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216 Cards in this Set
- Front
- Back
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what are the four adrenergic drugs?
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dobutamine (Dobutrex)
epinephrine (Adrenaline) midodrine (ProAmatine) norepinephrine (Levophed) |
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What drug type has the MOA that mimic the effects of the SNS neurotransmitters between the nerve and innervated organ?
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adrenergics
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what is the difference between direct acting and indirect acting adrenergic drugs?
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Direct binds to receptor to cause a reaction.
Indirect stimulates the release of catecholamines. |
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vasoconstriction, GI relaxation, uterus/bladder contraction, male ejaculation, decreased insulin release and pupil dilation are effects of what type of drug
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adrenergics
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increased cardiac contractility, increased AV node conduction, increased HR, cardiac stimulation are effects of what adrenergic stimulation
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beta 1
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bronchodilation, uterine relaxation, stimulates glycogenesis, increased renin secretion are effects of what adrenergic stimulation
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beta 2
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albuterol is commonly used for what disorders?
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asthma and bronchitis
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epinephrine is the drug of choice for what disorders?
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acute asthma attacks and anaphylaxis
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dobutamine is used for what disorder?
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chronic heart failure
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pseudoephedrine is used for what?
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nasal decongestion
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HA, restlessness, excitement, insomnia, euphoria, palpitation, dysrhythmias, tachycardia, vasoconstriction, HTN, anorexia, loss of appetite, dry mouth, n/v and seizures are adverse effects of what drugs?
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adrenergics
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out of all the adverse effects of adrenergic drugs, which 2 are the most serious?
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seizures and CVA due to hypertension
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drug interaction effects: TCA - adrenergics
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increased vasopressor effects and respiratory depression
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drug interation effects: alpha - beta
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antagonist effect
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drug interaction effects: anesthetic - adrenergics
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cardiac dysrhythmias
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drug interaction effects: adrenergic - MAOIs
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HTN crisis
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drug interaction effects: adrenergic - antihistamine/thyroid
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increased adrenergic effects
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lab interaction for Alpha-adrenergics cause...
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increased serum levels of corticosteroids, cortisol, corticotropin levels and glucose
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what are the four adrenergic blocker drugs?
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phenotolamine (Regitine)
carvedilol (Coreg) metoprelol (Lopressor, Toprol XL) propanolol (Inderal) |
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what drug type has a MOA that blocks the adrenergic receptors before a neurotransmitter can?
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adrenergic blockers
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difference between nonspecific beta blockers and cardioselective beta blockers
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nonspecific blocks all beta receptors. cardioselective blocks receptors on the heart
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what are the effects of alpha-adrenergic blockage?
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vasodilation, decreased BP, miosis, suppressed ejaculation, and some stimulate uterine contractions
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what are the cardiac effects of beta 1 blockers?
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decreased HR, slowed conduction through the AV node, prolonged SA node recovery, decreased O2 myocardial demand
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Ergot alkaloids are used to treat what disorder?
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migraines (constrict dilated vessels)
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Prazosin (minipress) is used for what disorder?
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HTN
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phentolamine (regitine) is used for what disorder?
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extravasation of vasopressor agents
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cardioselective beta blockers are commonly used for what disorder?
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post MI
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what can happen if a beta blocker is abruptly stopped?
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exacerbation of underlying angina, HTN
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what are adverse effects of beta blockers?
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impaired glucose levels, dizziness, depression, decreased HR, etc.
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Why might hypoglycemia occur with nonspecific beta blockers?
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impaired glycogenolysis; glucose is not mobilized in response to hypoglycemia
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Why might hyperglycemia occur with nonspecific beta blockers?
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insulin secretion is impaired, which increases blood glucose
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what are the three cholinergic drugs?
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bethanechol (Urecholine)
donepezil (Aricept) physostigmine (Antilirium) |
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what is the MOA of cholinergic drugs?
