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chapter 19 & 35 for test

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Term
Definition
PAIN   an unpleasant sensory & emotional experience associated w/ actual/potential tissue damage  
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PAIN EXPERIENCE   highly/larger subjective and influenced by behavioral, physiologic, sensory, emotional & cultural factors for a particular person under a certain set of circumstances  
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PAIN PERCEPTION (nociception)   an individual's awareness of the feeling/sensation of pain  
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PAIN THRESHOLD   the point at which an individual first acknowledges/interprets a sensation as being painful  
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PAIN TOLERANCE   the individual's ability to endure pain  
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ACUTE PAIN   arises from sudden injury/illness to the structures of the body  
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SYMPTOMS IN NERVOUS SYSTEM WHEN PAIN INCREASES   -elevated heart rate -nausea -elevated pulse -diaphoresis -elevated respirations -dilated pupils -elevated blood pressure -elevated glucose level  
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CHRONIC PAIN   slower onset & lasts longer than 3 months beyond the healing process  
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MALIGNANT   cancer  
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NON-MALIGNANT   non-cancer; causes other than cancer  
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NOCICEPTIVE   the result of a stimulus to pain receptors (eg: chemical, thermal, mechanical)  
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SOMATIC PAIN   pain originating from the skin, bone, joints, muscles, or connective tissue (eg: arthritis)  
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VISCERAL PAIN   pain originating from the abdominal and thoracic organs  
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4 STEPS IN NOCICEPTION   1. transduction 2. transmission 3. perception 4. modulation  
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NEUROPATHIC PAIN   results from injury to the peripheral or central nervous system (eg: trigeminal neuralgia); stabbing/burning; (phantom limb pain)  
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IDIOPATHIC PAIN   non-specific pain of unknown origin (eg: anxiety, depression, stress)(pelvis, neck, shoulders)  
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ANALGESICS   drugs that relieve pain w/out producing loss of consciousness or reflex activity  
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OPIATE AGONISTS   is a chemical that acts in ways similar to an opiate, but its real purpose is to trick the brain  
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OPIATE PARTIAL AGONISTS   activates the opioid receptors in the brain, but to a much lesser degree than a full agonist  
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OPIATE ANTAGONISTS   drugs which are competitive antagonists that bind to the opioid receptors with higher affinity than agonists but do not activate the receptors. This effectively blocks the receptor, preventing the body from responding to opioids and endorphins  
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PROSTAGLANDIN INHIBITORS   an agent that prevents the production of prostaglandins. An example is a nonsteroidal antiinflammatory drug  
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ACETAMINOPHEN   an analgesic drug used to treat headaches, arthritis, etc., and also to reduce fever, often as an alternative to aspirin. Proprietary names include Tylenol  
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SALICYLATES   a salt or ester of salicylic acid  
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NON-STEROIDAL ANTI-INFLAMMATORY   a class of analgesic medication that reduces pain, fever and inflammation  
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OPIATE RECEPTORS   stimulation of these receptors by the opiates blocks the pain sensation  
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DRUG TOLERANCE   when a patient requires increases in dosing to receive the same analgesic relief  
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PHYSICAL DEPENDENCE MAY DEVELOP???????   AFTER 3 - 6 WEEKS  
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WITHDRAWAL PEAKS AT   36 - 72 HOURS  
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WITHDRAWAL CAN TAKE THIS LONG TO SUBSIDE   5 - 14 DAYS  
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CEILING EFFECT   contrary to the action of the opiate agonists, a larger dose does not produce a significantly greater analgesic effect  
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RANGE ORDERS   pain medications ordered on PRN basis  
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DECREASED CARDIAC OUTPUT   the amount of blood put out by the left ventricle of the heart in one contraction is called stroke volume  
