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238 Cards in this Set
- Front
- Back
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Other NSAIDS
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pg 313
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List three NSAIDS?
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ibuprofen, naproxen, indomethacin
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What is their mechanism?
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reversibly inhibit COX 1 and 2. Blocks PG synthesis
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What is their clinical use (3As)?
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Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
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What are common toxicities?
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renal damage, aplastic anemia, GI distress, ulcers
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COX 2 Inhibitors
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pg 314
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Where is cox2 found?
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in inflammatory cells and mediates inflammation and pain
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Why is cox2 inhibition better than cox1?
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cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)
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Clinical Use?
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RA and osteoarthritis
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Acetaminophen
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pg 314
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What is its mechanism and where does it work?
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reversibly inhibits cox, mostly in CNS. Inactivated peripherally.
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What are its 2 As?
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antipyretic, analgesic but NOT anti-inflammatory.
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Overdose effects?
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hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver
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cardiovascular therapy
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pg 314
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Changes in CO affect two major pathways?
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1. Carotid sinus firing, sympa discharge 2. Renal blood flow, renin-ang pathway
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What is the effect of the following drugs: 1. Positive inotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII antagonists 5. Vasodilators and 6. Diuretics
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1. Increases cardiac output. 2. Inhibit renin release. 3. Inhibit ACE 4. Inhibits effects of AngII including increasing the preload, increasing the afterload and remodelling. 5. Decrease the preload and afterload. 6. Decrease the preload and afterload
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antihypertensive drugs
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pg 315
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What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics
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1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia 2. Hypokalemia, met alk, hypotension, ototoxicity
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These are wahat class of drugs: clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?
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sympathoplegics
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Adverse effects of clonidine?
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dry mouth, sedation, severe rebound HTN
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Adverse effects of methyldopa?
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sedation, positive coombs test
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Adverse effects of ganglionic blockers?
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orthostatic HTN, blurred vision, constitpation, sexual dysfuncction
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Adverse effects of reserpine?
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sedation, depression, nasal stuffiness, diarrhea
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adverse effects of beta blockers?
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impotence, asthma, cardiovascular, cns
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Adverse effects of guanethidine?
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orthostatic and exercise Hypotension, sex dysfxn, diarrhea
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Adverse effects of prazosin?
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1st dose orthostatic hypotension, dizzy, headache
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The following are what class: hydralazine, minoxidil, nifedipine, verapamil, nitroprusside
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vasodilators
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which one causes lupus like syndrome? Other toxicities?
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hydralazine, nausea, headache, reflex tachycardia, angina, salt retention
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adverse effets of minoxidil?
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hypertrichosis (hair growth - think Rogaine with minoxidil!), pericardial effusion, reflex tachycardia, angina, salt retention
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Side effects of nifedipine, verapamil?
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dizziness, flushing, constipation, nausea
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which one causes cynide toxicity?
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nitroprusside
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Adverse effects of ACE-I Captorpil? Think CAPTOPRIL
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C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension, P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L: lower angiotensin. Also hyperkalemia.
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Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia
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angiotensin II, fetal renal, hyper
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Hydralizine
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pg 315
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Which two anti-htn drugs do you use with B blockers to prevent reflex tachycardia, diuretic to block salt retention?
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hydralizine, minoxidil
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What is hydralizine's mechanims and clinical use?
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increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins. Reduces afterload. Used for severe HTN or CHF
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Calcium channel blockers, name three
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pg. 315 - nifedipine, verapamil, diltiazem
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Mechanism: block _____ chanels of cardiac and smooth muscles to reduce contractility
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voltage dependednt L type Ca
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Rank their effects on vascular smooth muscle ad on the heart.
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smooth muscle nifed> diltia > verapamil heart: vera> diltia> nifedepine
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What is the calcium channel blockers use?
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HTN, angina, arrythmias (not nifedipine)
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ACE -I, name three
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pg 316 - captopril, enalapril, lisinopril
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Mechanim considering bradykinin and renin release?
