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Pharm U5 Terms

Pharmacology: Unit 5 terms

QuestionAnswer
Cerebral cortex contains cell bodies of neurons (gray matter) that control voluntary activities of the body
Electroencephalogram (EEG) recording of electrical activity of the cortex; useful in diagnosing various brain disorders
Cerebral medulla composed of myelinated axons (white matter); includes basal ganglia (group of cell bodies (gray matter) sometimes called extrapyramidal system (EPS); regulates skeletal muscle tone and movement
Dopamine functions as neurotransmitter in basal ganglia of brain; blocked by antipsychotic drugs
Brainstem 10 of 12 cranial nerves originate from this part of the brain; includes thalamus, hypothalamus, pons, medulla oblongata
Thalamus regulates sensory impulses traveling to cortex; evaluates sensory information, directs it to appropriate cortex centers
Hypothalamus controls many body functions (temp, water balance, appetite, sleep, ANS, certain emotional/behavioral responses)
Pons located below hypothalamus; regulates respiration, serves as relay station for nerve fibers traveling to other areas of the brain
Medulla oblongata lies just above spinal cord; three vital centers – cardiac, vasomotor, respiratory; injury to this area frequently results in death
Cerebellum lies behind brainstem and below cerebrum; coordinates body movements, posture, maintains body equilibrium
Reticular formation diffuse network of nerve fibers that travel throughout brainstem and cerebrum; composed of excitatory and inhibitory fibers
Reticular activating system (RAS) excitatory fibers responsible for consciousness, arousal, degree of alertness, a filter process that allows for concentration
Inhibitory fibers decrease activity of RAS and, consequently, degree of arousal/alertness; decrease usually occurs in period of rest/sleep
Limbic system collection of neurons that form a specific neural pathway; most structures of system located around hypothalamus, lower portions of cerebrum; involved w/ emotional & behavioral responses, learning & memory
Extrapyramidal system somatic motor pathway located in CNS that affects skeletal muscles; associated w/ coordination of muscle group’s movement and posture
Inhibitory neurotransmitters GABA (gamma-aminobutyric acid), dopamine
Excitatory neurotransmitters glutamate (primary); also ACh, NE, Epi, serotonin
Sensation of pain occurs with local irritation sensed by nociceptors, followed by recognition within the CNS
Nociceptors located in skin, muscle, joints, bones, viscera; respond to tissue injury; quiet if no injury present
Pain management/selection of appropriate analgesic dependent upon the type and duration of pain
Analgesics relieve pain without affecting consciousness
Factors that lower pain threshold anxiety, sleeplessness, tiredness, anger, fear, fright, depression, discomfort, pain, isolation
Factors that increase pain threshold symptom relief, sleep, rest, diversion, empathy, specific medications (analgesics, antianxiety agents, antidepressants)
Pain classifications acute/chronic; visceral/somatic; nociceptive/neuropathic; slow/fast
Acute pain state in which individual experiences presence of severe discomfort or uncomfortable sensation; sudden onset that usually subsides with treatment; ex. myocardial infarction, appendicitis, kidney stones
Chronic pain persistent or recurring pain that continues for more than six months; may be difficult to treat effectively; ex. cancer, rheumatoid arthritis
Visceral source of pain origin in smooth musculature or sympathetically innervated organ systesm; often difficult to localize since it is dull and aching and may also be referred
Somatic source of pain arises from activation of nociceptors in skeletal muscles, fascia, ligaments, vessels, or joints; usually localized, constant; may be described as aching/throbbing
Nociceptive pain can only occur when all neural structures (nerve cell, nerve endings, spinal cord, brain) are functioning properly; can be acute or chronic
Neuropathic pain pain resulting from abnormal signals or nerves damaged by entrapment, infection (i.e. HIV, amputation, diabetes); usually chronic, but may be intermittent
Fast pain pain signal through A-delta fibers
Slow pain pain signal through C-fibers
Referred pain occurs when nerve fibers from visceral & somatic areas converge in same area in dorsal horn are processed in such a way that pain is perceived as originating in same area of somatic sensory A-delta fiber rather than visceral C-fiber
Opioid (agonist) analgesics include opiates, narcotic analgesics that produce the same pharmacological effects as opium.
