Miscellaneous

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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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. ⁠
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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⠀
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👉🏻 Clopidogrel – antiplatelet medication⁠⠀
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👉🏻 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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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. 🧠⁠

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Pharmacokinetics⠀

⭐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)⠀

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Anion Gap Acidosis -

Mind the Gap- HAGMA

Anion Gap Acidosis -
⭐️ High anion gap metabolic acidosis (HAGMA) occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body.⁠
💊 Several drugs and toxins have been implicated as direct or indirect causes of HAGMA. The three most common ones to consider are methanol, ethylene glycol and salicylates.⁠
🌬️ Symptoms are generally non-specific, with dyspnea being common secondary to stimulation of the central respiratory center. Screening for toxic ingestions, including over-ingestion of aspirin and acetaminophen, is important. ⁠
🌟 Additionally, screening for features suggestive of diabetes (e.g., polyuria, polydipsia, polyphagia) or renal failure (e.g., nocturia, pruritus, anorexia) is essential.⁠
🌟 Primary treatment of high anion gap metabolic acidosis requires correction of the underlying cause

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IV Fluids Review

💦 ⁠ IV fluids – What the tonic? ✏️The human body is composed of 60% water 💦 ⁠ -Two-thirds of it is available INTRAcellularly (space INside cells)⁠ -One-third of it is stored EXTRAcellularly (EXTERNAL space in blood vessels and around cells)⁠ ⁠ ⭐ There are different types of fluids with varying chemical compositions of salt and electrolytes that are designed to bring fluid into cells or keep fluid within the bloodstream.⁠ ⁠ 🔑 Key Tips:⁠ -Water flows where sodium (or particles) goes!⁠ -Solutions want to have the same ratio or balance of solvents (water) to solute (particles such as salt)⁠ -Water will flow from an area of low particles to an area of high particles⁠ -Semi-permeable membranes allow water to pass through but not particles⁠ ⁠ ⭐ First, think of the starting point as the space within blood vessels (or intravascular space) since IV fluids are infused directly into the bloodstream 🩸⁠ ⁠ ⭐ ISOtonic fluids: “ISOlated in the vasculature”⁠ -Equal amounts of water and particles so there is no movement between the compartments⁠ -Water from IV fluids stay ISOlated in the vasculature – used in situations where there is fluid loss and replacement is needed (ex: hemorrhage, diarrhea, vomiting)⁠ -Examples include: 0.9% sodium chloride (normal saline), dextrose 5% in water (D5W), lactated ringer (LR)⁠ ⁠ ⭐ HypOtonic fluids: “Out of the vasculature”⁠ -Low amounts of particles compared to water⁠ -Water flows OUT of the vascular into the cells⁠ -Used in situations where we have intracellular dehydration (ex: DKA, HHS)⁠ -Examples include: 0.45% sodium chloride (1/2 normal saline), 2.5% dextrose in water ⁠ ⁠ ⭐ HypErtonic fluids: “Enter the vasculature”⁠ -High amounts of particles compared to water ⁠ -Water ENTERS the highly concentrated vasculature from cells⁠ -Used in situations where there are swollen cells (ex: cerebral edema) or hyponatremia⁠ -Examples include: 3% sodium chloride (hypertonic saline), dextrose 10% in water (D10W) ⁠

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ketamine mnemonic

Ketamine Properties

ketamine mnemonic
📖 Ketamine is a medication primarily used for starting and maintaining anesthesia. It induces dissociative anesthesia, a trance-like state providing pain relief, sedation, and amnesia.⁠ ⁠ ⭐ The distinguishing features of ketamine anesthesia are preserved breathing and airway reflexes, stimulated heart function with increased blood pressure, and moderate bronchodilator.⁠

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Drug Mechanisms of Action Mnemonics/Tips

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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Cholinergic Muscarinic Agonist Effects

👉🏻 Cholinergic muscarinic agonists are drugs that bind to and activate muscarinic cholinergic receptors and increase the activity of the parasympathetic nervous system. They are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder, and eye. They may also be used to reduce heart rate. ⁠ ⁠ 👉🏻 Direct cholinergic agonists work by resisting acetylcholinesterase, thus preventing its breakdown. Drugs in this class include bethanechol, carbachol, and methacholine, and pilocarpine.⁠ ⁠ 👉🏻 Indirect cholinergic agonists work by inhibiting the acetylcholinesterase enzyme preventing the degradation of acetylcholine. Drugs in this class include neostigmine, physostigmine, galantamine, donepezil, and rivastigmine. ⁠

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