ITE CA2 pharm 2 Flashcards
Meperidine’s beneficial effects which receptor
Meperidine’s beneficial effects are multimodal and center around the kappa opioid receptor.
opioid associated with increases in heart rate and why
Meperidine has structural similarities to atropine. Which is why meperidine is the only opioid associated with increases in heart rate following administration. Meperidine also has some weak local anesthetic effects.
mu receptor subclasses
The µ1 receptor produces the analgesic and physical dependence properties of most opioids
µ2 receptor results in respiratory depression, miosis, euphoria, decreased gastrointestinal motility, and physical dependence.
µ3 receptors are unknown but may mediate some anti-inflammatory activity.
kappa receptor
The κ receptor mediates analgesia but also dysphoria, sedation, miosis, and inhibits antidiuretic hormone release.
delta receptor
The δ receptor is responsible for analgesia, physical dependence, and perhaps antidepressant effects.
nalbuphine recetpors
Nalbuphine works as a kappa-agonist/mu-antagonist analgesic.
methadone
receptors
types of pain to use it for
important side effect
Methadone exerts significant effects on the mu opioid receptor.
Methadone also acts on the NMDA receptor as an antagonist. NMDA receptor antagonism explains methadone’s effect for neuropathic pain and in opioid tolerance. Furthermore, the NMDA antagonism and serotonin reuptake inhibition make methadone an effective choice for chronic neuropathic pain as well as modulation of some of the psychological concerns of patients living with chronic pain.
Methadone does prolong the QT interval and should be monitored.
morphine
- receptor
- metabolism
- active metabolite
Morphine has its main effect on the mu opioid receptor.
Morphine is metabolized by the liver to morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G). More morphine is metabolized to M3G than M6G.
However M6G is an active metabolite of morphine.
Remifentanil
- receptor
- metabolism
Remifentanil has its main effect upon the mu opioid receptor. Remifentanil is unique with a very short half-life which is not affected by the infusion time. Remifentanil is metabolized by nonspecific plasma and tissue esterases.
Mesna
Mesna is an antioxidant that prevents cyclophosphamide induced hemorrhagic cystitis.
Common Chemo-Toxicities: Cisplatin, Carboplatin: Vincristine: Bleomycin, Busulfan: Doxorubicin: Trastuzumab: Cyclophosphamide: 5-FU, 6-MP, methotrexate:
Common Chemo-Toxicities: Cisplatin, Carboplatin: acoustic nerve damage, nephrotoxicity Vincristine: peripheral neuropathy Bleomycin, Busulfan: pulmonary fibrosis Doxorubicin: cardiotoxicity Trastuzumab: cardiotoxicity Cyclophosphamide: hemorrhagic cystitis 5-FU, 6-MP, methotrexate: myelosuppression
Roc clearance
Approximately 25-30% of rocuronium is renally excreted. It is cleared primarily by hepatic uptake and hepatobiliary excretion.
More importantly, rocuronium is primarily excreted through the hepatobiliary system and prolonged paralysis can be seen in patients with cirrhosis and liver failure.
NMBs not affected by renal failure
Of the commonly used NMBs, only succinylcholine and cisatracurium have minimal renal excretion and predictable durations of action in patients with renal failure.
Renal disease effect of half life on
Roc
vec
panc
The half-lives of vecuronium and pancuronium are significantly prolonged due to the accumulation of active metabolites that are renally excreted. In fact, 80% of pancuronium is renally excreted unchanged in the urine. By contrast, the half-life of rocuronium is only slightly prolonged (1.2-1.6 hours in normal patients vs. 1.6-1.7 hours in patients with end stage renal disease) since there are no active metabolites
Metabolites and their effects
Meperidine
Morphine
How they’re excreted and why it matters
The active metabolite in meperidine, normeperidine, causes seizure activity.
Morphine’s primary active metabolite, M6G, has a 100-fold greater potency, but exhibits an equal or decreased affinity for μ-receptors compared to morphine. Accumulation of M6G can result in respiratory depression. Morphine’s inactive metabolite, M3G, may cause myoclonus and allodynia. As morphine and meperidine metabolites are typically excreted via the kidneys, their side effects are prolonged in the setting of renal failure. ≈
Barbiturates in renal failure
Barbiturates have decreased protein binding in renal failure which leads to higher concentrations of free active molecules.
Allodynia
feeling pain from stuff that shouldn’t cause pain
Mivacurium in renal failure
How is it metabolized
Mivacurium activity is also independent of renal dysfunction because it is hydrolyzed by pseudocholinesterase.
