Med Chem Final Spring 2011

MOA: Congener of meprobamate- central sedative properties and spinal cord block of intraneuronal activity

Occasional idosyncratic reaction including allergy

Cenrally-acting agent

MOA: enhances spinal cord brain stem GABA-mediated presynaptic inhibition resulting in muscle relaxtion

Centrally-acting agents

MOA: Acts centrally at the brain stem level on descending serotonergic pathways to reduced tonic motor activity, No peripheral effects on skeletal muscle fibers or neuromuscular junction.

Ineffective in spasm due to CNS disease

Similar structurally to TCAs

MOA: Unknown- structurally related to GABA but NOT GABA agonist

Recently used for management of postherpetic neuralgia (intense burning/tearing pain)

No hepatic induction or inhibition

Dosage is function of Crcl

MOA: unknown details but appears to modulate sodium channels

Warnings: Serious rashes including Stevens-Johnson syndrome, not recommended during lactation, photosensitization possible

Less effective as analgesic and less respiratory depression than morphine

Full agonist at the mu receptor

Opiate agonists- Phenathrenes: Semi-Synthetic agents

Discontinued November 19 2010 due to risk of caridac toxicity

DO NOT use in patients that are suicidal or addiction prone, patients using other tranquilizer or antidepressant medication, do not use with alcohol- one of the major cuases of drug related deaths.

MOA: binds to mu receptors and prevents reuptake of norepinephrine and serotonin in the CNS

Non-schedule agent with narcotic agonist (Opioid) activity

Modify dose interval if Crcl is <30

5-HT1 Receptor Agonist

Nasal spray is one spray per nostril (5mg) 20 mg dose has higher side effects, do not increase with MD consultation

Antidopaminergic agents - Non-Phenothiazine agent

If extrapyramidal symptoms occur administer 50 mg diaphenhydramine IM.

Off-label use: stimulates production of lactation

Seretonin 5-HT3 receptor antagonist

N/V: unlabled N/V due to APAP poisoning, tx of acute levodopa-induced vidual hallucinations, prostacyclin induced N/V, reduction in bulimic episodes in bulimia, social anziety disorders, spinal or epidural morphine-induced pruritus.

• Benzodiazepine
• Intermediate acting

Indications: anxiety, PMS, panic disorder with or without agoraphobia, depression

Many drug interactions

No well documented fatal overdosage due to oral use without multiple drug ingestions

• Patient Information:
• Take with food or water if stomach upset occurs
• Do not discontinue use abruptly if long term use has occured
• Do not take concurrently with antacids due to decreased rate of absorption
• Avoid alcohol or other CNS depressants
• May cause drowsiness-use caution

Benzodiazepine

Intermediate acting

Indications: anxiety, parenteral for preanesthetic use, status epilepticus, chemotherapy induced N/V, acute alcohol withdrawl, psychogenic cataonia, chronic insomnia

MOA: unknown has affinity for seretonin 5-HT1A (partial agonist) and D2-dopamine receptors, but has NO anticonvulsant activity nor muscle relaxant properties.

Indications: management of anxiety diorders, PMS

Often takes 3-4 weeks to see results

Oxidative liver metabolism with active metabolites

MOA: subcortical area CNS-depressant, a rapid acting true ataraxic (calmative)

Indications: anxiety and tension, prior to dental procedures, acute emotional problems, alcoholism, allergic conditions with emotional overlap, anxiety caused by heart disease, pruritus, parenteral antiemetic and adjunct analgesia

TCA's: Tertiary Amines

Depression: tablets and injections

Inhibit NE and 5-HT reuptake: 5-HT Selective

Many side effects: seizures, sedation, hypotension, weight gain, sexual effects

TCA: Secondary amine

Depressioin: not recommended for children

Moderate NE and high serotonin uptake blocking activity and moderate anticholinergic effects

Slight orthostatic hypotension

MOA: related to phenethylamines and mechanims is a reuptake inhibitor of NE and dopamine

• Indications:
• Depression and smoking Cessation

Photosensitivity possible, associated with seizures and frequency increases with dosage, less sexual dysfunction, weight gain or sedation

SNRI: Phenethylamine

MOA: potent inhibiots of serotonin and NE reuptake

Depression and GAD

Photosensitivity possible, notify MD if a rash or hives or other allergic reactions occur.

SSRI

Obsessive-complusive disorder, depression, bulimia nervosa and other unlabeled use

Half life 1-348 hours - takes 28 days to reach steady state

SSRI

Obessive compulsive disorder, depression, panic disorders, social anxiety disorders, and other unlabled uses

Elderly or devilitated patients with severe renal or hepatic impairment-start as 10 mg/day but do NOt exceed 40 mg/day

Use caution on withdrawl- may cause development of psychiatric problems such as severe behavioral symptoms

• SSRI
• Obsessive compulsive disorder, depression, panic disorder, post traumatic stress disorder, and unlabeled uses.

Half-life 26-104 hours - takes 7 days to reach steady state

Hepatic metabolism

• SSRI
• S-enantiomer = Lexapro
• Depression, panic disorders, social anxiety disorders, and other unlabeled uses

Half-life 35 hours, takes 7 days to reach steady state

Hepatic impairment- 20 mg/day. Use caution

Claim to have favorable SE profile: no assocaiated weight gain, lower potential CYP450 drug interactions, insomnia, anxiety, agitation, nervousness and fatigue

CI: concurrent use or within 14 days of discontinuation of MOAI; cisapride and fluvoxamine

MOA: inhibition of CNS neuronal reuptake of serotonin (5-HT)- highly selective agent

Enantiopure drug- Sentantiomer of Celexa- 100X more potent than the R-enantiomer

10 mg recommended in hepatic impairment

Metabolized by 3A4, 2C19, and modest inhibitory effect on 2D6

1st generation anti-psychotic

Indications: psychotic disorders, anxiety, acute headache in the ER, commonly used antiemetic

Moderate sedative effects, 7.5 times more potent than chlorpromazine

• 2nd generation anti-psychotic
• Thienobenzodiazepine

Indications: Schizophrenia, bipolar mania, dementia related Alzheimer's disease

Dosing in debilitated patients: 5 mg to start with max of 20 mg/day

Heavily sedating with less weight gain as a side effect

2nd generation anti-psychotic agents

MOA: partial agonist at D2 and 5-HT1A receptors and antagonistic activity at 5-HT2A receptors

Orthostatic hypotension due to antagonistic activity at alpha 1 adrenergic receptors

Primary metabolite is de-hydro-aripiprazole via 2D6 steady state reached in 14 days

99% plasma protein bound- primarily albumin

Can be taken with or without food

• 2nd generation anti-psychotic agent
• Benzthiazole

Indications: schizophrenia

Initial dose 20 mg bid taken with food

>80 mg not recommended due to dose dependent QT elongation

No inhibition effect on CYP enzymes

Dopaminergic Agents

MOA: direct agonist activity at the dopamine receptors in the striatum (D3 only)

Indications: treatment of the signs and symptoms of idiopathic Parkinson's disease with or without levedopa/carbidopa

Approved for restless leg syndrome

• Antiparkinsons agent
• Indications: must be given concurrently with levodopa for parkinsons, carbon monoxide poisoning and maganese toxicity

MOA: inhibits peripheral decarboxylase enzyme that is responsible for decarboxylation of levodopa to produce dopamine - inhibits the action of pyridoxine HCl (vitamin B6)

Does not cross BBB

High protein diets inhibit carbidopa absorption

Do not administer to nursing mothers or use in children <18 years old

Max daily dose of carbidopa should not exceed 200 mg per day

Watch for blepharospam (eyelid spams) as a sign of excess dosage

MOA: prodrug converted by central decarboxylase into dopamine in CNS following active transport across the BBB

Peripheral blood dopamine is responsible for drug side effects: N/V, anorexia, dystonic movements, dry mouth, numbness, darkening of urine and sweat

Use in extreme caution in: wide angle glaucoma, severe CV disease, or pts with suspected skin lesions or a hsitory of melanoma, do not use in lactating mothers or chidren <12 years, can interfere wtih urine tests for sugar or ketones

CI: pts taking MAOI

Watch for on-off phenomenon- try drug holiday, keep dosage as low as possible

MOA: Centrally acting reversible cholinesterase inhibitor

Indications: mild to moderate Alzheimer's disease

Dosage is adjusted based on serum transaminase leves

MOA: Orally active N-methyl-D-aspartate (NMDA) uncompetitive open-channel antagonist--blocks the action of the neurotransmiter glutamate by binding to the NMDA receptor-operated cation channels.

Indication: moderate to severe Alzheimer's disease- first drug for severe stage of disease

Persistant activation of CNS NMDA receptors by glutamate

Helps relieve symptoms only -- not curative-- low incidence of side effects

Side effects observed-- dizziness, headache, constipation

Anything acidifies urine will increase excretion.

MOA: non-benzo modulation of the GABA-BZ receptor chloride channel macromoleculare complex

No myorelaxant or anticonbulsant properties

Indications: Short-term treatment of insomnia

Benzodiazepine

MOA: potentiates GABA neuronal inhibition by interacting with the GABA chloride ion channel receptor complex.

Indication: Insomnia

• Barbiturate
• MOA: Enhances GABA mediated chloride influx (GABA inhibition)

Indications: Grand mal seizures in pediatric patients, status epilecticus

Can cause CNS depression, drowsiness, and associated in decreased IQ in chronically treated children.

Stimulates P450 enzymes

Non-barbiturate/Benzodiaxepine Hypnotic

MOA: unknown, believed to result from GABA-receptor complexes at binding domains located close to or allosterically coupled to benzodiazepine receptors.

Insomnia--difficulty falling asleep and staying asleep

Looks safe for long term use - no loss of efficiancy

MOA: general CNS depression - no direct effect on muscle

Indications: adjunct to rest, physical therapy and other measures for the relief of discomfort associated with acute, painful, musculoskeletal conditions.

Use in caution with hepatic dsyfunction- conduct liver function tests

Possible teratogen, inform patients to watch for signs of liver dysfunction

MOA: inhibits muscarinic action of acetylcholine via direct anti-spasmotic effect on smooth muscle relaxing the bladder smooth muscle -primarily the R stereoisomer

Indications: overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency

Contraindicated in urinary retention, gastric retention or uncontrolled narrow-angle glaucoma

MOA: potently inhibits muscarinic action of acetylcholine via a direct antispasmotic effect on smooth muscle relaxing the bladder smooth muscle - very selective for the M3 muscurinic receptor over others

Indictions: overaction bladder with symptoms of urge urinary incontinence urgency and frequency

Contraindicated in urinary retntion, gastric retention or uncontrolled narrow angle glaucoma; No effect on QT elongation

Most common side effects: dry mouth, constipation, blurred vison, heat prostration

MOA: inhibits muscarinic action of acetylcholine via a direct anti-spasmotic effect on smooth muscle relaxing the bladder smooth

Indications: overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency

Contraindicated in urinary retention, gastric retention or uncontrolled narrow angle glaucoma; appears to prolong QT interval as dosage is increased

MOA: competitive inhibitor of muscarinic action of acetylcholine on the bladder smooth muscle

Indications: overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency

Higly bound to alpha acid glycoprotein

Dose dependent effect on QT elongation

Contraindicated in urinary retention, fastric retention or uncontrolled narrow-angle glacoma

MOA: produces a sustained depolarization by slowing the rate of voltage-activated Na channels-prevents hyperexitability

Indications: tonic-clonic (grand mal), psychomotor, status epilepticus, cardiac arrhythmias

Ineffective in absence seizures

Use a single manufacturers product bioavailability issues

Serum therapeutic level 5-20 micrograms/ml

Chronic use toxicity includes gingival hyperplasia, hirsutism, and overdoseage is manifest by atazia, nystagmus, vertigo, blurred vision, confusion, lethargy, hallucination

Many drug interactions inhibitio and induction

Never IM

• Benzodiazepines
• Indications: petit mal, akinetic or myoclonic seizures alone or as an adjuct

Therapeutic conc: 20-80 ng/ml

Be aware of additive sedative effects

MOA: reduces polysynaptic responses and blocks post-tetanic potentials

Indications: partial seizures, grand mal and mixed seizures, trigeminal neuralgia pain relief, psychiatric disorders, alcohol, cocaine, and benzo withdrawl

Warning: aplastic anemia and agranulocytosis, blod dyscrasias and hypersensitivity reactions, stevenspjohnsons syndrome

MOA: reduction of the ketone to the hydroxy group is the pcol active compound which produces blockage of the voltage sensitive sodium channel

Indications: monotherapy of adjunct use in adults and children 4-16 years of age suffering from partial seizures, atypical panic disorders

Monitor for blood dyscrasias and hypersensitivity reactions, use ethanol cautiously due to additive sedation

MOA: unknown mechanism except it binds to the alpha2-delta site (an auxiliary subunit of voltage-gate ca2 channels) in the CNS and appears to decrease the release of several neurotransmitters

Structural analog of GABA but does NOT bind these receptors nor the benzo receptors

Indications: neuropathic pain associated with postherpetic neuralgia, diabetic peripheral neuropathy, partial onset seizures in adults and the first drug approved for fibromyalgia

MOA: unknown details but appears to modulate sodium channels

Indications: epilepsy as a sole therapy in adults and as adjucnt therapy in pediatric use (2 years and older)

Warning: serious rashes including Stevens-Johnson syndrome

Often confused with other medications due to similarity of names

MOA: appears to increase levels of GABA

Indications: Petit mal and mixed seizures with absence, grand mal, and myoclonic seizures; bipolar manic-deressive illness, migraine prophylaxis

Warning: hepatotoxicity, teratogenic, pancreatitis

Will interfer with urine ketone tests, >5 years decreased bone density in young children

