Final Study Guide Flashcards
(50 cards)
What are opiate receptors, and what are their general effects?
Opiate receptors are receptors in the body that, when bound by opioids, produce effects such as analgesia (pain relief) and euphoria (pleasure). There are three main types: mu (best analgesia, most abuse liability), kappa, and delta.
What are naturally occurring opiates?
Naturally occurring opiates are derived from the opium poppy seeds and include morphine and codeine.
The Sumerians referred to opium as the ‘joy plant’ as early as 4000 B.C.
What are the acute effects of heroin use?
Acute effects of heroin use include depressant effects, pleasure (euphoria), analgesia, sedation/sleep, cough suppression, and constipation. Other effects on the body can include nausea and vomiting (initially), pupil constriction, lowering of blood pressure, flushing and warming of skin, and decreased sex hormone levels, diminished erection, sex drive, and fertility, and a decrease in REM sleep (‘nodding off’). Overdose can lead to death. Heroin can be administered through snuffing (intranasal), IV injection, smoking (opium), and ‘chasing the dragon.’
What are the chronic effects of heroin use?
Chronic heroin use can lead to physical dependence, tolerance (rapid to analgesia and euphoria but slow or non-existent to pupil dilation and constipation), and psychological dependence. It can also act as a cancer promoter by interfering with the ability to repair damaged DNA. Indirect effects include problems related to money, disease from needles (HIV, hepatitis), and lifestyle, leading to a much higher death rate for addicts.
Describe heroin withdrawal.
Heroin withdrawal typically begins 6-12 hours after the last drug use, peaks at 26-72 hours, and lasts about a week. While unpleasant, it is generally not as dangerous as alcohol or barbiturate withdrawal.
What are compensatory effects in the context of heroin withdrawal?
The sources do not explicitly define compensatory effects in the context of heroin withdrawal. This may be a concept discussed in the lectures or other materials not provided.
What is cross-tolerance in the context of opiate use?
Cross-tolerance refers to the development of tolerance to other opiates and sometimes to alcohol as a result of using a specific opioid.
What are the medicinal uses of opiates?
Medicinally, opiates are used primarily for analgesia (pain relief). They work by regulating the release of pain-signaling neurotransmitters (substance P, glutamate) in the spinal cord and through pain regulation from the brain stem. Morphine, an opiate, is used medicinally.
What are the non-medicinal uses of opiates?
Non-medicinal uses of opiates include achieving pleasure and euphoria. This can lead to misuse and addiction.
What brain areas are affected by opiate use?
Opioids act in the central nervous system (CNS), affecting areas such as the periaqueductal gray (brain area for pain perception), amygdala (aversive emotion associated with pain), frontal cortex, and brain stem (respiratory, vomiting, cough).
What is Substance P, and what role does it play in pain?
Substance P is a pain-signaling neurotransmitter that is released by nociceptive sensory neurons in the dorsal horn of the spinal cord. Its release is regulated by endogenous endorphins.
What was responsible for the spread of opiates out of the Mediterranean?
The sources mention that opium spread outward from the Mediterranean, but they do not specify by whom.
What are potential non-pharmaceutical effects of chronic opiate use?
Potential non-pharmaceutical effects of chronic opiate use include money problems, contracting diseases from needle sharing (HIV, hepatitis), lifestyle changes, and a significantly increased death rate. Chronic opioid use can also hinder social functioning and pose a huge financial strain.
How do endorphins and opiates modulate pain?
Endogenous endorphins are the body’s natural morphine-like neurotransmitters that regulate the release of pain-signaling neurotransmitters like substance P and glutamate in the spinal cord. Opioids, as exogenous substances, bind to opiate receptors and mimic the effects of endorphins, thus modulating pain. Pain regulation also comes from the brain stem.
Describe the opioid epidemic in America and its causes.
The opioid epidemic in America began in the 1990s when doctors became more aware of pain burdens. Pharmaceutical companies aggressively marketed opioids as safe and effective for all types of pain, leading to a flood of prescriptions. Doctors, facing pressure to treat pain seriously and efficiently, readily prescribed them. This made the US the world leader in opioid prescriptions. As access to painkillers increased, so did misuse and addiction. Over time, many users transitioned to stronger and cheaper opioids like heroin and illicitly manufactured fentanyl, which further fueled the crisis. The epidemic was exacerbated by a lack of access to addiction treatment, with only a small percentage of people with drug use disorders receiving specialty care. Socioeconomic and mental health issues also contributed. The crisis has led to a significant increase in overdose deaths, contributing to a drop in US life expectancy.
