💊 5-HT3 Inhibitors (ex: ondansetron)
🤢🤮 Nausea and vomiting are two of the most common presenting complaints
5-HT3 inhibitors (such as ondansetron) are one of the top 200 drugs prescribed and are used for the prevention of:
🌟 chemotherapy-induced nausea and vomiting
🌟 radiation-induced nausea and vomiting
🌟 postoperative nausea and vomiting
🌟 off-label for nausea and vomiting associated with pregnancy
Vancomycin belongs to a class of antibiotics called glycopeptides. Drugs in this class are composed of a cyclic peptide bound by two sugar molecules (glycogen), hence the name glycopeptides!
MOA: binds to D-alanyl-D-alanine on the outer surface of cell membranes preventing cross-linking. This interferes with cell wall synthesis and results in bacterial cell death.
Another way to think of it: cell walls are like LEGO pieces linking together. The more that are linked, the stronger the structure is. Vancomycin prevents this cross-linking leading to an unstable structure.
Vancomycin = think mainly gram-positive coverage including MRSA! (gram-negatives do NOT have a thick cell wall and lack the D-ala-D-ala sequence, making vancomycin useless against them)
NOTE: Recently, the term “red man syndrome (RMS)” has been replaced and is now recognized as “vancomycin flushing syndrome” or “vancomycin infusion reaction”.
Mind the Gap- HAGMA Read More »
⭐ This is a great way to remember the names of antiretrovirals ⭐ Antiretroviral medications are used to treat HIV by blocking different stages of the virus’s life cycle (e.g., blocking entry into the host’s CD4 lymphocyte, inhibiting viral DNA from replicating, etc.) 😖 However, learning the names of antiretroviral medications is horribly difficult. There are lots of drugs, with a dizzying array of names, abbreviations, and combination tablets. Hopefully, this will help you not to completely BLANK on which drug belongs to which type of antiretroviral! 🤓
Vasopressors and Inotropes
Vasopressors and inotropes OH NO! 🙇🏻♀️ These medications are commonly used in the critical care setting in patients with shock (or those with extremely low blood pressure) leading to end-organ damage (acute kidney injury, increased LFTs, etc.).
👉🏻 Vasopressors are drugs that cause vasoconstriction, therefore increasing mean arterial pressure (MAP). Vaso refers to blood vessels and pressor means to put pressure on or constrict making up the word – VASO-pressor. 🩸
Examples of vasopressors include:
⭐ Norepinephrine
⭐ Epinephrine
⭐ Vasopressin
⭐ Phenylephrine
👉🏻 Inotropes are drugs that affect cardiac contractility (or the force of muscular contractions). They can also be used as chronotropes (drugs that increase heart rate). THINK: Ino = strength; Chrono = time. Some vasopressors may also have effects on contractility and are called inopressors.
Examples of positive inotropic agents include:
⭐ Milrinone
⭐ Dobutamine
⭐ Dopamine
⭐ Isoproterenone
🧠 With the many different types of vasopressors and inotropes, it is important to understand how they work to use them effectively. Choosing the wrong agent or using it inappropriately, can harm the patient.
Vasopressors and Inotropes Read More »
IV chemotherapy agents with high emetic risks Read More »
Drugs that cause Constipation Read More »
It is common for learners to struggle with memorizing antibiotic coverage when they are first introduced to the subject. With so many unfamiliar bacteria and antibiotics to know, it can be more than enough to get your head spinning.
In school, you probably learned the spectrum of activity for antibiotics by grouping bacteria into 3 common classifications:
Gram-positive bacteria (e.g., Streptococcus, Staphylococcus, Enterococcus)
Gram-negative bacteria (e.g., E. coli, Klebsiella, Salmonella, Shigella, Pseudomonas)
Atypicals (e.g., Chlamydophilia, Legionella, Mycoplasma)
Additionally, you learned that they are then further subclassified into aerobes, anaerobes, lactose-fermenting, and non-lactose-fermenting. But wait, don’t get cross-eyed just yet! Memorizing the spectrum of activity of antibiotics does not have to be that difficult. In this article, I’ll share some memorization tips on remembering the common bugs and what drugs cover them.
BUGS AND DRUGS
A great tip for remembering antibiotic coverage starts with memorizing the antibiotics that cover the major categories of bacteria including anaerobes and atypicals as well as resistant pathogens such as methicillin-resistant staphylococcus aureus (MRSA) and pseudomonas. From there, you can build upon your knowledge of other less commonly seen bacteria or infections through the application of the material during class, rotations, and clinical practice.
Needless to say, these are a MUST for you to know for exams. Review the mnemonics below and quiz yourself to see how much you remember.
