FallExam1Drugs.txt

• Class: Antihistamine
• Use: Prophylactic treatment of asthma (not affective after asthma attack has started)
• MOA: Inhibits immunologically triggered degranulation of mast cells in the lungs. Prevents release of histamine and other in products of degranulation. The latter makes this most efficient.

• Class: Antihistamine
• Use: Prophylactic treatment of asthma (not affective after asthma attack has started)
• MOA: Inhibits immunologically triggered degranulation of mast cells in the lungs. Prevents release of histamine and other in products of degranulation. The latter makes this most efficient.

• Class: 1st Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Urticaria, OTC cold remedies, allergic rhinitis, hay fever, seasonal conditions
• UniqueTrait: Metabolized by CYP3A4.
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor. Toxicity: Sedation, antimuscarinic, anti-alpha-adrenergic.

• Class: 1st Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Motion sickness, Parkinsonism, allergies.
• UniqueTrait: Can't use with premees or newborns and contraindicated with ototoxic antibiotics
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor. Toxicity: Don't use in newborns or with ototoxic antibiotics. Sedation, antimuscarinic, anti-alpha-adrenergic.

• Class: 1st Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Motion sickness
• UniqueTrait: Affective in motion sickness
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor. Toxicity: Sedation

• Class: 1st Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Seasonal allergies
• UniqueTrait: Can cause cardiac toxicity if CYP3A4 inhibited and terfenadine accumulates. Noramlly metabolized to fexofenadine which is not cardiotoxic.
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor. Toxicity: Cardiac toxicity with antimicrobial agents, P450 inhibitors, or conazoles. Sedation, antimuscarinic, anti-alpha-adrenergic.

• Class: 2nd Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Allergy
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor
• Toxicity: Less sedating that 1st generation because can't enter CNS (less lipid soluble).

• Class: 2nd Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Allergy; UniqueTrait: Lower risk of arrhythmia when Terfenadine is converted to fexofenadine
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor. Toxicity: Less sedating that 1st generation because can't enter CNS (less lipid soluble).

• Class: 2nd Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Long acting allergy treatment;
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor
• Toxicity: Less sedating that 1st generation because can't enter CNS (less lipid soluble).

• Class: 2nd Gen. H1 Receptor Antagonist (Antihistamine)
• Use: Allergy
• MOA: reversible inhibitor (competitive antagonist) of H1 receptor
• Toxicity: Less sedating that 1st generation because can't enter CNS (less lipid soluble).

• AKA(prostacyclin)
• Origin: Arachadonic Acid via cyclooxygenase (COX pathway)
• Action: dec plate aggregation, vasodilation (+cAMP), dec uterine tone, bronchodilation (+cAMP), GI (-acid, +mucus, +blood), Kidney (+blood, +diuresis)
• Uses/Drug Analogs: Pulmonary hypertension/Epoprostenol(IV), Iloprost(inhaled), Treprostinol(subQ/IV)

• Origin: Arach Acid via COX
• Action: vasodilation (+cAMP for PGE1, +IP3 and +Ca2+ for PGE2), bronchodilation (+cAMP), inc. Temp, inc. uterine tone, dec plate aggreg, dec intraocular pressure, GI (-acid, +mucus, +blood), Kidney(+blood, +diuresis, -ADH)
• Uses/Drug Analogs: PGE1 (Misoprostol, Alprostadil), PGE2 (Dinoprostone)

• Origin: Arach Acid via COX
• Action: dec intraocular pressure, vasoconstriction(+IP3 and +Ca2+), bronchoconstriction(+IP3 and +Ca2+), inc Uterine contraction (+oxytocin)
• Uses/Drug Analogs: Latanoprost, Carboprost

• Origin: Arach acid via COX
• Action: vasoconstriction(+IP3 and +ca2+), platelet aggregation, bronchoconstriction(+IP3 and +Ca2+), inc uterine contaction(+oxytocin), kidney(dec bloodflow)

• Origin: Arach acid via Lipoxygenase (LOX)
• Action: bronchoconstriction(+IP3 and +Ca2+), inc vascular permeability (-BP)
• Assoc Drugs: Zafirlukast and Montelukast(singulair) are LT antagonists used to treat asthma

• class: PGE1
• Use: Erectile dysfunction, maintain patent ductus arteriosis in congenital diseases (transposition of the great arteries) before surgery

• class: PGE1 analog
• Use: NSAID related ulcers, abortifacient

• class: PGE2
• Use: labor induction, abortifacient
• SE: nausea, vomitting, diarrhea

