a) Caffeine ---- coffee (most widely consumed stimulant in the world)
b) Theophylline ---- tea
c) Theobromine --- cocoa

a) blockade of adenosine receptors
b) increase in cAMP by inhibition of phosphodiesterase
c) translocation of extracellular calcium

Note (a) and (b) produce same main effect - increase cAMP levels.

What effects do methylxanithines have on seizure threshold?

 When might this effect be clinically useful?

1. Seizure threshold is lowered

2. It is useful in ECT for psychiatric patients.

Low doses- ganglionic stimulation by depolarization

High doses- ganglionic blockade

Nicotine receptors are found multiple places throughout the CNS

Cocaine is an ester. Is it a benzoic-acid ester or a para-amino-benzoic-acid (PABA) ester?

What is the mechanism of action of cocaine?

How is cocaine unique among local anesthetics? 

1. Cocaine is a benzoid-acid ester.

2. Cocaine blocks the reuptake of monoamines (norepi,

    serotonin, & dopamine) into presynaptic terminals    

    from which these neurotransmitters are released.

3. Cocaine is unique as a local anesthetic because no

    other local anesthetic blocks NEPI reuptake. This

    makes it useful for surgical procedures because it

    causes vasoconstriction (ENT surgeons used to 

    administer it frequently intranasally because it

    provided local anesthesia and reduced bleeding). It

    also explains unique behavioral effects of cocaine.

A very agitated young male was brought to the ER by the police. Psychiatric Examination revealed that he had snorted cocaine several times over the past few days, the last time being 10 hours previously. He was given a drug that sedated him, and he fell asleep. The drug was used to counter this patient's apparent cocaine withdrawal was very likely:

A. Phenobarbital

B. Lorazepam

C. Cocaine

D. Hydroxyzine

E. Fluoxetine

The gen objectives of pharmacotherapeutic intervention in cocaine toxicity are to reduce CNS and cardiovascular effects of drugs by using benzo initially and then controlling tachycardia and hypertension.

B. The anxiolytic properties of benzodiazepines, such as

    lorazepam, make them the drugs of choice in

    treating the anxiety and agitation of cocaine

    withdrawal. Phenobarbital has hypnotic properties,

    but its anxiolytic properties are inferior to those of

    benzodiazepines. Cocaine itself could counteract the

    agitation of withdrawal, but its use would not be

    proper therapy. Hydroxyzine, an antihistamine, is

    effective as a hypnotic, and it is sometimes used to

    deal with anxiety, especially if emesis is a problem.

    Fluoxetine is an antidepressant with no immediate

    effects on anxiety.

A 30-year-old male presents with chest pain following cocaine administration. EKG is remarkable for multifocal PVCs. What medications would you use to treat this patient? Note, the text has several inaccuracies concerning the treatment of cocaine toxicity. See

http://emedicine.medscape.com/article/813959-overview

See Link

In general you need to address agitation (benzodiazepines), hypertension, arrhythmias, and coronary ischemia (caused by vasospasm). The only specific agent that may be present on the test will be benzodiazepine/lorazepam.

The effects of amphetamine on CNS and peripheral nervous system are indirect (like cocaine). That is they both depend upon elevation level of catecholamine neurotransmitters in synaptic spaces.

Amphetamines achieve this by releasing intracellular stores of catecholamines. This causes major behavior effects from the combination of dopamine and norepi release. This leads to increased alertness, decreased fatigue, depressed appetite, and insomnia. At high does psychosis and convulsions can ensue. Also, in sympathetic nervous system, Amphetamine act on the adrenergic system, indirectly stimulating the receptors through norepi release.

LSD binds to and activates serotonin receptors and causes a greater than normal activation of the receptor. This in turn causes rapid emotional swings, altered perceptions, and delusions.

Cannabis which has the cannaboinoid THC (the intoxicating one) takes effect by acting upon cannabinoid receptors, triggering the release of dopamine.

PCP works primarily as an NMDA (N-methyl d aspartate) receptor antagonist which blocks the activity of NMDA receptor. The NMDA receptor allows for the transfer of electrical signals between neurons.