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reduce lvels of ang II, prevent inactivation of bradykinin, renin release is increased to to loss of feedback inhibition
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what is the clinical use of these?
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HTN, CHF, diabetic renal disease
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Diuretics- site of action
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pg 316
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What is the site of action of 1. Acetazolamide, 2. Osmotic agents, 3. Loop agents, 4. Thiazides, 5. Potassium sparing, 6. ADH antagonists
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1. PCT 2. PCT, thin desc limb, CD 3. Thick ascending limb 4. Distal conv tubule 5. DCT a bit later 6. CD in inner medulla
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How does mannitol an osmotic diuretic work?
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increase tubular fluid osmolarity, producing increased urine flow
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what is the use and toxicity?
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Use: shock, drug overdose, decrease intracranial pressure. Toxicity - pulmonary edema, dehydration. Contraindicated in anuria, CHF
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Acetazolamide
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pg 317
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Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.
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Carbonic anhydrase, self-limited NaHCO3, reduction.
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What electrolye disturbace does it treat? Does it cause?
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treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.
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Other toxicity?
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neuropathy, NH3 toxicity, sulfa allergy
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uses?
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glaucoma, urinary alk, met alk, altitude sickeness
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Furosemide
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pg 317
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This sulfonamide loop diuretic inhibits _______cotransport
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NA, K, 2CL
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Furosemide also works by?
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abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium
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The three uses for this loop diuretic?
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edematous states, htn, hypercalcemia
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Toxicity using the OH DANG?
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ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout
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Ethacrynic Acid
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pg 317
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How is this drug different from furosemide? And how does that affect its use?
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Although both have the same action, ethacrynic is a phenoxyacetic acid derivative not a sulfonamide. Therefore use this drug when you are allergic to sulfa.
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What drug can be used to treat acute gout?
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ethacrynic acid
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AUTHOR
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Stacy Ugras
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Hydrochlorothiazide
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p.318
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Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule
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NaCl; early distal tubule
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Does hydrochlorothiazide increase or decrease the excretion of calcium ion?
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decrease
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A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium
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hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)
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K+-sparing diuretics
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p.318
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Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule
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aldosterone; cortical collecting tubule
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Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct
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Triamterine and amiloride
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Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect
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Gynecomastia (antiandrogen effect)
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Name three K+-sparing diuretics
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Spironolactone, Triamterene, Amiloride (The K+ STAys.)
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Diuretics: electrolye exchange
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p.318
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Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?
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All of them!
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Which types of diuretucs increase urine K+?
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All except K+-sparing diuretics. Carbonic anhydrase inhibitors, loop diuretics, thiazides.
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Do carbonic anhydrase inhibitors increase or decrease blood pH?
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Decrease, cause acidosis
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Do K+-sparing diuretics cause acidosis or alkalosis?
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Acidosis, decreases pH
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Do loop diuretics cause acidosis or alkalosis?
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Alkalosis, increases pH
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Do thiazide diuretics cause an increase or decrease in blood pH?
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Increase, cause alkalosis
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Do loop diuretics increase or decrease levels of urine calcium ion?
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Increase
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Do thiazide diuretics increase or decrease levels of urine calcium ion?
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Decrease
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Antianginal therapy
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p.319
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Name four determinants of the level of myocardial oxygen consumption
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There are five: end diastolic volume, blood pressure, heart rate, contractility, ejection time
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Do nitrates affect preload or afterload?
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preload
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Do Beta-blockers affect preload or afterload?
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afterload
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What is the effect of nitrates on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
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decrease EDV, decrease BP, increase contractility (reflex response), increase HR (reflex response), decrease ejection time
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What is the effect of Beta-blockers on: diastolic volume, blood pressure, contractility, heart rate, ejection time?
