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356 Cards in this Set
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what is lorazepam
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Benzodiazepine for relieving anxiety and for sleep
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what is buspirone
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Nonbenzodiazepine for anxiety
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What is trazodone
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An atypical Antipsychotic for promoting sleep
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What is chloral hydrate
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a non-barbiturate for promoting sleep
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what is ramelteon
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melatonin receptor agonist for promoting sleep
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what classes of drugs are used to relieve anxiety
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benzodiazepines for anxiety, Nonbenzodiazepines for anxiety, selective serotonin reuptake inhibitors, momoamine aoxidase inhibitors, tricyclic antidepressants, beta blockers
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what classes of drugs are used to promote sleep
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benzodiazepines for sleep, nonbenzodiazepines for sleep, atypical antipsychotic, nonbarbiturate hypnotic, barbiurates, melatonin receptor agonist
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what is GABA
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neurotransmitter that inhibits the cell from functioning
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what does the amygdala do
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recieves incoming sensory signals then communicates with the frontal lobes of the brain, can signal the brain that a threat is present and set off a fear response or anxiety
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What does the hippocampus do
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process the threatening or traumatic stimuli
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what are the stages of sleep
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NREM- Stage 1: light sleep, brain waves are irregular and rapid
Stage 2: brain waves are larger than in stage 1, with bursts of electrical activity Stage 3 and 4- deep sleep. REM sleep |
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What are SSRI's
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selective serotonin reuptake inhibitors and are a class of antidepressant drugs which are now considered first line therapy for anxiety disorders.
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How do SSRI's work?
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In severe stress, patients have low serotonin levels and they indirectly increase the amount of the neurotransmitter serotonin available in synapses
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How do tricyclic antidepressents worked
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same was as SSRI's but but they have a higher adverse effect profiles than SSRI's
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what are monoamine oxidase inhibitors
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oldest class of antidepressants , occasionally prescribed for panic disorder and social phobia. Have a serious risk for food-drug interaction
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What is monoamine oxidase
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the enzyme that degrades serotonin in the synapses and by inhibiting the enzyme more serotonin can remain
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what do beta blockers do for anxiety
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usually used to treat heart problems but they slow the heart rate for people who suffer from anxiety
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what are the pharmacotherapeutics of Lorazepam
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used in treating anxiety disorders, most frequently in GAD, and for short-term relief of anxiety that occurs with depression
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what are the pharmacokinetics of Lorazepam
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Administered: parenterally or orally
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what are the pharmacodynamics of Lorazepam
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Increases the effects of GABA
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what are the contraindications and precautions of lorazepam and all benzodiazepines
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psychoses, acute narrow angle glaucoma and use in children younger than 6 months
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what are the adverse effects of lorazepam
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mild drowsiness, ataxia, confusion, respiratory disturbances, bradycardia, and hypotension
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what are the core patients variables you should consider when administering lorazepam
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asses for renal and hepatic impairment, assess the patient for use of other CNS depressants, has a longer half life in Asians
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how do you maximize the therapeutic effects of lorazepam
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divide daily dosage and administer throughout the day because there is a fairly short duration of action
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how do you minimize the effects of lorazepam
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If GI distress occurs, administer with food, monitor for paradoxical reactions, dilute injectable lorazepam with an equal volume of compatible solution and assess for suicide effects and taper dose down slowly
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What drugs are in the same class as lorazepam
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anything that ends in -am and chlordiazepoxide and clorazepate
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what is buspirone
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an azaspirodecanedione that is not chemically or pharmacologically related to the benzodiazepines
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what is buspirone used for
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to treat symptoms of anxiety and intended for short-term therapy
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what is hydroxyzine
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a miscellaneous antianxiety drug, that exerts CNS depressant activity in subcortical areas. It rapidly produces a feeling of calm and relieve anxiety without impairing mental alertness and may be coadministered with narcotic to control pain while minimizing the nausea that may be an adverse effect from the narcotic
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what is meprobamate
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a non barbiturate used for short-term management of anxiety symptoms
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Where does meprobamate have selective effects
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multiple sites within the CNS including the thalamus and the limbic system
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What is the major problem with using benzodiazepines as a sleep aid
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category x pregnancy
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what is eszopiclone
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a nonbenzodiazepine hypnotic and is only drug approve for long term use for insomnia
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what are the benzodiazepines approved for sleep aids
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lorazepam, flurazepam, estazolam, quazepam, temazepam, triazolam
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what does eszopiclone do
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induces sleep quickly, prevent waking during the night
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What is zalephlon
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a sedative for short-term used and it is not chemically related to benzodiazepines but it does interact with the GABA-benzodiazepine complex
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what is zolpidem
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nonbenzodiazepine used for zolpidem used for shot-term treatment of insomnia. It induces sleep rapidly and should be taken immediately. interacts with GABA-BZ receptor
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How do melatonin receptor agonists work
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increases melatonin which is released in response to darkness and involved in the maintenance of the circadian rhythm
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What is ramelteon used for
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used in the treatment of insomnia when the patient has difficulty falling asleep
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what is trazodone
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an atypical antidepressant and causes significant sedation as an adverse effects. Most commonly used to promote sleep
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what is chloral hydrate
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a nonbrabiturate hypnotic used to induce sleep and cause preoperative sedation. It can be used as an adjunct to opiates and analgesics in pain control
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what are the advantages and disadvantages of sleeping drugs with a lower half-life
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drugs with lower half life experience less problems with daytime sedation but produce more early morning insomnia.