MOA: a sulfamate monosaccharide that exerts sodium channel blocking action, increases activity GABA at its receptor and antagonizes the effect of glutamate

Indications: adjunct therapy for patrial onset seizures in adults/kids and Lennox-Gastaut (LGS) syndrome in children

Dosage should be titrated as a fucntion of Crcl

Maintain fluid intake due to stone formation

MOA: unknown

Indications: adjunct in partial onset seizures in adults

Dosage must be individualized based on renal function

Possible teratogen

MOA: high affinity and partial agonist for the alpha4 beta 2 nicotinic acetylcholine receptor subtypes--simultaneously prevents nicotine binding. Although the drug binds and stimulates receptor mediated activity it is at a significantly lower level than nicotine. By competing with nicotine it blocks the stimulation of the central nervous mesolimbic dopamine system- blocks the reward reinforcement system

Indications: aid to smoking cessation treatment-appears to be the most effective drug available to treat tobacco dependence

Side effects: N/V, flatulence, insomnia, headache, abnormal dreams

Black box warning: exacerbations of pre-existing psychiatric illness-- agitation, hostility, depressed mood, suicidal ideation and behavior possible

MOA: inhibition of dihydrofolate reductase and thymidylate synthase--cell cycle specific agent? that inhibits DNA production

Do not take with food, avoid alcohol, salicylates and sun exposure, USE contraception, inform MD of any signs of neutropenia, bleeding, shortness of breath, yellow skin

Produces bone marrow depression, hepatotoxicity and death, diarrhea, lung disease not reversible, very nasty drug, inform patient of risks involved

• SNRI
• MOA: antidepressant and pain inhibitory actions related to its potentiation of serotonergic and noradrenergic actibity in the CNS.
• -potent inhibitor of neuronal serotonin and NE reuptake and less potent inhibitor of dopamine reuptake

Indications: 1. MDD- a major mood disorder characterized by one or more episodes of major depression with or without full recovery between episodes. 2. Fibromyalgia

Unlabeled uses: stress, and urinary incontinence, diabetic peripheral neuropathy

Duloxetine has no significantly affinity for dopaminergic, adrenergic, cholinergic, histaminergic, opiod, glutamate, and y-aminobutyric (GABA) receptors in vitro. Duloxetine does not inhibit monoamine oxidase

• Serotonin 5HT1b/5HT1D receptor agonist
• Highly specific for certain 5-HT receptor subtypes with no affinity for adrenergic alpha or beta receptors, dopaminergic receptors, muscurinic or opiod receptors

Not indicated for prophylaxis

Contraindicated in patients with ischemic heart disease

• Serotonin 5HT1 Receptor Agonist
• Not intended for prophylactic therapy

Dosing must be no more often than every two hours

• NSAID
• Sulfonamide

• NSAID
• Aryl-and Heteroaryl propionic acid derivatives

• NSAID
• Aryl-and heteroarylpropioinic acid derivatives

• NSAIDS
• At therapeutic concentrations inhibition of COX-1 does not occur:
• Advantageous when one does not want to inhibit COX-1: GI problems are apparently less due to continued COX-1 prostaglandin protection of the GI mucosa

Use linked to increased risk of MI event rate

• Central analgesic agents
• Agents that produce analgesia not mediated by opiate receptors but via other neruonal mechanisms

MOA: produces analgesia at both presynaptic and postjunctional alpha 2 adrenoceptors in the spinal cord that are responsible for pain transmission to the brain

Orally used as an anti-hypertensice agent, most off label uses of any drug

For analgesic activity it is given via the epidural route. Use in combination with opiates when opiates alone are ineffective

Not recommend for ostetrical, post-partum or peri-operative pain management

To treat heroin and other opiate addiction: First dosage form approved that can be prescribed in a doctor's office rather than at a treatment clinic

Opiod agonist- synthetic phenylpiperidines

Sublimaze injection: analgesic action of short duration during anesthesia and in post-operative pain relief

Transmucosal Lozenges: Oralet- pre-operative anesthesia, Actiq sugar free lozenge on a stick- breakthrough cancer pain only

Transdermal patches: Duragesic 25-100 mcg/hr delivery serious and life threatening hypoventilation possible

Transmucosal tablet: Fentora-breakthrough cancer pain only

Buccal Soluble film: Onsolis- breatkthrough cancer pain only

• Opiate Agonists - phenanthrenes: semi synthetic agents
• Full agonist at the mu receptor

Eqipontent as an analgesic (relief of moderate/sever pain) and less constipating effect, equipotent respiratory depression

Refrigerate suppositories

• Opiate agonist - phenanthrenes: Semi synthetic agents
• Full agonist at the mu receptor

Equipotent as morphine as an analgesic and cause of respiratory depression and constipation

• NSAID
• aryl and heteroarylacetic acid derivatives
• Patch and gel

• Salicylate
• MOA: all analogs are hydrolyzed to salicylic acid

Salicylic acid lowers body temp via vasodilation

1. ASA is a potent inhibitor of prostaglandin synthase by acetylating primarly COX-1. Cyclooxygenase is the first enzyme in the prostaglandin synthesis pathway

2. ASA and only aspirin: irreversible inhibitor of platelet aggregation (7-10 days) by preventing COX mediated synthesis of thromboxane A2 a mediator of platelet aggregation and a potent vasoconstrictor

3. ASA in large doses inhibits COX in arterial walls preventing synthesis of prostacyclin (PGI2) - a potent inhibitor of platelet aggregation this is why low doses are best in anti platelet applications


Lethal dose is 10-30 grams in an adult and 4 grams in children

Chewable tablets, gum tablets, enteric coated tablets, extended release tablets, delayed release tablets, suppositories included buffered produces

• 100 and 200tablets
• MOA: unknown, although it has wakeful-promoting effectst similar to sympathomimetic agents, however, its pharmacological profile does not resemble thes agents

Indications: narcolepsy- recurring episodes of sleep during the day and disrupted nocturnal sleep- genetic predisposition

Moderate CYP induction and 2c19 inhibitor

• A prodrug! That provides for once a day dosing with less abuse potential
• 30, 50, 70 mg capsule
• Can't shoot this drug IV b/c serum protease doesn't clip the amphetamine part

• Amphetamines - A CNS stimulant
• MOA: prevent reuptake of neurotransmitters NE and dopamine into the pre-synaptic neuron and increase the realse of these monamines into the extra-neuronal space- indirect agonist

CNS effects: increased arousal and wakefulness mood alteration- increased confidence, ability to concentrate, exhilaration, euphoria; increased motar activity, anorexia, insomnia

CV efffects: similar to sympathomimetic amines, CI in any CV abnormality

Indications: ADHD

Problems: addiction and tolerance, toxic psychosis with underlying undiagnosed psychosis, hypertension, angina, hyperthyroidism can be aggravated

MOA: mild CNS stimulant similar to amphetamines but with an unknown mechanism

Indications: ADHD, narcolepsy; unlabeled uses- treatment of depression in elderly, cancer and post stroke patients, post-anesthesia related hiccups

Patient info: take last dose prior to 6 pm to avoid insomnia, do not crush or chew SR products

MOA: selective inhibitor of pre-synaptic NE transporter

Indications: Attention Deficit/Hyperactivity Disorder in children and adults

1st new drug and non stimulant to treat this disorder in 3 decades

Not a schedule II or controlled substance

CYP2D6 followed by glucuronidation-slower metabolism

Patient info: can be taken with or without food, dosage adjustment necessary in moderate/severe hepatic insufficiency; dry mouth, insomnia, nausea, dizziness

• Opiate agonist- phenanthrenes: Natural products
• Full mu receptor agonist

Regular and controlled release tablets and capsules, solutions, injection and rectal suppositories

Indications: analgesic activity, and as an anesthetic agent preoperative

• Combined with atropine to prevent shooting
• Indicated in diarrhea

MOA: slows GI motility, no analgesic activity

Preferred in children 2-12 years old with the dose determined based on weight

Opiod Agonist: Synthetic diphenlheptanes

Indications: relief of severe pain (any pharmacy) detoxification and maintenance of narcotic addiction- ie Heroin (only approved pharmacies as oral dose form only) milder withdrawl effects and longer actin

Not useful preoperatively to reduce anxiety or for induction

• NSAID
• Aryl and heteroarylacetic acid derivatives
• Prodrug

• NSAID
• aryl and heteroarylacetic acid derivatives

MOA: inhibits COX that is responsible for prostaglandidn synthesis

Indications: to promote closure of significant patent ductus arteriosus in infants in which 48 hours of usual medical supportive treatment fails

• Dibensothiazepine: 2nd generation antipshychotic
• Indications: psychotic disorders
• Multiple neurotransmitter receptor antagonist: 5-HT, Dopamine, Histamine, H1 and alpha 1 and 2

No anticholinergic side effects!! no binding to muscarinic receptors

Moderately sedating, less weight gain is a side effect, increased heart issues when compared wih other atypicals

Anticholinergic Agents - usually less effective than levodopa

Indications: idiopathic, postencephalitic, arterosclerotic and drug/chemical induced (neuroletpics) parkonsonims

CI: children <3 years old

MOA: binds to specific retinoic acid nuclear receptors but not cytosolic receptor proteins - modulates cellular differentiation, keratinization and inflammatory processes

Potential for teratogenicity - topical application studies unknown

Combo with benzoyl peroxide- Epiduo

Agents used to treat glaucoma- Prostagladin analog

MOA: opthalmic solutions that reduce intra-ocular pressure by increasing trabecular meshwork and uveoscleral outflow of aqueous humor

Indications: reduction of intraocular pressure in open-end glaucoma if other medications have failed

These drugs can cause permanent change in eye color

Do not administer while wearing contact lens

Eventual systemic systemic distribution and hepatic metabolism

Agents used to treat glaucoma- Prostagladin analog

• MOA: opthalmic solutions that reduce intra-ocular pressure by increasing
• trabecular meshwork and uveoscleral outflow of aqueous humor

Indications: reduction of intraocular pressure in open-end glaucoma if other medications have failed

These drugs can cause permanent change in eye color

Do not administer while wearing contact lens

Eventual systemic systemic distribution and hepatic metabolism

Agents used to treat glaucoma- Prostagladin analog

• MOA: opthalmic solutions that reduce intra-ocular pressure by increasing
• trabecular meshwork and uveoscleral outflow of aqueous humor

Indications: reduction of intraocular pressure in open-end glaucoma if other medications have failed

These drugs can cause permanent change in eye color

Do not administer while wearing contact lens

Eventual systemic systemic distribution and hepatic metabolism

MOA: relatively selective dual H1-receptor antagonist and a inhibitor of histamine and other mediator release from mast cells by acting as a mast cell stabilzer- dual mechanism

Indications: prevention of itching associated with allergic conjuctivitis

No alpha adrenergic, dopaminergic or muscurinic type 1/2 receptor effects

Important patient info: remove contact lenses prior to use and leave them out for 10 minutes following use-- soft lenses can absorb the benzalkonium chloride preservative

MOA: unknown but beleved related to immunomodulating and anti-inflammatory properties

Normally used as an immunosuppressants in organ transplantation

Centrally acting agent

MOA: hyperpolarization of afferent nerve terminals and by binding to GABA receptors

Indications: oral-spasticity due to MS, spinal cord injuries and diseases, intrathecal- management of sever spasticity of spinal cord origin when unresponsive to oral dosing-- can be used with constant infusion pump (do single dose testing first) this rout allows 100X decrease in dosing

Elimination as the parent drug by urinary excretion, abrupt discontinuation may cause hallucinations, may cause painful urination

• SNRI
• Main metabolite of venlafaxine

Metabolized by 3A4

Discontinuation can be more severe thatn SSRI's increased diastolic BP and more dangerous in overdosage situations

• Thiazide and thiazide-like related diuretics
• Diuretics that act at the Distal convoluted tubule

• Diuretics that act on collecting tubule
• Potassium sparing agents- diuresis with no concomitant K loss

MOA: competitive inhibitor of aldosterone (induces the synthesis of transport proteins including the Na/K/ATP ase carrier system protein and luminal channel protein sythesis) preventing Na reabsorption and K echange for Na -- sparing K. Overal preventing na reabsorption of 2-3% of the filtered NA

SE: hyperkalemia and acidosis in cases of poor renal function, gynecomastia, breast tenderness, menstrual disturbances, GI disturbances, skin rashes

Drug interactions: anticoagulants (antagonize), ACE inhibitors, potassium preparations (hyperkalemia), salicylates (antagonixes the diuretic effect)

• Diuretic that acts on collecting tubule
• Potassium sparing agents- diuresis with no concomitant K loss

MOA: plugs the sodium channels preventing electrogenic reabsorption of 2-3% of the filtered NA

Indications: secodnary hyperaldosteronism, edema from CHF and cirrhosis of the liver, ascites, nephrotic syndrome, hypokalemia

SE: hyperkalemia, formation of renal stones, N/V, leg cramps, dizziness

Do NOT use alone for hypertension treatment or in patients with renal impairment

• Drug interactions: amantadine (increases plasma levels and apperance of toxicity), ACE inhibitors, potassium preperations (hyperkalemia), cimetidine (increase triamterene bioavailability, decreases hydroxylation and renal clearance)
• Indomethacin- concurrent use has lead to acute renal failure

Isolated from plants like foxgloves flowers and some other common household and yard plants

MOA: inhibition of the Na/K/ATP-ase pump located on the sarcolemma membrane of cardiac muscle. Makes more Ca available to the actin and mysoin resulting in an increase in the force of contraction

Works best for low output failure: diuresis, alleviates symptoms of right sided failure (venous congestion, edema) and left side failure (dyspna, orthopnea, cardiac asthma)

Narrow therapeutic range

Pay attention to the dosage dispensed. Do not change dosage forms without monitoring plasma levels.

