can be used for mild/moderate acute migraine attacks b/c act as vasoconstrictors

includes: aspirin, diclofenac, ibuprofen, indometacine, ketoprofen, naproxen

Zolmitriptan

Rizatriptan

Elitriptan

Almnotriptan

Frovatriptan

serotonin agonists that can be used during moderate/severe migraine attacks

are vasoconstrictors, neurogenic inflamamtion inhibitors, and dec pain transmission

Ergotamine

Dihydroergotamine

effective medications if taken during prodrome of a migraine attack

1st causes long-lasting vasoconstriction that is cumulative

inhibit NMDA receptors - blocks toxic effects assoc w/ excess Glu

used for moderate to severe AD

anticholinesterase in the brain -> stimulates N receptors in brain to release more Ach

used for mild to moderate AD

anticholinesterase in the brain

used for mild to moderate AD

anticholinesterase in the brain

used for mild to severe AD

long half-life and potent -> may be best Rx to give

crosses BBB where it metabolized into DA in order to act on post-synatpic R

parkinson drug

DOPA decarboxylase inhibitor -> helps prevent DOPA metabolism in the peripheral circulation

when combined w/ levodopa = Sinemet

minimized adverse effects of levodopa

does NOT cross BBB

DA agonist that will act on the post-synaptic R

useful for delayin onset of L-dopa therapy

DA agonist that will act on the post-synaptic R

useful for delaying the onset of L-dopa therapy

13X more potent that bromocriptine

DA agonist that will act on the post-synaptic R

useful for delaying onset of L-dopa therapy

can be used as a monotherapy or adjunct

DA agonists that will act on the post-synaptic R

useful for delaying onset of L-dopa

can be used a monotherapy or adjuct

drugs that affect CYP1A2 will affect clearance

Entacapone

Tolcapone

COMT inhibitors

adjuncts to be given w/ L-dopa

do NOT cross BBB

inhibits DA reuptake, blocks Ach and Glu R

used to reduce choreic movt

narrow therapeutic range

causes livedo reticularis

Trihexyphenidyl HCL

Benztropine Mesylate

anticholinergic (monotherapy or adjunct)

useful for reducing tremor

predopaminergic therapy

MAO-B inhibitor (monotherapy or adjunct) + inhibits DA reuptake

when used as monotherapy delays need for L-dopa by 9mos (avg)

may dec production of free radicals

inc DA stores in neurons

viable strain of mycobacterium bovis

MOA: activation of macs and other immune cells

USE: immunization against TB, immunostimulant in the tx of superficial bladder cancer

pt will always be PPD+, approved for enhancing bone marrow recovery after chemotherapy

grp of protein hormones from epith cells of the thymus (human or bovine)

MOA: conveys T cell specificity to uncommitted lymphoid stem cells; stimulates maturation of pre-T cells

USE: DiGeorge Syndrome (thymic aplasia aspect)

synthetic agent

MOA: antiparasitic drug that enhances T-cell mediated immune response and delayed hypersensitivity

USE: approved for combo w/ flurouracil in tx of Duke's Class C colorectal cancer

some efficacy in RA but causes agranulocytosis in HLA-B27pos ppl

cytokine; recombinant interferon a2A

MOA: inhibits cell proliferation and viral protein synthesis

USE: Kaposi's sarcoma, malignant melanoma, hepB, hepC

Cytokine; recombinant interferon B1b

MOA: inhibits cell proliferation and viral protein synthesis

USE: RRMS

SIDE EFFECTS: flu-like s/s, neurotoxicity, renal and CV abnormalities

MOA: dec IFN-a upregulation of MHC-II, inc Th2 cytokines, dec Th1 cytokines, inc IL-10 secretion

USE: MS

recombinant human colony stimulating factor (G-CSF)

MOA: inc number and size of hematopoietic progenitors

USE: neutropenia following stem cell/bone marrow transplant; after intense chemotherapy

cytokine; recombinant IL-2

MOA: promotes production of CTL and activates NK cells

USE: adjunct for renal cell carcinoma

SIDE EFFECTS: profound CV toxicity, pulmonary edema

may be useful for AIDS

lymphocyte immune globulin from hyperimmune serum of lg animals (horse); made by immunization w/ human T cells

