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Lowers maximal heart rate about 20-30 bpm from what the person would have achieved without the beta blocker o People can still get a cardiac training effect while on a beta blocker Orthostatic hypotension (dizzy if they stand up suddenly) Psychotropic effects, especially in older men (depression, lethargy) o
What do vasodilators do, and what are some of the adverse effects? Directly inhibit smooth muscle contraction in the vascular smooth muscle Indications: high blood pressure, heart failure Examples: minoxidil (Loniten) also causes hair growth Adverse effects: o Reflex tachycardia an increase in heart rate to try to bring blood pressure back up o Postural or orthostatic hypotension o Dizziness o Headaches o Edema and fluid retention How does the renin-angiotensin system work? The renin-angiotensin system normally helps to control a variety of physiological processes, especially blood pressure regulation If blood pressure suddenly falls, renin is released from kidneys Renin allows angiotensinogen to be converted into angiotensin I o Both angiotensinogen and angiotensin I are precursor molecules and are inactive Angiotensin I will come into contact with a substance called angiotensin converting enzyme (ACE), especially the lungs, and is thus converted to angiotensin II Angiotensin II is the most powerful vasoconstrictor in the human body If the body is subjected to chronic angiotensin II, vascular remodeling and occlusion may occur What do the ACE inhibitors do, and what are some of the adverse effects? Inhibits the angiotensin converting enzyme (ACE), which consequently decreases the formation of excess angiotensin II o This prevents acute vasoconstriction and decreases blood pressure o Also prevents vascular hypertrophy from chronic overexposure to angiotensin II Indications: high blood pressure and heart failure Examples: many drugs ending in pril Adverse effects: o Slight allergic response/skin rash o Dry cough o Nausea o Dizziness What do angiotensin II receptor blockers do? Blocks the receptor to which angiotensin II binds on the heart The renin-angiotensin system is still active, but it will not be able to over stimulate the heart and blood vessels This prevents the detrimental effects of angiotensin II on the heart and peripheral vasculature It also has fewer side effects than ACE inhibitors
What do Ca2+ channel blockers do and what are the indications? Furthermore, what are some of the adverse effects and rehabilitation concerns? Limits or blocks the entry of excess calcium in to vascular smooth muscle and cardiac striated muscle Promotes vasodilation and stabilizes the heart rate Indications: high blood pressure (causes vasodilation of the periphery), angina, arrhythmias Examples: many druges eding in ipine Adverse effects and rehabilitation concerns: o Swelling in ankles and feet o Orthostatic hypotension o Altered heart rate o Short acting form = Increased risk of heart attack in older adults (because it lowers blood pressure too quickly)? o May increase the risk of cancer What is an example of an organic nitrate? Nitroglycerine, isosorbide dinitrate, etc. What are the primary effects of nitrates and what are some potential adverse effects? Primary effects: o Works by dilating peripheral vasculature Causes an increase in venous dilation, cardiac preload will be decreased (less blood is returned to the heart) Causes an increase in arterial dilation, cardiac afterload will be decreased (the heart doesnt have to work as hard to push out blood against constricted arteries) o Decreases demand of oxygen by the heart o Treats angina (chest pains) Potential adverse effects: o It is another form of vasodilators, so some headaches and dizziness can occur o Orthostatic hypertension o Exaggerated response to systemic heat (getting in a whirlpool, etc. could be life threatening) avoid at all costs o Check drug viability physically, they can get broken down (in the bottle) o Should have drugs available at all times during any form of exercise Describe what happens in heart failure: During heart failure, the heart is beating too fast and ineffectively Describe digitalis and what happens in toxicity: Digitalis is a group of agents derived from the foxglove plant and is primarily indicated in the treatment of heart failure. It has mechanical effect on cardiac pumping ability and autonomic effect on autonomic nervous control of the heart. o Mechanical effect: inhibits the sodium potassium pump; Less sodium leaves so more calcium is remaining intracellularly. This results in a stronger contraction and better cardiac function
Sympathetic effect: decreases heart rate by stimulating the vagus, causing increased parasympathetic discharge. Also inhibits sympathetic. This slows down the heart, allowing it to fill more effectively and can pump more blood each time. When digitalis reaches toxic levels in the blood stream, can be severe or fatal. Symptoms: o GI distress o Fatigue o Depression o Confusion o Blurred vision o Arrhythmias o
