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Final MDA Smith

DrugClass/IndicationMechanism of actionExtra Info
NaHCO3 GI (antacid) Acid neutralizing agents Pay attention to Na levels; can release CO2
CaCO3 GI (antacid) Release CO2 to increase pH to cause a metabolic alkalosis Too much can cause rebound acid production
Al(OH)3 GI (antacid) Acid neutralizing agents not aborbed; problem with patients with renal failure because they cannot filter out easily
Mg(OH)2 GI (antacid) Acid neutralizing agents more aborbed than Al; problem with patients with renal failure because they cannot filter out easily
Charcoal GI (Antiflatulents) XXX XXX
Simethicone GI (Antiflatulents) XXX silicone polymer
Cimetidine GI (H2-Receptor Antagonists) Inhibit histamin receptors to block acid production many drug interaction; useful for GERD and SRMD
Ranitidine GI (H2-Receptor Antagonists) Inhibit histamin receptors to block acid production many drug interaction; useful for GERD and SRMD
Famotidine GI (H2-Receptor Antagonists) Inhibit histamin receptors to block acid production many drug interaction; useful for GERD and SRMD
Nizatidine GI (H2-Receptor Antagonists) Inhibit histamin receptors to block acid production many drug interaction; useful for GERD and SRMD
Omeprazole GI (PPI) irreversibly inhibit proton pumps to decrease acid secretion more effective than H2-Receptor Antagonists; 2-5d delayed effects
Lansoprazole GI (PPI) irreversibly inhibit proton pumps to decrease acid secretion more effective than H2-Receptor Antagonists; 2-5d delayed effects
Rabeprazole GI (PPI) irreversibly inhibit proton pumps to decrease acid secretion more effective than H2-Receptor Antagonists; 2-5d delayed effects
Pantoprazole GI (PPI) irreversibly inhibit proton pumps to decrease acid secretion more effective than H2-Receptor Antagonists; 2-5d delayed effects
Esomeprazole GI (PPI) irreversibly inhibit proton pumps to decrease acid secretion more effective than H2-Receptor Antagonists; 2-5d delayed effects
Sucralfate GI (Mucosal Protective Agent) activated by stomach acid, binds to ulcers, becomes a barrier better affinity for duodenal ulcers
Bismuth salts GI (Mucosal Protective Agent) activated by stomach acid, binds to ulcers, becomes a barrier may decrease the action of H. pylori in peptic ulcer disease
Misoprostol GI (Mucosal Protective Agent) analog of prostaglandin E1 - decrease stomach acid production may increase mucous and bicarbonate secetion; contraindicated in pregnancy (uterine contraction)
Alginic Acid GI (Mucosal Protective Agent) floats to the surface of the gastric contents and protects the esophagus from gastric acid polymer from seaweed; component of antacids; used for GERD
Metoclopramide GI (Gastric Motility promoting) 5-HT4 agonist and dopamine antagonist --> stimulates myenteric Ach release --> increasing gastric motility XXX
Cisapride GI (Gastric Motility promoting) 5-HT4 agonist --> stimulates myenteric Ach release --> increasing gastric motility restricted use due to toxicity
Erythromycin GI (Gastric Motility promoting) stimulates motilin receptors increased gastric emptying but increased incident of diarrhea
Benzodiazepines GI (Antiemetic) anxiolytic effect reduces anticipatory N/V XXX
Dexamethazone GI (Antiemetic) XXX effective adjunct in tx of N/V in chemo regimens
Dronabinol GI (Antiemetic) antiemetic effect is primarily central (CTZ) through CB1 agonist major ingredient in marijuana; stimulates appetite; inhalation is better
Phosphorated carbohydrate solution GI (Antiemetic) reduce smooth muscle contraction maybe a good alternative to antiemetic drugs in pregnancy
Metoclopramide GI (Antiemetic) dopaminergic antagonists high doses --> Parkinson's like symptoms --> respiratory paralysis -->death
Prochlorperazine GI (Antiemetic) Antihistamine/ antimuscarinic high doses --> Parkinson's like symptoms --> respiratory paralysis -->death
Promethazine GI (Antiemetic) Antihistamine/ antimuscarinic high effects of both Antihistamine/ antimuscarinic
Meclizine GI (Antiemetic) Antihistamine/ antimuscarinic used for vestibular problems or motion sickness
Hydroxyzine GI (Antiemetic) Antihistamine/ antimuscarinic high antimuscarinic activity; can decrease GI spasms