Desired serum range: 0.5-2.2 ng per ml

Class III anti-arrhythmic agent

MOA: block of cardiac potassium channels to prolong the repolarization phase

Clearly demonstrated to decarease arrhythmia mortality in post-MI and heart failure patients

t 1/2 = 45 days, possible accumulation

Adverse effects: photosensitivity, blue-gray skin discoloration, hypo/hyperthyroidism, nightmares, corneal deposits, hepatotoxicity, pulmonary fibrosis;

Monitor: liver, pulmonary and thyroid function, ophthalmic exams, chest roentgenograms

DI: can cause increased levels of digoxin, flecainide, cyclosporine, phenytoin, quinidien, procainamide

Class III & II Anti-arrhythmic agents: Ethanolamine class

MOA: beta blocker and K channel blocker

Indications: suppression of ventricular arrhythmias

AE: bradycardia, hypotension, exaverbation of heart failure, tordades de pointes

Racemic mixture at hydroxy sterocenter-- the pure d enantiomer has been shown to increase mortality by 65%

• Phenylalkylamines
• Inhibition of CA influx is the basis of anti-arrhythmic activity

Does not bind in resting state but only after the channels is opened. Water soluble that diffuses into the open channel

• Benzothiazepine
• Inhibition of CA influx is the basis of anti-arrhythmic activity

Does not bind in resting state but only after the channels is opened. Water soluble that diffuses into the open channel

Incompatible for mixing with furosemide solutions

Use in extreme caution in patients with CHF

DI: histamine H2 antagonists (cimetidine), may increase bioavailability by 50%, Serum digoxin levels may be increased

Notify MD if the following occur: irregular heart beat, shortness of breath, edema of hands or feet, pronounce dizziness, constipation, nausea, hypotension

• Ca channel blocker
• 1-4 dihydropyridines
• Effective in open or closed state by diffusion through the lipid bilayer to reach its binding site

Avoid abrupt withdrawl of all calcium blocking drugs must be gradual and under medical supervision

Use caution in patients with hepatic dysfucntion since all these agents are extensively metabolxied by the liver

Pass through mothers milk

Food interactions: grapefruit juice

Do not chew sustained release formulations

Nitrate vasodilator products

Problems with use: tolerance, withdrawl must be gradual, avoid alcohol duet to severe hypotension, do not change brands, dont use with camp phoshodiaesterases

Direct peripheral vasodilator

MOA: alters intracellular CA movements in vascular smooth muscle

Problem: rebound renin/ATII response- fluid retention

Aggravation of angina-lupus like reaction is pssible >200 mg/day

• Nitrate vasodilator product
• Topical ointment, IV, Sublingual, translingual, transmucosal, transdermal

• Non- selectibe Beta blocker
• Propanolamine class
• 1st drug marketed

Indications: cardiac arrhythmias, MI, hypertrophic subaortic stenosis, pheochromocytoma, hypertension, migraine prophylaxis, angina, essential tremor, stage freight, PSTD

Selective beta 1 receptor beta blocker

Indications: hypertension, MI, angina

Dosage needs reduction in renal failure as a function of crcl

Diuretics that act at the thick ascending loop of henle

MOA: inhibits the Na/K/Cl carrier system primarily in the Loop of Henle, some trace of activity in the proximal and distal tubules

SE: hypokalemia, excessive fluid and electrolyte loss (reduced GFR and loss of efficacy), increase in resorption of agents normally excreted by the proximal tubule (can increase lithium toxicity, hyperurcemia), possible hypersensitivity due to sulfa, ototoxicity (additive with aminoglycosides), hyperglycemia, nausea, vomiting , myalgia

• Selective beta 1 blocker
• Indications: hypertension, MI, angina pectoris, CHF

Toprol XL given presurgical to prevent heart complications appears to increase the danger of stroke or death

New selective beta 1 blocker and the durg modulates nitric oxide system

MOA: new two fold mechanism. Produces vasodilation decreasing total peripheral resistance by modulation of nitric oxide release

Indications: approved for hypertension

Metabolism 2D6

Non-selective alpha and beta blocker

Indications: hypertension, clonidine withdrawl induced hypertension, phechromocytoma

IV use not compatable with basic solution (5% bicarbonate, furosemide, or other alkaline products)

Nonselective alpha and beta blocking agent

Indications: essential hypertension, angina, idiopathic cardiomyopathy & CHF including severe heath failure.

Not recommended in hepatic impairment, watch glycemic control

Several polymorphism identified but most important is the Arg-Gly at amino acid position 389 which has been associated with CVD

Selective alpha 1 adrenergic antagonist- peripheral acting

Marked first dose effect postural hypotension- take first dose at bedtime

Indications: hypertension, benign prostatic hypertrophy, treatment of CHF in conjunction with beta blockers and dig

1-4 dihydropyridines Ca channel blocker

Indications: chronic stable angina, vasospastic angina, hypertension (SR only)

Indications: Benign prostatic hypertrophy

38-fold greater affinity for alpha1a receptors which have a high density in prostatic smooth muscle--prevents contraction by antagonizing the receptors

Take with food to prevent orthostatis, 99% protein bound to alpha1 acid glycoprotein,

ACEI: di varbocyl containing agents

Indications: hypertension, heart failure and asymptomatic LVD

Ethyl ester prodrug, no food effect on absorption

ACEI

Indications: hypertension, heart failure, acute MI

100% urinary excretion (why so popular), impared renal function prolongs effect, reduce dosage as a function of glomerular filtration rate, no food effect on absorption

ACEI - dicarbocyl containing agents

Indications: hypertension

Ethyl ester prodrug, slight reduced food effect on absorption, dosage adjustment as fucntion of crcl

• ACEI
• Indications: hypertension, heart failure

Ethyl ester prodrug, reduce dosage as a function crcl

• ACEI
• Indications: hypertension, heart failure, post MI

Ethyl ester prodrug, slight reduced food effect on absorption, reduce dosage as a function of crcl

• ARB
• Contraindicated in pregnancy due to fetal damage and death

Less cough side effect than with ACEI drugs- no bradykinin buildup

Indications: hypertension, sustantial first pass effect by 2C9, 3A4, active metabolites, anti-platelet effect

Appears to cause zn depletion and complexes with cu

• ARB
• Contraindicated in pregnancy due to fetal damage and death

Less cough side effect than with ACEI drugs- no bradykinin buildup

Indications: hypertension

Double ester prodrug, no dosage adjustment needed in mild hepatic impairment, renal impairment can increase plasma conc

• ARB
• Indications: hypertension
• Very minor hepatic metabolism, major food effect on absorption, severe renal disease and hepatic impairment use caution in dosing, can casue a 20% increase in serum K

• ARB
• Indications: hypertension
• Use extreme caution in hepatic impairment- dose can not be reduced below 40 mg and be useful

• ARB
• Indications: hypertension
• 20 mg/day starting dose

Following ester hydrolysis during intestinal absorption no further metabolic events occur

Anti-hypertensive effect onset occurs within one week and largely manifested after 2 weeks

Direct non-peptide renin inhibitor

MOA: inhibits renin, the first and rate limiting step in the production of angiotensin I and II aldosterone

Indications: mild to moderate hypertension alone or in combo with other agents

No increase in bradykinin levels

Do not use during pregnancy tetratogenic

t 1/2 life approx 45 hours

HMG- CoA reductase inhibitor

A prodrug activated by liver hydrolysis of the lactone ring

Indications: familila and non-familial hypercholesterolemia including type IIa and IIb disease, artherosclerosis--CHD

Extensive 1st pass effect by 3A4, renal disease can lead to increased plasma levels, take with meals

• Compactin class: HMG-CoA reductase inhibitor
• Prodrug activated by liver hydrolysis of the lactone ring

Indications: familial, and non-familial hypercholesterolemia including type IIa and IIb disease, artherosclerosis--CHD

Extensive 3A4 can be taken without regard to meals

HMG- CoA reductase inhibitor compactin class

Indications: familial and non-familial hypercholesterolemia including type IIa and IIb hyperproteinemias, artherosclerosis, previous MI, or other coronary events

Extensive first pass effect via sulfunation, hepatic disease can lead to huge increases in plasma concentrations, food will result in decreased absorption

HMG- CoA reductase inhibitor non-compactin

Indications: familial and non familial hypercholesterolemia including type IIa and type IIb hyperproteinemias, Type III dysbetalipoproteinemia, Type IV elevated serum triglycerides

Extensive 1st pass 3A4 (active metabolites), renal disease does not increase plasma levels, hepatic diease can lead to huge increases in plasma conc, can be taken without regard to meals

Atorvastatin phototoxi

HMG-CoA reducase inhibitor non compactin class

Indications: familial and non familial hypercholesterolemia including type IIa and IIb disease

Very minor 1st pass by 2C9 resulting in N-demethylation, no effect on 3A4

50% decrease in absorption if taken concurrently with antacides--2 hour rule applies, sulfonamide

• Anti-hyperlipidemic agents
• Fibric acid derivative

MOA: inhibits peripheral lipolysis, decreases hepatic extraction of free fatty acids, decreases VLDL synthesis and its carrier molecule synthesis

Indications: Type IV and V hyperlipidemia in patients at risk fro pancreatitis with tirglycerides of 1000-2000 mg/dl, patients at risk of CHD in which all other approaches have failed

Selective beta 1 blocker

Indications: hypertension

Dosage adjustment may be necessary in renal or hepatic failure

Selective alpha 1 adrenergic antagonist - peripheral acting

Indications: hypertension, benign prostatic hypertrophy

Minimal 1st pass effect

Marked 1st does effect-postural hypotension- take 1st dose at bedtiem

Fibric acid dervative

MOA: unknown but appears to inhibit triclyceride and VDLD synthesis

• ndications: Type IV and V hyperlipidemia in patients at risk fro
• pancreatitis with tirglycerides of 1000-2000 mg/dl, patients at risk of
• CHD in which all other approaches have failed

• Bile acid sequestrant
• MOA: form insoluable compelx with fatty acids and bile acid sterols which are excreted from the gall bladder. Complex passes out with the stool

Anion-exchange resins - do not use at the same time as anionic drugs, can reduce folate absorption

Often as combinatin therapy with HMG-CoA reductase inhibitors or with nicacin, take before meals, do not take in dry form, do not chew tablet dose forms

Indications: elevated LDL Type IIa hyperlipidemia in combination therapy with other agents, adjunct in treatment of type II diabetes

• Anti-hyperlipidemia agent
• Lipase inhibitor

MOA: selective inhibits intestinal absorption of cholesterol and other phytosterols at teh brush border area of the intestinal membrane

Indications: hyperlipidemia can be used in combination with the statin agents or fenofibrate

Inhibits the lipase enzymes by acylation of the enzyme active site nucleophile

MOA: platelet aggregation inhibitor bia phosphodiesterase inhibition leading to increased cAMP, prevents adenosine reuptake into red blood cells, inhibition of thromboxane A2 synthesis (activator of platelet aggregation)

Indications: adjunctive to coumarin anticoagulants in the preventionof post-operative thromboembolic complication of cardiac valve replacement, prevention of MI and stroke-in combo with ASA

• MOA:
• 1. inhibits ADP binding to platelet receptor
• 2. inhibits induction of the adhesion receptor glycoproteing IIb/IIIa adhesion of platelets
• 3. Effective for the entire life of the platelet
• 4. Does not inhibit cAMP phosphodiesterase

• Indications:
• 1. reduction of artherosclerotic events associated with MI, stroke or other peripheral artery disease, stent deployment-- DES stents more likely to experience late-stent thrombosis than BMS post discontinuation
• 2. Acute coronary syndrome

Inform dentist ---bleeding time is much longer

Metabolized intestinal esterase and hepatic metabolism

Need 2C19 so interact with PPIs that inhibit 2C19

Low molecular weight Glycosaminoglycans: LMW heparin

Less plasma protein binding, increased bioavailability and duration, less thrombin activity with potent factor Xa inhibition

Indications: post-surgical prophylaxis for DVT with or without PE, abdominal surgery, unstable angina, non-Q wave MI, other unlabeled uses related to surgery and trama

• Advantages:
• 1. self administered in outpatient setting
• 2. improved control of bioavailability
• 2. more selective for factorXa
• 4. less potential of thrombocytopenia

Vitamin K reductase inhibitor

Indications: prophylaxis and treatment of venous thrombosis, pulmonary embolism, and atrial fibrillation

Dosage must be individualized

Watch for signs of bleeding - Petechiae

Displacement is major cause of drug interactions

Do not switch brands

• 2C9 metabolizes S enantiomer-5x more potent
• 3A4 metabolizes R enantiomer

• 3 types of drug-drug interactions:
• 1. pharmacokinetic
• 2. pharmacodynamic
• 3. new drug interaction mechanicsm identified

Watch drinking with cranberry juice, and taking with ginseng

MOA: selective inhibitors of cyclic guanosine monophosphate (cGMP) specific phosphodiesterase 5 enhances effects of NO by preventing the degradation of cGMP--leads to smooth muscle relaxation and inflow of blood to the corpus cavernosum

SE: high plasma levels will cause abnormal color vision (blue/green); sudden hearing loss which may include tinnitus, vertigo an ddizziness

3A4 and 2C9

CI: any patient taking organic nitrate -- dangerous hypotension, known QT elongation

Use caution: in patients with pre-existing CV disease, anti-hypertensices, 4 hour or longer erection seek immediate medical attention

• MOA: selective inhibitors of cyclic guanosine monophosphate (cGMP) specific phosphodiesterase 5 enhances effects of NO by preventing the degradation of cGMP--leads to smooth muscle relaxation and inflow of
• blood to the corpus cavernosum

• SE: high plasma levels will cause
• abnormal color vision (blue/green); sudden hearing loss which may include tinnitus, vertigo an ddizziness
• 3A4 and 2C9

