Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
135 Cards in this Set
- Front
- Back
- 3rd side (hint)
lovastatin, pravastatin, simvastatin
Site of Action Effect on LDL Effect on HDL Effect on TG Side Effects |
HMG-CoA reductase inhibitors
Site of Action: Liver Effect on LDL: --- Effect on HDL: + Effect on TG: - |
Side Effects:
Myositis, increased LFT (must monitor) |
|
ezetimibe
Site of Action Effect on LDL Effect on HDL Effect on TG Side Effects Side Effects |
Cholesterol absorption inhibitors
Site of Action: Intestines Effect on LDL: -- Effect on HDL: 0 Effect on TG: 0 |
Side Effects:
Myalgias, possible increased LFT |
|
gemfibrozil, fenofibrate
Site of Action Effect on LDL Effect on HDL Effect on TG Side Effects |
Fibric acids
Site of Action: Blood (all stimulate lipoprotein lipase)Effect on LDL: -- Effect on HDL: + Effect on TG: --- |
Side Effects:
Myositis, increased LFT (must monitor) |
|
cholestyramine, colestipol, colesevelam
Site of Action Effect on LDL Effect on HDL Effect on TG Side Effects |
Bile acid sequestrants
Site of Action: Blood (all stimulate lipoprotein lipase)Effect on LDL: -- Effect on HDL: 0 Effect on TG: 0/+ |
Side Effects:
Bad taste, GI upset |
|
Niacin
Site of Action Effect on LDL Effect on HDL Effect on TG Side Effects |
Site of Action: Liver
Effect on LDL: -- Effect on HDL: ++ Effect on TG: - |
Side Effects:
Facial flushing, nausea, paresthesias, pruritus, increased LFT, insulin resistance, exacerbates gout |
|
ASA
Indications Cardiovascular Benefits Contraindications |
Indications:MI prevention; during and after MI.
Cardiovascular Benefits: - thrombosis risk |
Contraindications:
High risk of GI bleeding |
|
Clopidogrel
Indications Cardiovascular Benefits Contraindications |
Indications:During angina and MI; after PTCA.
Cardiovascular Benefits: - thrombosis risk |
Contraindications:
High risk of GI bleeding |
|
abciximab, eptifibatide
Indications Cardiovascular Benefits Contraindications |
GP IIb/IIIa inhibitor
Indications:During angina and MI; after PTCA or thrombolysis. Cardiovascular Benefits: - thrombosis risk |
Contraindications:
High risk of GI bleeding, thrombocytopenia |
|
Nitroglycerin
Indications Cardiovascular Benefits Contraindications |
Indications:During angina and MI.
Cardiovascular Benefits: - venous pressure causing - in preload & end-diastolic volume; as a result, blood pressure, ejection time, and O2 consumption - while contractility & heart rate + |
Contraindications:
Significant hypotension |
|
β-Blocker
Indications Cardiovascular Benefits Contraindications |
Indications:MI prevention; during angina; during and post-MI.
Cardiovascular Benefits: - blood pressure, contractility, heart rate & O2 consumption; + end-diastolic volume & ejection time; - mortality following MI |
Contraindications:
Long-term use w/ PVD, asthma, COPD, DM (can mask hypoglycemia), and depression (can worsen symptoms) |
|
ACE-I
Indications Cardiovascular Benefits Contraindications |
Indications:Post-MI
Cardiovascular Benefits:- afterload leading to - O2 consumption & blood pressure ; - mortality following MI; particularly helpful w/ comorbid CHF or DM |
Contraindications:
Pregnancy |
|
statins
Indications Cardiovascular Benefits Contraindications |
HMG-CoA reductase
Indications: Post-MI Cardiovascular Benefits: - risk of atherosclerosis progression by - LDL level |
Contraindications:
Use of multiple lipid-lowering medications |
|
Heparin
Indications Cardiovascular Benefits Contraindications |
Indications: Immediately post-MI, inpatient setting.
Cardiovascular Benefits: Decreases risk of thrombus formation |
Contraindications:
Active hemorrhage |
|
Warfarin
Indications Cardiovascular Benefits Contraindications |
Indications: Post-MI
Cardiovascular Benefits: - risk of thrombus formation |
Contraindications:
Pregnancy, active hemorrhage |
|
Morphine
Indications Cardiovascular Benefits Contraindications |
Indications: During and immediately post-MI
Cardiovascular Benefits: No direct cardiac benefit, but - pain during MI leading to - heart rate, blood pressure, and O2 consumption |
Contraindications:
Respiratory distress |
|
t-PA, urokinase
Indications Cardiovascular Benefits Contraindications |
Thrombolytics
Indications:Immediately post-MI, inpatient setting Cardiovascular Benefits: Breaks up thrombus; - mortality if used within 12 h post-MI |
Contraindications:
High bleeding risk |
|
Quinidine, procainamide
Mechanism of Action Potential Uses |
IA: Na-channel blockers (prolong action potential).