Propofol in renal failure
In general, propofol pharmacokinetics are similar between healthy patients and those with renal failure. Volume of distribution may be larger in uremic patients due to decreased albumin concentrations in that population. Total body clearance of propofol has been shown to be increased in uremic patients, which may seem counterintuitive. This is thought to be due to accelerated hepatic biotransformation in patients with renal failure. After a bolus dose of propofol, blood concentrations have been found to be lower between the 2-10 minute mark in renal failure patients.
2 categories of calcium channel blockers and 3 drugs in each
Dihydropyridine calcium channel blockers -Nifedipine -Nicardipine -Amlodipine Non-dihydropyridine calcium channel blockers: -Nimodipine -Diltiazem -Verapamil
Compare DHP CCB to non-DHP CCBs
Dihydropyridine CCB: decrease SVR
Non-DHP CCB: increased selectivity for myocardium, cardiac conduction system, coronary arteries; decreased platelet aggregation
Digoxin mechanism potentiated by results in what electrolyte change half life antidote
Decrase Na/K ATPase activity, leads to increased intracellular Na/Ca exchange leads to increased contractility
potentiated by hypokalemia, thiazide diuretics, amiodarone, decreased renal fxn
results in hypercalcemia
half life 40 hours
antidote: digibind
Cardiovascular effects of milrinone
The cardiovascular effects of milrinone can be summarized as: increased inotropy, increased lusitropy, increased ejection fraction, increased stroke volume, increased cardiac output, decreased afterload, decreased preload, pulmonary vasodilation, and systemic vasodilation.
TrueLearn Insight : Milrinone has been shown to improve mixed venous admixture through its reduction in myocardial oxygen consumption.
Since it does not act on the adrenergic alpha and beta receptors, milrinone has been proven effective as an inotrope in the setting of beta blockade and in the setting of beta receptor down-regulation (e.g. CHF). Milrinone is commonly used synergistically with adrenergic agents (e.g. epinephrine, norepinephrine). Milrinone is unique in its ability to increase cardiac index without increasing myocardial oxygen demand. It also improves myocardial relaxation (lusitropy) and augments coronary circulation.
milrinone MoA
Milrinone is a phosphodiesterase III (PDE3) inhibitor which increases inotropy. Both an arterial and venodilator.
Milrinone, therefore, increases cAMP levels which causes its inodilator properties.
Ketamine psychomimetic reactions decreased by
Ketamine is associated with a high incidence of psychomimetic reactions early in the recovery period. The incidence of these reactions can be decreased by coadministration of benzodiazepines, propofol, or barbiturates.
Etomidate
effects on cortisol
mechanism of effects on cortisol
Etomidate inhibits the synthesis of cortisol transiently in all patients and should be avoided in patients with adrenal insufficiency. Etomidate specifically inhibits 11β-hydroxylase and 17α-hydroxylase in the cortisol pathway in a reversible dose-dependent fashion.
Nicardipine metabolism and elimination
Nicardipine is metabolized by the liver and eliminated via gastrointestinal tract. Renal insufficiency has no effect on nicardipine use. Severe hepatic insufficiency results in significantly prolonged nicardipine half-life (normal half life is 60-100 min).
Nicardipine effects
coronary and peripheral arterial dilator.
Nicardipine (intravenous and oral) can cause an increase in heart rate in about 25% of the people. This tachycardia is NOT due to baroreceptor response, rather due to sympathetic activation. Nicardipine decreases systemic vascular resistance, but also increases cardiac contractility (C). The exact mechanism of this positive inotropic effect is unknown.
Nicardipine affected how by renal insufficiency effect on renal blood flow effect on GFR effect on renovascular resistance
Nicardipine dosage is not affected by renal insufficiency (D). The use of nicardipine increases both renal blood flow and glomerular filtration rate and also decreases renovascular resistance.
Metoclopramide
effects at what dosing
It is used perioperatively as an antiemetic. By promoting gastric emptying and increasing gastroesophageal sphincter tone, it may decrease the risk of pulmonary aspiration.
Per ASA guidelines, “Metoclopramide is a weak antiemetic and at a dose of 10 mg is not effective in reducing the incidence of nausea and vomiting.”
Higher doses (25-50 mg) may be necessary to have discernible benefit, but carry the risk of more side effects such as extrapyramidal symptoms. Metoclopramide has little effect on gastric acidity
Metoclopramide and succinylcholine interaction
Metoclopramide inhibits plasma cholinesterase and can increase the duration of action of succinylcholine
half life of
flumazenil
midazolam
The duration of action of midazolam (half-life 1.7-2.6 hours) exceeds that of flumazenil (half-life 0.7-1.3 hours).