CI: any patient taking organic nitrate -- dangerous hypotension, known QT elongation

• Use caution: in patients with pre-existing CV disease, anti-hypertensices, 4
• hour or longer erection seek immediate medical attention

MOA: Selective inhibitor (>10,000X) of cyclic guanosine monophosphate (cGMP) specific phosphodiesterase 5 (PDE5)

Metabolized by 3A4 to catechol metabolite

SE: high plasma levels will cause abnormal color vision (blue/green), sudden hearing loss which may include tinnitus, vertigo and dizziness

CI: any pt taking an organic nitrate--48 hours before admin possible, dangerous hypotension, known QT elongation

Use caution: 4 hour or longer erection seek immediate medical attention

• 2nd generation Sulfonylureas
• No active metabolites
• MOA:
• 1. Stimulate insulin release from pancreatic beta islet cells by binding to and blocking an ATP-ase sensitive K channel
• 2. This causes depolarization and an increase in intracellular Ca which leads to the release of the hormone
• 3. May also decrease the hepatic clearance of insulin

• Adverse effects:
• 1. Hypoglycemia-most common in the elderly taking agents that have long half-lives--this may appear as an acute neurologic emergency stroke--check blood glucose
• 2. DI caused by inhibition/induction of CYP systems
• 3. 10-15% patients will experience a disulfram-like reaction with ehtanol especially with chlorpropamide

Dosage must be individualized

CI: patients with IDDM, pregnancy, lactation or hepatic and renal failure

• 2nd Generation Sulfonylureas
• Weakly active metabolites
• MOA:
• 1. Stimulate insulin release from pancreatic beta islet cells by binding to and blocking an ATP-ase sensitive K channel
• 2. This causes depolarization and an increase in intracellular Ca which leads to the release of the hormone
• 3. May also decrease the hepatic clearance of insulin

• Adverse effects:
• 1. Hypoglycemia-most common in the elderly taking agents that have long
• half-lives--this may appear as an acute neurologic emergency
• stroke--check blood glucose
• 2. DI caused by inhibition/induction of CYP systems
• 3. 10-15% patients will experience a disulfram-like reaction with ehtanol especially with chlorpropamide

Dosage must be individualized

CI: patients with IDDM, pregnancy, lactation or hepatic and renal failure

• 3rd Generation Sulfonylureas
• Active metabolites
• MOA:
• 1. Stimulate insulin release from pancreatic beta islet cells by binding to and blocking an ATP-ase sensitive K channel
• 2. This causes depolarization and an increase in intracellular Ca which leads to the release of the hormone
• 3. May also decrease the hepatic clearance of insulin

• Additional mechanisms of action:
• 1. Appears to cause translocation of GLUT-4 glucose transporter to the cell surface from the cytoplasm- insulin like activity
• 2. May bind to a different protein than the usual sulfonylurea receptor on the beta islet cell

• Adverse effects:
• 1. Hypoglycemia-most common in the elderly taking agents that have long
• half-lives--this may appear as an acute neurologic emergency
• stroke--check blood glucose
• 2. DI caused by inhibition/induction of CYP systems
• 3. 10-15% patients will experience a disulfram-like reaction with ehtanol especially with chlorpropamide

Dosage must be individualized

CI: patients with IDDM, pregnancy, lactation or hepatic and renal failure

Thiazolidinediones

MOA: Increase the activity of teh nuclear receptor PPAR-gamma that regulate genes responsible for the control of glucose and insulin metabolism in adipose, liver and skeletal muscle tissues-increase tissue sensitivity

Indications: Type 2 diabetes alone or in combo with a sulfonylurea or insulin

These drugs work only work in presence of insulin

Watch for possibility of hepatic failure- monitor transaminase levels before and after starting therapy

Can be taken with or without food

Metabolized by 2C8 lesser extend by 2C9

Thiazolidinediones

• MOA: Increase the activity of teh nuclear receptor PPAR-gamma that
• regulate genes responsible for the control of glucose and insulin
• metabolism in adipose, liver and skeletal muscle tissues-increase tissue
• sensitivity

Indications: Type 2 diabetes alone or in combo with a sulfonylurea or insulin

These drugs work only work in presence of insulin

Watch for possibility of hepatic failure- monitor transaminase levels before and after starting therapy

Can be taken with or without food

Metabolized by 3A4. Decreases the efficacy of OC's- suggest alternate method of BC, monitor ALT for hepatotoxicity

MOA: Decrease hepatic gluconeogenesis and intestinal glucose absorption, increases peripheral tissue insulin sensitivity, does NOT cause insulin release in the pancreas

Indications: Type 2 diabetes with diet and exercise or in combination with a sulfonylurea

Can cause decrease B12 and folate absorption,

CI: In hepatic and renal failure or a history of lactic acidosis, Stop taking if MI occurs or septicemia

No protein binding, no metabolism with rapid renal excretion

Recombinant/chemically modified insulins

Forms microprecipitates in Sub-Q tissue prolonging duration from 18-26 hours

• Recombinant/chemically modified insulins
• Rapid acting 3-5 hours duration, take 15 minutes before meals or immediately after eating

• Recombinant/chemically modified insulins continued
• Rapid acting 3-5 hour duration, take 5-10 minutes before meals

Recombinant/chemically modified/synthetic polypeptides

Incretin mimetic or glucagon-like peptide-1 (GLP-1) receptor agonist that binds the GLP-1 receptor on beta islet cells causing insulin synthesis and excretion

• Thyroid Hormone
• T4
• DI: amiodarone, warfarin, dicoumarol, iopanoic acid, sulfonamides and heparin (interfer with T4 binding to plasma transport protein)

In the diabetic patient: If you start thyroid replacement therapy you must also monitor blood glucose levels closely and increase insulin and hypoglycemic medications

• hyroid Hormone
• T3

• DI: amiodarone, warfarin, dicoumarol, iopanoic
• acid, sulfonamides and heparin (interfer with T4 binding to plasma transport protein)

In the diabetic patient: If you start thyroid replacement therapy you must also monitor blood glucose levels closely and increase insulin and hypoglycemic medications

H2 antagonists

Indications: duodenal ulcer, benign gastric ulcer, erosive GERD, pathological hypersecretory conditions, GI bleeding , (heart burn, acid indigestion, sour stomach -OTC)

Does not inhibit cyp 450 enzymes

• Proton Pump Inhibitor
• MOA: at acidic pH within the parietal cells these prodrugs undergo an intramolecular rearrangement generating a sulfenamide that covalently reacts with thiol functional groups forming a disulfide on the extracellular luminal domain of the pump protein

These are permanent inhibitors of the pump system until protein/membrane turnover occurs which takes 3-5 days

Indication: delayed release capsules for duodenal ulcer associated with/without H. Pylori, erosive esophagitis, GERD, hypersecretory conditions, posterior laryngitis

Hepatic disease can increase bioavailability

• Proton pump inhibitor
• MOA: at acidic pH within the parietal cells these prodrugs undergo an intramolecular rearrangement generating a sulfenamide that covalently
• reacts with thiol functional groups forming a disulfide on the extracellular luminal domain of the pump protein

These are permanent inhibitors of the pump system until protein/membrane turnover occurs which takes 3-5 days

Indications: delayed release tablets for duodenal ulcers, GERD, maintenance of healing of GERD, hypersecretory conditions and for H. pylori eradication

CYP450 metabolized- no dosage adjustment in patients with mild to moderate dysfunction use caution in severe impairment

Take before eating

• Proton Pump Inhibitors
• MOA: at acidic pH within the parietal cells these prodrugs undergo an intramolecular rearrangement generating a sulfenamide that covalently
• reacts with thiol functional groups forming a disulfide on the extracellular luminal domain of the pump protein

These are permanent inhibitors of the pump system until protein/membrane turnover occurs which takes 3-5 days

Indications: Short term treatment of GERD

Can be taken with or without food

Accumulation in hepatic dysfunction is possible-use caution if concurrent C19 and 3A4 inhibitors are used

Enteric coated--low stomach pH will destroy the compound, can be taken with antacids or food

• H₂ antagonist
• Indications: duodenal ulcer, benign gastric ulcer, erosive GERD, pathological hypersecretory conditions

Does not inhibit CYP 450 enzymes

Stagger doses of antacids and H₂ blockers to maximize bioavailability

• Proton Pump Inhibitor
• S enantiomer of omeprazole

Indications: Erosive esophagitis, GERD, triple therapy for duodenal ulcer associated with H. Pylori

Capsules can also be opened and taken in a smiliar manner as lansoprazole in patients that have difficulty swallowing capsules: suspension for use down feeding tubes

• Proton Pump Inbitior
• MOA: at acidic pH within the parietal cells these prodrugs undergo an intramolecular rearrangement generating a sulfenamide that covalently
• reacts with thiol functional groups forming a disulfide on the extracellular luminal domain of the pump protein

These are permanent inhibitors of the pump system until protein/membrane turnover occurs which takes 3-5 days

Indications: delayed release capsules for duodenal ulcer associated with/without H. pylori, erosive esophagitis, GERD, hypersecretory conditions, dual and triple therapy, approved for children age 1-11 for GERD

For patients who have difficulty swallowing the capsules can be opeaned and sprinkled on applesauce, cottage cheese or yogurt or fruit juices if swallowed immediate upon mixing; Take before eating

• DPP-IV inhibitor of incretin
• MOA: Dipeptidyl protease IV inhibitor--prolongs the biological levels of the natural incretins GLP-1 and GIP--thereby increasing insulin release and decreasing release of glucagon

Modify dosage in moderate to end-stage renal failure as a function Crcl excreted via OCT tubular secretion as unchanged drug

Indications: monotherapy for type 2 diabetes (Do Not use for type I)

Potential adverse side effects: other peptides as cleaved by DPP-IV such as neuropeptides, cytokines, chemokines--what is the consequence of inhibiting their metabolims

MOA: A locally acting selective Cl- channel activator of ClC2 that produces a Cl-rich intestinal fluid without alteration of Na and K serum levels. This fluid production increases GI motility clearing the intestinal of stool

Indication: idiopathic chronic consitpation in adults (24 mcg bid with food)

Low systemic activity or absorption past the GI epithelia membrane. Not cyp metabolized but processed by carbonyl reductase in the stomach and jejunum

CI: pts with history of mechanical bowel obstruction

Short acting agent, beta 1 activity <beta 2 activity, PO onset 30 minutes with duration 4-8 hours, inhalation onset 5 minutes with duration of 3-6 hours, third most poten beta 2 agent--most widely used agent bia a nebulizer in ER

Short acting agent, a solution for inhalation. Reported to have much less beta1 activity thatn racemic mixture

Beta 1 activity < beta 2 activity, inhalation onset 20 minutes with duration of 12 hours, greatest beta 2 potency available (2X isoproterenol)

• Anti-cholinergic brochodilators
• Solution for inhalation, aerosol, nasal spray

MOA: Synthetic quaternary anticholinergic parasympatholytic ammonium compound chemically related to atropine which antagonize the effects of acetylcholine to decrease the intracellular concentrations of cGMP

CI: Food allergy to soy bean or peanut products

• Patient info:
• 1. avoid contact of solutions with the eyes since temporary blurred vision, precipitation or worsening of narrow-angle glaucoma or eye pain will result
• 2. If mixed with albuterol for nebulizer use the solution must be used within 1 hour
• 3. Nasal spray pumps require priming of up to 7 actuations

• Leukotriene Receptor Antagonist
• MOA: selective and competitive CysLT₁ receptor antagonist of leukotriene C₃ D₄ and E₄ which are components of slow-reacting substance of anaphylaxis (SRSA) preventing bronchoconstriction

Indications: prophylaxis and chronic treatment of asthma in adults and children one year of age and older, 4 mg oral granules for children 0.5-5 years old for perennial allergic rhinitis

Metabolized by 2C9 and 3A4

Tablets and chewable tablets, oral granules-once daily in the evening and with or without food

• Respiratory corticosteriod inhalation products
• MOA: adrenal corticosteriods with basic glucocorticoid activity and actions--exact mechanism in the lung tissue is unknown--local lung delivery can reduced the systemic glucocorticoid activity

Indications: tx including maintenance and prophylaxis of chronic asthma pts including those that require systemic corticosteriods of those that could benefit from systemic dose reduction/elimination

After withdrawl of systemic agents it takes several months for hypothalamic-pituitary-adrenal function to return to normal. Adrenal insufficiency will manifest itself during trauma, surgery or infection--use extreme caution--be on the lookout for severe asthmatic attack

Patient Information: rinse mouth out with water following use without swallowing to avoid oral candidiasis, do not abruptly stop use or use to treat acute attack, immediately contact MD if exposed to chicken pox or measles or if sore mouth or throat occurs

• Respiratory corticosteriod inhalation products
• MOA: adrenal corticosteriods with basic glucocorticoid activity and
• actions--exact mechanism in the lung tissue is unknown--local lung
• delivery can reduced the systemic glucocorticoid activity

• Indications: tx including maintenance and prophylaxis of chronic asthma
• pts including those that require systemic corticosteriods of those that
• could benefit from systemic dose reduction/elimination

• After withdrawl of systemic agents it takes several months for
• hypothalamic-pituitary-adrenal function to return to normal. Adrenal
• insufficiency will manifest itself during trauma, surgery or
• infection--use extreme caution--be on the lookout for severe asthmatic
• attack

• Patient Information: rinse mouth out with water following use without
• swallowing to avoid oral candidiasis, do not abruptly stop use or use to
• treat acute attack, immediately contact MD if exposed to chicken pox or
• measles or if sore mouth or throat occurs

• Respiratory Corticosteriod Intranasal product
• MOA: Adrenal corticosteriods with basic glucocorticoid activity and actions--exact mechanism in the nasal tissue is unknown (decreased inflammatory mediators)

