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150 Cards in this Set
- Front
- Back
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classes of Rx for HTN (4)
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1)diuretic
2) sympathopleggics (b blocker, alpha1, central agents) 3) direct vasodilators 4) ACEI/ARBs |
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hydralazine and minoxidil must be given with what to tx HTN
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beta blockers to prevent reflex tachycardia
(these are direct vasodilators) |
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nitroprusside
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a direct acting vasodilator for HTN
SE: CN toxicity |
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besides b blockers what sympathoplegics are used for HTN
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central: clonidine, methyldopa
inhib NE rel: reserpine, guanethidine alpha1=prazosin nicotinic Ach R antagonist=hexamethonium |
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acetazolamide, mech, where acts
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- carbonic anhydrase causing NaHCO3 diuresis, act PCT
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use acetazolamide (besides HTN)
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urinary alkalinization, metabolic alkalosis, altitude sickness, glaucoma
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toxicity of acetazolamide
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hyper Cl metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
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how acetazolamide affect acid/base of body
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causes systemic acidosis (gets rid of alkaline)
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furosemide actions
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sulfa loop diuretic
1) inhibit Na/K/Cl TAL 2) abolishes hypertonicity of medulla 3) increases Ca excretion |
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toxicity furosemide
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OH DANG: ototoxicity, hypokalemia, dehydration, allergy (ssulfa), nephritis (interstitial), gout
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ethacrynic acid, type Rx, use
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phenoxyacetic acid derivative acts like furosemide but NOT sulfa. use diuresis in those allergic to sulfa
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hydrochlorothiazide, mech, where acts
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thiazide diuretic - DCT Na reabsorb, decr Ca excretion
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summary 3 most impt diuretics
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1) loop-Na/K/Cl of TAL, lose Ca
2) thiazide-(-)Na reabsorb DCT, hold onto Ca 3)spironolactone-competit aldosterone R antagonist in CD |
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which diuretic for Ca kidney stone
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thiazide (holds onto Ca, less Ca in urine)
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mannitol use
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shock, Rx OD, to decrease ICP/IOP
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toxicity mannitol, contraindications
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pulmonary edema, dehydration
CI: anuria, CHF |
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toxicity hydrochlorothiazide
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hypoK metab alkalosis, low Na, hyperGLUC (Glycemia, Lipidemia, uricemia, calcemia)
also sulfa allergy |
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name K sparing diuretics
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Spironolactone, triamterene, amiloride, eplereone
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mech spironolactone
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competitive aldosterone R antagonist in CD
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toxicity spironolactone
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hyperK, gynecomastia, antiandrogen
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amiloride, use, mech
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K sparing diuretic, blocks Na in CD
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triamterene, use, mech
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K sparing diuretic, blocks Na in CD
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hydralazine
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vasodilator arterioles>veins (afterload reduction)
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mech hydralazine
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incr cGMP causes s.m. relaxation
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toxicity hydralazine
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compensatory tachycardia (give w b blocker), fluid retention, Lupus-like
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mech of CCB
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block voltage dependent L type Ca channels of cardiac and smooth muscle, reduce contractility
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compare 3 CCBs effect heart, vascul
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verapamil works greatest on heart least on sm m, nifedipine opposite, diltiazem is inbetween
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toxicities CCB
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cardiac depression, edema, flushing dizziness, constipation
verapamil/dilt: bradycardia, AV block |
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how tx nephrogenic DI
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HCTZ
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mech ACEI
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inhibit ACE
-decr AII -prevent inactiv bradykinin (vasodilator) but renin increases |
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toxicity ACEI
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CAPTOPRIL + hyperkalemia
cough, angioedema, proteinuria, taste changes, hypOtension, Preg, Rash, Increased renin, Lower angII. |
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isosorbide dinitrate, mech
veins > or < arteries? |
a longer acting nitroglycerin, vasodilate by releasing NO, causing incr cGMP and sm m relaxation.