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they mimic the effects of the PSNS neurotransmitters between the nerve and innervated organ
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how do indirect-acting agents work?
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increase amount of ACh available by inhibiting acetylcholinesterase (AChE)
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what is stimulating the intestine/bladder causing increased gastric secretions, motility, urinary frequency, miosis- decreased ocular pressure, increased salivation and sweating, decreased HR, vasodilation and bronchoconstriction the effects of?
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cholinergics
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what is the acronym used to describe the effects of cholinergic OD?
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S-salivation
L-lacrimation U-urinary incontinence D-diarrhea G-gastrointestinal cramps E-emesis |
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what are the indications for using of cholinergic drugs?
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decrease intraocular pressure in glaucoma, increase bladder and GI motility, diagnosis and treatment of myasthenia gravis and alzheimers
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what is a cardiac, respiratory and GI adverse effects of cholinergics?
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cardiac- bradycardia, hypotension. respiratory- bronchospasms, increased secretions. GI- abdominal cramps, n/v
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describe symptoms associated with cholinergic crisis
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circulatory collapse
hypotension bloody diarrhea shock cardiac arrest |
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what three classes of drugs antagonize cholinergics?
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anticholinergics, sympathomimetics, and antihistamines
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what 3 medical disorders should cholinergics be used cautiously with?
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peptic ulcer disease, asthma, bradycardia
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what are the three cholinergic blocker drugs?
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dicyclomine (Bentyl)
atropine tolterodine (Detrol) |
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what is the MOA of cholinergic blockers?
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compete with ACh for binding receptors at the PSNS muscarinic receptors
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what is mydriasis, cycloplegia (relaxed eye), decreased GI motility/secretions and salivation, increased HR, decreased bladder contraction-retention, decreased sweating, dry mucus membranes, bronchodilation the effects of?
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cholinergic blockers
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why are cholinergic blockers used for parkinson's disease?
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they decrease muscle rigidity and tremors
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what is the difference between high doses and low doses of cholinergic blockers?
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low doses slow the heart rate. high doses increase the heart rate
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what GI disorders are treated with cholinergic blockers?
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peptic ulcer disease, IBS, hypersecretory
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what patient populations are at risk for toxicity of cholinergic blockers?
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infants, elderly, fair skinned kids with down's syndrome, kids with spastic paralysis or brain damage
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why is "Hot as a hare, blind as a bat, dry as a bone and mad as a hatter" used to describe cholinergic toxicity?
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hot= decreased sweating
blind= mydriasis dry= decreased salivation mad= irritable, disoriented etc. |
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what classes of drugs result in additive effects with cholinergic blocking drugs?
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antihistamines, phenothiazines, tricylic antidepressants, MAO inhibitors
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what are the two heart failure drugs?
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lisinopril (Prinivil)- ACE inhibitor
digoxin (Lanoxin)- Cardiac Glycoside |
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what "tropic" effect influences the force of muscular contractions?
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inotropic
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what "tropic" effect influences the rate of the heart beat?
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chronotropic
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what "tropic" effect influences conduction with in the heart tissues?
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dromotropic
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how do ACE inhibitors impact the "renin-angiotensin-aldosterone" system?
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prevents Na+ and water resorption by inhibiting aldosterone secretion
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what are the indications for ACE inhibitors?
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HTN, heart failure, acute MI
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what are the adverse effects of ACE inhibitors?
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thrombocytopenia, dysrhythmia, nausea, hypotension, angina, hypokalemia, tremor
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how do cardiac glycosides help pt with heart failure?
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they treat tachydysrhythmias during atrial fibrillation
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what are the 3 tropic effects of digoxin (Lanoxin)?
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1. positive inotropic effect
2. negative chronotropic effect 3. negative dromotropic effect |
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what are the indications for cardiac glycosides?
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heart failure, atrial fibrillation, and atrial flutter
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what are the adverse effects of cardiac glycosides?
