- 8/1/2024
Introduction to Antibiotics
What are antibiotics.
How bacterial infection is cured.
How to kill bacteria.
What are antibiotics.
How bacterial infection is cured.
How to kill bacteria.
Category
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LearningTranscript
00:00Hey, you! Welcome to my new antibiotics course, the best antibiotics discussion in the whole freaking world.
00:07Antibiotics have been around for a little less than a hundred years, but they are not going away anytime soon.
00:16If you think that artificial intelligence is gonna make them obsolete, you're wrong.
00:22Bacteria is here to stay.
00:24I know it's hard, but I'll try my best to make it easy and simple.
00:29Here is hepatotoxicity and here is nephrotoxicity,
00:34because most of these antibiotics are either metabolized in the kidney or in the liver, metabolized slash excreted.
00:42Therefore, it's not a shocker that they can cause hepatotoxicity or nephrotoxicity.
00:48This is Linda. She's a Catholic nun.
00:52Linda reminds me of clindamycin.
00:55Clindamycin covers MRSA, especially if the MRSA is localized and mild.
01:01But clindamycin can lead to something bad called pseudomembranous colitis by the nasty C. difficile.
01:11With that being said, now let's get started.
01:13Here are just some quick side effects to remember forever.
01:17Clindamycin can lead to pseudomembranous colitis.
01:20Chloramphenicol can lead to gray baby syndrome.
01:23It's not actually gray, it's cyanosis to be honest, but it's close enough.
01:28This is vancomycin, the van.
01:31It can lead to red man syndrome.
01:33Here is a red man.
01:35Vancomycin covers gram-positive cocci and rods.
01:40Next is the metronidazole. Here is your metro.
01:43It's used to cover giardiasis, trichomonas vaginalis, and intamoeba histolytica.
01:51It can also treat the cholestridium difficile, which was caused by the clindamycin.
01:57Side effects of the metronidazole include metallic taste, mucosal inflammation,
02:03disulfiram-like effect, inflammation of the bladder or urinary tract problems,
02:09as well as peripheral neuropathy, and maybe some rash.
02:14So here is the deal. Clindamycin can cause pseudomembranous colitis.
02:20Vancomycin and metronidazole can treat the pseudomembranous colitis,
02:25which is caused by the nasty cholestridium difficile.
02:30Now let's make some assumptions.
02:32Whenever I use these symbols, I mean those kind of words.
02:36When I use this, I mean the uses, the clinical uses of the drug.
02:40These are the pharmacokinetics.
02:42Resistance. How does the bacteria resist the antibiotics?
02:46Adverse effects. Hepatotoxicity is the angry liver.
02:50Nephrotoxicity is the sad kidney.
02:53This is liver enzyme inducer. By liver enzyme, it's usually the P450 system.
02:58It induces the P450 system. This means it inhibits the P450 system.
03:03This is an oral drug. The blue one is an intravenous drug.
03:07The dark red one is intramuscular drug.
03:10This is chlamydia, the famous clam. This is a topical drug.
03:14This is drug-drug interaction. When you add two drugs together,
03:18you're not supposed to add them together.
03:21This is a gram-positive cocci and a gram-positive rods
03:24because they stain purple on the gram stain.
03:28These are gram-negative cocci and rods because they stain pink.
03:32This means that the drug is bactericidal because it killed the bacteria.
03:36This means that the drug is bacteriostatic.
03:39This means that the drug is toxic to your brain and might cause seizure.
03:44This denotes neuropathy. This depicts myopathy.
03:49This means myelosuppression, which means bone marrow suppression,
03:53which will lead to thrombocytopenia, anemia, and leukopenia,
03:58making you tired, more likely to bleed, and at a greater risk of infection.
04:04This means the drug will lead to upper respiratory tract infection.
04:07Here is your trachea. This means nausea, vomiting, diarrhea,
04:11which means GI distress. This means thrombocytopenia
04:15and some purpura, ecchymosis, or petechiae.
