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110 Cards in this Set
- Front
- Back
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Pilocarpine
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-MOA: Direct acting muscarinic agonist
-Clinical: Glaucoma (topically) Dry mouth (Srogen disease) Sweat test (Cystic fibrosis patients) |
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Bethanecol
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-MOA: Direct acting muscarinic agonist
-Clinical: Paralytic ileus (post-op) Urinary retention (diabetic neuropathy) |
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Carbachol
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-MOA: Direct acting muscarinic agonist
-Clinical: Glaucoma (topically) |
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Physostigmine
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-MOA: Indirect acting muscarinic agonist (anticholinesterase)
-Clinical: **Antidote in atropine OD Glaucoma -SE: Lots but especially bradycardia (AV block) -enters CNS |
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Neostigmine
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-MOA: Indirect acting muscarinic agonist (anticholinesterase)
-Clinical: Paralytic ileus Urinary retention Myasthenia Reversal of non-depolarizing NM blockers -SE: Lots but especially miosis and bradycardia (AV block) -NO CNS entry |
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Pyridostigmine
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-MOA: Indirect acting muscarinic agonist (anticholinesterase)
-Clinical: Paralytic ileus Urinary retention Myasthenia Reversal of non-depolarizing NM blockade -SE: Lots but especially miosis and bradycardia (AV block) -NO CNS entry |
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Edrophonium
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-MOA: Indirect acting muscarinic agonist (anticholinesterase)
-Clinical: **Diagnosis of myasthenia -SE: Lots but especially miosis and bradycardia (AV block) -Short-acting so do NOT use for myasthenia treatment |
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Isoflurophate(DFP)
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-MOA: Indirect acting muscarinic agonist (anticholinesterase)
-Clinical: Glaucoma -SE: bradycardia (AV block) -Organophosphate insecticide, **irreversible inhibitor |
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Pralidoxime(2-PAM)
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-MOA: Reactivates cholinesterase enzyme
-Clinical: Antidote to organophosphate pesticides and chemicals |
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Atropine
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-MOA: Muscarinic receptor antagonist
-Clinical: Antispasmotic Antisecretory Management of AchE inhibitor OD Antidiarrheal Opthamology -SE: Cardiotoxicity, Convulsions, Coma -Long-acting drug |
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Scopolamine
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-MOA: Muscarinic receptor antagonist
-Clinical: Antimotion sickness Sedation and short-term memory block -SE: Cardiotoxicity, Convulsions, Coma |
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Ipratropium
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-MOA: Muscarinic receptor antagonist
-Clinical: Asthma and COPD -SE: Cardiotoxicity, Convulsions, Coma -NO CNS entry |
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Trimethaphan
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-MOA: Competitive nicotinic receptor antagonist
-Clinical: Reduction of blood pressure during surgery Hypertensive emergencies |
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Nicotine
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-MOA: Depolarizing nicotinic receptor antagonist
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Hexamethonoium
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-MOA: Depolarizing nicotinic receptor antagonist
-Clinical: NO clinical use |
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Tubocuranine
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-MOA: Competitive nondepolarizing neuromuscular blocker
-Clinical: Diagnostic agent for myasthenia gravis Adjunct to anesthesia for intubation |
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Pancuronium
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-MOA: Competitive nondepolarizing neuromuscular blocker
-Clinical: Muscle relaxant during anesthesia and surgery |
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Vecuronium
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-MOA: Competitive nondepolarizing neuromuscular blocker
-Clinical: Muscle relaxing agent used as adjunct to general |
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Succinylcholine
