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Meharry Pharmacology
Drugs for Heme, Lymph and M/S
| Question | Answer |
|---|---|
| ABCIXIMAB | Blockade of PLATELET GP IIb/IIIa RECEPTORS-->prevents platelet aggregation IIb/IIIa receptor for fibrinogen; deficient in Kazar Glanzmann’s; Abciximab used in cardiac cath lab for Percutaneous Coronary(PCTAs); prevent blood clotting |
| ANTITHROMBIN III | Endogenous anticoagulant; inactivates serine proteases (IIa, IXa, Xa, XIa, and XIIa) Defects-->increased risk of venous thrombosis; potentiated by heparin |
| CLOPIDOGREL/PLAVIX | Inhibits ADP platelet pathway-->reduces platelet aggregation Used to prevent thrombosis Fever adverse effects than Ticlopidine; Tx for stroke |
| ASPIRIN (ASA) | prevent infarcts; < 300mg/day --> reduces platelet aggregation 300mg – 2400mg/day --> antipyretic & analgesic 2400mg-4000mg/day --> AI LOW: decreases uric acid secretion (causes hyperuricemia) HIGH: DECREASES uric acid reabsorption (causes uricosuria). |
| HEPARIN | Binds antithrombin III-->inhibits serine proteases (clotting factors) Thrombocytopenia; Ax: protamine sulfate; PTT shows its use (intrinsic); water sol; pregnant no placenta cross |
| LEPIRUDIN | Binds directly to the active site of thrombin-->inhibits thrombin’s downstream effects Use in patients with thrombosis related to HIT No antidote |
| LMW HEPARIN | MOA: binds ATIII then affects factor Xa directly (they DON’T AFFECT THROMBIN) Monitoring: cannot use aPTT to monitor reliably Antidote: Protamine partially reverses the effects of LMW heparins |
| RETEPLACE | Fibrolytic Recombinant human t-Pa Use for acute MI or acute ischemic stroke |
| t-PA | Fibrolytic Endogenous activator of plasminogen Used in severe deep vein thrombosis, acute MI, acute ischemic stroke expensive |
| WARFARIN | Blocks gamma-carboxylation of glutamate residues on prothrombin Factor II, VII, IX, X are vitamin K dependent-->incomplete coagulation Contraindication: Pregnant Women Antidote-vitamin K, fresh-frozen plasma, prothrombin complex, recombinant factor VIIa |
| PTT (Partial Thromboplasmin Time) | Screens for the function of the proteins in the intrinsic pathway Factors II, V, VIII, IX, X, XI, XII Heparin Prolonged PTT can be due to deficiency or dysfunction of the factors, prothrombin, or fibrinogen |
| PT (Prothrombin Time) | Assesses function of the proteins in the extrinsic pathway Warfarin Prolonged PT can result from deficiency or dysfunction of Factor V, VII, X, prothrombin, or fibrinogen |
| Hemophilia A | A (Factor 8 Deficiency) Essential cofactor for factor 9 X-linked recessive (males and homozygous females) Case: Hemarthroses, easy bruising, massive hemorrhage after trauma or operative procedures Lab: PROLONGED PTT, NORMAL PT, Prolonged Bleeding Time Tx: |
| Hemophilia B | B (Factor 9 Deficiency) Much more rare than Hemophilia A X-linked recessive (males and homozygous females) Essential cofactor for factor 8 in the coagulation cascade No petechia Case: Hemarthroses, easy bruising, massive hemorrhage after trauma or operati |
| Phototherapy | Treatment in Psoriasis (the big one) UVB Slows the rapid proliferation of epidermal cells leading to the Psoriasis PUVA (Photochemotherapy) Psoralen plus UVA |
| 1 - ACNE Tx | OTC ( gel, lotion, cream, soap, pad) Occlusion-keratolytics (salicylic acid, urea, lactic acid), retin A, isotretinoin, azelaic acid Sebum/Increased secretion-antibiotics and azelaic acid-stop/slow growth of bacteria and reduce inflammation |
| 2 - ACNE Tx | Glandular hyperplasia-antibiotics + isotretinoin (Acutane)-not given to pregnant women, oral contraceptive pill Benzyl peroxide-kills P. acnes, reduce oil production |
| 3 - ACNE Tx | Resorcinol, salicylic acid, and sulfur-help breakdown blackheads and whiteheads Salicylic acid-reduces shedding of cells Tretinoin, retinoid-blocks new comedones Creams and lotions-provide moisture |
| 4 - ACNE Tx | Oral antibiotics-cephalosporins and penicillins-reduce growth of bacteria and inflammation Oral and topical combined (benzyl peroxide with clindamycin/erythromycin Others: tetracycline (not given to pregnant women), minocycline, doxycycline |
