DIP Episode 112 - The “Clutch” Pharmacology Podcast Round 2
Topic
Pharmacology; Autonomic Nervous System Agents; Anti-hypertensives; Antibiotics; Antivirals; Psychopharmacology; Cardiac Drugs; Oncology.
Key Takeaway
Mastering the mechanism of action, clinical indications, and critical contraindications for major drug classes (e.g., {ACE} inhibitors, calcium channel blockers, anti-epileptics, antibiotics) is essential for high-yield board performance.
Episode Notes
Source / episode info
- Episode: 112
- Title: Divine Intervention Episode 112 – The “Clutch” Pharmacology Podcast Round 2
- Published: 2019-06-11
- Source: Episode page
One-liner
This episode provides a massive review of pharmacology, covering everything from autonomic agents and cardiac drugs to complex antibiotic classes (e.g., -lactams, aminoglycosides), anti-cancer chemotherapies, psychotropics, and critical drug interactions for board exams.
High-yield summary
- Autonomic Agents: Use selective _1 blockers like tamsulosin for BPH to avoid systemic hypotension; use muscarinic agonists (e.g., bethanechol) for urinary retention or post-operative atony.
- Cardiac Drugs: Recognize the differences between Dihydropyridine ({Ca}^{2+} channel blockers, cause peripheral edema) and Non-dihydropyridine ({Ca}^{2+} channel blockers, rate control); use {ACE} inhibitors/AR Bs for renal protection in diabetes or scleroderma renal crisis.
- Antibiotics: Know the spectrum of coverage (e.g., Vancomycin only covers Gram+; Aminoglycosides cover Gram-; Ceftriaxone is preferred for suspected meningitis). Remember that -lactams are generally safe, but specific generations target different pathogens ({Sepremomycin} for atypical infections).
- Psychopharmacology: Be aware of the side effects and management protocols: Isoniazid (INH) depletes Vitamin B6 (risk of peripheral neuropathy/seizures); Dopamine agonists are first-line for prolactinoma; Triptans must be used cautiously in patients with coronary artery disease due to vasoconstriction.
- Oncology: Understand the mechanism and toxicity profiles: Taxanes stabilize microtubules; Vinca alkaloids depolymerize them; Cisplatin is nephrotoxic/ototoxic, requiring NAC for protection.
Learning objectives
- Differentiate between \alpha-adrenergic receptor blockers and their clinical applications (BPH vs. phaeochromocytoma).
- Apply knowledge of autonomic pharmacology to manage conditions like urinary retention, ileus, and cholinergic crisis.
- Select appropriate antibiotics based on the suspected pathogen's Gram stain and resistance profile.
- Understand the mechanism and management of complement deficiencies (PNH) and coagulation disorders (TPA reversal).
- Correlate drug side effects with their mechanisms of action (e.g., \text{INH}/B6 depletion, \text{A ChE Is}/GI upset, \text{Ca}^{2+} channel blockers/edema).
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Phaeochromocytoma | Paroxysmal hypertension | Phenoxybenzamine (irreversible _1 blocker) | Always block _1 receptors first, then . |
| Myasthenia Gravis | Fluctuating muscle weakness | Pyridostigmine ({A ChE} inhibitor) | Long-acting A ChEI is preferred for chronic management. |
| Cholinergic Crisis | Miosis, salivation, diarrhea, bradycardia | Organophosphates/Nerve Gas | Treat with Atropine (muscarinic antagonist) or Pralidoxime ({A ChE} reactivator). |
| PNH | Intravascular hemolysis | Eculizumab ({C}5 inhibitor) | Requires prior vaccination due to risk of infection. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| -Blockade | Prazosin/Doxazosin cause orthostasis. Tamsulosin is selective for the bladder neck. | BPH management | Use tamsulosin to minimize systemic hypotension risk. |
| Thyroid Storm | Initial treatment with Proprenolol, followed by PTU. | Thyroid crisis management | Remember _2 agonists (e.g., Albuterol) can treat hyperkalemia. |
| {ACE} Inhibitors/AR Bs | Both are renally protective in diabetes and scleroderma renal crisis. | Hypertension/Nephroprotection | Contraindicated in bilateral renal artery stenosis or history of angioedema. |
| TPA Reversal | Minocripic acid or Tranexamic acid ({TXA}). | Massive bleeding after thrombolysis | {TXA} is preferred for life-threatening, non-trauma bleeds (e.g., delivery). |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| A patient with a history of BPH presents and requires _1 blockade without causing systemic hypotension or affecting bladder neck function. | Tamsulosin (Selective _1 blocker) | It selectively blocks receptors in the prostate/bladder neck, minimizing systemic side effects seen with Prazosin/Doxazosin. |
| A patient presents with a cholinergic crisis following organophosphate poisoning and requires immediate reversal of muscarinic blockade. | Atropine / Physostigmine (Muscarinic antagonist) | Atropine blocks the excess acetylcholine; Physostigmine is used to reverse atropine overdose by inhibiting A ChE. |
| A woman with suspected PNH presents, and complement pathway inhibition is required due to a {GPI} anchor deficiency associated with a PIGA mutation. | Eculizumab (C5 inhibitor) | It blocks the terminal complement component ({C}5), preventing intravascular hemolysis in PNH. |
| A patient with chronic diarrhea and suspected irritable bowel syndrome requires treatment that increases gut motility via muscarinic agonism. | Neostigmine / Bethanechol (Muscarinic agonist) | These agents stimulate parasympathetic activity, increasing peristalsis. |
| A patient presents with a history of acute myocardial infarction and is being treated with thrombolytics; massive bleeding develops requiring reversal. | Minocripic acid or Tranexamic acid ({TXA}) | {Minocripic} acid (or {TXA}) are antifibrinolytics used to stabilize clots and reverse excessive bleeding after TPA administration. |
| A patient with chronic urinary retention due to bladder detrusor underactivity requires medication that stimulates the parasympathetic system. | Bethanechol / Carbachol (Muscarinic agonist) | These agents stimulate the detrusor muscle, promoting urination. |
Differential diagnosis / distinguishing features
Anti-hypertensive Agents
| Key Features | Distinguishing Findings | Next Step |
| {ACE} Inhibitors | Block {Ang I} -> {Ang II}. Risk of dry cough, angioedema. | Monitor for renal function; use AR Bs if cough/angioedema occurs. |
| AR Bs (Losartan) | Block {AT}_1 receptor. No bradykinin accumulation risk. | First-line choice if AC Ei is contraindicated due to cough or angioedema. |
| Calcium Channel Blockers | Dihydropyridine ({Nifedipine}): Peripheral edema, used for HTN/Angina. Non-dihydropyridine ({Verapamil}): Rate control, Prinzmetal angina. | Select based on primary goal (vasodilation vs. rate slowing). |
Anti-seizure Medications
| Key Features | Distinguishing Findings | Next Step |
| Valproic Acid | Hepatotoxic; treats bipolar disorder/epilepsy. | Monitor LF Ts closely due to hepatotoxicity risk. |
| Carbamazepine | Treats trigeminal neuralgia. | Use with caution in pregnancy (teratogenic). |
| Lamotrigine | High risk of SJS syndrome. | Titrate dose slowly when initiating therapy. |
Management pearls
- For suspected phaeochromocytoma, always administer \alpha-blockade (\text{Phenoxybenzamine}) before any \beta-blocker to prevent hypertensive crisis.
- In a patient with acute mesenteric ischemia from an embolus (often originating in the left atrial appendage), immediate resuscitation and surgical intervention are paramount; do not delay diagnosis based on symptoms alone.
- When managing severe sepsis/septic shock, initial fluid resuscitation and vasopressors (\text{Norepinephrine}) are standard; remember that \text{Epinephrine} is reserved for anaphylactic shock.
- For suspected acute cholecystitis or cholangitis, prompt imaging (ultrasound) and cultures should guide antibiotic selection, prioritizing broad-spectrum coverage if sepsis is present.
Don't miss
Integration & clinical reasoning
- Cardiology & Pharmacology: The use of \text{ACE} inhibitors/AR Bs to treat peripheral edema associated with Dihydropyridine CC Bs (e.g., Nifedipine) is a classic, high-yield association because they dilate postcapillary venules, counteracting the increased hydrostatic pressure from arterial dilation.
- Endocrinology & Pharmacology: The management of Cushing syndrome requires understanding that \text{Metyrapone} inhibits 11\beta-hydroxylase, leading to decreased cortisol and increased ACTH/precursor hormones in a diagnostic test setting.
- Neurology & Pharmacology: The differential diagnosis between peripheral neuropathy caused by anti-cancer agents (e.g., Vinca alkaloids) versus other causes requires careful review of the drug's mechanism (microtubule interference).
OMM / COMLEX integration
- Acute Mesenteric Ischemia: Standard emergency management (resuscitation, vascular imaging, surgical consultation) takes absolute priority over OMT. The primary goal is rapid reperfusion and source control.
- Adrenal Crisis/Shock States: In any unstable patient (septic shock, adrenal crisis), the focus must be on immediate stabilization with fluids and vasopressors; pharmacological interventions like \text{ACTH} replacement or mineralocorticoid supplementation are critical components of resuscitation protocols.
Concept connections / cross-references
- For detailed coverage on \text{ACE} inhibitors, AR Bs, and Renin-Angiotensin System pathophysiology: [ Episode 105 ]
- For comprehensive review of anti-infective agents and antibiotic resistance patterns: [ Episode 98 ]
- For deep dives into the management of adrenal insufficiency and shock states: [ Episode 72 ]
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Phaeochromocytoma | _1 blockade (Phenoxybenzamine) | Blocks peripheral vasoconstriction. | Must be given before -blockade to prevent hypertensive crisis. |
| Myasthenia Gravis | Pyridostigmine ({A ChE} inhibitor) | Increases acetylcholine concentration at the neuromuscular junction. | Long-acting A ChEI is preferred for chronic management. |
| Organophosphate Poisoning | Cholinergic Crisis | Excess Acetylcholine (A Ch) buildup. | Treat with Atropine (muscarinic antagonist) and Pralidoxime ({A ChE} reactivator). |
| PNH | Eculizumab ({C}5 inhibitor) | Blocks the terminal complement component {C}5. | Prevents intravascular hemolysis; requires vaccination before therapy. |
Key terms glossary
| Term | Definition | Context | Example |
| _1-blocker | Drug class blocking alpha-one adrenergic receptors. | BPH, Phaeochromocytoma management. | Tamsulosin (selective); Prazosin (non-selective). |
| Muscarinic Agonist | Drug that stimulates parasympathetic receptors ({M}_1-{M}_5). | Urinary retention, post-op atony. | Bethanechol, Carbachol. |
| {A ChE} Inhibitor | Drug class preventing the breakdown of acetylcholine. | Myasthenia Gravis, Ileus. | Pyridostigmine (long-acting), Neostigmine. |
| Antifibrinolytics | Drugs that stabilize blood clots and prevent excessive bleeding. | Massive hemorrhage after TPA administration. | Tranexamic acid ({TXA}), Minocripic acid. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Autonomic Pharmacology | Create flowcharts for drug selection based on the specific receptor target (e.g., _1 vs. muscarinic). | High | Review board-specific mnemonics and classic clinical scenarios. |
| Antibiotics/Antivirals | Use a grid system to compare coverage, mechanism of resistance, and toxicity for major classes (-lactams, Aminoglycosides, etc.). | Medium-High | Focus on the "Red Flags": {MRSA}, Pseudomonas, or specific organ toxicities. |
| Cardiology/Renal Drugs | Understand the physiological consequence of each drug class (e.g., how AC Ei reduces intraglomerular pressure). | High | Practice questions linking drug mechanism to clinical outcomes (e.g., peripheral edema with CC Bs). |
Question pattern recognition
- Pattern: History of \text{BPH} requiring \alpha_1 blockade, but systemic side effects must be avoided -> Use Tamsulosin (selective blocker).