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-MOA: Depolarizing neuromuscular blocker that acts as agonist at Nm receptor to induce paralysis through persistent membrane depolarization
-Clinical: Rapid muscular relaxation during procedures |
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Phenylephrine
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-MOA: Direct acting a1 receptor agonist
-Clinical: Decongestant Mydriasis without cycloplegia |
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Methoxamine
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-MOA: Direct acting a1 receptor agonist
-Clinical: Paroxysmal atrial tachycardia -**Elicits vagal reflex (increasing bp to elicit the reflex bradycardia) |
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Metaraminol
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-MOA: Direct acting a1-receptor agonist
-Clinical: Hypotension due to hemorrhage Spinal Anesthesia Shock associated with brain damage |
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Clonidine
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-MOA: Direct acting a2 receptor agonist, decreases sympathetic outflow, decreases TPR and HR
-Clinical: Hypertension (initial increase in BP through some a1 activity followed by a decrease to treat HTN) Opiate withdrawal -SE: CNS depression Edema -***Drug interactions: tricyclic antidepressants decrease antihypertensive effects of a2 agonist |
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a-Methyldopa
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-MOA: Direct acting a2 receptor agonist, decreases sympathetic outflow, decreases TPR and heart rate
-Clinical: Hypertensive management in preganancy -SE: ***Positive Coombs test CNS depression Edema -***Drug interaction: tricyclic antidepressants decreases antihypertensive effects of a2 agonists |
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Tetrahydralozine
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-MOA: Direct acting a1 receptor agonist
-Clinical: OTC eye drops and nasal sprays -SE: Severe nausea and vomiting Seizures or coma |
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Isoproterenol
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-MOA: Non-selevtive Beta receptor agonist
-Clinical: Bronchospasm (B2) Heart block (B1) Bradyarrythmias -SE: Flushing, angina, and arrythmias |
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Dobutamine
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-MOA: Beta receptor agonist primarily selective for B1
-Clinical: Acute CHF |
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Terbutaline
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-MOA: Selective B2 receptor agonist
-Clinical: Asthma |
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Albuterol
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-MOA: Selective B2 receptor agonist
-Clinical: Asthma |
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Metaproterenol
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-MOA: Selective B2 receptor agonist
-Clinical: Asthma |
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Norepinephrine
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-MOA: Mixed agonist but primarily a1 and B1
-Does NOT act on B2 receptors |
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Epinephrine
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-MOA: Mixed agonist that predominates as alpha agonist at high doses and beta agonist at low-medium doses
-Clinical: **Anaphylaxis Cardiac arrest Adjunct to local anesthetics Glaucoma -Unlike NE, Epinephrine DOES activate B2 receptors |
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Tyramine
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-MOA: Indirect acting adrenoreceptor agonist, NE releasers and displace NE from mobile pool
-Clinical: Increases pressor response -**Drug interaction with MAO inhibitors (hypertensive crisis) -Classic situation is wine and cheese party with depression -NO CNS entry |
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Amphetamine
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-MOA: Indirect acting adrenoreceptor agonist, releases NE from mobile pool
-Clinical: ADHD Short-term weight loss Narcolepsy -Enters CNS inducing release of NE and dopamine -Dangerous to take recreationally while on MAO inhibitors |
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Ephedrine
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-MOA: Indirect acting adrenoreceptor agonist, releases NE
-Clinical: Decongestant (found OTC in cold medication) |
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Dopamine
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-MOA: Indirect acting adrenoreceptor agonist, at low doses activates D1 receptors, at medium doses activates B1 receptors, at high doses activates a1 receptors
-Clinical: Low dose = Increases renal blood flow and filtration Medium dose = Management of shock states High dose = Increase in blood pressure |
