Health 2 days ago A full and comprehensive drug classifications chart is available per the DEA in part of the Title 21 Code of Federal Regulations, 3 but the chart below is a list of some of the most commonly abused substances and their current scheduling.
Legal Drug Classifications Chart. Health 5 days ago Our templates are of high quality, free of charge, and provide an accurate type of document for you to be able to properly document your medication intake. Through a series of eye catching charts , the 5th edition of Pharmacological Classification of Drugs, with Doses and Preparations presents a systematized and updated listing of easy to remember drug classifications , which are also therapeutically meaningful.
Drugs are also classified by their chemical makeup and the way they interact with the brain and body. Some common classifications include: Depressants.
The two-digit categories are the major class and comprise subcategories e. Health 7 days ago 1. Its fundamental purpose is to provide a regulatory framework which controls the availability of, …. Drug classes that are defined by common modes of action i. Schedule III. Among the substances so classified by the Drug Enforcement Agency are glutethimide and various analgesic compounds containing codeine.
The Prescription Drug List is a list of medicinal ingredients that when found in a drug, require a prescription. It does not include medicinal ingredients that when found in a drug, require a prescription if those ingredients are listed in Controlled Drugs and Substances Act Schedules.
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Scheduling and Drug Classification Charts Nova Recovery Health 2 days ago A full and comprehensive drug classifications chart is available per the DEA in part of the Title 21 Code of Federal Regulations, 3 but the chart below is a list of some of the most commonly abused substances and their current scheduling.
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Category: Pharmacy , Hospital Detail Drugs. Units of measure and conversions 2. Ratio, proportions and percent strength 3. Stock solutions and alligation 4. Clinical-based calculations 5. The RXinsider review programs are designed to …. Trauma Score. Health 7 days ago their prescriptions at the pharmacy. Formulary Files Formulary files are the lists that are referenced by the EHR based on the identifiers returned by the PBM with a prescription eligibility response message.
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Health 3 days ago 1 Log in to the Providence Internal Career section. The body develops antibodies to HIV. This is called seroconversion , and it's what the poor patient above was going through for 2 or 3 weeks feeling like he had the flu.
Then it enters a "clinical latency" phase that can last for years. Meanwhile, the number of HIV copies in the body is steadily increasing. On a graph, it looks like this:. Eventually, CD4 counts get so low that "weird diseases that don't infect healthy people" start showing up. Untreated, HIV is indeed a death sentence It's normally a respiratory infection or similar that technically ends up "killing" the patient. We'll go into more specifics of the virus life cycle when we talk about the actual treatments for HIV.
That way we can see what each drug class does to affect each stage of viral replication. But, we'd be remiss to not mention this one bit about retroviruses in general. It's also extremely error prone. It's like that friend you have that never has her shit together.
She's always late. She's forgets to bring her pencil to class. She locks her keys inside her car. She's clutzy. She just spilled coffee on herself again. That's what reverse transcriptase is. Like your friend, reverse transcriptase means well. But inevitably it always makes a mistake. Because a virus that mutates all the damn time is a pain in the ass to treat. It quickly gains resistance to a given drug or a regimen. Meaning that even stable patients will periodically need to check their viral loads and CD4 counts.
If either starts going in the wrong direction, then it's time to run another genotype to see if there's new resistance. So now we've got the background and patho under our belts. We've also looked at a small glimpse of what a patient might experience in the early days of an HIV infection. As practitioners, we have to ask ourselves "Now what? First things first, we're gonna need to get some information. Some more intel.
Some deets. However, while we're at it, we should also grab the viral genotype. And the patient's fasting lipid profile and liver panel. Finally, for an added bonus, we're going to throw in the HLA test too. There's a lot deeper we can dig as far as lab work goes. But this is a good "Start Here" list that will get you through most scenarios.
That's a lot of information. What do we need all of that for? So we measure and monitor CD4 counts for for a couple of reasons. There isn't a consensus on this though. There's not necessarily a right or wrong answer here It's kind of like debating which way to load a toilet paper roll but with slightly more at stake. You'll get strong proponents from each side. And each will have a list of reasons why they are right. If you read that link, you'll see it's a pretty strong recommendation.
So it's probably "more right" much like loading the toilet paper "top down" is more right. Just be aware that you could see differing recommendations and practices.
Anyway, we also need a baseline CD4 count because certain drugs I'm looking at you, nevirapine cannot be initiated if the CD4 count is too high. We'll get more in why that is as we delve deeper into each drug class. Spoiler alert : For nevirapine, it's because of liver toxicity.
We'll also continue to monitor CD4 count throughout treatment as a way to determine the effectiveness of the regimen. In general, you're looking for an increase in CD4 count If you notice that the CD4 count is decreasing, it's time to re-evaluate the patient's therapy. Most likely you're either dealing with resistance from HIV or a lack of compliance from the patient.