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increase EDV, decrease BP, decrease contractility, decreased HR, increase ejection time
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The effects of using nitrates and Beta-blockers together will: a) decrease myocardial oxygen demands by the same amount as using either alone, b) decrease myocardial oxygen demands by an amount greater than if each were used alone, or c) have no effect on myocardial oxygen demand
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b) Decrease myocardial oxygen demands by an amount greater that if each were used alone
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Nifedipine blocks -- channels
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calcium
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In its effects on myocardial oxygen consumption, is Nifedipine similar to Nitrates or B-blockers?
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Nitrates (Nifedipine is similar to Nitrates)
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In its effects on myocardial oxygen consumption, is Verapamil similar to Nitrates or B-blockers?
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B-blockers
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Nitroglycerine, isosorbide dinitrate
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p.319
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Dose nitroglycerin dilate arteries or veins more?
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Veins>>arteries
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Does nitroglycerin increase or decrease cGMP in smooth muscle?
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Increase
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In industrial exposure to nitroglycerine, weekend withdrawal is characterized by which three symptoms?
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Tachycardia, dizziness , and headache ("Monday disease")
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Toxic dosage of nitroglycerine causes which three symptoms?
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Tachycardia, hypotension, headache
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Cardiac drugs: sites of action
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p.320
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Digitalis has its action on which cell membrane transporter?
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Na/K ATPase
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Ryanodine has its action on which channel?
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Calcium release channel in the sarcoplasmic receptor
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Calcium enters cardiac cells through which channel?
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Voltage-gated calcium channel
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Cytoplasmic calcium concentrations in cardiac cells can be decreased by sequestering calcium in the sarcoplasmic reticulum. Calcium enters the SR through which transporter?
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Calcium pump in the wall of the SR
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Calcium channel blockers have their effect on which calcium transporters?
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Voltage-gated calcium channel
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Cardiac Glycosides
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p.320
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What is digoxin's effect on the intracellular Na+ level?
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Increase
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What is digoxin's effect on the intracellular calcium level?
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Increase
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Name two ECG changes ellicited by digoxin administration
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There are 4: increase PR, decrease QT, scooping of ST segment, T-wave inversion
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Name three symptoms of digoxin toxicity
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Nausea, vomiting, diarrhea, blurry vision, arrhythmia
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Which potentiates the effects of digoxin- hypo- or hyperkalemia?
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hypokalemia
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Antiarrhythmics- Na+ channel blockers (classI)
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p.321
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Which phase of the cardiac action potential do antiarrhythmics decrease the slope of?
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Phase 4 depolarization
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What type of antiarrhythmic is Amiodarone?
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Class 1A (Class 1A includes Quinidine, Amiodarone, Procainamide, Disopyramide, "Queen Amy Proclaims Diso's pyramid."
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Do class 1A antiarrhythmics increase or decrease the effective refractory period, AP duration, and QT interval?
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Increase ERP, increase AP duration, increase QT interval
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What do class 1B antiarrhythmics do to the AP duration?
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Decrease AP duration
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What type of antiarrhythmic is mexiletine?
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Class 1B (includes Lidocaine, mexiletine, tocainide)
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What type of antiarrhythmic is encainide?
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Class IC (includes flecainide, encainide, propafenone)
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What effect do class 1C antiarrhythmics have on the AP duration?
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No effect!
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Antiarrhythmics- Beta-blockers (classII)
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p. 322
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What does esmolol do to the cAMP in cardiac cells?
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decreases cAMP (a beta-blocker)
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What does atenolol do the calcium currents in cardiac cells?
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decreases calcium current (beta-blocker)
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Timolol decreases the slope of which phase of the cardiac AP cycle?
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Phase 4 (a beta-blocker)
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What does propanolol do the the PR interval?
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Increases interval (beta-blocker)
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Is esmolol a short- or long-acting beta blocker?
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short-acting
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Antiarrhythmics- K+ channel blockers (class III)
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p. 322
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Does amiodarone increase or decrease AP duration?