- Pattern: Acute severe diarrhea/vomiting in the setting of suspected organophosphate poisoning -> Treat with Atropine (muscarinic antagonist) and Pralidoxime (\text{A ChE} reactivator).
- Pattern: Patient presenting with signs of hemolysis, \text{GPI} anchor deficiency, and loss of complement regulatory proteins CD55/CD59 -> complement-mediated intravascular hemolysis -> Suspect PNH; treat with Eculizumab.
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Okay, welcome. My name is Devine. I am a PGY-1, a transitional year resident. That's ultimately going to be studying radiology soon. This is episode 112 of the Devine intervention podcast and I am going to basically do around two of the Clutch Farm podcast. I will try to hopefully get all of it done today so that we don't have to go through around three. But we'll see how far I can go. So let's just jump right into it. So last time I talked about how you have alpha one agonist like phenoliferin or effedrine. Right, remember you can use those to treat like profound hypotension like in the setting of like getting anesthesia and then the person gets hypotensive. Classically on MBM is those people get phenoliferin or effedrine because those are alpha one agonists. And then remember your phenoxybenzamine and phentolamine. Remember those are classically used in the setting of if a person has a fiochromositoma right before they go for surgery. Remember you want to block out for receptors first before your block beta. So you can use the irreversible alpha one agonist. I mean alpha one antagonist, a phenoxybenzamine or the reversible alpha one antagonist phentolamine. I can already envisage how they could test that in the context of the mechalism and kinetics. And then don't forget your alpha one blockers prazosin and doxazosin. Remember that those they are used to treat a BPH in the short term.
Remember BPH long term therapies you are fin- your five alpha-in-doctase inhibitors like a finasteride, you testaride. And remember that prazosin, doxazosin can cause orthostatic hypotension because they are not selective only for the alpha one receptors in the bladder neck. They also they also attack the alpha one receptors that you find in the bloodstream. For tamsulocin right, tamsulocin is what you you'll go to if you want to just block things in the bladder neck and not sort of cause like the weirdness with regards to a high potential with the alpha one blockers. And then alpha methyl dopa is tested in the context of being one of the anti-hypertensives that are safe in pregnancy. Okay. Remember alpha methyl methyl dopa is also associated with with drug induced lupus and those anti-histonantibides. And then again other anti-hypertensives that are safe in pregnancy like your hydrozine, your labidolol, your niphetamine, remember hydrozine can cause a reflex tacky cardia. Remember it's also a three-door drug induced lupus. Remember labidolol is an alpha beta blocker, right? Remember classically it's useful hypertensive emergencies on NBM Es and then remember niphetamine as well. That's a dihydroperidina calcium channel blocker. I talked about clonidine last time. And again remember if a person comes in with a cocaine overdose right you want to avoid a beta blocker, right? So that you don't cause on-opposed alpha stimulation.
And then remember I talked about a thyroid storm, how thyroid storm is at first you give proprenolol, right? And then after that you give Ptu and then after that you can basically do whatever you want pretty much. But usually on NBM Es the graftar proprenolol first, that's the first drug you always want to give and then you can give Ptu afterwards. Remember Ptu can cause a granuloseitis, right? Like any other anti-thyroid medication. And then remember you're a beta 2 agonist, right? So like a beta raw, classically on exams, you use those for asthma. Remember you use that as short term like rescue therapy in asthma. And remember you can also use a beta raw for the treatment of hyperchylenia, right? Because it increases the activity of the sodium potassium ETP spump, right? So that's something that's tested quite frequently on exams. Our beta raw is a short actin, beta 2 agonist. Don't forget that we have some beta raw for motor raw, those are labas, right? Those are long actin and beta agonist. Remember before you institute a laba in asthma, the first thing you do is so you give a sabre first, if the sabre is not caught in it, you add an inhale, cortical steroid, if that's not caught in it, you add a laba. Remember never use a laba as monotherapy. And then if that's not caught in it, that's where you go to like a Pio steroids.
And one high yield thing to keep in mind is that a laba can actually be substituted for a laba, can actually be substituted for like your luchotrain inhibitors like xafrella cast and Montelocast, okay? So something to keep on the back of your mind. And then remember the beta 2 agonist, tributer lean, tributer lean, riddle drain, those are beta 2 agonists, you can actually use them as two colitis, if you want to delay pregnancy for a bit, okay? That's how the tested on MBM is. And then remember for person has an affelactic shock, your drug of choice is epinephrine, right? Your drug of choice in an affelactic shock is epinephrine. Contrast that with septic shock where your drug of choice is not epinephrine. For person has cardiogenic shock, you probably want to think more about an I-Notrope, right? So you want to use something like like a debutamine, which is a beta 1 agonist. Alternatively, you can use merinone. Merinone is a phosphodiesterase inhibitor. It ups your levels of cyclic AMP. Remember, cyclic AMP causes increased contractility in cardiac muscle, but it actually causes relaxation of smooth muscle. So basically, the thing that happens on the other circumstances is you increase the cardiac output because it's a positive I-Notrope, right? Because it's a phosphodiesterase inhibitor in all kinds of muscles. So you increase cardiac output, but you also decrease after load because it's causing visual dilution of your blood vessels.
Okay, because your blood vessels contain a smooth muscle. And then remember these drugs like Bethanychol and Carbacol, right? So Bethanychol Carbacol, they are classically used on NBM Es for the treatment of... You can either use them to treat like, what does it called? Because they are most grainy agonists, you can use them to treat uh... come on divine think. You can use them to treat um... um... overflowing continents, right? Because again, in overflowing continents, your bladder muscles are not contracting like they should. So pretty much you just give those people something that's a most grainych agonist. Remember, your prasin pathetic system rest and digest. So that essentially encourages those people to to um... encourages those people's blooders to work so that you can pee. Alternatively, you can also use Bethanychol in the treatment of like Ogilvys syndrome on NBM Es where the person essentially has their um... let's say like post anesthesia, they have like colonic... massive colonic dilution with no real obstruction. You can give them a maceramic agonist like a Bethanychol for those purposes. You can all use a Carbacol by Bethanychol, choose of more common Lyon NBM Es. And then if a person has a glaucoma, right? One thing you can actually do is to give a maceramic agonist to increase drainage through the canals of Schlem because if you give a maceramic agonist, you'll cause meiosis, right? So you'll clench down on the poopyels.
And when you do that, you basically like open up the highway of the canal of Schlem for drainage. So you can use drugs like a pylocarpin for that. Remember pylocarpin as a maceramic receptor agonist is also used on NBM Es in the treatment of um... uh... showgreens, right? So remember showgreens, those people are not making like spits pretty much, right? So you can actually remember by giving a maceramic agonist, you encourage the production of saliva, right? So that sort of relieves some of the symptoms. And then don't forget your acetylcholinesteries inhibitors, right? So like neo-stigmin, pyridosterigmin, phyzo-stigmin. So remember that you get rid of myastinia or pyridosterigmin, right? Because remember in myastinia, you have all the antibodies that are attacking the uh... the nicotinic acetylcholine receptor, you'll find out that you're a muscular junction. So if you give an acetylcholinesteries inhibitor, a long actin acetylcholinesteries inhibitor, like pyridosterigmin, you bump up the person's levels of acetylcholine and those will outcompete those nasty antibodies that you're finding on the surfaces of those cells. And then neo-stigmin again, acetylcholinesteries inhibitor, bumps up your acetylcholine, you classically use it to treat ilias on NBM Es, right? So like ogel viscendram, because neo-stigmin will bump up your acetylcholine and that will make your balls move. Remember your presence, pathetic system, mix you poop and mix you pee, okay?
And then remember, you can use phyzo-stigmin to fix an atropine overdose, right? Because remember, if a person overdose is an atropine, atropine has muscarinic receptor blocking activity. So if you give phyzo-stigmin, phyzo-stigmin will inhibit acetylcholinesteries, your levels of acetylcholine will go up and you can outcompete atropine on the muscarinic receptors. And then remember your acetylcholinesteries inhibitors like adonepyzo, galantamin and rivastigmin. Remember, if a person has Alzheimer's, right? They have a destruction of the bison nucleus of minor. So if you destroy the bison nucleus of minor, try to have an acetylcholine deficiency. Another way they can test that symptoms is to say that people with Alzheimer's have decreased activity of colon acetylcholine transferies. So if you basically have an acetylcholine deficiency, you try to give a pro-choline energy agent in the treatment of Alzheimer's, and you can give the acetylcholinesteries inhibitors adonepyzo, galantamin and rivastigmin for those are purposes. And then remember your organophosphate. Remember, organophosphate poisoning organophosphates, the acetylcholinesteries inhibitors, right? So the inhibitor acetylcholinesteries, and the thing is, when the inhibitor acetylcholinesteries, so this is essentially nerve gas. So a organophosphate nerve gas in pathophysiology. The inhibitor acetylcholinesteries, your levels of acetylcholine build up, and you have a colonergic toxic drum.
So they have a lot of like lacrimation, vomiting, diarrhea, sweating. They'll have like, pupillary meiosis, they'll have bradycardia on an NVME exam, right? Because remember acetylcholine, most chrysanctrogenic receptor agonist, slows conduction down the AV node. So the treat organophosphate poisoning, obviously you want to give something that can reverse those colonergic symptoms. So you can give a most chrysanctrogenic receptor antagonist like atroping, but you can actually try to regenerate the acetylcholinesteries by giving a drug like a pre-eduxy. And then methecolin. Methhecolin is actually a drug that's used in as a provocative test for asthma, right? Because methecolin is a most chrysanctrogenic receptor agonist. It's a most chrysanctrogenic receptor agonist, so it can trigger bronchospasm. So the thing is, if you use very dilute concentrations on a normal individual, it doesn't cause any problems, but if you give it to a person that is bronchospastic or has like predeliction for bronchospasm like an asthmatic, that dilute concentration will cause a decrease in FEV1 by more than like 20%. And then that helps you make your diagnosis of asthma. And then a diaphonium may shop on an NVME exam in the context of a diagnostic test for my astinia gravies. Remember, a diaphonium is used in the tensileant test. It's a very short active acetylcholinestrius inhibitors. Acetylcholinestrius inhibitor, not inhibitors, that's bad English.
