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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