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bradycardia, a/n/v, colored vision, helo vision, dyrhythmias, GI issues, confusion, headache, increased myocardial contractions
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what is the normal therapeutic level for digoxin (Lanoxin)?
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0.5-2 ng/ml
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what electrolyte imbalance increases digoxin toxicity?
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potassium > or = 5 mEq/L
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what type of diuretics increase digoxin toxicity?
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potassium wasting diuretics
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what decreases the absorption of digoxin?
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antilipemics
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why check a patient's pulse for 1 full minute prior to giving digoxin?
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drug may exasterbate the pulse and cause dysrhythmias
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is it good or bad for a pt to eat 2 bowls of bran cereal with digoxin?
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bad b/c it effects the bioavailability
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what are the four antianginal drugs?
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isosorbide mononitrate (Imdur)
nitroglycerin (Nitrostat)(NitroBid) diltiaxem (Cardizem) |
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what is the MOA for nitrates?
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they dilate all blood vessels, esp. venous vascular beds and reduce venous return; have a potent dilating effect on coronary arteries
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what are the indications for using nitrates?
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stable/unstable/vasospastic angina
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what are some adverse effects of nitrates?
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headache, tachycardia, postural hypotension
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what are some contraindications of nitrates?
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decreased tissue O2 resulting in anemia and head trauma
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what is reflex tachycardia?
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rapid heartbeat caused by a variety of ANS effects such as BP changes, fever or emotional stress
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what is nitrate tolerance?
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tolerance to antianginal effects and cross-tolerance when recieving more than one dosage
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what is the MOA of Calcium channel blockers?
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they block calcium in the excitation-contraction process of heart and vascular muscle cells which promotes relaxation of heart and vessels; also decreases automaticity of and conduction through SA and AV node which decreases heart rate
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what are some indications for using Ca+ channel blockers?
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angina, HTN, supraventricular tachycardia, coronary artery spasms, A fib and flutter, migraines
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what are some adverse effects of Ca+ channel blockers?
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peripheral edema, confusion, worsening HF, orthostatic hypotension, bradycardia, and heart failure because the slowing of blood flow slows everythine else down
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what are the four antihypertensive drugs?
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clonidine (Catapres)- adrenergic drug
captopril (Capoten)- ACE inhibitor losartan (Cozaar)- angiotensin II receptor blocker hydralazine HCl (Apresoline)- vasodilator |
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what is the MOA of clonidine (Catapres)?
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stimulates the alpha2 receptors which reduce the sympathetic outflow which reduces BP
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what is the MOA of captopril (Capoten)?
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decreases the work of the heart by lowering BP
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what is the MOA of losartan (Cozaar)?
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interferes aldosterone with binding to angiotensin II beta receptors
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what is the MOA of hydralazine HCl (Apresoline)?
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causes direct relaxation of the vessels
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what type of an agent is clonidine (Catapres)?
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centrally acting Alpha2 receptor agonist
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what are adverse effects of adrenergic drugs?
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bradycardia, reflex tachycardia, orthostatic hypotension
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what other drugs should the nurse be careful with when taking adrenergic drugs?
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CNS depressants such as alcohol, benzodiazepines, and opioids
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what are the indications for taking ACE inhibitors?
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HTN, to stop the progression of ventricular remodeling post MI
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what are adverse effects of ACE inhibitors?
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annoying non-productive cough, loss of taste, hyperkalemia, rash, pruritis, anemia, neutropenia, thrombocytosis, agranulocytosis
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what can be the cause of drug interactions with ACE inhibitors?
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antihypertensive effect and acute renal failure
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what are the adverse effects of angiotensin II receptor blockers?
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nasal congestion, dyspnea, insomnia, diarrhea, sinusitis
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what is the indication for using vasodilators?
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moderate to severe HTN
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what are the adverse effects of vasodilators?