04:19This means that the drug is administered subcutaneously.
04:22Look at the narrow angle. And this means that the drug is given
04:27through IV infusion, which means slowly.
04:32Here's the deal. Learning antibiotics or anything in life in general
04:36is a mind game. It's a mindset. Whatever the mind can conceive
04:42and believe, it can achieve. If you believe that you can do it,
04:46you will do it. If you believe that there's no way in the world
04:50that I'm going to understand antibiotics ever,
04:53you will never understand antibiotics, like ever.
04:57When I say antibiotics, I do not necessarily mean antibacterials.
05:02Antibiotics are here. They are called the antimicrobials.
05:06They could be antibacterial, antifungal, antiviral, or antiparasitic.
05:12Antibacterial or against your nasty bacteria.
05:16And they include the antituberculosis drugs,
05:20which will be divided into primary and secondary.
05:23The primary is the famous ripe. R is for rifampin.
05:27I is for isoniazid. P is for pyrazinamide.
05:31And E is for ethambutol, which causes green and red color blindness.
05:37Antifungals include the azoles. Not only the azoles,
05:41but also amphotericin B, nystatin, echinocandins,
05:46flucitazine, griseofolvin, etc, etc, etc.
05:50Antiviral could be divided into anti-HIV,
05:54also known as, sorry, HIV, also known as the heart therapy,
06:00which stands for highly active antiretroviral drug.
06:04The HIV virus is a retrovirus. Why do we call it retrovirus?
06:10Not because it wants to go back to the good old days,
06:13but because it has a reverse transcriptase,
06:17which will get the RNA and transform it back to its original form,
06:24which was the DNA. Because most of us go from DNA to RNA,
06:30thanks to the RNA polymerase. But the HIV virus is a retrovirus
06:35because it wants to go back to the DNA. Antiviral drugs also include
06:41anti-influenza, anti-hepatitis, and anti-herpes.
06:46Most of them have the root vir in their name.
06:51Then the last one is the antiparasitic. We can divide them into two broad categories.
06:56The antihelminths, or antihelminthic drugs, as well as antiprotozoal drugs.
07:04Just remember that metronidazole is an antibacterial,
07:08but it's also antiprotozoal. Just let you know.
07:12Humans do not have a cell wall. They only have cell membrane.
07:18However, bacteria, they have a cell wall and it's made of beta-lactam.
07:24Fungi have a cell wall and it's made of beta-glucan.
07:28That's why when I say the word beta-lactam inhibitors,
07:33it means it's gonna inhibit the cell wall synthesis.
07:37It's gonna affect the bacteria, but not the human,
07:40because humans do not have a cell wall. Makes perfect sense.
07:45We can divide the bacteria into gram-positive, or gram-staining,
07:50and non-gram-staining. Non-gram-staining includes anything that's not gram-positive.
07:54By the way, gram-positive are either gram-positive cocci, like this,
07:58and they are gonna be purple, or gram-positive rods, like this,
08:03and they will be purple because they are gram-positive.
08:06Next are the non-gram-staining, include the gram-negative cocci and the gram-negative rods,
08:11as well as others. Others include anatomically gram-positive.
08:15They were supposed to be gram-positive, but they do not stain with gram-stain at all,
08:23such as the famous Mycobacterium tuberculosis, because it's acid-fast,
08:27it cannot be stained with gram, or Mycoplasma, because it does not have a freaking cell wall,
08:32so we cannot stain it by the gram-stain, but they were supposed to be gram-positive.
08:38Then we have anatomically gram-negative, which were supposed to be gram-negative,
08:42but we do not use the gram that much, such as the famous Chlamydia, or the clam,
08:47we use the Giemsa stain, or the silver stain, Rickettsia,
08:51which will cause Rocky Mountain spotted fever, typhus, and early chiosis,
08:56and for that we use the Veal-Felix reaction, and we treat with Doxycycline,
09:02especially for the Rocky Mountain spotted fever, and the others.
