Drugs Acting on the Central and Peripheral Nervous Systems

Key Terms

• Action Potential: Sudden change in charge of a nerve cell membrane, enabling information transmission.

• Afferent: Neurons that bring information to the CNS; sensory nerves.

• Axon: Long projection carrying information from one nerve to another.

• Dendrite: Short projection transmitting information to the neuron.

• Depolarization: Sodium channels open, allowing sodium ions influx, reversing membrane charge.

• Effector Cell: Stimulated by a nerve, may be muscle, gland, or another neuron.

• Efferent Neurons: Carry information from CNS to effectors; motor neurons.

• Engram: Short-term memory from a reverberating circuit of action potentials.

• Forebrain: Upper brain level for thinking and sensory/motor coordination.

• Ganglia: Group of nerve bodies.

• Neuron: Structural unit of the nervous system.

• Hindbrain: Primitive brain area (brainstem), controlling vital functions.

• Limbic System: Midbrain area controlling emotions.

• Midbrain: Contains hypothalamus and thalamus; includes limbic system.

• Neurotransmitter: Chemical released by a nerve upon stimulation, interacting with receptors.

• Repolarization: Membrane returns to resting state, sodium ions outside, negative inside.

• Schwann Cell: Insulating cell on axons, enhancing conduction speed.

• Soma: Cell body of a neuron; contains nucleus and cytoplasm.

• Synapse: Junction between a neuron and an effector cell.

Nervous System Overview

• Controls body functions, analyzes stimuli, integrates responses.

• Central Nervous System (CNS): Brain and spinal cord.

• Peripheral Nervous System (PNS): Sensory receptors and motor nerves.

Physiology of the Nervous System

• Operates via electrical impulses and chemical messengers to transmit information.

• Neuron properties are foundational for nervous system functions.

Neurons

• Neurons are the structural unit of the nervous system.

• Approx. 14 billion neurons exist in the human body; 10 billion in the brain.

Neuron Structure

• Soma: Contains nucleus and organelles.

• Dendrites: Branch-like projections receiving signals.

• Axon: Elongated process carrying information away from the soma.

• Afferent Fibers: Nerve axons bringing information to the CNS.

• Efferent Fibers: Nerve axons carrying impulses away from the CNS to stimulate effector cells.

Action Potentials

• Nerves send messages through action potentials.

• Depolarization: Initial phase where sodium influx occurs.

• Repolarization: Membrane returns to resting state via the sodium-potassium pump.

Neurotransmitters

• Stimulate postsynaptic cells, either exciting or inhibiting them.

• Examples include:

  • Acetylcholine: Key in nerve-muscle communication and autonomic nervous system pathways.

  • Norepinephrine and Epinephrine: Released by sympathetic nervous system nerves; affect emotional responses and alertness.

  • Dopamine: Involved in impulse coordination and responses in specific brain areas.

  • GABA (Gamma-aminobutyric Acid): Inhibits neural activity, important for preventing over-excitement like seizures.

  • Serotonin: Regulates arousal, sleep, depression prevention, and motivation in the limbic system.

Page 23: Synaptic Transmission Sequence

• Steps: synthesis, uptake, release, diffusion, receptor interaction, second messenger activation, permeability change.

• Results in inhibitory or excitatory postsynaptic potentials leading to gland secretion or muscle contraction.

• Termination of neurotransmitter action involves enzyme inactivation, diffusion removal, or reuptake.

Nervous System Functions

• Controls body, analyzes stimuli, integrates responses through neurons.

• Neurons consist of a cell body, dendrites, and axons. Action potentials transmit information.

Action Potential Mechanics

• Sodium influx leads to membrane depolarization, followed by repolarization to restore resting membrane potential.

• Neurotransmitters released at axon ends stimulate postsynaptic reactions.

Central Nervous System (CNS)

• Comprises the brain and spinal cord; dominant nerve centers.

• Blood-Brain Barrier: Protective boundary against toxins influencing drug therapy.

• Circle of Willis: Distributes blood to protect neurons from oxygen/glucose deprivation.

