Pharm Exam Ii

Front 1

Mannitol

Back 1

Osmotic Diuretic

MOA: Inhibits water reabsorption throughout the tubule. It is a sugar alcohol that cannot be transported back into the system. It attracts water, allowing for excretion. Works at proximal tubule.
Use: Decrease IOP in glaucoma, decrease intracerebral pressure, oliguric states, rhabdomyolysis
SE: Acute hypovolemia

Front 2

Acetazolamide

Back 2

Carbonic Anhydrase Inhibitor
-Diuretic

MOA: Decreases H+ formation inside proximal tubule cell --> decreases Na/H antiport --> increases Na and HCO3 in lumen
Uses: Glaucoma, acute mountain sickness (treats edema and respiratory alkalosis), and metabolic alkalosis
SE: Bicarbonaturia and acidosis (loss of buffering capacity), hypokalemia, hyperchloremia (body adapts and absorbs Cl with Na), parethesia, renal stones, sulfonamide hypersensitivity

Front 3

Hydrochlorothiazide

Back 3

Thiazide
-Diuretic
-Antihypertensive

MOA: Inhibits Na/Cl transporter in distal tubule, causes increased luminal Na and Cl in DCT --> diuresis.
Uses: HTN, CHF, Nephrolithiasis (Ca stones), nephrogenic diabetes insipidus
SE: Hypokalemia/alkalosis, *hypercalcemia (increased Ca absorption). Causes decreased insulin release from pancreas --> hyperuricemia, hyperglycemia, hyperlipidemia

Front 4

Furosemide

Back 4

Loop Diuretic
-Antihypertensive

MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased reabsorption of Ca and Mg --> Increased diuresis
Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state
SE: Sulfonamide hypersensitivity, *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity
Drug Interactions: Digoxin

Front 5

Ethacrynic acid

Back 5

Loop Diuretic
-Antihypertensive

MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased back diffusion of K, decreased positive potential, decreased reabsorption of Ca and Mg.
Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state
SE: ***NO Sulfonamide hypersensitivity (use for pts with sulfa hypersensitivity), *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity
Drug Interactions: Digoxin

Front 6

Torsemide

Back 6

Loop Diuretic
-Antihypertensive

MOA: Inhibits Na/K/Cl transport in thick ascending loop. Causes decreased intracellular K, decreased back diffusion of K, decreased positive potential, decreased reabsorption of Ca and Mg.
Uses: DOC for acute pulmonary edema, heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic state
SE: Sulfonamide hypersensitivity, *Hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, *hyperuricemia, Ototoxicity
Drug Interactions: Digoxin

Front 7

Triamterine

Back 7

Diuretic - K+ Sparing
-Antihypertensive

MOA: Blocks Na/K antiport in collecting duct
SE: Hyperkalemia and acideosis

Front 8

Spironolactone

Back 8

Diuretic - K+ Sparing
-Antihypertensive

MOA: Aldosterone-receptor antagonist. Works at collecting duct principal cell.
Uses: Hyperaldosteronic state (elevated in CHF), corrects hypokalemic state, antiandrogenic uses (female hirsutism) because it blocks steroid receptors, CHF
SE: *Hyperkalemia and acidosis, antiandrogen

Front 9

Amiloride

Back 9

Diuretic - K+ Sparing
-Antihypertensive

MOA: Blocks Na/K antiport in collecting duct
SE: Hyperkalemia and acideosis

Front 10

Verapamil

Back 10

Antiarrhythmic: Type IV: Calcium Channel Blocker

MOA: Blocks slow cardiac Ca channels & blood vessels , decreases SA/AV nodal activity. Decreases CO and TPR.
Uses: Supraventricular tachycardia (Does NOT work on the Ca channels of blood vessels)
SE: *Peripheral edema, constipation, dizziness, flushing, hypotension, AV block

Front 11

Diltiazem

Back 11

Calcium Channel Blocker

MOA: Blocks slow cardiac Ca channels & blood vessels, decreases SA/AV nodal activity. Decreases CO and TPR.
Uses: Supraventricular tachycardia (Does NOT work on the Ca channels of blood vessels)
SE: Dizziness, flushing, hypotension, AV block

