Memorizing Pharmacology Video 6 of 7

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    A step-by-step view of pharmacology of cardiology moving through the various classes of medications paying special attention to drug stems and the drugs' relationship to each other. While the print highlights some of the main points, the written and video content work better in tandem than they do as individual works.

    Memorizing Pharmacology Video 6 of 7

    The cardiovascular system presents an opportunity to readily tie physiologic principles with pharmacology. By working backwards to those principles, these drugs tend to stay in long-term memory. I'll go into just enough detail on physiology in order to provide you a solid understanding of the drugs.

    OTC antihyperlipidemics and antiplatelet. There aren't many OTC cardiac medications, but let's look at three. First, the omega-3-acid ethyl esters form an important part of fish oil. Niacin or nicotinic acid helps reduce blood cholesterol levels. With very effective LDL lowering prescription drugs, we often see prescribers reaching for those first. Fish oil and niacin both have prescription forms as well. Common side effects include belching for fish oil and facial flushing for niacin.

    Aspirin is the OTC anti-platelet in this section. At 81mg, aspirin doesn't work as an anti-inflammatory as it does at 325 mg, but the low dose prevents platelet aggregation. This effect potentially reduces the chance of serious cardiac conditions such as heart attacks and strokes. We'll discuss other prescription only medications used for the same conditions.

    Have you ever overheard someone say that they forgot to take their water pill? As health practitioners we need to know generic, brand and these shortcut names patients use. Different diuretics work at different parts of the nephron, the functional unit of the kidney. It's critical to know basic renal physiology to help remember the drug classes in order from most to least potent diuretic.

    Mannitol, an osmotic diuretic, works in the proximal convoluted tubule (PCT) and furosemide in the ascending loop of Henle. The thiazide diuretic hydrochlorothiazide works in the distal convoluted tubule (DCT) with a little less diuresis. Two potassium-sparing diuretics, spironolactone and triamterene, work at the collecting duct, the last portion of the nephron's physiology. A more severe condition pathophysiologically like CHF might warrant furosemide, a less severe indication like initial hypertension warrants a lesser diuretic like hydrochlorothiazide. Diuretics that aren't potassium sparing are considered potassium wasting. Thiazide diuretics normally cause only a little reduction in potassium, but loop diuretics usually lose enough to warrant electrolyte replenishment.

    Alphas and betas.
    Doxazosin is an alpha-1 antagonist that opposes vasoconstriction and lowers blood pressure through vasodilation. Clonidine, an alpha-2 agonist, also lowers BP through the central nervous system (CNS) and is considered a negative feedback receptor. Thus when they are activated, they inhibit BP increasing norepinephrine, so norepinephrine inhibition lowers BP.
    Many beta-blockers end with -olol, but you have to memorize which are selective for beta-1 or non-selective. Beta-1 receptors, again, are primarily in the heart while beta-2 receptors are in the lungs. Activating beta-1 leads to increased heart rate (HR), while activating beta-2 leads to bronchodilation. Thus, a non-selective beta blocker such as propranolol will both lower HR and cause bronchoconstriction. Lower HR is good, but in patients with asthma, bronchoconstriction is undesirable.

    In patients with asthma, it's best to use a selective beta blocker like metoprolol tartrate or metoprolol succinate. The tartrate salt form is short acting while the succinate salt form is long acting. Either way, metoprolol blocks only beta-1 receptors, leading to lower HR. Third generation carvedilol opposes increased heart rate and vasoconstriction keeping the body from counteracting the medicine.

    Renin angiotensin aldosterone system (RAAS) drugs. When kidneys detect low blood flow, it produces more renin to convert angiotensinogen (not in the acronym) to angiotensin I. After further conversion to Angiotensin II via angiotensin converting enzyme (ACE), Angiotensin II increases aldosterone secretion, which makes the kidneys retain more sodium and water, and causes vasoconstriction thus increasing BP.

