DIP Episode 6 - 20 in about 20 minutes (Pharmacology Cases)

Okay, welcome. My name is Devine. I am a fourth-year medical student. Today we're going to be talking about the sixth episode of the Divine Intervention Podcasts. And today's topic is 2020. So in 20 minutes I'm going to discuss 20 pharmacology cases. And I'm going to try to integrate a lot of like other pharmacologies, some pathologies, some physiology and stuff like that. And just I can imagine the blood pressures of all the fourth-year medical students today. I can imagine it almost be really low with our expectations for match day tomorrow. So have a fun Thursday before you find out where you're going for the next, I guess anywhere from three to seven or eight years. Okay, so let's go ahead and begin. So the first case describes gynecomastia in a patient being treated for peptic concert disease. So gynecomastia in a patient being treated for peptic concert disease. Hopefully you're thinking about simedidine. Okay, simedidine is a H2 receptor antagonist. Okay, it's used to treat peptic concert disease. Remember by blocking those H2 receptors, you're preventing the enterochromophine, like cell medated stimulation of parietal cells, right through histamine H2 receptors that are GS coupled. So when you inhibit that stimulation, you have less sickly came in the parietal cell and you're sick with less acid. Okay, so this drug, it so happens that it has androgen receptor blocking activity.

So by blocking androgen receptors, it can cause a gynecomastia because it's sort of tilt you towards having, I guess like your estrogen to testosterone ratio, it tilt you towards having like more estrogenic effects. Okay, remember that simedidine is also an inhibitor of cytochromp 450. Good, next case. Seasures in a patient with a history of severe parietas between the finger webs, right? So if you see parietas between the finger webs, I really hope you're thinking about skb's. Okay, remember skb's is caused by sarcoptisus kbi. Okay, so the drugs you could use, the drug you should use in your patients is pymethrin. Okay, you can use pymethrin, but a circling agent is a drug known as lindain. Okay, it so happens that lindain has, it blocks gaba receptors. So by blocking gaba receptors, think about it. You're having a net glutamateurgic effect because gaba that normally comes you down no longer has that effect because you're blocking the receptors. So you could potentially get seizures with lindain. Okay, remember this is sort of similar to the way I sonyazine also causes neurotoxicity and seizures because I sonyazine depleted your vitamin B6 and vitamin B6 or pyridoxyl phosphate is a cofactor for glutamate decarboxylase, which helps you convert glutamate to gaba. Okay, so you have a net increase in glutamate and you can run into a lot of trouble. Also remember that glutamate decarboxylase is the enzyme that you make or want to bodies against in type 1 diabetes. Okay, good.

Next case, what is the preventive measure that could have been taken in a patient presenting with an EF of 25% three months after chemotherapy treatment of a lymphoma? Well, hopefully you're thinking about dilated cardiomyopathy. Okay, classically with your anthracyclins like doxandoneurubicin. Okay. So remember these drugs are intercalated intercaledian agents so they sort of stick themselves between gaining. So you begin to form all these like nasty cross links and stuff like that. It so happens that these anthracyclins are heavily bound by doxosyl like they are heavily bound by iron and that complex can cause the formation of a lot of superoxide radicals that can cause myocardial cell damage. Okay, so you can prevent that by giving an ion keeliter like dexerzoxy. Okay, giving an ion keeliter like dexerzoxy. Remember your anthracyclins cause an irreversible dilated cardiomyopathy. Contrast that will transduzium of that causes a reversible dilated cardiomyopathy. Okay, next case prevention of secondary hemochromatosis in a patient with a histrobeda thalmeja. Right, so patients with a histrobeda thalmeja they need to keep getting regular blood transfusions. Right, so that can cause a lot of ion loading. So you can treat that by giving a drug that's an ion keeliter. Like deferroxamine or deferacerox. Okay, remember those things have F-E in their names. I guess a deferacerox also has a F-E in its name so that helps you remember that those are ion keeliters.