Warning: Use caution in pts in systemic alternate-day corticosteroid treatment since HPA suppression likelihood may increase--local delivery can reduce the systemic glucocorticoid activity, some weak mineralcotoricoid activity

Localized infections from Candida albicans is rare but if any infection occurs anti-infective therapy must be used

Patient information: May dry and irritate the nasal mucosa, sneezing may occur, if problems persist after 3 weeks contact the MD, do not exceed recommended dosage, contact MD if exposed to chicken pox or measles

• Respiratory Corticosteriod Intranasal product
• MOA: Adrenal corticosteriods with basic glucocorticoid activity and
• actions--exact mechanism in the nasal tissue is unknown (decreased
• inflammatory mediators)

• Warning: Use caution in pts in systemic alternate-day corticosteroid
• treatment since HPA suppression likelihood may increase--local delivery
• can reduce the systemic glucocorticoid activity, some weak
• mineralcotoricoid activity

Localized infections from Candida albicans is rare but if any infection occurs anti-infective therapy must be used

• Patient information: May dry and irritate the nasal mucosa, sneezing may
• occur, if problems persist after 3 weeks contact the MD, do not exceed
• recommended dosage, contact MD if exposed to chicken pox or measles

• Respiratory Corticosteriod Intranasal product
• MOA: Adrenal corticosteriods with basic glucocorticoid activity and
• actions--exact mechanism in the nasal tissue is unknown (decreased
• inflammatory mediators)

• Warning: Use caution in pts in systemic alternate-day corticosteroid
• treatment since HPA suppression likelihood may increase--local delivery
• can reduce the systemic glucocorticoid activity, some weak
• mineralcotoricoid activity

Localized infections from Candida albicans is rare but if any infection occurs anti-infective therapy must be used

• Patient information: May dry and irritate the nasal mucosa, sneezing may
• occur, if problems persist after 3 weeks contact the MD, do not exceed
• recommended dosage, contact MD if exposed to chicken pox or measles

• Sympathomimetic Bronchodilators
• MOA: relative selectivity of a particular agent for alpha, beta 1 & 2 adrenergic effects determines it usefulness clinically--and predicts an agents SE that will be observed

200X higher affinity for beta 2 receptors over beta 1 (SS) is 1000X less potent as a beta 2 agonist than (RR) cpd

Also inhibitor of mast cell mediators such as histamine and leukotrienes

• An inhalation powder using the HandiHaler device
• Long-acting agent to be used once daily

• MOA: Synthetic quaternary anticholinergic parasympatholytic ammonium
• compound chemically related to atropine which antagonize the effects of
• acetylcholine to decrease the intracellular concentrations of cGMPCI: Food allergy to soy bean or peanut productsPatient info: 1.
• avoid contact of solutions with the eyes since temporary blurred
• vision, precipitation or worsening of narrow-angle glaucoma or eye pain
• will result2. If mixed with albuterol for nebulizer use the solution must be used within 1 hour3. Nasal spray pumps require priming of up to 7 actuations

2nd generation Antihistamines- Piperidine peripheral selective

Indications: seasonal allergic rhinitis (6 years of age or older) and chronic idiopathic urticaria

MOA: structurally related to tetracaine--anesthetizes stretch receptors in the respiratory areas dampening their activity reducing cough reflex at its source

Swallow capsules whole--do not chew or break

Estrogen replacement

• 2nd generation antihistamine
• 1 enantiomer drug
• Approved also for use in children 6-11 years of age - one half of a 5 mg tablet

• Additional indication of osteoporosis treatment
• Isolated from pregnant horse urine-sugar conjugates

FDA placed saftey monitoring list for possible angioedema

Selective Estrogen Receptor Modulator (SERM)

MOA: Estrogen receptor antagonist lacking estrogen activity in breast and uterine tissue, reduces bone resorption and turnover, increased bone mineral density

Indication: Osteoporosis tx

Extensive 1st pass metabolism

CI: women planning to become pregnant or pregnant, blood clot disorders

Use caution: discontinue use 72 hours prior to surgery or immobilization due to clotting potential, hepatic failure, not effective in treating hot flash disorders

• Progestin
• Specific indication: secondary amenorrhea, abnormal uterine bleeding due to hormonal imbalance, injectable contraceptive

Depo-Provera- Injectable--off label use-chemical castration of male sex offenders

Vaginal ring containing etonogestrel and ethynyl estradial

First transdermal skin patch approved for birht control

Contains ethinyl estradiol (Estrogen) and norelgestromin (Progestin)

A low dose but yeat effective agent when taken correctly containing norgestimate and ethinyl estradiol

Drospirenone (progestin) and ethinyl estradiol (estrogen activity)

Drospirenone is an analog of spironolactone--can cause increased K levels--measure during the 1st treatment period--watch for interactions wit other drugs that increase K

Claims less SE such as HA, N/V, breast tenderness, emotional lability

Decreases production of testosterone in ovaries and skin --a benefit in preventing mood symptoms

CI: renal, hepatic, or adrenal insufficency

Additionally Yaz is used for premenstrual dysphoric disorder for women that choose OC as a method of contraception

MOA: Inhibits steroid 5 alpha reductase preventing testosterone conversion to 5 alpha dihydrotestosterone

Indications: Benign prostatic hyperplasia

MOA: inhibits steriod 5 alpha reducatase preventing testosterone conversion to 5 alpha dihydrotestosterone

Indications: benign prostatic hyperplasia, androgenic alopecia

• Bisphosonate
• MOA: appears the bisposphoante is incorporated into the bone matrix and is imbibed by oseoclasts. this incapacitiates the osteoclas preventing resorption of the bone

All of these drugs are poorly absorbed in the intestine therefore take them at least 90 minutes before or after meals and only with water

Use caution in renal impairment, avoid Al or Mg containing antacids, may cause Nasuea and diarrhea

• Bisphosonate
• MOA: appears the bisposphoante is incorporated into the bone matrix and
• is imbibed by oseoclasts. this incapacitiates the osteoclas preventing
• resorption of the bone

• All of these drugs are poorly absorbed in the intestine therefore take
• them at least 90 minutes before or after meals and only with water

Use caution in renal impairment, avoid Al or Mg containing antacids, may cause Nasuea and diarrhea

Now available with CaCO3- Day 1 you take 35 mg of drug and days 2-7 one tablet of 1250 mg CaCO3

• New generation of bisphosphonate
• Indicated postmenopausal osteoporosis

Renal clearance is lineraly related to Crcl

New dosage form 150 mg tab taken once a month

Adrenocorticoal Steriods

MOA: decreases granulocyte phagocytosis and prevents leukocyte migration and lactate production, decreases inflammatory response to deposited crystals--an antimitotic agent- prebents spindle formation. Does not decrease plasma uric acid levels

Indications: Unique anti-inflammatory agent that is largely effective only in gout-can be used to relieve pain of an acute atttack or prophylactically; also some unlabeled uses-MS , cirrhosis and others

Natural product isolated from the flowering plant seeds and corn of colchicum autumale, a member of the lilly family

Always use with urcosuric agent

Perform periodic blood counts to look for leukopenia, not an analgesic nor an uricosuric agent, dc use at 1st sign of N/V, diarrhea or stomach pain; causes malabsorption of vit b12

MOA: inhibits xanthine oxidase which is responsible for the synthesis of urate from xanthine and hypoxanthine

Indications: Management of gout, management of patients with malignancies, calcium oxalate calculi

• Metabolism:
• 1. allopurinol is rapidly oxidized to the metabolite alloxanthine--this has a longer half life and accumulates contributing significantly to the overall therapeutic effects and side effects as dosage increases
• 2. inhibits liver microsomal enzymes cyp

Therapy should be started at low doses and tirated upward to prevent precipitation of a gouty attack, water consumption should be >2 liters/day useful agent in renal impairment when urcosuric agents do not work well

• Vitamin B12
• Primarly produced in microorganism
• Meats, eggs, seafood, dairy, and fermented products
• Water soluble
• Absorption is dependent on intrinsic factor
• A glycoprotein secreted by parietal cells of the gastric mucosa
• Deficiency leads to anema

• Vitamin B9
• Humans can not synthesize folic acid and get it from diet or microbial gut bacteria synthesis

Deficiency result of malabsorption or alcoholism

Need for folic acid increases during pregnancy

Anti-herpes agents- Synthetic nucleoside class of agent

MOA: following phosphorylation via first thymidine kinase, the triphosphate inhibits DNA polymerase and replication by being incorporated into DNA

Indications: HSV1 &2, shingles, epstein-barr, CMV, and chicken poz

Class B pregnancy--routinely used during pregnancy to suppress outbreaks and to aid in vaginal delivery to lower risk of offspring infection

Anti-infulenza- Neuraminidase inhibitor

MOA: ethyl eser prodrug that appears to inhibit influenza neuraminidase enzyme system thereby altering particle aggregation and release

Dosage reduction necessary in renal Ccr <30

75 mg capsules for adults--take without regard to food, suspension for kids plus 30 and 45 mg capsules

• Penicillin beta lactam antibiotic
• Indications: susceptible organisms causing Streptococcal, Pneumonoccal, Staphylococcal infections, rheumatic fever or chorea, Lyme's disease and mild to moderate anerobic infections.

Use extreme caution in Staph infections: resistance, Do Not use in cases of severe infection initially

Oral use only , May be taken with meals but blood levels higher if taken on empty stomach

Not penicillinase resistant, Not acid stable

Dosage adjustments are required in severe renal failure

Store reconstituted oral solutions in the regrigerator

Dosage typically 125-500 mg up to 4 times per day for 10-20 days

• Penicillin beta lactam antibiotics
• Aminopenicillins
• Indications: Spectrum of activity essentially identical to ampicillin except more active against Shigella spp., Chlamydia trachomatis in pregnancy

More complete absorption than ampicillin, 3X per day dosing, less diarrhea than ampicillin

Oral use only, Not penicillinase resistant, actid stable, May be taken with meals

Pediatric use: administer with milk, juice, or cold drink

• Penicillin beta lactam antibiotics
• Aminopenicillin
• Indications: Susceptible strains of organisms in lower respiratory infections, Otitis media and sinusitis, skin and skin structure infections, UTI

Oral use only, take with food if GI upset occurs

Penicillinase resistant due to clavulanate presence

Suspension and chewable tablets contain aspartame and should not be used by phenylketourics

First generation Cephalosporin Antibiotics: generally all agents are inactivated by beta lactamases

Indications: Respiratory tract infections, Otitis Media, skin and skin structure infections, bone infections, GU infections

Oral use only

Cross allerginicity with penicillins

• DI:
• Alcohol use may produced a disulfiram like reaction
• Aminoglycoside nephrotoxicity can be increased
• Anticoagulant effects can be potentiated
• Antacids can decrease plasma concentrations of oral agents
• Loop diuretics nephrotoxicity can be increased

Monitor renal function since all are renally excreted with the exception of cefoperazone

3rd generation cephalosporin antibiotic

Indications: Community acquired pna, acute exaccerbation of chronic bronchitits, acute maxillary sinusitis, pharnygitis, tonsillitis, skin and skin structure infections, acute otitis media

Oral use only, reduce in renal failure

Fluoroquinolines

DOC for inhalation anthrax

MOA: bactericidal agents that inhibit the enzyme DNA-gyrase (topoisomerase II) that is involved in introducing negative supercoils into circular duplex DNA. These coils relieve torsional stress in unwinding helical DNA therby permitting transcription and replication

Indications: Acute sinusitis, lower respiratory tract infections, nosocomial pna (IV only), skin and skin structure infections, bone and joint infections, UTI, chronic bacterial prostatitis, empirical therapy, for febrile neutropenia patients, complicated intra-abdominal infections, infectious diarrhea--agent of choice, thypoid fever, susceptible sexually transmitted diseases (oral)

Admix incompatibility with aminophylline, amozacillin, clindaymycin, floxacillin, heparin, maziocillin (alkaline solutions)

Photoactive drugs, may cause dizziness or lightheadedness, do not use magnesium or aluminum containing antacids, iron or zinc containing products or multiple vitamins 4 hours before or 2 hours after taking the medication. Do not take with milk or dairy products

2nd generation cephalosporin antibiotics

• Indications: Oral: respiratory tract infection, UTI, early Lyme disease, uncomplicated gonorrhea, skin and skin structure infections,
• Parenteral: as above plus septicemia, meningitis, bone and joint infections, mixed infections

Reduce dosage in renal impairment based on Crcl, may be taken with food, do not mix in the same IV as animoglycosides, or use sodium bicarbonate injection as diluent, do not chew tablets due to very bad taste, swallow whole

• Fluoroquinolines
• Indications: acute bacterial sinusitis, acute bacterial exacerbation of chronic bronchitis, community acquired pna

Oral use only

Can severely prolong the QT portion of an electrocardiogram in some patients, avoid use in patients with hypokalemia or ones taking Class Ia or III anti-arryhthmia drugs

Not recommend for patient with moderate or severe hepatic failure

• Fluoroquinolines
• Indications: acute maxillary sinusitis, acute bacterial exacerbation of chronic bronchitis, community acquired pna, skin and skin structure infections, UTI, acute pylelonephritis

Oral or IV use only

Dosage adjustment a fucntion of Crcl

Tetracycline

• MOA: bind 30s bacterial ribosomal subunit which prevents the binding of aminoacyl tRNA to the mRNA-ribosomal complex--leads to inhibition of bacterial protein synthesis
• Also binds to mammalian 30s but with much lower affinity, bacterial cells seem to concentrate tetracyclines--active (requires mg, and ATP) and passive transport

Indications: sensative organisms in URI, UTI inclduding acute gonococcal infections (single visit 300 mg immediately and 300 mg after 1 hour), syphilis, chlamydia infections, prevention of traveler's diarrhea at 100 mg/day