    If we block angiotensin-converting enzyme (ACE) then we never get angiotensin II and aldosterone won't be secreted. The vasodilation and lack of fluid retention causes BP to decrease. We can also block angiotensin II receptors with angiotensin II receptor blockers (ARBs) causing a similar BP lowering effect without a coughing side effect common with ACE inhibitors.

    Calcium channel blockers (CCBs). The foundational principle is that calcium is part of muscle contraction: skeletal, smooth, and cardiac. CCBs block these contractions only in smooth and cardiac muscles depending on the type of CCB. They don't block skeletal muscle because of a small physiological difference in channel structure.

    The two main drug classes include: dihydropyridines and non-dihydropyridines. Dihydropyridines all have the stem -dipine, think "dip in" blood pressure. These have little affinity for cardiac muscle. Dihydropyridines cause vasodilation in smooth muscle causing the decreased BP.

    Non-dihydropyridines have affinity for cardiac and smooth muscle. This imparts the antidysrhythmic properties. Medications in this class include diltiazem and verapamil.

    Vasodilator. Nitroglycerin is a representative vasodilator. It's used in emergencies when patients suddenly feel short of breath and have intense, crushing pain in their chest; two classic signs of angina or a heart attack. Nitroglycerin quickly opens up the blood vessels.

    Antihyperlipidemics. The HMG-CoA reductase inhibitors or "statins" are a keystone of therapy. HMG-CoA is the rate-limiting enzyme in creating cholesterol. By inhibiting that enzyme, less cholesterol forms. Statins are particularly good lowering LDLs, or 'bad' cholesterol. This medication class has been shown to reduce mortality in patients with cardiovascular diseases. Side effects to watch out for with these medications include liver toxicity and muscle inflammation. Fenofibrate reduces triglyceride levels, a different kind of cholesterol that's also important.

    Anticoagulants and antiplatelets. This section discusses the balance of bleeding versus clotting. Coagulating factors and platelets are constantly working to maintain equilibrium.
    I use four representative anticoagulants: enoxaparin, heparin, warfarin, and dabigatran. Notice the -parin stem, as well as-farin in warfarin and -gatran in dabigatran. Keep in mind INR checks are required for warfarin and regular checkups to reassess the patients' bleeding risk. Clopidogrel works a lot like low-dose aspirin to prevent platelets from sticking together. Like aspirin, it can improve heart attack prevention.

    Cardiac glycoside and anticholinergic. Two unique medications include digoxin and atropine. Digoxin increases the force of contraction of the heart and for patients with heart failure. Atropine is an anticholinergic or against acetylcholine, a neurotransmitter. It helps in certain cardiac emergencies.


    OTC antihyperlipidemics and antiplatelet
    OTC antihyperlipidemics
    Omega-3-acid ethyl esters
    OTC antiplatelet
    Diuretics - water slide
    Osmotic - PCT
    Loop - Loop of Henle
    Thiazide DCT
    Potassium sparing and thiazide
    Triamterene / hydrochlorothiazide
    Potassium sparing - collecting duct
    Electrolyte replenishment
    Potassium chloride
    Alphas and betas
    Alpha-1 antagonist
    Alpha-2 agonist
    Beta blockers - 1st generation - non-beta selective
    Beta blockers - 2nd generation - beta-selective
    Metoprolol tartrate
    Metoprolol succinate
    Beta blockers - 3rd generation - non-beta selective, vasodilating
    Renin angiotensin aldosterone system (RAAS) drugs
    Angiotensin converting enzyme inhibitors (ACEIs)
    Angiotensin II receptor blockers (ARBs)

    Calcium channel blockers (CCBs)
    Non-dihydropyridines - cause vasodilation and affect the heart
    Dihydropyridines - vasodilation only

    HMG-CoA reductase inhibitors
    Fibric acid derivatives - triglycerides

    Anticoagulants and antiplatelets

    Cardiac glycoside and anticholinergic
    Cardiac glycoside

    Last edit by Joe V on Jun 15, '18
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