USE: allograft rejection

SIDE EFFECTS: serum sickness, nephritis

MAb against CD3, prevents Th-APC interaction

USE: renal allograft rejection crisis

SIDE EFFECT: anaphylactoid rxns, cytokine release syndrome

Ab against Rho(D) Ag of the RBC

USE: prevent hemolytic dz of the newborn (Rh-)

SIDE EFFECT: anaphylactic shock rarely

humanized murine MAb against the alpha chain of the IL-2 receptor

USE: reversal of cardiac allograft rejection

Mab against Her-2/neu growth factor

USE: metastatic breast cancer w/ over expression of Her-2/neu

SIDE EFFECT: acute hypersensitivity rxns

murine immunoglobulin (IgG2a) -> adjuvant to other immunosuppressants in active kideny rejection

USE: forms complex w/ Ag to block FN of all T cells

SIDE EFFECTS: chills, fever, chest pain, GI, dyspnea, tremor

animal immunized w/ human lymphoid cells -> binds to T cells involved in Ag recognition and destroys T cells (blocks cellular immunity)

USE: in combo w/ cyclosporin A or cytotoxic drugs in bone marrow, renal, and heart transplantation

SIDE EFFECT: hypersensitivity, anaphylaxis, pain at injection site

immune globulin derived from horse -> binds to T cells involved in Ag recognition and destroys T cells (blocks cellular immunity)

USE: in combo w/ cyclosporin A or cytotoxic drugs in bone marrow, renal, and heart transplantation

SIDE EFFECT: hypersensitivity, anaphylaxis, pain at injection site

USE: prophylactic to prevent rejection

MOA: inhibits activation or action of cells of the immune system

SIDE EFFECT: cushingoid rxn, glucose intolerance, infections, hypotension, cataracts, skin fragility, bone dissolution, impaired growth in children

USE: can be used alone or as adjunct w/ prednisone in renal, hepatic, pancreatic, and cardiac transplant

MOA: bind to cyclophilin receptor -> inhibits Th activation and production of IL-2

SIDE EFFECTS: nephrotoxicity, HTN

cytochrome P450 metabolized at the double bond; when used in combo w/ other drugs nephrotoxicity will be dec

USE: can be used alone or as adjunct w/ prednisone in renal, hepatic, lung, and cardaic transplant

MOA: blocks FK-binding proteins -> specific inhibition of immune response

SIDE EFFECT: HA, nausea, vomiting, flushing

poorly absorbed after oral dosing

USE: can be used alone or as adjunct w/ prednisone in renal, hepatic, lung, and cardiac transplant

MOA: specific inhibition of immune response

SIDE EFFECT: HA, nausea, vomiting, flushing

used to be an antibiotic before but was taken off market b/c of immunosuppressive effects (now back on for these effects)

USE: renal transplantation, RA, non-specific inhibition of immune response

MOA: suppresses T-cell activity greater than B-cell activity

SIDE EFFECT: bone marrow suppression, GI disturbances, hepatic dysfunction

prodrug that is cleaved by metacaptopurine into active drug; given via IV

USE: combo w/ cyclosporine for bone marrow transplantation, monotherapy in autoimmune dz, inflammatory dz, RA

MOA: dihydrofolate reductase that inhibits replication and FN of T cells

SIDE EFFECT: hepatic fibrosis, cirrhosis

80-90% is excreted unchanged

USE: bone marrow transplant

MOA: non-specific inhibition of the immune response -> suppresses B cell>T cell

SIDE EFFECT: chemical irritation

activated by P-450

USE: RA pts who have undergone NSAID therapy for 3-4mos (takes 1-4mos to have effect)

MOA: slows progression of bone-articular dz, dec FN of inflammatory cells

SIDE EFFECTS: dematitis, eosinophilia, thrombocytopenia, leucopenia, pancytopenia

concentrated in many organs

USE: RA pts (low doses), leukemia/lymphoma (high dose)

2o MOA: folic acid analog - inhibits aminoimidazolecarboxamide and thymidylate synthetase -> dec neutrophil chemotaxis and dec lymphocyte and mac FN