PSVT, Afib, Aflutter, Vtach |
|
|
Lidocaine, tocainide
Mechanism of Action Potential Uses |
IB: Na-channel blockers (shorten action potential).
Vtach |
|
|
Flecainide, propafenone
Mechanism of Action Potential Uses |
IC: Na-channel blockers (no effect on action potential).
PSVT, Afib, Aflutter |
|
|
Propanolol, esmolol, metoprolol
Mechanism of Action Potential Uses |
II: β-Blockers.
PVC, PSVT, Afib, Aflutter, Vtach, MAT |
|
|
Amiodarone, sotalol, bretylium
|
III: K-channel blockers.
Afib, Aflutter, Vtach (not bretylium) |
|
|
Verapamil, diltiazem
|
IV: Calcium channel blockers.
PSVT, MAT, Afib, Aflutter |
|
|
Adenosine
|
K-channel activation, decrease in intracellular cAMP.
PSVT |
|
|
Thiazides (HCTZ, etc.); K- sparing (spironolactone, etc.); loop diuretics too potent for regular anti-HTN use
Mechanism of Action Prescription Strategy Side Effects |
Diuretics
Mechanism of Action: -circulatory volume to - CO & mean arterial pressure Prescription Strategy: Early; particularly effective in blacks and salt-sensitive patients |
Side Effects: + serum glucose, cholesterol, or TG; hypokalemia
|
|
Prazosin, doxazosin, terazosin
Mechanism of Action Prescription Strategy Side Effects |
α-blockers
Mechanism of Action: Block α-adrenergic receptors (primary controllers of vascular tone) to - total peripheral resistance Prescription Strategy: Adjunct to other medications; less commonly used |
Side Effects: Postural hypotension, headache, rebound HTN if stopped
|
|
Nonselective (propranolol, timolol); 1 β-selective (metoprolol, atenolol, esmolol)
Mechanism of Action Prescription Strategy Side Effects |
β-blockers
Mechanism of Action: - HR, contractility, CO, & - renin secretion to decrease total peripheral resistance. Prescription Strategy: Early; many important cardiac uses; more effective in white patients |
Side Effects: Sexual dysfunction in males, bronchoconstriction if non-β1 selective, HDL reduction, increased triglycerides
|
|
Nondihydropyridines (diltiazem, verapamil); dihydropyridines (nifedipine, amlodipine)
Mechanism of Action Prescription Strategy Side Effects |
Calcium channel blockers
Mechanism of Action: - influx of calcium during cardiac and vascular smooth muscle contraction to cause vasodilation Prescription Strategy: 2nd line; nondihydropyridines mainly effect myocardium; dihydropyridines mainly effect vascular smooth muscle & are utilized more often for HTN |
Side Effects: Hypotension, headache, constipation, + GI reflux
|
|
Hydralazine, minoxidil
Mechanism of Action Prescription Strategy Side Effects |
Vasodilators
Mechanism of Action: Direct relaxation of vascular smooth muscle Prescription Strategy: Adjunct to other medications; less commonly used |
Side Effects: Reflex tachycardia, possible adverse cardiovascular incidents
|
|
Lisinopril, captopril, enalapril
Mechanism of Action Prescription Strategy Side Effects |
ACE-I
Mechanism of Action: Block conversion of angiotensin I to angiotensin II and + circulating bradykinin to - angiotensin II vasopressor activity and aldosterone secretion, causing - in total peripheral resistance. Prescription Strategy: Early or second line; important cardiac and renal uses; more effective in young white patients |
Side Effects: Dry cough, azotemia, hyperkalemia, teratogenicity
|
|
Irbesartan, losartan
Mechanism of Action Prescription Strategy Side Effects |
ARB
Mechanism of Action: Block binding of angiotensin II to receptors to inhibit vasopressor activity and decrease aldosterone secretion Prescription Strategy: 2nd line |
Side Effects: Few side effects; high cost; teratogenicity
|
|
HTN w/ DM
Recommended Contraindicated |
Recommended: ACE-I,
Delays renal damage Contraindicated: Thiazide diuretic β-blocker Impaired glucose tolerance & Can mask signs of hypoglycemia |
|
|
HTN w/ CHF
Recommended Contraindicated |
Recommended: ACE-I, Diuretic
Improves mortality Contraindicated: Calcium channel blocker, Reduced rate/contractility can exacerbate heart failure |
|
|
HTN w/ Post-MI
Recommended Contraindicated |
Recommended: β-Blocker,
ACE-I Improves mortality |
|
|
HTN w/ Benign prostatic hypertrophy
Recommended Contraindicated |
Recommended: Selective α1-blocker
Reduces symptoms |
|
|
HTN w/ Migraine headache
Recommended Contraindicated |
Recommended:β-Blocker
May reduce symptoms |
|
|
HTN w/ Osteoporosis
Recommended Contraindicated |
Recommended:Thiazide diuretic,
