DIP Episode 111 - The “Clutch” Pharmacology Podcast Round 1
Topic
Cardiology pharmacology (Antiarrhythmics, CHF agents); Renal physiology (Diuretics, RTA); Infectious disease (Antibiotics, Prophylaxis)...
Key Takeaway
Pharmacology is a massive integration topic requiring mastery of drug mechanisms and side effect profiles; specific combinations (e.g., hyperkalemia + metabolic acidosis) are often tested to narrow the differential diagnosis.
Episode Notes
Source / episode info
- Episode: 111
- Title: Divine Intervention Episode 111 – The “Clutch” Pharmacology Podcast Round 1
- Published: 2019-06-09
- Source: Episode page
One-liner
This episode provides a comprehensive review of high-yield pharmacology across multiple systems, emphasizing drug mechanisms and critical associations in cardiology (antiarrhythmics, CHF agents), nephrology (diuretics, RTA), infectious disease (antibiotic spectrum/toxicity), endocrinology (thyroid management), and psychiatry.
High-yield summary
- Diuretic Combinations: Hyperkalemia + Metabolic Acidosis suggests Potassium-Sparing Diuretics (Amiloride/Triamterene); Hypokalemia + Metabolic Alkalosis suggests Loop or Thiazide diuretics; Metabolic Acidosis + Hypokalemia suggests Carbonic Anhydrase Inhibitors (Acetazolamide).
- Antiarrhythmics: Amiodarone is a Class III antiarrhythmic that can cause pulmonary fibrosis, blue-black skin discoloration, and thyroid dysfunction. Digoxin toxicity risk increases with hypokalemia.
- Antibiotic Stewardship: For MRSA coverage, Vancomycin (oral form for C. difficile) or Daptomycin are key; for Pseudomonas, use a third-generation cephalosporin like Ceftazidime or an aminoglycoside like inhaled Tobramycin in CF patients.
- Thyroid Storm Management: The standard sequence is Beta-blocker -> PTU -> Corticosteroids.
- Hormonal Replacement/Anabolic Agents: Teriparatide should be given in a pulsatile fashion to increase bone formation, but carries an increased risk of osteosarcoma.
- GI Protection: PP Is and H2 receptor antagonists are used for PUD; Misoprostol (a prostaglandin analog) is used to prevent NSAID-induced gastric injury.
Learning objectives
- Differentiate the mechanisms, indications, and toxicities of various classes of antiarrhythmic agents (e.g., Class I vs III).
- Apply knowledge of diuretic combinations to diagnose specific electrolyte imbalances (K+, Cl-, HCO3-).
- Select appropriate antibiotics based on pathogen coverage, resistance patterns, and patient risk factors (e.g., MRSA, Pseudomonas ).
- Understand the management protocols for thyroid storm and hyperthyroidism in pregnancy.
- Recognize the indications and contraindications of various psychotropic medications (e.g., SSR Is, antipsychotics) and their associated side effects.
Board exam buzzwords
| Condition | Key Finding | Association | Board Exam Tip |
| Hyperkalemia + Metabolic Acidosis | Potassium-Sparing Diuretics (Amiloride/Triamterene) | Block E NaC in collecting duct; cause K+ retention. | If you see this combination, think of potassium-sparing diuretics. |
| Hypokalemia + Metabolic Alkalosis | Loop or Thiazide Diuretics | Cause massive urinary wasting of K+ and HCO3-. | The strongest association with hyponatremia is the thiazides (HCTZ). |
| Thyroid Storm | High fever, altered mental status, tachycardia. | Order: Beta-blocker -> PTU -> Steroids. | Remember the sequence of treatment; PTU is preferred in pregnancy. |
| MRSA Infection | Skin/soft tissue infection. | Vancomycin (oral for C. difficile); Daptomycin (myotoxicity). | Oral vancomycin is the first-line agent for treating C. difficile. |
Rapid review table
| Topic | Key Point | Context | Exam Relevance |
| Diuretics | Loop: {Na}^+/{K}^+/2{Cl}^- symporter blocker; causes hypocalcemia/hypercalciuria. | Nephrolithiasis risk due to Ca loss. | If the question involves nephrolithiasis, think of loop diuretics. |
| Diuretics | Thiazides: {Na}^+/{Cl}^- symporter blocker at DCT; causes hyperglycemia/hypercalcemia. | K+ channel opener effect impairs insulin release. | Strongest association with hyponatremia is the thiazide group (HCTZ). |
| Anti-seizure | Carbamazepine: Used for Trigeminal Neuralgia. | Nerve root inflammation. | Classic drug choice for TN; also associated with granulocytosis. |
| Antibiotics | TMP-SMX/Metronidazole: Prophylaxis for Toxoplasma gondii or Neisseria meningitidis. | CD4 count <200 (for N. meningitidis) or <100 (for Toxo). | Remember the specific CD4 thresholds for prophylaxis indications. |
Board-speak -> diagnosis
| Board-speak / Vignette phrase | Diagnosis / Concept | Why it fits |
| A patient with a history of asthma presents with atrial fibrillation and requires rate control therapy. | Beta Blockers (Non-selective) | Non-selective beta blockers (e.g., Propranolol) are contraindicated in asthma due to risk of bronchospasm; alternative is CC Bs or calcium channel modulators. |
| A patient develops severe diarrhea after receiving a broad-spectrum antibiotic for suspected Clostridium difficile infection. | Oral Vancomycin / Fidaxomicin | Oral vancomycin and fidaxomicin are the preferred agents over metronidazole for treating C. difficile-associated diarrhea (CDAD). |
| A pregnant woman with hyperthyroidism is being treated, and her physician must select an agent that crosses the placenta safely. | Propylthiouracil (PTU) | PTU is preferred in the first trimester of pregnancy due to its ability to inhibit peripheral 5'-deiodinases (T4 -> T3 conversion). |
| A patient with chronic heart failure and an EF < 35% requires guideline-directed medical therapy. | ACE Inhibitors, Beta Blockers, AR Bs, Spironolactone, ICD | These agents improve survival in H FrEF; the combination of Isosorbide-dinitrate + Hydralazine is specifically noted for African American patients. |
| A patient presents with a history of GI tract surgery and develops acute mesenteric ischemia due to atrial fibrillation. | Embolus source: Left Atrial Appendage (LAA) | The embolus classically originates from the LAA thrombus, making anticoagulation critical. |
| A patient is being treated for hypercalcemia of malignancy and requires bone-modifying agents. | Bisphosphonates / Denosumab | These drugs are used to stabilize calcium levels; key side effects include osteonecrosis of the jaw (ONJ) and risk of pyalophagitis. |
Differential diagnosis / distinguishing features
Anti-diabetic Agents: Mechanism and Side Effects
| Key Features | Distinguishing Findings | Next Step |
| Sulfonylureas (Glyburide, Glipizide) | Stimulate insulin release; risk of hypoglycemia. | Monitor blood glucose closely due to high risk of severe hypoglycemia. |
| SGLT2 Inhibitors (Canagliflozin, Dapagliflozin) | Block renal glucose reabsorption in the urine. | Contraindicated in acute/chronic kidney injury or renal failure. |
| DPP-4 Inhibitors (Gliptins) | Inhibit breakdown of incretins; no risk of hypoglycemia when used alone. | Monitor for potential accumulation with other drugs. |
Anti-epileptic Drugs: Toxicity and Use
| Key Features | Distinguishing Findings | Next Step |
| Valproic Acid | Anticonvulsant agent. | Profoundly hepatotoxic; Never administer to a pregnant female. |
| Carbamazepine | Used for Trigeminal Neuralgia. | Associated with granulocytosis and drug-induced lupus. |
| Phenytoin | Anticonvulsant agent. | Associated with gingival hyperplasia and drug-induced lupus. |
Management pearls
- NSAID Nephroprotection: To prevent PUD from NSAI Ds, administer a prostaglandin analog like Misoprostol (or PP Is/H2 blockers).
- CHF Management Ladder: For H FrEF (\text{EF} < 35\%), the cornerstone drugs are AC Ei/AR Bs, Beta Blockers, and MR As (Spironolactone). Consider ICD placement.
- Antibiotic Choice for Pseudomonas : If resistance is suspected or if the patient has cystic fibrosis, use an aminoglycoside (e.g., inhaled Tobramycin) or a third-generation cephalosporin (Ceftazidime).
- Thyroid Storm Protocol: Immediate treatment involves \beta-blockers to control cardiac rate/temp, followed by PTU and corticosteroids.
Don't miss
Integration & clinical reasoning
- Cardiology/Nephrology Integration: The use of loop diuretics causes hypocalcemia and hypercalciuria; this mechanism is critical when assessing nephrolithiasis risk.
- Endocrinology/Pharmacology Integration: PTU's ability to inhibit peripheral 5'-deiodinases makes it crucial in the first trimester of pregnancy, linking thyroid metabolism directly to drug choice.