| 1 - ECZEMA Tx | Oral antihistamines Topical corticosteroids-betamethasone Antibiotics-flucloxacillin, erythromycon Topical tacrolimus/pimecrolimus-↓ T cell activity, ↓ calcineurin activity, block interleukin production |
| 2 - ECZEMA Tx | Systemic corticosteroids-azathioprine-inhibits purine synthesis-->prevents T cell proliferation Topical zinc pyrithione and selenium sulfide-antifungal Salicylic acid Ketoconazole |
| 3 - ECZEMA Tx | Emollients for skin for moisture—it reduces transepidermal water loss aka spongiosis. “Sponge soaks up water” making skin dry. Spongiosis is increased intracellular fluid in epidermis. It pulls keratinocytes away from each other |
| McCARDLE'S | Glycogen storage disease type V (GSD-V) muscle phosphorylase (myophosphorylase) deficiency |
| MYASTHENIA GRAVIS | Defective receptor at the NMJ Tensilon (edrophonium) short acting anti-cholinesterase inhibitor |
| OSTEOPOROSIS | Estrogen-Progestin inhibit osteoclast activity |
| Bisphosphonates 1 (OSTEOPOROSIS Tx) | Alendronate and Risdronate-anything anything in -ate) These nitrogen-containing compounds inhibit osteclast activity-->↓bone turnover and bone resorption--> ↑ bone mass, improved mineralization, ↓fractures |
| Bisphosphonates 2 (OSTEOPOROSIS Tx) | Act on the cholesterol biosynthesis pathway enzyme farnesyl diphosphate synthase which is in the osteoclast-->interferes with geranylgeranylation (attachment of the lipid to regulatory protein)-->osteoclast inactivation |
| Bisphosphonates 3 (OSTEOPOROSIS Tx) | also used to treat hypercalcemia and Paget’s |
| Bisphosphonates 4 (OSTEOPOROSIS Tx) | negative-erosive esophagitis/stomach ulcers, abdominal pain, nausea, indigestion, constipation, diarrhea, muscle or joint pain, and headache |
| Bisphosphonates 5 (OSTEOPOROSIS Tx) | Must be taken when you first get up, before you have eaten, and with a full glass of water. Do not lie down or eat for at least 1/2 hour after taking the drug. |
| Bisphosphonates 6 (OSTEOPOROSIS Tx) | Raloxifene-estrogen receptor modulator positive-reduces LDL cholesterol and total cholesterol level negative-hot flashes, leg cramps, flu-like symptoms, nausea, headache, DVT, and pulmonary embolism |
| Raloxifene (OSTEPOROSIS Tx) | Estrogen receptor modulator positive-reduces LDL cholesterol and total cholesterol level negative-hot flashes, leg cramps, flu-like symptoms, nausea, headache, DVT, and pulmonary embolism |
| PARATHYROID HORMONE | Increases the absorption of Ca and P from bone. Releases P not Ca in ditsal convoluted tuble; increases kidney production of Vit D; decreases serum Ca |
| PSORIASIS Tx - 1 | Topical steroids (flucinonide)-inhibits inflammation Vitamin D analogs (calcipotriene) and Retinoids (tazarotene)-inhibits proliferation Keratolytics (salicylic acid, urea, lactic acid)-remove hyperkeratosis |
| PSORIASIS Tx - 2 | Cyclosporine-inhibits inflammatory cell infliltration-blocks T-cell activation, decreases calcineurin activity-->inhibits production of IL-2, IL-3, and IFN-ɣ --> inhibits growth |
| PSORIASIS Tx - 3 | Photochemotherapy (moderate to severe psoriasis) 2 chemicals UVA-prep with sensitizer (psoralen) of side effects of UV light-inhibits proliferation UVB-doesn’t need sensitizer, used with other drugs (methetrexate/acitretin); increases the drug efficacy |
| PSORIASIS Tx - 4 | Systemic medication (for moderate to severe psoriasis) Biologics Cyclosporin Methotrexate Azathioprine Cortiocsteroids Oral retinoids Hydroxyurea Sulfasalazine 6-thioguanine |
| ACITRETIN | Tx for Psoriasis |
| ALEFACEPT | Immunosupressant; Tx for Psoriasis; CD2 Binding region |
| ALENDRONATE | A bisphosphonate used to treat osteoporosis, Paget’s, and hypercalcemia |
| CALCITONIN - 1 | Treatment for Osteoporosis, Hypercalcemia, Paget’s Released by the thyroid gland (naturally occuring) ↑ bone deposition of Ca++ and ↓ serum Ca++ ↓osteoclast activity-->slows bone loss in the spine |
| CALCITONIN - 2 | Salmon calcitonin: longer 1/2 life and > potency than human calcitonin Used to treat Paget’s Produces Type I hypersensitivity Most likely causes serum sickness (Type II hypersensitivity) negative-facial flushing, nausea, diarrhea, anorexia |
