Red Q Flashcards
Is theophylline a good choice of medication for asthmatic patients who experience seizures and insomnia?
No, it will likely lower seizure threshold and worsen insomnia
Theophylline has side effects including SNS activation, CNS activation, and cardiac stimulation, narrow therapeutic index, CYP issues, interactions with other drugs
Why are oral, long-acting beta2 receptor agonists (LABA) ineffective in treating ongoing, acute attacks of asthma?
1) oral would not work bc it needs to bind near those specific bronchial receptors, all b2 receptors, take too long to be effective
as a resp drug:
Salmeterol’s long, lipophilic side chain binds to plasma membrane lipids near bronchiolar beta(2)-receptors on smooth muscle, allowing the active site of the molecule to remain at the receptor site, continually binding and releasing. Beta(2)- receptor activation in the lung causes relaxation of bronchial smooth muscle, bronchodilation, and increased respiratory airflow.
Salmeterol’s long, lipophilic side chain binds to plasma membrane lipids near bronchiolar beta(2)-receptors
What are the drug treatment strategies for patients with stable COPD and an FEV1 value less than 70%?
Bronchodilators; both beta2 agonists and anticholinergics like ipratropium or tiotropium
Steroids are not first-line treatment unless there is a persistent asthma component
How does cimetidine increase the toxic side effects of many drugs?
Cimetidine is a potent CYP inhibitor, decreasing metabolism and increasing plasma levels of certain drugs
including warfarin, tricyclic antidepressants, lidocaine, calcium channel blockers, quinidine, oral sulfonylureas, phenytoin, theophylline, benzodiazepines, and beta-blockers (metoprolol and propranolol)
Why should bone density be monitored in patients taking proton pump inhibitors?
PPIs decrease HCl secretion, which can reduce calcium absorption and increase the risk of osteoporotic fractures
This is particularly important in patients at risk for osteoporosis
Why is acetaminophen not classified as an NSAID despite having a similar mechanism of action as aspirin?
Acetaminophen does not have anti-inflammatory properties and lacks the antiplatelet effect of aspirin
safe for gi bleeds and renal pts
Unlike NSAIDs, acetaminophen does not inhibit COX-1 and COX-2 in peripheral tissues, where inflammation occurs. It is a poor inhibitor in environments with high peroxide concentrations, which are present at inflammation sites. Its effects are more CNS-focused, affecting pain perception rather than peripheral inflammatory processes.”
True or False: Enteric coated ASA provides excellent protection against risks for GI bleeding.
somewhat true: The coating blocks the breakdown in a high acid environment. Does not break down until entering the duodenum where the environment is less acidic. So if your risk of GI bleed is only in the stomach, you can potentially get away with it, but usually if you have gastric ulcers, you probably have issues with your duodenum as well.
What should be done when glucocorticoid side effects appear?
When glucocorticoid side effects occur, it is not good medical practice to immediately withdraw treatment. Steroids need to be weaned d/t negative feedback loop to the hypothalamus that is created when administering exogenous steroids. They trigger the hypothalamus to decrease release of Corticotropin releasing hormone, decreasing release of ACTH by the ant. Pit. and thus decrease of steroids by the adrenal cortex. HPA axis gets suppressed.
How does the combined use of a δ-receptor antagonist and a μ-receptor agonist help with opioid tolerance?
The long-term treatment of pain associated with cancer is compromised by the development of tolerance to opioid medications.
Blocking the δ-receptor with an antagonist prevents tolerance while allowing analgesia from the μ-receptor agonist
This method can still produce side effects
How do NSAIDs alter the compensatory response of renal hypoxia?
Aspirin/NSAIDS can induce renal impairment, esp old peop. Renal hypoxia triggers the localized production of prostaglandins that induces renal vasodilation.
NSAIDs through the COX pathway decrease prostaglandins, so if you decr prostaglandins, you’re going to have a reduction in the ability for your nephron vasculature to vasodilate and bring more oxygen and nutrients to the kidney –> more kidney impairment
Remifentanil, another synthetic opioid receptor agonist, is commonly used in anesthesia practice. How does the unique mode of metabolism of this medication (as compared to other opioids) allow it to be used to precisely match its dose with the time frame of its desired clinical effects?
Remifentanil is considered a metabolic soft drug, one that is rapidly metabolized to an inactive form. Unlike other synthetic opioids which are hepatically metabolized, remifentanil has an ester linkage which undergoes rapid hydrolysis by non-specific tissue and plasma esterases. This means that accumulation does not occur with remifentanil and its context-sensitive half-life remains at 4 minutes after a 4-hour infusion.
Its context-sensitive half-life remains at 4 minutes after a 4-hour infusion
What medications are combined with hydrocodone in Vicodin?
Hydrocodone is one of the most widely prescribed drugs on the market and yet when given for the relief of pain its dose and the potential for addiction can be reduced when given in combination with other medications.
Acetaminophen + hydromorphone
This combination reduces the dose of hydrocodone and potential for addiction
Why is immediate-release opioid therapy recommended over extended-release for chronic pain?
ER formulations are more attractive for abuse due to higher concentrations and faster onset when manipulated. When ER formulations are crushed and then injected IV, not only is there a more rapid onset of action (a shorter Tmax) and higher Cmax (“dump” effect); there is also greater euphoria, an effect
that abusers desire.
Immediate-release formulations are safer and less likely to be abused
Q: A loss of libido in males and the development of amenorrhea and anovulation in females can become side-effects of opioid therapy. What is the mechanisms for these changes?
Opioids may decrease sexual function because they affect hormones in the hypothalamic-pituitary-gonadal pathways. These control the production of sex hormones by secreting gonadotropin-releasing hormone (GnRH). Opioids inhibit GnRH, leading to a decrease in the production of luteinizing hormone.