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What are the types of antidepressant drugs
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Selective serotonin reuptake inhibitors, tricyclic anti-depressants
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what is sertraline
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a selective serotonin reuptake inhibitor
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what is nortriptyline
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a tricyclic antidepressant
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what is a monoamine oxidase inhibitor
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phenelzine
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what is lithium
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a mood stabilizer
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what is major depressive disorder
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sympotoms cause impairment at work, and other social functions, don't get joy out of activities, change in appetite, weight, sleep or energy. Thoughts or attempts at suicide
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what is bipolar disorder
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when a person experiences symptoms of depression at some times and symptoms of mania at others
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what is mania
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when a person has an elevated or irritable mood lasting at least one week
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how long does it take for a therapeutic response in anti-depressants
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full affect is not seen until 4 week but more energy or other signs of improvement are seen within 1 to 2 weeks. Increased energy puts suicidal people at risk.
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what are the pharmacotherapeutics of sertraline
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depression, anxiety, PTSD
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What are the types of antidepressant drugs
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Selective serotonin reuptake inhibitors, tricyclic anti-depressants
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what is sertraline
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a selective serotonin reuptake inhibitor
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what is nortriptyline
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a tricyclic antidepressant
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what is a monoamine oxidase inhibitor
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phenelzine
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what is lithium
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a mood stabilizer
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what is major depressive disorder
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sympotoms cause impairment at work, and other social functions, don't get joy out of activities, change in appetite, weight, sleep or energy. Thoughts or attempts at suicide
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what is bipolar disorder
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when a person experiences symptoms of depression at some times and symptoms of mania at others
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what is mania
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when a person has an elevated or irritable mood lasting at least one week
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how long does it take for a therapeutic response in anti-depressants
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full affect is not seen until 4 week but more energy or other signs of improvement are seen within 1 to 2 weeks. Increased energy puts suicidal people at risk.
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what are the pharmacotherapeutics of sertraline
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depression, anxiety, PTSD
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what are the pharmacokinetics of sertraline
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Orally administered
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what are the pharmacodynamics of sertraline
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potent and selective inhibitor or neuronal serotonin reuptake and has a weak effect on norepinephrine and dopamine neuronal reuptake
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what are the contraindications and precautions of sertraline. Who should it be given with caution too?
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Patients with liver disease
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what are the adverse effects of sertraline
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gastrointestinal distress, headache, fatigue, insomnia and sexual dysfunction
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how do you maximize the effects of sertraline
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use with therapy, give time
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what are the symptoms of SSRI withdrawal syndrom
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FLUSH
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what are the pharmacotherapeutics of nortriptyline
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used to relieve the symptoms of depression and chronic pain
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what are the pharmacokinetics of nortriptyline
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Orally administered
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what are the pharmacodynamics of nortriptyline
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blocks reuptake of NE and serotonin into nerve terminals allowing increased concentration at postsynaptic effector sites
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what are the precautions of nortirptyline
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cardiovascular disorders
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what are the adverse effects of nortriptlyline
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disturbed concentration and confusion, headache, tremors, nausea, vomiting, bone marrow depression, urinary retention and sexual function disturbances hypotension
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how do you maximize the therapeutic effects of nortriptlyline
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monitor blood plasma drug levels
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what do MAOI's do
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inhibits enzymes that break down dopamine, epinephrine, norepinephrine and serotonin so more is available
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what is the pharamcotherapeutics of phenelzine
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used to treat depression
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what are the pharmacokinetics of phenelzine
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orally administered
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what are the precautions of phenelzine
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decreased liver function and congestive heart failure
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what are the adverse effects of phenelzine
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liver damage, anticholinergic effects, agrandulocytosis, leukopenia, thrombocytopenia and sexual dysfunction
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what health status should you get before administering phenelzine
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cardiovascular assessment and baseline labs
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how do you maximize the therapeutic effects of phenelzine
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platelet MAO enzyme activity is usually measure before therapy and during therapy
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how do you minimize the adverse effects of phenelzine
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numerous dietary and medication restrictions. monitor for symptoms of hypertensive crisis
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what are the drugs related to phenelzine
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isocarboxazid and traylcypromin and selegiline transdermal
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what are the pharmacotherapeutics of lithium
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a mood stabilizer and prevents extreme mood swings
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what are the pharmacokinetics of lithium
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administered: orally
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what are the pharmacodynamics of lithium
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competes with calcium, magnesium, potassium and sodium in body tissues and at binding sites.
