DIP Episode 28 - Antibiotics Part 2 (Protein Synthesis Inhibitors)

Hello, welcome. My name is divine. I am a fourth-year medical student. This will be the 20th episode of the divine intervention podcasts and today we're going to continue our story relating to the antibiotics. I'm going to primarily discuss the proteins synthesis inhibitors. So let's begin. Now remember the central dogma, right, of molecular biology where you basically start with DNA, okay? And then that DNA via the process of transcription is meeting to RNA. And then the RNA via the process of translation is meeting to protein. And there are certain raw materials you're doing fact need for translation, right? So you need like TRNA that has on the three-primary, it has the amino acid and then it also has the anti-codone, right? That pairs up with mRNA. The second raw material you need for the synthesis of proteins, right? You need the ribosome in bacteria, which is what we're trying to target today, right? We have a large subunit, that's the 50s subunit and a small subunit, that's the 30s subunit. And that together forms the 70s subunit contrast with humans that have a 60 and a 40s that mix up the EDS ribosome. And then we need an actual mRNA, right? Which was made by the process of transcription. So mRNA from the 5.3 to 3.3mN, right? It's loaded onto like the EPN A side of the ribosome, right? And the thing is the first TRNA, you should hopefully know that it goes to the P side, okay?

And the first amino acid that's classically meeting bacteria is a methyonine, a form of lethite, methyonine, okay? In fact, F-MET is something known as a PAMP, in the world of immunology. It's a pathogen, associated with molecular pattern. It's something that's not found in humans, right? So it's something that I need immune system recognizes to go after these nasty bugs. So the P side, right? So let me just hone in on some of these high-yield sites and just give a very quick overview of the pharmacology before going to the specific drug details. But the P side has 50 and 30 subunits that contribute to it, okay? And the thing is, if you work at the P side as an anti-baryco-inhibiting initiation. So the 50s contribution to the P side is inhibited by the nasolid, okay? We'll talk about it. It's a drug used to treat mercy and vr, it's an oral medication. Alternatively, the 30s contribution to the P side can be inhibited with the amino glycosides, right? So like a gentamysin, new amysin amicase, into bromysin and streptomycin. Now in regards to the A side, right? There are drugs that inhibit that A side, and if you're an A side inhibitor, it should make sense that you inhibit the long-dition step of protein synthesis, okay? And for the 30s contribution to the A side, that inhibition is done by your tetracyclins. Remember, you're unlike your amino glycosides that are bacteria's side, or your tetracyclins are bacteria's static, okay?

Now for the 50s contribution to the A side, the drugs that inhibit that side, the streptogram ends like daphyl pristine, quinopristine, the cover mercy, we'll talk about those later. And then for clandamysin and rhomysin, also the discostles together, clandamysin is in a different role class from rhomysin and rhomysin is a macrolid, okay? But your macrolids and clandamysin in general, they bind to the 50s subunit, and basically prevent movement along the messenger RNA, right? So you're basically inhibiting translocation, okay? Translocation is one of the sub-steps in the longation step of protein synthesis and translation. Now, peptidol transfer is, right? It's this high-yield enzyme that forms bonds between amino acids during the process of translation. That enzyme is inhibited by chloramphenicol, okay? So chloramphenicol inhibits peptidol transfer, it's a 50s inhibitor. The only 30s inhibitors that are protein synthesis inhibitors are your amino glycosides, which are bacteria's side, and your tetracyclins, which are bacteria's static. And the mnemonic, right? You'll probably hear this as you're studying for your USML exams, but by a 30 and sell at 50, okay? So the at 30, amino glycosides and tetracyclins are 30s inhibitors, and then the sell at 50, right? So like CCELL, right? So like clandamysin, clandamysin, clandamysin, erythromysin, and other macrolids, leneysolyde, and I believe the lincolstamides. Okay, so your amino glycosides, right?

