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Schedule I- high abuse potential, no accepted medical use, no prescription written, ex: Heroin, ghb, lsd
Schedule II- High abuse potential, accepted medical use, abuse may lead to dependence, most strict with DEA & physicians. ex: opioid, morphine, amphetamines
Schedule III- Lower abuse than 1 & 2, accepted medical use, may lead to moderate dependence, handwritten by physician, can be called in by physician only. ex: codeine, anabolic steroids
Schedule IV- lower abuse potential that III, accepted medical use, little dependence, signed by physicians. ex: benzodiazepines
Schedule V- Antitussive and antidiarrheals that contains small amounts of opioids, like Robitussin. lower abuse potential and very limited physical dependence.
"Half-life" determines drug dose interval NOT dose. If a drug's T1/2 is 3 hrs, you give pt this drug @0800, by 1100, 50% of this drug is gone due to metabolism and elimination process. To keep this drug at and above MEC level, you want to give another dose at least @ or before 1100. For a drug with long T1/2 , for instance 48 hrs, you give this drug @0800 Saturday, by 0800 Sunday, still more than 50% of this drug is available in patient's system. If you give this drug more than once a day (e.g., twice or three times a day), it could potentially cause overdose and adverse drug effects. Therefore, If a drug's half-life is >24 hours, it is not appropriate to give this medication more than once a day.
When patient is taking two highly protein-bond drugs, two drugs interact with each other by competing protein carriers. The effect of a highly protein-bound drug (A) will be increased when the second highly protein-bound drug (B) is given because drug B competes the protein carriers, force the drug A into unbound form or "free" form. The protein-bound drug is not active and has no drug effect; only "free" form drug (unbound drug) is active and has effect.
Scenario 1: Patient was taking drug A that is highly protein-bond, then the doctor prescribed drug B that is also highly protein-bond. Drug B competed and forced Drug A out of the protein carriers. In other words the new comer, drug B, freed drug A. I said in class: only free drug have active effect, protein-bond drug is inactive form. As a result , adding drug B increased drug A overall effect by releasing more protein-bond form of drug A into free form. Clinical implication: adding a second highly protein-bond drug could potentially lead to the risk of adverse effect caused by the highly protein-bond drug that the patient has been taking. Example: Patient is taking Coumadin, now the doctor prescribes Dilantin. Adding Dilantin could increase the risk of bleeding caused by increasingly available Coumadin freed by Dilantin.
Scenario 2: Patient was taking two highly protein-bond drugs: drug A and B. Now the doctor decided to discontinue Drug B due to medical necessity. Discontinuation of drug B made the protein carriers available for drug A. Free form of drug A that was working at action site quickly returned to blood stream to bind with those empty protein carriers. As a result, discontinuation of drug B reduced the overall effect of drug A by making more protein carriers available for drug A to be transferred into inactive form: protein-bond form. Clinical implication: Discontinuation of a highly protein-bond drug could potentially decrease the drug effect of another co-administered highly protein-bond drug by increasing its protein-bond form. Example: Patient is taking Coumadin and Dilantin, now the doctor discontinues Dilantin due to medical necessity. Discontinuation of Dilantin could reduce Coumadin's therapeutic effect, leading to the risk of blood clots.