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Anti-anginal
UVa med pharmacology block 3
| Question | Answer |
|---|---|
| Fill in the blank: Pain not responding to ___ tablets or lasting more than ____ minutes requires immediate medical attention | 3 tablets 20 minutes |
| What three blood gas/metabolites factors cause coronary vasodialation? | - Decrease in O2 (unlike pulmonary vessels) - Decrease in pH - Increase in metabolites (lactic acid, adenosine, PGE) |
| What are other names for stable angina? What is the etiology of the ischemia? | - classic or exertional angina - ischemia from vessel narrowing (artherosclerosis) |
| T or F: In stable angina, severity frequency and duration are unchanged for weeks to months | TRUE |
| What is the therapeutic mechanism of Beta blockers in angina? How do they differ from nitrates? | - decrease HR and contractility leads to increased perfusion time and decreased O2 demand - they DO NOT dialate coronary vessels, they may even constrict them due to B2 blockade |
| What is the single most common cause of death from ventricular failure or fibrilation? | MI |
| Stable angina is cause by: | an imbalance between O2 demand and O2 supply |
| At rest, what % of total body O2 supply is consumed by the heart? What % of CO goes to coronary vasculature? What does this mean? | - 11% of total O2 - 4% of CO goes to coronary vessels - VERY HIGH O2 EXTRACTION RATIO |
| What is the BOTTOM LINE (from ppt) in Ca channel blocker usage (3 parts) in angina? | - Both selective and non-selective blockers can be used for angina - Non-selective has been shown to be more efficacious and only ones SHOWN to prolong life - Non-selective are FIRST LINE, unless Ca blockers must be coadministered with B-blockers |
| How do neural/humoral factors affect coronary caliber? How important are these? | - a1 constrict - B2 dialate LESS important than chemical or physical events |
| What is the main limitation of nitrate therapy? How can in be prevented? | - TOLERANCE - It cannot be prevented, but can be reduced by giving regimen that allows 8 to 10 hours w/o drug or co-administering other drugs that reduce the ammount of nitrates (B blockers) |
| What is the treatment of unstable angina? WHY? | - Percutaneous revascularization and anti-thrombotics (like aspirin) - problem is thrombus formation |
| What is variant angina? What is another name for it? | - Angina cause by coronary vasospam, also caused by atheromatous disease, LESS COMMON - Printzmetal's Angina |
| Describe the neural cycle of anginal pain, starting with the effectors at the cardiac level | - pH and autocoids stimulate small afferent sympathetic fibers - fibers travel into spinal cord and are referred to shoulder, arm, or chest - pain activates sympathetic system which increases O2 consumption and leads to a vicious cycle |
| What is unstable angina? What are the clinical features? | - thrombus created by an atheromatous plaque rupture - angina at rest, changing anginal qualities, new-onsent angina, angina after MI, frequent acute episodes superimposed on chronic angina |
| What are some possible mechanisms for nitrate tolerance? | - decreased SH groups which are need for conversion to NO - reflexive increase in vasoconstrictor hormones - free radicals that destroy NO |
| What events increase cardiac O2 demand? | increases in: - HR - Contractility - preload -afterload - ejection time |
| What three physical events reduce the window for coronary flow? In practice, what is the main predominant factor? | 1) Increased heart rate 2) Decreased diastolic arterial pressure 3) Increased ventricular end-diastolic pressure ***HEART RATE IS THE MAJOR FACTOR IN PRACTICE |
| What are some counter productive effects of nitrates? | They can actually cause a reflexive increase in HR and contractility |
| What type of Ca channel blockers are Verapamil and Diltiazem? How are they used in angina treatment? | - NON-selective, meaning heart and vessels (as opposed to DHP's) - effective in angina for px's who are intolerant to B-blockers - reduced mortality in px's w/NORMAL LV FUNCTION - Do not co-administer with B-blockers because of depressed cardiac funt |
| How do nitrates derive their benefit in the treatment of angina? Give mechanisms. | - coronary vessel dilation *increase BF & collateral circ *increase subendocardial perfusion by decrease LVEDP - systemic vasculature dilation (veins > arteries) *relax great veins & decrease venous return (preload) *decrease TPR and pressure |
| What are contra-indications of B blockers in angina treatment? What are some side effects? | - Asthma and bradyarrythmias - impotence and fatigue |
| What circumstances favor and disfavor using a B-blocker as second line in addition to a nitrate in treating angina? | FAVOR: - post-infarction, LV dysfunction, high anxiety level DISFAVOR (aka use Ca channel blocker): - asthma, diabetes, hyperlipidemia, Printzmetal's angina |
| What type of channel blockers are DHP's? How are they used in angina? | - SELECTIVE blockers - First gen (nifedipine) must be co-administered w/B-blockers b/c of relfexive increase in HR - Second gen (amlodopine) do not need to be co-administered w/B-blockers - prevent coronary vasospasm, first line for Printzmetal's ang |
| What is the comined effect of nitrate plus B-blocker therapy? What is the BIG PICTURE MESSAGE? | Contractility: no change ED Volume: no change/DECREASE HR: DECREASED Ejection time: no change BP: DECREASED ***THE POINT IS, that each drug makes up for the detrimental effects of the other, leading to overall |
| What events decrease O2 supply? | - Increase HR and preload (reduced window for coronary flow) - Decreased coronary diameter (artherosclerosis) |
| What is the therapeutic status of B blockers in angina? | - for CHRONIC angine PROPHYLAXIS *NO USE in acute attack - Prevent excercise induced angina - can reduce nitrate dose (aka reduce tolerance) - CI'd in Printzmetal's Angina *can actually cause vasospasm via B2 blockade |
Created by:
sam.mrosenfeld
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