inhaled anesthetics, opiods, narcatiocs
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| Analgesia, euphoria, sedation | Agonist indications
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| Morphine effective against pain arising from the visceral, skeletal, and joints | Agonist indications
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| When morphine is added to volatile agents it increase the effects of anethesia | Agonist Indications
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| Morphine decrease cerebral blood flow in the absence of hypoventilation | Agonist clinical uses
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| Morphine reduces what during Myocardial infarctions | Preload also an Agonist clinical use
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| Demerol decrease what in post-op settings | Itching also a Agonist clinical use
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| Used independently to produce a limited level of analgesia | Agonist-Antagonist Indications
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| trhese drugs have the ability to produce Analgesia with limited risk of ventilation and physical dependence | Agonist-Antagonist
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| Partially reverses an agonist | Agonist-Antagonist
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| These drugs have a ceiling effect of analgesia | Agonist-Antagonist
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| Used to treat opiod respiratory depression | Antagonist Indications
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| Treat opiod induced respiratory depression do to maternal administration of opiods | Antagonist Indications
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| Treat deiliberate overdose | Antagonist Indications
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| Treat side effects of itching associated with neuraxial opiods | Antagonist Indications
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| 5X more potent than fentanyl, 1000x more potent morphine (strongest) | Sufentanil
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| Potency and lipid solubility Strongest to weakess | Sufentanyl> Remifentanyl> Alfentanyl> Morphine> Meperidine
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| Onset of action fastest to slow | Alfentanyl> Sufentanyl> Fentanyl> Morphine> Meperidine
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| Duration of action (longest to shortest) | Morhine> Meperidine> Fentanyl> sufentanyl> Alfentanyl> remifentanyl
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| Effect site equilibration | Fentanyl 6.4> Sufentanyl6.2> Alfentanl 1.4> Remifentanyl 1.1> Morphine 15-30 Meperidine
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| Partially reverse an agonist w/o completely reversing analgesic properties | Agonist-Antagonist Advantage
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| Limited risk of ventilator depression and physical dependency | Agonist-Antagonist Advantage
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| Insufficient analgesia properties for surgical anesthesia | Agonist-Antagonist Disadvantage
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| Ceiling effect | Agnist-Antagonist Disadvantage
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| One injection last for 48 hours | Clinical advantage of Morphine liposomal
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| no need for an indwelling catheter for continous infusion | Clinical advantage of Morphine liposomal
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| Designed for control of pain after major surgeries | Clinical advantage of Morphine liposomal
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| Not recommended for patients under 18 years old | Disadvantage of Morphine liposomal
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| Intrathecal admin has resulted in prolonged repsiratory depression | Disadvantage of Morhine liposomal
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| Most common side effect of neuraxial opiods | Pruritis
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| Most serious side effect of neuraxial opiods | Ventilation depression
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| Analgesia is dose dependent | Neuraxial Opiods
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| Neuraxial opiods __________ Mac for volatile anesthetics. | Decrease
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| Epidural admin of poorly lipid soluble opiods such as morphine will result in slower onset of action and longer duration of action. | Neuraxial Opiods
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| Sedation, CNS excitation, Neonatal Morbidity | Neuraxial Opiods
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| Main analgesia during labor & Delivery & after surgery | Meperidine
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| Effective in controlling post-op shivering | Meperidine
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| Meperidine is metaolized how? | in the liver
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| What's Meperidine primary route of elimination? | Urination excretion
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| Meperidine is metabolized into what | Normeperidine and Meperdinic acid
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| Common side effects of Morphine | Histamine release,nausea vomiting & pruritis
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| What is morphine's mechanism of action? | by acting on the mu receptors
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| What is Mu1 mechanism of action | produce analgesia and uphoria
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| What is Mu2 mechanism of action | responsible for hypoventilation, bradycardia, and physical dependency
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| How is Remifentanyl metabolized | only opiod not metabolized by liver, suscpetible to hydrolysis by plasma esteraase
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| What are advantages of remifentanyl | Quick onset, Short duration of action noncumulative effect
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| What are disadvantages of Remifentanyl | Cost, short duration of action could be disadvantage with long painful surgeries
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| Produced by anterior pituitary | growth hormone
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| produced by anterior pituitary | Prolactin
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| produced by anterior pituitary | Luteinizing hormone (gonadotropin)
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| produced by anterior pituitary | Adrenocorticotropic hormone (ATCH)
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| produced by anterior pituitary | thyroid stimulating hormone (TSH)
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| produced by posterior pituitary | ADH
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| produced by osterior pituitary | Oxytocin
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| How should patients with prior hypophysectomy be treated prior, during and after surgery? | Cortisol must be given continuously
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| How should patients scheduled for thyroidectomy be treated before ssurgery? | Thyroids have a long half life and may be omitted for a several days
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| What is the anti-inflammatory potency and Na retaining potency for Prednisolone? | Anti-inflammatory = 4 Na retaining potency .8
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| What is the anti-inflammatory potency and Na retaining potency for Prednisone? | Anti-inflammtory = 4 Na retaining potency = .8
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| WHat si the anti-inflammatory potency and Na retaining potency for Methylprednisone? | Anti-inflammatory = 5 Na retaining potency = 0.5
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| What is the anti-inflammatory potency and Na retaining potency for Betamthasone? | Anti-inflammtory = 25 Na retaining potency = 0
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| What is the anti-inflammatory potency and Na retainig potency for Dexamethasone? | Anti-inflammatory = 25 Na retaining potency = 0
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| What is Fludricortisone | Anti-inflammmatory = 10Na retaining potency = 250
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| What are the clinical uses of Oxytocin | causes uterine contractions
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| What are the clinical uses of ADH | Acts on the renal collecting ducts where it increases permeability of the cell to water; water is reabsorbed.