Brain Anatomy

• Divided into three major parts:

  • forebrain:

    • Two hemispheres coordinate sensory impulses and motor actions, important for speech and learning.

  • midbrain:

    • Comprised of thalamus and hypothalamus, aiding sensory information processing and basic bodily functions.

  • hindbrain:

    • Contains brainstem (pons, medulla oblongata) regulating vital functions (respiration, blood pressure).

    • Includes the reticular activating system (RAS) for arousal.

Limbic System Functions

• High levels of neurotransmitters; responsible for emotional expression.

• Related to drug therapy for emotional disorders.

Spinal Cord Anatomy

• Contains 31 pairs of spinal nerves with sensory (dorsal) and motor (ventral) roots.

CNS Functions

• Responsible for coordinating reactions and complex emotional responses beyond mere reflexes.

Anxiolytic and Hypnotic Agents

Key Terms

• Anxiety: unpleasant feeling of tension, fear, or nervousness in response to an environmental stimulus, real or imaginary.

• Anxiolytic: drug used to depress the central nervous system (CNS); prevents the signs and symptoms of anxiety.

• Barbiturate: former mainstay for treating anxiety, sedation, and sleep induction; associated with severe adverse effects and numerous drug-drug interactions, making it less desirable than newer agents.

• Benzodiazepine: drug that enhances gamma-aminobutyric acid (GABA) effectiveness, depressing the CNS to block anxiety signs; can induce sedation and hypnosis at higher doses.

• Hypnosis: extreme sedation leading to CNS depression and sleep.

• Hypnotic: drug that depresses CNS; induces sleep.

• Sedation: loss of awareness and reaction to environmental stimuli.

• Sedative: depresses CNS, resulting in loss of awareness of and reaction to the environment.

Drug List

• Benzodiazepines: midazolam, pentobarbital, promethazine, oxazepam, phenobarbital, ramelteon, alprazolam, quazepam, secobarbital, zaleplon, chlordiazepoxide, temazepam, zolpidem, clonazepam, triazolam.

• Barbiturates: buspirone, dexmedetomidine, estazolam, amobarbital, diphenhydramine, flurazepam, butabarbital, eszopiclone, lorazepam, mephobarbital, meprobamate.

Anxiolytic and Hypnotic Agents

• These agents alter individual responses to environmental stimuli:

  • Anxiolytics: prevent feelings of tension or fear.

  • Sedatives: calm patients and create unawareness of the environment.

  • Hypnotics: induce sleep.

  • Tranquilizers: produce tranquility in anxious patients.

States Affected by Anxiolytic and Hypnotic Drugs

• Anxiety: a feeling of tension, nervousness, or fear possibly leading to sympathetic stress reaction. Anxiolytic drugs address this feeling.

• Sedation: loss of awareness, often leading to drowsiness; sedative drugs also function as anxiolytics.

• Hypnosis: extreme sedation causing significant CNS depression, treated with hypnotic drugs to assist with sleep.

Drug Therapy Across the Lifespan

Children

• Use of drugs is challenging; responses may be unpredictable, often showing aggression, irritability, or tearfulness.

• Only a few benzodiazepines have established pediatric dosages, while barbiturates have established pediatric dosages but should be used with caution due to unexpected responses.

Older Adults

• More susceptible to adverse effects, including increased sedation and hallucinations. Dosages should be carefully calculated and monitored.

Adults

• Advised against driving or making legal decisions while under treatment. Liver function should be assessed regularly.

Summary

• Anxiolytics: minor tranquilizers that depress the CNS to treat anxiety. At higher doses, they function as sedatives or hypnotics, aiding patients who are very excited or afraid.

• Hypnotics: further depress the CNS to inhibit neuronal arousal and induce sleep.

• Benzodiazepines: react with GABA receptor sites to depress CNS, causing effects like drowsiness.

• Barbiturates: older class of agents with severe side effects; less desirable compared to newer options.

• Buspirone: new anxiolytic that does not cause sedation or muscle relaxation, suitable for driving or work.

• Newer hypnotics: affect serotonin (zaleplon, zolpidem) or melatonin (ramelteon) in the brain.