So let's get a little more granular with these drugs. And the thing is, again, I'm not going to just give you drug names to memorize. The step one loves to integrate material with multiple fields, so I'll talk about like the different ways these drugs are tested on exams, and then provide you the drug names. So the amino glycosides, right? So they include drugs like gentamysin, okay? Neomysin, amicasein, tubermycin, and streptomycin. They all end in mycin, okay? And they're bacteria side of, right? And one of the mechanisms they have is that the cost is reading of mRNA. If mRNA is not read properly, you make bad proteins. And it so happens that those bad proteins, they poke holes in the cell membrane, and by poking holes in the cell membrane, right? If you go, but if you think back to cell injury that you've probably learned as you're studying, pathoma, whatever, pathology resource you use, you see that when the cell membranes become permeable, that can cause death, right? Because every, that can cause cellular death, because all the cell soup is spilling out into the surroundings. So these drugs are bacteria side of, okay? And I've talked about how they work, they are 30 as inhibitors. Now the drug names again, gentamysin is here, Neomysin is another big one, okay? It's classically tested in the context of like prep before bowel surgery, because it's very good at killing of gram negatives, as you'll find out amino glycosides cover primarily gram negatives.

They do not very high up to know that they do not cover gram positives, they cover only gram negatives, okay? And the thing is Neomysin can actually be used in the setting of hepatic encephalopathy, because it's pretty good at killing of gram negatives. And one of the big constant when bugs in Eugenic tract are gram negative rods. So those are covered very nicely with Neomysin. Another drug you can use for that hepatic encephalopathy purpose is refaxing, it's an RNA polymerase inhibitor. Again, that is pretty good at killing of your GI flora. So you may see divine, come on. How do these drugs help in hepatic encephalopathy? The thing is, the bugs in your GI tract make a ton of ammonia, okay? And the thing is the GI tract with the exclusion of the stomach is primarily basic, so ammonia is pretty soluble. So it's actually reabsorbed in the GI tract. So one thing you could do is you could say, okay, let me try to take care of the source of the ammonia, just kill off all the bugs. Would refaximen RNA polymerase inhibitor or Neomysin? Aminoglycoside, okay? So that's how those work in the setting of hepatic encephalopathy. Remember, you could also give lactose for that purpose, right? To be galactic acid, acidify ammonia, you put it out as ammonium ions. Okay, now aminquisin is another amino glycoside to bromysin. The big context they test this with is patients that have cystic fibrosis.

Remember, patients with CF, classically, when they are less than 21, the most common cause of respiratory infections there is staff warriors. But as they become greater than 21, you're going into the territory of pseudomonas, okay? Sodomonas, you can perphylaxis against that in a CF patient by giving the inhaled form of to bromysin, okay? Again, because pseudomonas is a gram-negative rod. So it's covered very well by your amino glycosides. Streptomysin is another loyote amino glycoside. It's used to treat like drug resistant TB. Now, again, I said these drugs, the cover gram-negative is primarily including to the monos. The thing is, these drugs do not cover anaeropes because they actually need oxygen to get into a cell. So amino glycosides have no coverage against anaeropes. And one classic thing they test, and this is probably more step to territory, are GI cocktails for the treatment of, basically like, antibody cocktails for the treatment of GI infections. One cocktail that includes the amino glycosides is the MAG cocktail. I'm just making that word MAG, M-A-G, just to help you remember, Mectronidosol, Ampacillin, and Gentamysin, okay? And you do this because the Gentamysin and Ampacillin cover gram-negatives pretty well. Mectronidosol helps you cover the anaeropes, okay? Another classic GI cocktail is like Cipro, so Cipro-Floxacin in your Fluoroquineolones, and Mectronidosol. Again, Cipro, it's a Fluoroquineolone, very good gram-negative coverage, okay?