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| Suppression of HPA axis | warnings and adverse reaction of Corticosteroids
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| hypokalemisa is an advrse reaction of what | Corticsteroids
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| Metabolic acidosis is an adverse reaction of what | Corticosteroids
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| hyperglycemia is an adverse reaction of what | Corticosteroids
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| Developement of immune defiency may be caused by? | Corticsteriods
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| Inhibition of normal growth may be the effects of? | Corticosteroids
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| Peripheral blood changes may be caused by? | Corticosteroids
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| Osteoporosis and PUD are caused by? | Corticosteroids
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| Skeletal muscle myopathy is caused by | Corticosteroids
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| CNS dysfunction is caused by what? | Corticosteroids
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| What precautions should be taken with a patient who has chronic hypoadrenocorticism? | Dose of corticosteroid should be increased
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| Corticosteroid results in suppression of the ______ and leads to blunting normal release of | HPA axis and leads to blunting normal release of cortisol
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| How can you decrease the risk of patients having a CV collapse? | Increase the dosage of Corticosterods
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| What is SIADH (syndrome of inappropriate secretion of antiduretic hormone) | inappropriate and excessive secretion of ADH with subsequent water retension and dilutional hyponatremia.
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| What type of patients are prone to SIADH? | Head traumas, intracranial tumors, meningitis, pulmonary infections, & oat cell carcinomas
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| What antibiotic is used to treat SIADH | Demeclomycin (Declomycin)
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| What is the action of Demeclomycin | Promotes diuresis by antagonizing the effects of ADH on renal tubules.
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| What are the signs and synmptoms of SIADH? | Serum hypoosmality, HYPONATREMIA, most symptoms are associated with hyponatrmia
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| What factors speeds up induction from machine to alveoli? | anesthetic input, increased inspired partial pressure, increased ventilation, smaller the tube faster induction, increased FRC ratio
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| What speeds up inhaled anesthetics from alveoli to arterial blood? | low blood:gas partition coeffcient, low cardiac output, aveolar to venous partial pressure difference
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| What speeds up induction from arterial blood to brain? | Cerebral blood flow, arterial to venous pressure differnce, brain:blood partition coeffecient
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| Increasing the _______ in the inspired air will increase both the maximum tension that can be achieved in the alveoli and the rate increase in arterial tension. | anesthetic concentration
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| Increase ventilation, like PI, promotes input of inhaled anesthetics to offst ________ into blood | uptake
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| The net effect of increasing anesthetic concentration is a more rapid increase in PA and thus and increase in the ___________? | induction of anethesia
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| The greater the alveolar ventilation to FRC, the more _______ the increase in PA toward PI | rapid
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| What is the ratio of aveloalar ventilation to FCR ratio in neonates | 5:1
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| What is the ratio of aveolar ventilation to FCR in adults | 1:5
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| Indiction of anesthesia is slower with what? | more soluble anesthetic gases.
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| What drug characteristics may effect speed of induction of inhalational agents? | potency/solubility, oil:gas partition coeffceient.
