ADHD Overview and Therapeutic Approaches
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What are the core symptoms of Attention Deficit Hyperactivity Disorder (ADHD)?

  • Inattention and Hyperactivity
  • Hyperactivity and Excess Energy
  • Impulsivity and Anxiety
  • Inattention, Hyperactivity, and Impulsivity (correct)

    • What percentage of ADHD cases is believed to be genetic in origin?

  • 90%
  • 80% (correct)
  • 50%
  • 65%

    • Which of the following is considered a first-line non-pharmacologic intervention prior to medication trials for ADHD?

  • Alternative Therapies
  • Parent Training (correct)
  • Medication Trials
  • Dietary Interventions

    • What dietary intervention is mentioned as being beneficial for ADHD?

    <p>Omega-3 Fish Oil supplements</p> Signup and view all the answers

    What drug class is NOT directly associated with ADHD treatments as per the information provided?

    <p>Analgesics</p> Signup and view all the answers

    What environmental factors play a role in ADHD?

    <p>Excessive digital media consumption</p> Signup and view all the answers

    Between what years did the prevalence of diagnosed ADHD in children increase by 28%?

    <p>2007 to 2011</p> Signup and view all the answers

    Which system is implicated in the genetic origins of ADHD?

    <p>Dopaminergic system</p> Signup and view all the answers

    Which of the following statements regarding ADHD stimulants is true?

    <p>They are considered the first line of treatment for ADHD.</p> Signup and view all the answers

    Which behavioral intervention is NOT listed as appropriate for preschool children with ADHD?

    <p>Medication administration</p> Signup and view all the answers

    What is the primary mechanism of action for amphetamines in the treatment of ADHD?

    <p>Inhibition of dopamine and norepinephrine transporters</p> Signup and view all the answers

    What distinguishes lisdexamfetamine from dextroamphetamine?

    <p>Lisdexamfetamine has no effect until hydrolyzed</p> Signup and view all the answers

    Which of the following is a common adverse effect of amphetamines?

    <p>Weight loss</p> Signup and view all the answers

    What is the effect of alkaline urine on amphetamine elimination?

    <p>Decreases elimination</p> Signup and view all the answers

    Methamphetamine is known for having what characteristic compared to dextroamphetamine?

    <p>Increased central effects</p> Signup and view all the answers

    Which of the following medications is classified as a second line treatment for ADHD?

    <p>Atomoxetine</p> Signup and view all the answers

    What disorder is typically treated with ADHD-specific cognitive behavioral therapy?

    <p>Attention-deficit/hyperactivity disorder</p> Signup and view all the answers

    Which of the following compounds is typically NOT a controlled substance?

    <p>Atomoxetine</p> Signup and view all the answers

    What effect does chronic use of amphetamines have on mood?

    <p>Causes dysphoria</p> Signup and view all the answers

    Which is true regarding the pharmacological classification of stimulants?

    <p>Stimulants are first line, followed by non-stimulants.</p> Signup and view all the answers

    What is the mechanism of action for Atomoxetine?

    <p>Selective NE reuptake inhibitor</p> Signup and view all the answers

    Which of the following is true about neuromuscular blockers?

    <p>They cause muscle fasciculation before relaxation.</p> Signup and view all the answers

    Which type of neuromuscular blocker has a more rigid structure?

    <p>Non-depolarizing neuromuscular blockers</p> Signup and view all the answers

    What is the main effect of psychostimulants used in narcolepsy?

    <p>Improving wakefulness</p> Signup and view all the answers

    What kind of drugs are Guanfacine and clonidine classified as?

    <p>Presynaptic alpha2A-agonists</p> Signup and view all the answers

    Which feature characterizes non-depolarizing neuromuscular blockers?

    <p>They compete with acetylcholine at the neuromuscular junction.</p> Signup and view all the answers

    Which stimulant has reinforcing effects primarily due to the blockade of dopamine reuptake?

    <p>Cocaine</p> Signup and view all the answers

    What property do all neuromuscular blockers share regarding solubility?

    <p>Poorly lipid soluble</p> Signup and view all the answers

    Which xanthine is known for its central vasoconstrictive effects?

    <p>Caffeine</p> Signup and view all the answers

    What is the mechanism of action for spasmolytics?