Oral and IV use only, DO NOT use SC or IM

May be taking with food or milk

Highest lipid solubility of the TCN's

• Tetracycline
• MOA: bind 30s bacterial ribosomal subunit which prevents the binding of aminoacyl tRNA to the mRNA-ribosomal complex--leads to inhibition of
• bacterial protein synthesis
• Also binds to mammalian 30s but with much
• lower affinity, bacterial cells seem to concentrate
• tetracyclines--active (requires mg, and ATP) and passive transport

Indications: sensitive organisms in URI, UTI including syphilis, Chlamydia infections, sexually transmitted diseases in patients in which penicillins are contraindicated, meningoccal carriers, mycobacterium infections

May be taken with food or milk

Parenteral solutions are stable at room temp for 12 hours then discard

Macrolide agents

MOA: Binds selectively to a specific site on the 50s bacterial ribosomal subunit therapy preventing the translocation step of protein synthesis--it does not bind to mamamilan ribosomes

Indications: COPD bacterial infections, community acquired pna, genital ulcer disease, PID, suceptible sexually transmitted diseases including gonococcal and chlamydial infectiosn, URI, skin and skin structure infections,

New indication: one does tx for pediatric otitis media

IV and oral use only, do not administer as a bolus or IM

• Food decreases absorption by 50%
• Does not inhibit CYP

Macrolide agent

MOA: Binds selectively to a specific site on the 50s bacterial ribosomal subunit therapy preventing the translocation step of protein synthesis--it does not bind to mamamilan ribosomes

Indications: Upper and lower respiratory infections, mycobacterial infections, heliocobacter pylori double or triple therapy, greater potency agains a number of organisms when compared to base

Oral use only, may be given with or without food, no dosage adjustment in hepatic failure but with Crcl of <30 dosage adjustment necessary, 3A4 inhibitor

Markedly improved acid stability and oral bioavailability, reduced GI side effects

Use in CDAD

Avoid unnecesary use--carcinogenic

MOA: appears once metabolized binds DNA and prevents replication

Indications: anaerobic infections, intra-abdominal infections, skin and skin structure infections, gynecological infections, septicemia, CNS infections, lower respiratory tract infections, endocarditis, prophylaxis for colorectal surgery, hepatic coma, Crohn's disease, pseudomembraneous colitis, Helobacter Pylori

CDC recommended for bacterial vaginosis (single gram dose), giardiasis

Reduce dosage based on hepatic function, renally excrete metabolites, avoid alcohol, may cause metallic taste

Folate Reductase Inhibitor

• MOA: Some affinity for human folate reductase which causes some of the side effects in humans
• Microbes can not use dietary folic acid

• Sulfonamides MOA: competitive inhibitors of PABA--thes drugs are bacteriostatic
• By preventing folate coenzyme synthesis no deoxy thymidine for DNA synthesis is produced

These drugs with high pKa values are prone to crystalluria and resulting kidney damage

• Indications: UTI--perform susceptibility testing--may initiate therapy before results are obtained
• Use in caution in renal/hepatic failure

Phenytoin action is increased due to inhibition of hepatic metabolism

Nitrofuran: may be carcinogenic or mutagenic

MOA: may inhibit acetylcoenzyme A thereby intefering with bacterial carbohydrate metabolism, may inhibit cell wall synthesis

Indications: UTI in susceptible strains of E. coli, enterococoi, staphylococus aureus, klebsiella and enterobacter sp

Rapidly metabolized in the body-nitro reduction-carcinogenic-interaction with DNA, ineffective if Crcl is <40 may cause brown disocloration of the urine

• Anti- infectives and antiseptics
• MOA: inhibits the bacterial enzymes isoleucyl transfer RNA synthase

Indications: Impetigo caused by Staph and Strep Organisms

Systemic antifungal azole agent

MOA: some details are known-appears to inhibit funal cyp450 enzymes that are responsible for fungal sterol biosynthesis in particular lanosterol 14 alpha demethylase (azole or tazole group chelates iron in active site)

This is an enzyme in the pathway responsible for synthesis of ergosterol-the primary fungal sterol in cell membranes

Indications: oropharyngeal, esophygeal or vaginal candidiases, cryptococcal meningitis, prophylactic use in chemo or radiation therapy

Potent inhibitor of 3A4 therefore many drug interactions

Systemic Polyene

MOA: appear to bind cell wall sterols leading to disruption of the membrane and loss of cellular constituents especially K

Indications: Non-esophageal membrane GI candidiasis

• GI absorption is insignificant--pass out of the stool
• Oral tablets, mycostatin-also a vaginal product for candidiasis

Systemic antifugal azole agent

• MOA: some details are known-appears to inhibit funal cyp450 enzymes that
• are responsible for fungal sterol biosynthesis in particular lanosterol 14 alpha demethylase (azole or tazole group chelates iron in active
• site)

Indications: Systemic fungal infections, severe recalictrate cutaneous dermatophyte infections

Do not use fore fungal meningitis--poorly penetrates the CSF, topical use product also

Off label use: cushing disease and advanced prostate cancer--suppresses adrenal steroidogenesis

Potent inhibitor of 3A4, do not take with antacids delay 2 hours

Hepatotoxicity possible--monitor hepatic enzymes before and after starting tx

Anti-Malarials 7-chloro-4-aminoquinolines

• MOA: lots of mechanisms have been ruled out or still under investigation
• 1. Drug binding to ferriprotoporphyrin IX which by itself results in the lysis of erythrocytes and malaria protozoan cells-the drug complex is not a potent lysis agent
• 2. The drug (pka 8-9) gets trapped in the protozoan lysosome where the pH is normally pH 4.8-5.2. By raising the lysosome pH, the hemoglobin-digesting enzymes are inactivated--the parasite is deprived of amino acids

Indications: prophylaxis or treatment of acute attacks of malaria, lupus erythematosus, rheumatoid arthritis

Accumulate in liver, spleen, the heart, kidnesy and brain

Aromatase Inhibitors

MOA: inhibitors of the enzyme aromatase that is responsible for the covnersion of adrennaly produced androstenedione to estradiol--no effect on aldosterone synthesis

Reversible competitive inhibitor

Use caution in hepatic and renal impairment

1A2m 2C8/9, and 3A4 inhibitor at high dosages

MOA: immune response modulator that increases activity of CD3, CD4, CD8 and other immune cells, interferon alpha, infiltration of lymphocytes, macrophages

Indications: actinic keratosis, superficial basal cell carcinoma, external gential warts

Potassium replacement

HMG- CoA reductase inhibitor and 2-azetidinone (ezetibibe)

• MOA:
• Ezetimibe: inhibits absorption of cholesterol at the brush border of the small intesting
• Simvastatin: HMG-CoA reductase inhibitor

Indications: homozygous familial hypercholesterolemia, hyperlipidemias,

Dosage adjustment in chinese pts on niacin doses > 1 g/day

• Vitamin B3
• Indicated for hyperlipidemia to lower triglycerides and cholesterol (1-8 grams a day) ----NOT niacinamide

Seriou deficiency leads to a disease called pellagra (chronic alcoholism is major cause in US)

ARB and Thiazide Diuretic

Indication: hypertension, stroke risk reduction in pts with HTN and left ventricular hypertrophy

Sulfonamide derived drug

ARB

MOA: angiotension receptor antagonist.

Indications: hypertension alone or in combo with other antihypertensives, diabetic nephropathy in pts with type 2 diabetes, htn

Unlabeled uses: slow the rate of aortic root dilation in pediatric patients with Marfan's syndrome

Anticholinergic Agent and Beta 2 agonist

Indications: COPD in those pts who are currently on a regular bronchodilator who continue to have bronchospasms and require a 2nd bronchodilator

Contraceptive

Indications: prevent pregnancy, tx of acne, moder to sever vasomotor sx associated with menopause, prevetion of osteoporosis

Unlabeled uses: tx of hypermenorrhea, pain associated with endometriosis, dysmenorrhea, dysfunctional uterine bleeding

ARB and thiazide diuretic

Indications: combo therapy for the management of htn

Topical Analgesic

MOA: blocks both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, which results in inhibition of depolarization with reultant blockade of conduction

Indications: relief of allodynia (painful hypersensitivity) and chronic pain in postherpetic neuralgia

Thyroid product

MOA: exact mechanism is unknown, T4 is converted from T3

Indications: replacement or supplemental therapy in hypothyroidism

Opthalmic quinolone antibiotic

MOA: DNA gyrase inhibitor and inhibits topoisomerase IV.

Indications: Treatment of bacterial conjunctivitis caused by susceptible organisms

MOA: promotes immunity to seasonal influenza virus by inducing specfic antibody production.

Indications: Provide active immunity to influenza virus

May experience N/V. diarrhea, flu- like sx and redness & tenderness at injection site

Hydrocodone (analgesic, antitussive) and Chlorpheniramine (1st generation histamine h1 antagonist)

MOA: Suppresses cough in medullary center and competes with histamine for h1-receptor sites

ACEI and dihydropyridine Ca channel

MOA: Inhibits transmembrane influx of ca ions into vascular smooth muscle and cardiac muscle producing relaxation of coronary vasodilation and suppresses RAAS

Estrogen and Progestin combo

Indications: women with an intact uterus: tx of moderate to sever vasomoter sx associated with menopause, tx of moderate to severe vulvuar and vaginal atrophy due to menopause, postmenopausal osteoporosis

CNS stimulant

MOA: the more active d-threo-enantiomer or racemic methylphenidate. CNS stimulant blocks the reuptake of NE and dopamine and increases their release ino the extraneuronal space

Indications: ADHD

Response may take time, may experience decreased appetite or weight loss, restlessness, impaired judgment, HA, dry mouth or dizziness. Report unresolved rapid heartbeat, chest pain, difficutly breathing, excessive agitation, nervousness, insomnia, tremors, dizziness, or skin rash

Contraceptive

Indications: prevention of pregnancy

Unlabeld uses: tx of hypermenorrhea, pain associated with endometriosis, dysmenorrhea, dysfunctional uterine bleeding

ARB and Dihydropyridine Ca channel blocker

• MOA: Inhibits transmembrane influx of ca ions into vascular smooth
• muscle and cardiac muscle producing relaxation of coronary vasodilation
• and suppresses RAAS

Indications: htn

HMG-CoA and Dihydropyridine Ca blocker

Indications: for use when tx with both is appropriate

• Amlodipine: htn, chronic stable angina
• Atorvasatatin: dyslipidemias or primary prevention of cardivascular disease

Opthalmic 2nd generation H1 histamine antagonist

MOA: selective histamine H1-antagonist, inhibits release of histamine from mast cells. inhibits histamine induced effects on conjuctival epithelial cells

Indications: tx of the signs and sx of allergic conjuncitvitis

For eyes only, do not let tip touch eye, do not wear contacts if eyes are red, can cause cold-like symptoms and HA

Antibiotic and corticosteriod

MOA: cipro is quinolone antibiotic, dexamethasone is a corticosteriod used to decrease inflammatin accompanying bacterial infections

Indications: tx of otitis media in pediatric patients with typanostomy tubes or acute otitis externa in children and adults

Alpha 2 agonist ophthalmic agent (antiglaucoma)

MOA: selective antagonism for alpha 2 receptors causes reduction of aqueous humor formation and increased uveoscleral outflow

Indications: lowering of intraocular pressure in pts with open angle glaucoma or ocular htn

Antilipemic Agent

MOA: downregulates apoprotein c-III and upregulates the synthesis of apolipoprotein A-I, fattty acidt transport protein, and lipoprotein lipase resulting in an increase in VLDL catabolism, fatty acid oxidation, and elimination of triglyceride rich particles

Indications: adjunct to dietary therapy for tx of severly elevated serum triglyceride levels, to increase HDL, reduce LDL, and total cholesterol

MOA: natural steriod hormone that induces secretory changes in the endometrium, promotes mammary gland development, relaxes uterine smooth muscle, blocks follicular maturation and ovulation, and maintains pregnancy. When uses as part of an ART program in the luteal phase, progesterone supports embryo implantation.

Indications: prevention of endometrial hyperplasia in nonhysterectomized postmenopausal women who are receiving estrogen, secondary amenorrhea, abnormal uterine bleeding, part of assisted reproductive technology for infertile women

Intermediate to long acting insulin

MOA: intermediate to long acting insulin analog

Indications: tx of type 1 diabetes and type 2 to improve glycemic control

Corticosteriod

MOA: Controls the rate of protein synthesis, depresses the migration of leukocytes, fibroblasts; reverses capillary permeability and lysosomal staabilization at the cellular level to prevent or contol inflammation. Has potent glucocorticoid activity and weak mineralcorticoid activity

Indications: asthma, active crohns disease (oral)

2nd generation Histamine H1 antagonist

MOA: Histamine H1 receptor competitor

Indications: tx of seasonal allergic rhinitis and nasal pruritis, vasomotor rhinitis, eye itching

Androgen

MOA: principal endogenous androgen responsible for promoting the growth and development of the male sex organs and maintaining secondary sex characteristics in androgen deficient males

Corticosteriod

Estrogen Derivative

MOA: in studies for vulvar and vaginal atrophy in postmenopausal women, local estrogens have been shown to reduce vagina pH levels and mature the vaginal and urethral mucosa after 12 weeks of therapy, therby impoving vaginal dryness and mucosal atrophy

Indications: tx of moderate to severe vulvar and vaginal atrophy associated with menopause

Biguanide and thiazolidinedione- antidiabetic agent

• MOA:
• Pioglitazone is a thiazolidinedione antidiabetic agent that lowers blood glucose by improving target cell response to insulin, without increasing pancreatic insulin secretion. It has a mechanism of action that is dependent on the presence of insulin for activity.
• Metformin decreases hepatic glucose production, decreasing intestinal absorption of glucose, and improves insulin sensitivity (increases peripheral glucose uptake and utilization).