So basically, if you inhibit acetylcholinestrius with a diaphonium, you build up the levels of acetylcholin. When you build up the levels of acetylcholin, okay, so what happens? You transiently relieve the symptoms in my astinia gravies. And then one other drug I want to talk about here is scopolamine. Scopolamine is an anticholinergic agent it's very good for like motion sickness. That's literally all you need to know about it for an NVME exam. And then remember, if a person has something called urge incontinence, urge incontinence, right? So they give it to you on an NVME as a person that essentially has, they have like urinary urgency or they can't get to the bathroom in time before they pee on themselves. They love to test this a ton on NVME exams, right? It means that their blooders are overactive, right? And the thing is if a person has overactive bladder, remember I told you that your parents in pathetic system encourages pee and poop in. So if a person has overactive bladder, it means that their parents in pathetic system is working too well. So you give a more screening receptor antagonist for those purposes, right? And on NVME is the classic more screening receptor antagonists that are used in the treatment of urging incontinence are these drugs. There's this nomonic that I learned studying for step one. It's called the on the darn toilet.
So it's like O for oxybutinine, one the teeth for totaridine, the teeth for daryphenicine and sulfenicine, and then the other teeth for trospium, okay? So it's one of those high-eal things you want to keep at the back of your mind, for example. And then remember your hypertropium and the tiotropium, those are most screening receptor antagonists. You use those in the treatment of asthma, you can also use those in the treatment of COPD. Although in general, if a person has COPD and an NVME is forcing you to pick between a sabah, right? So basically like a buideral or a lumbar or a sama, right? So a short actin more screening antagonist, I would go more with the sama under those circumstances. Remember, hypertropium is short actin, tiotropium is longer actin. And then midodrine, it's classically used to treat like an autonomic instability on NVM Es, right? Midodrine is essentially like a viso constrictor. You can use it to treat like orthostatic hypotension in people. That's pretty much all you need to know about it. Hallopere doll already talked about it. Remember, it's a it's a first-generation typical anti-psychotic. It prolongs the QT interval, right? Remember, it can cause hyperprolactinemia because you're effectively blocking the tuberoidinformed Ebola pathway of dopamine. And remember that Hallopere doll already can cause all those fancies, mancy, extraperiodamidose symptoms. It's the most powerful first-generation typical anti-psychotic.
And then, remember, if a person is taking an isoniazid, right? Remember, isoniazid can cause it can cause a drug induced lupus. So remember that with your anti-histonantibodies? Remember, isoniazid also depletio vitamin B6, right? So you basically have decreased activity of a delthal amino levelinic acid synthetase, which is one of the real limiting enzymes in hym synthesis. So those people can get us a neuroblastic anemia. Remember, isoniazid in addition also has the ability to, again, by depleting B6, because I mean, that's why Dr. Seyfia, take an isoniazid, make sure that you take a vitamin B6, or what's another name for vitamin B6, but it does also force it alongside, because B6 is a cofactor for glutamate decarboxylase, which converts glutamate to GABA. So if you have a B6 deficiency, because you're taking isoniazid, you accumulate glutamate and you deplete GABA, right? So you can have seizures. And then, remember, isoniazid is nephrotoxic and hepatotoxic. The way I remember that is INH. Isoniazid is the IN, it's neurotoxic, H, it's hepatotoxic, okay? So that's another high thing you want to keep at the back of your mind for tests. And again, remember, isoniazid is classically used to treat the TB. And then remember, your levodopa carbidopa, those are classically used to treat Parkinson's. Levodopa is a dopamine precursor, pretty much. Carbidopa is a adopa decarboxylase inhibitor.
It basically prevents the peripheral breakdown of levodopa, so that you can cross the blood-brain barrier, get into the brain. And then you can use it to treat, you can use it to essentially treat Parkinson's and symptoms, because you're boosting those people's dopamine. And then don't forget this drug, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, intact, COMT inhibitors, so they can test those on MB Ms for the treatment of Parkinson's, because COMT is an inhibitor of, I mean, it breaks down dopamine, so if you give a COMT inhibitor, you have less dopamine breakdown, and you can potentially relieve the symptoms of Parkinson's. And then don't forget to cellulogen or acetylene, those are your MAB inhibitors, they are monoxide inhibitors, you can actually use them to treat Parkinson's as well, because again monamine oxidize B breaks down dopamine, so if you inhibit MAB, you don't break down dopamine, right, so you can fix symptoms of a Parkinson's. So don't remember that these MAB inhibitors are cellulogen or acetylene, they are like your classic MAB that you find in in a psychiatry, you don't want to give those agents in people that are taking a tyramine or rich foods. And then a man can also be used for Parkinson's, he was previously used for influenza, but no one does that stuff anymore because it, because it, there's essentially like 100% resistance.
And then there's some dopamine agonist I kind of want to talk about, right, so don't forget a primary pexol and repinarol, those are dopamine receptor agonists, they are classically used on MBM Es in the treatment of restless lex syndrome. Remember restless lex syndrome has an association with iron deficiency anemia, so iron supplementation is also a classic then the stesset on MBM Es, but yes, you can treat restless lex syndrome with a dopamine receptor agonist like primary pexol or repinarol. Alternatively, you can use a, there is this abatrate known as primidone, primidone is abatrate that's classically used in the treatment of restless lex syndrome. And then your dopamine agonist like bromocryptine, carburegulin, remember, you can use those to treat them, you can use those to treat them, what is it called? Oh, come on, divine thing. You can use those to treat a prolactinoma, right, because remember, another name for dopamine is prolactin inhibiting factor, so if you give a dopamine agonist like a bromocryptine, carburegulin, you can relieve the symptoms of a prolactinoma. And remember, prolactinomas, almost like 100% of the time the right answer on MBM Es is to give a dopamine agonist, resist the temptation to give surgery, even if the person's optic chiasm is being compressed, because the thing is once you start those dopamine agonists within hours to days, the tumor begins to shrink, okay?
It's only for a person who feels to respond to dopamine agonist therapy, that is when you can consider transphenoidal resection on MBM Es. Contrast that would like pitotra, the nomad that's secretion, I'm like, growth hormone, under those circumstances, your next step in management is a transphenoidal resection. And then don't forget like your halothane, succinocholine, halothane is an anaesthetic, succinocholine is depolarizing your musculub block in agent, those are classically used to treat, I mean, those just know how those things work, but basically remember that those are associated with malignant hypothermia. And if a person has malignant hypothermia, don't forget to give dantrolym, okay? Dantrolym, basically inhibits the release of calcium from the sarcoplasmic reticulum, and you can use it in the treatment of malignant hypothermia. And then I talked about how you could use seporeheptidine, seporeheptidine is an anti-histamine with serotonin receptor blocking activity that can be used to treat serotonin syndrome. Although remember, classically, your NBM is benzodiazepines, things you can explore first in the treatment of a serotonin syndrome. And then don't forget your benstruoping and a trihaxi phenodil. These are used to treat like the some of the extra pyramidal symptoms that are observed in Parkinson's, benstruoping trihaxi phenodil, those are musculine receptor antagonists, okay?
So by blocking the musculine receptor, you can actually use them to treat like the, what's this thing called? Like the acute dystonia or the Parkinsonian symptoms that are observed when a patient is taking an anti-psychotic. And then remember mementin, mementin is essentially like an anti-NMD receptor agent, right? So if blocks NMD receptors, it's basically used in the treatment of ALS because remember ALS, one of the theories of ALS, is this thing known as glutamate-excidotoxicity, okay? It's like when you get, when your neurons get glutamate, I mean, when your neurons get glutamate, yes, that's right, when your neurons get glutamate, they get super, super, super, super excited. And then that can cause destruction. I sort of think of it as like a young person, goes parties too hard and then they get into trouble and die, right? Sorry to use that morbid example, but you can get my point. So you can give an NMD receptor antagonism because glutamate acts through NMD receptors. So if you block those NMD receptors, you can sort of stem the tide of glutamate-excidotoxicity and you can relieve the symptoms of ALS, although it really doesn't, it really doesn't help much, it may be prolonged by like three months or something like that.
And then remember ketamine, ketamine, the big thing, one of the memories that it's like almost like a, things like a dissociative anesthetic, it also has a NMD receptor blocking activity, but just think of it as a dissociative anesthetic, that's probably all I'm going to say about that. I'm right, Luzol is another drug that's used to treat new garric disease, it also has NMD receptor blocking activity. And then don't forget ethosoxamide, ethosoxamide is a T-type counsel channel blocker, it's classically used on NVME exams to treat, to treat, come on the point, think, it's used to treat abson seizures, remember abson seizures and three hertz spike and slow with pattern on EE Gs. Remember Phenetoin, right, to remember Phenetoin, it's an anti-peleptic drug, it's a seradogen, so you want to try to avoid it if a patient is pregnant, but if a patient has been on it and it's control their symptoms and they're pregnant, on NVM Es do not stop the drug, continue the drug, very high you to know that the only anti-peleptic that you absolutely positively should stop in a pregnant woman on NVME exams is Valparic acid. And remember that Phenetoin, just like ethanol and aspirin has a zero-order elimination, okay, that's more of a step one question you may see.
And then don't forget a carbamazepine, right, you used to treat a tic-dolero, right, so like, by tic-dolero, I mean a trigeminal neurose, on NVME exam, remember carbamazepine is a teradogen, it can cause, it can cause a granulose itosis.
