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pharmacology
anesthesia - epi-norepi
| Question | Answer |
|---|---|
| the biosynthesis of catecholamines (norepi-epi) begins when? | conversion of phenylalanine to tyrosine in the cytoplasm of sympathetic nerve terminals. |
| what is the rate limiting step of catecholamine synthesis? | tyrosine hydroxylation to dopa by enzyme tyrosine hydroxylase. |
| what converts tyrosine to dopa? | hydroxylation, by enzyme tyrosine hydroxylase. |
| what happens to dopa in the making of catecholamine biosynthesis? | dopa converted to dopamine by dopa decarboxylase. |
| once dopamine is formed what does it do? | enters storage vesicles to be converted to norepi. |
| what is directly converted to norepi? | dopamine. |
| how is norepi released into the synaptic cleft? | action potential cause influx of calcium which cause vesicles to fuse with cell membrane of sympathetic nerve terminals to release norepi |
| inactivation of norepi is achieved by? | both reuptake and metabolism. |
| which is the majority pathway to cause inactivation of norepi? | the reuptake into nerve terminals. about 2/3rds |
| once reuptake of norepi occurs what happens next? | most pumped back into vesicles and the rest are metabolized by MAO IN THE cytoplasm. |
| norepi not reuptaked goes through what? | enters circulation to be metabolized by: 1. mao 2. comt |
| what blocks reuptake of norepi? | 1. TCA 2. COCAINE 3. AMPHETAMINES. |
| HOW IS EPINEPHRINE FORMED? | norepi converted into epinephrine in the adrenal medulla by PNMT |
| what enzyme causes the conversion of norepi into epinephrine/ | phenylethanolamine-n-methyltransferase PNMT. |
| Etomidate may be hazardous in what setting? why? | 1. ruptured globe - myoclonus activity 2. adrenosuppression in critically ill. |
| how does etomidate cause myoclonus? | supression of sub-cortical structures. |
| what may reduce. etomidate myoclonus activity? | premedication with versed or fentanyl. or valproate or clonazepam. |
| etomidate myoclonus may preclude its use in? | cardioversion. |
| list the drugs that may cause myoclonus? | 1. etomidate 2. normeperidine 3. opioids 4. metohexital 5. propofol 6. thiopental. |
| how does opioids cause myoclonus? | due to depression on inhibitory neurons. |
| how does normeperidine cause myoclonus? | a metabolite of meperidine. causes stimulation of the central nervous system. which manifest as myoclonus and seizures. |
| which drug may cause both seizures and myoclonus (not only myoclonus)? | meperidine metabolite - normeperidine. |
| which drug is an imidazole? | etomidate. |
| dose of etomidate? | 0.1-0.4mg/kg. |
| what is the cause of cns depression from etomidate? | gaba like activity. |
| awakening from etomidate is due to ? | redistribution. |
| how does etomidate make ssep monitoring more reliable/ | increases amplitude. |
| cns effect of etomidate? | 1. activates epileptic foci - careful in pts. with seizures 2. increase ssep amplitude 3. cerbral vasoconstrictor - decrease cbf and cmro2 by 25-35%. similar to thiopental. 4. has not analgesic affect/ |
| compared to thiopental the metabolism of etomidate is? | like thiopental, etomidate in hydrolyzed in the liver but five times greater then thiopental. |
Created by:
michelledaryanani
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