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765 Cards in this Set
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what are the types of drugs affecting lipid levels
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antihyperlipidemics
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what are the types of antihyperlipidemics
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statins, fibric acid derivatives, cholesterol absorption inhibitor, nicotininc acid, bile acid sequestrants
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what is the prototype drug of statins
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lovastatin
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what are high serum lipid levels associated with
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hypertension, coronary artery disease, coronary heart disease and other cardiovascular disorders.
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what are serum lipids
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fats found in the bloodstream
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what are the lipids found in the bloodstream
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cholesterol, cholesterol esters, phospholipids, triglycerides
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how are lipids transported in the blood
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by lipoproteins
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where is most of cholesterol produced
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liver
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what is the major cholesterol carrier in the blood
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LDL
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what is hyperlipidemia
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elevation of blood lipid levels
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what is hyperlipidemia a risk factor for
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atherosclerosis, coronary artery disease, and production of thromboses
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what is atherosclerosis
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narrowing of the arterial interior caused by buildup of hard, thick deposits and a hardening and loss of elasticity of the arterial wall
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how do cholesterol levels rise
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LDL binds to LDL receptors on cells and its cholesterol enters the cells but when too much cholesterol is in the cells, less receptors are available which means more LDL in the blood
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what do high cholesterol levels lead to
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atherosclerosis which leads to hypertension which leads to MI and stroke
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what are ideal cholesterol levels
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Total: less than 200
LDL: less than 100 HDL: 40-59 |
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what are the lifestyle changes to reduce LDL levels
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Diet, weight loss, increased physical activity
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what do most antihyperlipidemics do
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increase HDL, decrease triglycerides and LDL levels
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what do statins do
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lower blood cholesterol levels thus decreasing the uptake of modified lipoproteins by vascular cells and also restoring vascular endothelium. They also stabilize plaque and decrease thrombogenicity of blood.
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why should statins be coadministered
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most have metabolism effects on same isoenzyme in liver so if given together more of the drugs will not be metabolized and be available in the blood
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what is lovastatin
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a statin used in the treatment of primary hypercholesterolemia and combined hyperlipidemia. Also used in the secondary prevention of MI and stroke from thrombus formation.
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what are the pharmacodynamics of lovastatin and other statins
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competitiely inhibis HMG-CoA reductase, which is the enzyme that catalyzes the early rate-limiting step in cholesterol biosynthesis. This lowers LDL, total cholesterol and triglycerides and increases HDL.
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what are the contraindications and precautions of lovastatin
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active liver disease and pregnancy
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what is the pregnancy category of lovastatin
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X
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what are the adverse effects of lovastatin
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muscle and joint aches, weakness, cramps (myalgias), muscle damage, liver damage, rhabdomyolysis, elevated liver enzyme levels, myopathy
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what usually occurs in rhabdomyolysis
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brown urine
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what should you assess before giving lovastatin
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cholesterol levels and liver disease. Any other disease that contribute to increased blood cholesterol and LDL
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how do you minimize the adverse effects of lovastatin
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monitor liver function tests
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How do you maximize the adverse effects of lovastatin
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administer in evening
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how does provastatin differ form lovastain
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not metabolized in P-450 system so it doesn't have the sam drug interaction
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how does fluvastatin different from lovastatin
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metabolized via a different isoenzyme, does not raise digoxin levels
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which statin are asian subjects more sensitive too
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rosuvastatin
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what are fibric acid derivatives
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antihyperlipidemic that lowers triglyceride levels and increase HDL. Can lower or raise LDL levels. Most are coadministered with statins.
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what types of pateints generally use fibric acid derivatives
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diabetes or metabolic syndrome
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what are the types of fibric acid derivatives
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fenofibrate and gemfibrozil
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who is contraindicated with fenofibrate and gemfibrozil
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patient with hepatic or severe renal dysfunction, gall-bladder disease
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what is the cholesterol absorption inhibitor
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ezetimibe
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what is ezetimibe
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antilipid drug used to treat hypercholesterolemia.
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Who is ezetimibe restricted to in pediatrics
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children older than 10 with familal homozygous hypercholesterolemia
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What does ezetimibe do
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decreases LDL but has no effect on HDL or triglycerides
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What is the nicotinic acid
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niacin
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what are contraindications of nicotinic acid
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hepatic dysfunction, active peptic ulcer, severe hypotension and hemorrhaging.
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what are the bile acid sequestrates
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cholestyramine, colesvelam and colestipol
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what do bile acid sequestrants do
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just reduce LDL levels by promoting the oxidation of cholesterol to bile acids.
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what does the renal system include
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kidneys, ureters, and bladder
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what is osmolality
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strength or concentration of the urine produced
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what do the kidneys do
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play a major role in regulating acid-base balance and normal blood pH, reabsorption and secretion of electrolytes, and blood-pressure is also affected by the kidneys
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what causes hypervolemia
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excessive sodium and water retention. Edema may occur
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what does peripheral edema cause
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increase in cardiac workload and decrease tissue perfusion
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what are diuretics used for
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conditions in which fluid overload and edema has occurred such as in chronic heart failure, pulmonary edema, hypertension, cirrhosis, nephrotic syndrome, and kidney failure
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what is hydrochlorothiazide
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a thiazide that is used in the treatment of hypertension and treats edema from CHF, or hepatic or renal disease
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how does hydrocholorthiazide work
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acts in the distal tube and it increases the excretion of sodium and chloride in the distal convoluted tubule by slightly inhibiting the ion pumps that work in the sodium and chloride reabsorption
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what are the contraindications of hydrocholorthiazide
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severe renal impairment, anuria, hepatic coma
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what are the adverse effects of hydrocholorthiazide
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hypokalemia, hypoatremia, hypochloremia, and hypercalcemia
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what should be assessed when taking hydrochlorothizide
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allergies to sulfa and renal status and other contraindications. Assess access to toilet
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how do you maximize the therapeutic effects of hydrochlorothiazide
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administer dose in AM, monitor fluid intake, urine output and weight
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how do you minimize the adverse effects of hydrochlorothiazide
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correct any electrolyte imbalance prior to starting hydroclorothiazide therapy and monitor blood pressure, weight, intake and output and serum electrolyte levels during therapy
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what is furosemide
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a loop diuretic used to treat peripheral and pulmonary edema from CHF and hepatic and renal disease. also used to treat hypertension
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furosemide in the first choice diuretic for treating hypertension with preexisting what
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renal disease
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how does furosemide work
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inhibits the reabsorption of sodium, chloride and water in the ascending loop of henle
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what is the contraindication of furosemide
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anuria
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what are the adverse effects of furosemide
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electrolyte imbalance, especially hypokalemia ototoxicity, and alteration in glucose levels and permanent deafness.
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how do you maximize the therapeutic effects of furosemide
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titrate dose slowly and monitor blood pressure, edema, breath sounds, weight, intake and output, and serum electrolyte levels
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patients with severe CHF should be given furosemide how
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in a continuous infusion rather than equal dose given as IV bolus
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how do you minimize the adverse effects of furosemide
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closely monitor potassium levels and administer IV push slowly
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what assessments used be obtained while taking furosemide
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CBC, serum electrolyte and uric acid levels
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what do potassium sparing diuretics do
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promote sodium and water excretion in the distal tubule and potassium reabsorption
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what is triamterene
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a potassium sparing diuretic used as an adjunct to manage edema and hypertension
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how does triamterene work
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inhibits transport of sodium in the distal tubules independent of aldosterone
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what are the contraindications of triamterene
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kyperkalemia, renal or liver disease or if the patient is already receiving a potassium-sparing drug
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what are the adverse effects of triamterene
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hyperkalemia, nephrotoxicity, thrombocytopenia, elevated liver enzymes, headache and photosensitivity
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patients taking triamterene should avoid what
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eating potassium-rich food and potassium supplements
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what are the drugs significantly different from triamterene
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spironolactone, eplernone
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what is spironolactone
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potassium sparing drug that is an alderostone antagonist
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how do you minimize the adverse effects of triamterene
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monitor blood potassium levels and limit the intake of potassium
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how do you maximize the effects of triamterene
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administer in the morning
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what are osmotic diuretics
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increase osmotic pressure and pull fluid into the vascular space and prevent water sodium, and chloride reabsorption
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what is mannitol
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an osmotic diuretic that is used to treat acute renal failure, increased intracranial pressure in cerebral edema and reducing intraocular pressure
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how does mannitol work
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elevates blood plasma osmolarity that draws fluid from tissues and increases the concentration of molecules in the glomerular filtrate because it is not reabsorbed
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what are the contraindications of mannitol
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severe renal disease, pulmonary congestion, and intracranial bleeding
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what are the adverse effects of mannitol
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fluid or electrolyte losses, hypotension and tachycardia, hypovolemia
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how do you minimize the adverse effects of mannitol
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monitor patients hourly urine output, blood pressure pulse rate electrocardiographic tracings, intake to output ratios, renal function test results, and serum electrolyte levels. Give test dose for patients with marked oliguria or inadequate renal function
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how do you maximize the therapeutic effects of mannitol
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warm drug vial in water if crystals are seen and administer no warmer than body temperature using an in line filter
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what are the drugs related to mannitol
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glycerin, isosorbide, urea
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what is glycerin
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osmotic agent given to reduce intraocular pressure before ophthalmic surgery and during acute glaucoma attacks
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what is carbonic anhydrase
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an enzyme that plays a role in renal excretion of acid urine and reabsorption of sodium and potassium in the proximal tubule
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what does a carbonic anhydrase inhibitor do
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promotes excretion of sodium, potassium, bicarbonate, and water resulting in alkaline diuresis and decreases aqueous humor formation and decreases intraocular pressure
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what is acetazolamide
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a carbonic anydrase inhibitor that is used to treat chronic open angle glaucoma
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how does acetazolamide work
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prevents formation of aqueous humor and dcreases intraocular pressure. Also it inhibits carbonic anhydrase which is needed for active transport of ions across proximal tube
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what are the contraindications of acetazolamide
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kidney and liver disease, adrenocortical insufficiency, COPD, cirrhosis and closed angle glaucoma
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what are the adverse effects of acetaolamide
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anorexia, nausea, constipation, paresthesia, ataxia, tremor, tinnitus, bone marrow suppression
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how do you maximize the therapeutic effects of acetazolamide
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take every other day and use with miotics or mydratics for complementary effect when treating open angle glaucoma
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how do you minimize the adverse effects of acetazolamide
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allow kidney to recover and monitor CBC and platelet counts
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what is a life span alert in acetazolamide
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older adults may have hypotension and orthostatic changes
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what do anticholinergic agents do
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affect bladder contraction because receptors for these agents are found in the bladder and when they are blocked, bladder contraction cannot occur and urinary output decreases
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what are anticholineric agents used to treat
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overactive bladder
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what is tolterodine
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anticholinergic agent used to treat overactive bladder and incontinence
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how does tolterodine work
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blocks cholinergic muscarinic receptors in the bladder decreasing bladder function
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what are contraindications of tolterodine
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urinary retention, gastric retention, uncontrolled narrow angle glaucoma
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what are the adverse effects of tolterodine
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dry mouth, constipation, abnormal vision, urinary retention, and xerophthalmia (conjunctival dryness)
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how do you maximize the therapeutic effects of tolterodine
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administer drug on regular prescribed basis,
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how do you minimize the adverse effects of tolterodine
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decrease dosage with renal or liver disease
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what is flavoxate
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anticholinergic agonist used to treat cystitis, urethritis, prostatis, urethritis, or urethrocysitis
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what are the drugs affecting blood pressure
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antihypertensives and vasopressors
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what are the types of antihypertensives
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diuretics, beta blockers, calcium-channel blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors) andgiotensin II receptor blockers, selective aldosterone receptor blocker, alpha-beta blockers, centrally acting alpha-2 agonist, peripherally acting alpha-1 blockers, peripherally acting antiadrenergics, direct acting vasodilators,drugs used in hypertensice crisis
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what are adjuncts to hypertension treatment
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antihyperlipidemics, nitrates
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what is the prototype ACE inhibitor
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captopril
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what is the prototype angiotensin II receptor blocker
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losartan
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what is the prototype selective aldosterone receptor blocker
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eplerenone