dilates veins>>arteries |
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use isosorbide dinitrate
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(also NG) angina and pul edema
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toxicity isosorbide dinitrate
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tachycardia, hypotension, HA,
[[Monday disease-industrial exposure dev tolerance during week, Mon get tachycardic, dizzy, HA]] |
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how nitrates v. b blocker mainly tx angina
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nitrates mostly affect preload, b blocker mostly affects afterload
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5 ways to reduce myocardial O2 consumption
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1) EDV
2) BP 3) contractility 4) HR 5) ejection time |
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how do nitrates affect
1) EDV 2) BP 3) contractility 4) HR 5) ejection time |
(decr preload)
1) decr EDV 2) decr BP 3) incr contractility (reflex) 4) incr HR (reflex) 5) decr ejection time NET: decr MVO2 |
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how do nitrates and b-blockers given together affect
1) EDV 2) BP 3) contractility 4) HR 5) ejection time |
1) - EDV
2) decr BP 3) - contractility 4) decr HR 5) - ejection time NET big decr MVO2 |
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how do b-blockers affect
1) EDV 2) BP 3) contractility 4) HR 5) ejection time |
(afterload)
1) incr EDV 2) decr BP 3) decr contractility 4) decr HR 5) incr ejection time NET decr MVO2 |
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how do indiv CCB compare to b blocker/ nitrates in tx HTN
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nifedipine like nitrate, verapamil like b blocker
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compare digoxin and digitoxin
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digitoxin has grtr bioavail, much grtr t1/2 (168hrs) bc 70% protein bound, digoxin excreted in urine, digitoxin in biliary (no need adjust in RF)
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beware toxicity digoxin in the cases of:
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RF, hypoK, quinidine (decreases dig clrnc, displaces digoxin from tissue bind sites)
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toxicity digoxin
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N/V/diarrhea, blurry yellow vision, arrhythmia
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mech digoxin
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inhibit Na/K/ATPase but ultimately Na/Ca anitport - reulting in incr intracell Ca
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antidote dig toxicity
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normalize K, lidocaine, cardiac pacer, anti dig Fab
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use dig
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CHF, A fib (decr conduction AV node
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how dig affect EKG
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incr PR, decr QT, scooping of ST, T wave inversion
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diphenhydramine
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1st generation H1 blocker
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dimenhydrinate
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1st generation H1 blocker
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chlorpheniramine
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1st generation H1 blocker
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loratadine
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2nd generation H1 blocker
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fexofenadine
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2nd generation H1 blocker
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name 1st gen H1 blockers
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diphenhydramine, dimenhydrinate, chlorpheniramine
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name 2nd gen H1 blockers
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loratadine, fexofenadine, desloratadine
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toxicity 1st gen H1
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sedation, antimuscarinic, anti alpha adrenergic
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toxicity 2nd gen H1
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less sedation, antimuscarinic, anti alpha adrenergic
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use of H1 blocker
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allergy, motion sickness, sleep aid
(2nd gen just allergy) |
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LTB4
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neutrophil chemotactic agent
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LTC4
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bronchoconstriction, contraction sm m, incr vascular perm
(along with D4, E4) |
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PGI2
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inhibits platelet aggreg and incr vasodilation
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which Rx inhibit leukotrienes
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zafirlukast, montelukast
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affects thromboxane
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-incr plat aggreg
-incr vascular tone -incr bronchial tone |
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affects prostaglandins
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-incr uterine tone
-decr vascular tone -decr bronchial tone |
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affect prostacyclin
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decr plt aggreg, vascular tone, bronchial tone, uterine tone
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where do steroids work
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inhibit phospholipase A2 and protein syn leading to COX
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leukotrienes are derived from what
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lipoxygenase
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zileuton
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inhibits lipoxygenase
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classes asthma drugs
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1) STEROIDS!
2) b2 agonist 3) muscarinic antag 4) cromolyn 5) methylxanthine (theophylline) 6) anti-leukotrienes |
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salmeterol, use, SE
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long acting b2 for prophylaxis in asthma,
SE: tremor, arrhythmia |
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theophylline, mech, SE
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mech: inhibit phosphodiesterase incr cAMP causing bronchodilation
SE: cardiotoxicity, neurotoxicity with narrow therapeutic index |
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ex muscarinic antagonist used in asthma
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ipratropium
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cromolyn, mech, use, SE
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prevents rel mediators from mast cells.