    <p>Centrally acting muscle relaxants</p> Signup and view all the answers

    What is the effect of an R1 substituent being H on receptor action?

    <p>Preferential α-agonist action</p> Signup and view all the answers

    Which substituent configuration in R1 is associated with nonselective agonist action?

    <p>R1 = CH3</p> Signup and view all the answers

    What effect does the α-carbon substituent R2 = CH3 have on isomer types?

    <p>Both R and S isomers exist</p> Signup and view all the answers

    What effect does stimulation of central α1-receptors produce?

    <p>Sleeplessness, agitation, and restlessness</p> Signup and view all the answers

    How does a β-OH group affect CNS penetration?

    <p>It slows CNS penetration but does not stop it</p> Signup and view all the answers

    What happens to CNS penetration when R3 is H in nonphenolic compounds?

    <p>CNS penetration is significantly enhanced</p> Signup and view all the answers

    What is the relationship between the size of substituent R1 and receptor selectivity?

    <p>Different sizes of R1 influence which receptor subtype is stimulated</p> Signup and view all the answers

    Which class of stimulants is typically associated with nonselective agonist action?

    <p>Non-ADHD stimulants</p> Signup and view all the answers

    What is a consequence of the blood-brain barrier penetration being altered?

    <p>Increased effectiveness of drugs</p> Signup and view all the answers

    What receptor action occurs with a larger substituent at R1?

    <p>Decreased β action</p> Signup and view all the answers

    Which factor is crucial for the binding or efficacy of stimulants and muscle relaxants?

    <p>The presence of an arylethylamine moiety</p> Signup and view all the answers

    What kind of drug formulation is typically associated with improved absorption and sustained effect in medications?

    <p>Slow-release prodrug</p> Signup and view all the answers

    Which statement correctly describes the metabolic pathways relevant to stimulants and muscle relaxants?

    <p>Metabolite build-up can lead to adverse effects</p> Signup and view all the answers

    What characteristic of urine can influence the elimination of certain stimulants?

    <p>Acidity versus alkalinity of urine</p> Signup and view all the answers

    Which property is NOT considered when evaluating the physicochemical characteristics of stimulants and muscle relaxants?

    <p>Color of the tablets</p> Signup and view all the answers

    What is a common consequence of drug class instabilities in stimulants and muscle relaxants?

    <p>Loss of efficacy and potential for adverse effects</p> Signup and view all the answers

    What is a primary adverse effect associated with the use of amphetamines?

    <p>Hypertension</p> Signup and view all the answers

    How does acidic urine affect the elimination of amphetamines?

    <p>Increases elimination</p> Signup and view all the answers

    What distinguishes lisdexamfetamine from other amphetamines?

    <p>It is a pro-drug that provides a slow release and longer duration</p> Signup and view all the answers

    What condition is associated with possible psychosis due to prolonged use of amphetamines?

    <p>Dysphoria</p> Signup and view all the answers

    Which mechanism is primarily responsible for the stimulant action of amphetamines?

    <p>Inhibition of vesicular monoamine transporter 2</p> Signup and view all the answers

    Which drug exhibits increased central effects compared to dextroamphetamine?

    <p>Methamphetamine</p> Signup and view all the answers

    Which of the following is a characteristic of methylphenidate?

    <p>It inhibits monoamine oxidase</p> Signup and view all the answers

    What is true about the dextroamphetamine isomer?

    <p>It is a cationic amine</p> Signup and view all the answers

    What dietary intervention is suggested for ADHD management regarding food coloring?

    <p>Avoid red/orange food dye</p> Signup and view all the answers

    What effect does the β-OH group have in stimulant molecules?

    <p>Enhances receptor selectivity</p> Signup and view all the answers

    What effect does a larger substituent at R1 have on receptor action?

    <p>Reduces α-agonist action</p> Signup and view all the answers

    Which structure is associated with depolarizing neuromuscular blockers?

    <p>Flexible structure with two quaternary heads</p> Signup and view all the answers

    Which action is associated with β-OH in relation to CNS penetration?

    <p>Slows CNS penetration</p> Signup and view all the answers

    What type of isomers exist when R2 is set as CH3?

    <p>Chiral isomers</p> Signup and view all the answers

    What mechanism defines Atomoxetine's action?

