
Metformin remains the first-line therapy for type 2 diabetes, lowering glucose and cardiovascular risk by reducing gluconeogenesis and insulin resistance.
Compare GLP-1 analogs and DPP-4 inhibitors for type two diabetes, detailing their mechanisms, the cardioprotective role of GLP-1 analogs and sodium glucose cotransporter inhibitors, and related side effects.
Compare rapid, short, intermediate, and long-acting insulin, detailing mechanisms and postprandial hypoglycemia. Cover indications for type 1, type 2, gestational diabetes, timing, and common adverse effects like hypoglycemia and lipodystrophy.
Metformin treats type 2 diabetes by inhibiting gluconeogenesis via mitochondrial glycerol-3-phosphate dehydrogenase, increasing glycolysis and glucose uptake. Lactate accumulation can lead to lactic acidosis in renal insufficiency; use with caution.
Meglitinides, used with metformin for type 2 diabetes, bind beta-cell potassium channels to release insulin after meals, with hypoglycemia, weight gain, thyroid and liver tumor concerns, and renal failure contraindication.
Explain how sodium glucose cotransporter inhibitors (gliflozins) treat type 2 diabetes by blocking glucose reabsorption in the proximal tubule, providing cardioprotective benefits while causing glycosuria, dehydration, UTIs, and ketoacidosis risk.
Explore thiazolidinediones, which activate Ppargamma to boost insulin sensitivity and adiponectin, lower TNF-alpha and leptin, and feature long half-lives with risks of water weight gain, edema, heart failure, and osteoporosis.
Identify diabetes mellitus diagnosis criteria, including HbA1c above 6.5% and fasting glucose above 126 mg/dl. Compare type 1 autoimmune beta-cell destruction with type 2 insulin resistance, noting polydipsia, polyuria, polyphagia.
Understand type 2 diabetes: slow onset, symptoms include thirst, polyuria, weight loss, and fatigue, diagnosed by A1c >6.5 or fasting glucose >125, managed by lifestyle changes, weight loss, and exercise.
Learn how Amlodipine, a calcium channel blocker, treats hypertension and angina by dilating arteries, with dosing considerations for liver impairment and potential side effects like edema.
Digoxin inhibits the sodium-potassium ATPase in myocytes, increasing intracellular calcium and strengthening contraction. It also slows heart rate through the vagus nerve; toxicity risks hyperkalemia and arrhythmias.
Calcium channel blockers divide into dihydropyridines and non-dihydropyridines; dihydropyridines dilate vessels lowering blood pressure, while non-dihydropyridines like Verapamil reduce heart contraction, and Nimodipine prevents cerebral vasospasm after subarachnoid hemorrhage.
Explain nitroglycerin, isosorbide dinitrate, and mononitrate as venous dilators that lower preload via cyclic GMP, used for angina and acute coronary syndrome, with hypotension and reflex tachycardia as common effects.
Ranolazine lowers cardiac oxygen demand as a sodium channel blocker to treat refractory angina, used when other therapies or CABG are not feasible, with side effects such as headache.
Fludrocortisone acts as a synthetic aldosterone analogue with some glucocorticoid effects, used in primary adrenal insufficiency, and can cause hypervolemia, edema, hyperpigmentation, and infections via nuclear transcription of anti-inflammatory peptides.
Understand how infarction alters cardiac pathways and triggers arrhythmias. Explore class one a antiarrhythmics—quinidine, procainamide, disopyramide—sodium blockers that raise refractory period and QT, with cinchonism and drug-induced lupus risks.
Class one b antiarrhythmic drugs restore electrical flow through dead or semi-dead heart tissue after myocardial infarction, addressing arrhythmia, but may alter neuronal sodium levels, causing confusion and CNS depression.
Class ic antiarrhythmic agents, including fluocinonide and propafenone, are potent sodium channel blockers reserved for arrhythmias after options fail, prolonging the refractory period in severe atrial fibrillation or resistant tachycardias.
Class II antiarrhythmic agents are beta blockers that slow heart rate by acting on the SA and AV nodes, useful for supraventricular tachycardia and atrial fibrillation, though they mask hypoglycemia.
Verapamil, a class iv antiarrhythmic, slows sa and av nodes, raises the pr interval, and treats atrial fibrillation or atrial tachycardia, but is unsuitable for ventricular tachycardia and causes constipation.
Identify cardiotoxic drugs: trastuzumab, for Her2-mutated breast cancer causing reversible non-functioning cardiomyocytes; anthracyclines like doxorubicin and epirubicin cause irreversible fibrosis; theophylline raises cyclic AMP, and tricyclic antidepressants block sodium channels.
Explore hypertension medications that lower blood pressure using diuretics to reduce volume and calcium channel blockers to relax vessels, with ace inhibitors and arbs modulating angiotensin pathways.
Explore left- and right-sided heart failure, including pulmonary congestion, edema, and jugular venous distension. Learn acute and chronic management with oxygen, diuretics like furosemide, and vasodilators such as nitrates.
Isotretinoin, a vitamin A derivative, lowers sebum to shrink sebaceous glands and treat severe acne and related follicular conditions; requires pregnancy prevention and monitoring of liver function.
Antihistamines block H1 and H2 receptors, with first-generation H1 blockers also inhibiting muscarinic and alpha receptors, while second-generation blockers target only H1, used for allergy and peptic ulcers and gastritis.
Explore how minoxidil opens potassium channels to cause vasodilation and increase hair follicle blood flow, supporting hair growth in alopecia and indicating its antihypertensive origins.