Alters sodium transport in nerve and muscle cells |
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what are the precautions of lithium
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severe cardiovascular or renal disease, pregnancy or lactation, sodium imbalance
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what are the adverse effects of lithium
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coarse hand tremor, severe GI upset, blurred vision, drowsiness, and confusion. increased thrist, frequent urination
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lithium should be avoided with what
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alcohol, caffeine and thiazide diuretics and angiotensin-converting enzyme inhibitors
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what culture should be assessed with lithium
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Japanese
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how do you minimize adverse effects of lithium
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monitor serum levels regularly, assess for dehydration which increases risk of toxicity
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what is lithium toxicity
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slurred speech, unsteady gait, weakness, drowsiness, diarrhea, vomiting, confusion, and irregular heartbeat, possibly even seizure
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what are the other drugs used to treat bipolar disease
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carbamazepine, valproates, lamotrigine, antipsychotics
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what are the types of antipsychotics
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typical antipsychotics, atypical antipsychotics
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what are drugs for alzheimer-type dementia
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acetlycholinesterase enzyme inhibitors
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what is psychosis
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inability to perceive and interpret reality accurately, think clearly, respond correctly, and function in a socially appropriate manner
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what is the primary neurotransmitter related to thought processing
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dopamine
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what is schizophrenia
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a particular kind of psychosis that is characterized mainly by a clear sensorium but a marked disturbance in thinking
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what is dementia
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clinical syndrome of progressive, degenerate loss of memory and one or more of these abilities: Language skills, Higher-level skills, such as judgement, comprehension and problem solving. Ability to perform motor skills, ability to recognize or identify objects despite intact sensory function
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what is alzheimer disease
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form of progressive dementia
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what is vascular dementia
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results form damage to brain tissue, caused by cerebrovascular events such as transient ischemic attacks
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what is delirium
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sudden disruption in cognitive functioning, most often caused by a physical change in the body. Prevents brain from receiving some critical elements that it needs to function effectively
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what is haloperidol
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a typical antipsychotic used to treat psychotic disorders such as schizophrenia
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what are the pharmacokinetics of haloperidol
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protein bound, delayed onset of action
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what are the pharmacodynamics of haloperidol
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blocks dopamine, alpha and serotonin receptors
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what are the contraindications and precautions of haloperidol
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Parkinsons disease
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what are the adverse effects of haloperidol
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extrapyramidal symptoms, drowsiness, sedation, somnolence, lethargy and dysphoria
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what culture is different for haloperidol
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asians
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what is the difference between atpical and typical antipsychotics
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atypical target only specific dopamine receptors and treat both the negative and positive symptoms of schizophrenia
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what is olanzoapine
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an atypical antipsychotic that is used to treat psychotic symptoms in schizophrenia and for short-term treatment of acute bipolar disorder
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what are the pharmacokinetics of alanzapine
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highly protein bound
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what are the pharmacodynamics of olanzapine
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works by blocking several neuroreceptor sites, including serotonin, dopamine, muscarinic, histamine-1 and alpha-1
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what are the adverse effects of olanzapine
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type-2 diabetes, drowsiness, insomnia, agitation, nervousness, hostility, tardive dyskinesia, and nueroleptic malignant syndrome, hyperglycemia
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how do you minimize the adverse effects of olanzapine
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monitor glucose levels throughout therapy for all pts. give daily dose at bedtime
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what does acetylcholinesterase do
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enzyme that gets rid of acetylcholine
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what do AChEI's do
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inhibits AChE so it prolongs the activity of acetylcholoine on cortical cholinergic receptors and in the synapse which increase the concentrations of the memory regulating and cognition regulating neurotransmitter acetylcholine by reversibly inhibiting the enzyme cholinesterase
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what is rivastigmine
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an acetylcholinesterase enzyme inhibitor that treats dementia
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what are the pharmacokinetics of revastigmine
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administered orally
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what are the pharmacodynamics of rivastigmine
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carbamate derivative that enhances cholinergic function
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what are the adverse effecs of rivastigmine
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GI effects, dizziness, headache, chest pain, peripheral edema, vertigo, joint pain, agitation, and coughing
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what should be assed before giving drug
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cardiac coindition
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What are extra-pyramidal symptoms
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come from relative lack of dopamine stimulation and relative excess of cholinergic stimulation. 4 main symptoms. Parkinson like effects, akathisia (constant feeling of restlessness), acute dystonia, and tardive dyskinesia (involuntary lip smacking, chewing mouth movements ect.
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what are the positive symptoms of psychotic illness and what are they treated with
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delusions and hallucinations. treated by typical and atypical anti-psychotics
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what are the negative symptoms of psychotic illness and what are they treated by
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flat or blunted emotions, lack of pleasure or interest in things and limited speech. Treated by atypical anti-psychotics
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why is acute dystonia life threatening
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is spasms and prolonged muscle contractions and can occlude airway.
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what are the types of antiepileptic drugs
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antiepileptic drugs that decrease sodium influx, antiepileptic drugs that increase the effects of GABA (Benzodiazepines), antiepileptic drugs that decrease calcium influx, and antiepileptic drugs used in seizures related to pre-eclampsia and eclampsia
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What is phenytoin
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an antiepiletic drug that decreases sodium influx
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what is lorazepam
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a benzodiazepine that is used as an antiepileptic drug that increase the effects of GABA
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what is ethosuximide
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antiepileptic drug that decrease calcium influx
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what is magnesium sulfate
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antiepileptic drug used in seizures related to pre-eclampsia and eclampsia
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what are seizures
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loss of consciousness with generalized muscle twitching or mild alterations in consciousness with repetitive blinking
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what are the three main ways that antiepileptic drugs work
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decreasing the rate at which sodium flows into the cell, inhibition calcium flow rate into the cell through specific channels, increasing the effect of the neuroinhibitor gamma-aminobutyric acid (GABA)
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what do seizures result from
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high levels of glutamate or low levels of GABA which allow focus to take over the body
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what is focus when talking about seizures
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when a group of neurons exhibits coordinated, high-frequency discharge and when the focus spreads to other areas of the brain to join in the hyperactivity a seizure results
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what causes action potentials to be initiated in neurons
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influx of sodium into cell, influx of calcium through specialized voltage-dependent channels.