Indications: Management of type 2 diabetes mellitus (noninsulin dependent, NIDDM)

Laxative, bowel evacuant

• MOA: Bisacodyl acts on the colonic mucosa to increase peristalsis throughout
• the large intestine.
• Polyethylene glycol-electrolyte solution induces
• catharsis through strong electrolyte and osmotic effects.

Indications: Bowel cleansing prior to colonoscopy

5-Aminosalicylic Acid Derivative

• MOA: Mesalamine (5-aminosalicylic acid) is the active component of
• sulfasalazine; the specific mechanism of action of mesalamine is
• unknown; however, it is thought that it modulates local chemical mediators of the inflammatory response, especially leukotrienes, and is
• also postulated to be a free radical scavenger or an inhibitor of tumor necrosis factor (TNF); action appears topical rather than systemic

Indications: ulcertive colitis

Alpha/Beta Agonist

MOA: Stimulates alpha-, beta1-, and beta2-adrenergic receptors resulting in relaxation of smooth muscle of the bronchial tree, cardiac stimulation (increasing myocardial oxygen consumption), and dilation of skeletal muscle vasculature; small doses can cause vasodilation via beta2-vascular receptors; large doses may produce constriction of skeletal and vascular smooth muscle

• Indications: reatment of bronchospasms, bronchial asthma, viral croup, anaphylactic
• reactions, cardiac arrest; added to local anesthetics to decrease
• systemic absorption of intraspinal and local anesthetics and increase duration of action; decrease superficial hemorrhage

2nd generation Histamine H1 antagonist

MOA: Desloratadine, a major metabolite of loratadine, is a long-acting tricyclic antihistamine with selective peripheral histamine H1 receptor antagonistic activity and additional anti-inflammatory properties.

• Indications: Relief of nasal and non-nasal symptoms of seasonal allergic rhinitis
• (SAR) and perennial allergic rhinitis (PAR); treatment of chronic idiopathic urticaria (CIU)

Quinolone opthalmic antibiotic

MOA: Gatifloxacin is a DNA gyrase inhibitor, and also inhibits topoisomerase IV. DNA gyrase (topoisomerase II) is an essential bacterial enzyme that maintains the superhelical structure of DNA. DNA gyrase is required for DNA replication and transcription, DNA repair, recombination, and transposition; inhibition is bactericidal.

Indications: Treatment of bacterial conjunctivitis

Alpha 1 blocker

MOA: An antagonist of alpha1-adrenoreceptors in the lower urinary tract. Smooth muscle tone is mediated by the sympathetic nervous stimulation of alpha1-adrenoreceptors,which are abundant in the prostate, prostatic capsule, prostatic urethra, and bladder neck. Blockade of these adrenoreceptors can cause smooth muscles in the bladder neck and prostate to relax, resulting in an improvement in urine flow rate and a reduction in BPH symptoms.

Indications: Treatment of the functional symptoms of benign prostatic hyperplasia (BPH)

Topical Acne product

• MOA: Clindamycin and benzoyl peroxide have activity against Propionibacterium acnes in vitro.
• This organism has been associated with acne vulgaris. Benzoyl peroxide releases free-radical oxygen which oxidizes bacterial proteins in the sebaceous follicles decreasing the number of anaerobic bacteria and decreasing irritating-type free fatty acids. Clindamycin reversibly binds to 50S ribosomal subunits preventing peptide bond formation thus inhibiting bacterial protein synthesis; bacteriostatic or bactericidal depending on drug concentration, infection site, and organism.

Indications: Topical treatment of acne vulgaris

Corticosteriod

• MOA: Controls the rate of protein synthesis; depresses the migration of polymorphonuclear leukocytes, fibroblasts; reverses capillary
• permeability and lysosomal stabilization at the cellular level to prevent or control inflammation

Indication: Oral inhalation: Maintenance and prophylactic treatment of asthma; includes those who require corticosteroids and those who may benefit from a dose reduction/elimination of systemically-administered corticosteroids. Not for relief of acute bronchospasm.

ARB and Dihydropyridine Ca Blocker

Indications: Treatment of hypertension, including initial treatment in patients who will require multiple antihypertensives for adequate control

Osmotic laxative

MOA: Induces catharsis by strong electrolyte and osmotic effects

Indications: Bowel cleansing prior to GI examination

Aromatase Inhibitor

MOA: Nonsteroidal competitive inhibitor of the aromatase enzyme system which binds to the heme group of aromatase, a cytochrome P450 enzyme which catalyzes conversion of androgens to estrogens (specifically, androstenedione to estrone and testosterone to estradiol). This leads to inhibition of the enzyme and a significant reduction in plasma estrogen(estrone, estradiol and estrone sulfate) levels. Does not affect synthesis of adrenal or thyroid hormones, aldosterone, or androgens.

• Indications: For use in postmenopausal women in the adjuvant treatment of hormone receptor positive early breast cancer, extended adjuvant treatment of early breast cancer after 5 years of tamoxifen, advanced breast cancer with disease progression following antiestrogen therapy, hormone receptor positive or hormone receptor unknown, locally-advanced, or first-line (or second-line) treatment of advanced or metastatic breast
• cancer

Vasodilator

MOA: Nitroglycerin forms free radical nitric oxide. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation. Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronaryarteries and improves collateral flow to ischemic regions

Indications: Short-term management of pulmonary hypertension (I.V.); esophageal spastic disorders

Calcineurin inhibitor, immunosuppressant

• MOA: Suppresses cellular immunity (inhibits T-lymphocyte activation), by binding to an intracellular protein, FKBP-12 and complexes with
• calcineurin dependent proteins to inhibit calcineurin phosphatase activity

Indication: Prevention of organ rejection in heart, kidney, or liver transplant recipients

Antiretroviral Agent, Reverse Transcriptase Inhibitor (Nucleoside); Antiretroviral Agent, Reverse Transcriptase Inhibitor (Nucleotide)

• MOA:
• Nucleoside and nucleotide reverse transcriptase inhibitor combination;
• emtricitabine is a cytosine analogue while tenofovir disoproxil fumarate
• (TDF) is an analog of adenosine 5'-monophosphate. Each drug interferes
• with HIV viral RNA dependent DNA polymerase resulting in inhibition of
• viral replication.

• Indication:
• Treatment of HIV infection in combination with other antiretroviral agents

Alpha2 Agonist, Ophthalmic; Beta Blocker, Nonselective; Ophthalmic Agent, Antiglaucoma

• MOA:
• Brimonidine: Selective agonism for alpha2-receptors; causes reduction of aqueous humor formation and increased uveoscleral outflowTimolol: Blocks both beta1- and beta2-adrenergic
• receptors, reduces intraocular pressure by reducing aqueous humor
• production or possibly outflow; reduces blood pressure by blocking
• adrenergic receptors and decreasing sympathetic outflow, produces a
• negative chronotropic and inotropic activity by blocking beta1-adrenergic receptors

• Indications:
• Reduction of intraocular pressure (IOP) in patients with glaucoma or ocular hypertension

Proton Pump Inhibitor; Substituted Benzimidazole

• MOA:
• Suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump

• Indications:
• Short-term (4-8 weeks)
• treatment of active duodenal ulcer or active benign gastric ulcer;
• treatment of heartburn and other symptoms associated with
• gastroesophageal reflux disease (GERD); short-term (4-8 weeks) treatment
• of endoscopically-diagnosed erosive esophagitis; maintenance healing of
• erosive esophagitis; reduction of risk of upper gastrointestinal
• bleeding in critically-ill patientsOTC labeling: Short-term (2 weeks) treatment of frequent (2 days/week), uncomplicated heartburn

Alpha2-Adrenergic Agonist

• MOA:
• Stimulates alpha2-adrenoceptors in the brain stem, thus
• activating an inhibitory neuron, resulting in reduced sympathetic
• outflow from the CNS, producing a decrease in peripheral resistance,
• renal vascular resistance, heart rate, and blood pressure; epidural
• clonidine may produce pain relief at spinal presynaptic and
• postjunctional alpha2-adrenoceptors by preventing pain signal
• transmission; pain relief occurs only for the body regions innervated
• by the spinal segments where analgesic concentrations of clonidine
• exist. For the treatment of ADHD, the mechanism of action is unknown; it
• has been proposed that postsynaptic alpha2-agonist stimulation
• regulates subcortical activity in the prefrontal cortex, the area of the
• brain responsible for emotions, attentions, and behaviors and causes
• reduced hyperactivity, impulsiveness, and distractibility.

• Indications:
• Transdermal patch: Management of hypertension (monotherapy or as adjunctive therapy)

Corticosteroid, Ophthalmic

• MOA:
• Corticosteroids
• inhibit the inflammatory response including edema, capillary dilation,
• leukocyte migration, and scar formation. Loteprednol is highly lipid
• soluble and penetrates cells readily to induce the production of
• lipocortins. These proteins modulate the activity of prostaglandins and
• leukotrienes.

• Indications:
• Temporary relief of signs and symptoms of seasonal allergic conjunctivitis

Antidiabetic Agent, Meglitinide Derivative

• MOA:
• Nonsulfonylurea hypoglycemic agent which blocks ATP-dependent potassium
• channels, depolarizing the membrane and facilitating calcium entry
• through calcium channels. Increased intracellular calcium stimulates
• insulin release from the pancreatic beta cells. Repaglinide-induced
• insulin release is glucose-dependent.

• Indications:
• Management of type 2 diabetes mellitus (noninsulin dependent, NIDDM) as
• an adjunct to diet and exercise; may be used in combination with
• metformin or thiazolidinediones

Antiretroviral Agent, Protease Inhibitor

• MOA:
• Binds to the site of HIV-1 protease activity and inhibits cleavage of
• viral Gag-Pol polyprotein precursors into individual functional proteins
• required for infectious HIV. This results in the formation of immature,
• noninfectious viral particles.

• Indications:
• Treatment
• of HIV infection; should always be used as part of a multidrug regimen
• (at least three antiretroviral agents); may be used as a pharmacokinetic
• "booster" for other protease inhibitors

Anticholinergic Agent

• MOA:
• Blocks the action of acetylcholine at parasympathetic sites in smooth
• muscle, secretory glands and the CNS; increases cardiac output, dries
• secretions, antagonizes histamine and serotonin

• Indications:
• Transdermal: Prevention of nausea/vomiting associated with motion sickness and recovery from anesthesia and surgery

Proton Pump Inhibitor; Substituted Benzimidazole

• MOA:
• Proton pump inhibitor; decreases acid secretion in gastric parietal
• cells through inhibition of (H+, K+)-ATPase enzyme system, blocking the
• final step in gastric acid production

• Indications:
• Short-term (4 weeks) treatment of heartburn associated with nonerosive
• GERD; short-term (up to 8 weeks) treatment of all grades of erosive
• esophagitis; to maintain healing of erosive esophagitis for up to 6
• months

Antidepressant, Serotonin Reuptake Inhibitor/Antagonist

• MOA:
• Inhibits reuptake of serotonin, causes adrenoreceptor subsensitivity,
• and induces significant changes in 5-HT presynaptic receptor
• adrenoreceptors. Trazodone also significantly blocks histamine (H1) and alpha1-adrenergic receptors.

• Indications:
• Treatment of major depressive disorder

Antiemetic; Histamine H1 Antagonist; Histamine H1 Antagonist, First Generation; Phenothiazine Derivative

• MOA:
• Phenothiazine derivative; blocks postsynaptic mesolimbic dopaminergic
• receptors in the brain; exhibits a strong alpha-adrenergic blocking
• effect and depresses the release of hypothalamic and hypophyseal
• hormones; competes with histamine for the H1-receptor;
• muscarinic-blocking effect may be responsible for antiemetic activity;
• reduces stimuli to the brainstem reticular system

• Indication:
• Symptomatic treatment of various allergic conditions; antiemetic; motion
• sickness; sedative; adjunct to postoperative analgesia and anesthesia

Antimanic Agent; Antipsychotic Agent, Atypical

• MOA:
• Risperidone is a benzisoxazole atypical antipsychotic with mixed serotonin-dopamine antagonist activity that binds to 5-HT2-receptors in the CNS and in the periphery with a very high affinity; binds to dopamine-D2 receptors with less affinity. The binding affinity to the dopamine-D2 receptor is 20 times lower than the 5-HT2
• affinity. The addition of serotonin antagonism to dopamine antagonism
• (classic neuroleptic mechanism) is thought to improve negative symptoms
• of psychoses and reduce the incidence of extrapyramidal side effects.
• Alpha1, alpha2 adrenergic, and histaminergic
• receptors are also antagonized with high affinity. Risperidone has low
• to moderate affinity for 5-HT1C, 5-HT1D, and 5-HT1A receptors, weak affinity for D1 and no affinity for muscarinics or beta1 and beta2 receptors

• Indication:
• Treatment of schizophrenia; treatment of acute mania or mixed episodes
• associated with bipolar I disorder (as monotherapy in children or
• adults, or in combination with lithium or valproate in adults);
• treatment of irritability/aggression associated with autistic disorder

Antibiotic, Lincosamide

• MOA:
• Reversibly
• binds to 50S ribosomal subunits preventing peptide bond formation thus
• inhibiting bacterial protein synthesis; bacteriostatic or bactericidal
• depending on drug concentration, infection site, and organism

• Indications:
• Treatment of susceptible bacterial infections, mainly those caused by
• anaerobes, streptococci, pneumococci, and staphylococci; pelvic
• inflammatory disease (I.V.)