This makes recrudescence of benzodiazepine-induced somnolence after metabolism of flumazenil likely in this context.
what reversal agent can cause pulm edema
naloxone with large bolus doses
Milrinone metab/excretion?
Milrinone is excreted via the kidneys in its unconjugated form and therefore dosage should be adjusted in the setting of renal failure.
MIlrinone side effects
Common side effects of milrinone include tachycardia and hypotension. Thrombocytopenia was a clinical concern with the use of amrinone (renamed inamrinone) but is not significant with milrinone use after 48 hours of infusion. Higher doses of milrinone have been associated with atrial fibrillation.
Hepatopulmonary syndrome
- definition
- etiology
- how diagnose
- treatment
Hepatopulmonary syndrome is the triad of intrapulmonary vascular dilatations IPVDs, increased A-a gradient, and hepatic failure. Excessive levels of circulating NO result in significant ventilation-perfusion mismatching. A positive contrast-enhanced echocardiography (CEE) supports the diagnosis in a patient without underlying cardiopulmonary disease. Liver transplantation is the only definitive treatment and complete resolution of abnormal gas exchange may take up to a year following transplantation.
Hypoxia is improved when the patient lies flat (platypnea) and is worsened when the patient stands (orthodeoxia). The intrapulmonary vascular dilations cause increased perfusion relative to ventilation. Standing further worsens this ventilation-perfusion mismatch since gravity causes increased perfusion and pooling in the less-ventilated lower lung segments.
Common side effects of ondansetron include
Common side effects of ondansetron include QTc prolongation (20%, very rarely clinically significant), headache (11%), transient AST/ALT increases (5%), constipation (4%), rash (1%), flushing/warmth (< 1%), and dizziness (< 1%).
Intravenous administration of etomidate is associated with
Intravenous administration of etomidate is associated with pain on injection, postoperative nausea and vomiting, and superficial thrombophlebitis. Ways to prevent thrombophlebitis are to use larger veins, increasing the speed of injection, and pretreatment with lidocaine. Treatment options are controversial but include the use of NSAIDS and elastic stockings.
PGE1
uses
side effects
PGE1 is used to maintain patency or reopen the ductus arteriosus in “ductal dependent lesions” to improve blood flow to the lungs or systemic circulation depending on the nature of the congenital lesion. Side effects include apnea, hypotension, fevers, and CNS irritability.
Dexmedetomidine metabolism and excretion
Dexmedetomidine is extensively metabolized in the liver before being excreted in urine and feces.
Dexmedetomidine MoA and effects
Dexmedetomidine is a selective α2-adrenergic agonist (α2:α1 = 1600:1) that causes inhibition of presynaptic norepinephrine release from peripheral and central nervous system neurons (particularly those in the spinal cord and locus ceruleus in the brainstem). This results in analgesia, anxiolysis, sedation, and sympatholysis.
Dexmedetomidine
how many compartment model
context sensitive half time range
affected by renal failure?
Dexmedetomidine is rapidly distributed following intravenous administration and exhibits nonlinear three-compartment model pharmacokinetics. The three-compartment model consists of a central compartment and two peripheral compartments, one of which is a rapidly equilibrating compartment while the other is a slowly equilibrating compartment.
This pharmacokinetic model explains dexmedetomidine’s wide context-sensitive half-time range: four minutes after a 10-minute infusion versus four hours after an 8-hour infusion.
Interestingly, dexmedetomidine’s pharmacokinetics are not significantly affected by patient age, weight, or the presence of renal failure.
Upon which site does gabapentin most likely have its effect in treating chronic neuropathic pain conditions
Gabapentin is an anticonvulsant effective in several neuropathic pain conditions including post-herpetic neuralgia and painful diabetic neuropathy. Gabapentin has efficacy at the α2-delta subunit of calcium channels.
Site of action for these meds: lamotrigine topiramate carbamazepine levetiracetam drug class
lamotrigine: Ca channels
topiramate: GABAa, T-type Ca channels, glutamate receptors
carbamazepine: voltage-dependent sodium channels
levetiracetam: preseynaptic calcium channel glycoprotein SV2A
anti-convulsants
Medications that most commonly cause drug fever include
and what is the treatment
Medications that most commonly cause drug fever include amphotericin, cephalosporins, penicillins, phenytoin, procainamide, and quinidine. Other medications known to cause drug fever include cimetidine, carbamazepine, hydralazine, rifampin, streptokinase, and vancomycin.