Antidepressant Agents

Key Terms

• Affect: feeling experienced in response to environmental stimuli.

• Biogenic Amine: neurotransmitters (e.g., norepinephrine, serotonin, dopamine) thought deficient in depression.

• Depression: affective disorder with prolonged sadness exceeding precipitating events.

• MAOI: inhibits monoamine oxidase, raising norepinephrine levels and relieving depression with sympathomimetic effects.

• SSRI: selectively blocks serotonin reuptake; increases synaptic serotonin.

• TCA: blocks norepinephrine and serotonin reuptake, causing anti-cholinergic and sedative effects.

• Tyramine: dietary amine causing vasoconstriction; may lead to hypertensive crisis if consumed with MAOIs.

Drug List for Antidepressants

• Tricyclic Antidepressants: amitriptyline, doxepin, nortriptyline.

• MAOIs: phenelzine, selegiline, tranylcypromine.

• SSRIs: fluoxetine, paroxetine, duloxetine.

• Other Antidepressants: bupropion, trazodone, venlafaxine.

Affective Disorders

• Affect: Refers to people's feelings in response to their environment, which can be positive or negative, change in different situations, and usually are not extreme or long-lasting.

• Affective Disorders involve extreme reactions to positive/negative stimuli that change in situations but are often transient.

Depression and Antidepressants

• Depression, often misdiagnosed, manifests through energy loss, sleep disturbances, and overwhelming sadness.

Biogenic Amine Theory of Depression

• Depression theorized to stem from deficiencies of biogenic amines (norepinephrine, dopamine, serotonin).

• NE and serotonin regulate mood and arousal; deficiencies may occur due to:

  • Breakdown by monoamine oxidase (MAO).

  • Rapid neuronal firing leading to depletion.

  • Increased numbers or sensitivity of receptors.

Drug Therapy

• Effective treatment for depression alters neurotransmitter concentrations through:

  • Inhibition of MAO.

  • Blocking reuptake of neurotransmitters.

  • Regulating receptor sites and neurotransmitter breakdown.

Antidepressant Classifications

• Drug classes include:

  • Tricyclic antidepressants (TCAs): block reuptak

  • Monoamine oxidase inhibitors (MAOIs): prevent breakdown of neurotransmitters

  • Selective serotonin reuptake inhibitors (SSRIs): specifically inhibit serotonin reuptake

  • Other drugs that raise neurotransmitter concentrations.

Drug Therapy Across the Lifespan for Antidepressants

Children

• Antidepressants can increase suicidal ideation in children; monitoring is crucial, and long-term effects are often unclear.

Adults

• Medical causes of depression must be ruled out before therapy; effects of drugs may take weeks to manifest.

Older Adults

• Increased susceptibility to adverse effects; dosing adjustments are often necessary.

Summary

• Depression is common and often misdiagnosed; antidepressants increase biogenic amines in the brain.

• Antidepressant selection depends on individual tolerance to adverse effects; TCAs, MAOIs, and SSRIs have specific side effects.

Psychotherapeutic Agents

Key Terms

• Antipsychotic: treats thought process disorders; dopamine-receptor blocker.

• Attention-deficit disorder: behavioral syndrome characterized by an inability toconcentrate for longer than a few minutes and excessive

• Bipolar Disorder: involves depression alternating with hyperactivity.

• Major Tranquilizer: former name of antipsychotic drugs; the name is no longerused because it implies that the primary effect of these drugs issedation, which is no longer thought to be the desiredtherapeutic action

• Mania: phase of hyperexcitability in bipolar disorders.

• Narcolepsymental: disorder characterized by daytime sleepiness andperiods of sudden loss of wakefulness

• Neuroleptic: drug with neurological adverse effects used for psychosis.

• Schizophrenia: most common psychosis, characterized by hallucinations and delusions.

Drug List for Psychotherapeutic Agents

• Antipsychotic/Neuroleptic: risperidone, thioridazine, ziprasidone.

• Stimulants: armodafinil, dexmethylphenidate, atomoxetine.

Psychotherapeutic Agents

• Treat psychoses and targeted towards thought processes; help patients to function better socially.