- GI/Nephrology Integration: The combination of hyperkalemia and metabolic acidosis strongly points toward potassium-sparing diuretics (Amiloride/Triamterene) because they block E NaC, leading to K+ retention and subsequent acid trapping.
OMM / COMLEX integration
- Acute Mesenteric Ischemia/Sepsis: In any acute abdominal process or suspected ischemia, standard emergency management (NPO, IV fluids, resuscitation) takes absolute priority. Pharmacological agents are adjuncts only after stabilization.
- Drug Toxicity Management: When managing drug toxicity (e.g., severe hyperkalemia from a diuretic), the immediate goal is cardiac stability and electrolyte correction before considering specific antidotes or reversal agents.
Concept connections / cross-references
- For detailed information on the pathophysiology and treatment of adrenal insufficiency: Divine Intervention Episode 37 .
- For comprehensive coverage of GI anatomy and obstruction management: Divine Intervention Episode 105 .
- For advanced topics in renal physiology and RTA types: Divine Intervention Episode 98 .
High-yield association table
| Condition | Association | Mechanism | Clinical Significance |
| Hyperkalemia + Metabolic Acidosis | Potassium-Sparing Diuretics (Amiloride/Triamterene) | Block E NaC in the collecting duct, preventing K+ excretion and promoting H+ retention. | This combination is a classic board question pattern. |
| Thyroid Storm | -blockers, PTU, Corticosteroids | Beta-blockers control rate; PTU inhibits peripheral T4 to T3 conversion. | The sequence of treatment is critical for survival. |
| Osteoporosis/Hypercalcemia | Bisphosphonates / Denosumab | Inhibit osteoclast activity (resorption). | Side effects include ONJ and risk of pyalophagitis; PTH analogs increase this risk. |
| Acute Mesenteric Ischemia | Embolus source: Left Atrial Appendage (LAA) thrombus. | Source is typically atrial fibrillation-related embolization to the SMA. | Requires immediate anticoagulation therapy. |
Key terms glossary
| Term | Definition | Context | Example |
| Hyperkalemia | Elevated serum potassium level ({K}^+). | Often seen with K+ sparing diuretics or ACE inhibitors. | Amiloride/Triamterene use. |
| Metabolic Acidosis | Low plasma bicarbonate concentration ({HCO}_3^-) due to acid retention. | Seen with carbonic anhydrase inhibitor overuse (Acetazolamide). | Acetazolamide-induced metabolic acidosis. |
| PTU | Propylthiouracil; a thyroid hormone synthesis inhibitor. | Preferred anti-thyroid drug in the first trimester of pregnancy. | Used for hyperthyroidism during gestation. |
| LAA Thrombus | Clot forming in the left atrial appendage. | Source of emboli leading to acute mesenteric ischemia (e.g., in A Fib). | Requires anticoagulation therapy. |
Study optimization
| Topic | Study Approach | Priority | Resources |
| Pharmacology Mechanisms | Create flowcharts for drug action and side effects; focus on why a drug is used/contraindicated. | High (Must know mechanisms). | Review board-specific pharmacology guides (e.g., First Aid, Sketchy). |
| Electrolyte Imbalances | Practice linking the combination of two abnormal labs ({K}^+ + {HCO}_3^-) to a specific drug class/mechanism. | High (Pattern recognition). | Review diuretics and acid-base disturbances in tandem. |
| Antibiotics | Memorize coverage patterns, resistance mechanisms, and key toxicities for major classes (Pseudomonas, MRSA). | Medium-High (Must know spectrum). | Use flashcards or mnemonic devices for antibiotic associations. |
Question pattern recognition
- The "Combination of Two Things" Pattern: When presented with two abnormal lab values (e.g., hypokalemia + metabolic alkalosis), the answer is usually a drug class that causes both effects (Loop/Thiazides).
- The "Contraindication" Trap: Be wary of drugs contraindicated in pregnancy, renal failure, or specific comorbidities (e.g., Valproic Acid, SGLT2 inhibitors).
- The "Best Choice" Question: When multiple agents treat a condition (e.g., hyperthyroidism), the question often asks for the safest/most appropriate agent based on patient status (e.g., PTU in 1st trimester).
Test yourself
Common mistakes to avoid
Common traps
Original transcript with highlights
Original transcript with highlights
Okay, welcome to episode 111 of the Divine Intervention Podcast. And this podcast is one I will title the Clutch from a Colagy Podcast. I am going to go in completely around the border. I will try and cover most of the high-yield drugs that are tested on the USM list of one exam. I really do not know if I can compress, not even just on take that back. I will say on the USM-Lee exams. So basically, just say the drug and say the key associations for the drug. I do not know if this can be compressed into one podcast or require two or three podcasts, but I will try my best. So, basically the well-go about this is I will say the name of the drug and then we will keep going. So, first thing we have are the nitrates. So we know your nitrates, you know that you can use them in the setting of Pangina. And remember that nitrates because they cause visodilision, right, that can cause headache. Because we sort of think about it, viso-construction, like viso-constructive drugs, I used to treat headache, but visodilative drugs tend to cause headache, right? So, viso-construction, good for headache, visodilision, bad for headache. So that's one thing you want to keep in mind. And then remember your statins, remember your statins inhibit HMG query doctors. By inhibiting a HMG query, your doctors you decrease the synthesis of cholesterol. Your statins remember, right, they are hepatotoxic, they are myotoxic. And in general, you want to be careful if you are combining a statin and a fibrate.
Now, remember in myocene, right, it's one of those medications that I used to treat high cholesterol. It raises your HDL the best. And then remember like your cholesterol, amino, your cholesterol and cholesterol. Those drugs, they basically block the absorption of bylocytes. I remember that cholesterol, I mean if I'm not mistaken, can be used to bind up the C-defer toxin. And then your fibrates, right, again, remember your fibrates, they are very good at lowering your triglycerides. Again, they are myotoxic, they have a parotoxic, pretty much the same side effect profile as your statins. And then remember the joxin, remember the joxin is a sodium potassium ETP-spomp inhibitor. And by inhibiting the sodium potassium ETP-spomp, it's a positive inotropaid, but it also has a oscene receptor agonist activity, so it slows conduction down the EV node. So it's very good for the treatment of E-fib, but it's also a positive inotropaid. But remember, it actually does not improve survival in the setting of CHF. And because it inhibits the sodium potassium ETP-spomp, potassium doesn't get into the cell, so the joxin can cause hyperchylenia. But being hypochylemic actually predisposes you to the joxin toxicity, because the bind inside for the joxin and the sodium potassium ETP-spomp is the potassium site. So if you lack potassium, there is more space for the joxin to bind. And that increases your risk of ditched toxicity.
And remember, ditched toxicity usually manifests on exams as PV Cs, right? It can also manifest as like problems with vision, it can manifest as abdominal pain. So that's something I want to keep at the back of your mind. Now, don't forget Prokina Mide. Remember, it's a class 1e anti-rhythmic. Prokina Mide, remember the association with drug endus lupus, right? Remember, it's the drug of choice for the treatment of wolf Parkinson, white syndrome. Or if a patient has a fit, right? And the have WPW Prokina Mide is the drug of choice. It can cause drug endus lupus. Don't forget that with your anti-histonantibudits. And then, remember a mutorone. Remember a mutorone, it's a potassium channel block, it's a class 3e anti-rhythmic. It can basically do everything that. It basically works like every kind of anti-rhythmic. But the mechanism of actually one, remember, is that it's a potassium channel blocker. Remember, it can cause hypo or hyperthyroidism, beta through the Yod-B-Dal, or the wolf-chicoph effects. Remember, it can cause skin discoloration, remember it can cause pulmonary fibrosis, right? So those are things you kind of want to keep at the back of your mind with a mutorone. And then, remember your beta blockers. If you go from E through M, those are your selective beta blockers. But if you go from N going downwards, you have your non-selective beta blockers, right? So like proprylonal law, for example.
Non-selective beta blockers are contraindicated in people with asthma, right? Because it can cause like a bronchospastic effect. The classic NV Me question is a person that has state-fright. And state-fright is usually true to proprylonal law, but it tells you they have a history of asthma. You sort of want to live with the proprylonal law, right? And maybe go for a benzo under those circumstances. Then, don't forget your non-dihydroperidine calcium channel blockers. Those are actually very good for the... They actually are like negative vinyl tropes, right? Because they basically decrease the contractility of a person's heart. Those drugs are classically not used in the treatment of heart failure. They are used mostly on NV Me's for the treatment of e-fib, okay? So remember, e-fib, you can pursue like a rhythm control strategy. The rate control strategy, you can use a beta blocker, right? Or you can use a non-dihydroperidine calcium channel blocker like Verapamelto-Tayezan. And then, if a person also has a prince metal angina, those non-dihydroperidine calcium channel blockers are also good for that purpose. Then, remember the calcium channel blocker Nymo de Pín. If a person has like a recent stroke, if you want to prevent like a post stroke viso spasm, you can give Nymo de Pín. Nymo de Pín is a dihydroperidine calcium channel blocker that can be used for that purpose.