Treatment involves stopping an offending medication and is otherwise supportive.
How does hydrocortisone assist with septic shock
Hydrocortisone inhibits nitric oxide synthesis.
NSAIDs
MoA
Maximum analgesic effect?
NSAIDs are COX inhibitors that can be used as an effective mode of therapy for postoperative and chronic pain. They exhibit a “ceiling effect” meaning they are ineffective beyond a certain dose; unlike pure opioids agonists.
NSAIDs lead to a decrease in the production of prostaglandins. Prostaglandin E2 is the key mediator of both peripheral and central pain sensitization.
Cox 1 vs cox 2
COX-1 is the constitutive enzyme that produces prostaglandins, which are important for general “house-keeping” functions such as gastric protection and hemostasis. COX-2, on the other hand, is the inducible form of the enzyme that produces prostaglandins that mediate pain, inflammation, fever, and carcinogenesis.
NSAIDs in spine surgery
Both COX-1 and COX-2 play significant roles in bone fusion following fracture, and the use of the traditional NSAIDs has been found to inhibit the healing process, particularly following lumbar spinal fusion surgery
Cardiovascular medications that can be given intramuscularly include, but are not limited to:
Cardiovascular medications that can be given intramuscularly include, but are not limited to: atropine, glycopyrrolate, ephedrine, epinephrine, phenylephrine, and hydralazine.
Dexmedetomidine hemodynamic effects as bolus and infusion on
BP
CO
HR
Dexmedetomidine has varying hemodynamic effects depending on whether it is given as a bolus or as an infusion. A bolus can produce transient hypertension while an infusion may cause a slight decrease in pressure that returns to baseline as the infusion continues. Cardiac output and heart rate decrease to varying degrees with bolus and infusion dosing.
Why biphasic response precedex
The biphasic response occurs because alpha-2 receptors are located in two locations producing different responses. Initially, dexmedetomidine acts on peripheral alpha-2 receptors and causes vasoconstriction in the peripheral vasculature. Subsequently, the centrally located alpha-2 receptors are stimulated. The central receptors reduce the sympathetic tone and increase the parasympathetic outflow. It also acts to reset the baroreceptor system to a lower set blood pressure.
_____ is a neurotoxin that potently inhibits acetylcholinesterase, causing continual transmission of nerve impulses and inability to control respiratory muscles
Sarin
_____ inhibits fast sodium currents in myocytes, thus preventing contraction of respiratory muscles.
Tetrodotoxin
buprenorphine
Buprenorphine is a partial mu agonist. Its maximum opioid effects are less than those of full agonists.
standard initial therapy for tricyclic antidepressent (TCA) toxicity
sodium bicarb
EKG changes with methadone
QT prolongation; dose dependent especially greater than 120 mg/day,
Common medications that can lead to hyperkalemia and QRS widening include
Common medications that can lead to hyperkalemia and QRS widening include angiotensin converting enzyme inhibitors, angiotensin receptor blocking medications, potassium sparing diuretics, tacrolimus, succinylcholine, heparin, and certain antifungals.
Prolongation of the PR interval can be seen with
Prolongation of the PR interval can be seen with digitalis toxicity, and can increase to the point of first-degree atrioventricular block (C). This can also occur with high doses of beta antagonists and non-dihydropyridine calcium channel blocking medications.
Shortening of the PR interval
Shortening of the PR interval can occur when accessory tracts are present that allow atrial depolarization to reach the ventricles by means other than the atrioventricular node (D). The most common of these include Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL) syndromes.
Methadone additional MOA
Methadone has NMDA antagonistic properties in addition to opioid receptor agonism.
Effect on hepatic artery flow: angiotensin II Sevoflurane Glucagon Vasopressin
angiotensin II - decreases
Sevoflurane - decreases
Glucagon - increases
Vasopressin - decreases
Immediate temporizing therapy of clinically significant hypercalcemia includes
Immediate temporizing therapy of clinically significant hypercalcemia includes volume replacement with normal saline and loop diuretics.
phentolamine
alpha blocker
Effect of age on neuromuscular blocking drugs
how change induction dose
No change in the initial dose of a neuromuscular blocking agent is required for geriatric patients when compared to young adults. The effects of aging on neuromuscular blocking agents include: delayed onset of action, reduced requirements for maintenance dosing, and prolonged duration of action.