Mental Disorders and Their Classification

• Previously linked to environmental factors; now seen as brain dysfunction due to chemical imbalances.

Selected Mental Disorders

• Schizophrenia: Affects social functionality; strong genetic association with characteristics like hallucinations and delusions.

• Mania:Characterized by periods of extreme overactivity and excitement associated with bipolar disorder (manic-depressive illness).

  Bipolar Disorder: Involves alternating extremes of depression and hyperactivity, often reflecting biochemical imbalances and the inability of neurons to reestablish stability.

• Narcolepsy: Characterized by daytime sleepiness and sudden loss of wakefulness.

• Attention-deficit disorder: Behavioral syndrome seen in children and adults, marked by lack of concentration and hyperactivity

Drug Therapy Across the Lifespan for Psychotherapeutic Agents

Children

• Agents used cautiously; long-term effects are unclear, periodic monitoring of lithium levels is vital.

Older Adults

• Increased risk of adverse effects; caution with dosage and regular monitoring is necessary.

Adults

• Should be under regular care for monitoring and managing adverse effects.

Summary for Psychotherapeutic Agents

• Schizophrenia is marked by hallucinations and delusions; mania represents hyperexcitability.

• Lithium is key for treating bipolar disorder; its toxicity requires careful monitoring of levels.

• CNS stimulants increase RAS activity, improving attention in disorders like ADHD and narcolepsy.

Antiseizure Agents

Key Terms

• Absence Seizure: Type of generalized seizure, sudden loss of consciousness with brief (3-5 sec) episodes, previously termed "petit mal".

• Antiepileptic Drug: Designed to treat seizures by modulating excessive electrical activity in the brain.

• Convulsion: Muscular reaction to excessive electrical discharges in the brain.

• Epilepsy: Group of syndromes characterized by recurrent seizures.

• Generalized Seizure: Seizure that spreads rapidly from one brain area to both hemispheres.

• Partial (Focal) Seizures: Seizures localized to one brain area with no spread to the entire brain.

• Seizure: Sudden excessive electrical discharge from nerve cells in the brain.

• Status Epilepticus: Severe, rapidly recurring seizures, categorized as the most severe type of generalized seizure.

• Tonic-Clonic Seizure: Also known as "grand mal", marked by clonic-tonic muscle contractions and loss of consciousness.

Drug List

• Antiepileptic Drug Classes:

  • Partial: Rufinamide, Tiagabine, Topiramate

  • Benzodiazepines: Clonazepam, Diazepam, Clorazepate

  • Hydantoins: Phenytoin, Fosphenytoin

  • Succinimides: Ethosuximide

  • Gabapentinoids: Gabapentin, Pregabalin

Epilepsy

• Definition: Epilepsy is a collection of syndromes characterized by excessive electrical discharges from neurons in the brain.

• Symptoms: May lead to motor convulsions, or stimulate autonomic nerves causing different symptoms.

• Additional Effects: Not all seizures cause motor activity; some cause only lapses in consciousness or sensory symptoms.

• Management of Epilepsy: Utilizes antiepileptics or anticonvulsants to manage seizure activity.

Nature of Seizures

• Causes of Seizures: Often linked to abnormal neuronal activity. Primary seizures have no identifiable cause, whereas secondary seizures arise from identifiable stressors.

Classification of Seizures

• Categories:

  • A. GENERALIZED SEIZURES

    Characteristics: Initiate in one brain area and rapidly spread to both hemispheres, often leading to loss of consciousness.

    Further Details: Symptoms reflect extensive electrical activity throughout the brain region.

    Common Types:

    • Tonic-Clonic Seizures

    • Absence Seizures

    • Myoclonic Seizures

    • Febrile Seizures

    • Psychomotor Seizures

    • Status Epilepticus

  • B. PARTIAL SEIZURES

    Definition: Involve localized brain regions, originating from a specific focus without spreading.

    Types:

    • Simple Partial Seizures: Consciousness not impaired

    • Complex Partial Seizures: Consciousness impaired

Patient and Family Teaching

• Education Needs:

  • Understanding epilepsy stigma, diagnostic explanations, and actions during a seizure.

