HMG-CoA inhibitors (rate limiting step in cholesterol synthesis), fluvastain is least potent and atorvastain and rosuvastatin most potent

Rare adverse side effects of myopathy and rhabdomyoltsis

Femibrozil

Fibrate-Agonist of peroxisome proliferator activated receptor (PPAR-α), triglycerides decrease up to 50% and HDL increases up to 20%, LDL decrease up to 15%, work in combination with statins

increased LPL expression, decreased expression apo CIII (inhibitor of apocCII and LPL interaction) and increased hepatic oxidation of FA (decreased LDL and decreased TG synthesis), increased apoA1 (major HDL protein)

Fenofibrate

Fibrate-Agonist of peroxisome proliferator activated receptor (PPAR-α), triglycerides decrease up to 50% and HDL increases up to 20%, LDL decrease up to 15%, work in combination with statins

increased LPL expression, decreased expression apo CIII (inhibitor of apocCII and LPL interaction) and increased hepatic oxidation of FA (decreased LDL and decreased TG synthesis), increased apoA1 (major HDL protein)

Cholestyramine

Inhibitor of Bile Acid absorption-bind to bile acids, preventing enterohepatic circulation, LDL decreases by 28% and HDL increases by 5%, liver needs to synthesize more bile acids so takes in more cholesterol (increased LDL receptor expression)

Administered with a meal but can be associated with vit K def. (decreased fat absorption)

Colesevelam

Colesevelam most selective

Inhibitor of Bile Acid absorption-bind to bile acids, preventing enterohepatic circulation, LDL decreases by 28% and HDL increases by 5%, liver needs to synthesize more bile acids so takes in more cholesterol (increased LDL receptor expression)

Administered with a meal but can be associated with vit K def. (decreased fat absorption)

Colestipol

Inhibitor of Bile Acid absorption-bind to bile acids, preventing enterohepatic circulation, LDL decreases by 28% and HDL increases by 5%, liver needs to synthesize more bile acids so takes in more cholesterol (increased LDL receptor expression)

Administered with a meal but can be associated with vit K def. (decreased fat absorption)

Plant sterols

displace cholesterol from micelles leading to increased excretion into stool and deceased absorption

Ezetimibe

Inhibitor of cholesterol absorption-decreased (digested and biliary but biliary more important) cholesterol transport from micelles into the enterocye by inhibiting uptake through the brush boarder protein NPC 11, effective in combination with statin (compensatory increase in rate of synthesis not present)

Niacin

vitamin B3-reduces FA release from adipose tissue, increases plasma residence time for ApoA1 (HDL protein), decreased plasma LDL-cholesterol and TG concentration and increases HDL cholesterol, associated with changes in a G-protein coupled receptor, decreased adipocyre hormone-sensitive lipase activity

Side effects of flushing and pruritis, hyperuricemia, impaired insulin sensitivity, hepatotoxicity

Omega 3-Fatty Acids

EPA (eicosapentaenoic acid)

DHA (Docosahexaenoic acid)

Lovanza (prescription)  

Regulate nuclear transcription factors including SREBP-1c (cholesterol synthesis/uptake and FA biosynthesis) and PPAR alpha to reduce TG biosynthesis and increase fatty acid oxidation. Reduced plasma TG by 50%

digoxin

narrow therapeutic window, use with B blockers risk AV block, toxicity treated with antibodies or treating hypokalemia

Cardiac glycosides (1) in myocardium, inhibit plasma membrane Na/K ATPase leading to increased cytoplasmic Ca which results in positive inotropy (contraction strength), (2) inhibit sympathetic outflow and increase vagal tone (3) prolong effective refractory period and show conduction velocity at AV node

digitoxin

metabolized and excreted by liver, not kidney (better with renal failure)

Cardiac glycosides (1) in myocardium, inhibit plasma membrane Na/K ATPase leading to increased cytoplasmic Ca which results in positive inotropy (contraction strength), (2) inhibit sympathetic outflow and increase vagal tone (3) prolong effective refractory period and show conduction velocity at AV node