Diphenhydramine GI (Antiemetic) Antihistamine/ antimuscarinic high effects of both Antihistamine/ antimuscarinic
Ondansetron GI (Antiemetic) 5-HT3 Antagonists Antagonize 5-HT-mediatd N/V centrally and peripherally
Dolasetron GI (Antiemetic) 5-HT3 Antagonists Antagonize 5-HT-mediatd N/V centrally and peripherally
Granisetron GI (Antiemetic) 5-HT3 Antagonists Antagonize 5-HT-mediatd N/V centrally and peripherally
Palonosetron GI (Antiemetic) 5-HT3 Antagonists Antagonize 5-HT-mediatd N/V centrally and peripherally
Aprepitant GI (Substance P/NK1 antagonist) reduces vomiting associated with activation of these receptors useful in emetogenic chemo; PO; used with 5-HT3 antagonists and dexamethasone
Castor Oil GI (Stimulant Laxatives) ricinoleic acid increases intestinal motility Used for bowel preparation and intermittent with in OTC products; avoid id pregnant (unterine contractions); maybe dependent
Cascara GI (Stimulant Laxatives) plant alkaloids that stimulate colonic motility Used for bowel preparation and intermittent with in OTC products; avoid id pregnant (unterine contractions); maybe dependent
Senna GI (Stimulant Laxatives) plant alkaloids that stimulate colonic motility Used for bowel preparation and intermittent with in OTC products; avoid id pregnant (unterine contractions); maybe dependent
Bisacodyl GI (Stimulant Laxatives) synthetic colonic stimulant Used for bowel preparation and intermittent with in OTC products; avoid id pregnant (unterine contractions); maybe dependent
Psyllium seed GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Methylcellulose GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Bran GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Saline Cathartics GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Sorbitol GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
PEG solutions GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Lactulose GI (Bulk Forming Laxative) increase intralumenal fluid indirectly stimulating peristalsis strepoorly absorbed electrolytes cause water to rush in GI and have aggressive fluid evacuation
Mineral oil GI (Stool Softeners) Emulsification of intralumenal contents reduces pressure for defecation (esp in cardiac rehab and diverticula) not recommended for elderly because if can be absorbed and get mineral oil occlusion
Glycerin suppositories GI (Stool Softeners) Emulsification of intralumenal contents reduces pressure for defecation (esp in cardiac rehab and diverticula) not recommended for elderly because if can be absorbed and get mineral oil occlusion
Docusate GI (Stool Softeners) Emulsification of intralumenal contents reduces pressure for defecation (esp in cardiac rehab and diverticula) not recommended for elderly because if can be absorbed and get mineral oil occlusion
Diphenoxylate GI (Antidiarrheal) XXX opiate - contains atropine to prevent abuse
Loperamide GI (Antidiarrheal) opiate receptor agonist (enteric opiate receptors reduce peristalsis) can not be abused
Bismuth subsalicylate GI (Antidiarrheal) may inhibit binding of enteric E. coli toxins to mucosa dark coloration of tongue and feces is due to sulfide formation
Octreotide GI (Antidiarrheal) inhibits secretory peptide release by pancreatic tumors and those assoiciated with hypersecretory disorders XXX
5-ASA or Mesalamine GI (Inflammatory Bowel Disease) 5-ASA to the colon as an anti-inflammatory agent amino acid derivative of asprin; waits to be released unitl it gets to lower bowel
Sulfasalazine GI (Inflammatory Bowel Disease) 5-ASA to the colon as an anti-inflammatory agent pro-drug of the amino acid derivative of asprin
Olsalazine GI (Inflammatory Bowel Disease) 5-ASA to the colon as an anti-inflammatory agent pro-drug of the amino acid derivative of asprin
Balsalazide GI (Inflammatory Bowel Disease) 5-ASA to the colon as an anti-inflammatory agent pro-drug of the amino acid derivative of asprin
Hydrocortisone/ steroids GI (Inflammatory Bowel Disease) Immunosuppresants given as retention enema/foam; reduces systemic effects
Azathioprine GI (Inflammatory Bowel Disease) Immunosuppresants; inhibit the inflammation and minimice hematologic effects cytotoxic drug; low doses avoid bone marrow suppression