    <p>Selective norepinephrine reuptake inhibitor</p> Signup and view all the answers

    What is a significant consequence of the 3-hydroxy metabolite in steroidal muscle relaxants?

    <p>Accumulation causing prolonged paralysis</p> Signup and view all the answers

    Which drug primarily exhibits reinforcing effects due to dopamine reuptake blockade?

    <p>Cocaine</p> Signup and view all the answers

    What is a characteristic of non-depolarizing neuromuscular blockers?

    <p>Contain one or more quaternary nitrogens</p> Signup and view all the answers

    Which muscle relaxant is the first known neuromuscular blocking drug?

    <p>Tubocurarine</p> Signup and view all the answers

    What factor is key in the action of anorexiants in relation to CNS stimulation?

    <p>Secondary appetite-suppressant effect</p> Signup and view all the answers

    Study Notes

    Attention Deficit Hyperactivity Disorder (ADHD)

    • Core symptoms: Inattention, hyperactivity, and impulsivity
    • Origin: 80% genetic, implicated systems: Dopaminergic and adrenoceptor alpha 2 genes
    • Environmental factors: Can play a significant role
    • Prevalence: Increased 28% from 2007 to 2011, debate about overdiagnosis

    Therapies for ADHD

    • Prior to medication: First-line interventions include behavioral interventions, structured limit-setting, parent training, and dietary interventions.
    • Dietary interventions: Iron and Zinc supplements, omega-3 fish oil supplements, avoiding red/orange food dye, allergenic foods, sugar, and artificial sweeteners.
    • Behavioral interventions:
      • Preschool and School Age (6-11 years): Parent/family education on ADHD, training on behavioral modification, classroom management instruction for teachers
      • Adolescent: Breakup homework into short segments, structured schedule organizer (to-do lists)
      • Adolescent and Adult: ADHD-specific cognitive behavioral therapy (think before acting), metacognitive therapy (2 hours/week for 12 weeks)

    Pharmacologic Therapy

    • First-line: Stimulants, controlled (schedule II)
    • Second-line: Non-stimulants, not controlled agents, often used as adjuncts to stimulants, can be used alone
    • Stimulant mechanism of action: Amphetamine mimics neurotransmitters like dopamine (DA) and norepinephrine (NE), and to a lesser extent serotonin (5-HT).

    Amphetamine

    • Mechanism of action: Inhibits dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT) in the striatum and prefrontal cortex.
    • Inhibits vesicular monoamine transporter 2 (VMAT2): Inhibits the translocation of DA and NE from the cytosol into storage vesicles.
    • Increases DA and NE concentration in the synapse.
    • Inhibits MAO: Risk for serotonin syndrome and hypertensive crisis.

    Amphetamine Adverse Effects

    • Common: Decreased appetite, tachycardia, weight loss, insomnia, headache, irritability, and jitteriness.
    • Rare/Prolonged use: Dysphoria, zombie-like state, priapism, hypertension, and psychosis.

    Amphetamine Metabolism

    • Excretion: 30%-40% excreted unchanged
    • Alkaline urine: Decreases elimination
    • Acidic urine: Increases elimination

    Lisdexamfetamine

    • Pro-drug: Hydrolyzed in red blood cells (RBCs) to D-amphetamine, slow release and onset, longer duration, less abuse potential, smoother peak/trough effect.

    Methamphetamine

    • N-methyl analog of dextroamphetamine: Increased central effects, decreased peripheral effects compared to dextroamphetamine, increased abuse potential.

    Ephedrine and Pseudoephedrine

    • β-OH analogues of methamphetamine:
      • Ephedrine: Used in Chinese medicine for millennia, dietary supplements with ephedrine banned in the US.
      • Pseudoephedrine: Used as a precursor to make methamphetamine.

    Methylphenidate

    • Mechanism of action: Same as amphetamines, also inhibits MAO.
    • Isomers: Two chiral centers, four isomers, only threo used clinically, D-threo isomer causes the effect, dexmethylphenidate is the D isomer.