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Increase (K+ channel blocker)
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Does sotalol increase or decrease the effective refractory period?
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Increase (K+ channel blocker)
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Does bretylium increase or decrease the QT interval?
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Increase (K+ channel blocker)
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Name a symptom of sotalol toxicity.
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Torsades de pointes (K+ channel blocker)
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Name three of the symptoms of amiodarone toxicity.
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Pulmonary fibrosis, corneal deposits, hepatoxicity, skin deposits resulting in photodermatitis, neurologic effects, constipation, bradychardia, heart block, CHF, hypothyroidism/hyperthyroidism. (Therefore, should check PFTs, LFTs, and TFTs)
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Antiarrhythmics- Ca2+ channel blockers (class IV)
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p. 323
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Does verapamil increase or decrease the conduction velocity of the AV nodal cells?
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Decrease (calcium channel blocker)
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How does diltiazem affect the effective refractory period and the PR interval?
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Increases ERP, increases PR (calcium channel blocker)
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Other antiarrhythmics
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p. 323
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Name a potential use of Mg+ to treat arrhythmias.
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To treat torsades de pointes and digoxin toxicity
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Name a potential use of K+ to treat arrhythmias.
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Depress ectopic pacemakers, especially in digoxin toxicity
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Name a use of adenosine in treating arrhythmias.
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To diagnose and abolish AV nodal arrhythmias.
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Lipid-lowering agents
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p. 324
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What is the effect of cholestyramine on the serum triglyceride level?
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Slight increase (cholestyramine is a bile acid resin)
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What is the effect of colestipol on HDL?
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No effect! (colestipol is a bile acid resin)
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What is the effect of lovastatin on HDL?
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Increase (lovastatin is an HMG-CoA reductase inhibitor)
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Name 2 side effects of pravastatin.
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Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)
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What is the effect of Niacin on HDL?
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Increase
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What are the side effects of clofibrate?
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Incease LFTs and cause myositis (Clofibrate is a "Fibrate")
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Which increases HDL most: simvastatin, niacin, or gemfibrozil?
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Niacin
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Which decreases triglyceride level most: colestipol, Atorvastatin, niacin, or bezafibrate?
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Bezafibrate
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What is the main effect of ezetimibe?
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decrease serum LDL (a cholesterol absorption inhibitor)
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Gemfibrozil increases the activity of which enzyme?
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Lipoprotein lipase (which converts VLDL to IDL)
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AUTHOR
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Rafael Vazquez
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Arachidonic acid products
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p.325
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What enzyme breaks down membrane lipid into arachidonic acid?
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Phospholipase A2
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What two enzymes are responsible for the production of Hydroperoxides (HPETEs) and Endoperoxidases, respectively from arachidonate?
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Lipoxygenase= HPETE, Cyclooxygenases=endoperoxidases
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What major class of products do HPETEs give rise to?
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Leukotrienes
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What are the 3 major products of Endoperoxidases?
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Prostacyclin (PGI), Prostaglandins (PGE, PGF), Thromboxane (TXA)
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In general what effect do leukotrienes have on bronchial tone?
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Leukotrienes in general increase bronchial tone
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In the arachodonic acid pathway, what two enzymes do corticosteroids block?
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Phospholipase A2, COX-2
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NSAIDs, Acetaminophen and COX-2 inhibitors block which arachadonic acid pathway enzymes
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NSAIDs-non-selectively block COX-1 and COX-2, acetaminophen doesn't block COX-1 or COX-2, but instead it may block COX-3 in found in the brain, COX-2 inhibitors block COX-2
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What are the 4 major effects of Prostacyclin
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decrease platelet aggregation, decrease vascular tone, decrease bronchial tone, decrease uterine tone
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What are the 3 major effects of Prostaglandins
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increased uterine tone, decrease vascular tone, decrease bronchial tone
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What are the 3 major effects of Thromboxane
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increase platelet aggregation, increase vascular tone, increase bronchial tone
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Zileuton is a ________ pathway inhibitor?