Front 12

Nifedipine

Back 12

Calcium Channel Blocker
-Antihypertensive
-Antianginal

MOA: Blocks slow Ca channels in blood vessels. Causes decreased intracellular Ca. Decreases TPR (mostly works on blood vessels). Antianginal - Important for vasospastic angina
SE: Reflex tachycardia, *gingival hyperplasia

Front 13

Amlodipine

Back 13

Calcium Channel Blocker

MOA: Blocks L-type Ca channels in heart and blood vessels. Causes decreased intracellular Ca. Decreases TPR
Uses: HTN, angina
SE: Reflex tachycardia, *gingival hyperplasia

Front 14

Captopril

Back 14

ACE Inhibitor
-CHF
-Antihypertensive

MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation.
Uses: HTN, protective of diabetic nephropathy, CHF
SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema

Front 15

Enalaprilat

Back 15

ACE Inhibitor
-CHF
-Antihypertensive

Prodrug = Enalapril

MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation.
Uses: HTN, protective of diabetic nephropathy, CHF
SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema

Front 16

Lisinopril

Back 16

CHF - ACE Inhibitor

MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation.
Uses: HTN, protective of diabetic nephropathy, CHF
SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema

Front 17

Benazepril

Back 17

CHF - ACE Inhibitor

MOA: Block formation of Angiotensin II by inhibiting angiotensin converting enzyme. Decreases aldosterone and causes vasodilation.
Uses: HTN, protective of diabetic nephropathy, CHF
SE: Dry cough*, Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema

Front 18

Losartan

Back 18

Angiotensin I Receptor ANT (ARB)
-CHF
-Antihypertensive

MOA: Blocks AT1 R's on adrenal cortex and blood vessels.
Uses: HTN, protective of diabetic nephropathy, CHF
SE: Hyperkalemia (decreased aldosterone), acute renal failure in renal artery stenosis, angioedema

Front 19

Digoxin

Back 19

CHF: Cardiotonic Agent - Cardiac Glycoside

MOA: Inhibits cardiac Na/K ATPase --> Increases intracellular Ca --> Increases contractile force. Also inhibits neuronal Na/K ATPase, causes increased vagal and sympathetic stimulation
Pharmacokinetics: Long half life, requires loading dose. Large Vd (tissue protein binding) - Displacement by other drugs
Uses: CHF, Supraventricular tachycardia
SE: Early signs are GI - Anorexia, nausea, ECG and late signs are CNS - disorientation, visual effects. Toxic doses - Cardiac arrhythmias
Drug interactions - Quinidine and verapamil displace from tissue binding site

Similar to digitoxin, but longer-lasting effects

Front 20

Amrinone

Back 20

CHF: PDE Inhibitor

MOA: Increases cAMP in heart muscle, causing increased inotropy. Increases cAMP in smooth muscle, results in decreased TPR

Front 21

Milrinone

Back 21

CHF: PDE Inhibitor

MOA: Increases cAMP in heart muscle, causing increased inotropy. Increases cAMP in smooth muscle, results in decreased TPR

Front 22

Propranolol

Back 22

Beta Blocker (Non-selective)
-Antiarrhythmic: Class II
-CHF
-Antihypertensive
-Antianginal

MOA: Decreases HR, SV, CO. Also decreases renin release and aqueous humor production.
Use: Prophylaxis post-MI and supraventricular tachyarrhythmias
SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs
Caution: Asthma, vasospastic disorder, diabetes

Front 23

Sotalol

Back 23

Beta Blocker
-Antiarrhythmic: Class II
-CHF

MOA:
Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR. Also a K-channel blocker
Use: Life-threatening ventricular arrhythmia
SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs
Caution: Asthma, vasospastic disorder, diabetes

Front 24

Carvediolol

Back 24

Beta Blocker and Alpha Blocker
-CHF

Front 25

Quinidine

Back 25

Na Channel blocker
- Antiarrhythmic: Class I

MOA: Antiarrhythmic - Block fast Na channels, preferentially in the open/activated state. Increases AP duration and effective refractory period. Also blocks K+ channel. Also causes muscarinic receptor blockade, which can increase HR and AV conduction.
SE: *Cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation), hypotension, prolongation of QRS and increased QT interval associated with syncope (torsades)