Opioid (agonist) analgesics combine with mu, kappa, and delta opiate receptors within the CNS to produce analgesic effect by alter perception of pain; do not impair peripheral nerves
Opioid (agonist) analgesic side effects sedation, euphoria, dysphoria, constipation, urinary retention, miosis, respiratory depression, hypotension, bradycardia, bronchoconstriction, emesis, anti-emetic; different receptors (mu, kappa, delta) produce different effects
Morphine major analgesic drug contained in crude opium; prototype strong agonist; show high affinity for mu receptors, varying affinities for delta and kappa receptors
Agonist-antagonist agents drugs that stimulate one receptor but block another; effects of these agents depends on previous exposure to opioids; in opioid dependence will induce withdrawal symptoms due to blocking effects
Mixed opioid agonist-antagonist agents bind with kappa receptors and block or have minimal effects on mu receptors; have no antitussive effects and fewer GI effects than agonists do
Other analgesics centrally acting bind to mu opioid receptors; weakly inhibits re-uptake of NE and serotonin; used to treat moderate to severe pain; can cause seizures in pt taking serotonin reuptake inhibitors/antidepressants
Opioid antagonists compete with narcotics for receptor sites, thereby hindering narcotic effect; work only on opioid narcotic agonists; used for respiratory depression (drug-induced), opioid toxicity, opioid overdose, treatment of addiction; Narcan is the main agent
Naloxone (Narcan) opioid antagonist given IV, IM, or SC; drug of choice b/c does not produce respiratory depression; if this agent doesn’t work, indicates that patient overdosed on a non-opioid substance
Nonsteriodal anti-inflammatory drugs (NSAIDS) nonopioid analgesics; inhibit leukotriene and or prostaglandin pathways; can interact with cyclooxygenases (enzymes that produce prostaglandins)
Older NSAIDS non-opioid analgesic considered nonselective—any COX will do; produce analgesia (COX1 & COX2) or decreased platelet aggregation that are beneficial; adversely alters stomach lining, though
Newer NSAIDS non-opioid analgesics that relieve pain and inflammation but do not cause gastric problems by selectively inhibiting only COX2; analgesia equal to that of other NSAIDS
Non-steroidal anti-inflammatory drugs (NSAIDs) relieve mild to moderate pain without altering consciousness or mental function; reduce inflammation, relieve fever, releave vascular headaches, inhibition of platelet aggregation, myocardial infarction
Antiarthritic (antirheumatic) agents treats inflammation in patients not responding to other therapy; suppresses inflammation of synovial membrane in joints affected by arthritis during active stage disease; relieve pain, swelling, stiffness; can arrest progression of the disease
Uricosuric drugs (anti-gout) control acute inflammation of gout attack; increase excretion of uric acid, decrease production of uric acid
Gout inborn error of metabolism causing disorder in metabolism of uric acid; primarily affects males in middle age, and post-menopausal women; characterized by deposits of uric acid crystals in joints, especially big toe
Uricosuric drug contraindications/precautions aspirin can interfere with uric acid excretion causing exacerbation of gout
Generalized anxiety disorder characterized by at least six months of excessive anxiety and uncontrollable worry about everyday problems; primarily emotional experience giving individual sense of angst, unease, apphrehension; resulting distractibility and forgetfulness
Depression manifested by emotions of sadness, anhedonia, negative ruminations, somatic preoccupations, psychomotor retardation.