use: only prophylaxis (not acute) SE: rare |
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beclomethasone
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steroid often used in asthma
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name 2, give mech action steroids for asthma
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beclomethasone, prednisone
mech: inhibits syn of all cytokines. inactivates NFkB (t factor for TNFa). 1st line for CHRONIC ASTHMA |
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name antiluekotrienes and mech
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Zileuton-5-lipoxygenase inhibitor blocks conversion arachidonic acid to leukotrienes
Zafirlukast, montelukast-block leukotriene R |
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describe early and late response in asthma and tx
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early response= bronchoconstriction, tx b agonist, muscarinic antag, theophylline
late response=inflamm/bronchial hyperreactivity, tx steroids |
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compare/contrast b agonist, theophylline MOA
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both act to increase cAMP to cause bronchoconstriction, b agonist incr AC, theophylline - PDE (which degrades cAMP)
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compare/contrast where asthma Rx act on pathway causing symptoms
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cromolyn and steroids prevent mediator release, the others block mediators effects
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name H2 blockers (4)
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cimetidine, ranitidine, famotidine, nizatidine
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SE cimetidine
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1) inhibit P450
2) anti androgen 3) incr creatinine |
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SE H2 blockers
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minimal beside cimetidine
cimetidine SE: 1) inhibit P450 2) anti androgen 3) incr creatinine |
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use H2 blockers
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PUD, gastritis, mild GERD
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name PPI (2)
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omeprazole, lansoprazole
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mech PPI
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irreversibly inhibit H/K/ATPase in parietal cells
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use PPI (and how differ from H2 blocker)
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PUD, gastritis, GERD, ZE
(H2 don't use for ZE) |
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name 2 anti-ulcer agents
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bismuth, sucralfate
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sucralfate, MOA
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bind to ulver base and allow HCO3 to reestablich pH gradient--cannot be used with antacids of H2 blockers bc need acid to polymerize
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misoprostol, type Rx, use (3)
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PGE1 analog (increase production and sxn gastric mucous barrier).
use: prevent NSAID induced PUD, maintain PDA, induce labor |
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SE misoprostol
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diarrhea, abortifacient
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infliximab, mech, use
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monoclonal Ab TNFa,
use: Crohns, RA |
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infliximab toxicity
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respir infxn, F, hypotension
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sulfsalazine, mech, use
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combo of sulfapyridine (antibacterial) and mesalamine (anti inflamm)
use: UC, Crohns |
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toxicity sulfsalazine
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malaise, N, sulfonamide toxicity
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SE calcium carbonate antacid use
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hypercalcermia, rebound acid increase
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SE for ALL antacid over use
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hypokalemia
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SE AlOH antacid overuse
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constipation, hypophosphatemia
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advantages of LMWH
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-better bioavail
-(2-4)x t1/2 -no lab monitoring BUT not easily reversible |
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mech heparin
how monitor? |
activates antithrombin III, decr thrombin and Xa
MONITOR: PTT |
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PTT THINK:
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Heparin, intrinsic "HIT"
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PT think:
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warfarin, extrinsic "wet pet"
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lab monitor LMWH
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factor Xa (not usu necessary)
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heparin use
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immed anticoag (PE, stroke, angina, MI, DVT)
can be used in preg (doesn't cross placenta) |
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reversal of heparin, mech
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protamine sulfate positively charged binds negative heparin
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toxicity heparin
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bleeding, thrombocytopenia/HIT, drug-drug interactions
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mech Warfarin
monitor by |
interferes syn and gamma carboxylation vit K factors II, VII, IX, X, prot C, S
MONITOR: PT |
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compare contrast warfarin and heparin: structure
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heparin: large anionic, acidic polymer
warfarin: small lipid soluble |
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compare contrast warfarin and heparin: site action
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hep: blood
warfarin: liver |
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compare contrast warfarin and heparin: onset
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hep: rapid
warf: slow (limited by t1/2 of factors) |
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use warfarin
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chronic anticoag, cannot be used in preg (crosses placenta)
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toxicity warfarin
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bleeding, teratogen, drug-drug interactions
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compare contrast warfarin and heparin: reversal
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hep: protamine sulfate
warf: IV vit K, FFP |
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on initial starting of warfarin...
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start with heparin, bc warfarin can initially cause pro-coag state bc Prot C has shortest 1/2 life, is affected before the others
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mech of thrombolytics
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acitvate plasmin (major fibrinolytic ensyme), tPA specifically targets fibrin bound plasminogen
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what directly opposes thrombolytics
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aminocarpoic acid which inhibits fibrinolysis
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contraindications thrombolytics
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bleeding, hx intracranial bleed, recent sx, severe HTN
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name thrombolytics
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streptokinase, urokinase, tPA (alteplase), APSAC (anistreplase)
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does ASA affect PT, PTT?