Front 26

Procainamide

Back 26

Na Channel blocker
- Antiarrhythmic: Class I

MOA: Antiarrhythmic - Block fast Na channels, preferentially in the open/activated state. Increases AP duration and effective refractory period. Also blocks K+ channel.
SE: SLE-like syndrome (more likely with slow-acetylators), hematotoxicity, CV effects (torsades)

Front 27

Lidocaine

Back 27

Na Channel blocker
- Antiarrhythmic: Class I

MOA: Antiarrhythmic - Block fast Na channels, preferentially for tissues partly depolarized (slow conduction in hypoxic and ischemic tissues). Decreases APD due to block of the slow Na window currents, but this increases diastole and extends the time for recovery. Used for post-MI & open-heart surgery.
SE: CNS (seizures), LEAST cardiotoxic

Front 28

Phenyloin

Back 28

Na Channel blocker
- Antiarrhythmic: Class I

MOA: Antiarrhythmic - Block fast Na channels, preferentially for tissues partly depolarized (slow conduction in hypoxic and ischemic tissues). Decreases APD due to block of the slow Na window currents, but this increases diastole and extends the time for recovery.

*Class Ib antiarrythmic, but usually used as an antiepileptic

Front 29

Esmolol

Back 29

Beta Blocker (Cardioselective, B1)
-Antiarrhythmic: Class II

MOA: Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR
Use: Prophylaxis post-MI and supraventricular tachyarrhythmias
*Used as IV, used in acute SVTs
SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs
Caution: Vasospastic disorder, diabetes

Front 30

Acebutolol

Back 30

Beta Blocker (Cardioselective, B1)
-Antiarrhythmic: Class II

MOA: Prevent B-receptor activation, would would normally increase cAMP. Decreases SA/AV nodal activity. Decreases HR
Use: Prophylaxis post-MI and supraventricular tachyarrhythmias
SE: Cardiovascular depression (AV block), fatigue, sexual dysfunction, increases LDLs and TGs
Caution: Asthma, vasospastic disorder, diabetes

Front 31

Bretyllium

Back 31

K+ Channel Blocker (AP Prolongation)
-Antiarrhythmic: Class III

MOA: Blocks K+ Channel, slows repolarization of AP. Increases APD and ERP, especially in ventricular and Purkinje diseases

Front 32

Amiodarone

Back 32

K+ Channel Blocker (AP Prolongation)
-Antiarrhythmic: Class III

MOA: Blocks K+ Channel, slows repolarization of AP. Increases APD and ERP, especially in ventricular and Purkinje diseases
*Mimics classes I, II, III, IV - Increases APD and ERP in ALL cardiac tissues. Used for all arrhythmias.
*LONG half-life - binds extensively to all tissues, large Vd
SE: Pulmonary fibrosis, blue pigmentation of skin (smurf), phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfunction

Front 33

Adenosine

Back 33

Antiarrhythmic

MOA: Activates adenosine receptors to cause Gi-coupled decrease in cAMP - Decreases HR. Decreases SA and AV nodal activity
DOC: aroxysmal supraventricular tachycardias and AV nodal arrhythmias
SE: Flushing, sedation, dyspnea

Front 34

Clonidine

Back 34

alpha-2 Agonist
-Antihypertensive

MOA: Decreases sympathetic stimulation (negative feedback, decreases release of NE, decreases alpha1 and beta1 activation). Decreases TPR AND HR
Use: HTN, Opiate withdrawal
SE: CNS depression, edema

Front 35

a-methyldopa

Back 35

alpha-2 Agonist
-Antihypertensive

MOA: Decreases sympathetic stimulation (binds to alpha2 presynaptic R's and decreases release of NE, decreases alpha1 and beta1 activation). Decreases TPR AND HR
Use: HTN and HTN-management in pregnancy
SE: *Hemolytic anemia, CNS depression, edema

Front 36

Reserpine

Back 36

Antihypertensive: Interferes with storage vesicles (NE)

MOA: Prevents storage in vesicles (NE) - Decreases CO and TPR, decreases release of catecholamines
SE: *Severe depression, edema, increases GI secretions (PNS)

