Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
103 Cards in this Set
- Front
- Back
- Diuretic
- Effective for only a few days - Inhibit CA enzyme in luminal membranes of proximal tubule - blocks bicarb reabsorption - reduces Na reabosorption - increases Na/K exchange Tx: - met alkalosis - acute mtn sickness - glaucoma - alkalinize urine - adjuvant in epilepsy Tox: - renal stones - renal potassium wasting - hyperchloremic metabolic acidosis CI: - cirrhosis - sulfonamide hypersensitivity |
Carbonic Anhydrase inhibitors
|
|
- Carbonic anhydrase inhibiting diuretic
- Oral tx for acute mountian sickness |
Acetazolamide
|
|
- Carbonic anhydrase inhibiting diuretic
- Topical tx for glaucaoma |
Brinzolamide & Dorzolamide
|
|
- Loop diuretic
- Most ototoxic - Non sulfa drug |
Ethacrynic Acid
|
|
- Loop Diuretic
- enhances Ca excretion - Blk Na/K/2Cl cotransport (thick asc. loop) system - reduces resorption of Na - increases excretion of Mg & Ca - induce PG synthesis Tx: - pulm edema - acute renal failure - hyper-K - hyper- Ca SE: OH DANG! – Ototoxicity, Hypokalemia, Dehydration, Allergy(sulfa), Nephritis(interstitial), Gout CI: - NSAIDs - aminoglycosides (enhanced ototoxicity) - Lithium - CHF - renal failure - hepatic cirrhosis |
Furosemide
|
|
- newer loop diuretics
- Same MOA as fureosimide - available for tx of edema due to CHF - safe in hepatic & renal diseases |
Bumetanide & Torsemide
|
|
- Thiazide diuretic
- DOC: HTN |
Hydrachlorathizide
|
|
- Thiazide diuretic
- Less metabolic complications - Calcium Channel Blocker like effects - also a direct vasodilator |
Indapamide
|
|
- initial tx for uncomplicated HTN alone or combined
- reduce Na body stores, decrease blood volume & reduce CO - action can be inhibited by NSAIDS (dependent on PG synthesis) - activate potassium channels after 6-8 weeks to cause decline in peripheral resistance - More effective in blacks than whites and elderly rather than younger patients Used to Tx: - HTN, CHF - Nephrolithiasis - Nephrogenic diabetes insipidus SE: - increased plasma lipid concentration - Reduced glucose tolerance - Hypersensitivity (sulfonamide) - Hypokalemia - Hyperuricemia - Decrease Ca excretion - MG loss |
Thiazides
|
|
- Thiazide diuretic
- Diuresis in patients w/ reduced GFR |
Metolazone
|
|
- Thiazide diuretic
- Slower absorption, longer duration |
Chlorthalidone
|
|
- Selective Aldosterone antagonist K spaing Diuretic
- smilar MOA to spironolactone - lower incidence of endocrine related side effects |
Eplerenone
|
|
- Potassium sparing diuretics
- inhibit the Na/K xchange in distal renal tubule independent of aldosterone SE: - Hyper K |
Triamterene & Amiloride
|
|
- Diuretics
– inh. Aldosterone receptors in distal/collecting duct Tx: edema assoc w/CHF, cirrhosis, nephrotic syndrome |
Aldosterone Antagonists
|
|
- Diuretic
- act on late distal tubule & cortical collecting tubule - comprsed of Adlosterone antagonists & Direct sodium flux inhibitors - Inh Na/K exchange (collecting ducts) Tx: CHF, combined with K losing drugs, cirrhosis CI: Hyper-K -Triamterene -Amiloride – DOC for lithium induced DI |
Posassium Sparing Diuretics
|
|
- Aldosterone antagonist K sparing diuretic
- MOA: competitive inhibitor of aldosterone - oral admin - ↑ survival in CHF - most effective tx of hyperaldosteronism SE: - gynecomastia - impotence - caution with ACE inhibitors & ARBs (acidosis) |
Spironolactone
|
|
- K sparing diuretic
- DOC for lithium induced diabetes insipidus |
Amiloride
|
|
- Osmotic diuretic
- Organic compound compsed of two NH2 groups joined by a carbonyl |
Urea
|
|
