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Nervous System I
| question | answer |
|---|---|
| define general anesthesia | a global but reversible depression of the CNS and its functions, resulting in loss of response to and perception of external stimuli |
| what are the desirable effects of general anesthesia | amnesia, suppression of response to noxious stimuli, unconsciousness, myelorelaxation, immobility |
| what are the undesirable effects of general anesthesia | cardiovascular/respiratory instability, excitation convulsions, emesis, hypothermia |
| what things do you monitor during anesthesia | respiration, BP, blood flow to brain, intracranial pressure, post operative N&V |
| name 5 inhalation anesthetics | halothane (fluothane), isoflurane (forane), enflurane (ethrane), desflurane (suprane), sevoflurane (ultane) |
| name 4 parenteral anesthetics | propofol (diprivan), etomidate (amidate), ketamine (ketalar), thiopental (pentothal) |
| name 5 local anesthetics | cocaine, lidocaine (xylocaine), procaine (novacaine), tetracaine (pontocaine), bupivacaine (marcaine) |
| what are some of the effects of halothane | decrease BP by reducing cardiac output, assoc. with hepatotoxicity, can cause arrythmias, blocks sympathetic reflexes |
| Why is propofol used over thiopental | Its antiemetic effects |
| What do you call the condition when a patient is coming from under anesthesia where the body overreacts | emergence excitability |
| what can happen if a patient experiences emergence excitability | can have convulsions |
| what value do you monitor for patients using inhalation anesthetics | MAC50, minimum alveolar conc. |
| what is the MAC "dash bar" | conc. that can block autonomic reflex activity |
| what are the theories on anesthetic mechanism | unitary theory, protein theory, oxygen theory |
| what's the unitary theory | means one mechanism - anesthetic gets into lipid membrane and alters it so it doesn't function normally |
| what's the protein theory | says anesthetic effect not about lipid solubility but about ability to bind to certain proteins, specifically some kind of membrane receptor |
| what's the oxygen theory | says anesthetic changes availability of oxygen to specific brain tissues and results in anesthesia |
| when we block muscle movement where is the drug acting | spinal cord |
| what is thought to be the effect of anesthetic on GABA receptor | it binds to a site other than GABA binding site (possibly B3) and enhances the effect of GABA ==> influx of Cl- |
| how many of each subunit exists for the GABA A receptor | 6 alpha, 4 beta, 3 gamma |
| what is the most common mammalian structure | 2 alpha 1, 2 beta 2, one gamma 1 |
| which part of the nervous system has the most glycine receptors | spinal cord |
| are glycine receptors in the spinal cord strychnine sensitive or insensitive | strychnine sensitive |
| how do anesthetics affect glycine receptor | they enhance glycine receptor so glycine has more effect on it. |
| are glycine receptors inhibitory or excitatory | inhibitory |
| what's the effect of anesthetic on ACh nicotinic receptor in the brain | inhibition |
| True or false. NMDA is a major receptor for anesthetics | False |
| which anesthetic will act on NMDA receptor and what will it do | ketamine will block NMDA receptor |
| So basically what type of ion channels do anesthetics seem to act on and what are the results | Anesthetics seem to block calcium channels and open K+ channels |
| thiopental falls into what class of drugs | barbiturates |
| what type of action do we want from a parenteral anesthetic | fast onset and short duration |
| what causes the rapid onset of parenteral anesthetics | pharmacokinetics - redistribution |
| what do local anesthetics act on | they act on specific nerves. |
| on what type of nerves are local anesthetics more effective | pain nerves |
| what type of fibers are for pain | type C and A delta |
| what is the mechanism of action of local anesthetics | blocking Na+ channels |
| what do most local anesthetics come with to prolong duration | some other drug such as epi |
| how do local anesthetic additives prolong duration | by causing vasoconstriction which slows down removal of drug from site of action |
| what is lidocaine best know for when injected | it's one of the best anti-arrythmia agents |
| what type of arrythmias does lidocaine treat | ventricular |
| What other drug is used to treat arrythmias | procainamide |
| what is the mechanism of action of lidocaine and procainamide in treating arrythmias | blocking Na+ channels in heart |
| what is the first treatment for OCD | clomipramine |
| what differentiates clomipramine from imipramine | presence of Cl- on 3 position |
| what durgs are circulating in the body of someone on imipramine | imipramine and desipramine |
| what are some of the problems with tricyclic antidepressants | cardio, hepatotoxicities; cholinergic/histaminergic actions, some antagonize DA receptors |
| fluoxetine has an R and an S enantiomer. Which is more SERT selective? | The S enantiomer |
| The major metabolites of fluoxetine are also SERT selective. Which isomers are more potent and selective | The S enantiomer |