Front 37

Guanethidine

Back 37

Antihypertensive - Inhibits NE Release

MOA: Binds NE vesicles and inhibits NE release
SE: Diarrhea, edema

Front 38

Prazosin

Back 38

alpha-1 Blocker
-Antihypertensive

MOA: Arteriolar and venous vasodilation to decrease BP. Also inhibits SM contraction in prostate
Use: HTN, BPH
SE: Reflex tachycardia, "first-dose" syncope, *orthostatic hypotension, urinary incontinence (increases PNS)

Front 39

Hydralazine

Back 39

Antihypertensive: Direct-Acting Vasodilator - Nitric Oxide

MOA: Decreases TPR through arteriolar dilation
SE: SLE-like syndrome and slow acetylators, edema, reflex tachycardia

Front 40

Nitroprusside

Back 40

Antihypertensive: Direct-Acting Vasodilator - Nitric Oxide

MOA: Decreases TPR through dilation of both arterioles and venues
Use: DOC for hypertensive emergencies, IV
SE: Cyanide toxicity - co-administer with nitrites and thiosulfate

Front 41

Inamrinone

Back 41

CHF: Cardiotonic Agent - PDE inhibitor

MOA: Increases cAMP in heart cells (increases inotrophy) and SM cells (decreases TPR)

Front 42

Milrinone

Back 42

CHF: Cardiotonic Agent - PDE inhibitor

MOA: Increases cAMP in heart cells (increases inotrophy) and SM cells (decreases TPR)

Front 43

Nitroglycerine

Back 43

NO Precursor
-Antianginal

MOA: Pro-drug of NO. Venodilation decreases preload, which decreases O2 requirement. Nitrates decrease infarct size and post-MI mortality.
SE: Flushing, headache, orthostatic hypotension. Reflex tachycardia & fluid retention. Methemoglobinemia.
*Don't use with sildenafil (viagra)

Front 44

Isosorbide dinitrate

Back 44

NO Precursor
-Antianginal

MOA: Pro-drug of NO. Venodilation decreases preload, which decreases O2 requirement. Nitrates decrease infarct size and post-MI mortality.
SE: Flushing, headache, orthostatic hypotension. Reflex tachycardia & fluid retention. Methemoglobinemia.
*Don't use with sildenafil (viagra)

Front 45

Atorvastatin

Back 45

Statin
-Anti-atherosclerotic

MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia
SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity
*Cytochrome P450 inhibitors enhance toxicity of statins

Front 46

Simvastatin

Back 46

Statin
-Anti-atherosclerotic

MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia
SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity
*Cytochrome P450 inhibitors enhance toxicity of statins

Front 47

Lovastatin

Back 47

Statin
-Anti-atherosclerotic

MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia
SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity
*Cytochrome P450 inhibitors enhance toxicity of statins

Front 48

Pravastatin

Back 48

Statin
-Anti-atherosclerotic

MOA: Inhibits HMG-CoA reductase reduces liver cholesterol, increases LDL receptor expression, and decreases LDL. Decreased VLDL results in decreased triglyceridemia
SE: Myalgia, myopathy, rhabdomyolysis, hepatotoxicity
*Cytochrome P450 inhibitors enhance toxicity of statins

Front 49

Gemfibrozil

Back 49

Fibric Acid Derivatives
-Antiatherosclerotic Agent

MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia
SE: Hepatotoxicity

Front 50

Fenofibrate

Back 50

Fibric Acid Derivatives
-Antiatherosclerotic Agent

MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia
SE: Hepatotoxicity

Front 51

Clofibrate

Back 51

Fibric Acid Derivatives
-Antiatherosclerotic Agent

MOA: Induction of lipoprotein lipases, causes decreased VLDL and TGL. *Used for hypertriglyceridemia
SE: Hepatotoxicity

Front 52

Cholestyramine

Back 52

Bile Acid Sequestrant
-Antiatherosclerotic

MOA: Complex bile salts in gut. Causes decreased enterohepatic recirculation of bile salts, increased synthesis of new bile, decreased liver cholesterol, increased LDL-R expression, decreased blood LDL
SE: Increased VLDL and triglycerides, GI disturbances, malabsorption of lipid-soluble vitamins

Front 53

Colestipol

Back 53

Bile Acid Sequestrant
-Antiatherosclerotic

MOA: Complex bile salts in gut. Causes decreased enterohepatic recirculation of bile salts, increased synthesis of new bile, decreased liver cholesterol, increased LDL-R expression, decreased blood LDL
SE: Increased VLDL and triglycerides, GI disturbances, malabsorption of lipid-soluble vitamins