And then, also do not forget a class side effect of your dihydroperidine calcium channel blockers is Periferal Adema. Remember, they cause dilution of pre-capillary arterial. So that will increase the hydrostatic pressure in your capillaries. So that's how they cause Periferal Adema. So you can decrease that risk by essentially giving a post-capillary veniants like your ACE inhibitors. As the drugs of choice in the treatment of Periferal Adema, that's associated with your dihydroperidine calcium channel blockers. And then, don't forget mitroperside, right? You can use mitroperside for like hypertensive emergencies and emergencies. But you want to be careful, you don't want to put someone on an nitroperside drip for a prolonged period of time. Remember the association with Sanite Poisonin. So if you give your person that has hypertensive emergency, has been on an nitroperside drip for a long time and has lactic acid doses, you want to go ahead and stop the nitroperside drip because they are basically suffering from a Sanida toxicity. And then, don't forget your bisphosphonite. So your bisphosphonite, classically, on MBM, is they are used in the treatment of hypercalcine of malignancy. You can also use them in the treatment of osteoporosis. But some key things you want to remember is that your bisphosphonites, you have the cause of like a pylasophagitis, right?
And you have to drink tons of water, stand for like 30 minutes after taking them so that you have less interaction between the pylasophagitis. And your bisphosphonite is actually also caused like osteonecroses of the jaw. So that's a side effect. You want to keep at the back of your mind. And then, if you're thinking about terryparatide, remember terryparatide is a P-teach and a log. Remember if you give P-teach in a continuous fashion, it actually suppresses bone production. But if you give P-teach in a pulsatile fashion, it actually increases bone formation. So if you give terryparatide in pulsatile fashion over like two years, it causes an increase in bone density. But think about it. If you're giving a person a stimulating factor for bone, you can already begin to imagine that that can increase their risk of osteosarcoma. Remember, other things that classically increase risk of osteosarcoma in MBM is like retinoblastoma. So if you describe a kid that has a white reflexist of a red reflex, right? And also, Pages disease also increases your risk of osteosarcoma. And then don't forget, if you get a question about a patient that has preeclampsia, right? And they are beginning to get into the realm of aclampsia. Remember, you want to give magnesium on that of circumstances, right? So magnesium has multiple uses on MB Ms. You can use magnesium to treat aclampsia, right? To basically treat the seizures, right?
Another thing you can use magnesium for is for a very severe asthma attack. It's like your last line in the treatment of an asthma exacerbation. And then remember, your dopamine agonist like bromo cryptin or carburegoline, you can use those in the treatment of a prolactinoma. The very, I'll say almost always, a transphenoidal reception is the wrong answer. One MBM is for prolactinomas. Usually you go with dopamine agonist like bromo cryptin or carburegoline. And then don't forget your anticycotics, right? So like you have like your typical anticycotics like jaloparidol, flofelazine, trifloparazine. There's some low potency typical anticycotics like clopermazine, for example, right? Remember, your anticycotics, they prolong the cutin interval, right? So that's something you want to keep at the back of your mind. And your anticycotics, they can cause a hyper-prolactinemia, right? Because remember, another name for dopamine is prolactin inhibiting factor. So if you have a lot of dopamine on board, that inhibits the synthesis of prolactin. So if you gave something that blocks dopamine receptors, you'll actually have an increase in your prolactin, right? So that is one cause of hyper-prolactinemia through the tubero-informedibular pathway. So that's a class side effect with your anticycotics, right? And again, remember, your extra pyramidal side effects with your anticycotics, right?
So like the tardy dyskinesia, don't forget your acrophysia that you treat with beta blockers where the patient feels like they have to move around all the time. Don't forget your acute dystonia, right? That you can treat with an anticycolic energy like a Ben-stropin. Alternatively, you can use an antihistamine that has powerful anticycolic energy activity, like a Divein hydramin, right? So basically a Benadron, right? So those are kind of like key things you want to keep at the back of your mind. And then don't forget a metoclopromide. Metoclopromide is a dopamine receptor antagonist. It's actually used in the treatment of diabetic gastroprysis, right? But it's one of those classic NV Me exam causes of drug induced Parkinsonism, right? So drug induced Parkinsonism. And again, it does that because it has dopamine receptor antagonist activity. So they'll give you a person with a history of diabetes and gastroprysis that's treated, that then presents with like bradykinetic symptoms and like co-originity and all that stuff. If you see that think about metoclopromide toxicity, and usually the next step in management is to stop the drug, okay? And then if you're beginning to think about your eti-piglonti-psychotics, right? Remember, you have things like respiratory donk. respiratory donk has the biggest associated hyperprolectinemia. You have drugs like ziprasidone. Ziprasidone has the greatest ability to prolong the acute interval.
Remember quethyapine, quethyapine causes a cataract. Another thing with quethyapine that they love to test on exams is that it's essentially the only anti-psychotic on NBM is that you give to people that have in psychosis in the certain of treatment for Parkinson's, right? So remember in Parkinson's they have low dopamine. So you give them dopaminergic agents, right?
So like carbidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidopelidop and don't forget you'll land the pin remember all lands the pin can be used to treat OCD in fact remember OCD tells you the drugs that I used to treat OCD so the D is first line you antidepressants like SSR Is the C is second line so drugs like clomyperamine clomyperamine is a TCA and then you'll always all land the pin remember that all land the pin also has a strong association with a metabolic syndrome and then don't forget your clasping clasping is one of the two drugs in the world of psychiatry that has been shown to improve survival or decrease your risk of suicide pretty much right so the other drug there is lithium right so clasping remember that clasping can cause a granulose itosis it can cause a myocarditis it can cause like a hyper salivation so those are things you want to keep at the back of your mind and it is very unusual for you to start treating a person that has a schizophrenia with clasping not an NV Me test right it's something that you try after all else has failed pretty much and then don't forget our repeat prosol our repeat prosol is another typical anti-psychotic it does have a push it's a partial dopamine receptor agonist so in the presence of food dopamine is essentially acting as an antagonist that's pretty much all you need to know about our repeat prosol and then remember your tricyclic antidepressants right remember those things associated with anti-hamside effects so they have anti-heat-one effect
s so they can cause sedation they have anti-alpha one effect so they can cause an orthostatic hypotension right and they have anti-muscular unique effects so they can cause like urinary retention and they can cause like constipation and stuff like that and they can actually also cause arrhythmias and the way you treat like toxicity of tricyclic antidepressant is to give a sodium bicarbonate okay it's to give sodium bicarbonate so that's something you kind of want to keep at the back of your mind and remember these TCA is your tricyclics you cannot really use them to treat nocturnal aneurysis because you're effectively taking advantage of the anti-colonergic effects classically on NBM Es in e-premise is used for that purpose another drug you can actually use to treat nocturnal aneurysis is Desmopressin remember Desmopressin is an analog of ADHD right so by giving an ADHD analog you basically reabsorb more water from your urine right so you essentially have decreased the urine production or don't forget that Desmopressin right it can cause hyponitrimic seizures because if you keep reabsorb in water that will make you hyponitrimic and don't forget that Desmopressin can also be used to treat vanwylybredin disease right because if you remember it increases the release of vanwylybredin factor from Wibobo Paladi buddies that's a classically tested USMLE exam association and then if you go to your MLEO Is right so like your monoaminoxidase inhibitors right so like trinocipromin isocarboxacid right and phenols and phenols in is another one those drugs right the inhibit monoaminoxidase remember you want to avoid those drugs in the setting of a tyrimine rich foods right and although unusual with the contest that concept is with the MLEO being inhibitors that are used in the treatment of Parkinson's so like cellulogen or acetylene you also want to avoid tyrimine containing foods un
der those circumstances and then please do not forget that if you use multiple serotonergic agents together right you can get serotonin syndrome right classically that will present as like high fevers the patient will have myoclonus on an MBM exam usually your first step in management is like supportive care for the most part you can also use benzodiazepines but if the patient is not responding to a benzone then you want to consider proceeding to see prohibited in see prohibited in isananti histamine that has serotonin receptor blocking activity and then don't forget your SSR Is right so like your citalo pram isitalo pram peroxatine fluoxatine those drugs right the inhibit the reoptic of serotonin remember they have like a very mild increased risk of suicide remember these drugs have a sexual side effects right so they can cause a lot of sexual issues right so just something to keep at the back of your mind where you can actually take advantage of that in the treatment of premature ejaculation if you may and remember they are the first line drugs for the treatment of depression so major depressive disorder they're the first line for the treatment of anxiety right they are first line for the treatment of PTSD right so those are things you kind of want to keep at the back remember your isanri so like vanilla faxane deloxatine those are classically used in the treatment of a neuropathic pain right and remember that you have an association with hypertension if you see hypertension as a side effect of an anti-depressant think especially about vanilla faxane right your isanri and you also have the sexual dysfunction side effects but remember again deloxatine primarily for neuropathic pain all for like fibromyalgia on NVME accepts and then don't forget your anti-ri isanri penetring dopamine reoptic inhibitors like bupropune remember right it doesn't have the sexual side effec