What are serotonin agonists in the context of hallucinogens, and which drugs are examples?
Serotonin agonists are hallucinogenic drugs that primarily activate serotonin receptors, particularly the 5-HT2A receptor. Examples include LSD, DMT, psilocybin (mushrooms), and mescaline. General effects include alterations in perception, cognition, and mood, often involving distortions in thinking, illusions, and visual hallucinations, while maintaining a clear sensorium. The thalamus, which acts as a filtering station for incoming sensory stimuli, is a brain area involved in the hallucinogenic effects.
What are the pharmacokinetics of LSD?
LSD peaks in the blood in about 3 hours and its effects typically last for 6-8 hours. It is lipid-soluble, and only small amounts (25-300 micrograms) are required to produce effects. It has a relatively high therapeutic index (TI) of 280, and physical dependence does not develop.
What is the default mode network, and why might serotonin agonist hallucinogens be beneficial for treating depression and PTSD?
The default mode network is a brain network involved in the sense of self and filters information according to needs and priorities. Hallucinogens like LSD and psilocybin (serotonin agonists) may be therapeutic because they can ‘reset’ this network, potentially allowing for changes in thought patterns and emotional processing that could benefit conditions like depression and PTSD.
What are catecholaminelike hallucinogens, and which drugs are examples?
Catecholaminelike hallucinogens are drugs that affect norepinephrine (NE), dopamine (DA), and serotonin (5-HT). Examples include MDMA (ecstasy), DOM (STP), and nutmeg (myristicin, elemicin). They are structurally similar to amphetamine and enhance energy, endurance, sociability, and sexual arousal (due to effects on DA and NE). They also produce psychedelic symptoms like sensory-perceptual distortions, altered perception of color, sound, shape, hallucinations, a dreamlike state, and enhanced emotional responses (due to effects on 5-HT). Ecstasy has stimulant-like effects due to its influence on dopamine and norepinephrine.
What are the acute physiological effects of ecstasy (MDMA)?
Acute physiological effects of ecstasy include increased blood pressure and body temperature, jaw clenching, suppressed appetite, restlessness, insomnia, and impaired gait. Brain areas affected include the pre-frontal cortex (focused attention - DA), hypothalamus (homeostatic dysfunction, e.g., hyperthermia - excess 5-HT), amygdala (decreased ability to read negative emotions, increased positive attribution to others), and raphe nucleus (emotional well-being and stimulation/arousal - 5-HT). Neurotransmitters and hormones involved include dopamine (DA), serotonin (5-HT), and oxytocin (increased release, leading to increased empathy and bonding). There is also DA release in the nucleus accumbens (reward). Dangers of ecstasy include hyperthermia (potentially fatal), cardiovascular issues due to increased blood pressure, and potential long-term psychiatric problems with chronic use.
What are anticholinergic hallucinogens, and which drug is an example?
Anticholinergic hallucinogens are acetylcholine antagonists. An example is scopolamine, found in plants like deadly nightshade and jimsonweed. General effects include dry mouth, blurred vision, increased heart rate, and urinary retention. If the drug reaches the brain, it can cause sedation, amnesia, delirium, restlessness, hallucinations, and euphoria. It has also been used as a poison.
What are glutaminergic NMDA Receptor Antagonists, and which drugs are examples?
Glutaminergic NMDA Receptor Antagonists are drugs that block the NMDA receptor, a subtype of glutamate receptor. Examples include PCP (angel dust) and ketamine. PCP is a dissociative anesthetic that can cause agitation, excitement, delirium, disorientation, hallucinations, and a psychotic state. It can also lead to violent reactions, stupor, and coma. Ketamine, another dissociative anesthetic, is FDA-approved for quickly reversing severe depression and can be administered as a nasal spray. It also produces analgesia and amnesia.
Generally, what neurotransmitters are affected by hallucinogens?
Hallucinogens affect various neurotransmitter systems, including serotonin (5-HT), norepinephrine (NE), dopamine (DA), acetylcholine, and glutamate. Naturally occurring hallucinogens mentioned in the sources include mescaline (from peyote cactus), psilocybin (from mushrooms), and scopolamine (from plants like deadly nightshade and jimsonweed). Nutmeg also contains naturally occurring compounds with hallucinogenic effects.