Contraceptive; Estrogen and Progestin Combination

• MOA:
• Combination hormonal contraceptives inhibit ovulation via a negative
• feedback mechanism on the hypothalamus, which alters the normal pattern
• of gonadotropin secretion of a follicle-stimulating hormone (FSH) and
• luteinizing hormone by the anterior pituitary. The follicular phase FSH
• and midcycle surge of gonadotropins are inhibited. In addition,
• combination hormonal contraceptives produce alterations in the genital
• tract, including changes in the cervical mucus, rendering it unfavorable
• for sperm penetration even if ovulation occurs. Changes in the
• endometrium may also occur, producing an unfavorable environment for
• nidation. Combination hormonal contraceptive drugs may alter the tubal
• transport of the ova through the fallopian tubes. Progestational agents
• may also alter sperm fertility.

• Indications:
• Prevention of pregnancy; treatment of acne

Anorexiant; Sympathomimetic

• MOA:
• Phentermine is a sympathomimetic amine with pharmacologic properties
• similar to the amphetamines. The mechanism of action in reducing
• appetite appears to be secondary to CNS effects, including stimulation
• of the hypothalamus to release norepinephrine.

• Indications:
• Short-term (few weeks) adjunct therapy in obese patients with an initial body mass index (BMI) ≥30 kg/m2 or ≥27 kg/m2
• in the presence of other risk factors (eg, diabetes, hyperlipidemia,
• hypertension); therapy should be used in conjunction with a
• comprehensive weight management program.

Antidepressant, Alpha-2 Antagonist

• MOA:
• Mirtazapine is a tetracyclic antidepressant that works by its central presynaptic alpha2-adrenergic
• antagonist effects, which results in increased release of
• norepinephrine and serotonin. It is also a potent antagonist of 5-HT2 and 5-HT3 serotonin receptors and H1 histamine receptors and a moderate peripheral alpha1-adrenergic and muscarinic antagonist; it does not inhibit the reuptake of norepinephrine or serotonin.

• Indications:
• Treatment of depression

Expectorant

• MOA:
• Thought to act as an expectorant by irritating the gastric mucosa and
• stimulating respiratory tract secretions, thereby increasing respiratory
• fluid volumes and decreasing mucous viscosity

• Indications:
• Help loosen phlegm and thin bronchial secretions to make coughs more productive

Antiemetic; Histamine H1 Antagonist; Histamine H1 Antagonist, First Generation; Piperazine Derivative

• MOA:
• Has central anticholinergic action by blocking chemoreceptor trigger
• zone; decreases excitability of the middle ear labyrinth and blocks
• conduction in the middle ear vestibular-cerebellar pathways

• Indications:
• Prevention and treatment of symptoms of motion sickness; management of vertigo with diseases affecting the vestibular system

Laxative, Osmotic

• MOA:
• An osmotic agent, polyethylene glycol 3350 causes water retention in the stool; increases stool frequency.

• Indications:
• Treatment of occasional constipation in adults

Antifungal Agent, Topical; Corticosteroid, Topical

• MOA:
• Betamethasone
• dipropionate is a corticosteroid which controls the rate of protein
• synthesis; depresses the migration of polymorphonuclear leukocytes,
• fibroblasts; reverses capillary permeability and lysosomal stabilization
• at the cellular level to prevent or control inflammation. Clotrimazole
• is an antifungal agent that binds to phospholipids in the fungal cell
• membrane altering cell wall permeability resulting in loss of essential
• intracellular elements.

• Indication:
• Topical treatment of various dermal fungal infections (including tinea pedis, cruris, and corpora in patients ≥17 years of age)

Barbiturate

• MOA:
• Butalbital
• is a short- to intermediate-acting barbiturate. Barbiturates depress
• the sensory cortex, decrease motor activity, alter cerebellar function,
• and produce drowsiness, sedation, hypnosis, and dose-dependent
• respiratory depression. Acetaminophen
• inhibits the synthesis of prostaglandins in the central nervous system
• and peripherally blocks pain impulse generation; produces antipyresis
• from inhibition of hypothalamic heat-regulating center Caffeine
• increases levels of 3'5' cyclic AMP by inhibiting phosphodiesterase;
• CNS stimulant which increases medullary respiratory center sensitivity
• to carbon dioxide, stimulates central inspiratory drive, and improves
• skeletal muscle contraction (diaphragmatic contractility)

• Indications:
• Relief of the symptomatic complex of tension or muscle contraction headache

Iron Salt

• MOA:
• Replaces iron, found in hemoglobin, myoglobin, and other enzymes; allows the transportation of oxygen via hemoglobin

• Indications:
• Prevention and treatment of iron-deficiency anemias

Antilipemic Agent

• MOA:
• Mechanism has not been completely defined. Possible mechanisms include
• inhibition of acyl CoA:1,2 diacylglycerol acyltransferase, increased
• hepatic beta-oxidation, a reduction in the hepatic synthesis of
• triglycerides, or an increase in plasma lipoprotein lipase activity.

• Indications:
• Lovaza®: Adjunct to diet therapy in the treatment of hypertriglyceridemia (≥500 mg/dL)

Alpha2-Adrenergic Agonist

• MOA:
• An alpha2-adrenergic agonist agent which decreases excitatory
• input to alpha motor neurons; an imidazole derivative
• chemically-related to clonidine, which acts as a centrally acting muscle
• relaxant with alpha2-adrenergic agonist properties; acts on the level of the spinal cord

• Indications:
• Skeletal muscle relaxant used for treatment of muscle spasticity

Tension headaches, low back pain, and trigeminal neuralgia

Skeletal Muscle Relaxant

• MOA:
• Causes skeletal muscle relaxation by general CNS depression

• Indications:
• Adjunctive treatment of muscle spasm associated with acute painful musculoskeletal conditions (eg, tetanus)

Corticosteroid, Topical

• MOA:
• Stimulates the synthesis of enzymes needed to decrease inflammation, suppress mitotic activity, and cause vasoconstriction

• Indications:
• Short-term relief of inflammation of moderate-to-severe
• corticosteroid-responsive dermatoses (very high potency topical
• corticosteroid)

Antibiotic, Oral Rinse; Antibiotic, Topical

• MOA:
• The
• bactericidal effect of chlorhexidine is a result of the binding of this
• cationic molecule to negatively charged bacterial cell walls and
• extramicrobial complexes. At low concentrations, this causes an
• alteration of bacterial cell osmotic equilibrium and leakage of
• potassium and phosphorous resulting in a bacteriostatic effect. At high
• concentrations of chlorhexidine, the cytoplasmic contents of the
• bacterial cell precipitate and result in cell death.

• Indications:
• Skin cleanser for line
• placement, skin wounds, preoperative skin preparation; germicidal hand
• rinse; antibacterial dental rinse. Chlorhexidine is active against
• gram-positive and gram-negative organisms, facultative anaerobes,
• aerobes, and yeast. Orphan drug: Peridex®: Oral mucositis with cytoreductive therapy when used for patients undergoing bone marrow transplant

Anti-Parkinson's Agent, Dopamine Agonist

• MOA:
• Ropinirole has a high relative in vitro specificity and full intrinsic activity at the D2 and D3 dopamine receptor subtypes, binding with higher affinity to D3 than to D2 or D4 receptor subtypes; relevance of D3 receptor binding in Parkinson's disease is unknown. Ropinirole has moderate in vitro affinity for opioid receptors. Ropinirole and its metabolites have negligible in vitro affinity for dopamine D1, 5-HT1, 5-HT2, benzodiazepine, GABA, muscarinic, alpha1-, alpha2-,
• and beta-adrenoreceptors. Although precise mechanism of action of
• ropinirole is unknown, it is believed to be due to stimulation of
• postsynaptic dopamine D2-type receptors within the caudate
• putamen in the brain. Ropinirole caused decreases in systolic and
• diastolic blood pressure at doses >0.25 mg. The mechanism of
• ropinirole-induced postural hypotension is believed to be due to D2-mediated blunting of the noradrenergic response to standing and subsequent decrease in peripheral vascular resistance.

• Indications:
• Treatment of idiopathic Parkinson's disease; in patients with early
• Parkinson's disease who were not receiving concomitant levodopa therapy
• as well as in patients with advanced disease on concomitant levodopa;
• treatment of moderate-to-severe primary Restless Legs Syndrome (RLS)

Anticholinergic Agent

• MOA:
• Blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands and the CNS

• Indications:
• Treatment of functional bowel/irritable bowel syndrome

Analgesic, Urinary

• MOA:
• An azo dye which exerts local anesthetic or analgesic action on urinary tract mucosa through an unknown mechanism

• Indications:
• Symptomatic
• relief of urinary burning, itching, frequency, and urgency in
• association with urinary tract infection or following urologic
• procedures

Contraceptive; Estrogen and Progestin Combination

• MOA:
• Combination hormonal contraceptives inhibit ovulation via a negative
• feedback mechanism on the hypothalamus, which alters the normal pattern
• of gonadotropin secretion of a follicle-stimulating hormone (FSH) and
• luteinizing hormone by the anterior pituitary. The follicular phase FSH
• and midcycle surge of gonadotropins are inhibited. In addition,
• combination hormonal contraceptives produce alterations in the genital
• tract, including changes in the cervical mucus, rendering it unfavorable
• for sperm penetration even if ovulation occurs. Changes in the
• endometrium may also occur, producing an unfavorable environment for
• nidation. Combination hormonal contraceptive drugs may alter the tubal
• transport of the ova through the fallopian tubes. Progestational agents
• may also alter sperm fertility.

• Indications:
• Prevention of pregnancy; postcoital contraception

Anticonvulsant,

• MOA:
• The precise mechanism by which levetiracetam exerts its antiepileptic
• effect is unknown. However, several studies have suggested the mechanism
• may involve one or more of the following central pharmacologic effects:
• inhibition of voltage-dependent N-type calcium channels; facilitation
• of GABA-ergic inhibitory transmission through displacement of negative
• modulators; reduction of delayed rectifier potassium current; and/or
• binding to synaptic proteins which modulate neurotransmitter release.

• Indications:
• Adjunctive therapy in the treatment of partial onset, myoclonic, and/or primary generalized tonic-clonic seizures

Calcium Channel Blocker; Calcium Channel Blocker, Dihydropyridine

• MOA:
• Inhibits
• calcium ions from entering the “slow channels” or select
• voltage-sensitive areas of vascular smooth muscle and myocardium during
• depolarization, producing a relaxation of coronary vascular smooth
• muscle and coronary vasodilation; increases myocardial oxygen delivery
• in patients with vasospastic angina

• Indications:
• Treatment of hypertension

Corticosteroid, Topical

• MOA:
• Fluorinated
• topical corticosteroid considered to be of high potency. The mechanism
• of action for all topical corticosteroids is not well defined, however,
• is felt to be a combination of three important properties:
• anti-inflammatory activity, immunosuppressive properties, and
• antiproliferative actions.

• Indications:
• Anti-inflammatory,
• antipruritic; treatment of plaque-type psoriasis (up to 10% of body
• surface area) [high-potency topical corticosteroid]

Nonsteroidal Anti-inflammatory Drug (NSAID), Oral

• MOA:
• Reversibly inhibits
• cyclooxygenase-1 and 2 (COX-1 and 2) enzymes, which results in decreased
• formation of prostaglandin precursors; has antipyretic, analgesic, and
• anti-inflammatory propertiesOther
• proposed mechanisms not fully elucidated (and possibly contributing to
• the anti-inflammatory effect to varying degrees), include inhibiting
• chemotaxis, altering lymphocyte activity, inhibiting neutrophil
• aggregation/activation, and decreasing proinflammatory cytokine levels.

• Indications:
• Acute and long-term use in the management of signs and symptoms of
• osteoarthritis; rheumatoid arthritis and juvenile idiopathic arthritis
• (JIA); management of acute pain

Antimanic Agent

• MOA:
• Alters
• cation transport across cell membrane in nerve and muscle cells and
• influences reuptake of serotonin and/or norepinephrine; second messenger
• systems involving the phosphatidylinositol cycle are inhibited;
• postsynaptic D2 receptor supersensitivity is inhibited

• Indications:
• Potential augmenting agent for antidepressants; aggression, post-traumatic stress disorder, conduct disorder in children

ACEI

• MOA:
• Competitive
• inhibitor of angiotensin-converting enzyme (ACE); prevents conversion
• of angiotensin I to angiotensin II, a potent vasoconstrictor; results in
• lower levels of angiotensin II which causes an increase in plasma renin
• activity and a reduction in aldosterone secretion; a CNS mechanism may
• also be involved in hypotensive effect as angiotensin II increases
• adrenergic outflow from CNS; vasoactive kallikreins may be decreased in
• conversion to active hormones by ACE inhibitors, thus reducing blood
• pressure

• Indications:
• Treatment of hypertension, either alone or in combination with other antihypertensive agents; treatment of heart failure (HF)

Antidepressant, Tricyclic (Tertiary Amine)

• MOA:
• Increases the synaptic concentration of serotonin and norepinephrine in
• the central nervous system by inhibition of their reuptake by the
• presynaptic neuronal membrane; antagonizes the histamine (H1) receptor for sleep maintenance

• Indications:
• Depression; treatment of insomnia (with difficulty of sleep maintenance)

Antiarrhythmic Agent, Class IV; Calcium Channel Blocker; Calcium Channel Blocker, Nondihydropyridine

• MOA:
• Nondihydropyridine calcium channel blocker which inhibits calcium ion
• from entering the “slow channels” or select voltage-sensitive areas of
• vascular smooth muscle and myocardium during depolarization, producing a
• relaxation of coronary vascular smooth muscle and coronary
• vasodilation; increases myocardial oxygen delivery in patients with
• vasospastic angina

• Indications:
• Oral: Essential hypertension; chronic stable angina or angina from coronary artery spasm Injection:
• Control of rapid ventricular rate in patients with atrial fibrillation
• or atrial flutter; conversion of paroxysmal supraventricular tachycardia
• (PSVT)