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what is the neurotransmitter that is fired in seizures and what does it cause
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glutamate hyperexcitability
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what acts as a counterbalance to glutamate
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GABA preventing hyperexcitation
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what are the types of seizures
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partial-involves focus activity in one hemisphere or limited area of brain
generalized-involves focus activity within both hemispheres of brain;loss of consciousness |
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what are the types of partial seizures
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simple-muscle twitching, consciousness not impaired
complex-muscle twitching, consciousness impaired |
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what causes a focus
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head trauma, tumor growth, hypoxia, and inherited birth defects.
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What is phenytoin and what are its phramacotherapeutics
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Antiepileptic drug that decreases sodium influx into the cell and it is used to control partial and generalized seizures
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what are the pharmacokinetics of phenytoin
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administered orally and parentally
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what is status epilepticus
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a generalized seizure where one seizure follows anohter without recovery of consciousness between events or lasts longer than 5 minutes. Cause by stopping antiepileptic drug therapy and alcohol withdraw
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what is a tonic-clonic seizure
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generalized seizure where person experiences stiffness and rigidity and falls to the ground, they don't move, then convulsions occur with muscles alternating between contracting and relaxing
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what is an absence seizure
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generalized seizure where consciousness is lost for less then a minute, that is it. maybe excess blinking occurs.
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what are the pharmacodynamics of phenytoin
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Primary site of action is the motor cortex and it reversibly binds to sodium channels while they are in the inactive state.
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what are the contraindications and precautions of phenytoin
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bradycardia and sinoatrial block and AV block.
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what are the adverse effects of phenytoin
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most are in CNS such as dizziness, ataxia, dysarthria (bad speech), slurred speech, mental confusion, tremor. Also gingival hyperplasia
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how do you maximize the therapeutic effects of phenytoin
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monitor blood levels of drug and titrate the dose upward gradually because effects can change fast. Avoid coadministration with enteral tube feedings
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how do you minimize the adverse effects of phenytoin
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change dose in small increments, Give IV slow because of small therapeutic index
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what is a life span alert of phenytoin
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can cause fetal hydantoin syndrome, infant death form neonatal hemorrhage
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what are drugs significantly different from phenytoin that do the same thing
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carbamazepine, valproic acid, lamotrigine, topiramate, oxcarbazepine, levetiracetam, felbamate
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what should you teach the patient about phenytoin
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take medication with food
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what is ethosuximide and what does it do
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an antiepileptic drug that decreases calcium influx used to treat absence seizures
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what are the pharmacokinetics of ethosuximide
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administered orally
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what are the pharmacodynamics of ethosuximide
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inhibiting the influx of calcium ions, which play big role in mainly hypothalamus action potentials which cause absence seizures
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what are the adverse effects of ethosuximide
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drowsiness, dizziness, lethargy nausea and blood dyscrasias (abnormal material in blood)
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what are drug interactions of ethosuximide
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interacts with other antiepileptics
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what should you assess before giving ethosuxmide
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allergies, history of renal or hepatic dysfunction
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how do you minimize the adverse effects of ethosuximide
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assess complete blood count, urinalysis, and liver function studies.
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what are the antiepileptic drugs that increase effects of GABA
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benodiazepines, diazepam, clonazepam, clorazepate, midazolam
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what is diazepam
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a benzodiazepine used as antiepileptic drug used to treat status epilepticus. Can cause CNS depression.
