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Pharmacology Mod B

chapter 19 & 35 for test

TermDefinition
PAIN an unpleasant sensory & emotional experience associated w/ actual/potential tissue damage
PAIN EXPERIENCE highly/larger subjective and influenced by behavioral, physiologic, sensory, emotional & cultural factors for a particular person under a certain set of circumstances
PAIN PERCEPTION (nociception) an individual's awareness of the feeling/sensation of pain
PAIN THRESHOLD the point at which an individual first acknowledges/interprets a sensation as being painful
PAIN TOLERANCE the individual's ability to endure pain
ACUTE PAIN arises from sudden injury/illness to the structures of the body
SYMPTOMS IN NERVOUS SYSTEM WHEN PAIN INCREASES -elevated heart rate -nausea -elevated pulse -diaphoresis -elevated respirations -dilated pupils -elevated blood pressure -elevated glucose level
CHRONIC PAIN slower onset & lasts longer than 3 months beyond the healing process
MALIGNANT cancer
NON-MALIGNANT non-cancer; causes other than cancer
NOCICEPTIVE the result of a stimulus to pain receptors (eg: chemical, thermal, mechanical)
SOMATIC PAIN pain originating from the skin, bone, joints, muscles, or connective tissue (eg: arthritis)
VISCERAL PAIN pain originating from the abdominal and thoracic organs
4 STEPS IN NOCICEPTION 1. transduction 2. transmission 3. perception 4. modulation
NEUROPATHIC PAIN results from injury to the peripheral or central nervous system (eg: trigeminal neuralgia); stabbing/burning; (phantom limb pain)
IDIOPATHIC PAIN non-specific pain of unknown origin (eg: anxiety, depression, stress)(pelvis, neck, shoulders)
ANALGESICS drugs that relieve pain w/out producing loss of consciousness or reflex activity
OPIATE AGONISTS is a chemical that acts in ways similar to an opiate, but its real purpose is to trick the brain
OPIATE PARTIAL AGONISTS activates the opioid receptors in the brain, but to a much lesser degree than a full agonist
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
PROSTAGLANDIN INHIBITORS an agent that prevents the production of prostaglandins. An example is a nonsteroidal antiinflammatory drug
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
SALICYLATES a salt or ester of salicylic acid
NON-STEROIDAL ANTI-INFLAMMATORY a class of analgesic medication that reduces pain, fever and inflammation
OPIATE RECEPTORS stimulation of these receptors by the opiates blocks the pain sensation
DRUG TOLERANCE when a patient requires increases in dosing to receive the same analgesic relief
PHYSICAL DEPENDENCE MAY DEVELOP??????? AFTER 3 - 6 WEEKS
WITHDRAWAL PEAKS AT 36 - 72 HOURS
WITHDRAWAL CAN TAKE THIS LONG TO SUBSIDE 5 - 14 DAYS
CEILING EFFECT contrary to the action of the opiate agonists, a larger dose does not produce a significantly greater analgesic effect
RANGE ORDERS pain medications ordered on PRN basis
DECREASED CARDIAC OUTPUT the amount of blood put out by the left ventricle of the heart in one contraction is called stroke volume
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
RIGHT SIDED HEART FAILURE the right ventricle loses its pumping function and blood may back up into other areas of the body, producing congestion
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
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
HYPOVOLEMIA decreased volume of circulating blood in the body
NITRATE NITROGLYCERIN if no sting when given under the tongue=medication bad
NITROGLYCERIN IS GIVEN orally, topical ointment, transdermal patch, translingual spray, inhalation, IV
NITROGLYCERIN ADMINISTRATION give 1 tablet; if pain continues take another (up to three) q5min and call 911 after 1st tablet; can cause hypertension
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
FATTY OXIDASE ENZYME INHIBITOR ranolazine (Ranexa) -more rare; given if nitroglycerin does not work
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
HYPERTENSION INCREASES?? stroke heart failure decreased cardiovascular obesity
DIRECT VASODILATORS -stage 2 -taken by itself or w/ other meds -decreased flow to heart -relaxes arterial smooth muscle, reducing peripheral vascular resistance
DIRECT VASODILATORS hydralazine (Apresoline) -increase cardiac output -renal disease -hypertension w/ pregnancy
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
BETA ADRENERGICS BLOCKING AGENTS "lol" - ex: metoprolol -inhibit cardiac response to sympathetic nerve stimulation > block beta receptors; 1st and 2nd line drug
BETA ADRENERGICS BLOCKING AGENTS USES initial therapy for stage 1 and 2 hypertension; to decrease B/P
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
BETA ADRENERGICS BLOCKING AGENTS SIDE EFFECTS -peripheral vasoconstriction (purple, mottled skin) -heart failure -bronchospasm -wheezing -bradycardia -may mask hypoglycemia in diabetic patients
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
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
ACE INHIBITORS SIDE EFFECTS -nausea, fatigue, headache, diarrhea, orthostatic hypotension, -1/3 of patients develop a dry cough
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
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)
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
CALCIUM CHANNEL BLOCKERS DRUGS Amlodipine (Norvasc)
CALCIUM CHENNEL BLOCKERS SIDE EFFECTS -hypotension and syncope (1st week of tx) -edema -angina -preterm labor
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
DIURETIC FACTS -monitor I&O -daily weight -take in the morning -encourage fluids
DIURETIC DRUGS "Hydrochlorothiazide" common thiazide diuretic --Spironolactone, triamterene are potassium sparing
DIURETIC SIDE EFFECTS -low potassium levels (monitor potassium and glucose levels)
ANTICOAGULANTS Heparin, Lovenox, Coumadin, Pradaxa, ASA, Plavix
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
THROMBUS BLOOD CLOT
EMBOLISM BLOOD CLOT THAT MOVES TO VESSEL & CAUSES ISCHEMIA OR MI (DOES NOT BREAK CLOT DOWN)
HEPARIN interferes with conversion of pro-thrombin to thrombin (which prevents conversion of fibrinogen to fibrin)
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
HEPARIN ROUTE SQ (abdomen) 1/2 - 5/8" 25 - 28 guage IV by continuous infusion due to short half-life, duration is hours
HEPARIN FACTS -bleeding common -always double check vials -be aware of correct strength -control x 1.5
HEPARIN antidote PROTAMINE
COUMADIN "warfarin" inhibits vitamin K activity, which activates clotting factors II, VII, IX, and X (prevents clot formation)
COUMADIN LAB TEST C-O-U-M-A-D-I-N-P-T (INR)
COUMADIN ANTIDOTE Vitamin K; decreases effectiveness
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
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
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)
ENOXAPARIN (Lovenox) -low molecular weight heparin -given SQ in abdomen -more predictable response, frequent labs not required -Protamine is the antidote
LABORATORY TESTS TO EVALUATE CARDIOVASCULAR DRUG THERAPY -digoxin -PT, PTT -electrolytes: potassium level especially when diuretic therapy -GFR (Glomerular filtration rate)
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
LABORATORY TESTS FOR THROMBOEMBOLIC DISEASES DIAGNOSTIC TESTS -PT, aPTT, hematocrit, platelet count, Doppler studies, exercise testing, serum triglycerides, arteriogram, cardiac enzyme studies
Created by: Smccunn