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Cocaine
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-MOA: Indirect acting adrenoreceptor agonist, blocks reuptake of NE
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Phentolamine
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-MOA: Nonselective competitive alpha receptor blocker
-Clinical: Pheochromocytoma Local vasoconstricter overdose -SE: Reflex tachycardia Salt and water retention -Short-acting drug |
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Phenoxybenzamine
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-MOA: Nonselective irreversible alpha receptor blocker
-Clinical: **Short-term DOC for pheochromocytoma -SE: Reflex tachycardia Salt and water retention |
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Prazosin
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-MOA: Selective a1 receptor blocker ("zosins" are selective blockers), decreases arteriolar and venous resistance
-Clinical: Hypertension BPH -SE: ***Less reflex tachycardia bc NE feedback intact ***Orthostatic hypotension (first-dose syncope) Urinary incontinence |
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Tolazoline
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-MOA: Moderate alpha receptor blocking activity
-Clinical: Pulmonary artery anomalies |
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Propranolol
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-MOA: Nonselective Class II beta blocker, decreases SA and AV nodal activity, decreases renin release (HTN)
-Clinical: ***Hypertension ***Stable angina (NOT in vasospastic) ***CHF Prophylaxis post-MI Supraventricular arrhythmias Hyperthyroidism -SE: ***Cardiovascular depression (AV block) Fatigue Sexual dysfunction -Chronic use associated with increased LDL -Strong CNS sedation -Caution with asthmatics, vascular disorders, and diabetics |
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Metoprolol
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-MOA: Selective B1 receptor blocker
-Clinical: Angina Hypertension Post-MI Antiarrythmic -SE: ***Cardiovascular depression (AV block) Fatigue Sexual dysfunction Increased LDLs -B1 selective so has less effect on vasculature, bronchioles. uterus, and metabolism so safer in asthmatics, diabetics, and PVD -Caution with asthmatics, vascular disorders, and diabetics |
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Nadolol
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-MOA: Beta blocker
-NO CNS entry and long half-life |
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Timolol
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-MOA: Nonselective beta blocker
-Clinical: Hypertension Migraine Glaucoma -SE ***Cardiovascular depression (AV block) Fatigue Sexual dysfunction Increases LDLs -Caution with asthmatic, vascular disorders, and diabetics |
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Labetalol
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-MOA: Combined alpha and beta blocker activity
-Clinical: Hypertension and hypertensive crisis Pheochromocytoma -"alol" so NOT pure beta blocker -Combined alpha and beta blocker activity |
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Carvedilol
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-MOA: Combined beta and alpha blocking ability
-Clinical: CHF -"ilol" so NOT pure beta blocker -Drug has long half-life |
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Quinidine
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-MOA: Class Ia Antiarrhythmic drug (Na+ channel blocker), also causes muscarinic block which can increase HR and Av conduction, may also cause vasodilation via alpha block with possible reflex tachycardia
-Clinical: arrhythmias; atrial fibrillation, need initial digitalization to slow AV conduction -SE: ***Cinchonism Nausea and vomiting Hypotension Prolongation of QRS (tachycardia) Increased QT interval (torsades) |
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Procainamide
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-MOA: Class Ia Antiarrhythmic drug (Na+ channel blocker), less muscarinic block and no alpha block
-Clinical: arrhythmias -SE: ***Drug induced SLE with slow acetylators Hematotoxicity CNS effects CV effects (more likely to cause torsades) -***orally effective unlike quinidine because metabolized into active form which prolongs APD |
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Lidocaine
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-MOA: Class Ib Antiarrhytmic drug (Na+ channel blocker), blocks inactivated channel (preferentially slow conduction in hypoxic or ischemic tissue), decreases APD
-Clinical: ***IV use in arrhytmias post-MI DOC for arrhytmias following cardioversion Open heart surgery Due to digitalis -SE: ***Least cardiotoxic of conventional antiarrhytmics CNS seizures in severe OD |