Mercaptopurine GI (Inflammatory Bowel Disease) Immunosuppresants; inhibit the inflammation and minimice hematologic effects cytotoxic drug; low doses avoid bone marrow suppression
Infliximab GI (Inflammatory Bowel Disease) Immunosuppresants; monoclonal antibody against TNF-alpha mediator of he granulomatous inflammatory process in Chron's Disease
Alosetron GI (Inflammatory Bowel Disease) 5-HT3 Antagonists for diarrhea prominent IBS Restricted use due to ischemic colitic; shuts down normal vascular circulation in gut
Tegaserod GI (Inflammatory Bowel Disease) 5-HT4 agonist for constipation prominent IBS Side effect: diarrhea
Orlistat GI (Enteric Lipase Inhibitor) inihibts enteric lipase resulting in decreased fat absorption for wieght loss, reduces fat soluble vitmain absorption, increase defecation with fatty stool
Lubiprostone GI (Idiopathic Constipation) activates Cl channel --> increases Cl and water in LI lumen no significant absorption and effect on serum fluid and electrolytes; avoid when pregnant
Alvimopan GI (Postoperative Ileus) Mu antagonist with selectivity for enteric receptors (esp. effects on intestinal contraction) not for use in opiate dependent patients --> opiate withdrawl
Dietary Calcium and Vitamin D Osteoporosis enhance calcium absorption and inhibit PTH reduces bone turnover
Raloxifene Osteoporosis Estrogen receptor agonist increases osteoblastic differentiation; estrogen replacment works in the same way
teriperitide Osteoporosis Recombinant PTH; stimulates bone remodeling with osteoblastic enhancement pure PTH is counter-productive due to the loss of Ca
Calcitonin Osteoporosis inhibits osteoclastic activity good for advanced cases
Fluoride Osteoporosis low levels enhance bone mass; increase osteoblasts high levels inhibit osteoblastic activity
Alendronate Osteoporosis (Bisphosphonate) inhibition of cholesterol sythesis in osteoclasts high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Ibandronate Osteoporosis (Bisphosphonate) inhibition of cholesterol sythesis in osteoclasts high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Pamidronate Osteoporosis (Bisphosphonate) inhibition of cholesterol sythesis in osteoclasts high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Tiludronate Osteoporosis (Bisphosphonate) induction of apoptosis in osteoclasts due to phosphorylation of the drug high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Etidronate Osteoporosis (Bisphosphonate) induction of apoptosis in osteoclasts due to phosphorylation of the drug high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Risedronate Osteoporosis (Bisphosphonate) inhibition of cholesterol sythesis in osteoclasts high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Zoledronate Osteoporosis (Bisphosphonate) inhibition of cholesterol sythesis in osteoclasts high affinity for Ca in bone matrix; long half life; chronic treatment enhances bone mass
Saline Diuresis Hypercalcemia ??? follow by furosemide b/c enhances Ca excretion; only use if good renal function
IV Bisphosphonate Hypercalcemia inhibition of cholesterol sythesis in osteoclasts only use if there is a tumor
Calcitonin Hypercalcemia inhibits osteoclastic activity for acute cases
Phosphate Hypercalcemia XXX for extreme cases when there is no renal function ; can get reabsorbed --> renal stones
Erythropoietin Hematopoietic Agent (Normochromic, Normocytic Anemia) Stimulates burst forming units and late progenitor cells to amplify and commit to erythrocyte production, required for red cell production Produced by peritubular kidney cells in response to hypoxemia; used in chemotherapy, renal failure
Darbepoetin Hematopoietic Agent (Normochromic, Normocytic Anemia) Stimulates burst forming units and late progenitor cells to amplify and commit to erythrocyte production, required for red cell production Erythropoietin analog, has greater half-life (allows less frequent administration); used in chemotherapy, renal failure
Ferrous Sulfate Hematopoietic Agent (Microcytic, Hypochromic anemia) Replaces Iron deficiency (if absorption is not a problem) Used for microcytic, hypochromic anemia (monitored by plasma iron, ferritin, transferrin), oral
