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Parmacology
inhaled anesthetics, opiods, narcatiocs
| Question | Answer |
|---|---|
| Analgesia, euphoria, sedation | Agonist indications |
| Morphine effective against pain arising from the visceral, skeletal, and joints | Agonist indications |
| When morphine is added to volatile agents it increase the effects of anethesia | Agonist Indications |
| Morphine decrease cerebral blood flow in the absence of hypoventilation | Agonist clinical uses |
| Morphine reduces what during Myocardial infarctions | Preload also an Agonist clinical use |
| Demerol decrease what in post-op settings | Itching also a Agonist clinical use |
| Used independently to produce a limited level of analgesia | Agonist-Antagonist Indications |
| trhese drugs have the ability to produce Analgesia with limited risk of ventilation and physical dependence | Agonist-Antagonist |
| Partially reverses an agonist | Agonist-Antagonist |
| These drugs have a ceiling effect of analgesia | Agonist-Antagonist |
| Used to treat opiod respiratory depression | Antagonist Indications |
| Treat opiod induced respiratory depression do to maternal administration of opiods | Antagonist Indications |
| Treat deiliberate overdose | Antagonist Indications |
| Treat side effects of itching associated with neuraxial opiods | Antagonist Indications |
| 5X more potent than fentanyl, 1000x more potent morphine (strongest) | Sufentanil |
| Potency and lipid solubility Strongest to weakess | Sufentanyl> Remifentanyl> Alfentanyl> Morphine> Meperidine |
| Onset of action fastest to slow | Alfentanyl> Sufentanyl> Fentanyl> Morphine> Meperidine |
| Duration of action (longest to shortest) | Morhine> Meperidine> Fentanyl> sufentanyl> Alfentanyl> remifentanyl |
| Effect site equilibration | Fentanyl 6.4> Sufentanyl6.2> Alfentanl 1.4> Remifentanyl 1.1> Morphine 15-30 Meperidine |
| Partially reverse an agonist w/o completely reversing analgesic properties | Agonist-Antagonist Advantage |
| Limited risk of ventilator depression and physical dependency | Agonist-Antagonist Advantage |
| Insufficient analgesia properties for surgical anesthesia | Agonist-Antagonist Disadvantage |
| Ceiling effect | Agnist-Antagonist Disadvantage |
| One injection last for 48 hours | Clinical advantage of Morphine liposomal |
| no need for an indwelling catheter for continous infusion | Clinical advantage of Morphine liposomal |
| Designed for control of pain after major surgeries | Clinical advantage of Morphine liposomal |
| Not recommended for patients under 18 years old | Disadvantage of Morphine liposomal |
| Intrathecal admin has resulted in prolonged repsiratory depression | Disadvantage of Morhine liposomal |
| Most common side effect of neuraxial opiods | Pruritis |
| Most serious side effect of neuraxial opiods | Ventilation depression |
| Analgesia is dose dependent | Neuraxial Opiods |
| Neuraxial opiods __________ Mac for volatile anesthetics. | Decrease |
| Epidural admin of poorly lipid soluble opiods such as morphine will result in slower onset of action and longer duration of action. | Neuraxial Opiods |
| Sedation, CNS excitation, Neonatal Morbidity | Neuraxial Opiods |
| Main analgesia during labor & Delivery & after surgery | Meperidine |
| Effective in controlling post-op shivering | Meperidine |
| Meperidine is metaolized how? | in the liver |
| What's Meperidine primary route of elimination? | Urination excretion |
| Meperidine is metabolized into what | Normeperidine and Meperdinic acid |
| Common side effects of Morphine | Histamine release,nausea vomiting & pruritis |
| What is morphine's mechanism of action? | by acting on the mu receptors |
| What is Mu1 mechanism of action | produce analgesia and uphoria |
| What is Mu2 mechanism of action | responsible for hypoventilation, bradycardia, and physical dependency |
| How is Remifentanyl metabolized | only opiod not metabolized by liver, suscpetible to hydrolysis by plasma esteraase |
| What are advantages of remifentanyl | Quick onset, Short duration of action noncumulative effect |
| What are disadvantages of Remifentanyl | Cost, short duration of action could be disadvantage with long painful surgeries |