SIDE EFFECT: nausea, mucosal ulcers, hepatotoxicity

contraindicated in pregancy

USE: RA, Crohn's dz, AS, psoriatic arthritis

MOA: chimeric (human/mouse) anti-TNF Ab -> dec rate of new erosions

SIDE EFFECT: resp tract infection, nausea, HA, sinusitis, rash, cough, reactivation of latent TB

often given in combo w/ methotrexate

USE: RA, Juvenile Chronic Arthritis, Psoriasis, Psoriatic Arthritis, AS

MOA: recombinant fusion protein which binds TNF-a -> dec rate of new erosions

SIDE EFFECT: local pain and swelling (subC injection), resp tract infection, nausea, HA, sinusitus, rash, cough, reactivation of latent TB (less so then infliximab)

used to get around an inflammatory rxn to infleximab

Low Dose (81-300mg/dy) = anti-platelet

Intermediate Dose (300-2400mg/dy) = antipyretic and analgesic

High Dose (2400-4000mg/dy) = anti-inflammatory (OA, RA, other inflammatory joint disorders)

MOA: irreversible acetylation of COX isoenzymes

SIDE EFFECTS: Reyes Syndrome, GI irritation, gastric and duodenal ulcers, upper GI bleeding, fecal blood loss, hepatoxicity, asthma, rashes, renal toxicity, vomiting, tinnitus, dec hearing, vertigo

high 1st pass effect

USE: mainly analgesic, closing patent ductus arteriosus, anti-pyretic, anti-inflammatory

MOA: nonselective COX inhibitor

Side Effects: CV events, renal damage, GI distress, ulcers

can counteract anti-platelet effects of aspirin, more potent anti-inflammatory than aspirin

USE: analgesic, RA, OA, anti-inflammatory

MOA: nonselective COX inhibitor, LOX inhibitor

Side Effects: CV events, renal damage, GI distress, ulcers

pt w/ impaired renal FN will eliminate more slowly

USE: acute gout, patent ductus arteriosus, AS

MOA: nonselective COX inhibitor (possible phospholipase A/C inhibitor), dec neutrophil migration, dec T and B cell poliferation

Side Effects: CV events, renal damage, GI distress, ulcers, pancreatitis, HA, thrombocytopenia, aplastic anemia

USE: rheumatological disorders, suppress familial intestinal polyposis (may inhibits colon/breast/prostate cancer development)

MOA: sulfoxide prodrug metabolized to sulfide derivative, nonselective COX inhibitor

Side Effect: CV events, renal damage, GI distress, ulcers

undergoes enterohepatic cycling (prolongs duration of action)

USE: OA, RA, anti-inflammatory

MOA: ketone prodrug metabolized to acetic acid derivative; nonselective COX inhibitor

Side Effect: less GI adverse effects than other NSAIDS, pseudoporphyria, photosensitivity

non-acid NSAID

USE: post-op pain (potent analgesic, mod anti-inflammatory)

MOA: nonselective COX inhibitor

Side Effect: CV events, renal damage, GI distress, ulcers

USE: OA, RA

MOA: nonselective COX inhibitor

Side Effects: CV events, renal damage, GI distress, ulcers

short half-life so much give more freq doses (rarely used)

USE: OA, RA, reduce number of adenomatous colorectal polyps in FAP

MOA: COX-2 selective inhibitor

Side Effects: edema and water retention, asthma, thrombosis

contraindicated in pt w/ renal insufficiency, late pregnancy, metabolized by cytochrome P450, may reduce effects of ACE inhibitors, admin w/ fluconazole raises levels, admin will dec lithium levels

USE: analgesic, antipyretic (NOT anti-inflammatory or anti-platelet)

MOA: unclear -> COX-3 inhibitor (weak COX-1, COX-2 inhibitor)

Side Effect: hepatic necrosis (overdose, alcohol)

good to use in children w/ viral infection (no risk of Reye's Syndrome)

USE: acute gouty arthritis (early tx that has been replaced w/ NSAIDS)

MOA: bind tubulin of leukocytes -> inhibits migration and phagocytosis

Side Effects: diarrhea, nause, vomiting, rarely hair loss and bone marrow depression

may be used for prophylaxis in preventing recurrent attacks of gouty arthritis

USE: several bout of gout (chronic gout?)