Mechanisms of action of medications for aspiration prophylaxis:
Metoclopramide
H2 antagonists
Sodium citrate
Mechanisms of action of medications for aspiration prophylaxis:
Metoclopramide - increases LES tone and gastric emptying.
Ranitidine and other H2 antagonists - decreases both the amount and acidity of gastric secretions.
Sodium citrate - decreases the acidity of gastric contents.
NMDA receptor: type of receptor function activated by mediated by
The NMDA receptor is an inotropic glutamate receptor that
functions as a nonspecific ion channel when activated.
Activation only occurs when glutamate is bound to the receptor AND the cell is depolarized.
The receptor’s effects are primarily mediated via increased intracellular calcium.
Terbutaline
drug class
use
side effects
beta agonist (greater affinity for beta 2 than 1)
tocolytic
tachycardia, hypokalemia, hyperglycemia
lipophillic opioids
difference
fentanyl, alfentanil, sufentanil, remifentanil
lipophilic opioids rapidly cross the blood-brain barrier, producing more rapid analgesia effects compared to less lipophilic opioids such as morphine.
Lipophilic opioids are also cleared from the CNS more rapidly, explaining why fentanyl is cleared from the CNS faster than morphine
morphine
plasma half-life
analgesic action
half life 2 hours
analgesic action 4-5 hours
______ is the current gold standard for perioperative DVT and PE chemoprophylaxis due to its ability to decrease the incidence of venous thromboembolism while only minimally increasing the risk for major surgical bleeding.
Low molecular weight heparin (LMWH) is the current gold standard for perioperative DVT and PE chemoprophylaxis due to its ability to decrease the incidence of venous thromboembolism while only minimally increasing the risk for major surgical bleeding.
relative contraindications to beta blockers (if something else is available)
severe COPD and diabetes mellitus are relative contraindications to the use of beta-blockers
Labetalol receptor actions
β1 antagonist, partial β2 agonist, and an α1-receptor antagonist
Etomidate MoA
Etomidate exerts its clinical effect at the GABAA receptor by binding to specific sites on the receptor which enhances the affinity for GABA binding. Etomidate only directly activates the receptor at supra-clinical doses
Etomidate clearance
Etomidate is highly protein bound (~75%) and metabolized by liver ester hydrolysis to inactive metabolites that are primarily excreted by the kidneys
Name 3 potassium sparing duretics
A mnemonic for the potassium-sparing diuretics is: “The K+ STAys,” for Spironolactone, Triamterene, and Amiloride.
Thiazide diuretics metabolic derrangements
electrolyte abnormalities observed with thiazide diuretics include hypercalcemia, hyponatremia, hypokalemia, and hyperuricemia.
loop diuretics metabolic derrangements
Hypokalemia and hyponatremia can be observed after administration of loop diuretics such as furosemide and bumetanide
When avoid which uterotonics
Carboprost should be avoided in patients with a history of asthma and methylergonovine should be avoided in patients with hypertension or preeclampsia.
Sacubitril
Sacubitril is an antihypertensive drug that acts by inhibiting the enzyme neprilysin (the enzyme that breaks down ANP and BNP). It is currently available as a combination with valsartan. No specific guidelines are available relative to stopping or continuing sacubitril during the perioperative period.
Initial treatment for hypercalcemia
Initial treatment for hypercalcemia should be aimed at volume correction. With restoration of the patient’s fluid deficit furosemide can be used to decrease calcium levels.
Bisphosphonates are considered part of first-line therapy, however since they do not acutely decrease calcium levels they are not first choice for acute hypercalcemia.
Calcitonin is considered second-line therapy for hypercalcemia. Calcitonin takes 24-48 hours to work and 25% of patients may not have a response. Natural calcitonin is made by C-cell in the thyroid. Calcitonin antagonizes the effects of parathyroid stimulating hormone (PTH).
droperidol problems
extrapyramidal symptoms
QT prolongation
The maximum recommended dose of lidocaine that may be injected during tumescent liposuction is
The maximum recommended dose of lidocaine that may be injected during tumescent liposuction is 55 mg/kg.
The maximum recommended dose of epinephrine during tumescent liposuction is
The maximum recommended dose of epinephrine is 0.055 mg/kg (1:1,000,000 concentration).
For each day after interruption of any irreversible antiplatelet agent (aspirin, clopidogrel), approximately 10% to 14% of normal platelet function is restored thus it can take 7 to 10 days for an entire platelet pool to be replenished which irreversibly inhibits platelet function.