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Phenytoin
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-MOA: Class Ib Antiarrhytmic drug (Na+ channel blocker), blocks inactivated channel (preferentially slow conduction in hypoxic or ischemic tissue), decreases APD
-Clinical: Antiseizure drug Digitalis OD to reverse AV block |
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Esmolol
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-MOA: Nonselective class II beta blocker, decreases SA and AV
-Clinical: ***Prophylaxis post-MI *** IV in acute Supraventricular tachyarrhythmias |
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Acebutolol
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-MOA: Nonselective class II beta blocker, decreases SA and AV
-Clinical: ***Prophylaxis post-MI ***Supraventricular tachyarrhythmias |
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Sotalol
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-MOA: Two forms both which increase APD and ERP and one acts as a selective B1 blocker to decrease HR and AV nodal conduction
-Clinical: Prophylaxis of life-threatening ventricular arrhythmias CHF -SE: Lassitude Impotence Depression Torsades AV block |
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Bretylium
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-MOA: Class III Antiarrhytmic (K+ channel blocker), increases APD and ERP
-Clinical: IV use in life-threatening ventricular arrhytmias -SE: Arrhytmias (torsades) |
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Amiodarone
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-MOA: Activity mimics all antiarrhytmic drug classes, blocks Na, Ca, and K channels and beta receptors, increases APD and ERP
-Clinical: Arrhythmias -SE: ***Pulmonary fibrosis ***Blue pigmentation ("smurf" skin) ***Thyroid dysfunction Corneal deposits Phototoxicity Increased LDL Torsades Hepatic necrosis -Has a very, very long half-life -Remember "iod" in name for thyroid SE |
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Verapamil
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-MOA: Class IV Antiarrhytmic drug (Ca2+ channel blocker), decreases SA and AV nodal activity
-Clinical: Prophylaxis in reentrant nodal and atrial tachycardias Digitalis Toxicity -SE: ***GI distress (constipation) ***AV block (if slow AV node too much) - ***Drug interaction: avoid use with beta blockers in CHF patients |
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Adenosine
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-MOA: Antiarrhytmic drug, decreases SA and AV nodal activity by activating adenosine receptors
-Clinical: ***DOC for paroxysmal supraventricular tachycardias -SE: Flushing, sedation, dyspnea, bronchospasms |
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Reserpine
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-MOA: Destroys NE storage vesicles, decreases CO and TPR, decrease in NE, dopamine and serotonin in CNS
-Clinical: Hypertension -SE: ***Depression (often severe) Edema Increases Gi secretions |
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Guanethidine
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-MOA: Uses re-uptake pump to enter nerve terminal and binds vesicles inhibiting NE release
-Clinical: Hypertension -SE: Diarrhea Edema -***Drug interaction: tricyclic antidepressants block re-uptake |
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Pindolol
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-MOA: Non-selective beta blocker
-Clinical: Hypertension -SE: ***Cardiovascular depression (AV block) Fatigue Sexual dysfunction Increased LDLs -Caution with asthmatics, vascular disorders, and diabetics |
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Hyrdralazine
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-MOA: Direct-acting vasodilator, prodrug that decreases TPR via ***arteriolar dilation
-Clinical: Hypertension -SE: ***Drug-induced lupus with slow acetylators Edema Reflex tachycardia |
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Nitroprusside
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-MOA: Direct-acting vasodilator, prodrug that decreases TPR via dilation of ***both arteries and venues
-Clinical: ***DOC IV in hypertensive emergencies -SE: ***Cyanide toxicity (so only used short-term) |
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Nifedipine
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-MOA: Calcium channel blocker that decreases TPR
- Clinical: Hypertension ***Vasospastic angina -SE: ***Gingival hyperplasia Reflex tachycardia (bc lowering the bp through dilation) -So with the calcium channel blockers, verapamil works on the heart while nifedipine works on the blood vessels - think "dipines" work on blood vessels |
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Captopril