Maintains normal/high serum calcium |
|
|
HTN w/ Asthma/COPD
Recommended Contraindicated |
Nonselective β-blocker
Exacerbates bronchoconstriction |
|
|
HTN w/ Pregnancy
Recommended Contraindicated |
Contraindicated:Thiazide diuretic, Increased blood volume during pregnancy should be maintained
ACE-I & ARB, Teratogenic |
|
|
HTN w/ Gout
Recommended Contraindicated |
Contraindicated: Diuretic, Increase serum uric acid
|
|
|
HTN w/ Depression
Recommended Contraindicated |
Contraindicated: β-blocker, May worsen symptoms
|
|
|
albuterol, pirbuterol, bitolterol
Mechanism of Action Role |
Rapid-acting β2-agonists
Bronchodilators that relax airway smooth muscle; have rapid onset of action |
First-line therapy in mild intermittent cases and during exacerbations
|
|
salmeterol, formoterol, sustained-release albuterol
Mechanism of Action Role |
Long-acting β2-agonists
Bronchodilators that relax airway smooth muscle; have gradual onset and sustained activity |
Regular use in patients with moderate persistent or severe asthma
|
|
beclomethasone, flunisolide
Mechanism of Action Role |
Inhaled corticosteroids
- number and activity of cells involved with airway inflammation |
Mild persistent or worse cases; frequently combined with β2-agonist use
|
|
zafirlukast, zileuton
Mechanism of Action Role |
Leukotriene inhibitors
Block activity or production of leukotrienes that are involved in inflammation and bronchospasm |
Oral agents; adjunctive therapy in mild persistent or worse cases
|
|
cromolyn, nedocromil
Mechanism of Action Role |
Mast cell stabilizing agents
Stabilizes mast cells; anti-inflammatory prophylaxis |
Not useful acutely; anti-inflammatory prophylaxis in mild persistent cases
|
|
Theophylline
|
Bronchodilator
|
Former first-line therapy, but now replaced by β2-agonists because of side effects and interactions with other drugs; may be useful as adjunct in mild persistent or worse cases
|
|
ipratropium
|
Anticholinergic agents
Blocks vagal-mediated smooth muscle contraction |
Adjunctive therapy in moderate to severe cases
|
|
methylprednisolone, prednisone
|
Systemic steroids
Similar action to inhaled steroids; stronger effect than inhaled preparation |
Adjunctive therapy in severe, refractory cases
|
|
Asthma H/P= ≤2 times/week, Nocturnal awakening ≤2 times/month, May only occur during exercise
PEFR= >80% asymptomatic (LongTerm Control Exacerbation) |
Mild intermittent
No daily medications needed May use mast cell stabilizers if known trigger |
Inhaled short-acting β2-agonist
IV corticosteroids if persistent symptoms |
|
Asthma H/P=Bronchodilator use >2 times/week, Nocturnal awakening >every 2 weeks
PEFR= >20% fluctuations over time (LongTerm Control Exacerbation) |
Mild persistent
Inhaled low-dose corticosteroid Consider mast cell stabilizer, leukotriene inhibitor, or theophylline |
Inhaled short-acting β2-agonist
IV corticosteroids if persistent symptoms |
|
Asthma H/P= Daily symptoms
Daily bronchodilator use Symptoms interfere with activity Nocturnal awakening > times/week PERF=60%–80% (LongTerm Control Exacerbation) |
Moderate persistent
Inhaled low to medium dose corticosteroids and long-acting β2-agonist Consider leukotriene inhibitor or theophylline |
Inhaled short-acting β2-agonist
IV corticosteroids if persistent symptoms |
|
Asthma H/P= Symptoms with minimal activity
Awake multiple times/night Require multiple medications on daily basis PERF=Rarely >70%, FEV1 <60% |
Severe
Inhaled high-dose corticosteroids and long-acting β2-agonist Consider systemic corticosteroids |
Inhaled short-acting β2-agonist
IV corticosteroids if persistent symptoms |
|
calcium carbonate, aluminum hydroxide
Mechanism Prescription Strategy Adverse effects |
Antacids
MoA: Neutralize gastric acid Initial therapy, as needed |
Adverse Effects:
Constipation, nausea, diarrhea |
|
cimetidine, ranitidine
Mechanism Prescription Strategy Adverse effects |
H2 antagonists
MoA: Reversibly block histamine H2 receptors to inhibit gastric acid secretion For Patients not responding to antacids |
Adverse Effects:
Headache, diarrhea, rare thrombocytopenia; cimetidine may cause gynecomastia and impotence |
|
omeprazole, lansoprazole
Mechanism Prescription Strategy Adverse effects |
PPIs
MoA: Irreversibly inhibit parietal cell proton pump (H+/K+ ATPase) to block gastric acid secretion For Patients not responding to antacids |
Adverse Effects:
Well-tolerated; may + effects of warfarin, benzodiazepines, phenytoin, digoxin, or carbamazepine in some patients |
|
cisapride
Mechanism Prescription Strategy Adverse effects |
Pro-motility agents
MoA: Promote gastric emptying For Patients with poor LES fxn |
Adverse Effects:
Headache, diarrhea, cardiac effects |
|
Lispro, aspart, glulisine
Type of Insulin Time of Onset Peak Effect Duration Duration of Action |
Very-rapid-actinga
10 min 1 hr 2–4 hr |
|
|
Regulara
Type of Insulin Time of Onset Peak Effect Duration |
30 min
2–4 hr 5–8 hr |
|
|
NPH
Type of Insulin Time of Onset Peak Effect Duration |
2 hr
6–10 hr 18–24 hr |
|
|
Insulin glargine
Type of Insulin Time of Onset Peak Effect Duration |
2 hr
No peak 24+ hr |
|
|
Insulin detemir
Type of Insulin Time of Onset Peak Effect Duration |
2 hr
No peak 6–24 hr |
|
|
metformin
Mechanism Role Adverse Effects |
Biguanides
MoA: - hepatic gluconeogenesis, + insulin activity, - hyperlipidemia Role: Frequently first-line drug |
Adverse Effects:
GI disturbance, rare lactic acidosis, possible - vitamin B12 absorption; Contraindicated in patients with hepatic and renal insufficiency |
|
tolbutamide, glyburide, glipizide
Mechanism Role Adverse Effects |
Sulfonylureas
MoA: Stimulate insulin release from β-islet cells, reduce serum glucagon, + binding of insulin to tissue receptors Role:Frequently used after metformin or as first-line drug |
Adverse Effects:
Hypoglycemia; Contraindicated in patients with hepatic or renal insufficiency (greater risk of hypoglycemia) |
|
glitazones
Mechanism Role Adverse Effects |
hiazolidinediones
MoA: - hepatic gluconeogenesis, + tissue uptake of glucose Role:Adjunct to other drugs |
Adverse Effects:
Weight gain, + serum LDL, rare liver toxicity in some drugs |
|
acarbose
Mechanism Role Adverse Effects |
α-Glucosidase inhibitors
MoA: - GI absorption of starch and disaccharides Role: Monotherapy in patients with good dietary control of DM; adjunct to other drugs; may be used in patients with DM type |
Adverse Effects:
Diarrhea, flatulence, GI disturbance |
|
repaglinide, nateglinide
Mechanism Role Adverse Effects |
Meglitinides
MoA: Stimulate insulin release from β-islet cells Role: Used as 2nd drug with metformin or rarely as initial drug |
Adverse Effects:
Hypoglycemia; significantly more expensive than sulfonylureas with no therapeutic advantage |
|
acetazolamide
Site of Action Mechanism of Action Indications Adverse Effects |
Carbonic anhydrase inhibitors
SoA:Proximal convoluted tubule MoA: Inhibition of carbonic anhydrase causes mild diuresis and prevents HCO3- reabsorption Indications: Glaucoma, epilepsy, altitude sickness, metabolic alkalosis |
Adverse Effects:
Mild metabolic acidosis, hypokalemia, nephrolithiasis |
|
mannitol, urea
Site of Action Mechanism of Action Indications Adverse Effects |
Osmotic agents
SoA:Proximal convoluted tubule, loop of Henle, collecting tubule MoA: + tubular osmotic gradient + H2O excretion Indications: + intracranial pressure, acute renal failure (from shock or drug toxicity) |
Adverse Effects:
No effect on Na+excretion, relative hypernatremia |
|
furosemide
Site of Action Mechanism of Action Indications Adverse Effects |
Loop diuretics
SoA:Ascending loop of Henle MoA:Inhibits Na+/Cl-/K+cotransporter to -reabsorption and indirectly inhibits Ca2+ reabsorption Indications: CHF, pulmonary edema, hypercalcemia; rapid onset useful in emergent situations |
Adverse Effects:
Ototoxicity, hyperuricemia, hypokalemia, hypocalcemia |
|
hydrochlorothiazide
Site of Action Mechanism of Action Indications Adverse Effects |
Thiazides
SoA: Distal convoluted tubule MoA: Inhibits Na+/Cl- cotransporter to - reabsorption and indirectly + K+ excretion and + Ca2+ reabsorption Indications: HTN, CHF, hypercalciuria, diabetes insipidus |
Adverse Effects:
Hypokalemia, hyperuricemia, hypercalcemia |
|
spironolactone
Site of Action Mechanism of Action Indications Adverse Effects |
K+-sparing
SoA: Collecting tubules MoA: Aldosterone antagonist that inhibits Na+-K- exchange Indications: 2nd hyperaldosteronism, CHF, K+-preserving diuresis |
Adverse Effects:
Gynecomastia, menstrual irregularity, hyperkalemia |
|
ASA
Mechanism Role Adverse Effects |
MoA:Inhibits platelet aggregation by inhibiting cyclooxygenase activity to suppress thromboxane A2 synthesis
Role: Decreases thrombus risk in CAD and post-MI, decreases postoperative thrombus risk |
Adverse Effects