  • Encourage MedicAlert identification for emergencies.

  • Information about community resources and public transportation.

Drug Therapy Across the Lifespan

• Children: Special considerations around developmental impact and monitoring during treatment.

• Older Adults: Increased susceptibility to adverse effects; dosages often need adjustments.

Antiparkinsonism Agents

• Anticholinergic: Drug resisting acetylcholine effects.

• Bradykinesia: Characteristic slowness in movements of Parkinson’s Disease.

• Corpus Striatum: part of the brain that reacts with the substantia nigra tomaintain a balance of suppression and stimulation

• Dopaminergic: Drug enhancing dopamine's effects.

• Parkinson’s Disease: Degenerative disorder marked by loss of coordination.

• Parkinsonism: Symptoms similar to Parkinson’s due to adverse medication effects or brain injury-related issues.

• Substantia Nigraa: part of the brain rich in dopamine and dopamine receptors;site of degenerating neurons in Parkinson’s disease

• DRUG LIST

  • Anticholinergic Agents

  • Dopaminergic Agents

  • Adjunctive Drugs

Parkinson’s Disease

• Characteristics: Progressive, chronic neurological disorder. No known cure exists.

• Symptoms Management focus: Management rather than cure aims.

Parkinson’s Disease and Parkinsonism

• Characteristics:

  • Characterized by lack of coordination.

  • Does not affect higher cerebral cortex; patients may be alert but trapped in a degenerating body.

• Parkinsonism:

  • Refers to extrapyramidal symptoms resembling Parkinson's disease due to drugs or brain injuries, typically exhibiting tremors and bradykinesia.

• Manifestations:

  • Tremors develop gradually, leading to rigidity or weakness in muscle groups.

  • Difficulty maintaining posture; bradykinesia causes slow, difficult intentional movements.

  • Advanced stages show a shuffling gait, drooling, slow/slurred speech, and mask-like facial expressions.

Treatment Overview

• Current Treatment Approaches: Mostly focus on symptomatic management without halting neuron degeneration.

Drug Mechanisms

• Inhibition and Stimulation: Drugs are designed either to restore dopamine concentration or to block excitatory feedback in the neural pathways.

Drug Therapy Across the Lifespan

• Child Considerations: Limited safety data; require close monitoring.

• Adult and Older Adult Considerations: Risk of increased adverse effects, dosages require careful adjustment based on health status.

Muscle Relaxants

Key Terms

• Basal Ganglia Role: Coordination of unconscious muscle movements.

• Cerebellum: lower portion of the brain; Coordinates voluntary motion and balance actions.

• Extrapyramidal Tract: Communicates adjustments for unconscious muscle activities.

• Hypertonia: state of excessive muscle response and activity

• Interneuron: neuron in the CNS that communicates with other neurons, notwith muscles or glands

• Pyramidal tract: fibers within the CNS that control precise, intentional movement

• Spasticity: Characterized by sustained muscle contraction often due to neuronal damage.

• Spindle Gamma Loop System: Reflex pathway maintaining muscle tone through sensory detection.

Drug List

• Types: Centrally Acting and Direct-Acting agents such as baclofen and dantrolene.

Muscle Relaxants Overview

• Application: Treat muscle spasms due to injuries or spastic conditions through interruption of spasm cycles.

Nerve Function and Movement

• Motor Coordination: Relation of spinal motor neurons with brain areas responsible for muscle coordination.

Spinal Reflexes

• simplest nerve pathways that monitor movement and posture

• Spinal Reflexes

  • simple, involving an incoming sensory neuron and an outgoing motor neuron

  • complex, involving interneurons that communicate with the related centers in the brain

Neuromuscular Abnormalities

• Causes: Describes how neuronal injuries can lead to symptoms such as spasms or paralysis.

Muscle Spasm Causes

• Analysis: Typically caused by musculoskeletal injuries leading to involuntary contractions.

Drug Therapy Across Lifespan (Muscle Relaxants)

• Child Considerations: Specific pediatric dosing for metaxalone; monitoring for adverse effects.

• Older Adults: Susceptibility to adverse effects due to polypharmacy or chronic conditions.