09:05If Doxycycline is not there, you can use Chloramphenicol, but Chloramphenicol is archaic,
09:12it's historical. Doxycycline has replaced Chloramphenicol for almost all cases.
09:17Then the spirochetes, we have three of them, Tryponema pallidum, which causes syphilis,
09:22Borrelia, which causes Lyme disease, and Leptospira, which causes Leptospirosis.
09:27Spirochetes can be diagnosed by dark field microscopy.
09:31We can also use the VDRL, the Rapid Plasma Reagent, or RPR, these are screening tests.
09:39So the RPR and VDRL are screening tests.
09:44The confirmatory tests are the FTA, ABS, as well as something else called MHA, TP, or TPA, or TPAA, whatever.
09:54Let's get our terminology in order.
09:56What's the difference between Synergy, Additive, and Antagonist?
10:01Okay, Synergy means 1 plus 1 equals 3, which is a mathematical insanity, but a pharmacological reality.
10:11For instance, Penicillin plus Aminoglycoside are synergistic, which means it's better than either one of them alone.
10:18It's not just giving Penicillin alone, or giving Aminoglycoside alone.
10:22When you add them, you get two drugs. No, no, no, you get three drugs.
10:26This is called Synergy.
10:27Also, you can try it with Isoniazid plus Rifampin plus Streptomycin.
10:32These can be used to treat tuberculosis.
10:35Next is the Ciprofloxacin plus the Metronidazole.
10:38This will lead to an additive effect, 1 plus 1 equals 2.
10:43This is a good additive, but I can also show you a bad additive, such as adding Lupotirox to Aminoglycosides,
10:51because both of them are O2 toxic.
10:55This is a bad combination. That's a bad additive effect.
10:59Antagonist is 1 plus 1 equals 0.
11:02Penicillin plus Citricycline. Do not give them together.
11:07Here are some examples of good combinations.
11:09Please remember the first one, a beta-lactamase-sensitive Penicillin.
11:13Since it's beta-lactamase-sensitive, let's add a beta-lactamase inhibitor to prevent the destruction of this drug by beta-lactamase.
11:22And we'll talk about this soon.
11:24Anti-Pseudomonas, Penicillin plus Aminoglycoside for Pseudomonas.
11:27Third-generation Stiflosporin plus Aminoglycoside.
11:29Ampicillin plus Aminoglycoside.
11:31Have you noticed that Aminoglycosides are, like, everywhere, and it's very good for synergistic effect?
11:37It's a good combination when you combine them with beta-lactam antibiotics.
11:41The beta-lactam antibiotics are four categories.
11:45The Penicillins, the Stiflosporins, the Carbapenems, and the Monobactam.
11:53By the way, there is only one Monobactam. It's called Estreonam.
11:57Let's talk about the first one, antibacterials.
12:00Are either cell wall synthesis inhibitor or disruptor of cell membrane.
12:05They can inhibit the wall or the membrane of the freaking bacteria.
12:09Or they could be protein synthesis inhibitor.
12:13They inhibit translation and protein formation.
12:16Or nucleic acid synthesis inhibitor.
12:18By nucleic acid, I mean DNA and RNA and everything in between.
12:22And they are divided into direct acting or indirect acting.
12:26Direct acting, they will beat the living crap out of the DNA and RNA.
12:30Indirect acting, they will just inhibit the folate,
12:34which is a raw material important for synthesis of nucleic acid.
12:40Now, this is the most important diagram in this lecture.
12:43Antibacterials are either cell wall synthesis inhibitor, which include the cell membrane,
12:48because it's either a cell wall or a cell membrane.
12:51Both are lumped together in one category.
12:53Then we have protein synthesis inhibitor.
12:55And then we have nucleic acid synthesis inhibitor.
12:57It could be direct, which inhibit transcription or replication.
13:00Or indirect, they inhibit the folate.