- Osmotic diuretic
- decreased intracranial pressure - Neuro-sx prophylaxis |
Mannitol
|
|
- Diuretic
- not absorbed orally (if taken orally causes diarrhea), IV only - MOA: filtered but not reabsorbed in kidney (keeps water in tubules) - pharmacologically inactive SE: - Dehydration, hyper-Natremia - can produce pulmonary edema in CHF CI: severe CHF (early over-expansion of intravascular space) |
Osmotic diuretics
|
|
- Osmotic diuretic
- Vasodilator - Nitrite: sublingual (skip 1st pass), dilates veins →↓preload, - develop tolerance so not for long term use - reduces preload & afterload on heart - decreases damaging remodeling of heart |
Isosorbide
|
|
- Osmotic Diuretic
- also can be used to soften the stool |
Glycerin
|
|
- ADH agonist
- exogenous parenteral form of ADH |
Vasopressin
|
|
- ADH agonist
- synthetic longer acting analog of ADH - indicated in ruptured esophagus varix bleeding |
Desmopressin
|
|
- ADH antagonists
- Used for SIADH & other causes of elevated ADH |
Conivaptan & Tolvaptan
|
|
- ADH antagonist
- increases permeability in collecting duct - Produces nephrogenic DI - Used for SIADH & other causes of elevated ADH SE: Hyponatremia |
Lithium
|
|
- ADH antagonist
- increase permeability in collecting duct - Tetracycline ABX - Produces nephrogenic DI - Intermediate acting abx effects SE: - Hyponatremia - skin eruption after sunlight exposure |
Demeclocycline
|
|
- Inotropic CV drug
-Inhibits Na/K-ATPase - Ca enhances digitalis toxicity so digitalis toxicity is tx w/ potassium not w/ Ca - HR slows by vagal stimulation in normal hearts - CO increases in failing hearts - Cholestyramine reduces digitalis absorption & toxicity Tx: CHF, A-fib, A-flutter SE: - kidney diuresis from hemodynamic improvement - Gi vomiting & diarrhea (chemoreceptor trigger zone stimulation) - CNS vagal & chemoreceptor trigger zone stimulation (visual distrubances, color perception) - can stimulate arrhythmias & ventricular fibrillation (can lead to death) CI: - Wolf parkinson's white syndrome |
Digitalis
|
|
- inhibit phosphodiesterase
- increase cAMP - increase Ca influx - Vasodilating effect - IV admin - Increase CO acutely but decrease CO in long term SE: - thrombocytopenia - arrhythmias |
Bypyridines (Inamrinone, Milrinone)
|
|
- dopamine agonist
- sympathomimetic in tx of CVD - NT - Low dose activates D1 receptors - High dose activates beta 1 receptors on heart - increases renal flood flow (increases urine production) - increases CO - Used to tx cardiac shock w/out vasoconstriction |
Dopamine
|
|
- sympathomimetic in CVD tx
- selective Beta1 agonist - IV - Inotropic & chronotropic effects - used in a cardiac stress test - can increase renin release |
Dobutamine
|
|
- Inotropic CHF drugs
- experimental |
Calcium sensitizers (Levosimendan & Pimbendan)
|
|
- produced by ventricular muscle
- Endogenous concentrations are elevated in patients with heart failure |
B type natriruetic peptide
|
|
- B type Natriuretic peptide (recombinant form)
- Tx: acute decompensated CHF - improves symptoms of heart failure - tolerance does not develop requires close blood pressure monitoring to prevent symptomatic hypotension - will decrease pulmonary wedge pressure |
Nesiritide
|
|
- ACE inhibitor
- decrease BP -↓preload (↓ direct vaso-C) - ↓afterload (↓ aldosterone) - ↓tissue remodeling - ↓mortality, no reflex tachy SE: - dry cough (↑bradykinin) - hyper-K CI: - bilateral renal artery stenosis - pregnancy |
Captopril
|
|
- ACE inhibitor
- Similar to captopril |
Enlapril, Lisinopril, Ramipril
|
|
- reduce production of angiotensin II
