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Hepatoxic Drugs

👊🏻 Drug-induced liver injury 🥊⁠

💊 There are SO many medications that can cause liver injury through various mechanisms. However, some key medications have black box warnings for liver toxicity and are more well-known for their risk. These are the ones that you should know for exams! 🗒️⁠

🔺 Hepatoxic drugs are usually well tolerated unless high doses are administered. In most cases, the primary treatment is to STOP the drug, especially when liver enzymes (AST and ALT) rise 3 times above their upper limit of normal.⁠

🧠 Some other helpful memory tips:⁠
-Acetaminophen’s brand name is Tylenol which looks similar to ‘Tired Liver’. ⁠
-Nefazodone and Nevirapine are never used anymore due to their severe liver toxicity so think never-zodone and never-apine. ⁠
-KEToconazole can KILL your liver⁠

🤔Some of them are a stretch but if you’re willing to try them out and they help you retain the information then that’s a win in my books. ✌🏻⁠


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 Total Parenteral Nutrition (TPN)

“If the gut works, use it!” but when it doesn’t…⁠

✨ Check out this post to learn more!⁠

💉 Total parenteral nutrition (TPN), also known as parenteral nutrition (PN) is a form of nutritional support given completely via the bloodstream, intravenously with an IV pump. ⁠

🍞 TPN administers proteins, carbohydrates, fats, vitamins, and minerals.⁠

 

 

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Inhaled Corticosteroid Combinations

🧠Memory tips for inhaled corticosteroid combinations!⁠

🌬️Inhaled corticosteroids are first-line options for treating patients with asthma. But many of these inhalers are brand-name only and some come in combination with long-acting beta 2 agonists or inhaled anticholinergics. ⁠

🫁Inhaled corticosteroids work by reducing inflammation and swelling in the airways. Reducing inflammation makes it easier to breathe, which minimizes asthma attacks. But these medications have to be taken daily, and it may take several weeks before they’re fully effective.⁠

🧠Some of these brands are often used on exams and it is helpful to know what their combinations are: ⁠

TIP – we would never put two corticosteroids together so for example if the question asks about Symbicort – the answer should be ✅️budesonide with formoterol (ICS + LABA) NOT ❌️budesonide with fluticasone (ICS + ICS). ⁠


⁠👉🏻Quiz yourself on how well you know the combinations and some of my memory tips on remembering them!

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Sertraline

😳 Since one of sertraline’s common side effect is diarrhea 💩, I called this piece ‘Squirtraline’. 💦 🤣⁠

💊 Sertraline belongs to the class selective serotonin reuptake inhibitors. SSRIs are like the traffic controllers of your brain’s serotonin levels. They help ensure that serotonin sticks around longer, improving symptoms of depression and anxiety. ⁠

🧠TIP: Serotonin is your ‘feel-good’ neurotransmitter. It is responsible for regulating mood, emotions, and even appetite. Sertraline’s role is to increase the amount of serotonin available in the brain by inhibiting its reuptake. Notice how SERtraline looks similar to SERotonin. ⁠

🌟Common side effects to know: ⁠

-Nausea/diarrhea⁠
-Headache⁠
-Changes in sleep pattern⁠
-Decreased libido and erectile dysfunction⁠

👉🏻Other than sexual side effects, symptoms often improve or resolve with time. ⁠

🗒️ Note: Sertraline is the most likely of the SSRIs to cause diarrhea. Research shows it may occur in up to 20% of people. Don’t fret – educate your patients that it will usually get better within a few weeks and to use antidiarrheal medications (ex: loperamide) in the short term. ⁠

💊 Starting doses: 12.5-25 mg daily and may increase to 25-50 mg increments⁠

Sertraline Read More »

Amphotericin

If drugs came to life – Meet Ampho-terrible the fungal foe that packs a punch! 🥊 ⁠

🍄Amphotericin B is an antifungal medication that’s used to treat serious and life-threatening systemic fungal infections. But remember, with great power comes… well, some side effects! 😅⁠

✨The two main side effects to watch out for are nephrotoxicity and infusion-related reactions such as chills and fevers (often referred to as ‘shake and bake’). Because of its large side effect profile, it is often referred to as Ampho-TERRIBLE. ⁠

✨Some key things to keep in mind:⁠

-Liposomal amphotericin B (AmBisome) is a lipid formulation that a significantly improved toxicity profile compared to amphotericin B deoxycholate. ⁠