Mectronidosol helps you cover the anaeropes, right? So if you get a question about a patient that has like diverticulitis or colitisitis, and they're asking for a recommendation on an antibiotic regimen, you're going to pick either the MAG regimen of metro, ampicillin and Gentamysin, or the Cipro-Plus-Mectronidosol regimen. And another high-yield thing with the amino glycosides is they have some nicotinic receptor blocking activity, okay? Remember these nicotinic receptors, you find them at three high-yield spots in the body, right? So you find them at the neuromuscular junction, okay? You'll find those on the cell membranes of the post-ganglionic neuron, so the sympathetic nervous system, and also the parasympathetic nervous system, right? But in addition, you also find these receptors on the surfaces of chromafin cells. Remember, chromafin cells are kind of, they're part of the Adrenomadala, they are kind of modified post-ganglionic sympathetic neuro, okay, but they release epinephrine primarily because they express P and M T. So, amino glycosides, they can actually worsen your muscular blockade, right? So if a person is getting a neuromuscular block in agent, you probably want to be careful with the administrative amino glycosides in that population. Now, what are the side effects of amino glycosides, right? So the anephyrtoxic, in fact, is probably one of the most common causes of intra-renal azotemia, right? So like an intra-renal acrylophtiorea picture.

You amino glycosides are very nasty to cranial nerve-8, okay? So actually, you can apply this in the setting of mannier's disease, right? So remember, mannier's disease with a tread of very goldenodous and hearing loss. The pathophysiology there is like endolimpatic hydrops, right? So you have like hydropic swelling of the, from too much endolimp in your ear apparatus, right? So you can apply this to people, completely of ear fullness, and then you have like very goldenodous and hearing loss. You can actually treat that. Usually you try like a salt-restricted diet, you try like a diuretic, but if that doesn't work, symptoms are refractory. You can inject gentamysin into the ear, okay? So you can give gentamysin for that, an intra-like orychola injection, and that can basically terminate the mannier's disease, okay? So if you have a resistance to amino glycosides, don't forget, right? So if a bug encodes a transfer instance, I'm like an acetyl transferase, by adding that chemical group to the amino glycoside, the drug becomes inactivated, okay? And also, many bugs express porins. These porins like actively cause the amino glycosides to be extruded from the cells, or certain bugs also have mechanisms to prevent the amino glycosides from getting it, okay? So those are your big mechanisms of resistance with the amino glycosides. So now let's go to the next group, okay? So from, we've talked about the first 30-s amino glycosides, let's talk about the tetracyclin, right?

So the tetracyclin is the a30s inhibitors, the abactors static, okay? Remember the a3s, okay? The 30th contribution to the a3s, right? So the inhibit belongation. And the big drug names you want to remember here, right? So the all-endent cyclin, like the mechocycline, minocycline, doxycycline, tigacycline, tigacycline, I'll just say one word about this. It's a tetracyclin that has the ability to cover MRSA. So you're one of those things you want to file away, you'll bring some rates. One of the more new generation tetracyclins. It belongs to the drug class known as the glycosyclins. Now, what do these tetracyclins cover? So the cover-clamydia pretty well, okay? So you can use that for the treatment of UT Is. They cover Borrelia, Bokdovri, right? Remember that's the causative agent of Lyme disease, okay? Remember it's carried by the X-adistic. Don't forget for your exams that the X-adistic in addition to carrying Borrelia Bokdovri, that causes Lyme disease. It also carries Babesia microd, okay? Remember that multi-scross pattern in red blood cells. It can present as a Himalilic anemia. And remember, the X-adistic also carries an aplasma, okay? So an aplasmosis, Babesiosis, and Lyme disease can be caused by a bite from the X-adistic. Your tetracyclins also cover echatia, echatia, remember it's one of the causes of Rocky Mountain spotted fever, okay? Remember the rash on the palms and soles, okay? Remember the other causes of a rash on the palms and soles, right?

So like secondary syphilis, Kawasaki's disease, Koksaki A virus with hand-footed mouth disease, okay? And again, Riketsu, Riketsu. And actually, in Rocky Mountain spotted fever, this is actually one of the exceptions, where you can give a tetracycline to a kid that's less than eight years old. In general, you have a warming majority of the time if a kid is less than eight years old, they should not be getting a tetracycline. But if the disease they have is Rocky Mountain spotted fever, you usually take exception to that, because RMSF is pretty fatal, right? So you want to treat it really well and tetracycline's cover that bug extremely well, okay? Now, alternatively though, you could give a lower emphenicol for Rocky Mountain spotted fever. Remember, Rocky Mountain spotted fever is a peptidotransferase inhibitor. In fact, I'll say in general, in pregnant women that have Rocky Mountain spotted fever, usually the go-to drug is chloromphenicol, okay? Usually chloromphenicol. Now, your tetracycline's, they also cover Vibrio species, right? So you can use them for like Vibrio colorate, you can use them for Vibrio parhimolidicus and vognificus. Remember, those cause a watery diarrhea. Vognificus is particularly bad in people that have like liver disease, okay? Your tetracycline is also cover propione bacterium acne, right? So the causative organism in acne, they also cover Hpylori. In fact, if you, Hpylori has two kinds of therapies, right?

