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142 Cards in this Set
- Front
- Back
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Lipoxygenase
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-metabolizes arachidonic acid to straight-chain products, ultimately producing leukotrines
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Cyclooxygenase (COX)
COX I & II |
-cyclization of arachidonic acid, resulting in the production of prostacyclin, prostaglandins, or thromboxane
COX-1 – found in many tissues, the prostiglandins it produces important for a variety of normal physiological processes COX-2 – primarily in inflammatory cells, its products play an important role in tissue injury |
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Thromboxane
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-preferentially synthesized in platelets
-strongly activated platelet aggregation |
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Prostacyclin
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-synthesized in the endothelial cells of vessels
-endogenous vasodilator (vascular and bronchial smooth muscle) -inhibits platelet aggregation |
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SRS-A
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slow-reacting substance of anaphylaxis. Found in LTC4 and LTD4
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LTB4
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-chemotactic factor important in inflammation
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PGE1
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-significant protective effects on the gastric mucosa
-relax vascular smooth muscle |
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PGE2
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-endogenous vasodilator
-relax vascular smooth muscle -released in large amounts during menstruation and play a physiologic role in labor |
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PGF2-alpha
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-released in large amounts during menstruation and play a physiologic role in labor
-can cause dysmenorrheal associated with uterine contractions -reduces intraocular pressure |
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Dinoprostone
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-PGE2
-used to ripen the cervix at term before inducing labor with oxytocin -also used for abortion <28wks |
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Misoprostol
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-PGE1
-used with the progesterone analog, mifepristone, as an extremely effective and safe abortifacient combination. Also used in combination with methotrexate. Also used for prevention of peptic ulcers in patients who must take high doses of NSAIDs for arthritis and who have a history of ulcers associated with this use |
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Epoprostenol
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-PGI2
-use in severe pulmonary hypertension and to prevent platelet aggregation in dialysis machines |
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Alprostadil
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-PGE1
-used in treatment of impotence. Injection and insertion into the urethra |
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Latanoprost
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-PGF2-alpa
-treatment of glaucoma |
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Bimatoprost, Travoprost, Noprostone
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-newer drugs, similar to latanoprost. Increase outflow of aqueous humor, thereby reducing intraocular pressure
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Zileuton
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-selective inhibitor of 5-lipoxygenase thereby reducing the formation of leukotrines
-Prevents exercise- and antigen-induced. Also against “aspirin-allergy.” -Toxicity: elevation of liver enzymes |
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Zafirlukast, Montelukast, Pranlukast
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-inhibitors at the LTD4 receptor, used to treat asthma
-The LTE4 receptor is also blocked -Orally active and prevent exercise-, antigen-, and aspirin-induced bronchospastic attacks -NOT recommended for acute episodes -Toxicity: Rarely Chug-Strauss syndrome, allergic granulomatous angitis |
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Corticosteroids (mechanism related to eicosanoids)
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inhibit the production of arachidonic acid by phospholipases in the membrane. Also inhibit the synthesis of COX-2
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NSAIDs (mechanism related to eicosanoids)
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inhibit cyclooxygenase and the production of thromboxane, prostaglandin, and prostacyclin branches of the synthetic path. Most non-selectively inhibit both COX-1 and COX-2
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Celecoxib, Rofecoxib
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-selectively inhibit COX-2
-Celecoxib has a little COX-1 -no platelet effects (may still need aspirin) -INHIBIT sodium and water excretion (increase HTN and risk of heart disease) |
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Albuterol, Terbutaline, Metaproterenol
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-most important beta-2 selective agonists
-half life ~6hr |
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Salmeterol, Formoterol
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-long-acting B2-selective agonists
-half life ~12hr |
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Beta2-Selective Agonist Mechanism
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-act by stimulating adenylyl cyclase and increasing cyclic adenosine monophosphate (cAMP) in smooth muscle cells. The increase in cAMP results in a powerful bronchodilator response
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Beta2-Selective Agonist Toxicity
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- skeletal muscle tremor. At high clinical does, they can have some beta-1 effects. Some tachycardia is common. Arrhythmias may occur. Tolerance may also develop.