-Fevers, chills, and rigors are minimized by providing pre-medication with acetaminophen, diphenhydramine, and/or hydrocortisone 30–60 minutes prior to amphotericin B infusion.⁠

-The incidence and severity of nephrotoxicity can be reduced by providing 500–1000 mL bolus of normal saline before and after amphotericin B infusion.⁠

-Because it precipitates in normal saline, it must be given in a solution with 5% dextrose in water.⁠

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Atazanavir

⌛️ Time to get HIV Protease Outta Here with Atazanavir! 🦠💊 ⁠

🌟 Let’s talk about Atazanavir’s nickname, Bananavir. 🍌⁠

🌟 Atazanavir is used with other antiretroviral medications to treat human immunodeficiency virus (HIV). 🦠💊 It belongs to a class of drugs known as protease inhibitors. ⁠

🌟 One of the most common side effects with atazanavir is hyperbilirubinemia (35-49% of adults) causing yellow discoloration of the eyes and skin (jaundice) hence why this drug is often nicknamed BANANAVIR! 🍌Other common side effects include rash, nausea, headache, cough, fever, and hypercholesterolemia. ⁠

🌟 Key Points to Know For Exams⁠

-It is marketed under the brand name Reyataz⁠

-It works to inhibit HIV protease from breaking up large viral proteins into new mature HIV particles⁠

-It comes as a capsule and as a powder to be taken with food once a day to increase absorption⁠

-Hypersensitivity reaction can occur (Stevens-Johnson syndrome, toxic skin eruptions)⁠

-Beware of drug interactions as atazanavir is metabolized via CYP3A4 and it requires an acid gastric environment for optimal absorption (PPIs are contraindicated with use)⁠

-Atazanavir is often given with ritonavir to help boost levels of atazanavir concentrations⁠

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ototoxic drugs⁠

Ototoxic Drugs⁠

ototoxic drugs⁠

Hear me out as we discuss ototoxic drugs⁠

👂 Ototoxicity is a medication side effect involving damage to your inner ear. It can cause symptoms like ringing in your ears (tinnitus), hearing loss and balance problems.⁠

🌟 The risk for ototoxicity depends on the type of medication (common in some medications than others), the dose and duration of the medication, if you’re taking a combination of ototoxic drugs, and genetics. ⁠

🛑 The treatment is to stop the offending ototoxic agent. This often helps reverse the symptoms, although some ear damage may be permanent. ⁠

🌟 The most common drugs associated with ototoxicity includes aminoglycosides, chemotherapy such as cisplatin, loop diuretics, and salicylates. Check out today’s post to learn a fun mnemonic on other drugs that can cause ototoxicity. ⁠
.

Ototoxic Drugs⁠ Read More »

Dual Antiplatelets

Let’s talk DUAL ANTIPLATELETS 👏🏻

🌟WHEN do you use dual antiplatelet therapy (DAPT)?

1️⃣ Patients who have had acute coronary syndrome event (ACS) such as a heart attack

2️⃣ Patients who have stable ischemic heart disease and receive a stent placement (in other words, non-ACS setting)

🤫 pssst – if you don’t know what an ACS is – it is ANY condition brought on by a sudden reduction or blockage of blood flow to the heart. This is often caused by plaque rupture or clot formation in the heart’s arteries leading to sx of chest pain.

🌟 Okay great, we know when but WHY?

ACS is considered a medical emergency; treatment is needed to reopen the arteries and restore blood flow to the heart so it can work properly. This is usually done with a combination of medications + procedures such as a PCI (percutaneous coronary intervention) where a small structure called a stent is placed to open up the blocked blood vessel.

Afterward, the patient is at higher risk of future thrombotic events since they just had an occurrence and increased risk of stent thrombosis. This is where DAPT is recommended to prevent recurrent ischemic events.

🌟 Cool – but WHAT are dual antiplatelets?

Dual antiplatelet therapy recommendations include:

Aspirin PLUS ticagrelor, prasugrel, or clopidogrel

🌟 P2Y12 inhibitor considerations:

-Prasugrel is the most potent followed by ticagrelor, then clopidogrel (🧠TIP: Prasugrel is the most Potent ‘P’ for potent – but with increased potency comes increased bleeding risks. Avoid prasugrel in pt. age >75, hx of TIA/stroke, and hepatic dysfunction

-All of them are dosed once daily except ticagrelor which is dosed twice daily (🧠TIP: Ticagrelor is dosed ‘T’ for Twice daily) – can your patient be compliant?