There is triple therapy, that's usually first line. And then there's quadruple therapy. So triple therapy, you can remember it with a cap nomonic, right? So cap, so Cifoclarithromycin, that's a marker lead, is for amoxicillin. We talked about that in the previous podcast. And then the piece for PPI, like Omeperson, okay? But if that doesn't work, you can consider using quadruple therapy. And that's where your tetracycline's coming to play, right? So it's an MBTP, right? So M for metronidosol B for Bismuth, subsalicylic, the T's for the tetracycline, and then the PPI, okay? So that's quadruple therapy. Now, so your tetracycline is doing fat cover Hpylori, okay? And again, like I've said, they are contraindicated in case they're less than 80 or so. And one thing about the tetracycline is that they are very, they're bound very strongly by divalent ions. So you generally don't want to take a tetracycline with milk, right? Because milk contains calcium and magnesium ions, those can bind up the tetracycline, and it's not reabsorbed in the GI tract. But an interesting parallel to this is bones and teeth, contain a lot of divalent ions, right? So they are very good at chelithin tetracycline. So if you bind up these tetracycline, you can sort of imagine, you can sort of like stretch your thinking to imagine that this is potentially how tetracycline's cause a tooth discoloration, okay? And they also inhibit bone growth.

Again, that's why you don't give them to moms that are pregnant or kids that are less than 80 years old. So tetracycline's, right? Another big one is the mechlocycline. It actually inhibits the activity of ADHD at the principal cell of the collecting duct, okay? So the mechlocycline can actually cause nephrogenic diabetes in sypedas as a side effect. You can actually take advantage of that in the treatment of SIDH, right? So in SIDH, you're reabsorbing too much water because you have too much ADHD on board. So you can use the nephrogenic diabetes in sypedas side effect off the mechlocycline to treat SIDH. Remember, for SIDH, you can also use an ADHD receptor antagonist, your vaptans, like conivaptan or toe vaptan. Okay, now, l'anaisolid is a next drug I'll talk about. It's a 50s inhibitor. It belongs to a drug class known as the oxazolidinones, okay? You don't need to know that for step one. But it's a 50s inhibitor. It's bacterostatic. It's a P side inhibitor, right? So it inhibits the 50s contribution to the P side. So, what does this drug cover? The big things you want to know for your exam is it covers MRSA and VRE. That's essentially all you need to know about l'anaisolid. And it actually is a relatively clean drug. It's actually pretty expensive though. You've ever heard of Zyvox. That's l'anaisolid. It's a relatively clean drug. And many clinicians like it because it's an oral medication that can treat MRSA, okay?

Instead of giving like vancomycin, vancomycin is only available in general. As an IV formulation. Although you could use oral vancomycin in the treatment of C-Diff. Okay. So, relatively few side effects. But there's one that has started making its way to USMLA exams. And that's the fact that l'anaisolid can trigger serotonin syndrome when you're giving with another serotonergic agent, like St. John's Ward, or Sumatriptan, or other triptoms they use for migraines, or an SSRI, or an SNRI, or an MAOI, or tricyclic antidepressant. Okay? So, the pathophysiology behind that is that l'anaisolid actually has some weak monoramin oxidies in hebidin activity. So, because you can inhibit monoramin oxidies, it can boost your levels of serotonin. And again, it can trigger serotonin syndrome. Now, the next drug I'll talk about here is clean d'Amaisin. Okay, it's a 50-year inhibitor. Remember, I said it in hebid translocation, just like your marker lets. Okay? And it's back to your static. And the coverage of clean d'Amaisin is actually high up to now. You want to know that it covers MRSA really well, okay? In fact, clean d'Amaisin is used very commonly for MRSA skin infections like senolitis, for example. It's also pretty good at covering anoreubs classically. It covers anoreubs above the diaphragm, but that's a farce. It also covers anoreubs below the diaphragm. That doesn't really make much sense. But just classic, the classic classic teaching is anoreubs above the diaphragm, right?