Front 54

Niacin (Nicotinic acid)

Back 54

Antiatherosclerotic

MOA: Inhibition of VLDL synthesis, causing decreased plasma VLDL and LDL and **increased plasma HDL.
SE: Flushing, hyperglycemia

Front 55

Ezetimibe

Back 55

Antiatherosclerotic

MOA: Prevents intestinal absorption of cholesterol, decreases LDL
SE: GI distress

Front 56

Pilocarpine

Back 56

Muscarinic Agonist

MOA: Ophthalmic effects predominate - Contraction of sphincter muscle of the iris (miosis) and enhances tone of trabecular network. Contraction of ciliary muscle --> Accommodation.
Use: Glaucoma, dry mouth (Sjogren's)
SE: Topical - stinging & local irritation. Oral - Sweating and worsens asthma/COPD symptoms.

Front 57

Bethanecol

Back 57

Muscarinic Agonist

MOA: Mostly works on smooth muscles. GU - Increases detrusor tone and decreases resistance of internal sphincter. GI - Increases motility and secretion
Use: Gastric atony (increases motility) and urinary retention
SE: Bronchoconstriction, GI (nausea, vomiting, diarrhea), Miosis

Front 58

Carbachol

Back 58

Muscarinic Agonist

MOA: Non-selective cholinergic agonist
Use: Topically for glaucoma, increases aqueous humor outflow into the canal of Schlemm

Front 59

Physostigmine

Back 59

Anticholinesterase

MOA: Inhibits AChE. Readily crosses BBB.
Use: Antidote for anticholinergic delirium (from atropine overdose).

Front 60

Neostigmine

Back 60

Anticholinesterase

MOA: Inhibits AChE, increases accumulation of acetylcholine at neuromuscular junctions and synapses. Skel muscle - Reverses neuromuscular blockade. GU - Increased tone, motility and relaxation of sphincters. Heart - Decreased HR, contractility, and conduction velocity.
Use: Reverse nondepolarizing neuromusclar blockade (ex: coming out of surgical anasthesia), Myasthenia gravis.

Front 61

Pyridostigmine

Back 61

Anticholinesterase

MOA: Inhibits AChE, increases accumulation of acetylcholine at neuromuscular junctions and synapses. Skel muscle - Reverses neuromuscular blockade. GU - Increased tone, motility and relaxation of sphincters. Heart - Decreased HR, contractility, and conduction velocity.
Use: Myasthenia gravis.

Front 62

Edrophonium

Back 62

Anticholinesterase

MOA: Inhibits AChE
Use: Used to diagnose myasthenia gravis: Tensilon test - Increased ACh in NM junction able to overcome ACh receptor Abs leads to sudden improvement then decreased muscle strength. Also used to differentiate between cholinergic crisis (overmedication) and worsening myasthenia.

Front 63

Isoflurophate (DFP)

Back 63

Anticholinesterase

MOA: Organophosphate "nerve gas" - Suicide inhibitor of AChE. Accumulation of ACh at NM junctions and neuronal synapses.
Clinical: CNS - Coma, resp depression, seizures. Muscarinic - BRADYCARDIA. Nicotinic - Muscle twitching, fasiculations, weakness & flaccid paralysis.

Front 64

Pralidoxime (2-PAM)

Back 64

Antidote to Cholinesterase Inhibitor

MOA: Cholinesterase regenerator to organophosphate toxicity. ACh R blocker to decrease muscarinic hyperactivity that would otherwise cause potentially fatal bradycardia. Regeneration is due to pralidoxime's higher affinity for phosphorus.