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dizziness, headache, anxiety, tachycardia, edema, nasal congestion, dyspnea, dysrythmias
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what's important to assess first on a pt who is taking hydralazine (Apresoline)?
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blood pressure, potassium level, fluid loss (daily weights, accurate I&Os)
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why assess respiratory status and potassium serum levels prior to giving captopril (capoten)?
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causes non-productive cough and hyperkalemia
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why is abrupt withdrawl a serious concern?
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organ failure esp. brain, eyes and heart
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what are the four diuretic drugs?
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furosemide (Lasix)- loop diuretic
mannitol (Osmitrol)- osmotic diuretic spironolactone (Aldactone)- potassium-sparing diuretic hydrochlorothiazide (HydroDIURAL)- thiazide |
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why is it important that loop diuretics work even when creatinine clearance is low?
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loop diuretics will still work when rapid diuresis is needed
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what is the MOA of loop diuretics?
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potent diuresis with loss of fluid resulting in decreased fluid volume which decreases the return of blood to the heart or decrease filling pressures
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what are indications for using loop diuretics?
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edema with heart failure, hepatic or renal disease, and HTN
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what are adverse effects of loop diuretics?
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hypokalemia, dizziness, headache, tenitis
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what happens when a loop diuretic is given with ibuprofen (NSAIDs)?
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decreased diuretic activity
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what happens when a loop diuretic is given with digoxin?
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additive hypokalemic effect
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what is the MOA of osmotic diuretics?
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produces osmotic pressure in the glomerular filtrate which pulls fluid into the tubules causing diuresis
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what are the indications for using osmotic diuretics?
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early oliguric phase of acute renal failure, increased intracranial pressure, cerebral edema
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what are the adverse effects of osmotic diuretics?
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convulsions, thrombophlebitits, pulmonary congestion
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what is the MOA of potassium-sparing diuretics?
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binds to aldosterone receptors which blocks the resorption of water and sodium
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what are the indications for using potassium sparing diuretics?
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HTN, congestive heart failure, hyperaldosteronism
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what are the adverse effects of potassium-sparing diuretics?
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hyperkalemia, dizziness, headache, cramps, n/v, diarrhea, urinary frequency, weakness, gynacomastia, dysminuria
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what happens with the interaction between potassium sparing diuretics and ACE inhibitors?
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they're concurrent which increases potassium levels causing a potassium toxicity
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what is the MOA of thiazides?
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inhibits the resorption of sodium, potassium, and chloride which causes osmotic water loss; causes direct relaxation of arteriole leading to reduced afterload
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what are indications of using thiazides?
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heart failure, hepatic cirrhosis, edema, idiopathic hypercalciuria, diabetes insipidus
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what what are the electrolyte and metabolic disturbances associated with hydrochlorothiazide?
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decreased potassium levels, increased calcium, lipids, glucose, and uric acid
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what drugs do thiazides interact with?
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corticosteroids, digoxin, oral hypoglycemic
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what 3 things would you want to assess for the patient recieving a thiazide?
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blood pressure
volume status for fluids edema |
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what are two antidysrythmic drugs?
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lidocaine (Xylocaine)
amiodarone (Cordarone) |
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what is the MOA of antidysrhythmics?
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alter the action potential of cardiac cells making them less responsive to intrinsic electrical stimuli
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what are the indications for using antidysrhythmics?
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dysrhythmias by prolonging repolarization
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what type of dysrhythmias do lidocaine and amiodarone treat?
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lidocaine treats ventricular dysrhythmias.
amiodarone treats atrial and ventricular dysrhythmias |
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what are adverse effects of lidocaine (xylocaine)?
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CNS toxicities such as twitching, convulsions, confusion, anxiety, respiratory distress or arrest. cardiovascular effects such as hypotension, bradycardia, dysrhythmias
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what are adverse effects of amiodaron (cordarone)?