| DIAZEPAM | MOA Acts at GABA-A receptors linked to Cl- channels--> ↑frequency of chloride channels-->Hyperpolarization and ↑GABA activity |
| GLUCOCORTICOID | Low does prednisone is usually effective in reducing pain and morning stiffness associated with RA negative-can induce osteoporosis |
| HYDROXYZINE | used to relieve the itching caused by allergies and to control the nausea and vomiting caused by various conditions, including motion sickness. It is also used for anxiety and to treat the symptoms of alcohol withdrawal. |
| INFLIXIMAB | ↓T cell proliferation, ↓ neutrophil accumulation |
| ISOTRETINOIN | used to treat severe recalcitrant nodular acne (a certain type of severe acne) that has not been helped by other treatments, such as antibiotics. Isotretinoin is in a class of medications called retinoids - Vit A reg epithelial cell growth |
| METHOTREXATE - 1 | DMARD ( disease modifying antirheumatic drug) ***drug of first choice in treatment for RA Competitive inhibition of dihydrofolate reductase-->inhibits of dna synthesis—>inhibits growth of culprit autoimmune cells |
| METHOTREXATE - 2 | Concentration increased in the presence of hydroxychloroquine Typically anticancer drug negative-nausea, mucosal ulcers, hematotoxicity, hepatotoxicity, and teratogenicity |
| PYRIDOSTIGMINE | used to decrease muscle weakness resulting from myasthenia gravis. |
| RALOXIFENE | Treatment for osteoporosis SERM (selective estrogen receptor modulator)-->prevents bone loss negative-hot flashes, venous thromboembolism |
| TACROLIMUS | used along with other medications to prevent rejection (attack of a transplanted organ by the immune system of a person receiving the organ) in people who have received kidney, liver, or heart transplants; immunosupressant |
| TETRACYCLINE | Contraindicated in pregnant women and children used to treat bacterial infections, including pneumonia and other respiratory tract infections; acne; infections of skin, genital and urinary systems; and the infection that causes stomach ulcers |
| VITAMIN-D | Treatment for osteomalacia and hypoparathyroidism negative-headache |
| TNF-alpha | It is a cytokine that plays a central role in inflammation; It induces gene expression and protein synthesis in a variety of cells to mediate and promote inflammation |
| IL-11/Oprelvekin | Stimulates primitive megakaryocytic precursors & increases the number of platelets. Used in patients with thrombocytopenia after chemotherapy. SFx: fatigue, headache, dizziness, fluid retention, anemia, dyspnea and transient atrial arrhythmias. |
| G-CSF/Filgrastim | Accelerate recovery of neutrophils after chemo to treat neutropenia. Also used to mobilize HEMATOPOIETIC STEM CELLS (increase their concentration in blood). Side effects: Bone pain Pegfilgrastim: has a longer half-life than recombinant G-CSF. |
| GM-CSF/Sagramostim | Used to accelerate the recovery of neutrophils after chemotherapy & to treat other forms of neutropenia. Side effects: Fever, arthralgias, & capillary damage with edema |
| Hydroxyurea (but not in reference to sickle cell) | Inhibits ribonucleotide reductase, depleting dNTP and arrests cells in the S phase of the cell cycle. For sickle cell, it acts through poorly defined pathways to increase the production of fetal Hgb γ (HbF) which interferes with the polymerization of HbS |
| Erythropoietin | glycoprotein hormone that controls erythropoiesis, or red blood cell production. It is a cytokine for erythrocyte (red blood cell) precursors in the bone marrow. Made in liver and kidney. |
| Transfusion of RBC | MOA: replace blood plasma volume and cells in blood loss. SFx: acute hemolytic reaction, infusion of bacterially contaminated blood product, Graft-versus-host disease, transfusion-associated lung injury, severe allergic reaction or anaphylaxis |
| IgG | Ends in -mab; usually for cancers, tumors Rituxumab - follicular B-cell NHL (with fludarabine) Monoclonal IgG1 that binds CD20 on normal and malignant B-cells MOA - compelement mediated, induce apoptosis, Ab cellular cytotoxicity SFx: acute renal failure |