Okay, next case rapidly progressive neurological deficits. Okay, over weeks and some the lengths and a patient who was recently started on a drug. Okay, oligoclonal bands have previously been found with CSF studies in this patient. Well, the thing I'm really hoping you're thinking about here is a patient that has multiple sclerosis. Okay, remember the association with oligoclonal bands in the CSF. Okay, I remember you can see all these enhancing lesions on MRI that are separated by space and time. Okay, so the drug I'm talking about here is Nathaliezumab. Nathaliezumab is a monoclonal antibody against alpha-phointegrate and it has a strong association with the reactivation of the JC virus which can present as a progressive multi-focal lookance of a lopathy. Okay, and while we're on the topic of integrates, remember that an integrate deficiency is also associated with like the leukoset addition deficiency. Well, you give your question about a neonate that has like delayed separation of the umbilical cord. Okay, now next case severe hypotension and adrenal hemorrhage in a patient loss to follow up after receiving a two-year subscription of some drug. Fluocyte tomatry of a blood sample from this patient revealed an absence of GPI anchors. Okay, revealed an absence of GPI anchors, right? So if a patient has some disorder where they have no GPI anchors on fluocyte tomatry, I'm really hoping you're thinking of a PK gene mutation.

Okay, that's a proxiesum or noxional hemoglobinuria. Okay, so because those people don't have like CD55 and CD59 complement, comes and explodes the uh explodes the air itself. So it's a kind of intravascular hemolosis and in that case that person will basically have some kind of hemolytic anemia, right? So it's classically a young male that presents with hematuria in the mornings because complement is activated more often um at least at an increased level at night, okay? So remember the tributin of PNH is with aculesumab. It's a monoclonal antibody against C5, okay? So by basically creating a functional C5 deficiency, this person has an increased risk of uh nysserial infections, okay? And remember nysseria meningitis for example can cause water house refrigerants syndrome, which is where you have a adrenal hemorrhage, okay? So that's what I'm presenting with this case. Case number seven, management of a patient who presents with a white ton of 52,000, okay? Uh leukocyte alkaline phosphatise is decreased. leukocyte alkaline phosphatise is decreased. Well hopefully you're thinking about CML, okay? Chronic myeloid leukemia. Remember you have association with the 922 translocation where you create the BCR-Ebo um tyrosine kinase, okay? It's a fusion protein um that protein is uh operoglyphid in people that have a CML and the way you manage CML is by giving a drug known as a matnip, okay? Basically I'll just give you a trick right now.

Any drug that ends a nip is a tyrosine kinase inhibitor, okay? So you treat this condition with a matnip and the leukocyte alkaline phosphatise, I say it's uh it's low, that helps you differentiate CML from a luchomoid reaction where the leukocyte alkaline phosphatise is high. Remember that a matnip is also used to treat GI stromotrumors, okay? Because it also inhibits the C-ketatyrsine kinase receptor. Next case, case number 8, patient with a history of an apple correlation detected in abdominal CT feels to respond to therapy with an inhibitor of the epidermal growth factor receptor, okay? So uh apple correlation abdominal CT you're thinking of colon cancer, right? So colon cancer um uh many colon cancers for some bizarre reason over express the epidermal growth factor receptor, okay? So you could potentially treat a colon cancer by giving a monoclonal against the IGFR receptor, okay? So you can give a drug like say toxi-map, okay? But the thing is it so happens that Keras falls downstream of the epidermal growth factor receptor. So if you're taking an IGFR inhibitor and you're not recording any kind of effect, think about some kind of activity mutation in Keras, okay? And to sort of tie some things together for you. Uh your friends of the NBM, you want you to know the the adenoma carcinoma sequence with colon cancer, right? So like uh you can remember that with anomonic AK53, okay? So you start with an APC gene mutation and then you progress to a Keras mutation, okay?

Remember Keras is downstream of IGFR and then if you get a P53 mutation you get a full blown a colon carcinoma, okay? So uh next case food drop in a patient recently placed on some kind of chemotherapy regimen, right? So I really hope you're thinking of um peripheral neuropathy, okay? If many cancer drugs can cause peripheral neuropathy, but classically on board exams, the drug you want to think about is vincristine, okay? Vincristine. Remember vincristine is a vinka alkaloid, okay? So it binds to tubulin and essentially prevents the polymerization of microtubules, okay? And remember micro tubules, right? You need them for proponent neuronal function. If you want to get things to the synapse with those molecular models, you need micro tubules to make that happen. So that potentially explains the uh peripheral neuropathy you get with the vinka alkaloids. And remember that your vinka alkaloids sort of work like co-chasing, okay? Co-chasing also works by preventing the formation of the polymerization of micro tubules, okay? And I hope if you hear the words food drop, you're thinking of a common perinion nerve palsy, okay? Just an anatomy time there. Okay, case number 10, reduce the OCO and ASTLT elevations in a patient with a history of a snuestone appearance detected in a pelvic ultrasound, right? So snuestone appearance, pelvic ultrasound makes you think about an invasive mole, okay?

