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72 Cards in this Set

  • Front
  • Back
Antipsychotics are used to treat?
Psychotic disorders (Schizophrenia), disorders characterized by disorganized thinking which impairs the ability to recognize reality.
Anxiolytics are used for?
Neurotic disorders like anxiety, dissatisfaction, agitation, and hostility.
Antidepressants are used for?
Affective disorders like mania and depression, mood disturbances, hyperactivity, unrealistic optimism, and aggressiveness.
List 2 examples of a SSRI.
Fluoxetine, Sertraline, Paroxetine, Fluvoxamine, Citalopram, Escitalopram, Bupropion, Venlafaxine, Trazadone, Nefazodone.
List 2 examples of a TCA.
Amitriptyline, Amoxapine, Clomipramine, Desipramine, Doxepin, Imipramine, Nortriptyline, Protriptyline, Trimipramine, Mirtazapine.
List an example of a MOAI.
Phenelzine, Tranylcypromine, Isocarboxazid.
These are absorbed well orally, all are metabloized by hepatic P450, and their long half-life allows for once-a-day dosing.
SSRI's (considered the antidepressant of choice).
In regards to adverse effects, the most common is nausea and diarrhea *especially in this group and more frequently than with other antidepressants.
SSRI's
In regards to adverse effects, all of these may cause anxiety and restlessness, including insomnia so, it's important to give doses in the morning.
SSRI's but especially FLUOXETINE and SERTRALINE (because of stimulation of 5HT2C receptors).
What is a major current concern with SSRI's?
Increased suicide risk in children. (Paroxetine may increase suicide risk in adults).
Although SSRI's lack the ANS and CV side effects of TCA's, what should you be concerned about?
Increased bleeding (due to platelet inhibition).
This is a major concern when mixing SSRI's with other serotonin elevating drugs.
Serotonin Syndrome: mental status changes, tremor, convulsions, seizure, hyperthermia, and autonomic disturbances.
Venlafaxine and duloxetine.
SNRI's (block serotonin and norepi.)
Adverse effects: similiar to SSRI's
Hepatic Metabolism.
This drug blocks 5HT reuptake, is a partial agonist at 5HT receptors, blocks alpha adrenergic and H1 receptors, and down regulates beta adrenergic receptors.
Trazodone
This drug blocks dopamine reuptake.
Bupropion.
This atypical antidepressant has no effect on NE, 5HT, or dopamine reuptake. It blocks H1 receptors, presynaptic alpha 2 adrenergic receptors, increases NE and 5HT release and blocks 5HT2 and 5HT3 receptors.
Mirtazapine.
The use of this drug, which is also used for smoking cessation, is limited due to an increased risk of seizures.
Bupropion.
This class of antidepressants have little or no effect on sexual function.
Atypicals.
What are the first generation TCA's?
Imipramine, Desipramine, Amitriptyline.
What are the second generation TCA's?
Doxepin, Maprotiline, Amoxapine, Bupropion, Trazadone.
These agents enhance neurotransmitter action and effects by blocking the reuptake of NE and Serotonin in the CNS.
TCA's
These agents can cause a considerable amount of sedation.
TCA's.
These agents have a prominent anticholinergic activity in the autonomic nervous system.
TCA's (amitriptyline has the strongest anticholinergic action).
Due to the blocking of NE reuptake in the CV system, these agents may produce tachycardia.
TCA's.
At therapeutic doses, these agents can produce significant cardiovascular effects such as decreased BP, diminished CV reflexes, orthostatic hypotension, and cardiac arrhythmias.
TCA's
These drugs are not completely absorbed orally, are extensively bound to plasma proteins, have a large volume of distribution, are oxidized by hepatic P450 enzymes followed by glucuronidation, and have a long half-life of 10-50 hours.
TCA's.
List the relatively common adverse effects that can be seen with TCA's.
Dry mouth, constipation, blurred vision (antimuscarinic); sedation, weakness, fatigue, tremor, seizure and may turn depressed patient to manic phase (CNS); orthostatic hypotension, tachycardia, MI, CHF, and arrhythmias (CV).
TCA use can result in acute poisoning causing seizures, coma and death. How should you treat suspected acute TCA poisoning?
Treat arrhythmias as they arrise, must support vital functions. Physostigmine can reverse antimuscarinic, cardiotoxic, and neurotoxic effects. IV NaHCO3 can treat arrhythmia.
Other than depression, what are some other uses for TCA's?
Neuropathic pain, nocturnal enuresis, and fibromyalgia.
These agents block the metabolism of naturally occuring monoamines.
MOAI's.
These agents also have antimuscarinic, adrenergic blocking, and CNS effects and interfere with the conduction in the heart.
MOAI's.
Tyramine (commonly found in food), when combined with MOAI's can precipitate?
Hypertensive crisis.
As an anesthesia provider, it is important to note that phenelzine interferes with serum cholinesterase, how?
Serum cholinesterase activity may decrease in patients being treat with phenelzine, so succinycholine doses may need to be adjusted accordingly.
In patients being treated with MOAI's, the anesthesia provider may want to avoid this when administering a regional anesthetic.
Epinephrine.
Patients on Lithium Carbonate need what electrolyte balance checked along with the therapeutic index.
Sodium levels because decreased sodium can cause increased lithium levels and increased side effects.
Ace inhibitors, diuretics, and NSAIDs (increase or decrease) the renal clearance of lithium.
