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Now, That’s What I Call High-Yield: Pharmacology

I feel like too many of these installments start [INSERT SUBJECT NAME]….the bane of so many students’ studying. Sadly, pharmacology fits the bill. But, luckily, I absolutely love it and my day to day life in anesthesia is absolutely dependent on it! Ergo, I’ll make it “fun” and digestible for you.

As with all subjects, the way to approach pharmacology is systematic. Start with a brief overview of some general concepts. Move on to the autonomic nervous system, and where we find the ultra-high yield G-protein (e.g. alpha, beta) receptors. Understand the general toxidromes and big picture side effects of general classes, and the foundation is built.

When it comes to system specific drugs, while there is some overlap with this general chapter, we will cover those in each subject specific section.

Inhibitors (6.5) – Understand the difference between competitive and noncompetitive inhibitors. The Michaelis-Mentin kinetics and Lineweaver-Burk plots can get a little esoteric, and don’t offer too much in terms of being “high-yield,” but they might get you a question or 2 on the test.

Crammable equations (8.5) – There’s a ton of equations that lead to WILDLY EASY points on the test, IF you are able to memorize these equations on Test Day. It literally comes down to plugging 2 given numbers into a x = y/z sort of equation, and BOOM – there’s a correct answer. The downside? There are about 5 different equations here, including volume of distribution, clearance, half-life, and dosages. Best advice? Do what you can to memorize them the first time through, but don’t worry if you forget them. They will enter and exit your mind over and over throughout medical school. When you are in the final days leading up to the test, cram these equations into your head, so that when you forget them in 3 days time, Step 1 is done and done.

CNS/PNS layout (7.5) – This will come to play more in the neurology section, when you develop a proper framework of how the CNS and PNS are laid out. Key takeaways here are as follows:

  • Parasympathetic preganglionic AND postganglionic neurons use acetylcholine (ACh) as a messenger
  • Sympathetic preganglionic neurons use ACh, but sympathetic postganglionic neurons use epinephrine and norepinephrine (with the exception of sweat glands, which use the ACh for both)
  • Voluntary muscles use ACh as a messenger at a NICOTINIC ACh receptor
  • Muscarinic ACh receptors are found in the heart, brain, and smooth muscle (very clinically significant for bronchial dilation and constriction)

G-protein linked second messengers! (9.5) – Easily one of the most important parts of the chapter. Knowing which G-protein type (Gi, Gq or Gs) is associated with each receptor is a must. Even more important than that, knowing where different receptors are found in the body and their function will pay dividends both on test day and throughout your medical career. The most clinically relevant receptors are 𝝰1, 𝛃1, 𝛃2, M1, M2, H1, H2, and V2. A further description of these receptors (and the drugs and endogenous chemicals that agonize & antagonize them) will warrant its own post entirely.

Atropine (and antimuscarinic toxidrome) (7.5) – Atropine is a key drug, as it is part of your ACLS algorithm for symptomatic bradycardia. It blocks muscarinic (parasympathetic drive) on both sides of the blood-brain barrier, so can lead to a bit of mad[as a hatter]ness. If you remember the DUMBELSS of your cholinergic-crisis farmer in an organophosphate-laden crop maze, atropine will cause the opposite, and cure him at the same time. Classic tried-and-true mnemonic: Mad as a hatter, red as a beet, hot as a hare, dry as a bone, blind as a bat.

Sympathomimetics (9) – High, high-yield. Among the most important here is Epinephrine. The prefix epi-, greek for above, means epi hits all types of 𝝰 & 𝛃 receptors, with 𝛃 being affected more than 𝝰. Norepinephrine hits all the same receptors except (nor) 𝛃2. Isoproterenol (or iso𝛃roterenol) is isolated to 𝛃 receptors. Your “pure” 𝛃2 agonists, like albuterol, are most clinically relevant for bronchodilation. There is always a bit of overlap with 𝛃1 receptors, so administration can cause tachycardia. Do𝛃utamine whips the tired heart, and is used for acute decompensated heart failure. Rounding them out is dopamine, another pressor for shock.

Beta blockers (8.5) – Super-clinically relevant drug class. These drugs are used for hypertension, heart failure, angina, post-MI, supraventricular tachycardia, essential tremor, and even more. Be familiar with their function (block the stimulatory Gs protein!), adverse effect and toxicity (bradycardia, sedation, sexual dysfunction), and antidote (atropine and/or glucagon).

Toxicity treatment (7) – As a whole, you will definitely see a patient with some sort of drug overdose/intoxication on the exam. Which one? Who’s to say…Among the most important with their respective antidotes are Acetaminophen (N-actetylcysteine), benzodiazepines (flumazenil), carbon monoxide (100% [+/- hyperbaric] oxygen), heparin (protamine), methanol (fomepizole), opioids (naloxone), and warfarin (vitamin K and fresh frozen plasma).

Cytochromes (8) – Your inducers and inhibitors are long painful lists which aren’t going anywhere. Most common culprits are alcohol, -conazoles, erythromycin, amiodarone, omeprazole, metronidazole, phenytoin, carbamazepine, and rifampin.

Drug names (9) – To practice medicine, you need to speak the language. No brilliant way to get all of these internalized then to study them again and again, use flashcards, and spend a lot of time at the hospital.

This 23 page chapter of First Aid contains so much foundational information, it is worth at least a couple run-throughs. The knowledge of 𝝰 & 𝛃 receptors and their functions, agonists, and antagonists bears repeating. Stay tuned for a more in-depth look in our next post.

Check out our recent webinar on High Yield Neuro Pharmacology for the USMLE & COMLEX!