Dopamine

vasodialtes at low levels (D1 receptors), intermediate vasodialates (B2) and increases contractility and rate (B1), at high does vasoconstricts (alpha-1)

B Adrenergic receptor agonist- increase CAMP by activating G protein coupled adrenergic receptors, acting at cardiac B1-adrenergic receptors, agonists have positive inotropic (contractility) and lusitotropic (quicker relaxation)

Dobutamine

racemic mixture, (+) is alpha-1 antagonist and (-) is agonist (negate each other) so primarily acts on B1 receptor (increase contractility of heart) , 2.5 min half life, side effect of tachy and ventricular arrhythmia

B Adrenergic receptor agonist- increase CAMP by activating G protein coupled adrenergic receptors, acting at cardiac B1-adrenergic receptors, agonists have positive inotropic (contractility) and lusitotropic (quicker relaxation)

Epinephrine

non selective, low dose primarily B2 (vasodilation) and high dose primarily A1 (vasoconstriction), use in setting of cardiac resuscitation

B Adrenergic receptor agonist- increase CAMP by activating G protein coupled adrenergic receptors, acting at cardiac B1-adrenergic receptors, agonists have positive inotropic (contractility) and lusitotropic (quicker relaxation)

Norepinephrine

B1 agonist (contractility, diastolic relaxation and HR increase) and A1 agonist (vasoconstriction) so redistributes cardiac supply away from non-critical tissue, side effects of SA tachy

B Adrenergic receptor agonist- increase CAMP by activating G protein coupled adrenergic receptors, acting at cardiac B1-adrenergic receptors, agonists have positive inotropic (contractility) and lusitotropic (quicker relaxation)

Isoproterenol

Isoproterenol-synthetic B1 agonist (contractility, diastolic relaxation and HR) primarily but also B2 (vasodialation and hypotension)

B Adrenergic receptor agonist- increase CAMP by activating G protein coupled adrenergic receptors, acting at cardiac B1-adrenergic receptors, agonists have positive inotropic (contractility) and lusitotropic (quicker relaxation)

Theophylline

nonsepecific, earlier development

Phosphodiesterase Inhibitors -increase CAMP by inhibiting PDE enzymes that hydrolyze it, in cardiac myocytes, PDE inhibitors have positive inotropic (contractility) and lusiotropic (relaxation) effects, PDE inhibitors also relax vascular smooth muscle and thereby decrease preload (venodilation) and afterload (ateriodilation)

Inamirone

more specific for PDE3

Phosphodiesterase Inhibitors -increase CAMP by inhibiting PDE enzymes that hydrolyze it, in cardiac myocytes, PDE inhibitors have positive inotropic (contractility) and lusiotropic (relaxation) effects, PDE inhibitors also relax vascular smooth muscle and thereby decrease preload (venodilation) and afterload (ateriodilation)

Milirone

more specific for PDE3

Phosphodiesterase Inhibitors -increase CAMP by inhibiting PDE enzymes that hydrolyze it, in cardiac myocytes, PDE inhibitors have positive inotropic (contractility) and lusiotropic (relaxation) effects, PDE inhibitors also relax vascular smooth muscle and thereby decrease preload (venodilation) and afterload (ateriodilation)

Vesnarione

Phosphodiesterase Inhibitors -increase CAMP by inhibiting PDE enzymes that hydrolyze it, in cardiac myocytes, PDE inhibitors have positive inotropic (contractility) and lusiotropic (relaxation) effects, PDE inhibitors also relax vascular smooth muscle and thereby decrease preload (venodilation) and afterload (ateriodilation)

Levosimedndan

Calcium-Sensitizing Agents-enhances the sensitivity of troponin C to Ca which increases the extent of actin-myosin interactions without a substantial increase in myocardial oxygen consumption

Levosimedndan-also activate K channels, leading to peripheral dilation, used in HF

sulfanilamide

Sulfanomides: highly selective, microbes combat by increasing PABA synthesis, mutate PABA binding site and decreased permeability to sulfonamides, due to resistance usually admisnistered with triehtropim or pyrimethamine, compete with billirubin for binding sites (more unconjugated lead to kernitcterus and brain damage)