And then I already talked about Valparic acid, remember Valparic acid is hepato toxic, they love love love to test that stuff on NVME exams, Valparic acid is hepato toxic, okay, and then remember your topyramid and lamotrigine, topyramid lamotrigine, they are very good anti-peleptic agents, to pyramid can actually also be used for like, smoking cessation, okay, but remember to pyramid has a strong association with like mental doneness, so it sort of slows down the brain kind of like the patient say that oh, it can feel slow, and remember it has a very strong association with nephrolithiasis, and then remember lamotrigine has a very high risk of a stifle, John Senn's syndrome, and then remember your benzo that is epine, remember this mnemonic that Ben likes to have it more frequently, and then Barb likes to make it last longer, remember benzo's increased the frequency of opening of a gabar receptors, and then remember your barbiturates increased the duration, remember barbiturates, that's another nice mnemonic there, but barbiturates increased the duration of opening of a gabar receptors, and remember there's no reversal agent for barbiturates, you can reverse benzo's, benzo's, classically on mbm is you can use them as a first line agent, if a person has a, if a person comes in with a cocaine intoxication, you can actually use benzo's as your first line agent, that's one thing you can't consider, and then remember benzo's, you can use them for seizures, and remember your benzo's all ending pamm, and if a person has liver dysfunction, you should consider using a lot, so your lot benzo's, so the L for neurasapam, the O for oxazapam, and then the T for tamazapam, and classically on mbm exams, there is this, benzo long acting benzo in the hospital, many people know it as labrim, but it's actually used in the treatment of alcohol withdrawal, it's called a chlordiase of pero
xide, it's a very, very, very wonderful benzo for the treatment of alcohol withdrawal, and remember you can reverse benzo toxicity with something known as flomazane, although one thing your friends on the mbm love to do to people is they would give you a question about a person that maybe I don't know like they've got benzos, they got respiratory depression, and then you intubated them, right, and then they try to trick, and then they say that oh, this person is beginning to like thrash about and all that stuff, and then they say the next step in management, don't be scared actually to give those people more benzos, they have been intubated, so they're not, it's not like they're gonna like depress their respiration even more, okay, that's one like we're saying your friends on the mbm love to test, and then don't forget your, that you can use flomazane to reverse a benzo de azepins, and then don't forget gabapentin, gabapentin, and you want to kind of like slow down on the dose in a patient that has a renal dysfunction, and then remember that gabapentin can be used to treat a neuropathic pain on mbm's, same thing as a pregabaline as well, and then a proper for, remember proper for anesthesiologist love to refer to it as the milk of amnesia, okay, it's a very good anesthetic, remember it can cause respiratory depression, it can cause hypotension, and remember there is such a thing as a proper fall infusion syndrome where the person like becomes altered, they have like a lactic acidosis, and all that stuff, and remember a proper fall, right, if a person has a history of a familial hyper-trageless rightemia, you want to go ahead and avoid proper fall on an mbm exam, remember proper fall can cause hyper-trageless rightemia because it's delivered as an infusion with a lipid, and then let's see if a person has like a history of cerebral palsy and they have like muscle spasms
, you can actually give a baclofen for those purposes, and then let's see, remember for a person has what is it called, if a person has opioid toxicity, so they have like the pinpoint pool pills, and then in addition to the pinpoint pool pills they have like respiratory depression, so like meiosis and respiratory depression, on mbm is your first line of genus Naloxone, let me try to trick you on an mbm by giving you Naloxone and now Trexone, careful there, pick Naloxone, before Naloxone, Trexone kicks in the patient will be dead, so you don't want that, so I'm going ahead and give Naloxone, under those circumstances now Trexone is used more for to treat them like it kind of helps with like a smoking or a cessation, and then I remember your triptans, your triptans are your, come on divine, thank you, your triptans are your serotonin receptor agonists, they can be used to treat migraines, they can be used to treat migraines, although remember that you want to avoid in a person that has a histrop like coronary artery disease or like renotes phenomenon or like a histrop stroke, remember I said that earlier that viso constriction is good for headaches, so viso constriction, if you have a histrop viso spastic disease variant engineer, so like Prince Medellin, a tripton may not be the best idea in the world, and remember because your triptans have serotonin receptor agonist activity, they can actually trigger serotonin syndrome, okay, so if a person is taking a necessary, I want to think twice before you put them on a tripton, on an NBM exam, and they remember if a person has like a seizure, like what's the seizure called, a person has a cluster, sorry, not a seizure, a cluster headache, a cluster headache, you can abort the symptoms relatively quickly with 100% oxygen, and then remember if you give a person TPA and they are bleeding profoundly, you can go ahead and give a m
inocupric acid to reverse the effects of TPA, and then I already talked about how you can use my Modepine after an ischemic stroke, you can use it to prevent the post stroke visospasm, okay, actually sorry, it's more, you tend to give it more after a sub-archmode hemorrhage, like a brain bleed to prevent a post stroke visospasm, so that the patients don't have like an ischemic stroke superimposed on top of a hemorrhagic stroke, so you can give my Modepine for those of purposes, and then don't forget your Vegeph inhibitors, drugs like a bevacizumap and a runbizumap, right, you can use that to those agents to treat a wet macular degeneration, okay, and then remember your post stroke landing analogs like a latano post and travel post, you can use those to treat a glaucoma, and then remember as a zolomide, it's a carbonic and hydrism inhibitor, you can use it to treat central sleep apnea and NBM exam, so already explain the pathophysiology behind that in the prior podcast, you can also use acidosolomide as a diuretic, right, remember it has the unique cluster of side effects of a metabolic acidosis with hypochylemia, that is very unusual, usually when you see hypochylemia, you see metabolic alkalosis with that, or if you see hypochylemia, you see metabolic acidosis with that, but if you see like a diuretic that has the combination of metabolic acidosis and hypochylemia, think about acidosolomide on that of circumstances, and then you can also use acidosolomide, it's called diamoxin the hospital, to treat acidosolomide to more cerebride, acidosolomide is also known as idiopathic and trigranhypertension, it can also use it to treat like elevated IC Ps, it can also use it to treat glaucoma, okay, acidosolomide is a super super super high yield drug for NBM exam, and then this is not necessarily like a drug, but just don't forget your opioid, your endogenous opioid receptor ag
onists, so remember Bida endorphine attacks the new receptors, dinorphine attacks the capa opioid receptors, and then caffling goes after the the delta opioid receptors, those are things that they love to test on NB Ms, and then I already talked about your MEO Is, so drugs like phenylsene, tranylcypromine, and isocraboxazet, remember if you meet like pretty much a taken an SSR and you're about to study these MEO Is, you need to give like a two-week-lock period on NB Ms or else you can trigger serotonin syndrome, and remember that these drugs you want to avoid them in people that are taking a tyrimine or rich foods, and then don't forget your TCE, remember your TC Es have a anti-harm side effects, so they have anti-h1, anti-alpha one, and anti-muscranic effects, right, so the anti-h1 effects they can cost the addition, the anti-alpha one effects they can cost orthostatic hypotension, and the anti-muscranic effects they can cause urinary retention, and they can cause delirium in the elderly, so don't forget drugs, they're like amitriptoline, not tryptoline, the cipramine, in mepramin, amoxetine, doxetine, chlomypramin, those are all TC Es, remember in mepramin, classic Lyonendium is can actually be used in the treatment of nocturnal and uruses, right, because you're effectively taking advantage of its anti-cholinergic activity, right, so if a kid is peeing on himself too much, or you can sort of relieve those symptoms by giving something that can cause urinary retention, and then don't forget chlomypramin, chlomypramin is actually one of those drugs you can use to treat OCD on NVME exams, and that's all I'm going to say about that, and remember the other drug class that has those anti-harm side effects, those are drugs like, they are your first generation anti-psychotics, like your typical anti-psychotics, about the low-potency ones like a like clopromazine, for example, and
then don't forget your SSRI, right, so like fluoxetine, peroxetine, citraline, fluvoxamine, citalopramin, citalopramin, remember fluoxetine has the longest half-life of all the SSR Is, right, so it has like the least association with like SSRI, discontinuation, syndrome, and then don't forget your SNR, remember they cause hypertension on NVM Es, right, so don't forget like your vanilla vaccine, there's vanilla vaccine, do loxetine, melansiprin, remember the loxetine is classically used to treat an neuropathic pain, or fibromyalgia, on NVME exams, and then don't forget chrasodone, remember chrasodone can cause a big, big pain, penis, right, so it can cause it can cause a prior pizm, that's pretty, and the way you actually treat that because it has like alpha-wanna blockade activity, so if you kind of think about it this way, right, you essentially have like visual dilution of the blood vessels that feed the penis, right, so the person just has like way too much a blood going there, so they just have like their, their thinness sort of stand on it, right, so the way you can actually treat the issues, like the prior pizm that's associated with chrasodone, you can actually go ahead and give an alpha-wanna agonist like a phenoephrin, you actually go ahead and inject it into the penis, I know it's kind of morbid, right, we can inject it into the penis and that can kind of like relieve those symptoms, because if you actually leave the penis like erect like that for like a long time, there's a lot of problems that can come with that, I'll let you look that up on your own life.
Okay, and then don't forget mertazepine, mertazepine is an alpha-2 antagonist that's used to treat depression, especially depression in anorexic because it causes weight gain, it also causes sedation, so depression has depression and insomnia, mertazepine is an awesome drug for that, because by being an alpha-2 antagonist, right, it actually increases the release of anorepinephrine, because remember, the alpha-2 receptor is a GI coupled receptor, so it's like a negative feedback for your sympathetic nervous system, so it sort of shuts down the release of anorepinephrine, so if you give something that blocked an inhibitor, right, that will actually increase the synthesis of anorepinephrine, and then don't forget, it will propiate, and it's an NDRI, it's anorepinephrine dopamine reoptic inhibitor, you can use it to treat some depression, remember, avoided in patients that have something that can predispose them to seizures, right, so like, I don't know, like let's assume they have anorexia, what do you have bulimia, those are the classic patients on MDMA exams, and remember that it actually helps with weight loss, and it actually helps with a smoky sensation, and then, clasoping, right, it's an eti-biculant-type psychotic, remember, it can cause myocarditis, so they can present it as a, I appreciate that recently, static treatment for, for first schizophrenia, and then now they have like an S3 heart sound, they have like crackles, like basically signs of CHF, remember clasoping can also cause a hyper salivation, classically people call that the weaponocene drum, and remember that clasoping is also associated with Igrenolocytosis, once a person's white comb begins to drop on clasoping, your next step in management is to stop the drug, very high you'll know that, you need to stop the drug, in fact, in general, on MDMA, if a person is having a side effect from a drug, usua
lly the right answer, with very few exceptions, is to stop the drug, and remember that clasoping decreases the, is one of the, one of two agents in psychiatry that decreases the risk of suicide, the other one is Lithium, and then remember, again, I sort of mentioned this last time, but it's going to hide you, so I repeated again, remember of all the atypical anti-psychotics, respirators, associated with hyperprolatinemia, the most, the procedure don't prolongs the acute interval, clasoping is associated with cataract, and it's the drug that you can use to treat psychosis in the certain of Parkinson's, they love to test those on NVM Es, remember our repeat personal is a partial dopamine receptor agonist, it's one of the most benign atypical anti-psychotics, remember our lanzer pain can cause the metabolic syndrome, and it can also use it to treat OCD, remember Lithium and its tremors, remember Lithium it can also cause an effergenic diabetes in Sepedus, and then remember Lithium can cause a hypothyroidism, where the tell tale sign, on NVME exams of Lithium toxicity, is tremors, and then don't forget your Z drugs, right, so like your Zopidem, Zalaplon and Zopiclon, they are using the treatment of insomnia, they actually have a GABA receptor agonist activity, but remember that these drugs, they also actually have addictive potential, and the way you can actually reverse toxicity with these Z drugs, is actually to give flomazineal, and then remember our meltion, our meltion is a melatonin receptor agonist, you can also use it in insomnia, I think it's maybe called a remerion in the hospital, if I'm not mistaken, or I may be wrong, but our meltion is a thing you want to know for NVME exams, and it really doesn't have addictive potential, and then syvorexant, I believe in the hospital, it's called Belsomra, syvorexant is used to treat insomnia on NVME exams, right, so the th
ing is remember if patients have narcolepsy, they tend to have low levels of this thing, it's known as orrexin or hypochritin on NVME exams, so the thing is if an orrexin deficiency in your CSF makes you sleepy, because remember narcolepsy is a sleepy disorder, and you can kind of imagine that by giving an orrexin receptor antagonist like syvorexant, you can actually go ahead and treat insomnia on the other circumstances, so that's how it's tested on NVME exams, remember Bospiron, so Bospar, right, so Bospiron is used on NVME exams in the treatment of, of anxiety, okay, it's a partial agonist at serotonin receptor, so at 5 HT, I believe, 5 HT, 1 A or 2 A receptors if I'm not mistaken, and then remember your drugs of abuse, remember PCP, PCP usually shows up as a person that is like, like berserk, right, like super, super, super agitated, remember LSD usually presents as flashbacks on NVME exams, remember marijuana, right, so like marijuana usually shows up as hunger, and as like, like, conjunctival injection on NVME exams, right, so like red eye pretty much, and then remember that if a person is getting an adenosine based cardiac stress, we're gonna go ahead and avoid caffeine in those people, because caffeine contains, is a methyl-zanthane kind of like the ophelin as well, so it kind of reverses the effects of adenosine, that's actually one of those things that you're like, mmm, divine, that's a little too low yield, I promise you, I have taken many exams in my life, it's not a low yield factoid to keep at the back of your mind, and then remember a varanic clean, varanic clean is a nicotine receptor, a varanic clean, in fact mechanism of action probably doesn't matter, for NVME, so I'm gonna like let that go, because again I want to make this as high old as possible, but what varanic clean is classically, used on NVM Es to treat, um, um, smoking, uh, like a person that's
addicted to the cigarettes, although I guess if you really want that to know, varanic clean is a nicotine receptor agonist, right, that's your kind of mix sense, because you're using to treat something that kind of depends on nicotine, uh, nicotine are dependent, and then, um, don't forget your methylphenidate, remember methylphenidate is a stimulant, you can classically use it on NVME exams to treat, um, to treat, um, ADHD, right, or remember it can cause insomnia, it can cause wake loss, it can cause anorexia, so classically on NVM Es, if you see this agent atomoxetine, atomoxetine is a non-stimulant drug that can be used in the treatment of, uh, of ADHD.