HAART used to specifically mean 'triple therapy. But when we started moving to triple therapy as the standard of care, the name HAART became slightly less relevant. Either way, it's a term that is still used by basically everyone so now you're at least familiar with it. Young Anakin's viral load is even higher than Master Yoda's Image.
How many copies of HIV exist per ml of blood. Think of viral load as the opposite of CD4 count. So we use viral load as another marker along with CD4 counts to measure how therapy is progressing. If the viral load is decreasing, and CD4 count is increasing If the viral load starts to rise which will typically correlate with a decrease in CD4 , however, then it's time to reassess therapy.
We also check the viral load because if it's too high then it excludes certain drugs from being used. BMP - Primarily, this is all about renal function.
And every NRTI except abacavir requires a renal adjustment. Well how are we going know what renal function is without a BMP? Yes we could do a 24 hour urine collection and get an even more accurate picture of CrCl The BMP will also let you assess if electrolytes are out of whack and need correcting. It won't tell you anything specifically pertaining to HIV, but remember that HIV's calling card is making people sick with other infections.
It also gives a good baseline on where your patient stands in terms of anemia via hemoglobin and if they are a bleeding risk via platelets. Viral Genotype - Also known as the "resistance panel," you have to check this to see which HIV medications will be effective against the actual virus you're fighting.
As we mentioned in Part I of this series , retroviruses mutate all the damn time. This leads to resistance to medications and treatment failures. Just like bacteria have genes that make them resistant to methicillin, there are genes on the HIV genome that cause resistance to the entire class of NNRTIs. Checking the viral genotype will make sure we're selecting an appropriate combination of drugs.
Lipid Profile - We'll check this at baseline especially if the patient will be using protease inhibitors as part of their HAART regimen. Many of the protease inhibitors can do wacky things to your lipid panel, so we can use this as a way to monitor that. Please note that this test must be done in a fasted state. One of the most common causes for crazy numbers on a lipid profile test is the patient eating a Denny's Grand Slam before coming to their appointment.
That "fasted" bit has a habit of showing up on tests as well. I've seen more than one patient case study question that snuck in a patient eating before taking a lipid test. Liver Panel - First of all, it is unfortunately very common for HIV patients to be co-infected with hepatitis. So we should really check out what's going on with the liver. Getting a baseline LFT helps us monitor and prevent liver complications.
It's a protein that's on the surface of your macrophages. As pharmacogenomics has become more of a thing, HLA tests have played an increasing role in drug therapy. There are thousands of known variations polymorphisms of HLA. We've found that certain drugs do bad things to people if they have the "wrong" HLA type.
Basically their immune system goes apeshit. They have a pretty decent chance of developing a huge hypersensitivity reaction. They may go into shock and die. Either way, it's just something to avoid. It is one of the few HLA tests that are required before treatment.
If your patient has not had an HLA test, they cannot receive abacavir. The HLA type doesn't change, so it's just nice to grab an HLA test in the very beginning when you're initially working up the patient. Then you'll know from the get go if abacavir is ever an option. What is our end game here? Unfortunately, we cannot eradicate HIV at this time. Once contracted, you're pretty much a lifer.
That being said Patients can live normal lives for decades with the treatment advances that have been made. So what are our treatment goals? In the interest of time and space, what follows is far from an exhaustive list. There are phenomenal resources here if you really want some handy info. What follows is more of a tl;dr summary. And again, we'll be drilling down into a lot more drug-specific information when we go through each of the respective drug classes. Back in the day, one drug may have been enough.
Zidovudine monotherapy was pretty much our treatment strategy for much of the '80s AZT Break. So the standard of care is triple therapy. There are always exceptions, of course. But start by assuming that everyone gets triple therapy. What makes up that triple therapy? Lucky for us and patients , there are plenty of single tablet regimens out there to make things easy.
There's a growing list of options to choose from. These all contain an NRTI backbone and the "something else" in a convenient once daily tablet. They work, and they are tolerated with minimal side effects. Assuming your patient doesn't have resistance to one of the components which we check through the viral genotype , or some other baseline lab abnormality, you'd start them with one of the following regimens.
The brand name has been included if the regimen exists as a single-tablet combination pill. These are the preferred regimens. You'll notice that all of them contain an integrase inhibitor. You'll find these under "alternative" regimens. They're still good choices. But the new integrase inhibitors and their wonderful tolerability have moved them to the forefront.
You may also be confused by tenofovir alafenamide. You can read more about this new formulation of tenofovir on our post here. Remember from Part I , that we discovered HIV from otherwise healthy males becoming infected with a rare pneumonia. Opportunistic infections are things that don't normally cause disease in healthy patients. But when you lack a functioning immune system ala HIV, leukemia, etc then they can start showing up. With HIV specifically, we've been able to correlate when these infections start causing problems to a CD4 count.
There are 3 main bugs to worry about here. What you need to memorize are the CD4 counts where you'd need to begin prophylaxis. And the drugs we actually use for prophylaxis. For toxo, the count is So when you start a patient on PCP prophylaxis, you're also covering toxo.