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hypo/hypertension, goiter, corneal microdeposits, blue skin pigmentation, pulmonary fibrosis, pulmonary toxicity
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what is a key thing to know about drug interactions of antidysrhythmics?
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enhanced anticoagulant effect with anticoagulants and proarrhythmic effect with other antidysrhythmic agents
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which systems are important to assess with lidocaine?
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CNS and cardiovascular because of orthostatic BP
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why is INR (international normalized ratio) important with antidysrhythmics?
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the rate of bleeding will increase
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what conditions are important to assess when a pt is taking amiodarone?
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respiratory, thyroid, hepatic, hypertensive conditions
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how should IV antidysrhythmics be administered?
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via infusion pump
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what route(s) is lidocaine given?
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IV push or drip
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what route(s) is amiodarone given?
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IV for acute therapy
PO for chronic therapy |
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what CNS-related effects will you look for when giving lidocaine?
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bradycardia, dizziness, headache, chest pain, heart failure, peripheral edema, conduction disorders
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what should you assess when giving amiodarone?
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pulmonary function tests and thyroid function
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what are the three anticoagulant drugs?
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warfarin sodium (Coumadin)
enoxaparin (Lovenox) heparin |
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what are the two antiplatelet drugs?
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aspirin
clopidogrel (Plavix) |
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what is one thrombolytic drug?
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alteplase (Activase)
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define thrombus
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blood clot on the wall of a blood vessel
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define embolus
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dislodged blood clot that travels through the blood stream
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define pulmonary embolism
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embolus in the lung
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define deep vein thrombosis
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embolus in the leg
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what is the MOA of anticoagulants?
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prevents the process of coagulation to treat atherosclerosis, DVT, PE, stroke and MI
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how does warfarin effect vitamin K?
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inhibits Vit K synthesis
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what are the indications for using anticoagulants?
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preventing the formation of clots
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in what clinical situations would this anticoagulation therapy be warranted?
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pregnant women, thrombocytopenia, epidural catheter
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what are the adverse effects of anticoagulants?
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bleeding, heparin induced thrombocytopenia, bruising, brain anerysms, GI problems
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define heparin-induced thrombocytopenia
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allergic response resulting in small thrombosis that travel through the blood stream
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describe the symptoms of anticoagulant toxicity/overdose
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hematuria, melena (blood in stool), petechiae, ecchymoses, gum or mucous membrane bleeding
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what is the reversal agent for heparin?
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protamine sulfate
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what is the reversal agent for warfarin?
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IV injection of Vitamin K
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with what drugs cause an interaction of an increased anticoagulant effect with anticoagulants?
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acetomeinophen, furosemide, aspirin
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with what drugs cause an interaction of a decreased anticoagulant effect with anticoagulants?
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rifampin, sucralfate
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what labs should you assess when administering warfarin and what is the therapeutic range?
|
prothrombin time (PT)
international normalized ration (INR)- 2-3.5 |
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what route is enoxaparin (Lovenox) given?
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subcutaneous
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what labs should you assess before administering Lovenox?
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none are necessary unless they have bleeding issues or bruising near the injection site
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what route(s) is heparin given and describe the onset?
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subcutaneous- for acute therapy
intravenous- for chronic therapy |
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what is the MOA for aspirin?
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effects last 7 days, resulting in the dilation of the blood vessels and prevention of platelets from aggregating or forming a clot
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what is the MOA of clopidogrel (Plavix)?
|
inhibits platelet aggregation by altering the platelet membrane so that is can no longer receive the signal to aggregate and form a clot
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what antiplatelet drug is more effective at reducing the number of heart attacks, strokes, and vascular death?
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Plavix
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why is a deficiency of Vitamin K, GI ulcers, and traumatic injuries contraindicated with antiplatelets?
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blood is needed to clot with these effects
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what are the drugs that interact with antiplatelets?
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NSAIDs and steroids
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what is the MOA of alteplase (Activase)?
