Kaplan Section 4 Chapter 1 CNS Pharm - Drugs of Abuse
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| Name 2 drugs of abuse that are CNS stimulants | Cocaine, Amphetamines
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| What is the mechanism of cocaine? | In CNS, blocks reuptake of DA, NE, and 5HT; local anesthetic action from Na+ channel blockade
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| What is the mechanism of amphetamines? | 1. block the reuptake of DA and NE; 2. releases DA and NE from mobile pool --> more available; 3. weak MAO inhibitors --> less DA and NE inactivation --> more DA and NE available.
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| What is the effect of increased NE action when abusing CNS stimulants? | 1. inc HR and contractility, 2. BP changes, 3. mydriasis, 4. central excitation, 5. hyperactivity
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| What is the toxicity of excess NE? | 1. cardiac arrhythmias, 2. generalized ischmia with possible MI and strokes, 3. acute renal and hepatic failures
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| What is the effect of increased DA action when abusing CNS stimulants? | 1. psychotic episodes, 2. paranoia, 3. hallucinations, 4. possible dyskinesias, 5. endocrine disturbances
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| What is the toxicity of excess DA? | 1. Major psychosis, 2. cocaine delirium
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| What is the effect of increased 5HT action when abusing CNS stimulants? | 1. behavioral changes, 2. aggressiveness, 3. dyskinesias, 4. dec appetite
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| What is the toxicity of excess 5HT? | 1. possible serotonin syndrome
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| What is the toxicity of excess NE, DA, and 5HT? | 1. convulsion, 2. hyperpyrexia (excessive and unusual elevation of set body temperature greater than or equal to 41.1° Celsius (106°F) -- diff from hyperthermia, in which body's temp is way above nl set point), 3. death
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| What are the sx's of withdrawal from CNS stimulants? | 1. craving, 2. severe depression, 3. anhedonia (inability to experience joy), 4. anxiety
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| How would you manage withdrawal sx's from CNS stimulants? | Give anti-depressants
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| Name 3 groups of CNS depressants that people can abuse | 1. BZ's, 2. barbiturates, 3. EtOH
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| What is the mechanism of BZ's? | potentiates GABA binding to GABAa receptors at the BZ1 and BZ2 sites
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| What is the mechanism of barbiturates? | prolongation of GABA (imitates GABA at high doses) action on GABAa receptors
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| What is the mechanism of EtOH? | prolongation of GABA (imitates GABA at high doses) action on GABAa receptors
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| What is the effect of BZ's? | light-to-moderate CNS depression
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| What is the toxicity of BZ's? | sedation and anterograde amnesia (can't remember things after the insult/injury)
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| How do you treat BZ overdose? | Reverse with flumazenil
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| What are the withdrawal sx's of BZ's? | 1. rebound insomnia, 2. rebound anxiety
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| What is the effect of barbiturates? | CNS depression
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| What is the toxicity of barbiturates? | 1. severe CNS depression, 2. respiratory depression, 3. death
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| What is the effect of EtOH? | CNS depression
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| What is the toxicity of EtOH? | 1. severe CNS depression, 2. respiratory depression, 3. death
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| What are the withdrawal sx's of barbiturates? | 1. agitation, 2. anxiety, 3. hyperreflexia, 4. life-threatening seizures
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| What are the withdrawal sx's of EtOH? | 1. agitation, 2. anxiety, 3. hyperreflexia, 4. life-threatening seizures, 5. delirium tremens (delusions/hallucinations, associated with tactile hallucinations such as sensations of something crawling on subject - phenomenon known as formication)
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| What do morphine, heroin, methadone, and fentanyl have in common? | all are opioids
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| What is the mechanism of opioids? | 1. activate opioid receptors (mu, kappa, delta)
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| For opioids, the involvement of which receptor has the most intense abuse and dependence liability? | mu -- inc in DA transmission in the mesolimbic tracts
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| What is the effect of opioids? | 1. euphoria, 2. analgesia, 3. sedation, 4. cough suppression, 5. constipation, 6. strong miosis (not with meperidine)
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| What are the sx's of opioid toxicity? | 1. severe respiratory depression, 2. nausea, 3. vomiting
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| How do you treat respiratory depression caused by opioid toxicity? | give naloxone (a μ-opioid receptor competitive antagonist)
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| What type of drug is marijuana? | hallucinogen
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| What is the mechanism of marijuana? | Marijuana stimulates the dopamine pathway from the ventral tegmental area to the nucleus accumbens. Binds to cannabinoid receptors CB1 (CNS) and CB2 (periphery).
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| What is THC? | THC is the primary psychoactive component in marijuana.
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| How is THC metabolized in the body? | CYP450 system
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| What is the effect of marijuana? | 1. sedation, 2. euphoria, 3. inc HR, 4. conjunctival hyperemia (engorgement of the conjunctival vessels), 5. delusions, 6. hallucinations
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| What is the toxicity of marijuana? | Smoking --> possible flashbacks
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| What are the sx's of marijuana withdrawal? | irritability and anxiety
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| What is the mechanism of action of hallucinogens? | interaction with 5HT receptors
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| What is the effect of hallucinogens? | 1. hallucinations, 2. sympathomimetic, 3. dysesthesias (tactile hallucinations)
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| What is the toxicity of hallucinogens? | flashbacks likely
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| What is the toxicity of PCP? | 1. horizontal and vertical nystagmus, 2. paranoia, 3. rhabdomyolysis
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| What is the danger of PCP? | extremely toxic, OD is common, with convulsions and death
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| What is the toxicity of Ketamine? | more mild than PCP: 1. horizontal and vertical nystagmus, 2. paranoia, 3. rhabdomyolysis PLUS 4. hallucinations
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| What is the effect of ecstasy? (MDMA, MDA, MDEA) | amphetamine-like (stimulant) with strong 5HT activation --> hallucinogenic; neurotoxic
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