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Theophylline
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-important in treatment of asthma. Available in both prompt-release and sustained-release formulations
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Pentoxifylline
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remedy for intermittent claudication – decreased blood viscosity
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Methylxanthine Mechanism
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-inhibit phosphodiesterase (PDE), the enzyme that degrades cAMP to AMP, and thus increase cAMP. Requires high concentrations of the drug
-inhibit adenosine receptors (which normally promote bronchoconstriction) |
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Methylxanthine Effects
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bronchodilation, increased strength of contraction of the diaphragm. CNS stimulation, cardiac stimulation, vasodilation, slight increase in BP, and increased GI motility
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Methylxanthine Toxicity
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-Think caffeine OD
-GI distress, hypotension, cardiac arrhythmias, convulstions (OD). Beta-blockers can be used to counteract overdose effects. |
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Atropine
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-Muscarinic Antagonist NOT used any more for treatment of asthma
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Ipatropium
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quaternary antimuscarinic agent designed for aerosol use. Useful in 1/3 to 2/3 of all asthma patients. B2-agonists preferred, but in patients with COPD, ipatropium may work better
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Tiotropium
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-newer, longer-acting analog of ipatropium
-anti-muscarinic |
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Ipatropium (muscarinic antagonist) mechanism
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ipatropium (aerosol) competitively blocks muscarinic receptors in the airways and effectively prevents bronchocontriction mediated by vagal discharge. Systemically (not approved) acts like all other muscarinic antagonists
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Ipatropium (muscarinic antagonist) effects
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Ipatropium reverses bronchoconstriction in some asthma patients (children) and in many patients with COPD. NO anti-inflammatory effects
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Ipatropium Toxicity
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-very small systemic effects.
-If given in excess, minor atropine-like toxic effect may occur. -Does NOT cause tremor or arrhythmias. |
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Cromolyn (disodium cromoglycate), Nedocromil
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-extremely insoluble, therefore massive doses still result in low systemic blood levels.
-Given by aerosol for asthma |
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Cromolyn, Nedocromil Mechanism
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-involves a decrease in the release of mediators (such as leukotrines and histamine) from mast cells.
-NO bronchodilation, but can prevent bronchoconstriction. -Capable of preventing both early and late responses to challenge. |
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Cromolyn, Nedocromil Effects
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-only have local effects.
-Cromolyn has some oral efficacy in preventing food allergy. |
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Cromolyn, Nedocromil Toxicity
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-cough and irritation in the airway
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Beclomethasone, Budesonide, Dexamethasone, Flunisolide, Fluticasone, Mometasone
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-inhaled corticosteroids, first-line therapy for asthma
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Prednisolone, Hydrocortisone
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-IV for status asthmaticus
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Corticosteroid Mechanism
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-reduce the synthesis of arachidonic acid by phospholipase A2 and inhibit the expression of COX-2, the inducible form of cyclooxygenase
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Corticosteroid Effects
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-bind to intracellular receptors and activate glucocorticoid response elements (GREs) in the nucleus, resulting in synthesis of substances that prevent the full expression of inflammation and allergy.
-Inactivation of phospholipase A2 is particularly important to prevent bronchoconstricting leukotrines |
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Corticosteroid Toxicity
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-aerosol – very small adrenal suppression (rare). Changes in oropharyngeal flora resulting in candidiasis (flush).
-If oral therapy required, adrenal suppression can be reduced by alternate day therapy |
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Omalizumab
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-humanized purine monoclonal antibody to human IgE.
-It binds to the IgE on sensitized mast cells and prevents activation by asthma triggers and subsequent release of inflammatory mediators. -Use: prophylactic management of asthma. -Parenteral administration |
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Microcytic hypochromic anemia
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-caused by iron deficiency, most common type
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Megaloblastic anemias
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-caused by deficiency of vitamin B12 or folic acid, cofactors required for the normal maturation of RBCs
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Pernicious anemia
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-most common type of vitamin B12 deficiency anemia, is caused by a defect in the synthesis of intrinsic factor, a protein required for efficient absorption of dietary vitamin B12, or by surgical removal of that part of the stomach that secretes intrinsic factor
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Transferrin
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-transport protein that binds iron
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Ferritin
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-storage protein that binds iron
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Hemochromatosis
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-excess iron stores (increased GI absorption)
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Iron Absorption
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-absorbed as the ferrous ion (Fe2+) and oxidized in the mucosal cell to the ferric (Fe3+) form
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Iron Storage
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-Fe3+ is stored in the mucosa (bound to ferratin) or carried elsewhere in the body (bound to transferrin).