| Which receptors does fluoxetine bind to? | None |
| Which antidepressant drug shows virtually no receptor affinity and is the most potent binder of SERT? | Paxil |
| How is paxil dispensed (what isomer) | Pure (3S, 4R) trans enantiomer. |
| how is zoloft dispensed | as pure (1S, 4S) cis enantiomer |
| which antidepressant is the most SERT selective? | Citalopram |
| what does metabolism of citalopram cause | the metabolites increase NET acttivity |
| what substitution makes the SSRIs more SERT selective | Electronegative substitutions |
| what is the main thing to look out for when using fluvoxamine | drug interactions as it's a potent inhibitor of CYP450-2A |
| what cofactor is required to carry out oxidative deamination of monoamines | FAD |
| in what parts of body can you find MAOa | CNS, liver, GI, placenta |
| in what parts of body can you find MAOb | CNS, platelets |
| which isoform of MAO is important for the breakdown of serotonin, epi, norepi, and DA | MAOa |
| Clinically useful antidepressants target this MAO isoform | MAOa |
| What does MAOb break down | dopamine and trace amines (tyramine, tryptamine, etc.) |
| which types of drugs target MAOb | anti Parkinson's agents |
| what significant physiological changes occur with the use of MAOIs? | increased BP, heart rate/force |
| which drugs are contraindicated with MAOIs | drugs that are metabolized by MAO or inhibit MAO to a lesser degree (e.g. pseudoephedrine, dextromethorphan, ephedrine mists, H1 antagonists) |
| what will happen if you eat food containing tyramine while on MAOIs | you may suffer hypertensive crisis or worse |
| what is significant about tyramine in food | it's a potent vasopressor which is normally metabolized by MAO in the GI tract. |
| structures related to this compound have maximum MAO inhibition | amphetamine |
| phenelzine is what type of MAOI | Irreversible |
| Why is phenelzine an irreversible MAOI | it hydrazine group is metabolized to something that reacts with SH group in Cys residue of MAO. It lasts until new MAO is made (weeks). It's also a substrate. |
| what else is phenelzine responsible for | it inhibits GABA transaminase, the GABA inactivating enzyme ==> increases in GABA |
| which MAOI is reversible and irreversible | Parnate |
| this MAOI is selective for MAOb and at higher doses inhibits MAOa | Selegiline |
| define psychosis | a mental state in which thought and perception are impaired |
| what's a hallucination | a perception experienced without external stimulation of the sense organs. |
| what's a delusion | persistent belief contrary to the educational and cultural background of the individual |
| what is affective flattening | the near absence of emotional or facial expression |
| what is anhedonia | individual is unable to experience emotions such as pleasure or pain and feels detached from the environment |
| what is alogia | the absence of spontaneous production for the purpose of answering questions or expressing one's self |
| what is avolition | deficit in spontaneous goal directed behavior in which an individual may sit for prolonged periods of time and must be prodded into completing simple daily tasks |
| which receptors are important in schizophrenics and in what parts of the brain | D1 in frontal cortex, nucleus accumbens, amygdala and hippocampusand D2 in striatum and tuberoinfundibular pathway |
| what do we notice abut GABA levels in the brain of schizo | synthesis of GABA is decreased and GABA activity is reduced |
| in the brain, what happens when there is a deficit of GABA | increased activity in areas like cortex and hippocampus |
| what happens to dopamine levels in the cortex and limbic system of schizos | in cortex it is decreased (-ve symptoms) and in limbic system it is increased (+ve symptoms) |
| in schizos, what happens to the striatum if we block D2 receptors | we decrease dopamine activity and have increase in extrapyramidal side effects |
| in schizos, where do we want to decrease dopamine levels | in the limbic system |
| what receptors are stimulated more than normal in the cortex of schizos and what's the result | 5-HT2A, increase in negative symptoms |
| list some extrapyramidal side effects | involuntary irregular movements like tardive dyskinesia (face), restlessness, tremors, muscle spasms in neck. |
| what are the effects in schizos of drugs that block 5-HT2A | increases dopamine in striatum and decreases dopamine in limbic system |
| what antipsychotic drugs may cause hyperthermia | thorazine and mellaril |
| which class of phenothiazines has highest EPS and lowest side effects | piperazines |
| What effect does antimuscarinic activity have on EPS | it reduces EPS |
| how are phenothiazines metabolized and what do we need to look out for as a result | by CYP450; drug interactions. |
| the butyrophenone's are based on what analogue | meperidine |
| give 2 examples of butyrophenones | haloperidol and droperidol |
| how do the butyrphenones differ from the typical antipsychotics in terms of effects | they produce a high degree of EPS and tardive dyskinesia, but less sedation. |