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| What effect does a high oil:gas partician coeffecient have? | low MAC or higher potency
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| What effect does a low oil:gas partition coeffecient have? | High MAC or low potency
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| Define MAC | Minimal Alveolar Concentration is the concentration at 1 atm which causes immobility in 50% when expose to a noxious stimulus such as surgical stimulus
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| What patient characteristics increase MAC? | Hyperthermia, Hypernatremia, Hyperthyroid, chronic ETOH abuse,
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| What drugs increase MAC? | Cocaine, MAOI, Ephedrine, Levadopa
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| What patient characteristics decrease MAC? | Hypothermia, hyponatremia, elderly, acute alcohol ingestion, postpartum, BP<40 cardio-pulmonary bypass, anemia, metabolic acidosis hypoxia, pregnancy,
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| What drugs decrease MAC? | Benzos, clonidine, A2agonist, lithium, lidocaine, neuraxial oopiods,
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| what drugs decrease MAC? | Ketamine, Chlorpromazine, Physostigmine, Pancurium, Verapamil, Tetrahydrocanbinol hydroxine
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| All inhalational agents are excreted where | Lungs
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| Nitrous Oxide is metablized where and how much? | Gi tract and .004%
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| Deslflurane is metabolized by what and how much | .02% from P450
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| Isoflurane is metabolized how and how much | 2% from P450
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| Sevoflurane is metabolized how and how much | 5% FROM P450
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| How does volatile anesthetics arterial to venous pressure difference will effect the duration of actions? | The higher the solubility the more the agent will diffuse into the muscles or blood, thus prolonging induction.
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| In regards to volatile anesthetics which is the most soluble agent in use? | Isoflurane
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| What inhalational agent has the greatest analgesia and paralytic properties? | Nitrous Oxide
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| What is compound A? | Degredation product Sevoflurane and CO2 absorbers.
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| What risks are associated with Compound A | Neprotoxicity
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| What can be done to prevent formation of Compound A | Administer at least 2L of fresh gas flow to minimize formation of compound A
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| What is diffusion hypoxemia? | When Nitrous Oxide is discont it leads to a reversal of partial pressure gradients, N2O leaves the blood and entrs the alveoli and dilutes PAO2 and PCO2 in the alveoli
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| What can be done to avoid diffusion hypoxia? | Hyperventilate the patient with 100% O2 1-5 mins after turning off NO2.
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| What is the MAC, blood:gas partition coeffecient of NITROUS OXIDE? | Mac = 105 Blood:gas PC = 0.46 oil:gas PC = 1.4no vapor pressure
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| What is the MAC, VP, b:g partition coeffecient of ISOFLURANE | MAC = 1.2 B:G = 1.46 oil:gas = 98 VP = 240
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| What is the MAC, VP, B:G O:G partition coeffecient of SEVOFLURANE | MAC = 2 B:G = 0.69, O:G = 55 VP = 160
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| What is the MAC, VP, B:G, O:G partition coeffecient of DESFLURANE | MAC = 6 B:G = 0.42 O:G = 18.7 VP = 681
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| What are the advantages of Isoflurane | safer for kidneys, does not cause seizures, decrease ICP, decrease CMRO2 requirements, decrease BP but not CO,
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| What are the disadvantages of Isoflurane | Profound ventilation depression, tachepnia, Increased heart rate.
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| What are the disadvantages of Desflurane? | very pungent, airway irritant, increased coughing, increased incidence of laryngospasm, requires special heated vaporizer, decrease CO and BP, decrease cereberal blood flow
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| What are the advantages of Deflurane? | very little metabolism, unlikely to form neoantigens,
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| What are the advantages of Sevoflurane? | has no preservatives, but less stable, Reasonble MAC, non-irritating to airways, does not change heart rate.
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| What are the disadvantages of Sevoflurane? | less stable, breaks down in presence of soda lime, nephrotoxic, produces compounds A-F
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| What are the disadvantages of NO2? | either no effect or modest incerease in BP, does not increase CO2, provides analgesia, fast revrsible, weak trigger of MH
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| What are the disadvantages of Nitrous Oxide? | doe not relax skeletal muscles, cause diffusion hypoxia, depress vent response, can increase volume or pressure of air in gut, middle ear, lungs and head
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| What are s&s of fluoride toxicity? | Polyuria, hyernatremia, hyperosmolarity, increased serum creatinine, inability to concentrate urine.
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| What agent is fluortoxcity associated with? | Methoxyflurane
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| Inorganic fluoride metabolite is _________? | nephrotixic
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| Currently used anesthetics have significantly less metabolism and are less soluble thus | decreasing the nephrotoxic effects
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| What triggers MH | Succinylchloine and volatile anesthetics
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| True or false; all volatiel anesthetics can trigger MH | true
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| What is the most potent trigger of MH | Halothane although it is no longer used in the states.
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| What is the weakest volatile aneshtetic that can trigger MH? | Nitrous Oxide
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