Drug Abuse Management PDF

Psychoactive drug intoxication and withdrawal: Depressants: Intoxication (Nonspecific): Mood elevation, decreases anxiety, sedation, behavioural disinhibition, and respiratory depression. Withdrawal (Nonspecific): Anxiety, tremor, seizures, and insomnia. Alcohol (Ethanol): MOA: GABA agonist, Glutama...

Psychoactive drug intoxication and withdrawal: Depressants: Intoxication (Nonspecific): Mood elevation, decreases anxiety, sedation, behavioural disinhibition, and respiratory depression. Withdrawal (Nonspecific): Anxiety, tremor, seizures, and insomnia. Alcohol (Ethanol): MOA: GABA agonist, Glutamate antagonist (GABA-A receptor positive allosteric modulator). Intoxication: Emotional lability, slurred speech, ataxia, coma, blackouts, disinhibition, AST value is 2 x ALT (“ToAST 2 ALcohol”). The treatment is supportive, like for example fluids and antiemetics. Y puse una foto de Ethanol Treatment, espero que no pregunten eso (pero por si acaso). Withdrawal: The treatment consists of longer-acting benzodiazepines. Barbiturates: MOA: Barbiturates increase the duration of chloride channel opening (GABA-A receptor positive allosteric modulator). Intoxication: Low safety margin and marked respiratory depression. The treatment consists of symptom management (like for example, assist respiration and increase blood pressure). Withdrawal: Delirium, life-threatening cardiovascular collapse. Benzodiazepines: MOA: Benzos increase the frequency of chloride channel opening (GABA-A receptor positive allosteric modulator). Intoxication: Greater safety margin, Ataxia, minor respiratory depression. The treatment consists of flumazenil (which is a benzodiazepine receptor antagonist). Withdrawal: Seizures, sleep disturbance, and depression. Opioids: Mnemonic (Opioid OOOOOOOOOOOO’S, porque hacen yawning). MOA: Mu, Kappa, and Delta-Opioid receptor agonists (Opioid receptor modulator). Intoxication: Activation of µ receptors causes the prototype effects of pupillary constriction (pinpoint pupils), decreases GI motility, respiratory and CNS depression, euphoria, decreases gag reflex, and seizures. The most common cause of drug overdose is death. The treatment for overdose is naloxone. Withdrawal: Dilated pupils, diarrhea, flulike symptoms, rhinorrhea, yawning, nausea, sweating, piloerection (“cold turkey”), and lacrimation. The treatment consists of symptom management, methadone, and buprenorphine. Inhalants: MOA: Enhanced GABA signaling. Intoxication: Disinhibition, euphoria, slurred speech, ataxia, disorientation, and drowsiness. Effects often have rapid onset and resolution. Perinasal/perioral rash may be present. Withdrawal: Irritability, dysphoria, sleep disturbance, and headache. Basicamente lo que hay en Intoxication, es lo opuesto en Withdrawal. Stimulants: Intoxication (Nonspecific): Mood elevation, decreases appetite, psychomotor agitation, insomnia, cardiac arrythmias, tachycardia, and anxiety. Withdrawal (Nonspecific): Irritability, dysphoria, sleep disturbance, and headache. Amphetamines: MOA: Induces reversal of monoamine transporters (VMAT, DAT, SERT, NET), increases neurotransmitter release. Intoxication: Euphoria, grandiosity, mydriasis, prolonged wakefulness, hyperalertness, hypertension, paranoia, fever. Skin excoriations with methamphetamine use. Severe: cardiac arrest, seizures. The treatment consists of benzodiazepines for agitation and seizures. Withdrawal: Meth mites. Methamphetamine: MOA: Enhances release of monoamines (5HT, NE, DA). Intoxication: Pupil dilation, agitation, euphoria, tactile hallucinations, alertness, arousal, and wakefulness. Withdrawal: Sleepiness, hunger, and depression. Caffeine: MOA: Adenosine receptor antagonist. Intoxication: Palpitation, agitation, tremor, and insomnia. Withdrawal: Headache, difficulty concentrating, and flulike symptoms. Cocaine: MOA: Blocks reuptake of monoamines (5HT, NE, DA). Or Blocks reuptake of dopamine (DAT), serotonin (SERT), and norepinephrine (NET) transporters. Intoxication: Impaired judgement, pupillary dilation, diaphoresis, hallucinations (including fornication or they could be tactile hallucinations “sientes que alguien te esta tocando”), paranoia, angina, sudden cardiac death. Chronic use may lead to perforated nasal septum due to vasoconstriction and resulting ischemic necrosis. The treatment consists of benzodiazepines (diazepam). Phentolamine for cardiovascular management. If he has hyperthermia, immerse in cold water. If needed: Use nitroglycerin for refractory hypertension, or non-selective B-blockers. Closely evaluate the risk of ongoing MI, if yes (avoid Beta-blockers). Withdrawal: Restlessness, hunger, severe depression, and sleep disturbance. Nicotine: MOA: Stimulates central nicotinic acetylcholine receptors. Intoxication: Restlessness. Withdrawal: Irritability, anxiety, restlessness, decreases concentration, increases appetite/ weight. The treatment consists of nicotine replacement therapy (like for example patch, gum, lozenge); or bupropion/ varenicline. Hallucinogens: Lysergic acid diethylamide (LSD): MOA: 5-H𝑇2𝐴 receptor agonist (increases serotonin activity). Intoxication: Perceptual distortion (visual, auditory), depersonalization, anxiety, paranoia, psychosis, flashbacks (usually nondisturbing), mydriasis (dilation of the pupil of the eye). Withdrawal: None. Cannabis/ cannabinoids (Marijuana): MOA: Stimulate endocannabinoid CB1 and CB2 receptors or CB1 receptor agonist. Intoxication: Euphoria, anxiety, paranoid delusions, perception of slowed time, impaired judgement, social withdrawal, increases appetite “munchies”, dry mouth, conjunctival injection, and hallucinations. Withdrawal: Irritability, anxiety, depression, insomnia, restlessness, decreases appetite. MDMA (also known as Ecstasy): MOA: Blocks reuptake of 5HT and DA or Induces reversal of transporters for monoamines (SERT > DAT, NET), increasing their neurotransmitter release. Intoxication: Euphoria, hallucinations, disinhibition, hyperactivity, increases thirst, bruxism (grinding of the teeth), distorted sensory and time perception, mydriasis (dilation of the pupil of the eye). Life-threatening effects include hypertension, tachycardia, hyponatremia, and serotonin syndrome. Withdrawal: Depression, fatigue, change in appetite, difficulty concentrating, and anxiety. Phencyclidine (PCP): MOA: NMDA Receptor Antagonist. Intoxication: Violence, nystagmus (involuntary eye movement), impulsivity, psychomotor agitation, tachycardia, hypertension, analgesia, psychosis, delirium, and seizures. Withdrawal: Recurrence of intoxication symptoms caused by reabsorption in the GI tract; sudden onset of severe, random violence. *Dependence vs Addiction*: Dependence: If a person stops using the drug suddenly, their body might react because it misses the drug. This reaction is known as withdrawal, and it includes various symptoms that occur when the drug is no longer in the system. These symptoms together are called withdrawal syndrome. Addiction: When someone repeatedly uses addictive drugs, their body adjusts over time. This often means they need more of the drug to feel the same effects. This is called tolerance. In short, addiction involves needing more of the drug over time, while dependence is about the body’s reaction when the drug is missing. Physical dependence = Dependence. Psychological dependence = Addiction. Dependence naturally happens when someone uses a drug for a long time. The body gets used to the drug being present. Most people might experience this if they stop taking the drug suddenly. While many people develop dependence, only a few develop addiction. Addiction is when someone loses control over their drug use and develops a habit of seeking the drug compulsively. It involves psychological cravings and not just physical ones. In short, dependence is about the body’s adaptation to a drug, while addiction is about losing control over drug use due to strong psychological cravings. Dopamine is a “feel-good” chemical in the brain. Most addictive drugs increase dopamine levels in a specific brain area, making you feel happy or rewarded. The ERK (extracellular signal- regulated kinase) Pathway is like a communication line in cells. Drugs can activate this line, leading to changes in how cells behave. Calmodulin-related genes usually help with various cell functions. With drug use, these genes become less active (they decrease), affecting normal cellular processes. Drugs can increase the activity of genes that manage fats and the cell’s internal transport system (like a package delivery service within our cells), changing how cells grow and maintain themselves. This is known as the Lipid/Cholesterol and Golgi/ER Function. Glutamate and GABA receptors are like the brain’s on/ off switches. Drugs can affect these switches, altering brain communication, either exciting or calming the brain’s activities. Tolerance: Over time, the brain gets used to the drugs, so more is needed to feel the same effects. This is due to brain changes (either dialing up or down functions). Withdrawal: When you stop using the drug, these brain changes become obvious, leading to withdrawal symptoms as the body adjusts to being without the drug.