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what is the alpha beta blocker
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labetalol
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what is the centrally acting alpha-2 agonist prototype
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clonidine
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what is the prototype direct acting vasodilators
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hydralazine
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what is the prototype drug used in hypertensive crisis
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nitroprusside
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what is systole
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when the ventricles contract
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what is the formula for measuring blood pressure
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cardiac output time peripheral resistance
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what are the adrenergic receptors
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alpha-1, alpha-2, beta-1 and beta-2
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what happens when alpha-1 receptors are stimulated
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cause peripheral constriction and blood pressure increases
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what is sympathomimetic effect
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what happens in alpha-1 receptors stimulation
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what happens when alpha-2 receptor sites are stimulated
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inhibits the sympathetic system causing a sympatholytic effect which decreases the heart rate and decreases vasoconstriction
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where are alpha-2 receptors located
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brain
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where are beta-1 located
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heart
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what does stimulation of beta-1 receptors do
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increases heart rate, speed of cardiac conduction and force of cardiac contraction
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where are beta-2 receptors located
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bronchial and vascular mulsculature
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what happens when beta-2 receptors are stimulatedd
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induces bronchial and peripheral dilation which decreases blood pressure
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what does renin do
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produces angiotensin I
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what is angiotensin I
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inactive substance until it is converted to the active angiotensin II
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what converts angiotensin I to angiotensin II
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Angiotensin converting enzyme ACE
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what does angiotensin II do
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it is a potent vasoconstrictor and simulates secretion of aldosterone from adrenal medulla
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what does aldosterone do
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increases retention of sodium and water in the body which increases circulating volume which increase BP
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what are the two main categories of hypertension
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primary and secondary
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what is secondary hypertension
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occurs secondary to another condition such as renal stenosis or renal tumor
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what is a hypertensive crisis
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systolic blood pressure over 210 and distolic over 120
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what kind of diet does DASH recommend
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diet rich in fruits, vegetables, and non fat diary as well as reduced intake of saturated and total fat, but higher potassium and calcium intake
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what are lifestyle modifications to treat hypertension
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diet, weight loss, limiting alcohol intake, regular exercise and stopping smoking
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what is prehypertesion
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120-139/80-89
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what is stage 1 hypertension
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140-159/90-99
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what is stage 2 hypertension
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160+/100+
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when should thiazide diuretic be used in hypertension
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uncomplicated hypertension
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what is indicated for stage 2 hypertension
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combination therapy
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how do drugs reduce hypertension
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decrease cardiac output and dcreaseing peripheral resistance
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how is the cardiac output decreased
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decreasing heart rate, decreasing force of contraction and decreasing preload
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what does decreasing peripheral resistance do
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decreases afterload
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what are the drugs that decrease peripheral resistance
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diuretics, calcium channel blockers, ARBs, ACE inhibitors, alpha-beta blockers, alpha-2 stimulators
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what are the drugs that decrease heart rate
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beta blockers,alpha-beta blockers, alpha-2 stimulators
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what are the decrease force of contraction
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beta blockers, alpha-beta blockers
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what are the drugs that decrease preload
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diuretics, ARBs
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what is the primary therapy for beta blockers
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used to treat hypertension in patients with MI, stable heart failure, asymptomatic left ventricular dysfunction, atrial fibrillation and angina
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what is the primary therapy for diuretics
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hypertension in patients with isolated systolic hypertension, diabetes mellitus type 2, gout
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how do calcium channel blockers work
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inhibit the movement of calcium ions across the cell membranes, which decreases the mechanical contraction of the heart, reduces impulse formation and lessens conduction velocity and dilates coronary and peripheral arteries
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when are calcium channel blockers used
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hypertension with angina, atrial tachycardia and fibrillation and cyclosporine-induced hypertension
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how do ACE inhibitors work
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inhibits ACE so angiotensin I can't be converted into angiotensin II which is a vasoconstrictor
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when are ACE inhibitors used
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heart failure, asmptomatic left ventricular dysfunction, history of ST-elevation MI, history of non-ST elevation MI with an anterior infarct, diabetes, systolic dysfunction or proeinuric chronic renal failure
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when are ARBs used
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when patient can't take effects of ACE inhibitors
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how do selective aldosterone blockers work
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block mineralocorticoid receptors which lowers blood pressure and reduce end organ damage associated with hypertension
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what are the second line antihpertensives
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centrally acting alpha-2 stimulators, peripherally acting alpha-1 blockers, peripherally acting alpha-beta blockers direct acting vasodilators
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what is captopril
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angiotensin-converting enzyme inhibitor that is used to treat hypertension, chronic heart failure, diabetic nephropathy and left ventricular dysfunction
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how does captopril work
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inhibits that ACE needed to change angiotensin I to angiotensin II which causes vasoconstriction
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what are the contraindications of captopril
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2nd and 3rd trimester pregnancy and angioedema
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what are the adverse effects of captopril
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persistent nonproductive cough, angioedema, rash, hypotension, neutropenia, and dypnea
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what should you assess before starting captopril
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blood pressure
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how do you minimize that adverse effects of captopril
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monitor blood pressure for 2 hours after initial dose until stabilized and monitor patients blood pressure throughout therapy and assess blood reports for hyperkalemia, hyponatremia, and neutropenia, and assess urine for proteinuria
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how do you maximize the therapeutic effects of captopril
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administer captopril 1 hour before meals because food decreases absorption
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what is captopril
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an ACE inhibitor that is different from captopril that is a renin inhibitor
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what is losartan
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an angiotensin II receptor blocker that is used to treat hypertension, diabetic nephropathy (kidney failure in people with diabetes), and left ventricle dysfunction
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how does losartan work
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selectively blocks the binding of angiotensin II to the angiotensin I receptors in many tissues so vasoconstriction and aldosterone-secreting effects are blocked
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what are the contraindications of losartan
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women who are pregnant or breast-feeding
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what are the adverse effects of losartan
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hypotension, upper respiratory infections, dizziness, diarrhea, asthenia
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what should you assess before starting losartan
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health status and chronic conditions
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how do you maximize the therapeutic effects of losartan
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continue life style changes and avoid taking with grapefruit juice
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how do you minimize the adverse effects of losartan
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monitor creatinine, BUN, hemoglobin and hematocrit level, help patient out of bed and with ambulation
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what is eplerenone
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a selective aldosterone blocker that is used to treat hypertension and reduce endo organ damage that can occur in hypertension
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how does eplerenone work
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binds selectively to the mineralocorticoid receptors thereby blocking aldosterone from binding to these receptors
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what are the contraindications of eplerenone
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elevated potassium levels, severe renal failure, increased creatinine levels, type 2 diabetes with miroalbuminuria, concurrent administration of drugs that increase potassium levels
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what are the adverse effects of eplerenone
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hyperkalemia, diarrhea, albuminuria, gynecomastia, abnormal vaginal bleeding and hypercholesterolemia and hyponatremia
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what should you assess before giving eplerenone
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blood pressure and laboratory studies
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how do you maximize the therapeutic effects of eplerenone
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provide patient education prior and during therapy and take regularly, implement or continue lifestyle changes
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how do you minimize the adverse effects of eplerenone
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monitor patients potassium levels and renal function.
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what is labetalol
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an alpha-beta blocker that is used for hypertension most frequently with other agents especially thiazide and loop diuretics
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how does labetalol work
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adrenergic blocking agent that has a nonspecific beta blocking action at both the beta-1 and beta-2 receptor sites and a selective alpha-1 blocking action
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what are the contraindications of labetalol
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bradycardia, heart block, asthma, and cardiogenic shock non-compensated heart failure
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what are the adverse effects of labetalol
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diarrhea, dizziness, elevations in BUN and creatinine levels, tingling of scalp and fatigue
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how do you minimize the adverse effects of labetalol
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prepare IV carefully, observe patient for signs of heart failure, monitor blood pressure, discontinue long term use slowly, keep patient lying flat 3 hours after administration
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how do you maximize the therapeutic effects of labetalol
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administer oral labetalol with food to increase absolute bioavailabilty
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what should you assess before giving labetalol
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underlying pathology of hypertension
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what do centrally acting alpha-2 agonist do
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stimulate alpha-2 receptors in the medulla oblongata inhibiting the sympathetic nervous system which causes reduced sympathetic outflow form CNS resulting in decreased heart rate, decreased blood pressure and decreased vasoconstriction and decreased renal vascular resistance
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what is clonidine
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a centrally acting alpha-2 agonist used as a second-line drug to lower blood pressure and also relieves the discomfort of withdraw symptoms from narcotics
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how does clonidine work
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stimulates alpha-2 receptors centrally in the medulla oblongata inhibiting sympathetic nervous system
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what are the adverse effects of clonidine
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dry mouth, drowsiness, dizziness, sedation and constipation and rebound hypertension
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what do you assess before giving clonidine
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current medical status and any chronic diseases
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how do you minimize the adverse effects of clonidine
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gradually reduce dose, assess for sedation when medicine is started
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how do you maximize the theapeutic effects of clonidine
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give in combination with other antihypertensices, apply dosage patch to a hairless area of intact skin on the upper arm or torso every 7 days and rotate aplication
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what are the peripherally acting alpha-1 blockers
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prazosin, terazosin, and doxazosin
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what are the adverse effects of peripherally acting alpha-1 blockers
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due to the first pass effect orthostatic hypotension can occur
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what is hydralazine
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a direct acting vasodilators and is used adjunct to other antihypertensives
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how does direct acting vasodilators
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produces direct smooth muscle relaxation of the arterioles
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what are the contraindicatoins of hydralazine
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CAD, and mitral valvular disease
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what are the adverse effects of hydralazine
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arthralgia, dermatoses, fever, splenomegaly, and glomerular nephritis tachycardia, angina, anorexia, symptoms of systemic lupus erythematosus
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what should you assess before giving hydralazine
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blood pressure and drug history
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how do you maximize the therapeutic effects of hydralazine
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administering hydralazine with food promote bioavailability
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how do you minimize the adverse effects of hydraliazine
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administer hydralazine with a beta blocker or clonidine to decrease reflex tachycardia and with a diuretic to offset fluid retention
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what is nitroprusside
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drug used in hypertensive crisis
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how does nitroprusside work
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directly relaxes vascular smooth muscle, allowing dilation of peripheral arteries and veins
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what are the contraindications of nitroprusside
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aortic coarctation or arteriovenous shunting
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what are the adverse effects of nitroprusside
|
severe hypotension and cyanide poisoning
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what should you assess before giving nitroprusside
|
blood pressure and cnotraindications
|
|
|
how do you maximize the therapeutic effects of nitroprusside
|
infusion rate for nitroprusside must be titrated to reduce blood pressure without compromising organ perfusion and wrap diluted bad of drug in an opaque sleeve or aluminum foil to protect from light
|
|
|
how do you minimize the adverse effects of nitroprusside
|
start nitroprusside at a low rate and increase gradually until desired effects has been achieved
|
|
|
what is spironolactone
|
a drug significantly different from eplerenone and causes inability to achieve an erection, gynecomastia, irregular bleeding or postmenopausal bleeding hirsutism and deepening of the voice
|
|
|
what are the peripherally acting antiadrenergics
|
guanadrel, guanethidine, reserpine
|
|
|
what are the drugs different from hydralazine
|
minoxidil, epoprostenol and tolazoline
|
|
|
what is minoxidil
|
direct acting vasodilator that causes pericardial effusion, fluid retention and hypertrichosis (excess hair growth)
|
|
|
what is epoprostenol
|
directly dilates peripheral vessels and inhibits platelet aggravation and is used to treat primary pulmonary hypertension and has many adverse effects
|
|
|
what is tolazoline
|
used to treat pulmonary hypertension and can cause leukopenia, thrombocytopenia, hepatitis or renal failure
|
|
|
what are the drugs closely related to nitroprusside
|
diazoxide, fenoldopam, trimethaphan
|
|
|
what are the drugs used to treat hypotension resulting from shock
|
vasopressors-dopamine, dobutamine, isoproterenol, epinephrine, norepiniephrine, ehedrine, metaraminol, midodrine
|
|
|
what are the drugs to treat hypotension resulting from various mechanisms
|
phenylephrine
|
|
|
what are the drugs treating heart failure
|
ACE inhibitors, diuretics, beta blockers, cardiac glycosides, natriuretic peptides, ARBs, hydralazine, spironoloactone, nitroglycerin
|
|
|
what is the cardiac glycosides
|
digoxin
|
|
|
what is the natriuretic peptides
|
nesiritide
|
|
|
what is the cardiac output
|
volume of blood that leaves the left ventricle in 1 minute. stroke volume x heart rate
|
|
|
what is stroke volume
|
amount of blood that leaves the left ventricle with each contraction
|
|
|
what is the preload
|
what is the afterloadpassive stretching force exerted on the ventricular muscle created by the amount of blood that has filled the heart by the end of diastole
|
|
|
what is the afterload
|
amount of pressure the ventricular muscle must overcome to eject the blood into the systemic circulation
|
|
|
what is peripheral resistance
|
diameter of the vessel and pressure within the vessel. pressure x diameter of vessel
|
|
|
when does cardiac output decrease
|
when left ventricle is unable to eject the normal volume of blood during systole which decreases the ejection fraction
|
|
|
what happens to the heart when cardiac output decreases
|
cardiomyopathy occurs to provide more contractile force to try to imporve cardiac output
|
|
|
which side fails first in HF
|
left
|
|
|
what are natriuretic peptides
|
endogenous cardiac hormones
|
|
|
what do brain natriuretic peptides do
|
regulate cardiovascular homeostasis and fluid volume.
