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Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
Beta blockers and calcium channel blockers
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Beta blockers and calcium channel blockers

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  • 1.  Beta blockers and calcium channel blockers are widely prescribed for a range of conditions and are now widely used in the management of cardiovascular disease.  In 1958, the first beta blocker, dichloroisoproterenol, was synthesised by Eli Lilly Laboratories.  Sir James W Black in 1962, found the first clinically significant beta blockers – Propranolol and Pronethalol  Calcium channel blockers were first identified in the lab of German pharmacologist Albrecht Fleckenstein beginning in 1964 and are now widely used and have potent vasodialatory effect. . 
  • 2. Beta blockers, also known as beta-adrenergic blocking agents or beta antagonists, or betaadrenergic antagonists, are medications that reduce blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline.
  • 3.  Beta receptors are found on cells of the heart muscles, smooth muscles, airways, arteries, kidneys, and other tissues that are part of the sympathetic nervous system and lead to stress responses, especially when they are stimulated by epinephrine (adrenaline).
  • 4. Three types of beta receptors are known, designated β1, β2 and β3 receptors.  β1-adrenergic receptors are located mainly in the heart and in the kidneys.  β2-adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.  β3-adrenergic receptors are located in fat cells. 
  • 5. Angina pectoris  Atrial fibrillation  Cardiac arrhythmia  Congestive heart failure  Essential tremor  Glaucoma  Hypertension  Migraine prophylaxis  Mitral valve prolapse  Myocardial infarction 
  • 6.         Phaeochromocytoma, in conjunction with α-blocker Postural orthostatic tachycardia syndrome Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism Theophylline overdose Acute aortic dissection Hypertrophic obstructive cardiomyopathy Marfan syndrome (treatment with propranolol slows progression of aortic dilation and its complications) Prevention of variceal bleeding in portal hypertension
  • 7. cocaine-induced tachycardia  sinus bradycardia  partial AV block  peripheral vascular diseases  diabetes mellitus  chronic obstructive pulmonary disease (COPD) and  asthma 
  • 8.            Nausea diarrhea bronchospasm dyspnea cold extremities exacerbation of Raynaud's syndrome bradycardia hypotension, heart failure heart block fatigue
  • 9.          dizziness alopecia (hair loss) abnormal vision hallucinations insomnia nightmares sexual dysfunction alteration of glucose and lipid metabolism. Adverse effects associated with β2adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism)
  • 10.  Acebutolol (Sectral)  Atenolol (Tenormin)  Betaxolol (Kerlone, discontinued)  Betaxolol (Betoptic, Betoptic S)  Bisoprolol fumarate (Zebeta)  Carteolol (Cartrol, discontinued)  Carvedilol (Coreg)  Esmolol (Brevibloc)
  • 11. Labetalol (Trandate, Normodyne)  Metoprolol (Lopressor, Toprol XL)  Nadolol (Corgard)  nebivolol (Bystolic)  penbutolol (Levatol)  pindolol (Visken, discontinued)  propranolol (Inderal, InnoPran)  sotalol (Betapace)  timolol (Blocadren, discontinued)  timolol ophthalmic solution (Timoptic) 
  • 12.  Combining propranolol (Inderal) or pindolol (Visken) with thioridazine (Mellaril) or chlorpromazine (Thorazine) may result in low blood pressure (hypotension) and abnormal heart rhythms because the drugs interfere with each others' elimination and result in increased levels of the drugs.
  • 13. Dangerous elevations in blood pressure may occur when clonidine (Catapres) is combined with a beta blocker  Phenobarbital and similar agents may increase the breakdown and reduce blood levels of propanolol (Inderal) or metoprolol (Lopressor, Toprol XL). This may reduce effectiveness of the beta blocker.  Aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) (for example, ibuprofen) may counteract the blood pressure reducing effects of beta blockers by reducing the effects of prostaglandins. Prostaglandins play a role in control of blood pressure. 
  • 14.  Glucagon is the specific antidote for betablocker poisoning, because it increases intracellular cAMP and cardiac contractility  Patients who experience Bronchospasm due to the Beta2 blocking effects of nonselective beta blockers may be treated with anticholinergic drugs, such as Ipratropium, which are safer than beta agonists in patients with cardiovascular disease. Another antidote for beta blocker poisoning are Salbutamol and Isoprenaline.