- reduce afterload (bradykinin) & preload (decreased aldosterone secretion) - Lower blood pressure w/out compromising heart, brain or kidney - no reflex sympathetic activation (tachycardia) Oral - enhance antiHTN efficacy of diuretics - Diuretics inhance its effects SE: - cough - Angioedema - Acute renal failure in patients with bilateral renal artery stenosis CI: - 2nd & 3rd trimester of prengnacy - Don't combine w/ NSAIDs or K sparing diuretics |
Ace inhibitors (the prils)
|
|
- inhibit angiotensin II receptor
- similar side effects to ACE inhbitors minus the cough & angioedema - induce fetal toxicity CI: - pregnancy |
ARBs "Sartans" (Losartan, Candesartan, Valsartan)
|
|
- reduce mortality in CHF
- reduce renin secretion - decrease heart rate - reduce remodeling |
Beta blocker in CHF (metoprolol, Carvedilol)
|
|
- Vasodilator that acts through Nitric oxide
- Reduces both preload & afterload - decreases damaging remodeling of heart - IV only - Dilates arteries & veins - used to tx acute decompensated CHF SE: - reflex tachycardia - fluid retention (give w/ a ß-blocker and diuretic) - cyanide accumulation with longer tx (days) - excessive hypotension |
Sodium Nitroprusside
|
|
- Vasodilator that acts through Nitric oxide
- MOA similar to nitrities - direct effect on arteriolar smooth muscle - Oral - Dilates arteries - ↑CO - reduces preload & afterload on heart - decreases damaging remodeling of heart SE: - reflex tachycardia, fluid retention (give w/ a ß-blocker and diuretic) - Angina (common for all vasodilators) - HIP drug that can cause SLE |
Hydralazine
|
|
- Class II anti-arrhythmic agents
|
Beta blockers
|
|
- class 1a Sodium channel blocker
binds open & activated Na channels - decreases myocardial automaticity - Prolongs Action potentials - oral - Used to tx broad spectrum for most arrythmias SE: - GI upset (diarrhea) - CNS stimulation (convulsions) at high dose - Reflex tachycardia due to blocking alpha receptors - torsades & syncope - increases action of warfarin, digoxin & NMJ blockers - cinchonism CI: AV block |
Quinidine
|
|
- Class 1C sodium channel blocker
- Binds both activated and inactivated Na channels - oral Used to TX: - supra-ventricular arrhythmias & life threatening ventricular arrhytmias CI: CHF |
Flecainide
|
|
- Blocks both activated & inactivated Na channels
- Similar to Flecainide - used to tx life threatening arrhytmias - Oral |
Propafenone
|
|
- class 1a Sodium channel blocker
binds open & activated Na channels - similar to quinidine SE: - HIP drug that can cause SLE |
Procainamide
|
|
- MOA: bind open & activated Na channels leading lengthening action potential duration
- increased effective refractory period, QRS & QT durations leading to torsades |
Class 1a sodium channel blockers
|
|
- Block both activated & inactivated Na channels so no effect on duration of action potentials
- Potent sodium channel blockers - used to tx life threatening arrhytmias |
Class 1c sodium channel blockers
|
|
- Blocks inactivated Na chanels to shorten action potentials
- decrease effective refractory period w/ no change in QRS or QT |
Class 1b sodium channel blockers
|
|
- Chemically unrelated to any other anti-arrhythmic
- used to tx life threatening arrhytmias - Oral - 1A, 1B, 1C like effects |
Moricizine
|
|
- class 1a Sodium channel blocker
binds open & activated Na channels - Similar to quinidine - approved only for ventricular arrhythmias SE: - (-) inotropic effect - Anticholinergic effect (dry mouth etc) |
Disopyramide
|
|
-Class 1b sodium channel blocker