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what is the first choice to treat status epilepticus
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lorazapam
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what is clonazepam used to treat
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akinetic and myoclonic seizures (generalized seizures)
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what is clorazepate used for
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adjunctive treatment for partial seizures
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what are drugs different from barbituates but still work the same way
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gabapentin, pregabalin, phenobarbital, primidone, tiagabine, vigabatrin
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what are the classes of drugs that stimulate the central nervous system
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Centrally acting CNS stimulants, Anorectic agents, Respiratory stimulants
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what is the centrally acting stimulant
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dextroamphetamine
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what is the anorectic agent
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sibutramine
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what is the respiratory stimulant
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caffeine
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what are substance that are used to stimulate the CNS called
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analeptics
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what do anorectic agents do
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depress the appetite
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where does control of respiration occur
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pons and medulla
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how do CNS stimulants work
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provoke an increase release of neurotransmitters, a decreased reuptake of neurotransmitters or an inhibition of postsynaptic enzymes
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what do CNS stimulants help with
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narcolepsy, ADHD, obesity, and respiratory stimulation
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what is cataplexy
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brief sudden loss of motor control
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what are narcolepsy
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hypnagogic hallucinations are auditory, visual
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what is hypnagogic hallucinations
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hallucinations are auditory, visual, or kinesthetic sensations without stimuli, appearing transition period between wakefulness and sleep. associated with narcolepsy
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what is cataplexy
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brief sudden loss of motor control. related to narcolepsy
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what is hypercapnia
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buildup of carbon dioxide levels that may result from pulmonary compromise which depress the CNS
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what are centrally acting stimulants
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drugs that stimulate the CNS directly or indirectly
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What is dextroamphetamine and what is its used for
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A centrally acting stimulant that is used in the treatment of narcolepsy, ADHD and obesity
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how does dextroamphetamines treat obesity
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boost metabolism to burn fat easier
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what are the pharmacokinetics of dextroamphetamines
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administered orally
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what are the contraindications and precautions of dextroamphetamines
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cardiac disease, hyperthyroidism
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what are the adverse effects of dextroamphetamines
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Sudden death, stroke, MI, decrease appetite, rebound irritability, depression, headache, and jittery feeling increased blood glucose level
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what health statuses should you be aware of
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diebeties and pre-existing conditions
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how do you maximize the therapeutic effects of dextroamphetamine
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administer with food in the morning and no fewer than 6 hours
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what are the drugs closely related to dextroamphetamine
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methylphenidate
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what are the drugs significantly different from dextroamphetamines
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atomoxetine, modafinil, antihypertensive agents, antidepressants
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what is sibutramine and what is it used for
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it is an anorectic agents used to manage obesity by promoting weight loss
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what are the pharmacokinetics of sibutramine
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administered orally
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what are the pharmacodynamics of sibutramine
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inhibits central reuptake of dopamine, norepinephrine, and serotonin
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what are contraindications and precautions of sibutramine
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eating disorders, hypertension
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what are the adverse effects of sibutramine
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anorexia, constipation, insomnia, headache and dry mouth
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what are the drug interactions of sibutramine
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dextromethorhan, ergot alkaloids, lithium, MAOIs, meperideine, SSRIs, serotonin receptor agonists
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how do you maximize the therapeutic effects of sibutramine
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take daily on an empty stomach with diet and exercise
|
|
|
how do you minimize the adverse effects of sibutramine
|
refrain form using drugs that may induce serotonin syndrome or elevate the blood pressure
|
|
|
what are respiratory stimulants used for
|
manage postsurgical respiratory depression and apnea in preterm neonates
|
|
|
what is caffeine and what is its use
|
a respiratory stimulus used for managing neonatal apnea, asthma, drowsiness, and fatigue
|
|
|
what are the pharmacokinetics of caffeine
|
administered orally or IV. crosses placenta and blood-brain barrier
|
|
|
what are the pharmacodynamics of caffeine
|
direct stimulant at all levels of the CNS which also stimulates the cardiovascular system
|
|
|
what are the contraindications and precautions of caffeine
|
anxiety disorders, panic disorder, or insomnia
|
|
|
what are the adverse effects of caffeine
|
tremor, tachycardia, heightened attentiveness, diarrhea, excitement, irritability and insomnia
|
|
|
what are the drug interactions of caffeine
|
oral contraceptives, psychostimulants, sympathomimetic agents, lithium and MIAOs
|
|
|
how do you maximize the therapeutic effects of caffeine
|
do not crust extended-release form of medication
|
|
|
how do you maximize the therapeutic effects of sibutramine
|
take daily on an empty stomach with diet and exercise
|
|
|
how do you minimize the adverse effects of sibutramine
|
refrain form using drugs that may induce serotonin syndrome or elevate the blood pressure
|
|
|
what are respiratory stimulants used for
|
manage postsurgical respiratory depression and apnea in preterm neonates
|
|
|
what is caffeine and what is its use
|
a respiratory stimulus used for managing neonatal apnea, asthma, drowsiness, and fatigue
|
|
|
what are the pharmacokinetics of caffeine
|
administered orally or IV. crosses placenta and blood-brain barrier
|
|
|
what are the pharmacodynamics of caffeine
|
direct stimulant at all levels of the CNS which also stimulates the cardiovascular system
|
|
|
what are the contraindications and precautions of caffeine
|
anxiety disorders, panic disorder, or insomnia
|
|
|
what are the adverse effects of caffeine
|
tremor, tachycardia, heightened attentiveness, diarrhea, excitement, irritability and insomnia
|
|
|
what are the drug interactions of caffeine
|
oral contraceptives, psychostimulants, sympathomimetic agents, lithium and MIAOs
|
|
|
how do you maximize the therapeutic effects of caffeine
|
do not crust extended-release form of medication
|
|
|
what are the symptoms of caffeine withdraw
|
lethargy, anxiety, dizziness or headache
|
|
|
what are the classifications of drugs used to treat severe pain
|
strong narcotic agonists, mild narcotic agonists, and narcotic agonists-antagonists
|
|
|
what is the strong narcotic agonists
|
morphine
|
|
|
what is the mild narcotic agonist
|
codeine
|
|
|
what is the narcotic agonists-antagonists
|
pentazocine
|
|
|
what is pain
|
multidimensional subjective experience
|
|
|
what is transduction
|
term used to describe the phenomena associated with the initiation of a pain signal
|
|
|
where are pain receptors found
|
peripheral end plates of afferent neurons
|
|
|
what do opioids, serotonin, norepinephrine and GABA do in pain
|
bind with receptors on primary afferent and dorsal horn neurons to prevent further transmission of painful stimuli
|
|
|
what is nociceptic pain
|
caused by the activation of the delta and C nociceptors in response to painful stimuli
|
|
|
what is neuropathic pain
|
term used to represent pain in which the underlying pathology is abnormal processing of stimuli in the peripheral or central nervous systems. Damage to peripheral receptors, afferent fibers, or CNS or an impairment of he nervous system.