NOTE: Clindamycin, doxycycline, and Bactrim (generic: sulfamethoxazole/trimethoprim) cover community-acquired MRSA infections while vancomycin, ceftaroline, and daptomycin cover hospital-acquired MRSA infections. Other antibiotics not listed include: linezolid, telavancin, dalbavancin, oritavancin, tigecycline (this mnemonic story can get pretty long!)
NOTE: Atypical bacteria do not color with Gram staining (because they lack a cell wall) and remain colorless. They are neither gram-positive nor gram-negative; they are ATYPICAL! 🙂
NOTE: These are the main antibiotics that empirically cover anaerobes. There are other antibiotics that do have some anaerobic coverage but since anaerobes are hard to culture and identify, empiric therapy is often used in practice.
NOTE: Other antibiotics not listed include: cefiderocol, colistin, ceftolozane/tazobactam
TIPS FOR SUCCESS
QUIZ YOURSELF
A) Which of the following antibiotics can be used for a patient with MRSA+ pneumonia?
B) All of the following antibiotics cover pseudomonas EXCEPT for?
C) A patient is in need of anaerobic coverage for a diabetic foot infection, which of the following antibiotics would provide adequate anaerobe coverage?
D) Which antibiotic would provide coverage for atypical pathogens and streptococcus pneumoniae in a healthy patient diagnosed with community-acquired pneumonia (assuming local resistance is low)?
ANSWERS: A. 2, B. 3., C. 3., D. 3.
Hope these were helpful! If you have any additional memorization tips of your own, feel free to share them in the comments below.
If you are interested in learning more, check out our Antibiotics Pharmacology Coloring Book or Top 200 Drugs Made Easy Coloring Book for additional memorization tips!
Top Antibiotic Coverage Mnemonics Read More »
👶🏻 Preterm labor occurs when labor begins too early. If this happens before the 37th week of gestation, the fetal organs, especially the lungs, might not be fully developed.
💊 In these cases, labor can be suppressed with uterine relaxants that relax the uterine muscle and slow down contractions for up to 48 hours. It gives the fetus a few more days in the uterus as a corticosteroid is given to speed up the development of a preterm infant’s lungs. Steroids help the lungs mature and may promote the production of surfactant, a substance that prevents the collapse of alveoli (small sacs in the lungs where the air is exchanged).
💊 Uterine relaxants are also called tocolytics (toco = childbirth, lytic = terminate) and include several different types of drugs.
Uterine Relaxant Drugs Read More »
Antibiotic Renal Dosing Read More »
Ketamine Properties Read More »
Background
In this overview, we will be talking about how some of the most common antibiotics work. Let’s begin with a reminder of the structure of bacteria.
There are two main groups of bacteria – Gram-negative organisms and Gram-positive organisms. They are classified based on their Gram stain. What is a Gram stain? Gram stain is named after the Danish physician Hans Christian Gram who created this staining technique for visualizing bacteria; therefore, when you refer to Gram stains, use a capital “G.” Bacteria cell walls are made up of a substance called peptidoglycan, a polymer of amino acids and sugars that serves a fundamental role in the structure and integrity of the cell.
Bacteria differ in the types of walls they have. Gram-positive organisms have a thick peptidoglycan layer that retains crystal violet stain, making them purple after Gram staining. Gram-negative organisms have two distinct layers, a lipopolysaccharide (LPS) membrane that surrounds a thin layer of peptidoglycan. The LPS membrane does not retain crystal violet stain – they are stained later in the process by a pink counterstain called safranin, making Gram-negative organisms pink after Gram staining.
A great memorization tip is to keep your P’s together
Once you have made it passed the cytoplasmic membrane and cell wall, you have reached the organism’s cytoplasm wherein resides the organism’s ribosomes, genetic material, and other enzymes important to the bacterium’s survival – all things that antibiotics have been designed to target. Bacteria have ribosomes that translate messenger RNA into polypeptides and contain two subunits – the large 50S and small 30S subunits. Ribosomes are factories for protein synthesis. Proteins are responsible for all cell functions including things such as protective proteins, transport proteins, toxin proteins, and so much more!
Disrupt Cell Membrane:
There are two main antibiotics that work by disrupting the inner and outer membranes of bacterial cell wall, disrupting their function and leading to bacteria cell death, polymyxin and daptomycin.
Polymixins such as colistin and polymyxin B act like soap. Since these agents bind to the LPS layer, they have no activity against Gram-positive bacteria, which lack this layer.
Daptomycin inserts itself into the cytoplasmic membrane of Gram-positive bacteria, weakening the membrane and causing cations to leak out of the cytoplasm. This rapidly depolarizes the membrane potential, stopping processes essential for the life of the bacterium and killing it.