ts it doesn't cause weight gain so it actually helps with some weight loss it also helps with smoking cessation where remember classically on NVM Es you want to avoid bupropune in people that have a history of the soldiers that predispose them to seizures so patients that have anorexia nervosa or patients that have bulimia or patients that are taking isoniasid for TB and they are not taking B6 like the doctor recommends for those people you want to go ahead and avoid bupropune because it does lower the seizure threshold and then remember lithium lithium is used to treat bipolar disorder remember it's one of the drugs in addition to clausopen that has been shown to decrease the risk of suicide in the world of psychiatry remember it can cause hypothyroidism and remember lithium right it's the third element in the periodic table it's also in group one kind of like sodium so we can use that in a channel that you find that the principal cell of the collecting duct to go up and screw the second messenger cascade of EDH so it can cause an efferogenic diabetes in cipadas right so remember that's the one where you have failure of the urinary osmolality to rise by a significant amount after the administration of decimal present right after you've done like the first stage of the water deprivation test so those are key things you want to know with lithium and remember a classic tell tale sign on mbmi exams of lithium toxicity is tremors and then don't forget your vaptan's right so like honey vaptan told vaptan those drugs are 80 receptor antagonistic can be used in the treatment of side and then don't forget your drugs like like ipo like double poitin for example those are ipo analogues you can use those on mbmi's to treat the anemia that's associated with acronic kidney disease and then don't forget those drugs in a calcet in a calcet is a calcium sensing receptor modulator okay
that's pretty much probably all you need to know about it and then don't forget your diuretics right so you have like your loop diuretics right so like your ferozomide remember ferozomide works at the sodium potassium to chloride simporder now you'll find that the thick isndyl lumb of the loop of Henley remember that by blocking that channel you decrease the reabsorption of a potassium at that level of the nephron so you don't have that potassium diffusion of any more and you then don't have that coupled paracelular reabsorption of calcium right so loops actually cause a hypo calcium or remember they cause hypercalcuria right so those drugs are relatively contraindicated in patients that have a history of nephrolathiasis because you essentially don't more potassium more calcium in the urea don't forget your loops also cause a hypochylemia right they also cause hypo magnesiumia they cause hypo nitrimia but remember if you're thinking about a diuretic that is most strongly associated with hypo nitrimia think about your thiazide diuretics like HCTZ and where those HCTZ work remember HCTZ works at the distal convoluted tubule right it inhibits the sodium chloride simporder it has the strongest association with with hypo nitrimia like I mentioned and remember it causes a hypergloc side effect so you can cause like hyperdylysemia hyperlipedemia hyperlerosemia and hypercalcemia right the magnesium behind the hypercalcemia I describe that in one of my pharmacology podcasts I believe is like the cardiac pharmacology podcast or something like that and then I mean you may wonder like why does why do your thiazides cause all those hypergloc side effects again I describe this in one of my podcasts but I'll just give you a quick taste here basically it is believe that thiazides potassium channel are openers right so if you open up potassium channels for example in the pancreatic e
yelid cells right you probably will not be able to release as much insulin as you should right and that can potentially cause anything you see in a person that has an insulin deficiency or the umbiburum metabolized glucose well so they'll have hyperglycemia the umbiburum store plepids in a depo side so they can have hyperlipedemia so stuff like that the hypercalcemia again it's a more detailed mechanism but because this is a quick farm podcast I'm gonna keep going and then don't forget your case pairing diuretics right so you have like your amylo right and your triamterine remember those are inek channel blockers so they work at the level of the principle cell of the collecting duct remember that those drugs uh you they can cause they are one of the diuretics right that cause hypercalemia as a side effect instead of chypoclinia as you're used to and then don't forget that you can actually use those drugs in the treatment of the nephrogenic diabetes in sypedes associated with lithium use because again lithium ricks have a con the principle cell of the collecting duct by going through that inek channel so if you block that inek channel you could potentially decrease the presence risk of a nephrogenic diabetes in sypedes associated with lithium although classically on mbm is to treat nephrogenic d.i you give a thiazide diuretic and then your other case pairing diuretics don't forget your spirano lactone and a plerinone remember those are dosterone receptor antagonists so those drugs right they can potent uh remember spirano lactone is the one that can cause a dinechomastia right because in addition to blocking our dosterone receptors it also has the ability to block androgen receptors and remember a plerinone does not have that side effect it doesn't cause the dinechomastia and some other key things with spirano lactone right it's one of those pharmacological options you
have for the treatment of con syndrome right because again it blocks our dosterone receptors you can use it to treat the hersotism in the setting of PCOS because remember it actually inhibits five alpha reducties in the skin okay so that's one weird loyal thing that occasionally makes its way to the mbm is and remember that spirano lactone if a presence e-m drugs below 35 percent it's one of those drugs you can use as well it's actually one of the drugs that improves survival in the setting of heart failure right so what are the other drugs that improve survival in the setting of heart failure uh don't forget your ACE inhibitors right don't forget your beta blockers beta blockers to be more specific those are B-superlol um that's a selective beta one blocker don't forget your cavita law remember cavita law it's kind of like labeta law it's an alpha beta blocker and then don't forget your extended release metoprolol those are the three beta blockers that have been shown to improve survival in the setting of CHF and then spirano lactone is something you can also add to that list and then the combination of isosobidinitrate and hydrolyze and also known as bideol has been shown to improve survival in heart failure in African Americans okay so those are the drugs that improve survival in the setting of heart failure and again remember if a person has an EF list and 35 percent you want to go ahead and put an ICD right in those patients now don't forget your other diuretic acid azolomide acid azolomide right it's a carbonic anhydrase inhibitor right remember it's one of those drugs that because it inhibits carbonic anhydrase you waste by carbene your urine right so by wasting by carbene your urine you basically cause metabolic acid doses as a side effect so the thing is your acid azolomide is one of those red diuretics that has the cluster of metabolic acid doses as a side
effect in the setting of hypochylemia right usually if you see metabolic acid doses you see that with a concomitant hyperchylemia but if you see metabolic acid doses with hypochylemia you really want to think about acidosolomide on an NVME exam remember acidosolomide right I mean you may see why it was because hypochylemia it causes hypochylemia because by being a diuretic it basically makes you volume down so that increases the activity of your urine and your tensing out of the sterine system right so if our doeschron is going to mock right our doeschron waste potassium in the urine so you get a hypochylemia and don't forget that you can use a set of azolomide in the treatment of central sleep up here right because again because it causes metabolic acid doses as a side effect your body will try to compensate with a respiratory alkalosis the way you create a respiratory alkalosis is to hyperventilate okay so it almost like induces an electro an acid-based imbalance that causes your respiratory drive to increase and then don't forget that acidosolomide you can also be used in the treatment of idiopathic intra cranial hypertension or pseudo tumor cerebride right remember pseudo tumor cerebride will be an obese female that is taking like doxycycline like some drug for acne and then she complains of like headaches in the morning and like blurry vision may perform a physical exam I use observer papilladema okay so those are the big things you want to keep at the back of your mind with acidosolomide right if they want to test acidosolomide in the context of a renal tuberculosis remember it can cause a type 2 or proximal RTA okay contrast that with your spermolactone player known because they work at the level of the principle cell of the collecting duct and they basically antagonize our dose-troner receptors they essentially cause a high power dose to run state so those dru
gs are serial to type 4 RTA so those drugs your dose-troner receptor blockers they cause a metabolic acid or they cause a hyper-kilinear with that because they are blunt in the effects of our dose-troner so again just a quick summary because this is super high for pretty much all the USML Es if you see the combination of hyper-kilemia and metabolic acidosis think about your case pairing diuretics okay if you see the combination of hypochylemia and metabolic alkylosis think about your guardian variety diuretics like your loops and your thiazides well if you see the combination of metabolic acidosis and hypochylemia you want to think about your carbonic and hydrism inhibitors like acidosolomide and then don't forget manitol remember manitol is a non-reabsorbable sugar you can use it to treat elevated intracranial pressures when you can also use it to treat you can also use it as a diuretic okay now remember your anti-seizure medications right so the big one you probably want to remember is if those socks are mind remember if those socks are is a tea type calcium channel blocker it is used in the treatment of absente seizures remember that association with the three herds or the three per second spike and slow-wave pattern in a child that's not paying attention in class and has staring spells remember that carbamazepine carbamazepine is actually also a good drop for the treatment of seizures but on mbm is you use it primarily in the treatment of tig dolorer right so like trigeminal neuralgia remember it has an association with a granolocyteosis and then don't forget your feinitoline remember feinitoline you want to avoid it in a pregnant female because feinitoline can cause neuro tube defects because it sort of messes up the enzyme that helps you reabsorb fully in the gut the enzyme I believe is known as conjugase now feinitoline remember it's also a sythole drug in used