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Sulfanomides: highly selective, microbes combat by increasing PABA synthesis, mutate PABA binding site and decreased permeability to sulfonamides, due to resistance usually admisnistered with triehtropim or pyrimethamine, compete with billirubin for binding sites (more unconjugated lead to kernitcterus and brain damage)

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Sulfanomides: highly selective, microbes combat by increasing PABA synthesis, mutate PABA binding site and decreased permeability to sulfonamides, due to resistance usually admisnistered with triehtropim or pyrimethamine, compete with billirubin for binding sites (more unconjugated lead to kernitcterus and brain damage)

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Sulfanomides: highly selective, microbes combat by increasing PABA synthesis, mutate PABA binding site and decreased permeability to sulfonamides, due to resistance usually admisnistered with triehtropim or pyrimethamine, compete with billirubin for binding sites (more unconjugated lead to kernitcterus and brain damage)

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Sulfanomides: highly selective, microbes combat by increasing PABA synthesis, mutate PABA binding site and decreased permeability to sulfonamides, due to resistance usually admisnistered with triehtropim or pyrimethamine, compete with billirubin for binding sites (more unconjugated lead to kernitcterus and brain damage)

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Sulfatones:Dapsone-leprosy and pneumocytosis carnii pneumonia, side effect of methemoglobinemia

Antimicrobial Dihydroprotease Synthase Inhibitors- PABA analogues that competitively inhibit microbial dihydroprotease synthase and thereby prevent the synthesis of folic acid

Trimethoprim

Trimethoprim-bacterial, unchanged in urine (UTI Tx)

Antimicrobial dihydrofolate reductase inhibitors-folate analogues that competitively inhibit microbial DHFR and thereby prevent the regeneration tetrahydrofolate from dihdyrofolate

Pyrimethamine

Pyrimethamine- parisitic , effective for toxoplasmosis

Antimicrobial dihydrofolate reductase inhibitors-folate analogues that competitively inhibit microbial DHFR and thereby prevent the regeneration tetrahydrofolate from dihdyrofolate

Methotrexate

Methotrexate-little selectivity, reversible, arrest cells in S phase, use in chemo with leucovorin administered several hours after (rescues folinic acid in non-malignant cells), head, neck and breast CA

Antimicrobial dihydrofolate reductase inhibitors-folate analogues that competitively inhibit microbial DHFR and thereby prevent the regeneration tetrahydrofolate from dihdyrofolate

Aspirin

Aspirin- salicylate, long half life, irreversible on 1 and 2, lose dose for anthromobogenic prophylaxis, formation of aspirin-triggered lipoxins (15-epi lipoxn), side effects of anspirin induced airway hyperactivity (airway constriction) and Reye's syndrome (encephalopathy and liver steatosis in children)

Ibuprofen

Propionic Acid, used for RA, osteoarthrits, ankylosing spondylitis

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Naproxen

Propionic Acid, long half life, less GI effects than aspirin

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Propionic Acid

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Propionic Acid

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Inhibits neotrophil motility

Acetic Acids-incoroporate arachidonic acid into tricglyceride, making less available, used for RA, osteoarthrits, ankylosing sondylitis and other musculoskeltal disorders

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Acetic Acids-incoroporate arachidonic acid into tricglyceride, making less available, used for RA, osteoarthrits, ankylosing sondylitis and other musculoskeltal disorders

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Etodolac

Acetic Acids-incoroporate arachidonic acid into tricglyceride, making less available, used for RA, osteoarthrits, ankylosing sondylitis and other musculoskeltal disorders

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Diclofenac

Acetic Acids-incoroporate arachidonic acid into tricglyceride, making less available, used for RA, osteoarthrits, ankylosing sondylitis and other musculoskeltal disorders

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Ketorolac

Acetic Acids-incoroporate arachidonic acid into tricglyceride, making less available, used for RA, osteoarthrits, ankylosing sondylitis and other musculoskeltal disorders