Summary of Muscle Activity Control

• Higher-Level Control: Describes the balance of muscle activity management within the nervous system.

Consequences of Motor Neuron Damage

• Symptoms: How damage leads to spasticity and coordination difficulties.

Botulinum Toxin Applications

• Use Cases: Reduces severity of certain muscle-related conditions and aesthetically related applications.

Key Terms

Types of Pain Fibers

• A fibers: Large-diameter fibers transmitting touch and temperature sensations to the spinal cord.

• A-delta fibers: Small-diameter fibers transporting pain impulses.

• C fibers: Unmyelinated and slow fibers conducting pain signals slowly to the spinal cord.

Important Theories and Agents

• Ergot Derivative: A class of drugs causing vasoconstriction in the brain to relieve migraines but with notable adverse effects.

• Gate Control Theory: A theory explaining that the brain can modulate pain impulses via descending fibers that can close the ‘gate’ for pain transmission in the spinal cord.

• Migraine Headache: Severe, unilateral head pain with symptoms like light sensitivity and gastrointestinal upset, linked to brain arterial dilation.

• Narcotics: Drugs from opium that interact with specific receptors to induce effects across the body.

Classifications of Narcotics

• Narcotic Agonists: Stimulate opioid receptors to provide analgesia.

• Narcotic Agonists-Antagonists: Stimulate some opioids while blocking others.

• Narcotic Antagonists: Block opioid receptors, counteracting overdose effects.

• Opioid Receptors: Receptor sites on nerves responsive to endorphins, crucial for narcotic drug activity.

• Pain: A sensory and emotional experience indicating real or potential tissue damage.

Pain Transmission Pathway

• Spinothalamic Tract: Nerve pathway transmitting pain signals from the spine to the brain.

• Triptan: A selective serotonin receptor blocker that causes cranial vascular constriction for acute migraine treatment.

Drug List for Pain Management

Narcotics and Antagonists

• Antagonists: Examples include rizatriptan, naloxone, naltrexone.

• Narcotics: Sufentanil, codeine, fentanyl, hydrocodone, ergotamine, triptans (e.g., eletriptan, sumatriptan, methadone, morphine, etc.).

Overview

• Injuries can result in muscle spasms and pain, impacting normal function.

• Damage to CNS neurons may lead to chronic muscle contractions due to disrupted nerve signals.

• Treatments include skeletal muscle relaxants that act in the brain and spinal cord to alleviate pain cycles.

Pain

Nature of Pain

• Pain is tied to tissue damage, causing chemical release that stimulates sensory nerves.

Types of Pain

• Acute Pain:

  • Short-term pain following recent injury.

  • Emerges from recent tissue damage.

  • Alerts individuals to the injury prompting necessary care and behavior adjustments.

• Chronic Pain:

  • Persistent pain continuing past healing expectations, affecting daily life.

  • Persistent pain that may stress patients and interfere significantly with daily activities and sleep.

Pain Impulse Transmission

Nerve Fibers and Pain Sensation

• A-delta fibers: Myelinated, rapid response to acute pain.

• C fibers: Unmyelinated, slow response.

• Pain signals are processed in dorsal horn synapses, transmitting to the brain.

Pain Signal Pathways

• Ascending pathways: Carry pain signals from the periphery to the brain via the spinothalamic tract.

• Descending pathways: Modulate pain perception through the release of neurotransmitters like endorphins.

• Pain receptors activate through peripheral and central neurological pathways leading to brain response.

Pain Receptor

Opioid Receptors

• Definition: Receptor sites that respond to naturally occurring peptides, specifically endorphins and enkephalins.

• Location: Found in the central nervous system (CNS), on peripheral nerves, and on cells in the gastrointestinal (GI) tract.

• Functions in the Brainstem: Help to control various functions including blood pressure, pupil diameter, GI secretions, and the chemoreceptor trigger zone (CTZ), which regulates nausea and vomiting, cough, and respiration.

• Integration of Pain Information: In the spinal cord and thalamus, opioid receptors help to integrate and relate incoming information about pain.