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IMPAIRED VALVULAR FUNCTION   if coronary artery disease progresses to the point where papillary muscles become hypoxic or infarcted, then the impaired contractile function of these muscles can lead to a leaky tricuspid or mitral valve  
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RIGHT SIDED HEART FAILURE   the right ventricle loses its pumping function and blood may back up into other areas of the body, producing congestion  
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MYOCARDIAL ISCHEMIA   occurs when blood flow to your heart is reduced, preventing it from receiving enough oxygen. Due to partial/complete blockage of the coronary arteries  
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LEFT SIDED HEART FAILURE   when the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side, then blood backs up into the veins  
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HYPOVOLEMIA   decreased volume of circulating blood in the body  
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NITRATE   NITROGLYCERIN if no sting when given under the tongue=medication bad  
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NITROGLYCERIN IS GIVEN   orally, topical ointment, transdermal patch, translingual spray, inhalation, IV  
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NITROGLYCERIN ADMINISTRATION   give 1 tablet; if pain continues take another (up to three) q5min and call 911 after 1st tablet; can cause hypertension  
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NITRATES FACTS   -for angina pain (not enough oxygen; decreased blood flow) -take before increased activity to prevent angina -DO NOT take erectile dysfunction medications -bottle is dark to protect from light - 3-6 month shelf life  
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FATTY OXIDASE ENZYME INHIBITOR   ranolazine (Ranexa) -more rare; given if nitroglycerin does not work  
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FATTY OXIDASE ENZYME INHIBITOR FACTS   -decreased O2 required to produce energy for muscle contractions -decreased ischemia & angina symptoms -history of stable angina -no change on B/P or HR -prolongs QT interval on EKG  
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HYPERTENSION INCREASES??   stroke heart failure decreased cardiovascular obesity  
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DIRECT VASODILATORS   -stage 2 -taken by itself or w/ other meds -decreased flow to heart -relaxes arterial smooth muscle, reducing peripheral vascular resistance  
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DIRECT VASODILATORS   hydralazine (Apresoline) -increase cardiac output -renal disease -hypertension w/ pregnancy  
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DIRECT VASODILATORS SIDE EFFECTS   common: dizziness, numbness, tingling in legs, orthostatic hypotension, palpitations, tachycardia, nasal congestion, hair growth serious: fever, chills, joint/muscle pain, skin eruptions, gynecomastia  
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BETA ADRENERGICS BLOCKING AGENTS   "lol" - ex: metoprolol -inhibit cardiac response to sympathetic nerve stimulation > block beta receptors; 1st and 2nd line drug  
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BETA ADRENERGICS BLOCKING AGENTS USES   initial therapy for stage 1 and 2 hypertension; to decrease B/P  
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BETA ADRENERGICS BLOCKING AGENTS FACTS   -do not give w/ asthma or w/ peripheral vascular disease -cannot be stopped suddenly -can cause erectile dysfunction -zero effect on African americans  
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BETA ADRENERGICS BLOCKING AGENTS SIDE EFFECTS   -peripheral vasoconstriction (purple, mottled skin) -heart failure -bronchospasm -wheezing -bradycardia -may mask hypoglycemia in diabetic patients  
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ACE INHIBITORS   "pril" - ex: lisinopril -inhibit angiotensin I enzyme (ACE), disrupting the conversion of angiotensin I to angiotensin II -reduce B/P -preserve cardiac output -increase renal blood flow; decrease workload on heart  
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ACE INHIBITORS FACTS   -1st line decrease stroke volume resistance so heart has less resistance when ejecting; also block resorption of Na and H2O > diuresis -B/P less than 100; hold med DO NOT GIVE  
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ACE INHIBITORS SIDE EFFECTS   -nausea, fatigue, headache, diarrhea, orthostatic hypotension, -1/3 of patients develop a dry cough  
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ARBs ANGIOTENSIN II RECEPTOR BLOCKERS   "sartan" ex: valsartan, Losartan, valsartan, irbesartan -1st line -bind to angiotensin II receptor sites and block vasoconstrictor from binding to receptor sites in target organs -blocks aldosterone -decreases vascular resistance  
