Intravenous Medications and Adjuncts Flashcards Preview

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Flashcards in Intravenous Medications and Adjuncts Deck (48):

What is the treatment of malignant hyperthermia?

Dantrolene- developed as a muscle relaxant initially for the treatment of chronic spasticity.

Dantrolene blocks muscle spasm and thus heat production by preventing calcium release from the sarcoplasmic reticulum.


T or F: dantrolene must be reconstituted in 60 mL of normal saline.



T or F: pH of dantrolene is high (it is basic)



T or F: reconstituted dantrolene contains 3 gm of mannitol and brisk diuresis is likely to occur.



What is the half-life of dantrolene?

12 hours


T or F: once pt stabilized, dantrolene infusion must continue for 24 hours in ICU



T or F: dantrolene is metabolized in the liver.



T or F: alcohol-dependent patients will show cross-tolerance to barbiturates and benzos but not to opioids.



T of R: droperidol is a dopamine antagonist neuroleptic agent with antipsychotic and antiemetic action.

True- used for the treatment of PONV, duration of action does not correspond well with elimination half-life becasue its dissociation from the dopamine receptor site is slow.


By what mechanism of action does dexmedetomidine work?

An alpha-2 adrenergic agonist.

Similar to clonidine, dexmedetomidine has anxiolytic, sedative, and analgesic effects but has 8x higher affinity for the alpha-2 receptor.


T or F: Dexmedetomidine is water soluble. How is dexmedetomidine metabolized? Excreted?

True. It is metabolized in the liver, and the metabolites are excreted via the kidney.


T or F: when dexmedetomidine is abruptly discontinued after infusions of more than 24 hours, withdrawal symptoms may occur, including agitation, tachycardia, and hypertension.



T or F: a transient phase of hypertension after the loading dose may be induced by the binding of dexmedetomidine to vascular alpha-2 receptors and seldom requires action.

True- a large bolus has been reported to cause vasoconstriction and hypertension, followed by progressive hypotension. Whether the patient develops hypertension or hypotension depends on the patient's ability to mount a sympathetic response.

Dexmedetomidine is an alpha-2 agonist that binds to receptors in the locus ceruleus and spinal cord.


T or F: dexmedetomidine is associated with reduced opioid and hypnotic agent requirements around anesthesia, without producing significant respiratory depression. Added benefits include short duration, lack of effect on gut motility, and absence of active metabolites. May have renoprotective effect and blunts postoperative catecholamine surge. May induce significant bradycardia (seen in patients with hypovolemia).

True- a bolus dose of 2 mcg/kg has resulted in profound sinus bradycardia and even sinus arrest. This can be treated effectively with administration of anticholinergics such as glycopyrrolate or atropine.


T or F: tylenol has analgesic and anti-pyretic effects but minimal anti-inflammatory action.



T or F: tylenol has virtually no antiplatelet or GI effects.



T or F: hepatotoxicity from Tylenol occurs as a result of an accumulation of the toxic metabolite NAPQI, which ordinarily reacts with glutathione resulting in conjugates that can be renally excreted. When large amounts of Tylenol are ingested, glutathione becomes depeted and NAPQI accumulates, leading to hepatoxicity and hepatic necrosis.

IV acetylcysteine is the treatment of acetaminophen overdose.

When Tylenol is taken in large quantities, a minor metabolite called NAPQI accumulates. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to inactivate the toxic NAPQI. NAPQI then reacts with key hepatic enzymes, damaging hepatocytes, and leading to severe liver damage and even death by fulminant liver failure.

Acetylcysteine augments the glutathione reserves in the body and, together with glutathione, directly bind to toxic metabolites. These actions protect hepatocytes from NAPQI toxicity.


T or F: ketorolac is an NSAID drug that is metabolized in the liver and excreted by the kidneys. Adverse effects include GI irritation, ulceration, bleeding. Effects on platelets is reversible. What is the half-life?

True- Half life is 5 hours


T or F: Patients with asthma and chronic rhinitis are at increased risk of developing bronchospasm when given NSAIDs, particularly aspirin. Ketorolac should be withheld from patients with a history of NSAID-induced bronchospasm.



T or F: onset of anticoagulation of heparin is established immediately after IV administration.



T of F: heparin is eliminated via kidneys and hepatic metabolism. Monitoring of heparin should be via ACT. HIT is seen after repeated administration.