|
|
|
what is brain natriuetic peptides secreted by
|
ventricular tissue in response to changes in wall tension
|
|
|
how does brain natriuretic peptides regulate cardiovascular homeostasis and fluid volume
|
promotes natriuesis, diuresis, vasodilation, and smooth muscle relaxation and inhibits renin aldosterone axis
|
|
|
when is brain natriuretic peptides elevated
|
in CHF, MI, acute coronary syndrome, aortic stenosis, hypertension, end stage renal failure and cirrhosis with ascites
|
|
|
when does heart failure develop
|
when the heart cannot achieve the normal cardiac output for various reasons, a backlog of blood or congestion occurs
|
|
|
what are the ACE inhibitors used to treat CHF
|
captopril, fosinopril, lisinopril, enalapril, and quinapril
|
|
|
what are loop dieuretics used to treat in CHF
|
edema and to decrease fluid volume
|
|
|
what should be asseessed in patients taking leepdiuretics for CHF
|
BUN levels
|
|
|
when should beta blockers be administered
|
as soon as left ventricular dysfunction is diagnosed because it slows disease progression
|
|
|
what are the beta blockers used in CHF
|
bisoprolol, metoprolol, carvedilol
|
|
|
what are beta blockers used for
|
chronic CHF
|
|
|
what should be taken before beta blockers
|
diuretics because it prevents ana cute exacerbation of CHF caused by the slowing of the heart rte and decrease in contractile force that occurs with beta blockers and ACE inhibitors
|
|
|
what are cardiac glycosides
|
know as digitalis preparations used to maintain clinical stability and improve symptoms, quality of life and exercise tolerance in patients with all phases of CHF
|
|
|
what is digoxin
|
a cardiac glycosides, that is used in the treatment of CHF and atrial fibrillation
|
|
|
how does digoxin work
|
it exerts an indirect effect on the heart from stimulation of the autonomic nervous system and a direct action on both conduction system of the heart
|
|
|
what are the ARB drugs used in HF
|
valsartan, losartan, and candesartan
|
|
|
what is the ocnventional therapy for HF
|
ACE inhibitors, beta blockers, loop diuretics
|
|
|
what does digoxin do to the heart
|
increases the force of cardiac contraction, which increases the cardiac output
|
|
|
what is the indirect effect of digoxin on the heart
|
depresses the SA node to slow conduction to the AC node which slows the heart rate
|
|
|
what is the antidote for digoxin overdose
|
digoxin immune Fab
|
|
|
what are the major contraindications of digoxin
|
heart block, ventricular fibrillation, digitalis toxicity, sick sinus syndrome, and tachycardia
|
|
|
what are adverse effects of digoxin
|
dysrhythmias, anorexia, vominiting, diarrhea, headache, weakness, apathy, visual distubances, confusion, restlessness, disorientation, seizures, delirium, hallucinations, neuralgia, and psychosis, ventricular fibrillation, hypercalcemia, kypokalemia, hypomagnesemia, toxicity
|
|
|
what is the life span alert for digoxin
|
older adults have increased adverse effects because of impaired renal function. children often poisioned
|
|
|
how do you minimize the adverse effects of digoxin
|
narrow therapeutic index, monitor serum digoxin levels, assess for bradycardia (take pulse 1 min before giving drug), monitor and correct electrolyte imbalances and assess for noncardiac signs of digoxin toxicity
|
|
|
how do you maximize the therapeutic effects of digoxin
|
achieve rapid onset of therapeutic effect with a loading dose assess cardiac rhythm, weight and renal function before giving
|
|
|
what is nesiritide
|
a natriuretic peptide used in adults to treat acute, decompensated HF
|
|
|
how does nesiritide work
|
stimulates natriuretic peptide A/B receptors, promoting smooth muscle cell relaxation and dilation of veins and arteries, which reduces pulmonary capillary wedge pressure, decreased vascular resistance and decreased dyspnea and fatigue
|
|
|
what are the contraindications of nesiritide
|
cardiogenic shock, systolic blood pressure less than 90
|
|
|
what are the adverse effects of nesiritide
|
hypotension, injection site reactions, rash, sweating, itching, leg cramps, anemia, confusion, dimmed vision, increased creatinine levels, cough, apnea, and hemoptysis, cardiac arrhythmias (ventricular tachycardia, atrial fibrillation, AV node conduction abnormalities, bradycardia and angina) and angina
|
|
|
how do you maximize the therapeutic effects of nesiritide
|
use infusion pump to administer, must be reconstituted and then further diluted for infusion, and use the reconstituted nesiritide solution within 24 hours
|
|
|
how do you minimize the adverse effects of nesiritide
|
monitor the patients cardiac response to nesiritide therapy by keeping patient on continuous cardiac monitor, monitor blood pressure and pulse, ECG changes.
|
|
|
what is special about vasodilator-antianginal combinations like hydralazine-isosorbide
|
it is used to treat CHF in black patients
|
|
|
what should not be taken with hydralazine-isosorbide
|
erectile dysfunction drugs
|
|
|
what are drug different from nesiritide
|
inamirone and milrinone
|
|
|
what are the adverse effects of inamirone and milrinone
|
thrombocytpenia and hepatotoxicity most commonly in inamirone
|
|
|
what are the drugs to treat angina
|
nitrates, beta blockers, calcium-channel blockers, and adjunct treatment for angina
|
|
|
what is the prototype nitrate
|
nitroglycerin
|
|
|
what is the prototype beta blockers
|
propranolol
|
|
|
what is the prototype calcium channel blockers
|
verapamil
|
|
|
what are the drugs used in adjunct treatment for angina
|
anticoagulants/antiplatlets
|
|
|
what are other drugs used in adjunct treatment for angina
|
antihyperlipidemics and ACE inhibitors
|
|
|
what are the anticoagulants/antiplatelets used in adjunct treatment for angina
|
aspirin, clospidogrel and heparin
|
|
|
why does angina occur
|
because the heart is not receiving enough oxygen
|
|
|
how do drug therapies treating angina work
|
allows more oxygen to be delivered to heart or decreases the oxygen needs of the heart or both
|
|
|
what delivers blood to the heart
|
coronary arteries
|
|
|
when do oxygen requirements of the heart increase
|
when the heart pumps faster and works harder and if the heart has to overcome a greater peripheral resistance in the vessels to eject blood form the left ventricle
|
|
|
oxygen imbalance in the heart may be due to what
|
reduced coronary blood flow or form a need for increase oxygen
|
|
|
how are the four major risk factors associated with coronary heart disease and angina
|
cigarette smoking, diabetes, elevated blood lipid levels, and hypertension
|
|
|
what are the 4 types of angina
|
stable angina, unstable angina, prinzmetal or variant angina, or microvascular angina
|
|
|
what is stable angina
|
oxygen need exceeds ability of body to supply oxygen and occurs during exercise, stress or periods of increased physical exertion and is normally reversed with rest.
|
|
|
what is a myocardial infarction
|
a complete blockage of one of the vessels supplying blood and nutrients to the muscle of the heart
|
|
|
what is unstable angina
|
caused by severely decreased coronary blood flow. Pain occurs when resting and can even occur during sleep. May not be marked by chest pain but with some atypical findings
|
|
|
what drugs are also used in adjacent to the treatment of unstable angina
|
anticoagulants, antiplatelets and antiilipids
|
|
|
what is acute coronary syndrome
|
used to define a grouping of symptoms that are produced by acute myocardial ischemia; it represents a continuum of cardiovascular disease and vessel occlusion. ACS encompasses unstable angina
|
|
|
what are the symptoms of atypical unstable angina
|
SOB, nausea, profuse sweating, fainting, and pain in the arms, upper middle abdomen, shoulder or neck
|
|
|
what causes prinzmetal angina or variant angina
|
sudden coronary artery spasms that induce ischemia in the heart muscle which if lengthy can lead to sudden death. This is caused by emotional stress, medications, stree drugs or exposure to cold temperatures.
|
|
|
what is microvascular angina
|
patients experience chest pain but have no apparent coronary blockages. Pain results from impaired function of the tiny blood vessels that perfuse the heart, arms and legs
|
|
|
what is isosorbide dinitrate
|
a nitrate used in the treament and prevention of angina pectoris
|
|
|
what is atenolol
|
a beta blocker used to treat hypertension, angina pectoris and acute myocardial infarction
|
|
|
what is nifedipine
|
a calcium channel blocker used to treat angina pectoris, stable angina, and hypertension
|
|
|
what do beta blockers do in angina treatment
|
prevent the beta-adrenergic receptors from being stimulated and the effects decrease the oxygen demands of the heart and thereby decrease angina
|
|
|
what does calcium do to the heart
|
it is needed in the automatic and conducting cells of the heart to help create an action potential
|
|
|
what do calcium channel blockers do
|
inhibit calcium from moving across cell membranes which decreases in contraction, depression of impulse formation, and slowing of conduction velocity
|
|
|
what does calcium channel blockers cardiovascular effects do for the heart
|
decreasing the oxygen needs of the heart and they cause arteriolar dilation, and decreasing afterload
|
|
|
what do nitrates do
|
dilate vascular smooth muscle and both venous and arterial vessels
|
|
|
what does venous dilation do
|
decreases the returning blood flow to heart so preload is less
|
|
|
what does arterial dilation do
|
reduces systemic vascular resistance and arterial pressure which means afterload is less
|
|
|
how do nitrates help with angina
|
decrease workload on the heart and its oxygen needs
|
|
|
what are adjunct drug therapies used for for treating angina
|
not to decrease oxygen demands on heart but slow down the progression of coronary artery disease, prevent complication that may arise with angina, or minimize symptoms
|
|
|
what do adjunct drug therapies target in unstable angina
|
thrombus formation which is an important concern for unstable angina
|
|
|
what is aspirin used for
|
one drug that is used in chronic stable angina and unstable angina
|
|
|
what is clopidogrel
|
antiplatelet drug used in place or in addition to aspirin
|
|
|
what does glycoprotein IIb/IIIa receptor antagonists do
|
a platelet inhibitor and is used with MI and rehospitalization for acute coronary syndrome
|
|
|
what are the glycoprotein IIb/IIIa receptor antagonist drugs
|
abciximab, tirofiban and eptifibatide
|
|
|
what is heparin
|
an anticoagulant given by IV or SC route and is used in conjuncture with antiplatelets in unstable angina to prevent thrombus formation.