So that's why it's used for aspiration pneumonia. So if you describe a person that has pneumonia with false malinspeedum, you probably want to think about an anaerobic cause of that pneumonia. You want to go ahead and cover that with clean d'Amaisin. And remember the high-yield anoreubs that pop up every softener on USML exams, right? There's bacteriaoides, B-fragilis, there's fusobacterium species, okay? And then there's peptostreptococcus. I dare you to see that 10 times without flinching. Okay, peptostreptococcus. Now, clean d'Amaisin on exams as classically with them. So she's with the causing C-dif, okay? Because it kills off your GI floor, including the anaerobic, so C-dif can overgrow, okay? So you can get into trouble with that. And how do you treat C-dif colitis, right? You generally should have metronidazole. We'll talk about that in a different podcast. You can also treat it with urovencomisin, because eventcomisin is not reabsorbed. So you give it a release, these in the GI tract kills off the C-dif. If nothing works, you could also consider giving fidaxomaisin. Fidaxomaisin is one drug that inhibits RNA polymerase. It's using treatment of C-dif, but it's one of your last line meds. But if all that stuff doesn't work, you can then consider trying to fix transplant, okay? Now, real quick, I'll just go ahead and re-love the... Because I've been mentioning so many RNA polymerase inhibitors, so I think it probably makes sense to just reel them off right now.

So you can sort of remember all of them as a group. Fidaxomaisin is one, okay? It's used to treat C-dif colitis. Our ribavarian, right? Is another, okay? Remember ribavarian is used to treat hep C. You can also use it to treat RNA's V, although that's kind of controversial. Although, don't forget that ribavarian also has another mechanism of action as an inhibitor of I know sinmonophosphate dehydrogenase, okay? Which is the enzyme that's also inhibited by myocopenolipymofatil. Then, rifampin, that's used to treat TB, right? Remember the riboregimen is also an RNA polymerase inhibitor. And then, if you're going more into the word of toxicology, if you consume in mushrooms, like deadly mushrooms for some reason, alpha-amannitin is an RNA polymerase inhibitor as well. Now, the next drugs I'll talk about are your streptogrammines, right? Like quinoa-pristine, dalfoprystine, they bind to the A-sites. They basically inhibits the 50s contribution to the A-site, remember? I said the 30s contribution to the A-sites is inhibited by your tetracyclins. The 50s contribution is inhibited by your streptogrammines, okay? And these drugs actually back to our side, okay? They inhibited elongation, right? Because again, if you bind to the A-site to inhibiting elongation, I talked about the mechanism behind that earlier. And the drug names here again, quinoa-pristine, dalfoprystine, and the big coverage you want to know, in fact, probably the only coverage you need to know for any exam is MRSA.

These drugs cover MRSA. Now, chloramphenicol, it's a 50s inhibitor, right? I already said it inhibits peptidal transferries. Remember, this is the enzyme that basically forms peptide bonds between the aminoacet chains that you find in the P-site and the aminoacet that's just coming in the A-site, okay? And this drug, it so happens that it's cleared by phase two metabolism in the liver, right? So what's the poster child enzyme for phase two metabolism in the liver? That's UDPGT, right? So UDP, glucoronacyl transferries, okay? UDPGT. So when a kid is born, I mean, this enzyme is found pretty aggressively in adults, but when a kid is born, they have very little of this, okay? In fact, this enzyme generally is not induced until a kid is born, right? So it's something you generally don't have in you, right? So when a kid is born, they have very little levels of this. That's why, again, you generally want to, like, not give chloramphenicol to newborn, okay? Because of this UDPGT problem. So what are the bad side effects with chloramphenicol, right? So one bad side effect is a plastic anemia, okay? You can cause severe bone marrow suppression, right? So a classic example here will be like a kid that has been on chloramphenicol or some drug, they may not be chloramphenicol, but you may say kid has been on some drug for an isermin, for an isermin in gytis, meningitis, okay? In a developing country because chloramphenicol is actually pretty commonly used in a developing countries.