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activates plasminogen which forms plasmin to degrade fibrinogen and break up the thrombi so prevent re-occlusion of an infarcted blood vessel
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what are some indications for giving thrombolytics?
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acute MI, arterial thrombosis, DVT, occlusion of shunts or catheters, PE, acute ischemic stroke
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what are the adverse effects of thrombolytic drugs?
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bleeding, hypersensitivity, anaphylactoid reactions, n/v, hypotension, dysrhythmias
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what are some drugs that can cause interactions with thrombolytics?
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NSAIDs, steroids, non-aspirin NSAIDs
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for all coagulation modifiers, what tests should be assessed?
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CBC, Hgb, Hct, and clotting studies
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what areas should be avoided when injecting heparin?
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2 inches around the umbillicus, open wounds, acras, open or abraded areas, incisions, drainage tubes, stomas, areas of oozing or bruising
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regarding pregnancy/lactation, what is the preferred anticoagulation therapy?
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heparin
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how long should aspirin, NSAIDs and other antiplatelets be withheld prior to surgical procedures?
|
5-7 days
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prior to giving a thrombolytic, what pt history is important?
|
history of amiodarone with warfarin, or coumadin with warfarin and bleeding history
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what are symptoms of internal bleeding?
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hypotension, tachycardia, change in the level of consciousness, unexplained restlessness
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when rapid anticoagulation is needed, what is the drug of choice and what is it's reversal agent?
|
IV heparin; protamine sulfate
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what is the length of time a pt will be taking Lovenox?
|
5-10 days
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why will a pt be prescribed IV heparin plus warfarin sodium (coumadin)?
|
IV can't be given at home
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what should you assess for signs and symptoms of bleeding if the pt is on aspirin?
|
epitaxis, hematuria, hematemesis, easy or excessive brusing, blood in stool, bleeding of gums
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what is a common toxicity sign for aspirin?
|
constant ringing in the ears (tinnitus)
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what lab value(s) monitors heparin therapy and has a therapeutic value of 45-70 seconds or 1.5-2.5 times the control value?
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PTT and aPTT
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what lab value monitors warfarin therapy and should be 1.5 times the control or 18 seconds?
|
PT
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what are the four antilipemic drugs?
|
atorvastatin (Lipitor)- HMG-CoA reductase inhibitor
cholestyramine (Questran)- Bile Acid sequestrant niacin (Nicobid, Vitamin B3)- Niacin gemfibrozil (Lopid)- fibric acid derivative |
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what is the MOA of antilipemics?
|
used to reduce and maintain lipid levels in a desirable range; used to treat elevated serum cholesterol and triglyceride levels and reduce the risk of coronary artery disease
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what is the MOA of HMG-CoA reductase inhibitors?
|
reduces HMG-CoA reductase, that is needed by the liver, to decrease the production of cholesterol; statins decrease the rate of cholesterol production and augment LDL recycling
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what are indications for giving HMG-CoA reductase inhibitors?
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hypercholesterolemia, to decrease LDL, increase HDL and decrease triglycerides
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what is a contraindication of HMG-CoA reductase inhibitors?
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liver disease
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what are the adverse effects of HMG-CoA reductase inhibitors?
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mild, transient GI disturbances, rash, headache, myopathies/myalgias, increased in liver enzymes
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what is rhabdomyolisis and what can it lead to?
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breakdown of muscle protein accompanied by myoglobulinuria leads to acute renal failure and even death
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what should you be cautious when giving HMG-CoA reductase inhibitors with oral anticoagulants?
|
increased clotting times
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why is grapefruit juice reduced to 1 qt/day?
|
leads to rhabdomyolisis
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what is the MOA of bile acid sequestrants?
|
prevents the absorption of cholesterol by binding with bile acids from the small intestines; they lower the plasma LDL levels by enhancing efficacy of LDL remocal from plasma
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what are the indications for giving bile acid sequestrants?
|
primary or adjunct therapy for hypercholesterolemia, decreases LDL, increases HDL and increases triglycerides
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what are the most common adverse effects of bile acid sequestrants?
|
constipation, heartburn, nausea, belching, bloating, bleeding, headache, tinnitus, burnt color of urine
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what are some nursing implications for bile acid sequestrants?