Glutamate gamma-aminobutyric acid (GABA) major inhibitory NT; plays critical role in anxiety, depression, sleep
Sleep disturbances common disturbance in both clinical anxiety, depression
Sleep latency time it takes to fall asleep
Goals of management of sleep disorders reduce sleep latency, increase total time of sleep & sleep quality, enhance subjective sense of refreshment upon awakening in the morning
Benzodiazepines antianxiety agent; decreases excitability & functional activity of specific brain/spinal cord areas by potentiating GABA effects (increase Cl channel openings); greater degree of hyperpolarization & neuronal depression, which reduces activity of CNS areas
Benzodiazepine uses treatment of anxiety states, depression, preanesthesia, withdrawal syndromes, sustained seizures
Benzodiazepine antagonist—flumazenil (Romazicon) benzodiazepine receptor antagonist; admi IV to reverse depressant effects but not respiratory depressant effects of benzos; used in management of overdose; if pt. benzo dependent, can produce withdrawal reaction (seizure)
Azapirones nonbenzodiazopene; new class of antianxiety agent that also produces antidepressant effects; appear to act on serotonin receptors; main agent Is buspirone (BuSpar)
Piperazine derivatives nonbenzodiazepine agent; depresses CNS; tranquilizing effect produced primarily by depression of hypothalamus, brain stem reticular formation rather than cortical areas
Sedative an agent that produces state of calmness when given in divided doses; in high doses becomes hypnotic
Hypnotic agent given at bedtime to induce sleep; usually larger dose than a sedative
Sedative and hypnotics alleviate symptoms, but do not cure; dependence potential; induce rest by increasing amount of sleep, but do not necessarily produce restful REM sleep
Barbiturates in low doses, increases actions of GABA, reduces neuronal excitability; in high doses, causes general depression of entire CNS similar to actions of general anesthetics; main site of action is reticular formation and cerebral cortex
Barbiturates only used if nonbarbiturate doesn’t work; sedative (low dose) and hypnotic (high dose); operatively and as an anesthetic; anticonvulsant agent; causes excessive CNS depression, anxiety, hypersensitivity; very narrow therapeutic index, very addictive
Nonbarbituates diverse group of drugs with differing chemical structures and pharmacologic characteristics; newer drugs do not disturb sleep cycle, low risk for tolerance, dependency, withdrawal reactions; includes sleep aids (Sonata, Ambien, Lunesta)
Benzodiazepines depresses CNS by increasing GABA neuronal inhibition; used for insomnia, preoperative sedation, anxiety, sleep induction, hypnotic therapy, withdrawal syndromes; can cause CNS changes, hypotension, respiratory depression, CNS excitement
Alcohol GABA receptor antagonist; CNS depressant; sedation (low dose) & hypnotic/unconsciousness (high dose); effects are euphoria, depressed inhibitions, increase in activity, decreased fine motor skills, libido; diuresis (blocks ADH), appetite stimulation
Fetal alcohol syndrome set of congenital psychological, behavioral, cognitive, physical abnormalities appearing in infants whose mothers consumed alcoholic beverages during pregnancy
Disulfiran (Antabuse) used as treatment for compliant patients who refrain from alcohol; can cause severe complications if taken within 30 minutes of alcohol intake; flushin, diaphoresis, hypoventilation, copious vomiting, confusion, chest pain, breathing difficulty
CNS stimulant substance that quickens the activity of the CNS by increasing rate of neuronal discharge or blocking inhibitory NT
Therapeutic CNS stimulation restoring mental alertness/consciousness, stimulating respiratory center or depression, treating hyperkinetic children by acting as a depressant in a child; agents include amphetamines, anorexiants, analeptics
Amphetamines and amphetamine-like drugs stimulate release of NE, which causes increased alertness, less fatigue, elevated mood; used for treatment of narcolepsy, endogenous obesity, ADHD, mental depression, withdrawal symptoms
Narcolepsy syndrome characterized by sudden sleep attacks; due to lack of orexin in brain
Endogenous obesity obesity resulting from dysfunction of endocrine or metabolic systems
Attention deficit hyperactivity disorder (ADHD) childhood condition involving inattention, impulsivity, hyperactivity
Tachyphylaxis repeated administration of some drugs results in a marked decrease in effectiveness (tolerance)
Anorexiants (sympathomimetics) suppress appetite by acting on hypothalamus; used for weight reduction when accompanied by medical complications; similar side effects to those of amphetamines; tolerance and abuse are possible
Analeptics and methylxanthines stimulate CNS by acting on cerebral cortex and medulla; used to produce wakefulness and increase alertness, in OTC cold medicines and analgesics with caffeine; side effects include teratogensis, caffeinism, seizures, tolerance, abuse
Created by: michellerogers
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