And then they say the person starts having, like, worsening fever, the person's ulcers are dropping, and then they say you do like a bone marrow biopsy or whatever. And you get a dry tap, like, I guess, more bone marrow aspiration, you get a dry tap, or they could show you like a bone marrow histologic image, and you see lots and lots and lots of fat cells. If you see that, think about the plastic anemia from chloramphenicol, okay? It crosses the blood brain barrier very well, so it's very good for the treatment of meningitis, okay? Because it also covers gram negatives, supremely well. Another high outside effect of chloramphenicol is gray BB syndrome, okay? It's a lipid soluble agent, right? So it can deposit in the brain, deposit in other tissues, okay? And again, it happens because neonates have a UDPGT deficiency, okay? It's a physiologic, right? It's something that they build up with time, but initially they have this deficiency, so they can't clear the drug really well, okay? So they can get toxicity from the drug. And on usual, we can actually test this UDPGT business with a context of an adult, or like an older kid, is in the context of a person that has like an actual UDPGT deficiency, right? So like regular in a heart syndrome, like type 1 or type 2, or like Gilberts, right?

So if a patient has like Gilberts, in general, it's a symptom, but let's assume they're like severely ill septic in the ICU, you probably don't want to give them chloramphenicol as a drug, because when those people get sick, that UDPGT deficiency begins to become a little more symptomatic, okay? So you don't want to like compound their problems by giving them something bad like a chloramphenicol, that depends on UDPGT for metabolism. And again, chloramphenicol covers many bugs really well. Coverage gram positives, covers gram negatives. In fact, there's very little resistance to chloramphenicol, but the side effects just make it a very uncommon drug in clinical practice. Coverage nicere meningitis, again, because I said again, it crosses the blood brain barrier, and again, it's the drug of choice, very high up to notice. It's the drug of choice for the treatment of Rocky Mountain spotted fever in pregnant women, okay? Now, so you bar the gray baby syndrome or whatever turned on genetic effects come with chloramphenicol, pregnant women, Rocky Mountain spotted fever, get chloramphenicol. That's basically the only time chloramphenicol is ever used for any purpose in the in clinical practice, at least in the US. Now your microlit, they are 50s inhibitors, right? So the 50s subunit of the ribosome has a 23s, so think of it as a sub subunit. The 23s subunit of the 50s subunit of the ribosome is what is specifically inhibited by microlit, okay?

And by binding to that subunit, the microlit prevents translocation, okay? And I'll just go ahead and mention this now because I feel like this is the best place to slot this in, but that's actually the mechanism of resistance to microlit. If you methylene that 23s part of the 50s subunit of the ribosome, you basically prevent the microlit from binding, okay? And they lose their effectiveness. Now, the big things you want to, big drug names you want to remember for your microlit are like, is it through my send, the all-ending room ice-send, right? So is it through my send, Clarithromysend, Erithromysend, oligomysend, right? And they say, oh, microlit is there's not much we use them for. There's actually a lot of things that potentially exempt testable, but microlit, so I'm going to talk about them right now. First thing is, these microlit are cleared by the liver, okay? They're cleared by the liver, big deal. So the person has liver dysfunction, maybe reduce the dose of microlit that you give them. That's not a very testable factor, but a testable one is they are effective as motillary receptor agonists, okay? So motillin is a thing you'll find in the GI tract that activates motillary receptors and it causes, it's prokinetic, it increases GI motility. So if a patient has diabetic gastroperesis, you can actually treat that with metaclopromide.

