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NU 624
Exam 2 - Induction Agents
| Question | Answer |
|---|---|
| What are the 5 types of induction agents used in anesthesia? | Barbiturates, non-barbiturates, propofol, etomidate, ketamine |
| Identify 5 barbiturate induction agents. | Thiopental, methohexital, pentobarbital, secobarbital, phenobarbital |
| What is the trade name of thiopental? | Pentothal |
| What is the trade name of methohexital? | Brevital |
| What is the trade name of pentobarbital? | Nembutal |
| What is the trade name of secobarbital? | Seconal |
| What are all barbiturates derived from? | Barbituric acid |
| What two substances combine to form barbituric acid? | Urea and malonic acid |
| Which CNS neurotransmitter is linked to the action of barbiturates? | GABA |
| What element is involved with the use of barbiturates and how does it affect the nervous system? | Barbiturate use results in chloride ion movement into nerve cells |
| In what area can a substitution be made in the barbituric acid molecule to form different barbiturates? | Carbon atoms of the benzene ring |
| What change can be made to a barbiturate in order to increase its hypnotic activity? | Creating a branched chain substitution on the #5 carbon atom |
| Name two different categories of barbiturates. | Oxybarbiturates, thiobarbiturates |
| What is the molecular difference between oxy- and thio- barbiturates? | Oxybarbiturates retain an oxygen atom on the #2 carbon and thiobarbiturates retain a sulfur atom on the #2 carbon atom. |
| What changes can result from making substitutions in the molecular structure of a barbiturate? | Hypnotic potency, lipid solubility, anticonvulsant properties, duration of action |
| Methohexital is a commonly used type of ____________. | Oxybarbiturate |
| Why do anesthetists like using methohexital (Brevital)? | It is ultra-short acting |
| What are 4 different oxybarbiturates? | Methohexital, pentobarbital, secobarbital, phenobarbital |
| What are 2 thiobarbiturates? | Thiopental, thiamylal |
| What is the trade name of thiamylal? | Surital |
| What replacement occurs in an oxybarbiturate that makes it change into a thiobarbiturate? | The oxygen at on the #2 carbon is replaced with a sulfur atom |
| What are two ways that sodium thiopental can be abbreviated? | STP, NaTPL |
| What substitution enhances the anticonvulsant effect of barbituric acid? | A phenyl group at the #5 carbon |
| Give an example of a barbiturate with a phenyl group substitution. Where does this substitution occur and what does this enhance? | Phenobarbital--substitution at the #5 position, with a phenyl group, increases its anticonvulsant effect |
| The addition of a methyl radical to a nitrogen atom on the #5 carbon of barbituric acid results in what 3 changes? | More rapid onset, shorter duration, some convulsant effects |
| Give an example of a barbiturate with a methyl radical group substitution. | Methohexital |
| What are the side effects of methohexital? | Convulsant effects, manifested by involuntary but short-lived skeletal muscle movements. |
| Methohexital is a/an (long-acting/intermediate acting/short/acting/ultra short acting) barbiturate. | ultra short acting |
| How are barbiturates metabolized and excreted? | Metabolized by hepatic microsomal enzymes and renally excreted |
| The most significant metabolic pathway involves what position on a barbiturate and through what means of metabolism? | #5 carbon side chains via oxidation |
| What byproduct forms from the breakdown of a barbiturate? Is it active or inactive? | Thiopental carboxylic acid--inactive |
| After oxidation, the barbiturate becomes more (lipid/water) soluble. | Water |
| What metabolic pathway do thiobarbiturates undergo? | desulfuration |
| Desulfuration is a (Phase I/Phase II) reaction. | Phase I |
| How many steps are involved in the breakdown of thiopental? | 4 |
| What is the most commonly used thiobarbiturate? | Thiopental (Pentothal) |
| Describe the first step of thiopental metabolism? | Desulfuration converts thiopental to the oxybarbiturate, pentabarbital |
| Describe the second step of thiopental metabolism? | Oxidation of the side chain groups at the #5 carbon converts pentabarbital to water-soluble thiopental carboxylic acid |