13:03Let's talk about cell wall and cell membrane inhibitor.
13:06Let's start with the cell wall.
13:08You have three categories, beta-lactams, glycoproteins, and non-classified.
13:12This was the cell wall.
13:15How about the cell membrane, baby?
13:17The cell membrane is going to be the daptomycin or the polymyxins, including polymyxin B.
13:22Cool. Let's talk about the cell wall.
13:23You have three, beta-lactams, glycoproteins, and non-classified.
13:27Glycoproteins, vancomycin.
13:30Non-classified, base tracing.
13:31Thank you so much.
13:32How about the beta-lactams?
13:33You have four, penicillin, cephalosporin, carbapenem, and monobactam,
13:38such as the only one, astreonam.
13:41We are done with cell wall slash cell membrane inhibitor.
13:44Thank you very much.
13:45Let's talk about protein synthesis inhibitor.
13:48They are either 30S inhibitors or 50S inhibitors.
13:52What are the 30S and 50S?
13:54These are ribosomal subunits that are only present in bacteria, but not human.
14:00Human beings do not have the 30S and the 50S.
14:03Human beings just have 40S and 60S.
14:07So, in other words, the bacteria has 30S and 50S,
14:14and together we call them a 70S or a prokaryotic ribosome.
14:20This is bacteria.
14:22However, human beings have 80S chromosome, or I'm sorry, 80S ribosome,
14:29and it's made of 40S and 60S.
14:32These are the...
14:33Oh, but I thought like 30 plus 50 is 80.
14:36This is not a math class, honey.
14:37Get out of here.
14:38Cool, 30S inhibitors.
14:41They are only two, the aminoglycosides and the tetracyclines.
14:45Remember to add the S because there is a difference between tetracyclines,
14:49which is a group of medications, and tetracycline, which is an individual drug.
14:5550S inhibitors are many, including macrolides, glycosamides, such as clindamycin,
15:00streptogramine, chloramphenicol, and lenisolid.
15:03Just remember that the 30S are the aminoglycoside and the tetracycline.
15:07Amine no has the word no.
15:09This is an important mnemonic.
15:11Tetracyclines start with a T.
15:13They will cause teeth discoloration, and they will inhibit the teeth growth
15:17and the bone growth, and they will lead to growth stunting.
15:21Nucleic acid synthesis inhibitors are either direct-acting.
15:24They will beat the living crap out of the DNA, RNA, and everything in between,
15:28or indirect, which inhibit the raw material folate.
15:31Let's talk about the direct-acting.
15:33You have the quinolones or fluoroquinolones, such as ciprofloxacin
15:37or anything that has floxacin in it,
15:40nitroferantoin, which will cause your urine to be brown,
15:44rifamicin or rifampin, which will cause your urine to be red-slash-orange.
15:49Lovely colors.
15:51Folate inhibitors are TMP-SMX, combined together,
15:55or pyromethamine-sulfodiazine, combined together.
15:59We use this combination for toxoplasmosis.
16:03In the downloadable PDF, you have this diagram.
16:06Please try to memorize it, and then get a blank piece of paper
16:10and try to write everything here down.
16:13It will save you tons of hours.
16:16Since the Apple iOS 13 now has dark mode,
16:20let's add my dark mode of antibiotics.
16:22They are either antibacterial, antifungal, antiviral, or antiparasitic.
16:28Okay, we got it.
16:29What do we have here?
16:30We have the antibacterials include cell wall synthesis inhibitors,
16:35and if I want to write something here, what should I write?
16:39Like here, I should write protein synthesis inhibitor.
16:43Cool.
16:44And then if I want to add something here, I should add what?
16:47Nucleic acid synthesis inhibitor.
16:50All right.
16:51Protein synthesis are either 30S inhibitors or 50S inhibitors.
16:57Excellent.
16:57Nucleic acid synthesis inhibitors are either direct,
17:01which will be the living crap of DNA, RNA, and transcription, translation,
17:06stuff like that, or indirect.