And remember invasive, uh, I mean like, I mean, hydratideformals, they can progress and become invasive, I guess. The way you treat one way you can treat hydratideformals, I mean besides a suction cure attach, uh, actually you should do a suction cure attach, but let's assume it becomes invasive and whatnot, you can treat with methotrexate, okay? Remember methotrexate is a dihydrofolid reductase inhibitor, it has a very strong association with pulmonary fibrosis, right? So you can get a restrictive lung disease picture, that's why the DLCO is reduced and methotrexate is also hepato toxic, okay? And remember, you shouldn't give methotrexate to a pregnant woman so you don't give her a kid a neuro tube defect, okay? Next case, flushing in myoclonus in a patient who recently started oral antibiotic therapy against a gram positive, catalys positive and quaggolys positive organism. This patient has a history of generalized anxiety disorder, right? So basically I'm describing stuff for you, okay? So let's assume this person has MRSA, okay? One oral drug you could use to treat MRSA is Linizolid, okay? Remember Linizolid inhibits, um, inhibits initiation, okay? It binds to the 50s contribution to the P site of the ribosome, okay? Linizolid, it so happens, uh, has a, uh, some weak monoaminoxidys inhibition inhibitor activity, okay?

So for present, has a history of generalized anxiety disorder for which the drug of choice, uh, the SSR Is, you could potentially imagine a person getting a serotonin syndrome, okay? And uh, please don't forget that you treat serotonin syndrome with, uh, uh, like siper heptadine, which is, uh, it's a H1 blocker that also has a serotonin receptor blocking activity. Okay. Uh, so next case, uh, severe vomiting and flushing in a chronic alcoholic with a recent treatment for sedive colitis, okay? So sedive colitis, remember, it's your post antibiotic, um, diarrhea, okay? Uh, classically it's a watery diarrhea and the first line drop for treating a sedive colitis is metronidazol. Um, metronidazol has the disol from side effect, okay? So it inhibits as a toutahide dehydrogenase, so you can have a buildup of acetate aldehyde and you can begin to run into a lot of trouble if you're taking a boost on the side, okay? So that's your disol from effect. So the thing you want to think about with, uh, uh, your disol from effect, uh, think about that with metronidazol. Remember, this drug also causes a metallic taste and a mouth, okay? And remember, the other things you could use to treat sedive colitis, right? So you could use, uh, vancomycin, uro vancomycin, okay? You could use vidaxomycin, uh, it's a macrolated that also works as an RNA polymerase inhibitor and, uh, I guess your last link would also be a fickle transplant.

Okay, next case, he will go up in a five, white count of 500 and a pleatlet count of 20,000, right? So these are all abnormal in a patient, uh, treated for a monospot negative mononuclosis-like syndrome, okay? Monospot negative mononuclosis-like syndrome, right? So this prescient as CMV, okay? Remember the association with aldehyde inclusions, okay, on microscopy? And the way you treat CMV is with GANS-cyclover, okay? So GANS-cyclover, uh, basically, uh, inhibits DNA polymerase, but it needs to be activated by a UL-97 kinase, okay? So it's activated by UL-97 kinase, it's incorporated into the genome and then it causes a chain termination, okay? So GANS-cyclover has a stronger association with bone marrow suppression, okay? That's why this patient has this presentation, okay? And remember that CMV, if you have, uh, has many other things, it causes, right? So it can cause, um, like, red mites in a HIV patient or colitis in a patient with, uh, like a recent history of transplant, and it can also cause like linear ulcers, right? As of a gyitis in a patient with a history of a HIV. Okay, next case, CVIP gastric pain-reducing to the back in a patient recently started on some kind of pharmacotherapy. This patient has a history of inconsistent, uh, condom use. So history of inconsistent condom use should make you think about HIV, okay? Uh, one of the drug classes for the treatment of HIV or NRT Is includes drugs like stavidin and didenocin, okay?