|
|
|
what are lipid-lowering agents used with
|
used in conjunction with drugs to treat angina to slow the progression of coronary heart disease
|
|
|
when is an ACE inhibitor used with angina
|
used in patients with coronary artery disease if they also have diabetes, systolic dysfunction, or both
|
|
|
when is morphine used in angina
|
used to treat pain if unstable acute angina is not controlled by nitrates
|
|
|
how do nitrates improve the circulation to the heart itself
|
redistributing blood flow to the collateral vessels
|
|
|
what is nitroglycerine
|
a nitrate and use varies by route of administration
|
|
|
what is nitroglycerine given topical, sublingual or transmucosal or translingual spray used to treat
|
acute angina or to prevent chronic recurrent angina
|
|
|
what is an IV nitroglycerine used for
|
hypertension secondary to surgical procedures, to create controlled hypotension during anesthesia, to treat CHF associated with acute MI and to treat angina unresponsive to organic nitrates or beta blockers
|
|
|
how does nitroglycerine work
|
relaxes vascular smooth muscle and dilates both arterial and venous vessels
|
|
|
what are the contraindications with nitroglycerine
|
severe anemia and closed angle glaucoma
|
|
|
what are the adverse effects of nitroglycerine
|
headache, hypotension, postural hypotension, tachycardia, syncope, vertigo, anxiety, and weakness
|
|
|
what are the drug interaction of nitroglycerine
|
erectile dysfunction drugs
|
|
|
what should you assess before starting nitroglycerine
|
type of angina
|
|
|
how do you maximize the therapeutic effects of the nitroglycerine sublingual tablets
|
administer a tablet every 5 minutes up to three in 15 minutes if necessary. Have the patient lie down and avoid exposure to high temperatures or sunlight
|
|
|
how do you maximize the therapeutic effects of the nitroglycerine IV
|
dilute drug only into glass parenteral solution bottles and administer using tubing not made from polyvinyl chloride
|
|
|
how do you minimize the adverse effects of the nitroglycerine
|
assess the patients pulse and blood pressure before administering drug therapy, monitor for orthostatic hypotension and assist the patient to a standing position gradually when arising, treat any headache that develops with aspirin or acetaminophen
|
|
|
how often should transdermal nitroglycerine patch be removed and why
|
every 10-12 hours every 24 hours to prevent tolerance
|
|
|
what should you assess in IV nitroglycerine
|
alcohol intoxication and blood pressure and heart rate
|
|
|
what are drugs affecting cardiac rhythm
|
class I antiarrhythics, class II antiarrhytimics (beta blockers), class III antiarrhythmics, Class IV antiarrhythmics (calcium channel blockers), Postassium-removing resins
|
|
|
what are the types of Class I antiarrhythmics
|
Class 1A, Class 1B, Class 1C
|
|
|
what is the prototype class 1 antiarrhythmics
|
quinidine which is in class 1A
|
|
|
what are the types of Class II antiarrhythmics
|
beta blockers approved as antiarrhythmics and beta blockers not approved as antiarrhymics
|
|
|
what is the prototype class II antiarrhythmics
|
propanolol
|
|
|
what is the prototype class III antiarrhythmics
|
amiodarone
|
|
|
what are the types of class IV antiarrhythmics
|
calcium channel blockers approved as antiarrhythmics, non-calcium channel blockers, calcium channel blockers not approved as antiarrhythmics
|
|
|
what is the prototype Class IV antiarrhythmics
|
verapamil
|
|
|
what is the prototype potassium removing resins
|
sodium polystyrene sulfonate
|
|
|
what is arrhythmia
|
occurs any time the normal rate or rhythm of the heart is altered. The heart continues to beat but not in the expected pattern or manner.
|
|
|
what does dysrhythmia mean
|
Used interchangeably with arrhythmia and is preferred by many clinicians
|
|
|
what are the contractions of the heart dependent on
|
electrical conduction system of the cardiac muscle
|
|
|
what is the electrical system consist of
|
sinoatrial node, atrioventricular node, bundle of HIS, bundle branches and purkinje fibers
|
|
|
what are the waves of an EKG
|
P, QRS, T
|
|
|
what is the P wave
|
atrial depolarization
|
|
|
What is the PR segment
|
when the impulse leaves the atria and is slowed at the AV node so the atria and ventricles do not contract simultaneously
|
|
|
what is the PR interval
|
all electrical activity in the heart that takes place before the impulse reaches the ventricles. Has P wave and PR segment
|
|
|
What is the QRS wave
|
ventricle depolarization
|
|
|
what is the T wave
|
ventricular repolarization
|
|
|
what ions have an effect on the electrical changes in the heart
|
potassium (intracellular), sodium, calcium (extracellular)
|
|
|
what is the transmembrane potential
|
the electrical gradient that exits across the membrane of the cell because of the different concentrations of intracellular and extracellular ions
|
|
|
what is the action potential
|
all changes that occur in the transmembrane potential during an entire cycle of contraction and relaxation
|
|
|
what in the resting membrane potential
|
electrical charge of the transmembrane potential at rest -90mV.
|
|
|
when does depolarization occur
|
when sodium moves into the cell and transmembrane potential changes from negative to positive.
|
|
|
what is depolarization called
|
phase 0 of the action potential
|
|
|
what is repolarization
|
the movement of the transmembrane potential away from a positive value and toward the negative resting potential
|
|
|
what is phase 1 of the action potential
|
the initial downward movement toward zero after depolarization
|
|
|
what is phase 2 of action potential
|
plateau phase, where the calcium channels open slowly, positively charged calcium channels close, potassium channels open and potassium moves out of the cell. This is the difference between action potential of the cardiac muscle and skeletal muscles
|
|
|
what is phase 3 of action potential
|
rapid acceleration of repolarization
|
|
|
what is phase 4 of action potential
|
when full polarization is achieved and sodium and potassium have gradually returned to their original locations
|
|
|
hat is the refractory period
|
after the cell depolarizes and until it resores its normal electrical charge, it cannot be stimulated ot fire again
|
|
|
what is calcium need for in the heart
|
contraction of the heart. It links excitation to contraction. It goes into the cell and stimulates the release of calcium stored in the sarcoplasmic reticulum which induces a contraction
|
|
|
what is the main cause of cardiac arrhythmia
|
changes in the ionic currents through ion channels of the myocardial cell membrane
|
|
|
what do dysrhymias do to the heart
|
increase oxygen demand of the heart, and interfere with cardiac output, and disrupt function
|
|
|
what are the ways ionic changes allow arrhythmias to develop
|
through a disorder with formation, through a disorder of the impulse conduction system, or through a combination of both
|
|
|
what happens when a disorder of impulse formation is present
|
the rate of SA nodal discharges is altered allowing changes in the automaticity of the heart
|
|
|
what is automaticity
|
ability to generate an impulse spontaneously
|
|
|
what does decrease automaticity do
|
leads to sinus bradycardia,
|
|
|
what does an increase in automaticity lead to
|
sinus tachycardia
|
|
|
what does changes in automaticity come from
|
drug toxicity such as form digoxin or of excessive sympathetic activity
|
|
|
what are ectopic foci
|
a different problem with automaticy where the SA nodal rate decreases excessively and other excitable heart tissue reaches the threshold potential earlier than the SA node, generating an impulse
|
|
|
what causes ectopic foci
|
hypokalemia, myocardial ischemia, emotional stress, or hypoxia.
|
|
|
where will ectopic foci arise
|
in atrial, nodal, purkinje or ventricular muscles
|
|
|
what do disorders of impulse conduction result from
|
alteration in either the rate or the pathway of impulse conduction.
|
|
|
when does heart block occur
|
when conduction of the impulses through the AV node is delayed
|
|
|
what is the re-entry phenomenon
|
common source of alterations of impulse formation, where there is a block in a purkinje fiber or small branch fibers and the impulse cannot continue to travel in its normal forward path, so it re-enters the branch from the opposite side
|
|
|
what does re-entry cause
|
repetitive cardiac stimulation, firing, and arrhythmias
|
|
|
where do the arrhytmias occur
|
atria or ventricles
|
|
|
what is an atrial flutter
|
an arrhythmia originating in the atria, that has rapid atrial beating but a slower, regular or irregular, ventricular beating
|
|
|
what is atrial fibrillation
|
caused by rapid, irregular discharges form multiple atrial ectopic foci which leads to quivering of the atria without the occurrence of a true diastole or atrial contraction. Impulses are transmitted irregularly though the AV node, producing an irregular ventricular response
|
|
|
what are the types of AFib
|
first detected, recurrent, and permanents AFib. Recurrent has paroxysmal and persistent sub-groups
|
|
|
how do you manage AFib
|
rhythm control-cardioversion followed by maintenance of sinus rhythm with arrhythmic drugs
rate control-use of AV nodal blockers plus anticoagulation |
|
|
what is ventricular tachycardia
|
rapid ventricular beating arising from ventricular ectopic foci
|
|
|
what is ventricular fibrillation
|
quivering of the ventricle without a systolic beat. brain damage can occur
|
|
|
when do ventricular tachycardia and ventricular fibrillation occur
|
after an acute MI
|
|
|
what is used to treat arrhythmias
|
drugs and implantable cardioverter defibrillator (ICD) to prevent reoccurrence of some arrhythmias, can be treated with catheter ablation and antiarrhythmics
|
|
|
what are antiarrhythmic agents used for
|
prevent, suppress, or treat a disturbance in cardiac rhythm
|
|
|
what are the primary outcomes for antiarrhythmics
|
to decrease automaticity, decrease speed of conduction, and decrease reentry
|
|
|
what is proarrhythmia
|
antiarrhythmics can cause a new arrhythmia or exacerbate the arrhythmia they are treating because of their ability to modify the rhythm of the heart
|
|
|
what do class I antiarryhthmic drugs do
|
block sodium channels
|
|
|
what is the difference between class IA, IB, and IC antiarrythmic drugs
|
IB is fast, IC is slow, and IA is intermediate
|
|
|
What do class II antiarrhythmic drugs do
|
block adrenergic receptors (beta blockers) producing antisympathetic effects that slow heart rate, lengthen the time needed for conduction, and increase the force of contraction.
|
|
|
what are Class I antiarrhythmic drugs
|
local anesthetics or membrane-stabilizing agents that depress phase 0 in depolarization
|
|
|
what is quinidine
|
a Class IA antiarrhythmic drug used to treat atrial arrhythmias such as atrial flutter and fibrillation
|
|
|
how does quinidine work
|
decreases myocardial excitability, conduction velocity and contractility. The effective refractory period is prolonged so re-entry phenomena is prevented and conduction time is increased. And it also exerts an indirect anticholinergic effect which decreases vagal tone and may promote conduction in the AV junction
|
|
|
what are the contraindications of quinidine
|
cardiac arrhythmias related to conduction abnormalities (complete heart block, left bundle branch block, complete atrioventricular block, long QT syndrome, and drug-induced torsades de pointes) and myasthenia gravis
|
|
|
what are the adverse effects of quinidine
|
nausea, vomiting, abdominal pain, diarrhea, anorexia and cardiotoxicity
|
|
|
what should you assess on before giving quinidine
|
determine whether the patient has a type of atrial arrhythmia that is an indication for therapy and adequate potassium intake
|
|
|
how do you maximize the therapeutic effects of quinidine
|
adjust dose until reaching therapeutic range and maintain potassium at normal levels. monitor serum potassium levels
|
|
|
how do you minimize the adverse effects of quinidine
|
administer oral quinidine with food to prevent GI upset and thus avoid altered nutrition. Use infusion pump if given with an IV and monitor the EKG
|
|
|
what are the class IB antiarrhythmics
|
lidocaine and tocainide, mexiletine, moricizine, phenytoin
|
|
|
what do class IB antiarrhythmics do
|
depress phase 0 and unlike quinidine suppress automaticity and are used primarily with life-threatening ventricular arrhythmias and may shorten the duration of the action potential duration. Like quinidine they may also cause arrhythmias
|
|
|
what is lidocaine used for
|
all acute ventricular arrhythmias that are related to cardiac surgery or acute MI because they are life threatening.