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-MOA: Angiotensin-converting inhibitor that blocks the formation of angiotensin II resulting in prevent of AT1 receptor stimulation causing a decrease in aldosterone and vasodilation
- Clinical: Hypertension ***Protective of diabetic neuropathy ***CHF -SE: ***Dry cough ***Acute renal failure in renal artery stenosis Hyperkalemia Angioedema -***ACEI's prevent bradykinin degradation -"prils" are ACEI |
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Enalapril (Enalaprilat is active form)
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-MOA: Angiotensin-converting inhibitor that blocks the formation of angiotensin II resulting in prevent of AT1 receptor stimulation causing a decrease in aldosterone and vasodilation
- Clinical: Hypertension ***Protective of diabetic neuropathy ***CHF -SE: ***Dry cough ***Acute renal failure in renal artery stenosis Hyperkalemia Angioedema -***ACEI's prevent bradykinin degradation -"prils" are ACEI |
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Losartan
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-MOA: Angiotensin II receptor antagonist that blocks AT1 receptors resulting in decreased aldosterone and vasodilation
-Clinical: Hypertension ***Protective of diabetic neuropathy ***CHF -SE: ***Acute renal failure in renal artery stenosis Hyperkalemia Angioedema -ARBS do NOT interfere with bradykinin |
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Digoxin (Digitoxin)
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-MOA: Directly, it inhibits of the cardiac Na-K ATPase results in increased intracellular Na, decreased Na-Ca exchange, increased intracellular Ca, and overall increased contractile force. Indirectly, inhibits neuronal Na-K ATPase resulting in increased vagal and sympathetic stimulation
-Clinical: ***Acute CHF Supraventricular tachycardias (bc of vagal effects) -SE: ***Visual effects (halos), disorientation ***Cardiac arrythmias Anorexia, nausea -***Has a long half-life so in emergent situations need to give loading dose -***Use of Fab antibodies towards digoxin to manage toxicity - ***Drug interactions: Diuretics (hypokalemia) Quinidine and Verapamil |
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Amrinone
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-MOA: Phosphodiesterase inhibitors, increase cAMP in heart muscle results in increased isotropy but in smooth muscle results in decreased TPR
-Clinical: CHF -So get increased contractility in heart BUT vasodilation in smooth muscle with increased cAMP |
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Milrinone
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-MOA: Phosphodiesterase inhibitors, increase cAMP in heart muscle results in increased isotropy but in smooth muscle results in decreased TPR
-Clinical: CHF -So get increased contractility in heart BUT vasodilation in smooth muscle with increased cAMP |
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Dobutamine
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-MOA: Sympathomimetic that directly stimulates B1 receptors of the heart to increase contractility and stroke volume resulting in increased cardiac output
-Clinical: CHF |
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Nesiritide
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-MOA: Recombinant form of ANP that binds to ANP receptors increasing cAMP resulting in vasodilation
-Clinical: ***Used acutely resulting in vasodilation |
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Nitroglycerin
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-MOA: Nitrate that is prodrug of NO, causes smooth vessel dilation->decreased preload->decreased cardiac work->decreased oxygen requirement
-Clinical: Acute anginal attack -SE: ***Orthostatic hypotension, flushing, headache Reflex tachycardia and fluid retention -***Tachyphylaxis (tolerance) with repeated use |
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Isosorbide Dinitrate
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-MOA: Nitrate that is prodrug of NO, causes smooth vessel dilation->decreased preload->decreased cardiac work->decreased oxygen requirement
-Clinical: ***Chronic angina -SE: ***Orthostatic hypotension, flushing, headache Reflex tachycardia and fluid retention |
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Mannitol
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-MOA: Osmotic diuretic that inhibits water reabsorption mainly in the proximal tubule
-Clinical: Acute narrow angle glaucoma Intracerebral pressure -SE: Acute hypovolemia |
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Acetazolamide
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-MOA: Carbonic anhydrase inhibitor resulting in decreased H+ formation incite the proximal tubule, decreased Na-H transport, increased Na and HCO3- in lumen, and increased diuresis.