Increased risk of hemorrhagic stroke, GI bleeding |
|
clopidogrel, ticlopidine
Mechanism Role Adverse Effects |
Thienopyridines
MoA:Block ADP receptors to suppress fibrinogen binding to injury and platelet adhesion Role:Decreases risk of repeat MI or stroke in patients with prior MI, stroke, or PVD; decreases thrombus risk in postvascular intervention patients |
Adverse Effects
Increased risk of hemorrhage, GI bleeding |
|
abciximab
Mechanism Role Adverse Effects |
GP IIb/IIIa inhibitors
MoA:Inhibit platelet aggregation by binding to platelet GP IIb/IIIa receptors Role:Reduce risk of thrombus in unstable angina or following coronary vessel intervention |
Adverse Effects
Increased risk of hemorrhage, nausea, back pain, hypotension |
|
dipyridamole
Mechanism Role Adverse Effects |
Adenosine reuptake inhibitors
MoA:Inhibit activity of adenosine deaminase and phosphodiesterase to inhibit platelet aggregation Role:Used in combination with ASA in patients with recent stroke or with warfarin following artificial heart valve replacement |
Adverse Effects
Dizziness, headache, nausea |
|
Heparin
Mechanism Role Adverse Effects |
MoA:Binds to antithrombin III to increase activity and prevent clot formation
Role:Postoperative prophylaxis for DVT and PE, dialysis, decreases post-MI thrombus risk, safer than warfarin during pregnancy |
Adverse Effects
Hemorrhage, hypersensitivity, thrombocytopenia, narrow therapeutic window |
|
enoxaparin, dalteparin
Mechanism Role Adverse Effects |
Low molecular weight heparin
MoA:Binds to factor Xa to prevent clot formation Role:Postoperative prophylaxis for DVT and PE, safest option during pregnancy |
Adverse Effects
Hemorrhage, fever, rare thrombocytopenia |
|
lepirudin, argatroban
Mechanism Role Adverse Effects |
Direct thrombin inhibitors
MoA:Highly selective inhibitors of thrombin to suppress activity of factors V, IX, and XIII and platelet aggregation Role: Alternative anticoagulation in patients with history of heparin-induced thrombocytopenia (HIT) |
Adverse Effects
Hemorrhage, hypotension |
|
fondaparinux
Mechanism Role Adverse Effects |
Direct factor Xa inhibitors
MoA:Highly selective inhibition of factor Xa without activity against thrombin Role:DVT prophylaxis, anticoagulation following acute DVT or PE |
Adverse Effects
Hemorrhage, fever, anemia, edema, rash, constipation |
|
Warfarin
Mechanism Role Adverse Effects |
MoA:Antagonizes vitamin K-dependent carboxylation of factors II, VII, IX, and X
Role:Long-term anticoagulation post-thrombotic event or in cases of increased thrombus risk (postsurgery, Afib, artificial vales) |
Adverse Effects
Hemorrhage, numerous drug interactions, teratogenicity |
|
abacavir (ABC)
didanosine (ddI) lamivudine (3TC) zidovudine (AZT) Mechanism Adverse Effects |
Nucleoside reverse transcriptase inhibitors
Inhibit production of viral genome, prevent incorporation of viral DNA into host genome through reverse transcriptase inhibition |
Adverse Effects
Some have risk of bone marrow toxicity, neuropathy, pancreatitis, or hypersensitivity |
|
delavirdine (DLV)
efavirenz (EFV) nevirapine (NVP) Mechanism Adverse Effects |
Non-nucleoside reverse transcriptase inhibitors
Inhibit reverse transcriptase activity to prevent viral replication |
Adverse Effects
Possible hepatic toxicity, neurologic effects, rash |
|
indinavir (IDV)
nelfinavir (NFV) ritonavir (RTV) Mechanism Adverse Effects |
Protease inhibitors
Interfere with viral replication to cause production of nonfunctional viruses |
Adverse Effects
Hyperglycemia, hypertriglyceridemia, drug interactions, lipodystrophy |
|
Combivir
Trizivir Epzicom Mechanism Adverse Effects |
Combination agents
Combine multiple medications into same pill; ideal to reduce confusion of dosing schedules or to improve compliance |
Adverse Effects
Consistent with component drugs |
|
Cyclophosphamide, chlorambucil, ifosfamide, mechlorethamine
|
Nitrogen mustard alkylating agents
Free radical production causing cytotoxic alkylation of DNA and RNA |
|
|
Carmustine, streptozocin
|
Nitrosourea alkylating agents
Free radical production causing cytotoxic alkylation of DNA and RNA |
|
|
Busulfan
|
Alkyl sulfonate alkylating agents
Free radical production causing cytotoxic alkylation of DNA and RNA |
|
|
Thiotepa, hexamethylmelamine
|
Ethylenemine or methylmelamine alkylating agents
Free radical production causing cytotoxic alkylation of DNA and RNA |
|
|