And then, um, remember for a person who's been from alcohol, again, remember, don't forget to give them benzoes, remember aspirin on an NVME for a person has aspirin toxicity, the classic telltale sign is the combination of irrespiratory alkalosis and a metabolic acidosis, okay? Remember aspirin, it's an irreversibly inhibitor of cox one and cox two, remember it's an anti-plitlid agent if a person comes in with, uh, chest pain, the first thing you give them is 325 milligrams of aspirin, and aspirin, right, after a person, um, has, um, an MI and they get like a stent on one of the coronary vessels, you place them on a aspirin basically for, for life. And then, also don't forget that, uh, fish on NVM Es, this is actually like floridly high yield, on NVM Es you can actually use aspirin in the treatment of strokes, okay? in the treatment of strokes, very, very important to know that, a person has a stroke, on NVM Es, almost 99% of the time the right thing to do is to give them an anti-plitlid agent, either like aspirin or clopidogrel or diperidomol, okay?
So I think that's all I'm going to say about those, I already talked about the other anti-plitlid agents in the first, um, in the first, in the first, uh, like round one, pretty much, don't forget a ruflumilast, ruflumilast is a force for diastries inhibitor, it's used to treat a really, really bad COPD, uh, remember cell dynophilus and other force for diastries inhibitor, it's used to treat pulmonary arterial hypertension, but it is also used to treat, um, to treat the, what is it called? It's also used to treat, um, erectile dysfunction. And then remember, there's more press and I already talked about how you can use it to treat, um, olybran disease because it increases the release of olybran factor from our wibopaladi buddies and remember that it's also used to treat, um, central diabetes insipidus, right? And you can also use it to treat nocturnal injuries, so though you need to be careful because there's more press in, it's an edic receptor, um, agonist pretty much, it's an edic analogue, so if you're reabsorbent water in the nephrine, you can get hypoinitrumia and get seizures with that, so just sort of keep that in the back of your mind. And then remember, heprin, it's an anti-quagulant, it's not an anti-plitlid agent, it's an anti-quagulant, remember, the association with a heprin induced thrompocythopenia and remember that you can reverse heprin toxicity with, um, protein, okay?
And remember, heprin works by activating an antithrombin 3 to inhibit factors 10 and 2, um, lomolecular with heprin activates antithrombin 3 to inhibit factor 10 for the most part, that's why you can, if you, I mean, no one really does this in the real world, but you can follow lomolecular with heprin activity with a factor 10 A acid. And then remember your 10 inhibitors like a pixaban, riveroxaban, classically on ambient use those to treat tham heat. So the person has heat, you cannot give them a heprin containing product anymore. So your next step is to give a direct thrombin inhibitor, right? So you can use like bivaloridine or you can use dabygatran or you can use a gattroban or you can use a factor 10 inhibitor like a pixaban and a riveroxabin. And then remember that dabygatran, right? Remember, you can actually reverse it with an agent known as Idyrosisiumabvizis. And then I already talked about warfarin and predominant sulfate and fresh frozen plasma. I talked about how these days you can actually, the first line agent, if you need immediate warfarin reversal is something called a prothrombin complex concentric. And then remember TPA, TPA and exams use that to treat like strokes, right? For patients on ischemic stroke and they come in within like three and a half hours of the onset of symptoms, you can go ahead and give them TPA, TPA, the classic dingy cion ambient exams are like altar plays, ritter plays, tenecta plays.
And then remember TPA, you can reverse its effects, represents like bleeding too much, you can reverse TPA by giving a minocupric acid or you can give a trinexamic acid. Although an mbm is, I have seen trinexamic acid tested more in the setting of like a life threatening like obi-guin bleed. Because again, essentially given something that prevents the ability for a person to bleed, so you can use it to treat like a bad bad bad bad bad bad like delivery bleed, like delivery obi-guin bleed on a mbm exams. And then don't forget it, it lets you map. Aculizumab is a C5 inhibitor, it's used to treat paroxysmal moxonal hemoglobin remember that that has an association with a mutation in the pig aging. So you have like issues with your GPI anchors. So these people get like a bad bad bad hemolytic anemia. And remember that you can use a coulizumab for that purpose. But one thing you need to keep at the back of your mind is think about it by giving a C5 inhibitor, you're essentially using your, essentially using pharmacology to induce a terminal complement component deficiency. So before a person is studied on a coulizumab, they need to get vaccination against like the mycid, like against my seramine and gyridis. Remember people that have terminal complement component deficiencies have a high risk of recurrent niacereline infections. And they remember hydroxyorea, hydroxyorea, it's an inhibitor of ribonucleothyl reductase, remember it increases hemoglobin F.
So you can use it to treat sickle cell disease. But remember that you can also use hydroxyorea to treat some childhood malignant these. But those are like lower your think of hydroxyorea for sickle cell disease on NV Me exams. And then remember is a thioprin and a six-megapto purine. I remember the anti cancer agents. But one big thing you want to keep at the back of your mind is that these drugs are broken down by Zancthy Noxides. So if a person has, if a person has, if a person has gout and they have been treated for cancer, right, you do absolutely positively need to slow down or like decrease the dose of is a thioprin or six-megapto purine so that they don't get into, they don't get into trouble with toxicity. Because by giving a like alopeurino, for example, you're a hippy Zancthy Noxides, you can give it the breakdown of is a thioprin and six-megapto and you can get a lot of issues with that. And then remember methyl trexid, I already talked about methyl trexid, remember methyl trexid can cause a liver toxicity. It has multiple uses on NV Mes. You can use it to treat what is this thing called, molar pregnancy. I remember it works by inhibiting a dihydrofoli reductase. I already talked about like the Pyramethamine and Trimethoprim that also dihydrofoli reductase inhibitors. And how if a person has like profamboin virus suppression from a dihydrofoli reductase inhibitor, you can strongly consider rescuing the bone marrow with a drug known as a local worry.
And then remember the drugs that cause pulmonary fibrocytes, right? So drugs like Bliomisin, Busofan, Amudor and Methotrexid, although don't forget that Bliomisin works in the G2 phase of the cell cycle. It's one of those weird things you're like, oh, the vinyl is low yield. I promise you, it is absolutely not low yield on NV Me exams. And then remember, fibrocylurus, fibrocyling inhibits are familiar with synthase. Remember that it's an anti-cancer agent. And remember that if you give look over and look over in actually worsens the toxicity of fibrocytes. And another high yield thing to give you, I would five FU, there is this drug that's used to treat the, come on, divine, thank you. And enjoy this and it's patient. So crypto-coccus, crypto-coccus, crypto-coccus and new forms. Again, apologize for this thing being kind of like random. Again, I'm literally just sitting down and spewing facts from memory. So again, I sincerely apologize. So let's get back on topic here, right? So if a person comes in, they have crypto-coccus and enjoy this. Remember, usually right, you do like the latex particle agrotonition acid to make the diagnosis. Remember, it's also positive with the India inx stain. So you have like the soap bubble pattern. If a person comes in with crypto-coccus and crypto-coccal meningitis, you'll give them for terracing B, right? You can also give flu cytosine at the same time.
But after they have that issue for like a year, you actually need to place them on like five flu cytosine and prophylaxis. The thing is, five flu cytosine is actually converted by this enzyme, cytosine, the aminins to five FU. That's actually how it works. So just thought I'll go ahead and throw that out there. And then I already talked about in the prior podcast. The thing is, I'm just trying to you because it's my understanding that the first podcast, again, even like this one is infordent. So I'm just trying to give you like a small repetition real quick on some major things I talked about then. So don't forget cyclophosphamide, right? It's an alkalinity agent. It can cause hemorrhagic studies. You can reverse. You can prevent bladder problems with amnesia. And then remember your busufan. Busufan is an anti-cancer agent. It can cause a pulmonary fibrosis. Remember your doxorobecin and donor-becin. Remember those can cause an irreversible diluted cardiomyopathy, right? Remember those are your anthracyclins, their clasically used for breast cancer and mbim exams. Remember that these agents, they can cause, again, this diluted cardiomyopathy. And you can potentially prevent that diluted cardiomyopathy by giving a drug that inhibits the fentin reaction. I don't know if you remember that from from Pithuma. Maybe I don't know like studying your first year or second year or whatever. The drug that does that is a dixorzoxin. Dixorzoxin is an iron chelator.
And then don't forget, trust to Zumab. Trust to Zumab is a hertunu blocker. Someone who clone a antibody against hertunu. It's used in the treatment of breast cancer that expresses that hertunu receptor. Remember trust to Zumab can also cause a diluted cardiomyopathy. But unlike your anthracyclins, doxorobecin, it causes an irreversible not irreversible, irreversible diluted cardiomyopathy. And then remember, I tend to mycindee. I tend to mycindee. Remember on NBM exams, it is classically used in the treatment of ewings or ewings or coma. Remember that on your 11-22 translocation? It's also used to treat pretty much like childhood cancers, right? So like Wilms tumors on NBM exams. And then remember, you have been christened, then blasting. Those are anti-cancer agents that have a very strong association with bone marrow suppression. Remember, then blasting blast your bone marrow. That's a high thing you want to remember for your NBM exams. And then remember your pachylytaxel, dosytaxel. Those inhibits the depolymerization of... So you're... Henga. Your vincar alkaloids like vincristened, then blasting the inhibits the polymerization of microtubules. Your tuxels inhibits the depolymerization of microtubules. Remember that you have been christened, then blasting. You have a very strong association with peripheral neuropathy on NBM exams.