MOA: act at anion transport of renal tubules to inc uric acid secretion from the prox tubules

Side Effects: GI irritation, allergic dematitis

should NOT be used if pt is already excreting lg amt of uric acid

USE: chronic gout, prevent hyperuricemia from destruction of cancer cells by chemotherapeutic agents, inc effectiveness of merceptopurine (prevents its oxidation)

MOA: competitive inhibitor of xanthine oxidase + directly inhibits xanthina oxidase

Side Effects: GI disturbances, nausea, vomiting, diarrhea, hepatic toxicity, allergic skin rxn

used when probenicid and sulfinpyrazone cannot be used, urinary urate is grossly elevated (600-700mg), recurrent stone, pt w/ renal impairment

USE: drug of choise for 1o and 2o hypothyroidism

MOA: is converted to T3 inside tissues (mimics physiology)

Side Effects: reversible hyperthyroidism, heart palpitation, osteoporosis

USE: short term TSH suppression

MOA: exogenous sources of T3

Side Effect: cardiotoxicity

more active than LT4 but not recommended for tx of hypothyroidism b/c shorter half life and more severe side effects

USE: hyperthyroidism

MOA: thioamide - inhibits formation and coupling of idotyrosines in thyroglobulin + inhibition of T4 to T3 conversion

Side Effect: allergic rxn, reversible hypothyroidism, agranulocytosis, liver injuries

drug of choice in pregnancy and severe thyrotoxicosis b/c of the additional benefit of inhibition of T4 to T3 conversion

USE: hyperthyroidism

MOA: thioamide - inhibits formation and coupling of idotyrosines in thyroglobulin

Side Effects: allergic rxn, agranulocytosis, aplasia cutis (congenital defect)

drug of choice in tx of hyperthyroidism unless pt is pregnant b/c longer half-life (1-2X/dy)

USE: hyperthyroidism

MOA: inhibition of thyroglobulin proteolysis -> blocks release of thyroid hormone

Side Effects: crosses placenta -> fetal goiter, Jod-Basedow in susceptible individuals

useful for short-term managament of thyroid storm or prep for surgical thyroidectomy; rarely used as a monotherapy

USE: recurrent hyperthyroidism

MOA: beta emission causes parenchymal destruction of thyroid tissue

Side Effect: permanent hypothyroidism

Contraindication: pregnancy, breast-feeding

Precautions: postpone pregnancy 3mos after therapy, avoid close physical contact w/ anyone for 5dys  

USE: rapid acting insulin for DM-1 and DM-2

MOA: insulin w/ B28 and B29 reversed to favor monomer fomration

Onset: 10-15min

Peak: 30-90min

Duration: 3-5hr

Side Effects: hypoglycemia, weight gain, lipodystrophy

USE: rapid acting insulin for DM-1 and DM-2

MOA: insulin w/ aspartic acid at B28 -> inc dissolution

Onset: 10-15min

Peak: 30-90min

Duration: 3-5hr

Side Effects: hypoglycemia, weight gain, lipodystrophy

USE: rapid acting insulin for DM-1 and DM-2

MOA: insulin w/ lysine at B3 and glutamic acid at B29 -> inc dissolution

Onset: 10-15min

Peak: 30-90min

Duration: 3-5hr

Side Effects: hypoglycemia, weight gain, lipodystrophy

USE: short acting insulin for DM-1 and DM-2

MOA: insulin w/ minute amt of zinc -> rapid diffusion into circ

Onset: 30-60min

Peak: 2-3hr

Duration: 6-8hr

CHEAP

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

Neutral Protamine Hagedorn (NPH)

Humulin

USE: intermediate acting insulin for DM-1 and DM-2

MOA: insulin + protamine (basic protein) + zic complex causes slower dissolution into monomers

mixed w/ rapid/short acting insulin as combos

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

USE: intermediate acting insulin for DM-1 and DM-2

MOA: combo insulin = 30% semilente (insulin/low zinc) + 70% insulin/mod zinc

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

USE: long acting insulin for DM-1 and DM-2

MOA: insulin + high zinc

Onset: 4-6hr

Duration: 20-36hr

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

USE: long acting insulin for DM-1 and DM-2

MOA: insulin w/ AA residues changed to make it soluble in acidic pH (slow dissolution rate) + low zinc