Dacarbazine
|
Triazene alkylating agents
Free radical production causing cytotoxic alkylation of DNA and RNA |
|
|
Etoposide, vinblastine, vincristine
Paclitaxel, docetaxel Inhibition of DNA and RNA synthesis Antibiotics Bleomycin, dactinomycin, daunorubicin, doxorubicin, mitomycin Monoamine oxidase inhibitors Procarbazine Interference with enzyme regulation or DNA and RNA activity Antimetabolites Cytarabine, 5-flurouracil, methotrexate, mercaptopurine Platinum analogues Carboplatin, cisplatin Modulation of hormones to cause tumor remission Steroid hormones and antagonists Prednisone, tamoxifen, estrogens, leuprolide |
Vinca alkaloids
Taxanes Inhibition of spindle proteins to stop mitosis or cause cytotoxic polymerization |
|
|
Bleomycin, dactinomycin, daunorubicin, doxorubicin, mitomycin
|
Antibiotics Chemotherapeutic Drugs
Inhibition of DNA and RNA synthesis |
|
|
Procarbazine
|
Monoamine oxidase inhibitors
Inhibition of DNA and RNA synthesis |
|
|
Cytarabine, 5-flurouracil, methotrexate, mercaptopurine
|
Antimetabolites
Interference with enzyme regulation or DNA and RNA activity |
|
|
Carboplatin, cisplatin
|
Platinum analogues
Interference with enzyme regulation or DNA and RNA activity |
|
|
Prednisone, tamoxifen, estrogens, leuprolide
|
Steroid hormones and antagonists
Modulation of hormones to cause tumor remission |
|
|
Carbamazepine
MoA Indication Adversese Effects |
Inhibition of voltage-dependent Na channels
Monotherapy for partial or generalized convulsive seizures |
Nausea, vomiting, hyponatremia, Stevens-Johnson syndrome, drowsiness, vertigo, blurred vision, leukopenia
|
|
Phenytoin
MoA Indication Adversese Effects |
Inhibition of voltage-dependent Na channels
Monotherapy for partial or generalized convulsive seizures, Status epilepticuS |
Gingival hyperplasia, androgenic, lymphadenopathy, Stevens-Johnson syndrome, confusion, blurred vision
|
|
Lamotrigine
MoA Indication Adversese Effects |
Inhibition of voltage-dependent Na channels
Partial seizures, second-line drug for tonic–clonic seizures |
Rash, nausea, Stevens-Johnson syndrome, dizziness, sedation
|
|
Oxcarbazepine
MoA Indication Adversese Effects |
Inhibition of voltage-dependent Na channels
Monotherapy for partial or generalized convulsive seizures |
Hyponatremia, rash, nausea, sedation, dizziness, blurred vision
|
|
Zonisamide
MoA Indication Adversese Effects |
Inhibition of voltage-dependent Na channels
Second-line drug for partial and generalized seizures |
Somnolence, confusion, fatigue, dizziness
|
|
Ethosuximide
MoA Indication Adversese Effects |
Inhibition of neuronal Ca channels
Absence seizureS |
Nausea, vomiting, drowsiness, inattentiveness
|
|
Phenobarbital, pentobarbital
MoA Indication Adversese Effects |
Enhanced GABA activity
Nonresponsive status epilepticus |
Drowsiness, general cognitive depression, vertigo, nausea, vomiting, rebound seizures
|
|
Benzodiazepines
MoA Indication Adversese Effects |
Enhanced GABA activity
Status epilepticuS |
Drowsiness, tolerance, rebound seizures
|
|
Tiagabine
MoA Indication Adversese Effects |
Enhanced GABA activity
Second-line drug for partial seizures |
Dizziness, fatigue, nausea, inattentiveness, abdominal pain
|
|
Valproate
MoA Indication Adversese Effects |
Inhibition of sodium channels and enhanced GABA activity
Monotherapy or second drug for partial and generalized seizures |
Hepatotoxicity, nausea, vomiting, drowsiness, tremor, weight gain, alopecia
|
|
Topiramate
MoA Indication Adversese Effects |
Inhibition of NMDA-glutamate receptors and enhanced GABA activity
Second-line drug for partial and generalized seizures |
Weight loss, cognitive impairment, heat intolerance, dizziness, nausea, paresthesias, fatigue
|
|
Gabapentin
MoA Indication Adversese Effects |
Unknown
Monotherapy or second-line drug for partial seizures |
Sedation
|
|
Levetiracetam
MoA Indication Adversese Effects |
Unknown
Monotherapy for partial seizures, second-line drug for partial or generalized seizures |
Fatigue, somnolence, dizziness
|
|
Levodopa
MoA Indication Adversese Effects |
Dopamine precursor
Initial therapy Parkinson's Disease |
Nausea, vomiting, anorexia, tachycardia, hallucinations, mood changes, dyskinesia with chronic use
|
|
Carbidopa
MoA Indication Adversese Effects |
Dopamine decarboxylase inhibitor that reduces levodopa metabolism
Combined with levodopa to augment effects |