Decrease (enhancing toxicity).
This drug is just as effective as lithium, is generally better tolerated, and is replacing lithium?
Valproate.
This drug is less effective than lithium?
Carbamazepine.
What opioid should be avoided in patients taking MOAI's?
Meperidine.
What are analeptics?
Agents that remove inhibition from CNS neurons, increase synaptic excitation or alter axonal membrane properties resulting in CNS stimulation.
List examples of Xanthines.
Caffeine, Theophylline, Theobromine.
List examples of Amphetamines.
D-amphetamine, mixed amphetamine salts (Adderall), methamphetamine, dexmethylphenidate, pemoline, phentermine, sibutramine.
How do amphetamines work?
They release NE, 5HT, and dopamine from nerve terminals resulting in mood elevation, euphoria, alertness, and reduced fatigue.
List the clinical uses for amphetamines.
Narcolepsy, attention deficit-hyperactivity disorder, and appetite suppression.
This drug is a local anesthetic with sympathomimetic effects.
Cocaine.
This drug is a non-amphetamine stimulant used to treat narcolepsy. This drug has recently been approved for the treatment of patients with excessive sleepiness due to sleep apnea and shift work sleep disorders.
Modafinil.
This drug is used to treat ADHD but is not a stimulant.
Atomoxetine.
What effects does alcohol have on the CNS?
Alcohol increases GABA resulting in mediated inhibition (may cause sedation or ataxia). Alcohol also inhibits NMDA receptors causing blackouts and acts on neural membranes altering the fluidity of the membrane.
Can acute intoxication be lethal? Why or why not?
Yes, due to the depression of the medullary respiratory and cardiovascular centers.
Why is it common to see behavioral stimulation after one or two drinks of alcohol?
This is a result of depression of the inhibitory control mechanism of the reticular activating system.
List the effects that chronic alcohol use has on the endocrine system.
Diuretic effect, decreased testosterone, increased estrogen and corticotropin secretion, amennorrhea, gynecomastia, and testicualr atrophy. In relation to the blood, alcohol can cause nutritional anemia and increase susceptibility to infection.
These two drugs can be used to block withdraw symptoms in patients WITHOUT liver disease.
Chlordiazepoxide or diazepam.
This drug should be used to treat seizures experienced during alcohol withdraw.
Phenytoin (seizure threshold is decreased during alcohol withdraw).
This drug is used to promote abstinence from alcohol and will cause nausea, vomiting, pulsating headache, palpitations, vasodilation, hypotension, and hyperventilation that can last for several hours if alcohol is ingested.
Disulfuram.

Contraindicated in patients with severe heart disease or a history of psychosis.
This drug is used to promote abstinence from alcohol and works by blocking the rewarding effects of alcohol (hint: opioid antagonist).
Naltrexone.
This drug is used to promote abstinence from alcohol use by decreasing the craving for alcohol suggesting that it balances GABA and glutamate activity in the brain.
Acamprosate.
What are the therapeutic uses of ethanol?
Over the counter cold preparations and methanol intoxication.
How does ethanol work to treat methanol intoxication?
Ethanol can compete with methanol for alcohol dehydrogenase and decrease the rate of methanol oxidation (slowing the production of methanol's toxic metabolites).
This drug is a competitive inhibitor of alcohol dehydrogenase and can decrease the rate of metabolism of methanol or ethylene glycol to toxic metabolites but is very expensive.
Fomepizole.
What are the signs and symptoms of methanol poisoning?
CNS depression, slow metabolic acidosis produced by formic acid (major cause of death), and damaged retinal cells from formic acid leading to blindness.
This is a solvent for drugs and is also known as antifreeze. Large doses produce excitation followed by an alcohol-like depressant syndrome.
Ethylene glycol.
In alcohol-tolerant patients, should smaller or larger amounts of general anesthetics be considered?
Typically, larger amounts of general anesthetics are required but, there is an increase in CNS depression.
What can be expected when alcohol and opiates are used together?
Potentiation of the CNS depressnat effect of alcohol can be expected.
What interaction does alcohol and warfarin have?
The chronic use of alcohol decreases the half-life of warfarin. However, the anticoagulant effect may be enhanced when liver disease is present.
What can occur when amitriptyline and alcohol are used together?
Deaths have been reported with amitriptyline and alcohol use.
This increases the metabolism of alcohol and decreases its effects.
Fructose.
When chloramphenicol or ethionamide are combined with alcohol this can happen?
Disulfuram-like reaction and psychological abnormalities.
What happens when alcohol is combined or used with CNS stimulants like amphetamine or caffeine?
There is an antagonistic effect of the CNS depression but no improvement in motor function.
Diuretics and alcohol?
May increase blood alcohol levels and potentiate alcohol effects.
Nitroglycerin and alcohol?
Alcohol potentiates hypotension and may result in cardiovascular collapse.
Alcohols effects on anesthesia?
Acute alcohol use will contribute significantly to the CNS depressant drugs used in anesthesia.
Chronic alcohol use will induce the metabolism of some drugs, requiring more to produce the desired effects.
What should anesthetists pay particular attention to during anesthesia in patients on disulfuram?
Decreased metabolism of benzodiazepines and unexpected hypotention during general anesthesia because of inadequate NE stores. (Therefore, indirect acting sympathomimetics may not work well to increase BP).