These drugs have a very strong association with pancreatitis, okay? In fact, that's probably the biggest side effect you want to remember with those medications. Okay, next case, severe diarrhea, full body rash and abdominal pain in a patient who was recently started on pharmacologic management, uh, for HIV. This patient died three days after presentation. So this patient, this, uh, toxic drug I'm showing you, so it looks like a hypersensitivity reaction. So hopefully you're thinking about a back-a-veer, okay? A back-a-veer causes a very severe hypersensitivity in certain and susceptible patients that could actually present as death, okay? It could be fatal. And the pathophysiology behind this is there's a HLEB 57 gene, uh, protein product that can be bound by a back-a-veer. And normally that protein product is not immunogenic, but when a back-a-veer binds to it, it causes some kind of structural modification that basically shuts down whatever tolerance you build up in, I guess, your embryonic ears. And you'll form cytotoxic T cells against that complex and that can cause a very severe hypersensitivity reaction. So in general, before a person gets a back-a-veer, which is an N-R-T-I, you need to perform some kind of HLEB 57 testing. Okay. Now, drug of choice, so next case, drug of choice in the management of a diabetic, presenting with very high-feevers and severe sinus tenderness. So hopefully you're thinking of micro-micosis, okay?

Classically caused by like rhizopause species. You want to go ahead and give amphotericin B. It's the only drug that has, like, rescued some people. This can actually be pretty fatal. Remember, amphotericin B works by binding a gastro, okay? It's very never toxic, but if you give the liposomal form, you could potentially reduce toxicity. And remember that you could also use, you could actually use amphotericin B to treat a cryptococcal meningitis. You typically add a five flu sideos into that. Okay. Next case. After in popularity defect, in a patient with a recent history of hemoptysis, with a chest X for showing a riboprylobe, cavitory infiltrate. Right? So this is clearly TB, okay? So how do you treat TB? You can treat it with a rib regimen, right? So like rifampin, isoniasid, pyrazinamide, and ethymbutol. Ethymbutol works by inhibiting an enzyme known as aerobinocel transferase that helps you make some substrate that's bound by my colleague acid as you synthesize the cell wall of fungi. Okay? So ethymbutol is used to treat TB, okay? It's associated with optic neuritis, which again can present as an afferent popularity defect, okay? So don't forget they could easily tie this in with the Swingin flashlight test that you learned about in yourology. Okay. Next case. Neonit in a developing country is unresponsive on presentation. It was rushed to the hospital by ambulance, a reveal of his chart, reveals a medication error.

This child was recently treated with a dihydrofoli reductis inhibitor for some congenital infection, okay? For some congenital infection, right? So hopefully you're thinking about bacteria, okay? Try methyprin, so from ethymboxes all. You generally do not want to give this to a neonate, okay? Because it can cause connectors. And the mechanism behind that is chronic, the mechanism behind that is TMPSMX can displace indirebular ribin, okay, from albumin. And that indirebular ribin can cross the blood-brain barrier and cause a lot of problems in the neonate, okay? And remember that thrimethyprin, right? It's dihydrofoli reductis inhibitor. The SMX part, sofymethoxazole, works by inhibiting a dihydrophyridocyanthesis. But basically those two drugs work together to inhibit the synthesis of folate in bacteria. And remember that that's the drug of choice in the prophylaxis against the hemosistis-durevetsi in a HIV patient when the CD4 counter plummet will lower 200. Next case. Rising PCO2 in a patient, being treated with amicasein, for an aggressive pseudomonas infection. And EMG reveals a reduced amplitude of contraction with phrenic nerve stimulation, right? So anicasein is clearly an amino glycoside, right? And remember you amino glycosides, they basically work by inhibiting the 30th contribution to the P side. So the inhibiting initiation. I remember there are the only protein synthesis inhibitors that are generally bacteria side of, okay? So the covasoidomonas really well.