lupus so don't forget that with your anti-histona antibodies and then Valparic acid it's the most heterogeneous of all the anti-piliptic drugs you absolutely positively do not want to give Valparic acid to a pregnant female okay and remember that the telltale sign on mbm is of Valparic toxicities elevation you LF Ts of Valparic acid is profoundly hepatotoxic okay and then don't forget your drugs that I used to treat hyperthyroidism right so like your pt and methamazole remember those drugs essentially inhibit multiple steps in the synthesis of thyroid hormone remember methamazole is actually the preferred agent in most circumstances but in the setting of pregnancy you want to go ahead and consider pt instead so remember the p in pt for the p in pregnancy especially in the first trimester but to be honest with you I won't go with like those hardcore specifics or the most part if you see a pregnant female that is hyperthyroid go with pt on an mbm and then one special thing you kind of want to keep at the back of your mind with pt is that it has the ability to inhibit the peripheral 5-prem diodeonies that converts t4 to t3 so that is why pt is used quite extensively in the treatment of thyroid storm now in thyroid storm right there is a certain order of pharmacology you want to select if a person has thyroid storm your first step in treatment is always a bit of blocker most specifically perpranol okay and then your next step is pt and then after that you can consider the addendums like you can consider steroids you can consider um um um uh yeah actually I think those are the big things you actually use I mean you can also use like um legal solution to transiently block the reabsorption of iodine by by your thyroid gland but that's that's kind of low yield so I'm not even gonna go there even more and remember again your pt methemazole they have the association with e plege
ocudis right so the heterodogins and they also have the association with e plegeocytosis now if you're going uh delving more like deeper right so into pharmacology so again apologize if this is super random I am literally just sitting on my bed and just spewing out from a ecology facts I know that I classically tested in no in no certain order on uh on nbm is right so let's sort of go to the drugs that cover MRSA right so don't forget your drugs that cover MRSA the first one is vancomycin remember vancomycin is nephrotoxic and auto toxic and remember that it causes the red man syndrome and the way you can treat that is to basically slow down the infusion of vancomycin or you can give um you can give an anti histamine um or you can give an answer before you start the vancomycin infusion and remember that vancomycin right again it covers MRSA it's also good for sedive in fact vancomycin oral vancomycin is the first line medication for the treatment of sedive it's no longer metronidousok it is now vancomycin now don't forget daptomycin daptomycin is also good for the treatment of MRSA remember daptomycin don't forget the association with myotoxicity and then don't forget lenezolid remember lenezolid is a 50s inhibitor remember that lenezolid is also associated with a serotonin syndrome because it has weak monoamine oxidies inhibition activity and then um don't forget that um you can also treat MRSA with RIFAMPIN remember RIFAMPIN is one of your TB medications remember it causes like red urine right and then don't forget um this drug um come on divine think um tigus cycling it's like a new generation tetracycline it also covers MRSA pretty well so those are kind of like the big big drugs that cover MRSA on mbmi exams and then the drugs that covers the domonus don't forget your cephepine remember cephepine is a fourth generation cephalosporing it causes profound diarrhea a
nd like a like stomach upset don't forget septazidin septazidin is the only third generation um only third generation um what's the drug class called cephalosporing that is used to treat us to domonus and then remember as trionam remember it's a monobactam it also covers pseudomonas remember as trionam is notable in the sense that it has very little cross reactivity with the other penicillins and then don't forget your amino glycosides right so like gentamysin your mysin amicasein tuberomycin um those drugs are all can all be used to treat um pseudomonas especially like inhaled a tuberomycin it's used to decrease the incidence of pseudomonas and patients with um cystic fibrosis remember cystic fibrosis prior to the age of 20 is staff orders that causes your pneumonia if you're post past the age of 20 you're thinking more about the pseudomonas remember right you amino glycosides they also have that unique combination of nephrotoxicity and auto toxicity right the nephrotoxicity classically on mbmi is manifest as acute tubular necrosis right so you'll find like your pigmented epithelial cells your body brown cast on a sedimentation of the of the urine and then another drug set of drugs that also cover um pseudomonas are your fluoroquine alons like sypro-floxicin remember classically on exams sypro-floxicin is used in the treatment of UT Is right you can use it for cystitis you can use it for pylon and fritis remember you don't want to give um sypro to a kid right because it's uh it can cause like teachylysthenan rupture you want to give it to a pregnant woman and remember that your fluoroquine alons right you can actually prolong the cute interval kind of like your macrolids and kind of like your um anti-psychotics okay so those are the drugs that cover pseudomonas uh also don't forget your papyracidantes or back time um sozocin vitamin Z as it's fondly called in the hosp
ital also covers a pseudomonas a pretty well and then if you're venturing into some more antibiotics right so don't forget your colistine remember colistine is profoundly uh never toxic it's like your last last last line medication for the treatment of a serious uh gram um uh serious uh infections uh in the hospital and then don't forget your trimethoprim sophomethoxazole remember on mbm is you use it as prophylaxis against the nemosisidiservetis if the cd 4 count drops below 200 remember it's also very good prophylaxis against toxo right so like toxoplasma gondii when the cd 4 count dips below 100 remember that tmp smx remember that it in hip works by uh at least the trimethoprim part works by inhibiting dihydrofolory doctase contrast that with the smx part that works by inhibiting dihydroptory to synthathase right and if a person has profound bone marrow suppression from taking tmp smx because again it inhibits the synthesis of folate you can actually go ahead and treat that by rescuing the bone marrow of folinec not folic folinec acid analog known as a look of war now uh another similar drug to tmp smx is the combination of pyramethamine and sulfurdyesine pyramethamine is an inhibitor of dihydrofolory doctase sulfurdyesine is an inhibitor of dihydroptory to synthathase classically pyramethamine and sulfurdyesine is used in the treatment of toxoplasmosis or can you remember the ring and hansin lesions in the brain of a patient that has a hhivere remember another thing your differential there is a primary cns salam fuma but there are some like nucleomedicine tests that you can true radiology that you can use to differentiate between both but that's not for the purpose of of the usml exams and then don't forget uh easy thromicin it's a macrolate remember your macrolates prolong the cutine interval remember your macrolates are motylene receptor agonists so you can actual
ly use them in the treatment of diabetic gastroperesis but that also kind of gives your clue to why diureia is a classic side effect of the macrolates remember your macrolates again the prolong the cutine interval they are very good for the treatment of atypical pneumonia so remember the word macrolate mcl so there's an m that's for micro plasma there's a c that's for chlamydia there's an l that's for legionella those drugs are good in the coverage of atypical pneumonia and then don't forget that your macrolates right erythromycin especially if you use it very early when a kid is born that's associated with a pyloric stenosis on mbmi exams and then also don't forget that the macrolate is etromycin you can actually use it as part of triple therapy in the treatment of a hpylory and then is etromycin you can actually also use it as prophylaxis if a patient that has hiv has a cd 4 count that dips below 50 against a microbacteria maivyoma intracellularis and then your macrolates on mbmi exams they also used in the treatment of bordertella pertosis so like whooping cough remember that's like the 100-day cough so those people the people that will have like an infection where it's a bacterial infection but you respond with like a very high white count that is predominantly lymphocytes not neutrophils as you'd expect to right then remember if a person has pertosis if you're a close contact you need to be prophylaxis against as well with with macrolate and then don't forget septraaxone septraaxone is a very high-yout third generation cephalospory remember classically on mbmi it is used to treat meningitis right it covers my cereals really well and remember that septraaxone can also be used as prophylaxis if you're a close contact of a person that has a nice cereal meningitis right so what the preferred agent on mbmi is rifampin right you can use rifampin is the preferred agent y
ou can use septra or you can use a septraaxone obviously the patient is pregnant and they wear a close contact of a person meningitis you cannot give them rifampin you cannot give them septra because those are both teratogeans so in those circumstances you elect to go with septraaxone okay and remember that septraaxone especially in like neonates it can cause an intra hepatic or colostesis in general if you see a pediatric very nasty infection like a septic pediatric patient go ahead and consider giving those kids septal taxing think of septal taxing as baby septraaxone on mbmi exams okay now don't forget your penicillins right your penicillins the inhibitor transpeptidys remember penicillins that steal the drugs of choice for the treatment of syphilis remember penicillins can also cause like hypersensit it's kind of like a rash it's something called the jairish hex hymer reaction and describe that in more detail in my dedicated ammicroaffirmacology podcast well encourage you to sort of go after those as well and then don't forget your your amino penicillins right so like I'm picellin that's like IV penicillin I mean that's like essentially like IV amoxicillin okay remember amoxicillin has an oin the name so it's orom and picellin has an i in the name so it's IV okay remember that am picellin is the drug of choice on mbm is for the treatment of listeria monocyte touchin is right so if you see a mom that consumed like delimits or like soft cheeses and pregnancy think about listeriosis okay and remember that listeria is the third most common cause of of like pneumonia or like severe infections in the new units remember the number one is gruby strap number two is equal line and then number three is a listeria and then don't forget a cyclover it's cyclover covers herpes really well right so like HSV it also covers visi v pretty well on mbm exams remember a cyclover is ass