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Piroxicam

Oxicams, long half life, better tolerated than naproxen/ibuprofen and equally effective, inhibits collagenase and oxidative burst

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Mefenamate

Fenametes:antagonize prostanoid receptors to various degrees, less effective and more toxic than aspirin

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Melcofenamate

Fenametes:antagonize prostanoid receptors to various degrees, less effective and more toxic than aspirin

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Nabumefetone

Ketones, preference to COX-2, less GI side effects, associated with dizziness and HA

Nonseteroidal anti-inflamamtory drugs (NSAIDs)-inhibit COX-1 and COX-2, decreasing biosynthesis of downstream eiconosoids and thereby limiting the inflammatory response, only suppress signs of underlying inflammatory response but may not necessarily reverse or resolve the inflammatory process, associated with gastroathy (dyspepsia, gastrotoxicity, etc)

Acetaminophen

Weak inhibitor of peripheral COX's, (insignificant anti-inflammatory) predominant effect may be inhibition of COX-3 in the CNS, hepatotoxic on overdose (cytochrome P450)

Celecoxib

Selective COX-2 inhibitor, no COX-1 so no anti-platelet, unsure safety profile (associated with thrombogenity-CVA)-reduced PGI2 formation, but less GI bleeding (although now disbuted), use with RA, ankylosing spondylitis, acute pn, and dsysmenorrhea, and familial adenomatous polyposis (decreased activity of PPAR receptor alpha)

Etanercept

TNF receptor with IgG attached, Cytokine inhibitors-inhibit TNF-alpha (pro-inflammatory cytokine), Tx of RA and other autoimmune, increased risk of TB, fungal infection, hep B

Infliximab

humanized mouse monocolonal antibody against TNF alpha

Cytokine inhibitors-inhibit TNF-alpha (pro-inflammatory cytokine), Tx of RA and other autoimmune, increased risk of TB, fungal infection, hep B

Adalimumab

IgG antibody/Fab fragment against TNF-alpha

Cytokine inhibitors-inhibit TNF-alpha (pro-inflammatory cytokine), Tx of RA and other autoimmune, increased risk of TB, fungal infection, hep B

Golimumab

IgG antibody/Fab fragment against TNF-alpha

Cytokine inhibitors-inhibit TNF-alpha (pro-inflammatory cytokine), Tx of RA and other autoimmune, increased risk of TB, fungal infection, hep B

Certiolizumab

IgG antibody/Fab fragment against TNF-alpha

Cytokine inhibitors-inhibit TNF-alpha (pro-inflammatory cytokine), Tx of RA and other autoimmune, increased risk of TB, fungal infection, hep B

Anakinra

cytokine inhibitor, inhibits IL-1 (pro-inflammatory cytokine), Tx of RA when others have failed

Prednisone

Gluccoroticoids- inhibit COX-2 action (repress gene and enzyme expression, repress cytokines that activate COX-2 and limit substrate AA) and PG biosynthesis by inducing lipocortinsm activating endogenous anti-inflammatory pathways and other mechanisms, interfered with phosphopliase A2 (less AA available), induce annexins

Prednisolone

Gluccoroticoids- inhibit COX-2 action (repress gene and enzyme expression, repress cytokines that activate COX-2 and limit substrate AA) and PG biosynthesis by inducing lipocortinsm activating endogenous anti-inflammatory pathways and other mechanisms, interfered with phosphopliase A2 (less AA available), induce annexins

Gluccoroticoids- inhibit COX-2 action (repress gene and enzyme expression, repress cytokines that activate COX-2 and limit substrate AA) and PG biosynthesis by inducing lipocortinsm activating endogenous anti-inflammatory pathways and other mechanisms, interfered with phosphopliase A2 (less AA available), induce annexins

Gluccoroticoids- inhibit COX-2 action (repress gene and enzyme expression, repress cytokines that activate COX-2 and limit substrate AA) and PG biosynthesis by inducing lipocortinsm activating endogenous anti-inflammatory pathways and other mechanisms, interfered with phosphopliase A2 (less AA available), induce annexins