| Describe the third step of thiopental metabolism? | Conjugation with glucuronic acid |
| Describe the fourth step of thiopental metabolism? | Excretion by the kidneys as glucuronide |
| What three products combine to give propofol its milky white appearance? | 10% soybean, 2.25% glycerol, 1.2% purified egg phophatide |
| What does the soybean/glycerol/egg phosphatide formulation support? | Bacterial growth |
| What have recent reports on propofol revealed? | Bacterial contamination of the emulsion has led to post-op infections |
| What two pharmaceutical companies have created additives to combat the bacterial growth in propofol? | AstraZeneca and Baxter Labs |
| What component did AstraZeneca add to propofol to inhibit bacterial growth? | EDTA (ethylenediamenetetraacetate) |
| What component did Baxter Labs add to propofol to inhibit bacterial growth? | 0.025% sodium meta-bisulfite |
| Propofol is highly bound to what component? | Protein |
| Where and through what pathway is propofol metabolized? | In the liver via conjugation |
| What is significant about the clearance rate of propofol? | Clearance exceeds hepatic blood flow, suggesting extra hepatic methods of metabolism |
| How is etomidate classified? | Nonbarbiturate anesthetic |
| The use of etomidate causes ________ effects to produce a __________ state. | CNS, hypnotic |
| How is etomidate chemically classified? | Ethyl ester of a carboxylated imidazole derivative |
| What are two important facts regarding the benefits of etomidate? | Wide range of safety, maintains cardiovascular stability |
| What are two side effects of etomidate use? | Pain with injection and myclonia |
| What is myoclonia? | Involuntary, rapid, nonrhythmic muscle contractions |
| What types of enzymes are used to break down etomidate? | Hepatic microsomal enzymes and plasma esterases |
| What is the primary means of etomidate metabolism and where does it occur? | Ester hydrolysis in the liver and plasma |
| What type of adrenocortical effects does etomidate have and what does it lead to? | Adrenocortical hypofunction leads to decreased levels of cortisol |
| What are beneficial uses of cortisol in the body? | BP management, reduced inflammation, strengthened immune system |
| How long do the adrenocorticol effects of etomidate last? | 4 days after initial administration |
| Adrenocorticol hypofunction as a result of etomidate is (reversible/irreversible). | Reversible |
| Ketamine is a derivative of __________. | Phenylcyclidine |
| Why has ketamine decreased in popularity? | Causes serious psychic disturbances, including hallucinations and delirium |
| What type of neurological state does ketamine result in? | Dissociative state |
| What do dissociative anesthetics distort and what do they produce? | Distort perceptions of sight and sound to produce feelings of detachment from the environment and self |
| What effects occur in a dissociative state of anesthesia? | Catatonia, split personality |
| BONUS: What is a unique characteristic of optical isomers? | Their sequence of atoms and bonds creates a 3D structure |
| Bonus: What are chiral molecules? | Non-superimposable mirror images of molecules |
| What are two characteristics of the molecular structure of ketamine? | It is optically active with a chiral center that consists of two optical isomers |
| The racemic mixture of ketamine contains (equal/different) amounts of isomers. | Equal |
| What are the two optical isomers in ketamine? | S(+) and R(-) |
| What effects on patients does the S(+) isomer in ketamine have? | Less spontaneous motor activity, more calm in recovery, fewer complaints of pain |
| What effects on patients does the R(-) isomer in ketamine have? | Hallucinations, combativeness, delirium on emergence |
| Which isomer in ketamine is responsible for hallucinations and combativeness? | R(-) |
| Where and through what system is ketamine metabolized? | Liver by hepatic microsomal enzymes |
| What two Phase I metabolic processes occur in the metabolization of ketamine? | Demethylation and hydroxylation |
| What does the demethylation and hydroxylation of ketamine produce? | Glucuronide derivative |
| How is the glucuronide derivative of ketamine metabolism excreted? | Renally excreted after it undergoes conjugation |
Created by:
philip.truong
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