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Lipoxygenase
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Zariflukast is associated with what enzymes?
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Lekukotrienes
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Asthma drugs
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p 326
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Bronchodilation is mediated by what molecule
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cAMP
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Bronchoconstriction is mediated by _________ and ___________
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Ach and adenosine
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How many asthma drug categories are there?
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7- (1) nonspecific B-agonists, (2) B2 agonists, (3) Methylxanthines, (4) muscarinic antagonist, (5) cromolyn, (6) corticosteroids, (7) Antileukotrienes
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What is the only nonspecific B-agonist drug and what are its effects?
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Isoprotenerol-relaxes bronchial smooth muscle (B2) and tachycardia (B1) (adverse effect).
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What are the two B2 selective agonist asthma drugs?
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Albuterol- relaxes bronchial smooth muscle (B2), Salmetrol
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What are the indications for Albuterol and Salmetrol, respectively?
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Albuterol- use during acute exarcebation, Salmetrol- long-acting agent for prophylaxis
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what are the notable adverse effects of B2 agonist?
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arythmias and tremor
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B2-agonists activate this enzyme in bronchial smooth muscle that leads to an increase in ________ = bronchodilation
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B2 agonists activate adenylate cyclase and increase conversion of ATP to cAMP
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What are the likely mechanism of action theophylline?
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bronchodialation by inhibition phosphodiesterase (PDE), decreasing cAMP hydrolysis and antagnonizing adenosine action
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Why is usage of theophylline limited?
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limited b/c narrow therapeutic index (cardiotoxicity, neurotxicity)
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What kind of drug is Ipratropium?
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muscarinic antagonist
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How does mechanism of action of Ipratropium?
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competitive block of muscarinic receptors= prevention of bronchoconstriction
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cromolyn works by inhibiting the release of _______ from ______ cell?
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prevents release of medicators from mast cells
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Cromolyn is mainly used for the ______ of athsma and it is not indicated for _______ treatment of athsma?
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Used only for prophylaxis, not effective during acute episode. Also, toxicity rare
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__________and ________ are two major corticosteroids used for treatment of what kind of asthma?
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Beclomethasone and prednisone are 1st line therapy for chronic asthma
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What is the mechanism of action of corticosteroids?
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inhibits the synthesis of virtually of cytokines-->inactivates NF-KB, the transcription factor that induces the production of TNF-a, amonth other inflammatory agents.
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Zileuton blocks the conversion of _______ to ________.
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zileuton is a 5-lipoxygenase pathway inhibitior. Blocks the conversion of arachidonic acti to leukotrienes
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Zafirlukast works by_______ ________ ________
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bloking leukotriene receptors
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What the most basic asthma treatment strategy?
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avoidance of exposure to antingen (dust, pollen, etc)
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After exposure to antigen crosslinks IgE on mast cells. This is prevented by the following drugs: _________ and ________
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cromolyn and steroids
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Following allergen exposure mediators are released (ex. _______ and _________). This triggers an ______ asthmatic response characterized by ________ and may be treated with the following 3 asthmatic drug categories to treat the symptoms.
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examples of mediators are leukotrienes and histamine. Following allergen exposure an early asthmatic response characterized by bronchoconstriction that can be treated with B-agonsists, methylxanthines, and muscarinic antagonists.
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Also, mediators elicit a ________ response is which leads to bronchial __________ and is treated with __________.
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mediators elicit a late response and this leads to bronchial hyperactivity. This is best treated with steroids.
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GI therapy
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p. 327
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the following questions are from the diagram at the top of the page
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_____ cells are predominatly found in the antrum and _________ cells are predominatly found in the fundus.
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Gastrin cells are predominant in the antrum and parietal cells are predominant in the fundus.
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What are the 3 main stimuli of acid secretion?
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Ach, histamine, gastrin
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Gastrin stimulates the ECL cells to secrete histamine that stimulates ______ cells. Gastrin also activate the ______ cells to increase expression of _______ that increases ______secretion.