Sodium Ferric Gluconate Complex Hematopoietic Agent (Microcytic, Hypochromic anemia) Replaces Iron deficiency (if absorption is a problem) Used for microcytic, hypochromic anemia (monitored by plasma iron, ferritin, transferrin), parenteral
Iron Sucrose Hematopoietic Agent (Microcytic, Hypochromic anemia) Replaces Iron deficiency (if absorption is a problem) Used for microcytic, hypochromic anemia (monitored by plasma iron, ferritin, transferrin), parenteral
Iron Dextran Hematopoietic Agent (Microcytic, Hypochromic anemia) Replaces Iron deficiency (if absorption is a problem) Used for microcytic, hypochromic anemia (monitored by plasma iron, ferritin, transferrin), parenteral, used by Z-technique (has high-frequency of allergic reactions)
Deferoxamine Iron Chelator Chelates plasma iron and filters it out Removes excess plasma iron
Vitamin B6 Hematopoietic Agent (pyridoxin anemia) Replace vitamin B6 to treat hemoglobin synthesis being impaired and iron accumulating inside the mitochondria, which results in an increase in sideroblasts in the circulation Anemia can occur in malnourished individuals or people with tuberculosis (on pyrazinamide and isoniazid treatment)
Vitamin B12 (oral) Hematopoietic Agent (pernicious anemia) Replace vitamin B12 in cases of malnutrition Hematological manifestations of deficiency include megaloblastic anemia (large erythrocytic precursors in circulation), can have myelin degeneration
Vitamin B12 (parenteral) Hematopoietic Agent (pernicious anemia) Replace vitamin B12 in cases of malabsorption (absence of intrinsic factor) of B12 from the ileum Hematological manifestations of deficiency include megaloblastic anemia (large erythrocytic precursors in circulation), can have myelin degeneration; is intranasal, SC, IM
Folic Acid Hematopoietic Agent (megaloblastic anemia) Required for replication for purine biosynthesis Myelin degeneration will not occur & will not correct neurological deficit produced by Vitamin B12 deficiency, recommended during pregnancy
G-CSF Hematopoietic Agent (Neutrophil deficiency) Stimulates proliferation & differentiation of progenitors committed to neutrophil production; activates & prolongs life of circulating neutrophils, mobilizes stem cells into peripheral blood Treats neutropenia in chemotherapy, allows for extraction of blood and stem cells
G-CSF Pegylated Hematopoietic Agent (Neutrophil deficiency) Stimulates proliferation & differentiation of progenitors committed to neutrophil production; activates & prolongs life of circulating neutrophils, mobilizes stem cells into peripheral blood Treats neutropenia in chemo, allows for extraction of blood & stem cells, pegylation increases bulk of protein (by using glycades), decreasing ability to be degraded & requiring less frequent administration
Sargramostim (GM-CSF) Hematopoietic Agent (Neutrophil deficiency) Induce Recovery of Neutrophils Useful in chemo and as an adjunct for bone marrow & stem cell transplantation
Oprelvekin (IL-11) Hematopoietic Agent (Platelet Production) Stimulates Megakaryocytic precursors Increases platelet production, useful for thrombocytopenia secondary to chemotherapy
Heparin Anticoagulant Accelerates binding antithrombin III to thrombin (IIa) and Xa, resulting in delayed clot formation (process accelerated 1000x) Instantaneous, monitored by aPTT, parenteral, cleared by reticuloendothelial system, prevent/treat pulmonary embolism & deep venous thrombosis, can induce thrombocytopenia or heparin-induced thromboembolism
Protamine Heparin Overdose Inactivates circulating heparin (does not inactive LMW heparins) Given in 1:1 complex, alone can act as anti-coagulant
Desirudin Anticoagulant (Thrombin Inhibitor) Direct antithrombin effect independent of antithrombin III Related to hirudin, can be monitored by aPTT, can replace heparin if adverse rxn occurs, prevent deep vein thrombosis
Lepirudin Anticoagulant (Thrombin Inhibitor) Direct antithrombin effect independent of antithrombin III Related to hirudin, can be monitored by aPTT, can replace heparin if adverse rxn occurs, for heparin-induced thrombocytopenia/thromboembolism
Bivalirudin Anticoagulant (Thrombin Inhibitor) Direct antithrombin effect independent of antithrombin III Related to hirudin, can be monitored by aPTT, can replace heparin if adverse rxn occurs, for unstable angina (undergoing angioplasty)
