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58 Cards in this Set
- Front
- Back
Stable/Exertional Angina |
Only occurs when there is exertion |
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Variant/Vasospastic Angina |
Occurs at rest |
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2 ways to treat coronary ischemia |
Reduce oxygen demand and workload on heart, or increase oxygen supply to heart through vasodilation (minimal) |
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CAD |
Coronary artery disease - cardiac ischemia due to narrowing of the coronary arteries |
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CAD pathogenesis |
Atherosclerosis, thromoembolism, hypertension, diabetes, sudden coronary vasospasm |
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Which drug classes reduce oxygen demand and workload of heart? |
Nitrates, B blockers, and CCBs |
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Which drug classes increase oxygen supply to the heart? |
Nitrates and CCBs |
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Nitrates mechanism of action |
Prodrugs that release NO, which increases cGMP to relax smooth muscle cells - main action is venodilation (capacitance) to reduce preload - also dilate arterioles (resistance) at higher doses
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Nitrates best used for |
Acute angina - tolerance develops |
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Nitrates typical route of administration |
Sublingually, transdermally, or huge oral dose - first pass metabolism |
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Inhaled NO |
For pulmonary hypertension |
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Nitroglycerin metabolite activity |
Not very active |
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Isosorbite dinitrate metabolite activity |
Isosorbide mononitrates are active |
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Isosorbide 5-mononitrate |
Excellent bioavailability (no significant first-pass) - can be given orally |
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Nitrate tolerance causes |
True vascular tolerance (reduced capacity to convert to NO) or pseudotolerance (mechanisms extraneous to vessel wall) |
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Isosorbide clinical uses |
Acute symptomatic relief of angina, prophylactic management, long-term prophylactic management of stable angina, and perioperative hypertension |
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Sodium nitroprusside |
Nitrovasodilator - unlike nitroglycerin, no tolerance - dilates both arterioles and venules |
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Sodium nitroprusside therapeutic uses |
Primarily for hypertensive emergencies (short-term preload and afterload reduction) - also lower BP during acute aortic dissection, improve CO in CHF with pulmonary edema not responding to other treatments, decrease O2 demand after acute MI |
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Is sodium nitroprusside used for long-term hypertension management? |
No - can cause cyanide poisoning when used continuously |
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Drug Holiday |
Used for nitrates - Nitrate Free Interval to overcome tolerance |
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Nitrate tolerance |
Highest in nitroglycerine, less with isosorbide dinitrate. None in sodium nitroprusside |
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Beta antagonists effects |
Reduced HR, contractility, renin release, afterload, workload on heart |
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Metoprolol |
B1 blocker |
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Atenolol |
B1 blocker |
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Beta antagonist adverse effects |
Reduced exercise tolerance, asthma, PAD worsens, cold hands and feet, bad dreams, depression, ED, altered plasma lipids |
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CCBs |
Calcium channel blockers - block L-type Ca2+ channels - reduce HR, afterload - negative inotropic effect |
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DHP affinity |
Higher for smooth muscle than cardiac muscle, so useful for hypertension |
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CCBs adverse effects |
Flushing, bradycardia (with verapamil or diltiazem), tachycardia (nifedipine), ankle edema, cardiac depression, other smooth muscle - constipation, urinary retention, headache |
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DHP effect on heart rate |
Increase through reflexive tachycardia |
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CCBs vs nitrates |
CCBs act on vasculature and heart while nitrates act mostly on vasculature. CCBs are predominantly arteriolar dilators, while nitrates are predominantly venodilators |
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Is skeletal muscle effects by CCBs? |
No - relies on intracellular Ca2+ from sarcoplasmic reticulum |
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Do nitrates or CCBs dilate coronary arteries? |
CCBs |
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Dihydropyridines (DHPs) |
CCB class - more arterial dilation and little cardiac effect - used as antihypertensive agents - slow |
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Benzothiazepines |
CCB class - used for angina - cardiac effect |
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Phenylalkylamines |
CCB class - greater suppressive cardiac effect than benzothiazepines |
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Nifedipine |
Dihydropyridine CCB
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Amlodipine |
Dihydropyridine CCB |
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Diltiazem |
Benzothiazepine CCB |
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Verapamil |
Phenylalkylamine CCB |
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Different CCB classes have different |
Binding sites on L-type channel |
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Nifedipine and diltiazem bind |
Synergistically |
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Nifedipine and verapamil bind |
Inhibit each other's binding |
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Nifedipine vs amlodipine |
Amlodipine has higher bioavailability, longer half-life, OD dosing, slow onset, less intense effect, significantly less tachycardia (which can worsen ischemia in nifedipine use) |
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CCB contraindication |
Heart failure (especially verapamil and diltiazem) |
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Diltiazem and verapamil are not to be used with |
B blockers (cardio-depression |
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Nifedipine can increase risk of |
Myocardia ischemia (due to tachycardia) |
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Which CCB to use in hypertension? |
Amlodipine |
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Which CCB to use in angina? |
Diltiazem (but verapamil as well according to later slide) (and can be either stable or variant angina) |
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Which CCB to use in some types of arrhythmias? |
Verapamil |
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Major side effects of CCBs |
Constipation and flushing, especially in dihydropyridines
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Why not use DHPs for angina? |
Reflex tachycardia |
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B blockers used for |
Stable angina |
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B blocker caution |
Unopposed a1 coronary vasoconstrction |
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B blockers vs nitroglycerin |
B-blockers have longer duration of action and tolerance is less problematic, so more suited for chronic prophylaxis of stable angina |
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Diltiazem and verapamil key mechanism of angina relief |
Coronary vasodilation |
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Can B1 blockers be used in mixed angina? |
Yes |
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B1 blockers are not to be used in which kind of angina? |
Vasospastic/variant/Prinzmetal angina |
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Pentoxifylline |
Used for PVD symptoms of vasospasm causing lower body pain and inability to walk - PDE inhibitor, TNFa inhibitor, adenosine antagonist - reduces blood viscosity, promotes red cell deformability, helpful in vascular dementia - effect in intermittent claudication (pain in leg from exercise) - can walk further in a set period of time |