17:07They are just folate antagonists.
17:10And of course, they can lead to megaloblastic anemia
17:13because they inhibited your folate.
17:16Think, people.
17:17Let's talk about cell wall synthesis.
17:19I mean the cell wall and the cell membrane.
17:22Cell wall and cell membrane.
17:24Let's start with the cell wall.
17:25Beta-lactams, they are only four groups.
17:27Penicillins, cephalosporins, carbapenems, monobactams.
17:32There is only one monobactam.
17:34It's the one and only.
17:35Astreonam.
17:37The glycoproteins are vancomycin and telavancin.
17:40The non-classified are basitracin, which is only used topically.
17:44Basitracin, just to trace some cream over your lovely skin.
17:51That was the cell wall inhibitors.
17:52How about the cell membrane disruptors?
17:54The daptomycin, which can lead to muscle problem.
17:58And the polymexin.
17:59The poly are like tied pods.
18:02They will form pores in the membrane.
18:05Hashtag osmosis.
18:07Here is another important diagram.
18:09Please download the PDF and print it.
18:12Cool.
18:12This is the bacterial cell.
18:14First, we have the cell wall on the outside.
18:17OK, I got you.
18:18And then we have the cell membrane on the inside.
18:21Let's inhibit the cell wall.
18:23You have beta-lactams, vancomycin and basitracin.
18:25Thank you so much.
18:26Let's disrupt the cell membrane.
18:28You have daptomycin, polymexin B.
18:30Thank you so much.
18:32Now, let's talk about all of this nonsense.
18:33We start with PABA or para-amino-benzoic acid, DHF, which is dihydrofolate.
18:39There is a famous, very famous enzyme here called dihydrofolate reductase,
18:43which will convert the dihydrofolate into tetrahydrofolate.
18:46Tetrahydrofolate will form DNA and then DNA will become RNA.
18:51This is called RNA polymerase.
18:53Normally, we go in this direction.
18:56HIV, however, wants us to go in the opposite direction
18:59because it has the reverse transcriptase.
19:02But forget HIV now.
19:03We're talking about bacteria, not virus.
19:05OK, after RNA, you get protein.
19:08From DNA to RNA, it's called transcription.
19:10From RNA to protein, it's called translation.
19:13Let's inhibit those steps by folate antagonists.
19:17These are indirect nucleic acid synthesis inhibitors,
19:21such as TMP-SMX or pyrimethamine sulfadiazine.
19:26Next, we have, you can interfere with the DNA.
19:29We can beat the living crap out of the DNA.
19:31These are the quinolones and your nitroferantoin.
19:35We can inhibit the RNA synthesis by inhibiting the RNA polymerase.
19:40You can use rifamicin or rifampin, which will make your urine red slash orange.
19:46But nitroferantoin will make your urine brown.
19:49We can inhibit the protein synthesis here
19:52by either inhibiting the 30S subunit or the 50S subunit.
19:57Let's inhibit the 30S.
19:58You only have two groups.
20:00Aminoglycosides, they have the word no.
20:02Tetracycline, they start with a T.
20:05And you can inhibit the 50S.
20:07We have many.
20:07We have macrolides.
20:09We have clindamycin, streptogramine, chloramphenicol, and lenisolate.
20:13Let's talk about the story of the Staph aureus, which became resistant.
20:19In the beginning, Staph aureus was sensitive to methicillin.
20:23We called it methicillin-sensitive Staph aureus, or MSSA.
20:32Then the Staph became resistant to methicillin.
20:36So we developed a new drug called vancomycin,
20:41because now the Staph is resistant to methicillin,
20:44and we call it MRSA, methicillin-resistant Staph aureus.
20:49So we invented a new drug called vancomycin to treat the MRSA.
20:54But then the MRSA is smart.
20:57It became vancomycin-resistant Staph aureus, or Versa.