ociated with a crystalline effropathy so it can cause kidney stones and remember that if a person has like HSV that's resistant to a cyclover you can give the pyrophosphate analogous force carnate okay force carnate and then if a person has CMV remember CMV you treat that with a gun cyclover remember that you get resistance to CMV when you have a mutation in something called a UL97 kinase okay and if again if you have CMV that's resistant to gun cyclover proceed to the pyrophosphate analog force carnate okay now let's see let my brain sort of settle for a while okay so let's jump into some autonomic or cardio active medications right so if we start with the alpha receptors remember your alpha one receptors right you can block those with drugs like phenoxybenzamine it's an irreversible alpha one blocker and then you have phentolamine that is irreversible alpha one blocker how do you see those tested on the mbm's you see those tested on the mbm's in the setting of a fiochromosyptoma before you take a person to surgery for fiochromosyptoma remember that you want to block alpha receptors first with either phenoxybenzamine of phentolamine before you then go ahead and block a beta receptors and then don't forget your drugs like carvide law and labid law member carvide law labid law alpha beta blockers right and then if you're thinking about those alpha receptors don't forget your alpha one agonist like phenol effort and phenol effort and classically on mbm's is used to treat like hypotension it's also used to treat like allergic rhinitis okay the classic description is the hotel you on the mbm your patient gets an anesthetic be get hypotensive you can give them an alpha one agonist like phenol effort or effedering okay remember those drugs can cause a perforation of the nasal septum that's something that's tested quite commonly on mbm's cocaine is also associated with that
side effect and then if you're thinking about your alpha to agonist your alpha to agonist drugs like clonidin and guanfesting they're used to treat opioid withdrawal on mbm's they're also very good for treatment of like resistant hypertension it's just like the number of times you need to take them that's kind of like off-putting for many people but they are very good at controlling blood pressure and don't forget clonidin is also used in the treatment of so it's used to treat opioid withdrawal the alpha to agonist like guanfesting also clonidin right they are used to treat our Tourette okay remember Tourette you can also use an anticycolic like caloparydol or an eti-bicol like respiratory dome but in general for Tourette's study at the alpha to agonist okay and then if you're looking at your beta receptors again beta blockers there is for many things right they're used to treat like heart failure right the improved survival in heart failure especially like your metoprolol like you extended release metoprolol your carvidi lul and that be so pro-lul okay and then remember your beta blockers you don't want to give them to a person that comes in with like cocaine intoxication right and remember because they'll have like on opposed alpha activation on like a profound hypertension and remember your beta blockers are your class two anti-rhyd mix right remember your beta blockers you can rest your patient from beta blocker toxicity by giving glucagon right glucagon essentially resurrect cyclic AMP by using a different receptor I've already described this multiple times in multiple podcasts and then don't forget that you can use your beta blockers like prepare a lot to treat thyroid storm okay don't forget that you can also use your beta blockers to treat blocoma right especially like your partial beta agonist that might essentially by being partial agonist the access beta bl
ockers so drugs like acybutolol and pindolol okay let's see who else can use beta blockers for beta blockers this is more of a usmly step one question but beta blockers we can ask you about like urine and your tensing out of the system responds to a beta blocker don't forget that those drugs right remember there are beta one receptors at the afrin at your level of the nephron so beta one receptors when you block them you actually have a decreased release of rene so you can sort of fully them from there to what happens to your levels of outoster for example okay now um let's see um what are the drugs that I talk about let's see let's give me some seconds let me think I know there are many drugs I've not talked about okay so remember your ppi's right so like homepricot, pantoprosol those drugs irreversibly inhibit the sodium potassium um I mean the sodium hydrogen and antipotor that you find on the surfaces of parietal cells remember you make antibodies against those uh and those uh transporters in a perniscience andemia right so uh those drugs irreversibly inhibits that transporters so you decrease the secretion of uh acid into the lumen of the stomach remember your ppi's right stay the inhibitor sideogram p450 that's a high u thing you want to keep in mind your ppi's they can constitute part of triple therapy or quadruple therapy in the treatment of Hpylory and if you're testing for Hpylory you want to hold your ppi for a bit right you want to hold those ppi's for like a few days before you um you test for Hpylory so you don't get a false negative and then remember ppi's are associated with osteoporosis the associated with aspiration pneumonia's right so those are things you kind of want to keep at the back of your mind and ppi's high those ppi's you can use them to treat girt right you can use them to treat biretsisophagus um so that's what i'll see with those um you
r H2 receptor antagonists they also used in the treatment of um of like uh like peptic ulcer disease remember symetadine is a big big big big one it's an inhibitor of cytogram p450 and it causes gynecomastia okay because it has like some anti-adrogena effects so that's something you want to keep at the back of your mind and then um um don't forget your um um what are these drugs i want to talk about so don't forget your um gnr-analogues like lupraline right so you can use those to shrink the size of a lio maio mass or a fibrillate before you go to surgery if you also give those drugs in a pulsatile fashion right you can actually use them to um promote fertility um remember that you can also use um those drugs in a continuous fashion to treat like metastatic like testicular cancer right or like metastatic prostate cancer because they effectively shut down the hbg access remember though other drugs you can use for like metastatic prostate cancer you can use your uh androgen receptor blockers right so like flutamined and bica lutamined and then don't forget tamoxifen right so tamoxifen is a serum remember it's an estrogen receptor antagonist in the breast but it's an agonist in the bone and uterus so it does increase your risk of um of endometrial cancer but it actually does decrease your risk of osteoporosis contrast that we're a loxifen relax ifn is also a serum it's an antagonist in the breast it doesn't act in the uterus it's an agonist in bone so it decreases your risk of osteoporosis what it does not increase your risk of endometrial cancer and then um don't forget of this drug peg visomant it can be used to treat them acromegaly it's a growth hormone receptor antagonist right and then don't forget um dexamethasone right it's a steroid you can use it to treat adrenaline and sufficiency um remember hydrochorizone hydrochorizone has glucocoricoid and mineral ocoricoi
d properties uh don't forget fluidocorizone fluidocorizone has primarily mineralocoricoid activity and then don't forget um your your um phosphodistory is inhibitors like cell denafilter dialafilter remember you can use those to treat um erectile dysfunction you can also use those to treat pulmonary arterial hypertension remember those drugs are contraindicated in patients that are taking another visodiliter like a nitrate or an alpha one blocker right so that they don't get into trouble with like like profoundly low blood pressures and then remember aspirin aspirin is an irreversible inhibitor of cox 1 and 2 okay aspirin is the first drug you essentially give a person comes in with an mi right or a person comes in with chest pain remember aspirin right can cause a peptic ulcer disease okay and remember if you want to prevent the peptic ulcer disease as a pseudo like taking an inset you want to go ahead and give a drug like misoprostal right because it's a prostaglandin analogue and then don't forget your um your drugs like a clopidogrel, prostogrel, tycagrel, remember those are your P2 Y2 receptor blockers the antiplitlet medications you can use them in the treatment of strokes in fact i'll tell you this most of the time if a person has a stroke on an mbmi given an antiplitlet agent like aspirin or P2 Y2 drug uh basically another antiplitlet agent like your P2 Y2 receptor blockers or like um dipyridomol remember dipyridomol is a phosphodiesterase inhibitor um you can actually use those to treat our strokes right like chronically to like decrease the risk of getting other strokes and then don't forget that a dipyridomol can be used in the stress um can be used in stress tests by taking advantage of the coronary as still principle um because it's a viso dilator right because remember if you bump up if you inhibit phosphodiesterase you raise up your levels of cyclic AMP, cy
clic AMP causes um relaxation of smooth muscle but cyclic AMP causes contraction of cardiac muscle okay and then don't forget a closely related uh phosphodiesterase inhibitor that's also an antiplitlet medication cellostasol it's used in the treatment of peripheral arterial disease on mbmi's okay because again it causes a viso dilation by increasingly clik AMP and relax in smooth muscle now don't forget this drug um your your GP2 B3 A inhibitors right so like um um ab 6imab right and uh epthiphythythite anti-rofiban right those are also antiplitlet medications remember those those that's almost like a pharmacologic means of inducing um immune thrombocytopenic apypure because remember ITP is where you make autoantibodies against a GP2 B3 A um although please don't confuse that with um glansmantrombostinia where you have a deficiency of GP2 B3 A or brinatulis syndrome where you deficiency of GP1 B9 or brinatulis where you have a deficiency of brinatulis syndrome okay now also don't forget your haparin remember it's an activator of um anti thrombin 3 um remember that haparin well classically on mbmi's is this in the context of HIPT so person gets like and it's usually it's almost always a surgery question you get a haparin product your platelet count drops like a stone by more than 50% within like five to seven days you think about it your next step in management for those people is to give a direct thrombin inhibitor so factor two inhibitor like your agatroban your dabigatran your bivaliridin right remember dabigatran is known as uh dabigatran is one of those agents you can actually reverse these days with a monocloral antibody known as a idarosisumab okay so that's something that's pretty classically tested on mbmi's exams and then um don't forget your factor teni inhibitors right so like they all have x in their name like a pixaban river oxaban a doxaban right and then don't f