Argatroban Anticoagulant (Thrombin Inhibitor) Direct antithrombin effect independent of antithrombin III Related to hirudin, can be monitored by aPTT, can replace heparin if adverse rxn occurs, for heparin-induced thrombocytopenia/thromboembolism
Dalteparin Anticoagulant (LMW Heparin) Accelerates binding antithrombin III to thrombin (IIa) and Xa, resulting in delayed clot formation, but more selective for Xa Not require aPTT monitoring, treat acute venous thromboembolism & acute coronary syndrome, less likely to produce thrombocytopenia
Enoxaparin Anticoagulant (LMW Heparin) Accelerates binding antithrombin III to thrombin (IIa) and Xa, resulting in delayed clot formation, but more selective for Xa Not require aPTT monitoring, treat acute venous thromboembolism & acute coronary syndrome, less likely to produce thrombocytopenia
Tinzaparin Anticoagulant (LMW Heparin) Accelerates binding antithrombin III to thrombin (IIa) and Xa, resulting in delayed clot formation, but more selective for Xa Not require aPTT monitoring, treat acute venous thromboembolism & acute coronary syndrome, less likely to produce thrombocytopenia
Ximelagatran Anticoagulant (Direct Thrombin Inhibitors) Direct antithrombin effect independent of antithrombin III (orally active) Not approved in US, resulted in liver toxicity and bleeding, others in development to replace warfarin
Fondaparinux Anticoagulant (Factor Xa Inhibitor) Selective inactivation of Xa with antithrombin III For prophylaxis of deep venous thrombosis; SC or IV
Warfarin Anticoagulant Antagonizes the vitamin K dependent carboxylation of Factor II, VII, IX, X, as well as anticoagulant proteins C & S (orally effective) Protein C & S are natural anti-coagulating proteins, monitored by prothrombin time adjusted to INR, takes 3-5 days to work (use LMW heparins until start to work), many drug interactions occur due to competition for binding
Vitamin K1 Warfarin Overdose Bypasses reduction step, allowing carboxylation to occur, forming prothrombin Antagonizes bleeding
Urokinase Thrombolytic Agent Directly converts plasminogen to plasmin Not fibrin specific, can induce fibrinogen degradation independent of fibrin, occurs anywhere through circulation
Alteplase Thrombolytic Agent (tissue plasminogen activator) Converts plasminogen to plasmin in the presence of fibrin May lose fibrin specificity at high doses (lead to systemiclytic state), bleeding is common
Reteplase Thrombolytic Agent (tissue plasminogen activator) Converts plasminogen to plasmin in the presence of fibrin May lose fibrin specificity at high doses (lead to systemiclytic state), bleeding is common
Tenecteplase Thrombolytic Agent (tissue plasminogen activator) Converts plasminogen to plasmin in the presence of fibrin May lose fibrin specificity at high doses (lead to systemiclytic state), bleeding is common
Drotrecogin Thrombolytic Agent (Recombinant Human Activated Protein C) Replaces Protein C consumed in severe sepsis Rarely used with warfarin, used to manage coagulopathy
Aspirin Antiplatelet Agent Inhibits Cyclooxygenase-mediated synthesis of thromboxane A2 via irreversible acylation of enzyme Anucleated platelets cannot generate new enzyme, long lasting antiplatlet effect, bleeding & allergies are problem
Ticlopidine Antiplatelet Agent (ADP Antagonist) irreversibly bind to ADP receptor on platelets, inhibiting aggregation For oral administration
Clopidogrel Antiplatelet Agent (ADP Antagonist) irreversibly bind to ADP receptor on platelets, inhibiting aggregation For oral administration
Cilostazol Antiplatelet Agent (PDE III Inhibitor) Inhibition of phosphodiesterase resulting in increased cAMP and inhibition of aggregation & vasodilation Orally administered, useful for intermittent claudication (pain in lower extremities due to walking)
Abciximab Antiplatelet Agent (IIb/IIIa antagonist) Monoclonal antibody against IIb/IIIa complex (site of fibrinogen binding to platelets) IV administration, for acute coronary syndrome & primary prophylaxis of restenosis in angioplasty
Eptifibatide Antiplatelet Agent (IIb/IIIa antagonist) Monoclonal antibody against IIb/IIIa complex (site of fibrinogen binding to platelets) IV administration, for acute coronary syndrome & primary prophylaxis of restenosis in angioplasty