Cell Wall Inhibitors:
A few antibiotics target the creation of the cell wall itself, including Fosfomycin, beta-lactams (penicillin, cephalosporin, carbapenems), monobactam, and vancomycin. Fosfomycin inhibits an enzyme that catalyzes the first step of cell wall synthesis. Beta-lactam antibiotics like penicillins, cephalosporins, and carbapenems contain beta-lactam rings that irreversibly bind to enzymes on the cell membrane in bacteria called penicillin-binding proteins, or PBPs. This stops the final step in the creation of the peptidoglycan layer of bacterial cell walls, making the cell walls defective and unstable, leading to a series of events that ultimately kills the bacteria. Aztreonam, a monobactam antibiotic, also works this way. its mechanism of action is similar to a Trojan horse sneaking into the cell.
Vancomycin is a glycopeptide antibiotic that also works on cell wall biosynthesis. Glycopeptides are too big to get through the outer layer of Gram-negative bacteria, so, unlike beta-lactam antibiotics, glycopeptides only work on Gram-positive organisms. They bind to the D-alanyl-D-alanine (D-ala-D-ala) precursor – D-alanyl-D-alanine is an important component of the peptidoglycan layer, so when glycopeptides block its formation, they are stopping cell walls from being built. The lipoglycopeptides telavancin, dalbavancin, and oritavancin are like cousins to vancomycin that work the same but with an added mechanism of action similar to daptomycin that disrupts the cell membrane causing it to depolarize and become permeable, killing the cell.
Protein Synthesis Inhibitors:
Several antibiotics act on the ribosome, a complex molecule that serves as the factory for protein synthesis:
Aminoglycosides like gentamicin, tobramycin, and amikacin and tetracyclines like tetracycline, doxycycline, minocycline, tigecycline, are protein synthesis inhibitors that irreversibly binding to the small 30S ribosomal subunit.
Clindamycin, macrolides, oxazolidinones (linezolid and tedizolid), and lefamulin are protein synthesis inhibitors that interact with the big 50S ribosomal subunit, interfering with polypeptide chain synthesis leading to bacteria cell death.
Folic Acid Synthesis Inhibitors:
Folic acid is synthesized by bacteria from the substrate, para-amino-benzoic acid (PABA), and all cells require folic acid for growth. However, folic acid cannot cross bacterial cell walls by diffusion or active transport. For this reason, bacteria must synthesize folic acid from PABA. Sulfonamide antibiotics such as sulfamethoxazole and trimethoprim work synergistically with one another by interfering with folic acid production within the bacterium. Trimethoprim binds dihydrofolate reductase, and sulfamethoxazole competitively inhibits dihydrofolic acid synthesis by mimicking p-aminobenzoic acid, or PABA, preventing the final step of the process.
To help you remember this, think of the ‘FO’ in sulFOnamides as inhibiting FOlic acid synthesis.
Nucleic Acid Inhibitors
Lastly, a few antibiotics work against nucleic acids, the primary molecules that make up DNA, either directly or indirectly by inhibiting their production or repair.
Fluoroquinolones like ciprofloxacin, levofloxacin, moxifloxacin, and delafloxacin inhibit enzymes called DNA topoisomerases (DNA gyrase and topoisomerase 4), interfering with DNA replication, transcription, repair, recombination, and transposition.
Fidaxomicin works specifically on Clostridioides difficile RNA polymerases, making it useful for treating only that bacterium.
Metronidazole targets only anaerobic bacteria like Bacteroides species and protozoa like Giardia – it may be metabolized into a molecule that disrupts DNA and inhibits its synthesis, but we don’t really know how it works. It isn’t the only common antibiotic that we don’t know for sure how it functions – nitrofurantoin, an antibiotic helpful only for treating urinary tract infections, is also metabolized into molecules that may inactivate ribosomes, DNA, and RNA, but we don’t know for sure.
Mechanism of Action Mnemonic:
Let’s review some quick mnemonics on how to remember the MOA of some of the antibiotic classes discussed:
Cell membrane/wall inhibitors: remember this mnemonic:
Destroys Protective Fortification & Murders Various Bacteria.
The first two antibiotics in the mnemonic disrupt bacteria cell membrane and the rest work on the bacteria cell wall.
Protein synthesis inhibitors:
You’re AT 30th st. (30S) and you want to COM to 50th st. (50S)
Inhibit folic acid synthesis:
Think of the ‘FO’ in sulFOnamides as inhibiting FOlic acid synthesis
Inhibits DNA/RNA synthesis:
Think of the F in the first letters of these antibiotics as standing for DNA/RNA “Fiber”. The “x” in the middle of fidaxomicin also looks like a chromosome.
Antibiotics 1: Mechanisms of Action Simplified Read More »