- Blocks inactivated Na chanels to shorten action potentials - no change in QRS or QT - IV as antiarrhythmic - Used to tx ventricular arrythmia - Can cause Convulsions (CNS) - Least negative inotropic effects among the antiarrhytmics - interactions w/ protein binding p450 Local anesthetic (amide) - Intermediate axn - long T1/2 in system - epidural anesthesia - local |
Lidocaine
|
|
-Class 1b sodium channel blocker
used to Tx: - painful diabetic neuropathy - ventricular arrythmias in lodocaine resistant patients |
Mexiletine
|
|
-Class 1b sodium channel blocker
- Used for patients w/ lidocaine allergy, ventricular arrhythmia |
Tocainide
|
|
-Class 1b sodium channel blocker
- Blocks inactivated Na chanels to shorten action potentials - decrease effective refractory period w/ no change in QRS or QT - prolongs Na channel inactivation - Induces P450 - dose dependent elimination - oral/IV - DOC for tonic clonic seizure Used to Tx: - partial & tonic-clonic seizures - digoxin induced ventricular arrythmias SE: gingival hyperplasia, hirsutism nystagmus - double vision |
Phenytoin
|
|
- Class 3 antiarrhytmic agent
- blocks K channels - binds inactivated Na channels - increases QRS & QT - has class Ca channel blocking effects some alpha blocking (peripheral vasodilation) - Oral with long half life (13-100 days) so loading takes 15-30 days - decreases HR & conduction - Used to tx broad arrhythmias SE: - Elvira (brown eyes, gray skin) - brady cardia - pulmonary fibrosis |
Amiodarone
|
|
- K channel blockers
- prolong repolarization |
Class 3 antiarrythmic agents
|
|
- Non selective beta blocker
- prolongs APs - Oral - has class II & III effects - Used to tx ventricular & supraventricular arrythmias SE: -Torsades - Beta block |
Sotalol
|
|
- decrease heart rate & contractility
|
Ca channel blockers (Class 4)
|
|
- Ca channel blocker
- inbetween verapamil & nifedipine - improves myocardial perfusion - suppresses SA & AV nodes (prevents reflex tachycardia) Used to tx: - PSVT, Afib/flutter - Prinzmetal's angina - Vasodilation SE: - can cause bradycardia (node suppression) CI: - pts with SA or AV node abnormalities - CHF |
Diltiazem
|
|
- Ca channel blocker
- Class IV anti-arrhythmic - Blocks slow (L type) Ca channels - Slows AV nodal conduction (decreases HR) Used to Tx: - Reentrant supraventricular Tachycardia - reduces ventricular rate in atrial flutter & fibrillation - HTN & Angina Toxicity: - GI intolerance (constipation) - Bradycardia, AV block - Constipation CI: - Don't combine with beta blockers cause both reduce ventricular contractility - suppresses SA & AV nodes (prevents reflex tachycardia) so don't give to people with nodal abnormalities |
Verapamil
|
|
- Miscellaneous Antiarrhythmic
- Occurs naturally in body - 10 secod half life - enhances K conductance & inhibits Ca influx - Directly inhibits AV conduction - IV administration DOC: Paroxysmal supraventricular tachycardia (PSVT) Toxicity - Flushing, shorntess of breath, chest burning |
Adenosine
|
|
- Miscellaneous anti-arrhythmic agent
- causes resting potential depolarization & membrane stabilization - both hypo & hyperkalemia are arrhytmogenic |
Potassium
|
|
- Miscellaneous Anti-arrhytmic
Used to tx: - seizures in prreeclampsia & eclampsia - Cardiac glycoside induced arrhytmias - Tosade de pointes (polymorphic ventricular tachycardia) |
Magnesium Sulfate
|
|
- used in combination w/ thiazides & Loop diuretics to decrease K loss
- Don't use with other K sparing drugs |
Potassium sparing diurectics
|
|
- MOA: stimulate presnyaptic alpha 2 recepters to reduce NT release & postsynaptic receptors to inhibit neurons