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therapy initiated in low dosages, take drugs with meals esp. fiber and fluids
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bile acid sequestrants will reduce the absorption of concurrent drugs so when should the drug be administered?
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1 hour before or 4-6 hours after
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bile acid sequestrants will decrease absorption of what vitamins?
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A, D, E, K
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what is the MOA of niacin?
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reduce the metabolism and catabolism of cholesterol
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what are the indications of niacin?
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to decrease LDL, increase HDL and decrease triglycerides
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what are the adverse effects of niacin?
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flushing, pruritus, GI distress
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what are some nursing implications when administering niacin?
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give aspirin or NSAIDs 30 minutes before
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what is the MOA of fibric acid derivatives?
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activates lipoprotein lipase to break down cholesterol; suppresses the release of fatty acids from adipose tissue; inhibits synthesis of triglycerides in liver; increases the secretion of cholesterol into bile
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what are the indications of fibric acid derivatives?
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decreases LDL (Lipitor), increases HDL (Questrin), and decreases triglycerides (Lopid)
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what are the most common adverse effects of fibric acid derivatives?
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abdominal discomfort, diarrhea, nausea, headache, blurred vision, increased risk for gall stones, prolonged PT
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what should be assessed with fibric acid derivatives?
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contraindications such as hypersensitivities, biliary obstruction, liver dysfunction or disease, lipid levels and possible drug interactions
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when should questran be given with other meds?
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30 minutes before other meds or 4-6 hours after
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what are the three tropic effects of digoxin (lanoxin)?
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+ inotropic
- chronotropic - dromotropic |
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Ca+ channel blockers are used to prevent angina. What else are they used for?
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vasodilation and migraines
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name 3 nitrates and their route of administration
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Nitrostat- sublingual
Nitrobid- topical Imdur- PO Cardizem- PO |
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what's most important to assess prior to giving nitrates and why?
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risk for orthostatic hypotension
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your pt is taking digoxin (Lanoxin) and furosemide (Lasix), what worries you the most and why?
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hypokalemia because Lasix causes the risk which increases the risk for digoxin toxicity
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describe how diuretics reduce BP
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potent diuresis= loss of fluid Na+ and H2O excretion
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which 2 classes of diuretics cause hypokalemia?
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loop and thiazides
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what electrolyte imbalance may occur with spironolactone (aldactone)?
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hyperkalemia
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what's the most common side effect of captopril (Capoten)?
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cough
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your pt is takin losartan (Cozaar) for HTN. the dr has added isosorbide (Imdur) to his meds. what concerns you the most?
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decrease in BP
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name 2 drugs that are classifies as antidysrhythmics
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lidocaine & amiodarone
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name the 4 pharmacologic classes of antilipemics
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HMG-CoA reductase inhibitors
Bile Acid sequestrants Niacin Fibric Acid derivatives |
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what's the most serious side effects associated with amiodarone (Cordarone)?
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pulmonary toxicity
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which class of antilipemics would be avoided in a client with elevated triglycerides?
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questran
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why are 'statins' more effective at night?
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because liver produces cholesterol at night
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name 2 drugs classified as anticoagulants
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heparin (coumadin) & Warfarin
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what lab values do you assess for effectiveness of warfarin sodium?
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PT & INR
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your pt is receiving aspirin 325 mg PO daily. most likely this is for?
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anticoagulation therapy to prevent MI and stroke
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how is altepase different than heparin?
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altepase breaks up the clot and heparin just keeps the blood flowing
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your pt is receiving IV heparin. what will you be assessing?
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bleeding, bruising, thrombocytopenia, gums, IV site
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