But it so happens that these drugs also have the ability to bind to the presynaptic calcium channel that you find at synapses, okay? So that can prevent the release of acetylcholine. So these drugs actually associated with a neuromuscular blockade, okay? Another drug class that also has the side effects that you are calcium channel blockers. Your non-dihydroperidina calcium channel blockers, like I'm loaded, sorry, like a verapamele and deltaiazene, okay? Remember this is sort of similar to the pathophysiology behind the lumbarid etymyastenic syndrome, which is classically associated with small cell lung cancers, one exam, one exams, okay? So last case, so hemoglobin of 4.5, bleeding account of 15,000, and white count of 500 in a child with a history of somnolence and nocorrigidity. CSF studies revealed very low levels of glucose, elevated protein levels, a preponderance of neutrophilts, and gram-negative diplococsine that ferment more tos and glucose, okay? And then I add some addendum at the end above the adult presentation, okay? So this patient basically has an e-plastic anemia, okay? You can imagine that you have my seramine meningitis, meningitis, okay? So remember your CSF studies in bacterial infections. So let's assume this person was in a developing country with very few resources, and he got a chloromphenicol, because chloromphenicol is very good at crossing the blood-brain barrier.

Remember it works by inhibiting peptidal transferates, so it's a 50s inhibitor, but it can cause a plastic anemia as a side effect, okay? Another thing I would go ahead and see with regards to chloromphenicol toxicity, right, is that it can cause the gray baby syndrome, because it's metabolized by UDP glucoronacyl transferates, right? So you generally don't want to give chloromphenicol to a new unit, because they have like, in general, they have very low levels of UDPGT, okay? So they do not metabolize the drug, so they can get more toxicity from chloromphenicol, okay? In fact, one high yield, I'll say probably the only time you see chloromphenicol giving on an endemic exam is in the setting of re-catsia re-catsia infection in a pregnant female, okay? Chloromphenicol is actually indicated for that. Now, one adult presentation that where they could give you a very unusual endemic question, where a person has like chloromphenicol toxicity, is with cradlenohar syndrome, okay? Remember, it can cause, this is one of those GI disorders, where you get an indirect type of bilirubinemia, because you have a UDPGT deficiency, okay? So it could present with a chlor, they could easily give you a question, person has a UDPGT deficiency like cradlenohar syndrome, and it's asked which of the following drugs is contraindicated, okay? Chloromphenicol would be one of those drugs, okay? So just something to keep in mind.

I know this took a little over 20 minutes, I spent some time agreeating you guys at the beginning, and I guess I'm talking about some other fluff, but I wish you all the best. If you spot any errors, or you have any questions, just shoot me a message, okay? Or make a comment in the podcast, and I'll try to answer them as quickly as possible. Have a wonderful day, and all the best to the fourth year is with a match tomorrow. Thank you.

$\text{H}2$ receptor antagonist.

Lindane blocks GABA receptors, leading to a net glutamatergic effect (excitatory).

Anthracyclines (e.g., doxorubicin).

Anthracyclines cause irreversible dilated cardiomyopathy; Tacrodizium causes reversible cardiomyopathy.

Ganciclovir (used for CMV).

It inhibits aldehyde dehydrogenase ($\text{ALDH}$), leading to a disulfiram-like reaction.

Zidovudine and Didanosine.

It has androgen receptor blocking activity, shifting the estrogen-to-testosterone ratio toward more estrogenic effects.

The drug displaces indiredribulin from albumin, leading to riboflavin deficiency and potential neurological issues in the neonate.

Low $\text{LAP}$ helps differentiate $\text{CML}$ (myeloproliferative) from a leukemoid reaction, where $\text{LAP}$ would be high.

$\text{APC}$ mutation $\rightarrow$ $\text{Keras}$ mutation $\rightarrow$ $\text{p}53$ mutation.

Aminoglycosides (e.g., gentamicin).

Optic neuritis/Afferent pupillary defect ($\text{APD}$). This can be tested using the swinging flashlight test.

It has androgen receptor blocking activity, shifting the estrogen-to-testosterone ratio toward more estrogenic effects.

The drug displaces indiredribulin from albumin, leading to riboflavin deficiency and potential neurological issues in the neonate.

Low $\text{LAP}$ helps differentiate $\text{CML}$ (myeloproliferative) from a leukemoid reaction, where $\text{LAP}$ would be high.

$\text{APC}$ mutation $\rightarrow$ $\text{Keras}$ mutation $\rightarrow$ $\text{p}53$ mutation.

Aminoglycosides (e.g., gentamicin).

Optic neuritis/Afferent pupillary defect ($\text{APD}$). This can be tested using the swinging flashlight test.