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Gastrin stimulates the ECL cells to secrese histamine that stimulates parietal cells. Parietal cells are also activated by gastrin to increase the expression of the H,K ATPase that increases acid secretion.
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This type of drug acts by inhibiting M1 and M3 receptors on ECL cells and Parietal cells, respectively.
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muscarinic antagonists block M1 receptors in ECL cells and M3 receptors in parietal cells.
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This type of drug inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the _____ receptor.
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H2 blocker inhibits the ability of the ECL cell to stimulate acid secretion by interfering with the parietal H2 receptor.
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The most direct way of inhibiting acid secretion is by using this type of drug which acts on this enzyme.
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the most direct way of inhibiting acid secretion is by using proton pump blockers which inhibit the H,K ATPase on parietal cells.
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____________ acts by binding to the ulcer and increasing its healing. It may interfere with drug absorption in the stomach.
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sucralfate binds to the ulcer base and provides physical protection. It allows HCO3- secretion to reestablish pH gradient in the mucus layer.
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What hormone binds ECL cells and decreases acid secretion?
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somatostatin
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These type of drugs used to decrease pH in the stomach.
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antacids
.duh
.jk. (I was instructed to make a question of every word)
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questions not from the diagram
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____________, ___________, ___________, and ___________ are examples of H2 blockers and they act by (reversibly/irreversibly)
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cimetedine, ranitidine, famotidine, nizatidine reversilbly block H2 receptors.
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This H2 blocker is the only one that has many side effects which include potent inhibition of ______, _____ effects, and _____ renal excretion of creatinine.
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cimetedine is a potent inhibitor of P450, it has antiandrogenic effect and decrease renal excretion of creatinine. Other H2 blockers are relatively free of these effects.
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_________ and _________ (reversibly/irreversibly) inhibit the H/K ATPase in the stomach _______cells.
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Omeprazole and Iansoprazole irreversibly inhibit the H/K ATPase in stomach parietal cells
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Proton pump inhibitors are indicated for peptic ulcer, ________, _______, and _________ syndrome
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peptic ulcer, gastritis, esophageal reflux, and Zollinger-Ellison syndrome
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T/F: Bismuth and sucralfate allow HCO3- secretion.
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True: bismuth and sucralfate bind to ulcer base and provide physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucus layer=increased ulcer healing
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T/F: misoprostol is a PGE2 analog and increases the production and secretion of gastric mucous barrier.
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False: misoprostol is a PGE1 analog and it increases the production and secretion of gastric mucous barrier.
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What are the 3 indications for misoprosol?
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prevention of NSAID-induced peptic ulcers, maintains a PDA and used to induce labor
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In what population is misoprostol contraindicated?
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women of childbearing potential (abortifacient). It also casues diarrhea
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Infliximab is ___________ against ______.
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monoclonal antibody to TNFa
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The clinical indication for Infliximab is:
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Crohn's, along with fistula healing
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T/F: Infliximab can cause respiratory infection, fever, hypotension
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TRUE
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GI Drugs (cont.)
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p. 328
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This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases ______ and _______.
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sulfasalazine: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory effects). It is used for Ulcerative colitis and remission of Crohn's.
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T/F: Side effects of the above include: malaise, sulfonamide toxicity, neutropenia
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false: side effects: malaise, nausea, sulfonamide toxicity
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___________ is a powerful central-acting antiemetic. It acts by antagonizing the______ receptor.
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Ondansetron: is a powerful antiemetic. Think: you will not vomit with ondansetron, so you can go on dancing.
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T/F used to treat vomiting preoperatively and for cancer chemo therapy pts.
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False: it is used to treat vomiting postoperatively.
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Headache and __________ are side effects
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constipation (can't vomit or poop)
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Antacid overuse can affect:_________, __________, or ______ excretion of other drugs by altering ______ and ______ pH or by delaying gastric _________.