Learn to diagnose urticaria and hives with history, skin tests, including autologous serum skin test; manage with allergen avoidance, second-generation antihistamines, dose escalation, and steroids for severe cases.
Tacrolimus, an immunosuppressant to prevent chronic organ transplant rejection, inhibits interleukin-2 transcription to suppress T-lymphocytes and causes nephrotoxicity with gout, tremors, hyperglycemia, alopecia, gingival hypertrophy, and infections and cancers.
Explore how ACE inhibitors (pril drugs) lower blood pressure by reducing angiotensin II and increasing bradykinin, treat hypertension with diabetic kidney protection, and note dry cough and angioedema.
Acetazolamide inhibits renal carbonic anhydrase, depleting bicarbonate to cause metabolic acidosis and alkalize urine for aspirin overdose, altitude sickness, pseudotumor cerebri, glaucoma, and optic nerve fenestration if medical therapy fails.
Explain loop diuretics that inhibit the Na-K-2Cl cotransporter in the ascending loop of Henle, causing diuresis and decreased medullary tonicity, used for edema, hypertension, hypercalcemia; include ototoxicity and sulfa allergy.
Explore potassium-sparing diuretics like spironolactone, eplerenone, triamterene, and amiloride, which block collecting duct sodium channels to promote diuresis, treat hyperaldosteronism, heart failure, hyperandrogenism, arthritis, with risks of hyperkalemia and gynecomastia.
Angiotensin II receptor blockers (sartans) like losartan reduce blood pressure by blocking angiotensin II receptors, without bradykinin-related cough. They protect diabetic nephropathy but can cause transient creatinine rise and hyperkalemia.
Thiazide diuretics act on the distal ducts, inhibiting sodium chloride reabsorption and calcium excretion to produce diuresis, used for hypertension and heart failure with osteoporosis considerations.
Explore thioamides, including a proprietary uracil derivative and methimazole, as thyroid peroxidase inhibitors used to treat hypothyroidism; warn about hepatotoxicity, teratogenicity, and agranulocytosis, and stop if agranulocytosis occurs.
Levothyroxine, a T4 supplement, and liothyronine, a T3 active form, treat hypothyroidism by boosting thyroid hormones. Pregnancy raises thyroxine binding globulin, so higher levothyroxine doses may be needed in pregnancy.
Cinacalcet sensitizes parathyroid cells to circulating calcium. It lowers parathyroid hormone, may cause hypercalcemia, and treats primary hyperparathyroidism, parathyroid carcinoma symptoms, and secondary hyperparathyroidism in chronic kidney disease with hemodialysis.
In iodine-deficient individuals, hypothyroidism upregulates thyroxine receptors that respond to little iodine, and relocation to iodine-rich areas can trigger Jod-Basedow effect and thyroxine storm, countered by exponentially small iodine doses.
Explore how TSH stimulates T4 production, how organs convert T4 to T3 during stress, and why sick euthyroid syndrome arises from high T3 demand despite normal TSH and T4.
Classify antiepileptic drugs by mechanism of action, including calcium channel blockers, sodium channel blockers, gabaergic drugs, and dual-action agents. Highlight key side effects and exam-ready notes.
Explore neuroleptic malignant syndrome, a dangerous reaction to antipsychotics such as haloperidol and risperidone, with fever, altered mental status, muscle rigidity, and autonomic dysfunction.
Identify serotonin syndrome risks tied to antidepressants such as SSRIs and SNRIs, TCAs, and monoamine oxidase inhibitors, plus non antidepressants like triptans, carbamazepine, opioids, lithium, and illicit drugs.
Prioritize therapies over medications, emphasizing behavioral therapy, educational therapy, and family therapy. Recognize that medications are not first-line; antipsychotics and antidepressants require caution with herbal and dietary supplements.
Analyze how antipsychotics stored in fatty tissues cause long-lasting side effects, including hyperprolactinemia with gynecomastia and galactorrhea, dry mouth, constipation, sedation, metabolic syndrome, orthostatic hypotension, and QT prolongation.
Daptomycin disrupts the bacterial wall and, with polymyxin, treats resistant bacteria like MRSA and VRE; monitor CPK with statins, and avoid lung infections due to surfactant binding.
Metronidazole is an antibacterial and antiprotozoal free radical generator that treats anaerobic infections including amoebas, C. difficile, Giardia, and H. pylori; it can cause a disulfiram-like reaction with alcohol.
Explore corticosteroids in dermatology, detailing step up and step down therapy, topical vs systemic use, and when to employ intralesional or systemic steroids for inflammatory conditions, with key side effects.
Welcome to the Pharmacology Master Course.
We’ll discuss every medication that you will see in your practice as a healthcare professional. At the end of the course, you’ll be able to recognize any medication and immediately know the key features.
We will achieve this goal by breaking the medications into specific families. Each family of medication act the same and generally have similar side effects. However, there are distinctive features for each medication, those are important to recognize, especially for exam-takers, as they are points of high-yield.
The discussion will start by explaining the mechanism of action and the physiological effects. Once this is understood, the uses and side effects become easily apparent.
To help you memorize the complex points, the course has many quizzes and external resources with tons of mnemonics and notes.
The course focuses on high-yield and commonly used medications, such as oral diabetic therapies and anti-hypertensive agents. Knowing these medications byheart is imperative, which is why they get a larger slice of the pie. Uncommon medications will be covered as well, but we will focus on their key features and unique characteristics.
Nevertheless, you will learn the mechanisms of action, side effects, indications, and contraindications of all medications.