If you see peripheral neuropathy in the setting of an anti-cancer drug, the one and only thing I really want you to think about is been christened, then blasting. Because again, they can inhibit microtubules, right? And then don't forget your cisplatin, caboplatin, oxaliplatin. Those are also acolytine agents. Remember cisplatin is nephrotoxic and auto-toxic. You can decrease the risk of the nephrotoxicity with a drug known as a emifosten. And then remember, there is this class side effect of nephrotoxicity and auto-toxicity that are held by four groups of drugs on NBM exams, right? So remember cisplatin for that purpose. Remember you amino glycosides, right? So like gentamizing, you'mizing, amicasing, tubramizing, streptomycin. Remember your lube diuretics, they are also nephrotoxic and also remember vincomizing. And then remember your topo... Your topo isomerase inhibitors like ironoticant, topo-ticant, those anti-cancer agents. Remember ironoticant, topo-ticant, tend to inhibit topo isomerase 1, a topo site, a nipo site, tend to inhibit topo isomerase 2, okay? Remember, etopo site sounds an awful lot like etopo site. So that helps you remember that even inhibit topo 2. And then there's this trick. I just want to keep at the back of your mind for the future. If you ever see a drug that ends in nip, if a drug ends in nip, that pretty much tells you that it's a tyrosine kinase inhibitor, okay?
So elotinib, dasatinib, whatever, those are all in matinib, those are all of tyrosine kinase inhibitors. And then remember the tyrosine kinase inhibitor in matinib. Remember in matinib is used to treat CML. Remember that with your 9-22 translocation, if you're in a delfiochromozone, right where you create the BCR Abel fusion protein. Remember retoximab, retoximab is a monoclonal antibody given CD-20 in the pleatial B cell population. You can use it to treat many, many, many, many problems like most of these B cell lymphomas on NBME exams. And then remember tamoxifen, reloxifen already talked about the key differentiating factors. Remember, those are serums tamoxifen, estrogen receptor antagonist in the breast, but it's an agonist in bone, so it decreases your risk of osteoporosis, but it's also an agonist in the uterus, so it increases your risk of endometrial cancer. And then reloxifen is an estrogen receptor antagonist in bone. It's an estrogen receptor antagonist in breast, so it decreases your risk of breast cancer, but not as effective as tamoxifen. It's an estrogen receptor agonist in bone, so it actually decreases your risk of osteoporosis, and it's an estrogen receptor. It has no effects on estrogen receptors in the uterus. Okay, that's all I'm going to say about that. And then remember that tamoxifen, right, if you're a glean breast cancer chemoprophylaxis in a premenopausal woman on NBME exams, go with tamoxifen, okay?
But if you're glean breast cancer chemoprophylaxis on NBME exams in a lady that is postmenopausal, go ahead and consider an aromatis inhibitor like an astrozole or electrozole or ex semesting, okay? Remember once you hit menopause, you're always pretty much shut down, right? So if you're over shut down, then you just need something that you just need something that can prevent, because most of your estrogen once your postmenopausal comes from your double-sides using aromatis to convert androgens to estrogen. So if you inhibited aromatis, that can help you on that those are circumstances. Although, another thing I want you to keep in mind is that these aromatis inhibitors, right? Notice, they are doming down your production of estrogen. So those drugs actually increase your risk of osteoporosis, contrast that with your tamoxifen that decreases your risk of osteoporosis. I pro- again, you may see divine. These facts you're spewing, you're saying a lot of low-yield crap. I promise you, this is not low-yield crap. Again, I've treated thousands of people and I've taken lots of exams and thankfully done well. These things are very, very, very high yield to know for NBME exams. And then don't forget your phenastride, your test ride, you use those to treat BPH in the long term, okay? In the long term, you can use those to treat a BPH, okay?
Because remember the inhibitor five-hour inductees, so you prevent the formation of DHT because DHT is a thing that drives the growth of the prostate. And then remember your Epoanalogs like a double poetin, you remember the double poetin, a rhithropoetin, you use those to treat the anemia of chronic disease associated with CKD. And then if a person has chemotherapy and they have profound bone marrow suppression and severe, severe, severe, severe neutropenia, you can actually give them a drug like Philgrass stem or Sagra most stem. Remember stem, remember stem to tell you that they are stimulators of the bone marrow, okay? Stimulators of the bone marrow, they are GCSF analogs. And then don't forget this drug on Dancetron, so basically Zofrin. Remember it's a serotonin receptor antagonist, it's used to treat chemotherapy induced at MSS. And then don't forget your neurocline in one receptor antagonist, right? So drugs like aprepetent, you can also use those in the treatment of chemotherapy associated with MSS. And then don't forget metoclopromide. Meloclopromide is an anti-psychotic, basically it's a dopamine receptor antagonist, it's used to treat diabetic gastroperesis. But remember because it has dopamine receptor blocking activity, it can actually cause extra pyramidal side effects on NBM is the love to test this aton where they present a person that's like bradykinetic, has like hoggoye rigidity and all that crap.
And he started like over like the last three months and then they tell you that they have a histral diabetes and then they list all their drugs for you and then you are like, oh wait, stins metoclopromide on this drug list. So it's one of those weird things you sort of kind of want to keep at the back of your mind. And then remember all trans red noi casady uses, you treat acupromynocytic leukemia, remember that that's associated with our rods, right? Remember that also don't forget that with your 1517 translocation. And then on NBM is if a person has multiple myeloma, one drug you should actually keep in mind is one drug that never used to show up before but it has started showing up quite a bit in recent times is this drug known as bortezomib. Bortezomib is a proteasome inhibitor that's actually very useful in the treatment of in the treatment of multiple myeloma. And then don't forget your sglt 2 inhibitors again for diabetes, can I get flows in, that I get flows in, and I get flows in. Remember by inhibiting sglt 2 inhibiting like sodium glucose linked transporter. So you stop reabsorbing glucose in your urine. So you essentially peel glucose, peel glucose, guess what happens? Bugs love to have a great party in your urinary tract. So those drugs increase your risk of uti and again you absolutely want to avoid these drugs in patients that have a history of of renal insufficiency. And then don't forget drugs like a coni-vaptant, dou-vaptant.
You can use those drugs to treat SID, HTH, the adi receptor and antagonists, they are super expensive. And then don't forget your manitol. Manitol you can use it to treat elevated intracranial pressures. Remember it's a non-reabsorbable trigger. Although you want to kind of avoid it in patients that have a history of CHF because before it mobilizes stuff to your urine, right? I mean it's not like you're injecting manitol into the person's kidneys, no, that makes zero sense, right? You inject it into the bloodstream, right? So because the non-reabsorbable trigger, it would increase the aquatic pressures in your vascular tree. So that can fluid overload a person that has like a history of CHF for example. So that's one thing you sort of kind of want to keep at the back of your mind. And then remember your lube diuretic. Again remember your lube diuretic is because hypocaucemia, because hypomagnesemia, because hypochylemia, because nephronotoxicity, and remember that your lube diuretics, you kind of want to maybe avoid them in a patient that has a history of nephronolithiasis because they basically don't cause you in your urine. And remember that your lube diuretics, they all have an association with a sofa allergy with one exception, ethycrenic acid. Ethycrenic acid is the lube diuretic that you can give to people that have a really severe soft allergy, although of all the lube diuretics, the one that is the most nephronotoxicity, guess what? It's ethycrenic acid.
So that is one high yield thing you want to keep at the back of your mind. And then don't forget your thiozides, remember those work at the level of the distal-conferralitubial on your lube diuretics that work at the thick ascended limb of the lube of Henley. Your thiozide diuretics remember they have the strongest association hypochylemia. Remember your thiozides you can use those to reduce the incidence of nephronolithiasis because they cause hypochylemia and they do that by increasing the absorption of calcium from your urinary tract. Remember your thiozides and those hypochylgloca side effects are already talked about those in your in the prior podcast. And don't forget your thiozides, your friends at the NV Me, they've stopped putting HCTZ a lot because they know everyone get it right right, hydrochlorothiazide. How hard is that? Right? So they're beginning to use other drugs like Clothalidone, metolazone and indapamide. Those are all thiozide diuretics you want to be able to recognize from NV Me exam. And then don't forget probenesid. Probenesid is used to treat gout. Remember that probenesid is a uricosuric agent, right? So it basically increases the expression of a uric acid. But this drug is very rarely used in the real world because there are so many restrictions on its use. Before you can prescribe probenesid, the patient has to you need to for sure know that they are on the excretors of uric acid. They need to not have Hacto-fide.
They need to not have had nephrolithiasis from uric acid like from uric acid. So it's just so many restrictions but just so to keep that at the back of your mind. And then don't forget your adustrine receptor antagonis, epleronone and sperinolactone. Those are used to treat the remember you are a sperinolactone, right? It actually decreases, sorry, increases survival in CHF. You can use it to treat con syndrome because it has adustrine receptor blocking activity. You can use it to treat the hersortism that's found in PCOS because in addition to blocking adustrine receptors, it also blocks adustrine receptors. And then don't forget that sperinolactone can cause gynecomastia again because it has that adustrine receptor blocking activity. And then another thing that it can actually sperinolactone can be used for on NBM Esys, you can use it to treat chronically. You can use it to treat a person that has like an avidate bottle pressures and so for geoviruses. And then remember if you want to avoid the whole shindig with, I don't know if that's even a correct term, but if you want to avoid the whole deal with the gynecomastia with sperinolactone, you can give epleronone. Epleronone is an adustrine receptor antagonist but it doesn't have those adustrine receptor blocking activities. And then don't forget ameloride and triumturing. Remember those are potassium sperin diuretics.
You can use them to treat the nephrogenic diabetes and sypidosisosteroneathium because they are inectchannel blockers. Remember that inectchannel at the principal cell of the collecting duct. So if you block that inectchannel, you basically prevent lithium from gaining access to the principal cell and wrecking havoc on the second messenger cascade of adh. And they don't forget alescreen. Alescreen is a direct renein inhibitor that's literally all you need to know about it. It's a diuretic. And then don't forget your acin inhibitors. And alaprio, captopryl, ramepril, last lysinopryl. Remember your acin inhibitors are one of the drugs that have been shown to improve survival in the setting of CHF. Remember your acin inhibitors are contraindicated in people that have a histro bilateral rinolaristinosis. And remember that your acin inhibitors, you're also contraindicated in patients that have a histro of, come on divine, thank you, know this. They're contraindicated in people that have a histro of, oh yep, C1 estraisin inhibitor deficiency, right, so that they don't get like angiodema, right, so keep that at the back of your mind. And then remember that these are acin inhibitors, right, they basically decrease the conversion of angiotensin, 1 to 100 tensing, too, right.