NO peak (less likely to cause hypoglycemia)

Onset: 1-1.5hr

Duration: 11-24hr

cannot mix w/ other insulins

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

USE: long acting insulin for DM-1 and DM-2

MOA: insulin w/ FA sub for AA on B chain

basal insulin that is given once or twice daily; does not act as long as glargine

Side Effect: hypoglycemia, weight gain, lipodystrophy (rare)

Pramlintide

Symlin

USE: amylin mimetic for DM-1 and DM-2 that will complement insulin's actions

MOA: dec postprandial glucagon secretion, less fluctuation throughout dy, inc satiety

SC injection before every meal

Peak: 20min

Duration: 3hr

Side Effects: GI disturbances

USE: secretagogue for DM-2

MOA: closes K channels in B cells -> direct stimulation causes insulin release

Side Effects: hypoglycemia, mild weight gain

Contraindications: elderly pt w/ renal or hepatic dysfunction, pregnancy

1st generation: tolbutamide, chloropropamide, tolazamide

2nd generation: glyburide, glipizide, glimepride

USE: secretagogue for DM-2

MOA: inhibits ATP-sensitive K channels on B cells-> insulin secretion

only taken at meal time (fast acting)

Duration: 3-4hr

Side Effects: hypoglycemia, mild weight gain

Ex: Repaglinide, Nateglinide

USE: biguanide used for DM-2 (approved for adults and pediatrics)

MOA: targets HDAC -> dec hepatic glucose production, inc insulin sensitivity, dec blood TAG and FA, weight loss

1st line tx in DM-2

Side Effects: GI disturbances

Contraindications: ppl w/ impaired kidney FN, CHF

Pioglitazone (Actos)

Rosiglitazone (Avandia)

USE: thiozolidinedione for DM-2

MOA: bind peroxisome proliferation-activated receptor gamma (PPAR gamma) -> sensitize end organ to insulin, dec hepatic glucose output, inc HDL, dec TG and lipolysis

Onset: 6-14wks b/c transcription factor

use at beginning of therapy or pt will have impaired glucose tolerance to preserve B cell FN (dec insulin res)

Side Effects: fluid retention (edema), mild anemia, weight gain, fx

USE: a-glucosidase inhibitors for DM-2

MOA: blocks glucosidase -> inhibits intestinal hydrolysis of complex CHO -> dec digestion and absorption of starch

only modeslty effective in lowering glucose as monotherapy

Side Effect: flatulence, diarrhea, abdominal pain

USE: incretin mimetic for DM-2

MOA: bind GLP-1 R -> inc glucose dependent insulin sec, dec glucagon sec, slow gastric emptying, dec food intake (weight loss, postprandial glycemic control)

resistant to DPP-IV (enzyme that degreaded GLP-1)

inject SC 2x/dy

Side Effect: GI disturbance (nausea, vomiting, diarrhea), hypoglycemia w/ SU

USE: incretin enhancer for DM-2

USE: inhibits DPP-IV -> blocks GLP-1 degradation (post-prandial glycemic control)

does not inc occurence of hypoglycemia when used alone or in combo

Side Effects: URI, HA, abdominal pain, nausea, diarrhea

1st line tx in absence seizures

SE: GI, fatigue, dizziness, HA

good for kids

1st line tx in absence, myoclonic, tonic-clonic, and lennox-gastaut seizures

SE: CNS depressant, GI, liver toxicity, weight gain, teratogen

can also be used in preventative tx for migraine

will displace phenytoin off carrier protein if given together

1st line tx for tonic-clonic and partial seizures

SE: CNS sedation, agranulocytosis, aplastic anemia

can be used for tx of neuropathic pain and bipolar disorder

may aggrevate absence and myoclonic seizures

1st line tx in tonic-clonic, partial, and status epilepticus seizures

SE: CNS sedation, gum hyperplasia, hirsutism

recommended AED during pregnancy

carbamazepine and phenobarbital will dev levels

alcohol, diazepam, and methylphenidate will inc levels

used in acute tx of seizures and status epilepticus

SE: CNS sedation, tolerance, and dependence

rapid onset

Diazepam has rectal formulation