|
|
|
what is acute pain
|
meaning the immediate phase of response to an insult or injury, results from tissue damage.
|
|
|
what is chronic pain
|
may persist well beyond actual tissue injury and healing
|
|
|
what are the classifications that are normally used for pain menagement
|
opioid analgesics (narcotics) and non-steroidal anti inflammatory drugs (NSAIDs)
|
|
|
what is the main difference between opioids and NSAIDs
|
opioids work on the CNS
NSAIDs work on the PNS |
|
|
what are adjunct analgesics
|
when drugs are used secondarily for pain relief
|
|
|
what are the stypes of narcotic analgesics
|
opiate agonists, mixed agonist-antagonists, and antagonists based on their activity at opioid receptors
|
|
|
what is morphine and what is it used for
|
a strong narcotic agonist that is used for moderate to severe acute or chronic pain
|
|
|
what are the pharmacokinetics of morphine
|
administered orally, parentally, rectal or taopically.
|
|
|
what is the pharmacodynamics of morphine
|
agonist at the mu, kappa and possibly delta opiate receptors and reduces release of neurotransmitters in presynaptic space and produces hyperpolarization of postsynaptic dorsal horn neurons which prevent transmission of nociceptor pain
|
|
|
what are the contraindication and precautions of morphine
|
respiratory conditions because it causes respiratory depression, increased ICP, CNS depression
|
|
|
what are the adverse effects of morphine
|
CNS effects, respiratory depression, apnea, respiratory arrest, circulatory depression, cardiac arrest, shock, and coma
|
|
|
what is the antidote of morphine
|
naloxone
|
|
|
what is codeine and what is it used for
|
a mild narcotic agonist used to treat mild-to-moderate pain
|
|
|
what are the pharmacokinetics of codeine
|
IV or orally
|
|
|
what are the pharacodynamics of codeine
|
acts at specific opioid receptors in the CNS to produce analgesia, euphoria and sedation
|
|
|
what are the contraindications of codeine
|
don't give with other narcotics
|
|
|
what are the adverse effects of codeine
|
drowsiness, sedation, dry mouth, nausea and vomiting and consitpation
|
|
|
what are the drug interactions of codeine
|
antihistamines, phenothaizines, barbituates, tricyclic antidepressants, cimethidine, and alcohol
|
|
|
how do you minimize the adverse effects of codeine
|
avoid use if pateints health status requires a stong cough
|
|
|
what is pentazocine
|
a narcotic agonist-antagonist and is an agonist to control pain
|
|
|
what are the pharmacokinetics of pentazocine
|
absorbed orally and from SC and IM sites
|
|
|
what are the pharmacodynamics of pentazocine
|
mixed agonist-antagonist. It stimulates kappa receptors much as morphine does but also exhibits weak antagonist effects at the mu receptors
|
|
|
what are the contraindications of pentazocine
|
respiratory depression other CNS depressants
|
|
|
what are the adverse affects of pentazocine
|
nausea, vomiting, dizziness, light-headedness and euphoria, respiratory depression
|
|
|
what should you teach patients who are taking pentazocine
|
steer clear of alcohol and other CNS depressants
|
|
|
what should you asses on patients taking pentazocine
|
contraindications and hepatic disease and abuse potential
|
|
|
how do you maximize the therapeutic effects of pentazocine
|
provide environmental controls to reduce sensory stimuli and to aid relaxation
|
|
|
what is the type of drug that treats mild to moderate pain, fever, inflammation, and migraine headache?
|
Nonsteroidal anti-inflammatory drugs (NSAIDs)
|
|
|
What are the types of NSAIDs
|
Salicylates, NSAIDs (prostaglandin synthetase inhibitors) Para-aminophenol derivatives and serotonin-selective agonists.
|
|
|
what are the two responses in acute inflammation
|
vascular and cellular responses
|
|
|
what is the salicylates drug
|
aspirin
|
|
|
what is the NSAIDs drug
|
ibuprofen
|
|
|
what is the para-aminophenol derivatives drug
|
acetaminophen
|
|
|
what are the serotonin-selective agonists drug
|
sumatriptan
|
|
|
what are the stages of vascular response in inflammation
|
margination of WBCs to the periphery of the blood vessels, emigration of WBCs, chemotaxis, phagocytosis
|
|
|
what does the enzyme cyclooxgenase do
|
converts arachidonic acid to prostaglandins
|
|
|
what are the two forms of COX
|
COX-1 and COX-2
|
|
|
what does COX-1 do
|
synthesizes prostaglandins that are involved in the regulation of normal cell activity
|
|
|
what does COX-2 do
|
sppears to produce prostaglandins mainly at sites of inflammation
|
|
|
what is platelet aggregation
|
clumping of platelets
|
|
|
what are the two types of migraine headaches
|
migraine with aura, migraine without aura
|
|
|
what types of drugs are used to treat inflammation and fever
|
salicylates, NSAIDs, and para-aminophenol drugs
|
|
|
what are salicylates used for
|
managing conditions ranging from a simple headache to acute myocardial infarction
|
|
|
what are NSAIDs used for
|
anti-inflammatory drugs and analgesics
|
|
|
what is acetylsalicylic acid and what does it do
|
it is aspirin which is a salicylate which is used to treat mild-to moderate pain and prevent platelet aggregation
|
|
|
what are the pharacokinetics of aspirin
|
highly protein bound
|
|
|
what are the pharmacodynamics of aspirin
|
fever: inhibited PGE2 synthesis in hypothalamus
Inflammation: peripheral inhibition of prostaglandin Antiplatelet: irreversible inhibition of thromboxane A2 |
|
|
what are the contraindications of aspirin
|
peptic ulcer disease, bleed disorders and children with illness, renal or hepatic failure
|
|
|
what are the adverse effects of aspirin
|
renal failure, abnormal bleeding, GI upset, drowsiness, confusion
|
|
|
how do you maximize the therapeutic effects of aspirin
|
give with milk or food to decrease GI upset. Use uncoated aspirin when using for cardiovascular problem
|
|
|
who shouldn't recieve aspirin
|
children with varicella
|
|
|
what are the differences between salicylates and NSAIDs.