|
|
|
what do class II antiarrhythmic drugs do
|
beta blockers that depress phase 4 depolarization. They slow heart rate by suppressing the SA node, slow the speed of conduction through the AV node, and decrease the force of contraction
|
|
|
Who are class II antiarrhythmic drugs used on
|
reduce mortality in patients who have had recent MI, those with symptomatic heart failure and those with congenital long QT syndrome
|
|
|
Beta blockers are the most effective drugs for what
|
controlling the ventricular rate in AFib
|
|
|
what is propranolol
|
class II antiarrhythmic drug used for treating cardiac arrhythmias, specifically ventricular arrhythmias post-MI, tachyarrhythmias secondary to digoxin toxicity, and SVT (AFib or atrial flutter)
|
|
|
what do class III antiarrhythmic drugs do
|
produce a prolongation of phase 3 (repolarization). It prolonges action potential duration and refractory periods leading to reduction in membrane excitability of all myocardial tissue
|
|
|
What is amiodarone
|
a class III antiarrhythmic drug used in life threatening arrhythmias such as recurrent or life-threatening ventricular fibrillation, and recurrent, hemodynamically unstable ventricular tachycardia
|
|
|
how does amiodarone work
|
prolongation of the refractory period and noncompetitive alpha and beta adrenergic inhibition
|
|
|
what are the contraindications and precautions of amiodarone
|
severe sinus-node dysfunction, 2nd and 3rd degree AV block, severe sinus bradycardia
|
|
|
what are the adverse effects of amiodarone
|
pulmonary toxicity, exacerbation of the arrhythmia and liver disease, CNS effects, GI effects, photosensitivity, hypotension in IV use
|
|
|
how do you maximize the therapeutic effects of amiodarone
|
administer loading doses, mix the drug in glass bottles or polyolefine bags, use a volumetric infusion pump to prevent underdosage
|
|
|
how do you minimize the adverse effects of amiodarone
|
correct pre-existing electrolyte disturbances, use pulse oximetry or arterial blood cases to assess for changes in respiratory function, assess for symptoms of visual impairment, monitor blood pressure and EKG, adjust IV dose to control ventricular arrhythmia
|
|
|
what are the drugs related to amiodarone
|
sotalol, bretylium, ibutilide, dofetilide
|
|
|
what do the Class IV antiarrhythmic drugs do
|
depress phase 4 depolarization and lengthen phases 1 and 2 of repolarization
|
|
|
what is verapamil
|
a class IV antiarrhythmic drug and calcium channel blocker used for chronic atrial flutter or fibrillation, used with digoxin for repetitive paroxysmal supraventricular tachycardia and to treat supra-ventricular tachyarrhythmias and angina and hypertension
|
|
|
how does verapamil work
|
inhibits the movement of calcium ions across the cardiac and arterial muscle cell membrane which slows conduction, depresses automaticity, depresses myocardial contractility, and dilates coronary arteries and peripheral arterioles
|
|
|
what are the contraindications of verapamil
|
sick sinus syndrome, 2nd or 3rd degree heart block, hypotension, severe left ventricular dysfunction, severe chronic heart failure, or cardiogenic shock
|
|
|
what are the adverse effects of verapamil
|
constipation, dizziness, headache, nausea, hypotension, and peripheral edema and ventricular arrhythmias
|
|
|
what is the life span alert of verapamil
|
IV route in contraindicated in neonates and infants and older adults are more sensitive to hypotensive effects
|
|
|
how do you maximize the therapeutic effects verapamil
|
verify that the IV line is patent before IV administration, shield drug solution form light, give with digoxin
|
|
|
how do you minimize the adverse effects of verapamil
|
monitor ECK and blood pressure constantly while on IV, and monitor periodically throughout oral therapy, do not dilute it with sodium lactate and don't give with beta blockers
|
|
|
what do potassium-removing resins do
|
because hyperkalemia may lead to cardiac arrhythmias, potassium-removing resins are drugs used to prevent arrhythmias form occurring.
|
|
|
How do potassium-removing resins work
|
bind with potassium and allow it to be excreted
|
|
|
what is sodium polystyrene sulfonate
|
a potassium-removing resin used in treating hyperkalemia which can lead to arrhythmias
|
|
|
how does sodium polystyrene sulfonate work
|
release sodium ions that are replaced with potassium ions
|
|
|
what are the contraindications of sodium polystyrene sulfonate
|
anyone who cannot tolerate a small increase in sodium intake, extremely high potassium levels who need fast acting effects
|
|
|
what are the adverse effects of sodium polystyrene sulfonate
|
hypokalemia, other electrolyte imbalances, gastric irritation, anorexia, nausea, vomiting, and constipation
|
|
|
how do you maximize the therapeutic effects of sodium polystyrene sulfonate
|
give a cleansing enema first and leave resin in place at least 30 minutes after administering as enema, create a suspension of the powdered formula with water or syrup
|
|
|
how do you minimize the adverse effects of sodium polystyrene sulfonate
|
monitor serum electrolytes and EKG and if there is severe hyperkalemia, used othr methods to reduce potassium
|
|
|
what are the drugs affecting coagulation
|
hypercoagulation and hypocoagulation drugs
|
|
|
what are the types of hypercoagulation drugs
|
anticoagulants, direct thrombin inhibitors, antiplatelets, hemorhegologics, thrombolytics
|
|
|
what are the types of hypocoagulation drugs
|
clotting factors and hemostatics
|
|
|
what is the prototype anticoagulant
|
heparin
|
|
|
what is the prototype direct thrombin inhibitor
|
warfarin
|
|
|
what is the prototype antiplatelet
|
clopidogrel
|
|
|
what is the hemorheologic
|
pentoxifylline
|
|
|
what is the prototype thrombolytics
|
alteplase, recombinant
|
|
|
what is the prototype clotting factor
|
antihemophilic factor
|
|
|
what is the prototype hemostatic
|
aminocaproic acid
|
|
|
what is hemostasis
|
series of events that happens when body starts to blood. Slow blood flow, stop blood loss at the injury site, and prevent extensive blood loss
|
|
|
what does hypercoagulation result in
|
a thrombus (blood clot)
|
|
|
what is hemophilia
|
uncontrollable bleeding
|
|
|
what is fibrinolysis
|
the process of breaking down a formed clot
|
|
|
what are substances that promote coagulation
|
platelets, progocagulatns and cotting factors
|
|
|
what are clotting factors
|
plasma proteins that cause blood clotting
|
|
|
what is the clotting cascade
|
it is the act that is initiated by tissue damage and platelet activation, which mobilize the clotting factors circulating in the blood which then work with calcium to form fibrin
|
|
|
what are the two pathways to the clotting cascade
|
intrinsic and extrinsic
|
|
|
how is the intrinsic pathway activated
|
by injury to blood vessel
|
|
|
what does the intrinsic pathway lead to
|
formation of thrombin and then fibrin stabilized which means a stable blood clot is made
|
|
|
what activates the extrinsic pathway
|
tissue damage
|
|
|
how does the extrinsic pathway end
|
same way as intrinsic with the formation of thrombin and a fibrin stabilized clot
|
|
|
what are the key inhibitors of coagulation
|
tissue factor pathway inhibitor, antithrombin, and protein C pathway
|
|
|
what is fibrinolysis
|
process that lyses the fibrin in a clot after the bleeding stops
|
|
|
what lyses a blood clot
|
plasmin
|
|
|
when does coagulation occur
|
when blood flow is impeded and slowed in an area which leads to formation of a thrombus
|
|
|
what is an embolism
|
any undissolved matter carried in a blood or lymph vessel to another location where it lodges and occludes the vessel
|
|
|
what is a thromboembolus
|
when a portion of a thrombus breaks off, the fragment may travel through the blood stream and lodge in a vessel
|
|
|
what happens when a thromboembolus is lodged in a coronary vessel
|
a myocardial infarction occurs
|
|
|
what happens when a thromboembolus is lodged in a brain vessel
|
CVA or stroke occurs
|
|
|
what makes up an arterial thrombosis and what does an arterial thrombosis lead to
|
it is made up of platelet aggregates held closely together by fibrin and is the most common cause of MI, stroke, and limb gangrene
|
|
|
what makes up a venous thrombosis and what does it lead too
|
made up of mostly red cells and fibrin and leads to pulmonary embolism and postphlebitic syndrome
|
|
|
where do venous thrombi most often occur
|
in the deep vessels of the lower limbs (DVT)
|
|
|
what causes blood to slow in vessels
|
narrowing of lumen or fatty deposits in lumen cause lumen to constrict
|
|
|
what does decrease blood flow cause
|
stasis, which leads to blood coagulation
|
|
|
when doesn't blood clotting occur
|
when clotting factors are deficient
|
|
|
what are 3 hemophilic conditions caused by inherited deficiencies of specific clotting factors
|
hemophilia A (classic hemophilia)
Hemohilia B (christmas disease) von Willebrand disease |
|
|
decreased synthesis of clotting factors usually indicates what kind of disease
|
liver such as hepatitis and cirrhosis because thats where most clotting factors are created
|
|
|
when does fibrinolysis normally occur
|
balance with blood coagulation
|
|
|
what makes heparin
|
mast cells located in the connective tissue throughout the body
|
|
|
what do anticoagulants do
|
interfere with the clotting cascade and prolong blood clotting time
|
|
|
what are the two types ow anticoagulants
|
parenteral and oral
|
|
|
how do parenteral anticoagulants work
|
preventing the conversion of fibrinogen to fibrin
|
|
|
how do oral anticoagulants work
|
preventing synthesis of factors dependent on vitamin K for synthesis
|
|
|
what is heparin
|
a parenteral anticoagulant that interferes with the final steps of the clotting cascade. It prevents formation or extensions of blood clots but has no effect on existing blood clots
|
|
|
how does heparin work
|
rapidly promotes the inactivation of factor X, which, in turn, prevents the conversion of prothrombin to thrombin and also effects fibrin limiting the formation of a stable clot.
|
|
|
what are the contraindications of heparin
|
thrombocytopenia, bleeding disorders, and active bleeding other than DIC
|
|
|
what are the adverse effects of heparin
|
bleeding and thrombocytopenia
|
|
|
what is the life span alert for heparin
|
the anticoagulant that can be used during pregnancy
|
|
|
what is the safety alert for heparin
|
check concentration of heparin carefully. use of the wrong concentration for the route of administration is a common medication error
|
|
|
what should you review before giving heparin
|
allergies or prolonged bleeding times
|
|
|
how do you maximize the therapeutic effects of heparin
|
monitor laboratory values, allow heparin levels to reach steady state before aPTT is measured
|
|
|
how do you minimize the adverse effects of heparin
|
assess for signs of bleeding, Use IV pump, if aPTT during treatment exceeds the desired range, the dosage should be decreased
|
|
|
what is the antidote for heparin
|
protamine sulfate
|
|
|
what is warfarin
|
oral from of an anticoagulant that is used prophylactically for patients with a long term risk for thrombus formation (when mitral valve has been replaced or when hypercoagulability is a chronic concern related to venous stasis) or used right after heparin therapy to complete treating a thrombus or embolism
|
|
|
how does warfarin work
|
competitively blocks vitamin K at its sites of action
|
|
|
what are the contraindications of warfarin
|
active bleeding or bleeding disorders, ulcerations of the GI tract or bleeding disorders
|
|
|
what are the adverse effects of warfarin
|
bleeding, hemorrhage and fetal warfarin syndrome
|
|
|
what is the life span alert for warfarin
|
pregnant women
|
|
|
how do you maximize the therapeutic effects of warfarin
|
warfarin dosage should be individualized until PT or INR is in therapeutic range
|
|
|
how do you minimize the adverse effects of warfarin
|
monitor for signs of bleeding, antidote is vitamin K.