Tirofiban Antiplatelet Agent (IIb/IIIa antagonist) Monoclonal antibody against IIb/IIIa complex (site of fibrinogen binding to platelets) IV administration, for acute coronary syndrome & primary prophylaxis of restenosis in angioplasty
Dipyridamole Antiplatelet Agent Inhibits cyclic nucleotide phosphodiesterase and reuptake of adenosine (reduce platelet aggregation and activity) For prevention of postoperative thromboembolic complications of cardiac valve replacement
Anagrelide Antiplatelet Agent Selectively reduces platelet counts by reduction in megakaryocyte maturation Inhibits platelet aggregation, oral, for thrombocythemia
Cholestyramine Hypolipidemic Agent (Bile Acid-Binding Resin) Non-absorbable cationic exchange resin which binds bile acids in the gut and eliminates them through the feces, interference w/enterohepatic circulation of bile acids produces a cholesterol-lowering effect Bile acid go to feces, enterohepatic cholesterol lowers, liver take cholesterol from periphery, lowers LDL, cholesterol enters liver to produce bile acids
Colestipol Hypolipidemic Agent (Bile Acid-Binding Resin) Non-absorbable cationic exchange resin which binds bile acids in the gut and eliminates them through the feces, interference w/enterohepatic circulation of bile acids produces a cholesterol-lowering effect Bile acid go to feces, enterohepatic cholesterol lowers, liver take cholesterol from periphery, lowers LDL, cholesterol enters liver to produce bile acids
Colesevelam Hypolipidemic Agent (Bile Acid-Binding Resin) Non-absorbable cationic exchange resin which binds bile acids in the gut and eliminates them through the feces, interference w/enterohepatic circulation of bile acids produces a cholesterol-lowering effect Bile acid go to feces, enterohepatic cholesterol lowers, liver take cholesterol from periphery, lowers LDL, cholesterol enters liver to produce bile acids
Niacin Hypolipidemic Agent Decreases the hepatic esterification of triglycerides and reduction in VLDL, excreted as inactive metabolite & as unchanged drug in urine Lowers cholesterol & triglycerides at doses much greater than vitamin requirement, can prevent itching and vasodilation w/aspirin, liver function testing necessary
Gemfibrozil Hypolipidemic Agent (Fibric Acid derivative) Ligand of PPAR-alpha; reduces VLDL particle secretion from liver through increased oxidation Better tolerated than Niacin, increases lipoprotein activity (decrease VLDL triglycerides), increase HDL cholelithiasis risk
Fenofibrate Hypolipidemic Agent (Fibric Acid derivative) Ligand of PPAR-alpha; reduces VLDL particle secretion from liver through increased oxidation Better tolerated than Niacin, increases lipoprotein activity (decrease VLDL triglycerides), increase HDL cholelithiasis risk
Atorvastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Fluvastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Lovastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Pravastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Rosuvastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Simvastatin Hypolipidemic Agent (HMG-CoA Reductase Inhibitor) Inhibit HMG-CoA Reductase, decreasing production of cholesterol in the liver; LDL is pulled out of the periphery to increase enterohepatic cholesterol Metabolized by CYP3A4 & 2C9 (increase risk of drug interaction), most effective agent at lowering LDL, may have anti-inflammatory effect, high first pass extraction by liver
Zetia Hypolipidemic Agent (Cholesterol Absorption Inhibitor) Inhibits absorption of cholesterol (transporter protein interaction) from jejunal intestine, reducing circulating cholesterol, LDL, and triglycerides Synthesis and reuptake of cholesterol are blocked synergistically when agent is combined with a statin
Fomepizole Alcohol poisoning inhibits the conversion of alcohols to aldehydes if not avail. use ethanol for methanol poisoning
Disulturam Ethanol aversion inhibitor of acetaldehyde deHase generally without effects in absence of alcohol will make the patient sick if they consume alcohol
Created by: clamattina
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