L11 Flashcards

1
Q

What are CNS depressants, and how do they work?

A

CNS depressants, like ethanol and barbiturates, act by enhancing GABA receptor activity, leading to sedation and relaxation. Overdose can cause respiratory depression.

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2
Q

How do cocaine and amphetamines affect neurotransmitter systems?

A

They block the reuptake of dopamine, norepinephrine, and serotonin, increasing their levels and causing stimulant effects.

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3
Q

What is the main mechanism of action of opioids?

A

Opioids act on opioid receptors, inhibiting adenylate cyclase, reducing calcium influx, and increasing potassium efflux, leading to neuronal inhibition and pain relief.

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4
Q

How does ethanol affect the CNS?

A

Ethanol enhances GABA activity, inhibits NMDA receptors, and suppresses calcium channel opening, causing CNS depression.

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5
Q

What is the role of disulfiram in treating alcohol dependence?

A

Disulfiram inhibits aldehyde dehydrogenase, causing a buildup of acetaldehyde, which produces unpleasant effects to discourage alcohol consumption.

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6
Q

What are the pharmacological effects of nicotine on the CNS and autonomic systems?

A

Nicotine acts on nicotinic acetylcholine receptors, causing arousal, reduced anxiety, tachycardia, and increased blood pressure.

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7
Q

What are the main actions of cannabinoids on the CNS?

A

Cannabinoids act on GPCRs, inhibiting adenylate cyclase and calcium channels while activating potassium channels, leading to reduced synaptic transmission.

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8
Q

What toxic effects are associated with chronic smoking?

A

Smoking causes lung cancer, heart disease, chronic bronchitis, and fetal development issues. Nicotine and tar are primary contributors.

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9
Q

How does caffeine work as a CNS stimulant?

A

Caffeine inhibits adenosine receptors, increasing neuronal activity and causing wakefulness and alertness.

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10
Q

What is MDMA’s primary mechanism of action?

A

MDMA (ecstasy) inhibits serotonin uptake, increasing serotonin levels and causing euphoria and enhanced sensory perception.

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11
Q

Explain the pharmacological mechanisms of ethanol metabolism and its toxicological effects.

A

Ethanol is metabolized in the liver by alcohol dehydrogenase to acetaldehyde, which is then converted to acetate by aldehyde dehydrogenase. Acetaldehyde accumulation can cause toxicity (nausea, tissue damage). Chronic ethanol use leads to liver damage (cirrhosis), neurological degeneration, and dependence. Drugs like disulfiram inhibit aldehyde dehydrogenase to deter drinking.

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12
Q

Describe the mechanisms of action and effects of opioids on the CNS and the body.

A

Opioids bind to opioid receptors (GPCRs), inhibiting neurotransmitter release by reducing calcium influx and increasing potassium efflux. This inhibits pain signaling and produces euphoria. Chronic use leads to tolerance, dependence, and potential respiratory depression during overdose.

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12
Q

Discuss the harmful effects of chronic smoking and the pharmacokinetics of nicotine.

A

Smoking is linked to lung cancer, heart disease, and chronic bronchitis, with tar and nicotine as primary culprits. Nicotine is metabolized to cotinine, which has a longer half-life and is used as a biomarker for smoking. Nicotine also causes addiction through dopamine release in the brain’s reward pathway

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13
Q

Compare the mechanisms of action of CNS stimulants (caffeine, cocaine, and amphetamines) and their effects.

A

Caffeine blocks adenosine receptors, increasing neuronal firing and wakefulness. Cocaine and amphetamines block reuptake of dopamine, norepinephrine, and serotonin, causing euphoria and increased energy. Chronic use can lead to addiction and cardiovascular issues.

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14
Q

What are the pharmacological effects of cannabinoids and their potential therapeutic applications?

A

Cannabinoids act on CB1 receptors in the CNS, inhibiting neurotransmitter release. Effects include euphoria, relaxation, and altered sensory perception. Cannabinoids are being explored for treating pain, multiple sclerosis, and AIDS-related symptoms, but they may have long-term psychological effects.

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