-An accumulation of storage iron occurs in hemolytic anemias and in hemochromatosis |
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Iron Elimination
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-Minimal amounts of iron are lost from the body with sweat and saliva and in exfoliated skin and intestinal mucosa cells
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Iron Clinical Use
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-ONLY use is for iron deficiency anemia
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Signs/Symptoms of Iron Toxicity
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-necrotizing gastroenteritis, shock, metabolic acidosis, coma, and death.
-Chronic toxicity occurs most often in individuals who receive frequent transfusions and in those with hemochromatosis |
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Deferoxamine
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-used for treatment of acute iron intoxication
-chelates circulating iron |
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Cobalamin (definition and deficiency)
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-Vitamin B12
-a cobalt containing molecule that is a cofactor in the transfer of 1-carbon units in DNA synthesis -deficiency affects all cells, but b/c RBCs must be constantly made, so it is manifested first by anemia. -deficiency can also cause neurological defects that can become irreversible |
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Cobalamin Pharmacokinetics
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-produced only by bacteria
-absorbed in GI tract in the presence of intrinsic factor, a product of the parietal cells of the stomach. -Stored in the liver in large amounts (enough to last 5 years). -Plasma transport is accomplished by binding to transcobalamin II. |
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Cyanocobalamin, Hydroxocobalamin
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-Vitamin B12 products available
-hydroxocobalamin has a longer circulating half life |
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Vitamin B12 Essential Reactions
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-conversion of methylmalonyl-coenzyme A (CoA) to succinyl-CoA
-conversion of homocysteine to methionine |
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B12 deficiency and folic acid
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-In B12 deficiency, folates accumulate , the tetrahydrofolate supply is depleted, and the production of RBCs is slowed.
-Administration of folic acid to patients with B12 deficiency helps refills the tetrahydrofolate pool and partially or fully correct the anemia. -However, this does not correct the neurologic defects of B12 deficiency. |
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Clinical Use of B12 Products
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-treatment of naturally occurring pernicious anemia or anemia caused by gastric resecretion.
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Folic Acid Deficiency
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-required for normal DNA synthesis
-deficiency presents as megaloblastic anemia. -Deficiency during pregnancy increases the risk of neural tube defects in the fetus. |
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Folic Acid Pharmacokinetics
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-readily absorbed in the GI tract.
-Only modest amounts are stored in the body, so a decrease in dietary intake is followed by anemia within a few months. |
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Folic Acid Pharmacodynamics
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-converted to tetrahydrofolate by the action of dihydrofolate reductase.
-This is essential in DNA formation (dTMP cycle). -Thus, antifolate drugs are used in treatment of various infections and cancers |
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Folic Acid Clinical Use
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-deficiency most often caused by dietary insufficiency or malabsorption.