- Lower BP by decreasing vasoconstrictor tone & decreasing renin secretion - Clonidine or Methyldopa (prodrug) SE: - CNS effects (no monotherapy) - Sudden withdrawl of clonidine may cause HTN crisis - Methyldopa can cause hemolytic anemia with a positive coombs tests Drug interactions: - TCAs & Yohimbine inhibit clonidine's therapeutic action |
Alpha 2 agonist HTN sympathomimetics
|
|
- reduce CO, Renin secretion
- act in CNS to reduce sympathetic vasomotor tone - More effective in white/young than in black/elderly - recommended for monotherapy in young white males - Nebivolol works via Nitric oxide - Propanolol can cause bronchocontstriction - Beta blockated may mask symptoms of initial hypoglycemia & delay recovery from it Preferred drugs following: - angina, MI, or migraine CI: - Diabetes - Severe CHF - Asthma - Heart block |
Beta adrenergic antagonist tx of HTN
|
|
- Adrenergic neuron blocking agent used to tx HTN
- Inhibits vesicular uptake of NTs (NE, DA, 5HT) - lowers blood pressure by eliminating sympathetic tone - rarely used (unpleasant side effects) SE: - Sedation, depression, stuffy nose, dry mouth & GI disturbance |
Reserpine
|
|
- Adrenergic neuron blocker used in tx of HTN
- Replaces NE in the neuron vesicles - Blocks physiologic release of NE - rarely used (unpleasant side effects) SE: - postural hypotension - fluid retention - diarrhea - Retrograde ejaculation |
Guanethidine
|
|
- K channel regulator
- its actually a thiazide - Activates ATP sensitive K channels - Vasodilator & Hyperglycemic - Used in patients with insulinoma SE: - Hyperglycemia (ketoacidosis or non ketotic hyperosmolar coma) - Sodium & water retention - Hyperuricemia (because its a thiazide) - excessive hair growth (most frequently in children) |
Diazoxide
|
|
- K channel regulator used to tx HTN
- opens K channels & stabalizes membrane - dilates arterioles but not veins - Oral - in topical form it is Rogaine SE: - Hyper trichosis (abnormal amount of body hair growth) - angina (classic vasodilator effect) |
Minoxidil
|
|
- Block slow Ca channels to reduce intracellular Ca & relax smmm of arterys
- More effective in dilating arteries than veins - equally effective in monotherapy in mild to moderate HTN especially in elderly blacks - differences in tissue selectivity can result in opposite effects on heart rate as it would be increased by nifedipine but slowed by verapamil SE: - Inhibition of insulin secretion - interference with platelet aggregation |
Ca channel blocker vasodilation
|
|
- Ca channel blocker
- strongest vasodilator SE: - Reflex tachycardia due to pronounced vasodilation w/out inhibition of SA/AV nodes - angina (common vasodilating effect) - one of the 3 gingival hyperplasia drugs (also phenytoin & cyclosporin) |
Dihydropyridines (Nifedipine)
|
|
- Renin antagonist
- Non peptide - Hepatobiliary clearance Used to tx: HTN CI: - pregnancy risk category D in 2nd & 3rd trimesters |
Aliskiren
|
|
- due to Beta blockade at heart, kidneys & CNS
- both cardiac & vascular effects - ineffective in produing coronary vasodilation SE: - Bronchoconstriction can be life threatening in Asthmatics - Plasma tryglycerides can increase - Recovery from insulin induced hypoglycemia is delayed |
Beta blockers for vasodilation/angina tx
|
|
- Vasodilation (large veins > arteries)
- decreases Cardiac pre & after loads - Can cause reflex tachycardia - relax other smooth muscles in bronchi & GI/GU tracts - frequent exposure leads to tolerance - people working in explosive manufacturing are exposed to high nitrate levels and develop tolerance leading to "Monday disease" SE: - orthostatic Hypotension - tachycardia - Throbbing headaches |