| how is droperidol used | it's short acting and sedative. used in psych emergency and also as antiemetic and anesthetic |
| which neurotransmitter is haloperidol thought to be similar to | GABA |
| atypical antipsychotics look like which two structures together | a tricyclic and a piperazine |
| what sorts of problems have been associated with atypical psychotics | can lead to diabetes and obesity/weight gain |
| what about the SAR of atypical psychotics makes them more active | having tertiary terminal amines |
| activity at which receptor by antipsychotics leads to aggression, weight gain and sexual dysfunction | 5-HT1 and 2 |
| action of antipsychotics at which receptors will produce sedation | alpha 1 and 2, and hist 1 |
| name some atypical antipsychotics | olanzapine, clozapine, risperidone, quetiapine, ziprasidone, aripiprazole |
| which parts of the brain are targets for reducing anxiety | hippocampus and amygdala |
| which receptors seem to not be the right amount in people w/ anxiety issues and are these receptors increased or reduced | GABA receptors are reduced in number |
| what stage of sleep do we spend most time in | stage 2 |
| what are some of the uses of benzodiazepines | for anxiety, sedative hypnotic, skeletal muscle relaxer, anti-convulsant |
| which GABA subunits are required for anti-anxiety effects | alpha 1 and 2 |
| hypnotic agents only need to bind with this subunit | alpha 1 |
| what is the effect of benzo on sleep stages | stage 2 is increased, all other stages decreased. more REMs per night |
| how do benzos produce their muscle relaxing effect | they act in the spinal cord and interfere with synaptic transmission ==> reduced muscle tone |
| which benzos are most commonly used for anticonvulsant effects | klonopin and tranxene |
| what are the theories on why people develop tolerance to benzos | some think they can induce metabolism and thus get metabolized more rapidly. others think that regular use may lead to down regulation of receptors. |
| which benzos are ultrashort acting | midazolam (versed) |
| which benzos are short acting | xanax, ativan, serax (oxazepam) |
| which benzos are intermediate acting | klonopin |
| which benzos are long acting | valium, librium, tranxene |
| if dose of benzos is too high what can happen | can get vasodilation and blockade of neuromuscular junction |
| what effect do benzos have on GABA receptor | they cause it to open more often |
| which drug is used as an ultrashort acting hypnotic | zaleplon |
| which drugs are short acting hypnotics | zolpidem and halcion and rozerem |
| this drug is a melatonin receptor agonist | ramelteon |
| these benzos are intermediate acting hypnotics | temazepam, estazolam, eszopiclone |
| which tissue has the highest concentration of serotonin | pineal gland |
| what does the absence or presence of light affect | melatonin synthesis |
| melatonin is not a good hypnotic for which group of people | people whose melatonin level is normal |
| which group of patients would respond to exogenous melatonin better | older patients as their melatonin is lower than normal |
| what are the steps by which lack of light causes us to want to sleep | lack of light ==> stimulates hypothalamus to send signal to pineal gland to produce melatonin ==>melatonin sends signal to hypothal saying its time to go to sleep |
| where in the body do barbiturates generally work | brain, not in the periphery |
| which barbiturates are short acting | brevital and pentothal |
| name the intermediate/long acting barbiturates | secobarbital, pentobarbital, butabarbital, phenobarbital |
| what do barbiturates do to liver enzymes and how does affect other drugs in your system | barbiturates induce liver enzymes and cause duration of other drugs to shorten |
| what are the explanations for people developing tolerance to barbiturates | down regulation of GABA receptors; could be pharmacokinetic |
| what is chloral hydrate metabolized to and how is the drug dispensed | trichloroethanol; gel cap |
| the metabolite of what drug is the chemical found in the drug Soma | Meprobamate |
| where in the body does meprobamate work | brain and skeletal muscles |
| which benzo receptor subtype is more abundant | BZ1 |
| what change to benzo ring A will increase binding and anti-anxiolytic/hypnotic activity | adding an electronegative group to position 7 |
| what is needed in ring B of a benzo for it to work | must have a proton accepting group (C=O, C=S,etc) and the accepting group needs to be coplanar with ring A |
| what would you do to ring B of benzo to increase lipophilicity | Use N1 alkyl side chains |
| what does 3 - hydroxy group on ring B do to benzo | it causes faster excretion |
| what can you do to ring B of benzo to get higher affinity | anneal a 4th ring to it. |
| what substitutions on ring C of benzo retains activity and increases lipophilicity | ortho substitutions |
| when flumazenil blocks access to the BZ site on GABA how does it affect Cl- conductivity | it doesn't induce any Cl- conductivity |
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coolnuh
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