-Clopidogrel and prasugrel are affordable and available in generic versions while ticagrelor is not. Can your patient afford it?

 

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Diabetes

Let’s 👏🏻 talk 👏🏻 diabetes👏🏻!⁠

🌟American Diabetes Association (ADA) and the European Society of Cardiology (ESC) released new 2023 guidelines recently and I just had to do a doodle note on it. 🤓⁠

🌟There has been lots of debates regarding whether metformin should still be first-line for all patients with type 2 diabetes. ⁠

🌟 It still is a great first-line option for most patients due to it’s proven efficacy, safety, and low cost. There are also some speculation that it m-a-y have cardiovascular benefits as well considering many patients in the clinical trials were also on metformin. ⁠

💗🫘However, in patients with ASCVD or high ASCVD risks, heart failure, and chronic kidney disease, the ADA/ESC guidelines recommend starting a SGLT-2 inhibitor or GLP-1 agonists with cardiovascular and renal benefits regardless if they have type 2 diabetes. ⁠

🌟 It is still important to look at patient specific factors (cost, comorbidities, side effects) when deciding which agent to start first or to add on. ⁠

👉🏻GLP-1 agonists commonly have GI side effects and carry warnings for rare pancreatitis and gallbladder disease. It can cost patients $1000/month. Most of the agents are injectables and supply is not consistent.⁠

👉🏻SLGT-2 inhibitors are linked to genital yeast infections, and volume depletion. Cost is about $600/month but they do come in oral formulations.⁠


Reference: Diabetes Care. 2023 Jan 1;46 (suppl 1):S140-S157⁠

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H.Pylori

Let’s talk H. Pylori Treatment! 💊

⭐️ H. pylori is a type of bacteria that infects your stomach and causes damage to the tissue leading to peptic ulcers, inflammation, and gastritis.

⭐️ Treatment includes:

1️⃣ Medications that decrease stomach acid to help decrease damage to tissues (ex: PPI or H2-antagonist)

2️⃣ Medications such as bismuth subsalicylate (AKA Pepto-Bismol) that coats the stomach protecting it from stomach acid (also has anti-inflammatory properties and antimicrobial activity against H. Pylori)

3️⃣ At least 2 antibiotics in the regimen to prevent the bacteria from developing resistance to the antibiotics (ex: amoxicillin, tetracycline, metronidazole, or clarithromycin)

⭐️ Initial therapy for H. Pylori includes:

👉 Bismuth quadruple therapy and concomitant (non-bismuth quadruple therapy), both administered for 10-14 days, are recommended FRIST-LINE treatments.

👉 In penicillin-allergic patients, bismuth quadruple therapy is the preferred initial treatment. Consider referral for allergy testing in patients who fail initial therapy, since many patients who report penicillin allergy are not truly allergic.

👉 Alternative initial therapies include sequential, hybrid, levofloxacin-tripe, levofloxacin sequential, and LOAD therapies.

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Heart Failure Drugs

💔 Let’s talk about HF medications 👏🏻⁠

🧠 Understanding heart failure (HF) medications can be difficult if you don’t understand the underlying pathophysiology of the condition. ⁠

🤓 Check out the slides to learn more about the pathophysiology of heart failure that leads to the common symptoms seen. ⁠

✨ Goals of therapy are to manage structural heart disease, reduce morbidity and mortality, decrease Na+ and water retention, and eliminate or minimize HF symptoms. ⁠

✨ The cornerstones of HF treatment are medications targeted towards decreasing the activity of compensatory mechanisms and improving cardiac workload, controlling excess fluid, and enhancing cardiac contractility. ⁠

⭐️ Loop diuretics: control symptoms of fluid overload (e.g., shortness of breath, edema)⁠
⭐️ ACE/ARBs/ARNIs: shown to decrease mortality; recommended in ALL pt. with HFrEF ⁠
⭐️ Beta-blockers: shown to decrease mortality when added to an ACE inhibitor; recommended in ALL patients with HFrEF⁠


👉🏻 Check out the full review of HF medications in our F-R-E-E Heart Failure Guide which includes a mind map coloring page and heart failure drug table!