And remember that your acin inhibitors, you can actually use them to treat the peripheral adema associated with your dihydroperidine calcium channel blockers, like I'm looting, because remember, if you, your, your dihydroperidine calcium channel blockers, the cause peripheral adema by dilating pre-capillary arterial, so the increase the hydrostatic pressures in your capillaries. So if you wanted to treat that peripheral adema, you can work by dilating post capillary venials with drugs like your acin inhibitors. In fact, this is Florida, high-youtu, no the drug of choice, very high-youtu, no this, the drug of choice in the treatment of the peripheral adema associated with your dihydroperidine calcium channel blockers, are your acin inhibitors. And then don't forget your AR Bs, low sartan, herbasatan, can the sartan, tell me sartan, your AR Bs, you can use those to treat hypertension. Remember, classicalian MBA is really good if a patient has a history of like dry cough from taking an acin inhibitor. And one thing I want to go ahead and mention here is that your acin inhibitors are phenomenal for like the renal protective effects in a patient that has a history of diabetes. And I'll go ahead and see this. This is something that you actually test on step two and step three and like medicine board exams. Acin inhibitors are not an agent to institute first for hypertension in African-Americans. They just have decreased effectiveness in African-Americans.
The only time that you give an acin inhibitor as an anti-hypertensive on MBA exams to an African-American is if the African-American has a history of diabetes. Because remember your acin inhibitors, they are renal protective because they die lead the efferent arterials. So they basically reduce intraglomerular hypertension. And if a patient has a history of scleroderma to decrease the basically little trick scleroderma renal crisis, your drug of choice is an acin inhibitor. Okay, I know I spend time on this but this is actually like floridly high you to know for exams. And then this drug is used to treat um um there's this drug known as Iverbradine. So this drug known as Iverbradine, remember it inhibits the phony sodium channels. Um it's a great great great great great drug. It's used to treat angina. You can actually also use it to treat like a heart failure that's not like super well managed with beta blockers. And again remember it works by inhibiting that phony those are phony channels. I describe it in more detail in terms of like hardcore pathophysiology in the cardiac pharmacology podcast. So I'm not gonna be that uh be that horse too much. And then don't forget your class one a um anti-retarmix right? So your sodium channel blockers like di-supermide, quinidine, proquinamide. The big one you want to remember, remember quinidine with the synchonism.
Remember proquinamide has been the drug of choice for the treatment of wolf Parkinson's, and white liver pressure has like WPW and behalf AFIP right? So I ahead and give um proquinamide. Remember proquinamide is also a three-day drug in use lupus and those are anti-histona antibodies. And then don't forget your class one b anti-retarmix. Remember those actually shorten the duration of the action potential. So they shorten action potential duration. Drugs like lido kin, mixility, nanatokinide. Unlike your class one, your class one agents they make the QRS complex wider right? And they increase the risk of um torsad the point. Contrary to your class one b they actually again decrease the duration of the action potential. And then your class one c your flaky night and propaphenone. Those drugs they can cause like cutie prolongation and torsad the point. So you want to be careful with those with those agents. And remember your class one territ� mix are basically your beta blockers. I've talked about the beta blockers at NOSM. I've also talked about the class three agents. Your potassium channel blockers right? So drugs like amuterone, tronadeurone, ibiotolide, ophetolide, um, sodalol. One high you think you want to keep at the back of your mind though is that sodalol, they need test right? So you know obviously it's a potassium channel blocker and all that crap. But they may actually test it you know on especially on step on the usm at the step one example.
They love to test like oh what does this antiretmet do to like the PR interval for example. Sodalol will be one of those class three agents that can prolong the PR interval right? Because it's uh it essentially has beta blockin activity right? So it's slow conduction down your EV node. And then don't forget your non-dihydroperidine calcium channel blockers. Those are your class four agents like verapameo.taiazam. You can use those to treat the e-fib in a rate control strategy. You can use those to treat a prince metal angina. Remember prince metal angina these these is also known as a very ant angina. And uh yeah that's what I'm going to say about those. And you can actually also use them to treat a cluster headaches, okay? Cluster headaches. Now um remember your dihydroperidine calcium channel blockers remember your non-dihydroperidine calcium channel blockers are your class four antiretmics. Your dihydroperidine calcium channel blockers they are used as anti-hypertensives. Don't forget your clevide pin is one of those drugs that you can actually use to treat them a hypertensive uh like emergency or whatever. My cardipine is also another dihydroperidine calcium channel blocker that is super super super useful for the treatment of um hypertensive emergencies and our emergencies. And remember that my fedipine is one of the anti-hypertensives that has syphin pregnancy.
And then I already talked about the post-hemorrhagic stroke of visospasm that you can try to prevent with an amodipine. It's another example of a dihydroperidine calcium channel blocker. And then remember the joxin I talked about the joxin used in the prior podcast. Remember it's a positive I know trope. You can actually use it to treat a fib because it has most chronic receptor agonist activities so it slows down conduction through the AV node. Remember the joxin works by inhibiting the sodium potassium ATP spump. Remember that the joxin hypochylemia predisposes you to the joxin toxicity but hyperchylemia is a side effect of the joxin okay. I'll repeat that again. Hypochylemia predisposes you to the joxin toxicity but hyperchylemia so hyperchylemia is a side effect of the joxin. The reason behind that is you know what watch my podcast please listen to my cardio podcast. I talk about that in great detail so I'm gonna keep going. And then remember magnesium it's like a last-deach agent you can use in a really bad asthma exacerbation and you can also use mag to treat a aclamsia okay that's one thing I want to keep in mind. And then if a person has the joxin toxicity you can treat that with anti-deach fib fragments and I already talked about how you can use atroping.
You can use atroping to treat heart block okay or any like brady arrhythmia as part of like your ECLS algorithms and then don't forget that atroping you can also use it to treat toxicity from organophosphates or nerve gas on NVME exams because it's a most chronic receptor antagonist.
It speeds conduction down the EV node and they remember hydrozene hydrozene remember this can cause orthostatic hypertension it's a anterior viso dilator so it decreases after load right so it increases cardiac output but it can cause a reflex static cardiac remember it can also cause a peripheral adema and they remember nitroglycerin you can use it to treat angina on NVME exams remember you don't want to give that to a patient that has that's taking like a phosphodistory is inhibitor like cell dynaphyl so that you don't have an unsafe drop in blood pressure okay that's kind of like the voiceover for the cell dynaphyl ad but anyhow okay back to this and then remember nitroperside you can use it to treat like hypertensive emergency or urgency remember it contains a crap ton of cyanide so you can actually increase your risk for like lacticat like cyanide toxicity so you don't put people on an atroperside drip forever and then remember like your immunitrith sodium and thiosophic you can actually use those to treat a cyanide toxicity on NVME exams because remember immunitrith is a patholoxidizing agent so it converts Fe2 plus soferos iron to Fe3 plus opharic iron the ferric iron like Fe3 plus binds to cyanide really well Fe2 plus does not bind to cyanide very well okay so by using immunitrith you can read Fe2 plus Fe3 plus you bind up cyanide and then the sodium thiosophic converts the cyanide to thiosanide and then you can basically use that you can basically use that to essentially like ciphly excrete cyanide and then remember immunoxidil and diazoxide I mean oxidil and diazoxide immunoxidil is probably the big one you want to remember you can use it to treat like you can use it to encourage your hair growth in a man and remember that diazoxide it opens up that potassium channel that you find at the pancreatic eyelets so you may actually see it as a drug for the treatme
nt of insulin omnis on NVME exams because by basically even that potassium channel opener you basically make those cells not depolarized to square out insulin okay diazoxide keep it in mind that's literally the only thing I think you will ever see on NVM Es in that in that context and then remember this drug it's known as necerityte necerityte is a neprilizing inhibitor necerityte necerityte necerityte necerityte I feel like I'm confusing it with something else necerityte it's not a neprilizing inhibitor it's actually a BMP analog so you can use it with a treat heart failure remember BMP sort of promote dioresis and it's also a good viso dilator the neprilizing inhibitor I believe I'm thinking about is this drug it's not sort of an S Sacubitrile Sacubitrile is a neprilizing inhibitor remember neprilizing breaks down a ampion BMP so it basically it's I kind of think of it as almost like think of like your GLP1 agoness and your DPP4 inhibitors your GLP1 agoness the are like GLP1 is broken down by dipeptidyl peptidase 4 so if you inhibited DPP4 you'll increase your level of GLP1 so that's kind of like the same thing here yeah I had to think about that for a second necerityte is a BMP analog or you can decrease the breakdown of BMP by giving this drug Sacubitrile Sacubitrile is a neprilizing inhibitor and then remember your statins the amyotoxic the inhibited HMG coiriductase remember that you give high intensity statins to patients that have I've talked about like the indications for high intensity statin therapy in my medicine as shelf review videos it's like a tover study in 40 milligrams or sover study in 80 milligrams let's see and then don't forget your PC your PCSK9 inhibitors remember PCSK9 is an agent that basically breaks down LDL receptors so if you inhibited PCSK9 you have less breakdown of your LDL and you will essentially express more LDL receptors on the sur
face of your hepatocytes and you will basically be able to clear more LDL from your serum so those are drugs like alyrocumab and evolocumab they are very good inhibitors of PCSK9 and then don't forget your anti-staff lococopensillin so they cover MSSA drugs like methecellin, napcellin, oxacillin and dicloxacillin on mbm is pretty much these drugs are only used for the treatment of mastitis okay so that's something you sort of kind of want to keep at the back of your mind on exams and remember that these drugs have a stronger association with acute intensity on the Fridays where a patient has like fever they have a rash and they have eocenophils that are elevated in their blood on their and then don't forget sephazolin sephazolin is classically given before surgery on mbm exams surgeons affectionately refer to sephazolin as panseph I don't know surgeons have this panseph fetish but it works really well like as like anti-bacterial prophylaxis before a person who goes for surgery and then remember sephazolin is a first generation sephalosporin remember your sephalotitan your sephoxytins your sephyroxym those are second generation of sephalosporins and then don't forget sephatriaxone sephatriaxone is the drug of choice in the treatment of mycelian infections on mbm exams remember that sephatriaxone does not cover MRSA it does not cover pseudomonas okay and remember that sephatriaxone can cause intrahypatic holistasis on mbm exams and if you want to give especially in like kits right and if you want to give a person a sephatriaxone on an mbm exam and they are a kid so like a pediatric like like pediatric sepsis you can actually give sephotoxym sephotoxym is a broad spectrum fed generation broad spectrum fed generation sephalosporin that's used pretty commonly on mbm exams remember the only third generation sephalosporin that covers pseudomonas is sephtazody remember sephap
ym is a four generation sephalosporin it also covers them pseudomonas as well don't forget sephtarolins sephtarolins is a fifth generation sephalosporin that covers MRSA that's the high-yield thing you want to know with that don't forget your cava penems like imi penem meru penem erda penem and doripenem remember these drugs cover pseudomonas okay recover an aerobes recover a craft on a stuff in fact if you have an infection that is resistant to a cava penem that patient is in trouble pretty much and then don't forget astroenem astroenem is a monobactam it covers pseudomonas pretty well it is only used in the treatment of gram negative infections it does not cover gram positives remember vancomaisen vancomaisen binds to diala diala right so that you don't have basically transpeptidase needs to bind to diala for you to co-join the bacterial cell wall so if you bind to diala transpeptidase does not see aligning to bind to so you don't have a building of the cell wall in bacteria vancomaisen remember the mechanism of resistance where you convert diala diala to diala diala and remember vancomaisen and cause a red band syndrome you can treat that by giving an insid beforehand or you can slow down the infusion rate of the vancomaisen and remember that vancomaisen is never an auto toxic and remember that vancomaisen only covers gram positives and it doesn't cover gram negatives and remember that vancomaisen covers mercer really well and remember that vancomaisen oral vancomaisen can be used to treat cdiff in fact right now it is the first line medication for the treatment of cdiff on nbm exams oral vancomaisen.