-Anemia resulting is readily treated by oral folic acid supplements |
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Erythropoietin
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-produced by the kidney
-reduction in its synthesis is responsible for the anemia of renal failure. -Stimulates the production of red cells and increases their release from the bone marrow by activating specific receptors in the bone marrow. -routinely used for the anemias associated with renal failure and is sometimes effective for patients with other forms of anemia |
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Darbopoietin alpha
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-glycosylated form of Erythropoietin with a much longer half life
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Filgrastim
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-granulocye colony-stimulating factor (G-CSF)
-stimulates the production and function of neutrophils -mobilizes hematopoietic stem cells |
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Sargramostim
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-granulocyte-macrophage colony-stimulating factor (GM-CSF)
-stimulates the production and function of neutrophils. -also stimulates the production of other myeloid and megakaryocyte progenitors. -Toxicity: fever, arthalgian, capillary damage with edema |
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Pegfilgrastim
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-covalent conjugation product of filgrastim and a form of Polyethylene glycol (PEG)
-much longer serum half-life than Filgrastim (G-CSF) |
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Oprelvekin
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-(interleukin-11)
-stimulates the growth of primitive megakaryocytic progenitors and increases the number of peripheral platelets. -Used for the treatment of patients who have had a prior episode of thrombocytopenia after a cycle of cancer chemotherapy. In such patients, it reduces the need for platelet transfusions. -ADR – fatigue, headache, dizziness, and fluid retention |
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Ibuprofen
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-NSAID
-moderate effectiveness - ~2hr half-life |
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Indomethacin
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-NSAID
-greater anti-inflammatory effectiveness -can cause severe hematologic reactions -most toxic NSAID |
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Ketorolac
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-greater analgesic effectiveness than anti-inflammatory
-ONLY NSAID used parenterally -restricted to 72hr because of risk of GI and renal damage |
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Naproxen
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-moderate effectiveness
- ~12-24hr half-life -LOWEST risk of cardiovascular disease!! |
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Piroxicam
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-NSAID
-12-24 hr half-life -inhibits everything - leukocyte migration too -HIGHEST GI TOXICITY at high dose!! |
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Aspirin, NSAID Mechanism
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-COX converts arachidonic acid into endoperoxide precursors of prostaglandins.
-COX-1 is in noninflammatory cells, and COX-2 is in activated lymphocytes, polymorphonuclear cells, and other inflammatory cells. -Aspirin and other nonselective NSAIDs inhibit both forms of COX and therefore decrease thromboxane and prostaglandin synthesis throughout the body. -Aspirin acetylates and thereby irreversibly inhibits COX, while other NSAIDs are reversible. -Thus aspirin has a longer duration of its antiplatelet action. -Aspirin completely inhibits COX-1 and partially inhibits COX-2 |
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Aspirin, NSAID Effects
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-COX inhibitors reduce the manifestations of inflammation but do not affect the underlying tissue damage.
-Prostaglandin synthesis in the CNS that is stimulated by pyrogens is suppressed by NSAIDs, reducing fever. -Analgesia – diminished activation of peripheral pain sensors as a result of reduced prostaglandins. -Reduce prostaglandin-mediated cytoprotection in the GI tract and autoregulation of renal function. |
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Aspirin Toxicity
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-gastric upset, chronic use can result in gastric ulceration, upper GI bleeding, renal effects.
-Increases bleeding time. -Those with aspirin hypersensitivity may experience asthma. -At higher doses, tinnitus, vertigo, hyperventilation, and respiratory alkalosis are observed. -At very high doses, metabolic acidosis, dehydration, hyperthermia, collapse, coma, and death. -Children with viral infections increased risk for Reye’s Syndrome. |
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Nonselective NSAID Toxicity
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-GI disturbance, renal damage risk
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Phenylbutazone
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-NSAID
-should not be used chronically because it causes aplastic anemia and agranulocytosis |
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Celecoxib, Rofecoxib, Valdecoxib
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-COX-2 Selective Inhibitors
-reduced risk of GI effects including gastric ulcers and serious GI bleeding. -Do NOT have antiplatelet effects and so are not cardioprotective. -Not recommended in renal compromised patients because COX-2 is active in the kidney -Celecoxib is a sulfonamide |
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Methotrexate
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-DMARD
-cytotoxic drug -reduces the number of immune cells available to maintain the inflammatory response |
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Sulfasalazine
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-sulfapyridine moiety more important for antirheumatic action than the 5-aminosalicylic acid component
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Hydroxychloroquine
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-interferes with the activity of T lymphocytes
-decreases leukocyte chemotaxis -stabilizes lysosomal membranes -interferes with DNA and RNA synthesis -traps free radicals |
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Penicillamine
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-anti-inflammatory effects similar to hydroxychloroquine