What agent can be administered for the immediate reversal of heparin? What is the ratio of this agent to heparin?

Protamine- 1 mg of protamine inactivates 100 units of heparin.


What are adverse effects associated with the administration of protamine?

noncardiogenic pulmonary edema
pulmonary vasoconstriction
right heart decompensation
cardiovascular collapse
hypersensitivity reaction
causes direct histamine release


What is the mechanism of action of aspirin?

Irreversible inhibition of the production of thromboxane A2, which is an important factor involved in platelet aggregation and activation.


How long do the effects of aspirin last?

7-10 days


How many days before surgery should Plavix be discontinued?

7 days prior to surgery


What is the duration of cocaine intoxication if administered via a) IV and smoking, b) snorting, and c) oral ingestion?

15-30 minutes after IV injection and smoking
+/- 1 hour after snorting
3 hours after oral ingestion


What is the mechanism of action of cocaine?

Cocaine's sympathicomimetic and vasoconstrictive properties are caused by presynaptic reuptake blockade of serotonin and catecholamines and peripheral alpha-adrenergic agonistic activity.

Cocaine is also a sodium channel blocker, which in severe overdoses may lead to QRS-complex prolongation and negative inotropy.


T or F: Naloxone, succinylcholine, and beta blockers are contraindicated during cocaine intoxication. How does one manage cocaine intoxication therapy?

True- Supportive care, oxygen, benzodiazepines, and phentolamine are cornerstones of acute cocaine intoxication therapy.


T or F: furosemide inhibits the Na/K/2Cl co-transporter in the loop of Henle, resulting in diuresis with loss of Na, K, Ca, and Mg.



T or F: IV furosemide may elicit prerenal kidney failure in patients with pre-existing kidney disease.



T or F: ototoxicity is seen at high doses of furosemide or with rapid administration, expecially when combined with aminoglycosides or in patients with kidney failure.



Volatile anesthetic and chemotherapy contraindications:

Cyclophosphamide- halothane --> inhibits plasma cholinesterase, prolonging duration of action of Sch
Doxorubicin- cardiomyopathy
Methotrexate- nitrous oxide --> severe bone marrow suppression and mucositis



T or F: metoclopramide has significant adverse effects, including sedation, extrapyrimidal symptoms, and tardive dyskinesia.



T of F: metoclopramide is contraindicated in patients using levodopa and patients with epilepsy or pheochromocytoma. Reglan is not effective in paralytic ileus.



T of F: reglan is eliminated renally.



T or F: ketamine, in contrast to most other anesthetic drugs, is associated with a disorganized EEG pattern that is variable in all doses.



T or F: electrocortical silence, or an isoelectric state, cannot occur with anesthetic doses of ketamine, even in patients who are deeply anesthetized.

True- in fact, ketamine is associated with increased epileptiform activity.


T or F: opioids in general will cause a dose-related decrease in the frequency and an increase in the amplitude of the EEG waves.



T or F: Neuromuscular blockers can lower the processed EEG values.



T or F: barbiturates have been shown to lower ICP by inducing a dose-dependent reduction in CBF and CMRO2.

T- large doses of barbiturates casue the EEG to become isoelectric and the CMRO2 to be reduced by 45%.


T or F: flumazenil is a competitive benzodiazepine antagonist that has high affinity and great specificyt for the benzodiazepine receptor.

T- has minimal intrinsic effect. Onset of action is 3 min and is cleared rapidly, more rapidly than all the benzos, so it is possible that resedation may occur.


T or F: flumazenil reverse the hypnotic and respiratory effects of benzos more than the amnestic effects. HAs no negative side effects on the cardiovascular system.



T or F: dexmedetomidine decreases both CBF and CMR. This may be beneficial for patients with ischemic neurological injury.



When barbiturates are injected into the radial artery, what is the treatment?

The risk is prolonged vasoconstriction leading to gangrene. Treatment is stellate ganglion block.


T or F: ketamine increases ICP, CMRO2, and CBF.

True- contraindicated in patients with already increased ICP


T or F: metoclopramide can cause increased prolactin levels.

True- thus it must be avoided in patients in assisted reproductive therapy. Droperidol also causes increased prolactin levels.


T or F: phenobarbital, primidone, phenytoin, and carbamazepine are potent hepatic enzyme inducers.

True- the most noticeable effect is the short duration of clinical effect with aminosteroid neuromuscular blocking agents.