orget your warfarin right remember warfarin inhibits a vitamin key boxy reductis so it basically decreases the dama caboxylation of um factors 279 and 10 and 14 CNS remember you want a bridge with haparin so that you don't get um like like warfarin a crosses because you get uh you don't want to be because initially when you start warfarin you are transiently hyper-quaglubo and remember if you want to reverse warfarin right you can use vitamin k but if you want to reverse warfarin real quick uh previously on mbmi's the thing you'd go with is fresh frozen plasma and i mean obviously if that's like the answer you say you don't see this next thing i want to talk about choose a fresh frozen plasma about these days um there's this thing known as uh uh like it's called like the pro thrombin complex concentrate it's like the first line for the treatment of our warfarin toxicity these days and remember warfarin is also a terrarogen right and remember heparin you reverse heparin with protein right okay okay so um let's see remember nitrofyrantone you can only use it with tristis studies and females it doesn't work in any other um doesn't work in any other um sex or any other condition on mbmi's remember nitrofyrantone is also as you know that pulmonary fibrocess uh don't forget the other drugs that are pulmonary fibrocess right so like a busol fan right it's an anti-cancer drug a bleomysin remember bleomysin works specifically in the g2 phase it's also an anti-cancer drug it's one of those weird things that love to test on step three for some bizarre don't forget amute or run don't forget methotrexit remember methotrexit is a de-mart it's used in the treatment of rheumatoid arthritis remember it's a terrarogen so don't give it to a pregnant woman if a pregnant woman has rheumatoid arthritis on your test consider giving that pregnant woman hydroxychloroquine or um sulfosalazine
okay um and then um methotrexit right remember it's a dihydrofolio reductis inhibitor it can cause bone marrow suppression so you can use that to rescue the you can use a lukovorin the folinecacid analogue to rescue the bone marrow under those of circumstances and then don't forget that methotrexit is also hepato toxic right and methotrexit has some obi-guine applications like in the treatment of a choreocarsinoma for example and then don't forget your cyclophosphamide right cyclophosphamide um it's uh it's an alkalinity agent remember that it's um it can cause hemorrhagic estitis and it can increase your risk for bladder cancer remember that you can decrease the risk of hemorrhagic estitis associated with cyclophosphamide by giving this drug known as mesna okay by giving the drug known as mesna and then don't forget your your cisplatin cisplatin um it's the if you essentially see an anti-cancer drug that has causes like um auto toxicity on your mbmi's or causes like profound nausea and vomiting stop reading the question and pay for cisplatin okay remember cisplatin is nephrotoxic um in fact cisplatin is one of those unique drugs that has the combination of nephrotoxicity and auto toxicity the other two drugs on mbmi's that have that combination of side effects are your vancomycin and you know glycosides like a gentomycin okay so um uh cisplatin you can actually prevent the nephrotoxicity by giving this drug known as a amyphostin okay so am i fos ti okay and then um don't forget your um your vincar alkaloids like vinchristin vimblastin remember those prevent the polymerization so not depolymerization i mean polymerization so like p p for polymerization deprevent polymerization of micro two builds remember those drugs that have peripheral neuropathy on mbmi's and then um don't forget your pachyletaxel dosataxel those drugs prevent depolymerization of micro two builds r
ight those are also another set of cancer anti cancer agents and then don't forget your tnf inhibitors right so like adalimumab um a tonner sept right though remember a tonner sept is a decoy receptor for tnf and those drugs you want to check for TB where you want to do TB skin disease before starting those drugs um and then don't forget your um your ultransmit noic acid right remember you can use it to treat um acute pro myocytic leukemia remember that has the association with um um your 15 17a translocation um don't forget your immatineb remember immatineb is used to treat a cml right immatineb gasatinneb remember cml is associated with um the 922 translocation where you form the fusion protein a bcr able okay and then don't forget aculesumab aculesumab is a monoclonal antibody again c5 you can use it to treat paroxysmal nocturnal hemoglobinuria remember before you start aculesumab you want to essentially vaccinate those people against like nicere right because remember if uh by giving aculesumab you are effectively using pharmacology to induce a terminal complement component deficiency and that increases your risk for recurrent and nicerele infections and then don't forget adenosine right remember adenosine basically hyperpolarysic cells you can use it to treat a phab right or if a person has like an svt right if you want to basically like okay let's say less a phab more svt okay if you want to break the svt you give like six milligrams first if that doesn't work you give 12 milligrams if that doesn't work you give 12 milligrams okay and remember that adenosine right caffeine right or like fiorfelin antagonizes its effects um so that's something i want to keep at the back of your mind and then for like these cardiac stress tests somadenosin nonononomes like a regadenosin or apadenosin for example actually used in the these are cardiac stress again because this sort
of kind of tick advantage of the coronary steel principle and then don't forget your octriotide remember octriotide if a person has um come on divine thank you for pressing comes in with like a varsil bleed right to want to give octriotide in the acute phase remember for a person like chronically to decrease the arrest for having like re bleeding of the varsil whatever you can give spurnolactone you can give um come on divine thank you can give spurnolactone you can also give um proprylonol okay you can give spurnolactone you can give proprylonol don't forget your insulin like less pro aspirin and blue lysine those are like your rapid acting insolence I remember that insulin regular is your um your shodactin insulin your intermediate acting don't forget your np try to like your neutral perturbing hygidone or whatever it's called and then your long actin right don't forget your glargine your dead amere your degludeck those that tested quite commonly on exams and then remember metformin remember metformin it's a big one-eyed it's weak neutral right remember that um i have actually described the mechanism of uh metformin like the metformin mechanism basically remember if a person is getting contrast for I described that in a in one of my prior podcasts remember if a person is being studied on metformin whether you're taking metformin you want to stop the drug if you're getting contrast right because they can have like a life threatening a lactic acidosis and you also want to sort of kind of like forget metformin if a patient has a reno failure um don't forget your sulfonial ureas right so like your um those drugs remember the inhibits their potassium channel blockers right so the inhibits that uh ATP that uh um that potassium channel that depends on ATP right that you find in the pancreatic eye let's else remember these sulfonial ureas right so like proprprimide remembe
r proprprimide actually has an association with sideh um those drugs right the cause weight gain right and remember that these drugs they can actually trick you um in a person that's like they can be taken like so repetitious they're like factitiously on nbm exams so if a person is taking a sulfonial urea right the insulin will be high the acpeptide will be high and then you do the secretive ox screen and boom it's basically like a serum screen for sulfonial ureas okay um so that's something you want to keep at the back of your mind um don't forget your second generation of sulfonial ureas right so like your glee glee drugs so like gliburide is nephrotoxic uh glipyside is hepatotoxic there's also glimipride um and then don't forget your p-part gamma uh uh activators right so your tzds your thiozolidine diodes like pyoblidazone these are your glider drugs pyoblidazone rosy glidazone don't use them in a patient that has a CHF because they can cause fluid retention because they have p-part gamma receptors in the kidneys so they increase the reabsorption of water and then um these drugs remember they also cause a weak gain and then don't forget your your alpha glucosides inhibitors right so like your egg carburetles your migletal remember these drugs cause like a very nasty like phosphatine diarrhea it certainly don't want to be sitting next to these people on a pleenride um and then don't forget your g-lp 1 analogs right so like exenatide lyraglutide um those drugs they're contraindicated in patients that have a histro medallary thyroid cancer um and the associated olpankratitis as well right so that's something you want to keep at the back of your mind for mbm is and then don't forget your dpp 4 inhibitors right so your dipeptidol peptidase foine inhibitors right so like your um your glipthens right so like aloe glipthene lina glipthens ceraglipthens sacsaglipthene right
those drugs they are dpp 4 inhibitors um um um they actually again contraindicated in patients that have a histro medallary thyroid cancer um and remember like your lyraglutide it's actually been approved by geftd 4 weak loss okay so it's just something you want to keep at the back of your mind um and then let's see um don't forget your your um your your canagly flosen dapagly flosen those are your sglt 2 inhibitors right remember those are associated like urinary tract infections and they are contraindicated in patients that have a history of a renauphilia so i think this has gone on for long enough i'm going to make another clot from a colgipot cast but i hope you get a lot of use from this uh as i always say when i end the podcast i'd offer one on one tutoring for the u.s.m.