21:02So we invented a new drug to deal with the Versa,
21:05such as lenisolate, daptomycin, etc.
21:09So here is the story again.
21:11In the beginning, Staph aureus was sensitive to methicillin.
21:14Next, it became resistant to methicillin, called MRSA.
21:18We developed vancomycin.
21:19It became resistant to vancomycin, called Versa.
21:23So we developed lenisolate and daptomycin to deal with the Versa.
21:26Let me go back to the methicillin.
21:27You remember methicillin? Yes.
21:29Methicillin is very toxic to your kidney.
21:31It causes interstitial nephritis.
21:33So we do not use methicillin anymore.
21:35Okay, so how are you going to treat the methicillin-sensitive Staph aureus?
21:39We developed four new drugs.
21:42OX, CLOX, DICLOX, and NEF.
21:45OX, CLOX, DICLOX, and NEF.
21:47OXACILLIN, CLOXACILLIN, DICLOXACILLIN, and NEFICILLIN.
21:52NEF for Staph.
21:54So whenever I say the word methicillin-sensitive Staph aureus,
21:59I mean OX, CLOX, DICLOX, and NEF-sensitive Staph aureus.
22:04And when you hear me say the word MRSA,
22:06or methicillin-resistant Staph aureus,
22:08I mean OX, CLOX, DICLOX, and NEF-resistant Staph aureus.
22:13Because methicillin is now obsolete,
22:16because it caused interstitial nephritis.
22:19Syphilisporins have five generations.
22:23May God bless them.
22:25First generation, second generation, third generation,
22:27fourth generation, fifth generation.
22:29First and second generation cover the gram positive
22:32and, to a lesser extent, the gram negative.
22:35Generation three and generation four
22:37are more concerned with the gram negative
22:40and, to a very little extent, the positives.
22:44Antibiotics are either antibacterial, antifungal,
22:47antiviral, or antiparasitic.
22:49Antibacterials are either cell wall
22:51slash cell membrane inhibitors,
22:53protein synthesis inhibitor, nucleic acid synthesis inhibitor.
22:57Let's talk about the cell wall.
22:58Beta-lactams, glycoproteins such as vanco, and bacitracin.
23:02How about the cell membrane, dapto, and polymyxin?
23:05Next, we have protein synthesis inhibitor,
23:0730S inhibitors, amino, and tetra,
23:0950S inhibitors, all of the others.
23:11Nucleic acid synthesis inhibitor, direct,
23:13inhibit the DNA or RNA transcription translation,
23:16indirect, inhibit the folate.
23:18What are the direct?
23:19Quinolones such as ceprofloxacillin,
23:22nitroferantoin, which will make your urine brown,
23:24rifamycin or rifampin,
23:25which will make your urine red slash orange.
23:28The folate inhibitors, TMP with Esamax,
23:31pyrimethamine with sulfadiazine,
23:34and we use this for toxoplasmosis.
23:37We use this for urinary tract infection, among others.
23:41What are the four beta-lactams?
23:43Penicillin, cephalosporins, carbapenems,
23:46and monobactams such as the one and only,
23:48astreonam.
23:49Oh, let's have a case.
23:51A 35-year-old male presents with lesion down there.
23:55He is a sex worker and sexually active
23:58with multiple partners, including foreigners.
24:01He does not use protection during coitus.
24:04On physical exam, there is a single painless ulcer
24:08on his penis that measures 1 to 2 centimeter in diameter.
24:12The ulcer has a hard, indurated base
24:15with a heaped up border and a clean base.
24:19There is bilateral painless lymphadenopathy
24:23in the regional lymph node, in the groin or whatever.
24:26The patient recalls that it started
24:30as an elevated small mass on the penis,
24:34which secreted pus, but then now it's flat and ulcerative.
24:39What is the most likely diagnosis?
24:42Is it chancroid, chancre, condyloma lata,
24:45condyloma acuminata, gonorrhea, or chlamydia?
24:49Please pause.