|
|
|
what is an inherited trait that can effect warfarin
|
inherited variations of P-450 may alter drug response
|
|
|
what is PT and INR
|
prothrombin time and International Normalize Ratio
|
|
|
what are the drugs like heparin
|
enoxaparin, dalteparin, tinzaparin, fondaparinux
|
|
|
what are the drugs different from warfarin
|
anisindione
|
|
|
what are antiplatelet drugs
|
drugs that prevent platelet aggregation
|
|
|
when are antiplatelet drugs used
|
when overactive platelets pose long term risks for hypercoagulability
|
|
|
what kinds of patients are given antiplatelet drugs
|
those who have suffered MI, ischemic stroke or transient ischemic attack, or unstable angina and for primary prevention of a thromboembolic event in patients at risk
|
|
|
what is clopidogrel
|
an antiplatelet used to reduce atherosclerotic events (MI, stroke, and vascular death)
|
|
|
how does clopidogrel work
|
inhibits the binding of adensosine diphosphae (ADP) to its platelet receptor and the subsequent ADP-mediated activation of the glycoprotein IIb/IIIa complex and thus inhibits platelet aggregation which increases bleeding time
|
|
|
what are the contraindications of clopidogrel
|
active bleeding disorders such as peptic ulcers or intracranial hemorrhage.
|
|
|
what are the adverse effects of clopidogrel
|
bleeding, GI distress, and neutropenia
|
|
|
how do you maximize the therapeutic effects of clopidogrel
|
ensure that it is administered routinely
|
|
|
how do you minimize the adverse effects of clopidogrel
|
take clopidogrel with food to decrease GI problems, assess risk for falls and injuries and remove any hazards that can contribute to falls in the home
|
|
|
what do hemorheologic drugs do
|
act on RBCs to reduce blood viscosity and increase the flexibility of RBCs which prevent thrombus formation and increases oxygenations at cellular level
|
|
|
what are the drugs closely related to clopidogrel
|
aspirin, cilostazol, ticlopidine
|
|
|
what are drugs different from clopidogrel
|
dipyridamole, glycoprotein IIb/IIIa inhibitors, anagrelide
|
|
|
what is pentoxifylline
|
a hemorheolgoic drug used to manage symptoms of intermittent claudication from peripheral vascular disease. This durg improves the patients ability to walk for longer distances without pain
|
|
|
how does pentoxifylline work
|
increases flexibility of RBCs by increases cAMP levels which decreases platelet aggregation and promotes vasodilation. and increases cellular adenosine triphosphate levels which lowers blood viscosity
|
|
|
what are the contraindications of pentoxifylline
|
intolerance to methylxanthines (caffines)
|
|
|
what are the adverse effects of pentoxifylline
|
headache, dizziness, tremor, dyspepsia, nausea, vomiting and tachycardia.
|
|
|
how do you maximize the therapeutic effects of pentoxifylline
|
must be taken for several weeks before the full therapeutic effects are evident and peripheral circulation should be reassessed periodically to measure improvement
|
|
|
how do you minimize the adverse effects of pentoxifylline
|
give pentoxifylline with food to minimize GI upset
|
|
|
what do thrombolytic drugs to
|
assist in breaking down formed blood clots
|
|
|
how are thrombolytic drugs used in
|
patients who are diagnosed with an evolving acute MI; a PE; or acute ischemic stroke. also used to unclog central venous catheters
|
|
|
who are thrombolytic drugs used
|
only in emergency situations
|
|
|
what is alteplase, recombinant
|
a thrombolytic drug used to treat thromboembolic conditions in emergency situations
|
|
|
how does alteplase work
|
by binding to fibrin in a clot and converting the trapped plasminogen to plasmin and fibrinolysis occurs
|
|
|
what are the contraindications of alterplase, recombinant
|
active internal bleeding, especially intracranial, recent surgeries or medical events in which patient bled or which put patient at risk for bleeding now, seizure at onset of stroke, of severe uncontrolled hypertension
|
|
|
what are the adverse effects of alterplase, recombinant
|
internal or superficial bleeding,
|
|
|
what is the life span alert of alteplase, recombinant
|
current pregnancy or delivery of a child within the last 10 days and older adults are more likely to have intracranial bleeding
|
|
|
how do you maximize the therapeutic effects of alteplase recombinant
|
reconstitute alteplae, recombinant in sterile water for injection without preservatives, avoid vigorous shaking or agitation when reconstituting
|
|
|
how do you minimize the adverse effects of alteplase recombinant
|
closely and continually monitor vital signs and observe for signs of active bleeding. patient should be connected to a cardiac monitor, both during treatment and afterward, avoid venipuncture and arterial puncture, used pressure dressings when needed, handle patient gently
|
|
|
when should alteplase recombinant be used when treating ischemic stroke
|
3 hours
|
|
|
what are drugs closely related to alteplase, recombinant
|
thrombolytic enzymes: streptokinase, urokinase and anistreplase
|
|
|
what are drugs different from alteplase, recombinant
|
drotrecogin alfa
|
|
|
how do clotting factors work
|
replace absent clotting factors that are inherited
|
|
|
what is antihemophilic factors
|
clotting factors that provides factor VIII for those with hemophilia A. It is used to prevent and control excessive bleeding
|
|
|
how do antihemophilic factors work
|
provides factor VIII which is an essential component of blood clotting. it converts prothrombin to thrombin
|
|
|
what is a contraindication to antihemophilic factor
|
hypersensitivity to mouse protein
|
|
|
what are the adverse effects of antihemophilic factor
|
anaphlaxis, urticaria, nausea, chills, hemolytic anemia and transmission of hepatitis of HIV
|
|
|
how do you maximize therapeutic effects of antihemohilic factor
|
refrigerate AHF until use, before reconstitution warm the concentrate and the diluent to room temperature
|
|
|
how do you minimize the adverse effects of antihemophilic factor
|
after dilution administer AHF within 3 hours to precent bacterial growth, administer IV route only, monitor hematocrit and Coombs test result (hemolytic anemia)
|
|
|
who do hemostatic drugs work
|
stop blood loss by enhancing blood coagulation
|
|
|
what are the two types of hemostatic drugs
|
systemic agents and topical agents
|
|
|
how do systemic agents work
|
interfere with the breakdown of clots
|
|
|
how do topical agents work
|
used to control small amount of bleeding or oozing, uaually following surgery
|
|
|
what is aminocaproic acid
|
a hemostatic drug used to treat life threatening hemorrhage and bleeding from systemic hyperfibrinolysis or urinary fibrinolysis
|
|
|
how does aminocaproic acid work
|
blocks the action of plasminogen activators, interferes with the binding of active plasmin to fibrin
|
|
|
what are the contraindications of aminocaproic acid
|
use only in life-threatening situations and only when the overactivity of the fibrinolytic system is verified by laboratory testing, active intravascular clotting disorders
|
|
|
what are the adverse effects of aminocaproic acid
|
GI distress, headache, dizziness, seizures, hypotension, arrhythmias, tinnitus, nasal congestion, vomiting, abdominal cramps, diarrhea, diuresis, renal failure, rhabdomyolysis, thromboembolism
|
|
|
how do you minimize the adverse effects of aminocaproic acid
|
use IV pump, assess for bleeding or signs of thromboembolism, and place patient on cardiac monitor to detect arrhythmias, monitor vital signs throughout therapy, monitor intake and output and monitoring neurologic status
|
|
|
what are the drugs affecting the immune response
|
cytokines, immune modulators, antibodies
|
|
|
what is the prototype cytokine
|
interferon alfa-2a
|
|
|
what is the immune modulator prototype
|
cyclosporine
|
|
|
what is the antibodies prototype drug
|
rituximab
|
|
|
what are biologic modulators
|
group of biopharmaceuticals that are naturally occurring proteins used to alter the body immunologic responses
|
|
|
what is an autoimmune disease
|
when the body is inappropriately rejecting its self
|
|
|
what are antiangiogenesis
|
drugs that block blood vessel deveopmetn via the tyrosine kinase and teh VEGF pathways
|
|
|
what are tyrosine kinase inhibitors
|
agents targeted against cellular enzymes that are essential for tumor replication
|
|
|
what are monoclonal antibodies
|
can be engineered to attach to tumor cells for diagnosis or treatment of malignancies or target T lymphocytes to prevent or suppress T-cell recognition of tissue from outside the body
|
|
|
what is the immune system composed of
|
hematopoietic cells and multiple hematologic-immunologic production and storage sites
|
|
|
what is teh immune system composed of
|
hematopoietic cells and multiple hematologic-immunologic production and storage sites
|
|
|
what does the reticuloendothelial system include
|
immunologicaly active tissue and cells found in the lymph system, spleen, liver, lungs, GI tract, and brain
|
|
|
what do integrated immune response involving hematopoietic cells and immune tissues
|
provides the bodys nonspecific and specific response to invasion by antigens identified as nonself
|
|
|
what are the essential components of the immune response
|
hematopoietic cells, barrier defenses, the nonspecific immune response, the specific immune response and immunity
|
|
|
what are the two types of lymphocytes and what are they used for
|
T lymphocytes (T cells), B lymphocytes (B cells)
|
|
|
what are the 3 types of cells that T cells develop into
|
T4 helper cells, suppressor T cells, lymphokines
|
|
|
what do T4 helper cells do
|
stimulate other lymphocytes
|
|
|
what do suppressor T cells do
|
slow immune response, conserve energy,
|
|
|
what do lymhokines do
|
destroy foreign cells or maker them for destruction which causes the inflammatory response to be elicited
|
|
|
what is the cellular immune response
|
when lymphokines either directly destroy a foreign cell or mark it for destruction by phagocytes and elicit an inflammatory response
|
|
|
what are plasma cells
|
when B cells react with its specific antigen it changes into a plasma cell which produce antibodies or immunoglobins and react with their specific antigen and create antigen-antibody complex
|
|
|
what does the antigen-antibody complex do
|
reveals a new receptor site on the antibody that activates a series of plasma proteins in the body called complement
|
|
|
what do complement proteins do
|
destroy antigen by altering the membrane and allowing osmotic inflow of fluid that bursts the cell and induce chemotaxis and vasodilation
|
|
|
what are interleukins
|
chemicals secreted by active WBCs to influence other WBCs
|
|
|
what are teh four abnormal conditions that can weaken the immune system and stimulate immune response
|
neoplasms, viral invasion, autoimmune disease, and transplant rejection
|
|
|
what do neoplasms come from
|
the result from the growth of mutant cells
|
|
|
what does a viral invasion of a cell do
|
changes the cells membrane and antigenic presentation
|
|
|
what happens in autoimmune disease
|
the body responds to specific self-antigens by producing antibodies against self-cells (autoantibodies)
|
|
|
what does an organ transplantation do
|
weakens the immune system as the body reacts to the introduction of foreign cells
|
|
|
what are cytokines
|
chemical mediators released by WBCs in response to antigenic invasion of the blood or tissues
|
|
|
what do cytokines do
|
serve to enhance and accelerate the inflammatory and specific responses that will destroy the invading antigen
|
|
|
what are the properties of cytokines
|
generally proinflammatory but also have antiviral, antiproliferative, and antineoplasic properties
|
|
|
what is interferon alfa-2a
|
a cytokine used to treat hairy cell leukemia, AIDS related- kaposi sarcoma and chronic hepatitis and various cancers
|
|
|
how does interferon alfa-2a
|
inhibits the growth of tumor cells, prevents their multiplication and heightens the host immune responses to help protect the body from tumor cells. Blocks specifically viral infection by preventing viral replication
|
|
|
what are the adverse effects of interferon alfa-2a
|
pancreatitis, hepatic, renal disease, flue-like symptoms, lethargy, anorexia, nausea, and changes in taste, depression and suicidal ideation
|
|
|
what is the life span alert of interferon alfa-2a
|
avoid during pregnancy if possible
|
|
|
how do you maximize the therapeutic effects of interferon alfa-2a
|
reconstitute and store following manufacturers' instructions, obtain baseline blood counts and chemistries before therapy and at least monthly during therapy
|
|
|
how do you minimize the adverse effects of interferon alfa-2a
|
premedicate patients with drugs such as acetaminophen or diphenhydramine to reduce the flu-like adverse effects
|
|
|
what is rituximab
|
antibody drug used to treat relapsed or refractory B-cell non-hodgkin's lymphoma
|
|
|
how does rituximab work
|
a monoclonal antibody that binds specifically to the CD20 antigen found on the surface of normal and malignant B lymphocytes and cause cell lysis what are the ocntrain
|
|
|
what are the adverse effects of rituximab
|
nausea, urticaria, fatigue, headache, pruritus, bronchospasm,dyspnea, hypotension, angioedema, rhinitis, vomiting, flushing, pain and disease sites, and throat swelling
|
|
|
what is the span alert of rituximab
|
use birth control during therapy a for 1 year afterward and avoid breast-feeding during this time; use with caution in older adults
|
|
|
how do you maximize the therapeutic effects of rituximab
|
administer in saline or dextrose stored in plastic bags, not glass
|
|
|
how do you minimize the adverse effects of rituximab
|
premedicate patient to prevent infusion-related adverse effects, patients with cardiac of pulmonary risk factors should have continuous cardiac monitoring and frequent vital sign assessment
|
|
|
what is the health status you should assess for before giveing rituximab
|
respiratoy and cardiac conditions
|
|
|
what do immune modulators do
|
act directly on the function of T cells and B cells, stimulating or suppressing the immune response
|
|
|
what are lymphocytic modulators divided into
|
subcategories according to their primary chemical structure and pharmacologic properties
|
|
|
what is cyclosporine
|
an immune modulator used in the adjunct treatment to prevent rejection in solid organ transplantation and to prevent graft-vs-host disease in allogeneic bone marrow or stem cell transplant recipients
|
|
|
how does cyclosporine work
|
inhibits T-lymphocytes by causing cytotoxicity during the G0 and G1 phase
|
|
|
what are the contraindications of cyclosporine
|
hypersensitivity to polyoxyethylated
|
|
|
what are the adverse effects of cyclosporine
|
hepatotoxicity, nephrotoxicity, tremor, hirsutism, hypertension and gum hyperplasia
|
|
|
what are the life span alert of cyclosporine
|
children may need higher doses; therapy usually avoided during pregnancy
|
|
|
what should you assess before giving cyclosporine
|
assess current medications and exposure to crowds
|
|
|
ho do you maximize the therapeutic effects of cyclosporine
|
ensure that cyclosporine therapy is started soon after transplantation , oral form should be used as soon as possible
|
|
|
how do you minimize the adverse effects of cyclosporine
|
