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CHRONIC OBSTRUCTIVE PULMONARY DISEASE - PERMANENT, CHRONIC OBSTRUCTION OF AIRWAYS
- OFTEN RELATED TO CIGARETTE SMOKING
- EMPHYSEMA AND CHRONIC BRONCHITIS
- MANIFESTATIONS:AIRFLOW OBSTRUCTION ON EXPIRATION--OVERINFLATED LUNGS AND POOR GAS EXCHANGE
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Coordinating center for the nervous and endocrine responses to internal and external stimuli |
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The nervous system and the endocrine system work together to maintain internal homeostasis and to integrate the body's response to the external environment |
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Chemicals that are produced in the body and that meet specific criteria- also known as chemical messengers |
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Characteristics of Hormones |
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- produced in small amounts
- secreted directly in the bloodstream
- travel through blood to specific receptor sites throughout the body
- act to increase or decrease the normal metabolic processes of cells when they react with their specific receptor sites
- they are immediately broken down
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class II antiarrhythmic drug. treatment of cardiac arrhythmias especially supraventricular tachycardia, treatment of ventricular tachycardia induced by digitalis or catecholamines Actions: Competitively blocks beta-androgenic receptors in the heart and kidneys, has a membrane stabilizing effect and decreases the influence of sympathetic nervous system
adverse effects: bradyardia, CHF, cardiac arrhythmia, heart blocks, cerebrovascular accident, pulmonary edema, gastric pain, flatulence, nausea, vomiting, diarrhea, impotence, decreased exercise tolerance, antinuclear antibody development |
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drugs that effect the action potential of cardiac cells altering their automaticity, conductivity, or both |
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Class III Antiarrhythmics |
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blocks action K pump channels, prolonging phase 3 of the action potential, which prolongs repolarization and slows the rate and conduction of the heart. For life threatening ventricular arrhythmias |
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Drugs that block Na channels in the cell membrane during an action potential. they depress phase 0 of the action and change the duration of the action potential preferable in condition such as tachycardia in which Na gates are open frequently. indicated for treatment of potentially life-threatening ventricular arrhythmias and should not be used to treat other arrhythmias because of risk of proarrhythmic effects not to mixed with digoxin and other beta blockers |
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beta-adrenergic blockers, block beta receptors in the heart and kidney decreasing heart rate cardiac excitability and caridatc output. they also slow conduction through the AV nodes and decrease the release of renin. Lastly causing a depression of phase 4 of the action potential. Indicated for treatment of supraventricular tachycardias and PVC's. |
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Management of acute ventricular arrhythmias during cardiac surgery or MI Decreases depolarization, decreaseing automaticityof the ventricular cells; increases ventricular fibrillation threshold. metabolized in the liver and excreted in urine Adverse effects: Dizziness, light-headedness, fatigue, arrhythmias, cardiac arress, nausea, vomiting, anaphylactoid reaction, hypotension, vasodilation |
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beta-adrenergic blockers, block beta receptors in the heart and kidney decreasing heart rate cardiac excitability and caridatc output. they also slow conduction through the AV nodes and decrease the release of renin. Lastly causing a depression of phase 4 of the action potential. Indicated for treatment of supraventricular tachycardias and PVC's. |
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act to block Ca channels in the cell membrane, leading to depression of depolarizatio and a prolongation of phases 1 and 2 of repolarization which slows automaticity and conduction. For treatment of supaventricular tachycardia and to control the ventricular response to atrial flutter or fibrillation |
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Treatment of paroxysmal supraventricular tachycardia , atrial fibrillation, atrial flutter
Action: blocks the movement of ca ions across the cell membrane depressing the generation of action potentials, delaying phases 1 and 2 of repolarization and slowing conduction through the AV nodes
oral onset: 30-60min peak: 2-3 hr Duration:6-8 hrs iv onset: immediate peak: 2-3 min Duration: unknown
Adverse Effects: Dizziness, light-headedness, headach, asthenia, peripheral edema, bradycardia, AV block, flushing, nausea, hepatic injury. |
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stop the angiotensin I from convertion to angiotenson II in the lungs, stps the phase of renin-angiotenson system before vasoconstriction can occur or aldosterone can be released. remember most drugs end in -pril |
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Treatment of hypertension, CHF, diabetic nephropathy, left ventricular dysfunction after an MI.
Action: blocks ACE from converting to angiotension I to angiotensin II, eading to a decrease in blood pressure, a decrease in aldosterone production and a small icrease in serum k+ levels along with Na fluid loss.