-Clinical: ***Metabolic alkalosis Glaucoma Acute motion sickness -SE: ***Bicarbonaturia and acidosis ***Hypokalemia (when have metabolic acidosis with hypokalemia it's always CA inhibitors) ***Renal stones (losing H+ in urine so low ph can cause precipitation resulting in stones) -All CA inhibitors end in "zolamide" |
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Furosemide
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-MOA: Loop diuretic that inhibits Na-K-Cl transporter at thick ascending loop, results in decreased intracellular K+, decreased back diffusion of K+, decreased positive potential, decreased reabsorption of Ca2+ and Mg2+, and diuresis
-Clinical: ***DOC for acute pulmonary edema (HF) Heart failure Hypertension (increase PGs causing vasodilator) ***Anion overdose (losing all your ions) -SE: ***Sulfonamide hypersensitivity ***Hypokalemia, hypocalcemia and alkalosis Hyperuricemia (can exacerbate gout) -Drug interactions: ***Digoxin |
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Torsemide
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-MOA: Loop diuretic that inhibits Na-K-Cl transporter at thick ascending loop, results in decreased intracellular K+, decreased back diffusion of K+, decreased positive potential, decreased reabsorption of Ca2+ and Mg2+, and diuresis
-Clinical: ***DOC for acute pulmonary edema (HF) Heart failure Hypertension (increase PGs causing vasodilator) ***Anion overdose (losing all your ions) -SE: ***Sulfonamide hypersensitivity ***Hypokalemia, hypocalcemia and alkalosis Hyperuricemia (can exacerbate gout) -Drug interactions: ***Digoxin |
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Ethacrynic acid
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-MOA: Loop diuretic that inhibits Na-K-Cl transporter at thick ascending loop, results in decreased intracellular K+, decreased back diffusion of K+, decreased positive potential, decreased reabsorption of Ca2+ and Mg2+, and diuresis
-Clinical: ***DOC for acute pulmonary edema (HF) Heart failure Hypertension (increase PGs causing vasodilator) ***Anion overdose (losing all your ions) -SE:***Ototoxicity ***Hypokalemia, hypocalcemia and alkalosis Hyperuricemia (can exacerbate gout) -Drug interactions: ***Digoxin |
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Hydrochlorothiazide
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-MOA: Thiazide that inhibits Na-Cl transporter at the distal tubule, resoling in increased luminal Na and Cl and diuresis, also opens K+ channels
-Clinical: ***Hypertension, CHF -SE: ***Sulfonamide hypersensitivity ***Hypercalcemia (unlike loop diuretics) ***Hyperglycemia and hyperlipidemia -Drug interactions:***Avoid in diabetics Digoxin |
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Spironolactone
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-MOA: K+ sparing aldosterone antagonist at collecting duct (requires elevated aldosterone to function)
-Clinical: ***Adjunct to K+wasting diuretics CHF Hyperaldosteronic state -SE: ***Hyperkalemia and acidosis Antiandrogen (male using drug for CHF w/ gynecomastia) |
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Triamterene
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-MOA: K+ sparking drug that blocks Na+ channels at collecting duct
-Clinical: ***Adjunct to K+ wasting drugs -SE: Hyperkalemia and acidosis -***DO NOT use for CHF b/c have nothing to do with aldosterone |
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Amiloride
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-MOA: K+ sparking drug that blocks Na+ channels at collecting duct
-Clinical: ***Adjunct to K+ wasting drugs -SE: Hyperkalemia and acidosis Diabetes insipidus -***DO NOT use for CHF b/c have nothing to do with aldosterone |
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Diltiazem
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-MOA: Calcium channel blocker that resulting in vasodilation
-Clinical: Hypertention |
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Amlodipine
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-MOA: Calcium channel blocker resulting in vasodilation
-Clinical: Hypertension Chronic stable angina -SE: Reflex tachycardia with OD Hypotension and shock |
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Lisinopril
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-MOA: Angiotensin-converting inhibitor that blocks the formation of angiotensin II resulting in prevent of AT1 receptor stimulation causing a decrease in aldosterone and vasodilation
- Clinical: Hypertension ***Protective of diabetic neuropathy ***CHF -SE: ***Dry cough ***Acute renal failure in renal artery stenosis Hyperkalemia Angioedema -***ACEI's prevent bradykinin degradation -"prils" are ACEI |
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Benazepril
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-MOA: Angiotensin-converting inhibitor that blocks the formation of angiotensin II resulting in prevent of AT1 receptor stimulation causing a decrease in aldosterone and vasodilation
