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40 Cards in this Set
- Front
- Back
What are the effects of benzodiazepines? |
Anti-anxiety Sedative-hypnotic Amnestic Anticonvulsant Spinal Cord mediated Muscle Relaxation |
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What receptor does a Benzodiazepine act on? |
Benzos potentiate the activity of GABA which is an inhibitory neurotransmitter in the CNS leading to hyperpolarization of the cell membrane. |
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What is the volume of distribution, and protein binding for Benzos? |
Large Volume of Distribution and highly protein bound. |
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How are Benzos effect terminated? |
Redistribution Also has active metabolites when broken down |
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Do benzos have a small or large theraputic index? |
Large, the dose range is wide meaning a lot of medication can be given before reaching a toxic dose. |
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What are common side effects of Benzos? |
Fatigue Drowsiness Decreased Motor Coordination Impaired Cognitive Function Anterograde Amnesia |
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What is the PO and IM bioavailability of Midazolam? |
PO 50% and IM 80-90% Has high protein binding 95-96% Is water soluble in the syringe but becomes lipid soluble at biologic pH |
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How is the action of Versed terminated? |
Redistribution is Metabolized in the liver with a high hepatic extraction ratio. It is metabolized to 1-hydroxymidazolam (semi-active) and excreted by the kidney. |
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What are the systemic effects of Midazolam? |
CV stable Resp dose dependent changes in tidal volume CNS dose dependent reductions in CBF, amnesia, and cerebral metabolic requirement of O2 |
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What is the bioavailability of Diazepam |
PO 100% IM 50-60% Lipid soluble with large Vd (burns when IV) Extensive protein binding Has a low Hepatic Extraction Ratio Metabolites are active Nor Diazepam, Oxazepam, and Temazepam |
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What are the systemic effects of Valium? |
CV Minimal depression (similar to sleep) Resp Some depression with detectable increase in CO2 CNS amnesia Has anticonvulsant and muscle relaxant |
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Why does Lorazepam have a slower onset than other benzos? |
It has a lower lipid solubility. Has inactive metabolites (metabolized in the liver) Is a more potent Amnesic (5-10 x diazepam) Minimal depression of CV and ventilation |
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What are considerations of Flumazenil (Romazicon)? |
May be associated with onset of seizures, confusion, and agitation Has a shorter half life than benzos so could re-sedate. |
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What anticholinergic is the only one to cross the Blood Brain Barrier? |
Scopolamine causes CNS depression by combining with muscarinic cholinergic receptors in the brain preventing the neurotransmitter acetylcholine |
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What medication is utilized for patients with a family history or direct history of malignant hyperthermia? |
Propofol |
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What is the mechanism of action of propofol? |
It modulates the GABAA receptor by hyperpolarizing the membrane of the post synaptic neuron. |
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What are the actions of Diprivan? |
It is a hypnotic without analgesic or amnestic properties. Lipid soluble, in a soybean oil, glycerol, and egg products. Isotonic with a pH 7.0-8.5 Rapid metabolized, extensively distributed. Clearance from plasma exceeds Hepatic blood flow |
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What are the systemic effects of Propofol? |
CV hypotension with decreases in CO & SVR Decreases CBF and ICP Can reduce CPP Antipruritic, antiemetic, and Anticonvulsant |
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What is the mechanism of action for Etomidate? |
A modulator of GABAA receptors enhancing the affinity of the inhibitory neurotransmitter GABA. |
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What are the phamacokinetics of Etomidate? |
pKa of 4.2 (weak Base) Moderately lipid soluble Large Vd 76% albumin bound Redistribution accounts for awakening Metabolized by hydrolysis in the liver and plasma |
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Why should you administer narcotics with Etomidate? |
It is a IV hypnotic without analgesic activities. |
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What are the systemic effects of Etomidate? |
CV minimal effect Maintains CPP May activate seizure foci on EEG Causes adrenocortical suppression limiting response to stress (do not give to septic pts) Nausea and Vomitting are common Myoclonic muscle activity (pretreat with Narcs) |
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What are the properties of Barbiturates |
Its a Hypnotic with no analgesic properties Lipid Soluable with a rapid onset and LOC It has a short duration of Action It is an acid medication The chemical structure decides the class and action |
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Which medication is now used instead of Barbiturates? |
Propofol |
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How do barbiturates work? |
They have a direct and an indirect action on the GABAA Receptors. Directly it mimics GABA and attaches directly to the activating receptor Indirectly it attaches to the receptor and increases the affinity for GABA (ligand). Thus suppressing transmission of excitatory neurotransmitter (Glutamic acid) |
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How are barbiturates Metabolized |
By Hepatocytes and other extrahepatic sites. Has a low Hepatic Extraction Ratio, but is not dependent on hepatic enzyme activity for clearance (opposite of normal LHER) because the Liver has a high reserve capacity to oxidize Barbs Metabolites are inactive (will not Resedate) |
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Systemic Effects of Barbiturates? |
CV myocardial depression, vasodilitation, and transient hypotension. Resp transient respiratory depression or apnea (can cause histamine release) CNS decrease CBF, CMRO2, and ICP |
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What are two barbiturates? |
Sodium Thiopental Methohexital |
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What are the pharmacokinetics of Sodium Thiopental? |
High lipid solubility 72-86% bound to albumen Redistributes in 5min from brain to inactive tissue causing short duration of action. |
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What are some of the effects of Methohexital? |
Lowers Seizure threshold (used in ECT) Offers more rapid recovery than thiopental Can cause Myoclonus and pain on injection Hepatic Extraction Ratio is Larger than most Barbs (perfusion dependent) |
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What is the action of Ketamine? |
It is a dissociative anesthetic that can cause hallucinogenic effects. Binds to NMDA receptor inhibiting Glutamate by inhibiting the presynaptic release of it. |
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What are the pharmacokinetics of Ketamine? |
Highly lipid soluble (Crosses BBB) Low protein binding Large Vd Rapid distribution from plasma to tissues Metabolized by hepatic microsomal enzyme cytochrome P-450 High Hepatic Extraction Ratio |
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What are the systemic effects of Ketamine? |
CV increased HR, BP, CO, MVO2 requirements Resp no respiratory depression, decrease airway resistance (good for Asthma) CNS potent cerebral vasodilator, Increases CMRO2, CBF, ICP, and intraoccular pressure |
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What are precautions for the use of Ketamine? |
Increased IOP Risk of emergence delirium (psych hx, elderly, children(nightmares)) side effect less with concomitant use of Benzos. Inhalation agents prolong duration of action Use cautiously with CAD |
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What is the class and mechanism of action for Dexmedetomidine? |
Alpha2 adrenergic agonist Reduces symathetic outflow (sympatholytic) by inhibiting the release of NE (presynapse) causing sedation Postsynapse it inhibits symathetic activity decreasing BP and HR |
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How to remember which alphaadrenergic receptor works on what tissue? |
Alpha 1 Brains Alpha 2 Veins |
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Pharmacokinetics of Dexmedetomidine. |
Affinity for alpha2 verses alpha1 (1620:1) Rapid distribution half-life of 6 minutes Elimination half-life of 2 hours Biotransforms in the liver |
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Systemic effects of Dexmedetomidine? |
CV Moderate BP and HR reductions Profound decrease in catecholamine levels in the plasma Use caution in pts with advanced heart block |
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