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ARBs ANGIOTENSIN II RECEPTOR BLOCKERS SIDE EFFECTS   dyspepsia, cramps, diarrhea, headache, orthostatic hypotension, hyperkalemia (more common in pts w/ DM), -monitor potassium levels -discourage potassium or dietary supplements -can cause birth defects (DO NOT take when pregnant)  
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CALCIUM CHANNEL BLOCKERS   1st line drug for hypertension -blocks calcium channels in smooth muscles so they don't contract; they RELAX -slows the heart -effective for African americans, elderly, asthmatic, migraines  
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CALCIUM CHANNEL BLOCKERS DRUGS   Amlodipine (Norvasc)  
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CALCIUM CHENNEL BLOCKERS SIDE EFFECTS   -hypotension and syncope (1st week of tx) -edema -angina -preterm labor  
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DIURETICS (in conjunction with other classification)   -cause volume depletion, sodium excretion, vasodilation of peripheral arterioles -increase amount of urine produced by the kidney > decrease preload -use for hypertension  
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DIURETIC FACTS   -monitor I&O -daily weight -take in the morning -encourage fluids  
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DIURETIC DRUGS   "Hydrochlorothiazide" common thiazide diuretic --Spironolactone, triamterene are potassium sparing  
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DIURETIC SIDE EFFECTS   -low potassium levels (monitor potassium and glucose levels)  
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ANTICOAGULANTS   Heparin, Lovenox, Coumadin, Pradaxa, ASA, Plavix  
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ANTICOAGULANT ACTIONS   -inhibit formation of blood clots -used to prevent or treat blood clots, PE -prevent clotting of blood in arterial or heart surgeries, and major surgeries of chest/abdomen  
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THROMBUS   BLOOD CLOT  
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EMBOLISM   BLOOD CLOT THAT MOVES TO VESSEL & CAUSES ISCHEMIA OR MI (DOES NOT BREAK CLOT DOWN)  
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HEPARIN   interferes with conversion of pro-thrombin to thrombin (which prevents conversion of fibrinogen to fibrin)  
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HEPARIN LAB TEST   H-E-P-A-R-I-N-P-T-T (exact fingers) or H-E-P-A-R-I-N-A-C-T  
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HEPARIN ROUTE   SQ (abdomen) 1/2 - 5/8" 25 - 28 guage IV by continuous infusion due to short half-life, duration is hours  
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HEPARIN FACTS   -bleeding common -always double check vials -be aware of correct strength -control x 1.5  
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HEPARIN antidote   PROTAMINE  
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COUMADIN   "warfarin" inhibits vitamin K activity, which activates clotting factors II, VII, IX, and X (prevents clot formation)  
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COUMADIN LAB TEST   C-O-U-M-A-D-I-N-P-T (INR)  
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COUMADIN ANTIDOTE   Vitamin K; decreases effectiveness  
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COUMADIN FACTS   -OTC aspirin increases toxicity -must eat same amount of green leafy meal everyday -causes bleeding -half-life 0.5 - 3 days, duration 2 - 5 days  
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WHY A PERSON TAKES HEPARIN & COUMADIN TOGETHER   Warfarin usually takes a couple of days to reach the correct level, so you need the heparin to help treat the clot while the warfarin starts to act. Once the INR has been in the correct range for at least two days, the heparin can be stopped  
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dabigatran (PRADAXA)   -reduces risk of stroke w/ non-valvular atrial fibrillation -no labs/no antidote -thrombin inhibition -must swallow capsule whole renal excretion so be cautious if reduced kidney function -no drug antidote for bleeding: give FFP (fresh frozen plasma)  
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ENOXAPARIN (Lovenox)   -low molecular weight heparin -given SQ in abdomen -more predictable response, frequent labs not required -Protamine is the antidote  
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LABORATORY TESTS TO EVALUATE CARDIOVASCULAR DRUG THERAPY   -digoxin -PT, PTT -electrolytes: potassium level especially when diuretic therapy -GFR (Glomerular filtration rate)  
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LABORATORY TESTS FOR THROMBOEMBOLIC DISEASES COAGULATION TESTS   -PT (prothrombin time) = monitors warfarin therapy -aPTT (activated partial thromboplastin time) = monitors heparin therapy -INR (international normalized ratio) = monitors warfarin therapy -PLATELET COUNTS  
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LABORATORY TESTS FOR THROMBOEMBOLIC DISEASES DIAGNOSTIC TESTS   -PT, aPTT, hematocrit, platelet count, Doppler studies, exercise testing, serum triglycerides, arteriogram, cardiac enzyme studies  
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