For each day after interruption of any agent, approximately 10% to 14% of normal platelet function is restored thus it can take 7 to 10 days for an entire platelet pool to be replenished which irreversibly inhibits platelet function.
Scopolamine MoA timing common side effects contraindications
Scopolamine is an antimuscarinic drug that, when applied as a transdermal patch, can help prevent or treat PONV for up to 72 hours. The patch should be applied at least four hours prior to the need for its antiemetic action (peak 24 hours). The patch should never be cut or otherwise damaged as this can alter drug delivery. Common side effects include blurred vision, dry mouth, and agitation. Scopolamine is relatively contraindicated in patients with glaucoma since the drug’s mydriatic and cycloplegic effects can raise IOP.
CNS depression secondary to anticholinergic medication can be reversed by
CNS depression secondary to anticholinergic medication can be reversed by physostigmine, an anticholinesterase that crosses the blood-brain barrier.
Pyridostigmine mnemonic: pyramids are large, large things cannot cross the blood-brain barrier.
(alternatively) pyramid base has 4 edges/corners, quaternary structures do not cross the blood-brain barrier.
dexmedetomidine excretion
Dexmedetomidine undergoes almost complete biotransformation in the liver through the cytochrome P450 system with very little excretion of unchanged medication. Approximately 95% of the metabolites are excreted in the urine although there is little known about the activity of the metabolites. Because of this, patients with hepatic failure may need a decreased dose and patients with renal failure may have an accumulation of metabolites with larger doses and prolonged infusion.
chloroprocaine metabolism
Chloroprocaine is rapidly metabolized by plasma cholinesterase (half-life in the plasma is about 20 seconds), therefore leaving very little drug available to cross the placenta.
Local anesthetics site and mechanism of action
Local anesthetics facilitate peripheral nervous blockade by reversibly binding to the intracellular portion of the voltage-gated sodium channels.
side effects of NSAIDs in elderly
In elderly patients, 10-20% will experience dyspepsia with NSAID use. There is an increased risk of atrial fibrillation, development of congestive heart failure, renal toxicity, and gastrointestinal bleeding. However, these risks are lower than that of dyspepsia.
3 mechanisms for nitroprusside toxicity
Nitroprusside is metabolized to cyanide ions and toxicity can occur following lengthy infusions. The three major mechanisms for nitroprusside toxicity are
1) Cyanide ions bind to cytochrome c oxidase and inhibit cellular aerobic respiration.
2) Formation of cyanmethemoglobin which is unable to carry oxygen.
3) Thiocyanate production which causes CNS-related effects.
CYP3A4 inhibitors
Patients taking CYP3A4 inhibitors may be at increased risk for lidocaine toxicity. A few examples include: grapefruit juice, verapamil, diltiazem, amiodarone, and omeprazole.
Pancuronium elimination
Pancuronium should be avoided in renal disease. Pancuronium elimination occurs by kidneys at approximately 80%.
Vecuronium elimination
Vecuronium and rocuronium are primarily biliary excreted with about 20% renal elimination.
Mivacurium elimination
Mivacurium is degraded by plasma cholinesterases, and therefore not affected by renal failure.
Best meds to relieve opioid-induced biliary colic
Atropine, papaverine, and naloxone can relieve opioid-induced biliary colic.
Misoprostol
Misoprostol is a commonly used synthetic analog of prostaglandin E1 which causes cervical ripening and increases in uterine tone. It may be administered by oral, sublingual, buccal, vaginal, or rectal routes. Uterine rupture is a possible side effect when misoprostol is used for induction of labor in patients with a history of cesarean section. Other uncommon side effects include diarrhea, nausea, and vomiting.
magnesium effect on BP and mechanism
Vasodilation occurs with magnesium therapy and causes a decrease in blood pressure and in some cases hypotension.
Vasodilation occurs by calcium antagonism in vascular smooth muscle and by increased production of nitric oxide and prostacyclin I2.
Sugammadex is a synthetic, modified γ-_______
Sugammadex is a synthetic, modified γ-cyclodextrin (an 8-glucose ring). Accordingly, a patient with hypersensitivity to cyclodextrins is at significantly increased risk for an anaphylactic reaction to sugammadex and its use is contraindicated.
Sugammadex is physically incompatible with ___
Sugammadex is physically incompatible with ondansetron, ranitidine, and verapamil and should not be co-administered with these medications. If sugammadex and one of the above drugs are to be administered in the same line, the line should be adequately flushed with saline between administration of the two drugs.