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Gold sodium thiomalate and aurothiglucose (parenteral),
Auranofin (oral) |
-Organic gold substances
-alter the activity of macrophages and suppress phagocytic activity by polymorphonuclear leukocytes |
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Leflunomide
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-prodrug that is rapidly metabolized to a compound that inhibits dihydroorotate dehydrogenase, an enzyme required by activated lymphocytes for synthesis of the pyrimidines that are needed for RNA synthesis
-causes cell arrest in lymphocytes |
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Infliximab, Adalimumab
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-monoclonal antibodies that bind to and prevent the action of tumor necrosis factor-alpha (TNF-a), a cytokine that appears to play a key role in chronic inflammation
-given via injection |
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Etanercept
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-recombinant fusion protein comprising 2 TNF receptors linked to immunoglobulin
-acts as a "decoy" decreasing the cellular actions of TNF-a -given via injection |
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Acetaminophen
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-only OTC non-anti-inflammatory analgesic
-analgesic and antipyretic agent lacking anti-inflammatory and antiplatelet effects |
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Phenacetin
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-toxic prodrug that is metabolized to acetaminophen
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Acetaminophen Mechanism
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-weak COX-1 and Cox-2 inhibitor in peripheral tissues
-may also inhibit COX-3 in the CNS |
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Acetaminophen Pharmacokinetics
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-same indications as intermediate dose aspirin
-useful as an aspirin substitute in children with viral infections or patients with any aspirin intolerance -well absorbed orally and metabolized in the liver |
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Acetaminophen Toxicity
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-if taken in overdosages or by patients with severe liver impairment, can ne hepatoxic
-toxicity requires oxidation to cytotoxic intermediates by phase I CP450s -This occurs if substrates for phase II conjugation reactions (acetate and glucuronide) are lacking |
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Acetylcysteine
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-can be life saving after OD of acetaminophen
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Gout
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-associated with increased serum concentrations of uric acid
-acute attacks involve joint inflammation initiated by precipitation of uric acid crystals |
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3 Treatment Strategies for Gout
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1. reducing inflammation during attacks with colchicine, NSAIDs, or glucocorticoids
2. accelerating renal excretion of uric acid with uricosuric drugs (probenecin, sulfinpyrazone) 3. reducing (with allopurinol) the conversion of purines to uric acid by xanthine oxidase |
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Potent NSAIDs Used for Gout
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-Indomethacin (preferred [or a glucocorticoid] for acute treatment)
-inhibits inflammation of acute gouty arthritis -reduces prostaglandin formation and inhibits crystal phagocytosis by macrophages -may cause renal damage or bone marrow depression |
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Colchicine
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-selective inhibitor of microtubule assembly
-reduces leukocyte migration and phagocytosis -may also reduce production of leukotrine B4 and decrease free radical formation -causes GI disturbance, particularly diarrhea -can damage the liver and kidney |
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Glucocorticoids Used for Gout
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-short courses can cause behavioral changes and impaired glucose control
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Probenecid, Sulfinpyrazone
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-Uricosuric Agents
-weak acids that compete with uric acid for reabsorption in the proximal tubules of the kidney -may also compete with uric acid for secretion, however, and sometimes can actually raise uric acid serum levels -act primarily in the kidney and inhibit the secretion of a large number of other weak acids (methotrexate, penicillin) in addition to the reabsorption of uric acid -NO use in acute gout -can precipitate an attack of acute gouty arthritis (can be prevented by simultaneous administration of colchicine or indomethacin) |
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Allopurinol
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-converted to oxypurinol (alloxanthine) by xanthine oxidase
-irreversible, suicide inhibitor of xanthine oxidase (so is oxypurinol) -increases the concentration of the more soluble hypoxanthine and xanthine, and decreases the concentration of the less soluble uric acid. -given orally for the treatment of chronic gout (1-2 weeks after an attack) -also used as an adjunct to cancer chemotherapy to slow the formation of uric acid from purines released by the death of a large number of neoplastic cells. |
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Xanthine Oxidase
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-enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid
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Allopurinol Toxicity / ADR
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-can precipitate acute gout attacks
-causes GI upset, rash, and rarely peripheral neuritis, vasculitis, or bone marrow dysfunction, including aplastic anemia -INHIBITS the metabolism of mercaptopurine and azathioprine |
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Deferasirox
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-oral treatment of chronic iron toxicity
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Romiplostim
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-increases platelet # and activity
-decreases bleeding -binds to thrombopoetin and maxes out the number of platelets |
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Regranex