list step one two ck two cs and step three exams the internal medicine training exam and the abim board exam right and then if also preclinical exams study a shelf exams in med school and then if you're in undergrad and you need tutoring for like all chem gen chem physics um physiology biochemistry histology i offer tutoring for all those subjects and then if you're a med student applying to residency so an ERS application or college student applying to med school so an AMCA's application i do offer one on one like consulting for those so like application prep interview prep personal statement i did in um application preparation and stuff like that so if you need any of those things reach out to me through the website or you can send me a direct email at divine intervention podcasts podcasts with an sbn that gmail.com so have a wonderful rest of your day i will see you next time and god bless you thank you
Practice questions — USMLE style
Question 1 — Nephrology/Pharmacology
A 72-year-old woman with a history of hypertension is started on hydrochlorothiazide for blood pressure control. After two weeks, she presents to the clinic complaining of muscle weakness and fatigue. Laboratory studies reveal hypokalemia (K+ 3.0 mEq/L), metabolic alkalosis, and mild hypercalcemia. Which mechanism best explains this electrolyte disturbance?
- A) The thiazide diuretic inhibits carbonic anhydrase in the proximal tubule, leading to potassium wasting.
- B) The drug increases sodium reabsorption in the distal convoluted tubule, promoting potassium excretion via exchange mechanisms.
- C) The drug causes direct tubular damage, resulting in impaired calcium reabsorption and subsequent hypocalcemia.
- D) The diuretic inhibits aldosterone receptors, preventing adequate mineralocorticoid action and causing hyperkalemia.
Answer: B. Thiazide diuretics work by inhibiting the sodium-chloride symporter in the distal convoluted tubule. This increased sodium delivery to the principal cells of the collecting duct enhances potassium excretion (potassium wasting), leading to hypokalemia and metabolic alkalosis. The podcast notes that thiazides are associated with hypercalcemia, which is a common side effect related to their mechanism of action on calcium handling in the distal nephron.
Question 2 — Cardiology/Pharmacology
A patient with chronic heart failure (CHF) is being managed for atrial fibrillation and has been taking digoxin. The nurse notes that the patient's serum potassium level dropped from 4.5 mEq/L to 3.0 mEq/L this morning. Which finding should prompt immediate concern regarding potential drug toxicity?
- A) New onset of peripheral edema, suggesting calcium channel blocker overdose.
- B) Development of paroxysmal ventricular contractions (PV Cs), which is a classic sign of digoxin toxicity.
- C) Increased heart rate and palpitations, indicating inadequate beta-blocker effect.
- D) Mild nausea and vomiting, suggesting gastrointestinal side effects from the antiarrhythmic agent.
Answer: B. Digoxin inhibits the Na+/K+ AT Pase pump. The podcast explicitly states that hypokalemia increases the risk of digoxin toxicity because the binding site for digoxin on the Na+/K+ AT Pase pump is the potassium site. Low serum potassium levels increase the concentration gradient and thus the binding affinity, significantly increasing the risk of arrhythmias, which classically manifest as PV Cs.
Question 3 — Endocrinology/Pharmacology
A patient with Type 2 Diabetes Mellitus (T2 DM) presents for routine follow-up. The physician prescribes an SGLT2 inhibitor to improve glycemic control. Which of the following conditions should be monitored closely before initiating this medication, and why?
- A) History of chronic kidney disease; because the drug is nephrotoxic and can cause acute tubular necrosis.
- B) Pregnancy; because the drug crosses the placenta and poses a risk to the fetus.
- C) Severe heart failure; because it causes peripheral vasodilation and may worsen cardiac contractility.
- D) Renal impairment; because the drug relies on renal excretion, and impaired function increases the risk of lactic acidosis.
Answer: D. SGLT2 inhibitors (like canagliflozin or dapagliflozin) work by blocking glucose reabsorption in the proximal tubule. The podcast notes that these drugs are contraindicated in patients with a history of renal failure because they rely on renal excretion, and impaired kidney function increases the risk of metabolic complications like acidosis.
Question 4 — Hematology/Pharmacology
A patient is scheduled for elective surgery and requires prophylactic anticoagulation. Given their high bleeding risk, the physician orders an antiplatelet agent. Which class of drugs should be administered to prevent thrombosis, and what is a key consideration regarding its administration?
- A) Warfarin; requiring a bridging anticoagulant like unfractionated heparin due to slow onset of action.
- B) Aspirin; which must be avoided if the patient has active peptic ulcer disease.
- C) P2 Y12 inhibitors (e.g., clopidogrel); these agents are effective for stroke prevention but require careful monitoring for bleeding risk.
- D) Direct Thrombin Inhibitors (DT Is); they should only be used in acute settings and not prophylactically.
Answer: C. The podcast discusses antiplatelet medications, including aspirin and P2 Y12 inhibitors (like clopidogrel). These agents are commonly used for stroke prevention. While all options listed relate to coagulation/antiplatelets, the question asks for a general prophylactic agent class. P2 Y12 inhibitors are standard therapy for preventing thrombotic events post-stroke or stent placement. The key consideration is that while they prevent clotting, they increase bleeding risk, necessitating careful monitoring (as implied by the need for prophylaxis).
Quick fire review
What is the primary mechanism of action of statins?
They inhibit HMG-CoA reductase, thereby decreasing cholesterol synthesis in the liver.
Which antiarrhythmic drug is associated with both Drug-Induced Lupus and is the drug of choice for WPW syndrome?
Amiodarone (or Propafenone).
What class of diuretics causes a strong association with hypomagnesemia and hyperglycemia?
Thiazide diuretics (e.g., HCTZ).
Which anti-psychotic medication is known to cause hyperprolactinemia due to dopamine receptor blockade?
Most antipsychotics, especially those that block dopamine receptors.
What combination of lab findings suggests the use of a carbonic anhydrase inhibitor like Acetazolamide?
Metabolic acidosis and hypochloremia.
Which antiplatelet agent is used in both stroke prevention and stress testing because it inhibits phosphodiesterase, increasing cAMP?
Dipyridamole (or Cilostazol).
What drug class should be avoided in patients with asthma due to bronchospastic effects?
Non-selective beta blockers (e.g., Propranolol).
Name three drugs that are contraindicated or require caution when a patient has severe renal impairment.
Metformin, NSAI Ds/ACE inhibitors (in specific contexts), and potentially certain antibiotics like aminoglycosides.
What is the key difference in side effect profile between Spironolactone and Eplerenone?
Spironolactone can cause gynecomastia because it also blocks androgen receptors; Eplerenone does not have this side effect.
Which anti-psychotic medication has a unique association with causing cataracts?
Quetiapine.
What is the preferred agent for treating hyperthyroidism in a pregnant woman, and why?
PTU (Propylthiouracil); because it is safer than Methimazole during the first trimester of pregnancy.
Which drug class causes profound diarrhea and stomach upset due to its mechanism of action against H. pylori?
Cephalosporins (specifically, Septazidime).
What are the two primary drugs used for prophylaxis in a patient with HIV whose CD4 count drops below 200 cells/mm³?
Trimethoprim/Sulfamethoxazole (TMP/SMX) and Pyrimethamine/Sulfadiazine.
Which class of antibiotics is known to cause nephrotoxicity AND ototoxicity, requiring careful monitoring?
Aminoglycosides (e.g., Gentamicin).
Quick recall / Anki-style questions
Name three drugs that are contraindicated or require caution when a patient has severe renal impairment.
Metformin, NSAI Ds/ACE inhibitors (in specific contexts), and potentially certain antibiotics like aminoglycosides.
What is the key difference in side effect profile between Spironolactone and Eplerenone?
Spironolactone can cause gynecomastia because it also blocks androgen receptors; Eplerenone does not have this side effect.
Which anti-psychotic medication has a unique association with causing cataracts?
Quetiapine.
What is the preferred agent for treating hyperthyroidism in a pregnant woman, and why?
PTU (Propylthiouracil); because it is safer than Methimazole during the first trimester of pregnancy.
Which drug class causes profound diarrhea and stomach upset due to its mechanism of action against H. pylori?
Cephalosporins (specifically, Septazidime).
What are the two primary drugs used for prophylaxis in a patient with HIV whose CD4 count drops below 200 cells/mm³?
Trimethoprim/Sulfamethoxazole (TMP/SMX) and Pyrimethamine/Sulfadiazine.
Which class of antibiotics is known to cause nephrotoxicity AND ototoxicity, requiring careful monitoring?
Aminoglycosides (e.g., Gentamicin).