MAC is covered with either azithromycin preferred or clarithromycin. To summarize:. That's all for now. In Part III, we start breaking down each drug class. We'll start with NRTIs, as they make up the backbone of most regimens. Stay tuned! But before I go on, there's another distinction I have to make.
There are actually both nucleo side and nucelo tide reverse transcriptase inhibitors. We lump them into the same "NRTI" bucket because they work in exactly the same way. But they are technically different from each other. I never thought my bachelors degree in Molecular Genetics would come in handy, but here goes. Let's time travel back to the stuff you learned about in your own genetics pre-pharm classes.
All the way back to DNA base pairs. A nucleo tide is the same thing. But with a a phosphate attached to it. So you might have something like 5'-Adenosine monophosphate. When a nucleotide loses it's phosphate through hydrolysis or any other means , it becomes a nucleoside. Back to our NRTIs. All of them are nucelosides Tenofovir is the only nucelotide of the bunch. As far as I know, there is no active research into getting more NRTIs nucleoside or nucleotide , so this is going to be the landscape for a while.
Does any of this really matter much to you in terms of pharmacy school? No, not really. But you're here to learn right? You might win something on HIV drug trivia now.
Or you can be like one of those smug people that go around correcting everyone on their english. Get it? Cause it's an owl. Owls say "who" Image. Anyway, that's enough "science" for now. Let's get on with it. NRTIs are designed to mimic natural nucleotides in structure, but not in function.
To try and describe how this works: imagine you run an evil corporation that makes knock-off cell phones. You go out to get some source material to make these cellphones, and some guy in a suit sell you what looks like gold and feels like gold for your circuits. When you go and try to make your phones, the "gold" basically mucks up your systems.
Your factory shuts down and you die of dysentery for some reason like you were on the Oregon Trail. In the same way, NRTIs muck up reverse transcriptase by inserting themselves into the genome, but then shutting down transcription. No reverse transcription? No viral replication. Or, to put it another way, think of when you were asked to recreate a drawing as a kid. You get that 4 crayon box with four colors AGTC. What NRTIs essentially do is come in like a bully and replace the Crayola crayons you had with some plastic colored sticks that don't color at all.
Now you can't recreate the drawing. You become sad, and you no longer function. The nucleotides of art. Doom and ruin Sauron's shit. The downside of NRTIs is that since they mimic actual nucleotides, they can also screw up human genome replication by screwing with DNA polymerase. Luckily, beautiful human creatures like ourselves have built in redundancy to correct mistakes made by DNA polymerase. HIV's Reverse Transcriptase does not have said redundancy.
Unfortunately, our redundancy process is not perfect and adverse effects still happen. We'll start with class side effects. These are things that can occur with any NRTI. Damage to DNA, particularly in the mitochondria the power house of the cell! Lactic acidosis , lipoatrophy if you don't know what this is, Google it and you will never forget , and peripheral neuropathy. A mantra that fellow HU youknow alumni will recognize is "lactic acidosis and hepatic steatosis.
It rhymes. And it's a black box warning for every single NRTI. Moving on to individual agents, we're going to do something a little different. There are several NRTIs, and each has its own quirks. The tl;dr way. For starters, tenofovir is worthy of a special mention. It is included in a lot of combination regiments, it's also used to treat HBV, and it's recently been getting a formulation makeover from Gilead.
TAF has better cell penetration, so it can be given at a lower dose and maintain the same efficacy. There's solid data showing that it has lower toxicity in the two main "problem" areas for tenofovir renal failure and osteoporosis. We've been writing about a lot of the new agents as they've been approved by the FDA. Anyway, for your convenience, here's a handy list of the "cousins" that currently exist.
As for the other individual NRTIs, we've got some dosing tables for you. What you'll see in the tables below includes the pertinent dosing and dose adjustments you need for each agent. The tables will also highlight some important characteristics worth noting about each drug ex.
We tried to make it nice and easy by breaking things down in tables. It's not an exhaustive resource on each drug. Editor's Note: You'll notice as you go through these tables that the three-letter abbreviations are used for each drug. While it's not absolutely necessary to know the three-letter abbreviation, it is incredibly helpful.
You'll just have to memorize those. Anyway, we're using the abbreviations throughout the rest of this post. So consider this a heads up. Again, they're not completely necessary to commit to memory As noted earlier, TDF is the only nucleotide of the bunch.
Structurally similar to Lamivudine Epivir, 3TC. They're like cousins. So avoid the combination. Cause that's just weird. In fact, they ran into each other at an Easter gather up this past year. This is the only NRTI that does not require a renal adjustment But do note: Alcohol dehydrogenase is the mechanism of choice, so if anything no drinky and abacaviry.
Abacavir can cause hypersensitivity reactions that lead to organ failure and death. You'll find them together along with lamivudine in the combination product Triumeq.
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