| Produced by anterior pituitary | growth hormone |
| produced by anterior pituitary | Prolactin |
| produced by anterior pituitary | Luteinizing hormone (gonadotropin) |
| produced by anterior pituitary | Adrenocorticotropic hormone (ATCH) |
| produced by anterior pituitary | thyroid stimulating hormone (TSH) |
| produced by posterior pituitary | ADH |
| produced by osterior pituitary | Oxytocin |
| How should patients with prior hypophysectomy be treated prior, during and after surgery? | Cortisol must be given continuously |
| How should patients scheduled for thyroidectomy be treated before ssurgery? | Thyroids have a long half life and may be omitted for a several days |
| What is the anti-inflammatory potency and Na retaining potency for Prednisolone? | Anti-inflammatory = 4 Na retaining potency .8 |
| What is the anti-inflammatory potency and Na retaining potency for Prednisone? | Anti-inflammtory = 4 Na retaining potency = .8 |
| WHat si the anti-inflammatory potency and Na retaining potency for Methylprednisone? | Anti-inflammatory = 5 Na retaining potency = 0.5 |
| What is the anti-inflammatory potency and Na retaining potency for Betamthasone? | Anti-inflammtory = 25 Na retaining potency = 0 |
| What is the anti-inflammatory potency and Na retainig potency for Dexamethasone? | Anti-inflammatory = 25 Na retaining potency = 0 |
| What is Fludricortisone | Anti-inflammmatory = 10Na retaining potency = 250 |
| What are the clinical uses of Oxytocin | causes uterine contractions |
| 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. |
| Suppression of HPA axis | warnings and adverse reaction of Corticosteroids |
| hypokalemisa is an advrse reaction of what | Corticsteroids |
| Metabolic acidosis is an adverse reaction of what | Corticosteroids |
| hyperglycemia is an adverse reaction of what | Corticosteroids |
| Developement of immune defiency may be caused by? | Corticsteriods |
| Inhibition of normal growth may be the effects of? | Corticosteroids |
| Peripheral blood changes may be caused by? | Corticosteroids |
| Osteoporosis and PUD are caused by? | Corticosteroids |
| Skeletal muscle myopathy is caused by | Corticosteroids |
| CNS dysfunction is caused by what? | Corticosteroids |
| What precautions should be taken with a patient who has chronic hypoadrenocorticism? | Dose of corticosteroid should be increased |
| Corticosteroid results in suppression of the ______ and leads to blunting normal release of | HPA axis and leads to blunting normal release of cortisol |
| How can you decrease the risk of patients having a CV collapse? | Increase the dosage of Corticosterods |
| What is SIADH (syndrome of inappropriate secretion of antiduretic hormone) | inappropriate and excessive secretion of ADH with subsequent water retension and dilutional hyponatremia. |
| What type of patients are prone to SIADH? | Head traumas, intracranial tumors, meningitis, pulmonary infections, & oat cell carcinomas |
| What antibiotic is used to treat SIADH | Demeclomycin (Declomycin) |
| What is the action of Demeclomycin | Promotes diuresis by antagonizing the effects of ADH on renal tubules. |
| What are the signs and synmptoms of SIADH? | Serum hypoosmality, HYPONATREMIA, most symptoms are associated with hyponatrmia |
| 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 |
| What speeds up inhaled anesthetics from alveoli to arterial blood? | low blood:gas partition coeffcient, low cardiac output, aveolar to venous partial pressure difference |
| What speeds up induction from arterial blood to brain? | Cerebral blood flow, arterial to venous pressure differnce, brain:blood partition coeffecient |
| 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 |
| Increase ventilation, like PI, promotes input of inhaled anesthetics to offst ________ into blood | uptake |
| The net effect of increasing anesthetic concentration is a more rapid increase in PA and thus and increase in the ___________? | induction of anethesia |
| The greater the alveolar ventilation to FRC, the more _______ the increase in PA toward PI | rapid |