• Modulation of Pain: Endorphins and enkephalins normally modulate the pain information coming into the brain. Endorphins are released during stress to block the sensation of pain.

Pain Perception

Factors Affecting Pain Experience

• Past Experiences: Affect how pain is perceived or feared.

• Learned Responses: Influence reactions to pain based on social and cultural upbringing.

• Environmental Context: The setting may affect a person's willingness to express or address pain in presence of others.

Summary

Pain Mechanism Overview

• Pain occurs from tissue injury inducing chemical release, which stimulates specific sensory nerves leading to the spinal cord.

• Opioid receptors help modulate these signals through endogenous peptides.

Function of Narcotics

• Derived from opium, narcotics interact with opioid receptors for pain alleviation but may cause adverse effects like constipation, respiratory depression, and dependency.

Pharmacological Insights

• The unique effects and adverse reactions of each narcotic depend on their affinity for distinct opioid receptor subtypes

Understanding Narcotic Interactions

• Narcotic Agonists-Antagonists: Less addictive, stimulate some receptors while blocking others. Useful for managing pain with reduced addiction potential.

• Narcotic Antagonists: Essential in overdose scenarios to reverse narcotic effects.

Characteristics of Migraines

• Defined as severe, unilateral headaches possibly linked to arterial changes in the brain.

• Treatment Options: Involve ergot derivatives for vasoconstriction and triptans, a newer class with fewer systemic effects.

General and Local Anesthetic Agents

Key Terms

• Amnesia: Loss of memory associated with surgical procedures.

• Analgesia: Absence of pain sensation.

• Anesthetic: Drug which induces loss of sensation.

• Balanced Anesthesia: Combined drug approach to achieve optimal anesthesia effects with minimal side effects.

• General Anesthesia: Induces unconsciousness and analgesia for surgical procedures.

• Induction: time from the beginning of anesthesia until achievement of surgical anesthesia

• Local Anesthesia: Prevents pain in a specific area without affecting consciousness.

• Plasma Esterase: Enzymes that quickly break down ester-type anesthetics to mitigate effects.

• Unconsciousness: loss of awareness of one’s surroundings

• Volatile Liquids: Inhaled anesthetics that vaporize at room temperature for quick induction.

General and Local Anesthetic Agents

Anesthetic Classifications

• General Anesthetics: CNS depressants inducing loss of pain sensation and consciousness.

• Local Anesthetics: Target specific areas for pain relief without systemic effects.

A. General Anesthesia

• Involves administering a combination of various anesthetic agents to achieve:

  • Analgesia: Loss of pain perception.

  • Unconsciousness: Loss of awareness of surroundings.

  • Amnesia: Inability to recall events during the procedure.

• Combines drugs for optimal effects while minimizing adverse effects.

• Blocks body reflexes:

  • Prevents involuntary responses to injury, protecting cardiac, respiratory, gastrointestinal (GI), and immune functions.

  • Reduces muscle reflexes to avoid movements that could compromise surgical success.

Risk Factors Associated with General Anesthesia

Risk Factor

• CNS Factors: Neurological disorders may complicate reactions to CNS depressants.

• Cardiovascular: History of heart diseases increases surgery risks.

• Respiratory Factors: Pre-existing pulmonary disorders complicate anesthesia delivery.

• Renal and Hepatic Function: Conditions impacting metabolism lead to complications post-anesthesia.

Balanced Anesthesia

Balanced Anesthesia

• Involves combining several drugs, each with a specific effect, to achieve:

  • Analgesia: Pain relief.

  • Muscle Relaxation: Reduces muscle tension.

  • Unconsciousness: Loss of awareness of surroundings.

  • Amnesia: Inability to recall events during the procedure.

• Many drugs are given before the general anesthetic to facilitate the process; some continue during surgery to enhance effects at lower doses.

• Careful selection of appropriate agents, along with patient monitoring and support, helps alleviate many issues.

Common Agents in Balanced Anesthesia

• Preoperative Medications: May include anticholinergics to decrease secretions for easier intubation and prevent bradycardia associated with neural depression.

• Sedative–Hypnotics: Used to relax the patient, aid amnesia, and decrease sympathetic stimulation.