That's a dopamine receptor antagonist, but you could also use Erithromysend, motillary receptor agonist to treat diabetic gastroperesis. In fact, this explains why GI offset is probably one of the most common side effects with macrolates. Erithromysend, how you think Erithromysend, in fact, in general, Erithromysend, you try to avoid it in newborns because the thing is, it can cause an intra hepatic holostasis, because it can actually precipitate in ballas Erithromysend estolate, okay? And that can cause intra hepatic holostasis that will present as like elevations and alkaline phosphatase in a newborn, okay? And another thing where Erithromysend, right, it's actually associated with an increase risk of pyloric stenosis, especially if you give it within the first like eight weeks of life, okay? I remember pyloric stenosis presents as non-bilias vomitting in a kid that's less than, usually less than eight to 12 weeks old on exams, okay? You classically can diagnose it with an ultrasound, you see a target sign. I talked about those high-yield radiological signs in, I think, like episode 26 of our podcast. Now, let me just go ahead and see this. Many times on exams, especially NBME exams, if you pay attention to age ranges, you can usually pick out the right answer or very quickly exclude wrong answers. The thing is, in general, if a kid is one year old, they cannot get pyloric stenosis on NBME exams, okay?

Pyloric stenosis almost always shows up within the first three months of life. It's very high yield to know that, okay? So Erithromysend also being a fast-borne meal, right? Those all increase your risk of pyloric stenosis. Okay, now, the thing with the microlysis, they also have like some mild potassium channel blocking activity, okay? So they can actually prolong the cutie interval and cause that towards that point, okay? Clarithromycin, I already talked about it in the context of triple therapy for each pylory. Oligomycin is actually a microlit, and I'm sure you may be like, hmm, where have I heard of Oligomycin? Well, hopefully you've heard about it from reading the biochemistry chapter in first state, okay? Oligomycin is actually a microly that's used for its search purposes. It inhibits ATP-Synthase, complex 5, okay? So it's just one of those bizarre factors you do want to memorize for step one especially. Now, what do these microlytes cover, right? So microlytes, they cover a typical box, right? So like, especially the typical causes of pneumonia, like microplasma, chlamydia, and legionella, right? An easy way to remember that is if you spell out the word microlit, it has an M, it has a C, and it has an L in the name, okay? Actually, one of the med students at my med school were the ones that have thought me this nice to money there. So, covers MCL, microplasma, chlamydia, and legionella, okay? They also cover a vaccine preventable illnesses pretty well, right?

As a general principle, like corainy-bacterium diphtheria, right? So if you see like, bulls neck in an immigrant or a person from like California, like an anti-vaxxer person, think about potentially treating that with a microlit, okay? Corainy-bacterium diphtheria, another high-yod vaccine preventable illness, or a body-teller pertosis, right? So like, whooping cough, whooping cough, remember it classically presents as a person that has like a nasty cough, and then they have like an inspiratory whoops, or they essentially never put that inspiratory whoops, everyone has memorized that crap for example, they don't put that anymore. The thing they will probably put is a person that has cough, and the cough is so severe that they vomit after the cough, or they could say, oh, the person has cough, and then they have a subconjung type of hemorrhage. If you ever see that, think about body-teller pertosis, okay? And remember, it's a bacterial infection, and usually if a person has a bacterial infection, you respond to that bacterial infection by a proliferation of neutrophils, right? So your polymophone, nuclear leukocytes. The thing is, body-teller pertosis is actually typically in that respect. It's a bacterial infection that's accompanied by lymphocyteosis. In fact, these people's white counts will go to like 70,000, okay? That's another unique feature of body-teller pertosis.

And body-teller pertosis, you treat this with, I mean, you should obviously get the vaccine to not have it in the first place. But, and I'll just say this right now, vaccines do not cause autism. Okay, good. So you could treat with a whooping cough with a macrolid, or you could profilax, especially close contacts of a person that has whooping cough. You would profilax with macrolids as well. Is it through my sin? Is another macrolid, right? I remember they can test this in the context of HIV-8s, because it inhibits, sorry, it covers micro-bacterium, avium, intercellularity, right? Remember, your magic number is a CD4 count less than 50. You want to go ahead and give you the thromice and as profilaxis against macrolid. Now, I'll just go ahead and also say that the macrolid is the inhibits, cytokrom P450, okay? Remember, your P450 inhibitors and inducers are high yield things you want to know for your exam. The inhibitors, right? So there's this no money, you've probably read in many resources, right? The crack amigos no money, right? So like the P450 inhibitors, right? So like a CIPRA floxacin and your fluoroquinolone is the C, return of your. Remember, that's a pretty Zinhibra. Talk about that in a different podcast. I'm going to run the class three anti-anothermic, simedadine. It's a H2 receptor blocker. It's used to treat peptic ulcer disease. Remember, it also has antigen receptor blocking activity, so it can cause gynecomastia.