What are oral anticoagulants? Oral anticoagulants inhibit regeneration of vitamin K in the liver o Vitamin K promotes clotting factor synthesis in the liver o Once used, vitamin K needs to be regenerated in the liver. Coumadin decreases the regeneration of vitamin K and thus slows synthesis of certain clotting factors that are dependent on vitamin K In essence, this slows down the formation of clotting factors so that there are not as many available in the blood stream Drawback to Coumadin: there is a big time lag (3-4 days) between the time of starting the oral anticoagulant and the time in which it becomes effective What does warfarin (Coumadin) do, and how is it often used in tandem with heparin? Drawback to Coumadin: there is a big time lag (3-4 days) between the time of starting the oral anticoagulant and the time in which it becomes effective Typically, the patient begins with heparin to quickly get clotting under control Then they add in Coumadin or switch to Coumadin as long as needed (may be indefinitely) What do antithromobotics do? Inhibit platelet activity to decrease platelet induced clots How does aspirin work? Aspirin controls blood coagulation by affecting the formation of prostaglandins and thromboxane. When it reaches the cell, it directly inhibits the cyclooxygenase enzyme. Cell cannot make the first prostaglandin and thus cannot make any other prostaglandins, including thromboxane. o Thromboxanes naturally increase platelet activity and aggregation o Aspirin thus inhibits platelet function and prevents arterial thrombogenesis Less tendency for platelets to clump together and form clots What do thrombolytics do? Initiates break down of a clot (thrombus) that has already formed by activating plasmin Especially good for dissolving clots in coronary and carotid arteries Types: streptokinase, recombinant tissue plasminogen activator (like what the body makes naturally) Thrombolytics restore blood flow and helps prevent or reverse damage during myocardial infarction and/or ischemic stroke o Myocardial infarction taking a thrombolytic can decrease mortality by ~50%. One agent is specifically better than another agent; rather, time is the critical factor (effective if taken within 3-6 hours after onset of symptoms) o Ischemic stroke must rule out hemorrhagic stroke/be aware of this risk; recombinant tissue plasminogen activator seeps to be superior to streptokinase in this instance. Administer within 2-3 hours of symptom onset How are statins used to treat hyperlipidemia? Hyperlipidemia abnormal lipid profiles in the bloodstream
Statins inhibits the enzyme (HMG CoA reductase) that synthesizes endogenous cholesterol in the liver and helps with hepatic LDL breakdown. May also help increase HDL proteins and decrease triglycerides o LDL = bad o HDL = good Lipitor and Zocor are examples of statins
What are the adverse effects of antilipid agents? Side effects: nausea, diarrhea, bloating, neuromuscular problems! o Myalgia, myositis, weakness, parasthesias o Unexplained muscle pain or weakness = HUGE red flag!! Send back to physician!! o Can be life threatening!
Describe what antihistamines do and some problems with them: Block effects of histamine on upper respiratory tract Used to treat histamine mediated coughing, sneezing, irritation Newer agents are non sedating do not cross the blood brain barrier (Claritin) Problems o If crosses blood brain barrier, incoordination, blurry vision, sedation, fatigue Rehab concerns o Sedative effects o Dry out respiratory tract What is histamine? Causes irritation, scratchy throat, discharge, watery eyes, etc. What are the 3 classes of bronchodilators? Beta adrenergic agonists Xanthine derivatives Anticholinergics What happens when Beta 2 receptors are stimulated? Causes relaxation on airway smooth muscle Cell increases the production of cyclic-AMP Leads to bronchodilation Albuterol is a beta-selective type Epinephrine is nonselective and binds to B1, B2, A1, and A2 What are some ways Beta-adrenergic agonists can be administered and Inhalers push, then inhale at the right time Spacers between inhaler and mouth Nebulizer inhaled more slowly over a longer period of time What are some of the primary problems associated with Beta-adrenergic agonists? Bronchial irritation/constriction = mostly because of over reliance Cardiac stimulation, even with beta-2 receptors CNS stimulation (nervousness, etc.) What are the effects of anticholinergic drugs on bronchials? Acetylcholine stimulates bronchial smooth muscle contraction Anti acetylcholine drug = Dilation Blocks acetylcholine receptors Fairly selective for receptor on the lung Limited by side effects What are the inhaled glucocorticoids used in asthma, COPD and what are some problems with them? Anti-inflammatory steroids applied directly to the airway Oral administration is very dangerous Problems
o o
General catabolic (breakdown) effect on bone and muscle Limited daily dosage minimizes problems
What is the effect of cromones on histamine and when should they be taken? Usually in nasal sprays Prevent the release of histamine from mast cells and other inflammatory cells that lie in the respiratory tract Desensitizing cells that release the histamine so that when cells encounter an allergen, they do not produce a response Can only prevent an attack if taken before exposure, not after What are leukotriene modifiers? Leukotrienes mediate inflammatory responses; similar to prostaglandins in the airway (produced from same precursor). Play an important role in inflammation Receptor blockers once leukotriene is produced = Singulair (do not prevent production of leukotrienes, only block the receptors) Lipooxygenase (zyflo) inhibits production of leukotrienes Some concern over hepatic toxicity Know newer strategy of managing asthma vs traditional management Traditional Method o Inhaled beta-2 agonist for rescue therapy, supplemented with daily oral theophylline o But patients progressed, and at some point they add oral glucocorticoid (severe side effects) Newer Method o Begin anti-inflammatory inhaled glucocorticoids early o Can still have beta-2 drug available o Include other drugs as needed