Nitrates & Nitrites
|
|
- Nitrate
- has such a high first pass effect that it has to be given sublingually instead of orally - Used for immediate anginal relief due to rapid onset and short duration of action SE: - throbbing headache is the hallmark sign for its adverse effects |
Nitroglycerin
|
|
- ED drug
- selective inhibitor of cyclin guanosine monophosphate (Specific phosphodiesterase type 5) - P450 metabolism SE: - visual impairment (pilots can't take for at least 8 hours before flying because it makes white lights appear blue) CI: - Pregnancy, lactating, children - Creates an excessive drop in blood pressure when combined with nitrites - combination with alpha blockers may lead to symptomatic hypotension |
Sildenafil (Viagra)
|
|
- Faster onset of action than Sildenafil
- More selective for PDE5 than for PDE6 in the retina - similar to sildenafil |
Vardenafil (Levitra); Tadalafil (cialis)
|
|
- Endothelin receptor antagnoist
- Endothelins counterbalance the effects of NO Used for tx of severe pulmonary HTN SE: - eleveates hepatic enaymes - multiple drug interactions - inducer of CYP 3A4 CI: - preganacy (teratogen) |
Bosentan
|
|
- partial fatty acid oscidation inhibitor
- "Other" drug used in vasodilation/angina tx |
Ranolazine
|
|
- Large cationic resin insoluble in water
- bind bile acids & prevent intestinal absorption SE: - Constipation & bloating - Gallstone formation - hypoprothrombinemia due to vitamin K malabsorption - can impair absorption of other drugs |
Bile acid binding resins (Cholestyramine, Colestipol, Colesvelam)
|
|
- Water soluble vitamine excreted by urine
- lowers plasma VLDL & LDL by inhibiting VLDL secretion - inhibits hepatic cholesterologenesis - Increases levels of HDL (Most effective agent at doing this) - Give for high Cholesterol & Triglycerides Used to Tx: - Heterozygous familial hypercholesterolemia & combined hyperlipoproteinemia SE: - Vasodilation (prostaglandin dependent so give w/ aspirin to avoid) - GI discomfort - impairs glucose tolerance - elevates aminotransfersases or alkaline phosphatase - severe hepatotoxicity - Hyperuricemia (its an acid so it will compete with uric acid to get excreted) |
Niacin (Nicotinic acid & vitamin B)
|
|
- inactive statins that must be hydrolyzed to their active form (structural analogs of HMG-CoA reductase)
- reduce plasma LDL by inhibiting reductase to increase high affinity LDL receptors - decrease plasma triglycerides & increase HDL cholesterol |
Lovastatin, Simvastatin
|
|
- Main therapeutic effect is lowering LDL
- Give for high Cholesterol & Triglycerides - decrease C reactive protein - enhance endothelial NO production - Given in the evening (to effect the diurnal pattern of cholesterol synthesis) SE: - Liver damage - increased serum creatine kinase acitivity - Rhabdomyolisis - CYP3 metabolism |
HMG CoA inhibitors "Statins"
|
|
- already active forms ofstructural analogs of HMG-CoA reductase
- reduce plasma LDL by inhibiting reductase to increase high affinity LDL receptors - decrease plasma triglycerides & increase HDL cholesterol |
Atorvastatin & Fluvastatin
|
|
- function as ligand for nuclear transcription regulator PPAR alpha
- inhibit hepatic cholesterologenesis They produce: - lipoprotein lipase activity (promotes VLDL catabolism) - Triglycerides (by lowering [VLDL]) SE: - Cholelithiasis or gallstones - potentiate anticoaglulant action of warfarin - inhibit metabolism of statins - May increase LDL in some patients |
Fibric acid derivatives (Gemfibrozil, Clofibrate, Fenofibrate)