24:51And the answer here is, of course, B, chancre.
24:55This is primary syphilis.
24:57Classic.
24:58The lesion on the penis is painless.
25:02The regional lymph nodes are enlarged and painless.
25:06All right, miticosis, why not chancroid?
25:09Chancroid is painful.
25:11The lesion on the penis is painful,
25:14and the regional lymph nodes are painful.
25:17Here is another distinction.
25:19Primary syphilis, the chancre, is just one, a single lesion.
25:24But in chancroid, they are usually multiple lesions
25:27on the penis.
25:28How about condyloma lata?
25:29Condyloma lata is rash in secondary syphilis,
25:35not primary syphilis.
25:37And this is primary syphilis.
25:38How about condyloma acuminata?
25:40It has nothing to do with syphilis.
25:42Condyloma acuminata is HPV, human papillomavirus.
25:47How about gonorrhea or chlamydia?
25:48It doesn't seem like it because there is painless
25:52lymphadenopathy and painless ulcer on the penis,
25:55and it's classic for primary syphilis
25:57because it has a hard, indurated base
26:02with a heaped-up border, but the base is clean.
26:05There is no yellow pus in the base.
26:07But in chancroid, there is yellow pus in the base.
26:11Cell wall synthesis inhibitors include beta-lactam,
26:14vancomycin, and base hydration.
26:15The only thing that I want you to know about base hydration
26:18for now is that it's only topical.
26:21Let's talk about the cell membrane,
26:22not the cell wall, but the membrane.
26:24We have daptomycin, polymyxin B.
26:26The only thing that I want you to remember
26:28about daptomycin is it causes rhabdomyolysis.
26:33It destroys your muscles, baby.
26:35We will add more about daptomycin
26:37in the upcoming lectures.
26:39Polymyxin B starts with a P, and as you know,
26:43it will form pores in the membrane
26:46and disrupt the integrity of the cell membrane.
26:49Here is a great mnemonic, and this is from OnlineMedEd.
26:52It's a great website, by the way,
26:54and this doctor has a very good video on YouTube
26:58called the Antibiotics Ladder.
27:01Okay, cool.
27:02If you have an anaerobic infection,
27:04an infection caused by an anaerobe,
27:07a bacteria that's an anaerobe, it needs no oxygen.
27:11How do you treat it?
27:12It depends on the location of the infection.
27:15If the location is in your abdomen or pelvis,
27:18treat it with the metro, metronidazole.
27:21But if the infection is anywhere else,
27:24treat it with clindamycin.
27:26Remember Linda, the Catholic nun.
27:28So, where is the anaerobic infection?
27:30Doctor, it's in my GI tract,
27:33such as pseudomembranous colitis, colon.
27:35It's in my abdomen, slash pelvis.
27:38Give metronidazole.
27:40Doctor, it's in my pelvis.
27:42Give metronidazole.
27:44Doctor, it's on my skin.
27:46Give clindamycin.
27:48Doctor, I have aspiration pneumonia in my lungs.
27:52Give clindamycin.
27:53Again, it depends on the location.
27:56What are the anti-pseudomonial antibiotics?
27:59Very, very, very, very, very, very important.
28:03Okay, so here are the four beta-lactams.
28:05Penicillins, cephalosporins, monobactam, and carbapenem.
28:10All right, let's start with them.
28:11Let's start with the penicillin.
28:12Anti-pseudomonial penicillins.
28:14Not all penicillins, but a group of them
28:16called anti-pseudomonial, such as carbenicillin,
28:19ticercillin, pepericillin, azlucillin.
28:22How about cephalosporin?
28:23Only the third and fourth generation.
28:26How about the fifth?
28:27The fifth covers MRSA, but it does not cover pseudomonas.
28:31And the one and only estreonam, which is a monobactam,
28:34as well as carbapenem, such as amipenem,
28:38which has to be combined with celestatin.
28:41Otherwise, your kidney will suffer.