    SAR of Phenylethylamines

    • Amine substituent (R1): A cationic amine is essential for adrenoceptor binding, size influences receptor subtype stimulation.
      • R1 = H: Preferential α-agonist action, used as vasoconstrictors
      • R1 = CH3: Nonselective agonist action, used predominantly for α-agonist action
      • More R1: More β action, less α action
    • α-Carbon substituent (R2): R2 = CH3 introduces asymmetry, R and S isomers exist, penetration of the blood-brain barrier occurs if no phenolic hydroxyls are present.
    • β-Carbon substituent (R3):
      • R3 = OH: Introduces asymmetry, R and S isomers exist, slows CNS penetration.
      • R3 = H: CNS penetration enhanced, especially when R1 or R2 is CH3.

    ADHD Stimulants

    • Atomoxetine is a selective NE reuptake inhibitor.
    • Guanfacine and clonidine are presynaptic alpha2A-agonists.
    • Cocaine blocks reuptake of NE, 5-HT, & DA.
    • The main effect of cocaine is due to blockade of DA reuptake.
    • Cocaine is very addictive.

    Non-ADHD Stimulants

    • Xanthines are non-selective adenosine receptor antagonist.
    • Caffeine has central vasoconstrictive effects.

    Muscle Relaxants

    • Two types of muscle relaxants: Neuromuscular blockers, Spasmolytics
    • Neuromuscular blockers interfere with transmission at the neuromuscular end plate and lack central nervous system (CNS) activity
    • Spasmolytics are “centrally acting” muscle relaxants
    • Neuromuscular blockers are used during surgical procedures and in the intensive care unit (ICU) to produce muscle paralysis.
    • Depolarizing agents have a flexible structure connecting the two quaternary heads.
    • Non-depolarizing agents have a more rigid structure with the quaternary and protonated heads being part of bulky groups.
    • Succinylcholine is a depolarizing neuromuscular blocking agent that is a dimer of acetylcholine.
    • Non-depolarizing neuromuscular blockers are competitive nACh antagonists.
    • Non-depolarizing agents are either isoquinoline derivatives or steroid derivatives.
    • Neuromuscular blockers are poorly lipid soluble and therefore unable to enter the CNS.
    • The duration of action of neuromuscular blockers are limited by hydrolysis of the esters present in the drug.
    • Although often, the metabolites show partial activity, with steroidal muscle relaxants 3-hydroxy metabolites are usually 40-80% as potent as the parent.
    • Spasmolytics are centrally acting muscle relaxants, used to reduce spasticity in a variety of painful conditions.

    Stimulants

    • Pharmacophores are important for potency and binding.
    • Arylethylamine moiety is a common pharmacophore in stimulants.
    • N-substitution is crucial for stimulant activity.
    • Metabolites can build up and cause adverse effects.
    • Acidic urine can increase excretion of some stimulants.
    • Slow-release pro-drugs can be used to prolong stimulant effects.

    Muscle Relaxants

    • Acidic vs. alkaline urine can influence the excretion of muscle relaxants.
    • Pharmacokinetic properties can vary significantly between muscle relaxants.
    • Adverse effects are a concern with muscle relaxants.
    • Drug of choice for specific indications should be considered.
    • SAR provides insights into the structure-activity relationships of muscle relaxants.

    First-line Interventions Prior to Medication Trials

    • Behavioral Interventions: Structure, boundaries, and parental training are crucial for managing ADHD.
    • Dietary Interventions:
      • Iron and Zinc Supplements: Necessary if deficiencies exist.
      • Omega-3 Fish Oil Supplements: May be beneficial, sometimes combined with primrose oil (omega-6).
      • Food Dye Avoidance: Red and orange food dyes in processed meats should be avoided.
      • Allergenic Food Avoidance: May be a factor in some cases.
      • Sugar and Artificial Sweeteners Avoidance: May contribute to behavioral issues.

    Amphetamine MOA

    • Structure: Similar to neurotransmitters dopamine (DA) and norepinephrine (NE), and to a lesser extent serotonin (5-HT), due to the shared arylethylamine moiety.
    • Sympathomimetic Action: Mimics the actions of adrenaline and norepinephrine.
    • Serotonin Transporter (SERT) Inhibition: Affects the striatum and prefrontal cortex.
    • Vesicular Monoamine Transporter 2 (VMAT2) Inhibition: Prevents DA and NE from entering storage vesicles.
    • Increased Synaptic Concentration: Raises DA and NE levels in the synapse.
    • Monoamine Oxidase (MAO) Inhibition: Potential for serotonin syndrome and hypertensive crisis.

