparations
    - active: nasal spray, gum, lozenge, sublingual tablet, inhaler
    - passive: patches

-a large percent of patients using nicotine replacement are not smoking at 6 weeks but only 20% are abstinent for one year

37
Q

Pharmacotherapies for smoking cessation

A
  • bupropion

- Varenicline

38
Q

bupropion

A
  • antidepressant
  • used as a sustained release preparation
  • reduces craving and lessens some of the nicotine withdrawal symptoms (esp depression)
  • side effects: insomnia, dry mouth
39
Q

Varenicline

A
  • partial agonist of nicotinic receptors
  • rationale: reduce craving by activating the nicotinic achetylcholine receptor; will not desensitize like nicotine itself, also blocks the effects of nicotine if the person smoke (partial antagonist effect)
40
Q

Side effects for varenicline

A
  • nausea, headaches, constipation

- FDA concern for increase suicidal thoughts and depression

41
Q

other drugs used to treat ADHD that are not classified as stimulants

A
  • atomoxetine

- clonidine

42
Q

atomoxetine

A

-selective norepinephrine reuptake inhibitor (SNRI); antidepressant

43
Q

Clonidine

A

alpha 2 adrenergic receptor agonist

44
Q

Guanfacine

A

alpha 2 adrenergic receptor agonist

PDA Block 3 (16 decks)

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