arrange for periodic blood tests to monitor for renal, hepatic, and hematologic effects of the medication
|
|
|
what are the types of drugs affect corticosteroid levels
|
steroid hormone agonists , steroid hormone antagonists and mineralocorticoids
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what are the types of steroid hormone agonists
|
glucoscortioids, inhaled glucocorticoids, topical glucocorticoids, intra-articulary injected glucocortioids
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what is the prototype glucocorticoid
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prednisone
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what are the steroid hormone antagonists
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aminoglutethimide
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what are the mineralocorticoids prototype
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fludrocortisone
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what are corticosteroids used for
|
replacement therapy to maintain adequate levels of hormones in patients with inadequate adrenal function
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what are the parts of the adrenal gland
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medulla and cortex
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what do the medulla and cortex do
|
crucial to metabolism, the body's stress response, and fluid and electrolyte balances
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what does the medulla do
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synthesizes and secrete catecholamines- epinephrine and norepinephrine
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what does the cortex do
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synthesis and secretion of glucocorticoids and mineralocorticoids from plasma-derived, low-density lipoproteins and high density lipoproteins
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what are glucocorticoids produced in the adrenal gland
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cortisol and cortisone
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what do glucocorticoid steroids do in glucose metabolism
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increase blood glucose concentrations
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what does cortisol do
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sensitizes the arterioles to norepinephrine for vasopressor effects and allows epinephrine and glucagon to activate gluconeogenesis and glycogenolysis
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what is the most prevalent mineralocorticoid
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alderosterone
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what do mineralocorticoids do
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exert a major influence on regulating potassium, sodium and water balance
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what are the two forms of adrenal insufficiency
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primary and secondary
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what is primary adrenal insufficiency
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addison disease-results form the destruction of the adrenal cortex caused by infection or hemorrhage which results in hyosecretion of all adrenocortical hormones including cortisol and aldosterone
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what are the characteristics of addison disease
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glucocorticoid defciency effects: hypoglycemia, anorexia, nausea, vomiting, flatulence, diarrhea, hyperpigmentation of skin, anxiety, depression, and loss of mental acuity
mineralocorticoid deficiency: fluid and electrolyte imbalance, orthostatic hypotension, hyponatremia, hyperkalemia, general malaise, muscle weakness, muscle pain and cardiac arrhythmias |
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what is an addison crisis
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severe hypotension, hyponatremia, dehydration, hyperkalemia and hyperthermia
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waht is secondary adrenal insufficiency
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the deficiency of cortisol secretion is secondary to insufficient secretion of ACTH by the anterior pituitary
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what is the common cause of secondary adrenal insufficiency
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long-term treatment of nonendocrine disorder disorders with pharmacologic doses of glucocorticoid drugs
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what is cusing syndrome
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a rare disorder resulting from increase adrenocortical secretion of cortisol, resulting in chronic elevation in glucocorticoid and adrenal androgen hormones.
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what are the causes of cushing's syndrome
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ACTH-dependent adrenocortical hyperplasia, tumor, ACTH-secreting tumor, long-term administration of large doses of any steroid that is a potent glucocorticoid
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what is salt-losing adrenogenital syndrome
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a congenital condition that is characterized by an inherited enzymatic interference with the normal biosynthesis of glucocorticoids and mineralocorticoids. This results in abnormal testosterone levels resulting in masculinization
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what is hyperaldosteronism
|
excessive amouints of aldosterone are made causing hypertension secondary to sodium and water retention and hypokalemia-induced muscle weakness.
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what are cortisol and cortisone used for
|
replacement therapy in patient with adrenal insufficiency
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how do glucocorticoids work
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by binding to a specific cytoplasmic glucocorticoid receptor
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what happens when you abruptly stop taking glucocorticoids
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acute adrenal insufficiency
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what is a common adverse effect of synthetic glucocorticoids administered in high doese for anti-inflammatory and immunosuppressant effects
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suppression of HPA axis
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what is prednisone
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anti-inflammatory and immunosuppressive effects
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how does prednisone work
|
primarily glucocorticoid activity, although some mineralocorticoid activity is present and more apparent when the drug is administered in high doses
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what are the contraindications of prednisone
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systemic fungal infections
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what are the adverse effects of prednisone
|
CNS complaints of euphoria, headache and vertigo, GI complaints of of nausea, vomiting, increased appetite, weight gain, dyspepsia, anxiety, mood swings, insomnia, menstrual irregularities, hyperglycemia,
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how do you maximize the therapeutic effects of prednisone
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administer according to established schedule, increase dosage in times of stress to prevent drug induced adrenal insufficiency
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when is the most opportune time for administration of glucocorticoids
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early in the morning
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how do you minimize the adverse effects of prednisone
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give with meals or antacids, monitor patient, especially surgical patient for signs of infection
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administration of prednisone can lead to what
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peptic ulcer disease
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what happens if you abruptly stop taking prednisone
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acute adrenal insufficiency
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what is aldosterone
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naturally occurring mineralocorticoid that is expensive and requires parenteral administration
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what is fludrocortisone
|
a mineralocorticoid used for partial replacement for primary adrenocortical insufficiency
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how does fludrocortisone work
|
acts on the distal renal tubule to enhance the reabsorption of sodium and to increase the urinary excretion of both potassium and hydrogen ions
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what are the contraindications of fludrocortisone
|
systemic fungal infections and conditions not requiring intense mineralcorticoid activity
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what is fludrocortisone used for
|
adrenal insufficiency (addison disease)
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what are the adverse effects of fludrocortisone
|
sodium retention and increased urinary potassium excretion, chronic heart failure, cardiomegaly, and hypokalemic alkalosis
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what should you assess in patients taking fludrocortisone
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diet because of Na retention and K loss
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how do you maximize the therapeutic effects of fludrocortisone
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increase the dosage in time of stress to prevent drug-induced adrenal insufficiency, assess for drugs that may interact with and decrease its efficacy
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how do you minimize the adverse effects of fludrocortisone
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monitor blood pressure, fluid balance, and electrolyte status and review the importance of following a diet high in potassium-rich foods
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what should you monitor in taking fludrocortisone
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monitor for edema, weight gain, hypertension, cardiac arrhythmias, or muscular weakness
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what do steroid hormone antagonists do
|
steroid hormone antagonists act to inhibit or suppress the adrenal cortex, thus controlling the symptoms of cushing syndrome
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what is aminoglutethimide
|
a steroid hormone antagonist used to treat hypercortisolism (cushing syndrome)
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how does aminoglutethimide
|
inhibits enzymatic conversion of cholesterol to pregnenolne and suppresses adrenal cortical function
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what are the adverse effects of aminoglutethimide
|
drowsiness, skin rash, nausea, headache, myalgia, and anorexia, orthostatic hypotension and tachycardia
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what should you assess before giving aminoglutethimide
|
assess CBC and thyroid levels
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how do you maximize the therapeutic effects of aminoglutethimide
|
advise the patient to carry medical identification and inform health care professionals that this drug is being taken, provide supplemental doses of steroids during times of injury, infection, or illness
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how do you minimize the adverse of aminoglutethimide
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suppression of aldosterone production may cause orthostatic or persistent hypotension, help patient change positions slowly to decrease the risk of injury related to orthostatic hypotension, take drug with small, frequent meals
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what are the drugs affecting hematopoiesis
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erythropoiesis, colony-stimulating factors, interleukins
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what is the prototype colony-stimulating factor
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filgrastim
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what is the prototype erythropoiesis stimulant
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epoetin alfa
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what is the prototype interleukin
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oprelvekin (interleukin-11)
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what is hematopoieis
|
production and differentiation of blood cells, normally occurs within bone marrow
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what is hematopoesis
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production and differentiation of blood cells
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what does the immune system composed of
|
hematopoietic cells and multiple hematologic production and storage sites
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what are the hematopoietic cells
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WBCs, erythrocytes, platelets
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what makes up the reticuloendothelial system
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immunologically active tissue and cells found in the lymph system, spleen, liver, lungs, GI tract and brain
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what stimulates production of RBCs
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erythropoietin which is caused by a decrease in oxygen by some way
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what are the types of WBCs
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granulocytes, monocytes, and lymphocytes
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what are neutrophils
|
most common type of granulocyte considered the first line of defense against pathogens that gain entry into the body past the barriers and work by phagocytosis
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what happens when there is hematologic failure
|
inadequate cell production to meet bodys demands for oxygen transportation, blood coagulation, or prevention of infection
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what does aplastic mean
|
when all cell production is deficient
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what is anemia
|
reduced circulating RBCs
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what causes anemia
|
deficient cell production
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what is thrombocytopenia
|
low platelet count
