Held the evening before the paper, 3 September 2026. 11 standing scope rules and 12 answered questions, each with the timestamp it came from. This is the only place he says what is and is not being asked.
tools/check_pharm_review.py before this page
is written, with those corrections applied to the transcript rather than to the quote, so
the check cannot be fooled by the cleanup.“I would not get so hung up on indications other than generally like what kind of bugs is it treating or if there's notable bugs that it treats”
Asked to go over the treatment of the conditions named under each antibiotic, he said that is not where the course is yet. The pneumonia and syphilis examples in the lectures were context, not content — he is not asking for the treatment of choice for syphilis, and he is not expecting aminoglycosides for pneumonia until the pulmonology block later in the year.
What he does want off that axis: the notable organisms — he named MRSA, Pseudomonas and Clostridioides difficile — and the broad strokes, meaning does the agent cover anaerobes, does it cover atypicals.
“if we were doing a derm question about acne, for example, there you would want to know what kind of antibiotics you'd want to use and when”
He drew the line himself. The general antibiotic indications are out; the dermatology ones are in, because that material has been taught. The specific distinction he named is topical against oral — knowing which you reach for, and when.
“No, it'll be more, again, the broad strokes here”
Asked how much gram-positive and gram-negative detail is needed, he said to group by class. The two comparisons he gave as the right level:
“a patient has an infection, a skin infection. Do you think it's a gram-positive bacteria? Which one of these would be most likely to treat it?”
He described the item outright, including how the distractors are built: three agents with strictly gram-negative coverage and one good gram-positive agent, and you identify it. That is the level of discrimination being asked for — not which single drug treats one named organism.
“I'm never trying to trick you. It's just read the questions, see what I'm looking for and either know it or you don't”
He explained the statistic he checks after a paper — the point-biserial, which asks whether the people who did well overall got a given question right and the people who did poorly got it wrong. A high value means the item is measuring knowledge rather than puzzle-solving, and he said his run well. Read the stem for what it is asking; there is no second layer.
“As long as you know that it inhibits ergosterol synthesis and inhibits the ability for that cell wall or cell membrane to function and causes the cell to die, then that's good enough for my purposes”
He does not want the exact binding target of each antifungal class. What he would rather you could do is tell an antifungal from an antiviral from an antibiotic, so you know what you are treating.
The one place mechanism detail does matter is synergy. When two drugs are used for the same problem you need to know their mechanisms differ, because complementary mechanisms are the point of combining them.
“on the PANCE, you will only get the generic”
He gives both names wherever he can, deliberately, because in practice people say Lasix rather than furosemide and Rocephin rather than ceftriaxone, and he wants the association built early. But the board exam is generic-only, so the generic is the one you must have.
“most my questions will ultimately come down to four individual drugs”
Both halves of this matter, and they pull in opposite directions.
Learn the material by category. His example: every cell-wall-active drug is bactericidal — penicillins, cephalosporins, carbapenems, vancomycin, the polymyxins — so there is no point memorizing that fact drug by drug. Do the same for mechanism of action and the common contraindications. “Do big bins instead of individual agents.”
But the answer choices are individual drug names. He said most of his questions come down to four named drugs. So the skill being tested is seeing a drug name and placing it back in its bin — you read ceftriaxone, you think third-generation cephalosporin, and everything you know about that class becomes available.
That is exactly the drill the Drug Classes Drill and the other drills on this site are built to rehearse.
“don't know specific values. If I'm using any values, I will tell you what those are in the question itself”
He is asking why you look at a value, never what the number is. His worked contrast, which is worth knowing in full:
Same test, opposite target, for opposite reasons. That is the kind of question he is describing.
“pharmacology is not a what class, it's a why class”
He drew the contrast with anatomy, which he called closer to brute-force memorization, and with physiology, which is a why class — how the body normally works, how it goes wrong, how you then treat it. Pharmacology sits with physiology.
“I can read a drug reference if I wanted to know all the facts. I want you to know: why am I selecting this drug? What are the things I need to look for? How do I communicate this to my patient?”
“if you ever find yourself asking did he mean this or this you're already in the weeds”
Reading the stem. His shortcut is to read the last sentence first to see what is being asked, then go back through the stem for the context you need. He does not pad questions — there is no patient's favorite color in there, so every detail present is there for a reason. “Keep it simple, students.”