|
NSAIDs work by reversibly inhibiting COX and decreasing prostaglandins and thromboxane and salicyates irreversibly inhibit them
|
|
|
what is the black box warning on NSAIDs
|
increase risk of MI and stroke
|
|
|
what is ibuprofen and what does it do
|
it is an NSAID used to treat arthritis, mild to moderate pain, primary dysmenorrhea, migraine headache and fever
|
|
|
what are the pharmacokinetics of ibuprofen
|
highly protein bound
|
|
|
what are the pharmacodynamics of ibuprofen
|
inhibited synthesis or release of prostaglandins
|
|
|
what are the contraindications of ibuprofen
|
GI disease
|
|
|
what are the adverse effects of ibuprofen
|
GI upset and bleeding, hepatotoxicity, acute renal failure
|
|
|
how do you maximize the therapeutic effects of ibuprofen
|
give with milk or food to decrease gastric distress
|
|
|
what are para-aminophenol derivatives used for
|
analgesia and antipyretic
|
|
|
what is acetaminophen
|
a para-aminophenol used to treat fever or mild pain
|
|
|
what are the pharmacokinetics of acetaminophen
|
administered orally
|
|
|
what are the pharmacodynamics of acetaminophen
|
primarily centrally acting; inhibits prostaglandin synthesis in the CNS
|
|
|
what are the contraindications of acetaminophen
|
hepatic disease, viral hepatitis or alcoholism
|
|
|
what are the adverse effects of acetaminophen
|
usually tolerated well. can have rash, urticaria and nausea and renal or hepatic failure
|
|
|
Acetaminophen is the drug of choice for who
|
infants and children with flu and analgesic of choice during pregnancy
|
|
|
how do you minimize the adverse effecs of acetaminophen
|
coordinate periodic CBC, platelet count, and liver and renal function tests for patients on lon term therapy
|
|
|
what are triptans
|
serotonin-selective drugs
|
|
|
what are serotonin-selective drugs used for
|
to relieve pain and inflammation related to migraine headache. first line drugs for migraines
|
|
|
what is sumatriptan
|
serotonin-selective drug used to treat acute migraine headaches and cluster headaches
|
|
|
what are the pharmacokinetics of sumatriptan
|
administered orally, intranasally or subcutaneously
|
|
|
what are the pharmacodynamics of sumatriptan
|
vasoconstricts cranial blood vessels by being selective for 5-HT receptors located on cranial blood vessels and sensory nerves of the trigeminovascular system
|
|
|
what are the contraindications of sumatriptan
|
coronary artery disease and ischemic cardiac diseases
|
|
|
what are the adverse effects of sumatriptan
|
coronary artery vasospasm, cardiac dysrhythmias, angina, myocardial ischemia and dizziness
|
|
|
how do you minimize the adverse effects of sumatriptan
|
assess for history of cardiovascular or cerebrovascular disease
|
|
|
what are the drug classifications of drugs treating rheumatoid arthritis and gout
|
Disease-modifying antirheumatic drugs (DMARDs), Tumor necrosis factor inhibitor and antigout drugs
|
|
|
what are the DMARD drugs
|
methotrexate
|
|
|
what are the tumor necrosis factor inhibitors
|
etanercept
|
|
|
what are the antigout drugs
|
colchicine (acute gout)
allopurinol (chronic gout) |
|
|
what is rheumatoid arthritis
|
an autoimmune disease that is a systemic inflammatory disease. can cause inflammation of glands, the linings of the heart, the lungs and the vascular system
|
|
|
what is gout
|
a disease of purine metabolism and occurs when hyperurcemia forms monosodium urate crystals, which precipitate into the synovial fluid and initiate and inflammatory response,
|
|
|
how are DMARDs used
|
in conjunction with salicylates and NSAIDs or as monotherapy
|
|
|
where do disease modifying antirhemumatic drugs get there name
|
they are capable of arresting the progression of RA and can induce remission in some patients
|
|
|
what is pannus
|
destrusctive grandular tissue that extends through synovial space, damaging articular cartilage in RA
|
|
|
what is ankylosis
|
extreme stiffness or joint fusion
|
|
|
what is methotrexate
|
a DMARD that is a folate antimetabolite used in treating various malignancies and rheumatoid arthritis
|
|
|
what are the pharmacokinetics of methotrexate
|
administered orally or parenterally
|
|
|
what are the pharmacodynamics of methotrexate
|
exerts immunosuppressive effects by inhibiting the replication and function of T lymphocytes that stimulate the production of cytokines
|
|
|
what are the contraindications of methotrexate
|
immunosuppression, blood dycrasia, pregnancy
|
|
|
what are the adverse effects of methotrexate
|
rash, headache, nausea and vomiting, diarrhea, stomatitis, alopecia, suppression of bone marrow and blood dyscrasias
|
|
|
how do you maximize the therapeutic effects of methotrexate