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no
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toxicity ASA
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ulcer, bleeding, Reye's syndrome, tinnitus, hypervent
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ticlopidine
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inhibits plat aggreg by irrev blocking ADP R, inhibits fibrinogen binding by preventing gpIIb/IIIa expression
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clopidogrel
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inhibits plat aggreg by irrev blocking ADP R, inhibits fibrinogen binding by preventing gpIIb/IIIa expression,
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abciximab
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binds gp R IIa/IIIb on activated platelets
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toxicity clopidogrel, ticlopidine
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neutropenia (ticlodipine)
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toxicity abciximab
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bleeding, thrombocytopenia
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summarize anti coag agents
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-ASA via COX - TXA2
-ADP R blockers (clopidogrel, ticlopidine) -gpIIb/IIIa R blocker (abciximab) |
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leuprolide, mech, use
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GnRH analog agonist when pulsatile, antagonist when continous
use: 1) infertility (pulse), 2) prostate ca (cont), 3) uterine fibroids |
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toxicity leuprolide
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antiandrogen, N/V
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propylthiouracil, mech, use
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inhibit organification and coupling thyroid H syn, decr peripheral conversion T4 to T3
use: hyperthyroidism |
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methimazole, mech, use
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inhibit organification and coupling thyroid H syn
use: hyperthyroidism |
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toxicity methimazole
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rash, aplastic anemia, agranulocytosis (rare)
note: same SE as for PTU |
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toxicity PTU
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rash, aplastic anemia, agranulocytosis (rare)
(same SE as methimazole) |
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name antiandrogens and use (4)
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finasteride (5a reductase inhib, BPH, baldness)
flutamide (inhib androgens at testost R, prostate ca) ketoconazole, spironolactone (inhib steroid syn, used polycistic ovarian syn to prevent hirsutism) |
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ketoconazole
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inhib steroid syn used polycystic ovarian syn to prevent hirsutism
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name glucocorticoids (5)
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hydrocortisone, prednisone, dexamethasone, beclomethasone, *triamcinolone
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triamcinolone
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glucocorticoid
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finasteride
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5a reductase inhib,
use: BPH, baldness |
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flutamide
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inhib androgens at testost R,
use: prostate ca |
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use steroids
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addison's, inflamm, immune suppression, asthma
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toxicity steroids
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iatrogenic Cushing-buffalo hump, moon facies, truncal obesity, mscl wasting, thin skin, bruising, osteo, adrenocortical atrophy, PUD
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tx erectile dysfxn (3), mech
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sildenafil, vardenafil, tadafil
mech: - cGMP PDE causing incr cGMP, sm m relax in corpus cavernosum, incr BF, erection |
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toxicity sildenafil
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HA, flushing, dyspepsia, blue-green vision
**risk hypotension w nitrates |
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clomiphene, mech, use
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partial agonist at estrogen R in pituitary, preventing feedback inhib cause incr rel LH, FSH
use: infertility |
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toxicity clomiphene
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hot flashes, ovarian enlargement, multiple preg, visual
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mifepristone, mech, use
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competit inhib progestins at progesterone R
use: abortion AKA RU-486 |
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toxicity mifepristone
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heavy bleeding, N/V, anorexia, abd pain
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tx acute gout
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NSAIDs, often indomethacin
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colchicine, mech, use
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depolymerizes microtubules - leuko chemotaxis and degranulo,
use: acute gout, but not commonly used 2/2 SE (esp GI when given orally) |
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probenecid, mech, use
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- uric acid (also inhib sxn PCN),
use: chronic gout |
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complication probenacid
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inhib sxn PCN
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allopurinol, mech, use (2)
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inhibits xanthine oxidase (conversion xanthine to uric acid)
use: chronic gout, tumor lysis syndrome |
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advantages, disadvantages OCP
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+: reliable, decr endomet and ovarian ca, decr ectopic preg and pelvic infxn
-: daily, no protection STDs, incr TG, hypercoag, wgt gain, N, depression, HTN |
