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30 Cards in this Set
- Front
- Back
adrenergic blocking agents?
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-used for htn, ht failure, arrhythmias, angina
-usefullness comes form neg inotropic (red forces of ht’s contraction) & neg chronotropic (red rate of ht beats) effects that - the amount of work the ht needs to do -can be used in several types of cv conditions -CO is - which lowers bp |
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diuretics?
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-induce urination
-lowers bp, dec amount of h20 in the system, - bld volume & thus bp -complicated homeostatic/homeodynamic mech after initial fld loss -acts on kds -used to tx many conditions, htn, chf, other edematous conditions |
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thiazide diuretics?
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-most commonly rx & are among the most rx of all meds
-the distal convoluted tubule is impermeable to h20. about 10% of sodium chloride is reabsorbed into teh interstitial fld here through the na+ Cl- transporter, which is sensitive to thiazide diuretics -k+ depleting -Ca++ sparing, actually causes small net - in Ca++ loss in urine |
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ex of thiazide diuretics?
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hydrochlorothiazide (HCTZ) most common
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actions of thiazide diuretics?
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-sodium water retention, less bld volume, less co, less peripheral resistance, dec bp
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thiazide diuretics se?
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-hyperuricemia, can lead to gout
-orthostatic hypotension -hyperlipidemia -hyperglycemia & red control of bld sugar level in diabetes *people allergic to sulfa drugs may also be allergic to thiazides |
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thiazide diuretics drug interactions?
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-can - effects of anticoagulants & insulin
-inc effects of anesthetics, lithium, vit d -NSAIDS - effects thiazides -lethal reaction between thiazide & quinidine |
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loop diuretics?
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-work in A loop of henle, accounts of 25-30% of NaCl reabsorption
-drug of choice for pulmonary edema of ht failure & emergency conditions -cause excretion of Ca++ & Mg+, in pts w/norm serum ca, much is reabsorbed in distal tube, hyperclacermia is life threatening condition tx’d w/high dose of loop diuretics -K+ depleting |
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loop diuretics ex?
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furosemide (lasix)
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loop diuretics se?
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-can lead to:
ototoxicity-prob hearing & balance precipitate a rapid & severe loss of bld volume & can result in hypotension, shock, cardiac arrhythmias -not to be used w/lv cirrhosis |
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loop diuretics drug interactions?
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-inc effects of anesthetics, lithium, vit di
-potentiate anitcoagulants -aminoglycoside antib & cisplatin can + otoxicity of loop diuretics |
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diuretics se?
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-potassium depletion
-diet can slow down or reverse this -k+ rich foods: bananas, citrus, prunes. limit Na+ |
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potassium sparing diuretics?
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-work in the collecting tubule, inhibiting Na+ reabsorption & K+ excretion
-often in conjunction w/other diuretics -considered ca sparing, causes small net + in ca lost in urine -ex: spirolactone has an anti-androgen effect. it is sometimes used in hormone therapy for trans-women. many be used for hair loss & acne in women & topically for tx of male baldness |
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herbs w/diuretic effects?
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qu ma, tong cao, fu ling, ma huang, ze xie
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chm interactions w/diuretics?
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-gan cao: + pot loss & cause hypertension
-fan xie ye: + pot loss -lu hui: + pot loss when used w/thiazide diuretics & corticosteroids |
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vasodiatlators mech of action ?
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-cause smooth muscle relaxation in bld vessel
-unique target sites -when smooth muscle of bld vessel relax, tpr is - (dilation of bld vessels) -nito causes both arterial & venous relaxation, this will red the amount of work the ht has to do, by dilating coronary arteries, more o2 bld will flow to ht |
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vasodilators?
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-nitrates include: isosorbide mono-and di- nitrate and nitroglycerin. these drugs are commonly used for angina
-high doses cause postural hypotension, facial flushing, tachycardia -tolerance may be an issue |
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vasodilators ex?
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nitroglycerin (nitro): used to tx angina, also tx chf & hypertensive emergencies
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platelet inhibitors?
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-tx & prevent cv occlusive dzs
-used to maintain vascular grafts -used to keep arteries patent -thrombolytic therapy -also tx pain |
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platelet inhibitors ex?
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-aspirin (white willow bark) & other compounds of ASA: acetylsalicylic acid
-plavix (clopidogrel) |
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anticoagulants?
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-prevent & tx thrombosis & embolism & thromb-embolic disorders
1. thrombus: end product of norm clotting cascade in response to inflammation (bld clot), pathological when not appropriately broken down as par of norm resolution of clotting/inflammation ie. deep vein thrombosis 2. embolus: something carried in circulation & causes blockage elsewhere ie. pulmonary embolism |
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Oral anticoagulants?
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-coumarins, warfarin
-inhibit regeneration of vit k (necessary for clotting synthesis) |
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non-oral anticoagulants?
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prevent coagulation & clot formation by binding & inactivating certain clotting factors
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anticoagulants adverse effects?
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-hemorrhage: signs include petechiae, bld from gums & mucous membranes
-bld monitoring necessary *warfarin is highly pro bound was well as narrow ti. pts must be monitored to maintain an appropriate ability to clot. chm not recommended -warfarin is abortifacient (can cause abort) & teratogenic (birth defects) |
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chm which may potentiate anti-platelet/anti-coagulant effects?
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dan shen, dang gui, chaun xiong, gan cao bai shao, bai zhu, san qi, tao ren
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chm anticoagulants interactions?
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*chm from stop bld cat can counter the effects
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inflammation?
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-is normal & healthy process
-is: norm response to tissue injury caused by infection, physical trauma, noxious chemicals, bodys effort to inactivate/destroy invaders, remove irritants & set the stage for tissue repair -when the healing process is complete, the inflammatory process generally subsides |
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inflammation look lie?
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-rubor: redness
-calor: heat -tumor: swelling -dolor: pain -dysfx *the 1st 4 are caused by previously described inflammatory process |
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pathway of inflammation?
arachidonic acid/cox/lox |
-arachidonic acid is mobilized into interior of mast cells by phospholipases, phospholipase A2 in particular
-AA is then transformed into other inflammatory mediators by 5-lox (5 liooxygenase) or a cox (cyclo-oxygenase) enzyme *recall that the products of 5-lox activation are leukotrienes-which are potent bronchconstrictors |
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cyclo-oxygenase enzymes?
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-cox 1: found norm in most cells, generally associated w/norm physiological fx, reguired for protection of gi mucosa, maintenance of renal fx, control of hemostasis - on a norm basis
-cox 2: induced by the infla process, upregulated by cytokines & other cellular signals |