• class: PGF2a analog (stable so long lasting)
• Use: glaucoma, ocular hypertension
• SE: brown pigmentation, dry eyes

• class: PGF2a analog (stable so long lasting)
• Use: glaucoma, ocular hypertension
• SE: brown pigmentation, dry eyes

• class: PGF2a analog (stable so long lasting)
• Use: glaucoma, ocular hypertension
• SE: brown pigmentation, dry eyes

• class: PGF2a analog
• Use: Abortifacient and labor induction (less potent than dinoprostone)

• class: PGI2 (prostacyclin)
• Use: primary pulmonary htn (IV)

• Class: PGI2 analog
• Use: Primary pulmonary htn (inhalation)

• class: PGI2 analog
• Use: primary pulmonary htn (subQ/IV)

• class: LT receptor antagonist
• Use: Asthma, seasonal allergies (singulair)

• class: LT receptor antagonist
• Use: Asthma

• class: 5-LOX inhibitor (prevents LT production)
• Use: Asthma

• Effects: Analgesic, antipyretic (-PG), anti-inflammatory, anti-coagulant, Cox-2 procoagg(-PGI)
• Use: RA and Chronic Inflammation

GI irritation, increased bleeding time (TXA inhibition), Negative kidney effects, delayed onset of labor (PGE and PGF inhibition), Hypersensitivity (increased LT due to inhibition of COX pathway)

• Irreversible NSAID
• inhibits COx-1 and COX-2 by acetylation
• irreversibly inhibits platelet aggregation. Associated with Reyes syndrome, resp. and met. acidosis and salicylism. At high doses can stay in system for up to 13 hours (low does ~15 min). Stop prior to surgery to prevent hemmorhage.

• NSAID
• less effective COX inhibition than ASA; less side effects and no renal toxicity

• NSAID
• opthalmic surgery pain or topical use in solar keratosis
• Phenyl acid derivative
• Short acting (2hrs) and metabolised in the liver (CYP3A4 and CYP2C9)

• NSAID
• cancer pain and dental surgery
• salicylic acid derivative

NSAID

• NSAID
• Analgesic and Anti-inflammatory at high doses (only analgesis at low doses)
• Short acting (2hrs) and metabolized in the liver (CYP2C8)
• Assoc. with fluid retention, kidney failure, hepatitis, tinnitis, rash and GI problems

• NSAID
• Used to treat patent ductus arteriosis (PDA) by decreasing PGE2 synthesis (normally increased metabolism of PGE2 at birth closes this naturally), gout, ankylosis spindolytis.
• Potent indole derivative
• 30% must discontinue use due to psychosis and hallucinations

• NSAID
• Slow release and short acting (2hrs)
• Also inhibits LOX pathway

NSAID

NSAID

• NSAID
• Long acting (12 hrs)
• free fraction is 40% higher in females

NSAID

• NSAID
• treats familial intestinal polyposis
• increases serum aminotransferase Associated with cholestatic liver damage

• NSAID
• No anti-inflammatory or anti-coag effects. Antipyretic and analgesis (most active in CNS). Used instead of ASA in children to prevent Reyes Syndrome.
• Assoc. with hepatic necrosis (glutathione depletion can cause toxic accumulation in the liver).
• Treat OD with N-Acetylcysteine (regenerates glutathione for phase II metabolism)

• COX-2 selective NSAID
• Less GI SE but does not affect platelets. Less potent COX2 inhibitor.
• Renal dysfunction and same SE as typical NSAID

• COX-2 selective NSAID
• Preferential to celecoxib and less selective for COX2. Treat osteoarthritis.

• Corticosteroid (immunosuppressant)
• Autoimmune disease, allograft rejection and transplantation inflammation, Hypersensitivity. Regulates trancription of genes with glucocorticoid response elements. Chronic use (over 2wks) is assoc. with hyperglycemia, osteoperosis, increased infections, and ulcers

• Calcineurin Inhibitor (immunosuppressant)
• Inhibition of calcineurin phosphatase prevents IL-2 cytokine production and impairs Tcell response. GVHD (graft v host disease) after bone marrow transplant, aplastic anemia, kidney, liver and heart transplants, autoimmune diseases. Nephrotoxicity (sirolimus makes this worse), neurotoxicity, hypertension (vasocons.), hyperlipidemia, hypercholesterolemia, hyperurecemia, hepatotoxicity.