| Whole Blood | combined with an anticoagulant during the collection process, but is generally otherwise unprocessed transfusion |
| Factor Viii | treats hemophilia A (classic hemophilia) plasma derived so doesn’t cause hypersensitivity reactions (in contrast to some other drugs she told us to remember like G-csf, etc.) |
| Factor IX | Hemophilia B (christmas disease) plasma derived as well |
| Cx - Neutrpenia/Thrombocytopenia 1 Gold Compounds | Gold compounds is an analgesic/anti-inflammatory agent that can cause neutropenia MOA: via Hepten-induced antibodies |
| Cx - Neutrpenia/Thrombocytopenia 2 Valproic Acid | Valproic acid MOA: induces neutropenia via dose-dependent inhibition of maturation of granulocyte precursors |
| Cx - Neutrpenia/Thrombocytopenia 3 Doxorubicin | Doxorubicin MOA: induces neutropenia via direct toxicity for myeloid precursors |
| Cx - Neutrpenia/Thrombocytopenia 3 Clozapine | Clozapine MOA: induced neutropenia via apoptosis |
| Fluorouracil | nonmelanoma skin cancer & actinic keratosis fluorine at pos 5 of the uracil ring-->makes(5-Fdump intead of dumP)-->can’t methylate ring to convert dUMP to dTMP with Thymidylate Synthetase->DNA ->RNA b/c can’t transcribe; cells can’t identify the analog |
| 5-FU SFx | negative-anorexia, nausea, stomatitis, diarrhea, alopecia, acute cerebellar syndrome, cardiac toxicity |
| Cisplatin | Melanoma Tx; Mukherjee-causes alkali (adds a group) of 7 nitrogen of Guanine-->DNA becomes unstable and damaged Alter structure and function of DNA by cross-linking and/or fragmenting of DNA strands (Lippincott) negative-nephrotoxicity, bone problems |
| Cyclophosphamidine | Mechanism-becomes a phosphomide mustered nitrogen. The enzyme becomes affected. |
| Mechlorethamine | Mechanism (same as Cisplatin)-causes alkali of 7 Nitrogen of Guanine-->DNA becomes unstable and damaged |
| Melphalan | Select in Nitrogen mustard MoA-alkinates (put a group there) the purine molecule of the DNA-->DNA ruptureàburnàlots of cytokines and neutrophils come to the area-->more hydrogen peroxide is released-->oxidizes the double bone of purines and pyrimidine |
| Procarbazine | Mechanism-increase or decrease MAO (liver enzyme) |
| Doxorubicin | Antitumor Antibiotic-interact directly with DNA in the nucleus of cells-->interfere with cell survivial Others Bleomycin - SFx: Pulmonary toxicity Daunorubicin - SFx: Cardiotoxicity Doxorubicin - SFx: Cardiotoxicity |
| Doxorubicin MOA | Inhibits DNA and RNA synthesis Affects the S phase of the cell cycle b/c there you have DNA synthesis |
| Colchicine | Gout Tx negative-myelosuppression, neuromyopathy, diarrhea, nausea, abdominal pain, increased serum creatine kinase (liver function) Caution in patients with renal and hepatic insufficiency Alternatives-NSAID (except aspirin) |
| Colchicine MOA | Selective inhibitor of microtubule assembly-->reduces leukocyte migration and phagocytosis-->reduces production of LTB4 and free radical formation |
| Allopurinol | Chronic gout Tx |
| Allopurinol MOA | Inhibits uric acid production by inhibiting xanthine oxidase-->reduces urate sytnthesis |
| Indomethacin - 1 | Nonselective Cox inhibitor, may also inhibit Phospholipase A and C, reduce neutrophil migration and decrease T and B cell count popular for gout and ankylosing spondylitis |
| Indomethacin - 2 | common side effects tinnitus, headaches, dizziness, like any other non selective cox inhibitor severe side effects: pancreatitis, psychosis, thrombocytopenia, aplastic anemia |
| Methotrexate - 1 | Antimetabolite-similar to the building blocks of DNA or RNA. Changed from natural chemical so that when they block the cells ability to form RNA or DNA-->prevents cell growth. Used during the S phase of the cell cycle. Also treats rheumatoid arthritis. |
| Methotrexate - 2 | Competitive inhibition of dihydrofolate reductase->inhibits DNA synthesis—>inhibits growth of autoimmune cells SFx:bone marrow suppression, nausea, mucosal ulcers, hematotoxicity, hepatotoxicity, Impaired renal function Contraindication: Pregnancy |