Front 65

Atropine

Back 65

Muscarinic Antagonist

Use: Antidote for physostigmine overdose
SE: "Red as a beet, blind as a bat, dry as a bone, hot as a hare, and mad as a hatter." - flush, blurred vision, decreased secretions, hyperthermia, delirium, hallucinations

Front 66

Scopolamine

Back 66

Muscarinic Antagonist

Use: Motion sickness prophylaxis.
SE: "Red as a beet, blind as a bat, dry as a bone, hot as a hare, and mad as a hatter." - flush, blurred vision, decreased secretions, hyperthermia, delirium, hallucinations

Front 67

Ipratropium

Back 67

Muscarinic Antagonist

MOA: Decreased bronchoconstriction and bronchial secretions.
Use: COPD!! and asthma
SE: Dry mouth & sedation

Front 68

Norepinephrine

Back 68

Alpha Adrenergic Agonist

MOA: Peripheral vasoconstriction and increased BP.
Use: Severe hypotension (used in ICU)
SE: Reflex bradycardia

Front 69

Epinephrine

Back 69

MOA: Stimulates a1, a2, B1 and B2 R's. B is predominant at low doses and alpha at high doses. Net effect is equivalment to sympathetic stimulation.
Use: Cardiac arrest, cardiogenic shock, severe HTN
SE: Can precipitate MI or arrhythmias.

Front 70

Dopamine

Back 70

MOA: Precursor to NE, stimulates D1>B1>a1. Low doses - D1 predominates - Renal and splanchnic vasodilation. Medium dose - B1 predominates, Increased CO.
Use: Decompensated CHF - Treat with medium doses
SE: Arrhythmias

Front 71

Dobutamine

Back 71

Beta Adrenergic Agonist
-Stimulates B1>>B2
-CHF

MOA: Increases cardiac contractility and CO.
Use: Decompensated congestive heart failure
SE: Arrhythmias

Front 72

Amphetamine

Back 72

alpha=B

MOA: Causes release of endogenous NE after presynaptic uptake
Use: ADHD
SE: Restlessness, dependence

Front 73

Ephedrine

Back 73

B>alpha

MOA: Stimulates release of NE from sympathetic neurons. Net effect is to increase HR and Co, and variably increase TPR to increase BP.
Use: Nasal decongestant
SE: HTN

Front 74

Cocaine

Back 74

Indirect Agents Affecting Adrenergic NTs

MOA: Blocks reuptake of catecholamines (potentiates NE > Epi). CNS stimulation --> depression. CV (moderate doses) --> tachycardia, arrhythmia & MI.
SE: Myocardial ischemia

Front 75

Phenylephrine

Back 75

alpha1 Agonist

MOA: Reduces mucosal blood flow by causing vasoconstriction of superficial blood vessels, causing the fluid in the interstitial space draining through the veins, reducing edema.
Use: *Vasopressor, nasal decongestant
SE: Reflex bradycardia and *hypertension

Front 76

Methoxamine

Back 76

alpha1 Agonist

MOA: Vasoconstriction of skin and splanchnic vessels. Increases TPR.
Use: Hypotension. Also used to treat tachycardia (due to reflex bradycardia)
SE: Reflex bradycardia via baroreceptors

Front 77

Metaraminol

Back 77

Alpha Adrenergic Agonist
a1 >> B1

Use: Hypotension, particularly as a complication of anesthesia. Used for priapism.

Front 78

Tetrahydrozoline

Back 78

alpha1 Agonist

MOA: Decreases redness by limiting blood flow to eye surface
Use: VISINE

Front 79

Clonidine

Back 79

alpha2 Agonist

MOA: Works to suppress sympathetic outflow.
Use: HTN and drug withdrawal
SE: Sedation, dry mouth, *rebound hypertension

Front 80

Phenoxybenzamine

Back 80

Non-selective alpha blocker

MOA: IRREVERSIBLE antagonist. Alpha blockade causes dilation of vascular SM, decreases BP. Also inhibits neuronal extraneuronal NE reuptake.
Use: HTN, specifically pts with *pheochromocytoma
SE: Orthostatic hypotension, reflex tachycardia

Front 81

Tolazoline

Back 81

Alpha Antagonist

Used in vet medicine... -_-

Front 82

Phentolamine

Back 82

Non-selective alpha blocker

MOA: Competitive antagonist. Alpha blockade causes dilation of vascular SM, decreases BP
Use: HTN, pheochromacytoma
SE: Orthostatic hypotension, reflex tachycardia

Front 83

Isoproterenol

Back 83

Beta Agonist - B1-B2

MOA: Stimulates Beta R's - B1 increases HR & inotropy. B2 causes vascular SM relaxation. Net effect is increased HR and CO.
Use: Bradycardia, heart block and arrhythmias.
SE: Arrhythmias, flushing, angina