Adverse effects: Tachycardia, MI rash pruitus, gastric irritation, aphthous ulcers, peptic ulcers, dysgeusia, proteinuria, bone marrow suppression, cough
oral, onset:15 min peak:30-90min |
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in the blood vessels to prevent vasoconstriction and in adrenal cortex to prevent the release of aldosterone that is caused by reaction of these receptors with angiotensin II. Leads to a decrease in blood pressure caused by decreased in total peripheral resistance and blood volume. remember most drugs end in -sartan |
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Alone or as part of combination therapy for the treatment of heypertension, treatment of diabetic nephropathy with an elevated serum creatinine and proteinuria in patients with type 2 diabetes and hypertension
action: Selectively blocks the binding of angitension II to specifice tissue recpetors found in the vascular smooth muscle and adrenal glands, blocks the vasoconstriction and release of aldosterone associated with the renin-angiotensin system
oral, onset:varies peak:1-3 hrs duration 24hrs
Adverse effects: dizziness, headache, diarrhea, abdominal pain syptoms of upper respiratory tract infection, cough, back pain, fever, muscle weakness, hypotension |
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prevents the movement of ca into the cardiac and smooth muscle cells when the cells are stimulated. Decrease cardiac work load most drugs end in -dipine, with the exception of Diltiazem. |
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treatment of essential hypertension in the extened-release form
Action: inhibits the movement of ca ions across the membranes of cardiac and arterail muscle cells, depressing the impulses and leading to slowed conduction decreased myocardial, and dilation of arterioles which lowers blood pressure and decreases myocardial O2 consumption
oral,er onset:30-60min peak: 6-11hr duration:12hrs
Adverse effects: Dizziness, light headedness, headache, peripheral edema, bradycardia, atrioventricular block, flushin and nausea |
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produced relazation of the vascular smooth muscle, decreasing, peripheral resistance and reducing blood pressure, used in severe hypertension or hypertensive emergencies. |
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hypertensive crisis, maintenance of controlled hypotension during anesthesia, acute CHF
Action: acts directly on vascular smooth muscles to cause vasodilation and drip blood pressure; does not inhibit cardiovascular reflexes and tachycardia, renin release will occur
IV onset:1-2min peak: rapid Duration:1-10min
Adverse effects: apprehension, headache, retrosternal pressure, palpations, cyanide toxicity, diaphoresis, nausea, vomiting, abdominal pain, irritation at the injection site |
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Treatment of CHF, atrial fibrilation
Actions: Increases intracellur Ca and allows more Ca to enter the myocardial cell during depolarization, this caused a (+) inotropic effect (increased force of contraction), increased renal perfusion with a diuretic effect and decrease in renin release, a (-) chronotropic effect (slowers HR) and slowed conduction through the Av node
oral onset:30-120min peak:2-6hrs duration: 6-8days IV onset:5-30min peak:1-5hrs duration: 4-5days T1/2: 30-40hrs largely excreted unchanged in the urine Adverse effects: headache, weakness, drowsiness, visual disturbances, arrhythmias, GI upset |
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affect the intracelluar Ca levels in the heart muscles, leading to increased contractility. |
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short-term treatment of CHF in patients who have not responded to digitalis, diuretics or vasodliators
Action: blocks the enzyme phosphodiesterase, which leads to an increased in myocardial cell cAMP, which increased Ca levels in the cell, causing a stronger contraction and prolonged response to sympathetic stimulation, directly relaxes vascular smooth muscles
IV onset:immediate peak: 10min duration: 2hrs
adverse effects: arrhythmias, hypotension, nausea, vomiting, thrombocytopenia, pericarditis, pleuritis, fever, chest pain, burning at injection site |
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treatment of life-threatening ventricular arrhythmias, maintenance of sinus rhythm to delay the time to recurrence of atial fibrillation/flutter in patients with symptomatic atrial fibrillation/flutter who are currently in sinus rhythm
Action: blocks beta-adrenergic receptors in the heart, as well as K channels, prolonging phase 3 of the action potential, which prolongs repolarization and sloes the rate and conduction of the heart
oral onset: varies peak: 3-4hrs duration: 8-12hrs t1/2: 12hrs largly excreted unchanged in urine
adverse effects: laryngospasm. respiratory distress, CHF, cardiac arrhythmias, heart block, CVA, pulmonary edema, gastric pain, flatulence, nausea, vomiting, diarrhea, impotence |
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drugs that act directly on smooth muscle to cause relaxation and to depress muscle tone |
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treatment of acute angina, prophylaxis of angina, intravenous treatment of angina unresponsive to beta-blockers or orgainc nitrates, peroperative hypertension, CHF, associated with acute MI, produced controlled hypotension during surgery
action: relaxes vascular smooth muscle with a resultant decrease in venous return and decreases in arterial blood pressure, reducing the left ventricular workload and decreasing myocardial O2 consumption
adverse effects: hypotension, headache, dizziness, tachycardia, rash, flushing, nausea, vomiting, sweating, chest pain
half life: 1-4min, metabolized in the liver and ex thru urine iv onset: 1-2 min duration:3-5min sublingual onset: 1-3min duration:30-60min translingual spray onset: 2 min duration:30-60min transmucosal tablets onset: 1-2min duration:3-5hrs oral, SR tablet onset: 20-45mn duration:8-12hrs topical ointment transdermal onset: 30-60mn dur: 4-8hrs transderman onset:30-60min duration:24hrs |
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