28:43OK, next, we have the aminoglycosides,
28:47which are used for aerobic infections only,
28:51especially if they are gram-negative,
28:53and the quinolones, such as the ciprofloxacin.
28:57Quinolones are a nucleic acid synthesis inhibitor,
29:00specifically direct nucleic acid synthesis inhibitor.
29:04Here is case number two.
29:06By the way, this is the same patient from the last case.
29:09The question is, if this lesion on the penis is left untreated,
29:14what will happen to this ulcer?
29:16A, transformed into malignant neoplasm,
29:19or it's going to resolve on its own, increase in size and number,
29:23ooze its yellow purulent fluid, and then malignantly transform,
29:27becomes indurated, fluctuant, then forms a large,
29:31draining sinus and buboes.
29:34Please pause.
29:36And the answer here is B.
29:39It's going to resolve on its own.
29:40That's why many patients who have syphilis
29:43do not seek medical attention.
29:45After all, the lesion on the penis just went away.
29:49So they think, oh, I'm fine now.
29:52There is no need to go to the doctor.
29:55But the trypanema is still there in their body,
29:58waiting until it becomes secondary syphilis,
30:03with its chondylomalata and rash,
30:06including rash on the palms and the soles.
30:09And then it goes away.
30:11So the patient doesn't seek medical attention.
30:13Then it becomes tertiary syphilis.
30:17And this is ugly.
30:18This is the gamma, which is a caseating granuloma.
30:21This is the tabes dorsalis.
30:23This is the neurosyphilis that can eat your brain alive,
30:28leading to memory problems, personality changes,
30:33ataxia, etc.
30:34This is also the aortitis,
30:37specifically in the ascending aorta at the junction
30:40between the ascending aorta or the aortic arch
30:43and the brachiocephalic artery,
30:46which is the first branch of the aortic arch.
30:49This can lead to aortic regurgitation on auscultation.
30:53Aortic regurgitation is diastolic decrescendo murmur.
30:58If this is S1 and this is S2
31:01and this is S1 of the next cardiac cycle,
31:03aortic regurgitation is like this.
31:06It's diastolic, in the diastole,
31:08and decrescendo, which means it's downward sloping.
31:11Lop-dsh, lop-dsh, lop-dsh, lop-dsh, lop-dsh.
31:19And here is the most important diagram in this video.
31:22I just said that five times before.
31:23Okay.
31:24Here is the penicillin, syphilis-4, carbapenem,
31:26monobactam, the one and only S3 and M,
31:28vancomycin, amine, neo, glycosides, tetracycline,
31:32macrolides, clindamycin, sulfonamides,
31:34quinolone, and mitronidazole.
31:36This means gram-positive cocci,
31:38this gram-positive rod,
31:40this is a gram-negative cocci,
31:42and this is the tryponema pallidum.
31:44This is a spirochete under dark-field microscopy.
31:48So penicillin covers gram-positive cocci,
31:50gram-positive rods, gram-negative cocci,
31:53such as nocerea meningitidis,
31:55and tryponema pallidum for syphilis,
31:57such as the last patient who had primary syphilis.
32:00How about syphilisporin?
32:01They cover gram-positive cocci and rods,
32:04gram-negative cocci and rods.
32:06Next, we have carbapenems.
32:08They cover the anaerobes,
32:10gram-positive cocci, gram-negative rods.
32:14And you go all the way like this,
32:16and you memorize everything you need to know
32:18about antibiotics just in one diagram.
32:20Just genius.
32:22Thank you so much for watching.
32:23This is Medicosus Perfectionalis,
32:25where medicine makes perfect sense.
32:27If you need anything, you can go to my website,
32:30medicosusperfectionalis.com.
32:32If you need to send me an email,
32:33just send it to medicosusperfectionalis at gmail.com.
32:38Thank you so much for watching,
32:40and I'll see you in the next video
32:41when we talk about the beta-lifetimes.
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