|
stay hydrated to prevent nephrotoxicity
|
|
|
what health status should you assess for in methotrexate
|
comorbid conditions
|
|
|
who should you give methotrexate cautiously to
|
elderly and young
|
|
|
how do you minimize the adverse effects of methotrexate
|
take vitamin B, stay out of sun if photosensitivity occurs
|
|
|
why are DMARDs usually given with glucocorticoid steroids, NSAIDs or other DMARDs
|
because you can have smaller doses of both to decrease chance of adverse effect
|
|
|
what is the 'gold standard' for RA treatment
|
a tumor necrosis factor inhibitor and methotrexate
|
|
|
what is etanercept
|
a tumor necrosis factor inhibitor used in managing RA
|
|
|
what are the pharmacokinetics of etanercept
|
weekly subcutaneous injection
|
|
|
what are the pharmacodynamics of etanercept
|
binds specifically to circulating TNF, prevents it from binding to TNF receptors on the cell membranes, and prevents the TNF mediated cellular response
|
|
|
what is a Tumor necrosis factor
|
used to fight disease and drug inhibits it so you get sicker easier
|
|
|
what are the contraindications of etanercept
|
immunosuppression, blood dyscrasias, infections
|
|
|
what are the adverse effects of etanercept
|
nausea, headache, upper respiratory infections, injection-site reactions, severe infections, blood dyscrasias
|
|
|
how do you maximize the therapeutic effects of etanercept
|
administer weekly as prescribed, rotate injection sites
|
|
|
how do you minimize the adverse effects of etanercept
|
use aseptic technique for injections. Do not administer live-virus vaccines
|
|
|
what is the most important patient education for etanercept
|
high risk for severe infection
|
|
|
what is the first line drugs for acute gout
|
NSAIDS
|
|
|
what are the second line drugs for gout
|
colchicine and glucocorticosteroids
|
|
|
what does the antigout drug therapy focus on
|
decreasing the inflammatory response caused by hyperuricemia or reducing hyperuricemia
|
|
|
what is colchicine
|
an antigout drug used to treat acute gout and as presurgical prophylaxis to prevent gout. decreases inflammatory reaction of acute gout
|
|
|
what are the pharmacokinetics of colchincine
|
administered orally or IV
|
|
|
what are the pharmacodynamics of colchincine
|
inhibits the activity of leukocytes by decreasing their migration into the affected area
|
|
|
what are the contraindications and precautions of colchicine
|
cardiac disease, hepatic disease and renal disease
|
|
|
what are the adverse effects of colchicine
|
mostly related to GI system. Nausea, vomiting, diarrhea, abdominal pain, and paralytic ileus, blood dyscrasias, bone marrow supression
|
|
|
what are the drug interactions of colchincine
|
radiation therapy, drugs that depress bone marrow function and cyancobalamin
|
|
|
how do you maximize the therapeutic effects of colchicine
|
administer with full glass of water at evenly spaced intervals throughout the day. Adherence to diet and alcohol restrictions decreases hyperuricemia
|
|
|
who do you minimize adverse effects of colchincine
|
start medications at the first sign of an attack then take until symptoms start to resolve
|
|
|
what is the most important patient education for colchincine
|
dietary and alcohol restrictions to lower chance of hyperuricemia
|
|
|
what do uricosuric drugs do
|
treat chronic gout and balance urate concentrations
|
|
|
why aren't uricosuric drugs used for treating acute gout
|
they have no anti-inflammatory or analgesic activity
|
|
|
what is allopurinol
|
a drug used to treat chronic gout and is used to treat chronic gout, recurrent calcium renal stones, and hyperuricemia
|
|
|
what are the pharmacokinetics of allopurinol
|
administered orally or with IV
|
|
|
what are the pharmacodynamics of allopurinol
|
decreases the production of uric acid by inhibiting the action of xanthine oxidase
|
|
|
what does xanthine oxidase do
|
an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid
|
|
|
what are the contraindications of allopurinol
|
coadministration with drugs that induce myelosuprression
|
|
|
what are the adverse effects of allopourinol
|
pruritus, maculopapular rash, nausea and vomiting elevated LFTs and acute gout symptoms. Blood dyscrasias and severe dermatologic disorders
|
|
|
when should you administer allopurinol
|
after meals
|
|
|
how do you maximize the effects of allopurinol
|
administer in conjunction with colchicine, adhere do diet that limits uric acid production
|
|
|
how do you minimize adverse effects of allopurinol
|
ingest 2.5-3 liters of fluid daily
|
|
|
how early should DMARDs be used in diagnosis
|
3 months because joint destruction begins early in RA even without symptoms
|
