Theophylline: mechanism of action, what is the achieve serum concentration at steady state?, adverse events (with the dose 5and toxicities 9), what type of inducers and metabolized what?
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This inhibition leads to an increase in intracellular cyclic adenosine monophosphate (cAMP) levels, which in turn causes bronchodilation, diuresis, and central nervous system (CNS) stimulation. It also has a weak antagonist effect at adenosine receptors. Show more…
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6. What reactions are involved in phase II drug metabolism? (3 marks) 7. Theophylline and aminophylline can be used to treat asthma. Unfortunately, these drugs have a narrow therapeutic index and plasma concentrations of these drugs must be monitored regularly. a.) Name 3 drugs when co-administered with theophylline that will cause theophylline to have a toxic effect. (3 marks) b.) How do these 3 drugs cause theophylline to become toxic? (2 marks) c.) Name 3 drugs when co-administered with theophylline that will lead to theophylline having a reduced therapeutic effect. (3 marks) d.) How do these 3 drugs cause theophylline to have no therapeutic effect? (2 marks)
Adi S.
1. Dopamine, epinephrine (or norepinephrine) and histamine are important neurotransmitter agonists. When these ligands interact with their cellular receptors, how do they mainly elicit their responses? Activate adenylyl cyclase directly, leading to increased intracellular cAMP levels Activate phospholipase C Induce or inhibit synthesis of ligand specific intracellular proteins Open or close ligand gated ion channels Regulate intracellular second messengers through G-protein-coupled receptors 2. A patient with chronic-stable angina is on prophylactic beta-blocker therapy, with sublingual nitroglycerin used PRN (as needed) for managing acute angina. One day he experiences particularly severe angina and takes the usually recommended dose of sublingual nitroglycerin (NTG). His discomfort is not reduced at all. Seeking relief, he repeats the usual recommended dose of NTG dose 6 times over a period of about 10 minutes, and now has taken far too much of the nitrovasodilator. An electrocardiogram taken by the paramedics, who were called for the patient’s emergency, shows changes consistent with myocardial ischemia. The patient incurs a massive infarction, goes into cardiac arrest, and cannot be resuscitated. Which of the following is the most likely cause of or contributing factor to the patient’s ultimately fatal response to the excessive dosage of NTG? Assume the patient was taking no other drugs except the NTG and a beta-blocker. A. Cyanide, or toxic metabolite of NTG, accumulated. B. NTG directly induced coronary vasoconstriction. C. NTG lowered arterial (coronary perfusion) pressure excessively D. Beta-blocker counteracted the effects of NTG and increased the risk of ischemia 3. A 65-year old man with heart failure is unable to climb a flight of stairs without experiencing dyspnea. After several years of therapy with carvedilol, captopril and furosemide, the therapeutic plan probably needs to change now. You empirically add digoxin to improve cardiac muscle contractility. Within 4 week he has a marked improvement in his symptoms. Which of the following best describes the main cellular action of digoxin that accounts for its ability to improve his cardiovascular function? A. Activates beta1-adrenergic receptors B. Facilitates GTP binding to specific proteins C. Increases mitochondrial calcium (Ca++) release D. Inhibits sarcolemmal Na/K-ATP-ase 4. A patient has frequent episodes of paroxysmal supraventricular tachycardia (PSVT). Which of the following drugs would be most suitable for outpatient prophylaxis of these events? A. Adenosine B. Lidocaine C. Nifedipine D. Verapamil
Sri K.
A patient receiving procainamide therapy for cardiac arrhythmia is given an IV loading dose resulting in a serum concentration of 6 µg/mL. The therapeutic range is 4-8 µg/mL and the half-life is 4 hours. Four hours after the initial loading dose, another equivalent dose is given as an IV bolus resulting in a serum concentration of 7.5 µg/mL. Does the serum concentration after the second dose seem appropriate? If not, what would be the predicted serum concentration at this time? What factors would influence the rate of elimination of this drug?
Madhur L.
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