- Clinical: Hypertension ***Protective of diabetic neuropathy ***CHF -SE: ***Dry cough ***Acute renal failure in renal artery stenosis Hyperkalemia Angioedema -***ACEI's prevent bradykinin degradation -"prils" are ACEI |
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Lovastatin
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-MOA: HMG-CoA reductase inhibitor, results in decreased liver cholesterol, increased LDL receptor expression, and decreased plasma LDL, also decreased VLDL synthesis result in decreased triglyceremia
-Clinical: Antiatherosclerosis -SE:***Myalgia, myopathy (check creatine kinase) ***Hepatotoxicity (check liver function test) Rhabdomyolysis -Drug interaction: ***Cytochrome P450 inhibitors enhance toxicity of statins Gemfibrozil -Can be used in combined hyperlipidemia |
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Atorvastatin
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-MOA: HMG-CoA reductase inhibitor, results in decreased liver cholesterol, increased LDL receptor expression, and decreased plasma LDL, also decreased VLDL synthesis result in decreased triglyceremia
-Clinical: Antiatherosclerosis -SE:***Myalgia, myopathy (check creatine kinase) ***Hepatotoxicity (check liver function test) Rhabdomyolysis -Drug interaction: ***Cytochrome P450 inhibitors enhance toxicity of statins Gemfibrozil -Can be used in combined hyperlipidemia |
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Simvastatin
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-MOA: HMG-CoA reductase inhibitor, results in decreased liver cholesterol, increased LDL receptor expression, and decreased plasma LDL, also decreased VLDL synthesis result in decreased triglyceremia
-Clinical: Antiatherosclerosis -SE:***Myalgia, myopathy (check creatine kinase) ***Hepatotoxicity (check liver function test) Rhabdomyolysis -Drug interaction: ***Cytochrome P450 inhibitors enhance toxicity of statins Gemfibrozil -Can be used in combined hyperlipidemia |
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Pravastatin
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-MOA: HMG-CoA reductase inhibitor, results in decreased liver cholesterol, increased LDL receptor expression, and decreased plasma LDL, also decreased VLDL synthesis result in decreased triglyceremia
-Clinical: Antiatherosclerosis -SE:***Myalgia, myopathy (check creatine kinase) ***Hepatotoxicity (check liver function test) Rhabdomyolysis -Drug interaction: ***Cytochrome P450 inhibitors enhance toxicity of statins Gemfibrozil -Can be used in combined hyperlipidemia |
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Cholestyramine
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-MOA: Bile acid sequestrant that retains bile salts in the gut resulting in decreased recycling of bile salts, increased synthesis of bile salts by liver, decreased liver cholesterol, increased LDL receptor expression, and decreased blood LDL
-Clinical: Antiatherosclerosis -SE: ***GI disturbances -Drug interactions: ***Orally administered drugs ***Malabsorption of fat-soluble vitamins (Vitamin K deficiency) Increased VLDL and triglycerides |
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Colestipol
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-MOA: Bile acid sequestrant that retains bile salts in the gut resulting in decreased recycling of bile salts, increased synthesis of bile salts by liver, decreased liver cholesterol, increased LDL receptor expression, and decreased blood LDL
-Clinical: Antiatherosclerosis -SE: ***GI disturbances -Drug interactions: ***Orally administered drugs ***Malabsorption of fat-soluble vitamins (Vitamin K deficiency) Increased VLDL and triglycerides |
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Niacin (Nicotinic Acid)
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-MOA: Inhibits VLDL synthesis resulting in decreased plasma VLDL, decreased plasma LDL, and increased plasma HDL
-Clinical: Antiatherosclerotic -SE: Hypersensitivity reaction (***use aspirin) Hepatotoxicity |
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Gemfibrozil
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-MOA: Activates lipoprotein lipase resulting in decreased VLDL, some decrease in LDL, increased HDL
-Clinical: Antiatherosclerotic agent used in hyperlipidemia -SE: ***Gallstones (pure lipids build up) Myositis (when use with statins) -***Drug can increase LDL so contraindicated in hypercholesterolemia patients -Drug interaction: Statins |
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Fenobrilate
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-MOA: Activates lipoprotein lipase resulting in decreased VLDL, some decrease in LDL, increased HDL
-Clinical: Antiatherosclerotic agent used in hyperlipidemia -SE: ***Gallstones (pure lipids build up) Myositis (when use with statins) -***Drug can increase LDL so contraindicated in hypercholesterolemia patients -Drug interaction: Statins |