• Calcineurin Inhibitor (immunosuppressant)
• 100x more potent than cyclosporin A. Inhibition of calcineurin phosphatase prevents IL-2 cytokine production and impairs Tcell response. GVHD (graft v host disease) after bone marrow transplant, aplastic anemia, kidney, liver and heart transplants, autoimmune diseases. Same SE as cyclosporin A.

• Antiproliferative agent (immunosuppressant)
• Blocks IL-2 mediated Tcell activation and proliferation. Used to treat GVHD, transplant rejection, Autoimmune disease. May produce tolerance, complication in renal transplant patients, anemia, K+ imbalance, fever, increased risk of lymphoma and infection, hyperlipidemia (worse with cyclosporin A), thrombocytopenia, leukopenia, and hypotension.

• Cytotoxic drug (immunosuppresant)
• Coverted to thioinsoinate which is a competitive inhibitor of inosinic acid (A and G precursor). Prevents purine production and T cells. Used to treat RA and Transplant rejection. Toxic with allopurinol. Assoc. with myeolosuppression, GI toxicity, hepatic toxicity, and infection.

• Cytotoxic drug (immunosuppressant)
• Inhibits inosine monophosphate dehyrogenase (needed for purine biosynthesis) so prevents B and T cell proliferation. Used to treat transplant rejection along with corticosteroids and cyclosporine. Decreased absorption with antacids (due to magnesium and aluminum hyroxides).

• SIP-R agonist (immunosuppressant)
• Sequesters lymphocytes in lymph nodes and peyer's patches to prevent entry into circulation. Use to treat acute transplant rejection (few weeks) along with cyclosporin and prednisone. Can cause reversible lymphopenia and increase heart rate in 30% of patients.

• Antibody (immunosuppressant)
• Horse/Rabbit anti Human-T cell Ig (removes T cells from circulation). Use to treat Acute renal transplant rejection along with corticosteroids and azathioprine.

• Antibody (immunosuppressant)
• Mouse anti CD3 Ig (prevents antigen recognition by T cells and thus transplant rejection). Used to treat acute transplant rejection. Can cause cytokine release syndrome (fever, chills, nausea, vomitting, headache, and weakness), pulmonary edema, CNS disorders and cardiorespiratory disorders.

• Antibody (immunosuppresant)
• Mouse/human anti- IL-2 receptor Ig (prevents T cell activation by IL-2). Use to treat transplant rejection along with cyclosporin and corticosteroids. No toxcities!

• anti-TNFalpha Antibody
• Use for RA and Crohn's Disease along with Methotrexate. Can cause increased risk of infection including TB activation.

• TNFaplpha receptor recombinant
• Use for RA and Crohn's Disease along with Methotrexate. Can cause increased risk of infection including TB activation.

• Antibody against anti-Rh Ig (anti-D Ig)
• Used to prevent hemolytic disease of the newborn (Rh- mother with Rh+ fetus).

• Treats bladder cancer
• strain of mycobacterium bovis which stimulates T-cells and Nk cells. Can cause severe hypersensitivity and shock.
• (Drug class: Bio Response Modifier)

• Treat AIDS and Cancer
• Natural cytokine which increases B and T cell proliferation and differentiation. Also increases NK cell actions
• (Drug class: Bio response modifier)

• Treat cancer and congential diseases
• Natural cytokine which stimulates clonal expansion and differentiation of hematopoetic cells (inc. WBC). Can cause hypersensitivity
• (Drug class: bio response modifier)

• Treat cancer and congential diseases
• Natural cytokine which stimulates clonal expansion and differentiation of hematopoetic cells (inc. WBC). Can cause hypersensitivity
• (Drug class: bio response modifier)

• Treat anemia from AIDS, cancer chemotherapy, and kidney disease
• ATHLETES USE THIS ILLEGALLY TO BOOST RBC AND INCREASE AEROBIC CAPACITY AND INDURANCE. Can cause seizures, coagulation, and encephalopathies
• (Drug class: Bio responce modifier)

• Treat multiple myeoloma patients. Both newly diagnosed cancer and refractory cancer. Pro-apoptotic anti-proliferative properties (inhibit NK-kb and Bcl2). Inhibit tumor growth. Can cause constipation, peripheral neuropathy, and sedation
• (Drug class: bio response modifier)

• Treat multiple myeoloma patients. Both newly diagnosed cancer and refractory cancer. Pro-apoptotic anti-proliferative properties (inhibit NK-kb and Bcl2). Inhibit tumor growth. Can cause constipation, peripheral neuropathy, and sedation
• (Drug class: bio response modifier)