Reduces adverse effects of levodopa by allowing smaller dosage
|
|
Bromocriptine
MoA Indication Adversese Effects |
Dopamine receptor agonist
Increases response to levodopa in patients with declining response |
Hallucinations, confusion, nausea, hypotension, cardiotoxicity
|
|
Selegiline
MoA Indication Adversese Effects |
Monoamine oxidase type B inhibitor
Early disease; may help delay need to start levodopa |
Nausea, headache, confusion, insomnia
|
|
Amantadine
MoA Indication Adversese Effects |
Increases synthesis, release, or reuptake of dopamine
More effective against rigidity and bradykinesia |
Agitation, hallucinations
|
|
Antimuscarinic agents (e.g., benztropine)
|
Block cholinergic transmission
Adjuvant therapy Parkinson's Disease |
Mood changes, dry mouth, visual abnormalities, confusion, hallucinations, urinary retention
|
|
Phenylephrine
Indication in ICU MoA Effect |
Sepsis, shock
|
MoA:Agonist for α-adrenergic receptors (α1 > α2)
Effect:Vasoconstriction, reflex bradycardia |
|
Norepinephrine
Indication in ICU MoA Effect |
Shock
|
MoA:Agonist for α1- and β1-adrenergic receptors
Effect:Vasoconstriction, mildly increased contractility |
|
Epinephrine
Indication in ICU MoA Effect |
Anaphylactic shock, septic shock, post-bypass hypotension
|
MoA:Agonist for primarily β1 and to lesser extent α1- and β2-adrenergic receptors; α effects (vasoconstriction) predominate at high doses
Effect: Increased contractility (increased CO), vasodilation at low doses; increased contractility and vasoconstriction at higher doses |
|
Dopamine
Indication in ICU MoA Effect |
Shock (renal sparing)
|
MoA:Agonist for β1-adrenergic receptors (low dose) and α-adrenergic receptors (high dose); binding with dopaminergic receptors causes renal vascular vasodilation
Effect: Increased heart rate and contractility (increased CO), vasoconstriction (high dose only), increased renal blood flow |
|
Dobutamine
Indication in ICU MoA Effect |
CHF, cardiogenic shock
|
MoA:Agonist for β1-adrenergic receptors
Effect:Increased heart rate and contractility (increased CO), mild reflex vasodilation |
|
Isoproterenol
Indication in ICU MoA Effect |
Contractility stimulant in cardiac arrest
|
MoA:Agonist for β1-and β2-adrenergic receptors
Effect:Increased heart rate and contractility (increased CO), vasodilation |
|
Vasopressin
Indication in ICU MoA Effect |
Resistant septic shock, second vasopressor
|
MoA:ADH analogue with weak pressor effect
Effect:Vasoconstriction |
|
fluoxetine, sertraline, paroxetine, citalopram, escitalopram
Drug/Class Indications Mechanism Adverse Effects |
Drug/Class
Selective serotonin-reuptake inhibitors (SSRIs) Indications First-line treatment for depression Mechanism Block presynaptic serotonin reuptake to increase synaptic free-serotonin concentration and postsynaptic serotonin receptor occupancy |
Adverse Effects
Require 3-4 weeks of administration before they take effect; sexual dysfunction, decreased platelet aggregation, may increase risk of suicidal ideation in adolescents |
|
venlafaxine, duloxetine
Drug/Class Indications Mechanism Adverse Effects |
Selective serotonin/norepinephrine-reuptake inhibitors (SNRIs)
Indication First-line treatment for depression with comorbid neurologic pain; second-line treatment for patients failing SSRIs Mechanism Inhibit reuptake of both serotonin and norepinephrine in similar fashion to TCAs |
Adverse Effects
Nausea, dizziness, insomnia, sedation, constipation, HTN; side effects more benign than TCAs |
|
imipramine, amitriptyline, desipramine, nortriptyline
Drug/Class Indications Mechanism Adverse Effects |
Tricyclic antidepressants (TCAs)
Indications Mechanism Second-line treatment for depression; can be useful in patients with comorbid neurologic pain Block norepinephrine and serotonin reuptake to potentiate postsynaptic receptor activity |
Adverse Effects
Easy to overdose and may be fatal at only 5 times therapeutic dose (due to cardiac QT interval prolongation that causes arrhythmias), sedation, weight gain, sexual dysfunction, anticholinergic symptoms |
|
Bupropion
Indications Mechanism Adverse Effects |
Indications
Depression with fatigue and difficulty concentrating or comorbid ADHD Mechanism Poorly understood; may be related to inhibition of dopamine reuptake and augmentation of norepinephrine activity |
Adverse Effects
Headache, insomnia, weight loss |
|
phenelzine, isocarboxazid, tranylcypromine, selegiline