Heart Failure Drugs Read More »

Insulin

1️⃣ In Type 1 Diabetes, the pancreas is unable to produce insulin⁠

2️⃣ In type 2 diabetes, the body does not respond normally to insulin, and over time, the pancreas starts to produce less and less insulin⁠
⭐️ What is insulin?⁠
IN-sulin is a hormone that helps glucose get IN-side cells to be used as energy⁠
⭐️ Counseling Tips:⁠
👉🏻 Educate patients on the symptoms of hypoglycemia (fatigue, hunger, increased anxiety dizziness, palpitations)⁠
👉🏻 Inject the exact dose of insulin subcutaneously into the abdomen (preferred), upper arms, thighs, or buttocks⁠
👉🏻 Rotate injection sites every 1-2 weeks⁠
👉🏻 Monitor blood glucose in frequent intervals (2- 4 times a day) as directed by the doctor⁠.

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Drug Mechanisms of Action Part II

⭐ Continuing on with PART TWO ✌🏻 of this series, let’s look over some tips and tricks on remembering the mechanisms of action of the following drugs: ⁠⠀
⁠⠀
👉🏻 Canagliflozin, dapagliflozin, empagliflozin – antidiabetic medications ⁠⠀
⁠⠀
👉🏻 Pantoprazole (Protonix)– anti-acid medication⁠⠀
⁠⠀
👉🏻 Levothyroxine, liothyronine – thyroid replacement medications⁠⠀
⁠⠀
👉🏻 Clopidogrel – antiplatelet medication⁠⠀
⁠⠀
👉🏻 Lantoprost, bimatoprost – antiglaucoma agents⁠⠀
.⁠⠀
.⁠⠀

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Drug Mechanisms of Action Part I

💊 In pharmacology, the mechanism of action (MOA) is the specific biological process through which a drug produces its pharmacological effect AKA how it works. ⁠⠀
⁠⠀
📚 Not only is knowing the mechanism of action important for exams and NAPLEX (as they are popular test questions), it gives you a baseline to understand/remember the drug indication, side effects, and underlying pathophysiology of the disease state.⁠⠀
⁠⠀
⭐ Some MOAs are more complicated than others while some MOAs are unknown. Often, we get lucky and the drug class hints at the mechanism of action such as calcium channel blockers, angiotensin receptor blockers, beta-blockers, etc. but this may not always be the case. ⁠⠀
⁠⠀
🧠 Check out some tips and tricks on how to remember the MOA of some other common medications below:⁠⠀
⁠⠀
-Rivaroxaban, apixaban, edoxaban – anticoagulants⁠⠀
⁠⠀
-Montelukast (Singulair) – used for allergic rhinitis and asthma⁠⠀
⁠⠀
-Sulfamethoxazole – used in combination with trimethoprim as an antibiotic ⁠⠀
⁠⠀
-Metformin (Glucophage) – antidiabetic medication⁠⠀
⁠⠀
-Nitroglycerin – antianginal agent⁠⠀
⁠⠀

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Drug Interactions Review

 Let’s talk drug-drug interactions 💊

🌟 With millions of potential drug interactions, figuring out what you need to commit to memory can be overwhelming 😵 . However, with the right approach and some (or a lotta 😆) practice, you’ll be able to see more of a pattern.

✨ TIPS FOR SUCCESS: ✨

1. Know the interactions that are STRONG. 💪🏻 A strong inhibitor or inducer can lead to 5x the concentration of a drug while a weak inhibitor or inducer will cause less of a change. Higher concentrations lead to adverse side effects. Check out today’s post to help you remember the major inducers and inhibitors of CYP450 enzymes.

2. Know the interactions where the outcome is BAD. ❌ For example, tamoxifen is a prodrug. Strong 2D6 inhibitors such as fluoxetine, paroxetine, and bupropion can prevent the conversion of tamoxifen to its active form, therefore, increasing the risk that your patient will experience a reoccurrence of cancer. The same goes for the antiplatelet prodrug clopidogrel.

3. Start with the most COMMON drug interactions seen as they will likely be on exams and boards. 📝 Check out today’s post to see some examples of some of the major drug interactions.

4. Understand the MECHANISM of the drug interaction. 🧐 Inducers can ramp up the metabolism of a medication leading to decrease drug levels while inhibitors block the enzymes that break down the drug leading to higher drug concentrations.


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