The K4ketoconazole, that's an isole, it's an antifongo medication. Acute alcohol use, okay? Actually, inhibits CIPP450, contrast that with chronic alcoholism, then actually induces cytokrom P450. Okay? Your macrolid is already mentioned, also inhibitors. That's the M of CIPP450. I so niacet, that's one of your TB drugs, okay? Inhibits CIPP450, group-frujus, or Meprosol, that's your O, and other PPI is also inhibits CIPP450. And also your cell phonomites. Remember, those are dihydroperethythesensin inhibitors. I'll talk about that when I talk about bacteria. Okay? Your P415 induces, right? So don't forget your, the numonic there is like Guinness, coronas, and PB Rs. Induced chronic alcoholism, right? So like Guinness, the G's are greasy of woven coronas, carburemase, a pin. That's an anti-seasure medication. That's also used to treat trigeminal norrausia, or tic dolororo. That's an inducer of cytokrom P450. PB Rs, right? So the P stands for feintitone. Remember, that has zero-order metabolism. And then the B stands for the babituri. Try to remember those are gubber receptor agonists. There's no risk agent for those. The R stands for rifampin. Remember, that's an RNA polymerase inhibitor. That's used to treat TB. So PB Rs, the S stands for St. John's Ward. It's one of those harboh supplements that has some mild SSR activity. So it's used to treat depression. You can induce P450. And classic here on exams, these P450 inducers, they test them in the context of birth control.

Like a lady that's taking birth control and one of these other agents, and then she becomes pregnant because she's getting reduced effectiveness of the birth control pills. So Guinness, coronas, PB Rs induce chronic alcoholism, right? So chronic alcoholism also induces P450. Contrast that with, again, with acute alcoholism that inhibits P450. So I think this is going along enough. I think that's all I want to say about the protein synthesis inhibitors. The next time we meet in a different podcast episode, I'll go into the TB meds, the sulfonamides, and some other high-yodros like the fluoroquinolones and polymixins and blah, blah, blah. Okay, so have a wonderful rest of the day. I hope you're enjoying your Sunday, and this, I believe, is the first day of the Eastern Conference Final. I'm a Cleveland Cavalier supporter, so I hope they win. I wish you the best rest of the day. Have a wonderful week ahead, and God bless. Thank you.

70 S subunit (composed of a 50 S large subunit and a 30 S small subunit).

Chloramphenicol.

Inhibiting translocation (a sub-step in elongation) by binding to the 50 S subunit.

Aminoglycosides (e.g., Neomycin).

By a 30 and sell at 50 (Aminoglycosides/Tetracyclines at 30; Macrolides/Lincosamides/Chloramphenicol at 50).

Nicotinic receptor blocking activity, potentially worsening muscle weakness.

Aminoglycosides (e.g., Gentamicin).

Treatment of Rickettsial spotted fever (pregnant women) or Meningitis (due to BBB penetration and broad coverage).

Lincosamides (Linezolid) or Streptogramins (Quinupristin/Dalfopristin).

UDPGT (UDP glucuronosyltransferases).

Rifampin (for TB) and Ribavirin (or Cidofovir/Fidaxomicin, depending on context).

They can act as motilin receptor agonists, leading to increased GI motility (prokinetic effect).

Aminoglycosides (e.g., Gentamicin).

Treatment of Rickettsial spotted fever (pregnant women) or Meningitis (due to BBB penetration and broad coverage).

Lincosamides (Linezolid) or Streptogramins (Quinupristin/Dalfopristin).

UDPGT (UDP glucuronosyltransferases).

Rifampin (for TB) and Ribavirin (or Cidofovir/Fidaxomicin, depending on context).

They can act as motilin receptor agonists, leading to increased GI motility (prokinetic effect).