Drug/Class Indications Mechanism Adverse Effects |
Monoamine oxidase inhibitors (MAOIs)
Indications Second-line treatment for depression; can be particularly useful in treatment of depression with neurologic symptoms or in refractory cases Mechanism Block monoamine oxidase activity to inhibit deamination of serotonin, norepinephrine, and dopamine and increase levels of these substances |
Adverse Effects
Dry mouth, indigestion, fatigue, headache, dizziness; consumption of foods containing tyramine (cheese, aged meats, beer) can cause hypertensive crisis |
|
Trazodone
Indications Mechanism Adverse Effects |
Indications
Depression with significant insomnia Mechanism Poorly understood, but related to serotonin activity |
Adverse Effects
Hypotension, nausea, sedation, priapism; seizure risk at high doses |
|
Mirtazapine
Indications Mechanism Adverse Effects |
Indications
Depression with insomnia Mechanism Blocks α2-receptors and serotonin receptors to increase adrenergic neurotransmission |
Adverse Effects
Dry mouth, weight gain, sedation |
|
St. John's Wort (Hypericum perforatum)
Indications Mechanism Adverse Effects |
Indications
Used as first-line agent in Europe but only considered an alternative therapy in United States Mechanism Decreases reuptake of serotonin and, to a lesser extent, norepinephrine and dopamine |
Adverse Effects
GI distress, dizziness, sedation; drug interactions common |
|
alprazolam, clonazepam, diazepam, lorazepam
Drug/Class Indications Mechanism Adverse Effects |
Benzodiazepines
Indications Alprazolam has a rapid onset and short half-life and is particularly useful to break panic attacks; clonazepam and diazepam are more useful for prolonged therapy Mechanism Increase GABA inhibition of neuronal firing |
Adverse Effects
Sedation, confusion; stopping alprazolam usage is associated with withdrawal symptoms of restlessness, confusion, and insomnia (especially with frequent use) |
|
Buspirone
Indications Mechanism Adverse Effects |
Indications
Anxiety disorders in which abuse or sedation is a concern Mechanism Unclear, but related to serotonin and dopamine receptors |
Adverse Effects
Headaches, dizziness, nausea |
|
clozapine, risperidone, olanzapine, sertindole, quetiapine, ziprasidone, paliperidone
Drug/Class Indications Mechanism Adverse Effects |
Atypical antipsychotics
Indications First-line drugs for maintenance therapy for psychotic disorders Clozapine is most effective neuroleptic, but is reserved for refractory psychosis because of risk of agranulocytosis Mechanism Block dopamine and serotonin receptors |
Adverse Effects
Anticholinergic effects, weight gain, arrhythmias, seizures; clozapine carries risk of agranulocytosis; frequency and severity of side effects is significantly less than seen with traditional neuroleptics |
|
haloperidol, droperidol, fluphenazine, thiothixene
Indications Mechanism Adverse Effects |
Traditional high-potency antipsychotics
Indications Strong positive symptoms Emergency control of psychosis or agitation Frequently second-line drugs for maintenance therapy Mechanism Block D2 dopamine receptors |
Adverse Effects
Extrapyramidal effects (dystonia, parkinsonism), tardive dyskinesia, anticholinergic effects (sedation, constipation, urinary retention, hypotension), confusion, sexual dysfunction, hyperprolactinemia, neuroleptic malignant syndrome, seizures, arrhythmias; least anticholinergic effects of traditional antipsychotics but highest rate of extrapyramidal effects |
|
trifluoperazine, perphenazine
Drug/Class Indications Mechanism Adverse Effects |
Traditional medium-potency antipsychotics
Indications Strong positive symptoms Frequently second-line drugs for maintenance therapy May be used in patients exhibiting significant extrapyramidal and anticholinergic side effects with other traditional neuroleptics Mechanism Block D2 dopamine receptors |
Adverse Effects
Similar to other traditional drugs; mix of moderate extrapyramidal and anticholinergic effects |
|
thioridazine, chlorpromazine
Drug/Class Indications Mechanism Adverse Effects |
Traditional low-potency
antipsychotics Indications Strong positive symptoms Frequently second-line drugs for maintenance therapy Mechanism Block D2 dopamine receptors |
Adverse Effects
Similar to other traditional drugs; less extrapyramidal effects than more potent traditional antipsychotics, but more anticholinergics effects |