Daptomaisen remember it basically is it only covers a gram positive organisms also covers mercer on nbm exams remember your amino glycosides the cover gram negatives are really well remember that you can use tubermaisen it's an amino glycoside you can use it to treat in here to promote insid to prevent a pseudomonas in patients that have an cystic fibrosis remember that gen tamaisen is never toxic and auto toxic remember it does not cover an aerobes because it needs oxygen to be able to gain access to a cell and then don't forget that your amino glycosides can cause acute tuberlinic process right so you may see muddy brown cast in the urine of a patient that takes an amino glycoside on nbm exams and then don't forget your tetracycline right here remember your amino glycoside it's a it's a bactericidal 30s inhibitor your tetracycline are bacterostatic 30s inhibitors your key tetracycline remember your tetracycline are very good for zoonotic infections like Lyme disease from a borelia borgdophory and the exodistic they are very good for the treatment of um divine think they are very good for the treatment of Lyca rickettsia rickettsia and like Rocky mountain spotted fever um although remember that your tetracycline you want to avoid it in a in a kid that's less than eight years old okay so if a person has like Lyme disease and they are less than eight years old on nbm exams give a moxicillin okay but rickettsia rickettsia if a kid is less than eight years old and they have Rocky mountain spotted fever doxycycline is the drug of choice on that those are circumstances basically if you have Rocky mountain spotted fever you always get doxycycline on nbm exams the only exception to that rule is a pregnant woman if a pregnant woman has Rocky mountain spotted fever on an nbm exam you give chloramphenicol that is pretty much the only time you ever use chloramphenicol on an nbm
exam now remember that your tetracycline they are they can cause a photosensitivity remember the way to remember that is like um there um there's this numonic uh you know I'm learning to when I'm studying for step one I think it's like this numonic uh sap for photo to basically help you remember the agents the drugs that are uh half photosensitivity as a side effect so drugs like uh your sofonymize does the S in sap your amyodorone is also has a photosensitivity issues and then your tetracycline that's the sap for photo that's a nice way to remember that and then remember that your tetracycline they can cause like tooth discoloration they can cause multiple issues there okay and remember the mechlocycline is a tetracycline that you can actually use in the um treatment of acne okay I'm sorry I mean the mechlocycline causes nephrogenic diabetes in sypedus so you can actually use that side effect to your advantage in treating si a yes you can use that to your advantage in treating a si a d h and then uh remember your tetracycline can be used to treat acne okay and they're also very good for the treatment of like uh like uh cholera so like vibriol uh cholera okay and then don't forget that tigacycline is like a new generation tetracycline that covers merse and then don't forget lignisolate lignisolate covers merse uh covers uh vre very well on mbmi exams and remember that lignisolate has weak monamine oxidies inhibitor activity so it can cause a serotonin syndrome um and I think I'm gonna go ahead and stop here this has gone on for quite long enough so I'm really sorry but there has to be around three but now I can actually confidently make the promise that around three will be the last round of the plot from ecology podcast and as I always say when I end any podcast I do offer one and one to learn for step one two ck two cs and step three and the medicine in training exa
m and the medicine ebi in board exam and then if you have a college student friend that needs to learn for biochemistry physics general chemistry organic chemistry uh physiology histology alpha tutoring for all those things and then if you're a medicine applying to residency so an amca s application an ira s application or a college student applying to med school so an amca s application I do offer one and one like consulting for those who like application prep um application advise in personal statement writing interview prep and all that stuff so I wish all the best have a wonderful rest of your day and god bless you I'll see you next time
Practice questions — USMLE style
Question 1 — Pharmacology/Cardiology
A 68-year-old African American man with a history of Type 2 diabetes mellitus and hypertension presents for routine follow-up. His blood pressure is elevated, and his primary care physician recommends initiating an antihypertensive agent. Given the patient's specific risk factors, which class of medication should be prioritized for its renal protective effects?
- A) Calcium channel blockers (e.g., Nifedipine)
- B) Angiotensin II Receptor Blockers (AR Bs)
- C) Alpha-1 adrenergic agonists (e.g., Phenylephrine)
- D) ACE inhibitors (e.g., Lisinopril)
Answer: D. In African American patients with diabetes, ACE inhibitors are highly recommended as an antihypertensive agent because they provide superior renal protection by reducing intraglomerular hypertension through efferent arteriole dilation. While AR Bs also offer renal protection, the transcript specifically highlights that ACE inhibitors are particularly beneficial in this demographic for diabetic nephropathy management.
Question 2 — Neurology/Pharmacology
A 45-year-old woman presents with fluctuating muscle weakness and ptosis that worsens throughout the day. Physical examination reveals generalized muscle weakness without evidence of neuromuscular junction damage upon rest. The physician suspects Myasthenia Gravis (MG). Which pharmacological class is used to treat MG by increasing the concentration of acetylcholine at the postsynaptic membrane?
- A) Acetylcholinesterase inhibitors
- B) NMDA receptor antagonists
- C) Alpha-2 adrenergic agonists
- D) Cholinesterase acetyltransferase inhibitors
Answer: A. Myasthenia Gravis involves antibodies attacking nicotinic acetylcholine receptors (nA ChRs) at the neuromuscular junction. Acetylcholinesterase inhibitors (e.g., pyridostigmine, neostigmine) increase the concentration of acetylcholine in the synaptic cleft by preventing its breakdown, allowing the remaining functional nA ChRs to outcompete the autoantibodies.
Question 3 — Infectious Disease/Pharmacology
A patient is admitted with suspected Methicillin-resistant Staphylococcus aureus (MRSA) skin and soft tissue infection. The infectious disease specialist must select an antibiotic that reliably covers this resistant organism while minimizing nephrotoxicity risk associated with aminoglycosides. Which drug class represents the most appropriate choice?
- A) Cephalosporins of the third generation
- B) Tetracyclines
- C) Vancomycin
- D) Aminoglycosides
Answer: C. MRSA is a common concern in hospital settings, and vancomycin remains a cornerstone treatment due to its reliable coverage against resistant Gram-positive organisms like MRSA. Cephalosporins (even third generation) are often ineffective against MRSA. Tetracyclines and aminoglycosides have different spectrums of activity and may not be the first choice for severe MRSA infections.
Question 4 — Endocrinology/Pharmacology
A patient with Type 2 diabetes mellitus is started on a new oral hypoglycemic agent. The drug class belongs to the sodium-glucose linked transporter (SGLT) inhibitor family. Which of the following adverse effects is most characteristic and requires monitoring in this patient population?
- A) Hyperkalemia due to potassium retention
- B) Metabolic acidosis with hypochloremia
- C) Increased risk of urinary tract infections (UT Is)
- D) Peripheral edema due to vasodilation
Answer: C. SGLT2 inhibitors work by blocking glucose reabsorption in the proximal tubule, causing glycosuria. This mechanism increases the osmotic load and urine volume, which significantly raises the risk of UT Is. While these drugs can cause metabolic acidosis (B), the increased risk of UTI is a highly emphasized and common adverse effect that requires patient education and monitoring.
Quick fire review
What is the drug class used to treat urinary retention?
Anticholinergic agents (e.g., Oxybutynin, Solifenacin).
Which anti-psychotic agent is associated with a high risk of hyperprolactinemia and cataract formation?
Chlorpromazine (and other typical antipsychotics).
What is the mnemonic used to remember common anticholinergic agents for urinary urgency/overactive bladder?
"One the teeth for Tiotaridine, the teeth for Daryphenicine and Sulfenicine, and then the other teeth for Trospium." (Oxybutynin, Tolterodine, Darifenacine, Solifenacin, Trospium).
What is the drug of choice for anaphylactic shock?
Epinephrine.
Which anti-hypertensive class is contraindicated in patients with bilateral renal artery stenosis due to risk of worsening renal function?
ACE Inhibitors (and AR Bs are generally avoided/used cautiously).
What specific side effect must be monitored when administering Isoniazid for TB treatment?
Hepatotoxicity and depletion of Vitamin B6, which can lead to peripheral neuropathy or seizures.
Drug class used to treat severe asthma exacerbations (acute)?
Magnesium sulfate (Magnesium).
What is the primary mechanism by which Methotrexate works in treating ALS?
NMD receptor antagonism (blocking glutamate excitotoxicity).
Which drug class of anti-hypertensives are contraindicated in patients with a history of bilateral renal artery stenosis?
ACE Inhibitors.
What specific side effect is associated with the use of Lamotrigine, and what should be monitored for?
High risk of Stevens-Johnson Syndrome (SJS).
Which drug class are used to treat restless legs syndrome, and which agent is a partial dopamine receptor agonist?
Dopamine agonists; Pramipexole or Ropinirole.
What is the key difference in mechanism between an ACE inhibitor and an ARB regarding renal protection in SRC?
ACE inhibitors dilate the efferent arteriole (reducing intraglomerular pressure); AR Bs block AT1 receptors.
Which drug class of antibiotics are bactericidal, and which are bacteriostatic?
Aminoglycosides are bactericidal; Tetracyclines are bacteriostatic.
What is the most common side effect associated with taking a PPI (Proton Pump Inhibitor) in combination with other drugs that can cause metabolic acidosis?
None of the above (This question tests knowledge recall, but if forced to pick a high-yield association: The general class of GI acid suppressants are often linked to electrolyte imbalances). Correction for Anki: What drug is used to treat urinary retention by blocking muscarinic receptors? A: Anticholinergics.
Quick recall / Anki-style questions
Drug class used to treat severe asthma exacerbations (acute)?
Magnesium sulfate (Magnesium).
What is the primary mechanism by which Methotrexate works in treating ALS?
NMD receptor antagonism (blocking glutamate excitotoxicity).
Which drug class of anti-hypertensives are contraindicated in patients with a history of bilateral renal artery stenosis?
ACE Inhibitors.
What specific side effect is associated with the use of Lamotrigine, and what should be monitored for?
High risk of Stevens-Johnson Syndrome (SJS).
Which drug class are used to treat restless legs syndrome, and which agent is a partial dopamine receptor agonist?
Dopamine agonists; Pramipexole or Ropinirole.
What is the key difference in mechanism between an ACE inhibitor and an ARB regarding renal protection in SRC?
ACE inhibitors dilate the efferent arteriole (reducing intraglomerular pressure); AR Bs block AT1 receptors.
Which drug class of antibiotics are bactericidal, and which are bacteriostatic?
Aminoglycosides are bactericidal; Tetracyclines are bacteriostatic.
What is the most common side effect associated with taking a PPI (Proton Pump Inhibitor) in combination with other drugs that can cause metabolic acidosis?
None of the above (This question tests knowledge recall, but if forced to pick a high-yield association: The general class of GI acid suppressants are often linked to electrolyte imbalances). Correction for Anki: What drug is used to treat urinary retention by blocking muscarinic receptors? A: Anticholinergics.