  • 15.  A calcium channel blocker (CCB) is a chemical that disrupts the movement of calcium (Ca2+) through calcium channels. Calcium channel blockers are used as antihypertensive drugs.
  • 16.  CCBs used as medications primarily have three effects:  by acting on vascular smooth muscle they reduce contraction of the arteries and cause an increase in arterial diameter, a phenomenon called vasodilation (CCBs do not work on venous smooth muscle)  by acting on cardiac muscles (myocardium), they reduce the force of contraction of the heart  by slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
  • 17. 1.      Dihydropyridine Dihydropyridine calcium channel blockers are derived from the molecule dihydropyridine and often used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina This CCB class is easily identified by the suffix "-dipine" Amlodipine (Norvasc) Aranidipine (Sapresta) Azelnidipine (Calblock)
  • 18. 2.Non-dihydropyridine  Phenylalkylamine  Phenylalkylamine calcium channel blockers are relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina  EXAMPLES ARE:  Verapamil (Calan, Isoptin)  Gallopamil  Fendiline
  • 19. 3.Benzothiazepine Benzothiazepine calcium channel blockers belong to the benzothiazepine class of compounds and are an intermediate class between phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels.  EXAMPLE :Diltiazem (Cardizem) (also used experimentally to prevent migraine) 
  • 20. 4.Nonselective  While most of the agents listed above are relatively selective, there are additional agents that are considered nonselective. These include mibefradil, bepridil, flunarizine 5. Ziconotide  Ziconotide, a peptide compound derived from the omega-conotoxin, is a selective Ntype calcium channel blocker that has potent analgesic properties.
  • 21. AMLODIPINE (NORVASC)  CLEVIDIPINE (CLEVIPREX)  DILTIAZEM (CARDIZEM),  FELODIPINE (PLENDIL),  ISRADIPINE (DYNACIRC),  NIFEDIPINE (ADALAT, PROCARDIA),  NICARDIPINE (CARDENE),  NIMODIPINE (NIMOTOP),  NISOLDIPINE (SULAR), AND  VERAPAMIL (CALAN, ISOPTIN). 
  • 22.         CCBs are used for treating high blood pressure, angina, and abnormal heart rhythms. They also may be used after a heart attack They also are used for treating: pulmonary hypertension, Raynaud's syndrome, cardiomyopathy, and subarachnoid hemorrhage. CCBs are also used in the prevention of migraine headaches
  • 23.       AMLODIPINE (NORVASC®): Adult (usual) Angina: 5-10 mg po qd. BEPRIDIL (VASCOR®): usual dose: 300 mg/day; maximum daily dose: 400 mg CLEVIDIPINE -CLEVIPREX ® Intravenous infusion of Cleviprex at 1-2 mg/hour.
  • 24. DILTIAZEM (CARDIZEM ®):  Adult (usual) Oral:usual dose 180-360 mg po daily (ANGINA)  usual dose 120-180 mg bid (HYPERTENSION)  FELODIPINE (PLENDIL®):  Adults: hypertension: Oral: 2.5-10 mg once daily.  NIFEDIPINE (PROCARDIA®):  10-30 mg 3 times/day as capsules 
  • 25. Constipation  nausea  Headache  Rash  edema (swelling of the legs with fluid)  low blood pressure  drowsiness and dizziness  sexual dysfunction. 
  • 26.  Verapamil and diltiazem decrease the elimination of a number of drugs by the liver. Through this mechanism, verapamil and diltiazem may reduce the elimination and increase the blood levels of carbamazepine (Tegretol), simvastatin (Zocor), atorvastatin (Lipitor), and lovastatin (Mevacor). This can lead to toxicity from these drugs.
  • 27. Mild CCB toxicity is treated with supportive care  For severe overdoses, treatment usually includes close monitoring of vital signs and the addition of vasopressive agents and intravenous fluids for blood pressure support. IV calcium gluconate (or calcium chloride if a central line is available) and atropine are first-line therapies. 
  • 28.  Cardiovascular disease remains the leading cause of morbidity and mortality among transplant recipients. Therefore, antihypertensive therapy should focus on those agents with proven benefit in reducing the progression of cardiovascular disease. Despite their effectiveness, CCB's often have a high mortality rate over extended periods of use, and have been known to have multiple side effects. Beta-blockers, however, have been, are, and will remain the cornerstone for the treatment of heart failure

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