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Antacid overuse can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
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Constipation and (hypo/hyper) phosphatemia is seen with overuse of ________________
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aluminum hydroxide - Aluminimum amt. of feces
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Magnesium hydroxide overuse = ___________
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diarhea; Mg = Must go to the bathroom
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Calicium carbonate= hypercalcemia and (increase/decreased) acid
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causes hypercalcemia and increased acid.
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T/F: hyperkalemia can be seen with AlOH, MgOH, CaCO2
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False! hypokalemia
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Hematologic Drugs
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p328
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heparin
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Catalyzes activation of ____________, decreases ________ and __________. It has a ____t1/2. check PTT
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catalyzes the activation of antithrombin III, decreases thrombin and Xa. It has a short t1/2
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It is used for immediated anticoagulation for pulmonary embolism,_______, _______, MI, and ________. Follow PTT
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used for pulmonary embolism, stroke, angina, MI, and DVT.
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T/F: Is used during pregnancy
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true: it is used during pregnancy because it does not cross the placenta.
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It can cause bleeding,___________, and drug-drug interactions.
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thrombocytopenia
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___________ is used for rapid reversal of heparization (it is a _______ charged molecule that binds the ________ charged heparin)
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protamine sulfate is used for rapid reversal of heparinization (it is a positively charged molecule that binds the negatively charged heparin).
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Newer________________ (enoxaparin) act more on _____, have better bioavailability and 2-4 times longer t1/2. Can be administered subcut and (with/without) lab monitoring.
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lower-molecular-weight heparins (enoxaparin) act more on Xa, have better bioavailabitlity and 2-4 times longer half-life. Can be adm. Subcut and without lab monitoring.
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warfirin (coumandin)
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p. 328
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Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent factors ___, ___, ___, and ___, also, ___ and ___ via ______ antagonism.
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Interferes with normal synthesis and gamma-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X, protein C and S via vitamin K antagonism.
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t1/2 (short/long)
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long
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Used for _______ anticoagulation. Follow PT
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WEPT - Warfirin affects the Extrinsic pathway and prolongs PT
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T/F: is used during pregnacy
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False! (warfarin, unlike heparin, can cross the placenta).
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Toxicity: bleeding, _________, drug-drug interactions
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teratogenic
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heparin vs. warfarin
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p. 329
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Heparin is a (large/small) _____charged acicid polymer while Warfarin is (large/small) (charged/neutral) molecule
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Heparin is a large negatively charged acidic polymer while Warfarin is a small neutral charged lipid-soluble molecule
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T/F: Heparin is given orally while warfarin is given SC/IV
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False! Heparin is given IV/SC and warfarin is give oral
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Site of action: heparin _________, warfarin ______
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heparin's site of action is the blood; warfarin's site of action is the liver (synthesises clotting factors)
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Onset of action of _________ is slow; the onset of action of ______ is rapid
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onset of action of heparin is rapid (secs) and the onset of action of warfarin is slow, limitd by t1/2 of normal clotting factors.
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Warfarin works by imparing the synthesis of _______ dependent factors __, ___, ___, and ___ also _____, and ____; heparin activates _____, ____ and ___
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Warfarin works by imparing the synthesis of vitamin K dependent factors II, VII, IX, and X also protein S and protein C; heparin activates ATIII, Iia (thrombin) and Xa.
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Heparin 's duration of action is (acute/chronic); warfarin's duration of action is (actue/chronic)
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Heparin's duration of action is actute and warfarin's duration of action is chronic.
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Tx of acute OD: Heparin = _________; warfarin=______
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Tx of heparin OD is protamine sulfate; Tx of warfarin= IV vit. K and fresh frozen plasma.
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Warfarin is monitored by _________ while Heparin is monitored by ___________.
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Warfrin is monitored by PT (extrinsic pathway) (WEPT) and heparin is monitored by PTT (intrinsic pathway)
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