Dazobixen

inhibit thromboxane synthase

Thrmoboxane antagonisits- inhibit thromboxane synthase or antagonize thromboxane receptor, investigational agents, inhibit platelet activity, not clinically more effective than aspirin and more expensive

Pirmagrel

inhibit thromboxane synthase

Thrmoboxane antagonisits- inhibit thromboxane synthase or antagonize thromboxane receptor, investigational agents, inhibit platelet activity, not clinically more effective than aspirin and more expensive

Ridorgrel

TXA2 receptor antagonist

Thrmoboxane antagonisits- inhibit thromboxane synthase or antagonize thromboxane receptor, investigational agents, inhibit platelet activity, not clinically more effective than aspirin and more expensive

Zileuton

Lipoxygenase inhibitor, inhibits 5-lipoxygenase, which catalyzes the formation of leukotrienes from arachadonic acid, used in asthma, IBS and RA, limits ability of lipoxygenase to utilize nonheme iron (chelates), low bioavailability and potency but high liver toxicity

Monotelukast

Leukotriene Receptor Antagonist- selective antagonist of cystinyl leukotriene type-1 receptor (CysLT), used to treat bronchoconstriction (most effective for asthma against antigen), improve bronchial tone

Zafirlukast

Leukotriene Receptor Antagonist- selective antagonist of cystinyl leukotriene type-1 receptor (CysLT), used to treat bronchoconstriction (most effective for asthma against antigen), improve bronchial tone

Diphenhydramine

Ethanolamines, Diphenhydramine- motion sickness/nausea (chemo), insomnia (but cause next day sedation)

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Carbinoxamine

Pyrilamine

Ethylendimanies, insomnia (but cause next day sedation)

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Chlorpheniramine

Alkylamines, First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Chlorpheniramine

Promethazine

promethazines, motion sickness/nausea (chemo)

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Hydroxyzine

Piperazines-anti pruritic

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Cylclizine

Melclizine

Piperazine, motion sickness/nausea (chemo)

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Doxepin

Tricyclic dibenzoxepins, anti pruritic, used preferentially in depressed patients

First generation H1 antihistamines-inverse agonists that bind preferentially to the inactive conformation of the H1 receptor and shift the equilibrium to the inactive receptor site, general structure of two aromatic rings linked to a substituted ethylamine backbone, neutral at physiologic pH so can penetrate blood-brain barrier (drowsiness etc)

Cetirizine

Piperazines

Second generation H1 anti-histamines-inverse agonists that bind preferentially to the inactive conformation of H1 receptor and shift the equilibrium toward the inactive receptor site, ionized at physiologic pH so does NOT cross blood-brain barrier

Levocertizine

Acrivastine

Loratadine

Azelastine

Phthalazoinones, topical used for nasal congestion

Second generation H1 anti-histamines-inverse agonists that bind preferentially to the inactive conformation of H1 receptor and shift the equilibrium toward the inactive receptor site, ionized at physiologic pH so does NOT cross blood-brain barrier

Olopatadine

Tricyclic dibenzoxepins, topical used for nasal congestion

Second generation H1 anti-histamines-inverse agonists that bind preferentially to the inactive conformation of H1 receptor and shift the equilibrium toward the inactive receptor site, ionized at physiologic pH so does NOT cross blood-brain barrier

Cimetidine

H2 receptor antagonists-inhibit histiamine induced gastric acid secretion (GERD and peptic ulcer diseae), adverse effect of inhibition of cytochrome P450 drug metabolism

H2 receptor antagonists-inhibit histiamine induced gastric acid secretion (GERD and peptic ulcer diseae), adverse effect of inhibition of cytochrome P450 drug metabolism

H2 receptor antagonists-inhibit histiamine induced gastric acid secretion (GERD and peptic ulcer diseae), adverse effect of inhibition of cytochrome P450 drug metabolism

H2 receptor antagonists-inhibit histiamine induced gastric acid secretion (GERD and peptic ulcer diseae), adverse effect of inhibition of cytochrome P450 drug metabolism