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Clofibrate
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-MOA: Activates lipoprotein lipase resulting in decreased VLDL, some decrease in LDL, increased HDL
-Clinical: Antiatherosclerotic agent used in hyperlipidemia -SE: ***Gallstones (pure lipids build up) Myositis (when use with statins) -***Drug can increase LDL so contraindicated in hypercholesterolemia patients -Drug interaction: Statins |
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Ezetimibe
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-MOA: Prevents intestinal absorption of cholesterol resulting in decreased LDLs
-Clinical: Antiatheroscletic agent -SE: GI distress |
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Heparin
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-MOA: Catalyzes the binding of antithrombin III (a serene protease inhibitor) to factors IIa, IXa, XIa, and XIIa, resulting in their rapid inactivation
-Clinical: ***Rapid anticoagulation for thrombosis, emboli, unstable angina, DIC, etc. -SE: ***Bleeding ***Heparin-induced thrombocytopenia (HIT) Osteoporosis Hypersensitivity -Water-soluble -NO placental access (can use in pregnancy) -Low molecular weight heparins cause less HIT |
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Warfarin
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-MOA: Decreases hepatic synthesis of Vitamin K dependent factors II, VII, IX, X
-Clinical: ***Longer-term anticoagulation for thromboses, emboli, post-MI, heart valve damage, antiarrhythmias -SE: ***Bleeding ***Skin necrosis with low protein C ***Drug interactions (highly protein bound) -***Transient protein C deficiency on initiation -Lipid-soluble, given orally -Placental access (do NOT use in pregnancy) |
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Vitamin K
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-MOA: Antagonist of warfarin, increases cofactor synthesis, slow onset, given as fresh frozen plasma
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Steptokinase
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-MOA: Thrombolytic that catalyzes the formation of plasmin
-Clinical: IV for short-term emergency management of MI DVT Pulmonary embolism Ischemic stroke -SE: ***Bleeding ***Hypersensitvity and hypotension Intracerebral hemorrhage -***Early administration(3 hrs) crucial post-MI |
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Urokinase
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-MOA: Thrombolytic that catalyzes the formation of plasmin
-Clinical: IV for short-term emergency management of MI DVT Pulmonary embolism Ischemic stroke -SE: ***Bleeding Intracerebral hemorrhage -***Early administration crucial post-MI |
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Tissue plasminogen activator (t-PA)
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-MOA: Thrombolytic that catalyzes the formation of plasmin
-Clinical: IV for short-term emergency management of MI DVT Pulmonary embolism Ischemic stroke -SE: ***Bleeding Intracranial hemorrhage -Clot-specific so NO allergy problems |
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Asprin
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-MOA: Antiplatelet drug that irreversibly binds COX in platelets decreasing their activation
-Clinical: ***Low doses prevent MI and recurrence Higher doses for inflammation Prophylaxis in atrial arrhythmias -SE: NO side effects at low doses |
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Ticlopidine
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-MOA: Antiplatelet drug that blocks ADP receptors on platelets decreasing their activation
-Clinical: Post-MI Stable angina -SE: ***Leukopenia and thrombocytopenic purpura Hemorrhage |
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Clopidogrel
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-MOA: Antiplatelet drug that blocks ADP receptors on platelets decreasing their activation
-Clinical: Post-MI Stable angina -SE: ***Leukopenia and thrombocytopenic purpura Hemorrhage (particularly Ticlopidine though) |
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Abciximab
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-MOA: Antiplatelet dug that binds to glycoprotein IIb/IIIa receptors thus decreasing aggregation by preventing cross-linking reaction
-Clinical: ***Acute coronary syndromes Post angiplasty |
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Eptifibitide
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-MOA: Antiplatelet dug that binds to glycoprotein IIb/IIIa receptors thus decreasing aggregation by preventing cross-linking reaction
-Clinical: ***Acute coronary syndromes Post angiplasty |
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Tirofiban
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-MOA: Antiplatelet dug that binds to glycoprotein IIb/IIIa receptors thus decreasing aggregation by preventing cross-linking reaction
-Clinical: ***Acute coronary syndromes Post angiplasty |