|
|
- give for high triglycerides
|
Gemfibrozil
|
|
- inhibitor of cholesterol intestinal absorption
- Give for high Cholesterol & Triglycerides - Reduces LDL cholesterol in monotherapy - synergistic effects in combo with a statin |
Ezetimibe
|
|
- Heterogenous mix of sulfated mucopolysacharides
- unfractionated so has high molecular weight - MOA: affects Xa & thrombin - onset of action is immediate - used in pregnancy to replace warfarin SE: - Hemorrhage (tx: stop therapy or protamine sulfate) - Heparin induced thrombocytopenia CI: - Renal or hepatic dysfunction - actively bleeding patients - bleeding disorders - during or after surgery of brain, spinal cord or eye |
Heparin
|
|
- Low molecular wt heparin
- only inhibits factor Xa - can be injected subcutaneously - Lower incidence of heparin induced thrombocytopenia - protamine sulfate doesn't reverse effect of LMW heparins completely (no effect on fondaparinux) |
Enoxaprin, Dalteparin, Danaparoid
|
|
- Direct thrombin inhbitors
- Bivalrudin inhibits platelets too - given as alternative in Heparin induced thrombocytopenia CI: - renal dysfunction |
Lepirudine & Bivalrudin
|
|
- Factor Xa inhbitor (oral)
- rapid onset CI: - renal failure - liver disease |
Rivaroxaban
|
|
- Clotting factor synthesis inhibitor
- inhibits reduction of vitamin K in vivio - Many conditions affect it - many drug interactions - used to prevent development of emboli (no effect on already formed thrombi) - Given chronically - oral admin CI: - pregnancy |
Warfarin
|
|
- MOA convert plasminogen to plasmin
- used for lyses of clots - given IV or intra-arterially SE: - serious bleeding (tx w/ tranexamic acid and or whole blood) |
Thrombolyttic (fibrinolytic) agents
|
|
- Thrombolytic agent
- Recombinant protein - Clot selective (higher activity for fibrin bound plasminogen vs plasma plasminogen) - effective in establishing coronary reperfusion SE: high risk of stroke |
Tissu plasminogen activator (t-PA)
|
|
- Thrombolytic agent
- protein synthesized by streptococci - MOA: forms complex w/ plasminogen, increasing fibrinolytic activity - Not clod fibrin specific (generalized systemic fibrinolysis) - As effective as other fibrinolytics when used w/ aspirin SE: can cause allergic responses, anaphylaxis & pyrexia |
Streptokinase
|
|
- Thrombolytic agent
- MOA: mixture of plasminogen & stertokinase that has been rendered inert by acylation; in blood acyl group hydrolyze it making it fibrinolytic - More clot selective than stretokinase and administered more rapidly - long duration of action |
Anistreplase
|
|
- Antifibrinolytic
- used to tx bleeding disorders & for reversal of fibrinolytic therapy - MOA: inhibits plasminogen activation to prevent formation of plasmin SE: - intravascular thrombosis - Hypotension - myopathy CI: - DIC - upper GU bleeding |
Aminocaproic acid & Tranexamic acid
|
|
- MOA: phosphdiesterase 3 inhibitor
- promotes vasodilation and inhibits platelet aggregation - Used to tx intermittent claudication (DVT) |
Cilostazol ( no picmonic)
|
|
- MOA: irreversible inhibition of COX enzyme
- primary prevention of MI CI: - shouldn't be taken before dental procedures or surgery |
Aspirin
|
|
- inhibitor of ADP induced platelet aggregation
- MOA: irreversibly block the ADP receptor on platelets - Used in patients who are allergic to aspirin - DOC: prevent thrombosis inpatients uncergoing placement of coronary stents |
Clopidogrel
|
|
- inhibitor of GPIIb/IIIa receptor
- MOA: decrease platelet aggregation by inhibiting receptor from binding fibrinogen - given IV |
Abciximab
|