| What is the ratio of aveloalar ventilation to FCR ratio in neonates | 5:1 |
| What is the ratio of aveolar ventilation to FCR in adults | 1:5 |
| Indiction of anesthesia is slower with what? | more soluble anesthetic gases. |
| What drug characteristics may effect speed of induction of inhalational agents? | potency/solubility, oil:gas partition coeffceient. |
| What effect does a high oil:gas partician coeffecient have? | low MAC or higher potency |
| What effect does a low oil:gas partition coeffecient have? | High MAC or low potency |
| 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 |
| What patient characteristics increase MAC? | Hyperthermia, Hypernatremia, Hyperthyroid, chronic ETOH abuse, |
| What drugs increase MAC? | Cocaine, MAOI, Ephedrine, Levadopa |
| What patient characteristics decrease MAC? | Hypothermia, hyponatremia, elderly, acute alcohol ingestion, postpartum, BP<40 cardio-pulmonary bypass, anemia, metabolic acidosis hypoxia, pregnancy, |
| What drugs decrease MAC? | Benzos, clonidine, A2agonist, lithium, lidocaine, neuraxial oopiods, |
| what drugs decrease MAC? | Ketamine, Chlorpromazine, Physostigmine, Pancurium, Verapamil, Tetrahydrocanbinol hydroxine |
| All inhalational agents are excreted where | Lungs |
| Nitrous Oxide is metablized where and how much? | Gi tract and .004% |
| Deslflurane is metabolized by what and how much | .02% from P450 |
| Isoflurane is metabolized how and how much | 2% from P450 |
| Sevoflurane is metabolized how and how much | 5% FROM P450 |
| 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. |
| In regards to volatile anesthetics which is the most soluble agent in use? | Isoflurane |
| What inhalational agent has the greatest analgesia and paralytic properties? | Nitrous Oxide |
| What is compound A? | Degredation product Sevoflurane and CO2 absorbers. |
| What risks are associated with Compound A | Neprotoxicity |
| What can be done to prevent formation of Compound A | Administer at least 2L of fresh gas flow to minimize formation of compound A |
| 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 |
| What can be done to avoid diffusion hypoxia? | Hyperventilate the patient with 100% O2 1-5 mins after turning off NO2. |
| 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 |
| What is the MAC, VP, b:g partition coeffecient of ISOFLURANE | MAC = 1.2 B:G = 1.46 oil:gas = 98 VP = 240 |
| What is the MAC, VP, B:G O:G partition coeffecient of SEVOFLURANE | MAC = 2 B:G = 0.69, O:G = 55 VP = 160 |
| 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 |
| What are the advantages of Isoflurane | safer for kidneys, does not cause seizures, decrease ICP, decrease CMRO2 requirements, decrease BP but not CO, |
| What are the disadvantages of Isoflurane | Profound ventilation depression, tachepnia, Increased heart rate. |
| 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 |
| What are the advantages of Deflurane? | very little metabolism, unlikely to form neoantigens, |
| What are the advantages of Sevoflurane? | has no preservatives, but less stable, Reasonble MAC, non-irritating to airways, does not change heart rate. |
| What are the disadvantages of Sevoflurane? | less stable, breaks down in presence of soda lime, nephrotoxic, produces compounds A-F |
| 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 |
| 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 |
| What are s&s of fluoride toxicity? | Polyuria, hyernatremia, hyperosmolarity, increased serum creatinine, inability to concentrate urine. |
| What agent is fluortoxcity associated with? | Methoxyflurane |
| Inorganic fluoride metabolite is _________? | nephrotixic |
| Currently used anesthetics have significantly less metabolism and are less soluble thus | decreasing the nephrotoxic effects |
| What triggers MH | Succinylchloine and volatile anesthetics |
| True or false; all volatiel anesthetics can trigger MH | true |
| What is the most potent trigger of MH | Halothane although it is no longer used in the states. |
| What is the weakest volatile aneshtetic that can trigger MH? | Nitrous Oxide |
Created by:
boharris6928
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