Front 84

Albuterol

Back 84

Beta Agonist - B2 >> B1

MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation
Use: Bronchospasm in asthma, bronchitis, and COPD
SE: Tremor. Sinus tachycardia

Front 85

Terbutaline

Back 85

Beta Agonist - B2 >> B1

MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation
Use: IV for treatment of status asthmatics. Also used to suppress premature labor

Front 86

Metaproterenol

Back 86

B2 >> B1

MOA: B2 activation causes increased cAMP and relaxation of SM and bronchodilation
Use: Bronchospasm in asthma, bronchitis, and COPD
SE: Tremor. Sinus tachycardia

Front 87

Metoprolol

Back 87

Beta Blocker
-HTN

MOA: Selectively inhibits B1 R's. Decreases HR (acts as a Class II antiarrhythmic). Also decreases inotropy. Overall decreases O2 demand
Use: Ischemic heart disease, HTN, arrhythmias
SE: Bradycardia

Front 88

Nadolol

Back 88

Beta Blocker - Non-selective

MOA: Selectively inhibits B1 R's. Decreases HR (acts as a Class II antiarrhythmic). Also decreases inotropy. Overall decreases O2 demand
Use: Ischemic heart disease, HTN, arrhythmias, portal HTN, thyrotoxicosis, migraine prevention.
SE: Bradycardia, *bronchospasm

Front 89

Timolol

Back 89

Beta Blocker - Non-selective
-HTN

MOA: Decreases HR, SV, CO. Also decreases renin release and *aqueous humor production (can be used as eye drops)
Use: Glaucoma

Front 90

Carvediol

Back 90

Beta blocker (also alpha1) - Non-selective
-CHF

MOA: Decreases HR, SV, CO & TPR. Vasodilatory due to alpha1 blockade.
Use: Compensated heart failure (Improves symptoms, ejection fraction and survival)
SE: Hypotension, bradychardia.

Front 91

Labetalol

Back 91

Beta blocker (also alpha1) - Non-selective

MOA: Decreases HR, SV, CO & TPR. Vasodilatory due to alpha1 blockade.
Use: HTN

Front 92

Nicotine

Back 92

Depolarizing Ganglionic Blocker

MOA: Agonist for nicotinic ACh R's. Nm causes skeletal muscle contract. Nn stimulates both SNS and PNS. Epinephrine release, increase HR, peripheral vasoconstriction, Increased gut motility and secretion, increased respiratory rate.
Use: Aid smoking cessation
SE: Dependence

Front 93

Hexamethonium

Back 93

Depolarizing Ganglionic Blocker

MOA: Competitive antagonist of Nn receptors at PNS and SNS ganglia.
Use: Hypertensive crises - no longer used because of the many side effects that result from loss of all autonomic tone.

Front 94

Tubocurarine

Back 94

Competitive Neuromuscular Blocker

Use: Muscle paralysis during surgery or intubation
MOA: Antagonize receptor at neuromuscular endplate, inhibiting muscle contraction

Front 95

Pancuronium

Back 95

Competitive Neuromuscular Blocker

MOA: Nondepolarizing blockade causes skeletal muscle paralysis that can be overcome by stimulation or administration of cholinesterase inhibitor
Use: Induce paralysis (surgery)
SE: Histamine causes flushing, edema, erythema, hypotension, tachycardia. Increased HR and CO.

Front 96

Vecuronium

Back 96

Competitive Neuromuscular Blocker

MOA: Nondepolarizing blockade causes skeletal muscle paralysis that can be overcome by stimulation or administration of cholinesterase inhibitor
Use: Induce paralysis (surgery)
SE: Histamine causes flushing, edema, erythema, hypotension, tachycardia. Increased HR and CO.

Front 97

Succinylcholine

Back 97

Depolarizing Neuromuscular Blocker

MOA: Binds nicotinic (Nm) Ach R's, causing depolarization of membrane. Drug is NOT inactivated by acetylcholinesterase - prolonged depolarization. Causes depolarizing blockade that cannot be overcome.
Use: Paralysis for surgical procedures
SE: Malignant hyperthermia

Front 98

Trimethaphan

Back 98

Competitive Ganglionic Blocker

Use: Muscle paralysis during surgery or intubation
MOA: Antagonize receptor at neuromuscular endplate, inhibiting muscle contraction