• Antiemetics: To decrease the nausea and vomiting associated with the slowing of GI activity.

• Antihistamines: To decrease the chance of allergic reaction and help to dry up secretions.

• Narcotics: To aid analgesia and sedation.

Administration of General Anesthesia

• Induction:

  • Starting point until surgical anesthesia is achieved.

  • The transition to surgical anesthesia, often involving rapid-acting agents to navigate through potentially dangerous stages efficiently.

• Maintenance:

  • Keeping the patient anesthetized during surgery.

  • Consistent anesthetic management through gas anesthetics from stage three until surgery completion.

• Recovery:

  • Restoring consciousness post-procedure.

  • Continuous monitoring for adverse reactions is crucial during recovery until the patient regains full functionality.

B. Local Anesthesia

• refers to a loss of sensation in limited areas of the body

• Local anesthesia can be achieved by several different methods:

  • topical administration

  • Infiltration

  • field block

  • nerve block

  • intravenous regional anesthesia

Topical Administration

• Involves applying a cream, lotion, ointment, or drop of local anesthetic to traumatized skin or mucous membranes (e.g., in the eye, nose, throat) for pain relief or to facilitate procedures.

• Systemic absorption is rare but can occur if tissue is damaged.

Infiltration

• Involves injecting the anesthetic directly into tissues (e.g., for suturing or cutting) to block nerve impulse transmission.

Field Block

• Involves injecting anesthetic around the area affected by a procedure or surgery, providing a more intense effect than infiltration.

• Often used for dental procedures like tooth extractions.

Nerve Block

• Involves injecting anesthetic at a point along the nerves that supply the area for pain relief or muscle paralysis.

• Blocks are performed at a distance from the surgical field and involve a greater area, risking more adverse effects.

  • Types of Nerve Block:

    • Peripheral Nerve Block: Blocks sensory and motor aspects of a specific nerve.

    • Central Nerve Block: Injection into the roots of the spinal nerves.

    • Epidural Anesthesia: Injection into the epidural space near the spinal cord.

    • Caudal Block: Injection into the sacral canal.

    • Spinal Anesthesia: Injection into the subarachnoid space of the spinal cord.

Intravenous Regional Local Anesthesia

• Involves draining blood from a limb, securing a tourniquet, and injecting anesthetic into the limb's vein to prevent systemic circulation.

Neuromuscular Junction Blocking Agents

Key Terms

• Acetylcholine Receptor Site: Key area on muscle membrane for signal reception leading to contraction.

• Depolarizing Neuromuscular Junction (NMJ) Blocker: Causes stimulation of a muscle cell, leading to contraction without allowance for repolarization and restimulation; characterized by initial contraction followed by paralysis.

• Malignant Hyperthermia: A severe reaction to some NMJ drugs in susceptible individuals, characterized by extreme muscle rigidity, severe hyperpyrexia, acidosis, and potential fatality.

• Neuromuscular Junction (NMJ): The synapse between a nerve and a muscle cell.

• Nondepolarizing Neuromuscular Junction (NMJ) Blocker: Prevents depolarization and stimulation of the muscle cell by blocking the effects of acetylcholine.

• Paralysis: Lack of muscle function.

• Sarcomere: The functional unit of a muscle cell, composed of actin and myosin arranged in layers, giving a striped appearance.

• Sliding Filament Theory: Explains muscle contraction as a reaction between actin and myosin molecules when freed to interact due to the inactivation of troponin following calcium entry during depolarization.

Neuromuscular Junction (NMJ)

• The connection where a motor neuron communicates with a skeletal muscle fiber, leading to muscle contraction.

• NMJ-blocking agents interfere with normal muscle function at the nerve-muscle junction.

• Muscle function requires a nerve impulse arrival at the motor terminal, releasing acetylcholine (ACh) into the synaptic cleft.

• A balance of excitatory and inhibitory impulses maintains muscle tone.

Key Points

• The nerves and muscles communicate at the NMJ.

• ACh acts as the neurotransmitter at the NMJ.

• NMJ blockers interfere with muscle function.