And the one he repeated hardest, twice, including as his closing line: do not change your answers. He called it one of the worst habits, the one he hears constantly from students who struggle. Trust the gut instinct unless you have a very obvious reason to change it — you have had a week with this material and it is already in there.
Asked: “Are there any adverse effects we should focus on specifically?”
“whenever you hear hoofs beating, normally you should be thinking horses. Sometimes it's a zebra”
Zebras are the uncommon effects that are unique to one particular drug. His example is the alcohol interaction with metronidazole — most patients on it for an infection will not be drinking, but it costs nothing to warn them.
The shortcut: commons belong to the group, not the drug. Asked whether the common side effects of penicillins, cephalosporins and carbapenems need learning separately, he said “no, they're all the same” — do not spend the headspace. Spend it where a class breaks the pattern instead, and his example there is the tetracyclines: calcium binding, the bone effects, and photosensitivity that the patient genuinely needs advice about.
Where to aim: “Any time you see those killers or the zebras, those are always things you should look at.” The commons cover a good share of what he asks; the idiosyncratic ones are each worth about one question — he named vancomycin infusion syndrome, and slowing the infusion to two hours, as exactly that kind of one-off.
Asked: “Should we focus on the categories, mechanism and adverse effects of the autonomic drugs, or what they are used for?”
“what their mechanisms are will inform you on what they are used for in a lot of cases”
He said you do not learn the indications separately — you derive them. The same antimuscarinic mechanism treats chronic drooling and urinary incontinence; it is one action in two organs. Glycopyrrolate tends to be used for the first and oxybutynin for the second, but that is marketing and licensing rather than a real pharmacological divide, and either would work.
His example question: which of these would be most likely to slow a rapid heart rate? There is more than one right road — a beta blocker, or a muscarinic agonist, or an acetylcholinesterase inhibitor raising acetylcholine. Recognize the category and what it does, and the answer follows.
The reasoning chain he wants you running: this drug is an antimuscarinic → what do muscarinic effects look like → I am blocking those → so what should I see? That is where the mad as a hatter, dry as a bone picture comes from, rather than being memorized as a list.
Asked: “For conditions treatable with multiple drugs, like bradycardia, will the answer be clear?”
“I would not include both atropine and epinephrine. I would have like three drugs that lower the heart rate further and then like one that didn't”
He will not make you choose between two right answers. Asked whether a condition with several valid treatments would be ambiguous, he described how he builds the item instead: three drugs that would make the problem worse, and one that would not. He said he writes them that clearly on purpose — “I hate it when students challenge my question” — so most distractors are not even theoretically reasonable.
The clinical content he gave with it: for symptomatic bradycardia he follows the advanced cardiac life support guidelines. Atropine first — an antimuscarinic, so blocking the muscarinic receptors on the heart raises the rate. If that is not enough, move to beta-1 activation: dobutamine, epinephrine, norepinephrine or isoproterenol, all sharing that one action. In the guidelines epinephrine is the usual next step after atropine.
Asked: “For the antifungals, do we need to know the exact organism — for example that posaconazole treats Aspergillus?”
“I would not get hung up on memorizing each individual type of fungus that the drugs treat”
No. He said the fungi do not sort into clean categories the way bacteria do with gram-positive and gram-negative, and that the organism lists were there to give a sense of what is being treated, not to be memorized.
What he wants instead is that you can identify the type of antifungal, and above all tell an antifungal from an antiviral. His example item: a patient is influenza A positive, which of these is the best treatment — with an antifungal sitting among the options for you to reject.
Asked: “How many questions are there per lecture?”
“There are five questions per technical hour of lecture”
Five questions per scheduled hour of lecture. He does not set the hours — the course director does — but the ratio is fixed. Dermatology was scheduled three hours, which is more than he thinks it needs, and it still earns fifteen questions.
His split: 15 from the first deck, 15 from the second, and the remainder from the third. He was not certain of the total, talking himself between 40 and 45 and settling on “I think it's 45 … I need to double check”. It is written here as he said it rather than tidied into a figure he did not commit to.
He also mentioned, unprompted, that his class averages usually land in the upper eighties.