    Amphetamine Adverse Effects

    • Common: Decreased appetite, tachycardia, weight loss, insomnia, headache, irritability, and restlessness.
    • Rare/Prolonged Use: Dysphoria, zombie-like state, priapism, hypertension, and psychosis (especially with prolonged use).
    • Excretion: 30-40% excreted unchanged.
    • Urine pH Influence: Alkaline urine decreases elimination, while acidic urine increases elimination.

    Lisdexamfetamine (Vyvanse)

    • Lysine Amide Derivative: Prodrug that is hydrolyzed to D-amphetamine in red blood cells.
    • Slow Release: Hydrolysis occurs slowly, resulting in a gradual onset and longer duration of action.
    • Less Abuse Potential: Smoother peak and trough effect compared to other stimulants.

    Dextroamphetamine (Dexedrine)

    • D-Isomer of Amphetamine: More potent than the L-isomer.
    • Aka S-Isomer: The dextro form is the more active isomer.

    Methamphetamine (Desoxyn)

    • Increased Central Effects: Stronger central nervous system effects than dextroamphetamine.
    • Decreased Peripheral Effects: Weaker peripheral effects compared to dextroamphetamine.
    • Higher Abuse Potential: More addictive due to its potency.
    • N-Methyl Analog: Structural modification of dextroamphetamine.

    Ephedrine and Pseudoephedrine

    • β-OH Analogs of Methamphetamine: Similar structure to methamphetamine.
    • Ephedrine in Chinese Medicine: Utilized for centuries in traditional medicine.
    • Ephedrine Supplements Banned in the US: Dietary supplements containing ephedrine are prohibited.
    • Pseudoephedrine as Meth Precursor: Used as a precursor in the production of methamphetamine.

    Methylphenidate (Ritalin)

    • MOA: Similar to amphetamines, inhibiting reuptake of DA and NE.
    • MAO Inhibition: Also inhibits monoamine oxidase, similar to amphetamine, although to a lesser extent.

    EP2651892B1 (Concerta)

    • Chiral Centers: Two chiral centers result in four isomers.
    • Threo Isomer Used Clinically: The threo isomer is the most clinically effective, with the erythro having greater side effects.
    • D-Threo Isomer: Responsible for the therapeutic effect.
    • Dexmethylphenidate: D-isomer of methylphenidate is available as a separate medication.

    Phenylethylamine SAR (Structure-Activity Relationships)

    • Amine Substituent (R1):
      • Cationic Amine: Essential for binding to adrenoceptors.
      • Size Influence: Determines which receptor subtypes are stimulated.
      • R1 = H: Preferential α-agonist action, primarily used as vasoconstrictors.
      • R1 = CH3: Non-selective agonist action, mainly used for α-agonist effects.
      • Larger R1: Increase in β-action and decrease in α-action.
    • α-Carbon Substituent (R2):
      • R2 = CH3: Introduces asymmetry, leading to R and S isomers.
      • Blood-Brain Barrier Penetration: No phenolic hydroxyls allow for entry into the CNS.
      • Central α1-Receptor Stimulation: Causes sleeplessness, agitation, restlessness, and appetite suppression.
    • β-Carbon Substituent (R3):
      • R3 = OH: Induces asymmetry with R and S isomers. Slows but does not prevent CNS penetration.
      • R3 = H: Enhanced CNS penetration, particularly when R1 and/or R2 are CH3.

    Atomoxetine (Strattera)

    • Selective Norepinephrine Reuptake Inhibitor: Selective due to the methyl group at the 2-position on the aryl ring.

    Guanfacine and Clonidine

    • Presynaptic Alpha2A-Agonists: Work by stimulating alpha2A receptors in the presynaptic neuron.

    Cocaine

    • MOA: Blocks reuptake of DA, NE, and 5-HT (serotonin).
    • Reinforcing and Stimulant Effects: Primarily due to DA reuptake blockade.
    • Amphetamine-like Psychological Effect: Short-acting and intense compared to amphetamine.
    • High Addiction Potential: Highly addictive due to its rapid and potent effects on the brain’s reward system.

