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blockers of beta 1: increase heart rate increase contractility; increase renin release |
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beta 2 blocker cause relaxation of vascular bronchial and uterine smooth muscle ; increase glycogenolysis; increase insulin release; increase tremor
**** bronchial**** and ****uterine smooth muscle*** |
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blockers of beta 3 increase lipolysis increase urinary bladder relaxation |
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alpha 1 blockers cause vasoconstriction, mydriasis ( pupil dialation) , piloerection( hair standing up) and increase in glycogenolysis |
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Definition
decrease neuronal transmitter release, increase platelete aggregation, decrease lipolysis decrease insulin release |
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Definition
Antagonize (block) the B1 and B2 receptors Decrease heart rate Decrease contractility Decrease renin release (decrease angiotensin II) |
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Mechanisms specific to heart failure |
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Definition
Restore heart rate variability( patients see a big difference in resting heart rate) Prevent arrhythmia occurrence Prevent/slow remodeling process (hypertrophy) Inhibit renin secretion
NE still in heart in MI patients need to be advised that effects are bad at first but get better over time |
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Beta blockers place in therapy |
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Definition
Have long been considered one of drugs of choice for initial therapy Recent data shows less of a stroke benefit than other classes; clinically important increase in new diabetes No longer liked for hyper tension PB because it increases diabetes |
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Term
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Definition
Gold standard for heart failure (and post-MI) Symptoms will worsen initially, but slow improvement Slow titration: 3.125-6.25-12.5-25-50 or 12.5-25-50-100-200 ( push until you see side effects stop) Target dosing shown to be effective **** Important because Heart failure if you dont have target dose*****
High blood pressure use low dose until HPB comes in line *****exercise intolerance***** |
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Beta blockers remaining questions |
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Definition
Remaining questions: Role in therapy? ... younger patients, HF risk, angina What about newer beta-blockers? **** you cant rely on symptoms because all patients will feel worse initially***** |
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Selective Agents Metoprolol Atenolol Bisoprolol Betaxolol Nebivolol Acebutolol Esmolol |
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Definition
beta 1 most important group, selective cardio affinity for beta 1 receptor --good for pulmonary effect---Relatively selective especially in big doses ---dont give to people with COPD---Mild to high dose will show bronchial effect |
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Intrinsic Sympathomimetic Activity (ISA) |
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Definition
Pindolol Acebutolol Mimic sympathetic partially NO HF NO NO ANGINA Beneficial decreased side effects |
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Carvedilol (alpha1-antagonist)***in addition to blocking alpha it also blocks beta**** Nebivolol (increased NO) Labetolol (alpha1-antagonist) |
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Term
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Definition
Inhibit transmembrane influx of calcium Act at SA/AV node &/or vascular smooth muscle Vasodilation &/or Decreased heart rate
Other effects specific to class ***2main groups** Diltiazem and Verapamil (very limited) Negative inotropic and chronotropic effects
Dihydropyridines No effects on conduction in vivo |
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Definition
Blocks entry into cell and is essential for muscle contraction**** works by relaxing the vascular muscle |
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Calcium channel blockers group1 |
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Definition
Verapamil Diltiazem stronger on heart vascular |
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calcium channel blockers group 2 |
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Definition
dihydropyridines (DHP)do nothing on heart but great on vasodilation |
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Calcium Channel BlockersCommon Adverse Effects |
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Definition
Headache ***brain does not like** Flushing ***vasodilating** Pedal edema***especially dependent edema- common with DHP*** Constipation*****verapamil*** Hypotension ***both** Reflex tachycardia ***more with DHP*** Bradycardia, AV Block, CHF ********effects heart---hint verapamil & diltiazem******* said as a reminder |
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Calcium Channel Blockers Drug Interactions |
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Definition
Verapamil and Diltiazem ***can directly slow enzymes that effect other drugs*** Can cause many drug interactions Change metabolism and/or transport of drugs
Nifedipine, Felodipine, others Subject of many interactions Sensitive to changes caused by other drugs ******victims and perpetrators ******* |
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