Asked: “Any tips on last-minute studying, or things we really should focus on?”
“if you hear me spending like five minutes talking about something, chances are I think that's really important”
Re-listen rather than re-read. It is only three lectures. He said outright that time spent is his own signal — five minutes on something means he thinks it matters and probably wrote a question on it — and that the slides are not the whole picture, because the context, illustrations and stories are where the concepts lock in.
Group study, which he made the strongest case for: you cannot become fluent in a language through an app, you become fluent by talking to people who will catch what you have wrong. There is what you know, what you know you do not know, and what you do not know you do not know — and working alone is how that third category survives until the exam finds it.
“The first rule of PA school is being comfortable with being uncomfortable.”
Asked: “Can we go over the acne treatments in order for the different levels of acne?”
“start easy, start simple stuff first and then kind of work your way up to the big guns”
Before anything: ask what the patient has already tried, and what did and did not work. He was blunt about why — prescribe something they have already failed and they will conclude you were not listening.
Maximize the dose before you add or switch. If a product is partly working, go up in strength first.
Why going systemic costs you something. A topical works only where you put it, so the side effects stay local. Systemic antibiotics bring gastrointestinal upset, photosensitivity with the tetracyclines, and food and drug interactions — his example is a patient on a prenatal vitamin whose calcium and iron bind up the doxycycline.
Isotretinoin's price: heavy drying and desquamation, photosensitivity, light toxicity in the eyes, and worsening depression with possible suicidal ideation.
Also available: intralesional steroids for large inflammatory pustules, though he called that a specialty use.
And the contrast worth remembering: with an acute infection you do not hesitate — you go straight to what treats it. With a chronic condition like acne, “it's a marathon, it's not a race”, and you can work up the ladder finding what suits the patient.
Asked: “Would pilocarpine be preferable to carbachol because carbachol has more adverse effects?”
“the cholinergic agents are not really preferred for management of glaucoma”
He said he does not think either is clinically worse than the other, whatever the slide lists. The real answer is that the whole class is not preferred in glaucoma until you reach a third or fourth line agent.
Why: they cause miosis and impair the ability to re-accommodate the lens, so the patient gets poor vision and an induced short-sightedness, plus headaches from straining to see. He singled out younger patients with full vision as the worst fit. First-line is a prostaglandin or a beta blocker instead.
“I typically break them up into three categories. There's the killers, the commons and the zebras”
Asked which adverse effects to focus on, he gave a framework rather than a list. Sort every side effect you have learned into one of these three, and you will know what he is asking for.
Asked: “Does flaccid paralysis happen in phase one or phase two of the depolarizing agents?”
“So that would be in phase two”
Succinylcholine is two acetylcholine molecules joined together. In phase one it activates the nicotinic receptor at the neuromuscular end plate and depolarizes it — which is what produces the fasciculations, and what makes it a depolarizing agent. It then keeps sitting on the receptor until the receptor desensitizes from being over-activated, and that is phase two, when the flaccid paralysis appears.
His mnemonic, back from the autonomic lecture: the days of the week — Friday for fasciculations first, then Wednesday for weakness. Fasciculations come first because they are phase one; the weakness, and then the paralysis, is phase two.
Asked: “If they all inhibit acetylcholinesterase, why can't they be used interchangeably?”
“I need something that's able to get across the blood brain barrier and actually be able to treat the CNS effects there”
The real axis is whether the drug crosses into the brain.
Neostigmine in surgery is his worked example. Rocuronium and vecuronium are non-depolarizing blockers — they sit on the nicotinic receptor and keep acetylcholine off it, which paralyses the patient. Neostigmine blocks acetylcholinesterase, acetylcholine builds up, outcompetes the blocker and knocks it off the receptor, and neuromuscular function returns so the patient breathes for themselves.
And an honest caveat he added: some of the choice is not pharmacology at all. A myasthenia clinic may simply prefer pyridostigmine. He called it clinical inertia — “this was how I was trained” — and said there is often no concrete reason.
Asked: “What is the difference in mechanism between the polyenes, azoles and allylamines?”
“With the polyenes, for example, those are more so like kind of poking holes in the actual membrane itself to cause like leakage of contents”
He said the shared endpoint is enough: ergosterol synthesis is inhibited, the membrane stops working, the cell dies.