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-Platelet derived growth factor (doesn't increase growth of platelets)
-used in skin ulcers in diabetes -associated with increased cancer risk |
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Eltrombopag
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-oral
-binds to thrombopoetin and makes more platelets and increases maturation -treats thrombocytopenia -BLACK BOX warning - increased clots in hepatitis patients -hemotoxic -thrombocytopenia returns when drug discontinued |
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PGs, TXs, LTs, PGIs
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Prostaglandins, Thromboxanes, Leukotrines, Prostacyclins
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Omega 6 vs. Omega 3
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-Omega 6 forms PG1 (good) and PG2 (bad)
-Omega 3 forms only PG1 |
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Kosta says this will be a question
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"use of eicosanoids by immune cells determines which macrophages to spew out. transform from monocytes to macrophages"
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COX-2 Inducers
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-growth factors
-tumor promoters -cytokines -endotoxins (LPS) |
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Carboprost
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-PGF2a
-2nd trimester abortion -more powerful uterine contractor than oxytocin |
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Dinoprost tromethiamine
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-PGF2a
-abortion of longer than 15wks |
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Doxaprost
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-PGE
-prevents bronchospams -better than isoproterenol but irritates the respiratory mucosa so can't be used as an inhalant |
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Arbaprostil, Enprostil, Enisoprost, Deprostil, Rioprostil, Trimoprostil
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-Prostaglandin analogs
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Fenofibrate, Losartan (with regard to gout)
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-work on uric acid reabsorption (or secretion) similarly to probenecid of sulfapurizone
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Febuxostat
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-inhibits xanthine oxidase
-for patients with gout that can't tolerate allopurinol -potent, so must wait longer to start treatment |
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Poegloticase
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-PEG Uricase injections
-remove uric acid by degrading/metabolizing it -take every 1-2 weeks |
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Levomefolate
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-oral contraceptive with folate (metabolite of folic acid)
-increases folic acid levels |
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Ferumoxytol
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-IV drug for adults with anemia
-iron oxide with a carbohydrate shell |
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Mesalamine
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-5-aminosalicylate
-suppository because destroyed in the GI -for IBD |
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Meloxicam
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-NSAID
-preferential COX-2 over COX1 10x -no platelet effect -more cardiovascular activity, less GI toxicity |
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Dicolfenac
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-NSAID
-very toxic |
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Bromephenac
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-analog of diclofenac pulled from the market
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Etodolac
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-NSAID
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Flurbiprofen
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-NSAID
-very toxic (don't focus on very toxic drugs) |
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Ketoprofen
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-NSAID
-inhibits lipoxygenase too |
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Nabumetone
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-NSAID
-prodrug |
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Oxaprozine
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-NSAID
-50 hour half life -can be used in gout |
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Sulindac
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-NSAID
-"Excellent Drug" -prodrug -no GI toxicity -no kidney toxicity -HIGH liver toxicity -decrease risk of colin cancer (especially in people with polyps) |
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Rank by groups by toxicities:
1. Indomethacin, Tolmetin, Peroxicam 2. Naproxen 3. Aspirin, Salicylates, and Ibuprofen |
1. most
3. less toxic 2. least cardiovascular risk of ANY NSAID |
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Albuterol, Albuterol/Ipatropium, Levalbuterol, Metaproterenol, Bitolterol, Ephedrine, Pirbuterol, Salmeterol, Epinephrine, Formoterol, Sameterol/Fluticasone, Terbutaline/Formoterol, Isoetharine, Isoproterenol, Terbutaline, Isoproterenol
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Beta-2 Agonist Drugs Used for Asthma
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Theophylline ADR
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-Cimetidine, Erythromycin INCREASE plasma theophylline levels
-Phenytoin, Quinolones DECREASE |
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Beclamethasone, Budesonide, Flunisolide, Triamcinolone, Fluticasone, Mometasone, Fluticasone/Salmeterol
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Inhaled Corticosteroids Used to Treat Asthma
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PG's Mediating Heat
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PGE1, PGE2
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PGs Mediating Vasodilation/Redness
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PGE1, PGE2, PGD2, PGA2
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PGs Mediating Edema
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PGE, PGI1, PGI2
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PGs Mediating Pain
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PGI2 (~30 min), PGE1, PGE2 (~2hr)
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