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what is an erythropoiesis stimulant
|
drug used to create RBC that is a 165-amino-acid glycoprotein
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how is the erythropoiesis stimulant manufactured
|
by DNA technology
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how do erythropoiesis sitmulants work
|
the human eyrthropoietin gene is introduced into the mammalian cells, which then introduce erythropoietin that has the same biologic effects as endogenous erythropoietin
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what does improving Hb levels do
|
decrease fatigue
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what are colony-stimulating factors
|
glycoproteins that assist in the production of blood cells
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how do colony-stimulating factors work
|
by binding to specific cell surface receptors and stimulating proliferation, differentiation commitment and some end-cell functional activation
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what is neutropenia
|
low neutrophil levels
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what is the difference between oprelvekin and other interleukins
|
it primarily altershematopoietic activity and stimulates the production of platelets
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|
drugs that produce increased production of blood cells should not be given when
|
at same time as chemotherapy
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|
what are antimicrobials, anti-infectives and antibiotics
|
drugs used to manage infections
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|
how do you classify antimicrobial drugs
|
by susceptible organism and by mechanism of action
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what are the major classifications by susceptible organism
|
antibacterial drugs, antiviral drugs, antiretroviral drugs, antifungal drugs, antiparasitic drugs, antiprotozoal drugs, and antihelminthic drugs
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what are the classifications by mechanism of action
|
inhibition of bacterial cell wall synthesis, inhibition of protein synthesis, inhibition of nucleic acid synthesis, inhibition of metabolic pathways, disruption of cell wall permeability, inhibition of viral enzymes
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what are bacteriostatic drugs
|
inhibit bacteria, but their effect is reversible if the drug is removed unless the host defense mechanisms have eradicated the organism
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what are bacteriocidal
|
drugs antibiotics that actually kill bacteria
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what is the postantibiotic effect
|
organisms may not resume growing for several hours after exposure to the drug, despite undetectable drug levels
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how do antimicrobial drugs inhibit bacterial wall synthesis
|
weaken the cell wall, allowing the cell to absorb water which causes bacterial death. Penicillins and cephalosporins bind to specific proteins located within the bacterial cytoplasmic membrane which decreases stops the final step of cell wall synthesis
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what happens when drugs disrupt the integrity of the bacterial cell wall
|
cause the cell to leak components that are vital to its survival
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what do polyene antimicrobials do
|
bind to membrane components that are present only in microbial cells
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|
what do the imidazole antifungal agents do
|
act as selective inhibitors of enzymes involved in the synthesis of sterols
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what is selectivity toxicity
|
the ability to suppress or kill an infecting microbe without injury to the host
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what is antimicrobial resistance
|
the resistance of the microbe to the drug
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what are contributing factors
|
production of drug-inactivating enzymes, changes in receptor structure, changes in drug permeation and transport, development of alternative metabolic pathways, emergence of drug-resistant microbes, spontaneous mutation, conjugation
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what is spontaneous mutation
|
a change in the genetic composition of the microbe that may just be a random occurrence
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what is conjugation
|
a form of sexual reproduction in which two individual microbes join in temporary union
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|
What is MRSA resistant too
|
methicillin, aminoglycosides, tetracyclines, erythromycin and clindamycin
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what is the drug of choice for MRSA and MRSE
|
vancomycin
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what are the antibiotics affecting the bacterial cell wall
|
penicillins, cephalosporins, monobactum antibiotics, carbapenems, vancomycin
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what are the eypes of penicillins
|
narrow-specturm penicillins, broad-spectrum penicillins, extended-spectrum penicillins, penicillinase-resistant penicillins, beta-lactamase inhibitors
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|
what are the types of cephalosporins
|
1st generation through 4th generation
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what is the bacteria cell wall responsible for
|
maintaining the integrity of the internal cellular environment
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|
what is the osmotic pressure of the interior cell
|
high
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what happens if the bacterial cell wall is not intact
|
the internal osmotic pressure draws fluid into the cell until it bursts
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how does bacterial resistance occur in antibiotics affecting the bacterial cell wall
|
the drug can't reach binding sites within the cell, or the bacteria produce an enzyme that inactivates the drug
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|
what are the difference between gram positive and gram negative bacteria
|
gram positive bacteria have cell envelope only has two layers and gram negative have an additional out membrane and cell wall is much thinner.
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|
what are beta-lactamases
|
enzymes that disrupt the beta-lactam ring which inactivates the beta-lactam drugs
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|
what is the prototype penicillin
|
penicillin G
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|
what are beta-lactam antiboiotics
|
antibiotics that have characteristics of the beta-lactam ring, which is essential for antibacterial patterns
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what are penicillinases
|
enzymes that affect penicillins
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|
what are chephalosporinases
|
enzymes that affect cephalosporins
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|
how is the antibiotic from the cephalosporins class picked
|
depends on the sensitivity of the involved organism, preferred route of administration and sometimes the cost of therapy
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|
what are the major difference between cephalosporin generations
|
include their activity against gram-negative bacteria, their resistance to beta-lactamases, and their ability to distribute into cerebrospinal fluid
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|
what generation has the least activity against gram-negative bacteria
|
first generation cephalosporins and 4th generations have the highest
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|
what generation has the most resistance to betalactamases
|
4th, 1st have the least
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|
what generations have poor distribution into cerebrospinal fluid
|
1st and 2nd, 3rd and 4th have good distribution
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|
|
what are monobactam antibiotics
|
inhibits bacterial cell wall synthesis
|
|
|
what is monobactam antibiotics used for
|
gram negative aerobic bacteria
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|
what is good about monobactam antibiotics and carbapenems
|
can give safely to penicillin-allergic patients
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|
what are carbapenems used for
|
very broad spectrum antibiotics to treat gram-positive cocci, gram-negative cocci, and bacilli. most effective beta lactam antibiotics for use against anaerobes
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|
|
what is vancomycin
|
complex and unusual tricyclic glycopeptide antibiotic
|
|
|
when is vancomycin used
|
because of its toxicity it is only used when other antibiotics fail to resolve an infection
|
|
|
what kind of bacteria vancomycin get rid of
|
gram positive
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|
|
what is VRE
|
vancomycin resistant enterococci
|
|
|
what are signs of cochlear toxicity
|
tinnitus, hearing loss
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|
|
what are signs of vestibular toxicity
|
ataxia, vertigo, nausea and vomiting, nystagmus
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|
what is red man caused by
|
vancomycin and the histamine release that causes paresthesias, flushing, rash, or redness in face, neck, upper body, arms, or back
|
|
|
what are the types of antibiotics affecting protein synthesis
|
aminoglycosides, lincosamides, macrolide antibiotics, oxazolidinones, streptogramins, tetracyclines
|
|
|
what are the two processes of protein synthesis
|
transcription and translation
|
|
|
what is transcription and where does it occur
|
occurs in the nucleus and produces messenger ribonucleic acid (mRNA). mRNA goes through different types of maturation including one called splicing, during which the noncoding sequences are eliminated
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|
where does translation occur
|
in cytoplasm
|
|
|
what happens in translation
|
polypeptide is made
|
|
|
why are aminoglycosides ineffective against anaerobes
|
they don't have oxygen which is required to disrupt protein synthesis
|
|
|
when should lincosamides be used
|
situations with infections by bacteria with known sensitivity
|
|
|
what are oxazolidinones used for
|
treating methicillin-resistant staphylococcus aureus infections (MRSA)
|
|
|
what are streptogramins used for
|
eradicated superbugs resistant to other antibiotics
|
|
|
what do tetracyclines affect
|
gram-positive and gram-negative
|
|
|
what are the drugs that are miscellaneous antibiotics
|
quinolones/fluoroquinolones, cyclic lipopeptides, miscellaneous antibiotic
|
|
|
how do miscellaneous antibiotics work
|
an action other than disrupting the cell wall or protein synthesis of bacteria
|
|
|
what are quinolones affective against
|
gram positive and gram negative
|
|
|
what are subsequent generations of quinolones called
|
fluoroquinolones
|
|
|
what are first-generation quinolones used for
|
treat uncomplicated UTIs
|
|
|
what are second generation fluoroquinolones used for
|
have increased gram-negative and systemic activity
|
|
|
what do third generation fluoroquinolones do
|
extended activity against gram-positive pathogens but less active than second generation drugs against psudomonas
|
|
|
what do fourth generation fluoroquinolones do
|
have extended activity against psudomonas
|
|
|
what is arthropathy
|
joint disease
|
|
|
what is a benefit of daptomycin
|
its ability to retain potency against antibiotic-resistant gram-positive bacteria
|
|
|
what are the types of drugs treating urinary tract infections
|
sulfonamides, urinary tract antiseptics, urinary tract analgesics
|
|
|
what disorders can be classified as UTIs
|
cystitis, acute urethral syndrome, prostatitis, and acute pyelonephritis
|
|
|
how are urinary tract infections classified
|
complicated or uncomplicated
|
|
|
what is an uncomplicated UTI
|
bacterial infection
|
|
|
what is complicated UTI
|
also caused by bacteria and associated with some anatomical or structural abnormality
|
|
|
what are upper UTIs associated with
|
fever, nausea, vomiting, and flank or back pain
|
|
|
what are lower UTIs associated with
|
dysuria (painful urination), hematuria (blood in urine), urgency, and frequency
|
|
|
what is asymptomatic bacteriuria
|
when patient has no symptoms but urinalysis shows significant numbers of bacteria
|
|
|
what is cystitis
|
an infection of the lower urinary tract caused by introduction of a pathogen into the bladder.
|
|
|
what are results of cystitis
|
redness, inflammation, irritation and edema of the bladder mucosa with multiple submucosal hemorrhages and sometimes pus
|
|
|
what are the symptoms of cystitis
|
urgency, grequency, incontinence, dysuria, hematuria, burning or a felling of warmth on urination, bladder cramps or spasms, perineal itching, suprapubic discomfort, mild backache, or a low grade fever
|
|
|
what are factors that increase the risk of cystitis
|
pregnancy, diaphragm with spermicide use, sexual intercourse, and delayed postcoital micturition
|
|
|
what is urethritis
|
syndrome of STD's
|
|
|
what are the characterizations of NGU
|
redness, irritation and edema of the urethral mucosa
|
|
|
what are the common pathogens of urethritis
|
chlamydia trachomatis, ureaplasma urealyticum, mycoplasma hominis, mycoplasma genitalium, or trichomonas vaginalis
|
|
|
what is prostatitis
|
associated with urethritis or cystitis and organism can infect the prostate gland through blood stream or ascending from urethra
|
|
|
what is acute pyelonephritis
|
infection of kidneys and renal pelvis
|
|
|
what causes acute pyelonephritis
|
E. coli
|
|
|
what are symptoms of acute pyelonephritis
|
chills and fever, flank pain, hematuria, general malaise or fatigue, headache, and costoverebral angle tenderness
|
|
|
how do you diagnose UTI
|
subjective description of symptoms and positive urine dipstick test or urinalysis in pregnant women, age over 55, men with urinary symptoms and pateints with recurrent symptom
|
|
|
how are sulfonamides characterized
|
short, intermediate, topical, long acting
|
|
|
what are urinary tract antiseptics
|
antiseptics that work by local action because high serum levels are not achievable
|
|
|
what are mycobacteria
|
slow-growing microbes that require prolonged treatment, generally with multiple medications
|
|
|
where is TB most frequently found
|
lungs
|
|
|
what to mycobacteria cause
|
tuberculosis, leprosy and mycobacterium avium complex
|
|
|
what are the types of TB
|
mycobacterium tuberculosis hominis and bovis
|
|
|
how does human TB spread
|
droplet nuclei because it is an airborne disease
|
|
|
what are symptoms of active TTB
|
night sweats, cough, low grade fever, fatiuge, weight loss, and anorexia
|
|
|
what is leprosy
|
chronic infectious disease cause by M. leprae that effects skin, peripheral nerves, mucosa of upper respiratory tract and eyes
|
|
|
what is mcobacterium avium complex
|
term used to describe an opportunistic infection
|