| Infliximab | MOA (similar to etanercept) Targets TNF-alpha (monoclonal antibody to TNF-alpha) Approved for treatment of Crohn’s dz, RA, ankylosing spondylitis, psoritic arthritis negative-uticaria, chills, pruritus, rash, headache, cough, pharyngitis, heart failure |
| Sulfasalazine | Treatment of RA (DMARD)-antiinflammatory and antimicrobial effects MOA negative-myelosuppression, hepatoxicity, rash |
| Penicillin G & Cephalothin | Beta-lactams against Gram-+ve; inhibits cell wall synthesis |
| Ampicillin & Amoxycillin | Synthetic penicillin against G+ and G-; inhibits cell wall synthesis |
| Streptomycin & Gentomycin | Aminoglycosides against G+ and G-; inhibits protein synthesis via 30S RSU |
| Erythromycin | Macrolide against G+, G-, Neisseria, Legionella, Mycoplasma; inhibits protein synthesis via 50 RSU |
| Rifampicin | Rifamycin against G+, G- and TB; inhibits RNA polymerase via DdRp |
| Tetracyclines | G+, G- and Rickettsia; inhibits protein synthesis via 30S RSU |
| Doxycycline | Synthetic Tetracycline against G=, G-, Riickettsia and Borrelia; inhibits protein synthesis |
| Chloramphenicol | Against G+ and G-; inhibits protein synthesis via 50S RSU |
| SCA & Leukemimia Tx | Hydroxyurea Targets myeloproliferative leukemias, such as CML Treats Sickle Cell MOA Inhibits ribonucleotide reductase, and has a predilection for the S-phase of the cell cycle, where 39% of anti-neoplasic drugs work |
| Bleomycin SFx | pulmonary toxicity/fibrosis (NB: Kaplan videos also notes that Amiodarone, an anti-arrythmic drug used in patients with Afib, also causes this.) |
| Doxorubicin and Daunorubicin SFx | irreversible cardiotoxicity (due to oxygen free radicals); also causes bone marrow suprresion, alopecia (hair loss), GI distress, and stomatitis. |
| Sulfonamide/Trimethoprim MOA | inhibit synthesis of DNA; trade name - Bactrim; Example of Drug Synergy, overcome resistance. Sulfonamide inhibits dihydropterate synthetase, while trimethoprim inhibits dihydrofolate reductase; no synthesis of tetrahydrofolate (THF). |
| B-Lactams/Vancomycin | inhibit cell wall synthesis |
| Floroquinolones/Rifampin | inhibit DNA synthesis Fluoroquinolones--e.g. Etoposide, inhibit DNA gyrase/Topoisomerase II Rifampin--inhibits RNA polymerase (a portion of the drug cocktail used to treat tuberculosis infections). |
| Alkylating Drugs and Antimetabolites | Cytarabine, hydroxyurea, 6-mercaptopurine, methotrexate, 6-thioguanine - antimetaboltes; SFx: BONE MARROW SUPPRESS; xanthine oxidase metabolizes 6-mercaptopurine; XO inhibited by allopurinol in the Tx of gout, increase 6-mercaptopurine -> hepatotoxic. |
| The neurophysiologic correlates of chronic psychological stress, major depression, and chronic inflammatory “sickness behavior” | High levels of circulating cytokines in the periphery are associated with an increase in depression and mood disorder. |
| How inflammatory mechanisms might physiologically alter healthy CNS processes that relate to mood symptoms | monoamine neurotransmitter metabolism; derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan, and the thyroid hormones by the action of aromatic amino acid decarboxylase enzymes |
| How neuroendocrine processes are potentially altered by chronic inflammation and how those alterations could effect mood. | Plasticity- Excessive/prolonged activtn of cytokines (2* to chronic stressors): diminished neurotropic support; low neurogenesis; increased oxidative stress; increased glutamate; astrocyte/oligodendrite apoptosis; dysregulation of glial/neuronal interxns. |
| Most importantly, in lecture, I described a clinical case and the implications of this inflammatory processes on mood and how it should be addressed (with an example from the medical literature). | Eg: study about PTs who had psoriasis; influence on MDD; PTs who were given anti-inflammatory meds along with the anti-depressant meds had a better overall improvement in mood. Not doing so can affect disease course, treatment, and additional health risk. |
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