Let’s review a new drug! ⁠

✨You guys! – my new favorite hobby is mind mapping so let’s take a minute and learn about a new injectable diabetes medication together using this tool.⁠

💉Mounjaro (generic name: tirzepatide) is a new injectable medication indicated for Type 2 Diabetes. It is also called an Incretin mimetic.⁠

🤔But what is incretin?⁠

Incretin is a hormone or peptide that gets secreted by the gut in response to ingested food (helps the body regulate glucose). You can think of incretin as an acronym for:⁠

🧠INtestinal seCRETion of INsulin in response to food. ⁠

The two most important incretins in our body account for 90% of all incretin hormones: ⁠

👉🏻GLP-1 (glucagon-like peptide 1)⁠
👉🏻GIP (glucose-dependent insulinotropic peptide) ⁠

To understand the mechanism of action of tirzepatide, you need to understand what GLP-1 and GIP do. ⁠

GIP-1 and GIP help to regulate glucose control in the body by increasing insulin secretion, delaying gastric emptying, and activating the satiety center in the brain (makes us feel full)⁠

⭐️Tirzepatide is unique from other incretin mimetics because it has a dual mechanism of action by working on both GLP-1 and GIP. ⁠

👉🏻You can get your own mind map worksheet here!⁠

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?



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


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.

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!


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.

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⠀

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⠀

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.


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.

Antibiotic Coverages

⭐ Knowing antibiotic coverage starts with memorizing the antibiotics that cover the major categories of bacteria such as anaerobes, atypical, MRSA, and pseudomonas. ⁠

⭐ Studying for an upcoming exam? >>LISTEN<< These are a MUST for you to know. Review the post and quiz yourself to see how much you can remember. 🧠⁠

Hypertension in Pregnancy

Anti-hypertensives in pregnancy 🤰🏻⁠

✏️ Hypertension is defined as systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg. Chronic hypertension occurs before pregnancy or before 20 weeks gestation and gestational hypertension occurs after 20 weeks⁠

⚠️ Complications of high blood pressure include increased risks for preeclampsia/eclampsia/stroke for the mother and preterm delivery for the baby⁠

📖 As with most medications in pregnancy, antihypertensives have not been evaluated in robust randomized controlled trials. Check out the post for the preferred anti-hypertensive drugs used in pregnancy. ⁠

⭐ Methyldopa is recommended first-line due to its proven safe and effective use in pregnancy due to its long history of safety in pregnancy but its use in clinical practice may be less due to adverse reactions (e.g., fatigue, dizziness).⁠


Aminoglycosides – ‘The 3 Amigos’⁠

⭐ AMINOglycosides are antibiotics comprised of AMINO acid sugars that are linked together. ⁠

3️⃣ The three most commonly used are (mnemonic: TAG): ⁠

Other agents include plazomicin, streptomycin, and neomycin. ⁠

⭐ They are used for serious infections caused by gram-negative bacteria such as complicated UTIs, sepsis, or intraabdominal infections. They can also be used in combination with other agents for infectious caused by gram-positive bacteria in endocarditis. ⁠

⭐ MOA: they kill bacteria by binding onto 30S ribosomal subunits inhibiting the bacteria’s ability to synthesize proteins, leading to cell death⁠

⭐ Other key facts to know:⁠
-Adverse effects include nephrotoxicity and ototoxicity⁠
-They are approximately 70-95% excreted renally⁠
-They are concentration-dependent bacterial killers, which means bacterial killing increases with rising drug concentrations⁠
-Monitor serum drug levels (troughs and peaks), serum creatinine, BUN, urine output, and hearing⁠.


🌟 The thyroid gland produces thyroid hormones (T3 and T4, with T3 being the more active form) that affect metabolism, brain development, respiration, cardiac, nervous system functions, body temperature, muscle strength skin dryness, and so much more!⁠⠀
👉🏻 HYPOthyroidism is a result of an UNDERactive thyroid vs. HYPERthyroidism is an OVERactive thyroid. ⁠⠀
👉🏻 Common causes of hypothyroidism: having low levels doesn’t feel good – HAIL⁠⠀
-Hashimoto’s disease⁠⠀
-Iodine deficiency/interferons⁠⠀
👉🏻To compensate for an UNDERactive thyroid, synthetic versions of thyroid hormones are administered. Levothyroxine is the drug of choice due to its once-daily dosing, low cost, and more uniform potency. ⁠⠀


⭐Test your knowledge and check your answers on the second slide.

🚶🏻Think of pharmacokinetics (PK) as the drug’s journey into, through, and out of the body. This journey passes through four phases that can be remembered using the mnemonic ADME or “add me”. ⠀

-Absorption: the process of the intake of the drug into the body⠀
-Distribution: the process of the dispersion of the drug into the bloodstream and tissues⠀
-Metabolism: the process of the parent compounding into daughter metabolites⠀
-Excretion: the process of eliminating the drug from the body⠀

🗻 This journey varies depending on patient-specific factors such as renal function, sex, age, and genetics. All of these factors can affect the drug’s half-life, rate of elimination, and distribution and subsequently lead to toxicity or therapeutic failure. Knowledge of pharmacokinetics can assist with adjusting doses correctly especially in drugs that require therapeutic drug monitoring. ⠀

☝🏻 Additionally, drugs go through different processes of metabolism and elimination called first-order and zero-order kinetics. The biggest difference is that zero-order kinetics undergo constant elimination regardless of the plasma concentration while first-order kinetics depends on concentration. A good analogy is relating the concentration of drug to cake: 🎂⠀

-Regardless of how big of a cake you are served, you can only eat one bite (a certain amount) at a time, that’s zero-order kinetics (15 mg/hr)⠀
-With first-order kinetics, you suddenly can eat portions of the cake at a time so the bigger the cake the bigger the portion of cake you can eat (eliminate) at a time (50%/hr)⠀

Calcium Channel Blockers⁠

💊 Calcium channel blockers (CCBs) are used in the treatment of many cardiovascular conditions including hypertension and angina so needless to say they easily make the top 200 drugs prescribed.⁠⠀
👉🏻 They are divided into subclasses, non-dihydropyridines, and dihydropyridines and differ by their pharmacokinetic properties, clinical uses, response, and selectivity. ⁠⠀
👉🏻 Dihydropyridine CCBs end in the suffix ‘-ine’: ⁠⠀
👉🏻 Non-dihydropyridine CCBs don’t end in the suffix ‘-ine’ hinted by the name of the subclass, NOn-dihydropyridINE:⁠⠀