    Xanthine MOAs

    • Non-Selective Adenosine Receptor Antagonists: Block adenosine receptors throughout the body.
    • Caffeine: Causes central vasoconstriction.

    Narcoleptics (Psychostimulants)

    • Wakefulness Enhancement: Used primarily for narcolepsy and other conditions characterized by excessive daytime sleepiness.
    • Cardiovascular Effects: May increase blood pressure and heart rate, but usually mild.
    • Mechanism of Action: Not fully elucidated, but likely involves effects on the brain’s arousal centers.

    Anorexiants/Anti-Obesity Agents

    • Appetite Suppression: Not directly affecting the appetite center in the brain; rather, it works indirectly through CNS stimulation.
    • Chiral Compounds: Most are chiral compounds, with the dextro isomer showing psychostimulant and appetite-suppressing activity.
    • Phenylethylamine SAR: Larger substituents on the nitrogen atom (N) lead to greater β-action and less α-action.

    Muscle Relaxants (Neuromuscular Blocking Agents)

    • Clinical Use: Used during surgical procedures and in the ICU for muscle paralysis.
    • Adjuncts to General Anesthesia: Used to optimize surgical conditions and facilitate intubation for ventilation.
    • Muscle Relaxation: Relax skeletal muscles during surgery, primarily those of the limbs, chest, and abdomen.
    • Respiratory Effects: Respiration is the last muscle function affected.
    • General Anesthetic Reduction: Allows for lower doses of general anesthetics, reducing surgical risk and recovery time.

    Tubocurarine

    • First Known Neuromuscular Blocking Drug: Used by indigenous tribes in South America as early as 1510.
    • Structure: Initially misclassified as containing two quaternary ammonium salts.

    Neuromuscular Blocker Classification

    • Depolarizing: Drugs that mimic acetylcholine (ACh) and initially stimulate muscles before causing paralysis.
    • Non-Depolarizing: Drugs that block the action of ACh at the neuromuscular junction, preventing muscle contraction.

    Neuromuscular Blocker SAR

    • Depolarizing Agents: Flexible structure connecting two quaternary heads.
    • Non-Depolarizing Agents: Rigid structure with quaternary and protonated heads within bulky groups.

    Succinylcholine (Depolarizing NM Blocker)

    • Acetylcholine Dimer: Two acetylcholine molecules linked together.
    • MOA: Acts as an agonist at nicotinic acetylcholine receptors (nAChR).
    • Muscle Fasciculation: Causes initial muscle twitching before relaxation.

    Non-Depolarizing Neuromuscular Blockers

    • Concealed “Double-Acetylcholine” Structure: Two types of bulky structures: isoquinoline derivatives and steroid derivatives.
    • Common Feature: One or two quaternary nitrogen atoms.
    • Lipid Solubility: Poorly lipid soluble, preventing entry into the central nervous system (CNS).
    • MOA: Competitive antagonists of nAChR, blocking ACh binding.

    Non-Depolarizing Neuromuscular Blockers: Atracurium and Cisatracurium (Steroidal Derivatives)

    • Administration: Not absorbed orally, but well distributed after intramuscular (IM) or intravenous (IV) administration.
    • CNS Entry: Too polar to cross the blood-brain barrier.
    • Duration of Action: Limited by enzymatic hydrolysis of ester groups within the molecules.
    • Metabolite Activity: Metabolites exhibit partial activity, which can be an issue with prolonged ICU use.
    • 3-Hydroxy Metabolites: More potent than the parent compounds and can accumulate, leading to prolonged paralysis.

    Spasmolytics (Centrally Acting Muscle Relaxants)

    • Spasticity Reduction: Used to alleviate spasticity in various painful conditions:
      • Chronic back pain
      • Fibromyalgia
      • Spinal injury
      • Cerebral palsy
      • Multiple sclerosis
      • Stroke
      • Acute spasm due to injury
    • MOA: Work by acting on the central nervous system to reduce muscle tone and spasm.

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    Description

    Explore the core symptoms, genetic and environmental factors contributing to ADHD. Understand various therapies including behavioral interventions, dietary changes, and more. This quiz covers key aspects necessary for effective understanding of ADHD management.

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