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Nervous System by Mind Map: Nervous System

1. PNS

1.1. Motor

1.1.1. Somatic

1.1.2. Autonomic Parasympathetic Sympathetic

1.1.3. Receptors Adrenergic Alpha 1 Alpha 2 Beta 1 Beta 2 Dopamine Adrenergic DRUGS Cholinergic Nicotinic N Nicotinic M Muscarinic Cholinergic DRUGS

1.2. Sensory

2. CNS

2.1. Brain

2.1.1. The Hindbrain The medulla oblongata The pons The cerebellum

2.1.2. The Midbrain Two pairs of dorsal enlargements The superior and inferior colliculi

2.1.3. The Forebrain Two hemispheres Cerebral cortex Gray matter Basal ganglia Rostral end of the neural tube Diencephalon Thalamus Hypothalamus

2.1.4. CN 12: On Old Olympus Towering Tops, A Fin And German Viewed Some Hops Olfactory Optic Oculomotor Trochlear Trigeminal Abducens Facial Auditory (Vestibulocochlear) Glossopharyngeal Vagus Spinal Accessory Hypoglossal

2.2. Spinal Cord

2.3. Receptors

2.3.1. Mu Receptors Location CNS Function Analgesia Respiratory Depression Euphoria Sedation

2.3.2. Kappa Receptors Location CNS Function Analgesia Sedation

2.3.3. Serotonin

2.3.4. GABA GABA is an Inhibitory neurotransmitter that is widely distributed throughout the brain

2.3.5. Glutamate Glutamate is the primary excitatory neurotransmitter in CNS Works on 2 receptors: NMDA and AMPA

2.3.6. Opioid Analgesics and Antagonists Pure Opioid Agonists: activate Mu and Kappa. Morphine Fentanyl Oxycodone Hydrocodone (vicodin) Agonist-Antagonist Opioids: produce analgesia. Agonist on Kappa, Antagonist on Mu Limited response of respiratory depression, increases workload on heart Pure Opioid Antagonists: Naloxone. Reversal of overdose Drugs which block the effects of opioid agonist @ Mu receptor Treatment of opioid overdose Reversal of coma and respiratory depression Relief of opioid induced constipation Management of addiction Narcan


2.4.1. Antiepileptics Suppression of Sodium Influx Activated state: Na+ influx into the cell Inactivated state: After Na+ entry; cells are closed Normal: quickly return to activated state Medications: Reversibly bind to Na+ channel while they are in the inactivated state, prolonging inactivation Suppression of Calcium Influx In axon terminals, influx of Ca+ through voltage gated Ca+ channels promotes transmitter release Drugs block this and suppress transmitter release Promotion of Potassium Efflux: affect of repolarization Ezogabine Medication that acts on voltage gated K+channels to facilitate K+ efflux; slows repetitive neuronal firing Antagonism of Glutamate: primary excitatory transmitter Glutamate is the primary excitatory neurotransmitter in CNS Works on 2 receptors: NMDA and AMPA Drugs block the action of glutamate Potentiation of GABA: decrease neuronal excitability GABA is an Inhibitory neurotransmitter that is widely distributed throughout the brain Drugs decrease neuronal activity, suppressing a seizure

2.4.2. Antipsychotics FGAs Block receptors for dopamine in the CNS Cause serious movement disorders (Extra Pyramidal Symptoms EPS) Classified by Potency Adverse Effects Toxicity SGAs Produce only moderate blockage of dopamine receptors; stronger blockage for serotonin Less risk of EPS than FGAs Mechanism of action Therapeutic use Pharmacokinetics: rapid absorption after oral administration, highly protein bound, hepatic metabolism, renal and fecal excretion Adverse effects: Agranulocytosis, Seizures, DM Atypical Antipsychotics Risperidone (Resperdal) Mechanism of action: Pharmacokinetics: rapid absorption, hepatic met., renal excretion, long half life Therapeutic effects: Treatment of Schizophrenia and Bipolar disorder Adverse effects: Depot Preperations Long-acting, injectable formulations used for long-term maintenance therapy of schizophrenia Three depot preparations available

2.4.3. Depression Drugs SSRIs Produce selective inhibition of serotonin reuptake Produce CNS excitation Primarily used to treat major depression Other uses Adverse Effects Drug Interactions SNRIs (Venlafaxine) Indications Blocks NE and serotonin uptake Serious reactions if combined with MAOIs Side effects Tricyclic Antidepressants (TCAs) Drugs of first choice for many patients with major depression Most common adverse effects: sedation, orthostatic hypotension, and anticholinergic effects May increase risk of suicide early in treatment Block neuronal reuptake of two monoamine transmitters Indications Other uses Side Effect Toxicity MAOIs 2nd- or 3rd-choice antidepressants for most patients As effective as TCAs or SSRIs, but more dangerous Risk of triggering hypertensive crisis if patient eats foods rich in tyramine Drug of choice for atypical depression Therapeutic uses Adverse effects Hypertensive Crisis with Dietary Tyramine Atypical Antidepressants Bupropion (Wellbutrin)

2.4.4. Bipolar Disorder Drugs Mood stabilizers (Lithium) Relieve symptoms during manic and depressive episodes Do not worsen symptoms of mania or depression; do not accelerate the rate of cycling Prevent recurrence of manic and depressive episodes Lithium Antipsychotics Given during severe manic episodes Antidepressants Given during depressive episodes

2.4.5. Sedative-Hypnotic Drugs Drugs that depress CNS function Primarily used to treat anxiety and insomnia Antianxiety agents or anxiolytics Distinction between antianxiety effects and hypnotic effects is often a matter of dosage

2.4.6. Panic Disorder Drugs Antidepressants Selective serotonin reuptake inhibitors Tricyclic antidepressants Monoamine oxidase inhibitors Benzodiazepines Drugs of choice to treat insomnia and anxiety Used to induce general anesthesia Used to manage seizure disorders, muscle spasm, panic disorder, and withdrawal from alcohol Safer than general CNS depressants Potential for abuse Fewer drug interactions Adverse effects

2.4.7. Insomnia Drugs Drugs used for treatment Benzodiazepines Benzodiazepine-like drugs: zolpidem (ambien), zaleplon, and eszopiclone (lunesta) Ramelteon melatonin agonist Trazodone Causes excessive fatigue. Use with caution in elderly Antihistamines No longer used in children. Benadryl Alternative medicines melatonin Sleep hygiene